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Q: Android google maps release API key Can somebody explain me how to generate Google Api release key.
Google maps works perfectly on Virtual Device Manager, but on the phone not.
A: You need to generate a new key for the release build. Pls go through the info mentioned in this official page. Moreover, you can add the SHA1 for both your release and debug build, if you want to use a single key for both debugging and release purposes.
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"redpajama_set_name": "RedPajamaStackExchange"
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\section{General solution for emitter system}
\subsection{Steady-state solution of density matrix}
As mentioned in the main text, in the limit of the vanishing coupling between the emitter and detector, the detector can be regarded as a passive object and does not cause backaction on the emitter.
Therefore, we can separately solve and discuss the part of the motion equation describing the evolution of the emitter, that is,
\begin{eqnarray}
\dot{\rho_{\sigma}}=-i [\textit{H}_{A},\rho_{\sigma}] + \gamma_{1} D[\sigma_{ge}]\rho_{\sigma} + \gamma_{2} D[\sigma_{ae}]\rho_{\sigma}, \label{secS1a-1}
\end{eqnarray}
where $\textit{H}_{A}= \Omega \sigma_{eg} + \Omega_r \sigma_{ga} + H.c $ is the Hamiltonian of the emitter, and $\rho_{\sigma}$ represents the reduced density matrix of the emitter.
And under steady-state conditions, we get the analytical solutions of the density matrix elements of the emitter
\begin{eqnarray}
\rho_{gg}=&\frac{\Omega_r^2(2\gamma^2 + \Omega^2 + 2\Omega_r^2)}{M} , \nonumber \\
\rho_{aa}=&\frac{\Omega^4 + \Omega_r^2(2\gamma^2 - \Omega^2 + 2\Omega_r^2)}{M} , \nonumber \\
\rho_{ee}=&\frac{2\Omega^2\Omega_r^2}{M} , \nonumber \\
\rho_{ge}=&\frac{2i\gamma\Omega\Omega_r^2}{M} , \nonumber \\
\rho_{ae}=&\frac{-\Omega^3\Omega_r + 2\Omega\Omega_r^3}{M} , \nonumber \\
\rho_{ga}=&\frac{-i\gamma\Omega^2\Omega_r}{M} ,
\label{secS1a-2}
\end{eqnarray}
where $M=\Omega^4 + 2\Omega_r^2(2\gamma^2 + \Omega^2 + 2\Omega_r^2)$ (we assume $\gamma_1=\gamma_2=\gamma$ for simplicity). It can be seen that when the DC field is removed, the state $|a\rangle$ become a dark state on which all the populations are focused.
\subsection{Analytical expression of fluorescence spectrum}
\begin{figure}
\includegraphics[draft=false, width=0.8\columnwidth]{picture2/3LS_spectrum_NA.pdf}
\caption{(Color online) The analysis results (solid line) of the fluorescence spectrum according to Eqs.~(\ref{secS1b-7}) and (\ref{secS1b-13}) are compared with the numerical results (dotted line) to verify the accuracy of the theory in this section. The parameters applied in (a) and (b) are the same as that in Figs.1(c) and (d).\label{fig-3LS_spectrumNS}}
\end{figure}
The steady-state fluorescence spectrum for the transition $|e\rangle\rightarrow|a\rangle$ in the far-zone is given by
\begin{eqnarray}
S_{ea}(\omega)=Re\int_0^{\infty}d\tau \lim\limits_{t\rightarrow\infty}\langle \sigma_{ea}(t)\sigma_{ae}(t+\tau)\rangle e^{i\omega \tau},
\label{secS1b-1}
\end{eqnarray}
and can be calculated by means of the quantum regression theorem~\cite{Lax1963_Formal, Carmichael1993_An}.
In the equivalent weak excitation regime, i.e., $\Omega_r\ll\gamma^{*}$, the analytical expression of the fluorescence spectrum can be obtained by the perturbation method as
\begin{eqnarray}
S^{ew}_{ea}(\omega) = S^{ew}_{c}(\omega) + S^{ew}_{n}(\omega) + S^{ew}_{b}(\omega).
\label{secS1b-2}
\end{eqnarray}
Here $S^{ew}_{c}(\omega)$ represents the coherent part of the the fluorescence and is given by
\begin{eqnarray}
S^{ew}_{c}(\omega) = \gamma |\rho_{ae}|^2\delta(\omega).
\label{secS1b-3}
\end{eqnarray}
$S^{ew}_{n}(\omega)$ represents the incoherent narrow spectral components of the the fluorescence and is given by
\begin{eqnarray}
S^{ew}_{n}(\omega) = \frac{-i\rho_{ge}\Omega^2 + \rho_{ae}\gamma \Omega_r}{\Omega}\frac{\gamma^{*}}{\omega^2+\gamma^{*2}},
\label{secS1b-4}
\end{eqnarray}
with $S^{ew}_{b}(\omega)$ represents the incoherent broad spectral components and is given by
\begin{eqnarray}
S^{ew}_{b}(\omega) = \rho_{ae}\Omega\Omega_r\frac{1}{\omega^2+\gamma^2}-\frac{2i\rho_{ge}\Omega^3}{\gamma}\frac{\gamma^2-\omega^2}{(\gamma^2+\omega^2)^2}.
\label{secS1b-5}
\end{eqnarray}
It can be obtained that the ratio between the total intensities of the broad and narrow spectral components is
\begin{eqnarray}
\frac{\int_{\infty}^{\infty}d\omega S^{ew}_{b}}{\int_{\infty}^{\infty}d\omega S^{ew}_{n}} = \frac{\Omega^2}{\gamma^2},
\label{secS1b-6}
\end{eqnarray}
which is much less than 1. Therefore, the broad spectral components can be ignored, and the analytical expression of the fluorescence spectrum can be reduced as
\begin{eqnarray}
S^{ew}_{ea}(\omega) = S^{ew}_{c}(\omega) + S^{ew}_{n}(\omega),
\label{secS1b-7}
\end{eqnarray}
which is in good agreement with the exact numerical result according to Fig.~\ref{fig-3LS_spectrumNS}(a). We see that the fluorescence spectrum exhibits a single-peak structure whose linewidth is the equivalent decay rate $\gamma^{*}$, which means that the spectral width of the fluorescence can be much smaller than the intrinsic linewidth of emitter $\gamma$ as shown in Fig.~\ref{fig-3LS_spectrumNS}(a).
In the equivalent stronger excitation regime, i.e., $\Omega_r\gg\gamma^{*}$, the analytical expression of the fluorescence spectrum can be obtained as
\begin{eqnarray}
S^{es}_{ea}(\omega) = S^{es}_{c}(\omega) + S^{es}_{n}(\omega) + S^{es}_{b}(\omega).
\label{secS1b-8}
\end{eqnarray}
Here $S^{es}_{c}(\omega)$ represents the coherent part of the the fluorescence and is given by
\begin{eqnarray}
S^{es}_{c}(\omega) = \gamma |\rho_{ae}|^2\delta(\omega).
\label{secS1b-9}
\end{eqnarray}
$S^{es}_{n}(\omega)$ represents the incoherent narrow spectral components of the fluorescence and is given by
\begin{eqnarray}
S^{es}_{n}(\omega) = -\frac{i}{4}\rho_{ge}\Omega (\frac{2\gamma^{*}}{\omega^2+\gamma^{*2}} + \frac{\gamma^{*}}{(\omega-2\Omega_r)^2+\gamma^{*2}} + \frac{\gamma^{*}}{(\omega+2\Omega_r)^2+\gamma^{*2}}).
\label{secS1b-10}
\end{eqnarray}
$S^{es}_{b}(\omega)$ represents the incoherent broad spectral components and is given by
\begin{eqnarray}
S^{es}_{b}(\omega) = \rho_{ae}\Omega\Omega_r\frac{1}{\omega^2+\gamma^2}.
\label{secS1b-11}
\end{eqnarray}
It can also be obtained that the ratio between the total intensities of the broad and narrow spectral components is
\begin{eqnarray}
\frac{\int_{\infty}^{\infty}d\omega S^{es}_{b}}{\int_{\infty}^{\infty}d\omega S^{es}_{n}} = \frac{\Omega^2-2\Omega_r^2}{2\gamma^2},
\label{secS1b-12}
\end{eqnarray}
which is far smaller than 1. Therefore, the broad spectral components can be ignored, and the analytical expression of the fluorescence spectrum can be reduced as
\begin{eqnarray}
S^{es}_{ea}(\omega) = S^{es}_{c}(\omega) + S^{es}_{n}(\omega),
\label{secS1b-13}
\end{eqnarray}
which is in good agreement with the exact numerical result according to Fig.~\ref{fig-3LS_spectrumNS}(b). We see that the fluorescence spectrum exhibits a Mollow-like triplet~\cite{Mollow1969_Power, Wu1975_Investigation}.
The spectral width of each peak also depends on the equivalent decay rate $\gamma^{*}$, thus is much smaller than the natural linewidth of the excited state in the parameter regime concerned here.
Moreover, since the two ultranarrow sidebands arise at frequencies $\omega_L\pm 2\Omega_r$, one can infer that all the spectral components of fluorescence are concentrated in a bandwidth of $4\Omega_r$, which is much smaller than the natural linewidth of emitter as shown in Fig.~\ref{fig-3LS_spectrumNS}(b).
\subsection{Analytical expression of correlation function}
\begin{figure}
\includegraphics[draft=false, width=0.4\columnwidth]{picture2/3LS_g2t_NA.pdf}
\caption{(Color online) The analysis results (dotted line) of the correlation function according to Eq.~(\ref{sec3c-1}) are compared with the numerical results (solid line) to verify the accuracy of the theory in this section. The parameters used here are the same as that in Fig.1(e).\label{fig-3LS_g2tNS}}
\end{figure}
In the weak excitation regime, the analytical expression of the normalized second-order correlation $g^{(2)}_{ea}(\tau)$ can be obtained according to the quantum regression theorem as
\begin{eqnarray}
g^{(2)}_{ea}(\tau)=1 - \cos(2\Omega_r\tau)e^{-\gamma^{*}\tau} - \frac{\Omega^2-2\Omega_r}{2\gamma\Omega_r}\sin(2\Omega_r\tau) e^{-\gamma^{*}\tau},
\label{sec3c-1}
\end{eqnarray}
which is in good agreement with the exact numerical result according to Fig.~\ref{fig-3LS_g2tNS}. We can see from Eq.~(\ref{sec3c-1}) that the time evolution of the second-order correlation $g^{(2)}_{ea}(\tau)$ depends on the equivalent decay rate $\gamma^{*}$ and Rabi frequency $\Omega_r$ of the DC field, both of which are determined by the external coherent fields and thus can be easily manipulated in experiment.
In contrast, in the same parameter regime, the second-order correlation function of a normal two-level system (i.e., $g_{T}^{(2)}(\tau)=(1 - e^{-\frac{\gamma_{t}}{2}\tau})^2$) depends entirely on the intrinsic natural linewidth $\gamma_{t}$, which is difficult to modify artificially.
\section{Example implementation}
\subsection{Transition $F_{g}=1\rightarrow F_{e}=0$ of $D_{2}$ Line of ${}^{87}$Rb}
\begin{figure}
\includegraphics[draft=false, width=0.5\columnwidth]{picture2/Rb87level.pdf}
\caption{(Color online) (a) Schematic diagram of the level configuration for the transition $F_{g} = 1 \rightarrow F_{e} = 0 $ of the $ D_{2}$ line of ${}^{87}$Rb, where the transitions from the ground and excited states and between the ground-state Zeeman sublevels are, respectively, driven by $\sigma^{+}$-polarized laser field ($\textbf{E}$) and transverse magnetic field ($\textbf{B}_{T}$). The transition paths involved in Eqs.~(\ref{secS2-9}) and (\ref{secS2-10}) are exhibited in (b) and (c), respectively. (d) Schematic diagram of the equivalent three-level system of the emitter in (a) in the weak excitation regime.\label{fig-Rb87_level}}
\end{figure}
In order to demonstrate the experimental feasibility of SPS scheme proposed on the main text, we choose the closed transition $F_{g}=1\rightarrow F_{e}=0$ of the $D_{2}$ line of ${}^{87}$Rb as the emitter, where $F_{g} $ and $F_{e}$ respectively represent the total angular momentums of the ground and excited states. And many platforms, e.g., the single ${}^{87}$Rb atom loaded into an optical dipole trap reported in Refs.~\cite{Volz2006_Observation, Hofmann2012_Heralded, Leent2020_Long-Distance}, can be the potential candidates for the scheme implementation. As shown in Fig.~\ref{fig-Rb87_level}(a), the ground hyperfine state $F_{g} =1$ is composed of three Zeeman sublevels $|1,-1\rangle, |1,0\rangle, |1,1\rangle$, and the excited hyperfine state $F_{e} =0$ is composed of one Zeeman sublevel $|0,0\rangle$.
The transition $|1,-1\rangle\leftrightarrow|0,0\rangle$ is driven by a $\sigma^{+}$-polarized laser field $\textbf{E}$, and we set the quantization axis (z axis) along the direction propagation of the light beam.
We consider a static magnetic field $\textbf{B}_{T}$ perpendicular to the direction of light propagation is applied to drive the transitions between the ground-state Zeeman sublevels, whose direction is set along the x axis.
In spite of the above magneto-optical system, the transitions between the ground-state Zeeman sublevels can also be replaced by an optical scheme, i.e., stimulated Raman processes in large detuning condition (not shown here).
The fluorescence emitted from the excited state to the ground state is collected by a detector, which is modeled by a quantized harmonic oscillator with bosonic annihilation operator $s$ as in Sec.2 of the main text. In the frame rotating at the laser frequency $\omega_L$ and within the rotating wave approximation, the Hamiltonian of the combine system composed of the emitter and the detector can be given by
\begin{eqnarray}
\textit{H}_{Rb}=\textit{H}_{0} + \textit{H}_{I} + \textit{H}_{B} + \textit{H}_{S}. \label{secS2-2}
\end{eqnarray}
$\textit{H}_{0}$ is the nonperturbed Hamiltonian of the emitter
\begin{eqnarray}
\textit{H}_{0}=\Delta_e |F_{e},m_{e}\rangle \langle F_{e},m_{e}|+H.c . \label{secS2-3}
\end{eqnarray}
where $\Delta_e$ is the detuning of the transition $|1,-1\rangle\leftrightarrow|0,0\rangle$ frequency from the laser.
$H_I$ represents the laser-atom interaction Hamiltonian
\begin{eqnarray}
\textit{H}_{I}=\sum_{g_{i}} V_{eg_{i}} |F_{e},m_{e}\rangle \langle F_{g},m_{g_{i}}|+H.c . \label{secS2-4}
\end{eqnarray}
According to the Wigner-Eckart theorem~\cite{Woodgate2000_Elementary, Brink1994_Angular, Meunier1987_A-simple}, the interaction energy for the transition $|F_{g},m_{g_i}\rangle\rightarrow|F_{e},m_{e}\rangle$ can be given by
\begin{eqnarray}
V_{eg_{i}} = -\langle F_{e},m_{e}|\textbf{d}|F_{g},m_{g_{i}}\rangle\cdot\textbf{E} = (-1)^{F_{e}-m_{e}+1}\left(\begin{array}{ccc}F_{e} & 1 & F_{g} \\ -m_{e} & q & m_{g_{i}} \\
\end{array}\right)\Omega_{L} , \label{secS2-5}
\end{eqnarray}
where $\textbf{d}$ is the electric dipole operator, $ \Omega_{L} = \left\langle F_{e}\parallel \textbf{d}\parallel F_{g}\right\rangle E $ is the Rabi frequency of the light field, and $q=0, \pm1$ denotes the spherical components.
$H_{B}$ represents the magnetic-atom interaction Hamiltonian
\begin{eqnarray}
\textit{H}_{B} = -\mu_{B}g_{F}\textbf{F}\cdot \textbf{B}_{T} = \mu_{B}g_{F}B_{T}\sum_{g_{i},g_{j}} \langle F_{g},m_{g_{i}}|\textbf{F}|F_{g},m_{g_{j}}\rangle \cdot\textbf{e}_{x} |F_{g},m_{g_{i}}\rangle \langle F_{g},m_{g_{j}}| , \label{secS2-6}
\end{eqnarray}
where $\mu_B$ and $g_F$ denote the Bohr magneton and the gyromagnetic factor of the ground states, respectively. And
\begin{eqnarray}
\langle F_{g},m_{g_{i}}|\textbf{F}|F_{g},m_{g_{j}}\rangle
=&\left\langle F\parallel \textbf{F}\parallel F\right\rangle (-1)^{F_{g}-m_{g_{i}}} \left(\begin{array}{ccc}F_{g} & 1 & F_{g} \\ -m_{g_{i}} & q & m_{g_{j}} \\
\end{array}\right) . \label{secS2-7}
\end{eqnarray}
$\textit{H}_{S}$ is the Hamiltonian describing the detector and its coupling with the emitter
\begin{eqnarray}
\textit{H}_{S} =& \Delta_{s} s^{\dag}s + (g A_{d}s^{\dag} + H.c ), \label{secS2-8}
\end{eqnarray}
where the operator $A_d$ is defined as $A_d\equiv \left|1,d\right\rangle \left\langle 0,0\right|$ ($d=0,\pm1$), and denotes the atomic transition coupled with the detector.
In the weak excitation regime, i.e., $V_{eg_{-1}},\Omega_{B}\ll\Gamma$, we can deduce that there exist two main fluorescence emission paths where the shelving effect similar to that in the transition path in Eq.(1) of the main text can arise, that is, path 1 as shown in Fig.~\ref{fig-Rb87_level}(b)
\begin{eqnarray}
|1,-1\rangle\leftrightarrow|0,0\rangle \stackrel{decay}{\longrightarrow}|1,0\rangle \leftrightarrow|1,-1\rangle ,
\label{secS2-9}
\end{eqnarray}
which dominates the emission from the spontaneous decay $|0,0\rangle\rightarrow|1,0\rangle$,
and path 2 as shown in Fig.~\ref{fig-Rb87_level}(c)
\begin{eqnarray}
|1,-1\rangle\leftrightarrow|0,0\rangle \stackrel{decay}{\longrightarrow}|1,1\rangle \leftrightarrow|1,0\rangle \leftrightarrow|1,-1\rangle .
\label{secS2-10}
\end{eqnarray}
which dominates the emission from the spontaneous decay $|0,0\rangle\rightarrow|1,1\rangle$.
In path 1 and 2, because the magnetic field driving the transition between the ground states is weak, the emitter can stay in the states $|1,1\rangle$ and $|1,0\rangle$ for a long time, and thus these two states are both the shelving states.
Therefore, it is expected that the shelving effect similar to the scheme in the main text can emerge in the fluorescence emitted from the spontaneous decays $|0,0\rangle\rightarrow|1,0\rangle$ and $|0,0\rangle\rightarrow|1,1\rangle$.
On the other hand, similarly to the case in the main text, equivalent dissipations are introduced into the degrees of freedom of the ground states due to the adiabatic elimination of the excited state, i.e.,
$\mathcal{L}_{eff}\rho_{g'}=\sum_{i=-1}^{1}\Gamma^{*}_{i} D[\sigma_{g_ig_{-1}}]\rho_{g'}$,
where $\Gamma^{*}_{i} = 4\Gamma_{i} |V_{e g_{-1}}|^2/\Gamma^2$ is the equivalent decay rate from the states $|1,-1\rangle$ to $|1,i\rangle$.
Therefore, the emitter in Fig.~\ref{fig-Rb87_level}(a) can be equivalent to a three-level system driven coherently by the magnetic field as shown in Fig.~\ref{fig-Rb87_level}(d).
And, the equivalent decays $|1,-1\rangle\rightarrow|1,0\rangle$ and $|1,-1\rangle\rightarrow|1,0\rangle$ correspond to the decays involved in path 1 and 2, respectively.
\subsection{Fluorescence Properties and Detection Response}
\begin{figure}
\includegraphics[draft=false, width=0.8\columnwidth]{picture2/Rb87_fluorescence.pdf}
\caption{(Color online) The spectral property, second-ordering correlation and detection response for the fluorescent photon emitted from the transitions $|0,0\rangle\rightarrow|1,0\rangle$ and $|0,0\rangle\rightarrow|1,-1\rangle$ are, respectively, exhibited in (a)-(c) and (d)-(f). In (a) and (d), fluorescence spectrum for $\Omega_B=10^{-3}\Gamma$ and $V_{eg_{-1}}=10^{-2}\Gamma$ ($\Gamma =2\pi\times6.0666$MHz). In (b) and (e), normalized second-ordering correlations as a function of delay $\tau$ for $V_{eg_{-1}}=10^{-2}\Gamma$ with different $\Omega_B$. In (c) and (f), normalized two-photon correlations of the detector as a function of detection linewidth $\kappa$ and the interaction energies of coherent fields with $\Omega_B=V_{eg_{-1}}$.\label{fig-Rb87_fluorescence}}
\end{figure}
The fluorescence spectrum of the transitions $|0,0\rangle\rightarrow|1,0\rangle$ and $|0,0\rangle\rightarrow|1,1\rangle$ are shown in Figs.~\ref{fig-Rb87_fluorescence}(a) and (d).
Multi-peak structures arise as the case in the main text, which can also be understood by mean of the equivalent level system in Fig.~\ref{fig-Rb87_level}(d). Taking transition $|0,0\rangle\rightarrow|1,0\rangle$ as an example, we explain the origin of the spectral structure.
As mentioned above, the equivalent decay $|1,-1\rangle\rightarrow|1,0\rangle$ shown in Fig.~\ref{fig-Rb87_level}(d) corresponds to
the two-photon process composed of the transition $|1,-1\rangle\rightarrow|0,0\rangle$ driven by the laser and the subsequent spontaneous decay $|0,0\rangle\rightarrow|1,0\rangle$.
According to the standard dressed-state theory, there are four sidebands located at the frequencies $\pm\sqrt{2}\Omega_{B}$ and $\pm2\sqrt{2}\Omega_{B}$ in the emission of equivalent decay $|1,-1\rangle\rightarrow|1,0\rangle$~\cite{Zhang2019_Absorption}.
And since the laser frequency is constant, the transition $|0,0\rangle\rightarrow|1,0\rangle$ exhibits the same
spectral structure as that in the equivalent decay $|1,-1\rangle\rightarrow|1,0\rangle$.
Therefore, one can infer that all spectral components of fluorescence are concentrated on a narrow bandwidth about $4\sqrt{2}\Omega_B$, which can be much smaller than the natural linewidth of emitter.
From another perspective, we can conclude that thanks to the dominant positions of path 1 and path 2 in the formation of the fluorescence from the transitions $|0,0\rangle\rightarrow|1,0\rangle$ and $|0,0\rangle\rightarrow|1,1\rangle$, respectively, the global spectral narrowing caused by the shelving effect similar to the case in the main text can occur in the scheme considered here.
In addition, the simple relationship between the sidebands with ultranarrow linewidth and the magnetic field provides the theoretical possibility of the precision measurement of magnetic field.
In Figs.~\ref{fig-Rb87_fluorescence}(b) and (e), the statistical properties of fluorescence emitted from the transitions $|0,0\rangle\rightarrow|1,0\rangle$ and $|0,0\rangle\rightarrow|1,1\rangle$ are exhibited, respectively.
Similarly to the scheme in main text, the normalized second-order correlations of these two transitions can both remain a value very close to zero for a long delay which is much larger than the natural lifetime of the excited state.
These features of the correlations confirm that the shelving effects in paths 1 and 2 are, respectively, dominant in the processes emitting the corresponding fluorescence.
Moreover, because path 2 has a longer period than path 1, the corresponding second-order correlation can be maintained near zero for a longer time.
According to the above discussion, we see that the nontrivial spectral and statistical properties of the SPS scheme similar to that in the main text can be well realized in the transitions $|0,0\rangle\rightarrow|1,0\rangle$ and $|0,0\rangle\rightarrow|1,1\rangle$ of transition $ F_{g}=1\rightarrow F_{e}=0$ of the $D_{2}$ line of ${}^{87}$Rb. Accordingly, the corresponding excellent single-photon responses on the detector with a bandwidth approaching and even much smaller than the natural linewidth of emitter are predicted, which is confirmed in Figs.~\ref{fig-Rb87_fluorescence}(c) and (f).
In addition, because the shelving effect in path 2 is more prominent than that in path 1, the single-photon response for the fluorescent photon from the transition $|0,0\rangle\rightarrow|1,1\rangle$ on the detector is more conspicuous.
\subsection{Other realizable candidates of single-photon emitter}
\begin{figure}
\includegraphics[draft=false, width=0.8\columnwidth]{picture2/otherLevel.pdf}
\caption{(Color online) Schematic diagram of the implementation scheme of narrowed single photon source in transitions (a) $F_{g}=2\rightarrow F_{e}=1$ (b) $F_{g}=1\rightarrow F_{e}=1$. The transitions between the ground states and the excited states are driven by a $\sigma^{+}$-polarized laser field, and photons with multiple polarizations are emitted in spontaneous decays. A transverse magnetic field is applied to drive the transitions between the ground-state Zeeman sublevels (the driving between the excited-state Zeeman sublevels is weak compared to the spontaneous emission process, and thus is ignorable). Choosing the fluorescent photon with a polarization different from the laser as the detection target, the SPS scheme proposed in the main text can be realized.\label{fig-otherLevel}}
\end{figure}
Besides the closed transition $F_{g}=1\rightarrow F_{e}=0$ of the $D_{2}$ line of ${}^{87}$Rb, the scheme of ultranarrow SPS proposed in the main text can also be implemented in many transition structures based on various alkali-metal atoms, e.g., in other kind of transition $F_{g} \rightarrow F_{e}=F_{g}, F_{g}\pm1$.
Similar to the scheme in the main text, a circularly polarized laser drive resonantly the transitions between the ground and excited states, while a magnetic field perpendicular to the light propagation direction drives the transitions between the ground-state Zeeman sublevels, as shown in Fig.~\ref{fig-otherLevel}.
In the weak excitation regime of the laser and magnetic fields, due to the shelving effect similar to that mentioned in the main text, the SPS with an ultranarrow bandwidth can be realized in the transitions with polarization different from the laser.
One can see that the difference between the magnetic quantum numbers of the detected and laser photons is 1 or 2. Therefore, to reload the emitter, the transitions between the ground-state Zeeman sublevels are required, which can be realized easily by the transverse magnetic field.
In such schemes of emitter, the single-photon emission is controlled by two external coherent fields, and thus the linewidth and brightness of the SPS can be manipulated conveniently.
\bibliographystyle{apsrev4-2}
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{"url":"https:\/\/www.iacr.org\/cryptodb\/data\/paper.php?pubkey=12309","text":"## CryptoDB\n\n### Paper: Random Switching Logic: A Countermeasure against DPA based on Transition Probability\n\nAuthors: Daisuke Suzuki Minoru Saeki Tetsuya Ichikawa URL: http:\/\/eprint.iacr.org\/2004\/346 Search ePrint Search Google In this paper, we propose a new model for directly evaluating DPA leakage from logic information in CMOS circuits.This model is based on the transition probability for each gate, and is naturally applicable to various actual devices for simulating power analysis. We also report on our study of the effects of the previously known countermeasures on both our model and FPGA, and show the possibility of leaking information, which is caused by strict precondition for implementing a secure circuit. Furthermore, we present an efficient countermeasure, \\textit{Random Switching Logic}(RSL), for relaxing the precondition, and show that RSL makes a cryptographic circuit secure through evaluation on both our model and FPGA.\n##### BibTeX\n@misc{eprint-2004-12309,\ntitle={Random Switching Logic: A Countermeasure against DPA based on Transition Probability},\nbooktitle={IACR Eprint archive},\nkeywords={implementation \/ side-channel attaks, CMOS, leakage model, transition probability},\nurl={http:\/\/eprint.iacr.org\/2004\/346},\nnote={ dice@iss.isl.melco.co.jp 12755 received 3 Dec 2004},\nauthor={Daisuke Suzuki and Minoru Saeki and Tetsuya Ichikawa},\nyear=2004\n}","date":"2021-09-19 01:25:00","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 0, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 1, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.18151530623435974, \"perplexity\": 7956.951732492787}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.3, \"absolute_threshold\": 20, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2021-39\/segments\/1631780056656.6\/warc\/CC-MAIN-20210919005057-20210919035057-00329.warc.gz\"}"}
| null | null |
module Marketplace
require 'active_model'
require 'marketplace/order_validators'
class ListOrder < Order
include ActiveModel::Validations
include Marketplace::OrderValidators
include Marketplace::ListOrderDateAttributes
attr_accessor \
:order_status,
:fullfillment_channel,
:payment_method,
:buyer_email,
:seller_order_id,
:max_results_per_page,
:path,
:action
validates \
:created_after,
presence: true,
if: ->(order) do
order.last_updated_after.blank?
end
validates \
:last_updated_after,
presence: true,
if: ->(order) do
order.created_after.blank?
end
validates_with CreatedAfterValidator
validates_with LastUpdatedAfterValidator
def initialize(options)
options.each { |k,v| self.send("#{k}=", options[k]) }
end
def self.create(options)
new(options).parameters
end
def path
"orders"
end
def action
"ListOrders"
end
end
end
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 303
|
ETH Library is the largest public scientific and technical library in Switzerland.
As the central university library and knowledge hub of ETH Zurich, the ETH Library ensures the provision of scientific and technical information. Furthermore, it also offers resources for the public and for companies in research and development. Particular emphasis is placed on electronic information for university members and on the development of innovative services.
Collection focuses
ETH Library collects media from the following fields:
Architecture
Building sciences
Engineering
Natural sciences and mathematics
System-oriented natural sciences
Management and social sciences
Special libraries
ETH Library's four special libraries are responsible for supplying subject-specific literature to the corresponding departments and institutes at ETH Zurich. Their holdings are also generally available to the interested public. The special libraries include:
Architecture and Civil Engineering Library: architecture, urban and spatial planning; Material Collection:
Earth Sciences Library: geosciences
GESS Library: humanities, social sciences, economics, law and politics
Green Library: agricultural and food science, environmental science
Collections and Archives
ETH Library's Collections and Archives contain valuable original holdings of scientific and cultural-historical relevance. The Collections and Archives include:
Rare Books: works from the 15th to the 20th century
#Image Archive: historical photographs, aerial photographs, press photographs, portraits, postcards and much more.
Earth Science Collections: fossils, minerals, rocks and reliefs
ETH Zurich's Collection of Prints and Drawings: Switzerland's largest collection of printed works
University Archives: Administrative Archives of ETH Zurich and the ETH Board, personal papers of scientists
Maps: historical and modern, topographical and topical maps
Material Collection: building and historical materials
Max Frisch Archive: personal papers Max Frisch, primary and secondary literature
Cultural Assets Collection: art objects, art in architecture, the Sternwarte Collection
Thomas Mann Archive: personal papers Thomas Mann, primary and secondary literature
Image Archive
The Image Archive of ETH Library safeguards, indexes and mediates the library's image holdings. Its nationally and internationally significant image holdings document the development ETH Zurich, research expeditions to far-off lands, settlement development and changes in society, politics and technology in Switzerland.
ETH Library's Image Archive was launched in 2000 as an ETH Library organisational unit. It curates a large number of image holdings that have been taken over by the library in recent decades, such as within the scope of academic legacies. Searches and online access to the Image Archive's digitized holdings via E-Pics Bildarchiv Online. A growing number of sub-holdings are also available on Wikimedia Commons. In the series Image Worlds (photographs from ETH Library's Image Archive), the archive's core holdings are presented thematically in texts and pictures.
Content-related focuses
ETH Library's Image Archive includes image holdings with a direct relation to the history of ETH Zurich and its architectural and staff development. In particular, this includes:
scenes (from around 1860 onwards): historical photographs of buildings, institutes, lecture theaters and laboratories at ETH Zurich
portraits: portraits of former members and students of ETH Zurich and notable scientists
photograph collections from institutes at ETH Zurich: e.g. Geobotanical Institute/Rübel Foundation, Geological Institute, Institute of Aerodynamics, Institute of Building Conservation (Georg Mörsch) or the Photographic Institute
photographs and drawings from the personal papers of former professors at ETH Zurich: e.g. Albert Frey-Wyssling, Immanuel Friedlaender, Albert Heim, Arnold Heim, Robert Maillart, Leopold Ruzicka, Carl Schroeter, Leo Wehrli or Hans Leibundgut
The Image Archive has some extensive image holdings bearing a broader relation to science and technology and topics such as civil aviation, landscape and settlement development, (industrial) architecture or nature photography:
Foundation Luftbild Schweiz Archive (1918–2011): aerial photographs by Walter Mittelholzer from flights over Switzerland and to Persia, South Africa, Chad, Abyssinia, Svalbard or as the first to fly over Kilimanjaro, portrait and landscape shots of Switzerland, taken by the Swissair Photo AG
Swissair Photo Archives (1931–2001): photographs and films on civil aviation, the aviation business and aircraft and destinations of the former Swiss airline Swissair
Comet Photo AG Archive (1952–1999): media images on topics such as architecture, culture, nature, politics, prominence, sport, technology, transport with a relation to Switzerland
Scenes (from around 1860 onwards): landscapes and views of locations (primarily Switzerland)
Other private image holdings: Photo archive of the foundation Documenta Natura, photo archive of the Industriekultur Foundation of Dr Hans-Peter Bärtschi, aerial image archive of Air Color SA (Meyrin), nature photographs by Albert Krebs and orchid photographs by Hans R. Reinhard
The image materials serve as a primary information source and reference material for studies on image production and usage. Last but not least, the copies, negatives, glass slides and individual films also document the technical development of the image as a medium.
Selected key figures for ETH Library's holdings
ETH Library's holdings comprise around 8 million analogue and around 550,000 digital resources. As of September 2021, these include:
Analogue resources
Digital resources
The holdings of all ETH Zurich libraries, as well as more than 490 libraries across Switzerland, are available on ETH Library @ swisscovery. ETH Library @ swisscovery therefore provides access to more than 30 million books, series, journals and non-book materials.
Digital search platform
Research Collection
The Research Collection is ETH Zurich's publication platform. University members can publish their scientific full texts open access as well as archive their research data and make them accessible to the public. Furthermore, the Research Collection records all publications produced at ETH Zurich and serves as a source for publication lists in the academic reporting and on ETH Zurich's websites.
Other nationally relevant platforms operated by ETH Library (a selection)
e-rara.ch: digitized prints from Swiss libraries from the 15th to the 19th century
e-manuscripta.ch: digitized handwritten sources from Swiss libraries and archives
E-Pics: digitized photographs, image documents and 3D scans from collections, archives, institutes and units of ETH Zurich and external partners
E-Periodica: digitized Swiss journals in the fields of science and culture from the 18th century to the present day
Thomas Mann: manuscripts and press articles on Thomas Mann
Selected services
Circulation courier
Library customers have the option of having documents from the institutions participating in Swiss Library Service Platform delivered to the library of their choice.
DOI Desk
ETH Zurich's DOI Desk is located at ETH Library and acts as a central DOI registration centre for universities and research institutions in Switzerland. This service is also provided in collaboration with DataCite.
Research Data Management and Digital Curation
The specialist Research Data Management and Digital Curation office advises researchers at ETH Zurich on aspects of handling research data and digital data in general. The ETH Data Archive provides the technical infrastructure for the electronic long-term archiving and publication of this data.
E-Publishing office
As a central contact point for open access within ETH Zurich, ETH Library helps members of ETH Zurich to publish their dissertations, articles, reports and much more in a freely accessible way online.
DigiCenter
"The Digitization Centre at the ETH Library is service provider and competence centre in the fields of digitization and the handling of metadata. In cooperation with various institutions of ETH Zurich and Swiss libraries, it carries out large-scale and high-quality digitization projects".
Ongoing projects
ETH Library conducts a number of future-oriented projects, which ensure that the service and product portfolio is geared towards the needs of the target groups".
References
External links
ETH Library at ETHorama
ETH Search Portal
Website Image Archive
ETH Zurich's Collections and Archives
E-Pics Bildarchiv Online
Academic libraries in Switzerland
ETH Zurich
Swiss digital libraries
|
{
"redpajama_set_name": "RedPajamaWikipedia"
}
| 6,414
|
Too good to be true?
When Eulalia first met Fenno, she found him thoroughly irritating! So she was alarmed when her attraction to him escalated to uncomfortable levels. And it certainly didn't help that he was engaged to another woman.
Eulalia had more important things to take care of—like finding a home for herself and her young cousin. But her mysterious inheritance of a country cottage made her suspicious. Was fate—or Fenno—giving her a helping hand?
"Do not provoke me. I have a nasty temper, and don't be impertinent,"
he said.
Mr. van Linssen came a little farther into the shop and Eulalia saw how tired he was. She said, "I'm sorry. It's my tongue—it runs away with me. I do try to think before I speak, but I don't always remember." She smiled at him. "You're tired and that makes you cross. You should have a holiday, away from the hospital and London."
"And my patients?" He was amused and all of a sudden brisk. "Now, these flowers—something rather special this time, I think."
Lucky Ursula, reflected Eulalia. She only hoped the wretched girl realized it. It seemed unlikely, but perhaps she really did love him in her way, and she thought he must love her.
Romance readers around the world were sad to note the passing of Betty Neels in June 2001. Her career spanned thirty years, and she continued to write into her ninetieth year. To her millions of fans, Betty epitomized the romance writer, and yet she began writing almost by accident. She had retired from nursing, but her inquiring mind still sought stimulation. Her new career was born when she heard a lady in her local library bemoaning the lack of good romance novels. Betty's first book, Sister Peters in Amsterdam, was published in 1969, and she eventually completed 134 books. Her novels offer a reassuring warmth that was very much a part of her own personality, and her spirit and genuine talent live on in all her stories.
Fate Takes a Hand
Contents
CHAPTER ONE
CHAPTER TWO
CHAPTER THREE
CHAPTER FOUR
CHAPTER FIVE
CHAPTER SIX
CHAPTER SEVEN
CHAPTER EIGHT
CHAPTER NINE
CHAPTER ONE
THE LITTLE FLOWER shop, squeezed between two elegant boutiques, was empty save for a girl in a cupboard-like space at its back, making up a bouquet. It was a charming bouquet, of rose-buds, forget-me-nots and lilies of the valley, suitable for the littlest bridesmaid for whom it was destined, the last of six which she had been left to fashion while the owner of the shop had gone off on some mission of her own. She was tying a pale pink ribbon around it when the shop door was thrust open and a customer came in. A giant of a man, elegantly dressed, no longer young, and wearing a look of impatient annoyance upon his handsome features.
He came to a stop in the middle of the floral arrangements and said curtly, 'I want a couple of dozen roses sent to this address.'
'Red roses?'
'Certainly not. Yellow—pink, it really doesn't matter.'
He stared at her, and really she was worth being stared at: a big girl with generous curves, short dark curly hair, large grey eyes and a pretty face.
He said abruptly, 'What is your name?'
'Eulalia Warburton,' she replied promptly. 'What is yours?'
He smiled thinly. 'The roses are to be sent to this address.' He handed her a card. 'How much?'
'Fifteen pounds and two pounds for delivery.' She glanced at the card. 'This afternoon—this evening? Tomorrow?'
'This evening, before six o'clock. Make sure that they are fresh...'
She gave him an outraged stare. 'All the flowers in this shop are fresh.'
She took the money and thumped the cash register with some force. Thoroughly put out, she said snappily, 'If you doubt it, have your money back and go somewhere else.'
'Dear, dear.' He spoke with infuriating blandness. 'Are you having a bad day?'
'It was a perfectly good day before you came in,' she told him. A good thing Mrs Pearce wasn't here—she would have been given the sack on the spot. She handed him an ornate little card. 'You will wish to write a message?'
She took it back when he had written on it, handed him his change and bade him a coldly civil good day. She got a grunt in reply.
She watched his broad back disappear up the street and took a look at the card. It was to a Miss Ursula Kendall and, after a careful scrutiny of his scrawled message, she gathered that he was sending his apologies. Well, thought Eulalia, if he was as rude to her as he had been here, a nice piece of jewellery would be more in order.
She finished her bouquet and began to arrange the yellow roses in their Cellophane sheath; somehow pink didn't go well with a name like Ursula.
Mrs Pearce came back presently, approved of the bouquets and, since it was almost time to close, told Eulalia to deliver the roses. 'I know it's out of your way, so take a taxi—the money's in the till.' She bustled around, rearranging this and that. 'You'll have to take the bouquets round in the morning. Half-past nine—another taxi, I suppose—but it's a good order.'
It had been a pleasantly warm June day, but now that the afternoon was slipping into early evening there was a cool breeze. Eulalia donned a navy blue jacket over her navy and cream patterned dress, gathered up the roses and left the shop, taking a breath of air as she waited for a taxi. Even there, in London, from time to time one had a faint whiff of really fresh air.
The roses were to be delivered to an address close to Eaton Square. She paid the driver and mounted the steps to the front door of a Georgian terraced house. The girlfriend, if it was a girlfriend, lived in some style, thought Eulalia, and pressed the bell. The door was flung open at the same moment and a young woman stood frowning at her.
'I'm just going out...'
She was a handsome girl. Her features were too strong to be called pretty but she had beautifully dressed fair hair and large blue eyes, which for the moment held no warmth; moreover, she was dressed in the very height of fashion.
'Miss Kendall?' asked Eulalia sweetly. 'I was asked to deliver these to this address before six o'clock.'
Miss Kendall's perfectly made-up mouth thinned. She snatched the flowers and tore open the little envelope attached to them, glanced at the note and pushed the flowers back into Eulalia's arms. 'Throw them with the rubbish,' she demanded angrily. 'If he thinks he can—' She stopped. 'And don't just stand there—take the beastly things and go!'
'I simply cannot throw them in the bin,' said Eulalia firmly. 'They're fresh and beautiful.'
'Then take them home with you—eat them for your supper for all I care.' Miss Kendall turned suddenly and went into the house and banged the door.
They deserved each other, decided Eulalia, walking briskly to the nearest bus-stop. She hadn't liked her ill-tempered customer; she didn't like Miss Kendall either. A well-matched couple. She dismissed them from her mind and boarded a bus to take her home.
Home was a basement flat in Cromwell Road—not the best end by any means, but it was on the edge of respectability and the flats in the rest of the house were occupied by quiet people. It was dark and poky but it had a narrow strip of garden at the back and she had been lucky to get it. It was a worrying thought that the five-year agreement she had would run out before the autumn, but she had been a good tenant and she hoped that the landlord would renew it and not put the rent up. She tried not to think what she would do if he did that...
She went down the steps and opened the narrow door. The room beyond was fair-sized, with a window at the back as well as the barred one beside the door, and it was nicely furnished with chairs and tables and a heavy sideboard which must have come from a larger house. The curtains were chintz, drawn back from the net-curtained windows, and the floor was covered with a rather fine if shabby Turkish carpet. There were two doors along the inner wall, and one of them opened now to reveal a boy of eight or so, who came through followed by an elderly woman with rosy cheeks and a round face crowned by grey hair strained back into a bun.
Eulalia put down the roses and hugged the boy. 'Hello, Peter, have you had a good day at school? Tell me about it presently. Trottie, dear, I'm sorry I'm a bit late. I had to deliver these but they weren't wanted, so I brought them home.' She laid the roses down on a table, one arm round the boy. 'Did that man come about the leak in the bathroom?'
'That he did, Miss Lally, and a fine mess he left behind him too. Said he'd send the bill. Supper's ready when you are.'
'Two ticks,' said Eulalia, and went through the door to a narrow lobby with three doors. She opened one of them and, with Peter still with her, went into her room. It was very small, with one window, barred like all the others, but there was a colourful spread on the narrow bed, and cushions and a pretty bedside lamp. She hung her jacket in the corner cupboard, peered at her face in the old-fashioned looking-glass and said cheerfully, 'Let's have supper. I'm famished, and Trottie will have something delicious...'
Trottie had laid the table under the back window, and Eulalia went through the second door into the narrow kitchen and helped carry through the toad-in-the-hole and jacket potatoes, while Peter filled their glasses with water. It was a simple meal but eaten off old and beautiful china salvaged from her old home, as were the knives and forks and spoons, rat-tailed eighteenth-century heavy silver. Trottie wrapped them up carefully each evening and put them in a felt bag and hid them under her mattress. The discomfort was worth it, she had observed, for if they should be burgled even the worst of villains would hesitate to get an elderly lady out of her bed. Eulalia wasn't sure about that but she forbore to say so.
She found it a cheerful meal, listening to Peter's comments on his day at school, exchanging gentle gossip with Trottie, telling, with a wealth of detail, of the customer who had bought the yellow roses and how they had been rejected.
'They must have cost a pretty penny,' observed Trottie, and when Eulalia told her she said, 'My goodness gracious, we could eat like fighting cocks for a week on that.'
'What's fighting cocks?' said Peter, which led inevitably to the vexed question as to whether it would be unkind to have a rabbit in a hutch in the garden. They had decided against a dog long since, for there was no one to take him for walks. Eulalia was out all day, Trottie had the house to see to and Peter was at school. Even a cat would be risky, with so much traffic along the busy road.
'As soon as I've made my fortune,' said Eulalia, 'we'll move to a very quiet road with trees and big gardens and we'll have a cat and a dog and a rabbit too.'
'I suppose we couldn't go to the country?' asked Peter wistfully.
A wish she silently echoed. Oh, to be back in her old home in the Cotswold village where she had been born, in the nice old house to which her grandmother had whisked her when her parents had died in a car crash. She had been eight years old then and had spent the rest of her childhood there, and later, when her grandmother had grown frail, she had taken over the housekeeping with Miss Trott's aid. It was only on the old lady's death that she had discovered that the house was mortgaged and that there were debts...
She had paid them off and then, with Miss Trott's staunch company, had set off for London with the small amount of money she had salvaged and the promise of a job in the flower shop run by a sister of one of her grandmother's old friends.
She had laid out most of her money on the flat, its rent low because of the recession, signed a lease for five years and, with her wages and Miss Trott's pension, they had carved a life for themselves. It wasn't much of a life but neither of them complained; they had a roof over their heads and enough to eat. It had been towards the end of the third year that she had had a letter from her grandmother's solicitor. A cousin—one she had never known that she had—and her husband had been killed in a plane disaster, leaving a small boy. There were no members of the family save herself, and was she prepared to give the boy a home?
She had gone to see the solicitor and was assured that the facts set out in his letter had been true; the child, unless she was prepared to give him a home, would have to go to an orphanage. There was a little money, she had been told, enough to send him to prep school and, provided he could win a scholarship, pay for his further education. Of course she had agreed to have him, her kind heart wrung by the thought of the lonely little boy, and she had never regretted it. Between them, she and Trottie had helped him with his grief, found a decent school not too far away from the flat, and turned themselves into a family.
They finished their early supper, discussing quite seriously where it would be nice to live, the puppy they would have, a kitten or two and a rabbit—because of course the garden would be large enough to house all three... It was a kind of game they all played from time to time, Peter firmly of the opinion that one day it would all come true, while Eulalia and Trottie hoped for the best. Miracles did happen, after all.
Eulalia helped Peter with his homework presently, while Trottie cleared away the supper things, and when that was done they read a chapter from The Wind in the Willows together before a noisy bath-time in the minute bathroom leading off the kitchen. Peter went to bed, and once he was asleep Eulalia sat down at the table to do her anxious sums and count the money in the house. They managed, the pair of them, to keep their heads above water but there was never any money over. Peter was growing fast, the children's allowance was barely enough to keep him adequately clothed, and as for shoes...
She sat chewing the top of her ballpoint, ways and means for the moment forgotten, while she admired the roses displayed in a vase on the sideboard. Which, naturally enough, led her to think of the man who had bought them. He might, even at that very moment, be with his Ursula, apologising abjectly... No, he wouldn't! she corrected herself. He wouldn't know how to be abject... Then, neither would his Ursula. They would stare coldly at each other, concealing bad tempers in a well-bred manner. 'And good luck to them,' said Eulalia, so loudly that Trottie jumped and dropped a stitch of her knitting.
* * *
EULALIA HAD TO explain about the rejected roses when she got to the shop in the morning. 'It was too late to bring them back, and besides, Miss Kendall tore the wrapping.'
'Can't be helped,' observed Mrs Pearce. 'No point in bringing them back—he paid for them, didn't he?' She added, 'Men do such silly things when they're in love.'
Eulalia agreed, although she didn't think that he had behaved like a man in love. Very tight-lipped. He wouldn't do for me, she reflected, preparing to gather up the wedding bouquets and convey them in a taxi.
Her destination was a palatial mansion in Belgravia, the home of the bride and, judging by the coming and going, the wedding was going to be a day to remember. She was admitted at the side door, bidden to wait, and then led through a bleak passage into a kitchen and out again through a baize door to the entrance hall—a gloomy place with a lot of marble about and a very large chandelier hanging from its lofty ceiling. Here the bouquets were taken from her by a vinegar-faced lady in a black dress and borne away up the wide staircase. 'Wait here,' she was told sourly, and since there were no seats she wandered around, studying the large paintings on the walls. They were as gloomy as the hall, depicting scenes of battle, dying ladies in white robes, and dead ducks lying in a most unlikely fashion beside bowls of fruit and bunches of flowers.
'Absolutely awful,' said Eulalia in her clear voice, and turned round to see if there was anything better on the other wall.
The man who had bought the roses was standing at the foot of the staircase watching her. He looked rather splendid, in a morning coat with a carnation in his buttonhole, and she felt an unexpected pang at the thought of him marrying his Ursula, who most certainly didn't love him. He would be hard to love, of course, with that air of knowing best all the time...
She eyed him, her lovely head on one side. 'You look magnificent,' she told him, 'and I dare say you'll be very happy. She's quite beautiful and I dare say you made it up. Well, you'd have to, wouldn't you, since you're getting married...?'
'Your impertinent remarks are wide of the mark, Miss—er. I am not the bridegroom, nor indeed do I find it any of your business.'
He was as cross as two sticks, but she was glad he wasn't getting married. 'So sorry,' she told him cheerfully. 'I brought the bouquets, you know.'
'I did not know, nor am I the least interested. Why are you waiting here?'
'I was told to. By someone in a black dress. She had a sharp nose.'
His thin mouth quivered just a little. 'Then I will leave you to await her return. Good day to you, Miss—er.'
He crossed the hall and disappeared through a doorway and shut the door after him. At the same time the vinegar-faced lady came back, told her that the bouquets were satisfactory and that she might go. 'Through the side door.'
'I expect you're tired, and overworked and cross,' said Eulalia kindly, and nipped back down the bleak passage and out through the side door, to catch a bus and be borne back to the shop.
She was kept busy all day, for Mrs Pearce had built up quite a reputation for the perfection of her floral arrangements and there was a steady stream of customers, carried away by the sight of the flowers displayed so enticingly in the June sunshine. Besides, Eulalia was a very pretty girl and knew just how to please them, waiting patiently while they pondered their choice.
She didn't go home for lunch; the bus cost money, for one thing, and for another, if the shop stayed open during the lunch-hour there was always a sprinkling of office workers, mostly husbands wanting flowers sent to their wives for an anniversary. Eulalia, a romantic girl, took great pains with them.
She worked on Saturdays, too, which meant that Peter, home from school, had to rely on Trottie's company, but they spent their Sundays together, taking picnics to the parks in the summer and visiting museums in the cold weather. It wasn't ideal but it couldn't be helped. Mrs Pearce closed the shop on Mondays, which meant that Eulalia could stay at home and do the washing and ironing and then go to the local shops and stock up with groceries for the week. It worked well enough; since she and Peter spent their Sundays away from the flat, it gave Trottie a day to herself.
Going home that evening in a crowded bus, she planned what they would do at the weekend. They would take a bus, riding on the top, of course, and feed the ducks in St James's Park. Banana sandwiches as well as Marmite, she decided, apples, and she would make some sausage rolls before she went to bed on Saturday. Orange squash, because he liked it, and some chocolate... He was a contented child and wise beyond his years, for he never asked her for something he knew she couldn't afford.
* * *
IT WAS A splendid morning as they left the flat on Sunday. It would be warm later, but now, in the comparative quiet of a Sunday morning, it was pleasantly cool. The bus was half-empty, so they had an upstairs front seat. At times, reflected Eulalia, parts of London were delightful. There would be no hardship in living in one of the elegant houses which lined the streets through which the bus lumbered. Peter, as though he had read her thoughts, said, 'I'd like to live here. Do you suppose we could move one day?'
'Just as soon as I make my fortune,' she promised him, 'but that may take a little time!'
'You could marry a very rich man, Aunt Lally.'
'Indeed, I could. Perhaps you will find him for me, dear.'
They were nearing the park, and made their way down to the platform, where they exchanged the time of day with the conductor and got off at the next stop.
There weren't many people about, for it wasn't ten o'clock yet. They wandered along, looking at the bright flowerbeds and presently feeding the ducks, before going to sit down in the sun.
There were plenty of people about now. They wandered on and presently sat down again to eat their lunch, and since Peter wanted to walk and there was plenty of time before they need go back again for tea, they had a last look at the lake and crossed the park to the Mall, crossed into Green Park and turned into Piccadilly, where Eulalia suggested that they might get a bus. However, Peter wanted to walk through the elegant streets with their big houses. 'We can go as far as Park Lane,' he pointed out, 'and catch a bus there.' Nothing loath, she agreed. She seldom had the chance to walk for any distance and, although the streets of London, however elegant, weren't a patch on the country roads in the Cotswolds, it was pleasant enough to walk through them.
'I dare say dukes and duchesses live here,' said Peter. 'Do you suppose they're very grand inside?'
'Certainly—lovely curtains and carpets and chandeliers...' She enlarged upon this interesting subject as they walked, until in one of the quiet streets they came upon a magnificent dark grey Bentley and Peter urged her to stop while he took a good look at it. He circled it slowly, admiring it from all angles.
'I shall have one, when I'm a man,' he told her, and laid a small, rather grubby hand on its bonnet.
'Peter, don't touch. The owner would be very angry if he were to see you doing that.'
She let out a great gusty breath when a quiet voice said in her ear, 'A wise caution, Miss—er. You should exercise more control over your son.'
They had been standing with their backs to the terrace of grand houses. Now she shot round to face someone who was beginning to crop up far too frequently. 'It's you,' she said crossly. 'I might have known.'
'Now, why do you say that?'
'No reason at all. I'm sorry if Peter has annoyed you; he had no intention of doing so.' She moved away and took Peter's hand. 'Apologise to this gentleman, dear. I know you meant no harm but we mustn't forget our manners.'
The boy and the man studied each other. 'I'm sorry,' said Peter finally, 'but it's a super car and I wanted to look at it.'
The man nodded. 'Goodbye, Peter; goodbye Miss—er.'
He watched them go, smiling a little. A pity he couldn't remember her surname, and they were hardly on such good terms that he could address her as Eulalia.
'You look cross, Aunt Lally,' said Peter, as they reached a bus-stop and joined the short queue.
'Not with you, love; that man annoyed me.'
'Was he rich?' Peter wanted to know. 'He must be if he lives in one of those houses and drives a Bentley.'
'I dare say he is, but I really don't know. Here's our bus.'
Peter told Trottie all about it when they got home. 'Aunt Lally was a bit cross with him,' he explained.
At Trottie's enquiring look Eulalia said, 'It was the man who bought the roses,' in a voice which didn't invite questions.
* * *
A WEEK WENT by. Eulalia, fashioning bouquets and taking orders for beribboned, Cellophaned flowers to be sent to wives and girlfriends and mothers, longed silently for her old home, with its large untidy gardens and the fields beyond. She hoped that the people who had bought it were taking proper care of it and had left the frogs in the pool at the bottom of the garden in peace. It would have been nice to show them to Peter.
She gave her head a shake. Moaning over what was past and couldn't be helped would do no good. Rather, she must think of ways and means for Peter and Trottie to have a holiday once school was over. Somewhere not too far from London, and cheap. A farm, perhaps...
The fine weather had come to stay, at least for a time, and they planned a trip to the Serpentine on Sunday. Trottie was going to have her dinner with one of her elderly friends and Eulalia saw her off before she and Peter, carrying their picnic lunch, set out.
They had got off the bus and were waiting to cross the road when a bunch of youths on motorbikes raced past. They were in high spirits and the road was almost empty and they were going too fast. The last one of all went out of control, mounted the pavement and knocked Peter down, narrowly missing Eulalia, and tearing away.
Peter lay awkwardly, his head on the kerb, an arm bent awkwardly under him. She knelt down beside him, panic-stricken but fighting to keep sensible.
'Peter—Peter, darling? Can you hear me?' When he didn't answer she felt for his pulse and was relieved to find his heart beating strongly. She took off her cardigan and slid it under his head but she didn't move his arm in case it was broken. Then she stood up as a bus came lumbering along on the other side of the road. She waved and shouted to the driver and he stopped his bus, and the conductor came running across the street.
'He was knocked down,' said Eulalia in a voice which shook just a little. 'I must get him to hospital...'
The conductor was a spruce little man and he looked helpful. 'The bus passes Maude's 'ospital. We'll have him aboard—quicker than waiting for an ambulance or a taxi.'
'Bless you. He's concussed and I think that arm's broken.'
'Leave it to me, miss. You go ahead of me; 'e can lie on yer lap. We'll have 'im right as rain in no time.'
Between them they lifted Peter, and Eulalia lifted the arm gently and laid it across Peter's small chest and then hurried to the bus. There was only a handful of passengers aboard and no one complained at the delay as she got in, received Peter on to her lap and held him close as the bus pulled away. The hospital was indeed only a very short drive and the driver took his bus into the forecourt and down the ramp to Casualty and then got down to help his conductor carry Peter in. Eulalia paused just long enough to apologise to the other passengers for the delay, and ran after them.
They were standing, the two of them, explaining to a nurse as Peter was laid on a trolley. ''ere she is,' said the conductor. 'She'll give yer the details.'
He and the driver shook hands with her, looking bashful at her thanks. 'Can't keep the passengers waiting,' said the driver. ''Ope the nipper'll be OK.'
'Your names?' asked Eulalia. 'Quickly, for I must go to Peter.'
''E's Dave Brown and I'm John 'Iggins, miss. Glad to 'ave 'elped.'
She kissed them on the cheek in turn and hurried after the trolley.
Peter had his eyes open now and she took his hand in hers. 'Peter? It's all right, love. You fell down, you're in hospital and a doctor will come and see if you're hurt.'
'If you'll give the details to the receptionist,' said the nurse, 'we'll get him comfy and get someone to look at him. An accident, was it?'
Eulalia told her briefly and took herself off to the reception desk, and by the time she got back Peter was on an examination couch. His clothes had been taken off, the sleeve of his injured arm cut to allow the small arm to be exposed. He was trying not to cry and she went and held his good hand, wanting to weep herself.
The young doctor who came in said, 'Hello,' in a cheerful voice, then, 'so what's happened to this young man?'
He was gently examining Peter's head as he spoke. He peered into his eyes, then turned his attention to the arm. 'Can you squeeze my finger, old chap?' he wanted to know, and at Peter's whimper of pain, said, 'I think an X-ray first of all, don't you? So we can see the damage.'
He smiled at Eulalia. 'We'll take care of him. If you'll wait here?'
She went and sat down on a bench, oblivious of her torn dress and dishevelled person. There were few people around: two or three at the other end of Casualty, talking quietly, and near them were curtains drawn round one of the cubicles. The curtains parted presently and a big woman with an air of authority came out, followed by a man in a long white coat. She would have known him anywhere because of his great size, and she watched him go and speak to the group near by with a feeling that she was never going to be rid of him. Hopefully, he'd go away without seeing her...
But he had. He shook hands with the two women, and with the man with them, and trod without haste towards her.
He looked different, somehow, and he was different. He was someone in authority, ready to help and capable of doing just that. She stood up to meet him, her skirt in tatters around the hem, dust from the street masking its colour. 'It's Peter, he was knocked down by a motorbike—we were on the pavement. He hit his head and I think his arm is broken. He's been taken to X-Ray. I was told to wait here.'
She was pale with worry and her voice shook and so did her hands, so she put them behind her back in case he should see that and think her a silly woman lacking self-control.
'Where did it happen?'
She told him. 'And those two men on the bus, they were so quick and kind. I don't know what I would have done without them.'
'I suspect that you would have managed. Sit down again. I'll go to X-Ray and see how things are.'
She put a hand on his sleeve. 'Do you work here? I mean, you're a doctor in Casualty?'
'Not in Casualty, but I work here upon occasion. I am a surgeon.' He added, 'Orthopaedics.'
'Bones,' said Eulalia. 'You'll help Peter?'
'It seems that since I'm here I might as well.'
She watched him walk away. He had spoilt everything with that last remark. She had been beginning to like him a little but she had been mistaken; he was a bad-tempered man and rude with it. All the same, she hoped he would do something for Peter. Quite unexpectedly, two tears escaped and ran down her pale cheeks. She brushed them aside impatiently, and just in time as he came back.
'Mild concussion, and he has a fractured arm just above the wrist. We will give him a local anaesthetic, align the bones and put on a plaster. We'll keep him overnight for observation...' And at her questioning look he added, 'No, no, nothing to worry about. Routine only. You can fetch him in the morning, but telephone first. Keep him in bed for a couple of days and no school for a week.'
'He's all right?'
He said impatiently, 'Have I not said so? Come and see him before we put the plaster on.'
He turned on his heel and walked away, and she followed him through a door and into a small room where Peter lay on a table. He grinned when he saw her. 'He said I was brave,' he told her. 'I'm going to stay here tonight. You will fetch me, won't you?'
'Of course, dear.' She glanced around. There was no sign of any doctor, only a male nurse and a student nurse busy with bowls of water and plaster bandages.
'Like to stay?' asked the nurse, and gave her a friendly look.
'May I?'
'No problem.' He turned away and lifted Peter's good arm out of the blanket. 'Here's Mr van Linssen. He'll have you as good as new in no time at all.'
So that was his name. She watched as he slid a needle into Peter's broken arm. He did it unhurriedly and very gently, talking all the time to the boy. 'You're a lot braver than many of the grown-ups,' he told him. 'In a minute or two we're going to straighten your arm—you won't have any pain, but you'll feel us pulling a little. Keep still, won't you?'
Peter nodded. His lip quivered a little but he wasn't going to cry. It was Eulalia who felt like crying. She was sure that Peter couldn't feel any pain but she closed her eyes as Mr van Linssen began to pull steadily while the nurse held the arm firmly.
'You can look now,' he said in a hatefully bland voice, so she did. He was holding the arm while the nurse began to slide on a stockinette sleeve and then start to apply the plaster. It didn't take long and Peter hadn't made a sound.
Mr van Linssen was smoothing the plaster tidily when Sister put her head round the curtains. 'Why, Mr van Linssen, I thought you had left ages ago. You'll be late for that luncheon party.' Her eyes fell on Peter. 'Had a tumble?'
'Knocked down by a motorbike. I'd like him in for the night, Sister. Get a bed, will you? And we'll make him comfortable. He's been a model patient.'
She went away and the nurse started to clear up. Mr van Linssen took off his white coat and the student nurse took it from him gingerly. Rather as though he might bite, thought Eulalia. She got up. 'Thank you very much for your help—' she began.
She was cut short. 'No need, all in the day's work, Miss—er?'
He raised his eyebrows, standing there looking at her.
'Warburton,' she snapped.
He nodded. 'Your son's a nice little chap,' he said, and walked away.
She turned to the nurse. 'I'm Peter's cousin,' she told him. 'I did tell the receptionist—he's an orphan.'
'Makes no odds,' said the nurse, and smiled at her; she was very pretty and she had cheered up his day a bit. 'You were in luck. Mr van Linssen wasn't even on duty—came in to see the relations of a patient who died—had a hip op here and got knocked down late last night. He may be a consultant and a bit high and mighty but I know who I'd like to deal with my bones if I broke them.'
Sister came back then and Peter was borne off to the children's ward, sleepy now but rather proud of his plastered arm. Eulalia saw him into his bed and was told by the ward sister that there was no need to come back with pyjamas and toothbrush. 'He's only here for the night,' she said in a comfortable voice. 'Mind you phone first and we'll have him ready for you.'
Eulalia thanked her, kissed Peter and went out of the Casualty entrance. At the top of the ramp there was a dark grey Bentley and Mr van Linssen was sitting in it. He opened the door as she reached the car.
'Get in. I'll drive you home.'
'No, thank you. There's a bus—'
'Get in, Miss Warburton, and don't pretend that you aren't upset. All mothers are when their small children get hurt. Where do you live?'
She got in without another word after she had told him, and they drove in silence until he stopped before the flat. As she got out she said, 'Thank you, you're very kind. And I'm not Peter's mother, only his cousin.'
CHAPTER TWO
MR VAN LINSSEN had expressed no surprise, only grunted, nodded and driven away, leaving her wondering why on earth she had told him. Luckily she wouldn't have to see him again; she would feel such a fool...
She went indoors and was relieved to see that Trottie wasn't back yet. It would give her time to change her torn dress and tidy herself up and compose herself before telling her old friend what had happened. She made a pot of tea and sat down to drink it, reflecting what a good thing it was that she didn't go to work on Mondays; Mrs Pearce was a kind employer but she expected value for her money. She wasn't over-generous with her wages but she was fair. She was also a businesswoman who would have no compunction in giving Eulalia the sack if business fell off, and if Eulalia were to take too many days off she might look around for someone else. Once Peter was home Trottie would look after him, she thought worriedly. Dear Trottie, always willing and good-tempered, and hating the flat as much as she did.
She got up and began to get tea. The sandwiches were still in her bag—they had better have those...
Trottie came in presently, took one look at Eulalia's face and asked, 'What's happened? Where's Peter? You look like a ghost.'
When she had been told she said, 'Poor little fellow. But don't you worry, Miss Lally, he'll be as right as rain in no time. What luck that you're at home tomorrow, and he'll be no trouble—remember how good he was when he had the measles?' She gave Eulalia a sharp glance. 'Did you have any lunch?' She shook her head. 'I thought not. We'll have a nice tea and you can tell me about that doctor. Fancy meeting him like that, and him a medical man. Like it was meant...'
Before she went to bed that night Eulalia phoned the hospital to be told that Peter was asleep after eating a light supper with gusto. Everything was fine, and would she ring after tomorrow's round at noon? He would have been seen by then and an X-ray taken to make sure that the bones were in the right position.
She couldn't imagine Mr van Linssen making any mistakes about bones—after all, it was his work. A tiresome man, not worth sparing a thought for. All the same, it was difficult not to think about him, since he was all part and parcel of their disastrous day.
She fetched Peter home the next afternoon, and since he was to go straight to bed for another two days she took him in a taxi, a rare treat which delighted him. He was full of his stay in hospital; he had enjoyed it, he told her, the nurses had been fun, and the doctor who had seen him in Casualty had come to see him before he went to sleep, and in the morning the big man who had told him that he was brave had come to see him too. 'He wasn't alone,' explained Peter. 'There was Sister with him and two nurses and another doctor and someone who wrote in a book when he said something. I liked him, Aunt Lally, he's not a bit cross really. He carried a silly little girl all round the ward with him because she was crying.'
'I'm very grateful to him, Peter, and so thankful that you weren't really badly hurt. Did he explain that you have to stay quietly in bed for a few days? Dr Burns will come and see you then, and tell us when you can go back to school.' She put an arm round his small shoulders. 'Here we are, home again, and there's Trottie waiting for us.'
He didn't complain at going to bed but sat up happily enough with a jigsaw puzzle. He hadn't a headache but, all the same, Eulalia wouldn't let him read but read to him instead, and presently he settled down and slept, leaving her free to catch up on the household chores.
She began on a pile of ironing while Trottie rested her elderly feet. 'It's no good,' said Eulalia, 'you'll have to have a holiday. Somewhere that will suit you both. The seaside would be nice, or somewhere in the country—a farm, perhaps...'
'Give over, Miss Lally, where's the money to come from?' said Trottie.
'I'll go to the bank and get an overdraft...'
'And what about you?'
'Me? Oh, I'm fine, Trottie, and anyway, I can never have a holiday at this time of year. We're too busy in the shop. I'll wait until the tourist season is over.'
'You said that last year and you didn't go anywhere.'
'Well, things cropped up, didn't they?'
'You mean gas bills and new trousers for Peter and me having to have new spectacles.'
'Yes, well, we'll see. Now, what shall we eat tomorrow? I'll nip out and shop, if you like. Mrs Pearce won't mind if it's only for ten minutes.'
'How about a nice macaroni cheese? That's light enough for Peter—fish would be the thing, but I don't trust fish on Mondays. Mashed swede with a bit of butter, and I'll cream the potatoes. A little egg custard for afters.'
It was a good thing, reflected Eulalia later that evening, that Peter seemed to be quite well again. She had phoned the doctor and he had promised to look in some time tomorrow.
She went back to work in the morning, leaving Trottie to ask questions of their doctor when he came and get his advice. 'I know it's nothing much,' she said, 'but he had an awful bang on his head.'
Mrs Pearce was sympathetic but she didn't offer to let Eulalia go home early. She said with casual kindness, 'Boys will be boys, won't they?' Just as though it had been Peter's fault, and added, 'Luckily you have Miss Trott to look after him. I'll want you to stay a bit later today—Lady Bearsted is sending her secretary for the flowers for her dinner party some time after six o'clock.'
Because she was worried about Peter the day went slowly. Mrs Pearce went home at five o'clock, leaving Eulalia to lock up once the flowers had been fetched. Six o'clock took twice as long as usual to come, and even then there was no sign of the secretary. She came finally, half an hour later, apologetic and harassed. 'These dinner parties,' she confided to Eulalia, 'they're ghastly. I'm supposed to get these flowers back and arranged on the table and round the rooms before everyone arrives about eight o'clock...'
Eulalia took the flowers out to the waiting taxi, watched it drive away and tore back to get her jacket and lock up. At least the rush hour was almost over and it wouldn't take too long to get home.
All the same, it was well after seven o'clock when she reached the flat, to stop short on the pavement. Drawn up to the kerb was a dark grey Bentley.
A jumble of thoughts chased themselves round her head. Peter had been taken ill and their doctor had rung the hospital and Mr van Linssen had come to examine Peter. One heard of delayed collapse after concussion—Peter might be desperately ill. She flung open the door, almost tumbling down the steps in her hurry.
Trottie was standing at the table, a teapot in her hand. She looked up as Eulalia came in. 'You are late, love; you must be tired, and famished into the bargain.'
'Where's Peter? What's that man's car doing outside? Why is he here?'
She had spoken a good deal louder than usual and Peter called from his room.
'Aunt Lally—Mr van Linssen's here—we're playing draughts...'
Eulalia was feeling as anyone would who had believed the worst had happened and found that there was nothing to worry about. She had a wish to burst into tears but she swallowed them and went to Peter's little room. Most of it seemed to be taken up by Mr van Linssen's bulk. 'Why are you here?' she wanted to know, and then at Peter's puzzled look she bent to kiss him and smile.
Mr van Linssen stood up, bending his head to avoid cracking it on the ceiling. 'I happen to know your doctor,' he told her smoothly. 'We decided that it would save time if I were to come and check on Peter's progress, since if he were to come he would still need to inform me of his findings.'
'Peter's all right?'
'My dear Miss Warburton, if he were not, would we be playing draughts?'
She glared at him. What a nasty way he had of making her feel a fool. She was wondering if he would go now that she was home, and hoped that he would, but Trottie's voice from the living-room begged them to come and have a nice cup of tea. 'And I'll give Peter his supper,' she finished, and appeared a moment later with the tray. 'Go and pour the tea, Miss Lally, I'm sure you could both do with a cup, and the doctor can tell you about Peter, for I can see you're all of a fret.'
Eulalia, aware that Mr van Linssen was looking at her with an air of amusement, frowned and led the way, since there was nothing else she could do. Show him the door, of course, but that would be unthinkable. She should be grateful...
There was one of Trottie's Madeira cakes on the table beside the teapot. She poured the tea, offered the cake and passed him the sugar-bowl.
'You work long hours,' he observed, and bit into the cake.
'I had to wait to deliver some flowers. How is Peter, Mr van Linssen?'
'He is perfectly fit, but before he returns to school I want him to be X-rayed again...' At her look of fright he added, 'No, no, don't panic. I merely want to satisfy myself that the bones are correctly aligned and that there is no misplacement. Let me see—it is Tuesday today. Let him stay at home for the rest of this week. Bring him to the hospital tomorrow at ten o'clock.'
He saw the look on her face. 'No—stupid of me, you would be at your shop. I'll arrange for him to be fetched and brought back here. Trottie could accompany him, perhaps?'
'You're very kind.' She was always telling him that, she thought. 'I'm glad he's quite well. He's such a dear little boy.'
'Yes.'
He passed his cup and she refilled it and passed him the cake. 'Are you having a day off?' she asked politely.
'Er—no.' He thought back over his busy day, which had begun with an emergency operation at four o'clock in the morning and was by no means at an end. 'This is a delicious cake.'
She offered him more. It would spoil his supper or dinner, or whatever he had in the evenings, but he was a large man. He might have missed his tea.
He had missed his lunch too, but he didn't tell her that.
He went presently to say goodbye to Peter and to tell him that he would be going to the hospital in the morning for an X-ray. 'And you can go back to school on Monday.'
'Oh, good. Will you come and see me again?'
'Ah, yes, we still have to finish our game of draughts—I'll see if I can find the time.'
Peter was reluctant to let him go. 'Are you very busy every day?'
'Yes, old chap, but now and again I have a day off.'
'I think perhaps I'll be a surgeon when I grow up.'
'A splendid idea!' They shook hands, and Mr van Linssen shook hands with Trottie too, but when Eulalia took him to the door he bent and kissed her, opened the door and went up the stone steps two at a time without a backward glance.
She banged the door shut. 'He's outrageous,' she said furiously.
'You're a pretty girl, Miss Lally. Men like pretty girls.'
Eulalia ground her splendid teeth.
* * *
MR VAN LINSSEN drove himself home. He had enjoyed kissing Eulalia but he wasn't sure why he had done so. She was very pretty—indeed, beautiful when she wasn't looking cross—but he had known and still did know other pretty women and felt no urge to kiss any of them. True, he kissed Ursula from time to time, but always circumspectly, as she was fussy about her make-up being spoiled. Their engagement was a well-conducted affair, with no display of emotion.
He had decided to marry her because she was so suitable to be his wife, and since he was no longer a young man and had decided that there was no ideal woman in the world for him. He had known from the first that Ursula didn't love him; she liked him, was fond of him, and very content to marry him, for he had wealth and position and a certain amount of fame in his profession. They would get on well enough together, although she had revealed a pettishness and desire to have her own way which she had been careful not to let him see before they had become engaged. She had lost her temper once or twice and then apologised very prettily, but they had come near to quarrelling when he had told her that for part of the year they would live in Holland. 'My home is there,' he had pointed out reasonably. 'I have beds in several hospitals. My home is in the country and I think that you would like it.'
She had screamed at him—at the idea of burying herself alive in some miserable little village with no shops and none of her friends. She would go mad. Of course, she would go there with him just to visit, but certainly not for more than a week or so. Perhaps they could take some of her friends with them...
He had given her a long, thoughtful look and had walked out of her mother's house, so angry that he couldn't trust himself to speak, and then later he had sent her the roses...
He left the main road presently and turned into an elegant little street off Cavendish Square. His house was at the end of a short terrace of Regency houses and was a good deal smaller than the others, with only two storeys, but it had the advantages of easy access to the mews behind and a minute garden at the back. He got out of his car, got his bag from the back seat and trod the three steps to his front door.
A thin middle-aged man opened it. He had a long face with an expression of resigned disapproval upon it, and his staid, 'Good evening, sir,' held reproach.
Mr van Linssen clapped him on the shoulder. 'Good evening, Dodge. I'm late—I got delayed.' He started down the elegant little hall towards his study.
'Nothing serious, I hope, sir.'
'I got carried away playing a game of draughts and quite forgot the time.'
Dodge looked astonished. 'Draughts, sir? Would you like dinner served very shortly?'
Mr van Linssen, his hand on the study door, nodded. 'Please.'
Dodge coughed. 'Miss Kendall telephoned shortly after seven o'clock, sir. She asked if you were home. She seemed somewhat agitated, so I took it upon myself to say that you had been detained at the hospital over an urgent case. I was to tell you that she intended to go to the theatre with her friends as arranged.'
'Oh, lord, I forgot.' He glanced at his watch. 'Well, it's too late to do anything about it now. I'll have dinner and phone later this evening.'
Dodge's face didn't alter, his, 'Very good, sir,' was uttered in his usual rather mournful tones, but once in the kitchen he informed Mabel, his cat, that it served that Miss Kendall right, always expecting the master to frivol away his precious free time at the theatre and suchlike, when all he wanted to do was to have a quiet evening with a book or in the company of his own friends.
Dodge shook his head sadly and began to dish up. He was a splendid cook, and with the aid of a daily cleaner ran the little house to perfection. He disliked Mr van Linssen's choice of a bride. He considered her rude and arrogant and spoilt; moreover, despite his mournful manner, he was romantic at heart, and wished for nothing better than a love-match for his master.
Mr van Linssen enjoyed his dinner, finished an article he had been writing for The Lancet, made several phone calls to the hospital and then sat back idly in his chair. There was plenty of work for him to get on with on his desk, but he ignored it. He was mulling over his visit to Peter. A nice child, unspoilt too, and happy despite his orphaned state and lack of a father or uncle. Eulalia was doing her best, he had seen that for himself, and Trottie, waxing chatty over a cup of tea, had told him a good deal. Miss Lally was an angel, she had confided, and never had any time to herself. Even on a Monday, when she was free, there was the washing and ironing and shopping.
Mr van Linssen, who had only a vague idea about the running of a household, had nodded sympathetically. 'What she wants is a good husband,' Trottie had said, and had poured more tea.
She was an impetuous girl, he reflected now, outspoken too—not every man would want her for a wife. She was, of course, undeniably pretty. It was a pity that they had got off on the wrong foot, and she had made it obvious that she had no liking for him, although she had thanked him for looking after Peter and meant it.
He shrugged his shoulders, a little irritated at his interest in her, and lifted the phone.
Ursula's voice, high with bad temper, caused him to wince. 'I have had a wretched evening,' she told him, 'making excuses for you, and of course we were a man short for supper afterwards. Fenno, you will have to give up your appointments at all those hospitals—there's no need. You've private patients enough, and think of the private hospitals there are—you could pick and choose and enjoy a social life.'
It was an old argument which he had always brushed aside. Now he said, 'But I don't want to give up my appointments, either here or in Holland, Ursula, nor do I intend to.'
She did some quick thinking. 'Oh, darling, don't be cross. I've had a beastly time—the play was a bore and some fool spilt wine down my dress—it's a ruin. I'll have to go looking for another one, and shopping is so tiring.'
He thought of Eulalia's tired face when she had got home that evening and fought a rising tide of impatience. 'I'm sure you'll find something just as pretty as the frock which is spoilt.'
'I'll find something you will like, darling, be sure of that. Don't let's quarrel about something which isn't in the least important.'
Mr van Linssen controlled his rage with an effort. 'I have to ring off. I'll phone you tomorrow.'
When, hopefully, he would feel more tolerant.
He fetched Peter the next morning, much to that little boy's delight. 'We thought there'd be an ambulance,' explained Trottie. 'Shall I come with him? However will he get back?'
'I'll bring him back, and there's no need for you to come, Miss Trott.'
'There's coffee on the stove if you could find time for a cup, sir.'
Mr van Linssen sat himself down at the kitchen table, accepted the coffee and a slice of cake and remarked carelessly, 'You must find this very different from the Cotswolds.'
'Indeed I do, and so does Miss Lally. Made up her mind to go back there one day she has, bless her, though how she'll manage that, bless me if I know.'
'Perhaps she has prospects of marrying? An old friend—an admirer?'
'Admirers enough,' said Trottie, 'but that's not her way—too proud to accept help. Besides, she's not found the right man yet.' She gave a sniff. 'Besides, he'll have to be a proper man, if you know what I mean, able to take her troubles on to his shoulders. She's not one of these modern young women wanting to be something big in the business world, but she's no doormat, neither—'
She broke off as Peter came into the kitchen, his small face alight with excitement. 'Are we going in your car? Is that why you're here?'
'Indeed it is. Are you ready? We'd better be off or we'll be late.'
Mr van Linssen allowed Peter to chatter away as he drove to the hospital, but presently he asked casually, 'Do you want to go to the Cotswolds too, Peter?'
'Yes, 'cos Aunt Lally does. We shall go one day. She said so—she's going to make her fortune and we'll go to the village where she was a little girl and she's going to open a flower shop there and we'll have a dog and a cat and a rabbit and there will be a garden.'
'You might have to wait a bit, old chap.'
'That's what Aunt Lally says too, but I don't mind. When I'm a man I'll be a doctor like you, and then I can give her the money.'
Mr van Linssen's rather stern face broke into a smile. 'And why not?' he wanted to know.
He parked the car and led Peter to the X-ray department, and, when he had been X-rayed, handed him over to Casualty Sister, who fed him chocolate biscuits and a glass of lemonade until Mr van Linssen came back to say that everything was splendid and that he was to come back and have a fresh plaster put on his arm in three weeks' time. 'You'll have to keep that one for another five or six weeks, Peter, but you can use your arm as much as you like, as long as you keep it in a sling if it feels tired.'
'Aunt Lally will be pleased. I'll tell her.'
'Maybe I'll come along some time and explain it to her. Now we must go back.'
'Are you very busy?' asked Peter, as they went back to the car.
'Not this morning, but this afternoon I'm going to operate.'
'Oh, I'd like to watch you.'
'So you shall, when you are a medical student and I'm grey-haired and elderly.'
Peter laughed at that. 'With a beard and floppy moustache and specs!'
'I do wear spectacles occasionally,' said Mr van Linssen apologetically.
He didn't stay when they reached the flat. 'Everything's just as it should be, Miss Trott,' he said. 'I'll let your doctor know how things are, and I've no doubt he will get in touch with Miss Warburton.' He sounded all at once very like a medical man, kind in a distant manner, but quite impersonal.
* * *
WHEN EULALIA GOT home that evening she listened first of all to Peter's excited account of his visit to the hospital, and then to Trottie. Everything was all right, it seemed, and she was grateful to Mr van Linssen for taking so much trouble. She had no reason to suppose that he would leave any message for her; all the same, she felt a vague disappointment.
* * *
THE WEATHER TURNED suddenly wet and chilly, which meant that on Sunday, instead of their usual trip to one or other of the parks, she and Peter took a long bus ride, sitting on the front seat on top, sharing a bag of buns and pointing out everything which took their attention. And on Monday Peter went back to school.
It was halfway through the week when Mr van Linssen walked into the flower shop. Eulalia was alone, for it was the lunch-hour and Mrs Pearce had gone home for a while, leaving her to eat her sandwiches and get on with making bouquets for yet another wedding. She sighed as the doorbell tinkled, hoping it was someone who knew what they wanted and wouldn't keep her for minutes on end while they decided what to do. She put down the roses in her hands and went into the shop.
Mr van Linssen, looming over the floral displays, looked larger than ever and bad-tempered to boot.
Eulalia went delightfully pink, and to cover her sudden shyness said, 'Good afternoon, more yellow roses?'
It annoyed her then that she felt shy; from his forbidding appearance he had no recollection of kissing her, and certainly when he spoke it was quite without warmth, ignoring her remark.
'It is only proper that I should inform you of the result of Peter's X-ray, Miss Warburton, and as I was passing this way it seemed as good an opportunity as any at which to do it.'
'It's all right? Trottie said—'
'It is perfectly satisfactory. He must return for a new plaster in three weeks' time and continue to wear it for a further few weeks. He must use his hand normally. Do not get it wet, of course, and if it aches at all there is no reason why he shouldn't have a sling.'
'Thank you for telling me. I really am most grateful.'
He nodded impatiently. 'Do you not close the shop for your lunch-hour?'
'Heavens, no. Lots of customers come between one and two o'clock.'
'When do you take your lunch-hour?'
'Well, I don't. I mean, I have sandwiches and eat them when there's time.'
'The owner?'
What a lot of questions, thought Eulalia. 'Oh, Mrs Pearce goes home. She has a husband to feed, and she has to see wholesalers and so on—it's convenient to do that over lunch.'
His growl was so fierce that she wondered what she had said to annoy him. A quick-tempered man, no doubt. 'You will be good enough to send some flowers to Miss Kendall. What do you suggest?'
'Well, it depends, doesn't it? If it's just a loving gesture, red roses are for love, aren't they? But if it's by way of saying you are sorry about something, then a mixture of flowers—roses and carnations and some of those lilies there and an orchid or two...'
'Perhaps you will make up a bouquet and have it sent round?'
'A large bouquet? Any particular flowers?'
'No. Make your own choice. I'll write a card.'
She watched him scrawl on the card and put it in its envelope.
'It's a waste of money,' she told him cheerfully. 'Miss Kendall threw the yellow roses at me, you know.'
'Indeed?' He gave her a bland look. 'Don't you have a delivery boy?'
'Good heavens, no, that would be eating the profits.'
'You enjoy your work, Miss Warburton?'
'I like flowers and arranging them.'
'But you do not enjoy living in London and working in this shop?'
It wasn't really a question, just stating a fact, and she wasn't sure how to answer him. 'I'm glad to have a job.' She added with sudden asperity, 'And I can't think what business it is of yours.'
'Upon reflection, nor can I. Good day to you.'
He shut the door gently behind him as he left.
'High-handed,' said Eulalia loudly, 'as well as bad-tempered. If I hadn't disliked that Miss Kendall on sight, I'd be sorry for her.'
* * *
IT WAS ALMOST the end of the following week when Peter rushed to meet her when she got home. 'Aunt Lally, oh, Aunt Lally, something splendid—Mr van Linssen's going to take me round his hospital on Sunday afternoon. He knows I'm going to be a surgeon like him and he said I deserved a treat because I've been a good boy. Do say I can go—he says he'll fetch me in his car and bring me back.'
Eulalia took off her jacket and kicked her shoes from her tired feet.
'Darling, when did he say all this?'
'He stopped here on his way home and he said he was sorry you weren't here but he hoped you'd let me go with him. Two o'clock,' added Peter.
She looked down at the eager little face. He didn't have many treats. His small school-friends had fathers and mothers who took them to fun-fairs and the zoo, and in the summer to the sea for a holiday, but he had never voiced a wish to do that, although she was quite sure that he longed to do the same. She might not like Mr van Linssen, but for some reason or other she trusted him. She said at once, 'Darling, how lovely. Of course you can go, and how kind of Mr van Linssen to ask you. Did you thank him?'
'Yes, of course I did, but I said I'd have to ask you first.'
'Well, I think it's a splendid idea. How are you going to let him know?'
'He said he'd be driving past tomorrow morning and it's Saturday so I'll be here.' He lifted a happy face to her. 'Won't it be fun?' His face clouded. 'Only, what will you do, Aunt Lally? Because Trottie's going to her friend's for dinner...'
Eulalia glanced across to the table, where Trottie was arranging knives and forks and spoons. 'I've so many odd jobs to do—not housework, just nice little jobs like sewing on buttons—and I can read the Sunday papers.'
Trottie's eyes were on her face, and for a moment it seemed as though she would speak, but she only smiled. 'Sounds nice and peaceful to me,' she said finally. 'Dear knows you don't get much time to yourself.'
'You must remember every single thing you see,' said Eulalia, as they sat down to their supper.
* * *
SUNDAY CAME WITH blue skies and bright sunshine, and the three of them went to church before Trottie went to catch her bus. 'There's everything ready for your dinner,' she told them. 'Be sure and have it early so's not to keep Mr van Linssen waiting. I'll be back around seven o'clock, same as usual.'
It was a nice dinner but Peter was too excited to eat much. He was ready and waiting for a long time before two o'clock. 'Perhaps he won't come,' he said, for the tenth time.
'He said two o'clock, dear, so don't worry—there's still ten minutes left.'
He came five minutes later and she went to open the door to him.
Her, 'Good afternoon, Mr van Linssen,' was coolly polite. 'This is very kind of you.'
He stood looking at her. 'A pleasure. It has struck me that it might be sensible if you were to come too.' At her frown, he added, 'There is always the small chance that I might be called away urgently and Peter cannot be left alone. Do you dislike the idea very much?'
Upon reflection, she didn't dislike the idea at all. 'I don't want to spoil Peter's afternoon.'
'Don't worry, we'll leave you somewhere in safe hands.'
A remark which ruffled her feelings. She was on the point of making a suitably telling reply when Peter joined them. 'Are we ready? What a pity you can't come with us, Aunt Lally.'
'She is coming,' said Mr van Linssen, and shut the door.
'Do go and fetch whatever you need to fetch. Peter and I will plan our route round the hospital—you can have five minutes.'
Her eyes sparkled with temper. 'I don't—' she began with dignity. She caught his eye then. It was very compelling. She mumbled, 'All right, I won't be long.'
Thank heaven she hadn't changed out of the dress she had worn to church; she had intended to get into an old cotton dress and turn out a few cupboards. She brushed her hair, powdered her nose, added some more lipstick, found her bag and went back to the living-room. The pair of them were crouched over a large sheet of paper spread out on the table. A plan of the hospital, she supposed.
'Won't anyone mind?' she asked, as she got into the back of the car. 'Us walking round?'
'Not if you are with me,' he told her gravely.
They went to Casualty first, for once almost empty, and then to the outpatients' hall, before taking the lift to the first floor to inspect each ward in turn, and in each one he introduced them to the ward sister. 'Friends of mine,' he explained, which she found rather high-handed of him. She hardly knew him, and what conversation they had engaged in had hardly been of a friendly nature.
When they reached the theatre block she was left with Theatre Sister in her office and given a cup of tea while Peter, speechless with excitement, was taken to see one of the operating theatres. They were gone a long time, and when they got back Mr van Linssen had a cup of tea too, and Peter a glass of lemonade. Somehow Eulalia hadn't thought of the operating theatre allied to cups of tea. Sister's office was quite cosy, too, and she was young and pretty and obviously Mr van Linssen's slave.
She was one of the junior sisters, she had confided to Eulalia. The theatre superintendent, an awesome lady who ruled the theatres with a rod of iron, only scrubbed for major surgery and always for Mr van Linssen. 'There are two other sisters, but we aren't allowed to scrub for him, more's the pity. He's quite a dish, isn't he? Going to get married soon—he never talks about it, though.'
They went unhurriedly back through the hospital and into Casualty once more, where Mr van Linssen explained with patience exactly what happened to a patient when he arrived, answering Peter's endless questions with apparent tirelessness.
They got back into the car presently and he said casually, 'I hope you will both come and have tea with me. I'm sure Peter hasn't finished with his questions...?'
'Tea?' asked Peter. 'Oh, please.' He turned to look at Eulalia. 'Aunt Lally, can we go?'
It was impossible to refuse without being rude and spoiling the day for Peter. 'That would be nice,' she said pleasantly, and caught him looking at her in his side mirror.
She had supposed that they would go to one of the cafés in any of the parks, but instead he kept to the streets, their surroundings becoming more elegant with every minute. When he stopped before his house and got out and opened her door, she got out too, and stood looking at his house.
'You live here?' she asked.
'Yes. Very convenient for my work.' He went off to help Peter out, locked the doors and ushered them across the pavement and in through the door being held open by Dodge.
'I've brought some friends for tea, Dodge, if you would let us have it shortly.'
Peter held out his hand. 'How do you do, Mr Dodge? I'm Peter.'
Dodge shook his hand carefully. 'How do you do, Peter? I see you've been in the wars.'
'Miss Warburton and her cousin Peter, Dodge.' And Mr van Linssen smiled a little as Eulalia shook hands too.
CHAPTER THREE
EULALIA GAVE A small sigh as she went into the drawing-room. It was a long room, taking up the whole of one side of the little house, with a bay window at its front and doors opening on to the little garden at the back. It was furnished very much to her taste, with comfortable chairs, an enormous sofa before the hearth, splendid rugs on the polished wood floor, and mulberry silk curtains blending nicely with the chair-covers. There were little lamp-tables too, arranged just where they were needed, and a handsome bureau cabinet in marquetry. She knew a little about good furniture; this she thought was probably a William and Mary piece. It went very well with the cabinet of walnut with floral marquetry on the other side of the hearth, which was of the same period. She might not see eye to eye with her host, but she had to admit that he had excellent taste in furniture.
The doors to the garden were open and Peter had gone at once to look at it. 'Have a look round, Peter,' invited Mr van Linssen, and to Eulalia, 'Please sit down—tea will be here in a few moments. I hope we haven't spoilt your afternoon.'
She sat. 'No, I enjoyed it. It was very kind of you to give Peter a treat.'
'You have his sole charge?' he asked idly. 'Guardian to a small boy is no easy matter.'
'There wasn't anyone else,' she said simply. 'At least, the solicitor couldn't trace anyone from his father's family, and my cousin was an only child whose parents had died. I didn't even know her. Peter's a dear little boy. Trottie and I often wonder how we lived without him.'
'He's hell-bent on living in the country...'
'I know, and we will one day. I don't know how, but we will. Do you like the country, Mr van Linssen?'
'Yes—it's an entirely different way of living, isn't it?'
He talked on, putting her at her ease, slipping in a question here and there, and she, lulled by his quiet friendliness, answered readily.
Dodge came in presently and spread a magnificent tea on the table by the doors. 'The young gentleman will be more at ease sitting at the table,' he explained, and went away to fetch the teapot.
Peter came in from the garden. 'There's a cat in the garden, sitting on a chair,' he told them breathlessly. 'I stroked him and he purred. Aunt Lally, couldn't we have a cat?'
'That will be Mabel, Dodge's cat,' said Mr van Linssen. 'I expect it wouldn't be quite safe to have a cat at Cromwell Road, Peter—all that traffic rushing to and fro. I should wait until you get to the country.'
Eulalia frowned. Talking so much about the country wasn't much help. That she was determined to get there one day was a fact, but he made it sound as though it was a certainty in the not so distant future.
Peter nodded cheerfully and applied himself to his tea. Dodge, despite his sombre appearance, had a warm heart; there were sandwiches, strips of hot buttered toast, buttered scones, chocolate biscuits and a fruit-cake. Peter worked his way steadily through them all, and Eulalia, since she was hungry, saw no point in being lacking in appetite. There was a good deal of her to nourish, after all. Mr van Linssen, long ago resigned to his Ursula's finicky ways and professed inability to eat any but the choicest of foods, derived a good deal of amused pleasure from her unselfconscious enjoyment.
He was an excellent host, although he had no great love for social occasions; he talked of this and that, drank several cups of tea and ate a scone he didn't want, and had to admit to himself that he was enjoying his afternoon. He had refused an invitation to go with Ursula to friends in the country for the weekend, pleading pressure of work. Well, he had had a busy week, and to spend his free Sunday, before beginning on an even busier one, in the company of Ursula's friends with whom he had little in common, would have given him little pleasure.
They were still sitting round the table while Peter ate the last chocolate biscuit, when the doorknocker was thumped, and a moment later Dodge opened the door, to be thrust aside by Miss Kendall.
'Darling, how naughty of you, I do believe—' She stopped. 'What on earth is she doing here? It's the girl from the flower shop, isn't it? And that boy.' Her charming smile turned to tight-lipped offence. 'I came back early, thinking you might like to spend the evening with me, but I can see it's not necessary.'
She turned her back on Eulalia and Peter. 'You said you were going to be busy over the weekend.' She tossed her head and added spitefully, 'With this shop girl, I suppose.'
Mr van Linssen had risen to his feet, listening impassively to this outburst. 'My dear Ursula, shall we overlook this little outburst?' His voice was quiet and cool. 'This is Miss Warburton, who works in the flower shop as you already know, and this is her cousin Peter. We have spent an hour or so at the hospital, a reward for his pluck when he broke his arm recently.'
Peter had left his chair too and had come to stand by him, and now he held out a small hand. 'How do you do?' he said, mindful of Eulalia's teaching of good manners.
Miss Kendall ignored the hand, and after a moment Peter let it fall and turned a puzzled look on Eulalia. She sat, outwardly serene, inwardly seething, waiting to see what would happen next.
Mr van Linssen, apparently untroubled by his fiancée's ill humour, put an arm around Peter's bony shoulders, for he had seen the boy's lip tremble. He said now, 'I don't know when I have had such a delightful afternoon, Peter. We must do it again some time.'
Oh, no, we won't, reflected Eulalia, and caught his eye. He smiled at her, knowing exactly what she was thinking, and she frowned at him. 'We have indeed had a lovely time, Mr van Linssen, but I think we should be getting home now.'
'Of course.' He turned to Ursula, sulking in a chair. 'Coming with us, Ursula?'
'Whatever for? I'll wait here, and when you get back you can take me out for a meal. I've had a very boring weekend.'
'Just as you like.' He watched as Eulalia and Peter wished her goodbye, only to be ignored, and then ushered them out to the car while Dodge stood at the street door. They wished him goodbye too, and Eulalia said, 'It was a lovely tea,' and smiled at him very sweetly.
'A pleasure, miss, and a joy to see the young gentleman enjoying it.'
No one spoke as they drove away until Peter observed, 'I like Mr Dodge—he looks sad, but he isn't, is he?'
Mr van Linssen laughed. 'Not in the least. I believe him to be quite happy inside.'
'Oh, good. Why was that lady cross?'
'Hush, Peter,' said Eulalia, in what he called her 'aunt' voice, so he hushed.
At the flat Mr van Linssen got out, opened her door and helped her out and did the same for Peter, and then stood looking down at her while she started on her thank-you speech. She had barely begun it when he said, 'Shall we go inside and see if Miss Trott is back?'
She stopped in mid-sentence. 'Come inside? You want to come inside?'
'Shall I not be welcome?'
'Of course you are welcome, and do come in, only I thought—I thought you'd want to get back home quickly.'
He didn't answer but followed her down the steps, took the key from her and opened the door. Peter skipped ahead of them to hug Trottie and gabble the excitements of the afternoon to her. She kissed his happy face and said, 'Darling, how very nice. You shall tell me all about it presently, but here's Mr van Linssen... Can we offer you tea? And how nice to see you again,' added Trottie in her soft country voice.
She offered a hand and he took it and bent to kiss her cheek as well.
'We have just had tea, Miss Trott, at my house.' He glanced at Eulalia. 'I, for one, have enjoyed a most pleasant afternoon.'
'But the lady was cross,' said Peter, and was immediately hushed by Eulalia.
Trottie saw the look on her face and launched into an account of her own day. 'And such lovely weather—you can't beat our English summers.'
'But, Trottie, it rains a lot—'
'Of course it does, things have to grow, don't they? You're a foreign gentleman, sir, what do you think of our weather?'
'Delightful, on the whole. Holland is flat and there is always a wind, and it can be very cold in winter.'
Without quite knowing how it had happened, Eulalia discovered that they were all sitting round the table, and there they stayed for the next half-hour, while Mr van Linssen led Trottie on to talk about her younger days until he said reluctantly, 'I must go back home, I'm afraid, and I dare say it's Peter's bedtime.'
He made his farewells briskly and this time he didn't kiss Eulalia.
When he had gone Trottie said, 'Well, that was a nice little visit to end the day, wasn't it? I'll start the supper, Miss Lally, while you get Peter bathed and ready for bed. I dare say he could eat something in his dressing-gown, for once.'
It was over supper that Peter, warm from his bath and wrapped in his dressing-gown, brought up the subject of Miss Kendall again.
'Why was she so cross?' he wanted to know.
'Well, dear, I think she was surprised to find us there. You see, she wanted Mr van Linssen to take her out and I dare say we spoilt her evening.'
'She was rude,' he persisted. 'She didn't shake my hand, and if she's going to marry Mr van Linssen why didn't she kiss him?'
'I expect she'll do that when he gets home. Now, eat your supper, darling, and then off to bed. School in the morning, remember.'
Later that evening, Trottie said, 'That Miss Kendall doesn't seem the right kind of wife for dear Mr van Linssen. Such a good man. He needs a loving wife, not a woman with a nasty temper and no manners.'
'I dare say she's quite different when she's with him, Trottie.'
'You may depend upon that; that's how she caught him in the first place.' She nodded her elderly head. 'Depend upon it too that she doesn't care twopence for him. Smart, is she, as well as pretty?'
Eulalia thought back. 'Yes—very smart—lovely clothes, Trottie, and perfect make-up. Let's be honest, she's the kind of a wife a man in his position needs—you know, dinner parties and so on.'
Trottie gave her a sharp look over her spectacles. 'If that's what you think a man needs in a wife, then you're much mistaken, Miss Lally.'
'Anyway,' said Eulalia defiantly, 'he has a bad temper and he can be very rude. I dare say they'll get on very well together.'
'You don't like him,' said Trottie flatly.
'I don't know him well enough to have an opinion about him,' said Eulalia which, although not quite true, put an end to the conversation.
* * *
SHE TOOK PETER to school in the morning and then went back to do the chores which Trottie was beginning to find tiring and, those done, she fetched her basket and went shopping, laying out the housekeeping money in a prudent fashion, and all the while her thoughts, which should have been centred on groceries, kept straying to Mr van Linssen.
She didn't like him, of course, but she had to admit that he had been very kind to Peter. He had a nasty temper, all the same, and she didn't think that his Ursula would improve that—a very unpleasant young woman and, as she had reminded herself so often, deserving of him and he of her.
She went back and had her lunch with Trottie and embarked on the ironing. There were never enough hours in a Monday.
* * *
IT WAS TEN days later when he came into the shop once more. Eulalia, on her own as it was lunchtime, was sitting on a stool at the back of the shop, eating her lunch out of a paper bag: cheese sandwiches and an apple, and a mug of tea which Mrs Pearce allowed her to brew.
She put the sandwich, half eaten, back in the bag, and in a voice thickened by bread and cheese, wished him good afternoon.
'More flowers?' she wanted to know. 'You must be a very quarrelsome man.'
'What an impertinent girl you are! I never seek a quarrel, and I might point out that it is no concern of yours if I choose to quarrel.'
'True. Is it to be red roses this time?'
It gave her quite a jolt when he said yes. So he did love Ursula, after all. She felt an unexpected pang of regret. 'A dozen? Two dozen?'
'Two dozen. Send them by Interflora to this address.'
He gave her a card with the address—it was somewhere in Holland—and she wrote it down in the order-book and asked, 'Is this place a town? Will there be an Interflora shop there?'
'No, Leiden is the nearest place.'
'I can look it up in our international directory. We get a good many of our roses from Aalsmeer, they'll be beautifully fresh. Do you want to send a message with them?'
Pen poised over the form she was filling in, she waited.
'Yes—happy birthday, and sign it "Fenno".'
'That's an unusual name,' observed Eulalia, busy writing.
'So is Eulalia.'
'Yes, well—this will cost you a pretty penny.'
'That, again, is no concern of yours.'
She raised large grey eyes to him, allowing the lashes full play. 'We make it a custom to mention the cost before the customer pays—just in case they can't afford it!' She gave him a kind smile and a motherly nod of the head, and saw his mouth set like a rat-trap. Why, she wondered, did she feel the need to annoy him when they met? Why didn't she treat him with a cool indifference and be polite? If Mrs Pearce heard her she would be given a week's notice for cheeking a customer.
She began to work out the cost, doing most of it on her fingers.
'Do you not use a calculator?' he wanted to know impatiently. 'I cannot stand here all day while you add and subtract like a schoolchild.'
'I never was any good at maths, and please don't interrupt me or I'll have to start all over again.'
'I'm surprised that you keep your job.'
'Well, you see, Mrs Pearce always takes Interflora orders, only she's not here.' She added her sums and told him the total and dealt with his credit card. 'I'll see that it gets phoned through today,' she told him. 'Does it matter if it's delivered morning or afternoon?'
'Morning.' He turned to go and at the door paused. 'How is Peter?'
'Very well. His plaster is covered with his friends' names and rude messages. We had a note from the hospital to say that he must go there to have a new plaster tomorrow.'
'That is convenient for you?'
She looked her surprise. 'Well, no, but nothing's convenient, if you see what I mean, not when I'm here all day, but Trottie will take him and bring him back.'
'I'll fetch him and take him home again. He'll be going to Outpatients?'
'Yes, but we can't impose on your kindness again. Trottie will—'
He cut her short. 'I have said that I will take him and bring him home—I shall be taking Outpatients' orthopaedic clinic.' He opened the door, wished her a curt goodbye over his shoulder and went into the street.
When she got home that evening she told Trottie and Peter what Mr van Linssen had arranged.
'There,' said Trottie. 'Didn't I know what a good man he is—so thoughtful of others, knowing as how you weren't free to take Peter yourself?'
'Oh, magnificent,' said Peter, who was forever trying out long words. 'Perhaps he'll have time for a game of draughts when he brings me home.'
'Not very likely,' said Eulalia sharply. 'He has to work like anyone else.' Which remark earned her surprised looks from her companions.
* * *
MR VAN LINSSEN, driving back to the hospital, told himself that it was interest in Peter which had driven him to offer to take him back to Outpatients in the morning. Certainly it was not his intention to please Eulalia: a tiresome girl and far too outspoken. She needed a firm hand and she wasn't likely to get it, for it would be hard to find a man prepared to put up with her ways. Of course, he conceded, she was devoted to the boy and very protective of Miss Trott, hard-working too, and not easily discouraged. She deserved some sympathy, although she would probably throw it back in the face of anyone offering it.
He parked the car and stalked into his clinic where, contrary to his custom, he snapped the heads off his two housemen, a handful of students and an unfortunate nurse who dropped a pile of notes on the floor.
His clinic lasted longer than usual and his temper, although once more in control, was no better. When he remembered that he was taking Ursula to the opera that evening it grew decidedly worse. To go home and change into a dinner-jacket, go without his dinner and spend the evening being sociable to her many friends, have supper with them afterwards and get home too late to work at the series of lectures he was to give was more than he could tolerate, although he saw no help for it. For once, however, Fate was to treat him kindly, even if she hadn't been as kind to the elderly man knocked down in the street outside the hospital and rushed inside. He was preparing to leave Sister's office, where he had been discussing his list for the following afternoon, when the phone went and he was asked if he would go to Casualty. Theatre Sister was surprised at the cheerful manner with which he responded.
The man was severely injured: a fractured pelvis, fractures of one leg and an arm. Mr van Linssen forgot all about Ursula and the opera and spent several hours in Theatre, putting the bones together again. It was late when he left to go home to Dodge and the kind of meal only Dodge could conjure up at a moment's notice. He was sitting at the table, finishing his coffee, when Dodge told him that Miss Kendall had telephoned twice and he had informed her that his master was delayed at the hospital. He didn't add that she had carried on something shocking, but said smoothly that she had seemed a little upset.
'I'll ring her presently.' He glanced at his watch. 'No, it's too late now. I'll have to do it tomorrow when I've finished the clinic.'
* * *
PETER WAS WAITING for him when he drove to the flat in the morning. 'I knew you'd come,' he said happily. 'Grown-ups don't always do what they say they're going to, but you do, don't you?'
'As far as possible, old chap. Jump in or we shall be late.' He bade Trottie goodbye and settled the boy beside him and, once at the hospital, handed him over to the young doctor who had first seen him. 'Give me a ring when you're ready. I'll be in Theatre for half an hour, then in Outpatients.'
It was rather more than half an hour by the time Peter was dealt with, and a nurse was detailed to take him over to Outpatients. Here he was sat on a bench and told to wait until Mr van Linssen came for him, something he was delighted to do, for there was so much to see—patients going in and out, nurses, doctors, porters wheeling trolleys and, best of all, presently Mr van Linssen himself in a long white coat, surrounded by the registrar, his housemen, several students and Sister. He looked, thought Peter, like one of the men in his book of heroes. His small chest swelled with pride because they were friends.
Mr van Linssen lifted a hand in greeting and disappeared through another door, and after ten minutes or so came out again, this time without his white coat.
'Trottie said she'd have coffee ready,' said Peter hopefully in the car.
'Just what I need, but I can only stay for five minutes. I'm operating this afternoon and I must go round the ward first.'
'Yes, of course,' agreed Peter solemnly. 'I'm sure Trottie will understand.'
Mr van Linssen, nicely filled with coffee and a slice of Trottie's cake, went back to work. He had quite forgotten Ursula.
She phoned that evening soon after he got home and he listened patiently to her cross voice telling him just what she thought of him and, since he felt guilty, he apologised handsomely. It was after he had put the receiver down that it occurred to him that he would have to send more flowers...
* * *
EULALIA HAD JUST opened the shop when he got there the next morning. At the sight of him she said, 'Peter's all right—Trottie said so.' She eyed him anxiously. 'Is something wrong?'
He gave her a pointed good morning. 'Of course not. How you do fly into a panic at the sight of me—am I such a harbinger of bad news?'
'Each time I see you I think it will be the last,' she declared. 'Not more flowers? Hadn't it better be a diamond brooch from Cartier?'
He gave her a level look. 'Do not provoke me. I have a nasty temper, and don't be impertinent!'
He came a little further into the shop and she saw how tired he was. She said, 'I'm sorry, it's my tongue, it runs away with me. I do try to think before I speak but I don't always remember.' She smiled at him. 'You're tired and that makes you cross. You should have a holiday, away from the hospital and London.'
'And my patients?' He was amused and all of a sudden brisk. 'Now, these flowers—something rather special this time, I think.'
Lucky Ursula, reflected Eulalia. She only hoped the wretched girl realised it. It seemed unlikely, but perhaps she really did love him in her way, and she thought he must love her. 'How about pale mauve orchids and fern in one of these vases? They're a bit expensive because they're nineteenth-century Staffordshire—Mrs Pearce goes around the antique shops and buys up the real thing when she can find it.' She held it up for his inspection. 'I'm sure Miss Kendall would love it...'
He said without much interest, 'Very well, send it to her home, will you—some time today?' He paid her, and with a brief goodbye left the shop. She watched him cross the street and get into his car and drive away. Perhaps this really was the last time she would see him...
He hadn't written a card. His car had disappeared into the stream of traffic and there was nothing to do about it. She told Mrs Pearce when she arrived, and was told to write a card herself and take the flowers in her lunch-hour. 'I'll stay here until you get back,' said Mrs Pearce. 'You can go more easily than usual—there'll be plenty of buses around noon.'
It was nice to be away from the shop, even if it was her lunch-hour. Eulalia rang the bell of Ursula's home and a severe woman in a black dress and apron opened the door.
'Flowers for Miss Kendall,' said Eulalia.
She was about to hand them over when she heard Ursula's voice call out, 'Who is it?' and she came into the hall. She eyed Eulalia with dislike. 'You again. More flowers.' She turned to the woman. 'All right, you can go, Mrs Parkes. Hasn't he got more sense than to send flowers? Good God, I get flowers from everyone.' Her eyes narrowed. 'Perhaps he likes to go to your shop and talk to you—is that it? After him, are you? I know your kind, on the look-out for a rich husband, although probably you wouldn't mind if he wasn't your husband.' She sniggered.
Eulalia went pale with rage. 'Here are your flowers. You are a very vulgar woman and spiteful...'
She had thrust the carefully wrapped vase and flowers at Ursula, who took them and then deliberately dropped them on the ground, lifted up a foot and stamped on the orchids.
'They're only flowers,' said Eulalia slowly. 'They never did you any harm and they were beautiful—so was the vase.'
'You haven't heard the last of this,' declared Ursula, and went indoors and banged the door shut.
Eulalia, shaking with rage, told Mrs Pearce when she got back to the shop.
'Oh, dear, they're good customers too, and we were to do the wedding-flowers. You'd better apologise, Eulalia—the customer's always right, you know.'
Eulalia stared at her. 'Mrs Pearce, she was unforgivably rude to me. I didn't start it, you know.'
Mrs Pearce shrugged her shoulders. 'Apologise, all the same, Eulalia—she could lose me a lot of custom, telling tales to her friends; she knows a great many people, you know.'
Eulalia said steadily, 'I'm sorry, Mrs Pearce,' and went to serve a customer.
She told Trottie when she got home that evening, after Peter was in bed and asleep. 'Mrs Pearce was annoyed because I wouldn't apologise, but Trottie, what would I apologise for, and how dare that woman say things like that? She made me feel cheap...'
'A very nasty person,' Trottie allowed, 'and don't you say you're sorry, Miss Lally, whatever happens.'
'Whatever' did happen; Eulalia was given a week's notice when she got to work next Tuesday. 'I'm sorry to lose you, Eulalia,' said Mrs Pearce, 'but I can't afford to lose any business. I'll give you a good reference and you'll get another job easily enough, I dare say.' She paused. 'You won't reconsider apologising?'
'No, Mrs Pearce. Miss Kendall was rude and abusive; she is the one who should apologise. Unfortunately she has money and influence on her side, hasn't she?'
Mrs Pearce looked uncomfortable. 'If you could overlook it...' she began, but seeing the stubborn look on Eulalia's face said no more.
Trottie took the news with a solid calm. 'You did right, Miss Lally, and don't you go regretting it. We've had hard times before, and got through them, and you'll get a job in no time. What have we got in the bank?'
They spent the evening doing sums, plotting and planning. Peter's school fees were safe, tied up in a trust, even if she had wanted to get at them—which she most definitely didn't. It was a question of cutting down on their already tight budget until she found work.
There was little chance to go job-hunting during that week, and she couldn't bring herself to ask for time off to try for any of the likely jobs advertised. She went home on Saturday evening, her last pay-packet in her purse, feeling scared and defiant at the same time. As Trottie had said, they had weathered worse storms...
She hadn't told Peter and she didn't intend to until she had found other work. She spent the next week applying for any likely job. She had a good reference, and there were a number of likely offers. She wrote letters, telephoned, even took long bus journeys in the hope of getting some work, but luck was against her—she was too old, too young, lived too far away. At the end of the following week she was taken on as an interviewer for a new brand of soap powder, stopping passers-by and asking for their opinion about rival soap powders. It was a thankless task: busy housewives didn't want to stop, young women were flippant, old ladies either chillingly dismissive or garrulous. Besides, it was hard on the feet and it rained for most of the time, but she was glad to be earning some money and, more than that, it was a job of sorts. 'Out of work' sounded so hopeless.
She had been given Southampton Row and Bloomsbury Way as her stamping ground. The agent who had employed her had decided that she was pretty and looked—to use that old-fashioned word—ladylike; people were more likely to stop for her, especially in that area.
* * *
IT WAS ON her last day that Mr van Linssen, driving himself away from Great Ormond Street hospital, caught sight of her, standing with her board and pen poised. He slowed the car, the better to see what she was doing, and saw her approach a woman with a Harrods bag on her arm, who halted briefly, waved her away and walked on. He drew into the side of the road and watched her, oblivious of the traffic warden making his way towards him. Eulalia had stopped another woman now, with more success it seemed, for she was writing something down and the woman was talking.
The warden tapped on the car window and he turned round; at the same time the man saw his 'Doctor on Duty' ticket, nodded and walked away, which left Mr van Linssen free to stare his fill. What was Eulalia doing so far from the flower shop and why was she doing it? He started the car and drove on, already late for the first of his private patients.
It was two days before he could find time to visit the shop, to be greeted by a prim girl with glasses, and as thin as a wafer, a cruel contrast to Eulalia's opulent person.
'Miss Warburton?' he enquired, and Mrs Pearce came from the back of the shop.
'You wanted to speak to Eulalia? I'm afraid I had to dismiss her. One of my best customers complained about her rudeness. She was a very outspoken girl at times, but a good worker.' Her eyes strayed to her new assistant, listlessly bunching stocks.
Mr van Linssen drew a bow at a venture. 'Was the customer by any chance Miss Kendall—my fiancée?'
Mrs Pearce, scenting the likelihood of substantial orders in the future, answered readily. 'Yes—so unfortunate—and I do apologise for Eulalia's sharp tongue. Do you care to order any flowers today?'
He gave her a cold look. 'Thank you, no. I merely wished to speak to Miss Warburton.'
He got back into his car. He had a list that afternoon, and it would be evening before he was free to seek Eulalia out, but he just had time to go and see Ursula before he was due at the hospital.
She was at home, getting ready to go out to lunch with friends.
'Fenno—how lovely—are you free? I'm lunching with the Abbotts and they won't mind if you come with me—we're meeting at Claridge's. You've got your car? Good, I needn't get a taxi.' She stopped and looked at him then. 'What's the matter? You look angry—' she smiled '—but not with me, I hope?'
'Yes, with you, Ursula. Do you know that your complaint about Eulalia at the flower shop resulted in her dismissal? What exactly occurred?'
'Oh, darling, such a fuss about nothing—such an impertinent girl...'
'Why was she impertinent?'
Ursula shrugged. 'Oh, I really can't remember, and she was so clumsy that I dropped the flowers and the vase.' She put a hand on his arm. 'Nothing to worry about, Fenno. Let's go.'
His eyes were hard. 'I'm operating. I'm already in danger of being late. I'll see you some time.'
He left her, and after a minute she shrugged again and told the maid to ring for a taxi. She would have to be extra charming so that he would be his usual patient and tolerant self with her. She was a vain young woman and she had no fear of rivals.
* * *
MR VAN LINSSEN, preparing to leave in the late afternoon, found himself back in Theatre once more, dealing with an emergency, and it was late evening by the time he let himself into his house. Dodge, looking more sorrowful than ever, served him his dinner, observed that Miss Kendall had telephoned twice, and expressed the opinion that his master could do with a good night's sleep.
'I shan't be going in to the hospital until the afternoon,' he was told. 'I'll have a quiet morning catching up with the paperwork.'
Dodge shook his head sadly and went away to bring in the coffee-tray. At least his master had shown no desire to phone that Miss Kendall.
Mr van Linssen had his breakfast at the usual time, spent an hour at his desk and then fetched his car and, with a word to Dodge that he would be back for lunch, drove himself away.
I wonder where he's off to? reflected Dodge. Mad as fire, he is. Never a nasty word, but seething all the same.
Mr van Linssen stopped in the Cromwell Road outside Eulalia's flat and went down to its front door, gave the knocker a thump and waited with well-concealed impatience. Trottie opened the door, gave him one look and said, 'Oh, sir...' and then added, 'How nice to see you—you'll come in? I'm doing the housework, if you don't mind the mess.'
He took her hands in his. 'Miss Trott, what has happened? I saw Eulalia near Great Ormond Street hospital, canvassing people. I went to the shop and was informed she had been dismissed. I was told one side of the story, now I want to hear the other.'
Trottie didn't find it strange that he should ask. 'I'll make us a cup of coffee and I'll tell you,' she promised, and presently sat down opposite him. 'Miss Lally's out looking for work. That was only a temporary job, asking people about soap powder—you know—they call it a survey. And I'll tell you why she got sacked, only perhaps I shouldn't, because you may be angry.'
He drank some of his coffee; there was no cake, he noticed. 'No, I promise I won't be that.'
'Well, I don't know what Miss Lally'll say when I tell her—you see, it was things said about you and her, and it was your future intended who said them.'
He smiled at her. 'Miss Trott, if it is what I suspect, then I need to know—is it something Eulalia wouldn't tell me herself even if I asked her?'
'Lord, she'd rather run a mile, sir. That upset she was...' Trottie told him then, and when she'd finished she said, 'So you see how it is, sir, she wasn't going to apologise for something she hadn't said or done.'
'Of course not. I'm sorry this has happened and perhaps it would be better to say nothing to Eulalia. I will forget what you have told me, so that if ever she and I should meet in the future she need never know that I am aware of what was said.' He smiled suddenly. 'And the amusing thing is that she can't stand the sight of me!'
Trottie didn't answer that; sometimes it was best not to interfere with Fate's antics.
'Forgive me for asking, but are the three of you able to manage until she finds another job?'
Trottie was a simple soul and she trusted him. 'Well, Peter's fees are safe—they are in some kind of trust that I don't really understand. We've cut down as much as we can but, you see, we've never been able to save more than a few pounds. It's kind of you to ask, sir, but it's more than my life's worth to accept anything from you—you see that, don't you?'
He nodded. 'Yes, Miss Trott, I do.' A vague, ridiculous plan was taking shape at the back of his head—a pity he had no time to examine it now. He got up, kissed Trottie's elderly soft cheek, left some pocket-money on the table for Peter—and took himself off.
Driving back to his house, he began to laugh. The idea was so preposterous, it might work!
CHAPTER FOUR
MR VAN LINSSEN was unable to pursue his preposterous idea until late that night, when his long day was finished and he was at home sitting at his desk, roughing out a paper on bones which he was to read at a seminar in Holland within the next few weeks. Presently he laid down his pen and sat back and allowed his thoughts to dwell on it. Then he opened his appointment-book and studied it carefully. With a few adjustments and the help of his invaluable secretary, he should be able to give himself a weekend free from patients.
On Friday evening he told Dodge that he would be away for the weekend. 'Ah, yes, sir,' said Dodge, looking more unhappy than ever. 'You will be seeing Miss Kendall?'
'Miss Kendall? No, Dodge, I'm spending it in the Cotswolds.'
He left early on the Saturday morning and drove down the M4 until he turned off for Malmesbury, where he stopped to enquire the way, driving on presently through the quiet countryside through small side-roads until he reached the village he sought—Brokenwell, a fair-sized place with a wide main street, a village green with a cluster of houses, shops and an ancient church. He stopped outside the village pub, the Boy and Horseshoe, and went unhurriedly into the bar where he had coffee, since it was too early for a drink, and enquired if he might stay the night.
There was a room, agreed the landlord, and he was welcome to it.
'Come far, have you, sir?'
'London. I'm looking for someone and I don't know where to start. A family called Warburton lived here, I believe, and I want to get in touch with their solicitor. I don't suppose you could help me?'
'Well, now, that's something I don't know, but if you tried Mrs Tagge at the post office, she'll know, seeing as how she sorts the post and so on.'
Mr van Linssen thanked him, observed that he would be back presently, and crossed the green to the small general stores and post office.
Mrs Tagge was old, rather deaf and short-sighted. That didn't matter, though, as she gave him the information he sought. 'Wanting 'im for a bit of business?' she wanted to know. 'Well-known in these parts, 'e is.'
'So I understand. Thank you, Mrs Tagge.'
He went back to the pub, looked up the solicitor's phone number and dialled it. There was just the chance that there would be someone there on a Saturday morning. There was: the solicitor himself, sounding impatient. 'I'm on the point of going home for the weekend,' he pointed out. 'It would have to be a matter of urgency if you want to see me.'
Mr van Linssen didn't waste his words. 'You were the Warburton family's solicitor, I believe. I know Miss Warburton. She has fallen on hard times and I am anxious to help her, since it is the fault of a close connection of mine that this has happened. I need your help.'
Mr Willett's voice became more friendly. 'Eulalia? Well, yes, I am prepared to see you, Mr—I didn't quite get your name.'
'Van Linssen. When will it be convenient to you? I must be back in London by eight o'clock on Monday morning at the latest. I'm staying at the Boy and Horseshoe.'
'Perhaps you would come to my office this afternoon. Two o'clock. Cirencester—you know the address? Good. I must tell you that this is most unusual, but Eulalia is a dear girl and she hasn't had a very happy life, I imagine, since she left Brokenwell.'
Mr van Linssen agreed, rang off, and took himself off to the pub for bread and cheese and beer, agreed with the landlord that steak and kidney pie with young beans and jacket potatoes would suit him very well that evening, then went to his room—a spotlessly clean apartment, the window of which overlooked the back garden—donned a light jacket and drove himself to Cirencester, a matter of eight miles or so.
Mr Willett was in his office, an elderly man with a serious face. He shook hands, pointed out again that he wasn't in the habit of seeing clients on a Saturday afternoon, but since it was Eulalia... 'You are a friend of hers?'
'Hardly, although we have met. But I am good friends with little Peter.'
'Ah, yes, the little boy who was orphaned. Very sad. She came at once to the rescue, you know. Before we go any further, may I enquire your purpose in helping Eulalia?'
'As I said, it was through a close connection of mine that she lost her job. Peter broke his arm recently and I have been looking after him. It was Miss Trott who told me that they had fallen on bad times.'
'Trottie—of course, she went with Eulalia—a dear soul. You are their doctor?'
'No. I'm in orthopaedics at Maude's. That is how I came to know Peter.'
'Ah, yes, I see. And in what way can I help you?'
'This may sound a little out of the ordinary,' observed Mr van Linssen, 'but if you will hear me out...'
Two hours later he was back at the pub, drinking the strong tea the landlord had offered and eating a lardy cake to go with it. 'Mrs Wedge, the wife that is, is a rare cook. Happen you'll enjoy it, sir.'
Mr van Linssen, contented with his day's work, did.
The next day, Sunday or no Sunday, he was agreeably surprised how willing people were to do business with him when instant payment was offered. No one could have been more helpful than the house agent in Malmesbury, disturbed while browsing over the Sunday papers. He had long ago decided that the cottage this placid gentleman was willing to buy without more ado would never sell—only to a fool who hadn't any idea what it would cost to put it to rights. Although this particular gentleman didn't look like a fool.
Still, business was business. He readily undertook to deal with the purchase as speedily as possible and pocketed Mr van Linssen's cheque before he could change his mind.
Mr van Linssen, aware of the house agent's opinion, smiled to himself and went back to London. He could safely leave the rest to Mr Willett.
Dodge didn't fail to notice his look of satisfaction. 'A pleasant weekend, I trust, sir?' he enquired discreetly.
'Splendid, Dodge, thank you.' He was leafing through the letters and messages on the hall table. There was nothing that required his immediate attention, so he went to his study with the pleasant prospect of a quiet evening and one of Dodge's well-cooked dinners.
The phone rang as he sat down. Ursula, wanting to know where he had been. 'And don't tell me you were at the hospital because they said you weren't.'
'Quite right. I've been out of town on business.'
'What business?'
He was still feeling pleased with himself. 'You don't need to concern yourself with such a dull thing as business, Ursula.'
She gave a tinkling laugh. 'I should hope not. I had a lovely day out in the country—the Thornefolds' place—town's so boring this time of year, darling. Couldn't you take a teeny-weeny holiday? We could have a week or two in the Bahamas. The Thornefolds are going—they've rented a villa on one of those islands. We could be alone.'
Mr van Linssen, without going too deeply into the reason, didn't particularly wish to be alone with his Ursula. 'My dear girl, a holiday, even a couple of days, is quite out of the question. I've an appointment-book bursting at the seams, and besides, I'm due back in Holland within the next week or so. You could come back with me if you like?'
'Don't be silly, Fenno. Holland would be as bad as London—probably worse. All those sausages and cheese...'
He let that pass. She was entitled to her views; perhaps she would alter them when they were married. He frowned at the thought, and said quickly, 'I'll try and get away early tomorrow evening—we might go out to dinner somewhere—in the country, if you like?'
'Oh, all right. Somewhere decent—I don't want to be hemmed in by yokels.' She sounded peevish. 'Call for me about seven-thirty.'
She rang off and he put the phone down, sat down at his desk and opened the first of the folders on it and became immersed at once in its contents, Ursula forgotten, although, strangely enough, the memory of Eulalia standing in a corner of the street with a clip-board, earning a precarious living, persisted in coming between him and the patient's notes before him.
* * *
EULALIA HAD FOUND another job. Putting leaflets about some newfangled washing-machine through letterboxes. Temporary, of course, and she was in a way thankful, for it was boring and tiring and kept her on her feet for the entire day. However she was paid for it—a miserable sum, but better than nothing. It lasted for ten days, and on the day after that, two days before Peter would start his holidays, the postman brought a letter. She didn't open it at once; it was an expensive envelope and it looked official, and she dreaded to open it in case it was some unexpected demand for money. She turned it over in her hand and put it down on the table.
'Go on,' said Trottie, 'open it, Miss Lally.'
The letter inside was on the same expensive paper, and she glanced at the heading and frowned. 'It's from Mr Willett—you remember, Trottie?—our solicitor at Cirencester. Whatever can he be writing about?'
Trottie tutted impatiently. 'Read it and find out,' she suggested.
Eulalia read the letter and then, with a rather pale face, re-read it.
'Trottie,' she said in a strange voice, 'did you know that there was a great-uncle living in Australia? He's died and I'm his only living relation. He's left fifty-six thousand pounds and a cottage in Brokenwell. I don't believe it!'
'If it's from Mr Willett and written in black and white, then you'd best believe it, Miss Lally.'
Eulalia handed over the letter and Trottie got her spectacles and read it in her turn. 'And why not?' she wanted to know. 'There's nothing strange in family going off to the ends of the earth and getting forgotten.' She looked sternly at Eulalia over her glasses. 'And here's me been praying night and day for a bit of help and here it is. You'll go and see Mr Willett, Miss Lally, and take a look at that cottage and see if we can live in it.'
'I'll have to find work, Trottie. I know it seems a lot of money, but the interest won't be enough to live on.' She smiled suddenly. 'Oh, Trottie, if I opened a flower shop...?'
'Just the thing, love. Won't Peter be happy?'
'There's Gormer's close by—a prep school for boys—he could go there!'
'It's meant, Miss Lally. You'd better go tomorrow.'
'Yes, if I catch an early train, I could see Mr Willett first and then take a look at the cottage and come back on the last train.'
'You take care, Miss Lally, it's a wicked world these days.'
Eulalia, her head gloriously filled with rather wild ideas, hardly heard.
Waiting at the school gates for Peter, she wondered what he would say when she told him. Perhaps he might want to stay; he was happy at this school. She need not have doubted his delight when she gave him the news as they walked back to the flat.
'A puppy,' breathed Peter, 'and a cat and a rabbit. Is there a garden, Aunt Lally?'
'I don't know, dear, but I dare say there is. I'm going there tomorrow to have a look. If the cottage is watertight, I dare say we could move into it quite soon.'
He skipped along beside her, full of questions, but presently he said, 'Will you tell Mr van Linssen? He'll want to know; I'm his friend and he'll miss me.'
'He's a busy man, Peter. I know—when we know we're going to move, you can write him a little note and tell him, and thank him for all he's done for you. Will that do?'
He considered. 'Yes, I expect so. I'd like to say goodbye to him.' He brightened. 'He'll want to come and see us before we go.'
'If he has time.'
He wouldn't come, of course, she reflected, he was a busy man; besides, he had his Ursula and his own life and why should he bother? She found herself regretting that.
She caught the earliest possible train to Cirencester the next morning and when she got there went at once to Mr Willett's office. He greeted her warmly, assured her that she was indeed the lawful owner of Ivy Cottage, High Street, Brokenwell, and the sum of fifty-six thousand pounds, and the odd hundred or so, on deposit at the bank. 'And if you should require an advance, Eulalia, I will give you a cheque now. There may be expenses...'
'Yes—well, yes, please. I'm out of work and we do need the money. If the cottage is habitable I intend to move in as soon as possible. Peter can start school at Gormer's at the start of the autumn term, if they'll take him, and I'm going to open a flower shop—just a small one. There are several big houses around the village.' She thought briefly of her own old home. 'I might be able to make a living, and there'll be the interest...'
'Very prudent,' commented Mr Willett, his hands clasped before him as though in prayer, not inappropriate since he was breathing silent pleas for forgiveness for telling such a pack of lies, even though they were in the best possible interests of the listener.
He gave her coffee, handed her the keys of the cottage, and suggested that when she had been to the bank she might take a taxi to Brokenwell. 'An extravagance,' he said, smiling at her, 'but for once to be condoned.'
Eulalia, with money in her purse, got out of the taxi, paid the driver and stood on the narrow pavement, looking at the property. It was an end cottage, one of a row in the centre of the village, its outside wall overlooking a narrow lane which petered out after a few hundred yards into fields. It looked solid, even if shabby, with a stout door and a window on either side and three smaller windows above. The door opened straight on to the pavement, and after a moment she put the key in the lock and went inside.
There was no hall; she found herself in a small room with faded wallpaper and a Victorian fireplace with an inglenook on either side of it. The door in the opposite wall led straight into the kitchen, its plastered walls discoloured and housing an ancient gas stove and a large white porcelain sink. The back door beside its small window opened on to the garden, and she went outside to have a look. It was in a woeful state, overgrown, with the tin cans and paper bags lying around, but it was quite large, with apple-trees at the end of it and a brick wall surrounding it. She sighed with delight. Peter could have his puppy at last...
Inside again, she opened the second door in the living-room to another small room, with the same old-fashioned fireplace and a deep window-seat and a door half-open on to a narrow twisting staircase. She went up slowly and found them solid enough, and at the top there was a tiny landing with three doors. The rooms were small but the views from them were delightful. No bathroom, but then, if she could find someone to put one in for her...
She went out into the main street and walked to the other end and up another small lane, and knocked on the door of a house with a workshop attached. The man who answered it was young, about her age, short and sturdy, with twinkling eyes.
'Lord love us, if it isn't Miss Lally. Here's a sight for sore eyes—come back to live, 'ave yer?'
'Yes. It's Jacob, isn't it?' She held out a hand and had it wrung. 'I wondered if your father could do some work for me.'
'Dad? 'E died two year ago. I'm carrying on the business. What do you want done?'
'I've inherited Ivy Cottage and I want to come and live in it. I haven't much money to spend, but it does need painting and repairing and I want a bathroom built on. Could you do it?'
'Don't see why not, Miss Lally. Tell you what, I'll come with you now and take a look and give you an idea of what it'll cost. It'll be an idea—just a rough one, mind.'
He took some time going over the little house, talking cheerfully all the time. 'The old dodger 'oo 'ad it, he went and died a year ago. Rented it, he did, never bothered much with paint and so on. But it's sound enough, needs a bit of plastering and a lick of paint, and a couple of the windows need to be rehung.'
'And a bathroom?' urged Eulalia.
'Well, now—got to get planning permission for that. Shouldn't be too 'ard, seeing as I'll build it on the back wall the other side of the back door.'
'How long before I could move in?'
'In an 'urry ter come back, are you? Well, we'll all be glad ter see you, Miss Lally. I'm not all that busy—give or take, a couple of weeks ter paint and plaster in and out, take a look at the roof. Don't want no paper on the walls?'
'No, just a nice creamy emulsion—you know—a kind of clotted cream.'
'Just the ticket. The bathroom'll take a bit longer but I could get Jim—the plumber 'oo works for me—ter put a washbasin in one of the bedrooms...'
'All of them, please, and what about hot water?'
'One of them gas boilers. Open fires?'
'Oh, yes. Can you give me some idea of how much it will cost? I know it'll be a rough guess.'
He sat down on the window-seat and produced pencil and paper. The sum he suggested would still leave more than fifty thousand in the bank.
'That's all right. Do you want something on account?'
'It'd be a help.'
She got out her new cheque-book. 'And if I came down in about two weeks, could you advise me about a cooking stove? I've got a washing-machine at the flat in London. It's pretty old but I dare say it'll do for another year or two.' She smiled at him. 'Jacob, it's lovely coming back home. I've still got Miss Trott with me and an orphaned nephew. He's eight, and just longing to get away from London. So are we.' They went out into the street together. 'I'll write to you when we'll be coming to look round, shall I?'
'You do that, Miss Lally. 'Ow you getting back now?'
'I expect there's a bus. I must get back to London this evening.'
'Tell you what, I'll run you back to Cirencester. You wait 'ere, I'll get the van.'
'But it's past your dinnertime.'
'The wife'll keep it 'ot. It's only a few miles anyway.'
She got home late that evening, tired but happy. Jacob had driven her to Cirencester and left her at the railway station and she had had a meal there, decided to take the late afternoon train, and taken herself to look at the shops. Curtains, she had thought happily, and fitted carpets in the bedrooms... By the end of the afternoon she had had a very good idea of what she should buy, and when she had passed the gas showroom windows, she had gone back and entered the shop, chosen a gas cooker and paid for it, feeling reckless.
Recounting her day to the interested Trottie, she observed, 'I do hope I haven't been extravagant, Trottie, but it was reduced because I paid for it at once, and they'll deliver it in a week's time. That'll give Jacob time to get the kitchen painted. Oh, Trottie, it's such a dear little place, I can't believe it's true. We'll be so happy there. It's as though it was meant to happen...'
* * *
MR VAN LINSSEN, who had meant it to happen, had a satisfactory talk over the phone with Mr Willett when he got home from the hospital. So far so good...!
* * *
THE POSTMAN CAME again the next morning, this time with a letter from Eulalia's landlord to inform her that when her lease expired within a few weeks, he regretted having to renew it at a higher rent.
It gave her great pleasure to write and tell him that she wouldn't be renewing the lease.
The next ten days were passed happily enough, plotting and planning about the future: colour schemes were discussed, curtain material decided upon, a furniture remover sought out who would take their household goods as a part-load on his way to Malmesbury and then, assured by Jacob that the cottage was going along nicely, they went, all three of them, to Brokenwell. There was a convenient bus this time, so that they got off in the village just before midday, and as they walked down the street they were stopped by people who remembered them, glad to see them again, so that by the time they reached Ivy Cottage, Peter was dancing with impatience.
It looked quite different now. Jacob had given its walls of Cotswold stone a good clean, painted the door and the windows and replaced the broken gutters. They went inside and found him there, painting the window-seat. He put down his brush as they went in, shook hands with Eulalia and Miss Trott and said, ''Ello, young 'un,' to Peter before taking them on a tour. He had worked miracles, it seemed to Eulalia; the whole place seemed larger now that the walls were painted.
'That's a fine sink,' said Trottie. 'Don't anyone go taking that away.'
'Never worry, Miss Trott, and I'll fix you up a few shelves wherever you want them.'
The bedrooms commanded instant approval. 'May I have a room in the front?' asked Peter. 'I can see right down the street for miles and miles.'
'I don't see why not. Trottie, do you want your room in front or at the back?'
'The back, if it's all the same to everyone. Now I'm up here I'll measure for curtains, and we can get them made before we come.' She took out a tape measure and a notebook and Eulalia took Peter into the garden.
He didn't say anything for a minute, and then looked up at her.
'Yes, dear, just as soon as we're settled in you shall have your puppy.' She was rewarded with a hug.
'And a cat and a rabbit?'
'Yes...'
Jacob asked, 'Likes animals, does 'e? The wife's cat's 'ad kittens. Reckon they'll be ready to leave 'ome by the time you're settled in.' He took some papers out of a pocket. 'I got planning permission—said it was urgent on account of there being no modern sanitary arrangement. Cast your eye over this, Miss Lally, and see if it suits. It'll be easy enough—I can have it done in no time—but it'll cost you a bit more. Got ter have Cotswold stone, you see. The plumber'll be along as soon as I've got it up—starting it tomorrow. The basins in the bedrooms is ready, 'ot water laid on. If you can use the outside convenience for a day or two, you could move in four or five days' time.'
She nodded. 'We'll do that, Jacob. The cottage is finished, isn't it, except for the cooker and the washing-machine? They promised the cooker for Monday—will you be here if they bring it and fit it?'
'Right you are, Miss Lally, I'll be here.'
'You'll need some more money.' She got out her cheque-book once more.
She explored the garden with Peter, discovering hidden rose-bushes, a clump of peonies, lilies, and a neglected strawberry-bed. There were two apple-trees, too, and a plum-tree bowed down with fruit. The brick wall was sound, too, though too high for Peter to see over. It faced south and she thought how it would be a blaze of colour in the spring, with daffodils and grape hyacinths growing at its foot.
Peter flung his arms round her waist. 'Aunt Lally, I'm so happy. Are you happy too?'
'Oh, darling, yes, won't it be fun?'
'Shall I ask Mr van Linssen to come and see us? I expect he'd like to be here and not in London.'
'Well, I'm not sure about that, Peter. You see, he doesn't live our kind of life. He's an important surgeon and has lots of important friends and he's going to be married soon. I doubt if he could spare the time.' Peter's lower lip trembled very slightly and she went on hastily, 'But I'm sure he'd like to have a letter from you.'
'All right. Will you want to read it?'
'No, dear; I'm sure you'll write it very well without any help from me.'
They went back to Cromwell Road that evening, tired and happy, and the next day Eulalia, leaving Peter with Trottie, took herself off to Oxford Street to buy curtain material. There were a lot of windows at the cottage but they were small. She found odd lengths going cheap and bore them back to the flat, where she and Trottie measured and cut, making linings from an old sheet, stitching by hand since they hadn't got a sewing-machine. And by the time they were finished it was time to start packing up.
* * *
IT WAS THE last day; the van was loaded and the flat empty. Eulalia turned the key in the lock for the last time and without a moment's regret, she told herself, shying away from the unbidden thought that she would have liked to see Mr van Linssen just once more. She still wasn't sure if she liked him, but he had been kind. Besides, she was sorry for Peter, who had looked each day for the Bentley to drive up with him at the wheel, but he hadn't come, nor had he written.
She told herself that a letter from a small boy could easily get overlooked in the mass of his post, but she said nothing to Peter, respecting his unhappy silence.
They would both have felt a lot better if they had known that Mr van Linssen had been to Holland to give urgent advice concerning a rare bone tumour about which he was a well-known authority. Peter's letter was in his pocket, but just for the moment his own affairs had to give way to his work. He operated, stayed long enough to make sure that his patient would make a recovery, and returned to England four days after Eulalia had moved to Brokenwell.
Any unhappy feelings they had were for the time swallowed up in the excitement of the move. Jacob had worked wonders with the cottage. The gas cooker had been installed, there were shelves in the kitchen just where Trottie wanted them, and washbasins in the bedrooms, and the chimney-sweep had been. It was late evening before they had got the beds up and made, the elderly, still handsome, Turkey carpet from their old home laid in the sitting-room and the more immediate necessities of life unpacked. They sat around the kitchen table eating beans on toast and drinking tea, before seeing a sleepy Peter into his bed.
'When can I have a bath?' he wanted to know.
'Tomorrow. We'll go over to the Boy and Horseshoe. Jacob says the landlord—Mr Wedge—will let us have baths until the bathroom is ready.'
Later Eulalia eagerly inspected the almost completed extension to the back of the cottage. It was small, just room for its basic equipment, but never mind its austerity, she thought, it was all they needed to make the cottage perfect.
They hung curtains the next morning, rearranged what furniture they had, and cleaned and polished until Trottie pronounced herself satisfied that there wasn't a speck of dust or dirt to be found, and, when Peter had arranged his toys in the cupboard in his bedroom, they had coffee then went into the back garden and spent an hour picking up the rubbish.
'I'll have to buy some garden tools,' said Eulalia, handing Jacob and his mate their elevenses.
'There's a car-boot sale on Saturday,' Jacob told her. 'You might pick up a spade and suchlike. Old Bob—remember him? He's still doing an odd job on and off, as you might say. He'd come and clear the garden for a fiver. Scythe down the grass and clear the worst of the weeds.'
'Would he? Is he still living in Water Lane? I'll go and see him.'
They went over to the Boy and Horseshoe presently and had their baths and a hot meal and, leaving Trottie to go back to the cottage, Eulalia and Peter went to call on old Bob—not all that old and still very fit.
'I heard you was back, Miss Lally, love. Plenty of us old uns remember you and your granny up at the 'ouse. In Ivy Cottage, are you? Nice little place and very sound. I'll be along one day and take a hand to that garden. Nice enough it was once—got a bit neglected.'
'Yes, I know, but if you'd give it a start I intend to get it going again. There's any amount of stuff swallowed up with weeds.'
He nodded. 'Couple of good apple-trees...'
'And a plum and a row of soft-fruit bushes...'
They nodded in agreed enthusiasm.
In two days they were more or less straight, with curtains at the windows, chairs and tables finally in the right places, and cupboards and drawers filled from the packing-cases; moreover, the bathroom was finished. Eulalia surveyed it with a pride tinged with regret that having the walls tiled and the floor laid was for the moment beyond the budget she had allowed herself. But she promised herself she would go to Cirencester to buy bright-coloured towels and a bathmat to give it an air of warmth.
She paid Jacob and the plumber and sat down to count her money. There was still some over without touching the fifty thousand in the bank. In a week or two, once they were settled in and she had arranged Peter's school, she would see if Jacob could turn the decrepit old shed halfway down the garden into something watertight where she could start her flower shop. Life was full of possibilities—Trottie was happy renewing old acquaintances in the village, and Peter was in the seventh heaven, and as for herself—she was happy too. She found herself wishing she could tell Mr van Linssen just how happy she was.
A wish which was to be granted.
* * *
MR VAN LINSSEN, back home again, immersed himself immediately in his work, spending long hours in the operating theatre, taking over Outpatients from his registrar, catching up with his private patients at his consulting-rooms. It was only when he had dealt satisfactorily with all these things that he permitted himself to think about Eulalia. She would have moved by now, of course. He phoned Mr Willett and was told that, yes, Eulalia had taken up residence at Ivy Cottage. She would be going to see Mr Willett some day next week. 'She has, I hear, made the place very attractive, knows exactly what she wants and goes after it. Very like her grandmother,' added Mr Willett drily.
Ursula, peevish at Mr van Linssen's determination to keep his handsome nose to the grindstone, had taken herself off with friends to the south of France, so he felt free to plan a day's outing to Brokenwell. He had to explain to Peter why he hadn't answered his letter, besides that he had a present for him.
It was a fine morning when he set out, and the traffic was heavy since it was a Saturday; all the same, he drew up at Ivy Cottage soon after ten o'clock. Peter, hanging out of his bedroom window, saw him at once and raced downstairs. 'Aunt Lally, he's here, I knew he'd come...' He opened the cottage door and flung himself at Mr van Linssen, which gave Eulalia time to peer into the little looking-glass in the kitchen and deplore her shining nose and untidy head of curls, but there was no time to do more than switch off the iron and go to meet him.
Her, 'Good-morning, Mr van Linssen,' was pleasantly friendly and was answered by his cheerful,
'Hello, Eulalia,' and a quick kiss on her cheek.
She ignored that, aware that her heart was thumping far too loudly. 'How did you know where we were?'
'Your landlord gave me the forwarding address.' He was a truthful man, but the lie slipped off his tongue without trouble; if he told the truth he would involve Mr Willett, who would never forgive him.
'Well, now you're here,' said Eulalia in a cool voice, 'will you have a cup of coffee? Trottie's shopping—she will be back presently and will be glad to see you.' She went a little pink at his amused look, and added clumsily, 'Well, we are all glad to see you. Do come in.'
'Thank you, but first I have something for Peter.' He went back to the car, and when he turned round there was a small puppy under his arm.
CHAPTER FIVE
'I HAD YOUR letter, Peter and thank you for it. I had to go to Holland for a while and had no chance to answer it, and when I got back I had rather a lot of work to do. I hope this little fellow will recompense you for your disappointment.'
'A puppy,' shouted Peter. 'For me? For my very own? I can keep him?'
Mr van Linssen put the little creature into Peter's arms. 'If Eulalia will allow you to keep him, he's yours.'
The puppy peered from under his arm, his round eyes wary. He was of no known breed, with large ears and a rough black coat with a white shirt-front. Eulalia reflected that Mr van Linssen hadn't put a foot wrong; someone less understanding might have turned up with a pedigree pup, but he had known just the kind of dog a small boy would want. She said quietly, 'Of course Peter may have him, it's one of his dreams come true. He's a darling little dog.'
She watched the small creature in Peter's arms, wriggling a little and then licking the small hand which held him. 'He likes me,' said Peter in a satisfied voice. 'Thank you very much, Mr van Linssen, he's just exactly what I would have chosen. Has he got a name?'
'Not yet, that's for you to decide, isn't it? I've brought his basket with me, and there's a little book telling you how to feed him and take care of him...'
He was still standing at the door, and Eulalia said quickly, 'Do please come in.'
'Thank you, and coffee would be delightful. I'll get the basket first, shall I?'
He came back from the car with it, carrying a box too. 'I wasn't sure whether you could get the right food, so I brought some with me.'
He followed her into the cottage with Peter keeping close, cuddling the puppy.
Trottie, returning from her shopping trip, came up behind them.
'Well, this is a lovely surprise. Sit yourself down, love—coffee's soon ready, and one of my cakes. Come far, have you?'
He bent to kiss her cheek. 'What a lovely warm welcome,' he observed, and Eulalia blushed. She had been lacking in manners; he must think her rude.
She said on an impulse, 'I'm sorry I wasn't more welcoming, Mr van Linssen, I—I was surprised.'
Trottie had gone to fetch the coffee and Peter had gone into the garden with the puppy. Mr van Linssen loomed over her. 'Oh, good—I thought for a moment that your strong feelings had got the better of you and you were going to show me the door.'
'That's absurd, besides, you brought the puppy and made Peter so happy.'
He smiled a little. 'And you, Eulalia, are you happy?' He looked around the comfortable little room. 'This is a charming little cottage, a far cry from Cromwell Road. Did you win the pools? The letter I had from Peter left me rather in the dark.'
She was very conscious of his nearness. 'It seems that I had a great-uncle in Australia, who left me the cottage and quite a lot of money—there isn't anyone else in the family, you see. I'd never heard of him, but he has my eternal thanks.' She drew rather a defiant breath. 'I'm going to open a shop—a flower shop.'
'What a splendid idea. Here in the village?'
She nodded. 'Not just yet, of course, but I'll have to make a living of some sort later on. There are any number of large houses scattered around, if I could get them interested, and there'll be weddings and funerals.'
He didn't say what he thought about her plans but bent and kissed her cheek very gently. 'I'm so glad you have had good luck for a change.' He moved away from her and added lightly, 'You don't mind me calling? I had to put matters right with Peter, but I promise you I won't bother you again.'
Before she could answer that, Trottie came in with the coffee. 'You'll stop for lunch,' she told him, and didn't look at Eulalia. 'Cold chicken and a salad and jacket potatoes, and an apple pie for afters.'
'Delicious. Thank you, Miss Trott, I should like that very much. And how do you like this village?'
'Bless you, love, I was born here, know every stick and stone in it, not to mention them as lives here.'
'Indeed?' He turned an enquiring face to Eulalia. 'So that is why you decided to come and live here. I suppose you could have sold the cottage and found something else.'
She handed him a slice of cake on a plate. 'As a matter of fact, I lived here too,' she told him. Her manner dared him to ask more questions.
He looked politely surprised. 'Well, well, that must be delightful for you. The village is well away from the main roads, isn't it?'
They discussed the surrounding countryside for a while until he said, 'May I find Peter and talk to him about the puppy? He's a bright little boy, but I'd better explain feeding times and so on.'
He took himself off to where Peter sat with his new companion, eating cake, sharing the slice between them. The garden was still unkempt and overgrown, but Peter had found an old wooden bench and Mr van Linssen sat down beside him. The bench groaned under his weight but didn't collapse, and the pair of them stayed there until Trottie called them in for their lunch.
'Wash your hands,' she warned them. 'There's our nice bathroom so you've no excuse.'
Mr van Linssen, meekly doing as he was told, looked around him. It was a very basic new bathroom, he considered, but Eulalia seemed to be managing very well. The cottage was repaired and painted but she hadn't wasted money on unnecessary furbishing. He wasn't sure about her plans for a flower shop, but it would be best not to mention it at the moment—he was, after all, supposed to have only a passing interest, and when he had said that he wouldn't come to see her again she hadn't replied...
He left shortly after their meal, saying all the right things to Trottie and kissing her elderly cheek, shaking hands with Peter and bidding Eulalia a coolly friendly goodbye which left her in no doubt about not seeing him again. Which was exactly what he had intended...
Watching the Bentley's elegant rear disappearing down the street, she reflected that he couldn't have made himself more plain; this had been by way of a farewell visit for Peter's sake. Certainly he had spent a good deal of time with the little boy, sitting out there in the garden. She wondered what they had talked about.
She went back into the cottage and helped with the washing-up, and then wandered into the garden where Peter was playing with the puppy.
'I must think of a name,' said Peter, 'and when I have I shall write and tell Mr van Linssen about it.'
'Well, dear...' began Eulalia, not quite sure how to go on.
'Don't you like him?'
'Yes, yes, of course I do, but I think he brought you the puppy as a kind of goodbye present, don't you?'
He shook his head. 'He's my friend.'
'That's nice—to have a friend, I mean. You must think of a really good name. I'll think, too, while I do a bit of gardening.'
She wasn't thinking about names as she toiled away at clearing the fruit-bushes, though, she was remembering Mr van Linssen's casual goodbye, and why she should mind that he had been so casual she didn't know. She attacked a gooseberry-bush quite fiercely, and told herself not to waste time thinking about someone who didn't matter at all when there were so many other important matters to decide upon.
They all went to church on Sunday morning, leaving the puppy happily asleep in his basket in the kitchen, and because there was a new rector since Eulalia had lived there with her grandmother, and several people in the congregation wanted to speak to her, their progress was slow as they left after the service. Peter said nothing, but the hand she was holding squeezed hers once or twice, just to remind her that he wanted to get back to his new companion, so she made the excuse that she had to get back to cook the Sunday dinner and left Trottie happily renewing old acquaintances.
'I've thought of a name,' said Peter as they reached the cottage. 'Charlie.'
'Just right,' declared Eulalia. 'Put on your sandals, dear, and take him into the garden and tell him.'
So Charlie became one of the family, and she thought of Mr van Linssen every time she looked at him.
It was during the following week that Jacob arrived with a ginger kitten tucked inside his jersey. 'A little lady,' he pointed out. 'As sweet a nature as you'd wish for. I heard as how you'd got a pup, so they'll be friends, like.'
Peter was over the moon. 'Aunt Lally,' he said excitedly, 'now we've got all we wanted, haven't we? Well, almost—there's still the rabbit and, of course, I would like you to have a big Bentley motor car like Mr van Linssen.'
'I'll settle for the rabbit,' declared Eulalia, not altogether truthfully.
After suitable correspondence, she took him to the new school, enrolled him for the autumn term and set about getting his uniform. That meant two or three trips to Cirencester with a Peter impatient to get back to his pets. He had named the kitten Blossom, and there was no denying the fact that he was now a very happy and contented small boy.
'It is such a pity that I shall never be able to thank that great-uncle,' she told Trottie one day. 'Just think, Trottie, we might still have been in Cromwell Road trying to find somewhere to live and me hunting for work. Which reminds me, once we've got Peter settled at school I must start thinking about the shop. You still think it's a good idea?'
Trottie nodded. 'It's worth a try. Start in a small way and see how it goes. You'll have to give it a year, and if it's paying its way by then you can open up a bit.'
Eulalia gave her a hug. 'Trottie, what would we do without you?' She stretched her arms open wide. 'Oh, isn't life just wonderful?'
'Never better, Miss Lally. All we want now is for some nice young man to come along and sweep you off your feet.'
'He'd need plenty of strength! I'm what is politely known as generously built, Trottie, and he'd have to be someone special, for he'd have to take Peter and you as well as me, not to mention Charlie and Blossom.' She sighed. 'He'd be hard to find.'
'That's as may be, but you ought to have a nice young man to take you out a bit, Miss Lally.'
'I'm very happy,' said Eulalia, and almost believed it. She had no right to be otherwise; everything she had wished for had come true, so why should she hanker after seeing Mr van Linssen again? Such a hopeless wish it was best forgotten at once.
She went into the garden and went on with clearing the fruit-bushes. With luck, they would have soft fruit enough next year, and very soon they could pick the apples. The plums were ripe, too; they were eating them every day and Trottie was in her element turning them into jam.
'I have no reason to feel the least bit unhappy,' said Eulalia to Charlie, who was helping her with the digging after his own fashion.
Most of the younger men and women Eulalia had known when she had lived with her grandmother were either married or had left home, but there were still one or two left. Once Peter was going to school she would accept their invitations for coffee or a game of tennis or supper. It would be very pleasant to renew old friendships, she reflected, and since Peter would have his lunch at school he would be away all day during the week. The rector's small son was already at the school, and the rector had suggested that he could give Peter a lift there and back when he took his own son, an offer which she had thankfully accepted.
By the time Peter's school started the autumn term, they had settled into a pleasant routine. Trottie, back in her own village, was shedding the years, going off to the village shops, cooking and bottling and making jam from the blackberries Eulalia and Peter had picked to go with the apples. As for Peter, he had filled out nicely, made friends in the village, and spent happy hours training Charlie and playing with Blossom. He was looking forward to school, too, his one regret that he couldn't take his pets with him.
'Well, dear,' said Eulalia cheerfully, 'you will be here to give them their breakfasts in the morning and take Charlie into the garden, and back here to give them their supper, and we might take Charlie for a walk before your supper.'
Peter, a reasonable child, agreed to this, only adding, 'It's a pity that Mr van Linssen can't see Charlie. You don't suppose he'll come to see us?'
'No, love, I don't expect that he will. He'll be getting married soon and he won't have any time.'
'He could write a little letter...'
'Important people like him have secretaries to write their letters.'
She went with the rector on Peter's first day at school, careful to keep in the background—small boys, she knew, were touchy about grown-ups tagging along. From a distance, she saw him and the rector's son go through the imposing front door of the school. 'I do hope he'll be happy,' she told her companion.
'No doubt of it! He's a happy child and well-liked. I'll bring him home with my son Jack this afternoon, and you'll find he's settled in without any trouble. You'll have more time to yourself now, won't you? You must come over to the Rectory for a game of tennis one afternoon. Do you remember the Woollands? Victor and Joyce have been in America but they're due back any day now—nice to meet old friends again...'
'Yes, I did know them—but not very well.' She hadn't liked Joyce much, a gushing girl who spread spiteful gossip, and as for Victor, unless he had improved out of all knowledge, she had no particular wish to see him again. He had had damp hands and an overpowering conceit. She couldn't refuse the rector's invitation, however. He had been very kind, helping her to slip into village life again, and perhaps Victor had improved since they had last seen each other...
She met him in the village street a few days later, and at first glance he didn't appear to have altered at all, and his hand when he grasped hers was still damp. 'Lally, we were told you were back—come into a fortune, I hear. Some people have all the luck!' He laughed heartily and she smiled a polite smile and hastened to disillusion him.
'Whatever you heard is nonsense, Victor. I've inherited Ivy Cottage and some money from a relative.'
He sniggered. 'Didn't suppose you'd admit it. Never very forthcoming, were you? Still got that boy with you?'
'Peter? Yes, and Miss Trott.'
'Nosy old bird...'
She fired up. 'How dare you talk like that of Miss Trott? I must be on my way. Give my love to Joyce...'
He put a hand on her arm. 'Got off on the wrong foot. Sorry, old girl. Just my joking. No offence. Joyce'll want to see you—may we come and see you one day? Renew old friendships, eh?'
She said levelly, 'We never were friends, Victor, but do bring Joyce if she would like to come.'
She told Trottie when she got back to the cottage. 'I couldn't refuse him, could I?' she asked. 'We used to play tennis together, but then there were the Cartwrights and the Kingsleys, so I never had much to do with Victor or Joyce. He behaved as though we'd been the best of friends instead of casual acquaintances.'
'Who is spreading tales about your fortune, I'd like to know?'
'I don't suppose anyone is. I think he was trying to find out if I'd come into a lot of money.'
Trottie snorted. 'Like his cheek, I never did like those two, Miss Lally. I remember them when they were quite small—a pair of mischief-makers, they were.'
'Well, we don't have to bother about them, Trottie. I expect they've got jobs and won't be around much.'
Wishful thinking. Joyce intended to stay at home for a while, declaring that her visit to the United States had unsettled her, and Victor, who had some mysterious job in Bristol, told anyone who asked him that he had been given leave in order to recover from some complaint which he didn't specify.
They came to see Eulalia one morning, and she gave them coffee and listened politely to their colourful accounts of their stay in America, regretted when asked that she was far too busy to return their visit at the moment, and hoped that she had seen the last of them. But they came again, and then Victor took to coming on his own and, never mind if she was gardening or busy about the cottage, he stood around, getting in her way until she begged him as nicely as possible not to call so often.
He had laughed that off with a speaking look. 'Oh, look, now Eulalia, we're old friends. I'm keen to resume our friendship and go a bit further.'
Her grey eyes flashed. 'That's a very silly remark; we never were friends, or have you forgotten? The odd game of tennis, seeing each other in other people's houses from time to time—so there's nothing to resume and certainly no reason for you to "go a bit further", whatever you may mean by that.'
'I'm thinking of settling down, Lally, and I've decided that I might marry you.'
'Don't call me Lally, and I don't care in the least what you have decided. I wouldn't marry you if you were the last man left on earth.'
He took it as a joke. 'Oh, come on, old girl. I'm quite a catch, you know—a fairly decent job, and there'll be some money when Mother and Father die, and until then we'll have your little nest-egg to fall back on.'
She looked at him with horror. 'What a perfectly dreadful thing to say. What gave you the idea that you could live off what you call my "little nest-egg"? Of all the colossal cheek. Go away, Victor, and stop bothering me. I don't like you and I'll be obliged if you don't come here again.'
He looked put out, but only for a moment. 'Taken you by surprise, haven't I? Think it over, Lally. Your future isn't exactly anything to get excited about, is it?'
'Get out,' said Eulalia. 'You're so conceited you can't see when you're not wanted or liked. Don't come back, either.' As he turned to go she added, 'And don't dare to call me Lally—that's only for my nearest and dearest.'
After he'd gone she stayed in the garden for a while; it would never do to upset Trottie. She dismissed his visit lightly when that lady asked what he had wanted and it wasn't until Peter was in bed that evening that Trottie said severely, 'I would like to know now, Miss Lally, what's upset you. It's that Victor, isn't it?'
So Eulalia told her, unaware that Peter was sitting at the top of the staircase listening to every word.
'He's pestering me, Trottie,' said Eulalia. 'He's got the idea that I've plenty of money and he thinks he can marry me and live on it—probably he'll want to live in this cottage too. I don't know what to do.'
Peter did, however. He crept back to bed and lay awake, his arm around Charlie. Here was a reason to write to Mr van Linssen, who had written his name and address and telephone number on a little card and given it to him when they had been in the garden together. It was a secret, he had said, just between the two of them, and if he was needed Peter was to write to him or telephone and he would come. 'You see,' Mr van Linssen had explained, 'Eulalia and Trottie haven't a man to look after them—you are a splendid help to them, but sometimes a man is needed.'
They had shaken hands on it.
Telephoning would be difficult but he could write a letter. He had enough money for a stamp, and when there was no one to see he took paper and an envelope from the kitchen drawer. He wrote it sitting up in bed the next night, addressed it carefully, stamped it and, when he went to the village shop with Lally after school, he posted it while she was buying the bacon Trottie wanted.
* * *
MR VAN LINSSEN, coming down to an early breakfast, found it beside his plate with the rest of his post and opened it first. He read the childish writing, frowning, and then giving a snort of laughter at Peter's urgent PS begging him to come quickly and marry his aunt Lally before Victor could!
He put the letter aside then and read the rest of his mail, applied himself to his breakfast and went to his study where he rang his secretary. That highly efficient lady listened to him without comment and then said, 'Well, Mr van Linssen, I'll do my best. You're due at the hospital in half an hour and I presume you will be there for most of the day. I'll contact your private patients with appointments for tomorrow morning and arrange for them to come on the following day or this evening. You have an outpatients clinic tomorrow afternoon at five o'clock.'
He thought for a moment. 'Do that, will you? I should be back some time during the late afternoon. I'll phone you then. Let me know later on how many patients will be coming this evening, will you?'
Dodge bowed a sorrowful head when he was told that his master would require breakfast at seven o'clock on the following morning. 'I need to go to the country, Dodge, but I should be back around four o'clock.'
'As you say, sir. May I remind you that you are taking Miss Kendall to lunch tomorrow?'
Mr van Linssen swore powerfully in his own language. 'Ring her, will you, Dodge? Tell her that I've been called away on urgent business.'
Dodge's voice was as mournful as it always was, but he hid a pleased smile. Miss Kendall didn't like him; indeed, he thought it likely that when she married Mr van Linssen she would see that he was dismissed. An observant man, he thought he had detected a certain reluctance on the part of Mr van Linssen to join in any of the social activities which his fiancée found so vital to her enjoyment of life. She would certainly be extremely put out, he reflected with relish, closing the door after his master.
Mr van Linssen worked his way through the day, operating all the morning, doing a ward round in the afternoon and then going straight to his consulting-rooms to see his private patients. It was almost eight o'clock by the time he put the key in his front door, to be met by Dodge with the observation that dinner would be on the table in twenty minutes or so, and would he like a drink at once?
'Give me ten minutes. I'll have a shower and change. No messages?'
'No, sir. I telephoned Miss Kendall and apprised her of the situation.'
'And?'
'She was a little put out, if I may say so, but will telephone you tomorrow evening.'
Mr van Linssen grunted a reply and took himself off upstairs, to come down presently, have a drink and eat his dinner, and now that he was free from his work he applied himself to the problem of Eulalia. She was becoming a liability, he told himself, and was quite old enough to take care of herself, but Peter's letter couldn't be ignored. It was best that he went to Brokenwell and saw what was happening for himself. Victor might be quite a decent chap, to whom Peter had taken a dislike, probably at the idea of his aunt getting married.
The September morning held a touch of chilliness as he got into his car and drove away. It was eight o'clock and the morning traffic was building up, but once he was free of the suburbs he sent the Bentley surging ahead. It was good to be free of London, even if only for a few hours, and it would be good to see Eulalia again, tiresome girl though she was.
He slowed the car through the village street very soon after ten o'clock and stopped before Ivy Cottage. The door was open and Trottie was polishing the brass knocker. Her nice elderly face creased into a wide smile as he got out. 'Well, I never did. Now, isn't this nice, and just in time for a cup of coffee. Peter's at school but Miss Lally's in the garden.' The smile went for a moment. 'That Victor's with her again. It don't matter what she says, he pesters her something shocking. Keep the front door locked and he climbs the fence into the back garden, if you please.'
Mr van Linssen bent to kiss her cheek. 'Ah, Victor—I hoped that I would meet him.'
'Is that why you're here? How did you know?'
'I think that had better be a secret, Miss Trott. Do you suppose that I might go into the garden?'
'You do that, my love. I don't doubt Miss Lally will be glad to see you.'
'The lesser of two evils?' suggested Mr van Linssen with a smile, and opened the back door.
Lally was at the bottom of the garden, picking the last of the apples, and Victor was leaning against a tree, facing the cottage, so that he saw Mr van Linssen first. Eulalia, who had been telling him in a forthright manner just what she thought of him, saw the look of surprise on his face and turned round to look herself. Mr van Linssen, treading lightly despite his size, was within a foot of her.
Before he could speak he had reached her, put a great arm round her shoulders and said breezily, 'Lally, my dear, I intended to phone you when I got back, but I thought I would surprise you.' He dropped a kiss on her cheek for good measure. 'Is this by any chance Victor, who has been so tiresome in his attentions?' He shook his head slowly. 'Really, young man, you must know by now that they are unwelcome. I suggest, in the friendliest manner, mind you, that you leave Eulalia alone—you mustn't poach on another man's preserves, you know.'
He smiled in a kindly way, aware of Eulalia bursting with rage at being called a preserve. 'I take it you understand me?' He was still smiling but his eyes were like cold steel, and Victor muttered that he was just going anyway.
'Good, good, and stay away, won't you?' suggested Mr van Linssen in the silkiest of voices. 'I trust that I have made myself plain?'
Victor mumbled again and hurried away, to be met at the kitchen door and ushered out of the cottage without waste of time by Trottie, who had been watching from the kitchen window. It was a pity that she had been unable to hear what had been said, but no doubt Miss Lally would tell her later. She took a newly baked cake out of the pantry and set it on the kitchen table with the coffee-cups, humming cheerfully.
Eulalia and Mr van Linssen watched Victor hurry away before she turned to face him. He spoke first. 'I must apologise for referring to you as my preserve—it seemed the best way of making that oaf understand.'
Having cut the ground neatly from under her feet, he waited quietly for her to speak. 'Yes, well, it did annoy me. It made me sound like a—a...'
'Preserve? Make no mistake, Eulalia, I could never think of you in that light. What a tiresome fellow he is.'
'Tiresome? Tiresome?' She was still angry and humiliated at having been found and taken by surprise. 'He's been the bane of my life.' She added defiantly, 'I've never encouraged him...'
'Well, no, I don't doubt that.' His tone was dry and she looked at him.
'Why are you here?'
'The warmth of your welcome flatters me, Eulalia!'
She went pink. 'I do beg your pardon, that was dreadfully rude. I'm a bit upset.' She gave a great sniff and looked away. 'Do you suppose he'll stay away from me now?'
'Yes. I think that I have given him to understand that I have—er—a prior claim.'
The pink which was ebbing away came flooding back. 'That's nonsense.'
'Of course it is. We must not forget that I am to be married at some future date, but this Victor doesn't need to know that, does he?'
'Well, it was very kind of you to—to pretend...' She paused and went on in a polite voice. 'I am most grateful to you, Mr van Linssen. Perhaps you would like a cup of coffee?'
'Thank you.' They started walking towards the kitchen door. 'Tell me, how is Peter enjoying his school?'
'He loves it, and he loves Charlie—the puppy. Trottie's got him in the sitting-room because he tried to bite Victor the other day.'
'Ah! I thought he was an intelligent dog when I got him!'
It seemed important to keep some sort of a conversation going. 'Do you have a dog?'
'Yes, in Holland. I live there for the greater part of the year.'
They had paused at the kitchen door. 'Do you?' asked Eulalia blankly. 'I thought you lived in London.'
He answered her gravely. 'When I am over here working, yes, I do.'
For some reason she felt snubbed, but some contrary imp moved her to ask, 'So Miss Kendall will live in Holland. Will she like that?'
He only smiled at her, so that she felt even more snubbed than before. Well, it had been silly of her to ask questions. She lifted her chin and invited him into the cottage.
The coffee was already on the table, and so was one of Trottie's cakes, already cut into generous slices. She poured his coffee, offered him cake and asked artlessly, 'Having a bit of a holiday, Mr van Linssen?'
'No, no, just a morning off. London is a delightful city, but now and again a breath of country air is pleasant.' He turned to Eulalia. 'Do you suppose that if I were to drive over to Peter's school I might be allowed to see him for a few minutes?'
'I don't know. They're a bit strict about strangers—not that you're a stranger, but they wouldn't know that.'
'In that case, perhaps you would phone them from the car and vouch for me? I can't come all this way without seeing him.'
They went out to the car presently and she phoned the headmaster and explained. 'And please don't tell Peter. Mr van Linssen would like to surprise him.'
So he went away shortly after that, saying that he'd call in to say goodbye on his way back, refusing Trottie's offer of steak and kidney pudding and one of her apple pies with real regret.
He was back within the hour, to stay only long enough to thank Trottie for the coffee and cake and express his hope to Eulalia that she would no longer be bothered by Victor's unwelcome attentions.
She brushed that aside. 'You saw Peter? He was surprised?'
He looked down at her pretty face, smiling a little. 'He seemed glad to see me. He looks very well. Country air suits him. It suits you too, Eulalia.'
He stood, still looking at her, and she thought with a pleasant little thrill that he was going to kiss her. He didn't, however, but got into the Bentley and drove away.
CHAPTER SIX
'WERE YOU surprised to see Mr van Linssen?' Eulalia asked Peter when he got home from school that afternoon.
'Yes, I was, but I did know he'd come and see me again, Aunt Lally.' He gave her a guileless look.
Mr van Linssen had told him that he had done quite the right thing in writing to him: 'For your aunt Lally mustn't be bothered by uncouth fellows like this Victor. Remember, Peter, that I will always come if you or she needs me.' He had smiled at the small trusting face lifted to his. 'You're happy here? I saw Charlie—he looks splendid, and Blossom is just the right companion for him.' He had told Mr van Linssen that he was very happy, adding that sometimes his aunt Lally looked sad.
'I suppose you can't do anything about that?' he had asked.
Mr van Linssen had looked grave. 'I think that perhaps in time I might be able to do just that,' he had said. He had gone away then, after slipping a pound into Peter's hand.
Of course, he wasn't going to tell Aunt Lally about their conversation, not that part of it, at any rate.
As for Trottie, she kept her own counsel. Gentlemen, especially those who had important jobs and were engaged to be married, didn't drive miles just to drink her coffee and eat her cake and arrive just when they were most needed... Someone had told him about Victor. She glanced at Peter, sitting at the table, doing sums. When presently Eulalia said suddenly, 'How did Mr van Linssen know about Victor?' she sounded suspicious.
Trottie said comfortably, 'The world's a small place, love. I dare say he met up with someone from round about here who mentioned it—you know what people are—and the rector was in London a week or so ago. Probably they go to the same club.'
A most unlikely thing, but since Eulalia knew as little about London clubs as Trottie did she agreed readily enough.
* * *
AS FOR MR van LINSSEN, he drove himself back to London, had the tea the faithful Dodge had ready for him, changed from country tweeds into sober grey suiting and equally sober silk tie, and took himself off to his clinic in Outpatients. He was invariably pleasant and very civil to those who worked with and for him, but today there was a warmth in his manner which surprised them. Outpatients Sister, a comfortable fortyish woman and married, remarked on it to her staff nurse.
'Perhaps he's in love.'
'Out of the question. He's engaged to that hoity-toity young woman who came last Christmas to see the decorations. A toffee-nosed creature she was, too.'
'He could still have fallen in love,' said the staff nurse shrewdly.
'And serve her right,' observed Sister.
Mr van Linssen was home again by seven o'clock, in time to change yet again, this time into a black tie, since he was invited with Ursula to a dinner party with some friends of hers. He had no wish to go, but he had seen very little of her lately and he must make amends.
She was looking particularly charming that evening in a dress of bright blue, the colour of her eyes, cut very low, which was a mistake, for her figure was what she described as boyish and the dress did nothing for her flat chest. Whatever Mr van Linssen's thoughts were about it he didn't give voice to them, but expressed a liking for the colour of the dress and suggested that they should be on their way.
'I've not had you to myself for days,' pouted Ursula, offering a cheek for his kiss, 'and do be careful of my hair, Fenno...'
He was acquainted with almost everyone there. His host and hostess were Americans who lived for a good part of the year in London in a large house in Hampstead, and their guests were as cosmopolitan as they were. Mr van Linssen's perfect manners concealed his boredom as he greeted everyone in turn, while Ursula flitted from one group to the next, trilling her light laugh, making amusing conversation, in her element. Watching her flirting with a youngish American he didn't know, he tried to imagine her as his wife and found it impossible.
Driving her back to her home later, he answered her remarks about their evening in an absent-minded manner so that she said crossly, 'Well you make it sound as though the whole evening was a bore. You really are getting a bore yourself, Fenno. Once we're married, I intend to entertain a lot—I've heaps of friends. Think how influential they will be—you'll get well known, you might even get a knighthood.'
He forbore to tell her that he was already well known in the medical world—a world which mattered to him; besides, how could he, a Dutchman be offered a knighthood? If his services to surgery ever merited it, then his own queen would reward him for them. He was suddenly tired, too tired to argue with Ursula. He saw her into her home, wished her goodnight, refusing an offer to go in for a cup of coffee, and drove himself to his own home, thankful that he had several appointments in Holland and would be leaving on the following day for a week or more.
He phoned Ursula when he got in and listened patiently while she grumbled at him for not letting her know sooner. 'That nice man I was talking to—he's from Chicago—invited us both to have lunch with him on Sunday. He's rented an apartment in Richmond while he's staying here—I said we would go, and now you've spoilt it all.'
'I am sorry I forgot to tell you. There's no reason why you shouldn't go without me, is there? Make my apologies. I cannot change any of the appointments I've made in Holland.'
'Oh, well, I'll go on my own—there'll be several of us there.' She added peevishly, 'You won't be able to carry on like this when we're married, you know.'
She rang off and he went along to his study to catch up on his paperwork. Then, after a busy day on the morrow, he caught an evening flight to Schiphol, where he was met by a grey-haired man who shook his hand and led him outside to where a dark blue Jaguar was parked.
Mr van Linssen, reverting to his mother tongue, remarked that it was nice to be back home. 'Everyone well, Pete?' he wanted to know as he took the wheel.
'Mevrouw arrived this afternoon. She hopes to see something of you while you are here, mijnheer, and that you will have time to see the rest of the family.'
'I shall be busy, Pete, but I should be home each evening with my mother, and I'll certainly find time to visit my sisters.' He glanced at his companion. 'You're well? And Anneke?'
'Both well, I am happy to say, mijnheer. We hope that you will be here for some time.'
'Ten days, no longer.'
'You will perhaps spend more time in Holland when you are married?'
'My fiancée isn't keen on the idea, Pete. I must bring her over for a few days to meet the family.'
Pete remained silent. He had been with the family since Mr van Linssen was a little boy, running the household while his wife did the housekeeping, and after so many years in the family service he was regarded as a friend. After a few moments he said, 'She could not be anything but happy to live here, so quiet and peaceful by the lake, and yet so near Amsterdam and Utrecht.'
Mr van Linssen had driven the short distance south to Aalsmeer and turned on to the Hilversum road, but some six miles before he reached that city he turned into a country road running between the lakes which stretched for some miles on either side of it. It was pleasant country, giving one no inkling of the nearness of Hilversum and Utrecht, with trees bordering the road, pleasant villas at the water's edge, and from time to time a village. He was going south now towards Utrecht, but only for a short distance before he turned between brick pillars into a short drive and stopped before the house at its end.
It was a solid house, built of rose-coloured bricks, with a gabled roof and a great many windows. Those on the ground floor were tall and wide, but the nearer the roof the smaller they became, with leaded panes and painted shutters. He got out of the car and went up the double steps to the canopied front door while Pete got his bags from the boot. The door opened at his touch and he went inside to the wide hall, with its panelled walls and high plastered ceiling, and was met by a very small, very thin woman with brown hair, barely streaked with grey, and brown eyes. She burst into voluble Dutch, wringing his hand and then smiling broadly as he bent to kiss her cheek.
'Anneke, it's good to see you again.'
'You are alone?' she wanted to know. 'The young lady is not with you? We had hoped to see her...'
'Not this time, Anneke. Is my mother in the drawing-room?'
'Yes, and waiting for you. I will bring coffee, and presently there is a good supper for you.'
'Good, I'm famished.' He smiled at her and crossed the hall to open the double doors at one side and go into the room beyond.
His mother came to meet him as he went in, a tall woman with silver hair worn in an old-fashioned style, framing an elderly face which must at one time have been beautiful. Her eyes were blue and just now they were alight with pleasure. 'Fenno, my dear, this is delightful. You did not mind that I came here before you had arrived? I wish to see as much of you as possible and I know you will be away for most of your day.'
He kissed her cheek. 'Mama, there is nothing I could wish for more but to find you here waiting for me. I hardly saw you when I was last in Holland.'
'You are alone? You have not brought your fiancée with you?'
He answered her briefly. 'No, she did not wish to come.'
His mother gave him a sharp glance. 'Of course, it would be dull for her as you will be away for so much of the time.' She smiled at him. 'I must wait until the wedding, perhaps?'
His 'Perhaps' was uttered casually as he went to open the doors into the grounds at the back, to be greeted by the dog who came bounding in at his whistle.
Anneke came in then, with coffee and the information that supper would be served in twenty minutes or so. 'You waited for me?' he asked his mother.
'Yes, dear, you may well be gone in the morning by the time I get down, and probably you will be too tired to talk much in the evening. Will you be operating?'
'Yes, at Leiden. I shall be there for three days and then I go to Utrecht and finally to Amsterdam. You will stay?'
'Willingly, Fenno.' She spoke readily but she searched his face anxiously. She understood him very well: reserved to the point of coldness, generous to a fault, a steadfast friend, a compassionate man towards his patients and, hidden away beneath his beautiful manners, a romantic. Now there was something wrong, and most likely something to do with this Ursula he intended to marry. Even though she had never met her, Mevrouw van Linssen had taken a dislike to her; she had sent excuses for not accompanying Fenno on several occasions now, and it was obvious that she had no wish to meet his family. She began to talk about his younger sister who had just had a second son, and presently, when they had supper together, she gave him a light-hearted account of his friends' and family's doings since he had been away.
It wasn't until the following evening as they sat before the fire in the drawing-room, the dog at their feet, that he told her about Peter.
'He sounds a nice child,' said his mother, and hoped for more. Into the companionable silence she asked, 'You say he's an orphan, poor boy. I suppose his lives with his grandparents?'
'No, a cousin, and an old housekeeper.'
More promising, reflected Mevrouw van Linssen. 'How dull for him—I hope he has lots of friends.'
'Not dull at all. His cousin is in her late twenties.' He paused and she waited for more, but all he said was, 'The housekeeper worked for Eulalia's grandmother until she died. She had nowhere to go, so they made a home together, and then took on Peter when his parents were killed.'
He began to talk about something else, leaving his mother thoughtful.
He didn't speak of it again until the day before he was to return to England, when he was driving his mother back to her small town house in den Haag, and then in reply to her carefully careless question.
'See Peter? I doubt it. He lives in the Cotswolds. Besides, his cousin dislikes me.'
His voice was harsh, and she contented herself by saying casually, 'The Cotswolds are lovely, aren't they? All those charming houses.' But she thought to herself, so it is this aunt with the pretty name. Why didn't she like Fenno? She had no idea how to answer that question. Instead she begged him to give her love to Ursula. 'And do tell her that she must come and meet me before you marry,' a remark which he replied to with a grunt which could have meant anything.
* * *
THE AUTUMN DAYS were shortening but the fine weather still held. Eulalia dug away at the garden, gradually reducing it to some kind of order, while old Bob, a bit too stiff for hard digging, saw to the fruit-trees and pruned anything that needed it. She had planted as she cleared, and already there were neat rows of winter cabbage, spinach, beet and turnips. It was a bit late in the year to plant, but the soil was good and the garden sheltered. When she wasn't busy in the garden she helped with the chores and did the shopping if Trottie's feet were painful. She had half expected to see Victor, but there was no sign of him. Mr van Linssen's bit of play-acting had frightened him off, and after a few days she stopped looking over her shoulder each time anyone went past the cottage, and on the following Sunday, although he was in church, sitting in his family pew, he avoided looking at her.
Trottie, who had been there too, remarked on that as they walked home with Peter between them. 'Depend on it, Miss Lally, he had a nasty fright; Mr van Linssen being such a big gentleman and with such a cold eye when it suits him. Happen that Victor thinks you're promised.'
Eulalia tried to look unconcerned and blushed instead, so that Peter wanted to know why she had got so red. 'And why does Victor think you're promised?' he enquired. 'And what does that mean?'
Eulalia had always done her best to be a good guardian and that meant telling the truth as much as possible when he asked awkward questions. 'It's a rather old-fashioned way of saying you're engaged.'
Peter gave a little skip. 'To Mr van Linssen? How absolutely super. He'll be my cousin too, won't he?'
'No, dear, I must explain. He—just pretended, so that Victor would stop bothering me. He's going to marry Miss Kendall. He was just doing a kind act.'
She couldn't bear to see Peter's disappointed face. 'Never mind, love, I'm on the look-out for a millionaire who'll look after all of us forever and ever!'
'Oh, well,' said Peter. 'I suppose he'll do if we can't have Mr van Linssen.'
'Well, no, we can't,' agreed Eulalia, and felt unutterably sad at the thought.
Presently, when they had had their dinner and Peter was in the garden with Blossom and Charlie, and Trottie was having what she called her 'lay down', she brushed the sadness away; she had no reason to be sad about the man. They disagreed every time they met and he had a nasty knack of making her feel foolish. She was, of course, grateful to him, for he seemed to have a way of turning up at the right moment, but he was, she told herself, an arrogant man, given to sarcasm and with the gift of bringing out the worst in her. She would, she told herself resolutely, forget him.
It wasn't easy, but, the garden dealt with for the moment, she was able to turn her attention to plans for the shop. She had renewed old acquaintances by now and Peter had friends in the village. She went out to coffee-mornings, afternoons of tennis and the occasional dinner party, so that by the time she was ready to open the shop there would be a number of people who would come and buy flowers, out of curiosity at first and then, hopefully, because the shop and its contents were attractive. It would have to be just before Christmas, when she might hope to get orders for flower arrangements as well as cut flowers.
She spent her evenings making lists, planning how much money she dared spend and debating ways and means with Trottie. She intended to get Jacob to put up a small glasshouse attached to the bathroom wall, and get planning permission to knock a hole in the side wall of the garden and put a gate there, something she had discovered could be done since it wouldn't alter the appearance of the cottage. She still had to go and see Mr Willett and get his advice, and before that make a few tentative enquiries in the village to see what people thought of the idea. Not everyone, of course, but the rector, and old Colonel Grimes up at the Manor, and the doctor, and Mr Wedge at the Boy and Horseshoe...
She went one morning to see him first, leaving Peter with Trottie. It was mid-morning and there were only two people in the bar, while Mr Wedge leaned on his elbows, discussing politics. Eulalia, waiting until he had made short work of the government and politicians in general, finally asked for a cup of coffee. 'And if you could spare five minutes—I'd like your advice.'
'Lor', Miss Lally that's given for free, likewise the coffee. Trouble, is there?'
'No, no, Mr Wedge, just an idea I want to tell you about.'
The two men leaning on the bar came nearer. They were both elderly, long since retired from working on local farms and eager to hear what she had to say.
'You'm Miss Lally,' said the oldest man. 'I remember you when you was a little maid. Living in that Ivy Cottage that gentleman bought.' He turned to Mr Wedge. 'Remember, Tim? Him with that great big car. 'Ad it all cut and dried 'fore you could say knife. Wanted to know where that Mr Willett 'oo saw to Mrs Warburton's business, poor soul, lived. Mark you, 'e were a fool to buy the place. Leastways, it seemed so, but Miss Lally 'ere 'as done it up a treat.'
It took Eulalia a few moments to realise what the old man was saying. She went so pale that Mr Wedge cast her an anxious look, not sure what was wrong but sensing that something was amiss. He said, 'How about another half-pint, William, though you ought to be getting home or you'll have your missus after you.' It was a relief when William nodded reluctantly and made for the door with a cheerful 'See you' and a wave.
He was barely out of the door when Wedge said loudly, 'I'll fetch that cup of coffee, Miss Lally, now it's quiet. Tim here's a bit deaf so you can say what you want.'
Eulalia said slowly, 'If you don't mind, Mr Wedge, I'll come back later—I've just remembered something...' And she followed William out of the door. He was already halfway up the street but she caught up with him easily.
'May I walk a bit of the way with you? I want to ask you something?'
'Why not, missy? Time's me own when the wife's not badgering me.' He gave her a shrewd glance. 'Something I said back there in the pub?'
'Yes, the gentleman who bought Ivy Cottage. Did he give his name, was he English?'
'Didn't give no name, not to me, anyway. As for being a foreigner I wouldn't know. Spoke the Queen's English a sight better than me. Quiet kind of man and 'andsome. Pots of money, no doubt, with that car. It were a Bentley motor car, like Sir Percy over at Bowle House drives.' He stopped and took a look at her. 'Know 'im, do you, Miss Lally?'
'Oh, yes,' said Eulalia, in a voice which boded ill for Mr van Linssen, 'I know him.'
She bade him goodbye presently and walked back to Ivy Cottage, going at a great pace, propelled by rage. Trottie looked up from her knitting as she went in. 'And what's upset you, Miss Lally? Don't tell me it's that Victor...'
Eulalia stood in the centre of the little room, magnificent in her rage. She said between her teeth, 'Not Victor. Mr van Linssen. How dare he?'
Trottie put down her knitting. 'Well, tell old Trottie all about it,' she invited.
'This cottage—he bought it. William Thorpe told me, at least, he was talking to Wedge and I asked him.' She gave a great heaving breath. 'Don't you see, Trottie, it belongs to him? There's something fishy about that; he's played a trick on me.' She stopped to think. 'Do you suppose that he bought it from that great-uncle in Australia? No, of course he couldn't, and besides, I've got the deeds. I don't understand.'
Trottie knitted half a row. 'You'd best go and see that Mr Willett. He'll have the answer, I've no doubt.' She finished the row. 'That old William's getting on a bit, doesn't always know what he's talking about.'
Eulalia said doubtfully, 'Yes, perhaps that's it. All the same, I'm going to take the deeds and catch the bus into Cirencester this afternoon.'
'You do that,' advised Trottie. 'Don't go blaming that nice Mr van Linssen until you know he's guilty.'
'If he is, I'll never speak to him again.'
'Well, you're not likely to see him, are you, love?' said Trottie briskly. She folded up her knitting. 'I'll get us a bite to eat and you go and tidy yourself. You can't go to Cirencester in that old dress.'
It was mid-afternoon by the time Eulalia arrived at Mr Willett's office and requested his clerk for a few minutes of his time. She didn't have to wait long. Mr Willett came out of his room to meet her, shook hands in the most friendly fashion and ushered her in. He had seen her white face and eyes dark with rage, and embarked most prudently upon a series of questions as to her health, the health of Miss Trott, the well-being of Peter and a lengthy observation concerning the pleasure of living in a village again after the drabness of the Cromwell Road.
Eulalia replied politely and waited until he paused for breath.
'Did you know,' she asked without preamble, 'that Mr van Linssen had bought Ivy Cottage? And what about the money—all that money? And was there a great-uncle in Australia?'
Mr Willett sat back, his hands before him in an attitude of prayer, and looked grave. 'First, will you tell me from whom you have heard all this?'
So Eulalia took a calming breath and told him, and then sat waiting for him to answer.
'It is not within my power to discuss this matter with you, Eulalia. You must understand that. I am not at liberty to disclose my clients' private affairs.'
'That's absurd—however am I to find out the truth if someone doesn't tell me?'
Mr Willett switched on his intercom and requested two cups of tea. 'I can but advise you. Since you are anxious to solve the matter, I suggest that you should write to Mr van Linssen and put the matter before him.'
The tea came and she sipped it while she thought. 'But you did know about it?' she wanted to know.
Mr Willett nibbled a biscuit. 'My dear Eulalia, I have already told you that I am not in a position to reveal such information.'
'He was your client, though?' said Eulalia. She got no reply other than an offer of a second cup of tea. She liked Mr Willett, who had done his best for her when her grandmother had died, and now she said, 'All right, I'll write to him and see what he says. Thank you for your advice.' She got up. 'I'll let you know about his reply.'
He escorted her to the door and shook hands. 'I'm sure it can be settled,' he assured her. 'Some misunderstanding!'
He went back to his office and sat down to think. His first impulse was to telephone Mr van Linssen and tell him what had occurred, but on second thoughts he decided against it. He suspected that Mr van Linssen had more than an ordinary interest in Eulalia and who was he to interfere?
As for Eulalia, she went back to Ivy Cottage, assured Peter, back from school, that she had gone to see Mr Willett about a trifling matter, and remarked to Trottie that it had been very pleasant in Cirencester but the days were getting rather chilly, and after their supper she helped Peter with his homework and saw him into bed, accompanied by Charlie and Blossom. Only when he was asleep did she sit down and tell Trottie what Mr Willett had said. 'I'm going up to London tomorrow morning,' she declared. 'If I catch an early train I can be there by eleven o'clock. I'll go to Maude's and find out if he's there, and if he isn't I'll go to his house and wait for him.'
'Supposing he does own this house and the money too, what will you do, Miss Lally? You can give him back almost all the money, but you can't give him back this place, leastways, if you do, we'd be out in the street. And Peter? I know his school fees are safe but he's got to live somewhere, hasn't he? And him so happy with the garden and Charlie and Blossom?'
'I thought about that on my way home, Trottie. I'll pay back the money I haven't spent and I'll get work, any work, so's we can go on living here, and I'll pay the rent. In that way we are not beholden to him.' She swallowed back tears. 'Oh, why did he do it?'
Trottie had her own ideas about that but she didn't say anything, only remarked presently that that seemed a sensible thing to do and what kind of job had Eulalia in mind?
'Anything—in a supermarket? I shouldn't think you need qualifications for that—only references—or in a café or a restaurant.' She looked at her old friend. 'I'm so sorry, Trottie—all those dreams...'
'At least we're out of London, love, you're young and strong and Peter's happy, and I'm content like I never was in Cromwell Road.'
Eulalia gave her a hug. 'You're an angel. I'll make us a hot drink and we'll go to bed.'
She told Peter at breakfast that she was going to London for the day. 'A bit of business, nothing to worry over. I'll bring you back a Beano from the bookstall.'
'Oh, thanks, Aunt Lally, and will you have time to see Mr van Linssen?'
She wasn't going to lie to him. 'Darling, I don't know where he is, he might be in Holland, but if I do see him—and that's not likely, is it?—I'll give him your love.'
As soon as she had taken him to school she caught her bus and then the train, had a cup of coffee at the station buffet and caught a bus going west which would take her almost to Maude's Hospital. All the way there she had rehearsed what she would say; she would be quiet and cool and businesslike. She had, she honestly thought, bottled up her rage and humiliation; she would guard her tongue and not answer him back, however infuriating he became. She realised that if it was a misunderstanding she was open to his ridicule, but that was a small risk.
She got off the bus and went along to the entrance of the hospital and enquired of the porter if Mr van Linssen was there. The head porter looked at her most suspiciously. 'Patient, are you? You're in the wrong door, miss, and his clinic isn't till one o'clock. Better come back in an hour or so and go to the outpatients' door round to the right as you go out.'
He turned to answer the phone and she went out into the forecourt again. She was in luck. She would join the patients for his clinic; he would have to see her then. It meant that she would have to catch an evening train back home and probably miss the last bus to the village, but she could get a taxi.
She wasn't far from the park and there was a small café near there where she could get a sandwich and some coffee. The walk did her good, and she sat for half an hour eating her small meal before going into the park and walking briskly along its paths. It was a fine autumn day but there was a nip in the air, and she wished she had worn something warmer. Her jersey dress and jacket looked good, and to boost her self-confidence she had worn a hat, a small-brimmed velvet one, years old but dateless. She wasn't sure why she had taken such care with her clothes, perhaps to impress upon Mr van Linssen that she wasn't penniless and didn't need his charity. She even went over her speech again as she walked, and presently made her way back to the hospital and walked boldly into the outpatients' hall. It was crowded, which suited her very well, and there were notices on the wall pointing out where the patients for the various clinics should sit. Mr van Linssen's benches were already almost full when she approached them, to be halted by a fussy little woman who asked for her card.
Eulalia gave her her brightest smile. 'I'm not a patient. I have to see Mr van Linssen on a private matter and I haven't time to go to his home. May I sit here and see him when his patients have been attended to?'
The little lady pursed her lips. 'It's most unusual. I don't know what Sister will say.'
'If I'm not a patient, surely she need not be bothered,' Eulalia pointed out.
'That's true. You are personally acquainted with Mr van Linssen?'
'Oh, yes. Over a period of some months. He is a friend of my cousin.'
'Oh, well, I dare say that's all right. Sit on the far side of the back row. You'll have to wait a while—he's got a very full clinic today.'
Eulalia sat down where she was told and looked around her. A sister was bustling to and fro, so were several nurses, and presently two young housemen crossed the hall and went through a door close to the front bench, followed almost at once by a woman in a white overall with a great many papers under her arm, and five minutes later there was a wave of shuffling and head-turning and Mr van Linssen, looking quite different in his long white coat, crossed the hall. He was talking to a younger man and didn't look at anyone. She watched his massive back disappear through the door and felt a pang of something. Panic? Fear at having to face him? Pleasure at seeing him again? She didn't pursue the thought.
The next three and a half hours seemed endless. She longed for a cup of tea but she didn't dare leave her seat in case he went away. The benches slowly emptied, few remaining patients were in the hall now, and very soon she would get her chance. She went over her prepared speeches once more and, as the last patient was called in, moved to the front bench.
The man came out again in ten minutes, followed by the two housemen, a nurse and the older man with Sister. That lady pulled up short when she saw Eulalia. 'You're very late. Where are your notes? I doubt if Mr van Linssen will see you.'
Eulalia had slipped past her. 'I'm not a patient but I have to see him before he leaves.' She closed the door in Sister's astonished face and stood looking at Mr van Linssen, writing busily at his desk.
He didn't look up. 'Sister, we'll admit that last man...' He did look up then. His blue eyes, suddenly alert and cold, studied her for a moment, then he got slowly to his feet.
'Oh dear, oh dear,' said Mr van Linssen, and gave her a mocking smile which tore to shreds all her coolness and calmness and dignity and reduced her speeches to utter nonsense.
CHAPTER SEVEN
HE CAME FORWARD and offered her a chair. 'Do sit down. I can see that you are bursting with the wish to give vent to your rage and to hurl abuse at my head.' He glanced at his watch. 'I can spare you ten minutes.'
Eulalia found her voice. It was rather shrill and not quite steady but she knew what she wanted to say. 'I do not care whether you can spare the time for me. I shall say what I have come to say, and if it takes more time than ten minutes, that's just too bad.'
He eyed her with appreciation; bad temper suited her. Her lovely grey eyes flashed, her cheeks were delightfully pink. She sat down deliberately, put her handbag on the floor and folded her hands on her lap. He saw that they were shaking and her charming bosom was heaving in a beguiling manner, and he sat back in his chair. He had been taken by surprise but he rather thought he was going to enjoy the next half-hour.
He said, as politely impersonal as a doctor to his patient, 'I'm listening, Eulalia.'
'Don't call me Eulalia,' she snapped.
'You shouldn't say that. I might be tempted to call you something else.'
'Oh, be quiet, do,' she snapped. Her carefully rehearsed speeches had flown out of her head. 'You tricked me, didn't you? There wasn't an uncle in Australia—how did you get Mr Willett to agree? And why did you do it?'
She paused, and he said smoothly, 'You are so sure that I have done this, but you have no proof. You may be mistaken, in which case your journey here, rather gratifying though it may be to myself, has been a waste of time and money.'
She stared at him, suddenly uncertain, and then remembered William.
'I have proof. William told me—he's an old man who lives in the village. He was in Wedge's bar when you were there. He remembered you because you had a Bentley motor car.'
Mr van Linssen laughed. 'How very lowering for my ego. Now that you have proof, what do you intend to do about it, Eulalia?'
'Give it all back, of course. I can't do that all at once, but I haven't used much of the money, and what I have used I'll pay back if it takes me the rest of my life. And we'll leave the cottage...'
His slow smile mocked her. 'Yes? And where will you go?'
'I'll find somewhere. I'm not a fool.'
'No, but pig-headed in the extreme. Come down off your high horse and use some sense. What about Peter and Miss Trott? Are they to suffer a homeless plight with you?'
He was sitting back in his chair, very much at his ease, and she felt rage bubbling up inside her again. She said in a cold voice with only the faintest quiver in it, 'I am not pig-headed.'
'No, no, of course not—a slip of the tongue. Let us say rather that you are a strong-minded female who likes her own way.'
The interview which she had planned so carefully had now become a fiasco and it was all his fault. Somehow she had been made to feel guilty. She sat silent, trying to regain her composure, not helped by him glancing at the watch he took from his waistcoat pocket.
'You are returning this evening to Brokenwell?'
'Yes.' She got up. 'There's no point talking to you. I'll go and see Mr Willett. I'll send you a cheque, and perhaps you would be good enough to tell me what rent you require?'
All he said was, 'You've missed your train. When is the next one?'
'Eight o'clock.'
'You won't be home until nearly midnight. Sit down, Eulalia.'
So she sat down again, quite glad to do so, for she was hungry and her feelings had left her tired and somewhat dispirited. Just for a moment she didn't care what was to happen next.
Mr van Linssen lifted the receiver and dialled. 'Dodge, will you go to the study and look in the phone book for the Boy and Horseshoe at Brokenwell and let me have the number?' In a few moments he said, 'Thank you,' and put down the receiver, to pick it up again and dial once more. 'Mr Wedge? Van Linssen here. Would you be good enough to send a message to Miss Trott at Ivy Cottage? Tell her that Miss Warburton will be staying as my guest until tomorrow morning and will return home some time during the day. Many thanks.'
He put the receiver down and Eulalia gasped, 'You can't do that...'
'I just have,' he pointed out in a reasonable voice, and sat back again, watching her.
Eulalia drew a long breath. She said in a voice that was getting rather shrill, 'I do not care for your arrangements, Mr van Linssen, I intend to go home.'
She got to her feet again and this time he did the same. 'Yes, yes.' He sounded impatient. 'But since I owe it to Miss Trott and Peter to return you safely to Brokenwell, you have no alternative but to do as I say.'
'You are an abominable man,' said Eulalia loudly, 'and I dislike you. I dislike you even more than I do Victor. You are high-handed and sarcastic and—and unkind, and if I had that money with me now I'd throw it at you, and the cottage as well.'
The absurdity of this remark didn't strike her, and whatever Mr van Linssen thought about it remained concealed by a perfectly expressionless face. He picked up the phone once more and spoke into it. 'Geoff? I've been called away. Will you collect the notes from Outpatients? I'll see to them later. Yes, in an hour or two.'
That done, he took Eulalia's arm and walked her briskly out of the room and across the hall and into the forecourt, bidding a surprised nurse and a porter goodnight as he went.
Eulalia went silently. There was a great deal she wanted to say, but she was so angry that her thoughts weren't making sense, and putting them into words would be useless. She sat beside him in the car, as still and stiff as a poker, her lovely nose in the air, vexed even more by Mr van Linssen's casual manner. He could have been delivering a parcel for all the notice he took of her.
She said suddenly, 'I am doing this against my will and I protest very strongly.'
'Don't be so silly,' observed Mr van Linssen in a voice to dampen down even the strongest feelings.
That was the extent of their conversation until they reached his house.
Dodge, advancing to meet them as they went in, showed no surprise, but inclined his head gravely and bade her good evening and stood listening to his master telling him to take Miss Warburton to the guest-room so that she might tidy herself.
'Miss Warburton has missed her train. She will spend the night here and return to Brokenwell in the morning. Could we have a tray of tea in ten minutes or so, and dinner at the usual hour? See that Miss Warburton has all she wants, will you?'
He turned to Eulalia. 'Do come down when you're ready. I'm sure you would like a cup of tea. The cure for all ills in this country, is it not?'
He waited until she had followed Dodge upstairs, and then went along to his study to let his registrar know that he would be back at Maude's in a couple of hours.
Eulalia was ushered into a charming room at the back of the house, overlooking the tiny garden beyond which there was a narrow road and on the other side of it a row of mews cottages. She looked out of the window and then turned to survey the room. It was quite small but most elegantly furnished, with a peach silk bedspread and curtains, a satinwood dressing-table and two small easy chairs and a thick cream-coloured carpet, and when she peered round a door beside the bed she discovered a bathroom, equipped with thick peach-coloured towels, soap, powder, bath essence... There was even a toothbrush and hairbrush and comb.
Perhaps Ursula comes here, thought Eulalia, unaware that it was Dodge's pride that unexpected guests would find everything they could need.
She poked at her hair, powdered her nose, applied lipstick and went downstairs, outwardly serene, inwardly quaking.
The drawing-room was as beautiful as she had remembered, more so now perhaps, since there was a bright fire in the steel grate and a small table had been drawn up to it on which was a silver teapot and delicate cups and saucers and a plate of fairy-cakes. Mr van Linssen drew a chair forward for her and asked her to pour out in a no-nonsense voice, and sat down again in a vast wing-chair. It was all very cosy and domestic, made more so by the presence of Mabel, curled up before the fire. It was all so normal, too, thought Eulalia. It seemed right that they should be sitting there facing each other, drinking their tea and eating Dodge's delicious little cakes. She gave herself a mental shake. She mustn't allow herself to be soothed; Mr van Linssen would take advantage of that and make some preposterous suggestion about the cottage and all that money...
He did no such thing, however, merely made absent-minded conversation, offered the cakes, had a second cup of tea, and then excused himself with the plea that he had some telephoning to do, leaving her with Mabel for company and a pile of newspapers.
She put these down presently and got up and wandered round the room, examining the pictures and the books housed in the handsome breakfront Georgian bookcase. They were handsomely bound, probably first editions, she thought, and some of them had titles in what she supposed was Dutch. She walked to the window and stood looking out into the already darkening evening. It was quiet, and she thought it was almost as peaceful as Brokenwell. She was still standing there when Mr van Linssen came back, offered her a drink and, when she had sat down, went to his chair again.
She answered his remarks with polite brevity, although this didn't appear to discompose him in the least, for he made easy conversation until Dodge came to tell them that dinner was served.
Eulalia, whose insides were hollow with hunger, was sensible enough to polish off lobster bisque, chicken à la king and chocolate pudding, as light as air and smothered in cream. It made no difference, she told herself, that she was at the table of a man she disliked; she had been famished and it was good sense to eat a meal, even though she sat unwillingly at his table. Mindful of her manners and swallowing her temper with the soup, she replied suitably to her companion's casual talk and had a second helping of pudding. They had their coffee at the table and, as soon as they had drunk it, Mr van Linssen got up.
'You'll forgive me if I leave you in Dodge's care? I have to return to Maude's and I may be back late. If I don't see you in the morning, tell him which train you wish to catch and he will see you on your way.'
He didn't wait for her answer but gave her a curt 'Goodnight' over his shoulder as he left the dining-room, and a moment later she heard the front door close. It was strange, she reflected, that she should feel lonely the moment he was out of the house.
Dodge ushered her back into the drawing-room, offered magazines, switched on the television set concealed in a corner of the room, and indicated that suitable night-things had been put in her room for her use.
'Early-morning tea at half-past seven, miss, if that is agreeable to you?'
'Yes—yes, thank you. I should like to catch the ten-forty train.'
'Certainly, miss. If there is something else you require, just ring the bell by the fireplace.'
'I think I'll go to bed early...'
'In that case, I wish you goodnight, miss. I trust you will sleep well.'
She thought it unlikely; there was too much on her mind. She had a long hot bath, doing sums in her head, calculating to the last penny how much she could pay back at once, and there was the rent...
She got into bed wearing the silk and lace nightie she had found draped over a chair. Whose? she wondered as she put it on, and then forgot about it as she climbed into bed and settled against the pillows. She still had a lot of thinking to do—she switched off the bedside lamp and lay in the dark. What was she going to tell Peter? She was asleep before she had the answer.
She woke to find a stout woman in a print overall arranging a small tray of tea by the bed. She drew back the curtains and wished Eulalia good morning in a cheerful cockney voice, adding, 'Breakfast in half an hour, miss,' and went away.
Eulalia sat up in bed and drank her tea and ate the wafer-thin slices of bread and butter. There was a lot to be said for luxury; she only hoped that Mr van Linssen's Ursula appreciated the prospect of a comfortable future. She had a shower, dressed, and went downstairs, torn between the hope that Mr van Linssen would be there and a wish never to set eyes on him again.
He was there at the breakfast-table in a charming little room at the back of the house. He got up as she went in, wished her good morning with impersonal politeness, expressed the hope that she had slept well and invited her to sit down. So she sat, poured her coffee, accepted the offer of scrambled eggs from Dodge and started her meal, turning over in her mind suitable topics for conversation. Never mind that she detested the sight of him sitting there so handsome and self-assured, good manners demanded that. While she was still formulating a remark about the weather, he got to his feet again. 'You will forgive me? I have an early appointment. Dodge will see you safely away.'
'Oh—I'll write—no, I won't. Mr Willett can write about paying back the money and the rent and...'
He said with barely concealed impatience, 'Yes, yes, do whatever you wish. Please give my regards to Miss Trott and my warmest greetings to Peter.'
'He asked me to give you his love.' She saw him glance at his watch and hurried on. 'And thank you for your hospitality, you have been most kind.'
His smile mocked her. 'You're too old to tell fibs,' he observed and went away, closing the door gently behind him.
She finished her breakfast, her thoughts in a fine muddle, and Dodge came presently to tell her that he would drive her to the station in good time to catch her train.
'There's really no need. I can get a bus and I'll leave with time to spare.'
'We have a small car for use in town, miss. Mr van Linssen asked me to see you safely on to your train.'
His look was so reproachful that she gave in.
The small car turned out to be a beautifully kept Rover. Still looking melancholy, Dodge drove through the traffic, parked the car and accompanied her on to the platform, pausing on the way to purchase a couple of newspapers and a magazine or two which he handed to her as she got into the train. She thanked him and shook his hand and he gave her a rare smile.
'I wish you a safe journey, miss, and hope to see you again.'
'Thank you, Dodge. I don't expect to come to London again. Thank you for making me so comfortable.'
He stood on the platform as the train drew away. His mournful expression didn't reflect his thoughts. She would be back if the master had anything to do with it. He dismissed Miss Kendall without a second thought—she hadn't a chance against this nice young lady...
Eulalia got back to Ivy Cottage in time to share her lunch with Trottie, and that lady, taking one look at her downcast face, said comfortably, 'No need to talk for the moment, Miss Lally, take off that jacket and sit down. I've some pasties in the oven and a cup of tea to wash them down.'
Over their second cup of tea Trottie observed mildly, 'That was kind of Mr van Linssen to send a message and look after you for the night. I was getting that uneasy.'
Eulalia put down her cup. 'I went to the hospital and saw him there. He—he found it amusing that I had found out about the cottage and all that money. He didn't make any excuse or give a reason—he called me pig-headed. I wish I had thrown something at him...'
'You always were an impetuous girl,' said Trottie. 'You came to some agreement?'
'Yes—no. I don't know, he just didn't care. I said I'd see Mr Willett and send back as much money as I had and pay rent for this cottage. He wasn't a bit interested,' she added crossly. 'He practically ordered me to spend the night at his house.'
'Well, love, London's a nasty place after dark for young women on their own. He did quite right.' She glanced at Eulalia's unhappy face. 'You won't be seeing him again?'
'Certainly not. Besides, he has no reason to come here.'
Trottie could think of a very good reason but she didn't say so. Mr van Linssen was old and wise enough to arrange his life to his own satisfaction. As for Lally, once she had simmered down and thought things over... Trottie, an incurable romantic, nodded to herself.
Eulalia said thoughtfully, 'I don't need to tell Peter anything, do I? I won't be able to open the shop this year. I'll get a job. It'll have to be part-time so that I can fit in the buses... I can tell him that I've decided to learn a bit more about it before starting on my own. Could we manage, Trottie?'
'Of course we can, Miss Lally. We'll have all the veg and fruit we need—we can splash out a bit at weekends when he's home.' She added bracingly, 'It's a sight better than Cromwell Road.'
'Oh, Trottie, I know, only I feel humiliated; he was amused, just as though it was a joke. I felt like someone to whom he's thrown money in the street.'
'Now, now, Miss Lally, you didn't ought to think that. He's a good man, only he don't let it show.'
'I hate him,' said Eulalia fierily.
All the same, she presented her usual serene face when Peter came back from school, gave him a suitably expurgated version of her visit to London, added Mr van Linssen's greetings and answered his eager questions as to how he had looked and what he had said.
He asked wistfully, 'He didn't say he'd come and see me?'
'Well, no, darling. He leads such a busy life. When he took me to his house yesterday evening he only stayed a little while, because he had to go back to the hospital, and in the morning when I went down to breakfast he had to go within a few minutes.'
'When he marries,' said Peter, 'his wife and children won't see him very often, will they?'
She had a quick mental picture of him sitting at the head of his breakfast-table with a smiling wife facing him and children on either side of him—several children, she reflected, he was a man to want a family. She shook the thought away; if he married his Ursula he would be lucky to have one lonely child, and he or she would probably be out of sight in the nursery. She felt a sudden pang of pity for him. She must stop thinking about him, and when she did, it must be with dislike.
* * *
HER PITY WAS wasted, of course. Mr van Linssen needed none; he was in complete command of his destiny, even though it would need some rearranging before it was to his liking. Even the arrival of Ursula on the following evening did nothing to destroy his calm.
She brushed past Dodge as though he wasn't there and flung into the dining-room where Mr van Linssen was eating his dinner.
'Where were you last night?' she demanded. 'Dulcie Shaw saw you in the car with a girl. Who was she and why was she with you?'
He put down his napkin and got to his feet. 'My dear Ursula, this is an unexpected pleasure. You won't mind if I finish dinner? I had no time for lunch today. Can Dodge bring you something?'
'I dined hours ago,' she snapped, 'at the Shaws'—Dulcie was there, of course, sniggering about it. You should have been with me...'
Mr van Linssen selected cheese and took a biscuit. 'My dear Ursula, I seem to remember that you refused my invitation to the theatre yesterday evening on the grounds that you would be bored and would much prefer the Shaws' company.'
'That's quite different. It's a boring play, from all accounts, and why should I have to spend a tedious evening when I might be having fun?'
'Why, indeed? Do you find me tedious, Ursula?' He was watching her under lowered lids.
She pouted and said in a wheedling tone, 'Well, you are rather dull, darling. You still haven't told me who she was.'
'I don't intend to tell you, Ursula. Shall we go to the drawing-room for coffee?'
Her face became ugly with temper. 'I'm going, and I hope you'll be sorry for being so beastly to me—and don't think you can get round me with a stupid bunch of flowers.'
She flounced into the hall, and Dodge, looking suitably grieved, opened the door for her and bade her goodnight in a doleful voice before going off to his kitchen, where he fell to whistling cheerfully while he collected the plates and cutlery ready for the daily woman to clean when she came in in the morning. Very satisfactory, he decided. Now it only needed a bit of luck...
* * *
WHICH, AS IT turned out, was by no means as unlikely at it seemed. It was a Saturday afternoon and Trottie and Peter had gone to the village shop, leaving Eulalia at home, writing careful answers to the offers of work in the local weekly paper. They didn't intend to buy much: a tin of corned beef—Trottie was clever at serving it up in a hundred and one different guises—dog food, cat food and, since it was the weekend, Peter had his pocket-money to spend. Fifty pence a week wasn't much but he laid it out carefully, and Mrs Trusk, who owned the shop, allowed him to take his time deciding between fruit-gums and humbugs. She wasn't busy, anyway, and she and Trottie had plenty to gossip about.
He made his choice, and Trottie moved away from the counter, caught her foot on the corner of a box of oranges and fell. She was a stout little person and fell hard. Peter had rushed to help her up but she put out a shaking hand. 'No, love—leave me—I've hurt my leg.' She gave him a lop-sided smile and fainted.
Mrs Trusk, bending over Trottie, said unnecessarily, 'She's fainted. Oh, dear, whatever shall we do?'
'Ring the doctor,' said Peter, 'and get a glass of water.' He picked up one of Trottie's hands. 'Trottie—it's all right, we'll look after you.'
His voice quavered a bit; he was, after all, only eight years old, despite his efforts to be calm, like his idol Mr van Linssen.
Trottie opened her eyes. 'I know you will, ducks—don't let anyone move me.'
The doctor was on his rounds and his wife didn't know where exactly. By then several people had gathered round. 'Ring the ambulance,' said Mr Wedge and then, 'Someone get a cushion for Miss Trott's head.' He looked around him. 'And someone fetch Miss Lally.'
Peter slipped behind the counter again and went to the phone. Glad that he had Mr van Linssen's phone number, he dialled it, and when someone answered he said in a rush, 'I must speak to Mr van Linssen, it's very important. Tell him it's Peter.'
He sighed gustily when the well-remembered voice said in his small ear, 'Peter, what's wrong? Can I help?'
'It's Trottie, she's fallen down and she can't get up because of her leg and the doctor isn't here. They've sent for an ambulance but it's got to come from Cirencester and someone's gone to fetch Aunt Lally...' He paused on an indrawn breath, determined not to cry but wanting to very badly.
'Good man. You did quite right to ring me. Now, listen very carefully. I am going to get into my car and drive to Cirencester. It so happens that I have a good friend there. He'll allow me to take a look at Trottie and do anything that's necessary. Lally will have to go with Trottie. I want you to find Mr Wedge and ask him to go with you to the cottage and stay there until I come. I shall have Dodge with me and he will stay with you as long as it is necessary. I should be with you in a couple of hours. There's no need to tell Lally; she has enough to worry about. Tell her you'll be quite all right until she gets home. Have you got all that, Peter?'
'Yes, Mr van Linssen. I knew you'd come.'
He put the receiver back and joined the group around Trottie. Eulalia was kneeling beside her now, holding her hand and talking to her in a quiet voice, and above the babel of voices was the raucous sing-song of the ambulance. Peter touched Eulalia on the arm. 'You'll go with Trottie?' he asked. 'I'll be all right until you get home.'
'But someone must stay with you.'
'I'll get Mr Wedge—I know he will.'
Eulalia nodded. 'That's splendid of you, Peter. Look, stay here with Trottie while I run back and get her overnight things. She may need to stay in hospital.' She gave his small shoulder a squeeze and darted away, and by the time the paramedics had Trottie on a stretcher, her leg tenderly encased in a plastic splint, she was back again.
'Go home with Mr Wedge, darling, and stay indoors. The key's on the hook. I should be back soon after tea, but you get a meal if you're hungry, and feed Blossom and Charlie.' She gave him a quick hug. 'Bless you, Peter.'
There was no time for more. He watched the ambulance drive away and then went home. Mr Wedge went with him, a comforting arm around his small shoulders. 'There's bound to be some news quite soon, and I'll stay just as long as I'm needed.'
The cottage was very quiet. Mr Wedge made some tea and cut some bread and butter. Peter, with his mouth full, explained about Dodge.
'Now that's a grand idea. Nice chap, is he, this Dodge?'
'Oh, yes, Mr Wedge. He looks after Mr van Linssen.'
Mr Wedge, his mind set at rest, poured the tea.
* * *
DODGE WAS IN the kitchen, preparing a béchamel sauce with which to coat the chicken he was preparing for that evening's meal—to be served earlier than usual, since Mr van Linssen was to escort his Ursula to some late evening function or other. He was quite unprepared for his master's sudden appearance.
'Ah, Dodge. Leave everything, pack two overnight bags, one for me, one for you. Ten minutes—you can have ten minutes.'
'Sir,' said Dodge in a pained voice.
'Yes, yes. I'll explain as we go. Now hurry, there's a good chap.'
Something in Mr van Linssen's voice made him do exactly that; within ten minutes he was coming down the stairs at twice his usual stately pace, a bag in each hand. A minute later he was sitting beside Mr van Linssen, listening to that gentleman's quiet voice explaining. Dodge had never looked anything other than melancholy all his life but now he allowed himself a smile. Here was a bit of luck, unless he was mistaken.
'Miss Kendall,' he ventured. 'You were to attend a function with her.'
'Oh, lord, yes. Dodge, pick up the phone and ring her now. Tell her that I'm called away on an urgent case.'
Dodge listened unmoved to Ursula's cross voice, expressed his regret and put the phone back. After that they didn't speak. The motorway was fairly empty: the weekenders had already gone and the evening traffic wouldn't start up for another two or three hours. Mr van Linssen sped along the fast lane and Dodge prayed that there would be no police patrols about.
They were nearing Cirencester when Mr van Linssen finally spoke. 'Dodge, I'll drop you off at Ivy Cottage. See to the boy, won't you? Get a meal if it's needed. I'll probably drive Miss Warburton back later, when we know what the damage is.'
He turned off the motorway and took the road to Malmesbury, and presently drove slowly through Brokenwell and stopped at Ivy Cottage. They both got out and Peter saw them from the window, and the next moment he had unlocked the door. He said in a small voice, 'I knew you'd come,' and Mr van Linssen put a great arm around him and turned to shake Mr Wedge's hand.
'Many thanks. I'm grateful,' he said quietly, and then, to Peter, 'Well, of course, friends help friends, you know, and how splendid of you to know what to do. I've brought Dodge with me. He's going to stay here while I go and see how Trottie is. He'll stay here tonight too, so if I don't bring your aunt Lally back by bedtime, you go to bed as usual.'
Peter nodded. 'All right, but you'll tell me if anything's wrong?'
'At once. That's a promise. Now I'm off. Tot ziens.'
'What does that mean?' asked Peter, as he and Dodge went back into the cottage, after waving goodbye to him and to Mr Wedge.
'See you later,' said Dodge. 'Now, how about us doing some cooking when we've had a cup of tea? I'm a dab hand at it.'
* * *
EULALIA SAT BY Trottie in the ambulance, holding her hand. Trottie's face was pale and her eyes were closed, but now and again she opened her eyes and smiled. 'Silly me,' she whispered. 'Ought to know better at my age.'
Eulalia murmured in a comforting voice, 'Mrs Trusk leaves boxes all over the shop. Don't worry, Trottie, we'll have you home again in no time at all.'
At the hospital she was asked to wait while Trottie was examined. It seemed an age before a nurse came to tell her that she could sit with her for a while. 'She's been X-rayed,' the nurse explained, 'but we'll have to wait for a little while until they're looked at. She's a bit drowsy—she was given something for the pain.'
Trottie was half asleep. 'It don't hurt now,' she assured Eulalia. 'I'll be all right, Miss Lally, do you go home to Peter.'
'In a little while. He's quite all right, Mr Wedge said that he would stay with him. He'll know what to do. Don't worry, Trottie, everything's fine.'
Trottie dozed off and Eulalia sat holding her hand, thinking about the future. It would have to be re-planned. She couldn't take a job until Trottie was fit again, and if it was a badly broken leg—and from the glimpse she had had of it when the paramedics had examined it, it certainly looked as if it was—then she would have to stay at home for some time. She couldn't work in the village even if there was work to be had, for everyone would want to know why she—possessed of her own cottage and a handsome bank balance—should need a job, and sooner or later Peter would hear of it...
A young doctor interrupted her thoughts, beckoning her away to tell her that Mr Wyatt, the consultant orthopaedic surgeon, would like a word with her. She was led away to a small office and found him sitting at a desk and Casualty Sister standing beside him.
'Miss Warburton?' He shook hands. 'You must be anxious about Miss Trott. The X-rays show that the two lower bones of her left leg are broken. Rather nasty breaks, I'm afraid, which will need surgery. This will mean a stay in hospital while the wound heals. The leg will be put in plaster and there is no reason why she shouldn't return home once she has got used to crutches. She has every chance of recovering completely.'
'When will you operate?'
'Within the next hour or so. Miss Trott is shocked—a brief rest is to her advantage.'
'I'd like to stay until the operation is finished.'
'Of course. Would you like to stay with Miss Trott now for a while? When she goes to Theatre, Sister will show you where you can wait.'
She went back to Trottie, who was awake now and rather tearful.
'It's all right, Trottie,' said Eulalia. 'I've seen the surgeon. He's going to see to your leg very soon and I'll stay until you are back in bed.'
As she spoke she was vaguely aware that someone had come into the department. There was a rumble of voices, and a moment later the cubicle curtain was drawn aside and Mr van Linssen, looking as calm and at ease as though he had just got out of his armchair, came to stand by the couch.
He nodded at Eulalia, smiling a little at her open-mouthed astonishment, and then turned his attention to Trottie, who looked up at him and smiled.
'Now I'll be all right,' she said.
CHAPTER EIGHT
MR VAN LINSSEN took her hand in his. 'Of course you will. Mr Wyatt and I are going to have a look at that leg, and presently we'll put the bones together and give you a plaster.' He looked across at Eulalia.
'If Eulalia would wait somewhere while we are doing it...'
She bent and kissed Trottie's cheek, not looking at him. 'I'll see you later, Trottie, when you are back in your bed.'
He gave her a searching look as she went past him. 'Don't worry—such an easy thing to say, but I promise you Trottie will be as good as new.'
She nodded because she believed him. Even though she disliked him, she told herself, he had never lied to her.
There was no one else in the waiting-room. She leafed through the pile of old magazines and drank the tea a nurse brought her, and tried not to think about Trottie in Theatre now, with Mr van Linssen bending over her unconscious little body. She found to her shame that she was snivelling, and wiped her eyes and blew her nose in a vain effort to stop the tears. They went on trickling down her cheeks and presently she gave up mopping them. There was no one to see...
Mr van Linssen, still in his green theatre kit, his mask pulled down under his chin, loomed in the doorway. 'You had better mop your face,' said he cheerfully. 'Trottie is already awake. If she sees you in tears she'll probably insist on going home.' He added, 'There's nothing to cry about, you know.'
Her hanky was sodden, and she wiped her eyes with the back of her hands like a child. 'I wish I knew the right words to tell you what I think of you,' she said in a watery voice, and then, remembering, 'But you've been very kind. I'm—I'm very grateful.'
'Yes, yes, leave the gratitude for the moment. Come and see Trottie.'
She got up then and went to the door. 'She's going to be all right? Was her leg very bad?'
'Nothing which couldn't be put right. I've set the bones and her leg is in plaster. Mr Wyatt will keep her here for a few days—I had to make a small incision in order to get the bones in alignment. Once the wound has closed she can come home. Come along, now.'
Trottie was in a small ward with half a dozen other patients, in a corner bed with the curtains still drawn round it. Mr van Linssen pulled them apart and gave Eulalia a small shove. 'You can have ten minutes,' he told her, and went away to where Sister was waiting for him at the other end of the ward.
Trottie was awake, nicely cushioned with pillows, her plastered leg under a cradle so that it would dry and allow the wound, visible through the little window cut in the plaster, to be inspected.
'I'm such a nuisance, Miss Lally.'
'Rubbish, Trottie. You've been marvellous. Mr van Linssen says you will be able to come home very soon and everything's fine. I'll be going home presently, but I'll come tomorrow with some more nighties for you. What about some books?'
'Just my knitting, love. Is Peter all right?'
'Yes. Mr Wedge is with him, and I'll be home in time to get his supper and get him to bed.' She saw Trottie's eyes close and bent and kissed her. 'Sleep well, Trottie, there's nothing to worry about.'
Trottie opened an eye. 'Well, of course not, with that dear man looking after us.' The eye closed, and in a few moments Eulalia left her.
Sister was in the ward talking to a nurse, but there was no sign of Mr van Linssen. Eulalia wondered why he had been there and supposed that he was called to any hospital which might need him. He was already on his way home, probably. Sister came to meet her.
'You'll be coming tomorrow? If you would bring a dressing-gown and more nighties—we shan't need to keep Miss Trott in for more than a few days, a week at the most. Come when you like in the afternoon or evening. Goodnight, Miss Warburton.'
Eulalia said goodnight and went slowly down the staircase. She would have to get a taxi to Brokenwell, for the last bus would have left by now. She stopped to count the money in her purse, afraid that she wouldn't have enough, and was interrupted by Mr van Linssen saying rather testily, 'Come along, Peter will be wondering what's happened to you...'
'You're still here...?'
'Well, of course I am. Now, do come along like a good girl. The car's on the other side of the forecourt.'
She hung back. 'I don't know how you got here,' she began. 'I mean, it was a surprise, but very lucky for Trottie, but you've taken care of her and there's no need to drive me home, it's out of your way.'
'Nothing of the sort. Dodge is with Peter and I fully expect that between them they will have got a meal for us.'
'Dodge?' asked Eulalia faintly. 'He's here too?'
She was thrust into the car without further ado and he got in beside her. 'Company for Peter.'
She turned to look at him as he drove away. 'I don't understand.'
'Peter had the good sense to phone me before the ambulance arrived.'
'Phone you?' She frowned. 'But we haven't got a phone. Besides...'
'The village shop has, and he used it.'
'And you came, just like that?'
'Yes.'
'But how did he know your phone number?'
'I gave it to him.'
She thought this over. 'Why?'
'Various reasons.' He had slowed the car and stopped outside the cottage, and its door was flung open at once and Peter came racing out.
'Is Trottie all right? Did you operate? Will you explain it to me later?' He beamed at Mr van Linssen and gave Eulalia a hug. 'You've been crying, your face is all blotchy.' He reached up to kiss her. 'Never mind, Aunt Lally, Mr Dodge has cooked a most gorgeous supper.'
Mr van Linssen was standing by the car watching them, and she said quickly, 'Please come in and have supper. You must be hungry, and I know Peter's dying to talk to you.'
He thanked her gravely, searching her face, and she turned away feeling shy all of a sudden, relieved to find Dodge standing just inside the door. He looked as downcast as usual as he greeted her. 'I have prepared a meal, miss, and I trust that you do not consider it presumption on my part. Young Peter has been of great assistance in its preparation.'
'How very thoughtful of you, Dodge. Supper would be lovely, and I'm sure Mr van Linssen is hungry.'
'Famished. Peter, if you'd like to sit here beside me I'll explain about Trottie while Eulalia tidies herself.'
'What you mean is,' said Eulalia very clearly, 'I must go and wash the tears from my face.' She glared at him, and went into the bathroom and stayed there for much longer than necessary, trying to regain her composure. When she went back into the kitchen, Dodge was dishing up and Mr van Linssen and Peter, heads together, were far too absorbed to notice her, or so she thought.
She offered to help Dodge, who accepted with dignity as he dished soup into the plates and removed a pie from the oven. 'I ventured to make sufficient pastry for a second pie, miss. I thought that you might like it for cold tomorrow. Steak and kidney with a trace of onion.'
'Did I have any steak and kidney in the house? I don't remember...'
'Peter and I visited the butcher, miss. He has excellent meat.'
Mr van Linssen had got up and was pouring sherry. 'Something smells delicious, Dodge. Have a glass of sherry before we start on it?'
'I haven't any sherry—' began Eulalia, and was interrupted by Dodge.
'We visited Mr Wedge, miss, in order to tell him that he had no more need to worry about Peter, and I, quite by chance, noticed a particularly good sherry there; a little stimulant is sometimes necessary.'
Mr van Linssen hid a smile and they drank their sherry and sat down to their supper.
The talk, naturally enough, was of Trottie. 'We'll fetch you directly after lunch tomorrow,' said Mr van Linssen. 'Trottie will be feeling quite herself by then and will no doubt be pleased to see visitors.'
Eulalia said quickly, 'There's no need—I mean, Peter and I can go, but you must want to return to London.'
'Certainly not. Pray don't deprive us of a day in the country. Dodge certainly deserves a day out, don't you, Dodge?'
'Indeed I do, sir, and I trust that I may have the opportunity of meeting Miss Trott—a lady of courage and spirit, I gather.'
Eulalia ate her soup and her pie and the crème brûlée Dodge had conjured up, and discovered that the future wasn't as black as she had thought it to be. Mr van Linssen had given her a detailed account of Trottie's injury and said confidently that there was no reason why she shouldn't be back and getting around with crutches in a very short time. 'And the sooner she is back pottering around the house the better. We'll have to change the plaster later on, and she'll need a quick check-up from time to time. That's no problem. I can drive down and see her here; there is no need for her to wait around at the hospital...I'll talk to Wyatt about that.'
'So you'll come again,' shrilled Peter happily.
'If Eulalia allows me to do so.'
He looked at her and gave her a small, mocking smile and she said coolly, 'Of course. You're very kind.' And because he was still smiling, she added, 'Peter, it's time you were in bed. You've had such a busy day and thank you for being so quick to help Trottie. I'm proud of you.'
'Well, Mr van Linssen wasn't here, so I had to get him, didn't I?'
He shook hands with Mr van Linssen, then with Dodge, and wanted to know if he had to have a bath.
'Have it in the morning, dear. I'll be up in two ticks to make sure you're in bed. Only clean your teeth.'
'While you're tucking him up, we'll wash up before we go.'
'Go? Not back to London?'
'No, no. Dodge, I feel sure, has booked rooms for us at Mr Wedge's.'
'Oh.' She stood uncertainly. 'I'm afraid I've not enough rooms here.'
'You have been most kind giving us supper.'
'Which Dodge cooked...'
'But you were not compelled to invite us.'
Peter came out of the bathroom then and she went upstairs with him, and when she came down again presently it was to find the washing-up done and Mr van Linssen arranging the spoons and forks tidily in their drawer while Dodge hung up the tea-towels. 'There was no need,' she began. 'You've both done all the work. Thank you.'
'Dodge is a dab hand at washing dishes, and I'm learning fast,' said Mr van Linssen. 'Goodnight, Eulalia.' He walked across the room to her, bent and kissed her, and went through the door, leaving her with her mouth open.
'Time for a nightcap before we go to bed,' observed Mr van Linssen to Dodge, and led the way down the street to the Boy and Horseshoe.
As for Eulalia, she stood for quite some time, doing nothing at all, trying to convince herself that she didn't like Mr van Linssen and having finally to admit that, despite his offhand manner and his tiresome habit of always being right, she liked him very much.
You can stop there, my girl, she told herself, he's all but a married man.
She went to bed presently, peeping into Peter's room to find him fast asleep with Charlie and Blossom curled up on the end of the bed. She thought of Mr van Linssen over at the Boy and Horseshoe and wondered if he was asleep too. It would be nice to see him tomorrow, she thought as she closed her eyes, but he shouldn't have kissed her. Not like that, for it hadn't been a social peck, far from it. And she had enjoyed it.
She and Peter went to church in the morning, then went back to eat Dodge's excellent pie before collecting such things as Trottie might want for the next few days, and that was barely done before the Bentley drew up before the door.
Mr van Linssen greeted them pleasantly, suggested that Charlie might go with them, settled the three of them in the back, waited patiently while Eulalia went back to make sure that Blossom was indoors, and with Dodge beside him drove to the hospital, where he persuaded Charlie to stay in the car and led his little party inside.
Trottie was sitting up in bed, looking small by reason of the cradle in the bed, but her colour had returned and her hair was brushed back into its usual severe bun. She beamed at them all and looked enquiringly at Dodge.
'Miss Trott, this is Mr Dodge, who runs my home for me.' Mr van Linssen smiled at them both in turn. 'I'm sure he'll want to tell you how much he likes Ivy Cottage. Eulalia and I are going to talk to Sister for a few minutes. When we come back, Peter, I don't think anyone would mind if we took a look round together.'
He looked at Eulalia then, an unsmiling look, and she found herself blushing under it, quite unable to look away from him. She might have stood there for untold moments if Peter hadn't said, 'Do hurry, Aunt Lally, there's such a lot to see.'
She walked beside him as they went down the ward and into Sister's office, where they were joined by the young doctor who had first seen Trottie in Casualty. He eyed Eulalia with open admiration and treated Mr van Linssen with a respect which made her realise what an important man he was in his profession. Miss Trott was doing well, he assured him, and continued in technicalities, leaving her to listen to Sister's reassuring remarks about Trottie. Presently they went back to the ward and Peter skipped away with Mr van Linssen, while she sat down beside Trottie's bed and listened to Dodge discussing the best method with which to make choux pastry, his usually sombre face positively animated. She glanced at Trottie, whose cheeks were nicely pink. She was smiling at him while she contradicted him flatly, something he took in good part.
Back at the cottage, it seemed only polite to ask them in for a cup of tea, an offer which Mr van Linssen accepted with alacrity. 'We shall be leaving shortly. I have an engagement this evening and we must get back. I'm sure that Trottie will go on well, but if you are worried please do not hesitate to let me know. I'll be in touch with Mr Wyatt, who will let you know when she may return home.'
She thanked him, poured the tea and watched the cake she had baked early that morning being demolished. Not a word had been said about their previous meeting. Presumably it wasn't to be referred to again and everything was to be left for Mr Willett to deal with.
They got up to go presently, and Peter asked eagerly if Mr van Linssen would come again soon.
As he always did, Mr van Linssen gave him a serious answer. 'Perhaps not here, Peter. I shall certainly go to the hospital when the time comes, to take off Trottie's plaster and put on a fresh one, and just to make sure that she's as good as new.'
'You wouldn't have time...?'
Eulalia said in a wooden voice, 'Peter, dear, Mr van Linssen's a very busy person. I expect he'll come if he has the time, but his time isn't always his own. He can't do what he likes...'
Mr van Linssen grinned.
* * *
DRIVING BACK TO London, he observed to Dodge, 'Miss Trott is rather a nice person, isn't she?'
'A charming little lady, sir. I must say I was much taken with her. We got on famously.'
A remark which gave his master a good deal of satisfaction. In the intervals of their desultory conversation he bent his powerful brain to set his plans for the future in motion. As they were nearing the end of their journey he said carelessly, 'I may want you to drive down again, take Miss Trott flowers and so on—I can't get away, and if there are any small problems you can let me know.'
'With pleasure, sir.' And Dodge did that rare thing, he smiled.
* * *
WATCHING THE BENTLEY'S tail-lights disappear along the village street, Eulalia reminded herself that allowing Mr van Linssen to occupy her thoughts was a waste of time, and downright dangerous now that she had at last admitted to herself that she liked him after all. Her efforts to forget him were frustrated by Peter, who wished to talk about him at length, and despite herself she found that she was talking about him with as much enthusiasm as Peter.
The next day, however, with Peter at school, she shut him from her mind, although he did have a nasty way of popping back into her thoughts at odd moments. Still, she had a lot to do before she caught the bus to visit Trottie in the afternoon. Peter was to go back with the rector's son until she got home, and Jacob had promised to feed and exercise Charlie and keep an eye on Blossom. The village, sympathetic to a man, were only too willing to help in any way that they could. She shopped quickly, prepared a meal for the evening, packed the things Trottie had asked for and caught the bus to Cirencester.
Trottie looked quite her old self. 'I've been out of bed,' she said proudly. 'Home by the end of the week, Mr Wyatt said. You're managing, Miss Lally?'
Eulalia assured her that she was, handing over the knitting, several magazines, more nighties and the last of the roses from the garden before sitting down to talk.
'That's a nice man, that Mr Dodge,' said Trottie. 'We got on a treat. Fair took to him, I did.'
'He is nice,' agreed Eulalia. 'He and Peter get on famously.'
'He's devoted to Mr van Linssen, thinks the world of him.' She looked at Eulalia over her spectacles. 'Says he works too hard, loves his work.'
Since Eulalia made no reply to this, she began to talk about something else and didn't mention him again. As Eulalia said goodbye she observed, 'Not very happy, are you, Miss Lally? Still bothering about the cottage and the money?'
'No, no, I'm going to see Mr Willett tomorrow and then forget about it.'
'But we can't manage unless you get a job, and I'll not be of much use for a bit.'
'Don't worry about it, Trottie, of course we'll manage, we always have. It'll be lovely to have you back, we do miss you. I'll be in tomorrow about the same time.'
Going back in the bus she pondered the future. She would have to ask Mr Willett to delay the payment of the rent for a few weeks. The money could be paid back at once, the sooner the better, although she would miss it fearfully, and as soon as Trottie could be left alone she would find work in Cirencester or Malmesbury. There was no good in brooding over it.
She showed a cheerful face to Peter when she collected him from the Rectory, and regaled him with a description of her visit to Trottie over their supper. 'I'm going again tomorrow, Peter, but I won't go the next day because it's your half-day from school and I thought we might go and look for cob-nuts.'
She saw Mr Willett the next day and was a little surprised that he agreed readily to return what money remained in the bank. 'As to the rent of the cottage, there is no hurry for that, for Mr van Linssen's solicitor hasn't decided how much it will be. I'll let you know in due course.'
When she saw Trottie she told her that everything had been arranged and there was absolutely no need to think any more about it. 'And I'll not come tomorrow, Trottie, since it's Peter's half-day, but I'll be in the following day.'
When next she saw Trottie she was sitting out of bed, her plastered leg supported on a pillowed stool and a vase of yellow roses on the table beside her. 'Nice, eh?' she wanted to know as Eulalia bent to kiss her. 'That nice Mr Dodge came to see me yesterday, would you believe it? Brought them roses and a great box of chocolates and stayed talking for an hour or more. Said he had a bit of time to himself and fancied a nice drive into the country. We had ever such a nice talk.'
'Trottie, you've got a beau!'
'Go on with you, Miss Lally, and me nigh on sixty. Mr Dodge—he's sixty next month—don't mean to leave Mr van Linssen's service, been with him for years.' Her usually cheerful voice sounded wistful. 'He did say he might pop down again some time—wants to show me an old cookery-book he had from his granny. He still uses the recipes in it.' She added, 'Mr van Linssen's been in Scotland, operating on some bigwig, then he went to Ireland to operate on some poor men who had their kneecaps shot away. He's a dab hand with bones, Mr Dodge said.'
The village rallied round when Trottie came home; the local taxi fetched her and refused to take his fare, the butcher supplied his choicest leg of lamb, the greengrocer carried up a basket of vegetables and the baker offered a cake, and Mr Wedge, not to be outdone, delivered a dozen bottles of milk stout. She held court for several days, sitting in the living-room, and stumped around on her crutches, making sure Eulalia was keeping the kitchen as she liked it. She slept in the dining-room, for the stairs were beyond her, on a bed Eulalia had borrowed from the Boy and Horseshoe, and life quickly settled down again. But it wasn't safe to leave her, Eulalia had decided. She would have to wait until Trottie had had her plaster changed and was quite confident on her crutches.
* * *
TROTTIE HAD BEEN home for two weeks when Mr Dodge arrived in the Rover. He had brought flowers again and a basket of fruit, not the apples and pears which were so easy to come by in the village, but pineapples and grapes and hot-house peaches. He stayed for tea, and since he had come soon after lunch Eulalia felt free to go into Cirencester once more and see Mr Willett. Not that she got any satisfaction from that gentleman. There was no news of the rent, she was told, these things took time. So she went back home and found Trottie and Mr Dodge in the kitchen making cucumber sandwiches and toasting tea-cakes. A prosaic occupation and yet she detected a distinct whiff of romance.
It wasn't until he was on the point of going that he handed Eulalia an envelope. It contained a scrawled note from Mr van Linssen, informing her that he would be coming the following morning to take Trottie to the hospital. 'About ten o'clock,' said Dodge, 'if Miss Trott could be ready by then. I am to say that there will be no need for you to accompany her and she will be brought back as soon as possible.'
'Is something wrong?' Eulalia looked anxiously at Dodge. 'There's nothing in this note...'
'I apprehend that Miss Trott is to be examined to make sure that the wound on her leg has healed properly.' He added with an air of reproach, 'Mr van Linssen would have told you if there was anything you should know.'
She agreed meekly.
Mr van Linssen arrived at ten o'clock the next day, pleasantly refused the coffee she offered, and lost no time in packing Trottie neatly into the car. His manner was brisk. Obviously he was a man with no time to waste, although he spared a moment to tumble Charlie and lay a gentle finger on Blossom. Rather daunted by his manner, Eulalia offered lunch on their return. It was refused with polite regret, so that she said with a sudden burst of temper, 'I can't think why you should spend your valuable time driving all this way. We are most grateful, of course, but I can easily hire a car next time.'
He turned at the door as he left the cottage, and gave her a look—it was a look to melt her bones and she took a step backwards, blinded by the sudden shock of it. This was neither the time nor the place in which to fall in love, and if she wasn't careful she would make a fool of herself. It was a mercy that he didn't like her overmuch; everything he had done for them was because he liked Peter...
He got into the car and drove away and she made herself smile and wave to Trottie, wedged into the back seat, but alone in the small sitting-room there was no need to smile. She felt overwhelming relief that she hadn't lost her head and flung herself at him, but he had looked at her...
She must have been mistaken. His manner had been brusque, even if polite. She would need to match her manner with his, and once Trottie was well there would be no need to see him again—she had said that several times already and each time Fate had stepped in.
Anxious to forget her unhappy thoughts, she flung herself into an orgy of housework.
The morning became noon and then afternoon and there was no sign of them. Eulalia ate a sandwich and made a cup of coffee and tidied herself. They would certainly want tea...
She was in the kitchen and didn't hear the Bentley's silent stop. They were in the sitting-room before she realised it. She cast a satisfied eye over the scones she had just taken from the oven, switched on the kettle and went to meet them.
Mr van Linssen was helping Trottie off with her coat. 'Everything is exactly as it should be,' he observed. 'In a few weeks the plaster can be changed and in the meantime she may get around on her crutches, as long as she doesn't get tired.'
'That's great. Tea's ready.' Eulalia didn't quite look at him.
'I must leave you to enjoy it. I've an engagement this evening.'
His Ursula, of course. She said brightly, 'Oh, I'm sorry you can't stay. Thank you for coming—it made it so easy for Trottie.'
She saw him to the door, looking no higher than his chin and longing for him to kiss her again. But he didn't. He said nothing at all, shook Trottie's hand and was gone, all within the space of a few minutes.
'I made some scones,' said Eulalia. 'I thought he might have stayed, but of course he wouldn't want to, would he? Not after the fuss about the money and the cottage. Perhaps I should have said something about it...'
'Best leave well alone,' said Trottie, 'and I could do with one of those scones, love. I had a nice lunch at the hospital while my plaster was drying. Ever so kind they were, all trooping around behind Mr van Linssen like the stars around the sun. Real famous he is, so one of the nurses told me, travels all over the place putting bones to rights.'
Eulalia listened eagerly. Any crumb of news about him was to be treasured and sorted and stored away. Loving him, she could see, would be a great waste of time but she wasn't sure how to stop it. Perhaps once she had got over the first delicious thrill of it she would be able to damp it down.
She fetched the scones and made the tea and listened to Trottie's account of her day, and presently she went to fetch Peter from the Rectory and the evening's activities swamped any private thoughts.
* * *
THE WEEKS WENT by, enlivened by visits from Dodge, carrying flowers for Trottie and sweets for Peter. They looked forward to seeing him although, to Eulalia's sorrow, he never mentioned Mr van Linssen. It was obvious that he was taken with Trottie and she with him; they went for short, careful walks together and Trottie looked ten years younger. It seemed very likely that they would marry, and Eulalia, while happy to know that her friend's future was secure, wondered how best she could rearrange her own. If and when Trottie married Dodge she would, of course, take her pension with her and there would be no money at all. The problem would be to find work which fitted in with being at home for Peter when he got back from school each day. It would have to fit in with the buses going either to Cirencester or Malmesbury and allow her to be at home when he returned. It was a worry which kept her awake at night, one which she felt she couldn't share with Trottie.
It wasn't until Dodge had driven away on one of the frequent visits that Trottie said, 'Miss Lally, dear, Dodge and me are wishful to marry, but not until the time's right. Dodge will tell Mr van Linssen and bide by what he says.'
Eulalia gave her a hug and wished her happy and said light-heartedly that she and Dodge were made for each other. 'He's a good man, Trottie, and I know you'll be happy. What fun to have a wedding in the family.' Later, though, when Trottie had gone to bed, she sat in the kitchen, staring at the wall, wishing with all her heart that by some mysterious means Fenno van Linssen would come and sort out her life for her.
* * *
HAD SHE BUT known, that was exactly what he was doing. Dodge had apprised him of his wish to marry Trottie and he had expressed pleased surprise, delighted that his attempt to play Cupid had been so successful.
'We would wish to remain in your service, sir,' said Dodge.
'Well, of course—I couldn't manage without you, Dodge, and having Miss Trott is a bonus, isn't it?'
'Certainly it is, sir. But what about Miss Lally?'
'Ah, yes, a matter which must be looked into as soon as possible.'
Dodge went back to his kitchen, leaving Mr van Linssen to sit back in his chair and allow his thoughts to dwell upon Eulalia. A proud piece, he reflected lovingly, who would probably deny her love out of sheer cussedness. It was, he decided, time to do something about that, but first things first.
He had had a long day—six hours in Theatre, a ward round, several private patients to see at the end of the afternoon—nevertheless, that evening he drove to Ursula's home. He should be feeling guilty, he thought, at putting an end to their engagement, but it had weeks ago become a farce. Ursula had relied on her pretty face and amusing manner to attract him, and once they had become engaged she had allowed her selfishness and impatience at his work to take over. He had known for some time that she was marrying him for his money and position and not because she loved him, and he, knowing this, had lost any feeling for her long ago—since, he had to admit, he had walked into the flower shop and seen Eulalia...
The maid answered the door, and when he asked if Miss Kendall was at home she said in a fluster, 'Yes, sir, in the drawing-room, but I don't know...'
He didn't wait to hear the rest of it but went up the staircase two at a time and opened the imposing door. Ursula was there, so was the American he had met at the dinner party. They were so closely locked in each other's arms that neither of them saw Fenno for a few moments.
He didn't say anything, but stood leaning against the door, smiling a little. Kindly Fate was helping his plans along very nicely. It was Ursula who broke the silence. 'So here you are, ready to spend half an hour with me out of your precious day—well, you needn't bother! I've decided not to marry you. I'd die of boredom within a month.' She gave him a defiant look. 'I'm going to marry Wilbur.'
Mr van Linssen strolled across the room. 'We met at a dinner party some weeks ago, did we not?' He shook hands with the man. 'Congratulations, and you, Ursula. I do hope you will be very happy.' He bent and pecked her cheek and she began to tug the ring off her finger. 'No. Oh, no, keep it. What would I want with a diamond ring?' He smiled a little. Eulalia would get his grandmother's old-fashioned sapphire and rose diamond ring, handed down from one bride to the next. He said blandly, 'I won't interrupt your plans for the evening. I'll see myself out.'
He left the house, whistling cheerfully. He wasn't in the least tired and he still had a good deal of plan-ning to do.
CHAPTER NINE
MR DODGE CAME on the following Friday, but he came in Mr van Linssen's car and Mr van Linssen was driving. Eulalia was in the kitchen baking an apple tart and it was Trottie who stumped to the door on her crutches and let them in.
She lifted her face with the unselfconsciousness of a child for Dodge's kiss, and was kissed in turn by Mr van Linssen. 'She's in the kitchen,' she said. 'Arthur, help me on with my coat. We'll go the the Boy and Horseshoe and get a bottle of sherry. I dare say there'll be coffee by the time we get back.'
Dodge allowed his features to relax into a smile and Mr van Linssen laughed. 'I haven't wished you happy yet. I do with all my heart—Dodge is a lucky man.'
Eulalia had heard their voices, and when he opened the kitchen door she was standing, the rolling-pin in her hand, her face pale, her heart thumping nineteen to the dozen. He closed the door gently behind him and said, 'Hello, Eulalia. Do you intend to whack me with that rolling-pin?'
She was having trouble with her breath. 'No, no. I—I'm surprised. I'm making apple tart—that's all.'
He came up to the table. 'Oh, good, for I have come, so to speak, holding an olive-branch in my hand.'
'An olive-branch?' she repeated stupidly. 'What for?'
'I believe that it is Peter's half-term on Thursday?' When she nodded, he added, 'I'm going to Holland that day—perhaps he might like to come with me, and you too, of course.'
'Go with you? To Holland?' She gathered her scattered wits together. 'We haven't passports.'
'A minor detail. Will you come, Eulalia?' He smiled at her then, and she picked up the rolling-pin again so that she need not look at him.
'We can't—Charlie and Blossom—and I won't leave Trottie alone.'
'Well, of course not. Dodge will come and stay with her and look after things.'
He had an answer for everything.
She tried again, still studying the rolling-pin. 'Miss Kendall—is she going to Holland with you?'
'No, no. I rather think that in the near future she will be going to the States. A most suitable match, I gather, although I deplore his taste in ties.' She raised her eyes long enough to inspect his—Italian silk, richly sombre and probably wildly expensive. He went on in a casual voice, 'We—er—agreed to differ on the subject of marrying.'
'None of this has anything to do with me,' said Eulalia in a high voice.
'Don't be a silly girl. All I am doing is offering Peter and you a few days' holiday. You will stay at my home but I shall be away almost all of the time. Is it not a good opportunity for Dodge and Trottie to get to know each other?' He added in a smug voice, 'We mustn't be selfish.'
She rolled the pastry for an unnecessary length of time. 'Would you take Peter alone? There's really no need for me to go with him.'
'My dear girl, am I expected to see that he changes his socks and washes behind his ears?'
'No. Isn't there another woman there to do that?'
She glanced up and saw his smile. 'Oh, yes, several. You will be quite safe, Eulalia.'
'Well, I'll have to think about it.' She tried to sound cool but her voice wobbled a bit at the thought of spending several days with him.
'By all means,' he agreed affably. 'You can tell me when we've had coffee.'
'I said think about it,' she said crossly, 'and I must ask Peter...'
'Without wishing to state the obvious, I suspect that he will want to go.' He wandered off to meet Trottie and Dodge as they came in, and Eulalia made coffee and found the biscuits, and if she didn't have overmuch to say for herself no one appeared to notice.
Dodge washed the cups and saucers, and she sat uneasily while Trottie and Mr van Linssen discussed the weather. 'It's getting chilly,' he observed. 'Holland always seems colder. Well, it is, of course. You had better bring something warm with you, Eulalia.'
Trottie looked suitably surprised. 'Going on a bit of a holiday, Miss Lally—and Peter too? Do you both good, that peaked you've been looking lately.'
Eulalia shot him a dark look. A mean trick, pinning her down to give an answer with Trottie there. 'I haven't...' she began, and caught his eye. He wasn't smiling but something in his steady look made her pause. She said weakly, powerless, it seemed, to prevent her tongue from uttering the words, 'Yes, we're going on holiday, Trottie—just for a few days—it's Peter's half-term.'
'I dare say Holland's as nice as England,' said Trottie. 'Well, almost. I've not much liking for foreign parts, myself.' She smiled at Mr van Linssen. 'Begging your pardon, though I don't count you as foreign.'
'You flatter me, Trottie. You shall come to Holland with Dodge later. He considers it quite a pleasant place.'
He got to his feet. 'Well, we must go. I'm sorry I can't stop to see Peter, but I've a list at three o'clock. If I'm to take some time off I must work a little harder first. Eulalia, get your passports from the post office—they'll only be temporary but we can get permanent ones later on. I'll be here quite early on Thursday morning and Dodge will be with me.' He bent to kiss Trottie's cheek and made way for Dodge before turning away. 'We shall go from Dover and get home in the late afternoon.'
He gave her an avuncular pat on the shoulder and went out to the car where Dodge joined him. She watched him drive away, torn between a great wish to go with him and annoyance at the high-handed way he had got her to agree to do as he wanted.
Peter, home from school, could hardly contain his excitement. 'Whereabouts in Holland?' he wanted to know.
'I'm not exactly sure...'
'Well, it doesn't really matter, does it? It's abroad, isn't it? Wait till I tell the boys at school. Aunt Lally, I'm so excited.'
Eulalia had to admit that she was excited too.
For the moment, she put aside her problems, fetched the passports, packed clothes for the two of them, and worried about money, which was a bit silly for she had almost none to worry about. In the end she went to Cirencester again and pawned her watch—a gold one her grandmother had given her on her twenty-first birthday.
* * *
THURSDAY CAME, AND with it Mr van Linssen and Dodge. No time was lost; greetings were exchanged, farewells said, Charlie and Blossom embraced for the last time, Eulalia ushered into the back of the car and Peter, to his delight, settled in the front seat. It had all been done, she reflected, without fuss or bustle; she would have encountered far more bustle catching the bus to Cirencester. She supposed that Mr van Linssen travelled so much that a mere trip to Holland was taken in his stride. She sat quietly, half listening to Peter's small voice and Mr van Linssen's deep tones as he drove south.
He broke the journey at a service station, telling them that he would meet them in the café in five minutes' time. Eulalia, hurrying Peter in the direction of the loos, was grateful for his matter-of-factness. They had sandwiches and coffee and got back into the car, Peter clutching a bar of chocolate. 'In case you get peckish,' said Mr van Linssen.
They had travelled on the motorways for almost all the distance, in the fast lane, and as far as Eulalia knew it was motorway until they reached Dover—as it proved to be. The Bentley made nothing of the distance; they were slowing down as they reached the harbour while she was still lost in daydreams.
Once on board they went on deck, so that Peter could watch as the ferry left Dover, and then they went to the restaurant for a meal, and all the while Mr van Linssen kept up a flow of easy talk about nothing in particular, answering Peter's flow of questions with patience, evading her attempts to ask the questions hovering on her tongue. When at last she got her chance he answered casually, 'My home is in a small village close to some lakes, a short distance from Utrecht and Hilversum. We'll drive up the coast into Holland. Once we are over the border it will be motorway again, I'm afraid, but it is the quickest way, and Peter will be needing his supper and bed.'
With that she had to be content.
Once they had landed, he took the road north out of Calais, following the coast into Belgium and to the border town of Sluis. It wasn't a fast road but it was almost free of traffic and, unlike the motorway to Antwerp and beyond, there was plenty to see—small villages, churches and neat villas. She suspected that he had come that way so that Peter wouldn't get bored. Breskens, where they would have to take another ferry, was only a few miles from Sluis and a ferry was waiting. It was a short crossing, but there was time to have a cup of coffee and then go on deck in the chilly evening so that Mr van Linssen could point out exactly where they were. They joined the motorway when they landed at Vlissingen.
'Just over a hundred miles now,' said Mr van Linssen, and joined the stream of traffic. It sounded a long way, but he put his large, well-shod foot down and raced along. Eulalia supposed that there were driving restrictions in Holland as well as in England, although the cars seemed to be going very much faster, perhaps because the country was so flat that one could see ahead for miles—no hedges, no corners, no hills. They were bypassing Breda in forty minutes and turning north to Utrecht. It was dark by the time they got there, but the lights from the city lit up the sky as they passed it, taking the motorway to Amsterdam now. Not for very far, though; he turned the car off the motorway and into a country road. There was a glimmer of water and trees, and presently a village, and few minutes later they were turning in between brick pillars to stop before his home.
'We're here, aren't we?' asked Peter, as Mr van Linssen unbuckled his belt, and he turned round to say, 'Aunt Lally, I'm so excited, aren't you?'
Of course she was; she was scared too. What on earth had she been thinking of to come all this way, meet any number of people she didn't know and who might not like her or Peter? Who were the people, anyway? She knew absolutely nothing about him or his home. She got out of the car when he opened the door for her, feeling a little mad. The sight of the house didn't reassure her either. It stood for so much: wealth and gracious living and a proud ancestry. No wonder he was so arrogant. No, not arrogant, just sure of himself...
The door had been opened, allowing light to stream out, and a grey-haired man came down the steps to meet them.
'Pete.' Mr van Linssen shook his hand. 'Eulalia, Peter, this is Pete, who runs this place with his wife Anneke. Pete, Miss Warburton and Peter.'
They shook hands and Pete said, 'A pleasure to meet you, miss, and Peter.'
Eulalia said quickly, 'Oh, you speak English. Peter and I can't speak Dutch, I'm afraid.'
'No worry, miss. Anneke speaks only Dutch, but I will be there too.'
They were inside the house by now and Anneke came to meet them, to be greeted with a hug by Mr van Linssen before they were introduced once more. He said something to the housekeeper, who took their coats while Pete fetched the luggage and Mr van Linssen said briskly, 'Let us find my mother. She will be expecting us.'
'Your mother?'
He took her arm. 'Did I not mention her? She stays here frequently, although she lives in den Haag. She will be in the drawing-room, I expect.'
He opened the double doors and ushered them inside. The room was magnificent—high-ceilinged, its walls hung with mulberry-red silk. There were high-backed armchairs on either side of the blazing fire in the great stone hearth, and a wide sofa, backed by a sofa table, facing it. Great bow-fronted cabinets stood against two walls and a brass stoelklok with its ponderous slow tick-tock hung between the long windows. There was a chandelier hanging from the ceiling, a glistening crystal waterfall, but it wasn't lighted; a number of small lamps stood around on the small tables set here and there around the room, casting a gentle glow, and there were ormulu wall-lights.
Eulalia heard Peter's gasp as they went forward to meet the elderly lady getting out of her chair. She was tall, as tall and as big as Eulalia, and still a good-looking woman. Her hair was grey and severely dressed and her eyes were as blue as her son's, and she was smiling.
'Fenno, you're here at last.' She lifted her face for his kiss. 'And this is Eulalia and Peter.' She offered a hand, adding, 'I may call you Eulalia? You do not mind? It is delightful to have you to stay. You shall tell me all the news from England, and I am looking forward to hearing about Peter's school.'
Mr van Linssen had gone to the French windows at the end of the room and opened them, and a large dog ambled in, to fall all over her master with delight, giving happy yelps. 'Come and meet Sally, Peter. She looks fierce but she's very friendly.'
She was a Bouvier, with a grey woolly coat, small yellow eyes and enormous teeth, a formidable beast if crossed, but just now grinning with pleasure and submitting to Peter's small hands. 'You like dogs?' asked Mevrouw van Linssen of Eulalia.
'Yes. Mr van Linssen gave Peter a puppy; we call him Charlie...'
Mevrouw van Linssen took her arm. 'You will want to go to your room and tidy yourself, my dear. Anneke shall take you and Peter upstairs, but don't be long, for we shall dine early so that Peter can go to bed.'
Anneke came then and clucked in a motherly fashion over Peter and led them across the hall to the staircase curving against one wall to the gallery above. It was a rather grand staircase with carved banisters, and the wooden treads were worn by generations of feet.
They had rooms side by side with a shared bathroom, and the moment Anneke left them Peter said in an awed whisper, 'Aunt Lally, it's very grand, like a palace. Mr van Linssen must have lots of money. I wonder why he works when he doesn't need to?'
'I think because he likes being a surgeon, dear.'
Peter nodded and said, 'Yes, I expect so.'
They explored their rooms together, charmed by the narrow canopied beds hung with muslin curtains, and their coverlets of toile de Jouy, the matching curtains and the William and Mary marquetry chests. In Peter's room there was a tulip-wood dressing-table on delicate castors and a small tub armchair, just right for his size. There were books too—children's books on the small table by the bed. Someone had gone to a great deal of trouble, thought Eulalia, inspecting in her turn her own room, with its Georgian dressing-table set between the two windows, a Dutch marquetry toilet mirror on it. There was a cheval-glass in one corner of the room too, and she took a quick look at her person. Her plain wool dress couldn't compete with her hostess's elegant outfit, but it would pass muster. She went into Peter's room, made sure that he had washed his face and hands, brushed his hair and went downstairs again.
There was sherry in the drawing-room and lemonade for Peter and ten minutes' pleasant talk before they crossed the hall to the dining-room. It was not as large as the drawing-room but equally grand, with a massive sideboard and an oval table which could seat a dozen without difficulty. They sat at one end of it, Mr van Linssen at the head, his mother on his right and Eulalia, with Peter beside her, on his left, while Pete served them with soup, chicken in a delicious sauce and a chocolate pudding rich with cream. They drank a white wine and Pete poured apple-juice for Peter.
Mr van Linssen was a splendid host, maintaining a gentle flow of talk which required no effort to answer, and talking to Peter too, keeping to general topics with his mother but never once giving a clue about his family or his life in Holland. Presently, waiting as Peter bade them goodnight, Eulalia was aware that he was watching her, but she looked away quickly, afraid that he might see how happy she was to be there, in his home with him.
He opened the door as they reached it and touched her on the arm. 'Come down again, Eulalia.'
She nodded at his waistcoat, very conscious of his hand.
Back in the drawing-room, once Peter had fallen asleep, she sat beside Mevrouw van Linssen on the sofa a little away from him in his armchair, while he suggested how she and Peter might spend their days. He sounded matter-of-fact and friendly. 'I don't need to go to Amsterdam until the afternoon. I thought we might go round the gardens and explore the house. I know Mother will love to gossip after I've gone.'
'Are you staying in Amsterdam?'
'No, no, but I shall be back very late, and I go to Utrecht on the following day and on to Leiden, but I should be home in the early evening. I wondered if you would like to come with me? Utrecht is worth a visit, and so is Leiden. I'll take you both to lunch and then drive to Leiden. I only need to be there for a couple of hours and, if you would like, I'll get someone to take you both round the hospital.'
'That would be marvellous. Peter will be thrilled. Won't we be a nuisance?'
'No, not at all. I'm afraid it is a very small glimpse of Holland.'
'But it's a start,' observed his mother. 'Leiden is a charming little city. I'm sure you'll enjoy it. And I'm looking forward to showing you the village, and we can walk to the lake...'
Eulalia said her goodnights presently and said, 'Please don't get up,' when Mr van Linssen walked to the door with her.
He took no notice at all, but with his hand on the door said, 'I think that you might try and call me Fenno, don't you? After all, we are old acquaintances.' He bent swiftly and kissed her. 'Goodnight, Eulalia.'
She wouldn't sleep, she fretted as she got ready for bed. He shouldn't have kissed her—it wasn't fair, with the business of the cottage and the money still a bone of contention between them—well, on her side at any rate, since he persisted in doing nothing about it or even mentioning it.
She got into bed, ready to lie and worry, but instead went to sleep at once.
The next day was over too soon. They spent the morning roaming round the gardens: acres and acres of lawns, rose-garden and a herb-garden, a walled kitchen-garden, a pond with carp, a gazebo, long walks bordered by herbaceous plants, lying dormant, and a vast greenhouse. Peter, with Sally beside him, ran ahead while Eulalia, quite forgetting her worries, stopped to peer and admire and ask questions.
'However many gardeners do you have, Mr van— I mean, Fenno?'
'Two, and a boy.' He tucked her hand in his. 'You aren't cold?'
'No, it's lovely, so different...'
'Very quiet, although we are very close to the motorway. You like a country life, don't you, Eulalia?'
She nodded. 'Yes. What's through that little door?'
'A paddock, with stables at the far end housing a pony, a chestnut mare and a donkey.'
Peter would have stayed there for hours, feeding them the carrots and sugar Fenno had brought with him, but they prised him away at last and went indoors to have coffee before looking round the house.
'There won't be time to see all of it. Mother will be delighted to take you round the old wing and the attics.' He took her hand and they went upstairs with Peter and Sally to begin their tour. There were several doors round the gallery and passages to the left and right, as well as half a dozen stairs leading to the back of the house. They went from room to room, each one perfect, until he glanced at his watch.
'I have to go—there's one more room I want to show you.'
He led the way to the front of the gallery and opened a double door. The room overlooked the front gardens, its three tall windows draped in pastel brocade, the bed a vast four-poster with curtains of the same brocade. There were tallboys and a vast chest against one wall, and a dressing-table with a triple mirror and a low stool, and all of them were in tulip-wood and marquetry. There were comfortable chairs too, and a day-bed at the foot of the four-poster.
Peter stared round him. 'It's like a room for the Queen.'
Mr van Linssen nodded gravely, his eyes on Eulalia.
He left soon after and they sat down to lunch with Mevrouw van Linssen, and afterwards walked to the village and took a look at the lake. Sally pranced along beside them and Peter ran to and fro, completely happy.
Eulalia, lying in her bed later that night, reflected that it had been a lovely day. Pete had taken Peter to the kitchen to watch Anneke cook, and she and Mevrouw van Linssen had toured the rest of the house—the old wing, seldom used now, a mass of small panelled rooms and narrow passages, and then the attic floor. Not really attics, for they had been made into a flat for Pete and Anneke and bed-sitting rooms for the two housemaids. Only the vast one over the wing was filled with a hotchpotch of discarded furniture, great cabin-trunks, and a cupboard filled with old-fashioned dresses and hats. They had poked around together while Mevrouw van Linssen chatted of this and that, slipping in a few questions from time to time, so unobtrusively that Eulalia hadn't noticed.
The one flaw in a perfect day had been the lack of Fenno, but tomorrow, she told herself, she would be with him all day.
She woke early, as did Peter, and together they went to look out of the window. It was a fine day but there was a wind, and clouds piling up on the horizon, and striding away down the drive was Fenno with Sally.
'I'd have gone with him if he had asked me,' said Peter.
Me too, thought Eulalia, and urged him to get dressed so that they would be downstairs when he came back.
He wished them a cheerful good morning, remarked that there was a cold wind and that they had better wear something warm, and, once breakfast was eaten, warned them that he wanted to leave in ten minutes.
'You're sure you don't mind?' asked Eulalia, already halfway to the door. 'Taking us, I mean...'
'I'm delighted to have your company, but don't keep me waiting.'
He drove them to a quiet street next to the cathedral in Utrecht, explained how they might reach the shopping streets, and warned them to be back at that spot in three hours' time. 'And don't try and climb the Dom tower, there are four hundred and sixty-five steps. Have you money with you?' He didn't look at her. 'You've had no time to get guldens, have you?' He fished in his pocket and handed her some notes, and seeing her attempt to refuse said, 'Don't be silly, you can pay me back later on. We'll have a quick lunch together, but you'll need coffee.'
He got back into the car and drove away. 'I should have liked to have gone with him,' said Peter.
And so, reflected Eulalia, would I.
They spent a long time in the cathedral, took a look at the Dom tower, then found their way to the shops and a café where they had coffee and a milkshake and, since she might as well use the money now that she had it, some luscious cream cakes. They were in a quiet corner, and she opened her purse and counted the guldens. More than five hundred—however did he think she could repay him if she were to spend them? She prudently put almost all of it with her sparse bundle of five-pound notes and calculated how much she could afford to borrow. That done to her satisfaction, they went shopping for presents for Trottie and Dodge—a cup and saucer for each of them in Delft blue, not the genuine china but pretty, nevertheless, and by then it was time to find their way back to the little side-street again, pausing to hang over the little arched bridges and watch the boats on the canals and gaze up at the old gabled houses.
The Bentley nosed its way round the corner as they turned into the street. 'Enjoyed your morning?' Fenno wanted to know. 'We'll have lunch and drive on to Leiden.'
He took them to the Café de Paris, smart and expensive, with a décor which left Peter's eyes wide open.
'Something quick,' he suggested.
'Whatever you suggest...'
'Omelettes? And french fries for Peter?' He gave the order and asked for coffee at the same time, and an orange drink for Peter, who plied him with questions about the hospital until a plate was set before him and he began on the french fries. It was a pleasant meal, even if they wasted no time over it; indeed, Peter was finished first, impatient to be gone since they were to go round the hospital in Leiden.
It was thirty miles to Leiden, a distance the Bentley covered in less than half an hour, and Mr van Linssen drove straight to the hospital. 'I shall be here for an hour or so—why not walk a little way along Rapenburg by the canal, and come back here in about half an hour? I'll leave word at the lodge. Just say who you are.'
So they walked a bit, and discovered the university and the Hortus Botanicus gardens, the library and a museum, and presently presented themselves at the porter's lodge and were handed over to a young doctor.
'Wim Bakker,' he introduced himself. 'Mr van Linssen asked me to show you round.'
'How kind, but shouldn't you be working?' Eulalia liked him at once.
'I have a few hours off duty.' His English was as good as hers.
'Then we're taking up your precious free time.'
'It is a pleasure, Miss Warburton.' He smiled down at Peter. 'You wish to be a great man like our Mr van Linssen? And why not? Let us start our tour.'
They were in the entrance hall an hour or so later when Mr van Linssen joined them, asked if they had enjoyed themselves, thanked Wim and swept them out to the car, his manner a mixture of the avuncular and the impatient, at least with Eulalia; with Peter he was painstakingly kind, answering questions and explaining things.
It was the same when they returned to his home, so that she became stiff and shy with him; she had been a fool in rose-coloured spectacles just because he had invited her and Peter for a few days' holiday and had broken off his engagement to Ursula. She went hot and cold at the thought that she had given herself away, and that evening, after Peter was in bed and they were sitting in the drawing-room, when Mevrouw van Linssen remarked that she and Peter had had a very full day, and Fenno capped that by observing that she must be tired, she seized on it as an excuse to take herself off to bed, where she wept herself to sleep.
They left for England the next morning. Mevrouw van Linssen kissed her warmly with the remark that a longer stay would have been very pleasant. 'But of course, Peter mustn't miss his schooling, must he?' she said, and waved them away cheerfully. She lifted her face for her son's kiss and said that she expected to see him again. 'Very soon,' she added with a wide smile.
The journey home was made with the ease Eulalia was beginning to expect from Fenno, with just enough time when they reached Calais to go on board and a quick getaway when they reached Dover. He stopped at a service station so that Peter might have egg and chips while he and Eulalia had coffee and sandwiches, and when they were once more on their way he delighted Peter by phoning Dodge from the car to let him know that they would be home in time for supper. He and Peter kept up a seemingly endless conversation for most of the journey, casting an occasional remark over their shoulders to her, so that she had all the time in the world to think. Not that she solved any of her problems.
They arrived at Ivy Cottage to a warm welcome and a pleasant flurry of activity from Dodge and Trottie, and they sat down to supper almost at once. Between them they had produced a meal fit for a king: prawn cocktails, minute steaks with creamed potatoes and baby sprouts, and one of Trottie's apple pies for afters, and, since Trottie was full of questions, Eulalia forgot her problems for the moment, thinking how delightful it was, all of them sitting round the table with Charlie and Blossom pacing to and fro in the hope of titbits, and of course Fenno sitting at its head.
She was taken quite by surprise when the meal had been cleared and Fenno said casually, 'Well, we must be off. You're ready, Dodge?'
'Off?' said Eulalia. 'You're going back to London now?'
'Like Peter, I have to work tomorrow.'
Trottie and Dodge were in the kitchen but Peter was standing by Fenno, so even if she had wanted to, there was no chance to say anything. What would she say, anyway? she wondered forlornly, as she expressed her thanks with suitable politeness.
'I'm glad you enjoyed your visit. Far too brief, though. We must do better next time.'
'There won't be a next time,' she said very fast, quite forgetting Peter.
'But, Aunt Lally, why can't we go again? I liked it, and I like being with Mr van Linssen.'
'He's a busy man, Peter. I'm sure he has very little time for—for...'
'His friends?' asked Fenno blandly. 'For those he loves? You are mistaken, Eulalia. He has all the time in the world.'
She didn't look at him, and Peter, happy again, went out to the car with him, and Dodge wished her goodbye and got in beside his master. The car was out of sight when she realised that Fenno hadn't said goodbye. She supposed that she had deserved that.
* * *
WITH PETER BACK at school, she picked up the threads of her life once more. The future was precarious and first she must talk to Trottie. That lady, when asked when she was going to marry, parried the question with a vague, 'Well, Miss Lally, it all depends...'
'On what, Trottie?'
'One thing and another. I'm not going up the aisle with my leg in a plaster, that's for sure.' Trottie looked up from the table where she was polishing glasses. 'And that reminds me, I'm to have another plaster on Friday. Mr van Linssen told Dodge he could take the Rover and fetch me. Such a kind man. Dodge'll be here around nine o'clock. You'll be all right on your own?'
'Of course.' Eulalia made her voice sound cheerful; after all, before long she would be on her own, wouldn't she? And Trottie, dear Trottie, who had shared everything with her without complaint, must marry just as soon as possible. It would be a good opportunity while she was at the hospital to collect as many newspapers as possible and look for part-time work. She knew to a penny how much she needed to keep Peter and herself, and there were one or two things she could sell. His school trust, thank heaven, was more than enough for the fees, so she could fit him out as he grew. She would manage. She asked, 'Are you going to live at Mr van Linssen's house when you are married? It's very nice there, not a bit like Cromwell Road. You'll like it.'
'Well, we'll wait and see,' said Trottie, infuriatingly refusing to give a plain answer.
It was hard to maintain a cheerful face, since Peter talked about Mr van Linssen incessantly and it seemed to her that Trottie encouraged him. If only she could go somewhere and have a good cry about it and then forget him.
Friday came and with it Dodge, driving sedately down the village street. He wished Eulalia a dignified good morning, when she wasn't looking kissed Trottie, and then helped her carefully into the car and drove away. They might not be back until the afternoon, he observed, and if Trottie was tired he hoped that Eulalia wouldn't object if he took her for some refreshment.
'Heavens, of course I don't mind, Dodge. Have a nice lunch or something—there are lots of good restaurants in Cirencester—and come back when you like. I'm going into the village now but I'll be in for the rest of the day.'
The moment the car was out of sight she got into her coat and hurried to the newsagent in the main street, where she bought every likely paper as well as The Lady magazine, and bore them back, and with Blossom on her lap and Charlie beside her, she spread them out on the kitchen table and began looking for work.
There weren't many jobs which she could do. Check-out at a supermarket, someone to deliver circulars in Malmesbury, someone to look after a frail elderly lady, hours to suit—she wondered what that meant, to suit her or the old lady? Someone to walk two dogs twice a day, a young lady to demonstrate a new brand of margarine at one of the supermarkets. She made a list and then, surrounded by newspapers, she composed a letter applying for each of them. A job, any job, was necessary, so that Trottie would feel free to go. With luck, she reflected, she might be able to fit in two part-time jobs, as long as they were both in Cirencester...
She was on her third attempt at an application when the knocker was thumped, and before she could get up the door was thrown open and Fenno came in.
'Well, really,' said Eulalia, short of breath and with her heart thumping against her ribs, torn between surprise and delight and rage. 'How did you get here?' she managed, as he closed the door behind him and locked it, put the key on the table and picked up her last effort.
He looked at her over the top of it. 'In my car. Although if it had been necessary I would have walked.'
'Walked all the way from London? Why?'
He fended off Charlie with a gentle hand. 'Because I wanted to see you and, come to that, I would walk from the other side of the world if I had to. Even though I would not be sure of my reception, for a more obstinate, pig-headed girl I have yet to meet!' He swept the newspapers off the table and pulled her gently into his arms, ignoring her indignant gasp. 'I took you to Holland because I had a sentimental wish to ask you to marry me while we were in my home, but you were so polite and distant. Why?'
She stared at his waistcoat buttons. 'I thought... Well, I'd only just discovered... What I mean is...'
Mr van Linssen considered this a sufficiently satisfactory answer to allow him to tighten his hold and kiss her soundly.
'I'm not pig-headed,' said Eulalia, 'or obstinate.'
He kissed her again lingeringly. 'You're both, my darling heart. Will you say yes if I ask you to marry me?'
'Yes,' said Eulalia. 'Am I really your darling heart, Fenno?'
'Forever and always, my dear love.'
'Is that why you bought this cottage and gave me all that money?'
'That is why.'
She smiled up at him, and Mr van Linssen, a man of flesh and blood, kissed her again, taking his time.
* * * * *
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ISBN: 9781460315729
Copyright © 1995 by Betty Neels
All rights reserved. By payment of the required fees, you have been granted the non-exclusive, non-transferable right to access and read the text of this e-book on-screen. No part of this text may be reproduced, transmitted, down-loaded, decompiled, reverse engineered, or stored in or introduced into any information storage and retrieval system, in any form or by any means, whether electronic or mechanical, now known or hereinafter invented, without the express written permission of publisher, Harlequin Enterprises Limited, 225 Duncan Mill Road, Don Mills, Ontario, Canada M3B 3K9.
This is a work of fiction. Names, characters, places and incidents are either the product of the author's imagination or are used fictitiously, and any resemblance to actual persons, living or dead, business establishments, events or locales is entirely coincidental. This edition published by arrangement with Harlequin Books S.A.
® and ™ are trademarks of the publisher. Trademarks indicated with ® are registered in the United States Patent and Trademark Office, the Canadian Trade Marks Office and in other countries.
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{"url":"https:\/\/med.libretexts.org\/Bookshelves\/Anatomy_and_Physiology\/Book%3A_Fluid_Physiology_(Brandis)\/Chapter_5%3A_Control_of_Water_Metabolism\/5.10%3A_Summary_of_Renal_Water_Handling","text":"# 5.10: Summary of Renal Water Handling\n\nThe kidney is the most important organ in the regulation of water balance in the body. Under normal circumstances, the sensitive hypothalamic osmoreceptors detect any change in extracellular tonicity and respond by altering secretion of ADH from the posterior pituitary. The volume receptors are much less sensitive and really function as a backup sensor. Most water intake is not due to thirst. The thirst mechanism functions as a backup effector mechanism.\n\n### The kidney is the effector organ for body water balance.\n\nGlomerular filtration rate (GFR) is very large (180 l\/day) in comparison to the amount of urine that is typically produced. Most of the water in the filtrate is reabsorbed because of renal processes which are independent of ADH action.\n\nThe diagram below summarises the percentages of water reabsorbed in the various renal segments. The two extreme examples of absence of ADH and maximal ADH production are outlined. The kidney adjusts the water reabsorption between these two extremes (under the influence of ADH) in order to maintain a constant plasma osmolality. The minimum (or obligatory) urine volume is determined by the size of the daily solute load and the maximal urine osmolality that can be achieved. The maximum urine osmolality decreases with increasing age in adults so the obligatory urine volume is higher for a given solute load in the elderly.\n\n### All water reabsorption in the kidney is passive.\n\nWater moves in response to osmotic gradients. These osmotic gradients are all directly or indirectly due to the reabsorption of solute particularly sodium. There are no water pumps in the body.\n\n## Quantitative Summary of Renal Water Handling\n\nGFR (180 l\/day)\n\n65% Reabsorbed Proximal Tubule\n\n15% Reabsorbed Loop of Henle (thin descending limb)\n\n20% of filtrate Enters Distal Tubule\n\n$$8 \\% \\text {Reab in CD} > 19 \\% \\text {Reab in CD}$$\n$$12 \\% \\text {of filtered } H_{2}O < 1 \\% {of filtered } H_{2}O$$","date":"2019-08-23 15:26:01","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 0, \"mathjax_display_tex\": 1, \"mathjax_asciimath\": 0, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.46387237310409546, \"perplexity\": 5621.214086727734}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2019-35\/segments\/1566027318894.83\/warc\/CC-MAIN-20190823150804-20190823172804-00388.warc.gz\"}"}
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Андрій Варфоломійович Семидідько (, село Ковалівка, тепер Шишацького району Полтавської області — , місто Москва) — український радянський діяч, голова колгоспу «Червона зірка» Шишацького району Полтавської області. Депутат Верховної Ради СРСР 2-го скликання.
Життєпис
Народився в бідній селянській родині. З 1916 року наймитував у заможних селян. Закінчив семирічну школу.
З початку 1930-х років — конюх, бригадир, комірник колгоспу «За урожай» на Полтавщині.
У 1935—1939 роках — голова колгоспу «Переможець» Шишацького району Полтавської області.
Член ВКП(б) з 1938 року.
З 1939 по 1941 рік — голова колгоспу «Червона зірка» села Ковалівки Шишацького району Полтавської області.
У 1941 році був евакуйований до Челябінської області РРФСР.
З грудня 1942 по 1945 рік служив у Червоній армії, учасник німецько-радянської війни.
З 1945 до 15 жовтня 1949 року — голова колгоспу «Червона зірка» села Ковалівки Шишацького району Полтавської області.
На пам'ять про Андрія Семидідька в селі Ковалівці Шишацького району було названо вулицю.
Нагороди
медаль «За взяття Кенігсберга»
медаль «За перемогу над Німеччиною у Великій Вітчизняній війні 1941—1945 рр.» (1945)
Джерела
газета «Радянська Україна» — Київ — січень 1946.
Члени КПРС
Депутати Верховної Ради СРСР 2-го скликання
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{"url":"http:\/\/math.stackexchange.com\/questions\/127992\/how-to-plot-this-function","text":"# How to plot this function\n\nI want to plot functions (using some software, any recommendations?) that looks like this below. Could someone suggest equations of functions that would look like the graph below?\n\n-\nThere are many of them: I have started to use Geogebra. \u2013\u00a0 user21436 Apr 4 '12 at 14:01\nThanks, could you give me an example? \u2013\u00a0 Gary Apr 4 '12 at 14:01\nHave you tried: gnuplot (free), mathematica, matlab, ...? The functions you list could be more or less anything - how about $b(x) = (x\/10)^2, h(x) = 1+b(x), g(x) = 2+b(x), f(x) = 3+b(x)$? \u2013\u00a0 Johannes Kloos Apr 4 '12 at 14:09\nThanks Johannes! \u2013\u00a0 Gary Apr 4 '12 at 14:51\n\nBesides the excellent suggestions made by Johannes Kloos\n\nHave you tried: gnuplot (free), mathematica, matlab, ...? The functions you list could be more or less anything - how about $b(x)=(x\/10)^2$, $h(x)=1+b(x)$, $g(x)=2+b(x)$, $f(x)=3+b(x)$?\n\nI'll add that fooplot is free, runs in a browser, and is very easy to use:\n\n-\n\nYou can also do the plots by using MAPLE as follows:\n\n[> with(plots):\n[> b := proc (x) options operator, arrow; (1\/100)*x^2 end proc:\n[> multiple(plot, [b(x), x = 0 .. 10, y = 0 .. 5,color and 0 .. 5,color = red, thickness = 3], [b(x)+1, x = 0 .. 10, y = 0 .. 5, color = green, thickness = 3], [b(x)+2, x = 0 .. 10, y = 0 .. 5, color = blue, thickness = 3], [b(x)+3, x = 0 .. 10, y = 0 .. 5, color = black, thickness = 3]);\n\n\n-\n@amWhy: Yes I wish I could go. Thanks, I am well but exhausted cause of 8 hours teaching. :-) \u2013\u00a0 Babak S. Oct 27 '13 at 18:10\n@amWhy: Honestly, I am addicted to be here Amy. Thanks for your supporting and warming words my dearest friend. ;-) \u2013\u00a0 Babak S. Oct 27 '13 at 18:32","date":"2015-04-18 17:18:30","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 1, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 1, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.6464000940322876, \"perplexity\": 502.72238685272254}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 5, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2015-18\/segments\/1429246635639.11\/warc\/CC-MAIN-20150417045715-00168-ip-10-235-10-82.ec2.internal.warc.gz\"}"}
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'Want,' a Horror Short Story
Mawr Gorshin Horror fiction, literature, science fiction, short story August 19, 2020 August 19, 2020 21 Minutes
"I can't believe you just did that, you humongous animal!" Dr. Will Cameron shouted in sobs as he looked up and watched his gigantic colleague, Dr. John Gula, licking human blood off his fingertips. "How could you just…pick up…Dr. Sanders and…eat her?"
"I was hungry," thirty-foot-high Dr. Gula said, then belched.
"You were hungry?" Cameron said. "That's all you can say, you cannibalistic monster!"
"It must be one of the bizarre side effects of Aggrandizin, the drug we were going to test on the diseased fish around this island…"
"And you're still hungry, after all those apes you ate," Cameron said, looking up at Gula in horror. "Making you grow to that monstrous size."
"Another…surprising…side effect of the drug," Gula said, pulling up the tarpaulin he had wrapped around his waist to cover his nakedness. "And you know I had to eat the drugged apes, to stop them from eating us. One of them almost got you."
"I'd rather we were eaten by the apes then to see this nightmare as it's unfolding! I keep hoping I'll wake up from a nightmare, but this…insane…moment seems all too real!"
"I find it as hard to believe as you do, Cameron."
"We were only supposed to dose marine animals with the Aggrandizin, to speed up their ability to heal wounds and recover from disease, after the exposure to the pollution and toxic chemicals surrounding the island. How did this simple experiment turn into such a nightmare?"
"That baby shark grew in size, and hunger. It bit Sanders, she bumped into me, and I accidentally injected myself with the drug. I already explained that to both of you."
"How much of the drug did you dose yourself with? Ten times the amount we gave that shark?"
"It must have been at least about ten times the amount we were going to dose the fish with," Gula said, without a trace of emotion.
"And you ate all those apes!"
"It was either that, or they were going to eat us. We saw how ravenous they got after they, it's more than safe to assume, broke into the phials of Aggrandizin in the boat, and how they grew like me, each time after they ate something. We saw how insatiable their hunger got, like mine, even to the point of eating what no animal of their species would normally ever eat, including flesh. We saw how they ate most of the plant and animal life here…"
"And you ate the rest, and Dr. Sanders, just now!"
"I couldn't help myself, Cameron! Try to understand! I'm not any happier about it than you are."
"You don't seem to give a shit, John!"
"You don't know the hunger that Aggrandizin causes!"
"I don't wanna know!" Cameron bawled. "How could this have happened? How could we have gotten this drug so horribly wrong? This is like something out of a B science fiction movie. How could a mere drug cause someone to grow into a giant, of all things, and to hunger so much, that he'd eat apes, and another human being?"
Speaking of hunger, Gula was looking down at Cameron and licking his lips.
"John, don't look at me like that," Cameron said, backing up a few steps, with trembling legs.
"I can't help it." Gula was drooling as his eyes explored Cameron's meaty body.
"John, only I can fit into the boat to go back out and get help for you. There's no more food for you to eat here."
"I'll go fishing by hand in the ocean after I eat you."
"The massive pollution in the water surrounding this island means that you won't be able to eat any edible marine life here," Cameron insisted. "That's why we chose this island to do our experiments: to dose the sick fish, and hopefully save them from the poisons in the water. You can't eat the marine life here. You'll get sick."
"The drug dose I took should be strong enough to repel any toxins from the dead fish near here." He licked his lips again at Cameron, who shuddered at the sight.
"The toxic chemicals dumped in the water are so poisonous that even your Aggrandizin dosage, as excessive as it was, surely won't be strong enough to counteract the toxicity of any dead fish floating around here."
"You don't know that for sure. You're only saying that because you want to believe it. But even if what you say is right, I'll go further out into the water. I'm getting larger and larger. I could conceivably wade far enough, with my gigantic size, to get past the polluted part."
"You can't swim, by your own admission, and the toxic chemicals are already spread out so far into the ocean around here that, even at your size, you won't be able to wade out far enough to get past the pollution surrounding the island. The ring of pollution is like a thick donut, and this island is like the small hole in the centre, there's so much donut out there."
Gula licked his lips and said, "Donut."
"OK, bad comparison," Cameron said, shaking spastically at how Gula's eyes were staring at him, appraising his tastiness. "Look, you need me alive to sail the boat back to the African mainland and get help. Just hang on, be patient, control your hunger, for God's sake."
Gula's hand reached down to pick up Cameron, who dodged the huge fingers and started running away. "You can't catch me; how can you expect to catch any fish by hand in the ocean?"
"I'll practice and get better." He reached for running Cameron and missed again.
"If you eat me,…you'll have…no food left." Cameron raced for the leafless trees that Gula and the apes had already fed on. "What will you do…after eating me…eat yourself? You eat, you grow…and only get hungrier. Aaaah!"
Gula grabbed him and picked him up.
"The tarp is slipping off your waist!" Cameron said, hoping to distract Gula and make him let go.
"So what?" Gula said as he brought Cameron up to his face. "Nobody else is here to see me with my cock and balls hanging out."
"After you eat me, the tarp won't…be big enough…to cover you! You'll rip out of it…the way you…ripped out…of your clothes…after eating…those apes!"
"Nobody will be here to see me."
"Exactly!" Cameron shouted. "Without me, you'll have…no one to help you! You'll be trapped…alone…on this island! With no more food!"
Gula opened his mouth wide enough to bite off Cameron's head. Cameron put his hands on Gula's upper lip, pushing away to keep from going in his mouth.
"Only I…can help you…find food!" Cameron shouted while kicking at Gula's chin and swinging away from his mouth. "The water's…toxicity…will damage…your skin…if you wade out…to find fish. The Aggrandizin…won't be strong enough…to heal you. If you eat me, you'll die!"
"Yeah, I probably will."
"Then, why won't…you resist…the temptation…to eat me? Unh!"
"I can't help it," Gula said, grabbing Cameron's legs and aiming the feet at his mouth. "It's in my nature to keep eating. I'm the scorpion, and you're the frog, like in that old fable."
He put Cameron's legs in his mouth, up to his thighs. Cameron was screaming and kicking at Gula's uvula, and at the roof of his mouth.
"No! John, don't!"
He felt Gula's sharp incisors bite through his waist, cutting through his skin and muscles, and cracking the bones. He screamed as he saw the blood spraying everywhere. His now-separated upper half hung loose and shook; his eyes and mouth were wide open in horrific disbelief. He passed out.
Gula was chewing, cracking the bones and sighing with relief that his hunger was being satisfied…for the moment. He felt his body vibrating, as it always did whenever he ate something since his Aggrandizin dosage. He grew by about a foot.
He looked down. Cameron was right. The tarpaulin had fallen from his waist and onto the sand on the beach. A breeze was caressing his balls.
He gulped down Cameron's masticated bottom half, licked the blood from his lips, and belched out loud.
"Goodbye, Cameron. Sorry about this."
His mouth was now big enough to stuff in, with the greatest of ease, all of the upper half of Cameron's body, so he did.
Crunch! Crunch! Crunch!
Blood splattered all over his face. The bald head of the chubby man looked like that of a giant baby's having eaten tomato sauce and soaked red all over his cheeks. The white tarpaulin would be his diaper. How appropriate.
Gulp. Burp!
He wiped the blood off his face and licked his hand. To see the day when he would actually find cannibalism to be appetizing…what a shock. His body vibrated again, and he grew another foot or so.
He picked up the tarp and wrapped it around his waist. "You were wrong about one thing, Cameron. It's still large enough to cover my dick and ass."
Then, he felt another pang of hunger.
"Oh, shit. What do I do now?"
He walked over to the edge of the shore, where the filthy water washed up pieces of plastic and dead fish. The water was a mix of blue and yellow from all the toxic waste in it.
"Eww," he groaned at the sight of the dead fish's unnatural colours. As hungry as I am, he thought, there's no way in hell that I'm eating any of those.
He looked far out to sea. Cameron was right again: the pollution went so far out that Gula couldn't see any pure blue water anywhere beyond the filth. Even at his enlarged size, he still couldn't see far enough.
I wonder if I can see the shark out there, he thought, straining his eyes. I'll bet it's gotten really huge by now. If I were to see it, I might consider going out there, trying to swim and risking drowning, then eating it if I caught it…or letting it eat me, even. I can't imagine wanting to continue living like this. A part of me actually wouldn't mind drowning or being eaten by the shark.
His stomach was growling.
To think, that shark was a baby, swimming just outside the periphery of the ring of pollution. We caught it in a net, Sarah Sanders held its wiggling body, and I stuck the needle of Aggrandizin in its side. I dosed it with a generous amount. Then it bit her on the arm.
The hunger in his gut was getting painful.
She screamed and jerked her arm. Her elbow nudged my arm, and I stabbed the needle into my left wrist. I accidentally pushed the plunger all the way in and injected a huge dose of the drug into my arm. Neither she nor Cameron noticed what I'd done, they were so busy fussing with the shaking, growing shark and throwing it back into the water, then worrying about treating her bite wound. Cameron said the baby shark had already grown to almost twice its size, just from the one bite.
Another stomach growl.
Back in the water, it caught a fish in its teeth and ate it. It grew some more. We saw it eat a few more fish; now it had grown to about the size of a great white shark…and like at the end of that old Spielberg movie, it attacked our boat.
Another hunger pang.
Cameron got out his binoculars, and after about half a minute of frantically searching for somewhere we could go to save ourselves from the shark, he spotted this island. Getting here would have been the fastest way to get to safety from the shark, which we saw eating more and more fish, and growing and growing, and trying to ram a hole in the side of our boat. We turned on the motor and raced over here. We'd already eaten all of the food on the boat, so I was holding back as best I could…as I am now—oh, this is getting difficult! Anyway, when we got here, I ran over to the trees and wolfed down as many of the leaves as I could stuff into my mouth. Cameron and Sanders were shocked at my behaviour. They left the boat and ran into the woods with me. Some apes must have gotten into our boat, found the phials of Aggrandizin, broke the glass, and drank from it; because soon after, they were growing and eating like the baby shark and me.
His hunger was getting unbearable.
As I, grabbing at leaves and grass to eat, was being chased by Cameron and Sanders, the apes that must have had the drug ran back into the woods with us. They ran around eating leaves and other animals, too. We ended up eating all the leaves off the trees on this tiny island. I was ripping out of my clothes. One of the enlarged, ravenous apes jumped on Cameron; in its new taste for flesh-eating, it would have eaten him, but I grabbed it and ate it. Again, Cameron and Sanders were shocked at my behaviour. I fought off the other attacking apes, and ate them.
Another stomach growl. "Unh!" he grunted.
After having feasted on the rest of the island's apes, plants and insects, Gula continued in his thoughts, I'd grown so big, I ripped out of my clothes. Sanders gave me the tarpaulin to cover myself with, then…I…ate her. How could I have done that? But…how could I not have…
Oh, the hunger…
He was shaking…gasping and wheezing…
"Aaaaaah!" he screamed, running into the water. It was slimy and disgusting. He grabbed a large shark's corpse and tried eating it out of desperation. It tasted so awful, he spat it out within a second. He waded out as far as he could go. The…liquid…more like piss than water, had reached his chin. Waves splashed on his face. Then he remembered: "I…can't…swim."
He turned around and rushed back, plodding in the water and almost falling into it, till he finally got back onto the land, soaking in caustic filth and sobbing in despair. The Aggrandizin managed to heal his skin reasonably well, but his stomach was growling so much, it was like having a huge second mouth…or many little mouths…in his belly.
"For God's sake," he said in gasps and sobs. "We made Aggrandizin…to make animals stronger, more immune…to disease and injury, not to make them…become giant gluttons!" We didn't see any of these side effects during the lab experiments on the rats, he thought. Granted, we gave them very small doses, unlike with the baby shark (or me, for that matter). We weren't in charge of feeding them afterwards, and we came out here quickly after what seemed successful experiments. I guess I was too proud to wait and see if there would be any undesirable after-effects. I just saw quick healing, and we all jumped to conclusions. There was an email or two from the people in the lab; we never got around to reading them—maybe the messages were a warning about such after-effects. I don't know—it's too late for me now.
He looked down at his arms.
They looked tasty.
He was salivating.
"Come on, John," he said. "You can't be serious."
The growing happens only after eating, he thought as he looked at that meaty flesh. My powers of healing, particularly strong after my large dose, could compensate for the bite wounds, at least to enough of an extent that, if a boat comes by, I can be taken away and saved.
His stomach growled again. He was shaking.
"I can't take this anymore. It's crazy, but I have to do it."
He bit off a huge chunk off of his left forearm. Blood sprayed everywhere.
"Aaaaah!" he screamed in clenched teeth as he began chewing.
The pain was excruciating, but the delicious flesh was satisfying in a way that made him forget the throbbing.
He swallowed. He felt the flesh enter his stomach, filling in the void.
"Aaaaah!" he sighed. Thanks to the Aggrandizin, the pain was subsiding, the blood clotted faster, and he felt every encouragement that the wound would soon just be a crater in his arm. He felt those familiar vibrations, and grew a tiny bit.
He enjoyed a few fleeting minutes of relief from his hunger. The pain in his arm disappeared.
"Wow," he said. "That was a fast recovery."
Then he felt another hunger pang.
"And that was fast, too," he said. "Fuck!" I can't just keep taking bites out of myself…but what else am I going to eat? My shit when I crap? (Funny thing: I've eaten so much, yet I never piss or shit…why is that? Is it another side effect of the Aggrandizin? What kind of bizarre voodoo drug did we synthesize in that lab?) "Am I drugged, or possessed of a devil?"
He looked at his left arm, where the freshly healed crater was. Then he looked at the flesh right next to it, just before his elbow.
Maybe a huge ship will sail by and find me here, he thought. Hope, hope.
Another pang…a sharp, stinging one.
He opened his mouth wide, and his head dove onto that arm.
"Unh!" he grunted as he sank his teeth into that coveted arm-flesh. His teeth dug deep enough to reach the bone, several square inches of which were exposed after his ripping the flesh off, spraying blood all over the place and making him groan muffled whimpers of pain as he chewed.
Again, when the flesh hit his stomach, the more important pain was gone…for the moment.
He trembled, then grew another tiny bit.
With my growing size, I should be more visible to ships, he thought, massaging his throbbing arm as it healed. Then again, I'm not growing as much as I was before. It must be because I'm eating myself instead of eating other living things.
Speaking of eating, he wanted more flesh. He felt like a pregnant woman whose belly was a womb with half a dozen hungry fetuses aching for food.
"I'm getting used to the pain," he said as he looked at his upper left arm. "If only I could get used to the hunger."
He bit off the bicep; again, the bite went all the way to the bone. His face was red with blood. He grunted in pain, but indeed, he found it more and more bearable.
His want of flesh continued to grow.
He looked over at his right arm now…and he coveted the flesh he saw.
All I do is want, want, want! he thought. I always want more! I only want more! I can never stop wanting! I'm wanting of flesh on my arms, and I only want to eat more. I have a surplus of want, and a lack of anything to eat other than myself! This is madness!
He bit off a chunk from his right forearm. He was so used to the pain now that he easily ignored it. His body wasn't growing anymore, though.
The only thing growing now was his hunger. He now felt as though his, so to speak, belly-womb was housing a dozen so-to-speak hungry fetuses instead of half a dozen.
The moments of relief were getting shorter and shorter. Within an hour, he'd ripped off and eaten all of the flesh on his arms. He'd chewed off the flesh on his hands and fingers. All that was left of them were bone and ligaments.
The sharp ends of his finger-bones were useful; he could use them to rip off flesh on parts of his body that he couldn't reach with his head.
Now that his arm flesh was all gone, he looked down at his legs.
He licked his lips.
Oh, so much meat, he thought.
Without even hesitating anymore, he dug his bony fingers deep into his upper right leg flesh, tore off a huge chunk, right down to the bone, and didn't seem aware of any pain in his leg as he brought the meat up to his grinning face. He munched on it with manic glee.
No sooner did he gulp it down and feel it hit his thankful stomach, but he felt more hunger pangs.
I'm slowly killing myself, he thought, but I can't help it. It's my nature. I'm the scorpion on the scorpion. I'm sitting on my own back, crossing the river and stinging myself.
He tore off a chunk of flesh from his upper left leg and stuffed the bloody mass into his greedy mouth. He chomped on it with a gory grin.
"Mmm!" He swallowed and belched.
Next, he ripped off his left calf and stuffed it in.
I am so high in protein! he thought, then let out a macabre laugh.
He shrank a little.
He ripped off his right calf and ate it. His hunger went on in an unbroken line—no more brief moments of relief, not even for a few seconds. He dug his fingers into the remaining flesh on his legs, tore it all off, and ate it. He shrank some more.
Within another hour, all four of his limbs were just bone and ligaments. His hunger, the only thing growing, was growing far faster than he was shrinking.
He dug his fingers into his cheeks, ripped them off, and ate them. The sight of all of his teeth, in what would have looked like a perpetual grin (were he to have looked at his reflection in the water), made no difference in terms of his facial expression; for if that cheek and lip flesh were to have remained on his face, he'd still have been grinning from ear to ear, his teeth just as fully exposed, he was enjoying his ghoulish meal so much.
The healing effects of the Aggrandizin were still working just enough to keep him alive, but they were abating, fading away little by little. Though his healing was slower, his growing urge to eat overshadowed the pain from the wounds so much that he seemed numb everywhere except in his stomach.
He ripped all the skin off of his face. After eating that, he felt himself shrinking again. He was now just slightly larger than his original size.
He looked out to sea; he saw no ships anywhere.
His stomach was growling, louder and louder, like a thousand voices inside, whining for food.
He felt his energy beginning to wane, too.
With effort, he ripped off the flesh on his chest and ate it. In his skeletal hands, he cupped the blood, as best he could, to stop it from dripping on the sand, then he drank it.
Still, he just got hungrier and hungrier.
He tore the flesh off his neck, all the way around from the front to the back. His neck bone, larynx, and esophagus were showing. He ate the flesh, chewing with lethargic slowness.
He looked down at his chest, where his upper ribcage was showing. Though he'd shrunk all the way back to his original size, his stomach was bloated with all the rest of his eaten body. Instead of being rotund, though, it oddly had a number of bumps on it.
Yet still, his stomach felt as if empty.
He ripped the flesh off of his buttocks and ate it. Then, amazingly, his cock and balls became appetizing, so he tore them off and ate them, his hunger so severe that he gave no thought to how disturbing it would be to lose them. There is no castration anxiety when one is as famished as he was, apparently.
He was sitting in a lake of reddened sand. All that was left of his body were his skull-like face, with his eyeballs showing because he'd ripped off and eaten his eyelids, his exposed skeleton—his ribcage being the only cover of his heart and lungs—and the skin on his back.
He couldn't bear the sight of his lower body. He'd have shuddered to think what his face must have looked like in the reflection in the water. What have I reduced myself to? he wondered. And the Aggrandizin is still keeping me alive…how?…even though I can feel my life slowly fading away. My energy is draining from me, little by little. The only energy I seem to have in large amounts is in my guts.
He looked out to the polluted sea…still, no ships to be seen anywhere out there.
He looked back down at his bloody, mutilated body, at the protrusions in his belly.
"There is nothing good to see, anywhere," he said. "And still, I'm hungry." His bony index fingers stabbed into his eyes. "Unghh!" He pulled them out of their sockets, each pull making a popping sound, then he popped them into his mouth.
He wanted to sob, but he had only blood for tears pouring out of the sockets.
His stomach felt about to burst, it was so stuffed.
Still, he hungered.
He began scratching his back for more flesh to eat, his diminishing strength making those scratches slower and shallower. As he stuffed his bony face with the bloody flesh, he felt the strain on his stomach.
And he was still hungry.
After ripping off all the flesh he could reach on his back and eating it, he tore into his guts, ripped out his pancreas, bits of intestine, and his kidneys. He stuffed the meat in his mouth. It tasted awful, but it gave some relief—not much—to his hunger.
How am I still alive? he wondered. I can feel myself slowly weakening, slowly dying, but I should have already been dead long ago. Was the dose I gave myself really so strong as to sustain me in this extremity?
His hunger pangs continued to grow, even as his energy was fading away.
I don't wanna live anymore, he thought. That's for sure. Maybe I can speed up my death. Destroying my vitals should do it. The apes that had the Aggrandizin died soon enough when I ate them; surely I can die soon enough if I keep eating myself, right to the bone. Surely the Aggrandizin won't keep me going forever.
He dug his hand under and behind his ribcage and tore out a lung. He ate it. Fantastically, he was still conscious and breathing. He tore out and ate the other lung: he still lived. He couldn't believe it—the drug apparently made breathing unnecessary to live. He ripped out his heart and ate it. The Aggrandizin was, to some extent, counteracting all of these mutilations, though his life was ever so slowly fading away.
Has the drug made me immortal? Am I hallucinating in my fading consciousness? Is that how these impossibilities are possible?
He felt a jiggling of those protrusions in his stomach—not the rumblings of hunger so much as the sensation of what seemed to be small living beings in there.
Am I immortal, or are there immortal beings inside me? Has the drug resurrected and regenerated all the bits of flesh that I've digested? Is Aggrandizin making us all immortal, me and those inside me? Or, in my delirium, am I hallucinating their existence?
With his energy level so low now, he couldn't lift his arms to rip off any more body parts to stuff into his mouth. Yet his hunger kept growing…especially the hunger of whatever had awoken and was growing and fidgeting around inside his belly.
Those things were poking bubbly bumps against his belly, making wavelike movements along the surface of his skin there. After a while of this continued pressure, one of the things poked a hole in his belly, spitting blood out of the opening.
It kept pushing, ripping a larger hole and spraying out more blood. The rest of his body lay still and, finally, he was dead. The thing pushed its way out of the hole, followed by all of the others, one by one, until the bloody belly lay empty on the soaking red sand.
Those things, kept alive by the Aggrandizin that they all shared, were blood-covered blobs, lumpy but basically spherical, with mouths that had serrated, teeth-like protrusions all along the edges. They looked like gruesome, deformed 3-D Pac-men, each about the size of a tennis ball. They rolled out over the sand in a blind search for food, their mouths flapping open and shut without ever tiring, while making grotesque grunting sounds: "Ngah-ngah-ngah-ngah!…" They quickly turned beige as more and more sand grains stuck to the blood on them.
Some rolled out to sea, eating the plastic and dead fish. They would die of food poisoning minutes after their exposure to the impurities in the water. Others rolled into the woods, eating the few remaining blades of grass and leaves on the trees. As they ate, they grew somewhat.
By the time they'd eaten everything alive on the island, they too found their energy waning as their insatiability only strengthened. Instinctively, as they had sensed while hibernating inside Gula's guts, they knew that eating each other was futile. Each of them about the size of a medicine ball now, they just lay on the ground, rocking from side to side as their mouths faced the sky, as if babies wishing to cry out to their mother for something to eat.
All of them were in the middle of the leafless forest, hidden by the trunks of the trees. Night was falling. They were saving what little energy they had left for any possible food that chance might provide. They didn't make the slightest sound.
Within an hour, the stars and moon offered the only light. A large, lost boat came ashore, filled with about twenty people—adults, elderly, and children.
"Where are we?" a ten-year-old boy among them said as they began disembarking.
"I don't know," his mother said. "It stinks here. Pollution in the water…Do I smell blood?"
Everyone got off the boat after a few minutes. Some of them, those who hadn't smelled the blood, wandered into the woods.
The eating blobs felt the vibrations from all the footsteps. Their mouths curled up into smiles.
Published by Mawr Gorshin
I'm merging the variety of topics I've blogged about--which include literary and film analyses, anarchism, socialism, libertarian-leaning Marxism, narcissistic abuse, and psychoanalysis--into a coherent philosophy centred on dialectical materialism, dialectical monism, and object relations theory. Now, one dialectical opposition is that between the erotic and the ascetic, so accordingly, my writing encompasses the sexual as well as the philosophical; the former can be found in my publications on the Literotica website, as well as my self-published (erotic) horror writing on Amazon. View all posts by Mawr Gorshin
Published August 19, 2020 August 19, 2020
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Dad and son drove teenager to South Shields car park to carry out 'revenge attack'
South Shields man shouted 'ah cushty' as he was shot by police, hears inquest
Jurors at an inquest into the death of a man who was shot by police have been played audio of him shouting "go for it" at firearms officers who had repeatedly told him to drop the gun he was carrying.
Monday, 12th November 2018, 4:03 pm
Updated Monday, 12th November 2018, 4:09 pm
James Carlo Wilson, inset, and the scene of the 2016 shooting.
James Carlo Wilson's father believed his son aimed to "go out in a blaze of glory" and wanted to be killed by a police marksman, the hearing in Newcastle was told.
Mr Wilson junior, 24, called Northumbria Police to demand armed response officers come to see him and was still on the phone when he was hit by first a plastic bullet then five seconds later by a rifle round which hit him in the chest.
Mr Wilson shouted "ah cushty" - slang for "great" - after the first round was fired.
A loud bang was recorded on the open mobile phone line then the police officer who fired the second round called out "shots fired, first aid required".
In the minutes before the confrontation, drunken Mr Wilson repeatedly asked the police call handler when the armed response officers were coming and made threats.
When the call handler said "so you're not going to be peaceful", he replied "I'm going to shoot them" before swearing.
Moments before the shot was fired, as officers told him "put it down", Mr Wilson shouted "Go for it, go, go, go."
Outlining the case to the jury, Newcastle coroner Karen Dilks said an air pistol was recovered from the scene outside his former partner's home in Frenchman's Way, South Shields.
Mr Wilson died in hospital on April 1, 2016, three days after he was shot.
In a statement read to the inquest, his father, Carl Wilson, said: "I think he wanted to go out in a blaze of glory. That's why he did it the way he did.
"I think he wanted the police to kill him and he used the police to commit suicide."
James Wilson, who was on crown court bail at the time, and his close friend Sean McLellan had shared 48 bottles of beer on the Easter Monday, with the shooting happening in the early hours of the next day.
At 12.57am Northumbria Police received an anonymous call, naming Mr Wilson as having a black 9mm gun and that he was in Frenchman's Way.
The three-week inquest at the Mansion House heard that a traffic officer was sent to drive past the address in an unmarked car and saw someone holding a black object.
At 1.15am there was a second call from the same number. Mrs Dilks said: "The caller, among other threats, said he would not put the gun down, he didn't care if anyone got hurt and he was going to shoot the officers who attended."
Armed officers drove to the scene and parked around 30 metres away from Mr Wilson, with in-car video showing him pointing his weapon "several times" towards the officers, the coroner said.
He did not put the gun down when he was told to, Mrs Dilks said, and he was shot with an "attenuated energy projectile" - a plastic bullet - before he was hit by the rifle round fired by another officer.
Police attempted to carry out first aid at the scene and he was taken to the Royal Victoria Infirmary where he died.
Mr Wilson was outside the home of his ex-partner Kayleigh Reay and she told the inquest they split up after he had been self-harming.
The jury heard there had been a previous cliff-top incident where he had to be saved by police.
Mrs Dilks said the jury may consider, among other issues, whether Mr Wilson provoked the police "with a view to officers ending his life".
Mr Wilson lived in South Shields with his mother Tracy Todd, who told the inquest she had never known her son to have a BB gun.
She said: "James is not the type of person to have a firearm."
Mr McLellan strongly disputed the theory that Mr Wilson wanted to go out in a "blaze for glory", adding that he hated his father and had rarely seen him.
Mr McLellan said: "James worshipped Kayleigh, all he wanted was a family with (her).
"There was a time up the cliffs when he was not in the right frame of mind. He never wanted to take his own life, never."
The inquest continues.
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{"url":"https:\/\/termpapernow.com\/samples\/using-audio-in-machine-learning-7990\/","text":"# Using audio in machine learning\n\nThe first and most vital step in order to be able to use audio in machine learning, is to understand how raw audio is being perceived by humans, and try to present in electronic format this information, in a way that resembles this perception. For this task, we extract features out of the audio signal.\n\nThe most basic information about the perception of human ear is going to be explored, without giving an excessive explanation on audio theory.\n\n\u2014\u2014\u2014\u2014-\n\nHire a custom writer who has experience.\nIt's time for you to order amazing papers!\n\norder now\n\nRecording of a music piece is the first step in audio representation on computers and devices.\nSound is, in a more simplistic approach, vibrations, or else changes in the air pressure \\cite{WesternElectricCo}.\\newline\n\nIn digital recording, the differences in air pressure at a particular time and space can be captured, and the sound is represented as a sequence of discrete numbers (a waveform). This is different from the analog signal, where the values are continuous \\cite{Proakis1992DigitalSP}.\nWe call every one of these numbers a sample, and we call sample rate the amount of samples per second. In reverse, these numbers can be converted back to sound when we listen to them from a device, with the opposite procedure.\\newline\n\nSample rate is an important element in sampling, as it should be above than the input frequency, otherwise the result will be of low quality and maybe not resembling correctly the waveform. Furthermore, the bit rate, the number of bits used to store each sample, is also an important factor where the quality of the recording depends to \\cite{PeterElsea}.\n\nGiving some examples, 8,000 Hz is the telephone standard rate, 22,050 Hz and 44,100 Hz are common rates used for audio CDs, and finally 48 kHz and larger sampling rates are used in high quality video recordings and on professional video equipment.\n\n\u2014\u2014\u2014\u2014-\n\nGiven the above information, it is obvious that the digital signal is a complex waveform, and the use of it to create a classifier, or for any other MIR application is not very viable, as it requires powerful hardware. Even if using a sampling rate smaller than the common 44,100 Hz, for example half of it, 22,050 Hz, the amount of arithmetic values that have to be stored and trained is still huge. In every second, 22,050 values are stored, meaning that for a one minute song, 1,323,000 samples are stored. As a result, the samples, or else, the waveform of the audio piece cannot be used directly. Another manipulation has to be done to the audio before is ready to be used.\\newline\n\nFor this reason, we extract features out of the music piece. Exist features that are relevant or irrelevant to the digital audio signal itself.\n\nMcKay and Fujinaga \\cite{McKay2004AutomaticGC} have proposed that features can be categorized into low-level, high-level and cultural features.\nThe low-level features can be obtained from the audio signal itself, and do not have a musical meaning. On the other hand, high-level features give musical information, such as the instruments used. At last the cultural features are based in social information \\cite{Bogdanov2009FromLT}\\cite{McKay2004AutomaticGC}. \\newline\n\nIn this section, and in the thesis in general we are going to focus on the low-level features of the audio.\n\nMany low-level audio features have been proposed and applied into different music genre classification systems.\nSome of the most important of them, that present the spectral or temporal information of the audio, are:\n\nTempo, Spectrogram, Log spectrogram, Mel-spectrogram, Log mel spectrogram, Mel-Frequency Cepstral Coefficients (MFCCs), Chroma, Spectral Centroid, Spectral Contrast, Spectral Flatness, Spectral Rolloff, Spectral Flux, Tonnetz, Zero Crossing Rate and Root-Mean-Square (RMS) energy.\\newline\n% temporal envelope, tempo histogram,\n% Spectral Spread, Spectral Flux, Measure\n% 159_Paper5.pdf\n\nFirstly, in order to give an understanding about feature extraction, it is important to provide some information about Fourier Analysis, as it consists the first step in many feature extractions.\n\nFigure \\ref{fig:Audio Waveform} \\cite{Haugen} shows an example of a sinusoid waveform display of a recorded audio piece. The x axis represents the time, while the y axis represents the amplitude.\\newline\n\n\\begin{figure}\n\\centering\n\\includegraphics[width=1.0\\textwidth]{waveform}\n\\caption[Audio Waveform]{Audio Waveform}\n\\label{fig:Audio Waveform}\n\\end{figure}\n\nIn this time domain representation, we do not have enough information about how the sound really is.\\newline\nTherefore, we have to get into the frequencies domain, the Spectrum, by decomposing the time series. This is were Fourier Transformation (FT) is used.\nIn general, FT and specifically Short-Time Fourier Transformation (STFT) is frequently used in audio signal processing \\cite{Cohen:1995:TAT:200604}.\\newline\n\nThe mathematical definition \\cite{Allen1977AUA} of STFT is :\n\n\\begin{eqnarray}\nX_m(\\omega) &=& \\sum_{n=-\\infty}^{\\infty} x(n) w(n-mR) e^{-j\\omega n}\\nonumber \\\\[10pt] &=& \\hbox{\\sc DTFT}_\\omega(x\\cdot\\hbox{\\sc Shift}_{mR}(w))\n\\end{eqnarray}\n\nwhere\n\\begin{eqnarray*}\nx(n) = \\hbox{input signal at time $n$}\\\\\nw(n) = \\hbox{length $M$\\ window function (\\textit{e.g.}, Hamming)}\\\\\nX_m(\\omega) = \\hbox{DTFT of windowed data centered about time $mR$}\\\\\nR = \\hbox{hop size, in samples, between successive DTFTs.}\\\\\n\\end{eqnarray*}\n\nWe break the signal into windows, (the time for which the signal is considered for processing) and we calculate the Discrete Fourier Transformation for every window. Usually the window function used is Hamming.\nThe data acquired in a window is called a frame.\n\nOver the time period measured, the signal is divided into its frequency components, which are also sinusoidal functions, having their own amplitude and phase \\cite{Allen1977AUA}\\cite{All}\\cite{Chauhan2015VoiceR}.\n\n% J. B. Allen, \u201cApplication of the short-time Fourier transform to speech processing and spectral analysis,\u201d Proc. IEEE ICASSP-82, pp. 1012-1015, 1982.\n\nIn Figure \\ref{fig:Audio Signal in Time and Frequency Domain} appears an example of an audio signal in the Time and Frequency Domain:\n\n\\begin{figure}[htbp!] \\centering\n\\includegraphics[width=0.5\\textwidth]{FFT}\n\\caption[Audio Signal in Time and Frequency Domain]{Audio Signal in Time and Frequency Domain}\n\\label{fig:Audio Signal in Time and Frequency Domain}\n\\end{figure}\n\n% https:\/\/www.nti-audio.com\n\nNow, being into the Frequency Domain, we have only frequency information, and the optimal would be to have also temporal information, as this is also the way humans perceive sounds in the cochlea. Therefore, Time\/Frequency representations (spectrograms) are used.\\newline\n\nSpectrograms are a time series of frequency compositions. Short Time Fourier Transformation is applied for a specific time where the signal is seemingly stationary, and the resulted diagram is rotated by 90 degrees. All these diagrams combined create the spectrogram.\\newline\n\nIn Figure \\ref{fig:Audio in Time, Frequency and Time\/Frequency Domains} \\cite{DavidForsyth} is presented an audio piece in its three representations: Waveform (Time Domain), Spectrum (Frequency Domain) and Spectrogram (Frequency\/Time Domain). With this frequency over time representation, it is possible to compare sounds as images.\nDetails about the features that are going to be extracted in this thesis are given bellow.\n\n\\begin{figure}[htbp!] \\centering\n\\includegraphics[width=0.5\\textwidth]{waveform-spectrum-spectrogram}\n\\caption[Audio in Time, Frequency and Time\/Frequency Domains]{Audio in Time, Frequency and Time\/Frequency Domains}\n\\label{fig:Audio in Time, Frequency and Time\/Frequency Domains}\n\\end{figure}\n\n% http:\/\/luthuli.cs.uiuc.edu\/~daf\/courses\/cs-498-daf-ps\/lecture%208%20-%20audio%20features2.pdf\n\n\\subsubsection{Spectrogram}\nThe spectrogram of an audio wave is extracted by following the steps analyzed above.\n\nThe two steps summarized are:\n\n1) Dividing the signal into frames.\n\n2) Compute the amplitude spectrum of the signal using Short Time Fourier Transformation.\n\nIt is basically a series of short term DFTs.\n\n%\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\n\\subsubsection{Log Spectrogram}\nHumans do not perceive loudness linearly, but almost logarithmic, and for that it is usual to get the logarithmic of the amplitude, creating the Log Spectrogram \\cite{Rabiner:1993:FSR:153687}\\cite{Logan2000MelFC}.\n\n%\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\n\\subsubsection{Mel Spectrogram and Log Mel Spectrogram}\nMel Spectrogram and Log Mel Spectrogram are used because the human ear, does not perceive frequencies and pitch linear (similar to the case of loudness). The cochlea acts like a filter, concentrating and emphasizing only certain frequencies. This scale of perception is called mel.\n\nWith mel spectrograms the spectrum is smoothed, emphasizing the most important frequencies, approximating better the way the human ear perceives sound. We perceive lower frequencies to be more important than the higher ones (we understand pitch changes better at low frequences). As a result, more mel frequency filters exist on the low frequency regions and less on the high ones.\n\nTo get into the mel scale, we use triangular overlapping windows like in Figure \\ref{fig:Mel frequency filters}.The mathematical formula \\cite{OShaughnessy2000SpeechC} for converting from frequency to Mel scale is:\n\n\\begin{eqnarray}\nm=2595\\log_{10}(1+\\frac{f}{700})\n\\end{eqnarray}\n\nGetting the logs of the powers at each of the mel frequencies is also common, and a necessity for extracting the MFCC feature \\cite{Rabiner:1993:FSR:153687}\\cite{Logan2000MelFC}.\n\n\\begin{figure}[htbp!] \\centering\n\\includegraphics[width=0.6\\textwidth]{mel}\n\\caption[Mel frequency filters]{Mel frequency filters}\n\\label{fig:Mel frequency filters}\n\\end{figure}\n\n%\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\n\\subsubsection{Mel Frequency Cepstral Coefficients}\n\nMel Frequency Cepstral Coefficients (MFCCs) are one of the most used features in music and speech recognition, as it can extract the features of human voice. They are used more in audio\/speech recognition and classification rather than simple mel spectrograms.\n\nOnce again, MFCC is based on the way human ear perceives sounds. In particular, humans do not perceive the sounds that are over 1000 Hz.\n\nTo extract this feature, after (a) dividing the audio signal into frames, (b) applying Fourier Transformation and (c) applying the mel filter, (d) we smooth the log mel spectrogram by using one more frequency transformation, the Discrete Cosine Transformation \\cite{doi:10.1080\/03043799808928258}\\cite{Muda2010VoiceRA}\\cite{Chauhan2015VoiceR}.\n\n\\subsubsection{Deltas and Deltas-Deltas}\nIn sound, the changes in the cepstral features over time are very important. Hence, we use Deltas, which represent the change of the MFCC coefficients over time.\n\nDelta feature gives the velocity, while double delta gives the acceleration \\cite{Muda2010VoiceRA}.\n\n% http:\/\/luthuli.cs.uiuc.edu\/~daf\/courses\/cs-498-daf-ps\/lecture%208%20-%20audio%20features2.pdf\n\n% Summary: Process of Feature\n% Extraction\n% \u2022 Speech is analyzed over short analysis window\n% \u2022 For each short analysis window a spectrum is obtained\n% using FFT\n% \u2022 Spectrum is passed through Mel-Filters to obtain MelSpectrum\n% \u2022 Cepstral analysis is performed on Mel-Spectrum to\n% obtain Mel-Frequency Cepstral Coefficients\n% \u2022 Thus speech is represented as a sequence of Cepstral\n% vectors\n% \u2022 It is these Cepstral vectors which are given to pattern\n% classifiers for speech recognition purpose\n% http:\/\/www.speech.cs.cmu.edu\/15-492\/slides\/03_mfcc.pdf\n\n\\subsubsection{Chroma}\nAs humans perceive pitch periodically, because of the way pitch traverses the helix, pithes that are octave related, are considered similar (they have the same harmonic role). Usually the chroma range is the twelve pitches of the chromatic scale (12 bins).\n\nIn chroma representations (chromagrams), for each time step in the spectrogram, the amplitudes of the frequencies with the same chroma bin are summed \\cite{Jiang}.\n% http:\/\/www.cs.northwestern.edu\/~pardo\/courses\/eecs352\/lectures\/MPM14-Chromagrams.pdf\n\n% coefficients that belong to the same chroma are summed.\n% that are perceived as similar, are presented as approximate colors.\n% A chroma representation of an audio can be derived by summing up all pitch coefficients that belong to the same chroma.\n\n\\subsubsection{Spectral Contrast}\nSpectral Contrast presents \u201cthe decibel difference between peaks and valleys in the spectrum\u201d \\cite{Yang2002SpectralCE}.\n\n\\subsubsection{Tonnetz}\nTonnetz, is a geometric representation that visualizes the relations between different notes or pitches \\cite{LeonhardEuler}.\n\n% of equal-tempered pitch intervals grounded in music theory.\n\n% \u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2013\n% \u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014-2.2\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014-\n% \u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2014\u2013\n\n\\section{Previous research}\n% Uncomment this line, when you have siunitx package loaded.\n%The SI Units for dynamic viscosity is \\si{\\newton\\second\\per\\metre\\squared}.\n% \\begin{figure}[htbp!] % \\centering\n% \\includegraphics[width=1.0\\textwidth]{minion}\n% \\caption[Minion]{This is just a long figure caption for the minion in Despicable Me from Pixar}\n% \\label{fig:minion}\n% \\end{figure}\n\nOn the last two decades, several studies have been made in the area of automatic music genre classification, and many different approaches and machine learning algorithms have been tested.\n\nFollowing, is presented briefly the state-of-the-art in automatic music genre classification. Due to the use of different databases and number\/type of genres explored in each research, the comparison of them in the face of accuracies is not completely objective.\n\nThe information given bellow is not a complete representation of all the features and systems used in automatic genre classification, but more of a presentation of the milestones in the field.\\newline\n\nIn general, the following traditional techniques have been explored in the field of automatic music genre classification:\n\\begin{itemize}\n\\item Gaussian models \\cite{Tzanetakis2002MusicalGC}\n\n\\item Gaussian Mixture Models \\cite{Tzanetakis2001AutomaticMG}\n\n\\item Support Vector Machines \\cite{Xu2003MusicalGC}\n\n\\item Hidden Markov Models \\cite{Jiang2}\n\n\\item k-Nearest Neighbour clasifiers \\cite{Tzanetakis2002MusicalGC}\n\n\\item Linear Discriminant Analysis \\cite{Tzanetakis2001AutomaticMG}\n\n\\item Neural Networks \\cite{Pons2016ExperimentingWM}\\cite{pikrakis}\\newline\n% \\cite{Dieleman}\n\n\\end{itemize}\n\n% Random Forests[] % Linear Prediction Coding\n% Explicit Time Modelling with Neural Network\n% Tree-based Vector Quantization\n\nFollowing is presented a number of research work in the field of music genre recognition:\n\\begin{itemize}\n\\item Tzanetakis et. al. were the first to introduce music genre classification, proposing classification based on extracting timbral texture (Spectral Centroid, Spectral Rolloff, Spectral Flux, MFCC), and rhythmic (Beat Histogram) and pitch content (Pitch Histogram), using a Gaussian Mixture Model classifier. They achieved an accuracy of 61\\% in ten genres. They continued using support vector machine and Linear Discriminant Analysis \\cite{Tzanetakis2002MusicalGC}\\cite{Tzanetakis2001AutomaticMG}.\n\n\\item Li et al., proposed a new feature extraction technique, Dubechies Wavelet Coefficient Histogram (DWCH), and concluded that for music genre classification the timbral texture provides better results than rhythmic or pitch content. They achieved an accuracy of 61\\% in 10 genres\\cite{Li2003ACS}.\n\n\\item Jiang et al. proposed that spectral contrast features give better results than MFCC \\cite{Jiang2}.\n\n\\item Xu et. al. used Support Vector Machines, using MFCC LPC-derived cepstrum, Spectrum power, ZCR and Beat spectrum \\cite{Xu2003MusicalGC}.\n\n% Meng et. al. [28] % Lidy et. al. [22]\n\n\\item Bergstra et al. proposed a classification by using a collection of frames of audio, instead of extracting a solo feature per song. They achieved an accuracy of 82,5\\% for 13,4 second segments \\cite{Bergstra2006AggregateFA}.\n\n\\item McKay and Fujinaga used a hierarchical classification system, and they considered the combination of features \\cite{McKay2008CombiningFE}\\cite{McKay2010ImprovingAM}.\n\n\\item Schindler and Rauber proposed a combination of audio and visual features, with positive results \\cite{Schindler2015AnAA}.\n\n\\item Pikrakis proposed the use of deep networks, using the rhythm signature of the audio pieces \\cite{pikrakis}.\n\n\\item Recently, with the rapid development of deep learning, it has been proposed by many the feature learning (spectral or temporal features) \\cite{Humphrey2013FeatureLA}\\cite{Sigtia2014ImprovedMF}\\cite{Deshpande}\\cite{Hamel2010LearningFF}.\n\n% [13]LEARNING TEMPORAL FEATURES USING A DEEP NEURAL\n% NETWORK AND ITS APPLICATION TO MUSIC GENRE\n% CLASSIFICATION\n\n% Il-Young Jeong and Kyogu Lee\n% Music and Audio Research Group Graduate School of Convergence Science and Technology, Seoul National University, Korea\n\n\\item With the development of machine learning, many researchers have used convolutional neural networks for automate music genre classification\n\\cite{DBLP}\n\\cite{DBLP:journals\/corr\/LeeN17a}\n\\cite{DBLP:journals\/corr\/HersheyCEGJMPPS16}\\cite{Choi2016AutomaticTU}\n\\cite{Choi2017ConvolutionalRN}.\n\n% [http:\/\/cs231n.stanford.edu\/reports\/2017\/pdfs\/22.pdf#cite.gwardys] % [5][8] % [13] % M. S. Keunwoo Choi, Gyorgy Fazekas. Automatic tagging\n% using deep convolutional neural networks. 2016.\n\n\\item Other researches have used deep recurrent neural networks \\cite{Freitag2017auDeepUL}\\cite{Irvin2016RecurrentNN}.\n\n% [Chun Pui Tang, Ka Long Chui, Ying Kin Yu, Zhiliang Zeng, Kin Hong Wong]\n\n\\end{itemize}\n\nEven though computer vision have reached very good results, and deep learning algorithms are being created continuously meliorating the results, research in automatic music genre recognition is not as popular.","date":"2019-02-23 08:23:27","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 1, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 0, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.4468011260032654, \"perplexity\": 1966.2856465432662}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.3, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2019-09\/segments\/1550249495888.71\/warc\/CC-MAIN-20190223082039-20190223104039-00601.warc.gz\"}"}
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Q: Añadir opción de subtítulos a un vídeo en HTML
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<video src="video.mp4" poster="imagen.png" controls=""></video>
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Buenas una vez más a tod@s,
Tengo que insertar un vídeo en una web, pero no sé cómo indicar en los controles que el subtítulo sea opcional. ¿Hay alguna manera sólo usando HTML?
Muchas gracias por adelantado.
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R.O.A est la marque du constructeur espagnol de motos, triporteurs et camionnettes Motorizadas Onieva installé à Madrid. Le nom de la marque est constituée des propres initiales de son fondateur, Rafael Onieva Ariza qui l'a crée en 1952. Plusieurs modèles de motos, tricycles ont été produis ainsi que des fourgonnettes Tempo Matador sous licence à partir de 1961. La société est renommée Tempo Ibérica SA en 1963, puis est rachetée et intégrée par Barreiros SA en 1966.
Histoire
La société Indústrias Motorizadas Onieva - IMO est créée en 1952 par Rafael Onieva Ariza. Elle débute la fabrication de motos de sa propre conception en utilisant un moteur Hispano Villiers, en 1953, commercialisées sous la marque R.O.A.
En 1958, IMO présente une « micro-car » à la Foire de Barcelone, une voiturette à trois roues animée par un moteur deux cylindres de 197 et 250 cm³ Hispano Villiers. La ligne s'inspire très fortement de l'Isetta du constructeur italien Iso Motors mais, en raison de son prix élevé, environ 45.000 pesetas à l'époque, elle n'est produite qu'à 6 exemplaires.
En 1960, IMO s'associe au constructeur de motos allemand BMW Motorrad pour assembler en Espagne les motos BMW R 27 destinées au groupe de la circulation de la Garde civile. Les motos et les triporteurs R.O.A. connaissent un grand succès commercial, avec plus de 40.000 unités produites au cours des 17 années d'activité du constructeur.
En 1960, IMO construit aussi une petite série de 12 exemplaires d'un mini porteur à quatre roues, inspiré du « Farmobil » allemand, équipé d'un moteur à essence BMW deux cylindres, quatre temps de 600 cm³ de cylindrée. Le projet doit être abandonné rapidement en raison du refus du constructeur allemand de délivrer une licence de fabrication et de l'impossibilité d'obtenir des licences d'importation pour les moteurs BMW : à l'époque, l'Espagne franquiste est soumise aux sanctions internationales de l'ONU qui interdit tout échange commercial sauf pour les produits agricoles.
Au début des années 1960, l'Espagne connait un fort développement interne et la demande de véhicules industriels augmente fortement. En 1961, IMO s'associe avec la société allemande Vidal & Sohn Tempo-Werk GmbH de Hambourg pour fabriquer les fourgons Tempo Matador en Espagne. La société Tempo Onieva SA est spécialement créée à cet effet, dans laquelle Industrias Motorizadas Onieva, Barreiros SA et Rheinstahl Hanomag, propriétaire de Tempo et déjà partenaire de Barreiros dans une société de fabrication de tracteurs agricoles, sont actionnaires à parts égales.
Ces fourgons ont une charge utile de 1,5 tonnes. Ils sont construits sur un châssis tubulaire et disposent de la traction avant. Ils sont équipés d'un moteur Diesel léger Barreiros de 55 ch. Ces véhicules sont les premiers fourgons sur le marché espagnol à être équipés d'un moteur diesel. À peine 4.000 exemplaires sont produits en 4 ans.
ROA a également fabriqué une série de 100 cabines en fibre de verre pour les premiers camions Barreiros.
En 1963, la société a été renommée Tempo Ibérica SA. En 1967, elle est rachetée et intégrée dans Barreiros SA.
Bibliographie
Histoire de Industrias Motorizadas Onieva SA.
Notes et références
Constructeur motocycle ayant son siège en Espagne
Constructeur automobile ayant son siège en Espagne
Constructeur automobile disparu
Entreprise fondée en 1952
Entreprise disparue en 1967
Entreprise espagnole disparue
Marque espagnole
Barreiros
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\section{Introduction}
\section{Introduction}\label{sec:intro}
In the last decades, much work has been devoted to networked control systems with a focus on cybersecurity aspects.
Communications over shared mediums potentiates the exploitation of vulnerabilities that may result in consequences, sometimes, catastrophic.
A central problem in networked multi-agent systems is the so-called consensus problem, where a set of agents interacting locally through a communication network attempt to reach a common value. In other words, the final value is the outcome of running a distributed algorithm among nodes which can communicate according to the network topology.
Therefore, the problem of consensus is the basilar stone of a multitude of applications, ranging areas such as: optimization~\cite{tsitsiklis1986distributed,johansson2008subgradient}; motion coordination tasks -- flocking and leader following~\cite{jadbabaie2003coordination}; rendezvous problems~\cite{cortes2006robust}; computer networks resource allocation~\cite{chiang2007layering}; and the computation of the relative importance of web pages, by PageRank like algorithm~\cite{silvestre2018pagerank}.
Notwithstanding, the consensus problem further appears as a critical subproblem of major applications.
A distributed Kalman Filter based on two consensus systems was proposed in~\cite{olfati2007distributed} to estimate the 2D motion of a target. The work was experimentally assessed in~\cite{alriksson2007experimental} to estimate the motion of a real robot.
Due to the relevance of consensus methods and the cybersecurity aspects, a crucial property to ensure in any consensus algorithm is its ability to overcome abnormal situations, i.e., achieve resilient consensus.
\textbf{Resilient consensus.}
Each agent in a network that works as expected must be able to filter erroneous information and be capable of reaching the consensus value that results from legit network information.
A new fault-tolerant algorithm to accomplish approximate Byzantine consensus in asynchronous networks is introduced in~\cite{haseltalab2015approximate}.
The method also applies to synchronous networks, to networks with communication paths with delay, and the authors extend the results to time-varying networks.
Subsequently, authors performed the convergence rate analysis of the fault-tolerant consensus algorithm of~\cite{haseltalab2015approximate}
in~\cite{haseltalab2015convergence}.
The work in \cite{silvestre2013SSVO} introduced a system to tackle worst-case and stochastic faults in the particular scenario of gossip consensus.
The developed method may be integrated into the consensus algorithm to achieve resilient consensus, making the nodes converge to a steady state belonging to the set resulting from the intersection of the estimates that each agent perceives for the remaining nodes~\cite{silvestre2014finite}.
The technique was extended to a wider family of gossip algorithms in \cite{silvestre2017automatica}.
These methods converge, and they offer a theoretical bound on the attacker signal, that can be computed \emph{a priori}. However, their computational complexity for the worst-case undetectable attack makes the approach inviable.
For detecting attacks, their computational complexity is, in general, worse than that of the new algorithm proposed in this work. For detecting attacks, their computational complexity is, in general, worse than that of the new algorithm proposed in this work. For attackers' isolation, the computational complexity in~\cite{silvestre2017automatica,ramossilvestresCDC,ramossilvestresIJoC} is exponential, contrasting with the proposed polynomial-time approach.
In~\cite{oksuz2018distributed}, two fault-tolerant and parameter-independent consensus algorithms are introduced to deal with misbehaving agents.
One of the approaches adaptively estimates, using a fault-detection scheme, how many faulty agents are in the network.
Whenever there are $f$ faulty agents the authors' method converges if the network of non-faulty nodes is $(f + 1)$-robust.
The other approach consists of a non-parametric Mean-Subsequence-Reduced algorithm, converging when both the network of non-faulty agents is $(f + 1)$-robust and the non-faulty agents possess the same amount of in-neighbors.
In~\cite{sundaram2018distributed}, the authors characterize the limitations on the performance of any distributed optimization algorithm in the presence of adversaries. Additionally, they investigated the vulnerabilities of consensus-based distributed optimization protocols to identify agents that are not following the consensus update rule.
The authors suggest a resilient distributed optimization method, and they provide lower bounds on the distance-to-optimality of attainable solutions under any algorithm, resorting to the notion of maximal $f$-local sets of graphs for cases where each agent has at most $f$ adversaries neighbors.
In~\cite{dibaji2015consensus}, the authors explore the scenario where each regular agent in a network refreshes its state based on local information, using a deliberated feedback law, and that malicious nodes update their state arbitrarily.
The authors present an algorithm for the consensus of second-order sampled-data multi-agent systems.
Assuming that the network has sufficient connectivity, the authors proposed a resilient consensus method, in which each node ignores the information of neighbors having large/small position values, considering that although the global topology of the network is unknown to regular agents, they know a priory the maximum number of malicious neighbor nodes.
Next, using similar reasoning, the authors in~\cite{kikuya2017fault} extend the previous work, presenting a consensus algorithm for clock synchronization in wireless sensor networks.
Subsequently, in~\cite{sundaram2016ignoring}, each agent may have a particular threshold for the number of extreme neighbors it ignores.
Under such a setup, the author draws network conditions that ensure reaching a consensus.
Further, the author presented conditions under which the consensus is asymptotically almost surely (with probability 1) achieved in random networks and with random node's thresholds.
In~\cite{usevitch2018resilient}, it is proposed a resilient leader-follower consensus to arbitrary reference values, where each agent ignores a portion of extreme neighbors. This consensus method guarantees a steady state value lying in the convex hull of initial agent states.
In a similar approach, the authors of~\cite{saldana2017resilient} presented a resilient consensus algorithm for time-varying networks of dynamic agents.
In~\cite{dibaji2017resilient}, the case of quantized transmissions, with communication delays and asynchronous update schemes is studied for update times selected in either a deterministic or random fashion.
In~\cite{chen2018attack}, the authors present a consensus+innovations estimator.
In the proposed method, each node in the network thresholds the gain to its innovations term. The authors ensure that if less than half of the agents' sensors fall under attack, then all of the agents' estimates converge with polynomial rate to the parameter of interest.
In~\cite{dibaji2019resilient}, the authors present a resilient fully distributed averaging algorithm that uses a resilient retrieval procedure, where all non-Byzantine nodes send their initial values and retrieve those of other agents. The convergence is ensured under a more restrictive than the conventional node connectivities assumption.
\textbf{Classes of consensus problems.}
We may classify the problems of consensus based on the domain of the time update as: discrete-time (discrete), as in~\cite{zhu2010discrete,cai2012average}; or as continuous-time (continuous), as in~\cite{ren2005consensus,cai2012average}.
Also, it can be classified based on the network communication: synchronous, see for instance~\cite{zhu2010discrete}; or asynchronous, see for example~\cite{tsitsiklis1986distributed,haseltalab2015approximate,liu2017asynchronous}.
Moreover, the communication between agents may be: deterministic, see~\cite{cai2012average} for example; or stochastic, as in~\cite{boyd2006randomized,antunes2011consensus,silvestre2018broadcast} for instance.
Lastly, the agents' network of communication can be categorized as: static, see~\cite{cai2012average,oksuz2018distributed,silvestre2018broadcast}; or dynamic, changing in time, see in~\cite{olfati2004consensus,zhu2010discrete,saldana2017resilient}.
Here, we propose a resilient consensus algorithm that can be used for discrete-time, synchronous or asynchronous communication and static or dynamic network of communication.
By synchronous we mean algorithms in which updates occur at the same time for all the nodes, whereas in an asynchronous setting, at each time, any non-empty subset of nodes may update their state.
\textbf{Reputation systems.}
The concept of reputation of an entity is an opinion about that entity that usually results from an evaluation of the entity based on a set of criteria.
Everyday, we implicitly assign a reputation to persons, companies, services, and many other entities.
We do so by evaluating the entity behavior and comparing to what we would expect, and, further, by assessing other important (with large reputation) entities opinion.
In fact, reputation is an ubiquitous, spontaneous and highly efficient utensil of social control in natural societies, emerging in business, education and online communities.
Hence, this ubiquitous concept has been ported to several important application with relative success, such as in ranking systems~\cite{li2012robust,saude2017robust,saude2017reputation,10.1145/3397271.3401278}, where reputation-based ranking systems are proposed and shown to cope better with attacks and to the effect of bribing.
It is also an important measure to assess in the field of Social Networks as in~\cite{josang2007survey,zhu2015authenticated}.
In~\cite{pujol2002extracting}, the authors propose a method to address the problem of calculating a degree of reputation for agents acting as assistants to the members of an electronic community.
For more related work on reputation systems, we refer the reader to the surveys in~\cite{josang2007survey,hendrikx2015reputation} and references therein.
\textbf{Main contributions:}
(i) we propose a (fully distributed) discrete-time, reputation-based consensus algorithm resilient to attacks that works for both synchronous and asynchronous networks; with this algorithm, each agent only needs to have a low computational power to do calculations with the neighbors' values;
(ii) we show that the proposed algorithm converges with exponential rate;
(iii) for attacks with some properties, we show, theoretically, that our method does not produce false positives and holds polynomial time complexity, although we observe the same behavior for other types of attacks.
\subsection{Preliminaries and Terminology}\label{sec:notation}
First, we recall some concepts of graph theory, and we set the notation that we will adopt in this manuscript.
A \emph{directed graph}, or simply a \emph{digraph}, is an ordered pair $\mathcal G=(\mathcal V,\mathcal E)$, where $\mathcal V$ is a set of $n>1$ \emph{nodes}, and $\mathcal E\subseteq \mathcal V\times\mathcal V$ is a set of \emph{edges}. Edges are ordered pairs which represent a relationship of accessibility between nodes. If $u,v\in\mathcal V$ and $(u,v)\in\mathcal E$ then the node $v$ directly accesses information of node $u$.
In the scope of consensus algorithms, we also refer to a digraph as a \emph{network}, and we further say that nodes are \emph{agents} of the network.
A \emph{complete digraph} or \emph{complete network} is a digraph such that all nodes can directly access information of every other node.
Given an agent $v\in\mathcal V$, we denote the set of nodes that $v$ can directly access information in the network $\mathcal G=(\mathcal V, \mathcal E)$ by $\mathcal N_v=\{v\}\cup\{u\,:\,(u,v)\in\mathcal E\}$, and they are the \emph{neighbors} of $v$. The proper neighbors of $v$ are $\bar{\mathcal N_v}=\mathcal N_v\setminus \{v\}$.
The \emph{in-degree} of a node $v\in\mathcal V$, denoted by $d_v$ is the number of neighbors of $v$, i.e.,
$d_v=|\mathcal N_v|$. Likewise, the \emph{out-degree} of a node $v\in\mathcal V$, $o_v$, is the number of nodes that have $v$ has neighbor, i.e., $o_v=|\{u\,:\,v\in\mathcal N_u\}|$.
A \emph{path} in $\mathcal G=(\mathcal V,\mathcal E)$ is a sequence of nodes $(v_1,v_2,\hdots v_k)$ such that $(v_i,v_{i+1})\in\mathcal E$ for every $i=1,\hdots, k-1$.
A convenient way of representing a digraph is by means of its adjacency matrix $A\in\mathbb R^{n\times n}$, where $A_{u,v}=1$ if $(u,v)\in\mathcal E$, and $A_{u,v}=0$, otherwise.
A \emph{subgraph} or a \emph{subnetwork} $\mathcal H = (\mathcal V',\mathcal E')$ of a digraph $\mathcal G=(\mathcal V,\mathcal E)$ is a digraph such that $\mathcal V'\subset \mathcal V$, $\mathcal E'\subset\mathcal E$.
If $\mathcal A$ denotes a set of nodes $\mathcal A\subset\mathcal V$, we denote by $\mathcal G\setminus\mathcal A$ the subgraph $\mathcal H$ of $\mathcal G$ that consists in $\mathcal H=(\mathcal V\setminus\mathcal A,\mathcal E')$, where $\mathcal E'=\{e\in\mathcal E\,:\,e=(u,v)\text{ and } u,v\notin\mathcal A\}$.
Given a finite and non-empty array of possibly repeated elements sorted by increasing order $\mathcal C=\{x_1,\ldots, x_n\}$, with $x_i\in\mathbb R$, with at least one $j\neq i$ and $x_i\neq x_j$, we define the following element:
$
\displaystyle\fmin_{x\in\mathcal C}x = y_f,
$
where, inductively defined as
\[
y_f = {\small\begin{cases}
x_1, & \text{if }f=1\\[0.2cm]
\min\left\{x\in\mathcal C\,:\,y_{f-1} < x < x_n\right\}, & \text{if }\displaystyle\mathop{\exists}_{x\in\mathcal C}y_{f-1} < x < x_n \\
y_{f-1}, &
\text{otherwise.}
\end{cases}}
\]
In other words, we are computing the $f$th smallest element of the set obtained from the array $\mathcal C$ by discarding repeated elements, but ensuring that it is not the maximum element.
This definition will be very important to the reputation-based consensus method we propose, because we need to normalize a set of values, dividing them by the difference between the maximum and the $\fmin$ element.
For instance, consider the sets of sorted elements $\mathcal C=\{1,2,2,2,3\}$.
If $f=1$ then $\displaystyle\fmin_{x\in \mathcal C}x=1$, and if $f\geq 2$ then $\displaystyle\fmin_{x\in \mathcal C}x=2$.
\section{Reputation-Based Consensus}\label{sec:rep_based}
Consider a network of agents $\mathcal G=(\mathcal V,\mathcal E^{(k)})$, with initial states $x_v^{(0)}\in\mathbb R$, for $v\in \mathcal V$.
In the non-attacked scenario, agents can reach consensus through the use of a distributed linear iterative algorithm with dynamics given by:
\begin{equation}\label{eq:dyn}
x^{(k+1)} = W^{(k)} x^{(k)},
\end{equation}
where $x^{(k)}$ is the vector collecting the $n$ agents states at time step $k>0$, and the matrix $W^{(k)}\in\mathbb R^{n\times n}$ is such that: (i) $W_{u,v}=0$ if the agents $u$ and $v$ do not communicate, and (ii) the agents converge to the same quantity, i.e., $\displaystyle\lim_{k\to\infty}x^{(k)}=x^\infty$.
Additionally, we consider a set of attacked agents $\mathcal A\subset\mathcal V$.
If the agents $a\in\mathcal A$ do not follow the update rule of the consensus procedure, then each regular agent, $v\in\mathcal V\setminus\mathcal A$, should be able to identify and discard the attacked agents' values in the computation of the consensus value. In order to solve the problem state
, we make the following assumption:
\noindent$\,\,\bullet\,\,$ For each regular agent, $v\in\mathcal V\setminus\mathcal A$, more than half of the neighbors are regular agents, i.e., $|\mathcal N_v\cap\mathcal A|<|\mathcal N_v|/2$ and the network of normal nodes is connected.
\noindent The assumption we made is a typical assumption in the state-of-the-art methods to achieve resilient consensus.
We remark that the assumption we do make is equivalent to the $r$-robustness ($(r,1)$-robust) defined in~\cite{kikuya2017fault}.
Further, observe that the previous assumption is reasonable, because each regular agent needs to be able to divide his neighbors into the set of normal nodes and the set of attacked ones, by comparing the information that it receives. Hence, if the majority of the information is not legitimate there is no redundancy to allow to identify the attacked neighbors.
\subsection{Attacker model}
In what follows, we consider an attacker that may corrupt the state of the nodes in the subset $\mathcal{A}$ by adding an unbounded signal. The attacked dynamics are a corrupted version of~\eqref{eq:dyn} as follows:
\setcounter{equation}{1}
\begin{equation}
x^{(k+1)} = W^{(k)} x^{(k)} + \Delta^{(k)},
\end{equation}
where $\Delta^{(k)}\in\mathbb R^n$, which entails the assumption that the attacker cannot corrupt the communication between nodes to send different messages to distinct neighbors.
Observe that this assumption allows the attacker to change the state of a subset of agents to (possibly) different values. For example, in a network with 10 agents, an attacker may change the state of agents 3 and 5 using different values, but it cannot change the network communication scheme.
Furthermore, the attacker cannot create artificial nodes nor change the network topology, i.e., the structure of $W^{(k)}$ and the dimension $n$ are fixed in (2).
Notice that if a malicious entity could create nodes in the network, it would be impossible to deter, as the attacked nodes would be the majority regardless of $n$.
Additionally, the attack cannot target the initial state, i.e., $\Delta^{(0)} = 0$, since this scenario would be undetectable. The sequences of state values for the attacked version would be the same as a normal execution of the algorithm with the attack value as initial state.
\subsection{Reputation-based consensus \emph{(\textsf{RepC})}}\label{sec:rbc}
Next, we propose a reputation-based consensus algorithm (\textsf{RepC}).
The idea behind the algorithm is that, each time an agent obtains information (states) from its neighbors, the agent measures how discrepant is, in average, the state from one neighbor regarding the states of the remaining ones and its own state.
The \textsf{RepC} is composed by two phases: (i) \textbf{identification of the attacked nodes}; (ii) computation of the \textbf{consensus}.
Notice that the proposed algorithm is a fully distributed discrete-time consensus algorithm that works for both synchronous and asynchronous networks. Also, each agent only needs to have a low computational power to do calculations with the neighbors' values.
\subsubsection{Synchronous communication \emph{\textsf{RepC}}}
Given the maximum number of allowed attacked nodes $f$, the identification of the attacked nodes is performed by the following iterative scheme:
{\small
\allowdisplaybreaks
\begin{align*}\label{eq:id}
&\textbf{Reputation update: }\\
\tilde c_{ij}^{(k+1)} & = \begin{cases}
1-
\displaystyle\displaystyle\sum_{v\in \bar{\mathcal N_i} }\frac{|x_j^{(k)}-x_v^{(k)}|}{|\mathcal N_i|}, & j\in\mathcal N_i\\
0, &\text{otherwise}
\end{cases}\\ &\textbf{Normalized Reputation update: }
\\[0.2cm]
\tilde\tilde c_{ij}^{(k+1)} & = \begin{cases} \displaystyle\frac{\tilde c_{ij}^{(k+1)}-\displaystyle\fmin_{v\in\bar{\mathcal N_i}}\tilde c_{iv}^{(k+1)}}{\displaystyle\max_{v\in\bar{\mathcal N_i}}\tilde c_{iv}^{(k+1)}-\displaystyle \fmin_{v\in\bar{\mathcal N_i}}\tilde c_{iv}^{(k+1)}}, & i\neq j\\
1, & \text{otherwise}
\end{cases}\\
& \textbf{Normalized Reputation update with confidence $\varepsilon$: }
\\
c_{ij}^{(k+1)} & = \begin{cases}
\,\tilde\tilde c_{ij}^{(k+1)}, &\text{if }\,\tilde\tilde c_{ij}^{(k+1)}>0, \\
\varepsilon^{k+1},& \text{otherwise}\\
\end{cases}\\
& \textbf{Consensus state update: }
\\
x_i^{(k+1)} & = \displaystyle\sum_{j\in\bar{\mathcal N_i}} c_{ij}^{(k)}x_j^{(k)}\bigg/\displaystyle\sum_{j\in\bar{\mathcal N_i}} c_{ij}^{(k)},\\
\end{align*}
}
{\small $c_{ij}^{(k+1)}=0$} if {\small $j\notin\mathcal N_i$}, and {\small $c_{ii}^{(k+1)}=1$}, and
where {\small $c_{ij}^{(0)}=1$} for {\small $j\in\bar{\mathcal N_i}$} and {\small $c_{ij}^{(0)}=0$} otherwise, and {\small $x_i^{(0)}$} is the initial value of each agent $i$.
Further, {\small $\varepsilon\in]0,1[$} is a \emph{confidence factor} which guarantees that each agent does not discard immediately values that are discrepant from its neighbors' average.
Notice that the selected value for $\varepsilon$ must be small to have a negligible impact on the agents' consensus states. Also, a large $\varepsilon$ may cause an agent to do not detect an attacked neighbor. This, in turn, makes the asymptotic consensus to deviate from the consensus without attacked agents towards a combinations of the attacked agents asymptotic states.
We illustrate this property in Section~\ref{sec:ill_exam}.
Further, notice that the proposed method computes a weighted average of the agents' values. Therefore, we can ensure that the final consensus state is a convex combination of the agents' initial states.
\subsubsection{Asynchronous communication \emph{\textsf{RepC}}}
The asynchronous version of algorithm \textsf{RepC} consists of, at each instance of time, the agents that communicate, $\mathcal A'\subset\mathcal A$, follow Equation~\eqref{eq:id}, where $\bar{\mathcal N}_i$ is replaced by $\bar{\mathcal N}_i\cap \mathcal A'$.
Another interesting fact is that the iterative scheme~\eqref{eq:id} may also be used in the scenario where the network of agents evolves with time.
The results in Section~\ref{sec:rbc} can be restated for this scenario by considering that the set of neighbors of a node is dynamic, and by verifying, at each time, that each agent has more than two neighbors and more than half of them are regular agents.
In Section~\ref{sub:dyn_net} and~\ref{sub:dyn_net_noisy}, we illustrate the dynamic network of agents and dynamic network with noisy agents scenarios.
The first important property to prove about \textsf{RepC} is that it converges.
To simplify the proof, we assume that we are in the scenario of synchronous communication.
The general proof follows the same steps, but it is more complex and it needs more complex notation to denote the set of neighbors with which a node communicates at each time.
Additionally, we assume that $x_i^{(k)}\in[0,1]$.
Notice that this corresponds to do a bijection of each $x_i^{(0)}$ as $\tilde x_{i}^{(0)}=( x_{i}^{(0)}-x_{\min}^{(0)})\big/(x_{\max}^{(0)}-x_{\min}^{(0)})$.
Further, in the following proofs and for technical reasons, we assume that each attacked agent shares a state that is converging to some value.
This simplification is needed in order to derive theoretical guarantees of the proposed method.
Although, in practice, the algorithm is still effective under other circumstances, as we illustrate in Section~\ref{sec:ill_exam}.
\begin{lemma}\label{lemma:conv}
If for any $i\in\mathcal V$ we have that $|\mathcal N_i|>2$, then each agent that follows the iterative scheme in~\eqref{eq:id} converges.
\end{lemma}
\begin{proof}
$
\left\|x^{(k+1)}-x^{(k)}\right\|_\infty = \displaystyle\max_{i}\left|x_i^{(k+1)}-x_i^{(k)}\right|
$
and, hence, assuming without loss of generality that $\|c_i^{(k)}\|_1\leq\|c_i^{(k+1)}\|_1$
{\small
\begin{align*}\label{eq:proof1}
\left|x_i^{(k+1)}-x_i^{(k)}\right| = \left|\frac{c_i^{(k+1)}\cdot x^{(k)}}{\|c_i^{(k+1)}\|_1}-\frac{c_i^{(k)}\cdot x^{(k-1)}}{\|c_i^{(k)}\|_1}\right| \\
= \left| \frac{c_i^{(k+1)}\cdot x^{(k)}}{\|c_i^{(k+1)}\|_1}-\frac{c_i^{(k)}\cdot x^{(k)}}{\|c_i^{(k+1)}\|_1}+\frac{c_i^{(k)}\cdot x^{(k)}}{\|c_i^{(k+1)}\|_1}
-\frac{c_i^{(k)}\cdot x^{(k-1)}}{\|c_i^{(k)}\|_1} \right|\\
\leq \left| \frac{c_i^{(k+1)}\cdot x^{(k)}}{\|c_i^{(k+1)}\|_1}-\frac{c_i^{(k)}\cdot x^{(k)}}{\|c_i^{(k+1)}\|_1}+\frac{c_i^{(k)}\cdot x^{(k)}}{\|c_i^{(k)}\|_1}
-\frac{c_i^{(k)}\cdot x^{(k-1)}}{\|c_i^{(k)}\|_1} \right|\\
= \left| \frac{c_i^{(k+1)}-c_i^{(k)}}{\|c_i^{(k+1)}\|_1}\cdot x^{(k)}+c_i^{(k)}\cdot\frac{x^{(k)}-x^{(k-1)} }{\|c_i^{(k)}\|_1} \right|\\
\leq \frac{\max_{j\in\mathcal N_i}|c_{ij}^{(k+1)}-c_{ij}^{(k)}|}{\|c_i^{(k+1)}\|_1}+\frac{\max_{j\in\mathcal N_i}|x_{j}^{(k)}-x_{j}^{(k-1)}|}{\|c_i^{(k)}\|_1}\\
\leq \frac{\max_{j\in\mathcal N_i}|c_{ij}^{(k+1)}-c_{ij}^{(k)}|}{\|c_i^{(k)}\|_1}+\frac{\max_{j\in\mathcal N_i}|x_{j}^{(k)}-x_{j}^{(k-1)}|}{\|c_i^{(k)}\|_1},
\end{align*}
}
because we are assuming that $x_v^{(m)},c_{ij}^{(m)}\in]0,1[$.
Now we need to compute $\max_{j\in\mathcal N_i}|c_{ij}^{(k+1)}-c_{ij}^{(k)}|$.
First, we notice that we cannot have that $\max_{j\in\mathcal N_i}|c_{ij}^{(k+1)}-c_{ij}^{(k)}|=|\varepsilon^{k+1}-\varepsilon^{k}|$, because there is always a $j\in\mathcal N_i$ such that $c_{ij}^{(k+1)}>\varepsilon^{k+1}$ and all the other $k\neq j\in\mathcal N_i$ are such that $c_{ij}^{(k+1)}\geq\varepsilon^{k+1}$.
Therefore, we need to consider only three cases:
{\small \begin{enumerate}
\item $c_{ij}^{(k+1)}=\varepsilon^{k+1}$ and $c_{ij}^{(k)}=\tilde\tilde c_{ij}^{(k)}$;
\item $c_{ij}^{(k+1)}=\tilde\tilde c_{ij}^{(k+1)}$ and $c_{ij}^{(k)}=\varepsilon^k$;
\item $c_{ij}^{(k+1)}=\tilde\tilde c_{ij}^{(k+1)}$ and $c_{ij}^{(k)}=\tilde\tilde c_{ij}^{(k)}$.
\end{enumerate}}
For case $1)$ we have that
{\small$
\left|c_{ij}^{(k+1)}-c_{ij}^{(k)}\right| = \left|\varepsilon^{k+1} - \tilde\tilde c_{ij}^{(k)} \right|
< \left|\,\tilde\tilde c_{ij}^{(k+1)} - \tilde\tilde c_{ij}^{(k)} \right|,
$}
since {\small $c_{ij}^{(k+1)}=\varepsilon^{k+1}$} implies that {\small $\tilde\tilde c_{ij}^{(k+1)}\leq 0$}.
Using the same reasoning, for case $2)$, we have that
{\small$
\left|c_{ij}^{(k+1)}-c_{ij}^{(k)}\right| = \left|\, \tilde\tilde c_{ij}^{(k+1)}-\varepsilon^{k} \right|
< \left|\,\tilde\tilde c_{ij}^{(k+1)} - \tilde\tilde c_{ij}^{(k)} \right|.
$}
We only need to compute $3)$
{\small \begin{equation}\label{eq:proof2}
\begin{split}
\left|\,\tilde\tilde c_{ij}^{(k+1)}-\tilde\tilde c_{ij}^{(k)}\right| = \frac{\left|\tilde c_{ij}^{(k+1)}-\tilde c_{ij}^{(k)}\right|}{\max_{v\in\bar{\mathcal N_i}}\tilde c_{iv}^{(k+1)}-\fmin_{v\in\bar{\mathcal N_i}}\tilde c_{iv}^{(k+1)}}\\
\leq |\tilde c_{ij}^{(k+1)}-\tilde c_{ij}^{(k)}|\\
= \frac{1}{|\bar{\mathcal N_i}|}\sum_{v\in \bar{\mathcal N_i} }\left(|x_j^{(k)}-x_v^{(k)}|-|x_j^{(k-1)}-x_v^{(k-1)}|\right)\\
\leq \frac{1}{|\mathcal N_i|}|\mathcal N_i|\left(|x_j^{(k)}-x_\alpha^{(k)}|-|x_j^{(k-1)}-x_\alpha^{(k-1)}|\right)\\
= \left(|x_j^{(k)}-x_\alpha^{(k)}| -|x_{\alpha}^{(k-1)}-x_{j}^{(k-1)}|\right.\\
+\left.|x_{\alpha}^{(k-1)}-x_{j}^{(k-1)}| -|x_j^{(k-1)}-x_\alpha^{(k-1)}|\right)\\
\leq \left(|x_j^{(k)}-x_j^{(k-1)}|+|x_\alpha^{(k)}-x_\alpha^{(k-1)}|\right)
\leq 2 \displaystyle\max_{j\in\bar{\mathcal N_i} }|x_j^{(k)}-x_{j}^{(k-1)}|,
\end{split}
\end{equation}}
\noindent where $\alpha=\displaystyle\underset{v\in\bar{\mathcal N_i}}{\arg\max} \left(|x_j^{(k)}-x_v^{(k)}|-|x_j^{(k-1)}-x_v^{(k-1)}|\right)$.
Now, plugging~\eqref{eq:proof2} in~\eqref{eq:proof1}, we have that
\[
{\small
\begin{split}
\|x^{(k+1)}-x^{(k)}\|_\infty \leq \frac{3}{\|c_i^{(k))}\|_1}\max_{j\in\bar{\mathcal N_i}}|x_j^{(k)}-x_{j}^{(k-1)}|\\
\leq \frac{3}{\|c_i^{(k)}\|_1}\|x^{(k)}-x^{(k-1)}\|_\infty\leq \frac{3}{|\bar{\mathcal N_i}|}\|x^{(k)}-x^{(k-1)}\|_\infty
\end{split}
}
\]
Therefore, the iterative scheme converges whenever $\frac{3}{|\mathcal N_i|+1}<1$, which is equivalent to $|\mathcal N_i|>2$.
\end{proof}
In fact, the requirement about the number of neighbors, i.e., each agent having more than 2 neighbors, agrees with the intuition. A regular agent should assess to, at least, 3 states to distinguish whether nodes are following the consensus update rule or not.
Otherwise, if there are only 2 neighbors then their reputation can be, for instance, alternating between iterations.
The previous result states that \textsf{RepC} converges (i.e. each agent converges to a state) but it is still missing to show that each regular agent converges to the same value, i.e., all regular agents \emph{agree}.
The next lemma assesses that: (i) either an agent $v$ converges to a unique value; (ii) or for any other agent, the reputation of agent $v$ is zero, i.e. $c_{uv}^\infty=0$.
\begin{lemma}\label{lemma:one_limit}
Consider the iterative scheme~\ref{eq:id}.
For any agent $j\in\mathcal V$ one of the following holds:
\begin{enumerate}
\item[$(i)$] $\displaystyle\lim_{k\to\infty}x_j^{(k)}=x^\infty$;
\item[$(ii)$] $\displaystyle\forall_{i\in\mathcal N_j}\lim_{k\to\infty}c_{ij}^{(k)}=0$ (neighbors of $j$ assign it reputation zero).
\end{enumerate}
\end{lemma}
\begin{proof}
By Lemma~\ref{lemma:conv}, we have that~\eqref{eq:id} converges for each agent $i\in\mathcal V\setminus\mathcal A$.
We just need to show that for a given node $u\in\mathcal V\setminus\mathcal A$ and for each of its neighbors $v\in\mathcal N_u$ either $(i)$ or $(ii)$ happens.
Let $u\in\mathcal V\setminus\mathcal A$ and $v\in\mathcal N_u$, we show by induction on the number of neighbors of $u$, $|\mathcal N_u|$, that for each neighbor either its reputation is zero or it converges to the same value as $u$.
The basis is when $|\mathcal N_u|=1$, and we have that $x^\infty_u=\frac{x^\infty_u+c^\infty_{uv}x_v^\infty}{1+c^\infty_{uv}}$. Thus, either $c^\infty_{uv}=0$, or $c^\infty_{uv}>0$ and $x_v^\infty=x_u^\infty$.
When $|\mathcal N_u|=N+1$, we have that
$
x^\infty_u = \sum_{j\in\bar{\mathcal N}_u}c_{uj}^\infty x_j^\infty\bigg/\sum_{j\in\bar{\mathcal N}_u}c_{uj}^\infty.
$
Since the reputation that $u$ assigns to itselft is $c^\infty_{uu}=1$, we can rewrite the previous expression as
{\small\begin{equation}\label{eq:step1}
x^\infty_u = \frac{x_u^\infty+\sum_{j\in\mathcal N_u\setminus\{v\}}c_{uj}^\infty x_j^\infty+c_{uv}^\infty x_v^\infty}{1+\sum_{j\in\mathcal N_u\setminus\{v\}}c_{uj}^\infty+c_{uv}^\infty}
\end{equation}}
Further, using the induction hypothesis, either $(i)$ or $(ii)$ is true for any set of $N$ neighbors of $u$. Hence, for $j\in\mathcal N_u\setminus\{v\}$ either $x_j^\infty=x^\infty$ or $c_{uj}^\infty=0$. In any of the cases, we have that
{\small \begin{equation}\label{eq:step2}
x_u^\infty+\sum_{j\in\mathcal N_u\setminus\{v\}}c_{uj}^\infty x_j^\infty = x^\infty\left(1+\sum_{j\in\mathcal N_u\setminus\{v\}}c_{uj}^\infty\right)
\end{equation}
}
By replacing~\eqref{eq:step2} in~\eqref{eq:step1}, it follows that
\[{\small
\begin{split}x^\infty_u = x^\infty & = \frac{x^\infty\left(1+\sum_{j\in\mathcal N_u\setminus\{v\}}c_{uj}^\infty\right)+c_{uv}^\infty x_v^\infty}{\left(1+\sum_{j\in\mathcal N_u\setminus\{v\}}c_{uj}^\infty\right)+c_{uv}^\infty},\\
\end{split}
}
\]
implying that either $c_{uv}^\infty=0$ or $c_{uv}^\infty>0$ and $x_v^\infty=x_u^\infty=x^\infty$.
By transitivity, we can apply the same to each neighbor of all neighbors of $u$, and so forth. Thus, the result yields for all $i\in\mathcal V\setminus\mathcal A$.
\end{proof}
As a corollary, we have that if a regular agent using \textsf{RepC} detects a neighbor as a faulty node, then it is a faulty node.
In other words, there are no false positives.
\begin{corollary}\label{cor:detection}
Let $v\in\mathcal V\setminus\mathcal A$ and $u\in\mathcal V$.
By using the iterative scheme~\eqref{eq:id}, if $c_{uv}^\infty=0$ then $u\in\mathcal A$.
\end{corollary}
The proof of Lemma~\ref{lemma:conv} also hints that half of each agent's neighbors should not be under attack, so that each normal node identifies the attacked agents correctly.
This is expressed in the following.
\begin{lemma}\label{lemma:rep}
Suppose that the iterative scheme~\eqref{eq:id} converges to a value different from that broadcasted by the attacked agents. If for each agent $i\in\mathcal V\setminus\mathcal A$, less than half of its neighbors are not attacked agents, i.e. $|\bar{\mathcal N_i}\cap \mathcal A|<|\bar{\mathcal N_i}\setminus \mathcal A|$, then $\displaystyle\lim_{k\to\infty}c_{ia}^{(k)}=0$, for $a\in\mathcal A$ and $\displaystyle\lim_{k\to\infty}c_{iv}^{(k)}=1$ for $v\in\bar{\mathcal N_i}\setminus\mathcal A$.
\end{lemma}
\begin{proof}
By Lemma~\ref{lemma:conv}, we have that the each regular agent using the iterative scheme in~\eqref{eq:id} converges to $x^\infty$. Let $y$ denote the value that all the attacked agents in $\mathcal A$ share with the neighbors.
Thus, for a regular agent $i\notin\mathcal A$, an attacked agent's reputation, $a\in\mathcal A$, satisfies
\[
{\small
\begin{split}
\tilde c_{ia}^\infty=&\lim_{k\to\infty}\tilde c_{ia}^{(k)} = 1-\frac{1}{|\mathcal N_i|}\sum_{v\in\mathcal N_i}\left|y-\lim_{k\to\infty}x_v^{(k)}\right|
\\= &
1-\frac{|\mathcal N_i\setminus\mathcal A|}{|\mathcal N_i|}\left|y-x^{\infty}\right|,
\end{split}
}
\]
and the limit of the reputation of a regular user, $j\notin\mathcal A$, is given as
{\small\[
\tilde c_{ij}^\infty= \lim_{k\to\infty}\tilde c_{ij}^{(k)}
=
1-\frac{|\mathcal N_i\cap\mathcal A|}{|\mathcal N_i|}\left|x^{\infty}-y\right|.
\] }
Since $|\mathcal N_i\cap\mathcal A|<|\mathcal N_i\setminus\mathcal A|$ and $y\neq x^{\infty}$, then $\tilde c_{ij}^\infty>\tilde c_{ia}^\infty$, and because reputations values are normalized to be between $0$ and $1$, we have that, for all $i$, $1=c_{ij}^\infty>c_{ia}^\infty=0$.
\end{proof}
Now, we need to show that a regular agent using \textsf{RepC} identifies the neighbors which are attacked nodes, and to study the convergence rate of method.
\begin{lemma}\label{lemma:complete}
Let $v\in\mathcal V\setminus\mathcal A$ and $u\in\mathcal V$.
By using the iterative scheme~\eqref{eq:id}, if $u\in\mathcal A$ and $|\mathcal A|\leq f$ then $c_{uv}^\infty=0$.
\end{lemma}
\begin{proof}
Let $a\in\mathcal A$ be an attacked node.
We want to show that for a regular agent, $v\in\mathcal V\setminus\mathcal A$, the reputation of agent $a$ strictly decreases with time.
Let $v\in\mathcal V\setminus\mathcal A$, we have that
$
|x_a-x_v^{(k+1)}|-|x_a-x_v^{(k)}
\leq|x_v^{(k+1)}-x_v^{(k)}|
$
\end{proof}
\begin{proposition}
Consider the iterative scheme in~\eqref{eq:id} and let $N=\displaystyle\min_{i\in\mathcal V}|\mathcal N_i|$ and $\lambda = \frac{3}{N+1}$. If $N>3$, then~\eqref{eq:id} converges with exponential rate and we have that $\|x^{(k+1)}-x^{(k)}\|_\infty\leq \lambda^k$. Further, to achieve an error of at most $\delta>0$ between the last two iterations, we need to run the iterative scheme at most $k=\lceil\log_{\lambda}(\delta)\rceil$ times.
\end{proposition}
\begin{proof}
Let $N=\displaystyle\min_{i\in\mathcal V}|\mathcal N_i|$ and $\lambda = \frac{3}{N+1}$.
Using the proof of Lemma~\ref{lemma:conv}, we have that
$
\|x^{(k+1)}-x^{(k)}\|_\infty \leq \frac{3}{|\bar{\mathcal N_i}|}\|x^{(k)}-x^{(k-1)}\|_\infty
\leq \lambda^k\|x^{(1)}-x^{(0)}\|_\infty\leq \lambda^k.
$
Hence, the iterative scheme converges with exponential rate of $\lambda^k$.
To achieve an error between iterations of at most $\varepsilon$, we need to have that
$
\lambda^k\leq\delta,
$
which is equivalent to have that
$
k\leq\log_{\lambda}(\delta)\leq \lceil\log_{\lambda}(\delta)\rceil.
$
Therefore, if we run the iterative scheme at most $\lceil\log_{\lambda}(\delta)\rceil$ times, we obtain an error between the last two iterations of at most $\varepsilon$.
\end{proof}
\subsection{Complexity Analysis}\label{sub:complexity}
Next, we investigate the complexity analysis of the proposed algorithm \textsf{RepC}, when the network communication is synchronous.
\begin{proposition}\label{prop:complexity}
Let $\mathcal G=(\mathcal V,\mathcal E )$ be a network of agents, $l=\displaystyle\max_{v\in\mathcal V}|\mathcal N_v|$, then, for $i$ iterations and for each agent, the iterative scheme~\eqref{eq:id} has time complexity of $\mathcal O(l^2i)$.
\end{proposition}
\begin{proof}
Given a network of agents $\mathcal G=(\mathcal V,\mathcal E )$, for time step $k$ and for an agent $v$, the time complexity of~\eqref{eq:id} is the sum of the time complexities of computing $\tilde c_{vu}^{(k)}$, $\tilde\tilde c_{vu}^{(k)}$, $ c_{vu}^{(k)}$, for each $u\in\mathcal N_i$, and $x_v^{(k)}$.
Computing $\tilde c_{vu}^{(k)}$ has computation complexity of $\mathcal O(|\mathcal N_v|^2)$, because there are $\mathcal O(|\mathcal N_v|^2)$ pairs of neighbors values to compute the absolute difference.
Each of the remaining steps has time complexity of $\mathcal O(|\mathcal N_v|)$.
Hence, the sum of each step time complexity is $O(|\mathcal N_v|^2)+4\times\mathcal O(|\mathcal N_v|)=O(|\mathcal N_v|^2)$.
Thus, if $l=\displaystyle\max_{v\in\mathcal V}|\mathcal N_v|$, then $\mathcal O(l^2)$ is a bound for the time complexity that each incurs.
Therefore, for $i$ iterations of the iterative scheme~\eqref{eq:id}, each agent incurs in $\mathcal O(l^2 i)$ time complexity.
\end{proof}
\section{Illustrative Examples}\label{sec:ill_exam}
Subsequently, we illustrate the use of \textsf{RepC} for different kinds of attacks.
Further, in the examples, we use $\varepsilon=0.1$.
\subsection{Same value for attacked nodes}
In the following examples, we consider the network of agents depicted in Fig.~\ref{fig:GA}~(a).
\begin{figure}[h!]
\centering
\subfigure[Network of agents $\mathcal G_A$.]{\label{fig:a}\includegraphics[width=0.42\textwidth]{ex1G.pdf}}
\subfigure[Network of agents $\mathcal G_B$.]{\label{fig:b}\includegraphics[width=0.38\textwidth]{exDiffG1.pdf}}
\caption{}
\label{fig:GA}
\end{figure}
First, we illustrate algorithm \textsf{RepC} in the scenario of a network of agents \textbf{without attacked nodes}. The set of agents is $\mathcal V_1=\{1,\hdots,5\}$ and, thus, the set of attacked agents is $\mathcal A=\emptyset$. We set the parameter $f=1$.
Figure~\ref{fig:C0} depicts the state evolution of each agent
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{Exp0.pdf}
\caption{Consensus of network $\mathcal G_A$ with agents $\mathcal V_1$ and set of attacked agents $\emptyset$.}
\label{fig:C0}
\end{figure}
Here, we explore the scenario where an \textbf{attacker} targets one agent to \textbf{share a value close to the consensus} of the network of regular agents, depicted in Fig.~\ref{fig:GA}.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{Exp1zoom.pdf
\caption{Consensus of network $\mathcal G_A$ with agents $\mathcal V_1$ and set of attacked agents $\mathcal A_1$ (zoomed around the attacker's value.)}
\label{fig:C1}
\end{figure}
The set of agents is $\mathcal V=\{1,\ldots,5\}$ and the set of attacked agents is $\mathcal A=\{1\}$.
Figure~\ref{fig:C1} depicts each agent consensus value.
We can see that although the attacker value is very close to the consensus value, the neighbors of the attacked node assign zero to its reputation, by using~\eqref{eq:id}. Hence the value that the attacked node shares is discarded.
Next, in Figure~\ref{fig:c2} -- Fig.~\ref{fig:c3}, we depict the evolution of the reputations that agents $2$ and $3$ assign to their neighbors.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{c2.pdf}
\caption{Evolution of the reputations that agent $2$ assigns to each of its neighbors.}
\label{fig:c2}
\end{figure}
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{c3.pdf}
\caption{Evolution of the reputations that agent $3$ assigns to each of its neighbors.}
\label{fig:c3}
\end{figure}
\subsection{Different values for attacked nodes}
Next, we illustrate the scenario where attacked nodes share different values.
For that end, we consider the set of agents $\mathcal V=\{1,\ldots,10\}$, with $\mathcal A=\{1,8\}$, and the network of agents depicted in Fig.~\ref{fig:GA}~(b).
We explore two scenarios with two attacked agents: (i) both attacked nodes share values (distinct) smaller than the consensus, see Fig.~\ref{fig:C2}; (ii) one attacked node shares a value larger than the consensus while the other uses a smaller value than the consensus, see Fig.~\ref{fig:C3}.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{ExDiff2.pdf}
\caption{Consensus of network $\mathcal G_B$ with agents $\mathcal V_3$ and set of attacked agents $\mathcal A_3$}
\label{fig:C2}
\end{figure}
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{ExDiff1.pdf}
\caption{Consensus of network $\mathcal G_B$ with agents $\mathcal V_2$ and set of attacked agents $\mathcal A_2$}
\label{fig:C3}
\end{figure}
\subsection{Asynchronous Communication}
We, now, illustrate the use of algorithm \textsf{RepC} in the case where the communication between nodes occur asynchronously. To simulate this scenario, at each time instance, a random subset of agents communicates.
The set of agents is $\mathcal V=\{1,\ldots,5\}$, the network of agents is $\mathcal G_A$, and the set of attacked agents is $\mathcal A=\{1\}$.
Figure~\ref{fig:repConAsyn} depicts the state evolution of each agent when using the asynchronous version of algorithm \textsf{RepC}. Each normal node identifies and discards the information of the attacked agent.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{repConAsyn.pdf}
\caption{Consensus of network $\mathcal G_A$ with agents $\mathcal V_1$, asynchronous communication, and set of attacked agents $\mathcal A=\{1\}$.}
\label{fig:repConAsyn}
\end{figure}
\subsection{Dynamic network}\label{sub:dyn_net}
Next, we test the scenario where the network of agents evolves with time and the attacked agents share the same value.
We consider two networks composed by 10 agents, as depicted in Fig.~\ref{fig:GD}, with set of agents $\mathcal V=\{1,\hdots,10\}$ and set of attacked agents $\mathcal A=\{1\}$.
\begin{figure}[h!]
\centering
\hfill
\subfigure[Network of agents $\mathcal G_D$.]{\label{fig:a}\includegraphics[width=0.46\textwidth]{exDynG2.pdf}}\hfill
\subfigure[Network of agents $\mathcal G_C$.]{\label{fig:b}\includegraphics[width=0.46\textwidth]{exDynG1.pdf}}
\hfill
\caption{}
\label{fig:GD}
\end{figure}
In the example, we consider that the dynamic network of agents for time instance $k>0$ is given by
$\mathcal G_1^{(k)}=\begin{cases}
\mathcal G_C &\text{if } k\leq 10\\
\mathcal G_D &\text{otherwise}
\end{cases}.$
The consensus value of each agent, utilizing the iterative scheme~\eqref{eq:id}, is depicted in Fig.~\ref{fig:C4}.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{ExDyn1.pdf}
\caption{Consensus of dynamic network $\mathcal G_1^{(k)}$ with agents $\mathcal V_1$, and set of attacked agents $\mathcal A=\{1\}$.}
\label{fig:C4}
\end{figure}
\subsection{Dynamic network with noisy agents}\label{sub:dyn_net_noisy}
Finally, we illustrate the scenario where not only the network of agents evolves with time, but also the attacked agents share different values, which are uniform random variables with a fixed mean value. These is captured in the example depicted in Fig.~\ref{fig:var1}.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{ExDynRand.pdf}
\caption{Consensus of dynamic network $\mathcal G_1^{(k)}$ with agents $\mathcal V_1$, and set of attacked (noisy) agents $\mathcal A=\{1,8\}$.}
\label{fig:var1}
\end{figure}
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{ExDynRand3.pdf}
\caption{Consensus of dynamic network $\mathcal G_1^{(k)}$ with agents $\mathcal V_1$, and set of attacked agents $\mathcal A=\{1,8\}$, where agent $1$ behaves as a noisy node and agent $8$ as an attacked node.}
\label{fig:var}
\end{figure}
\subsection{Stochastic communication}
When the communication between agents has a stochastic nature, we may still successfully apply \textsf{RepC}.
This is illustrated in the next example. We consider the network $\mathcal G_E$ in Fig.~\ref{fig:gStoc}, with $\mathcal V_1$, and the set of attacked agents $\mathcal A=\{1\}$. Further, at each time step, only a random subset of agents communicate between them. The described situation is depicted in Fig.~\ref{fig:stoc}, where the regular agents could effectively detect the attacked node and achieve the true consensus of the network.
\begin{figure}[h!]
\centering
\includegraphics[width=0.46\textwidth]{gStoc.pdf}
\caption{Network of agents $\mathcal G_E$.}
\label{fig:gStoc}
\end{figure}
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{stochastic.pdf}
\caption{Consensus using a \textsf{RepC} method, with network $\mathcal G_E$, set of agents $\mathcal V_1$, set of attacked agents $\mathcal A=\{1\}$ and stochastic communication.}
\label{fig:stoc}
\end{figure}
\subsection{\textsf{RepC} vs. state-of-the-art}
Here, we illustrate how the proposed algorithm competes with the state-of-the-art approaches, based on the idea that each agent discards a set of maximum and minimum neighbor values.
In the next examples, we use the two networks depicted in Fig.~\ref{fig:g1StateArt1}.
\begin{figure}[h!]
\centering
\subfigure[Network of agents $\mathcal G_F$.]{\label{fig:a}\includegraphics[width=0.25\textwidth]{gStateArt1.pdf}}
\subfigure[Network of agents $\mathcal G_G$.]{\label{fig:b}\includegraphics[width=0.48\textwidth]{gStateArt2.pdf}}
\caption{}
\label{fig:g1StateArt1}
\end{figure}
In the first example, consider the set of agents $\mathcal V_2=\{1,2,3,4\}$, with the complete network (Fig.~\ref{fig:g1StateArt1}~(a)) and attacked agents $\mathcal A=\{1\}$.
Using the state-of-the-art, i.e., when each agent discards the maximum and minimum neighbors' values, we obtain the result depicted in Fig.~\ref{fig:CStateArt1}. The method is not able to deter the attack and the regular agents converge to the attacker value.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{StateOfTheArt1.pdf}
\caption{Consensus using a \textbf{state-of-the-art} method, with network $\mathcal G_F$, set of agents $\mathcal V_2$, and set of attacked agents $\mathcal A=\{1\}$. The black line is the true consensus value.}
\label{fig:CStateArt1}
\end{figure}
Using \textsf{RepC}, as illustrated in Fig.~\ref{fig:COur1}, the regular agents converge to a value close to the true value, with a small deviation caused by the influence of the $\varepsilon$ parameter.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{Our1.pdf}
\caption{Consensus using \textsf{RepC}, with network $\mathcal G_F$, set of agents $\mathcal V_2$, and set of attacked agents $\mathcal A=\{1\}$. The black line is the true consensus.}
\label{fig:COur1}
\end{figure}
In the second example, we consider the network of agents depicted in Fig.~\ref{fig:g1StateArt1}~(b), the set of agents $\mathcal V_3=\{1,2,3,4,5\}$ and attacked agents set $\mathcal A=\{1\}$.
The example portraits the scenario where an attacker stubbornly sends to the neighbors the true consensus value
In Fig.~\ref{fig:CStateArt2}, we present the consensus states of the agents when using the state-of-the-art approach. We can see that the agents are not able to converge to the true consensus value.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{StateOfTheArt2.pdf}
\caption{Consensus using a \textbf{state-of-the-art} method, with network $\mathcal G_G$, set of agents $\mathcal V_3$, and set of attacked agents $\mathcal A=\{1\}$. The black line is the true consensus value.}
\label{fig:CStateArt2}
\end{figure}
Subsequently, we present the consensus state of the agents when using \textsf{RepC}. In this case, the agents are able to converge to the true consensus of the network.
\begin{figure}[h!]
\centering
\includegraphics[width=0.61\textwidth]{Our2.pdf}
\caption{Consensus using \textsf{RepC}, with network $\mathcal G_F$, set of agents $\mathcal V_3$, and set of attacked agents $\mathcal A=\{1\}$. The black line is the true consensus.}
\label{fig:COur2}
\end{figure}
\subsection{Consensus final error}
To explore how different is the final consensus value produced by \textsf{RepC} and the consensus value without attacked nodes, we use the complete network of $5$ agents depicted in Fig.~\ref{fig:GA}~(a), with agents' initial states
$x^{(0)}=\left[\begin{smallmatrix} 1 & 0 & 3 & 1.2 & 2.5 \end{smallmatrix}\right]^\intercal$, where agent $1$ is under attack and shares values from a Gaussian noise with mean $\mu$ and standard deviation $\sigma$.
The consensus value, without attacked nodes, is $1.489$.
We compute the absolute difference between the consensus value found with \textsf{RepC} in the non-attacked case and the consensus value obtained with \textsf{RepC} when the attacker follows the mentioned strategy.
Moreover, we ranged $\mu$ from $0$ to $1$ in steps of $0.005$ and ranged $\sigma$ from $0.1$ to $1$ in steps of $0.005$, repeating each attacking scenario $20$ times to compute the absolute average error.
The results of the experiment are depicted in Fig.~\ref{fig:error}.
\begin{figure}[H]
\centering
\includegraphics[width=0.46\textwidth]{rep_consensus_gaussian.pdf}
\caption{Absolute difference between the consensus resulting from Algorithm \textsf{RepC} when node one $1$ is under attack to share the a Gaussian noise with mean $\mu$ and standard deviation $\sigma$.}
\label{fig:error}
\end{figure}
We can see from Fig.~\ref{fig:error} that, in average, we obtain a small final consensus error. When $\mu$ is close to $1$ and $\sigma$ is close to $0.1$, the attacked node state value is close to what would be when in the non-attacked scenario ($x_1^{(0)}=1$) and it takes more time to be classified as an attacker by its neighbors, yielding a slightly larger final consensus error.
\section{Conclusions}\label{sec:conc}
In this work, we presented a reputation-based consensus algorithm (\textsf{RepC}) for discrete-time synchronous and asynchronous communications in a possibly dynamic networks of agents.
By assigning a reputation value to each neighbor, an agent may discard information from neighbors presenting an abnormal behavior.
Algorithm \textsf{RepC} converges with exponential rate and it has polynomial time complexity. More specifically, for a network of agents, if we run $i\in\mathbb N$ iterations of \textsf{RepC}, we incur in $\mathcal O(l^2i)$ time complexity, where $l$ is the greatest number of neighbors a node has in that network.
For attacks with certain properties, we proved that the algorithm does not produce false positives. For other types of attacks, we illustrate the behavior of the proposed algorithm, which also worked as envisaged.
Future work directions include extending the algorithm for continuous-time consensus and to introduce the reputation idea for other types of consensus algorithms.
Furthermore, an important additional theoretical property to prove (even if only for some sorts of attacks) is whether or not \textsf{RepC} may cause an agent to wrongly classify a neighbor as attacked, i.e., if there are false negatives.
{\small
\bibliographystyle{alpha}
|
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"redpajama_set_name": "RedPajamaArXiv"
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| 8,689
|
Matti [] ist ein männlicher Vorname.
Herkunft und Bedeutung
Matti ist die finnische Variante von Matthäus. Daneben wird er auch als Kurzform von Matthäus oder Matthias verstanden.
Der Name bedeutet: "Gabe des ", "Geschenk des ".
Verbreitung
Neben Finnland ist der Name auch in Estland, Schweden und Dänemark verbreitet.
In Deutschland wird der Name vor allem seit den 1990er Jahren vergeben und gewinnt seitdem an Popularität. Im Jahr 2021 belegte er Rang 82 der beliebtesten Jungennamen Deutschlands.
Namensträger
Matti Ahde (1945–2019), finnischer Politiker und Sportfunktionär
Matti Alahuhta (* 1952), finnischer Manager
Matti Aikio (1872–1929), norwegischer Dichter
Matti Aura (Politiker, 1943) (1943–2011), finnischer Politiker (Nationale Sammlungspartei), Verkehrsminister
Matti Braun (* 1968), deutscher Künstler
Matti Breschel (* 1984), dänischer Radrennfahrer
Matti Bye (* 1966), schwedischer Musiker und Komponist
Matti Fagerholm (* 1962), finnischer Rockmusiker, bekannt als Michael Monroe
Matti Geschonneck (* 1952), deutscher Regisseur
Matti Goldschmidt (* 1951), österreichisch-israelischer Choreograph und Autor
Matti Hagman (1955–2016), finnischer Eishockeyspieler
Matti Hakala (* 1984), finnischer Biathlet
Matti Hautamäki (* 1981), finnischer Skispringer
Matti Heikkinen (* 1983), finnischer Skilangläufer
Matti Helminen (* 1975), finnischer Radrennfahrer
Matti Järvinen (1909–1985), finnischer Speerwerfer
Matti Y. Joensuu (1948–2011), finnischer Journalist und Autor
Matti Kärki (* 1972), schwedischer Metalsinger
Matti Keinonen (1941–2021), finnischer Eishockeyspieler und -trainer
Matti Klemm (* 1975), deutscher Radio-, Fernseh- und Synchronsprecher
Matti Klinga (* 1994), finnischer Fußballspieler
Matti Klinge (1936–2023), finnischer Historiker
Matti Krause (* 1986), deutscher Schauspieler, Hörspiel- und Synchronsprecher
Matti Kuparinen (* 1984), finnischer Eishockeyspieler
Matti Laakso (1939–2020), finnischer Ringer
Matti Lähde (1911–1978), finnischer Skilangläufer
Matti Langer (* 1990), deutscher Fußballspieler
Matti Lehikoinen (* 1984), finnischer Mountainbikefahrer
Matti Lehtinen (1922–2022), finnischer Baritonsänger
Matti Närhi (* 1975), finnischer Speerwerfer
Matti Nykänen (1963–2019), finnischer Skispringer
Matti Oivanen (* 1986), finnischer Volleyballspieler
Matti Paasivuori (1866–1937), finnischer Politiker
Matti Pajari (* 1979), finnischer Radrennfahrer
Matti Pellonpää (1951–1995), finnischer Schauspieler
Matti Pietikäinen (1927–1967), finnischer Skispringer
Matti Pitkänen (* 1951), finnischer Skilangläufer
Matti Puhakka (1945–2021), finnischer Politiker
Matti Raivio (1893–1957), finnischer Skilangläufer
Matti Rantanen (Musiker) (* 1952), finnischer Akkordeonist
Matti Rantanen (Rallyefahrer) (* 1981), finnischer Rallyefahrer
Matti Repo (* 1959), finnischer Bischof
Matti Rönkä (* 1959), finnischer Journalist und Krimiautor
Matti Salminen (* 1945), finnischer Opernsänger
Matti Schindehütte (* 1975), deutsch-finnischer Pfarrer und Filmproduzent
Matti Siimanainen (1920–2010), finnischer Ringer
Matti Sippala (1908–1997), finnischer Speerwerfer
Matti Vanhanen (* 1955), finnischer Politiker
Nikolaus Matti Abdalahad (* 1970), syrischer Geistlicher und Patriarchalvikar
Einzelnachweise
Männlicher Vorname
Finnischer Personenname
Theophorer Personenname
|
{
"redpajama_set_name": "RedPajamaWikipedia"
}
| 3,118
|
talk about an important step we're taking to help our neediest citizens.
freedom, and democracy all around the world.
medical care just to pay the rent.
disabilities and to subsidize their rents.
Thanksgiving is alive every day of the year.
but was embargoed for release until the broadcast.
phase begins today with this conference.
50 international states and organizations represented here this morning.
invested so much in this process that it was a sound investment.
once investors see that the peace agreement truly is taking hold.
their hopes for the future; and there is no fear.
|
{
"redpajama_set_name": "RedPajamaC4"
}
| 4,738
|
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"redpajama_set_name": "RedPajamaGithub"
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| 360
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Have His Carcase
The eighth book in Dorothy L Sayers' classic Lord Peter Wimsey series, introduced by bestselling thriller writer Lee Child - a must-read for fans of Agatha Christie's Poirot and Margery Allingham's Campion Mysteries. 'D. L. Sayers is one of the best detective story writers' Daily TelegraphA young woman falls asleep on a deserted beach and wakes to discover the body of a man whose throat has been slashed from ear to ear . . .The young woman is the celebrated detective novelist Harriet Vane, once again drawn against her will into a murder investigation in which she herself could be a suspect.Lord Peter Wimsey is only too eager to help her clear her name.'She brought to the detective novel originality, intelligence, energy and wit.' P. D. James
2016 Lee Child
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"redpajama_set_name": "RedPajamaCommonCrawl"
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| 2,149
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In the new Gus Van Sant-directed film, Milk, Sean Penn shares a steamy kiss with co-star Mark Martinez, who says the Oscar-winner let the lip-lock go on a little longer than expected.
"I'm performing, and [Penn] comes onto the dance floor," Mark tells E!. "He grabs me, and he just slaps the biggest kiss on me…It felt like the kiss was forever. I'm like, is he going to stop? I had to close my eyes, I couldn't believe it."
In the film, Martinez plays the late cross-dressing disco singer Sylvester. In one scene, the actor, dressed in a purple, blue and silver kimono with a matching turban and black bell bottoms, performs Sylvester's 1978 hit, "You Make Me Feel (Mighty Real)"
"All of a sudden, Sean's pointing at me and he's talking to the assistant director," Martinez explains. "The assistant director comes up to me and says, 'Just to let you know, you are now going to break up Sean and [co-star] James Franco's conversation. You're going to grab Sean, and Sean's going to be really excited, and he's going to kiss you.'"
Martinez, whose professional name is Flava, tried to convince Van Sant to do another take. "I'm thinking, we gotta do this thing again. We just didn't get it right," Martinez says. "But Gus was like, 'It's perfect, perfect, perfect.' I said, 'No! It's not perfect! Sean was laughing at me!'"
It seems that Penn's lips have been working overtime lately! As reported exclusively by OK!, the oscar winning actor was spotted smooching a mystery woman outside the Westin St. Francis Hotel in San Francisco on Tuesday. Eyewitnesses say the unknown brunette accompanied Sean out of the hotel, kissing him goodbye before he jumped into his sports car and zoomed off.
In Dec., the actor announced that he and wife Robin Wright were divorcing after 11 years of marriage. In Feb. he raised eyebrows when he showed up at an Oscar party with model Petra Nemcova, igniting speculation that the two were an item.
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"redpajama_set_name": "RedPajamaC4"
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\section{Introduction}
The generation or consumption of reactive power by inverters has been explored by several researchers as a way to control voltage fluctuations in distribution circuits with a high penetration of distributed photovoltaic (PV) generation. See \cite{KostyaMishaPetrScott3} and references therein for an overview. These approaches have tended to fall near two extremes. One extreme considers centralized optimization \cite{KostyaMishaPetrScott} where computations are done by a single central authority which is assumed to have full observability of the system. Such a system requires two-way communications between the central authority and at least all of controlled inverters. The rate of these communications should be sufficient to respond to the fastest expected fluctuations of solar irradiance. At the other extreme are local policy-based methods that require no communications at all, except for perhaps between devices at a single node. These inherently suboptimal methods rely only on node-local measurements as inputs to a policy that converts the measurements into a control action. Such policies have been based on heuristics and physical reasoning \cite{KostyaMishaPetrScott2,KostyaMishaPetrScott3} and on Monte Carlo-like approaches \cite{kundu2013distributed} that use centralized optimization in off-line computations to find strong correlations between the local measurements and the optimal local control actions.
In \cite{kundu2013distributed}, it was found that a significant source of the suboptimal behavior of local policy-based methods was saturation of inverters. In this case, the local policy results in a {\it desired} control action that, when combined with the local power flow conditions, is beyond the capability of the inverter. In \cite{kundu2013distributed}, this generally occurred when the real power injection by the inverter was approaching the apparent power capacity leaving little room for reactive power generation or consumption. Instead of achieving the desired reactive power injection, the inverter saturated at its apparent power capacity. In a centralized approach, optimality is restored because the full observability of the central authority makes it aware of the saturation allowing it to compensate with extra reactive power generation (or consumption) from nearby nodes. Such a response suggests that nearest-neighbor communications may be used to restore optimality in capacity-limited or otherwise constrained systems. There are other reasons to expect that limited communications may provide significant advantages over policy-based control without the larger overhead of centralized communications. Primary among these is the ability to adapt to system configurations that were unforeseen in the development of a policy based either on heuristics or sampling methods.
In this manuscript, we explore distributed approaches to control reactive power from PV inverters in distribution circuits and show how to restore optimality and adaptability through an iterative message-passing algorithm. Although we invoke limited communications, we continue to rely solely on local computations which depend only on local measurements and the most current data communicated from the nearest-neighbor nodes. The suggested cyber-physical control scheme is decentralized but optimal.
The results in this manuscript are based on the observation that the convex optimization formulation of \cite{KostyaMishaPetrScott,KostyaMishaPetrScott2,KostyaMishaPetrScott3} is separable in the key optimization variables, i.e. the node voltages and the power flows along the circuit. Separability suggests application of modern methods of distributed computations such as the dual ascent method and the Alternating Direction Method of Multipliers (ADMM) \cite{Boyd2011,boyd2013}.
The ADMM algorithm converges significantly faster than the dual ascent algorithm, a property one expects from the general arguments expressed in \cite{Boyd2011}.
Furthermore, the dual ascent algorithm for a non-differentiable dual function does not always converge to the optimal solution, but can converge to its neighborhood \cite{bertsekas1999nonlinear,nedic2009distributed}.
Faster convergence of ADMM is largely confirmed in our experiments conducted over seven different distribution circuit configurations with different numbers of nodes and varying photovoltaic penetration and load profiles. In each experiment, we minimize the total loss of real power while constraining all node voltages to be within nominal operational bounds.
The dual ascent method has been considered by \cite{Zampieri13a, Zampieri13b, Zampieri13c}, where a slightly more general model of radial power flows was considered.\footnote{References \cite{Zampieri13a, Zampieri13b, Zampieri13c} approximate power flows along the lines assuming that voltage variations along the line is much smaller than the voltage magnitude at the head of the line. The LinDistFlow approximation of \cite{89BWa}, used in \cite{KostyaMishaPetrScott,KostyaMishaPetrScott2,KostyaMishaPetrScott3} and adopted in this manuscript to model power flows, assumes additionally that losses of real and reactive power anywhere along the feeder are much smaller than respective flows.}
Dual decomposition distributed algorithm with gradient ascent for voltage regulation was also proposed in \cite{zhang2012optimal}, where
it was shown to solve a convex relaxation of power flow equations.
We further note that an optimization algorithm for optimal load control for frequency regulation has been recently proposed \cite{zhao2013powerB}, where it was shown that a frequency-based load control together with the system dynamics and power flows act as a decentralized primal-dual algorithm that solves the global optimization problem.
The dual ascent and ADMM-based algorithm was also used to solve a semi-definite programming relaxation of optimal power flow problem, where communication was carried out between different segments of the distribution network \cite{dall2013distributed}. The semi-definite programming relaxation of power flow problem for optimization of real and reactive PV generation in a radial network was also used in \cite{Dall2013}, where it yields an exact solution of the original problem in a single-phase radial network.
After the initial submission of our manuscript to the arxiv, other methods of solving convex relaxation of power flow equations via ADMM were proposed \cite{Erseghe2014,magnusson2014distributed,peng2014distributed}.
The material in the remainder of this manuscript is organized as follows. Power flows in a distribution circuit and control of inverters as a global optimization are reviewed in Section \ref{sec:DF} and Section \ref{sec:optim}, respectively. Algorithms for distributed control based on nearest neighbor communications are described in Section \ref{sec_ADMM} and \ref{sec_noU}.
The algorithms are tested and compared in Section \ref{sec_cases}. Section \ref{sec_disc} presents our conclusions and a brief discussion of the path forward.
\section{Distributed Flow Formulation}
\label{sec:DF}
The flow of electric power in the quasi-static approximation is governed by Kirchoff's laws. The DistFlow equations \cite{89BWa,89BWb,89BWc} are these laws restated in terms of power flows and applied to radial or tree-like distribution circuit with a discrete set of loads. For the radial case, the DistFlow equations are
\begin{subequations}\label{DistFlow}
$\forall j=0,\ldots,n-1$,
\begin{eqnarray}
&&P_{j+1}\!=\! P_j\!-\!r_j\frac{P_j^2\!+\!Q_j^2}{V_j^2}\!-\!p_{j+1}, \label{Pj+1}\\
&&Q_{j+1}\!=\!Q_j\!-\!x_j\frac{P_j^2\!+\!Q_j^2}{V_j^2}\!-\!q_{j+1}, \label{Qj+1}\\
&&V_{j+1}^2\!=\!V_j^2\!-\!2(r_jP_j\!+\!x_jQ_j)\!+\!(r_j^2\!+\!x_j^2)
\frac{P_j^2\!+\!Q_j^2}{V_j^2},
\label{Vj2}
\end{eqnarray}
where $P_j+iQ_j$ is the complex power flowing away from node $j$ toward node $j+1$, $V_j$ is the voltage at node $j$, $r_j+ix_j$ is the complex impedance of the link between node $j$ and $j+1$, and $p_j+i q_j$ is the complex power extracted at the node $j$. Both $p_j$ and $q_j$ are composed of local consumption minus local generation due to the PV inverter, i.e.
\begin{eqnarray}
p_j=p_j^{(c)}-p_j^{(g)},\quad q_j=q_j^{(c)}-q_j^{(g)}.
\label{p_q}
\end{eqnarray}
Of the four contributions to $p_j+i q_j$, we assume that $p_j^{(g)}$, $p_j^{(c)}$, and $q_j^{(c)}$ are uncontrolled (i.e. driven by consumer load or instantaneous PV generation). In contrast, the reactive power generated by the PV inverter, $q_j^{(g)}$, can be adjusted within limits. Eqs.~(\ref{Pj+1},\ref{Qj+1},\ref{Vj2},\ref{p_q}) are solved with the following boundary conditions
\begin{eqnarray}
V_0=\rm{const},\quad P_n=Q_n=0. \label{boundary}
\end{eqnarray}
\end{subequations}
The schematic distribution circuit in Fig.~\ref{fig_feeder} helps to explain the notation.
\begin{figure}[b]
\centering
\includegraphics[width=8.5cm]{Figs2}\\~\\
\caption{
A schematic diagram of the distribution circuit illustrating the notation used in Eqs.~(\ref{Pj+1},\ref{Qj+1},\ref{Vj2},\ref{p_q}).
}
\label{fig_feeder}
\end{figure}
\section{Control of Inverters as a Global Optimization}
\label{sec:optim}
We aim to solve the following global optimization problem: minimize the total loss of real power while constraining the voltage within nominal operational limits and the reactive power generation to the inverters' apparent power capacity $s_j$:
\begin{subequations}\label{DistFlowOptimization}
\begin{eqnarray}
&\min\limits_{q^{(g)},P,Q,V}& \sum_{j=0}^{n-1} r_j\frac{P_j^2+Q_j^2}{V_j^2},\label{Loss}\\
& \mbox{s.t.}& \mbox{Eq.~(\ref{Pj+1},\ref{Qj+1},\ref{Vj2},\ref{p_q},\ref{boundary})},\nonumber\\
&& \forall j=1,\ldots,n:\quad \nonumber \\
&& (1-\epsilon)^2 V_0^2 \leq V_j^2\leq (1+\epsilon)^2 V_0^2,\label{Voltage}\\
&& \left| q_j^{(g)} \right| \leq \sqrt{s_j^2- \left(p_j^{(g)} \right)^2}. \label{PV_constraint}
\end{eqnarray}
\end{subequations}
Here, Eq.~(\ref{Voltage}) are the voltage constraints (with $\epsilon$ typically set to $0.05$, following the ANSI C84.1-2006 standard), and Eq.~(\ref{PV_constraint}) is the inverter apparent power constraint.
Under normal operations, the changes in voltage from node to node are small compared to the voltages and the loss of real and reactive power are small compared to the power flows themselves. In this limit, Eqs.~(\ref{DistFlowOptimization}) can be restated within the LinDistFlow approximation, i.e.,
\begin{subequations}\label{LinDistFlow}
\begin{eqnarray}
&\min\limits_{q^{(g)},P,Q}& \sum_{j=0}^{n-1} r_j\frac{P_j^2 + Q_j^2}{V_0^2}, \label{LossLinear}\\
&\mbox{s.t.}&
\forall j=0,\ldots,n-1: \nonumber \\
&& P_{j+1} = P_j-p_{j+1}^{(c)}+p_{j+1}^{(g)}, \quad P_n=0,\label{P-lin}\\
&& Q_{j+1}=Q_j-q_{j+1}^{(c)}+q_{j+1}^{(g)}, \quad Q_n=0,\label{Q-lin}\\
&& U_{j+1}=U_j-2(r_jP_j+x_jQ_j),\label{V-lin}\\
&& \forall j=1,\ldots,n: \nonumber \\
&& V_0^2 \left(\epsilon^2 - 2\epsilon \right) \leq U_j\leq V_0^2\left(\epsilon^2 + 2\epsilon\right),\label{Voltage-U}\\
&& \left| q_j^{(g)} \right| \leq \tilde{s}_j, \label{PV_constraint_1}
\end{eqnarray}
where $U_j=V_j^2 - V_0^2$ and $\tilde{s}_j=\sqrt{s_j^2-(p_j^{(g)})^2}$. We have assumed $V_j^2 \approx V_0^2$ in \eqref{LossLinear}.
Simulations in \cite{KostyaMishaPetrScott,kundu2013distributed} suggest that the LinDistFlow are well justified for a wide range of distribution circuits. This observation is powerful because the LinDistFlow formulation of Eqs.~(\ref{LinDistFlow}) is convex (a quadratic objective function with linear constraints). Convexity implies that this optimization can be solved efficiently provided each node can communicate with a central authority which performs the computations and distributes the optimal values of $q_j^{(g)}$ to all nodes \cite{KostyaMishaPetrScott,kundu2013distributed}. In the remainder of this work, we will focus on developing a decentralized optimization algorithm, which solves Eqs.~(\ref{LinDistFlow}) only by passing messages between nearest neighbors on the network.
We note that the $P_j$ are determined by solving Eq.~(\ref{P-lin}) for given $p_j^{(c)}$ and $p_j^{(g)}$, and the $P_j$ in Eqs.~(\ref{LossLinear},\ref{V-lin}) can be treated as constants and one can formulate the problem as an optimization over the
$Q_j$ by combining Eqs.~(\ref{Q-lin},\ref{PV_constraint_1}):
\begin{equation}
\left| Q_j - Q_{j-1} + q_j^{(c)} \right| \leq \tilde{s}_j, \quad Q_n = 0 \label{PV_constraint_1Q}.
\end{equation}
\end{subequations}
The actual control outputs are the $q_j^{(g)}$, but these can be inferred from Eq.~(\ref{Q-lin}), once the optimal solution is stated in terms of $Q_j$.
In the following, we present an ADMM-based distributed algorithm for the solution of the LinDistFlow problem.
We further present a dual-ascent distributed algorithm that solves a simplified LinDistFlow problem where the voltage constraints
are omitted and compare its performance with the ADMM algorithm (with and without voltage constraints).
\subsection{ADMM consensus distributed algorithm}
\label{sec_ADMM}
We adapt a consensus version of the ADMM algorithm to our problem. A general discussion of the method and proof of convergence is described in \cite{Boyd2011}. The consensus version assumes that each of the nodes in the network has its own local objective function and a local set of constraints which act on a global variable shared between all the nodes. Each node solves a local optimization problem for respective local copies of the global variables. The local optimization problem consists in finding the optimum for the local copies of the variables, subject to the condition that all local copies are equal to the global variable. The problem is solved iteratively, with all local copies eventually converging to the global optimal value.
For the problem described by Eqs.~\eqref{LinDistFlow}, each node $j$ will keep the local copies of the $Q_j$, $Q_{j-1}$, $U_j$ and $U_{j-1}$ variables, which we will denote $Q^{+}_j$, $Q^{-}_j$, $U^{+}_{j}$ and $U^{-}_{j}$ respectively. We note that the algorithm assumes that one can measure power flows $P_j$ between nodes which are treated as auxiliary constant parameters of the algorithm.
The optimization problem \eqref{LinDistFlow} formulated as a consensus problem becomes:
\begin{subequations}\label{LinDistFlowconsensus}
\begin{eqnarray}
&\min\limits_{Q}& \sum_{j=1}^{n} \frac{r_{j-1} \left(Q^{-}_j \right)^2 }{V_0^2}, \label{LossLinearQconsensus} \\
&\mbox{s.t.}& \forall j=1,\ldots,n: \nonumber \\
&& Q^{+}_j - Q^{-}_{j} + q_j^{(c)} - \tilde{s}_j \leq 0, \label{PV_constraint_1con} \\
&& -Q^{+}_j + Q^{-}_{j} - q_j^{(c)} - \tilde{s}_j \leq 0, \label{PV_constraint_2con} \\
&& Q^{+}_j = Q_j, \quad Q^{-}_j = Q_{j-1}, \quad Q_n = 0 \label{consensus} \\
&& V_0^2 \left(\epsilon^2 - 2\epsilon \right) \leq U^{+}_j\leq V_0^2\left(\epsilon^2 + 2\epsilon\right),\label{Voltage-Uconsensus} \\
&& U^{+}_{j} = U^{-}_j - 2(r_{j-1} P_{j-1}+x_{j-1} Q^{-}_{j}), \label{V-linconsensus} \\
&& U^{+}_{j} = U_j,\quad U^{-}_j = U_{j-1} ,\quad U^{-}_1 = 0 \label{V-consensus}
\end{eqnarray}
\end{subequations}
The conditions \mref{consensus,V-consensus} ensure that all local copies of the variables are equal to the global variables $Q_j$ and $U_j$
and hence the optimization problem \eqref{LinDistFlowconsensus} is equivalent to \eqref{LinDistFlow}.
We solve \eqref{LinDistFlowconsensus} using distributed ADMM method \cite{Boyd2011,boyd2013}, for which
the augmented Lagrangian is
\begin{subequations}
\begin{equation}
{\cal L}^{\rm{ADMM}} = \sum_{j=1}^{n} {\cal L}^{\rm{ADMM}}_j,
\end{equation}
where
\begin{eqnarray}
{\cal L}^{\rm{ADMM}}_j &=& \frac{r_{j-1} \left( Q^{{-}}_j \right)^2} {V_0^2} \label{LagrangianADMM} \\
&+& \frac{\rho}{2} \left( Q^{+}_j - Q_j \right)^2 + \frac{\rho}{2} \left( Q^{ -}_{j} - Q_{j-1} \right)^2 \nonumber \\
&+& \frac{\rho}{2} \left( U^{+}_j - U_j \right)^2 + \frac{\rho}{2} \left( U^{-}_{j} - U_{j-1} \right)^2 \nonumber \\
&+& \lambda^{Q^+}_j \left( Q^{+}_j - Q_j \right) + \lambda^{Q^{-}}_j \left( Q^{-}_j - Q_{j-1} \right), \nonumber \\
&+& \lambda^{U^+}_j \left( U^{+}_j - U_j \right) + \lambda^{U^{-}}_j \left( U^{-}_j - U_{j-1} \right). \nonumber
\end{eqnarray}
\end{subequations}
The quadratic terms in the objective function with $\rho/2$ prefactor represent penalties for the local variables being different from the global variables. These terms do not change the optimal value, as the constraints \mref{consensus,V-consensus} require that the local and global variables are equal at the optimum. The dual variables associated with \mref{consensus,V-consensus} are $\lambda^{Q^{+}}$, $\lambda^{Q^{-}}$, $\lambda^{U^+}_j$ and $\lambda^{U^{-}}_j$. Note that we do not include constraints \mref{PV_constraint_1con,PV_constraint_2con} in the Lagrangian, as the algorithm will be minimizing ${\cal L}_{\rm{ADMM}}$ in such a way that $Q^{+}$ and $Q^{-}$ will always stay within the feasible set, i.e. satisfy \mref{PV_constraint_1con,PV_constraint_2con}.
The ADMM distributed consensus algorithm is an iterative algorithm where the $k+1$-th iteration starts with values $Q_j(k)$, $Q_{j-1}(k)$, $Q_j^{+}(k)$,$Q_j^{-}(k)$, $\lambda^{Q^{+}}_j(k)$, $\lambda^{Q^{-}}_j(k)$, $U_j(k)$, $U_{j-1}(k)$, $U_j^{+}(k)$,$U_j^{-}(k)$, $\lambda^{U^{+}}_j(k)$, $\lambda^{U^{-}}_j(k)$ for each node $j$. One iteration of the algorithm consists of the following steps:
\begin{enumerate}
\item {\bf Minimization step}. For each node $j$, the following optimization problem is solved
\begin{eqnarray}
&& \min\limits_{Q^{-}_j,Q^{+}_j, U^{+}_j, U^{-}_j} {\cal L}^{\rm{ADMM}}_j \label{LocalLoss} \\
&& \mbox{s.t. Eqs.~\mref{PV_constraint_1con,PV_constraint_2con,Voltage-Uconsensus,V-linconsensus}} \nonumber
\end{eqnarray}
This minimization step is a convex optimization problem with quadratic objective function of four local variables $Q^{-}_j,Q^{+}_j, U^{-}_j, U^{+}_j$ with linear constraints and can be solved analytically by evaluating the corresponding Karush-Kuhn-Tucker conditions \cite{boyd2004convex}. However, the expressions are bulky and we do not present them here for the sake of brevity.
Each node $j$ can perform the minimization step independently, as the optimization is carried over the local variables at node $j$. The solutions to the local minimization problem in $k$-th iteration of the ADMM distributed consensus algorithm are denoted as $Q^{-}_j(k+1)$, $Q^{+}_j(k+1)$,
$U^{-}_j(k+1)$, $U^{+}_j(k+1)$.
\item {\bf Averaging step}. This step updates the global (shared) variables $Q$ and $U$. The update rules for each are the following:
\begin{eqnarray}
&& \forall j = 1,\ldots,n-1: \nonumber \\
&& Q_j(k+1) = \frac{1}{2} \left( Q^{+}_j(k+1) + Q^{-}_{j+1}(k+1)\right) \nonumber \\
&& U_j(k+1) = \frac{1}{2} \left( U^{+}_j(k+1) + U^{-}_{j+1}(k+1)\right) \nonumber \\
&& Q_n(k+1) = 0, \, Q_0(k+1) = Q^{-}_1(k+1),\, U_n = U^{+}_n \nonumber
\end{eqnarray}
This step requires communication between nearest neighbors, as they need to exchange their local variables in order for each node $j$ to calculate the new value for $Q_j$ and $Q_{j-1}$ which is the average of the respective local copies of neighboring nodes.
\item {\bf Lagrange multipliers update step}.
The Lagrange multipliers, which are also stored by each node locally, are updated according to the following rules for each node $j$:
\begin{eqnarray*}
{\lambda^{Q^{+}}_j}(k+1) &=& {\lambda^{Q^{+}}_j}(k) + \rho \left( Q^{+}_j(k+1) - Q_j(k+1) \right) \\
{\lambda^{Q^{-}}_j}(k+1) &=& {\lambda^{Q^{-}}_j}(k) + \rho \left( Q^{-}_j(k+1) - Q_{j-1}(k+1) \right)\\
{\lambda^{U^+}_j}(k+1) &=& {\lambda^{U^+}_j}(k) + \rho \left( U^{+}_j(k+1) - U_j(k+1) \right) \nonumber\\
{\lambda^{U^{-}}_j}(k+1) &=& {\lambda^{U^-}_j}(k) + \rho \left( U^{-}_j(k+1) - U_{j-1}(k+1) \right) \nonumber.
\end{eqnarray*}
All variables involved in this step have been calculated and communicated in the previous step, which means that the Lagrange multipliers are updated locally at each node $j$.
\end{enumerate}
The ADMM algorithm requires synchronized communication between the neighboring nodes where local variables ($Q^{+}_j$, $Q^{-}_j$, $U^{+}_j$ and $U^{-}_j$) are communicated between nearest neighbors.
These local variables can be interpreted as 'beliefs' of node $j$ about which reactive power should be flowing in and out of the node and what should be the voltage magnitudes. The consensus algorithm leads to convergence of these local variables between the neighboring nodes, thus finding a global optimal solution.
Once the algorithm converges, the local variables will actually correspond to an optimized feasible solution $Q_j$ and $U_j$ of problem \eqref{LinDistFlowconsensus}. The actual values of reactive power injected by inverters can be calculated by each node from its local variables as
\begin{equation}
q^{(g)}_j = Q^{+}_j - Q^{-}_j + q^{(c)}_j
\label{how_to_q_g}
\end{equation}
The above solution for $q^{(g)}_j$ is guaranteed to be within the allowed bounds given by the $\tilde{s}_j$, as the local variables always satisfy the conditions \mref{PV_constraint_1con,PV_constraint_2con}.
To test the performance of the ADMM algorithm, we compare its convergence with a dual ascent algorithm, which we derive for a simplified LinDistFlow problem without voltage constraints in Section \ref{sec_noU}.
As we will show in Section \ref{sec_cases}, the ADMM distributed consensus algorithm converges faster than the dual ascent algorithm, which is known to be its general main advantage \cite{Boyd2011}.
\subsection{Dual ascent algorithm for distributed control of the inverters with no voltage constraints}
\label{sec_noU}
We now formulate a dual ascent approach to solving the simplified optimization problem \eqref{LinDistFlow} without considering the voltage constraints \mref{V-lin,Voltage-U}.
The Lagrangian becomes
\begin{subequations}
\begin{eqnarray}
{\cal L}\left(Q,\zeta^+,\zeta^- \right) &=& \sum_{j=0}^{n-1}\Biggl[\frac{r_j Q_j^2}{V_0^2} + \\
&+& \zeta^+_j\left(Q_{j+1} - Q_j -\tilde{s}_{j+1}+q_{j+1}^{(c)}\right) \nonumber \\
&+& \zeta^-_j\left(-Q_{j+1}+Q_j-\tilde{s}_{j+1}-q_{j+1}^{(c)}\right) \nonumber \Biggr].
\label{Lagrangian}
\end{eqnarray}
\end{subequations}
The dual ascent algorithm consists of the following steps:
\begin{subequations}
\begin{enumerate}
\item Minimize ${\cal L}\left(Q,\zeta^+,\zeta^- \right)$ over $Q$ for given $\zeta^+, \zeta^-$, which
leads to the following update rule in $k$-th iteration
\begin{equation}
\label{ascent_minimization}
Q_j (k+1) = \frac{V_0^2}{2 r_j} \left( \zeta^{+}_j(k) - \zeta^{+}_{j-1}(k) + \zeta^{-}_{j-1}(k) - \zeta^{-}_{j}(k) \right).
\end{equation}
\item Update dual variables according to
\begin{eqnarray}
\zeta^{+}_j(k+1) &=& \max \left(0, \zeta^{+}_j(k) + \alpha \Delta^+_{j+1} \right) \label{ascent_alphaplus} \\
\zeta^{-}_j(k+1) &=& \max \left(0, \zeta^{-}_j(k) + \alpha \Delta^-_{j+1} \right) \label{ascent_alphaminus}
\end{eqnarray}
\end{enumerate}
where
\begin{eqnarray*}
\Delta^+_{j+1} &=& Q_{j+1}(k+1) - Q_j(k+1) + q_{j+1}^{(c)} - \tilde{s}_{j+1} \\
\Delta^-_{j+1}&=& - Q_{j+1}(k+1) + Q_j(k+1) - q_{j+1}^{(c)} - \tilde{s}_{j+1}.
\end{eqnarray*}
\end{subequations}
This scheme allows parallel implementation, where each node $j$ receives values of $\zeta^{+}_{j}(k)$ , $\zeta^{-}_{j}(k)$ from its right neighbor $j+1$ and sends values of
$\zeta^{+}_{j-1}(k)$ , $\zeta^{-}_{j-1}(k)$ to its left neighbor $j-1$. Node $j$ then calculates $Q_{j}(k+1)$ using those variables and then sends the result to neighbor $j+1$, while receiving $Q_{j-1}(k+1)$ from neighbor $j-1$. The communicated values are then used by node $j$ to calculate $\zeta^{+}_{j-1}(k+1)$ and $\zeta^{-}_{j-1}(k+1)$.
An advantage of the dual ascent algorithm is that it requires the nodes to perform trivial algebraic operations (which are simpler than the solution of Eq.~\eqref{LocalLoss}) and synchronously communicate their local variables $Q$, $\zeta^+$, and $\zeta^-$ to their neighbors.
However, based on discussion in \cite{Boyd2011}, the dual ascent method is expected to require a large number of iterations to converge. The speed of convergence is controlled by parameter $\alpha$, but the range of feasible $\alpha$ is limited---choosing $\alpha$ which is too large results in a failure to converge, while $\alpha$ chosen too small translates into a slow convergence.
We provide comparison of the dual ascent algorithm with the ADMM algorithm in Section \ref{sec_results}. Since the proposed dual ascent algorithm does not
consider voltage constraints, we will also consider a version of the ADMM algorithm without the voltage constraints (referred to as ADMM-noV), which can be straightforwardly obtained from the ADMM algorithm by excluding voltage variables $U_j, U^+_j, U_j^-$ and removing constraints \mref{Voltage-Uconsensus,V-linconsensus,V-consensus}.
\section{Experiments with distributed global optimization on different distribution circuit cases}
\label{sec_cases}
We explore the performance of our distributed optimization algorithms via simulations on a range of distribution circuit cases. We first introduce the considered feeder line configuration cases and then compare the performance of the dual ascent, ADMM and ADMM-noV algorithms on these cases. The global optimization
results from these algorithms are compared with the sub-optimal local optimization scheme proposed in \cite{KostyaMishaPetrScott}, where each node only uses its local information about $q_j^{(c)}$ to set its $q_j^{(g)}$. Finally, we compare losses and voltages calculated with the LinDistFlow equations with the ones calculated by DistFlow equations for the same set of injected reactive power $q^{(g)}$ in order to check the validity of the underlying approximation.
\subsection{Distribution circuit test cases}
The properties of the distribution circuit used in the simulations are summarized in the following table:
\begin{center}
\begin{tabular}{|c|cclll|}
\hline
{\bf Case} & {\bf Nodes } & {\bf PV-pen} & $\mathbf{p^{(c)}_{\rm{\bf max}}}$ & $\mathbf{p^{(g)}}$ & $\mathbf{s_{\rm{\bf max}}}$ \\
\hline
1 & 100 & 100\% & $4$ kW & $1$ kW & $1.1$ kW \\
2 & 100 & 50\% & $4$ kW & $1$ kW & $1.1$ kW \\
3 & 250 & 50\% & $2.5$ kW & $1$ kW & $2.2$ kW \\
4 & 250 & 50\% & $1$ kW & $2$ kW & $2.2$ kW \\
5 & 150 & 85\% & $4$ kW & $0.9$ kW & $1.1$ kW \\
6 & 200 & 100\% & $3.75$ kW & $0$ kW & $2.2$ kW \\
7 & 150 & 70\% & $2$ kW & $7.0$ kW & $10$ kW \\ \hline
\end{tabular}
\end{center}
The ``PV-pen'' column indicates the percentage of nodes in the distribution circuit that have PV generation installed. These nodes all inject the same power which is given in the column denoted as $p^{(g)}$. $s_{\rm{max}}$ is the apparent power capacity of the inverters which enters into the constraints in Eq.~\eqref{PV_constraint}. We set $s_j = s_{\rm{max}}$ for all the nodes with PV generation installed, and $s_j = 0$ for the rest. The real power consumed at each node, $p_j^{(c)}$, is chosen from a uniform distribution between $0$ and $p^{(c)}_{\rm{max}}$. The reactive power consumption is set to $q^{(c)}_j = 0.25 p_j^{(c)}$ for all the cases except for cases 5 and 7 where $q^{(c)}_j = f_j p_j^{(c)}$ with $f_j$ is drawn from a uniform distribution between $0.01$ and $1.0$ for case 5 and between $0$ and $1.0$ for case 7. The distribution circuit line resistance $r_j$ and reactance $x_j$ are $0.33\, \Omega/\rm{km}$ and $0.38\, \Omega / \rm{km}$ respectively, with the distances between the neighbors always set to
$0.25\,\rm{km}$. The voltage at the start of the distribution circuit is $V_0 = 7.2\,{\rm kV}$.
The considered distribution circuits are based on feeder line configurations used in our previous work \cite{KostyaMishaPetrScott,KostyaMishaPetrScott2, KostyaMishaPetrScott3} where suboptimal, policy-based control schemes were analyzed. Case 6 corresponds to higher loads with no generation but 100\% penetration (representing example of a nighttime case with high loads). This case is included because the node voltages violate the {\it minimum} voltage constraint without control of the $q^{(g)}$ (i.e., when all $q_j^{(g)} = 0$) . Case 7 corresponds to a scheme with high power generation and low consumption in the feeder line such that, without control, the voltage violates the {\it maximum} voltage constraint. The voltage rise above the allowed limit is a possible issue in networks with high distributed PV generation
\cite{tonkoski2012impact}.
\subsection{Global vs local optimization}
\label{sec:global_vs_local}
First, we compare the globally optimal solutions for the injected reactive power obtained with the distributed algorithms described above (denoted as $\tilde{q}_j^{(g)}$) with the local policy-based scheme proposed in \cite{KostyaMishaPetrScott}. In the local scheme, the inverters are set to supply the local reactive power consumption up to their apparent power capacity:
\begin{equation}
\label{q_local}
q^{(g)}_j({\rm{local}}) = \min \left( q^{(c)}_j , \tilde{s}_j \right).
\end{equation}
We compute the total circuit losses (using Eq.~\eqref{LossLinear}) for both global and local policy-based scheme (setting reactive powers to $\tilde{q}_j^{(g)}$ and $q^{(g)}_j({\rm{local}})$ respectively) and divide by the losses for the ``no-optimization scheme,'' i.e. with all $q^{(g)}_j$ set to zero. This scheme corresponds to the current situation for PV inverters which inject real power at a nominal power factor of $1.0$. The normalized losses from the globally-optimal solution of Eqs.~\eqref{LinDistFlow} (Loss$^{\rm glob}_{\rm lin}$) and the local policy control (Loss$^{\rm loc}_{\rm lin}$) are shown in the following table for cases 1-5: \\
\begin{center}
\begin{tabular}{|c|cc|}
\hline
{\bf Case} & {\bf Loss$^{\rm glob}_{\rm lin}$} & {\bf {\bf Loss$^{\rm loc}_{\rm lin}$}} \\
\hline 1 & $0.834$ & $ 0.845$ \\
2 & $0.941$ & $0.949$ \\
3 & $0.847$ & $0.890$ \\
4 & $0.954$ & $0.962$ \\
5 & $0.700$ & $0.771$ \\ \hline
\end{tabular}
\end{center}
In each case, both control schemes lower the total loss of real power, and except for cases 3 and 5, the local policy-based scheme performs nearly as well as the globally optimal solution. This should be expected because these cases are not so heavily loaded or over-generated that the voltage exceeds the normal operational limits. As was shown in \cite{kundu2013distributed}, the local policy in \eqref{q_local} is approximately an optimal policy until these limits are approached. However, this local policy is unable to respond appropriately when the voltage deviates beyond its normal operational limits.
Cases 6 and 7 are shown in the table below, along with the minimum (for case 6) and maximum (for case 7) voltages normalized with respect to its nominal value $V_0$.
The voltages shown in the table were calculated by solving the exact DistFlow eqs.~\eqref{DistFlow} using the values of $q_j^{(g)} = \tilde{q}_j^{(g)}$ for the global optimization of LinDistFlow eqs.~\eqref{LinDistFlow} scheme (V$^{\rm glob}$), $q_j^{(g)} = q^{(g)}_j({\rm{local}})$ for local policy control scheme (V$^{\rm loc}$), and $q_j^{(g)} = 0$ for the no-optimization scheme (V$^{\rm{noopt}}$) respectively.
The voltages in the no-optimization scheme violate the nominal operating limits for both cases. The local policy-based control is unable to fully correct this situation and, in the case of voltage in case 7, makes the situation worse. The global optimization scheme enables the voltage to be corrected to respect the constraints, which naturally leads to higher losses. We note that the minimum (maximum) normalized voltage calculated with LinDistFlow approximation is $0.95$ ($1.05$) for case 6 (case 7) for global optimization scheme, but the actual values obtained from DisFlow eqs.~\eqref{DistFlow} are slightly below the voltages calculated from the linear approximation \eqref{LinDistFlow}. The agreement between the linear approximation and the DistFlow equations will be further discussed in Section \ref{sec:validity}.
\begin{center}
\begin{tabular}{|c|ccccc|}
\hline {\bf Case} & {\bf Loss$^{\rm glob}_{\rm lin}$} & {\bf Loss$^{\rm loc}_{\rm lin}$}& {\bf V}$^{\rm glob}$ & {\bf V}$^{\rm loc}$ & {\bf V}$^{\rm{noopt}}$ \\ \hline
6 & $0.954$ & $0.941$ & $ 0.947 $ & $0.938$ & $ 0.920$ \\
7 & $1.11$ & $1.09$ & $1.045$ & $1.074$ & $1.071$ \\ \hline
\end{tabular}
\end{center}
\subsection{Performance of distributed optimization algorithms}
\label{sec_results}
\begin{figure}
\centering
\includegraphics[width=8.5cm]{referee_dual_ascent_figure}\\~\\
\caption{
The average absolute deviation from the optimal values for $q^{(g)}$ as a function of number of iterations for the dual ascent algorithm applied to cases 1-5. The cases 3 and 4 are shown in the inset, while the cases 1, 2 and 5 are plotted with the iteration axis scaled by the multiples of $10^4$ iterations.
}
\label{fig_ascent}
\end{figure}
\begin{figure}
\centering
\includegraphics[width=8.5cm]{referee_admm_figure}\\~\\
\caption{
The average absolute deviation from the optimal values for $q^{(g)}$ as a function of number of iterations. The data were obtained from ADMM-noV algorithm for cases 1-5.
}
\label{fig_admm}
\end{figure}
\begin{figure}
\centering
\includegraphics[width=8.5cm]{referee_admm_v_figure}\\~\\
\caption{
The average absolute deviation from the optimal values for $q^{(g)}$ as a function of number of iterations. The data were obtained from ADMM algorithm for cases 1-7, with cases 6 and 7 shown separately in the inset.
}
\label{fig_admm_v}
\end{figure}
For cases 1-5, where voltage constraints are satisfied even without explicitly including them in the optimization problem, the dual ascent, ADMM-noV and ADMM algorithms yield identical minimum real power losses. However, these algorithms do not have equal performance in terms of convergence.
For cases 1-5, we contrast the convergence properties of each algorithm by comparing the intermediate values of $q^{(g)}_j$ at iteration $k$ with the global optimum $\tilde{q}^{(g)}_j$ obtained by solving \eqref{LinDistFlow} with the CVX package \cite{cvx,gb08}. We plot on the y-axis the average absolute deviation as a function of number of iterations, defined as
\begin{equation}
{\rm{D}}(k) = \frac{1}{n} \sum_{j=1,\ldots,n} \left| q^{(g)}_j(k) - \tilde{q}^{(g)}_j \right|
\end{equation}
where $n$ is the total number of nodes in the feeder line. At each iteration, the values of $q^{(g)}(k)$ are calculated from the local variables. For the dual ascent algorithm, we utilize $Q(k)$ and \eqref{Q-lin} to obtain $q^{(g)}(k)$ while for ADMM-noV and ADMM we use the variables $Q^{-}(k)$, $Q^{+}(k)$ and Eq.~\eqref{how_to_q_g}.
The values of ${\rm{D}}(k)$ for dual ascent, ADMM-noV, and ADMM algorithms are plotted in Figs.~\ref{fig_ascent}, \ref{fig_admm} and \ref{fig_admm_v}, respectively. For all the algorithms, the initial value of $Q_j$ and of all Lagrange multipliers was chosen to be equal to $0$. The initial values of $U_j$ for the ADMM algorithm were taken from the solution of Eq.~\eqref{V-lin}, with $Q_j$ set to 0.
For the cases 1, 2, and 5, the dual ascent algorithm (Fig.~\ref{fig_ascent}) takes the order of $10^4$ iterations to converge while cases 3 and 4 only required a few tens of iterations. The fast convergence is primarily due to the optimal solution for those cases being close to the initial choice of $Q_j = 0$. The speed of convergence is controlled by the parameter $\alpha$ in Eqs.~\mref{ascent_alphaplus,ascent_alphaminus}. Via empirical experimentation, we find $\alpha = 0.05/V_0^2$ to give optimal convergence performance as choosing larger/smaller $\alpha$ caused numerical instability/slower convergence.
For cases 1-5, the ADMM-noV (Fig.~\ref{fig_admm}) and ADMM (Fig.~\ref{fig_admm_v}) algorithms converge to the optimal $q^{(g)}$ within tens of iterations. This rapid convergence dramatically outperforms the dual ascent algorithm in cases where the initial guess is not close to the optimal solution. In the cases 6 and 7, ADMM requires order of $10^3$ iterations (Fig.~\ref{fig_admm_v}, inset). The reduced performance in this case is because the voltage constraints are violated at some nodes, and this information needs to propagate throughout the entire distribution circuit.
In general, the dual ascent algorithm requires more iterations, and hence more rounds of communication between nodes, to converge. The adjustment of the $q^{(g)}$ should be carried out on the faster timescales than the $p^{(g)}$ and $p^{(c)}$ are changing. For PV generation, these changes can be on the order of one to several minutes. In some cases, the large number of interactions required for dual ascent would challenge the capability of grid communications systems.
\begin{figure}
\centering
\includegraphics[width=8.5cm]{referee_admm_v_fromqg0}\\~\\
\caption{
The average absolute deviation from the optimal values for $q^{(g)}$ as a function of number of iterations. The data were obtained from ADMM algorithm for cases 1-7.
The initial state was taken for $Q,\,Q^{+},\,Q^{-}$ and $U$ corresponding to solution of power flow equations when $q^{(g)}_j = 0$.
}
\label{fig_admmv_fromqg0}
\end{figure}
\begin{figure}
\centering
\includegraphics[width=8.5cm]{referee_admm_v_fromqglocal}\\~\\
\caption{
The average absolute deviation from the optimal values for $q^{(g)}$ as a function of number of iterations. The data were obtained from ADMM algorithm for cases 1-7.
The initial state was taken for $Q,\,Q^{+},\,Q^{-}$ and $U$ corresponding to solution of power flow equations when $q^{(g)}_j = q^{(g)}_j(\rm{local})$.
}
\label{fig_admmv_fromqlocal}
\end{figure}
\begin{figure}
\centering
\includegraphics[width=8.5cm]{referee_admm_fromqg0_then_admmv}\\~\\
\caption{
The average absolute deviation from the optimal values for $q^{(g)}$ as a function of number of iterations. The data were obtained from an algorithm which first ran ADMM-noV for 50 iterations and then used the measured values of voltage to initialize ADMM algorithm.
The initial state was taken for $Q,\,Q^{+},\,Q^{-}$ corresponding to solution of power flow equations when $q^{(g)}_j = 0$.
}
\label{fig_admmv_fromqlocalUafter}
\end{figure}
Our choice of initial condition in for Figs.~\ref{fig_admm}, \ref{fig_admm_v} was simple $Q = Q^+=Q^-=0$, $U$ was set in accordance with solutions of \eqref{V-lin} with $Q = 0$.
Such choice of $Q$ allowed for direct comparison between the dual ascent and ADMM algorithms, as they started from the same point. Note that the choice of nonzero initial $Q_j$ in the dual ascent algorithm would also require setting up nonzero Lagrange multipliers $\zeta^{+}_j, \zeta^{-}_j$, according to \eqref{ascent_minimization}, that would likely require additional (preemptive) communication between the nodes to agree on the multipliers.
The zero initial choice of $Q$ was sufficiently close to the actual optimal solutions in cases 3 and 4. However, other cases required more iterations to converge. On the other hand, the ADMM-noV algorithm converged within tens of iterations even in the other cases (1, 2 and 5) in spite of the fact that the final solutions for $Q$ were rather different from the zero initial guess. The ADMM algorithm, applied to the cases 6 and 7 where voltage constraints were violated in the unoptimized solution, took much longer ($O(10^3)$) to converge. Experimenting with the ADMM we have found that its convergence is rather sensitive to the initial guess of voltages. In particular, we tested the following two initializations:
(a) $Q$ and $U$ corresponding to the case where $q^{(g)}_j = 0$ for all nodes (the unoptimized solution), and (b) $Q$ and $U$ corresponding to the state where $q^{(g)}_j = q^{(g)}_j(\rm{local})$, where $q^{(g)}_j(\rm{local})$ is the local optimum defined by Eq.~\eqref{q_local}. Convergence of the ADMM is compared for these two initial states in Figs.~\ref{fig_admmv_fromqg0} and \ref{fig_admmv_fromqlocal} respectively. Note that the bare ADMM-noV (i.e. no voltage constraints) converged in tens of iterations for both (a) and (b) initiations. Convergence of ADMM initialized with $q^{(g)}_j=q^{(g)}_j(\rm{local})$ (Fig.~\ref{fig_admmv_fromqlocal}) matched convergence of the bare ADMM-noV for cases 1-5, as does ADMM when initialized from $Q_j = 0$ (Fig.~\ref{fig_admm_v}). However, the same ADMM initialized with $q^{(g)}_j = 0$ took $O(10^3)$ iterations to converge in the cases 3 and 4, presumably due to rather inaccurate voltage guess/initiation. One possible way to get around this problem is to run the ADMM-noV algorithm for few iterations, and then switch to the ADMM initializing voltages from the measured values at the nodes, as shown in Fig.~\ref{fig_admmv_fromqlocalUafter}.
The convergence of ADMM algorithms is further influenced by the choice of the parameter $\rho$ in the ADMM Lagrangian \eqref{LagrangianADMM}. We used $\rho = 1/V_0^2$, which we found, via empirical experimentation, to give the best convergence properties for our algorithm.
We have considered decreasing and increasing $\rho$ by a factor of 10 and 100. The choice which provides good convergence properties for all the cases and initial conditions considered is found to be $\rho = 1/V_0^2$, even though for some particular cases and choice of initial conditions, smaller or larger $\rho$ sometimes performs slightly better. The convergence rate is sensitive to the choice of $\rho$, as choosing too large or too small $\rho$ can lead to significant slowdown of convergence in some cases, as illustrated in Fig.~\ref{fig_admmv_rhos}.
Finally, we note that for the numerical implementation, the actual units of representation of voltage and reactive power can play significant role, as they balance the magnitude of the terms in the ADMM Lagrangian.
For our ADMM simulations, we represented $Q$ in kW and $U$ in $100$ kV$^2$ units. Choosing smaller magnitude for the representation of the voltages could lead to accumulation of errors due to the differences between the local variables $U^{+}, U^{-}$ and the actual value of $U$, which would then affect the convergence for algorithms where voltage constraints are violated typically at the last few nodes in the distribution circuit. Alternatively, one could consider having two different parameters $\rho_Q$ and $\rho_U$ and adapt them separately for optimal convergence.
\begin{figure}
\centering
\includegraphics[width=8.5cm]{referee_admm_rhos}\\~\\
\caption{
The average absolute deviation from the optimal values for $q^{(g)}$ for case 7 (in the main plot) and case 4 (in the inset) for different values of parameter $\rho$.
The initial state was taken for $Q,\,Q^{+},\,Q^{-}$ and $U$ corresponding to solution of power flow equations when $q^{(g)}_j = q^{(g)}_j(\rm{local})$.
}
\label{fig_admmv_rhos}
\end{figure}
\subsection{Validity of LinDistFlow approximation}
\label{sec:validity}
The optimization algorithms formulated above rely on the validity of LinDistFlow equations. To test the accuracy of this approximation, we take the $\tilde{q}_j^{(g)}$ solution of the global optimization formulated with the LinDistFlow equations \eqref{LinDistFlow} and substitute them into the DistFlow equations \eqref{DistFlow}. We then solve the DistFlow equations exactly and compare the relative losses (normalized with respect to the losses of the no-optimization scheme) of the DistFlow (Loss$^{\rm{glob}}_{\rm DF}$) and LinDistFlow equations (Loss$^{\rm glob}_{\rm lin}$).
We also compare the maximum difference between the normalized voltages calculated by LinDistFlow (V$^{\rm glob}_{\rm lin}$) and by DistFlow (V$^{\rm{glob}}$) equations for each case. We use the Matpower package \cite{matpower} to solve the DistFlow solutions, with the reactive powers set to values obtained by solution of the LinDistFlow optimization problem \eqref{LinDistFlow}. The table below shows these comparisons, with $\left| \delta V \right|$ defined as $\max_j \left| {V^{\rm glob}_{\rm lin}}_j - V^{\rm{glob}}_j \right|$.
In addition, we also solve the global optimization DistFlow problem with CVX package using a centralized algorithm from \cite{farivar2012optimal}, which finds the values of reactive power $q^{(g)}$ that solve Eqs.~\eqref{DistFlowOptimization}. The obtained relative losses for such a solution (shown in the table below as Loss$^{\rm{glob-nonlin}}$) are close to the relative losses calculated for the reactive powers $\tilde{q}_j^{(g)}$ obtained from our decentralized optimization of LinDistFlow equations.
\begin{center}
\begin{tabular}{|c|cccc|}
\hline
{\bf Case} & {\bf Loss$^{\rm glob}_{\rm lin}$} & {\bf Loss$^{\rm glob}_{\rm{DF}}$} & {\bf Loss$^{\rm glob-nonlin}$}& $\left| \delta V \right|$ \\
\hline
1 & $0.834$ & $0.828$ & $0.828$ & $0.000$ \\
2 & $0.941$ & $0.937$ & $0.937$ & $0.000$ \\
3 & $0.847$ & $0.821$ & $0.819$ & $0.001$ \\
4 & $0.948$ & $0.937$ & $0.937$ & $0.000$ \\
5 & $0.700$ & $0.687$ & $0.687$ & $0.000$ \\
6 & $0.954$ & $0.916$ & $0.920$ & $0.003$ \\
7 & $1.087$ & $1.112$ & $1.071$& $0.005$ \\ \hline
\end{tabular}
\end{center}
The relative losses Loss$^{\rm glob}_{\rm{DF}}$ agree within few percent with the values predicted by the LinDistFlow equations, and in most cases, the DistFlow relative losses are actually slightly lower than the ones obtained from LinDistFlow equations. For all the cases considered, the maximum difference between values of voltages are of the order of $10^{-3}$, which is a satisfactory precision since the algorithm needs to optimize objective function subject to (normalized) voltage constrained to between $0.95$ and $1.05$.
For the cases 6 and 7, where global reactive power control scheme is necessary to ensure voltage regulation within allowed bounds, the voltage magnitude calculated with LinDistFlow equations ($V^{\rm glob}_{\rm lin}$) slightly overestimates the exact value calculated from DistFlow equations ($V^{\rm glob}$). As a result, the actual voltage is in fact lower by $O(10^{-3})$. Hence, the global optimization of LinDistFlow equations leads to lower relative losses (Loss$^{\rm glob}_{\rm{DF}}$) than Loss$^{\rm glob-nonlin}$ obtained from optimization of DistFlow problem \eqref{DistFlowOptimization} for case 6 (where LinDistFlow optimization's minimum voltage is $0.947$), and higher relative losses for case 7, as the maximum normalized voltage obtained from LinDistFlow optimization is actually $1.045$, lower than the maximum bound $1.05$, which is attained with the global DistFlow optimization.
\section{Discussion}
\label{sec_disc}
In this work, we presented three distributed algorithms achieving global optimality of reactive power flows in power-distribution systems and tested these algorithms on multiple examples of circuits with high PV penetration. In this formulation of the optimization, the cost function and constraints are separable and this structure is explored to construct and compare three exact distributed algorithms that rely on local measurements, local computations and communications between nearest neighbors. The general advantage of this distributed implementation is that each node can have its own set of constraints as well as its own objective function, which do not need to be known to the other nodes. The dual-ascent algorithm allows for simple implementation, but in most cases requires significantly more iterations to converge. The consensus-based ADMM algorithms require more sophisticated local computations, however, overall they converge much faster than the dual ascent algorithm.
Our approach allows multiple generalizations. We highlight some, while emphasizing the importance of future theoretical, algorithmic and experimental (simulations and testbed) explorations:
\begin{itemize}
\item One can easily generalize our ADMM algorithm to different objective functions: for instance, some nodes can have an additional term in the objective function which depends on voltage, such as $\left( V - V_0 \right)^2$. This correction would improve the voltage quality for that particular node. Those rules can even be changed locally and on-the-go, without other nodes being aware of the adaptation.
\item Communications between different nodes do not need to be synchronized and may allow some degree of delay. It will be important to analyze the robustness of the scheme to delays, errors and corruptions, e.g. originating from targeted attacks. It is expected that the distributed nature of the algorithm makes it much more secure against localized and non-correlated attacks than centralized algorithms.
\item Our algorithm is naturally extendable to account for more complicated tree-like topologies and some (still separable) nonlinearities in power flows, of the type already discussed in \cite{Zampieri13c} for the dual ascent algorithm. It also allows generalization to account for binary PV-inverter selection such as discussed in \cite{Dall2013}.
\end{itemize}
\section{Acknowledgments}
The authors thank Sidhant Misra, Changhong Zhao and Steven Low for helpful advice and productive discussions. The work at LANL was funded by the Advanced Grid Modeling Program in the Office of Electricity in the US Department of Energy and was carried out under the auspices of the National Nuclear Security Administration of the U.S. Department of Energy at Los Alamos National Laboratory under Contract No. DE-AC52-06NA25396. The work at NMC is supported by the National Science Foundation award \# 1128501, EECS Collaborative Research ``Power Grid Spectroscopy".
\bibliographystyle{ieeetr}
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{
"redpajama_set_name": "RedPajamaArXiv"
}
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References
External links
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{
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\section{Introduction}
Spin valve, consisting of two or more layered conducting ferromagnetic (FM) materials, is a key element of spintronics \cite{MonLod,ParkWund}.
The electrical resistance of a
spin valve switches between high and low values depending on
whether the alignment of the magnetization in the layers is parallel (P)
or antiparallel (AP). The mechanism of this change is the giant
magnetoresistance (MR) effect \cite{Grunberg}, which is the
basis of modern commercial devices such as reading heads for computer hard drives or magnetic sensors. In the past decade, spin valve also attracted much attention in 2D materials, see {\it e.g.} Refs.~[\onlinecite{YeZhu,ModMog,LuoM,LinYang,CarSor,SongCai,HanKaw0}], which have easily tunable electronic properties.
Recently-discovered 2D van der Waals (vdW) magnets, notably Cr$_2$Ge$_2$Te$_6$ (CGT) \cite{GongLi} and CrI$_3$ \cite{HuaCla}, have easily-manipulated magneto-electric and magneto-optical properties \cite{BurchMand,GoZha}, and therefore are very promising for spintronics. In particular, the layered antiferromagnetic (LAF, {\it i.e.} two adjacent FM monolayers coupled antiferromagnetically) order confirmed in bilayer insulating CrI$_3$ \cite{HuaCla,JiangLi,JiangShan,SunYi} adds an intriguing dimension to develop 2D antiferromagnetic spintronics with low power consumption and robustness against perturbations from magnetic fields \cite{BalMan,JungMar}. A few proposals exploiting LAF have been put forward, including manipulating electron spin by high-intensity electric field \cite{GongSJ} and exotic topological phases by electro-optical effect \cite{ZhaiBlanter}. However, the intrinsic LAF systems usually have large band gaps, no or weak spin polarization or low electron mobility \cite{HuaCla,BurchMand,GoZha,JiangLi,JiangShan,SunYi,GongSJ}, which strongly limit their applications in design of electronic circuits with low energy consumption.
Recent progress made it possible to fabricate 2D structures composed of almost any layers on top of each other \cite{LiYang,ZhongSey,NovMish}. These structures display a higher variety of properties than natural materials, can be tailored to have predefined physical properties, and open a way to design high-performance devices based on unusual interface physics. Motivated by the latest advances on fabrication of four-layer vdW heterosystems (typically graphene/bilayer CrI$_3$/graphene \cite{SongCai} and WSe$_2$/bilayer graphene (BLG)/WSe$_2$ \cite{Island}) and a BLG-based device that allows for local bias control \cite{LiWang}, we propose an artificial four-layer LAF device [Fig.~1(a)] with two gated terminals linked by the central scattering region to realize a fully electrically controlled spin valve. Its operation mechanism is similar to that of existing giant MR devices \cite{Grunberg,YeZhu,ModMog,LuoM,LinYang,CarSor,SongCai,HanKaw0},
with the difference that it does not require magnetic field: By altering the mutual bias orientation in the two terminals, from
P to AP, the MR of in-plane transport varies significantly. Due to the magneto-electric coupling [Fig.~1(b)], the spin valve effect is transferred to the nonmagnetic vdW layers. We start with
a phenomenological model, and further use the density functional theory
(DFT) calculations to demonstrate the concept with a material platform$-$BLG encapsulated by two single layers of CGT.
Our proposed LAF spin valve has three advantages over the usual spin valves \cite{Grunberg,YeZhu,ModMog,LuoM,LinYang,CarSor,SongCai,HanKaw0}: ($i$) It is robust against environmental perturbations from magnetic or
null-stray fields due to antiferromagnetism \cite{BalMan,JungMar,GongSJ};
($ii$) It requires only small vertical bias to control, is reversible to operate, superior to traditional magnetic control \cite{Grunberg}; ($iii$) It is not sensitive to the presence of domain walls (DWs), thus enabling the device to possess strong anti-jamming of DWs. The two latter points are not trivial, and we demonstrate their validity here.
\begin{figure}
\centerline{\includegraphics[width=8.5cm]{Fig1.pdf}} \caption{
(a) Top: Sketch of a LAF spin valve based on BLG encapsulated by 2D FM insulators.
1 (2) marks the layer of BLG. The device consists of two LAF terminals [left (L), right (R)] and a linked central region (C, length $d$), where a collinear
DW (magnetic periodicity along $y$ is not drawn) is taken as an example. Local dual-gates in L/R are used to induce the vertical electric field $E_z$ and tune the Fermi energy $E_{\rm F}$ \cite{SongCai,LiWang}. Bottom: Typical bands are plotted to show how high MR is achieved for the P arrangement of $E_z$ in L and R. (b) A general picture of field-modulated layer- and spin-resolved density of states (DOS) for the case on the right. By shifting the layer-spin dependent states in energy, the LAF field in model~(\ref{Hami}) induces a band gap in BLG, and then $E_z$ drives fully spin polarization within the gap.}
\end{figure}
\section{Model and Theory}
Our model of four vdW layers in Fig.~1(a) contains the nonmagnetic conducting BLG with Bernal stacking \cite{McKosh,Neto} in the middle and two FM insulating layers located respectively on the upper and lower sides. As a typical conducting system, BLG has the advantages of highly-adjustable electron mobility \cite{McKosh,ZhaTan} and long spin relaxation length \cite{HanKaw,Suichen,XuZhu}, which can be very little affected by vdW proximity \cite{Island,YangTu} and suggest an easily-prepared platform to realize low-consumption devices. We assume that the two insulating layers are identical 2D magnets with out-of-plane magnetization (favorable to ultrahigh density data storage \cite{WelMos}), and do not contribute to the low-energy electronic bands except for proximity-induced magnetism. An effective low-energy Hamiltonian from an empirical tight-binding model (see Appendix A) reads
\begin{equation}\label{Hami}
\begin{split}
H_0=\upsilon_0(p_x\sigma_x+\xi p_y\sigma_y)-\frac{\gamma}{2}
\sum_{i=x,y}\tau_i\sigma_i+m_z\tau_zs_z
+\lambda_U\tau_z,
\end{split}
\end{equation}
where $\sigma_i$, $\tau_i$, $\bm s_i$ ($i=x,y,z$) are, respectively,
the Pauli matrices for sublattice isospin, layer isospin and real
spin. Here, $\xi=\pm1$ indicate two opposite valleys $K$, $K'$ of the
hexagonal Brillouin zone, $p_{x(y)}$ is the momentum component,
$\upsilon_0=3at/2$ is the Fermi velocity in graphene ($a$, $t$ are
the bond length and nearest-neighbor hopping, respectively),
and $\gamma$, $m_z$ and $\lambda_U$ denote the strengths of the
interactions. The first and second terms are, respectively, the massless Dirac term
and the interlayer nearest-neighbor coupling
(usually sufficient to capture the band features
\cite{McKosh,Neto}). The third term indicates the LAF field induced by short-range magnetic proximity from two FM layers \cite{TangZhang,CarSor}. The last term represents the vertical bias.
We also consider other possible interactions which might be present but do not qualitatively change the MR effect we concern with. They read \cite{KarpCum,Island,YangTu} $H'=H'_\Delta+H'_{\rm R}$, where $H'_\Delta=\Delta\sigma_z$ represents the
intralayer inversion-symmetry breaking induced by interface lattice mismatch
and $H'_{\rm R}=\lambda_{\rm R}(\sigma_xs_y-\xi\sigma_ys_x)/2$ \cite{KarpCum,ZhaiJin1,ZhaiJin2} is the proximity-induced Rashba interaction. For simplicity, we take $H'$ the same in both monolayers. Disregarding $H'_{\rm R}$, the low-energy four bands are solved as
\begin{equation}\label{band}
\begin{split}
E^2=&\upsilon_0^2p^2+\frac{\gamma^2}{2}+\alpha^2+\Delta^2\\
&-\frac{1}{2}\sqrt{4\upsilon_0^2p^2(4\alpha^2+\gamma^2)+\left(\gamma^2-4\alpha
\Delta\right)^2},
\end{split}
\end{equation}
where $\alpha=\lambda_U+sm_z$ ($s=\pm1$ denote spin up and spin down, respectively).
In the actual numerical calculations below (Fig.~2), weak $H'_{\rm R}$ is taken into account as well.
As sketched in Fig.~1(a), the system is divided into three regions, including the left (L), right (R) terminals and the central (C) scattering region. We use
an effective empirical potential \cite{SanPra} $\lambda_U(x)=U~{\rm erf}(x/d)$ and $U$, respectively, to simulate the AP and P bias configurations. Here, erf is the error function, and $x=0$ is the center of region C.
Depending on the sample quality, the system can be a pristine LAF crystal when no DW is present in region C ($dm_z/dx=0$). The simplest DW is collinear, as sketched in Fig.~1(a), and can be simulated by a smooth potential \cite{WahAug}
\begin{equation}\label{m_z}
m_z(x)=M_0\tanh\frac{\pi x}{d}.
\end{equation}
Here, the magnetization $m_z$ vanishes at $x=0$ due to
the destructive overlap between opposite spins. We can further consider
the noncollinear Bloch
($m_y^2=M_0^2-m_z^2$,
$m_x=0$) and N\'{e}el ($m_x^2=M_0^2-m_z^2$,
$m_y=0$) types of DW due to spin fluctuation \cite{WahAug} by adding in-plane magnetization terms $m_y\tau_zs_y$ and $m_x\tau_zs_x$ to Eq.~(\ref{Hami}), respectively. The in-plane magnetization of Bloch (N\'{e}el) type is parallel (perpendicular) to the DW,
and the sign of $m_{x}$ or $m_y$ indicates the DW chirality. The spin valve functions qualitatively the same with or without DWs, however, the details of scattering potential differ.
\begin{figure*}
\centerline{\includegraphics[width=17.5cm]{Fig2.pdf}} \caption{
Calculated results from the lattice model (see Appendix A) with parameters $t=2.7$~eV, $\gamma=0.39$~eV \cite{Neto}, $M_0=27$~meV, $\Delta=13.5$~meV and $\lambda_{\rm R}=0.9$~meV. (a) MR ratio versus $E_{\rm F}$ for different DW types (no, collinear, Bloch and N\'{e}el)
for an armchair-edged strip with $W=40\sqrt3 a$ under $U=-M_0$ and $T=0$. The symbols I to IV label four MR states with clear boundaries. (b) Contour plot of MR in the $(E_{\rm F},U)$ plane for the armchair-edged strip with collinear DW at $T=0$. The dashed line corresponds to the cross-section $U/M_0 = -1$ used in (a). (c) Band gap $E_g$ in terminal L (green dashed line). For comparison, the spin-dependent band gap $E_g^s$ is shown under $\lambda_{\rm R}=0$ (red circle for spin up, black rectangle for spin down). Blue circle points denote four gap values $E_{g,i}$ ($i=1$ to 4) under $U/M_0=\pm1$. (d) Influence of temperature on MR versus $E_{\rm F}$ under $U=-M_0$ for the collinear-DW case in (a).}
\end{figure*}
Taking the collinear DW in Fig.~1(a) for example, we illustrate a typical band-to-band
tunneling to realize the high MR state for the P bias configuration due to spin mismatch
between L and R. By tuning the direction of vertical bias, the LAF spin valve can be
switched on or off. The giant MR effect is understood from a general picture of phase transition in Fig.~1(b), seen from model~(\ref{Hami}), that the LAF field drives BLG to be insulating by moving the states with opposite spins in the same layer and the states with the same spin in opposite layers oppositely. The vertical bias induces a full spin polarization by moving the states in the opposite layers oppositely. More crucial for the realization of the entirely electric control of the spin valve effect is that the opposite bias induces the opposite spin polarization. We characterize the MR effect
by a resistance ratio
\cite{LinYang,Grunberg}\label{MR}
\begin{equation}
\rho_{\rm MR}=\frac{R_{\rm AP}-R_{\rm P}}{R_{\rm AP}+R_{\rm P}},
\end{equation}
where $R_{\rm P(AP)}=1/G_{\rm P(AP)}$ is the resistance for the P
(AP) case. The conductance can be calculated by using the nonequilibrium
Green's function method \cite{Datta} as
\begin{equation}\label{conductance}
G=\frac{e^2}{h}\int_{-\infty}^{+\infty}dE{\cal
T}(E) \left(-\frac{\partial}{\partial E}f(E-E_{\rm F})\right),
\end{equation}
with the transmission given by ${\cal T}(E)={\rm Tr}({\cal
G}\Gamma_{\rm L}{\cal G}^\dag\Gamma_{\rm R})$, where $\cal G$ is the
Green's function of the system, Tr denotes the trace, $\Gamma_{\rm
L, R}=i(\Sigma_{\rm L, R}-\Sigma_{\rm L, R}^\dag)$ represents the
broadening of L and R, and $f(E-E_{\rm F})$ is the
Fermi-Dirac distribution function.
\section{RESULTS AND DISCUSSION}
We first solve the model by performing calculations in an armchair-edged sample with the width $W=40\sqrt3 a$. Two terminals L and R are
assumed to be semi-infinite. A relatively-short scattering region with the length $d=10a$
is fixed, and the main electrically-tunable parameters are the bias voltage $U$ and the Fermi energy $E_{\rm F}$ (see details in Appendix B) and Ref.~[\onlinecite{GavLaz}]). We keep $\vert U \vert$ the same for P and AP configurations and fix the parameters $t=2.7$~eV and $\gamma=0.39$~eV from bare GBL \cite{Neto} and $M_0=27$~meV, $\Delta=13.5$~meV and $\lambda_{\rm R}=0.9$~meV.
When $U=-M_0=-27$~meV is fixed ($E_z\simeq-0.5$~V/nm \cite{ZhaTan}), our results of MR ratio versus $E_{\rm F}$ in Fig.~2(a) show that nearly-perfect MR effect, {\it i.e.} $|\rho_{\rm R}|\simeq100\%$, appears for $|E_{\rm F}|/M_0\in(0.5,1.5)$, independent of whether the DW is present or not. The MR ratio of this spin valve effect changes the sign if a DW appears. This is because the $m_z$-induced spin polarization near $E_{\rm F}$ changes sign in terminal R (is unchanged in L). Nontrivially, we find the giant MR effect is not sensitive to whether the DW type is collinear, Bloch or N\'{e}el, and meanwhile, the spin valve effect is irrelevant to the magnetic chirality of DW, confirmed by changing the sign of $m_x$ or $m_y$ in calculations. To illustrate the MR effect in more detail, we show the contour plot of MR ratio in the $(E_{\rm F},U)$ plane for the collinear DW in Fig.~2(b). The result shows that there is a sharp transition between the absence of the MR effect for lower $E_{\rm F}$ and the nearly-perfect MR effect for higher $E_{\rm F}$ [see also $|E_{\rm F}|/M_0<0.5$ in Fig.~2(a)]. This parameter regime of no MR, $G_{\rm P(AP)}\equiv0$, is attributed to either of the following two factors: One is the absence of transport states induced by band gap in two terminals, and the other is the spin mismatch for both P and AP bias configurations.
To precisely clarify the result in Fig.~2(b), we plot the band gap $E_g$ (green dashed line) for terminal L as a function of $U$ in Fig.~2(c).
For contrast, we also plot the spin-dependent band gap $E_g^s$ (circle for spin up, rectangle for spin down) by ignoring $\lambda_{\rm R}$ in calculations. It is found that the total band gap changes very little if $\lambda_{\rm R}$ is added due to $\lambda_{\rm R}\ll M_0,\Delta$.
In the presence of the DW in Eq.~(\ref{m_z}), the band gap in terminal R
can be directly obtained by interchanging the tabs for opposite spins in Fig.~2(c) due to the opposite magnetic orientation in two terminals. Thus, it is sufficient to get all the information of band gap by analyzing either of two terminals. After sorting four values $E_g^{s=\pm}(\pm U)$ for terminal L in order from lowest to highest, labeled as $E_{g,i}$ ($i$=1 to 4), we find considering the tunnelling mechanism in Fig.~2(b) that MR vanishes (I, $\rho_{\rm MR}=0$) for $|E_{\rm F}|<E_{g,2}/2$, and the nearly-perfect MR (II, $|\rho_{\rm MR}|\geq95\%$) occurs under the conditions $|E_{\rm F}|\in(E_{g,2},E_{g,3})/2$ for $U<0$ and $|E_{\rm F}|\in(E_{g,2},E_{g,4})/2$ for $U>0$. Likewise, the normal giant MR (III, $95\%>|\rho_{\rm MR}|\geq 25\%$ \cite{Grunberg}) holds for $|E_{\rm F}|\in(E_{g,3},E_{g,4})/2$, and weak MR (IV, $0<|\rho_{\rm MR}|<25\%$) happens for $|E_{\rm F}|>E_{g,4}/2$.
Without a DW, the dependence of $E_g(U)$ is identical for the two terminals, the condition for MR to vanish in Fig.~2(a) is strictly given by $|E_{\rm F}|<E_g(U)/2$ [see the blue region in Fig.~2(c)]. Independent of whether the DW is present or not, the nearly-perfect MR can work for the overlapping band gap region of opposite spins [see the yellow region in Fig.~2(c)] by tuning the magnitude of the bias which can be different for L and R, in addition to the sign of the bias.
\begin{figure*}
\centerline{\includegraphics[width=13cm]{Fig3.pdf}} \caption{DFT results for
CGT/BLG/CGT. (a) Side view of the optimized unit cell.
(b) The vertical electric field $E_z$ tuned energy difference on average per atom between FM and LAF states. (c) Energy bands for $E_z=0$ (left), $\pm0.2$ V/nm (right).
(d) Spin-dependent band gap as a function of $E_z$.}
\end{figure*}
Figure~2(d) further considers the influence of temperature, showing MR at $T=60$~K and 120~K, for the collinear DW at $U=-M_0$. Unsurprisingly, MR ratio versus $E_{\rm F}$ becomes smooth due to the presence of the Fermi-Dirac distribution in Eq.~(\ref{conductance}), in comparison with that in Fig.~2(a). The energy broadening induced by temperature can cover the whole band gap region, and thus enables giant MR effect when $E_{\rm F}$ lies inside the band gap. Note that the pattern of the curves in Fig.~2(d) remains the same even if the $T$-modified $M_0$ is considered in a specific system. This means, the proposed spin-valve mechanism remains operational up to the Curie temperature of the FM layers.
In particular, the numerical result $E_g^s$ for the finite-size strip in Fig.~2(c) agrees with the analytical result for the 2D bulk case $E_g^s(U)\simeq2(\gamma^2/2+\alpha^2+\Delta^2-|\gamma^2-4\alpha\Delta|/2)^{1/2}
=2|U+sm_z+\Delta|$ derived from Eq.~(\ref{band}) for $\gamma^2>4\alpha\Delta$. This reveals a negligible edge effect. Further calculations indicate that the edge effect on band gap can be ignored when $W$ exceeds a critical value $20\sqrt3a$ ($\sim$5~nm), consistent with the experimental report~\cite{YinJiang} for bare BLG. Additionally, it is argued that the electron mean free path can be estimated by $\ell\simeq\lambda_{\rm F}=h\upsilon_0/\sqrt{|E|\gamma}$ \cite{SanPra} ($\lambda_{\rm F}$ is the Fermi wavelength, $\ell\simeq248a=35.2$~nm for $E=0.01t$). The spin diffusion length may be estimated by $\ell_s^{-1}\simeq2\ell[\lambda_{\rm R}/(\hbar\upsilon_{\rm F})]^2$ (the Fermi velocity $\upsilon_{\rm F}=2\upsilon_0\sqrt{|E|/\gamma}$) in the Dyakonov-Perel mechanism \cite{DyaPerel}. The ballistic spin transport, on which we deliberately focus here, should always dominate for $d\ll\ell,\ell_s$ (see Appendix C, $\ell_s$ is usually on the ${\rm \mu m}$ scale). The nanoscale $W$ and $d$ here should be experimentally available \cite{YinJiang,WahAug}.
For zigzag-edged systems, the LAF field or vertical bias can
induce edge states \cite{ZhaiBlanter}, which reduce the MR ratio. However,
edge disorder or defects can increase the MR ratio by hindering the edge
transport. For both the armchair or zigzag-edged systems with $W<20\sqrt 3a$, the spin
valve effect can still hold in spite of strong quantum confinement, which only
leads to some quantitative variations in MR.
\section{Proposal for materials realization}
We now propose, based on DFT calculations \cite{KreFur,KreFurth,KreHaf,PerBur,TangSan}, that BLG encapsulated by CGT monolayers, each of which is a FM semiconductor \cite{GongLi,GoZha}, is feasible to realize the antiferromagnetism in our model.
There was a previous LAF prediction in CrI$_3$/BLG/CrI$_3$ \cite{CarSor}, but the formation of mixed low-energy bands from both BLG and CrI$_3$ strongly limits its superiority. For the compounds of graphene and CGT, the influence of spin-orbit couplings on low-energy bands are much smaller than other parameters and can be disregarded, as proved previously \cite{ZolGmi,ZolGmi20}.
In Fig.~3, we show the DFT results for CGT/BLG/CGT with
an average equilibrium interlayer spacing $d=3.65~{\AA}$ between CGT monolayer
and its close-contacted graphene monolayer. The unit cell in Fig.~3(a) is constructed with a $5\times5$ supercell of 50 carbon atoms per graphene layer and a $\sqrt3\times\sqrt3$ supercell of 12 chromium atoms per CGT layer. See Appendix D for other computable details. To clarify the magnetism of the ground state, we show the energy difference on average per atom ($\Delta E$) between the FM and LAF states in Fig.~3(b), which strongly suggests that the system has a LAF ground state robust against small $E_z$ that we focus on. In contrast, bilayer CGT itself is FM \cite{GongLi}, which becomes LAF
here when the layers are spatially separated.
We show the DFT band at $E_z=0$ in the left panel of Fig.~3(c), where the inset enlarges the local band near $E_{\rm F}$ and is well fitted by $\Delta=8.9$~meV, $m_z=-7.2$~meV, $t=2.441$~eV, $\gamma=0.396$~eV in our model and an additional interlayer next-nearest neighboring hopping $\gamma'=0.267$~eV.
Here, we have $m_z<0$ and $\Delta>|m_z|$, different from the assumptions in Fig.~2.
As expected, we show the contrasting spin polarization of the bands for $E_z=\pm0.2$~V/nm, which is much smaller than 1$\sim$3~V/nm experimentally accessible in vdW systems of BLG \cite{ZhaTan} and bilayer CrI$_3$ \cite{JiangLi}. We plot the spin-dependent band gap $E_g^s$ versus $E_z$ in Fig.~3(d), where spin-up and spin-down band gaps vanish for $E_z>0.23$~V/nm and $E_z<-0.1$~V/nm, respectively. This is beyond our model because CGT has a nonnegligible contribution to $E_g^s$ as $E_z$ increases.
\section{Conclusion}
Our proposal of antiferromagnetic spin valve based on
vdW magnetic proximity effect paves the way for engineering spintronic devices with low energy consumption by making full use of magneto-electric coupling. The appearance of nearly-perfect MR and the robustness of antiferromagneism against required vertical bias have revealed the superiority of our proposed device. Other adjustable quantities, {\it e.g.} stacking order, interlayer sliding, rotation angle or layer number, may bring rich opportunities for developing 2D antiferromagnetic spintronics.
\section*{ACKNOWLEDGMENTS}
This work was supported by the NSFC with Grant Nos.~12074193, 61874057 and 11874059,
the QingLan Project of Jiangsu Province (2019), Key Research Program of Frontier Sciences, CAS, Grant No. ZDBS-LY-7021, Beijing National Laboratory for Condensed Matter Physics, Natural Science Foundation of Zhejiang Province (Grant No. LR19A040002). We are grateful to S. Jiang for insightful experimental discussion.
\input{vdW_LAF_Spin_Valve.bbl}
\end{document}
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Q: Display json format with Three.js I am trying to display an object that had been imported to blender with stl format and i exported to json format by this exporter. Below is the json file
{
"normals" :[....]
"metadata": {
"normals": 2673,
"vertices": 2972,
"faces": 5380,
"uvs": 0,
"type": "Geometry",
"version": 3,
"generator": "io_three"
},
"name": "ForenBox demoGeometry",
"vertices": [....]
"faces": [...]
"uvs": []
}
My js loader works fine beacause i tested it with correct json formats.
What is mine json format missing?
The object has been imported to blender by stl format!
Thanks!
|
{
"redpajama_set_name": "RedPajamaStackExchange"
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\section{Introduction}
In this paper we study the complexity of some natural optimization problems in segment arrangements. Let $S$ be a set of straight-line segments in $\ensuremath{\mathbb{R}}^2$, $\mathcal{A}(S)$ be the arrangement induced by $S$, and $a, b$ be two points not incident to any segment of $S$ and in different cells of $\mathcal{A}(S)$.
In the {\sc $2$-Cells-Connection} problem we want to compute a set of segments $S'\subseteq S$ of minimum cardinality with the property that $a$ and $b$ belong to the same cell of $\mathcal{A}(S\setminus S')$.
In other words, we want to compute
an $a$-$b$ path that \emph{crosses} the minimum number of segments of $S$ counted without multiplicities.
The \emph{cost} of a path is the total number of segments it crosses.
In the {\sc All-Cells-Connection} problem we want to compute a set $S'\subseteq S$ of minimum cardinality such that $\mathcal{A}(S\setminus S')$ consists of one cell only.
In the {\sc $2$-Cells-Separation} problem we want to compute a set $S'\subseteq S$ of minimum cardinality that \emph{separates} $a$ and $b$, i.e., $a$ and $b$ belong to different cells of $\mathcal{A}(S')$ -- equivalently -- any $a$-$b$ path intersects some segment of $S'$.
Apart from being interesting in their own right, the problems we consider here are also natural abstractions of problems concerning sensor networks. Each segment is surveyed (covered) by a sensor, and the task is to find the minimum number of sensors of a given network over some domain that must be switched on or off so that: an intruder can be detected when walking between two given points ({\sc $2$-Cells-Separation}), or can walk freely between two given points ({\sc $2$-Cells-Connection}) or can reach freely any point ({\sc All-Cells-Connection}). Because of these applications, it is worth considering a variant where the segments lie inside a given polygon $P$ with holes and have their endpoints on the boundary of $P$, and the $a$-$b$ path must also stay inside $P$. See Fig.~\ref{fig:polygon} for an example of this last scenario. We refer to these variants as the restricted {\sc $2$-Cells-Separation} or {\sc $2$-Cells-Connection} in a polygon.
\medskip
\noindent
{\bf Our results.} We provide an algorithm that solves {\sc $2$-Cells-Separation} in $\mathcal{O}(n^2+nk)$ time, where $k$ is the number of pairs of segments that intersect. The same algorithm, with an extra logarithmic factor, works for a generalization where the segments are weighted. The algorithm itself is simple, but its correctness is not at all obvious. We justify its correctness by considering an appropriate set of cycles in the intersection graph and showing that it satisfies the so-called \emph{3-path condition}~\cite{t-egsnc-90} (see also \cite[Chapter 4]{mt-gs-01}). The use of the 3-path condition for solving {\sc $2$-Cells-Separation} is surprising and makes the connection to topology clear.
We show that both {\sc $2$-Cells-Connection} and {\sc All-Cells-Connection} are NP-hard even when the segments are in general position. The first result is given by a careful reduction from {\sc Max-$2$-Sat}, which also implies APX-hardness. The second one follows from a straightforward reduction that uses a connection to the feedback vertex set problem in the intersection graph of the segments and holds even if there are no proper segment crossings. Also, when any three segments may intersect only at a common endpoint, {\sc $2$-Cells-Connection} is fixed-parameter tractable with respect to the number of proper segment crossings.
Finally, we consider the restricted problems in a polygon. The restricted {\sc $2$-Cells-Separation} in a polygon is easily reduced to the general weighted version and thus can be solved efficiently. The restricted {\sc $2$-Cells-Connection} in a polygon remains NP-hard but can be solved in near-linear time for any fixed number of holes. The approach for this latter result uses homotopies to group the segments into clusters with the property that any cluster is either contained or disjoint from the optimal solution.
\begin{figure}[t]
\centering
\includegraphics[width=0.47\textwidth]{polygon}
\caption{A polygon with holes and a minimum-cost $a$-$b$ path.}
\label{fig:polygon}
\end{figure}
\medskip
\noindent
{\bf Related work.} Our NP-hardness proof for {\sc $2$-Cells-Connection} has been carefully extended by Kirkpatrick and Tseng~\cite{tseng-thesis}, who showed that the {\sc $2$-Cells-Connection} remains NP-hard even for \emph{unit-length} segments. However, their result does not imply APX-hardness for unit-length segments.
The related problem of finding (from scratch) a set of segments with minimum total length that forms a barrier between two specified regions in a polygonal domain has been shown to be polynomial-time solvable by Kloder and Hutchinson~\cite{KH07}.
The problems we consider can of course be considered for other geometric objects, most notably unit disks. To this end, closely related work was done by Bereg and Kirkpatrick~\cite{BK09}, who studied the counterpart of {\sc $2$-Cells-Connection} in arrangements of unit disks and gave a $3$-approximation algorithm. While the complexity of {\sc $2$-Cells-Connection} for unit (or arbitrary) disks is still unknown, there exist polynomial-time algorithms for restricted belt-shaped and simple polygonal domains~\cite{KLA07}. Simultaneously and independently to our work, Gibson et al.~\cite{gkv-ipud-11} have considered the problem of separating $k$ points in an arrangements of disks and provided a polynomial-time $O(1)$-approximation algorithm. Their approach is based on building a solution by considering several instances {\sc $2$-Cells-Separation} on arrangements of disks, which they can solve approximately.
\section{Separating two cells}
In this section we provide a polynomial-time algorithm for {\sc $2$-Cells-Separation}.
We will actually solve a weighted version, where we have a weight function $w$ assigning
weight $w(s)\ge 0$ to each segment $s\in S$. For any subset $S'\subseteq S$ we define its weight
$w(S')$ as the sum of the weights over all segments $s\in S'$.
The task is to find a minimum weight subset $S'\subseteq S$ that separates two given points $a$ and $b$.
Our time bounds will be expressed as a function of $n$, the number of segments in $S$,
and $k$, the number of pairs of segments in $S$ that intersect.
We first describe the algorithm, and then justify its correctness.
We assume for simplicity of exposition that the segment $\segment{ab}$ is vertical
and does not contain any endpoint of $S$ or any vertex of $\ensuremath{\mathcal{A}}(S)$.
Let $\gamma$ be a polygonal path contained in $\bigcup S$, possibly with self-intersections.
Because of our assumption on general position, no vertex
of $\gamma$ is on the segment $\segment{ab}$.
We define $N(\gamma;a,b)$ as the number of oriented intersections
of $\gamma$ with $\segment{ab}$: a crossing where $\gamma$ goes from the left to the right of $\segment{ab}$
contributes $+1$ to $N(\gamma;a,b)$,
while a right-to-left crossing contributes $-1$ to $N(\gamma;a,b)$.
We have $N(\reverse (\gamma);a,b)= -N(\gamma;a,b)$.
In a graph, we will use the term \emph{cycle} for a closed walk without repeated vertices.
A polygonal path is \emph{simple} if it does not have self-intersections.
\subsection{The algorithm}
\label{sec:algorithm}
From $S$ we construct its intersection graph
$\ensuremath{\mathbb{G}}=(S,\{ ss'\mid s\cap s'\not = \emptyset \})$.
See Fig.~\ref{fig:intersectiongraph}(a)-(b).
Note that $\ensuremath{\mathbb{G}}$ has $k$ edges.
To each edge $ss'$ of $\ensuremath{\mathbb{G}}$ we attach a weight (abstract length) $w(s)+w(s')$.
Any distance in $\ensuremath{\mathbb{G}}$ will refer to these edge weights.
For any walk $\pi$ in $\ensuremath{\mathbb{G}}$ we use $\length (\pi)$ for its length, that is, the sum of the weights on its edges
counted with multiplicity, and $S(\pi)=V(\pi)$ for the set of segments along $\pi$.
For any spanning tree $T$ in $\ensuremath{\mathbb{G}}$ and any edge $e\in E(\ensuremath{\mathbb{G}})\setminus E(T)$,
let $\ensuremath{\tau}(T,e)$ denote the cycle obtained by concatenating the edge $e$ with
the path in $T$ connecting both endpoints of $e$.
(The actual orientation of $\ensuremath{\tau}(T,e)$ will not be relevant.)
\begin{figure}
\centering
\includegraphics[width=\textwidth]{intersectiongraph}
\caption{(a) A set of segments $S$.
(b) The corresponding intersection graph $\ensuremath{\mathbb{G}}$ with some of its edge-weights.
(c) The polygonal path $\gamma(\pi)$ for the walk $\pi=s_2 s_1 s_4 s_6 s_7 s_5 s_4$.
(d) The closed polygonal path $\gamma(\pi)$ for the closed walk $\pi=s_2 s_1 s_4 s_6 s_7 s_2$.}
\label{fig:intersectiongraph}
\end{figure}
Consider any walk $\pi=s_0 s_1\cdots s_t$ in $\ensuremath{\mathbb{G}}$.
This walk defines a polygonal path, denoted by $\gamma(\pi)$,
which has vertices $x_0,x_1,\dots ,x_{t-1}$,
where $x_j=s_j\cap s_{j+1}$ for $j=0,\dots,t-1$.
If $\pi$ is a closed walk with $s_0=s_t$, then we take $\gamma(\pi)$ to be
a closed polygonal path whose last edge is $x_{t-1}x_0$, which is contained in $s_0$.
See Fig.~\ref{fig:intersectiongraph}(c)-(d).
The polygonal path $\gamma(\pi)$ is contained in $\bigcup S(\pi)$.
Note that even if $\pi$ is a cycle
the closed polygonal path $\gamma(\pi)$ may have self-intersections.
For any segment $r\in S$, let $T_r$ be a shortest-path tree in $\ensuremath{\mathbb{G}}$ from $r$;
if there are several we fix one of them.
We will mainly use polygonal paths arising from cycles $\ensuremath{\tau}(T_r,e)$,
where $e\in E(\ensuremath{\mathbb{G}})\setminus E(T_r)$.
Thus we introduce the notation $\gamma(r,e)=\gamma (\ensuremath{\tau}(T_r,e))$.
(Again, the actual orientation of $\gamma(r,e)$ will not be relevant.)
The algorithm is the following. We
compute the set
\[
P=\{ (r,e)\in S\times E(\ensuremath{\mathbb{G}}) \mid \mbox{$e\in E(\ensuremath{\mathbb{G}})\setminus E(T_r)$ and
$N(\gamma(r,e));a,b)\not = 0$}\},
\]
choose
\[
(r^*,e^*)= \arg~ \min_{(r,e)\in P}~ \length(\ensuremath{\tau}(T_r,e)),
\]
and return $S(\ensuremath{\tau}(T_{r^*},e^*))$.
This finishes the description of the algorithm.
For analyzing it, it will be convenient to use the notation
$\tau^*=\ensuremath{\tau}(T_{r^*},e^*)$ and $\gamma^*$ for the polygonal path $\gamma(\tau^*)$.
The algorithm, as described above,
can be implemented in $\mathcal{O}(n^3k)$ time in a straightforward way.
We can speed up the procedure to obtain the following result.
\begin{lemma}\label{le:time}
The pair $(r^*,e^*)$ can be computed in $\mathcal{O}(nk+ n^2\log n)$ time.
\end{lemma}
\begin{proof}
The graph $\ensuremath{\mathbb{G}}$ can be constructed explicitly in $\mathcal{O}(n^2)$ time by checking
each pair of segments, whether they cross or not.
Recall that $\ensuremath{\mathbb{G}}$ has $k$ edges.
For any segment $r\in S$, let us define
\begin{align*}
E_r ~~&=~~ \{ e\in E(\ensuremath{\mathbb{G}})\setminus E(T_r)\mid (r,e)\in P\} \\
&=~~ \{ e\in E(\ensuremath{\mathbb{G}}) \mid \mbox{$e\in E(\ensuremath{\mathbb{G}})\setminus E(T_r)$ and
$N(\gamma(r,e));a,b)\not = 0$}\}.
\end{align*}
Note that
\[
P=\bigcup_{r\in S} \{ r\}\times E_r,
\]
and therefore
\[
\min_{(r,e)\in P}~ \length(\ensuremath{\tau}(T_r,e)) =
\min_{r\in S}~ \min_{e\in E_r}~ \length(\ensuremath{\tau}(T_r,e)).
\]
Thus, $(r^*,e^*)$ can be computed by finding, for each $r\in S$,
the value
\[
\min_{e\in E_r}\length(\ensuremath{\tau}(T_r,e)).
\]
We shall see that, for each fixed
$r\in S$, such value
can be computed in $\mathcal{O}(k+n\log n)$ time.
It then follows that $(r^*,e^*)$ can be found in
$|S|\times \mathcal{O}(k+n\log n)=\mathcal{O}(nk+ n^2\log n)$ time.
\begin{figure}
\centering
\includegraphics[width=\textwidth]{intersectiongraph2}
\caption{(a) Tree $T_{s_1}$ for the scenario of Fig.~\ref{fig:intersectiongraph} assuming unit weights in the segments.
In this case $C_{s_1}(s_8)=s_2$ and $C_{s_1}(s_6)=s_4$.
(b) The polygonal paths $\gamma(T_{s_1}[s_8])$ and $\gamma(T_{s_1}[s_6])$.
(c) The polygonal paths $\gamma(p_{s_1}(s_8)s_8s_6 p_{s_1}(s_6))= \gamma(s_7s_8s_6 s_4)$
and $\gamma(C_{s_1}(s_6)s_1 C_{s_1}(s_8))= \gamma(s_4s_1s_2)$ that are used to compute $N(\gamma(s_1,s_6s_8);a,b)$
in Lemma~\ref{le:time}.
}
\label{fig:intersectiongraph2}
\end{figure}
For the rest of the proof, let us fix a segment $r\in S$.
Computing $T_r$ takes $\mathcal{O}(|E(\ensuremath{\mathbb{G}})| + |V(\ensuremath{\mathbb{G}})|\log |V(\ensuremath{\mathbb{G}})|) = \mathcal{O}(k+n\log n)$ time.
For any segment $s\in S$, $s\not =r$, let $T_r[s]$ denote the path in $T_r$ from $r$
to $s$. We define $N_r(s)=N(\gamma(T_r[s]);a,b)$
and define $C_r(s)$ to be the child of $r$ in the path $T_r[s]$.
See~Fig.~\ref{fig:intersectiongraph2}(a)--(b).
The values $N_r(s)$, $s\in S$, can be computed in $\mathcal{O}(n)$
time using a BFS traversal of $T_r$:
if $p_r(s)$ is the parent of $s$ in $T_r$, we can compute $N_r(s)$
from $N_r(p_r(s))$ in $\mathcal{O}(1)$ time using
\[
N_r(s)~=~ N_r(p_r(s))+ N(\gamma(p_r(p_r(s))p_r(s)s) ;a,b).
\]
Similarly $C_r(s)$, $s\in S$, can be computed in $\mathcal{O}(n)$ time:
we assign $C_r(s')=s'$ for all children $s'$ of $r$ and use
that $C_r(s)=C_r(p_r(s))$ for any $s$ not adjacent to $r$.
For $ss'\in E(\ensuremath{\mathbb{G}})\setminus E(T_r)$ we have that $N(\gamma(r,ss'):a,b)$ is equal to
\begin{align*}
N_r(s) + N(\gamma( p_r(s)ss' p_r(s'));a,b) - N_r(r,s') + N(\gamma( C_r(s')r C_r(s));a,b).
\end{align*}
See~Fig.~\ref{fig:intersectiongraph2}(b)--(c).
(The negative sign comes from the reversal of $T_r[s]$.)
Therefore, each $N(\gamma(r,ss');a,b)$ can be computed in $\mathcal{O}(1)$ time from the values $N_r(s)$, $N_r(s')$, $C_r(s')$, $C_r(s)$.
It follows that $E_r$ can be constructed in $\mathcal{O}(|E(\ensuremath{\mathbb{G}})|)=\mathcal{O}(k)$ time.
The length of any cycle $\ensuremath{\tau}(T_r,e)$ can be computed in $\mathcal{O}(1)$ time per cycle in a similar fashion.
For each vertex $s$, we store at $s$ its distance $d_\ensuremath{\mathbb{G}}(r,s)$ from the root $r$.
We also construct a data structure for finding lowest common ancestor ($\lca$) of two vertices in constant
time. Such data structure can be constructed in $\mathcal{O}(n)$ time~\cite{lca1,lca2}. The length of a cycle can then be recovered using
\[
\length(\ensuremath{\tau} (T_r,ss'))~=~ d_\ensuremath{\mathbb{G}} (r,s)+ w(s)+w(s') + d_\ensuremath{\mathbb{G}}(r,s') - 2 d_\ensuremath{\mathbb{G}} (r,\lca (s,s')).
\]
Equipped with this, we can in $\mathcal{O}(k)$ time compute
\[
\min_{e\in E_r}~ \length(\ensuremath{\tau}(T_r,e)). \qedhere
\]
\end{proof}
The following special case will be also relevant later on.
\begin{lemma}\label{le:time2}
If the weights of the segments $S$ are $0$ or $1$,
then the pair $(r^*,e^*)$ can be computed in $\mathcal{O}(nk+ n^2)$ time.
\end{lemma}
\begin{proof}
In this case, a shortest path tree $T_r$ can be computed
in $\mathcal{O}(|E(\ensuremath{\mathbb{G}})| + |V(\ensuremath{\mathbb{G}})|) = \mathcal{O}(k+n)$ time
because the edge weights of $\ensuremath{\mathbb{G}}$ are $0$, $1$, or $2$.
Using the approach described in the proof of Lemma~\ref{le:time} we spend $\mathcal{O}(k+n)$ per root $r\in S$,
and thus spend $\mathcal{O}(nk+n^2)$ in total.
\end{proof}
\subsection{Correctness}
Consider the set of closed walks
\[
\Pi = \{ \pi\mid \mbox{$\pi$ a closed walk in $\ensuremath{\mathbb{G}}$ with $N(\gamma(\pi);a,b)\not =0$} \}.
\]
We have the following property, known as 3-path condition.
\begin{lemma}\label{le:3-path}
Let $\alpha_0,\alpha_1,\alpha_2$ be 3 walks in $\ensuremath{\mathbb{G}}$ from $s$ to $s'$. For $i=0,1,2$,
let $\pi_i$ be the closed walk obtained by concatenating $\alpha_{i-1}$ and the reverse of $\alpha_{i+1}$,
where indices are modulo 3.
If one of the walks $\pi_0,\pi_1,\pi_2$ is in $\Pi$, then at least two of them are in $\Pi$.
\end{lemma}
\begin{proof}
\begin{figure}
\centering
\includegraphics[width=\textwidth]{3pathcondition}
\caption{(a) Scenario in the proof of Lemma~\ref{le:3-path}.
(b) The polygonal path $\gamma(\pi_2)$.
(c) The polygonal paths $\beta_1$ and $\beta_3$. (The bottom of $\beta_1$ lies on $s'$. We draw it outside because of the common part with $\beta_3$.)}
\label{fig:3pathcondition}
\end{figure}
(This result is a consequence of the group structure for relative $\ensuremath{\mathbb{Z}}_2$-homology.
We provide an elementary proof that avoids using homology.)
For $i=0,1,2$, let $a_i$ be the starting vertex of the polygonal path $\gamma(\alpha_i)$
and let $b_i$ be the ending vertex.
The polygonal paths $\gamma(\alpha_0),\gamma(\alpha_1),\gamma(\alpha_2)$
start on $s$ and finish on $s'$.
However, they may have different endpoints.
See Fig.~\ref{fig:3pathcondition}.
To handle this, we choose a point $p$ on $s$ and a point $p'$ on $s'$,
and define $\beta_i$ to be the polygonal path obtained
by the concatenation of $pa_i$, $\gamma(\alpha_i)$, and $b_ip'$.
A simple but tedious calculation shows that, using indices modulo 3,
\begin{align*}
N(\gamma(\pi_i);a,b)~~=~~ N(\beta_{i-1};a,b)- N(\beta_{i+1};a,b).
\end{align*}
Indeed, since
\[
N(a_{i+1} a_{i-1};a,b)= N(p a_{i-1};a,b) + N(a_{i+1}p ;a,b)
\]
and
\[
N(b_{i-1} b_{i+1};a,b)= N(p' b_{i+1};a,b) + N(b_{i-1}p';a,b),
\]
we have
\begin{align*}
N(\gamma(\pi_i);a,b)~&=~~~~ N(\gamma(\alpha_{i-1}) ;a,b)
+ N(b_{i-1}b_{i+1};a,b) \\
& ~~~~ + N(\reverse (\gamma(\alpha_{i+1}));a,b)
+ N(a_{i+1} a_{i-1};a,b)\\
&=~~~~ N(\gamma(\alpha_{i-1}) ;a,b)
+ N(p' b_{i+1};a,b) + N(b_{i-1}p';a,b) \\
& ~~~~ - N(\gamma(\alpha_{i+1});a,b)
+ N(p a_{i-1};a,b) + N(a_{i+1}p ;a,b)\\
&=~~~~ N(p a_{i-1};a,b) + N(\gamma(\alpha_{i-1}) ;a,b) + N(b_{i-1}p';a,b) \\
& ~~~~ - N(p a_{i+1} ;a,b) - N(\gamma(\alpha_{i+1});a,b) - N( b_{i+1}p';a,b)\\
&=~~~ N(\beta_{i-1};a,b)- N(\beta_{i+1};a,b).
\end{align*}
It follows that, using indices modulo $3$,
\begin{align*}
\sum_{i=0}^2 N(\gamma(\pi_i);a,b)
~~=~~ \sum_{i=0}^2\left(N(\beta_{i-1};a,b) - N(\beta_{i+1};a,b) \right)
~~=~~ 0.
\end{align*}
Therefore, if $N(\gamma(\pi_i);a,b)\not= 0$ for some $i$, at least another cycle $\pi_j$, $j\not= i$,
must have $N(\gamma(\pi_j);a,b)\not= 0$.\qedhere
\end{proof}
When a family of closed walks satisfies the 3-path condition, there is a general method to find a shortest element in the family.
The method is based on considering fundamental-cycles defined by shortest-path trees, which is
precisely what our algorithm is doing specialized for the family $\Pi$.
We thus obtain:
\begin{lemma}\label{le:shortest}
The cycle $\tau^*$ is a shortest element of $\Pi$.
\end{lemma}
\begin{proof}
It is a consequence of the 3-path condition,
that a shortest cycle in
\[
\{ \ensuremath{\tau}(T_r,e)\mid r\in S, e\in E(\ensuremath{\mathbb{G}})\setminus E(T_r), \ensuremath{\tau}(T_r,e)\in \Pi \}
~~=~~
\{ \ensuremath{\tau}(T_r,e)\mid (r,e)\in P \}
\]
is a shortest cycle in $\Pi$. That is, the search for a shortest element in $\Pi$
can be restricted to cycles of the type $\ensuremath{\tau}(T_r,e)$.
See Thomassen~\cite{t-egsnc-90} or the book by Mohar and Thomassen~\cite[Chapter 4]{mt-gs-01}
for the so-called fundamental cycle method.
(The method is described for unweighted graphs but it also works for weighted graphs.
See, for example, Cabello et al.~\cite{ccl-fsntc-10} for the generalized case of weighted, directed graphs.)
\end{proof}
The next step in our argument is showing that $\gamma^*$ is simple (without self-intersections)
and separates $a$ and $b$.
We will use the following characterization of which simple, closed
polygonal paths separate $a$ and $b$.
\begin{lemma}\label{le:jordan}
For any simple, closed polygonal path $\gamma$ we have $|N(\gamma;a,b)|\le 1$.
Furthermore, $\gamma$ separates $a$ and $b$ if and only if $N(\gamma;a,b)= \pm 1$.
\end{lemma}
\begin{proof}
Since $\gamma$ is simple, it defines an interior and an exterior by the Jordan curve theorem.
The crossings between $\gamma$ and $\segment{ab}$, as we walk along $\segment{ab}$,
alternate between left-to-right and right-to-left crossings because $\segment{ab}$ has
pieces alternating in the interior and exterior of $\gamma$.
Therefore $|N(\gamma;a,b)|\le 1$.
Assume that $\gamma$ separates $a$ and $b$, so that one is in the interior of $\gamma$
and the other in the exterior.
Then the segment $\segment{ab}$ crosses $\gamma$ an odd number of times, and it must be
$|N(\gamma;a,b)|=1$. Conversely, if $|N(\gamma;a,b)|=1$, then the number of intersections between
$\gamma$ and $\segment{ab}$ is odd, which implies that one of the points $a$ and $b$ is in the interior
of $\gamma$ and the other in the exterior.
\end{proof}
We can now prove that $\gamma^*$ is simple using a standard uncrossing argument.
Indeed, a self-crossing of $\gamma^*$ would imply that we can find a strictly
shorter element in $\Pi$, which would contradict the property stated in Lemma~\ref{le:shortest}.
\begin{lemma}\label{le:feasible}
The polygonal path $\gamma^*$ is simple and separates $a$ and $b$.
\end{lemma}
\begin{proof}
Assume, for the sake of contradiction, that $\gamma^*$ is not simple.
It is then possible to show the existence of two cycles $\tau_1$ and $\tau_2$ in $\ensuremath{\mathbb{G}}$ such that
$\length(\tau_1)<\length(\tau^*)$,
$\length(\tau_2)<\length(\tau^*)$,
and $N(\gamma^*;a,b)= N(\gamma(\tau_1);a,b)+ N(\gamma(\tau_2);a,b)$,
as follows.
\begin{figure}
\centering
\includegraphics[width=0.8\textwidth]{partition}
\caption{The polygonal paths defined by the cycles $\tau_1$ and $\tau_2$ from the cycle $\tau$ in Lemma~\ref{le:feasible}.}
\label{fig:partition}
\end{figure}
Let $s_0 s_1s_2\dots s_t$, with $s_t=s_0$, be the cycle $\tau^*$.
Start walking along $\gamma^*$ from $s_0\cap s_1$, until we find the first self-intersection,
which is defined by segments $s_i$ and $s_j$, with $i< j$.
Note that $2\le j-i$ because $s_i$ and $s_{i+1}$ cannot define a self-intersection of $\gamma^*$.
Consider the cycles $\tau_1 = s_i s_{i+1}\dots s_j s_i$
and $\tau_2=s_0\dots s_i s_j \dots s_t$. See Fig.~\ref{fig:partition}.
Note that
\[
N(\gamma^*;a,b) ~~=~~ N(\gamma(\tau_1);a,b) + N(\gamma(\tau_2);a,b)
\]
because the polygonal paths $\gamma(\tau_1)$ and $\gamma(\tau_2)$ form a disjoint partition
of $\gamma^*$, with orientations preserved.
Moreover, because $j-i\ge 2$ and $\tau^*$ is a cycle,
we have $\length(\tau_1)< \length (\tau^*)$ and $\length(\tau_2)< \length (\tau^*)$.
This finishes the proof of existence of $\tau_1$ and $\tau_2$.
Because $\tau^*\in \Pi$ we have
\[
0~~ \not= ~~ N(\gamma^*;a,b)~~ =~~ N(\gamma(\tau_1);a,b) + N(\gamma(\tau_2);a,b) .
\]
Therefore, $N(\gamma(\tau');a,b)\not = 0$ for some $\tau'\in\{ \tau_1,\tau_2\}$.
Since $\length(\tau')<\length (\tau^*)$ and $N(\gamma(\tau');a,b)\\ \not = 0$,
then $\tau'\in \Pi$. This contradicts the property that $\tau^*$ is a shortest
cycle of $\Pi$ (Lemma~\ref{le:shortest}).
We conclude that $\gamma^*$ must be simple.
Since $\gamma^*$ is simple, $N(\gamma^*)\in \{ -1,0,+1\}$ by Lemma~\ref{le:jordan}.
Since $\tau^*\in \Pi$, then $N(\gamma^*)\not = 0$, which implies $N(\gamma^*)= \pm 1$.
It then follows from Lemma~\ref{le:jordan} that $\gamma^*$ separates $a$ and $b$.\qedhere
\end{proof}
We can now prove the main theorem.
\begin{theorem}\label{thm:separation}
The weighted version of {\sc 2-Cells-Separation} can be solved in $\mathcal{O}(nk+n^2\log n)$ time,
where $n$ is the number of input segments and $k$ is the number of pairs of segments that intersect.
\end{theorem}
\begin{proof}
We use the algorithm described in Section~\ref{sec:algorithm}.
The algorithm returns a feasible solution because of Lemma~\ref{le:feasible}:
the cycle $\gamma^*$ separates $a$ and $b$ and
is contained in $\bigcup S(\ensuremath{\tau}(T_{r^*},e^*))$, therefore,
the set $S(\ensuremath{\tau}(T_{r^*},e^*)$ returned by the algorithm separates $a$ and $b$.
To see the optimality of the weight of $S(\tau^*)$, consider an optimal solution $S_*\subseteq S$.
Assume that we run the algorithm on $S_*$.
The algorithm would compute a cycle $\tau_*$ in the intersection graph of the segments $S_*$
and return $S(\tau_*)\subseteq S_*$. By Lemma~\ref{le:feasible},
the polygonal path $\gamma(\tau_*)$ is simple and separates $a$ and $b$.
Lemma~\ref{le:jordan} implies that $N(\gamma(\tau_*);a,b)=\pm 1 \not =0$,
and therefore $\tau_*\in \Pi$ (here $\Pi$ refers to the original problem, rather than the subproblem
defined by input $S_*$).
For any cycle $\pi$ of $\ensuremath{\mathbb{G}}$ we have $\length(\pi)= 2 |S(\pi)|$ because of the choice of the edge-weights in $\ensuremath{\mathbb{G}}$.
Since $\tau^*$ is a shortest cycle in $\Pi$ by Lemma~\ref{le:shortest},
we have
\[
w(S(\tau^*))~~=~~\tfrac 12 \length (\tau^*)
~~\le~~ \tfrac 12 \length(\tau_*)
~~=~~ w(S(\tau_*))
~~\le~~ w(S_*).
\]
It follows that $S(\tau^*)$ is a feasible solution whose weight is not larger than $w(S_*)$,
and therefore it is optimal.
The running time follows from Lemma~\ref{le:time}.
\end{proof}
\begin{corollary}\label{co:separation}
The weighted version of {\sc $2$-Cells-Separation} in which the segments have weights $0$ or $1$
can be solved in $\mathcal{O}(n^2+nk)$ time,
where $n$ is the number of input segments and $k$ is the number of pairs of segments that intersect.
\end{corollary}
\begin{proof}
In the proof of the previous theorem we use Lemma~\ref{le:time2} instead of Lemma~\ref{le:time}.
\end{proof}
In the case where the segments of $S$ are unweighted, the points $a, b$ are inside a polygon $P$ with holes, and the $a$-$b$ path must be contained in the interior of $P$, the problem can be easily solved by
assigning weight 0 to the edges $E(P)$ of the polygon $P$
and weight $1$ to the segments in $S$.
We can then apply Corollary~\ref{co:separation} on $S\cup E(P)$, and obtain the following.
\begin{corollary}
The restricted {\sc $2$-Cells-Separation} problem in a polygon with holes can be solved in $\mathcal{O}(n^2+nk)$ time, where $n$ is the total size of the input
and $k$ is the number of pairs of segments in $S$ that intersect.
\end{corollary}
\section{Connecting two cells}
\label{2cells}
We show that {\sc $2$-Cells-Connection} is NP-hard and APX-hard by a reduction from {\sc Exact-Max-$2$-Sat}, a well studied NP-complete and APX-complete problem(c.f.~\cite{Hastad01}):
Given a propositional CNF formula $\Phi$ with $m$ clauses on $n$ variables and exactly two variables per clause, decide whether there exists a truth assignment that satisfies at least $k$ clauses, for a given $k\in\mathbb{N}$, $k\leq m$.
Let $x_1,\dots,x_n$ be the variables of $\Phi$, $\ell_i$ be the number of appearances of variable $x_i$ in $\Phi$, and $\ell= \sum_i \ell_i$; since each clause contains exactly 2 variables, $\ell=2m$. The maximum number of satisfiable clauses is denoted by ${\rm opt}(\Phi)$.
Using $\Phi$ we construct an instance consisting of a set of segments $S=S(\Phi)$ and two points $a=a(\Phi)$ and $b=b(\Phi)$ as follows.
Abusing the terminology slightly, the term \emph{segment} will refer to a set of identical single segments stacked on top of each other. The cardinality of the set is the \emph{weight} of the segment. Either all or none of the single segments in the set can be crossed by a path.
There are two different types of segments, $\tau_1$, and $\tau_{\infty}$, according to their weight. Segments of type $\tau_1$ have weight $1$ (light or single segments), while segments of type $\tau_{\infty}$ have weight $20m$ (heavy segments). The weight of heavy segments is chosen so that they are never crossed by an optimal $a$-$b$ path.
\begin{figure}
\centering
\includegraphics[width=.43\textwidth]{idea_construction}
\caption{Idea of the construction with curved segments.}
\label{idea}
\end{figure}
We first provide an informal, high-level description of the construction that uses \emph{curved} segments. Later on, each curved segment will by replaced by a collection of straight-line segments in an appropriate manner. See Fig.~\ref{idea}. We have a rectangle $R_\infty$ made of heavy segments, with point $a$ at a lower corner and $b$ at an upper corner. For each variable $x_i$ we add a small vertical segment of type $\tau_{\infty}$ in the lower half of $R_\infty$.
From the segment we place $\ell_i$ horizontal light segments, denoted by $R_i$, going to the right and $\ell_i$ horizontal light segments, denoted by $L_i$, going to the left until they reach the outside of $R_{\infty}$. Roughly speaking, (things are slightly more complicated)
an optimal $a$-$b$ path will have to choose for each $x_i$ whether it crosses all segments in $L_i$, encoding the assignment $x_i={\rm T}$, or all segments in $R_i$, encoding the assignment $x_i={\rm F}$.
Consider a clause like $x_2\vee x_{n}$, where both literals are positive. We prolong one of the segments of $L_2$ and one of the segments of $L_n$ with a curved segment so that they cross again inside $R_\infty$ (upper half) in such a way that an $a$-$b$ path inside $R_\infty$ must cross one of the prolongations, and one is enough; see Fig.~\ref{idea}, where one of the prolongations passes below $R_\infty$. A clause like $\bar x_n\vee x_2$ is represented using prolongations of one segment from $L_2$ and one segment of $R_n$. The other types of clauses are symmetric. For each clause we always prolong different segments; since $L_i$ and $R_i$ have $\ell_i$ segments, there is always some segment that can be prolonged. It will then be possible to argue that the optimal $a$-$b$ path has cost $\ell+ (m-{\rm opt}(\Phi))$.
We do not provide a careful argument of this here since we will need it later for a most complicated scenario. This finishes the informal description of the idea.
We now describe in detail the construction with straight-line segments.
First, we construct a polygon, called the \emph{tunnel}, with heavy boundary segments of type $\tau_{\infty}$; see Fig.~\ref{chain}(a).
The tunnel has a `zig-zag' shape and can be seen as having $8$ corridors, $C_1,\ldots ,C_8$. It starts with $C_1$, the \emph{main} corridor (at the center of the figure), which contains point $a$, then it turns left to $C_2$, then right, etc., gradually turning around to $C_7$ and then to the \emph{end} corridor $C_8$ (at the top). The latter contains point $b$. To facilitate the discussion, we place a point $b'$ in the tunnel where the transition from $C_7$ to the end corridor occurs.
The tunnel has a total weight of $21\cdot 20m =\mathcal{O}(m)$.
The rest of the construction will force any $a$-$b$ path of some particular cost (to be given shortly) to stay always in the interior of the tunnel.
\begin{figure}
\centering
\includegraphics[width=.88\textwidth]{variable_chain}
\caption{(a) Tunnel and variable chain. Each gray trapezoid represents a piece with $\ell_i$ parallel segments. (b) Part of a chain piece close to the tunnel.}
\label{chain}
\end{figure}
Each variable $x_i$ of $\Phi$ is represented by a collection of 16 pieces, which form a chain-like structure. Each \emph{piece} is a group of $\ell_i$ nearly-parallel single segments whose ends are either outside the tunnel or lie on `short' heavy segments of type $\tau_{\infty}$ in the interior of the tunnel, referred to as \emph{obstacles}. For each variable, there is one obstacle in each of the corridors $C_1$, $C_2$, $C_7$ and there are two obstacles in each of the corridors $C_3$, $C_4$, $C_5$, and $C_6$. See Fig.~\ref{chain}(a), where we represent each piece by a light gray trapezoid and each obstacle by a bold, short segment. Pieces always contain a part outside the tunnel. The exact description of the structure is cumbersome; we refer the reader to the figures. The obstacle in $C_2$ contains the extremes of four pieces: two pieces, called $P_i$, go to the obstacle in the main corridor, one goes to an obstacle in $C_3$, and the fourth piece, which we call $N_i^l$ goes outside the tunnel. Symmetrically, the obstacle in $C_7$ contains the extremes of four pieces: two pieces, called $N_i$, go to the main corridor, one goes to the corridor $C_6$, and one, which we call $P_i^r$ goes outside the tunnel. We add pieces connecting the obstacles in $C_3$ and $C_4$, the obstacles in $C_4$ and $C_5$, and the obstacles in $C_5$ and $C_6$. From the obstacle in $C_3$ that currently has one piece we add another piece, which we call $P_i^l$ and whose other extreme is outside the tunnel. From the obstacle in $C_6$ that currently has one piece we add another piece, which we call $N_i^r$, whose other extreme is outside the tunnel.
The obstacles and the pieces of all variables should satisfy some conditions: obstacles should be disjoint, pieces can touch only the obstacles at their extremes, and pieces may cross only outside the tunnel. See Fig.~\ref{complete}. Some of the single segments of $P_i^r$, $P_i^l$, $N_i^r$, $N_i^l$ will be prolonged and rotated slightly to encode the clauses. For this, we will need that the line supporting a segment from $P_i^r\cup N_i^r$ intersects inside the end corridor the line supporting a segment from $P_j^l\cup N_j^l$. This can be achieved by stretching the end corridor sufficiently and placing the obstacles of $C_2$ and $C_7$ close to the tunnel boundary; see Fig.~\ref{chain}(b).
\begin{figure}
\centering
\includegraphics[width=.86\textwidth]{general_construction_2}
\caption{Example of overall construction.}
\label{complete}
\end{figure}
For each clause of $\Phi$ we prolong two segments of $P_i^r\cup P_i^l \cup N_i^r\cup N_i^l$ as follows; see Fig.~\ref{complete} for an example of the overall construction, where prolongations are shown by dashed lines. Each segment corresponds to some literal $x_i$ or $\bar x_i$ in the clause: in the first case the segment comes from either $P_i^r$ or $P_i^l$, while in the second one it comes from either $N_i^r$ or $N_i^l$. For the construction, these choices for each clause can be made arbitrarily, provided that one segment intersects the tunnel from the left side and the other one from the right. These segments are prolonged until their intersection point inside the end corridor. For each clause, two different segments are prolonged. Since the pieces corresponding to variable $x_i$ have $\ell_i$ segments, there is always some segment available.
Segments corresponding to different clauses may intersect only outside the tunnel; this is ensured by rotating the segments slightly around the endpoint lying in the obstacle. In this way, the end corridor is obstructed by $m$ pairs of intersecting segments such that any path from the intermediate point $b'$ to point $b$ staying inside the tunnel must intersect at least one segment from each pair.
The following lemma establishes the correctness of the reduction.
\begin{lemma}\label{sec2_lem:bothdirections}
There is an $a$-$b$ path of cost at most $8\ell + k$, where $1\le k \le m$, if and only if
there is a truth assignment satisfying at least $(m-k)$ of the clauses.
\end{lemma}
\begin{proof}
We denote by $S_i$ the set of segments in the pieces corresponding to the variable $x_i$.
We denote by $S_i^{\rm T}$ the segments in the pieces of $P_i$, the piece connecting $C_7$ to $C_6$, the piece $P_i^r$, and so on in an alternating manner along the chain structure. Note that $S_i^{\rm T}$ contains $P_i$, $P_i^l$ and $P_i^r$.
We denote by $S_i^{\rm F}$ the segments $S_i\setminus S_i^{\rm T}$. Note that $S_i^{\rm F}$ contains $N_i$, $N_i^l$ and $N_i^r$.
See Fig.~\ref{chain-posneg}.
Each of the sets $S_i^{\rm T}$ and $S_i^{\rm F}$ contains $8\ell_i$ segments. Inside the tunnel there is an $a$-$b'$ path disjoint from $S_i^{\rm T}$ and there is another $a$-$b'$ path disjoint from $S_i^{\rm F}$. We also denote by $T_j$ the two segments used for clause $C_j$ of $\Phi$.
\begin{figure}
\centering
\hfill
\includegraphics[width=.49\textwidth]{variable_chain-positive}
\centering
\hfill
\includegraphics[width=.49\textwidth]{variable_chain-negative}
\hfill
\caption{Removal of $S_i^{\rm T}$ (left) and $S_i^{\rm F}$ (right).}
\label{chain-posneg}
\end{figure}
Consider a truth assignment $\{x_i=b_i\}$, where each $b_i\in \{{\rm T} ,{\rm F} \}$, satisfying at least $(m-k)$ clauses. We construct a subset of segments $S'$ where we include the set $S_i^{b_i}$, for each variable $x_i$, and a segment of $T_j$, for each clause $C_j$ that is not satisfied by the truth assignment. Since $|S_i^{b_i}|=8\ell_i$, the set $S'$ contains at most $8\ell+ k$ segments. The removal of $S'$ leaves the points $a$ and $b'$ in the same cell of the arrangement. Equivalently, there is an $a$-$b'$ path inside the tunnel that crosses only segments from $S'$. If a clause $C_j$ of $\Phi$ is satisfied by the truth assignment, then at least one of the segments in $T_j$ is included in $S_i^{b_i}\subset S'$. If a clause $C_j$ is not satisfied, then one of the segments $T_j$ is included in $S'$ by construction. Thus, for each clause $C_j$ we have $T_j\cap S'\not= \emptyset$. It follows that $b'$ and $b$ are in the same cell after the removal of $S'$.
Conversely, note first that any $a$-$b$ path with cost at most $8\ell +k\le 16 m+m = 17m$ cannot intersect the tunnel boundary or an obstacle because segments of type $\tau_{\infty}$ have weight $20m$. Let $S'$ be the set of segments crossed by the path. If $P_i\subset S'$, then we define $b_i={\rm T}$; otherwise, we define $b_i={\rm F}$.
Note that when $P_i\not\subset S'$, then $N_i\subset S'$ because the $a$-$b$ path is inside the tunnel. (However it may be $N_i\cup P_i\subset S'$, so the assignment of $b_i$ is not symmetric.) We next argue that the truth assignment $\{x_i=b_i\}$ satisfies at least $(m-k)$ clauses.
Consider the case when $P_i\subset S'$. Inspection shows that
\[
|S'\cap S_i| \ge 8\ell_i + |S'\cap (N_i^l \cup N_i^r)|.
\]
Indeed, after the removal of $P_i\cup N_i^l \cup N_i^r$ any path from $a$ to $b'$ must still cross at least $6$ pieces. Similarly, inspection shows that when $N_i\subset S'$ we have
\[
|S'\cap S_i| \ge 8\ell_i + |S'\cap (P_i^l \cup P_i^r)|.
\]
Let $A_i= N_i^l \cup N_i^r$ if $b_i={\rm T}$ and $A_i= P_i^l \cup P_i^r$ if $b_i={\rm F}$. The previous cases can be summarized as
\[
|S'\cap S_i| \ge 8\ell_i + |S'\cap A_i|.
\]
We further define
\[
Y= \bigcup_i (S'\cap A_i).
\]
For each clause $C_j$ we have $S'\cap T_j\not= \emptyset$ by construction, as otherwise $a$ and $b$ cannot be in the same cell of $S\setminus S'$. If $C_j$ is not satisfied by the truth assignment $\{x_i=b_i\}$, then it must be $(S'\cap T_j)\subset S'\cap A_k$ for some variable $x_k$ in $C_j$. This means that
$T_j\cap Y\not=\emptyset$. Since the sets $T_j$ are disjoint by construction, the number of unsatisfied clauses is bounded by $|Y|$.
Using that
\[
8\ell + k~ = ~ |S'| ~=~ \sum_{i=1}^n |S' \cap S_i| ~\ge~ \sum_{i=1}^n (8\ell_i + |S'\cap A_i|) ~=~ 8\ell + \sum_{i=1}^n |S'\cap A_i|,
\]
we obtain
\[
\sum_{i=1}^n |S'\cap A_i| \le k.
\]
Therefore, the total number of clauses with value ${\rm F}$ is bounded by
\[
|Y| ~=~ \sum_i |S'\cap A_i| ~\le~ k.\qedhere
\]
\end{proof}
The construction can be easily modified by replacing every heavy segment with a set of $20m$ distinct parallel single segments such that every single segment in $S$ that originally intersected the heavy segment now intersects all the segments in the new set and such that no three segments have a point in common. We have the following:
\begin{theorem}\label{NP-hard}
{\sc $2$-Cells-Connection} is NP-hard and APX-hard even when no three segments intersect at a point.
\end{theorem}
\begin{proof}
NP-hardness follows form Lemma~\ref{sec2_lem:bothdirections} and the fact that the reduction produces $\mathcal{O}(nm)$ segments, whose coordinates can be bounded by a polynomial in $(n+m)$. APX-hardness follows from the fact that the reduction is approximation-preserving, as we now show.
First, since there is always an assignment that satisfies at least $3m/4$ clauses, we have that $m\le (4/3) {\rm opt}(\Phi)$. Recall that an optimal $a$-$b$ path costs $8\ell+ (m-{\rm opt}(\Phi))$, where $\ell=2m$. A polynomial-time $c$-approximation algorithm ($c>1$) for the problem would give a path that costs at most
\begin{align*}
c(8\ell+ (m-{\rm opt}(\Phi))) ~~&=~~ c(17m+{\rm opt}(\Phi))\\
&=~~ 17m-c\,{\rm opt}(\Phi)+17(c-1)m\\
&\le~~ 17m-c\,{\rm opt}(\Phi) + 17(c-1)(4/3){\rm opt}(\Phi)\\
&=~~ 17m-{\rm opt}(\Phi)(68/3-(65/3)c)\\
&=~~ 16m+\Bigl[ m-{\rm opt}(\Phi)(68/3-65c/3) \Bigr]
\end{align*}
and, by Lemma~\ref{sec2_lem:bothdirections}, a truth assignment that satisfies at least
${\rm opt}(\Phi)(68/3-65c/3)$ clauses. However, {\sc Exact-Max-2-SAT} cannot be approximated
above $21/22$~\cite{Hastad01}, which implies that $c$ must be larger than $(68/65 - 63/(22\cdot 65))\approx 1.002097\dots$
(A slightly better inapproximability result can be obtained using the better bounds that rely on the unique games conjecture~\cite{kkmo-oir-07}.)
\end{proof}
We can reduce {\sc $2$-Cells-Connection} to the minimum color path problem (MCP):
Given a graph G with colored (or labeled) edges and two of its vertices, find a path between the vertices that uses the minimum possible number of colors.
We color the edges of the dual graph $G$ of $\mathcal{A}(S)$ as follows: two edges of $G$ get the same color if and only if their corresponding edges in $\mathcal{A}(S)$ lie on the same segment of $S$.
Then, finding an $a$-$b$ path of cost $k$ in $\mathcal{A}(S)$ amounts to finding a $k$-color path in $G$ between the two cells which $a$, $b$ lie in.
However, MCP is NP-hard~\cite{BLWZ05} and W[1]-hard~\cite{FGK10} (with respect to solution size) even for planar graphs, it has a polynomial-time $\mathcal{O}(\sqrt{n})$-approximation algorithm and is non-approximable within any polylogarithmic factor~\cite{HMS07}.
\section{Tractable cases for connecting two cells}
We now describe two special cases where {\sc $2$-Cells-Connection} is tractable. First, we consider the case where the input segments
have few crossings, in a sense that is specified below. Then, we return to the special case where we have a polygon and provide an algorithm
that takes polynomial time when the number of holes in the polygon is constant.
\subsection{Segments crossings.}
Without loss of generality, we assume that every segment in $S$ intersects at least two other segments and that both endpoints of a segment are intersection points. We say that two segments cross if and only if they intersect at a point that is interior to both segments (a segment crossing).
Consider the colored dual graph $G$ of $\mathcal{A}(S)$ as defined after Theorem~\ref{NP-hard}. A face of $G$ (except the outer one) corresponds to a point of intersection of some $r\geq 2$ segments and has $r$ colors and, depending on the type of intersection, from $r$ to $2r$ edges.
For example, for $r=2$ we can get two multiple edges, a triangle, or a quadrilateral, with two distinct colors. See Fig.~\ref{fig:colored_dual}(a)-(c), where the colors are given as labels.
\begin{figure}[t]
\centering
\includegraphics[width=\textwidth]{colored_dual}
\caption{Examples of intersections in $\mathcal{A}(S)$ and colored edges in $G$.}
\label{fig:colored_dual}
\end{figure}
When any three segments may intersect only at a common endpoint and no two segments cross, $G$ can only have multiple edges (possible all with the same color), bi-chromatic triangles, and arbitrary large faces where all edges have different colors; See Fig.~\ref{fig:colored_dual}(d) for an example. In this case, since two segments can intersect only at one point, each color induces a connected subgraph of $G$, in fact a tree (where all but one multiple edges with the same color can be deleted) for there can be no monochromatic cycle in $G$. Then, {\sc $2$-Cells-Connection} reduces to a simple shortest path computation between the cells containing $a$ and $b$ in the (uncolored) graph resulting from $G$ by completing each monochromatic tree into a clique.
By contrast, note that {All-Cells-Connection} is still NP-hard for this special case; see Section~\ref{allcells}.
Generalizing this, if we allow $k$ segment crossings,
we can easily reduce the problem to $2^{\mathcal{O}(k)}$ shortest path problems as follows. Let $C \subseteq S$ be the set of the (at most $2k$) segments participating in these crossings. For a fixed subset $C'$ of $C$, we first contract every edge of $G$ corresponding to a segment in $C'$, effectively putting all segments of $C'$ into the solution. Then, we delete every edge corresponding to a segment in $C\setminus C'$ that still participates in a crossing, i.e., we exclude all crossing segments of $C\setminus C'$ from the solution.
In the resulting (possibly disconnected) graph $G'$, each of the remaining colors induces again a monochromatic subtree, thus we can compute a shortest path as before and add $C'$ to the solution. Finally, we return a minimum size solution set over all $2^{\mathcal{O}(k)}$ possible subsets $C'$.
Thus, we have just proved the following:
\begin{theorem}
{\sc $2$-Cells-Connection} is fixed-parameter tractable with respect to the number of segment crossings if any three segments may intersect only at a common endpoint.
\end{theorem}
\subsection{Polygon with holes.}
Let $P$ be a polygon with $h$ holes and $S$ be a set of segments lying inside $P$ with their endpoints on its boundary; see Fig.~\ref{fig:polygon}. We use $n$ as a bound for the number of vertices of $P$ and segments in $S$.
We consider the restricted {\sc $2$-Cells-Connection} problem where the $a$-$b$ path may not cross the boundary of $P$. This version is also NP-hard by a simple reduction from the general one: place a large polygon enclosing all the segments and add a hole at the endpoint of each segment.
We assume for simplicity that $a$ and $b$ are in the interior of $P$.
A boundary component of $P$ may be the exterior boundary or the boundary of a hole. For each boundary component $\beta$ of $P$, let $C_\beta$ be the connected component of $\mathbb{R}^2\setminus P$ that has $\beta$ as boundary, and let $z_\beta$ be an arbitrary, fixed point in the interior of $C_\beta$. If $\beta$ is the exterior boundary, then $C_\beta$ is unbounded.
Let $\beta$ and $\beta'$ be two boundary components of $P$; it may be that $\beta=\beta'$.
Let $S_{\beta,\beta'}$ be the subset of segments from $S$ with one endpoint in $\beta$ and another endpoint in $\beta'$. We partition $S_{\beta,\beta'}$ into clusters, as follows. Consider the set $X_{\beta,\beta'}$ obtained from $P\setminus \{ a, b \}$ by adding $C_\beta$ and $C_{\beta'}$. Note that $a$ and $b$ are holes in $X_{\beta,\beta'}$. For each segment $s=\segment{pq}\in S_{\beta,\beta'}$, with $p\in \beta$ and $q\in\beta'$, we define the following
curve $\gamma_s$: follow a shortest path in $C_\beta$ from $z_\beta$ to $p$, then follow $\segment{pq}$, and then follow a shortest path
in $C_{\beta'}$ from $q$ to $z_{\beta'}$. See Fig.~\ref{fig:polygon2}.
We say that segments $s$ and $s'$ from $S_{\beta,\beta'}$ are \emph{$a$-$b$ equivalent} if $\gamma_s$ and $\gamma_{s'}$ are homotopic paths in $X_{\beta,\beta'}$.
Since being homotopic is an equivalence relation (reflexive, symmetric, transitive), being $a$-$b$ equivalent is also an equivalence relation in $S_{\beta,\beta'}$.
Therefore, we can make equivalence classes, which we call \emph{clusters}.
The following two results provide key properties of the clusters.
\begin{figure}[t]
\centering
\includegraphics[width=0.9\textwidth]{polygon2}
\caption{Some of the curves $\gamma_s$ arising from Fig.~\ref{fig:polygon}, after a small perturbation, and the resulting clusters. In the left case, $\beta$ and $\beta'$ are boundaries of holes, while in the right case $\beta'$ is the exterior boundary.}
\label{fig:polygon2}
\end{figure}
\begin{lemma}\label{le:clusters1}
$S_{\beta,\beta'}$ is partitioned into ${\mathcal O}(h^2)$ clusters. Such partition can be computed in ${\mathcal O}(h n \log n)$ time.
\end{lemma}
\begin{proof}
Let $\Gamma_{\beta,\beta'}$ be the set of curves $\gamma_s$ over all segments $s\in S_{\beta,\beta'}$.
Note that two curves $\gamma_s$ and $\gamma_{s'}$ of $\Gamma_{\beta,\beta'}$ may cross only once, and they do so along $s$ and $s'$.
With a small perturbation of the curves in $\Gamma_{\beta,\beta'}$ we may assume that $\gamma_s$ and $\gamma_{s'}$ are either disjoint or cross at $s\cap s'$.
(We do not actually use that $\gamma_s$ contains shortest paths inside $C_\beta$ and $C_{\beta'}$ besides for this property of non-crossing curves inside $C_\beta$ and $C_{\beta'}$.)
We now describe a simple criteria using crossing sequences to decide when two segments of $S_{\beta,\beta'}$ are $a$-$b$ equivalent. We take a set $\Sigma$ of non-crossing paths in $X_{\beta,\beta'}$ that have the following property: cutting $X_{\beta,\beta'}$ along the curves of $\sigma$ removes all holes. Such set $\Sigma$ has a tree-like structure and can be constructed as follows. For each boundary $\alpha$ of $P$, distinct from $\beta$ and $\beta'$, we add to $\Sigma$ the shortest path in $P$ between $a$ and $\alpha$. We add to $\Sigma$ the shortest path in $P$ between $a$ and $b$. Finally, if $\beta$ or $\beta'$ is the exterior boundary of $P$, we add to $\Sigma$ a shortest path from $a$ to a point that is very far in $P$ union the the outer face. In total, $\Sigma$ has $O(h)$ polygonal paths in $X_{\beta,\beta'}$. Note that the curves in $\Sigma$ are non-crossing and a small perturbation makes them disjoint, except at the common endpoint $a$. See Fig.~\ref{fig:polygon3}. Each curve $\sigma\in \Sigma$ is simple and has two sides. We arbitrarily choose one of them as the right side and the other as the left side. We use $\sigma_1,\dots,\sigma_k$ to denote the curves of $\Sigma$.
\begin{figure}[t]
\centering
\includegraphics[width=0.9\textwidth]{polygon3}
\caption{The curves $\Sigma$ in solid and $\Gamma_{\beta,\beta'}$ in dashed style for the example of Fig.~\ref{fig:polygon2}, after a small perturbation.}
\label{fig:polygon3}
\end{figure}
To each path $\gamma$ in $\Gamma_{\beta,\beta'}$ we associate a crossing sequence $w(\gamma)$ as follows. We start with the empty word and walk along $\gamma$. When $\gamma$ crosses an arc $\sigma_i\in \Sigma$ from left-to-right we append $\sigma_i^\rightarrow$ to the word, and when $\gamma$ crosses $\sigma_i$ from right-to-left we append $\sigma_i^\leftarrow$ to the word. From the crossing sequence $w(\gamma)$ we can obtain the \emph{reduced crossing sequence} $w^R(\gamma)$: we iteratively remove contiguous appearances of $\sigma_i^\rightarrow$ and $\sigma_i^\leftarrow$, for any $i$. For example, from the crossing sequence $\sigma_1^\rightarrow \sigma_2^\leftarrow \sigma_3^\rightarrow \sigma_3^\leftarrow \sigma_2^\rightarrow$ we obtain the reduced crossing sequence $\sigma_1^\rightarrow$. A consequence of using $\{ \sigma_i \}$ to construct the so-called universal cover is the following characterization:
the curves $\gamma_s$ and $\gamma_{s'}$ are homotopic in $X_{\beta,\beta'}$ if and only if the curves $\gamma_s$ and $\gamma_{s'}$ have the same reduced crossing sequence. See for example~\cite{clms-04}. We conclude that $s$ and $s'$ from $S_{\beta,\beta'}$ are $a$-$b$ equivalent if and only if
$w^R(\gamma_s)= w^R(\gamma_{s'})$.
The union of $\Sigma$ and $\Gamma_{\beta,\beta'}$ forms a family of pseudosegments: any two of them crosses at most once.
Indeed, by construction different curves can only cross in $P$, but inside $P$ all those curves are shortest paths, and thus can cross at most once.
Furthermore, the segments $\Sigma$ do not cross by construction and the curves of $\Gamma_{\beta,\beta'}$ have common endpoints.
Mount~\cite[Theorem 1.1]{mount-90} has shown that in such case the curves in $\Gamma_{\beta,\beta'}$
define at most ${\mathcal O}(|\Sigma|^2)={\mathcal O}(h^2)$ distinct crossing sequences. Therefore, there are at most ${\mathcal O}(h^2)$ homotopy classes defined
by the curves in $\Gamma_{\beta,\beta'}$, and $S_{\beta,\beta'}$ defines ${\mathcal O}(h^2)$ clusters.
The procedure we have described is constructive: we have to compute $O(h)$ shortest paths in $P$ to obtain the curves of $\Sigma$, and then, for each segment $s\in S_{\beta,\beta'}$, we have to compute the corresponding crossing sequence. Such crossing sequence is already reduced. Note that for computing the crossing sequence of $\gamma_s$ we never have to construct $\gamma_s$ itself because all crossings occur along $s$.
This can be done in ${\mathcal O}(h n\log n)$ time using algorithms for shortest paths in polygonal domains~\cite{hs-oaesp-99} and data structures for ray-shooting among the segments of $\Sigma$~\cite{ray-shooting}.
\end{proof}
\begin{lemma}\label{le:clusters2}
For each cluster, either all or none of the
segments in the cluster are crossed by a minimum-cost $a$-$b$ path.
\end{lemma}
\begin{proof}
\begin{figure}[t]
\centering
\includegraphics[width=0.9\textwidth]{polygon4}
\caption{Figure for the proof of Lemma~\ref{le:clusters2}. Left: case when $s$ and $s'$ are disjoint.
Right: case when $s$ and $s'$ intersect. In both cases, the darker gray region represents the topological disk defined by $\pi[x,y]$ and $\segment{xy}$.}
\label{fig:polygon4}
\end{figure}
Let $s$ and $s'$ be two $a$-$b$ equivalent segments from $S_{\beta,\beta'}$.
This implies that $\gamma_s$ and $\gamma_{s'}$ are homotopic in $X_{\beta,\beta'}$.
Therefore, the path $\gamma$ obtained by concatenating $\gamma_s$ and the reversal of $\gamma_{s'}$ is contractible in $X_{\beta,\beta'}$.
Let $\pi$ be a minimum-cost path between $a$ and $b$ that crosses $s$ but does not cross $s'$.
We will reach a contradiction.
We take $\pi$ that minimizes the total number of crossings with $s$.
We may assume that $\pi$ is simple and disjoint from $\beta,\beta'$.
We use $\pi[x,y]$ to denote the subpath of $\pi$ between points $x$ and $y$ of $\pi$.
We distinguish two cases:
\begin{itemize}
\item $s$ and $s'$ do not intersect. In this case, the curve $\gamma$ is simple and contractible
in $X_{\beta,\beta'}$. It follows that $\gamma$ bounds a topological disk $D_\gamma$ in $X_{\beta,\beta'}$.
By hypothesis, $\pi$ crosses the part of the boundary of $D_\gamma$ defined by $s$ but
not $s'$. Therefore, $\pi$ must cross at least twice along $s$. Let $x$ and $y$ be two consecutive crossings of $\pi$ and $s$
as we walk along $\pi$. See Fig.~\ref{fig:polygon4} left. Consider the path $\pi'$ that replaces $\pi[x,y]$ by the segment $\segment{xy}$.
Any segment $s''$ crossing $s$ along $\segment{xy}$ crosses also $\pi$ because $\pi[x,y]$ and $\segment{xy}$ define a disk.
Therefore $\pi'$ crosses no more segments than $\pi$ and crosses $s$ twice less than $\pi$.
Thus, we reach a contradiction. (If $\pi'$ is not simple we can take a simple path contained in $\pi'$.)
\item $s$ and $s'$ intersect. In this case, the curve $\gamma$
in $X_{\beta,\beta'}$ has precisely one crossing. Let $\gamma'$ and $\gamma''$ be the two simple loops
obtained by splitting $\gamma$ at its unique crossing. It must be that $\gamma'$ and $\gamma''$ are contractible,
as otherwise $\gamma$ would not be contractible. See Fig.~\ref{fig:polygon4} right.
Therefore, we obtain two topological disks $D_{\gamma'}$ and $D_{\gamma''}$, one bounded by $\gamma'$ and another by $\gamma''$.
The path $\pi$ must cross the boundary of $D_{\gamma'}$ or $D_{\gamma''}$, and the same argument than in the previous item
leads to a contradiction.\qedhere
\end{itemize}
\end{proof}
A minimum-cost $a$-$b$ path can now be found by testing all possible cluster subsets, that is, $2^{{\mathcal O}(h^4)}$ possibilities.
\begin{theorem}
The restricted {\sc $2$-Cells-Connection} problem in a polygon with $h$ holes and $n$ segments can be found in $2^{{\mathcal O}(h^4)}\polylog n$ time.
\end{theorem}
\begin{proof}
We classify the segments of $S$ into ${\mathcal O}(h^4)$ clusters using Lemma~\ref{le:clusters1}. This takes ${\mathcal O}(h^3 n\log n)$ time. Because
of Lemma~\ref{le:clusters2}, we know that either all or none of the segments in a cluster are crossed by an optimal $a$-$b$ path. Each subset of the clusters defines
a set of segments $S'$, and we can test whether $S'$ separates $a$ and $b$ in ${\mathcal O}(n\polylog n)$ time~\cite{single-face1,single-face2}.
\end{proof}
\section{Connecting all cells}\label{allcells}
We show that {\sc All-Cells-Connection} is NP-hard by a reduction from the NP-hard problem of feedback vertex set (FVS) in planar graphs (c.f.~\cite{V01}): Given a planar graph $G$, find a minimum-size set of vertices $X$ such that $G-X$ is acyclic.
First, we subdivide every edge of $G$ obtaining a planar bipartite graph $G'$. It is clear that $G'$ has a feedback vertex set of size $k$ if and only if $G$ has one. Next, we use the result by de Fraysseix et al.~\cite{dFMP91} (see also Hartman et al.~\cite{HNZ91}),
which states that every planar bipartite graph is the intersection graph of horizontal and vertical segments, where no two of them cross (intersect at a common interior point). Let $S$ be the set of segments whose intersection graph is $G'$; it can be constructed in polynomial time. Since $G'$ has no triangles, no three segments of $S$ intersect at a point. Then, observe that all cells in $\mathcal{A}(S)$ become connected by removing $k$ segments if and only if $G'$ has a feedback vertex set of size $k$. Therefore we have:
\begin{theorem}
{\sc All-Cells-Connection} in NP-hard even if no three segments intersect at a point and there are no segment crossings.
\end{theorem}
It is also easy to see that if no three segments intersect at a point a $k$-size solution to {\sc All-Cells-Connection}
corresponds to a $k$-size solution of FVS in the intersection graph of the input segments.
For general graphs, FVS is fixed-parameter tractable when parameterized with the size of the solution~\cite{CFLLV08}, and has a polynomial-time $2$-approximation algorithm~\cite{V01}. We thus obtain the following:
\begin{corollary}
When no three segments intersect at a point, {\sc All-Cells-Connection} is fixed-parameter tractable with respect to the size of the solution and has a polynomial-time $2$-approximation algorithm.
\end{corollary}
\section*{Acknowledgments:}
We would like to thank Primo{\v z} {\v S}kraba
for bringing to our attention some of the problems studied in this abstract.
\bibliographystyle{alpha}
|
{
"redpajama_set_name": "RedPajamaArXiv"
}
| 2,147
|
Q: OneSignal with Apache Cordova Write-up i have been struggling with OneSignal getting the plugin to work correctly each time i try and debug I get an error such as JDK 1.8 required , or android licence agreement not accepted.
How can I solve this?
A: I'm new to onesignal and I have come across a few common and uncommon problems with setting up Onesignal with Cordova and thought I would do a write up of my experience.
When starting you need to follow the setup guide provided by onesignal
Remember to generate keys for GCM api, Google project key, and finally onesignal project key. You will need these along the setup process.
Next: Create a Apache Cordova project -> and build Solution.
Next: Update CLI to V6.4 or higher (with this you will need to install JDK 1.8 and point to it once installed go to Tools -> Options -> Tools for Apache Cordova -> Environment variables override and point to the JDK 1.8 file)
Test your app on your device at this point it should run without problems.
Install the Onesignal plugin from GitHub OneSignal Cordova SDK. And just in case test again to see that the app still launches.
You might receive an error saying you need to accept a licence agreement for android SDK 24 for this go to Tools -> Android -> Android SDK Manager and install Android 7.0 (API 24) this will allow you to accept license agreement.
Next: follow the OneSignal Cordova Setup Guide
Once you have completed the setup go to the oneSignal dash while running the app on your device it should automatically be subscribed if you are using Android. Then send yourself a notification.
|
{
"redpajama_set_name": "RedPajamaStackExchange"
}
| 6,434
|
Q: Choosing different colors for this loading dots script Here is a 10 loading dots animation script.
As you can see we can choose a single color for all dots but, I want to choose different colors for each dot, I have tried to create unique dots divs and take the control of their colors in CSS but that way the animation crashes.
Any help would be greatly appreciated.
here is the original code:
TweenMax.staggerTo(".dots", 2, {
x: 220,
backgroundColor: 'white',
repeat: -1,
ease: SlowMo.ease.config(0.3, 0.2, false)
}, 0.25);
TweenMax.staggerFrom(".dots", 2, {
opacity: 0,
scale: 0.7,
repeat: -1,
ease: SlowMo.ease.config(0.3, 0.2, true)
}, 0.25);
html {
width: 260px;
height: 32px;
overflow: hidden;
}
body {
background-color: transparent;
text-align: center;
padding: 50px;
}
.container {
background-color: transparent;
position: absolute;
left: 50%;
top: 50%;
transform: translate(-50%, -50%);
}
.dots {
position: absolute;
width: 1em;
height: 1em;
border-radius: 50%;
background-color: #d0c9d8;
opacity: 1;
left: -120px;
}
.dotss {
position: absolute;
width: 1em;
height: 1em;
border-radius: 50%;
background-color: #fcba03;
opacity: 1;
left: -120px;
}
.link {
position: absolute;
bottom: 20px;
right: 30px;
color: white;
font-size: 40px;
text-decoration: none;
}
<div class="container">
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
</div>
<script src="https://cdnjs.cloudflare.com/ajax/libs/gsap/2.1.3/TweenMax.min.js"></script>
<script src="script.js"></script>
<link rel="stylesheet" type="text/css" href="style.css">
A: You can use the "nth-child() Selector" .
The nth-child pseudo-class is specified with a single argument, which
represents the pattern for matching elements.
For your case;
TweenMax.staggerTo(".dots", 2, {
x: 220,
backgroundColor: 'white',
repeat: -1,
ease: SlowMo.ease.config(0.3, 0.2, false)
}, 0.25);
TweenMax.staggerFrom(".dots", 2, {
opacity: 0,
scale: 0.7,
repeat: -1,
ease: SlowMo.ease.config(0.3, 0.2, true)
}, 0.25);
html {
width: 260px;
height: 32px;
overflow: hidden;
}
body {
background-color: transparent;
text-align: center;
padding: 50px;
}
.container {
background-color: transparent;
position: absolute;
left: 50%;
top: 50%;
transform: translate(-50%, -50%);
}
.dots {
position: absolute;
width: 1em;
height: 1em;
border-radius: 50%;
background-color: #d0c9d8;
opacity: 1;
left: -120px;
}
.dots:nth-child(2n) {
background-color: red;
}
.dots:nth-child(3n) {
background-color: blue;
}
.dotss {
position: absolute;
width: 1em;
height: 1em;
border-radius: 50%;
background-color: #fcba03;
opacity: 1;
left: -120px;
}
.link {
position: absolute;
bottom: 20px;
right: 30px;
color: white;
font-size: 40px;
text-decoration: none;
}
<div class="container">
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
<div class="dots"></div>
</div>
<script src="https://cdnjs.cloudflare.com/ajax/libs/gsap/2.1.3/TweenMax.min.js"></script>
<script src="script.js"></script>
<link rel="stylesheet" type="text/css" href="style.css">
|
{
"redpajama_set_name": "RedPajamaStackExchange"
}
| 8,536
|
Georg Gartner (9 de julio de 1966 en Viena, Austria) es un cartógrafo y geógrafo austríaco.
Vida y carrera profesional
Gartner estudió geografía en la Universidad de Viena y comenzó a especializarse en cartografía desde el principio. En 1991 completó sus estudios y cambió a la Universidad Técnica de Viena, donde comenzó a escribir su tesis. Con algunas interrupciones por estancias en el extranjero en Nebraska (EE.UU.), Melbourne (Australia) y Cantón (China), entre otros, se convirtió en asistente universitario en el Instituto de Cartografía y Tecnología de la Reproducción de la Universidad Técnica de Viena. En marzo de 2007 fue nombrado catedrático universitario del Instituto de Geoinformación y Cartografía.
Gartner es el editor de la serie de libros "Lecture Notes in Geoinformation and Cartography" (Springer) y editor en jefe del "Journal on Location-based Services" (Taylor & Francis). Fundó la serie de conferencias "Location-based Services". Fue cofundador del Máster Internacional en Cartografía ("Cartography M.Sc.") junto con la Universidad Técnica de Múnich, la Universidad Técnica de Dresde y la Universidad de Twente.
De 2011 a 2015, Georg Gartner fue presidente de la Asociación Cartográfica Internacional (ACI). Durante este tiempo, entre otras cosas, la ACI fue admitida en el Consejo Internacional de Ciencias (ICSU, International Council of Science Union) como miembro de pleno derecho, su propio medio de publicación de la ACI, el International Journal of Cartography (IJC), y el Año Internacional de los Mapas 2015-2016 ("International Map Year 2015-2016") apoyado por las Naciones Unidas.
Enfoque de su investigación
En su trabajo de investigación, Gartner se ocupa principalmente de los servicios basados en localización (LBS por sus siglas en inglés), que se pueden clasificar en el campo de la telecartografía o cartografía multimedia.
El segundo foco de investigación de Gartner y sus colaboradores es considerar cómo hacer que el propio entorno se comunique, lo que se denomina 'entorno inteligente' e incluye, por ejemplo, 'pantallas públicas', pantallas instaladas frente a edificios. En informática, esto se conoce como computación ubicua . En cartografía, este concepto se utiliza para comunicar información espacial.
Publicaciones
Referencias
Hombres
Nacidos en 1966
Austríacos
Profesores de la Universidad Técnica de Viena
Geógrafos del siglo XXI
Cartógrafos del siglo XXI
|
{
"redpajama_set_name": "RedPajamaWikipedia"
}
| 7,090
|
Chocolates back then meant one and one thing. Cadbury's. There was Mr. Pop's, Break, Double Decker – all three of which have long disappeared into the distance. Then came Eclairs, Fruit & Nut Bars, Nutties – in their signature Red branding, and of-course, the festive-special metal tin boxes.
Then there was Amul. Big on taste, but low on promotional might – they couldn't quite compete with the marketing muscle of Cadbury's and later on, Nestle. But they sure did make some yummy chocolate. Sadly, most of the chocolates mentioned above, disappeared over the years. Low sales, changing taste and increased competition meant that some of my childhood favourites were discontinued. The ones that survived changed and lost their signature flavour, forever.
Then, one day, I spotted these giant, oversized Amul Dark Chocolate bars at a store. Biting into the slab, i felt like Anton Ego going back to his childhood in that memorable scene from the movie – Ratatouille. The dark chocolate was full of flavour – flavour that I'd long missed in the chocolates available here. I soon discovered that they came in this single origin packs, where each one of them, held their own on the flavour & taste scale.
Amul Chocolates were once again on the purchase list and I sought them whenever the occasion called for one. My latest discovery led me to the Amul Stall at Churchgate Station, where i got this – the Dark Passion.
A 'Kit-Kat' alternative to say – this one's again a lot more tastier than the Nestle version. Not too sweet, not to dry, it's got just the right amount of snap and flavour, to really melt in the mouth.
You think I'm kidding? I'm not. Go. Buy one for yourself and enjoy some sinful pleasures.
|
{
"redpajama_set_name": "RedPajamaC4"
}
| 1,056
|
by Mike Reid, reprinted with permission.
Two days ago, another man—a recent and very superficial convert to Islam—rammed and killed another Canadian soldier with his car.
I do not know the real political affiliations of either of the attackers, but clearly among their personal intentions we can list the intent to commit suicide. You don't expect to survive if you kill a soldier and then, by rushing into the seat of government, practically guarantee hero status for whoever shoots you.
In other words, both of these men sought a way out of this mortal coil, and decided that the best and most dignified way to get out would be to go on a killing spree against strangers in uniform until someone else killed them in return.
Whether or not these attackers were in any way authentically associated with ISIS or Muslim terrorism, politicians, newspeople, and the common man at his dinner table will associate them with it. The steady spread of plausible, self-confirming rumour about the evil of Islam will grow and accelerate.
Like all acts of Muslim-branded terrorism hitherto committed on North American soil, although the casualties are numerically minuscule, the symbols are profound.
Because the terrorists attacked soldiers and politicians, the very embodiments of Canadians' self-identification with the state, Canadians at large will feel that the terrorists have attacked them personally. Canadians will feel frightened and vengeful. We will find it psychologically very easy to dehumanize Muslims and Middle-Easterners. And we will feel more ready to kill them.
This is only one of the early incidents in a long and self-perpetuating cycle of vengeance, quasi-racist and quasi-religious xenophobia on both sides, and death, death, death for everyone.
Canadian politicians will shake their fists at the shadowy foe, and promise to send more brave Canadian soldiers, and especially more nice, clean bombs to go and kill the enemy.
Even if the enemy (ISIS? Militant Islam? Middle-Eastern sexist violence?) could be well-defined, when those bombs fall, they will kill and maim noncombatants, innocents, and children too.
Then the vengeful victims and their kin and those who feel some symbolic self-identification with them will cry out for more murdering.
And some new mentally unstable Canadian will adopt their cries for vengeance as a way to escape his own muddled life in a sudden act of purifying suicidal glory. And that mentally unstable fellow (almost always, it is a man) will kill some more Canadians, numerically insignificant but symbolically profound.
Killing some more of those Canadians will let you escape your life with glory, they say to their audience on Twitter and YouTube. Killing some more of those Arabs will bring peace to us and them, we whisper to our children as we tuck them into bed.
Either way, if collectivist violence continues to be accepted as a wise and honorable pursuit, the blood will flow until the sands of time blot it over with some new catastrophe.
There is, as far as I know, only one hope for peace. And that is the humble recognition that other humans are people too — not nations we can rescue or demons we can destroy. Just people.
Both of this week's amateur terrorists are dead. We can exact no further vengeance upon them for the fear they have struck in our hearts by attacking our symbols. If the politicians want (and they probably do), they can issue orders to have some more Canadian people kill some more Syrian or Iraqi or Turkish people. But that cannot resurrect our dead or erase our fears or refute their religions or save their nations.
It can just kill more people.
This year, weary and engaged more in fatherhood than in politics, I did not march to protest Canada's involvement in the latest vaguely defined bombing of Middle-Easterners.
And this morning, I have no tears or laughter. I have only sadness and sympathy for all those people who will wave the flag of a nation or a religion and kill other people, and die themselves.
This entry was posted in End of the Empire and tagged blowback, Canada. Bookmark the permalink.
|
{
"redpajama_set_name": "RedPajamaC4"
}
| 3,944
|
import React, {Component} from 'react';
import { Field, reduxForm } from 'redux-form';
import { connect } from 'react-redux';
import PlusIcon from 'react-icons/lib/fa/plus';
import { addFilter, removeKeywordFromFilter } from '../actions';
class AddCategoryFilter extends Component {
handleFormSubmit(formProps) {
if ('categoryName' in formProps && formProps['categoryName'].trim().length !== 0) {
this.props.addFilter(formProps.categoryName);
this.props.reset(); //reset form and clear fields
}
return
}
handleRemoveKeywordFromFilter(text) {
this.props.removeKeywordFromFilter(text);
}
renderFormControl() {
return (
<div>
<ul>
{this.props.filters.map((item) => {
return (
<div key={item}>
<li onClick={() => { this.handleRemoveKeywordFromFilter(item); }}>
{item}
</li>
</div>
);
})
}
</ul>
</div>
);
}
render() {
const { handleSubmit } = this.props;
return (
<div>
<div>
<p>过滤掉不想看的新闻类别, 单击取消过滤</p>
<form onSubmit={handleSubmit(this.handleFormSubmit.bind(this))}>
<Field name="categoryName" label="categoryName" component="input" type="text" className="form-control" />
<button type="submit"><PlusIcon /></button>
</form>
</div>
{this.renderFormControl()}
</div>
);
}
}
AddCategoryFilter = reduxForm({
form: 'AddCategoryForm', // a unique name for this form
})(AddCategoryFilter);
const mapStateToProps = (state) => {
const { filters } = state.newsListFilter;
return {
filters,
};
};
export default connect(mapStateToProps,
{ addFilter, removeKeywordFromFilter })(AddCategoryFilter);
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 8,536
|
package com.iticket.service;
import java.util.List;
import com.iticket.model.api.ClientMember;
import com.iticket.model.stadium.Stadium;
import com.iticket.model.ticket.Voucher;
import com.iticket.vo.TicketVo;
public interface TicketService {
/**
* 预售卖出
* @param member
* @param voucherId
* @param ticketType
* @param payMethod
* @param showPrice
* @param saleType
* @param disType
* @return
* @throws IException
*/
List<TicketVo> reserveSell(ClientMember member, Long voucherId,
String ticketType, String payMethod, String showPrice, Integer saleType, String disType)
throws IException;
/**
* 预售取消
* @param member
* @param voucherId
* @throws IException
*/
void reserveCancel(ClientMember member, Long voucherId) throws IException;
/**
* 重复打印
* @param member
* @param voucherId
* @return
* @throws IException
*/
List<TicketVo> repeatPrint(Stadium stadium, ClientMember member, Long voucherId, String reprintPass)throws IException;
/**
* 退款
* @param member
* @param voucherId
* @throws IException
*/
void refund(Stadium stadium, ClientMember member, Long voucherId, String refundPass) throws IException;
/**
* 根据凭证获取座位名称
* @param voucher
* @return
*/
String getSeatLabelsByVoucherId(Voucher voucher);
}
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 4,115
|
VIZf/x specializes in the creation and visualization of computer based environments.
VIZf/x was founded by and currently lead by Robert Staehle. Mr. Staehle is a registered architect licensed in several western states. Mr. Staehle obtained a B. Architecture from the University of Arizona '80. Between 1980 and 1992 Mr Staehle was employed as an architect in the traditional sense of the profession. He specialized in residential design and construction. Many designs completed by Mr. Staehle received notoriety and professional awards. Several designs are still published today in the Sunset Book series of publications.
In addition to his architectural credentials Mr. Staehle is a former Planning Commissioner having served in that capacity for four years, a member of the ASAI (American Society of Architectural Illustrators), and an Apple Consultant.
VIZf/x has provided services for institutional, corporate, and individual clients. We intentionally split our work load between construction product manufacturers and providing integrated services to the design process prior to project approvals. This split in services has helps us to work closely with the integration of CAD tools into the architectural design process. We have worked hand in hand with many of the popular CAD software developers. The knowledge gained while creating leading edge software tools enhances our ability to create computer based simulations which capitalize on the strength of the tools available. Pushing the envelope to create rapid, cost effective representations of proposed construction projects, in turn, helps us to guide developers in understanding the challenges faced by the automated processes of the design professional.
One of the best ways to contact us is via iChat. You can chat Mr. Staehle by clicking this link archiboy@mac.com. Or Click this link to ADD Mr. Staehle your buddy list.
VIZf/x is a founding member of The Rendertek Group. The group is a collaboration of outstanding independent consultants offering a wide range of computer based services to its' clients. By our alliance with The Rendertek Group VIZf/x is able to offer a complete range of services to our clients. From professional quality print campaigns to Architectural/Civil/Mechanical Engineering visualization including production of speaker support, legal litigation documents and entertainment content.
|
{
"redpajama_set_name": "RedPajamaC4"
}
| 4,537
|
I love this word. And I encourage you to love it, too, whether it's your word of the year or not.
When you are working in your business, you want to work to a place of sufficiency. You want to do enough to create the result you desire. Just ENOUGH. Not too much. Working beyond the point of satisfaction is inefficient, and inefficiency is where you stop getting a return on your dollars, time and mental space. They are all being wasted when you go past the point of ENOUGH.
And yet, I see women entrepreneurs overworking all the time. There is this constant striving that is absolutely draining and comes from a place of lack. If you believe you are enough, than at a certain point you must believe that your work is enough and there is no point in continuing to strive. But there lies the rub: you don't believe you are enough and this is why your efforts are endless, because they can never BE enough either.
So let's talk about the illusion of perfection.
There's an illusion of perfection that will absolutely prevent you from growing your business—it won't immediately destroy it, but perfection will fester in the background and make you a stagnant prisoner. Maintaining the illusion you've created is a full time job in itself. Juggling all of the "perfect" will prevent you from growing.
On paper, things look great, but you're working too hard, trying to do everything perfectly, and completely unable to try new things. You spend a lot of time in a defensive state, hiding your cards and avoiding getting real.
Perfectionism can look like obsessively working on the same thing rather than putting it out into the world, or it can look like a Vegas smoke and mirrors act, where you're constantly shining a light and focusing your energy on what's working… and completely ignoring where it's all falling apart. It can also look like fear of taking the next step in favor of resting on your current successes—because you're terrified the next step will break everything you've built.
Perfectionism usually comes with a fair amount of anxiety because you are trying to look like enough instead of just being enough.
So how can you let go of the perfectionism?
It takes practice. Practice sending that newsletter before the eighth round of editing. Practice not having 120 slides for your next presentation; hey, 60 slides is probably enough, right? Try sharing an imperfect picture of yourself on social media and leave out the perfect caption that perfectly explains the deep lessons learned. Don't wrap it all up in a neat bow; just be vulnerable … and enough.
The more imperfect I am in my business and my life, the more I get done and the more success I create. The more imperfect action my clients take, even in the face of fear, the more dollars and opportunities come their way.
It's not all perfect, but it's good ENOUGH—and good enough is sufficient.
To be clear, I don't have this all down perfectly (ha!), I still find myself overworking and aiming for perfection. Hence why ENOUGH is my word of the year.
PS: Ready to take some massive imperfect action in your business? We can help. Book a free Scale Session with my team to figure out your next imperfect steps to reaching your next level of success. Let's get something going.
|
{
"redpajama_set_name": "RedPajamaC4"
}
| 8,199
|
{"url":"https:\/\/www.physicsforums.com\/threads\/could-any-one-suggest-one-book-on-probability-theory-to-me.320195\/","text":"# Could any one suggest one book on probability theory to me?\n\n1. Jun 16, 2009\n\n### wdlang\n\ni am working on theoretical physics\n\ni hope i can get a book on probability theory\n\ni hope this book is a bit advanced to have detailed discussion of characteristic functions and their applications.\n\ni do not like the statistics applications. I hope that part is as small as possible.\n\nThanks!\n\n2. Jun 16, 2009","date":"2018-02-21 08:06:56","metadata":"{\"extraction_info\": {\"found_math\": false, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 0, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 0, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.8049908876419067, \"perplexity\": 1033.6679639388217}, \"config\": {\"markdown_headings\": true, \"markdown_code\": false, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2018-09\/segments\/1518891813571.24\/warc\/CC-MAIN-20180221063956-20180221083956-00285.warc.gz\"}"}
| null | null |
#region Copyright
#endregion
using System;
namespace Kodestruct.Common.Section.Interfaces
{
public interface ISectionIRolled: ISectionI
{
double k { get; }
double T { get; }
}
}
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 1,618
|
' Licensed to the .NET Foundation under one or more agreements.
' The .NET Foundation licenses this file to you under the MIT license.
' See the LICENSE file in the project root for more information.
Imports Microsoft.CodeAnalysis.Editor.UnitTests.SignatureHelp
Imports Microsoft.CodeAnalysis.VisualBasic.SignatureHelp
Namespace Microsoft.CodeAnalysis.Editor.VisualBasic.UnitTests.SignatureHelp
Public Class FunctionAggregationSignatureHelpProviderTests
Inherits AbstractVisualBasicSignatureHelpProviderTests
Friend Overrides Function GetSignatureHelpProviderType() As Type
Return GetType(FunctionAggregationSignatureHelpProvider)
End Function
<WorkItem(529682, "http://vstfdevdiv:8080/DevDiv2/DevDiv/_workitems/edit/529682")>
<Fact(), Trait(Traits.Feature, Traits.Features.SignatureHelp)>
Public Async Function TestAggregateFunctionInAggregateClause() As Task
Dim markup = <Text><![CDATA[
Imports System.Linq
Module Program
Sub Main(args As String())
Dim lambda = Aggregate i In New Integer() {1} Into Count($$
End Sub
End Module
]]></Text>.Value
Dim expectedOrderedItems = New List(Of SignatureHelpTestItem)()
expectedOrderedItems.Add(New SignatureHelpTestItem($"<{VBFeaturesResources.Extension}> Count() As Integer", String.Empty, Nothing, currentParameterIndex:=0))
expectedOrderedItems.Add(New SignatureHelpTestItem($"<{VBFeaturesResources.Extension}> Count({VBWorkspaceResources.expression} As Boolean) As Integer", String.Empty, Nothing, currentParameterIndex:=0))
Await TestAsync(markup, expectedOrderedItems)
End Function
#Region "EditorBrowsable tests"
<WorkItem(7336, "DevDiv_Projects/Roslyn")>
<Fact, Trait(Traits.Feature, Traits.Features.Completion)>
Public Async Function TestEditorBrowsable_FunctionAggregation_BrowsableStateAlways() As Task
Dim markup = <Text><![CDATA[
Imports System.Collections.Generic
Imports System.Runtime.CompilerServices
Imports System.Linq
Class C
Sub M()
Dim numbers As IEnumerable(Of Integer)
Dim query = Aggregate num In numbers Into GetRandomNumber($$
End Sub
End Class
]]></Text>.Value
Dim referencedCode = <Text><![CDATA[
Imports System.Runtime.CompilerServices
Imports System.Collections.Generic
Public Module Goo
<System.ComponentModel.EditorBrowsableAttribute(System.ComponentModel.EditorBrowsableState.Always)>
<Extension()>
Public Function GetRandomNumber(ByVal values As IEnumerable(Of Integer)) As Integer
Return 4
End Function
End Module
]]></Text>.Value
Dim expectedOrderedItems = New List(Of SignatureHelpTestItem)()
expectedOrderedItems.Add(New SignatureHelpTestItem($"<{VBFeaturesResources.Extension}> GetRandomNumber() As Integer", String.Empty, Nothing, currentParameterIndex:=0))
Await TestSignatureHelpInEditorBrowsableContextsAsync(markup:=markup,
referencedCode:=referencedCode,
expectedOrderedItemsMetadataReference:=expectedOrderedItems,
expectedOrderedItemsSameSolution:=expectedOrderedItems,
sourceLanguage:=LanguageNames.VisualBasic,
referencedLanguage:=LanguageNames.VisualBasic)
End Function
<WorkItem(7336, "DevDiv_Projects/Roslyn")>
<Fact, Trait(Traits.Feature, Traits.Features.Completion)>
Public Async Function TestEditorBrowsable_FunctionAggregation_BrowsableStateNever() As Task
Dim markup = <Text><![CDATA[
Imports System.Collections.Generic
Imports System.Runtime.CompilerServices
Imports System.Linq
Class C
Sub M()
Dim numbers As IEnumerable(Of Integer)
Dim query = Aggregate num In numbers Into GetRandomNumber($$
End Sub
End Class
]]></Text>.Value
Dim referencedCode = <Text><![CDATA[
Imports System.Runtime.CompilerServices
Imports System.Collections.Generic
Public Module Goo
<System.ComponentModel.EditorBrowsableAttribute(System.ComponentModel.EditorBrowsableState.Never)>
<Extension()>
Public Function GetRandomNumber(ByVal values As IEnumerable(Of Integer)) As Integer
Return 4
End Function
End Module
]]></Text>.Value
Dim expectedOrderedItems = New List(Of SignatureHelpTestItem)()
expectedOrderedItems.Add(New SignatureHelpTestItem($"<{VBFeaturesResources.Extension}> GetRandomNumber() As Integer", String.Empty, Nothing, currentParameterIndex:=0))
Await TestSignatureHelpInEditorBrowsableContextsAsync(markup:=markup,
referencedCode:=referencedCode,
expectedOrderedItemsMetadataReference:=New List(Of SignatureHelpTestItem)(),
expectedOrderedItemsSameSolution:=expectedOrderedItems,
sourceLanguage:=LanguageNames.VisualBasic,
referencedLanguage:=LanguageNames.VisualBasic)
End Function
<WorkItem(7336, "DevDiv_Projects/Roslyn")>
<Fact, Trait(Traits.Feature, Traits.Features.Completion)>
Public Async Function TestEditorBrowsable_FunctionAggregation_BrowsableStateAdvanced() As Task
Dim markup = <Text><![CDATA[
Imports System.Collections.Generic
Imports System.Runtime.CompilerServices
Imports System.Linq
Class C
Sub M()
Dim numbers As IEnumerable(Of Integer)
Dim query = Aggregate num In numbers Into GetRandomNumber($$
End Sub
End Class
]]></Text>.Value
Dim referencedCode = <Text><![CDATA[
Imports System.Runtime.CompilerServices
Imports System.Collections.Generic
Public Module Goo
<System.ComponentModel.EditorBrowsableAttribute(System.ComponentModel.EditorBrowsableState.Advanced)>
<Extension()>
Public Function GetRandomNumber(ByVal values As IEnumerable(Of Integer)) As Integer
Return 4
End Function
End Module
]]></Text>.Value
Dim expectedOrderedItems = New List(Of SignatureHelpTestItem)()
expectedOrderedItems.Add(New SignatureHelpTestItem($"<{VBFeaturesResources.Extension}> GetRandomNumber() As Integer", String.Empty, Nothing, currentParameterIndex:=0))
Await TestSignatureHelpInEditorBrowsableContextsAsync(markup:=markup,
referencedCode:=referencedCode,
expectedOrderedItemsMetadataReference:=New List(Of SignatureHelpTestItem),
expectedOrderedItemsSameSolution:=expectedOrderedItems,
sourceLanguage:=LanguageNames.VisualBasic,
referencedLanguage:=LanguageNames.VisualBasic,
hideAdvancedMembers:=True)
Await TestSignatureHelpInEditorBrowsableContextsAsync(markup:=markup,
referencedCode:=referencedCode,
expectedOrderedItemsMetadataReference:=expectedOrderedItems,
expectedOrderedItemsSameSolution:=expectedOrderedItems,
sourceLanguage:=LanguageNames.VisualBasic,
referencedLanguage:=LanguageNames.VisualBasic,
hideAdvancedMembers:=False)
End Function
<WorkItem(7336, "DevDiv_Projects/Roslyn")>
<Fact, Trait(Traits.Feature, Traits.Features.Completion)>
Public Async Function TestEditorBrowsable_FunctionAggregation_BrowsableStateMixed() As Task
Dim markup = <Text><![CDATA[
Imports System.Collections.Generic
Imports System.Runtime.CompilerServices
Imports System.Linq
Class C
Sub M()
Dim numbers As IEnumerable(Of Integer)
Dim query = Aggregate num In numbers Into [|GetRandomNumber($$
|]End Sub
End Class
]]></Text>.Value
Dim referencedCode = <Text><![CDATA[
Imports System.Runtime.CompilerServices
Imports System.Collections.Generic
Imports System
Public Module Goo
<System.ComponentModel.EditorBrowsableAttribute(System.ComponentModel.EditorBrowsableState.Always)>
<Extension()>
Public Function GetRandomNumber(ByVal values As IEnumerable(Of Integer)) As Integer
Return 4
End Function
<System.ComponentModel.EditorBrowsableAttribute(System.ComponentModel.EditorBrowsableState.Never)>
<Extension()>
Public Function GetRandomNumber(Of T)(ByVal values As IEnumerable(Of T), ByVal selector As Func(Of T, Double)) As Integer
Return 4
End Function
End Module
]]></Text>.Value
Dim expectedOrderedItemsMetadataOnly = New List(Of SignatureHelpTestItem)()
expectedOrderedItemsMetadataOnly.Add(New SignatureHelpTestItem($"<{VBFeaturesResources.Extension}> GetRandomNumber() As Integer", String.Empty, Nothing, currentParameterIndex:=0))
Dim expectedOrderedItemsSameSolution = New List(Of SignatureHelpTestItem)()
expectedOrderedItemsSameSolution.Add(New SignatureHelpTestItem($"<{VBFeaturesResources.Extension}> GetRandomNumber() As Integer", String.Empty, Nothing, currentParameterIndex:=0))
expectedOrderedItemsSameSolution.Add(New SignatureHelpTestItem($"<{VBFeaturesResources.Extension}> GetRandomNumber({VBWorkspaceResources.expression} As Double) As Integer", String.Empty, String.Empty, currentParameterIndex:=0))
Await TestSignatureHelpInEditorBrowsableContextsAsync(markup:=markup,
referencedCode:=referencedCode,
expectedOrderedItemsMetadataReference:=expectedOrderedItemsMetadataOnly,
expectedOrderedItemsSameSolution:=expectedOrderedItemsSameSolution,
sourceLanguage:=LanguageNames.VisualBasic,
referencedLanguage:=LanguageNames.VisualBasic)
End Function
#End Region
End Class
End Namespace
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 7,618
|
// ExpectedAndFound.java, created on Apr 19, 2012
package eu.fabiostrozzi.ceppo.terms;
/**
* Expected and found details.
*
* @author fabio
*/
public class ExpectedAndFound implements Term {
private Object[] found;
private Object[] expected;
/**
* @return the found
*/
public Object[] getFound() {
return found;
}
/**
* @param found
* the found to set
*/
public void setFound(Object[] foundWhat) {
this.found = foundWhat;
}
/**
* @return the expected
*/
public Object[] getExpected() {
return expected;
}
/**
* @param expected
* the expected to set
*/
public void setExpected(Object[] expectedWhat) {
this.expected = expectedWhat;
}
}
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 290
|
{"url":"https:\/\/encyclopediaofmath.org\/wiki\/Variational_calculus,_numerical_methods_of","text":"# Variational calculus, numerical methods of\n\nThe branch of numerical mathematics in which one deals with the determination of extremal values of functionals.\n\nNumerical methods of variational calculus are usually subdivided into two major classes: indirect and direct methods. Indirect methods are based on the use of necessary optimality conditions (cf. Variational calculus; Euler equation; Weierstrass conditions (for a variational extremum); Transversality condition; Pontryagin maximum principle), with the aid of which the original variational problem is reduced to a boundary value problem. Thus, the computational advantages and drawbacks of indirect methods are fully determined by the properties of the respective boundary value problem. In direct methods, the extremum of the functional is found directly. The optimization methods thus employed are a development of the idea of mathematical programming.\n\nThe subdivision of the numerical methods of variational calculus into direct and indirect methods is largely arbitrary. In some algorithms both approaches are utilized. Moreover, some methods cannot be classified as belonging to either class. Thus, methods based on sufficient optimality conditions form a separate group.\n\nThe first numerical methods of the calculus of variations appeared in the work of L. Euler. However, their most rapid development took place in the mid-20th century as a result of the spread of computers and the possibility, afforded by these techniques, to solve complicated problems in technology. The development of numerical methods in variational calculus mostly concerned the theory of optimal control, which, from the aspect of practical applications, is the most important (cf. Optimal control, mathematical theory of).\n\n## Indirect methods.\n\nWith the advent of the Pontryagin maximum principle (1956), variational problems can very often be reduced to boundary value problems.\n\nConsider the following problem in optimal control: Find a trajectory $x( t)$ and a control $u( t)$ for which the functional\n\n$$\\tag{1 } J = \\int\\limits _ {t _ {0} } ^ { T } f ^ { 0 } ( t, x, u) dt$$\n\nassumes its minimal value, given the differential constraints\n\n$$\\tag{2 } \\dot{x} = f ( t, x, u),$$\n\nthe boundary conditions\n\n$$\\tag{3 } x ( t _ {0} ) = x _ {0} ,$$\n\n$$\\tag{4 } x ( T) = x _ {T} ,$$\n\nand control restrictions\n\n$$\\tag{5 } u \\in U,$$\n\nwhere $x = ( x ^ {1} \\dots x ^ {n} )$, $u = ( u ^ {1} \\dots u ^ {m} )$ are the vectors of the coordinates of the phase and the controls, $f = ( f ^ { 1 } \\dots f ^ { n } )$, $U$ is a closed set in an $m$- dimensional space, and $t$( the time) is an independent variable.\n\nAccording to Pontryagin's maximum principle, the optimal control $u( t)$ must, for any $t$, produce the absolute maximum of the Hamilton function\n\n$$\\tag{6 } H ( {\\widetilde{u} } ) = \\max _ {u \\in U } H ( u) =$$\n\n$$= \\ \\max _ {u \\in U } \\left [ \\sum _ {i = 1 } ^ { n } \\psi _ {i} f ^ { i } ( t, x, u) - f ^ { 0 } ( t, x, u) \\right ] ,$$\n\nwhere $\\psi = ( \\psi _ {1} \\dots \\psi _ {n} )$ is defined by the system of equations\n\n$$\\tag{7 } \\dot \\psi _ {i} = - \\frac{\\partial H }{\\partial x ^ {i} } ,\\ \\ i = 1 \\dots n.$$\n\nThe control $u( t, x, \\psi )$ is found from condition (6) and is substituted in (2) and (7). As a result one obtains a closed boundary value problem for a system of $2n$ differential equations (2) and (7) with $2n$ boundary conditions (3) and (4).\n\nThe scheme of numerical solution which is most frequently employed for this boundary value problem involves the use of Newton's method of fractional steps [3]. One introduces the discrepancy vector\n\n$$\\tag{8 } \\phi _ {i} = x ^ {i} ( T) - x _ {T} ^ {i} ,\\ \\ i = 1 \\dots n,$$\n\nwhere the value of $x ^ {i} ( T)$ is obtained by solving the Cauchy problem for the system (2), (7) with initial conditions (3) and $\\psi _ {j} ( t _ {0} ) = \\psi _ {j0}$, $j = 1 \\dots n$. The discrepancies (8) are considered as functions of the unknowns $\\psi _ {10} \\dots \\psi _ {n0}$, defined by the system of equations\n\n$$\\tag{9 } \\phi _ {i} ( \\psi _ {10} \\dots \\psi _ {n0} ) = 0,\\ \\ i = 1 \\dots n.$$\n\nThe system (9) is solved by Newton's method (cf. Newton method); the partial derivatives involved,\n\n$$\\frac{\\partial \\phi _ {i} }{\\partial \\psi _ {j0} } ,\\ \\ i, j = 1 \\dots n,$$\n\nare numerically determined by the formula:\n\n$$\\frac{\\partial \\phi _ {i} }{\\partial \\psi _ {j0} } \\approx$$\n\n$$\\approx \\ \\frac{\\phi _ {i} ( \\psi _ {10} \\dots \\psi _ {j0} + \\Delta \\psi _ {j0} \\dots \\psi _ {n0} ) - \\phi _ {i} ( \\psi _ {10} \\dots \\psi _ {n0} ) }{\\Delta \\psi _ {j0} } ,$$\n\nwhere the values of $\\phi _ {i} ( \\psi _ {10} \\dots \\psi _ {j0} + \\Delta \\psi _ {j0} \\dots \\psi _ {n0} )$ are obtained by solving Cauchy's problem for the system (2), (7), with initial conditions (3) and conditions\n\n$$\\psi _ {l} ( t _ {0} ) = \\psi _ {l _ {0} } ,\\ \\ \\psi _ {j} ( t _ {0} ) = \\psi _ {j0} + \\Delta \\psi _ {j0} ,\\ \\ l \\neq j,$$\n\nwhere $\\Delta \\psi _ {j0}$ is a small increment of $\\psi _ {j0}$.\n\nThe partial derivatives may be determined by a more accurate, but more laborious, method [4], involving the integration of a system of $2n$ equations in variations for the system (2), (7).\n\nThe difficulties in Newton's method consist, in the first place, in the selection of a successful initial approximation for $\\psi _ {j0}$ and, secondly, in the unstability of the Cauchy problem, which is very strongly manifested on large intervals $[ t _ {0} , t _ {1} ]$. There is no generally valid procedure to overcome the first difficulty. A number of methods (cf. Cauchy problem, numerical methods for ordinary differential equations) are available to deal with the unstability of the Cauchy problem.\n\nIf the boundary conditions and the functional are given in a more general form than in (3), (4) and (1) (e.g. in the Bolza problem with mobile ends, in a variational problem with free (mobile) ends), the transversality condition is added to supplement the optimality conditions (6) and (7). After elimination of the arbitrary constants which appear in these conditions, a closed boundary value problem and a corresponding system of equations of the type (9) are obtained.\n\nThe solution of the system (9) may also be obtained by any other method used in solving non-linear systems.\n\nSpecific methods for solving boundary value problems of a special type have been developed. Thus, linear boundary value problems are solved by the method of transfer of the boundary conditions (shooting method). This method is also employed as a constituent element for the iterative solution of non-linear boundary value problems [1].\n\nProblems in variational calculus are very often solved with the aid of electronic computers, since in this way indirect methods can be effectively and relatively simply realized. However, such techniques are not applicable in all cases; for certain important classes of problems in variational calculus \u2014 e.g. problems involving phase restrictions \u2014 it is difficult to write down the necessary conditions and these result in boundary value problems with a complicated structure. Moreover, the boundary conditions need not ensure that the solution found in fact supplies an extremum of the functional. This must be verified by introducing sufficient optimality conditions. All this restricts the scope of application of indirect methods.\n\n## Direct methods.\n\nThe first direct method was proposed by Euler for the solution of the simplest problem in variational calculus. It is known as Euler's method of polygonal lines (or as Euler's finite-difference method). In this method the functional\n\n$$\\tag{10 } J ( x) = \\ \\int\\limits _ { t _ {0} } ^ { {t _ 1 } } F ( t, x, \\dot{x} ) dt$$\n\nis considered on continuous polygonal lines $x( t)$ which satisfy given boundary conditions\n\n$$\\tag{11 } x ( t _ {0} ) = x _ {0} ,\\ \\ x ( t _ {1} ) = x _ {1} ,$$\n\nand which consist of $N$ rectilinear segments with end points at given abscissas. Thus, the functional becomes a function of the ordinates of the vertices of the polygonal line, while the initial problem is reduced to the task of minimizing a function of several variables (cf. Euler method).\n\nSince the labour involved in such calculations is considerable, direct methods were neglected for a long time in traditional studies in variational calculus. They were taken up again early in the 20th century. New methods for the reduction to the problem of finding an extremum of a function of several variables were proposed. Of these, the most important one is the Ritz method, according to which the solution of minimizing (10) subject to condition (11) is to be found in the class of functions of the form\n\n$$x = \\phi _ {0} ( t) + \\sum _ {i = 1 } ^ { N } a _ {i} \\phi _ {i} ( t),$$\n\nwhere ${\\phi _ {i} } ( t)$, $i = 0 \\dots N$, are elements of a complete infinite system of linearly independent functions which satisfy the boundary conditions\n\n$$\\phi _ {0} ( t _ {0} ) = x _ {0} ,\\ \\ \\phi _ {0} ( t _ {1} ) = x _ {1} ,\\ \\ \\phi _ {i} ( t _ {0} ) = \\phi _ {i} ( t _ {1} ) = 0,$$\n\n$$i = 1, 2 ,\\dots.$$\n\nThe problem is reduced to finding a minimum of the function\n\n$$J = J ( a _ {1} \\dots a _ {N} )$$\n\nof $N$ variables. Ritz's method is sufficiently general. It is applied to the solution of variational problems in mathematical physics consisting of the minimization of a functional which depends on functions of several variables. A further generalization of the method to include this class of problems is the method, [2], in which the coefficients are considered to be unknown functions of one of the independent variables (e.g. if the problem involves two independent variables $t$ and $\\tau$, $a _ {i}$ may be given as ${a _ {i} } ( \\tau )$). The initial functional becomes dependent on $N$ functions ${a _ {i} } ( \\tau )$, which may be defined in terms of the necessary conditions, i.e., in the final count, by solving the boundary value problem for a system of $N$ Euler equations.\n\nPractical requirements enhanced the interest in non-classical problems of optimal control. The presence in technical problems of complicated restrictions on the phase coordinates and the control functions, the discontinuity of the right-hand sides of differential equations, the possible existence of singular and sliding optimal conditions, etc. \u2014 all this stimulated the development of new direct methods. The most popular methods are those involving the idea of descent in the space of controls and of successive analysis of variants (of the type of dynamic programming).\n\nDescent methods in the space of the controls are based on finding a sequence of controls $u _ {k} \\in U$ of the form\n\n$$\\tag{12 } u _ {k + 1 } ( t) = \\ u _ {k} ( t) + \\delta u _ {k} ( t),$$\n\nwhich corresponds to a monotone decreasing sequence of values of the functional. For instance, suppose it is required to find a minimum of the functional\n\n$$\\tag{13 } J = F ( x ( T))$$\n\nsubject to the conditions (2), (3) and (5) ( $U$ is a convex and simply-connected set). The increment $\\delta u _ {k} ( t)$ is found as follows. The variational equations for (2) and the conjugate system (7), subject to the conditions\n\n$$\\psi _ {i} ( T) = \\ - \\frac{\\partial F ( x ( T)) }{\\partial x ^ {i} } ,\\ \\ i = 1 \\dots n,$$\n\nat the right-hand end, are used to represent the linear part of the increment of the functional (13) as a result of the variation $\\delta u$, in the form\n\n$$\\delta J = - \\int\\limits _ {t _ {0} } ^ { {T } } \\frac{\\partial H }{\\partial u } \\delta u dt.$$\n\nIn order to decrease the value of the functional (13), the increment\n\n$$\\delta u _ {k} ( t) = \\ \\kappa \\frac{\\partial H }{\\partial u } ,\\ \\ \\kappa > 0,$$\n\nwhere the value of $\\partial H \/ \\partial u$ is calculated on the control ${u _ {k} } ( t)$ and on the corresponding trajectory ${x _ {k} } ( t)$, must be chosen for each iteration. The regularity of the linearization, and hence also the decrease in the value of the functional (13), is ensured by choosing a sufficiently small value of $\\kappa$. The descent process (12) begins from some ${u _ {0} } ( t)$ and is terminated when, as a result of the last iteration, $| \\delta J |$ becomes smaller than some given $\\epsilon$. In the case of a free right-hand end described above, the resulting algorithm is most simple [5], [6], [7]. Another method which does not involve linearization of the initial problem is very effective in solving problems with a free end [8]. If the right-hand end is also subject to boundary conditions, all algorithms become much more complicated. To deal with boundary conditions, a gradient projection procedure is employed in [5], while in [6] failure to satisfy the boundary conditions is penalized by considering the functional\n\n$$\\tag{14 } J = F( x( T)) + \\sum _ {i = 1 } ^ { n } \\lambda _ {i} ( x ^ {i} ( T) - x _ {T} ^ {i} ) ^ {2} ,\\ \\ \\lambda _ {i} > 0,$$\n\nrather than (13). The method in which the increment of the control is determined by solving an auxiliary linear programming problem, resembles the gradient methods [9].\n\nA large group of direct methods for the numerical solution of optimal control problems is based on the idea of optimal analysis of variants [10], [11], [12]. An important feature of this method is that it may be used to solve problems with phase restrictions of the kind\n\n$$\\tag{15 } x \\in G,$$\n\nwhere $G$ is a closed set in an $n$- dimensional space. Its principal disadvantage is the fact that its use rapidly becomes more difficult as the dimension of the space increases. In these methods the initial problem is reduced to a problem of non-linear programming of a special type. Two ways of effecting such a reduction are usually employed. The first method ultimately yields the problem of minimizing a function which depends only on the controls given at the points of a discrete grid on the axes [13]. In the second method controls are discarded and the task is reduced to minimizing a function of the type\n\n$$\\tag{16 } J ( x _ {0} \\dots x _ {N} ) = \\ \\sum _ {i = 0 } ^ { {N } - 1 } f _ {i} ( x _ {i} , x _ {i + 1 } ),$$\n\nwhere $x _ {i}$ is the value of the vector $x$ at the point $t _ {i}$, $i = 0 \\dots N$, subject to the restrictions\n\n$$\\tag{17 } x _ {i} \\in G _ {i} ,$$\n\nwhich follow from the restrictions (3), (4) and (15). The procedure employed for the minimization of (l6) subject to (17) may be geometrically interpreted as follows.\n\nFigure: v096210a\n\nEach family of vectors $\\{ x _ {0} \\dots x _ {N} \\}$ is put into correspondence with a polygon line, as shown in the figure, passing through $x _ {0} \\dots x _ {N}$ and lying in the hyperplanes $\\Sigma _ {i}$ defined by equations $t = t _ {i}$. The length of the polygon line $J ( x _ {0} \\dots x _ {N} )$ is the sum of the lengths $f _ {i} ( x _ {i} , x _ {i+} 1 )$ of its individual links. The domain of admissible $x _ {i}$- values is defined by (17), and is separated from the forbidden domain by some polygonal line (the forbidden domain is shown shaded in the figure). The problem is to find the minimum length of a polygonal line located in the admissible domain and connecting the hyperplanes $\\Sigma _ {0}$ and $\\Sigma _ {N}$. The algorithm by which this problem is solved is a multi-step process, during which a certain set of variants $\\Omega _ {i}$ known not to contain the optimal polygonal line is marked off at each stage $i$. The zero-th stage consists in defining the function\n\n$$l ( x _ {1} ) = \\min _ {x _ {0} \\in G _ {0} } \\ f _ {0} ( x _ {0} , x _ {1} ),$$\n\ni.e. the length of the shortest link connecting each point $x _ {1} \\in \\Sigma _ {1}$ with the hyperplane $\\Sigma _ {0}$. Since\n\n$$\\min _ {x _ {0} \\in G _ {0} } J ( x _ {0} \\dots x _ {N} ) = \\ l ( x _ {1} ) + \\sum _ {i = 1 } ^ { {N } - 1 } f _ {i} ( x _ {i} , x _ {i + 1 } ),$$\n\nthe set $\\Omega _ {0}$ of polygonal lines not containing the segment $l( x _ {1} )$ may be discarded. In the first stage one constructs the shortest polygonal line\n\n$$l ( x _ {2} ) = \\ \\min _ {x _ {1} \\in G _ {1} } \\ ( l ( x _ {1} ) + f _ {1} ( x _ {1} , x _ {2} ) ),$$\n\nconnecting each point $x _ {2} \\in \\Sigma _ {2}$ with $\\Sigma _ {0}$, and the set of polygonal lines $\\Omega _ {1}$ not containing the straight line $l( x _ {2} )$ is also discarded, etc. In the $i$- th stage one constructs the shortest polygonal line\n\n$$\\tag{18 } l ( x _ {i + 1 } ) = \\min _ {x _ {i} \\in G _ {i} } \\ ( l ( x _ {i} ) + f _ {i} ( x _ {i} , x _ {i + 1 } ) ),$$\n\nconnecting each point $x _ {i+} 1 \\in \\Sigma _ {i+} 1$ with $\\Sigma _ {0}$, and the set of polygonal lines $\\Omega _ {i}$ not containing the polygonal line $l( x _ {i+} 1 )$ is discarded. The last stage yields the solution of the initial problem \u2014 the shortest polygonal line connecting the hypersurfaces $\\Sigma _ {N}$ and $\\Sigma _ {0}$:\n\n$$l = \\min _ {x _ {N} \\in G _ {N} } \\ l ( x _ {N} ).$$\n\nFormula (18) is a recurrence relation which describes the multi-step process for finding the solution. It is the base of dynamic programming and of Bellman's optimality principle.\n\nIn accordance with (18), the minimum must be found on sets $G _ {i}$ with, generally speaking, the cardinality of the continuum. The numerical realization involves a finite-dimensional approximation of them. To do this one constructs \u2014 in addition to the grid with respect to $t$( e.g. with a constant step $\\tau$) \u2014 also a grid with respect to $x ^ {j}$ with step $h ^ {j}$( $j = 1 \\dots n$). The problem is then reduced to finding the shortest path in a special graph, with the grid nodes as vertices. Let $P _ {k} ( i)$ be the node $k$ lying in the hyperplane $\\Sigma _ {i}$; let\n\n$$l _ {ks} ( i) = f _ {i} ( P _ {k} ( i), P _ {s} ( i + 1))$$\n\nbe the length of the segment connecting two nodes $k$ and $s$ in neighbouring hyperplanes; and let $l _ {k} ( i)$ be the length of the shortest path connecting the node $P _ {k} ( i)$ with the hyperplane $\\Sigma _ {0}$. The recurrence relation (18) will then assume the form\n\n$$l _ {s} ( i + 1) = \\min _ { k } ( l _ {k} ( i) + l _ {ks} ( i) ),$$\n\nwhere the minimum is taken over the numbers $k$ of all nodes located in the admissible domain $G _ {i}$ of the hyperplane $\\Sigma _ {i}$. In the general case this minimum is found by inspecting all nodes. This method makes it possible to find a global extremum of the function (16), subject to (3), (4) and (15), with an accuracy determined by the steps $\\tau$ and $h ^ {j}$ of the grids. In order that the method converge to the solution of the initial problem, certain relations between these steps (e.g. of the type $h ^ {j} = o ( \\tau )$) must hold. The method requires the use of fast computers with large memories. For this reason, the first step in practical work is to find a solution on a coarse grid, after which a finer grid is used to obtain a more exact solution in a neighbourhood of the solution thus found. This is done with the aid of one of the methods for finding a local extremum (cf. Travelling-tube method; Local variations, method of; Travelling-wave method).\n\n#### References\n\n [1] N.N. Moiseev, \"Computational methods in the theory of optimal systems\" , Moscow (1971) (In Russian) [2] L.V. Kantorovich, V.I. Krylov, \"Approximate methods of higher analysis\" , Noordhoff (1958) (Translated from Russian) [3] V.K. Isaev, V.V. Sonin, \"Numerical aspects of the problem of optimum flight as a boundary value problem\" USSR Comput. Math. Math. Phys. , 5\u00a0: 2 (1965) pp. 117\u2013129 Zh. Vychisl. Mat. i Mat. Fiz. , 5\u00a0: 2 (1965) pp. 252\u2013261 [4] S. Dzhurovich, D. Makintair, Raketnaya Tekhn.\u00a0: 9 (1962) pp. 47\u201353 [5] V. Denkhem, V. Braison, Raketnaya Tekhn. i Kosmonavtika\u00a0: 1 (1964) pp. 34\u201347 [6] L.I. Shatrovskii, \"On a numerical method of solving problems of optimum control\" USSR Comput. Math. Math. Phys. , 2\u00a0: 3 (1962) pp. 511\u2013514 Zh. Vychisl. Mat. i Mat. Fiz. , 2\u00a0: 3 (1962) pp. 488\u2013491 [7] T.M. Eneev, Kosmicheskie Issl. , 4\u00a0: 5 (1966) pp. 651\u2013659 [8] I.A. Krylov, F.L. Chernous'ko, \"On a method of successive approximations for the solution of problems of optimal control\" USSR Comput. Math. Math. Phys. , 2\u00a0: 6 (1962) pp. 1371\u20131382 Zh. Vychisl. Mat. i Mat. Fiz. , 2\u00a0: 6 (1962) pp. 1132\u20131139 [9] R.P. Fedorenko, \"Approximate solution of some optimal control problems\" USSR Comput. Math. Math. Phys. , 4\u00a0: 6 (1964) pp. 89\u2013116 Zh. Vychisl. Mat. i Mat. Fiz. , 4\u00a0: 6 (1964) pp. 1045\u20131064 [10] R. Bellman, \"Dynamic programming\" , Princeton Univ. Press (1957) [11] V.S. Mikhalevich, \"Sequential optimization algorithms and their application. Part I\" Cybernetics , 1\u00a0: 1 (1965) pp. 44\u201356 Kibernetika (Kiev) , 1\u00a0: 1 (1965) pp. 45\u201356 [12] N.N. Moiseev, \"Numerical methods of optimal control theory using variations in the state space\" Cybernetics , 2\u00a0: 3 (1966) pp. 1\u201324 Kibernetika (Kiev) , 2\u00a0: 3 (1966) pp. 1\u201329 [13] Yu.M. Ermol'ev, V.P. Gulenko, \"The finite-difference method in optimal control problems\" Cybernetics , 3\u00a0: 3 (1967) pp. 1\u201316 Kibernetika (Kiev) , 3\u00a0: 3 (1967) pp. 1\u201320","date":"2020-08-14 22:31:47","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 1, \"mathjax_display_tex\": 1, \"mathjax_asciimath\": 0, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.7776206731796265, \"perplexity\": 290.7299325566996}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.3, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2020-34\/segments\/1596439740343.48\/warc\/CC-MAIN-20200814215931-20200815005931-00078.warc.gz\"}"}
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In the spoiler above is the complete list of every Magical Girl show I've seen. I excluded extra details like specials, movies and such, but included second seasons if available. I included Nanoha A's movie because it's a recap of the second season.
The only thing I can think to watch now is Pastel Yumi, which despite having the word Idol in the title is not about singing. It's on AnimeSols just like Creamy Mami so that makes things a tad easier.
Since I know you tend to like the witchy ones, how about Sugar Sugar Rune?
I also think you would enjoy the Magic Users Club OAV, It may have some fan service but Sae seems like the type of magical girl you would like.
I had always meant to experience Sugar Sugar Rune, but I'd been specifically told to choose the manga instead of the anime. I have low tolerance for reading manga on sites like mangahere and mangafox. I only managed to tolerate reading Sailor Moon because I could see the entire page on the tablet and could turn the pages with the touch screen.
Since I can't find any actual downloads for the English manga, I may have to settle for the manga.
Robot Girls Z; a magical girl spoof of the Mazinger Z franchise. Even if you don't know a lot about Mazinger its still hilarious. Powerpuff Girls Z is also a fun title.
you like shows about magical girls helping people right?
How about Saint Tail? She helps people get back their stuff.
I've been curious of watching Sugar Rune and Saint Tail myself. Are both good?
I like both of them, you're better off reading the manga if you can for both of them though.
I haven't seen much of Sugar Sugar Rune, but most fans are a bit disappointed in it and I dont know why exactly? But its still pretty cute from what I've seen. On the plus side the art and sound in it are fantastic.
I read up on Sugar Sugar Rune and it said they made the anime more magical girly? Plus it was running at the same time as the manga so there are differences. Honestly that doesn't bother me because I usually enjoy animes more than their manga counterparts. It just depends on how the characters are developed in each version.
Subject: Re: What to watch next?
|
{
"redpajama_set_name": "RedPajamaC4"
}
| 5,837
|
Q: Knex query event logs to winston file. I would like save all knex query event to winston file. I found somthing like this
http://knexjs.org/#Interfaces-Events . Its work good for my but now i have to add
.on('query-response', function(response, obj, builder)...
for each knex query.
I would like add one global function for all qnex query. It is possible?
A: You can export your knex object from a separate dbConnection file and import it in other file where you need. In your dbConnection file add event listener to knex. Like here:
In your dbConnection file write this:
const knex = require('knex')({
//Your db configuration here
});
knex.on('query', console.log);
module.exports = knex;
In your other file require it and use it.
const knex = require('/dbConnection');
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{
"redpajama_set_name": "RedPajamaStackExchange"
}
| 5,502
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Ryszard Doroba (ur. 3 marca 1928 w Łowiczu, zm. 14 stycznia 1985 w Łodzi) – autor powieści dla młodzieży, scenariuszy i dialogów do filmów animowanych. Autor tekstów piosenek do muzyki Zdzisława Daniela "Kiedy ujrzę cię (Kiedy ujrzę cię jeszcze raz)" (2004) i Zdzisława Pucka "Gdy zapytasz nie odpowiem". (2007) Pochowany na cmentarzu komunalnym Doły (Kwatera: XXII, Rząd: 15, Grób: 16).
Mieszkał w Domu Literatów przy al. T. Kościuszki 98.
Publikacje
Łechtanie Hioba (1962)
Tajemnica podziemnego lochu (Łódź 1972, 1980)
Baszta Szarej Sowy (1974)
Bliżej filmu (Warszawa 1980)
Mój przyjaciel Filon (1984)
Wakacje pana Fajki (1984)
Wakacje pod łunami (1985)
Scenariusze
Pies w kosmosie (1963) – scenariusz,
Ludzie rosną (1968) – scenariusz,
Colargol na Dzikim Zachodzie (1976) – dialogi,
Colargol Zdobywcą Kosmosu (1978) – dialogi.
Przypisy
Ludzie urodzeni w Łowiczu
Urodzeni w 1928
Zmarli w 1985
Pochowani na Cmentarzu Doły w Łodzi
Pisarze związani z Łodzią
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{
"redpajama_set_name": "RedPajamaWikipedia"
}
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\section{Introduction}
The classical theory of force-free motions of rigid particle systems has a long history in connection with investigation
in Mathematics and Mechanics. From the Differential Calculus, in the case of translational particle motions in
Euclidean space (Newton axioms of Mechanics), to the Riemann Geometry. Hence, the definition of geodesics has immediately concerned
with force-free particle motions on surfaces. The introduction of Riemannian manifolds and the geometry of their geodesics were
motivated by the mechanics of constrained particle systems. In the last few years, the study of force-free motion systems on
Riemannian manifolds of constant sectional curvature has attracted the interest of several authors \cite{carinera1}, \cite{C-F-G}, \cite{C-F-G2}, \cite{M}, \cite{N} and
\cite{S}.
In particular, in \cite{C-F-G} the authors define the notion of a pendulum on a surface of constant Gaussian curvature $K$ and they study the motion of a mass
at a fixed distance from a pivot. So, a pendulum problem on a surface of constant curvature is defined as a pivot point and a mass connected to
that point
by a rigid massless rod of fixed length $\rho$. It is assumed that the pivot is constrained to move along some fixed curve with prescribed motion.
The rod provides the only force on the mass in order to keep
the mass at the fixed distance from the pivot.
No torque is applied to the rod, (fig. 1).
In \cite{C-F-G} it is studied the pendulum problem when the pivot moves along a geodesic path, and the
space is a surface of constant (not zero) curvature. It is considered the surface immersed in $\R^3$ or $\L^3$ and it is obtained the
differential motion equation by Newtonian procedure doing a laborious calculation. Moreover, the cases $K>0$ and $K<0$ are necessary to come
from different forms.
In this work, we deal with the pendulum problem from an analytic point of view.
This procedure allows approach simultaneously the cases of positive
and negative curvature and also of zero curvature (as a limit case), with very simple computations.
The key of our study is a lagragian approach, which has a 1-dimensional configuration space.
As adirect consequence the internal curvature force is conservative and its potential function is easily calculated.
Moreover, this method can be used
to another related problems, as the elastic pendulum, or the quantum pendulum.
Mainly, this work concerns the case in which the pivot moves along a geodesic. Let $\zeta$ be the angle between the rod
and the motion direction of the pivot. We will assume the following convention:
\vspace{1mm}
\noindent If the constant curvature of the space is $K>0$,
$$\cos_K(z)=\cos(z\sqrt{K}),\quad \sin_K(z)=\sin(z\sqrt{K}),\quad \tan_K(z)=\tan(z\sqrt{K}) \, .$$
\noindent If the constant curvature of the space is $K<0$,
$$\cos_K(z)=\cosh(z\sqrt{-K}),\quad \sin_K(z)=\sinh(z\sqrt{-K}),\quad \tan_K(z)=\tanh(z\sqrt{-K})$$
The main result is the following:
{\quote {\it Suppose that the pivot of pendulum moves with constant speed $v$ along a geodesic on a surface with constant curvature $K$.
Let $\zeta(t)$ the angle at the time $t$ between the rigid rod and the direction of pivot motion. Then the Lagrangian of the system is
$${\cal L}(\zeta,\dot\zeta)=\frac{1}{2}m\dot{\zeta}^2\sin_K^2(\rho)\frac{1}{\mid K\mid}-\frac{1}{2}mv^2{\rm sgn}(K)\sin_K^2(\rho)\sin^2(\zeta).$$
\noindent Therefore, the motion equation is
\begin{equation} \label{P}
\frac{d^2\zeta}{dt^2}=-v^2K\sin_K(\zeta)\cos_K(\zeta).
\end{equation}}}
Using the previous result and geometric arguments, we obtain the motion equation of the system when the pivot accelerates
along a geodesic (see Section 4). Further developements are discussed in Section 5.
\begin{figure}
\centering
\begin{tiny}
\end{tiny}\includegraphics{pend1.eps}
\caption{Pendulum motion}
\label{fig 1}
\end{figure}
\section{Preliminaries}
It is well known that a complete, simply-connected Riemannian $n$-manifold with constant sectional curvature
is isometric to one of model spaces $\R^n$, $\S^n(R)$ or $\H^n(R)$ (see \cite{L}).
\vspace{2mm}
Let $(\S^2 (R),\langle\,,\,\rangle_1)$ be the 2-dimensional sphere of radius $R$,
endowed with the metric induced from $(\R^3, \langle\,,\,\rangle)$, where
$$\langle\,,\,\rangle=dx^2+dy^2+dz^2.$$
\noindent Consider the coordinate system $\{U_1, \Phi=(\varphi,\theta)\}$ in $S^2(R)$ with $U_1=\Phi^ {-1}((0,\pi)\times (0,2\pi))$ and
$\Phi^{-1}(\varphi,\theta)=(x,y,z)$, being
$$\left.
\begin{array}{l}
x=R\sin{\varphi}\cos{\theta}
\\ y=R\sin\varphi\sin\theta
\\ z=R\cos\varphi
\end{array}
\right\}$$
\noindent In this coordinate system the metric is given by
$$\langle\,,\,\rangle_1=R^2\, d\varphi\otimes d\varphi + R^2\sin^2\varphi\, d\theta\otimes d\theta,$$
\noindent and the non-zero Christoffel symbols are $\Gamma_{\varphi\theta}^{\theta}=\cot\varphi$ and
$\Gamma_{\theta\theta}^{\varphi}=-\sin\varphi\cos\varphi$.
\vspace{2mm}
Let's consider also the hyperbolic plane $(\H^2(R),\langle\,,\,\rangle_2)$, where $$\H^2(R)=\{(x,y,z)\in\R^3/x^2+y^2-z^2=-R^2\}$$
\noindent and $\langle\,,\,\rangle_2$ is the induced metric from the Lorentz-Minkowski spacetime $\L^3$.
\noindent Let $\{U_2, \Psi=(\alpha,\beta)\}$ be the coordinate system in $\H^2(R)$ with $U_2=\Psi^ {-1}((-\infty,\infty)\times(-\infty,\infty))$ and
$\Psi^{-1}(\alpha,\beta)=(x,y,z)$, where
$$\left.
\begin{array}{l}
x=R\cosh{\alpha}\sinh{\beta}
\\ y=R\sinh\alpha
\\z=R\cosh\alpha\cosh\beta
\end{array}
\right\}$$
\noindent The metric is given by
$$\langle\,,\,\rangle_2=R^2d\alpha\otimes d \alpha+R^2\sinh^2 \alpha \, d\beta\otimes d\beta$$
\noindent and the non-zero Christoffel symbols are
$\Gamma_{\alpha\beta}^{\beta}=\coth\alpha$ and $\Gamma_{\beta\beta}^{\alpha}=-\sinh\alpha\cosh\beta$.
\section{Rigid pendulum}
Firstly, we deal with the rigid pendulum problem in the case that the pivot moves along a geodesic of its space, with constant speed.
We will do analogously the study for
$K>0$ and $K<0$.
\subsection{ Spherical case, kinetic energy}
Note that in the case $K>0$ we must require that $\rho<\pi R$ to guarantee that the mass and the rod are on the same side of the geodesic line.
Suppose that the pivot moves along the geodesic $\varphi=\frac{\pi}{2}$ with constant speed. Let's take a reference associated to the pivot. Denote by
$\zeta$ the angle between the rigid rod and the direction of pivot motion.
The Lagrangian of the system has two components, on the one hand, the kinetic energy of the mass ${\bf T}$, and on the other hand,
the potential energy ${\bf V}$, which is due to the curvature of space, i.e., ${\bf V}=0$ if the space is flat.
Consider the isosceles geodesic triangle formed in an infinitesimal temporal interval, by the rod and the arc $dl$ traced by the mass (fig. 2).
\begin{figure}
\centering
\begin{tiny}
\end{tiny}\includegraphics[width=0.47\linewidth]{pend2.eps}
\caption{Infinitesimal triangle}
\label{fig 2}
\end{figure}
The Sine Theorem
for Spherical Geometry allows us to write
$$dl=R\,\sin(\rho/R)\,d\zeta=\frac{1}{\sqrt{\mid K\mid}}\sin(\rho\sqrt{\mid K\mid})\,d\zeta,$$
\noindent thus
$$\tilde v=\frac{dl}{dt}=\dot\zeta\sin(\rho\sqrt{\mid K\mid})\frac{1}{\sqrt{\mid K\mid}}.$$
\noindent Therefore, if the particle has mass $m$, the kinetic energy is given by
$${\bf T}=\frac{1}{2}m\dot\zeta^2\sin^2(\rho\sqrt{\mid K\mid})\frac{1}{{\mid K\mid}}.$$
\subsection{Spherical case, potential energy}
Consider the coordinate system $\{U_1, \Phi=(\varphi,\theta)\}$ with the metric $\langle\,,\,\rangle_1=R^2\, d\varphi\otimes d\varphi + R^2\sin^2\varphi\, d\theta\otimes d\theta,$ and suppose that the pivot moves
along the geodesic $\varphi=\frac{\pi}{2}$ with constant speed $v$. Obtain us the mass acceleration due to the curvature, so
suppose that the mass moves along the curve
$$\left.
\begin{array}{l}
\varphi=\varphi_0
\\ \theta=\frac{v}{R}t
\end{array}
\right\}$$
\noindent Its acceleration is given by
$$a=\frac{v^2}{R^2}\Gamma_{\theta\theta}^\varphi \frac{\partial}{\partial\varphi}=-\frac{v^2}{R^2}\sin(\varphi)\cos(\varphi)\frac{\partial}{\partial\varphi}.$$
As consequence, the external force that we must be to apply on the rod will be ${\bf F}_e=ma$ and the curvature potential energy ${\bf V}$ satisfies ${\bf F}=-{\rm grad}\,({\bf V})$,
where ${\bf F}=-{\bf F}_e$. Hence,
$${\bf V}=\int_{\pi/2}^{\varphi} R^2(-m\sin(\varphi)\cos(\varphi))\frac{v^2}{R^2}\,d\varphi=\frac{m}{2}v^2\cos^2\varphi$$
\noindent where we have taken $\pi/2$ as origin energy. Again, using the Sine Theorem (fig. 3) we obtain
\begin{figure}
\centering
\includegraphics[width=0.47\linewidth]{isosceles.eps}
\caption{Geodesic triangle}
\label{fig 3}
\end{figure}
$$\cos (\varphi)=\sin(\zeta)\sin(\rho/R) .$$
Thus
$${ \bf V}(\zeta)=-\frac{m}{2}v^2\sin^2(\rho/R)\sin^2(\zeta).$$
Now, we can enunciate the following Theorem,
\begin{teor} Suppose that the pivot of pendulum moves with constant speed $v$ along a geodesic on a surface with constant curvature $K>0$.
Let $\zeta(t)$ the angle at the time $t$ between the rigid rod and the direction of pivot motion. Then the Lagrangian of the system is
\begin{equation}
{\cal L}(\zeta,\dot\zeta)=\frac{1}{2}m\dot{\zeta}^2\sin^2(\rho/R)\frac{1}{K}-\frac{1}{2}mv^2\sin^2(\rho/R)\sin^2(\zeta)
\end{equation}
\noindent Therefore, the motion differential equation is given by
\begin{equation}\label{motion1}
\frac{d^2\zeta}{dt^2}=-v^2K\sin(\zeta)\cos(\zeta)
\end{equation}
\end{teor}
If we do $K\rightarrow 0$,
$$\sin(\rho)\simeq \rho\sqrt{\mid K\mid}$$
\noindent and
$$\lim_{K\rightarrow 0}{\cal L}=\frac{1}{2}m \dot\zeta^2\rho^2,$$
\noindent obtaining the Lagrangian function of the pendulum moving in the Euclidean plane, when the pivot moves along a straigh line with constant speed.
\subsection{ Hyperbolic case, kinetic energy}
Consider us now, the pivot moving along the geodesic $\alpha=0$, with constant speed $v$. Analogously to the spherical case, we take a reference
joint with the pivot and we denote $\zeta$ the angle between the rigid rod and the direction of pivot motion.
If we consider the isosceles hyperbolic differential triangle (fig. 2), and making use of the corresponding theorems of the Hyperbolic Geometry,
we can to conclude that the kinetic energy of the system is given by
$${\bf T}=\frac{m}{2}\dot\zeta^2\sinh (\rho/R)\,\frac{1}{\mid K\mid}.$$
\subsection{ Hyperbolic case, potential energy}
Reasoning as the in spherical case, we consider that the pivot moves along the geodesic $\alpha=0$. If the mass moves along the curve
$$\left.
\begin{array}{l}
\alpha=\alpha_0
\\ \beta=\frac{v}{R}t
\end{array}
\right\},$$
\noindent we can to calculate the curvature potential function,
$${\bf V}=\int_{0}^\alpha R^2(-m\sinh(\alpha)\cosh(\alpha))\frac{v^2}{R²}=-\frac{m}{2}v^2\sinh(\alpha) \, ,$$
\noindent where we have taken $0$ as origin energy. Again, using the Sine Theorem in the hyperbolic case, we obtain
$$\sinh(\alpha)=\sin(\zeta)\sinh(\rho/R).$$
Thus,
$${\bf V}=-\frac{m}{2}v^2\sinh^2(\rho/R)\sin^ 2(\zeta) .$$
\begin{teor} Suppose that the pivot of the pendulum moves with constant speed $v$ along a geodesic on a surface with constant curvature $K<0$.
Let $\zeta(t)$ the angle at the time $t$ between the rigid rod and the direction of pivot motion. Then the Lagrangian of the system is given by
\begin{equation}
{\cal L}(\zeta,\dot\zeta)=\frac{1}{2}m\dot{\zeta}^2\sinh^2(\rho/R)\frac{1}{\mid K\mid}+\frac{1}{2}mv^2\sinh^2(\rho/R)\sin^2(\zeta) .
\end{equation}
\noindent Therefore, the motion differential equation is
\begin{equation}\label{motion}
\frac{d^2\zeta}{dt^2}=v^2\mid K\mid\sinh(\zeta)\cosh(\zeta) .
\end{equation}
\end{teor}
With our convention, we can to enunciate (compare with \cite{C-F-G}, Theorem A):
\begin{teor}
Suppose that the pivot of pendulum moves with constant speed $v$ along a geodesic on a surface with constant curvature $K$.
Let $\zeta(t)$ the angle at the time $t$ between the rigid rod and the direction of pivot motion. Then the Lagrangian of the system is given by
$${\cal L}(\zeta,\dot\zeta)=\frac{1}{2}m\dot{\zeta}^2\sin_K^2(\rho)\frac{1}{\mid K\mid}-\frac{1}{2}mv^2{\rm sgn}(K)\sin_K^2(\rho)\sin^2(\zeta).$$
\noindent Therefore, the motion differential equation is
$$\frac{d^2\zeta}{dt^2}=-v^2K\sin_K(\zeta)\cos_K(\zeta).$$
\end{teor}
\begin{rema} {\rm
Suppose $K>0$ and consider the motion equation (\ref{motion1}). Making the change $u=2\zeta$, we obtain the differential equation
\begin{equation}\label{planar}
\frac{d^2u}{dt^2}=-v^2 K\sin(u) ,
\end{equation}
\noindent which is the equation of planar pendulum of length $1$ in Euclidean space subject to a constant gravitational field of magnitude $g=v^ 2 K$. Its stable and unstable equilibria at $u=0$ and $u=\pi$,
correspond to the stable $\zeta=0$ and unstable $\zeta=\pi/2$ equilibria of the pendulum on the spherical surface.
On the other hand, if $K<0$, making $u=\pi-2\zeta$ in the motion equation (\ref{motion}), we obtain, in similar form, that $\zeta=\pi/2$ is stable equilibria and $\zeta=0$ is unstable equilibria.
Moreover, it is well known that the equation (\ref{planar}) can be exactly solved in term of a elliptic integral of first kind (see \cite{San}, for instance), which cannot be evaluated in a closed form.
A first approximation to this problem in arbitrary constant curvature is given for small oscillations around the stable equilibria points of this physical system. That is, for small $u$, $\sin_K u
\simeq u$, and the equation of motion is approximated by
$$\frac{d^2u}{dt^2}=-v^2 \mid K \mid u.$$ Observe that the previous equation represents a simple harmonic oscillator of frequence $\omega = v \sqrt{\mid K \mid}$.
}
\end{rema}
\subsection{A first integral}
Since the Hamiltonian function ${\cal H}$ is time independent, it is an integral on phase space and it represents
the system energy. Using the standard notation $(q_\zeta,p_\zeta)$ in the phase space, we can write
$$p_\zeta=\frac{\partial {\cal L}}{\partial\dot\zeta}=m\dot\zeta \sin^2_K(\rho) \frac{1}{\mid K\mid}.$$
The Legendre transformations allow us to give
\begin{equation} \label{hamiltonian}
{\cal H}(\zeta ,\dot\zeta)=\frac{1}{2}m\dot{\zeta}^2\sin_K^2(\rho)\frac{1}{\mid K\mid}+\frac{1}{2}mv^2{\rm sgn}(K)\sin_K^2(\rho)\sin^2(\zeta).
\end{equation}
Moreover, it is easy to see that ${\cal H}$ is constant if and only if
$$2\Big(\frac{d\zeta}{dt}\Big)^2-K v^2\cos(2\zeta)$$
\noindent is constant (compare with \cite[Prop. 1]{C-F-G}).
\section{Accelerated pivot}
Suppose now that the pivot moves along a geodesic path with lineal acceleration $a(t)$. We come to compute the acceleration induced by the accelerated pivot at the mass making use of a geometric argument.
We follow the following steps:
\vspace{1mm}
\noindent a) Translate to the mass the pivot acceleration $a(t)$ .
\noindent b) Transform this acceleration in angular acceleration between the rod and the geodesic path traced by the pivot.
\noindent c) Project on the orthogonal direction to the rod.
\
\begin{figure}
\centering
\includegraphics[width=0.47\linewidth]{acelerated.eps}
\caption{Triangle}
\label{fig 4}
\end{figure}
\noindent Indeed, consider the geodesic triangle of the figure 4. The translated acceleration to the mass is given by
$$a(t)\cos_K(d),$$
\noindent and the angular acceleration by
$$\frac{a(t)\cos_K(d)}{R\sin_K(\rho)}.$$
\noindent Finally, in order to project, it is enough to multiply by $\cos(\mu)$
$$\frac{a(t)\cos_K(d)\cos(\mu)}{R\sin_K(\rho)}.$$
On another hand, taking into account the previous triangle, from the Pythagoras and Cosine Theorem in non-Euclidean geometries, we have
$$\cos_K(\mu)=\sin_K(\zeta)\cos_K(h)\ \ {\rm and}\ \ \cos_K(\rho)=\cos_K(d)\cos_K(h),$$
\noindent thus $\cos_K(d)\cos_K(\mu)=\cos_K(\rho)\sin_K(\zeta)$. As a consequence, the searched acceleration is
$$\sqrt{\mid K\mid} a(t)\cot_K(\rho)\sin_K(\zeta(t)).$$
So, we prove in a different approach the result (\cite[Theorem D]{C-F-G})
\begin{teor} Assume that the pivot moves with speed $v(t)$ along a geodesic on a surface with constant curvature $K$. Let $\zeta(t)$ the angle that the rigid rod makes with the direction of the motion of the pivot.
Then the pendulum satisfies the differential equation
$$\frac{d^2\zeta}{dt^2}=-v(t)^2 K \sin(\zeta(t)) \cos(\zeta(t))+\sqrt{\mid K\mid} \, a(t) \, {\rm cotan}_K(\rho) \, \sin(\zeta(t)),$$
\noindent where $a(t)=\frac{dv}{dt}.$
\end{teor}
\section{Some further physical applications}
As a first application,
consider us the case of a pendulum whose pivot moves along a geodesic on a surface of constant curvature with constant speed $v$ and whose rod is elastic. Let $k$ be the elastic constant of the rod,
let $\rho$ be the length of the rod and let $l(t)$ be the elongation of the rod at the time $t$. Our analytical approach allows us to initiate the study of dynamical system in similar form as the rigid case. So, it is not difficult to see that
its Lagrangian function is given by
$$
{\cal L} (\zeta,l,\dot{\zeta},\dot{l}) = \frac{1}{2} m \dot{\zeta} \sin_K^2 (\rho + l) \frac{1}{|K|} -\frac{1}{2} m v^2 {\rm sgn}(K) \sin^2_K (\rho + l) \sin_K^2 (\zeta) + \frac{1}{2} m \dot{l}^2 - \frac{1}{2} k l^2
$$
Secondly, we will make an approximation to the quantum system.
Denote $\overline{m}:=m \sin_K^2 (\rho )/\mid K \mid$. Then, (\ref{hamiltonian}) can be written, for $K >0$, in terms of $\zeta$ and $p_\zeta$ as
$$
{\cal H}(\zeta, p_\zeta)=\frac{p_\zeta^2}{2 \overline{m} }+\frac{1}{2} \overline{m} v^2 K \sin^2(\zeta).
$$ Observe that the same expression, up an additive term, is obtained for $K<0$.
Therefore, a suitable time independient Schrodinger equation for this system can be described as
$$
- \frac{ \hbar^2 }{2 \overline{m} } \frac{d^2 \psi}{d\zeta^2} + \frac{1}{2} \overline{m} v^2 K \sin^2(\zeta) \psi = E \psi,
$$ where $\psi(\zeta)$ is a complex function representing the wave function of the mass particle in this physical system. Observe that it is
expected that the energy should take quantized values. In fact, if it is assumed that $\psi$ is confined in a region where $\zeta$ is close to $0$, the
previous equation, in this first approximation, corresponds to the quantum harmonic oscillator, whose energy is found to be
$$
E_n = \hbar v \sqrt{|K|} \left(n+\frac{1}{2} \right) , \ \ {\rm for \ \ all} \ \ n\in\mathbb{N}.
$$ Observe that, within this simplification, in the quantum of energy, $\hbar v \sqrt{|K|}$, appears the speed of the rod and the
curvature of the ambient space.
\section*{Acknowledgments}
The authors are partially supported by the Spanish MEC-FEDER Grant MTM2010-18099.
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The corporation upholds the philosophy of "Be No.1 in high quality, be rooted on credit rating and trustworthiness for growth", will continue to serve outdated and new consumers from home and overseas whole-heatedly for Flange End Floating Ball Valve , Flange Connection Floating Ball Valve , Welded Floating Ball Valve , your coming mail will be remarkably appreciated.
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"redpajama_set_name": "RedPajamaC4"
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\section{Introduction}
In conventional superconductors, the attractive interaction responsible for superconducting (SC) pairs is mediated by lattice vibrations (phonons). The strength of this interaction is generally assumed to be field-independent, since the lattice vibrations are not directly coupled to the applied magnetic field ($H_{\rm ext}$). The influence of $H_{\rm ext}$ is usually treated as a perturbation that results in suppression or modulation of the SC order parameter.
In the case of uranium-based ferromagnetic (FM) superconductors UGe$_2$, URhGe and UCoGe, on the other hand, the pairing interaction is supposed to be mediated by FM spin fluctuations \cite{UGe2SC,AokiNature,UCoGe,Fay, Valls}, whose excitation spectrum can be strongly modified by $H_{\rm ext}$, as proved by recent NMR studies \cite{THattori,THattori2,YTPRL,YTPRB,Kotegawa}.
It is thus supposed that the pairing interaction can be affected by $H_{\rm ext}$, and indeed, such a field-dependent pairing mechanism has been suggested to be responsible for the unconventional SC properties of UCoGe \cite{THattori,THattori2,Mineev2011,Tada,Tada2,Wu},
and further, provide exotic field-induced SC in the case of URhGe \cite{YTPRL,YTPRB,Kotegawa,LevyScience,LevyNP,Hattori,Mineev2015}.
\begin{figure}[tb]
\begin{center}
\includegraphics[width=15.6 cm,keepaspectratio]{Figure1_YTnew.eps}
\caption{\footnotesize \setlength{\baselineskip}{3.5mm} Angle $\theta$ dependence of the upper critical field $H_{\rm c2}$ determined by resistivity measurements
in single crystals of (a) URhGe and (b) UCoGe \cite{AokiReview}.}
\end{center}
\vspace{-3mm}
\end{figure}
Among FM superconductors, URhGe and UCoGe have
the same crystal structure of the orthorhombic TiNiSi type and are both itinerant weak ferromagnets with Ising anisotropy along the $c$ crystal axis. These two compounds should thus offer similar bases for the SC mechanism. However, their upper critical field $H_{\rm c2}$, one of the
most fundamental SC parameters, exhibits remarkable
differences\cite{Wu,Aoki2009S,AokiReview}.
In Fig.\,1, we compare the $\theta$ dependence of $H_{c2}$ between UCoGe and URhGe \cite{AokiReview}.
For UCoGe [Fig.\,1(b)], $H_{c2}$ reaches a surprisingly large value, about 20 T for $H_{\rm ext}\|b$ ( $\sim30$ T for $H_{\rm ext}\|a$).
The value highly exceeds the Pauli limiting field, 1.84 $k_{\rm B}T_{\rm SC}/\mu_{\rm B}$, where $T_{\rm SC}=0.7$ K.
$H_{c2}$ is, however, extremely sensitive to the angle of the applied field; a small rotation of the field from the $b$ axis to the $c$ axis rapidly suppresses the $H_{c2}$.
In contrast, $H_{c2}$ in URhGe has no steep increase either around $H_{\rm ext}\|b$ or around $H_{\rm ext}\|a$. $H_{c2}$ exhibits only a weak $\theta$ dependence below 2 T [the inset of Fig.\,1(a)]. The anisotropy of $H_{\rm c2}$ is only about 2.5 between the $b$ and $c$-axis directions. Such moderate anisotropy would be mostly explained by the anisotropy of the effective electron mass.
Interestingly, the field-induced ``reentrant'' SC phase (RSC) appears around a field-induced tricritical point (TCP) located around $H_R\approx12$T for $H_{\rm ext}\|b$. At the TCP, the FM order is forced to align along the field direction ($\|b$) \cite{LevyScience,LevyNP}.
In this paper, we report the results of the Co-NMR spin-lattice relaxation rate $1/T_1$ measurements performed at lower fields for a 10\% Co-doped single crystal of URhGe.
The experiments reveal that spin fluctuations in URhGe are robust against magnetic field applied along any direction in the $bc$ plane.
This makes a clear contrast with the case of UCoGe\cite{THattori}, and provides further support for the mechanism of FM superconductivity mediated by spin fluctuations in these materials.
\section{Experimental Results and Discussion}
A 10\% Co-doped single crystal of URhGe (=URh$_{0.9}$Co$_{0.1}$Ge) was prepared by the Czochralski pulling method.
The substitution of Co for Rh is isostructural and only negligibly affects the magnetic properties of URhGe
\cite{Sakarya,Huy,YTPRL}.
The compound is thus regarded as a suitable proxy to investigate the nature of FM fluctuations in URhGe \cite{YTPRL,YTPRB}.
The $1/T_1$ measurements were performed at a fixed temperature of $T=1.6$ K, well below $T_{\rm Curie}$ = 11.8 K.
The $T_1$ values were determined by fitting the saturation recovery of the spin-echo intensity to the theoretical function for the central transition of the $I=7/2$ nuclear spins.
\begin{figure}[t]
\begin{center}
\includegraphics[width=15.8 cm,keepaspectratio]{Figure2_YTnew.eps}
\caption{\footnotesize \setlength{\baselineskip}{3.5mm} (a) The field-angular dependence of $1/T_1$ for URh$_{0.9}$Co$_{0.1}$Ge measured with several different fields, $H_{\rm ext}$=2, 3.3, 4.95 and 6.8 T. The dashed lines of the corresponding color indicate the $1/T_1(\theta)$ values calculated using the Eqs. (2) and (3) for fixed values of $(1/T_1)_b=155$ s$^{-1}$ and $(1/T_1)_c=63$ s$^{-1}$ and $H_{\rm int}=1.5$ T (see the text).
(b) The field-angular dependence of $1/T_1$ reported for UCoGe \cite{THattori}.
}
\end{center}
\vspace{-3mm}
\end{figure}
Figure 2(a) shows the field-angle dependence of $1/T_1$ in URh$_{0.9}$Co$_{0.1}$Ge.
Here the angle $\theta$ is defined as the angle from the $b$ axis in the $bc$ crystal plane; the magnetic field components are thus ($H_{\rm ext}^b$, $H_{\rm ext}^c$) = ($H_{\rm ext}\cos\theta, H_{\rm ext}\sin\theta$). $1/T_1(\theta)$ was measured for different field values, $H_{\rm ext}$=2, 3.3, 4.95 and 6.8 T.
In Fig.\,2(b), we plot $1/T_1(\theta)$ reported by Hattori {\it et al.} for UCoGe \cite{THattori}.
In UCoGe, $1/T_1(\theta)$ exhibits a strong field-angle dependence; a small rotation of $H_{\rm ext}$ from $\theta=0^{\circ}$ dramatically suppress the $1/T_1$. This leads to a cusp-like sharp peak around $\theta=0^{\circ}$, which becomes sharper with increasing $H_{\rm ext}$.
This behavior indicates a strong suppression of the longitudinal component of FM spin fluctuations by $H_{\rm ext}^c=H_{\rm ext}\sin\theta$ \cite{THattori,THattori2,Tada,Tada2}.
It is thus naturally expected that the suppression of the pairing strength by $H_{\rm ext}^c$ is at the origin of the anomalous $H_{\rm c2}$ behavior in UCoGe \cite{THattori,Tada}.
In contrast, we found that $1/T_1$ in URh$_{0.9}$Co$_{0.1}$Ge shows relatively weak $\theta$ and $H_{\rm ext}$ dependences at lower fields (at 2 and 3.3 T) [Fig.\,2(a)];
there is no dramatic suppression of the FM spin fluctuations by $H_{\rm ext}^c$.
As $H_{\rm ext}$ is increased, $1/T_1(\theta)$ variation increases, developing a broad peak centered at $\theta=0^{\circ}$.
However, compared with the case of UCoGe, the overall $\theta$ dependence is still not very strong even above 4 T.
In the following, we analyze the $1/T_1$ behavior shown in Fig.\,2(a), to demonstrate that, in contrast to the case of UCoGe, the field effects on the spin fluctuations are negligibly small in URhGe at lower field values.
In general, $1/T_1$ probes hyperfine field fluctuations perpendicular to the quantization axis of the nuclear spin.
In the paramagnetic state, the nuclear spin is quantized along the applied field direction, and hence
the $\theta$ dependence of the $1/T_1$ is expressed using the values $(1/T_1)_{b,c}$ that correspond to the fields applied along the $b$ and $c$ directions, respectively:
\begin{equation}
1/T_1(\theta)=(1/T_1)_b\cos^2\theta+(1/T_1)_c\sin^2\theta.
\end{equation}
\begin{figure}[t]
\begin{center}
\includegraphics[width=9.3 cm,keepaspectratio]{Figure3_YTnew.eps}
\caption{\footnotesize \setlength{\baselineskip}{3.5mm} (a) A schematic view of the nuclear spin quantized along the vector sum of the external and internal fields, \mbox{\boldmath $H_{\rm ext}+H_{\rm int}$}. (b) The $r$ dependence of the $1/T_1(\theta)$ calculated using the Eqs. (2) and (3) for fixed values $(1/T_1)_b=155$ s$^{-1}$ and $(1/T_1)_c=63$ s$^{-1}$.
(c) The measured $H_{\rm ext}$ dependence of $1/T_1$ at $\theta=0^{\circ}$ ($H//b$). The dashed line is the calculated $H_{\rm ext}$ dependence using the above given $(1/T_1)_{b,c}$ and $H_{\rm int}=1.5$ T. The $H_{\rm R}$ represents the critical field where the TCP appears. Both $1/T_1$ and $1/T_2$ diverge towards $H_{\rm R}$ \cite{YTPRL,YTPRB,Kotegawa} }
\end{center}
\vspace{-3mm}
\end{figure}
This equation was found to fully explain the $\theta$ dependence of $1/T_1$ in the paramagnetic state of UCoGe \cite{THattori}.
In the FM state, on the other hand, a typically large internal field $H_{\rm int}$ generally appears at nuclear positions.
Then, instead of being quantized along the direction of \mbox{\boldmath $H_{\rm ext}$},
the nuclear spin is quantized along the vector sum of the two fields, \mbox{\boldmath $H_{\rm ext}+H_{\rm int}$} [Fig.\,3(a)]. This requires the modification of Eq. (1) as
\begin{equation}
1/T_1(\theta)=(1/T_1)_b\cos^2\theta{'}+(1/T_1)_c\sin^2\theta{'},
\end{equation}
with
\begin{equation}
\tan{\theta{'}}=\frac{H_{\rm ext}\sin{\theta}+H_{\rm int}}{H_{\rm ext}\cos{\theta}}=\frac{\sin{\theta}+1/r}{\cos{\theta}}.
\end{equation}
These equations indicate that both the magnitude and $\theta$ dependence of $1/T_1$ depend on the ratio $r=H_{\rm ext}/H_{\rm int}$.
In the case of UCoGe, $H_{\rm int}$\ has been estimated from Co-NQR \cite{Ohta} to be $\sim$0.1 T directed parallel to the $c$ axis.
The value is more than an order of magnitude smaller than the $H_{\rm ext}$ used in NMR experiments (typically more than 1 T). This allowed the authors in the Ref. \cite{THattori} to use Eq. (1) even in the FM state.
In the case of URh$_{0.9}$Co$_{0.1}$Ge, on the other hand, the $H_{\rm int}$ has not been determined by Co-NQR. However, the ordered moment of $0.47 \mu_B$, estimated in the FM state, is nearly 10-15 times larger than that of UCoGe, implying the existence of a large $H_{\rm int}\sim1.5$ T at Co nuclear positions.
The value is of the same order as $H_{\rm ext}$, and thus must be fully taken into account in the $1/T_1$ analysis.
Figure\,3(b) shows the $r$ dependence of $1/T_1(\theta)$ calculated using the Eqs. (2) and (3) with fixed values of $1/T_1$, $(1/T_1)_b=155$ s$^{-1}$ and $(1/T_1)_c=63$ s$^{-1}$.
The same calculations are also plotted in Fig.\,1(a), to be compared with the experimental data. Here, we take the $H_{\rm int}=1.5$ T, that is, for example, $H_{\rm ext}=2$ T corresponds to $r=1.3$.
As seen in Fig.\,2(a), the two given values of $(1/T_1)_b$ and $(1/T_1)_c$ reproduce well the magnitude and $\theta$ dependence of $1/T_1$ obtained at the two low field values $H_{\rm ext}=2$ T $(r=1.3)$ and 3.3 T $(r=2.2)$.
That is, $1/T_1$ behavior below $\sim$4 T can be explained mostly by taking into account the tilting of the quantization axis of the nuclear spins with increasing $H_{\rm ext}$.
Conversely, it reveals that the field effect on spin fluctuations is negligibly small at the lowest fields.
The calculation, however, does not fully reproduce $1/T_1(\theta)$ at higher fields. To be more precise, it does not explain the development of the broad peak around $\theta=0^{\circ}$ in $H_{\rm ext}=4.95$ and 6.80 T [Fig. 2(a)].
The deviation between experiment and calculation
becomes significant with increasing $H_{\rm ext}$. This can be seen more clearly in Fig.\,3(c), where the calculated field dependence of $1/T_1$ at $\theta=0^{\circ}$ ($\|b$) is compared with the experimental data.
While the calculated value is nearly field independent, the experimental data rapidly increase above $H_{\rm ext}\sim$8 T \cite{YTPRL}.
As discussed in previous papers \cite{YTPRL,YTPRB}, this rapid increase of $1/T_1$ is connected to the enhancement of spin fluctuations when approaching the TCP around 13 T.
Around the TCP, the spin fluctuations diverge both along the $b$ and the $c$ axes, providing the divergence in $1/T_2$ and $1/T_1$, respectively \cite{YTPRL,YTPRB,Kotegawa,Misawa1,Misawa2}.
It should be remarked that the critical fluctuations in UCoGe are suggested to develop as a feature of the system close to the FM instability \cite{THattori,AokiJPSJ83,AokiReview}.
As mentioned, these critical fluctuations are in longitudinal mode ($H\|c$) and very sensitive to the $H_{\rm ext}$ applied along the same direction (i.e., parallel to the easy-magnetization axis) \cite{THattori,Tada}.
On the other hand, the present NMR results reveal that URhGe at zero field does not possess such critical fluctuations; in this system the FM instability
and related critical fluctuations emerge only under strong magnetic fields, when the system approaches to the TCP \cite{AokiJPSJ83,AokiReview,Nakamura2017,YTPRL,YTPRB}.
Then, the higher $T_{\rm SC}$ in UCoGe (0.7\,K) and in the high-field reentrant SC phase of URhGe (0.45 K), as compared to $T_{\rm SC}$ in URhGe at zero field (0.25 K), implies that these critical fluctuations are more favorable for the mechanism of the FM superconductivity.
\section{Summary}
In summary, the field-angle resolved NMR $1/T_1$ measurements reveal that spin fluctuations in the FM state of URhGe are robust against moderate magnetic field ($\lesssim4$ T) applied along any direction in the $bc$ crystal plane.
This makes a clear contrast with the case of its sister compound UCoGe, in which the rapid suppression of the FM spin fluctuations by a tiny field along the $c$ axis has been observed.
We show that such a difference in the character of spin fluctuations is reflected in their two distinct phase diagrams of the upper critical field $H_{\rm c2}$. This provides further support for the mechanism of superconductivity mediated by FM spin fluctuations in these materials.
\section*{Acknowledgment}
A part of this work was supported by JSPS KAKENHI Grant Number JP15KK0174, JP15H05745, JP15H05884, JP15H05882, JP15K21732, JP16KK0106, JP16H04006, 19K03726, JP19H00646, ICC-IMR, and the REIMEI Research Program of JAEA.
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ZAZ 1102 2005
2005 ZAZ 1102
Photo Information (Width: 340px, Height: 243px, Size: 9Kb)
More photos of ZAZ 1102
ZAZ 1102 Problems
Electricety
1995, there was born in the cables of selfe
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Drive wheels - Traction - Drivetrain: FR or RR
ZAZ 1102 Specs
2005 ZAZ 1102 specs, Fuel type Gasoline, Drive wheels FR or RR, Transmission Gearbox Manual
For the Soviet developmental psychologist, see Alexander Zaporozhets.
The Zaporozhets (Russian: Запоро́жец, zaporozhets (help·info); Ukrainian: Запорожець, Zaporozhets) was a series of subcompact cars designed and built from 1958 at the ZAZ factory in Soviet Ukraine ("Zaporozhsky Avtomobilny Zavod", or Zaporozhian Automobile Factory). Different types of Zaporozhets were produced until 1994. It had special features for disabled people such as ability to be fully controlled by hands and sometimes was given for free by the state to disabled people or war veterans.
The name Zaporozhets means a Cossack of the Zaporizhian Sich. It can also mean а man from Zaporozhye oblast.
Zaporozhets is still warmly remembered in many ex-USSR countries. Like the Volkswagen Beetle or East Germany's Trabant, Soviet Zaporozhets was destined to become a "people's car". It was the cheapest Soviet car and so the most affordable to common people. At the same time, it was rather sturdy and well suitable to Russian roads. The very looks of this car gave birth to several nicknames that stuck with it forever: "Zapor" (short for "Zaporozhets", but also means "constipation" in Russian), "hunchback" (due to ZAZ-965 insect-like form; ZAZ factory workers never used this nickname, using "Malysh" (Russian: малыш; English: Kiddy) instead ), "big-eared" (the car had air intakes on its sides to cool down the engine in the rear of the vehicle).
All Zaporozhets cars featured rear wheel drive (with engine in the rear) and aircooled engines.
The ZAZ-965 model was made between 1960 and 1969. Despite speculations that the design was copied from the Fiat 600, ZAZ representatives say the car was an exclusively Soviet design, created by Soviet ZAZ engineers jointly with colleagues from Moscow's NAMI and Moskvitch car plant. First prototypes were designated as Moskvitch-444.
» Read More About ZAZ 1102
2005 ZAZ 1102 specs, photos, mpg, towing capacity, size - Photos, Pics, Wallpapers, Images.
Used 2005 ZAZ 1102 For Sale, Fuel type Gasoline, Drive wheels FR or RR, Transmission Gearbox Manual.
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{
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Orlando Smeekes (born 28 December 1981) is a Curaçaoan former professional footballer who played as a winger.
Club career
Smeekes was born in Amsterdam, Netherlands. On 10 September 2008, he left Go Ahead Eagles and moved to German 3. Liga club Stuttgarter Kickers. After the relegation of Kickers he signed with FC Carl Zeiss Jena on 26 June 2009. In July 2010 joined for a trial week at Coventry City, which did not result in a full-time contract. He had further trials at Charlton Athletic with similar success. On 21 March 2011, he signed a contract with SV Wehen Wiesbaden and joined the club on 30 June 2011. He joined South African club Maritzburg United on 26 June 2012.
International career
Smeekes made two appearances for the Curaçao national team and four for the Netherlands Antilles national team.
References
External links
Profile at VI
1981 births
Living people
Dutch footballers
Dutch people of Curaçao descent
Footballers from Amsterdam
Dutch Antillean footballers
Curaçao footballers
Netherlands Antilles international footballers
Curaçao international footballers
Dutch Antillean expatriate footballers
Curaçao expatriate footballers
Expatriate footballers in Germany
Association football forwards
3. Liga players
FC Volendam players
SC Telstar players
TOP Oss players
Helmond Sport players
Go Ahead Eagles players
Stuttgarter Kickers players
FC Carl Zeiss Jena players
SV Wehen Wiesbaden players
Maritzburg United F.C. players
FC Den Bosch players
WKE players
Expatriate soccer players in South Africa
Flevo Boys players
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1. A box contains nine bulbs out of which 4 are defective. If four bulbs are chosen at random, find the probability that all the four bulbs are defective.
B. 125/126
E. 1/126
2. An automobile financier claims to be lending money at S.I., but he includes the interest every six months for calculating the principal. If he is charging an interest of 10%, the effective rate of interest becomes?
B. 10.25%
3. I. a2 + 8a + 16 = 0,
II. b2 - 4b + 3 = 0 to solve both the equations to find the values of a and b?
4. The sum of the squares of three numbers is 138, while the sum of their products taken two at a time is 131. Their sum is:
5. Jacob brought a scooter for a certain sum of money. He spent 10% of the cost on repairs and sold the scooter for a profit of Rs. 1100. How much did he spend on repairs if he made a profit of 20%?
6. 12(13/18) + 16(11/27) - 10(5/9) = ?
A. 182/3
B. 1831/54
D. 201/2
E. 211/3
7. Solve the equation for x : 19(x + y) + 17 = 19(-x + y) - 21
A. -1
B. -2
C. -3
D. -4
8. An amount of Rs.1560 was divided among A, B and C, in the ratio 1/2 : 1/3 : 1/4. Find the share of C?
9. (3-3 * 95/2) / (272/3 * 3-4) = ?
10. (800 / 64) * (1296 / 36) = ?
11. Walking with 4/5 of my usual speed, I miss the bus by 5 minutes. What is my usual time?
B. 30 min
D. 20 min
12. The difference between a positive proper fraction and its reciprocal is 9/20. The fraction is:
13. The third proportional to 1 and 2 is?
15. There are some rabbits and peacocks in a zoo. The total number of their heads is 60 and total number of their legs is 192. Find the number of total rabbits?
17. 4 men and 6 women can complete a work in 8 days, while 3 men and 7 women can complete it in 10 days. In how many days will 10 women complete it?
18. 125 liters of a mixture of milk and water contains in the ratio 3:2. How much water should now be added so that the ratio of milk and water becomes 3:4?
A. 20 liters
B. 30 liters
C. 40 liters
D. 50 liters
19. How many four digit numbers can be formed using the digits {1, 3, 4, 5, 7,9}(repetition of digits is not allowed)?
20. A pupil's marks were wrongly entered as 83 instead of 63. Due to the average marks for the class got increased by half. The number of pupils in the class is:
21. A sum of money amounts to Rs. 9800 after 5 years and Rs. 12005 after 8 years at the same rate of simple interest. The rate of interest per annum is?
23. The edges of a cuboid are 4 cm, 5 cm and 6 cm. Find the volume of the cuboid?
24. A and B started business in partnership investing Rs. 20,000 and Rs. 15,000 respectively. After six months, C joined them with Rs. 20,000. What will be B's share in the total profit of Rs. 25,000 earned at the end of 2 years from the starting of the business?
25. In a series of six consecutive even numbers, the sum of the second and sixth numbers is 24. What is the fourth number?
26. A and B start a business, with A investing the total capital of Rs.50000, on the condition that B pays A interest @ 10% per annum on his half of the capital. A is a working partner and receives Rs.1500 per month from the total profit and any profit remaining is equally shared by both of them. At the end of the year, it was found that the income of A is twice that of B. Find the total profit for the year?
27. Identify the greatest numbers: 450, 2100, 1625
D. All are equal
E. 2100, 1625
28. If one third of 3/4 of a number is 21. Then find the number?
29. How many liters of oil at Rs.40 per liter should be mixed with 240 liters of a second variety of oil at Rs.60 per liter so as to get a mixture whose cost is Rs.52 per liter?
A. 120 liters
B. 180 liters
C. 110 liters
D. 160 liters
30. Aman started a business investing Rs. 70,000. Rakhi joined him after six months with an amount of Rs. 1,05,000 and Sagar joined them with Rs. 1.4 lakhs after another six months. The amount of profit earned should be distributed in what ratio among Aman, Rakhi and Sagar respectively, 3 years after Aman started the business?
A. 7:6:10
B. 12:15:16
C. 42:45:56
C. if the relationship between a and b cannot be established.
32. The average age of students of a class is 15.8 years. The average age of boys in the class is 16.4 years and that of the girls is 15.4 years. The ration of the number of boys to the number of girls in the class is:
33. The denominator of a fraction is 1 less than twice the numerator. If the numerator and denominator are both increased by 1, the fraction becomes 3/5. Find the fraction?
34. Using all the letters of the word "THURSDAY", how many different words can be formed?
B. 8!
C. 7!
E. 6!
36. Two numbers have a H.C.F of 16 and a product of two numbers is 2560. Find the L.C.M of the two numbers?
37. A 25 cm wide path is to be made around a circular garden having a diameter of 4 meters. Approximate area of the path is square meters is
C. 4.5
39. In how much time would the simple interest on a certain sum be 0.125 times the principal at 10% per annum?
A. 1 1/4 years
B. 1 3/4 years
C. 2 1/4 years
D. 2 3/4 years
40. After decreasing 24% in the price of an article costs Rs.912. Find the actual cost of an article?
42. By selling 50 meters of cloth. I gain the selling price of 15 meters. Find the gain percent?
43. A man can row a boat at 20 kmph in still water. If the speed of the stream is 6 kmph, what is the time taken to row a distance of 60 km downstream?
A. 20/6 hours
B. 27/2 hours
C. 30 hours
D. 30/13 hours
44. A metallic sphere of radius 12 cm is melted and drawn into a wire, whose radius of cross section is 16 cm. What is the length of the wire?
A. 45 cm
B. 18 cm
D. 180 cm
45. A tank 3 m long, 2 m wide and 1.5 m deep is dug in a field 20 m long and 14 m wide. If the earth dug out is evenly spread out over the field, the level of the field will raise by nearly?
A. 0.299 cm
B. 0.29 cm
C. 2.98 cm
D. 4.15 cm
46. Two taps can separately fill a cistern 10 minutes and 15 minutes respectively and when the waste pipe is open, they can together fill it in 18 minutes. The waste pipe can empty the full cistern in?
A. 7 min
47. 3/20 is what percent of 12/25?
A. 42.75%
48. A man can row 30 km downstream and 20 km upstream in 4 hours. He can row 45 km downstream and 40 km upstream in 7 hours. Find the speed of man in still water?
D. 12.5 kmph
49. Two cars P and Q start at the same time from A and B which are 120 km apart. If the two cars travel in opposite directions, they meet after one hour and if they travel in same direction (from A towards B), then P meets Q after 6 hours. What is the speed of car P?
C. 120 km/hr
|
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Ландсберг () — місто в Німеччині, розташоване в землі Саксонія-Ангальт. Входить до складу району Заалє. Площа — 124,74 км². Населення становить ос. (станом на ).
1 січня 2010 роки до складу міста Ландсберг було включено село Оппін.
Галерея
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Офіційний сайт
Міста Саксонії-Ангальт
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303rd Intelligence Squadron (303 IS) is an intelligence unit of the United States Air Force located at Osan AB, South Korea. Also known as "Skivvy Nine," the squadron is a tenant unit of the 51st Fighter Wing, although it is operationally a component of the 480th Intelligence Wing. Most Skivvy Nine operations occur in the Korean Combined Operations and Intelligence Center (KCOIC). Together with the 6th Intelligence Squadron, the 303rd Intelligence Squadron comprises Distributed Ground Station 3 (DGS-3), a component of the Air Force Distributed Common Ground System. Founded 22 November 1950, the 303rd Intelligence Squadron is one of the most historic units in the U.S. Air Force, providing timely cryptologic support since the Korean War.
Mission
History
Lineage
Designated as the 6903rd Security Squadron and activated on 1 May 1970
Redesignated 6903rd Electronic Security Squadron on 1 August 1979
Redesignated 6903rd Electronic Security Group on 1 October 1981
Redesignated 303rd Intelligence Squadron on 1 October 1993
Assignments
Pacific Security Region, 1 May 1970
Pacific Security Region (1 May 1970 – 30 September 1980)
USAF Security Service (later Electronic Security Command), 31 Dec 1972
Electronic Security, Pacific (later Pacific Electronic Security Division, 692nd Intelligence Wing, 692nd Intelligence Group, 692nd Information Operations Group, 692nd Intelligence Group), 30 September 1980
694th Intelligence, Surveillance and Reconnaissance Group (30 September 1980 – Present)
694th Intelligence Group (later 694th Intelligence, Surveillance, and Reconnaissance Group), 1 April 2008 – present
Stations
Osan Air Base, Republic of Korea, 1 May 1970 – present
Awards
Air Force Outstanding Unit Award with Combat "V" Device
1 June 2002 – 31 May 2003
Air Force Outstanding Unit Award
1 May 1970 – 1 April 1971
2 April 1971 – 1 April 1972
1 January 1976 – 30 June 1977
1 July 1978 – 30 June 1979
1 July 1979 – 30 June 1981
1 July 1991 – 30 June 1993
1 October 1993 – 30 September 1994
1 October 1994 – 30 September 1995
1 October 1995 – 30 September 1996
1 October 1997 – 30 September 1998
1 October 1999 – 30 September 2000
1 June 2001 – 31 May 2002
1 June 2003 – 30 September 2004
1 October 2004 – 31 May 2005
1 June 2007 – 31 May 2009
1 June 2009 – 31 May 2011
Republic of Korea Presidential Unit Citation
19 August 1972 – 20 August 1972
References
Notes
Bibliography
External links
Air Force Intelligence, Surveillance and Reconnaissance Agency
Intelligence squadrons of the United States Air Force
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{"url":"http:\/\/www.ask.com\/question\/what-is-the-fraction-one-third","text":"# What Is the Fraction One Third?\n\nThe fraction one third is normally written as 1\/3. It represents one of the three equal parts of a whole. Fractions are numbers that represent part of a whole number. Usually, the whole number is 1, thus the whole is divided into smaller parts.\nQ&A Related to \"What Is the Fraction One Third\"\n 1. Find the fractions on a fraction chart to compare denominators up to 12. Find the lengths of the given fractions on the chart. The fractions that are closer to the left side of http:\/\/www.ehow.com\/how_8165358_compare-fractions-...\n 2 thirds is already a fraction, meaning 0.66667. It looks like the following: 2 --- 3 can also be written as 2\/3. It is equal to 4\/6, 6\/9 etc http:\/\/wiki.answers.com\/Q\/What_fraction_is_two_thi...\n The fraction for one third is 1\/3. Any more questions for me? http:\/\/www.chacha.com\/question\/what-is-the-fractio...\nTop Related Searches\nExplore this Topic\nGiven the shape and size of an iceberg, as little as 10% of its mass may be above the surface. The density of pure ice is about 920 kg\/m\u00b3, and that of sea ...\nOne third is a fraction used to describe a small area or portion of a larger whole. 1\/3 times 3 adds up to 1. The answer is 0.333333. For simplification purposes ...\nThe easiest way to figure fractions is to visualize what you are doing. Draw a circle on a piece of paper. Now the if the fraction is one third, draw three lines ...","date":"2014-03-14 14:05:46","metadata":"{\"extraction_info\": {\"found_math\": false, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 0, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 0, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.8116554617881775, \"perplexity\": 497.0093747070675}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 5, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2014-10\/segments\/1394678693350\/warc\/CC-MAIN-20140313024453-00025-ip-10-183-142-35.ec2.internal.warc.gz\"}"}
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Q: Prove ${\lim\limits_{m \to +\infty}} \ln{\left(1+\frac{r}{m}\right)} = \frac{r}{m}$ How do you prove ${\lim\limits_{m \to +\infty}} \ln{\left(1+\frac{r}{m}\right)} = \frac{r}{m}$, where $0 < r < 1$?
I encountered this problem while trying to reproduce the third to last step in this proof.
A: You don't. As $m$ is inside a limit on the left side of your equality, there should be no $m$ on the right side.
What you can say is that $\lim_{m\to+\infty}\frac{\ln(1+\frac rm)}{\frac rm} = 1$, and you can prove it by studying function $f;x\mapsto \frac{\ln (1+x)-x}{x}$.
A: $$\lim_{m\to+\infty} \ln\left(1+\frac{r}{m}\right) = \ln(1) = 0$$
$m$ goes to infinity, so the resulting limit can't have $m$ in it.
What's used in the proof is that $\ln(1+h) \sim h$, which is the same as saying $\lim_{h\to 0}\frac{\ln(1+h)}{h} = 1$
A: This formula is meaningless: a limit cannot depend on the dummy variable.
What is meant is probably that both sides are equivalent, denoted
$$ \ln\Bigl(1+\dfrac{r}{m}\Bigr) \sim_{m\to\infty} \frac{r}{m}$$
in the sense that
$$\lim_{m\to\infty}\smash[t]{\frac{\ln\Bigl(1+\dfrac{r}{m}\Bigr)}{\dfrac{r}{m}}=1}$$
(which does not imply the difference tends to $0$).
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{"url":"https:\/\/www.physicsforums.com\/threads\/extrapolating-schwarzschild-exterior-coordinate.294133\/","text":"# Extrapolating Schwarzschild exterior coordinate\n\n1. Feb 21, 2009\n\n### Jonathan Scott\n\nAs is well known, the relationship between the Schwarzschild radial coordinate (defined by the proper area of a spherical surface) and the proper distance in the radial direction is very different for the exterior and interior solutions. This makes it difficult to visualize what happens if we attempt to discuss the gravitational effect of a point mass, for example as in Schwarzschild's original paper (and he shows that he is well aware of this in his other paper, describing a sphere with uniform density). In terms of the model he uses in that paper, the exterior of a mass point which is located at the origin of his original coordinate system would have a proper surface area which corresponds to a Schwarzschild radial coordinate of $r = 2Gm\/c^2$ (now known as the \"Schwarzschild radius\"), but at the same time the central point of that same mass point (like the central point of any spherical mass) clearly has a Schwarzschild radial coordinate of 0. This contradiction obviously means that something is wrong, but as there are multiple unphysical assumptions are involved, this does not give a unique explanation of what is really happening.\n\nTo avoid such infinities, one can instead consider a finite mass and shrink it down. To avoid other complexities, that finite mass can take the form of a thin uniform shell. I believe that by Birkhoff's theorem, it should be possible to devise such a shell that has the same field externally as a spherical mass M. However, inside the shell, space is flat (again by Birkhoff's theorem). The proper area of the inside of a thin shell should be equal to the proper area of the outside, which would then correspond to the Schwarzschild radial coordinate of the surface, so the proper radius of the shell would be equal to its Schwarzschild radial coordinate.\n\nIf the shell changes in radius, the internal proper radius changes by the same amount as the Schwarzschild radial coordinate, but the radial proper distance from some point outside it to the surface changes proportionally to the radial component of the metric, $1\/\\sqrt(1-2GM\/rc^2)$. The exterior and interior parts of the range of the Schwarzschild radial coordinate are therefore physically quite different. However, it seems reasonable to attempt to extrapolate the exterior radial coordinate to the centre, by taking the proper radius of the sphere and assuming it to be scaled by the same radial metric factor as just outside the sphere. That is, if you poked a ruler through a hole in the sphere and measured the distance to the centre, through flat space, it might be reasonable to assume that the radial scale factor to convert that proper distance back to an extrapolated exterior radial coordinate would be the same as immediately outside that surface.\n\nThe proper distance to the centre is $r$ so the extrapolated radial coordinate distance to the centre is $r \\sqrt(1-2GM\/rc^2)$ which is the same as $\\sqrt(r (r - 2GM\/c^2))$. Note that this tends to zero as $r$ tends to $2GM\/c^2$.\n\nThis says that if you have a shrinking shell and extrapolate the distance to its centre in terms of the external radial coordinate, using continuity at the surface, then as the radial coordinate of the sphere approaches the Schwarzschild radius, the extrapolated remaining distance to the centre in terms of the external radial coordinate approaches zero.\n\nSkipping some calculation, if you express the radial coordinate of the shell as $r = R+2GM\/c^2$, where $R$ tends to zero as $r$ approaches the Schwarzschild radius, then for small $R$ the extrapolated location of the centre is external Schwarzschild radial coordinate $2GM\/c^2 - \\sqrt(2GMR\/c^2)$.\n\nThis seems to suggest that as such a shell shrinks down towards the Schwarzschild radius, the extrapolated distance to the centre (in terms of a continuation of the Schwarzschild coordinate just outside the surface) shrinks down to zero, which suggests that perhaps Schwarzschild's original solution is merely the hypothetical limit of an otherwise physically reasonable situation.\n\nDoes this seem valid? It obviously doesn't actually prove anything, but it does suggest that the Schwarzschild radial coordinate is nothing like as simple as it might seem at first glance.\n\n2. Feb 22, 2009\n\n### rrogers\n\nYou musn't carry unjustified intuitions into reasoning about GR. Some preconcieved ideas do carry, others don't. This makes up the history of understanding the GR model. It is necessary to understand Schwarzschild mentally (build intuition) before tackling the more complex situations; black holes that are charged, rotating, and both.\nDespite the fact that GR is a neat explanation\/model it is clear that QM has the \"final\" say in the matter. The singularities apparently violate our experimental results that lead to QM. An obvious discrepancy is the uncertainty principle versus the extreme localization at singularities. I don't consider the lack of renormalization serious because I think it's probably a lack of proper mathematical descriptive tools. I could very well be wrong.\nI consider the reality of multiple universe solutions to be decidable by measurements\/constraints we haven't acknowledged; like some cases included\/excluded in ODE's. There seem to be plenty of possibilities that can not be excluded a prior; negative energy regions and such (see the Casmir effect).\nMy favorite universe alternative model (to the big bang) was tossed when the accelerating expanding universe data came in; and rescued by Penrose.\nThe whole theory has a beauty and flexibility beyond anything I imagined when I started studying it. The flexibility lasts until more data and constraints are imposed. To bad QM came along sidetracked the TOE. Reality sometimes bites:)\n\nRay\n\n3. Feb 22, 2009\n\n### Hurkyl\n\nStaff Emeritus\nI should also point out that unless you plan on black hole diving, the exterior solution is all that's relevant.\n\n(P.S. the (exterior) Schwarzschild solution only has $r > 2GM \/ c^2$; the radial coordinate doesn't reach the Schwarzschild radius, let alone continue through to 0)\n\n4. Feb 22, 2009\n\n### Jonathan Scott\n\nIt appears that I need to point out that my model in the original post doesn't involve a black hole. It involves a hollow spherical shell which is just outside the Schwarzschild radius for its effective mass.\n\nWhat I'm pointing out is that in this case (where no black hole is involved) is that a ruler which is poked through the shell into the hollow region (which is flat) will say that in units of the Schwarzschild radial coordinate just outside the surface, the ruler distance to the center tends to zero as the shell radius (either proper radius or as Schwarzschild radial coordinate) tends to the Schwarzschild radius.\n\n5. Feb 22, 2009\n\n### rrogers\n\nOkay, now consider Flamm's Paraboloid http:\/\/en.wikipedia.org\/wiki\/Schwarzschild_metric\nand extend your ruler along the spacelike slice. I think that if you _infer_ the center distance from the local curvature around the constant r shell I think you will find it's nowhere near zero; even as you approach the horizon. An interpretation might be that a, infinitesimal, projection orthogonal the the shell will be pointing in what would be interpreted as a timelike direction by an external observer. Remember the inferred spacelike slices are defined by the observer coordinates, not by the geometry. In other words, although passage to the horizon can seem to occur in finite time to falling observer; it will take forever from the outside stationary frame.\nI haven't done the calculation, and I would rather wait till I have my books and the real computer; a couple of months, I am in transit. If you really think I am wrong, I will try to do the calculation without them, but I almost always get calculations wrong the first time even with them:)\n\nRay\n\n6. Feb 23, 2009\n\n### Jonathan Scott\n\nInside the hollow shell, the proper distance to the center AND the Schwarzschild radial coordinate of the shell both tend to the Schwarzschild radius, matching the curvature. However, just outside the shell, a radial ruler measuring proper distance is becoming infinitesimally small compared with the scale of the Schwarzschild radial coordinate as the Schwarzschild radius is approached. That means that if it is poked through the shell to measure the proper distance to the center, it would measure the expected value, but if the external radial coordinate is extrapolated along the ruler to the center (in a way which preserves at least approximate continuity compared with proper distance), the result approaches zero as the shell approaches the Schwarzschild radius.\n\n7. Feb 23, 2009\n\n### DrGreg\n\nI think you're thinking about it the wrong way round. Don't think of the \"radial coordinate\" distance approaching zero, think of it as the extrapolated ruler distance to the centre of the shell approaching infinity. And the reason it approaches infinity is that your ruler is properly-accelerating away from the centre at an ever-increasing rate (approaching infinity).\n\nNow if you poke your ruler through a small hole in the shell, remember the shell has huge mass concentrated in a very thin thickness, so a huge amount of spacetime curvature occurs within that tiny thickness. If your ruler is strong enough to withstand the huge tidal forces, then, yes, inside the the shell, ruler distance equals coordinate distance, and the ruler is not accelerating at all. (You'll need a very stretchy ruler to be accelerating outside the shell and simultaneously not accelerating inside the shell.)\n\n8. Feb 23, 2009\n\n### Jonathan Scott\n\nThe proper distance from the surface of the shell to the center as measured by a ruler isn't infinite; it is simply equal to the Schwarzschild radial coordinate of the shell. The proper distance from a point above the surface to the surface does of course become very large, but that's not what I'm talking about.\n\nThe Schwarzschild radial coordinate obviously changes scale abruptly at the surface of the shell. However, I was interested in the question of whether it is possible to say approximately where the center of the shell is located in terms of an extrapolated continuation of the external coordinate. One can extrapolate that coordinate by simply making the reasonable assumption that the rate of change of radial proper distance with coordinate distance is continuous through the surface. As space inside is flat, it also seems reasonable to continue that as an approximation to the center.\n\n9. Feb 23, 2009\n\n### rrogers\n\nBack to Flamm's paraboloid. Consider successive rings (shells); truncate the cone at various values of w\/r. Are these as your cases. You are restricted to the static case; on the manifold. The inferred center is not where your stepping is going to take you. i.e. the surfaces of the spheres are not going to get smaller at the rate you expect.\n\nRay\n\n10. Feb 24, 2009\n\n### Jonathan Scott\n\nYes, truncating the cone of Flamm's paraboloid with a flat plane at the bottom is equivalent to my cases. My ruler process is equivalent to taking a ruler, measuring the distance from the center of the truncated plane to the edge, then swinging that ruler down to align with the truncated edge of the cone and projecting it as a straight line, so that the radial coordinate of the lower end gives the apparent radial coordinate of the center as extrapolated from the outside, which will of course lie close inside the cone. A similar method can also be applied where the mass is solid, so the cone is rounded off at the bottom, giving a more continuous join.\n\nI feel that Schwarzschild coordinates are often treated as if they \"really\" describe space, even though they behave in odd ways near a dense mass, and in Schwarzschild's own \"point mass\" case the entire range of coordinates up to the Schwarzschild radius appear to be shrunk into a point, leading to apparent contradictions. I don't think the Flamm's paraboloid picture helps very much, as it is directly expressed in Schwarzschild coordinates itself.\n\nIf we take isotropic coordinates instead, we get a picture that rulers shrink uniformly as one gets towards the event horizon (which of course has a different coordinate value in isotropic coordinates), although of course we still get the same proper area in the limit.\n\n11. Feb 24, 2009\n\n### rrogers\n\nYes, Schwarzchild coordinates and such are just independent scalar fields laid down on a manifold; a description. Then the metric (actually the structure of the manifold) provides a mapping from vectors to covectors; alternately geodesics. The geodesic paths are required to remain fixed no matter how the coordinates\/scalar fields are chosen.\nThe other part of the mapping to our coarse reality is provided by the Einstein tensor. You have to learn a lot to realize how simple and beautiful the whole thing is:) Sort of a contradiction. The only reason for one coordinate system over another is to clearly bring out some features or provide separation of certain symmetries. like Cartesian, Polar, and Elliptical coordinates.\nRambling on and on:)\nRay\n\n12. Feb 24, 2009\n\n### rrogers\n\nA side note: The Schwarzschild coordinate patches (inside and outside) do not compose a \"Atlas\" because they don't overlap; the way real Atlases are required to do. This has led to the obfuscation of thinking that the event horizon is a membrane\/wall of some sort. It is a wall, but only to observation. Like comoving accelerating coordinates; the Rindler coordinate chart. This also has a \"event horizon\" (parts of space time become unobservable) but that is an observer function, and the real spacetime remains flat. Coordinate system alternatives to the Schwarzchild coordinates transition neatly; but are mathematically more complicated.\n\nThis comment is for readers of this thread that are unfamiliar with these aspects, and are interested.\nRay","date":"2018-12-17 10:21:09","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 1, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 0, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.8334711790084839, \"perplexity\": 459.26626080546515}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2018-51\/segments\/1544376828501.85\/warc\/CC-MAIN-20181217091227-20181217113227-00639.warc.gz\"}"}
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## Contents
1. Cover
2. Title Page
3. Contents
4. A Note from the Authors
5. Introduction
6. **PART I** **DEFINING THE PROBLEM**
1. 1 | What Is Your Source of Medical Information?
2. 2 | Does a Gluten-Free Diet Work for You?
3. 3 | Picky Eaters—Orthorexia and the Hygiene Hypothesis
4. 4 | Pitfalls and Perils of a Gluten-Free Diet
5. 5 | Supplements and Probiotics
6. 6 | A Word on Testing—What Do Antibodies Tell Us?
7. **PART II** **WHAT IS GOING ON IN THE GUT**
1. 7 | The Normal Gut and Digestion
2. 8 | The Gut in Disease
3. 9 | The Microbiome
4. 10 | The "Second Brain" in the Gut
8. **PART III** **THE FINGERS ON THE TRIGGER**
1. 11 | Gluten and Nongluten Grains
2. 12 | Carbohydrates and FODMAPs
3. 13 | Drugs
4. 14 | The Double Hit Theory
5. 15 | Inflammation
6. 16 | Intestinal Permeability—"Leaky Gut"
9. **PART IV** **PUTTING ORDER IN THE DISORDERS**
1. 17 | Celiac Disease
2. 18 | Gluten Sensitivity—the New Kid on the Block
3. 19 | Irritable Bowel Syndrome
4. 20 | Inflammatory Bowel Disease
5. 21 | Eosinophilic Esophagitis
6. 22 | Neuropathy
7. 23 | Diabetes
8. 24 | Wheat and Other Food Allergies
9. 25 | Fibromyalgia and Chronic Fatigue Syndrome
10. **PART V** **THE BRAIN-GUT-GLUTEN CONNECTION**
1. 26 | Autism Spectrum Disorders and ADHD
2. 27 | Schizophrenia—Revisiting "Bread Madness"
3. 28 | Brain Fog—Neurology or Meteorology?
4. 29 | The Stress of Holding Back
11. **PART VI** **NAVIGATING A GLUTEN-FREE LIFE**
1. 30 | Nondietary Therapies—the Drug Pipeline
2. 31 | Eating Healthy
3. 32 | Myths and Misconceptions
4. 33 | Food for Thought
12. Acknowledgments
13. APPENDIX A | Diets Through the Ages
14. APPENDIX B | Resources
15. APPENDIX C | Arsenic and Mercury Guidelines
16. APPENDIX D | Guidelines for Eating Gluten-Free
17. APPENDIX E | Scientific Articles and Studies
18. Glossary
19. Index
20. P.S. Insights, Interviews & More . . .*
1. About the Authors
2. About the Book
3. Read On
21. Praise
22. Also by Peter H. R. Green, M.D., and Rory Jones, M.S
23. Copyright
24. About the Publisher
# Guide
1. Cover
2. Contents
3. Chapter 1
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2. iii
3. iv
4. v
5. vi
6. vii
7. viii
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A Note from the Authors
All the information in this book is based on current scientific knowledge about the effect on the body of gluten and the many foods, drugs, and supplements that we ingest. It is derived from an in-depth analysis of current medical literature, extensive clinical experience, patient and professional interviews, as well as ongoing research into the various manifestations and conditions ascribed to gluten-related disorders.
Other medical experts may have differing opinions and interpretations of the medical literature. Wherever pertinent, the authors have attempted to note conflicting points of view on key issues as well as topics that have not as yet been scientifically resolved.
Many of the peer-reviewed articles we have consulted may not be readily accessible to all readers. For this reason, we have not included footnotes for all medical facts and figures. Instead, we have listed good basic review articles and books for different subjects in the appendices.
**All references to the "Center" refer to the Celiac Disease Center at Columbia University.**
NOTE: This book is not a self-diagnosis manual. It is intended to generate informed patients who know what questions to ask of their physicians and how to understand the answers.
Introduction
_The fewer the facts, the stronger the opinion._
—ARNOLD H. GLASOW
Simple solutions are always appealing. In the last few years, gluten has become the ultimate villain—the Wicked Witch, Darth Vader, the Joker, and Hannibal Lecter rolled into one devouring multisystem ravager. It is blamed for draining our brain, blowing up our bellies, invading our nervous system, and setting fire to our guts. A recent bestselling book claimed that: "Brain disease can be largely prevented by the choices you make in life . . ." If only it were that simple.
Almost a third of all American and UK consumers are trying to avoid gluten. By any reckoning, a significant portion of the buying public is focused on the gluten in our food supply and on their plates.
Gluten is implicated in everything from heart disease, neuralgia, sore muscles, exhaustion, "brain fog," headaches, autism, diabetes, arthritis, curious rashes, schizophrenia, dementia, weight loss, fibromyalgia, and irritable bowel syndrome to plain "it makes me feel sick-"itis. Yet most of these claims do not hold up.
In fact, it has become increasingly hard to swallow the story line written by the media as well as friends, family members, and various alternative health care professionals. The menu at this feast of confusion includes wheat and the different proteins within it, genes, germs, fungi, antibiotics, herbicides, enzymes, supplements, and anything else that travels through the intestinal tract. It is a multicourse, multisystem, increasingly nonscientific boiling pot.
Unfortunately, the food industry and general population got onto a gluten-free diet ahead of the medical community, which is now playing scientific catch-up. With the advent of the Internet, everyone has become a medical researcher. This has left room for the public to run away with ideas and point fingers at gluten as the cause for anything and everything.
Gluten has become a media-borne epidemic. **But beware: pseudoscience can be hazardous to your health.**
The Promise of Miracles
_He took a grain of truth and made a loaf of baloney._
—ANONYMOUS
The majority of the information available about the effect of gluten on the body is only partly correct or almost wholly incorrect, and few people have the background or knowledge to question its accuracy. Most of the claims touted by TV hosts, books by "experts," and websites featuring the words _natural_ or _doctor recommended_ do not withstand scrutiny.
Which is exactly what we intend to do. Starting in the gut and working up to the brain and back, we will explore the many claims, conditions, treatments, and diets to diagnose exactly what gluten does and does not cause or cure.
In 1996, Alan Greenspan, then the Federal Reserve Board chairman, used the phrase _irrational exuberance_ as a warning that the market might be overvalued. Today, this same phrase could be used to describe the emotions surrounding gluten, which is being blamed for many of the physical as well as psychological problems people suffer from. And it is becoming increasingly scientifically clear that this focus on gluten as the culprit behind "all that ails ye" is increasingly irrational.
Gluten—the "One Size Fits All" Myth
_There are in fact two things, science and opinion; the former begets knowledge, the latter ignorance._
—HIPPOCRATES
Occam's Razor is a principle utilized in medicine stating that among competing hypotheses, the hypothesis with the fewest assumptions should be selected. It seems to account for the spate of books that point to gluten as the reason behind every pain and drain in the body.
When a patient comes to the doctor—usually with a group of symptoms—the doctor needs to isolate and evaluate each issue separately, not necessarily as manifestations of the same condition. Doctors need to care for patients as a whole, and that requires a sensitive ear as well as appropriate tests and treatments. Holistic medicine is not just about including acupuncture, behavioral therapy, and mindfulness—treatments that we recommend to some patients—but isolating, testing, and treating each patient for every individual problem they have.
It is time to look at gluten differently and offer reliable science and guidance in navigating your way to a healthier and symptom-free life.
**Part I** exposes the many misconceptions surrounding gluten. The gluten-free diet works for many and is necessary for those with celiac disease. We now understand a great deal more about why it works, as well as the benefits and pitfalls of a gluten-free lifestyle. For others, the diet does not work—or works only for a short period of time—and understanding the reasons for that can help you reboot your health.
Where you get your medical and health information can determine whether you are being properly diagnosed, treated, and monitored on a diet that is not necessarily healthy. This includes taking a close look at your eating habits—you may be eliminating the wrong foods or your household may simply be too clean for your own immunological good. Most exclusion diets come at a price; you should know the precise value of what you are sacrificing.
We will examine the various temporary or expedient remedies that are being prescribed, including probiotics and supplements, to expose the underbelly, as it were, of this unregulated industry. We will explain the key tests that are used to analyze nutritional issues and symptoms that are often blamed on gluten but may mean something entirely different.
Having eliminated some of the myths, in **Part II** we will dive into the subterranean world of your gut, its many inhabitants, and how it communicates with your brain. Four of the hottest research topics today are the brain, the microbiome, inflammation, and the food we eat, gluten in particular. We have found new and intriguing connections between them.
We begin at the mouth, where food, drugs, supplements, tobacco, alcohol, "bugs" of all types, and anything else we knowingly or inadvertently swallow enter the body and travel through the digestive tract. But this is where the story gets interesting. For many, digestion is a torturous journey that creates gas, bloating, and pain in the gut. For others, food and other ingested substances create inflammation and multisystem disorders that radiate throughout the body.
Your gastrointestinal (GI) tract is in constant communication with your brain. Much of the story is actually narrated by our brains and the "second brain," the enteric nervous system in the gut. Thus, a dynamic interaction of multiple factors and "conversations" in the body determines not only your day-to-day but also your long-term health. In this section we will start to explore what happens when the gut talks to the brain and the brain answers back, and what each person can do to moderate this internal dialogue.
**Part III** examines the different elements that cause symptoms often attributed to gluten alone. This includes other portions of wheat and FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols)—an acronym for the many dietary culprits in the carbohydrate family. Drugs, infections, and other illnesses also affect the gut-brain axis and disturb the microbiome. Many cause a "double hit"—the first infection or illness predisposing the body to a sensitivity to gluten. This will come as no surprise for anyone who has gotten turista or a traveler's infection; the bathroom journey often continues for months after they return. A double hit may even set the stage for schizophrenia.
This takes us to the role of inflammation and the so-called leaky gut, two largely misunderstood aspects of the body's defense system. They are blamed for many things they do not do—and implicated in others that we are just beginning to understand.
**Part IV** focuses on the specific conditions where gluten plays a part. Each section clarifies and explains the role and relation of diet, inflammation, antibodies, genes, germs, and gut-brain cross-talk, as well as the latest treatment options.
In **Part V** we look closely at the brain and separate pseudoscience from the important studies being conducted on serious and damaging conditions like autism and schizophrenia. We will look at the relation of gluten to "brain fog" and the potential long-term effects of the gluten-free diet on a person's mind and behavior. It is becoming increasingly clear that the constant need to "hold back" when eating—one of the most normal and usually pleasurable aspects of daily living—may create additional stress on both the brain and the body. Putting yourself on a restrictive diet—any diet—may have unintended consequences on the stress circuits in your brain.
For those committed to a truly gluten-free lifestyle, finding the right balance of nutritional foods is crucial, and **Part VI** will help to guide you there. This section contains the latest updates on nondietary therapies for celiac disease (the pharmaceutical products being developed to supplement or eliminate the need for a gluten-free diet), as well as further thoughts on what the science about gluten means for the future of our gut-brain health.
With a growing array of gluten-free products hitting the market almost monthly, it is important to know what is safe, what is hidden, and what are some of the nongluten ingredients in these products that are worse for the body than gluten. We will look at "food glue"—processed food doesn't grow that way—as well as the many myths that still surround a gluten-free diet.
**Gluten is a piece in many medical puzzles but is the ultimate answer to only a few. We will help you determine if it is an answer to yours.**
_Science, my lad, is made up of mistakes, but they are mistakes which it is useful to make, because they lead little by little to the truth._
_—_ JULES VERNE, _JOURNEY TO THE CENTER OF THE EARTH_
_The scientific theory I like best is that the rings of Saturn are composed entirely of lost airline luggage._
—MARK RUSSELL
_Some people think that the truth can be hidden with a little cover-up and decoration. But as time goes by, what is true is revealed and what is fake fades away._
—ISMAIL HANIYEH
PART I
Defining the Problem
It started with an avalanche of bad things happening. Kind of an achiness and gluey feelings in my joints all the time, and it just started to escalate. A mysterious fatigue where I just felt drugged.
The joint stuff was so bad I couldn't walk upstairs and couldn't roll over in bed without hurting. The final straw was when I developed vertigo, which got me to go to the doctor. I thought, _I'm too young for this to be going on._
She did all these tests and scans, a neck X-ray, and everything was normal. She found "nothing wrong" with me. And yet I clearly was not functional.
Someone recommended removing things from my diet to see if it would help, and I started with wheat, dairy, sugar, and eggs. By the end of that first week I started to feel better and the vertigo went right away. It was literally like the tide going out. I was very disciplined and reintroduced each food, eggs first, then dairy, sugar, and wheat. When I reintroduced the wheat the back pain reappeared instantly.
(JILL, 50)*
I know a ton of people who don't eat gluten for a variety of things—or nothing.
(ANNABELLE, 33)
The gluten hysteria is killing the credibility of people with celiac disease. Because people think it's a fad thing, that we're watching our weight or we think it is healthier, that we're choosing this way of life, and they're discounting the fact that it's a medical illness. You'd think we'd be going in a different direction. We've gone a few steps back.
(ILYSSA, 39)
What Is Your Source of Medical Information?
_Science is a way of thinking much more than it is a body of knowledge._
—CARL SAGAN
_I observe the physician with the same diligence as the disease._
—JOHN DONNE
I understand that I don't really know where I am on that gluten spectrum because I haven't had any tests. And the other stuff is treated like hocus-pocus. So individuals draw their own wacky conclusions. I'd really like to know what a scientist thinks about it and what I should do.
(JILL, 50)
There are many sources today for health information and many reasons individuals do not go to a doctor to get it. Many people will see a doctor only in order to resolve a physical ailment that has either disrupted their life, will not resolve itself in the over-the-counter (OTC) drug aisles of the pharmacy, or because their spouse/child/friend/sister, etc. insisted that "it's time to get to the bottom of this." In fact, many do not see a doctor until their symptoms have seriously affected their ability to work, travel, or sleep. And even then, some arrive with a list of answers before asking the physician what they think is the matter.
When was the last time you:
• Self-diagnosed from Internet information?
• Self-treated with OTC drugs and/or diet?
• Gave a doctor a diagnosis _before_ you were examined?
Some people self-diagnose or seek alternative practitioners when medical tests fail to reveal a cause for ongoing symptoms and/or prescribed drugs fail to cure them. And many of them accept a food-related "diagnosis" as the solution to the problem. Given the current focus on foods as cause and cure, far too many roads lead to gluten. If you are looking to prove that gluten is the cause of your physical symptoms, you will undoubtedly find ammunition to justify this conclusion. As the scientist and mathematician John Lubbock noted: "What we see depends mainly on what we are looking for."
But if you type "gas, bloating, and fatigue" into your browser, you will find more than 90 other medical and psychiatric conditions on WebMD that cause the same symptoms. And your health depends on isolating, testing for, and treating the correct underlying condition.
My Doctor "Pooh-Poohs" Food Intolerances
When I don't eat gluten, I feel fine; when I do eat it, I don't. My doctor did all these tests and scans and X-rays, and everything was normal. She didn't say "it is in your head," but there was this long "Hmmmm. I don't have a diagnosis, but I think it's all about gluten."
(NANCY, 44)
Some physicians, aware of the popularity of the gluten-free diet and the susceptibility of people to dietary trends, dismiss nonceliac food intolerances as a legitimate cause for concern. These doctors may be dismissive of symptoms and therefore not interested in getting to the root of the problem, making diagnosis more difficult.
Doctors do not rely on Internet blogs, magazine articles, or website write-ups of scientific papers. They read and analyze the papers and base their diagnoses on peer-reviewed understanding of a condition. Medicine is a plastic science—studies change the understanding of diseases and their mechanisms regularly—so doctors treat conservatively rather than accepting what they may consider a diet that has no good "data" behind its efficacy. For this reason, some may believe that you are on a gluten-free diet for no real scientific reason.
Nevertheless, diagnosis is critical for social acceptance and accommodation—it confers legitimacy on a symptom or the patient. Thus, many people who feel marginalized by health care professionals turn to alternative practitioners to legitimatize their symptoms and solutions. This in turn undermines biomedical science and advocates self-diagnosis—an individual can avoid foods without a doctor's diagnosis. This can backfire if your problem has no relation to the food(s) you are eating. And if that is the case, you are postponing a proper diagnosis that might alleviate your symptoms.
Listening to the Media and the Masseuse
_Many readers do not go beyond an article's headline or its opening paragraph; it is also difficult for laymen to critically assess statements coming from apparent voices of authority._
—JEROME GROOPMAN, M.D., _HOW DOCTORS THINK_
Health advice is readily available on the Internet, TV shows, and from nutritionists or unlicensed "dietitians," health gurus, masseuses, bloggers, newspapers, and magazines. While the advice from alternative sources can be helpful in some cases and generally ensures a sympathetic ear, it should not be a substitute for or confused with medical advice from your physician.
You Rely on Internet Advice
My patient arrived with a fistful of material from the Internet, a list of tests she wanted to confirm the diagnosis she'd come to of her problem, and possible drugs to treat it. I asked her why she bothered to consult with a doctor.
(DR. F)
There are many medical resources on the Internet, but it can be hard to understand and interpret research studies. PubMed Central, an archive of biomedical and life sciences journal literature at the U.S. National Institutes of Health's (NIH) National Library of Medicine, posts the abstracts of all research studies (essentially the summary of what the study set out to do and its results and conclusions). While some studies are free, obtaining full-text articles that contain a discussion section is often difficult without academic access and a subscription. This key section outlines all the limitations of the study (e.g., a very small group was tested, requiring confirmation in a larger study; participants dropped out because of symptoms; a drug or test caused serious side effects in a significant amount of people, etc.) that are crucial for assessing its meaning.
Magazine articles often trumpet a study, drug, or breakthrough that comes on the heels of another less-publicized study with opposing or lukewarm results.
Some Listserv sites distribute messages with Q&A sections to a specialized electronic mailing list. The advice on these sites ranges from practical travel and eating-out advice to testing analysis. The former is helpful; the latter is dangerous, as it comes mainly from patients.
Some people rely on the Internet more heavily because it is often financially difficult for them to see a doctor until a medical crisis sends them to the emergency room. Nevertheless, most major medical centers today have excellent websites based on the different specialties and conditions they treat. These specific sites offer reliable medical guidance and can help you determine if a doctor's visit is essential and help you to find appropriate resources.
Conflicting advice is found online, and many people read articles that agree with what they have already decided is the solution. Many are looking not for medical information but advice and treatments from the articles and "experts" that confirm their own prejudices on the subject.
The Internet offers everything from PubMed Central to preposterous—it is not a place to go for a diagnosis or treatment.
You "Test" Online
Alternative tests for various food intolerances are available online. While the less said about them the better—you are paying a great deal of money for something that is scientifically meaningless—the reasons behind this statement deserve some explanation.
A biological marker for gluten sensitivity does not currently exist, although researchers are working to find one. (See chapter 18, "Gluten Sensitivity.") Despite that fact, fecal (stool) tests for this condition are available online along with other fecal tests for various food intolerances and allergies. The same "lab" also advertises a DNA genetic test for nonceliac gluten sensitivity (NCGS) even though no specific genes have been isolated for the condition.
Additionally, the markers they claim will determine the "diagnosis" (IgG antigliadin antibodies) are neither sensitive nor specific enough to diagnose either celiac disease or gluten sensitivity. (See chapter 6, "A Word on Testing.") It has been shown that 20 percent of non-gluten-sensitive individuals also have elevated levels of these antibodies for no apparent reason, which puts any "diagnosis" by these tests in serious doubt.
The danger of getting your medical information and diagnosis from what amounts to a self-test is that your problem may not be gluten sensitivity and you fail to get a proper medical evaluation, thereby missing a serious illness that then goes untreated and may progress.
You Do It "Naturally" with Alternative Sources
Inundated by headlines and articles exposing the dangers in our food supply, the side effects of drugs, the rise in hospital-borne infections, bacterial resistance to antibiotics, and many other environmental dangers, many patients want a more "natural" approach to health care. Others feel that they understand their bodies better than their doctors. While there may be some truth in this thinking, it can also border on the delusional. (See chapter 3, "Picky Eaters.")
Many people find their thinking about food and fatigue issues is more simpatico with that of a chiropractor, trainer, nutritionist, or acupuncturist and follow their dietary and supplement advice. Some of these practitioners push products that they claim will cure gastrointestinal issues, cleanse the body, and enhance your health, but are usually the modern version of snake oil—a quick quack remedy or panacea. The majority of these products will do little more than help your wallet lose weight, and some of them can be truly dangerous. (See chapter 5, "Supplements and Probiotics.") This can make patients fearful or unwilling to tell their doctors about the supplements, herbs, and potions they take in addition to prescription medications. The doctor is then unable to unravel a drug/supplement interaction that could be lethal and would be immediately apparent if the patient had come clean.
Doing it "naturally" or on your own can compound issues, especially when there are major problems or psychological issues.
Why Individuals Don't Go to Doctors
_Whenever I read anything, it says, "Consult your doctor before doing any exercise." Does anybody do that? I kind of think my doctor has people coming in with serious problems. I don't think I should be calling him and saying, "Hi, this is Rita, I'm thinking of bending at the waist."_
—RITA RUDNER
There are various reasons people do not rely on doctors for medical advice and treatment, but food and lifestyle issues seem to raise a red flag on both sides of the desk. Many with unresolved symptoms assume the doctor trivializes them as nonserious and therefore they avoid the discussion. Others state that they think the doctor views a gluten-free diet as a lifestyle rather than a health decision. And if going gluten-free is not to treat celiac disease, a wheat allergy, or another diagnosed condition but gives you a better quality of life, you both may be right.
My Doctor Doesn't Listen/Have Time
My doctor said, "You have celiac disease. Go on a gluten-free diet and I'll see you in six months." That's when we got really frustrated and really lost. My doctor sent me home without any guidance.
(ARLENE, 18)
Admittedly, not every doctor is a talented listener. Understanding the experience of illness comes with practice, and some physicians need to be reminded that the antibodies on the lab sheet are attached to a person. But there are two sides to this dialogue, and patients often fashion their narratives to give the doctor what they think the doctor wants to hear. The result can be unsatisfactory for both parties.
Allergies and food intolerances—along with celiac disease and other autoimmune diseases—have mushroomed in the past decade for reasons that are still being actively researched. Many physicians are therefore still examining the dietary and potential microbiotic aspects of their specialties, so you should request a professional referral for dietary counseling if your diagnosis requires a restricted diet.
Food restriction is currently the only treatment for those with celiac disease and food allergies, and a major component of others, such as diabetes and kidney stones. Trained and registered dietitians have the time to explore the nuances of these various diets, and you should turn to them for expert advice after—not before—diagnosis.
You Got Off on the Wrong Floor
_Where you stand depends on where you sit: your specialty can affect, even determine, your position._
—JEROME GROOPMAN, M.D., _HOW DOCTORS THINK_
Many people look to alternative sources for a diagnosis because they feel that their doctor "sees me only as someone with irritable bowel syndrome." Diagnoses stick until it can be proven that you have something else—and negative test results often leave people categorized and displeased with the answer. Patients with GI symptoms usually have GI issues; those with neurological symptoms usually have neurological issues. Doctors are taught in medical school that "the common occurs commonly." But frequently GI issues can cause neurological symptoms, as is seen in celiac disease and other malabsorption conditions that cause vitamin and mineral deficiencies leading to _ataxia_* (lack of coordination) and other gut-brain reactions.
If you need a raincoat, you won't find it in the shoe department. It is often necessary to run different tests or seek out a different specialist who is willing to change his/her position on an issue.
Financial Issues
The insurance and financial landscape of medicine is a reason cited by some people in the U.S. to explain their avoidance of medical care. If you continue to have unresolved symptoms and are self-diagnosing and self-treating without the benefit of medical testing, you should seek out a clinic or practice that will accommodate your needs, before an underlying condition sends you to the emergency room.
Where you get your medical information will ultimately determine your long-term health.
Ask yourself if you are seeking alternative sources of medical information mainly to justify a gluten-free diet as the answer for ongoing symptoms. As 19th-century French physiologist Claude Bernard said, "It is what we think we know already that often prevents us from learning."
Does a Gluten-Free Diet Work for You?
You have to decide that food is no longer the focus of your life.
(DINA, 28)
It's harming people with celiac disease because people are choosing the "diet of the month," and it's really impacting the people who medically are on a restricted diet.
(JEAN, 37)
Are You a PWAG?
PWAGs (pronounced _pee-wags_ ) stands for people who avoid wheat and gluten. It is a term coined by a group of gastroenterologists to encompass the huge numbers of patients they have been seeing who go on a gluten-free diet because of what they describe as an intolerance to wheat products in the absence of celiac disease.
Many of these patients have a higher prevalence of the genes associated with celiac disease (the HLA-DQ typing). And one study showed that PWAGs had a higher number of medical diagnoses for other food intolerances and _small intestine bacterial overgrowth (SIBO)_.
If you are a PWAG, there are many reasons you made this decision—disease treatment, symptoms relief, perception of a healthier way to be, recommended by a health care professional, etc. And an equal variation in its success.
First and Foremost—What Is Gluten?
_Gluten_ is the general term used to describe the storage protein of wheat. Wheat is approximately 10 to 15 percent protein—the remainder is starch. Gluten is what remains after the starch granules are washed from wheat flour. The gluten fraction that is most studied in celiac disease is _gliadin_ , but there are other proteins that chemically resemble _gliadin_ in rye (secalins) and barley (hordeins). These proteins are not strictly glutens, but are generally included in the term. There are other proteins in wheat (see chapter 11, "Gluten and Nongluten Grains") that may also be problematic for PWAGs and are part of the complex reason why the diet works for some, only partially for others, or not at all.
Why a Gluten-Free Diet Works
**You have celiac disease and the diet fixes the inflamed intestine.**
A gluten-free diet is a lifesaver for those with celiac disease and is a proven medical treatment. If followed carefully, it resolves symptoms, rebuilds nutritional stores depleted by a damaged intestinal lining, and, in children, rebuilds bone loss caused by malabsorption of calcium. (See chapter 17, "Celiac Disease.")
**You have nonceliac gluten sensitivity (NCGS) and the diet relieves symptoms (neurological, skin, gastrointestinal).**
Many individuals who feel or have been told that they have NCGS—again, there are currently no diagnostic tests for this condition—find relief with gluten withdrawal for neurological disorders, skin rashes, and GI symptoms such as gas and bloating. (See chapter 18, "Gluten Sensitivity.")
**You have irritable bowel syndrome (IBS), and elimination diets have resolved some or all of the gas, bloating, and pain.**
IBS may be due to a sensitivity to a food that most tolerate without problems. It is a diagnosis of exclusion—other tests having proven negative—and dietary restriction can be successful, often only partially, for those patients with carbohydrate intolerances. (See chapter 12, "Carbohydrates and FODMAPs," and chapter 19, "Irritable Bowel Syndrome.")
**You just think it works so it does.**
A placebo is not only the archetypal sugar pill but anything that impacts a patient's expectations.
Why a Gluten-Free Diet Does Not Work
**The main reason a gluten-free diet does not work is that gluten is not the issue and/or you may be missing treatment for another disease**.
This may include:
• SIBO
• Fructose intolerance
• Lactose intolerance
• Other food intolerances
• Microscopic colitis
• Gastroparesis (a condition where the stomach cannot empty properly)
• Pelvic floor dysfunction (weak muscles in the pelvic floor, often caused by childbirth)
• A problem related to a medication you are taking
After a thorough medical evaluation, we find that many PWAGs have a variety of conditions and may, in fact, be able to eat gluten again, symptom free, with proper diagnosis and treatment.
**You may be on a gluten-free diet but other types of carbohydrates, e.g., fructose, are the problem.** (See chapter 12, "Carbohydrates and FODMAPs.")
**You're under the impression that the diet is a cure-all for many health-related ailments.**
A survey by _Consumer Reports_ showed that 63 percent of North Americans think that a gluten-free diet improves physical or mental health, and 33 percent buy gluten-free products because they believe these foods will improve digestion and gastrointestinal function. Unless you have celiac disease or a specific carbohydrate intolerance, a gluten-free diet will not work for either of these issues.
The diet does not work to lower cholesterol or strengthen your immune system, even though many people believe it does.
**The diet is disrupting your intestinal flora—the microbiome—and causing symptoms.**
Restrictive diets—gluten-free, low-FODMAP—have been shown to reduce the richness and diversity of our intestinal microbiota, which in turn may cause persistent symptoms in patients with celiac disease and possibly other conditions. While it is unclear exactly what this disruption means or the long-term effects, it is generally believed that a diverse microbiome is healthier. While there is no one "healthy" microbiome, the studies on this should be watched. (For more, see chapter 9, "The Microbiome.")
People should make every effort to diversify their diets. This may be particularly important as people age. Aging is known to be associated with a reduced diversity of the gut microbiome, and this may lead to a compromised intestinal barrier and increased susceptibility to infectious diseases and infections.
If a disrupted microbiome is a side effect of a gluten-free diet, these consequences should be considered before you embark on a gluten-free regimen unless you have celiac disease.
Will It Work in Other Ways?
**Can I lose weight on a gluten-free diet?**
Some go on a gluten-free diet to lose weight. This works if you exclude but do not replace wheat as the main carbohydrate. In animal studies a gluten-free diet prevented the development of obesity and metabolic disorders. BUT, while gluten was eliminated from the diet, the mice were not fed replacements with gluten-free products. The no–white food or Atkins diet (no bread, pasta, potatoes, rice, cake, or cookies) will usually ensure weight loss but can be nutritionally inadequate if enough fruit and vegetables are not substituted for those carbohydrates. It is also hard to sustain.
**Will I have more energy?**
Unfortunately, if you do not have celiac disease, a gluten-free diet is not likely to make you the Energizer Bunny. Although many people insist that they feel logy or tired after eating gluten, there is little scientific evidence to support this. Postprandial fatigue (which occurs after eating) is common, especially after a large meal, when various hormones are released to aid digestion. These hormones act on the brain when released in the gut and cause the fatigue many report.
**Will I become a world-class athlete—or will thinking so make it better?**
The use of a gluten-free diet by famous people has enhanced its appeal. Publicized by Hollywood stars, it has also been endorsed by several high-profile athletes. The reasons behind this speak to our infatuations with celebrities and fad diets, and wanting to believe something enough to think it works—the placebo effect.*
An Australian study of nonceliac athletes, including eighteen world and/or Olympic medalists who followed a gluten-free diet 50 to 100 percent of the time, reported that self-diagnosed gluten sensitivity was the primary reason for adopting the diet. The leading sources of information on the gluten-free diet were online, a trainer/coach, and other athletes. Neither the diagnosis nor treatment was based on medical rationale, merely the perception that removing gluten provided "health benefits" and an "ergogenic edge."
If you do not have chronic symptoms that require medical treatment, the gluten-free diet can be both placebo and minefield. We advise staying tuned to your local news for updates—the latest dietary trend may be announced on _Entertainment Tonight._
If you are looking for more realistic scientific advice, the following chapters will explore what taking gluten and other foods out of your diet will really do to and for your body.
Picky Eaters—Orthorexia and the Hygiene Hypothesis
_Water surges, only to overflow._
—CHINESE PROVERB
Things turn into their opposites when they reach their extremes. And "healthy" eating is moving in that direction.
There are good reasons that we have food on our minds. According to the U.S. Centers for Disease Control and Prevention (CDC), half of all Americans have a chronic disease or condition such as high blood pressure, heart disease, or type 2 diabetes and have been instructed to think about fat, sugar, and/or salt. More than 9 percent have diabetes and must monitor their sugar/glucose intake multiple times every day. At least 35 percent of Americans are obese and cycle through different diets, gaining and losing weight every year. About 1 percent has celiac disease and avoids gluten. Up to 15 million people in the U.S. have a food allergy, estimated to affect 1 in every 13 children under the age of 18. A study by the World Health Organization reported that noncommunicable diseases were responsible for 86 percent of all deaths and 77 percent of the disease burden in the European Region and noted that this primarily included conditions caused by high blood pressure and cardiovascular diseases. Three of the priority interventions recommended were dietary.
Unfortunately, the National Eating Disorders Association notes that 20 million women and 10 million men suffered from a clinically significant eating disorder at some point in their life, including anorexia nervosa, bulimia, binge eating, or an eating disorder not otherwise specified. In the UK, a National Health Service (NHS) study estimated that more than 725,000 people are affected by an eating disorder and that eating disorders can affect people of any age.
The current obsession with food is not surprising; mankind has been on some kind of restricted diet—by need or choice—since the beginning of time (see Appendix A), but for some it has taken a turn into the obsessively unhealthy.
Orthorexia Nervosa—Healthy Eating as a Disease
_Food is an important part of a balanced diet._
—FRAN LEBOWITZ
I don't like anything "lite"—that's not my thing. I have one friend who goes to a chiropractor who tests you, and they take one thing after another out of your diet. He evaluates what you eat and decides what foods your body is not tolerating. She's currently living on kale.
(ILYSSA, 39)
The focus of the press and social media on "healthy eating" as the source of, or cure for, disease has taken hold to the point of creating a new condition termed _orthorexia nervosa._ Individuals eliminate one healthy food after another (gluten, corn, soy, meat, dairy, all fats, carbohydrates, etc.) in the belief that these foods are "unhealthy"—until they are barely receiving adequate nourishment. It can reach the point of anemia, bone loss, vitamin depletion, and malnutrition.
The condition is not as yet recognized in the _DSM-V_ (the _Diagnostic and Statistical Manual of Mental Disorders,_ used professionally to diagnose psychiatric disorders) but is being seen by many doctors evaluating patients for symptoms related to nutritional deficiencies.
The term _orthorexia_ was coined by Dr. Steven Bratman from the Greek _ortho_ (correct or proper) and _orexis_ (hunger or appetite). Unlike in anorexia, those with orthorexia focus on the _quality_ rather than the _quantity_ of food eaten. They start removing foods because they do not feel well, and when they do not feel better, they remove more and more until they are on an overly restricted and generally unhealthy diet.
Are You Orthorexic?
• Have you eliminated entire food groups from your diet? (Gluten, dairy, corn, and soy are the usual suspects as well as red meat, carbohydrates, etc.)
• Three or more food groups?
• Do you constantly worry about which foods may be unhealthy?
• Do you feel guilty when you eat food you consider unsafe?
• Do you have problems finding healthy foods?
• Do you have ritualized eating patterns?
• Are you anxious when eating out or traveling?
• Have you started avoiding lunches, dinner dates, and catered parties?
• Do you lecture your friends and family about unhealthy eating?
• Do you read medical journal articles about digestion, carbohydrates, protein, etc.?
• Do you challenge others who disagree with your food choices?
• Do you wish that you could just eat and not worry about the quality of foods?
• Do you have symptoms that do not fit any medical diagnostic category for which you blame gluten, dairy, or a specific food?
Orthorexia affects a small percentage of individuals, but is yet another food-related disorder that has evolved from the increased focus on food as cause and/or cure for symptoms and disease.
The Hygiene Hypothesis—Are We Too Clean for Our Own Immunological Good?
My daughter-in-law sterilizes everything that goes into my grandson's mouth. I raised four children on the 10-second rule—if it's been on the floor for less than 10 seconds, pick it up and eat it—and not one had an allergy or food issue. Now we're boiling the baby's fork and spoon after it comes out of the dishwasher, and every other person's child is allergic to peanuts or dairy or gluten. Something's wacky here.
(GERI, 64)
The diagnosis of allergies and autoimmune diseases has risen dramatically in the last few decades. While there are many underlying and complex mechanisms at work, a great deal of scientific interest is being focused on the "hygiene hypothesis." This states that childhood exposure to germs and certain infections helps the immune system develop normally, and that excessive cleanliness interrupts this process.
In other words, the young child's environment can be too clean to effectively challenge a maturing immune system. Frequent and repeated exposure to a variety of _microbial antigens_ and infections may lead to a more robust, i.e., healthier immune system.
While it is well documented that avoiding germs helps prevent the spread of infections, the hygiene hypothesis suggests that we have taken this too far. And with the advent of antibiotics and the great public health efforts of the last century, the immune system is no longer required to fight germs as actively as in the past.
Scientists based this hypothesis in part on the observation that, before birth, the fetal immune system's "default setting" is suppressed to prevent it from rejecting the mother's tissue. This is necessary before birth—when the mother is providing the fetus with her own antibodies. After birth the child's own immune system must take over and learn how to fend for itself. But the extremely clean household environments often found in the developed world do not provide the necessary exposure to germs required to "educate" the immune system so that it can learn to launch its defense responses to infectious organisms.
A critical part of this evolution is orchestrated by a child's developing microbiome, and a lack of diversity—reduced by exposure to fewer germs and infections—derails the period of immune growth after birth.
The hygiene hypothesis has been implicated in the growing number of people with allergies, autism, and autoimmune diseases.
MacDonald's Farm Had the Right Idea?
Since the hypothesis was first proposed by epidemiologist Dr. David Strachan in 1989, several studies have revealed a reduction in the sensitivity to allergens and atopic (skin) disease in children exposed to farm environments, those who have animals in their homes, and in those who have attended day care at an early age and were exposed to other children's infections.
Several lessons have come from studies comparing populations in Russian Karelia and neighboring Finland. These two populations live in completely different socioeconomic circumstances—they have one of the largest socioeconomic discrepancies in the world—yet share similar diets and genetic backgrounds.
The researchers determined that the children in Karelia are exposed to a large variety of different microbial infections that are significantly less frequent in Finnish children. Starting in 1999, numerous studies on autoimmune and allergic diseases show an incidence of type 1 diabetes that is six times lower in Russian Karelia. The incidence of celiac disease is 1 in 496 in Karelia and 1 in 107 in Finland using identical criteria. These studies appear to indicate that environmental factors play a role in our immune reaction to microbes and in the development of allergies and autoimmune conditions. While all of the factors initiating these conditions have not been identified, the hygiene hypothesis offers an intriguing approach.
The mechanisms by which microbes can reduce the development of autoimmune disease are not well understood. They are only part of a larger autoimmune and allergic response that is also affected by your genetic makeup, and a variety of factors that occur over a person's lifetime. It cannot be considered the sole determinant of a disease.
Before people start feeding their children from the floor or allowing them to share the dog's bowl, it should be stressed that many researchers feel that the hygiene hypothesis is far too simplistic an approach to understanding the causes of celiac disease or any other autoimmune disease.
This hypothesis does focus attention on the impact of microbes on disease, hopefully without discouraging good hygiene practices.
BOTH ORTHOREXIA AND the hygiene hypothesis are extreme examples, yet they illustrate what can happen when individuals become mesmerized by the message, and the human body is deprived of the many forms of nourishment it requires to develop, grow, and flourish. Both advanced in the name of "health."
What we deprive our body of is every bit as important as what we feed it.
Pitfalls and Perils of a Gluten-Free Diet
_Sooner or later everyone sits down to a banquet of consequences._
—R. L. STEVENSON
A gluten-free diet gives with one hand and takes away with the other. For individuals with celiac disease, it truly is a lifesaver yet requires constant vigilance and restrictions. Others find it gives them relief from symptoms like gas and bloating while taking many essential nutrients from their diets. The "giving hand" can also contain heavy metals, toxins, and excess fat and sugar. The "taking hand" dips into pocketbooks for more costly foods. The scale can get very unbalanced if individuals are not aware of the health risks in a gluten-free diet that are often hidden behind the hype surrounding it.
Studies on the real long-term effects of a gluten-free diet on the body and the brain are being published with increasing regularity since the awareness of celiac disease and popularity of the diet in the general public began about a decade ago. While many of the studies are on celiac disease patients who must follow a strict gluten-free diet, research has exposed some troubling issues that affect everyone following the diet.
Mostly we are doing it because we realized how good we can feel and believe it is healthy for us.
(ARIELLE, 33)
A gluten-free diet is many things to many people, but for most it is far from healthy.
Healthy or Hazardous?
Nutrition
Going "gluten-free" may cure symptoms for some, and is a necessity for those with celiac disease, but eliminating gluten from your diet also removes much of the fiber and some essential vitamins and minerals from your food supply.
Wheat, rye, and barley are flavorful, vitamin- and fiber-filled grains. Ironically, manufacturers also regularly fortify wheat flours as well as the cereals, breads, and other processed products made from them with the vitamins and minerals that might have been removed during processing. Conversely, gluten-free foods, with a few exceptions, have not caught up with this fortification. Some, like quinoa, may not need this as much as rice flour.
The breads, cereals, cookies, cakes, and snacks with gluten-free grains also put people at risk for potential problems with excess fat, sugar, and salt. These ingredients are used to bind gluten-free products—gluten is the "glue" that holds breads and cakes together—and to make them as tasty as their wheat-filled counterparts.
People with celiac disease who embark on a gluten-free diet without the help of a nutritionist can easily develop vitamin and mineral deficiencies, especially iron and the B vitamins. Calcium can also be deficient if dairy is restricted. This is a double problem because many start the diet already suffering from malabsorption due to the damage to their small intestine. Missing a favorite sweet or breaded dish, they often make poor food choices to satisfy a craving.
Lost fiber and nutrients need to be replaced with fresh fruits, nuts, beans, vegetables, and other gluten-free grains (e.g., quinoa, millet, buckwheat, sorghum) to maintain a "nutritional" diet. If you are going to take gluten out, put its nutritional value back in. (For more, see chapter 31, "Eating Healthy.")
Heavy Metal (Not of the Musical Variety)
Rice, a common substitute in a gluten-free diet, may contain high levels of arsenic as well as cadmium and mercury. Other heavy metals (e.g., tin, lead, and mercury) have also been found both in gluten-free food and flours and the people ingesting them.
While the raised levels do not approach toxic levels, there should be a warning. A greater number of patients with celiac disease develop neurological symptoms over the ensuing years after starting a gluten-free diet. While this has been attributed to the development of a new autoimmune disease, the recent concern about the occurrence of metals such as lead, mercury, and arsenic in people on a gluten-free diet may in fact be a manifestation of heavy metal toxicity.
_Arsenic with Your Rice?_
Arsenic occurs naturally in the environment and is also released into soil and water by fertilizers and pesticides as well as manufacturing practices. It is absorbed into anything growing in these environments—in particular, rice absorbs arsenic more readily than many other plants. The Environmental Protection Agency (EPA) published a "hazard summary" about arsenic in 2012 stating that "food is the major source of exposure" for most people and that chronic exposure can result in GI effects as well as central and peripheral nervous system disorders and certain cancers. Studies suggest that it may also affect a baby's immune system when ingested by a mother during pregnancy.
The Food and Drug Administration (FDA) has not released a finished assessment of the potential health risks associated with arsenic in rice and other foods made from rice, but _Consumer Reports_ and other studies urge caution.
_Consumer Reports_ tested several different rices from growing regions around the world and concluded that organic rice is no different from conventionally grown rice—they both take up arsenic in the same manner from soil and water. Brown rice often has the highest levels because metallic elements accumulate in the husk and bran, which are milled off when rice is processed. Nevertheless, brown rice still contains more nutrients and is more fibrous.
It is possible to reduce the risk of arsenic in cooked rice by rinsing the raw rice before cooking, and by using excess water during the cooking process and throwing it out before serving; this sacrifices some nutritional value but can reduce the arsenic content by almost a third.
Almost everything that's gluten-free has some rice in it. Suzanne Simpson, R.D., of the Celiac Disease Center at Columbia University cautions patients: "Rice doesn't have a lot of nutritional value. It doesn't have a lot of fiber or protein; it is basically just carbs. Most of the [gluten-free] breads, pasta, tortillas, cookies, and flour mixes contain rice. And people eat rice on top of it." Children who are on a gluten-free diet that also contains rice pasta, cookie, and bread products as well as cooked rice should be monitored to lessen arsenic exposure.
She recommends that people do not use rice pasta and minimize their rice intake for variety as well. We also advise people on a gluten-free diet to see a dietitian regularly to ensure that the diet is diverse and not simply various versions of rice. (See Appendix C, "Arsenic and Mercury Guidelines.")
_Corn Fungi_
The other grain staple of a gluten-free diet is corn. A recent study comparing the gluten-free diet of people with celiac disease versus those on a regular diet found a mycotoxin (a chemical produced by fungi/mold that is harmful to humans and domestic animals) in a number of corn products. The levels of this particular mycotoxin—a fumonisin associated with nervous-system and cancer-causing damage in animals—were high, raising concern regarding the long-term safety of various corn-based products.
The contamination of corn products with fumonisins has also been reported in other European studies, suggesting the potential of toxicity for anyone on a gluten-free diet ingesting a fair amount of corn-based products. While little is known about the fumonisin in the American diet, it is an area for further research and emphasizes the need to diversify the diet!
_Mercury and Other Metals_
Mercury is a naturally occurring heavy metal that appears to be increasing/accumulating in the food chain because of its use in medications, dental amalgams, thermometers, blood pressure machines, batteries, and fluorescent lightbulbs, and its presence in the fish we eat. Mercury can damage the nervous system, kidney, and lungs and remains in the body for a long time, where it affects inflammation and the immune system.
A recent study showed a fourfold increase in mercury blood levels of celiac disease patients following a gluten-free diet. No differences were found in their fish intake or number of amalgam fillings—both sources of mercury found to increase the amount of this metal in the body—but other dietary sources were not examined. Another study found elevated blood levels of mercury, lead, and cadmium and urinary levels of tin and arsenic in people eating a gluten-free diet, some with and some without celiac disease.
The reason for the increased levels in these people is unclear—whether it is food related, altered absorption, or response to mercury in these people. There might also be a genetic tendency in these people to accumulate it or to be more susceptible to specific toxic effects.
Additional studies to determine what is causing the increase in heavy metals in people following a gluten-free diet are needed. It is a potential pitfall that cannot be ignored.
Gluten Weighing In
The weight-loss potential of a gluten-free diet seems to be one of its biggest attractions for some people. Numerous Hollywood names attest to its effectiveness. If you cut out all bread, pasta, cake, cookies, and snacks and do not replace them with gluten-free alternatives, you will probably lose weight. It's called the no–white food, no-carb, gluten-free diet.
But many people following a gluten-free diet are surprised when they find themselves gaining weight from the many fat-, sugar-, and sodium-filled gluten-free products they are now eating to replace what has been removed. People with a double diagnosis of diabetes and celiac disease who must count carbohydrates are initially surprised to see that the gluten-free substitute is often much higher in carbs.
I was eating everything—and constantly—and lost 25 pounds in the year before I was diagnosed (with celiac disease). Once I went on a gluten-free diet, I ate the same amount and gained 30 pounds in about seven months. I went from sick and skinny to healthy and chubby. The pasta and bread and cakes were gluten-free and didn't go right through me, so I realized I had to retrain and restrain myself.
(SHEILA, 46)
People with celiac disease also often gain weight on a gluten-free diet because their intestine is healing and they are now able to digest food properly. Depending on how you define "going gluten-free," you may actually find that one of the things it "gives" is added pounds.
No Shelf Life Means More Money
The costs involved in buying shelf space from the retailer are prohibitive for the smaller manufacturer. It is one of the reasons why you see mainly larger national brands in your local stores. Also, the range and types of ingredients we use are more costly, and gluten-free products fit in the "natural" and "organic" world, where retailers often charge a premium over regular products. Many items are also made by smaller manufacturers who don't have the same big-company processing efficiency. These are some of the reasons gluten-free food is costlier.
—GEORGE CHOOKAZIAN, FOODS BY GEORGE
Gluten-free products are generally much more expensive and less widely available than their gluten counterparts. There are a number of reasons that manufacturers give for this.
Ingredients as well as facilities have to be certified and adhere to specific labeling regulations and testing, which incurs costs. Ingredients must also be grown and milled contamination-free and are often purchased in smaller batches than those used by larger manufacturers, again adding expenses. Many breads, cakes, and muffins are frozen to preserve their freshness. They have a shorter shelf life than preservative-filled products, and spoilage adds to their cost.
Some manufacturers have started lowering prices as competition in the market increases, but gluten-free products can still add to a family's grocery bill.
You Have Isolated the Wrong Issue
One of the biggest dangers of going on a gluten-free diet before properly isolating and testing for what is causing symptoms is postponing and/or missing a correct diagnosis. Numerous other serious medical conditions—including microscopic colitis, SIBO, inflammatory bowel disease (IBD), and irritable bowel syndrome (IBS)—often present with the same symptoms as food-induced dyspepsia or other GI complaints. Gas, bloating, pain, diarrhea, and constipation can be distress signals for almost any and every GI disorder and disease. And neuropathies, headache, and fatigue can signal a number of underlying autoimmune and neurological diseases.
Many people mistakenly believe that their symptoms can be treated and cured through food elimination. By the time you finally get to a doctor, the gluten-free diet may have intensified another condition and taken away your health.
You May Be Eating Gluten Anyway
The biggest hurdles? Contamination. If I had to sum it up, I'm very comfortable with the lifestyle, very comfortable feeding my family, the options are enormous, but I never sit down at a dinner and say, "This is perfectly right." The kids want pizza and pasta. But when they have gluten-free pasta on the menu I still worry that they don't know how to prepare it safely. I still struggle with it.
(ILYSSA, 39)
One pitfall in a gluten-free diet is trying to adhere to it when gluten is a hidden ingredient in or on your food. This may be due to contamination or confusion about gluten-free labeling and regulations or actual false labeling.
Cross-contamination and a lack of awareness in restaurants accounts for most of the "I got glutened" comments from people trying to follow a gluten-free diet. For preparing gluten-free meals, restaurant kitchens often use fryers or pasta water in which dishes that are breaded or contain gluten have been cooked. The cross-contamination that occurs in manufacturing also usually relates to shared equipment, confusion about barley and malt—which contain gluten but not from wheat, which is required to be listed as an allergen on labels—or gluten that finds its way from crops that share fields and storage facilities with nongluten grains.
Testing can be spotty. Several groups offer "gluten-free certification," but they are not all using the same ELISA (enzyme-linked immunosorbent assay) tests to ascertain gluten content. It is also physically impossible to test every batch of a cereal or packaged product to ensure that it contains less than 20 parts per million, the standard set by the FDA for all foods with a "gluten-free" label.
Reading labels and talking to food servers is crucial to avoiding hidden ingredients and cross-contamination. Doing so is a source of stress and disruption for many people.
We were in a restaurant with a gluten-free menu, so I probably didn't ask enough questions. But my daughter ate the salad and what looked like a plain chicken breast, and within 20 minutes she was vomiting all over the tablecloth. I knew she'd gotten gluten no matter what they told me.
(CISSY, 42)
Whenever we go away I go right to the head of food services in every hotel. I don't bombard them but ask how they can help me and how I can help them. So they have the knowledge for the next person who comes with celiac disease. We get amazing dedication and great service.
(ILYSSA, 39)
Less Microbiotic Diversity
Any restrictive diet reduces the diversity of the microbiota in the gastrointestinal tract, a potentially unhealthy change. While there is no one healthy microbiome, a gluten-free diet removes foods that the intestinal microbiota dine on. Studies show that the FODMAP diet may not be a healthy one to maintain for that reason, and patients are cautioned about the consequences of remaining on it for a long period of time. (See chapter 5, "Supplements and Probiotics.")
The Bottom Line
A gluten-free diet is lifesaving for people with celiac disease. It reduces symptoms for many with NCGS—people who have tested negative for celiac disease but who have similar symptoms—and IBS. But the long-term harm of the diet for people who do not really need it is still unknown.
What we do know is that a gluten-free diet is:
• low in fiber
• low in iron
• low in B vitamins
• high in sugar and fat
• associated with elevated levels of heavy metals in the body
• a risk for increased sensitivity to gluten
• potentially bad for your microbiome
Be advised that when embarking on a gluten-free diet you are potentially sitting down to a banquet of consequences. If you are thinking of replacing what is lost in a gluten-free diet with supplements and probiotics, read the next chapter carefully.
Supplements and Probiotics
I had watched a TV show with [a well-known doctor] when he talked about a supplement—garcinia cambogia—for weight loss. The doctor had a very good reputation, and he seemed to think it was a good thing. A number of my friends love the show, and it's impressive, very persuasive. I thought it seemed safe, and I took that for about a month. I didn't feel any different, and I didn't lose any weight but happened to see my doctor right before we were going on a trip to Mexico. The doctor called me over the weekend when he got my blood tests back and told me that I had hepatitis.
I thought, _What!?_ It was unbelievable! Garcinia cambogia was so popular and so heavily advertised, and I thought that it didn't seem like anything risky. My advice to someone taking something recommended on TV—don't trust them or take anything without talking to your doctor first. Vitamins and supplements are an unregulated industry. This could have killed me and severely damaged my liver. I seem to have recovered completely but have to be checked regularly. I thought, _It's just a plant_ —I guess there's nothing more lethal than nature.
(CAROL, 56)
Carol had acute drug-induced hepatitis that can be progressive and result in liver failure and even death. Luckily hers resolved because it was caught in time. She had a follow-up appointment at the Center early in the development of the disease, and a medical history showed that she had recently started taking garcinia cambogia for weight loss. She stopped taking the drug after blood tests pinpointed the problem. The literature prominently lists hepatotoxicity (liver toxicity) as a side effect of garcinia cambogia—weight loss is not.
Hepatitis does not cause symptoms early in the disease, just biochemical evidence of acute hepatitis in the form of elevated liver enzymes. Later, symptoms of liver failure develop, including nausea, vomiting, anorexia, confusion, and coma. Drug-induced liver failure may result in death if not caught early. Carol soon learned what "just a plant" meant—and that "natural" does not mean "harmless."
Half of all Americans take some type of herbal remedy, and more than $28 billion a year is spent on various vitamins, minerals, herbal preparations, and probiotics. This number is about $104 billion globally. While visits to medical professionals have remained steady over the past decade, consultations with alternative medical practitioners and health gurus have increased dramatically—along with the use of supplements.
A tsunami of herbs, minerals, vitamins, and probiotics fill the shelves in drugstores, natural food stores, and supermarkets. They are heavily advertised not just as dietary supplements but as good for your health and claim to treat a wide spectrum of conditions from prostate problems and depression to sexual dysfunction, anxiety, insomnia, thinning hair, weight loss, and more. They are also promoted as a pharmaceutical aid for diarrhea, gas, and bacteria lost through antibiotic use, vaginal yeast infections, oncoming colds and flu, and pain. Many believe that they are safer than prescription drugs whose adverse effects are stated in accompanying literature.
I read the warning label on the [drug] my doctor prescribed—it was longer than my college thesis. Looked as if it would probably cure me if it didn't kill me first. The labels on my supplements have no [listed] side effects of note.
(SHARON, 65)
They've been using these as medical cures in China for centuries.
(ANGELA, 33)
The fact that they have been used for thousands of years in the East may be the only justifiable claim many supplements can make. Although there is little scientific evidence to support the medical claims made in the popular media about the effectiveness of supplements, most people consider them "natural" and basically safe. But several recent and scientifically rigorous studies have proved that there are some very dangerous trends in this unregulated industry, and some supplements may have life-threatening consequences. A recent study in the _New England Journal of Medicine_ showed that approximately 23,000 emergency room visits each year—between the years 2004 and 2013—were due to "adverse events related to dietary supplements."
Laxatives in Your St. John's Wort?
A 2015 Canadian study tested popular herbal supplements and found that many of the bottles contained pills that were diluted or contained none of the product listed on the label. Others consisted entirely of fillers such as soybeans, wheat, and rice—ingredients that were not necessarily on the label. These were the only "plants" in the pill. One bottle of St. John's wort, the _New York Times_ reported, "contained only Alexandrian senna, an Egyptian yellow shrub that is a powerful laxative." Other supplements contained walnuts, potentially deadly for people with nut allergies. This study suggests that the problem may be widespread. It is especially troubling for those with a severe food allergy or requiring a strict gluten-free diet.
This study and others prompted the New York State attorney general in 2015 to issue a cease-and-desist order to several large chains selling supplements, requiring them to withdraw the products. He was joined by other state agencies. The aim of the initiative is to require manufacturers to address their own product issues so that supplements are not pulled from store shelves _after_ they have done harm.
If you are currently gluten-free and suddenly have a return of symptoms, you may need to look at the supplements you take instead of what you had for dinner the night before. Unfortunately, inspecting the label may not help—the "FACTS" section of a supplement label may show the product contains very little or none of this important "ingredient."
Another study published in the _Journal of the American Medical Association_ found that half of the FDA Class I recalls between 2008 and 2012—where there is a "reasonable probability that [their use] will cause serious adverse health consequences or death"—were supplements. And about two-thirds of the recalled dietary supplements that were analyzed still contained banned drugs at least six months after being recalled. These banned and/or prescription-only drugs found in supplements included:
• **Sibutramine** —a weight-loss drug that was withdrawn from the U.S. market in October 2010 since it is known to substantially increase blood pressure and/or pulse rate and may present a significant risk of heart attack and stroke in some people.
• **Sildenafil** —used for erectile dysfunction, it can cause hearing loss and low blood pressure and reacts with a number of other prescription drugs.
• **Fluoxetine** —trade name Prozac, this drug is sold only by prescription.
• **Phenolphthalein** —formerly the main component in laxatives, such as Ex-Lax, banned by the FDA in 1999 for sale in the U.S. due to the risk of causing cancer with long-term use.
• **Aromatase inhibitor** —used by prescription only in breast cancer treatments to lower estrogen levels.
• **Various anabolic steroids.**
A September 2015 recall by the FDA is particularly sobering. Two weight loss supplements were found to contain both sibutramine and phenolphthalein—neither of which were listed on the label. They were marketed under the names Pink Bikini and Shorts on the Beach and sold online. The FDA also noted that "these products may also interact in life-threatening ways with other medications a consumer may be taking."
Most of the FDA-recalled supplements were for bodybuilding, weight loss, and sexual enhancement. If you use these products, you may be getting an enhancement in the form of side effects you did not bargain for. Supplement labels may hide more than that pink bikini can.
When Your Doctor Advises Vitamin or Mineral Supplements
Vitamin deficiencies are often found in people with newly diagnosed celiac disease and require supplementation until the gut has healed and can absorb nutrients properly, and the deficiency is resolved. Anyone on a restricted diet or with another GI condition that involves malabsorption is also a candidate for supplementation.
We recommend choosing a gluten-free vitamin that has only the regulated amounts of vitamins. Try to avoid multivitamins that have megadoses of anything.
People who eat processed food are most likely getting their vitamins synthetically to begin with. Milk, fortified with vitamin D, is the primary source of D for most people who avoid the sun. Ironically, cereals, breads, flours, and canned foods all are fortified to replace the vitamins and minerals removed by processing. But manufacturers have just begun to fortify gluten-free foods, and this can pose problems for someone who has grown accustomed to obtaining their vitamins synthetically from processed food and is now on a gluten-free diet.
The pendulum can easily swing in the other direction. Many people still take megadoses of vitamins, assuming that if some is good, more must be better. We see more people with vitamin B6 toxicity than deficiency, due to excess supplementation.
Vitamin B6 (pyridoxine) is involved in many metabolic functions throughout the body. It is needed for brain development and function and involved in the process of making serotonin and norepinephrine, chemical transmitters in the brain. Although vitamin B6 is often promoted for "nervous system health," its toxicity is usually focused on the nervous system. A vitamin B6 deficiency is rare in the general population since it is found in many foods.
Test First
It is not surprising that many people, anxious about the amount of different vitamins they are getting in their diet, rely so heavily on vitamin and mineral supplements. What _is_ surprising is that they read the pros and ignore the cons—the toxicities, interactions with other vitamins and drugs, contamination, and mislabeling.
A vitamin or mineral deficiency can be ascertained by blood tests and addressed by some simple dietary changes.
A Word on Fatigue and L-Carnitine
L-carnitine is an amino acid that is produced by the body and a natural component of the diet. It helps the body produce energy and is used in Europe to treat fatigue and as a replacement supplement for people on a very strict vegetarian/vegan diet.
It is found in high levels in red meat and in lower levels in dairy products as well as pork, seafood, and chicken. High levels of carnitine are found in those who consume excess amounts of red meat. A natural compound, it is available by prescription as well as over the counter.
L-carnitine excess can cause a number of side effects including diarrhea, nausea, and cramps. It can interact with prescription drugs and is associated with increased risk of cardiovascular disease. You should take supplements only under a doctor's instruction. (See chapter 17, "Celiac Disease.")
Widely Used Supplements That Cause Drug Interactions
_We don't want to focus on the trees (or their leaves) at the expense of the forest._
—DOUGLAS R. HOFSTADTER, PROFESSOR OF COGNITIVE SCIENCE
Recently several large studies have examined the contents of various supplements. Many were tested and found to contain allergens, little or none of the herb or vitamin on the label, or a banned substance. Others are potentially dangerous in their interaction with common medications. A few are worth mentioning.
**St. John's Wort**
St. John's wort is one of the 10 best-selling supplements in the U.S. It is marketed as a mood elevator and is arguably the most popular supplement to treat depression. But St. John's wort can speed the breakdown of various prescription medicines by eliminating them from the body before they can take full effect. This includes anticoagulants (blood thinners), oral contraceptives, antidepressants, cancer drugs, and immunosuppressants (causing transplant rejection).
**Vitamin K**
Vitamin K helps in blood coagulation but in excess can block the effect of medications like warfarin (blood thinners) used to prevent blood clots. Because it is now added to many calcium supplements and found in multivitamins, it can quietly reach high levels in the body and trigger problems before someone is aware of any issue.
**Vitamin C**
Vitamin C will facilitate iron absorption. People with a tendency to absorb excess iron should be careful with this supplement.
**Zinc**
Taken by many to "shorten a cold," zinc has numerous GI side effects and interacts with antibiotics and antihypertensive medications.
**Ginseng**
Used in Chinese medicine for heart issues, this is another popular herb that can interfere with anticoagulant drugs like warfarin and can interact with some antidepressant medications. It has been implicated in neonatal death when taken by the mother.
The list is long. Licorice, black cohosh, echinacea, ginkgo, and many of the most popular herbs are the subject of questionable claims, drug interactions, and lack of quality control.
You should limit vitamin intake to the vitamins you are deficient in—validated through testing and as directed by your doctor.
Supplements for Those Age 50 and Up
While taking supplements can be harmful at any age, older adults are more likely to encounter problems. Older adults also usually take more and a wider variety of prescription drugs than younger people, and this increases the risk of a dangerous interaction with supplements. In addition, many patients do not tell their doctors about the nonprescription pills they ingest, and many doctors do not ask about them—leading to potentially serious consequences.
Supplements, like many prescription drugs, are metabolized and eliminated through the kidney and liver. Since older people have higher rates of kidney and/or liver disease, it may be harder for their body to process compounds found in supplements. The interactions with the cardiovascular system can be particularly problematic. Taking blood thinners or cardiovascular drugs with St. John's wort, vitamin K, zinc, or ginseng may cause serious problems.
Probiotic Intoxication
_We think, each of us, that we're much more rational than we are.
And we think that we make our decisions because we have good reasons to make them. Even when it's the other way around. We believe in the reasons, because we've already made the decision._
—DANIEL KAHNEMAN, PSYCHOLOGIST AND BEHAVIORAL ECONOMIST, NOBEL LAUREATE
_Probiotic_ is the term currently used to name the live bacteria/microorganisms taken by people to supposedly correct and/or maintain the natural balance of their gut and microbiome. This raises the question of what is a "natural" and "healthy" balance of microbiota—proportions that science has not yet been able to determine.
The balance of different bacteria varies from person to person, as well as culture to culture, depending on eating habits, genes, and environment. And while we know that a diverse microbiome is desirable, not everyone needs "rebalancing" to stay healthy.
A recent study of a tribe of hunter-gatherers in Africa, the Hadza people of Tanzania, showed that they lacked _Bifidobacterium,_ a bacterium that is found in probiotic foods and considered healthy. They also had other bacteria that are considered a sign of disease in Western populations.
The study underscores the need to redefine what is healthy and unhealthy in our microbiota and how different bacteria interact with each other. And more important, that a far more personalized approach to probiotics is needed if they are to be effectively utilized to treat human health.
Manipulating the gut microbiota may prove to be an effective way to control the development of diseases and influence treatment. While the benefits of probiotics are being actively studied, it is still scientifically unclear whether they work for specific diseases. You are consuming live bacteria with the assumption that it is a "good" versus "bad" bacteria. For those taking probiotics during antibiotic therapy, how do you know that the antibiotic is not killing the probiotic you are taking or interfering with its action? Probiotics are regulated as a food, not a drug. Which means that they are largely _un_ regulated. They need to be reported to your doctor along with any pharmaceuticals that you are taking.
More important, the safety of their use by young children, older adults, and anyone with a compromised or weak immune system is unclear and potentially dangerous.
While many people have had symptomatic relief through the use of probiotics, the health claims related to these products are often questionable and derived from animal studies that may not translate to humans, as well as studies of different types of bacteria (e.g., lactobacilli and bifidobacteria) that have huge differences within each species. For example, there are 170 species of _Lactobacillus_ , one of the most widely advertised and available probiotic bacterium. All are part of the normal gastrointestinal and vaginal flora and are used in a variety of commercial products. Yet only some strains have been tested; others lack any real data.
While probiotics are being tested in the treatment of many different medical conditions (allergies, obesity, liver disease, IBS, diarrhea caused by antibiotics, and stomach ulcers, to name a few), it is still too early to know if they are truly effective or safe for these conditions, though studies in irritable bowel syndrome look promising.
The Upside—Some Studies Are Very Promising
Some probiotics digest or alter gluten. One commercially available probiotic that contains eight different bacteria can reduce the toxicity of gluten when used in a fermentation process. A study of sourdough baked wheat products fermented by specific bacteria and funguses was shown to be safe for people with celiac disease.
Probiotics cannot at this point be recommended for the pharmaceutical treatment of celiac disease as they have not as yet been proven safe and effective, but they are an exciting area of research.
_Clostridium Difficile_ and Fecal Transplants
Fecal transplants and certain probiotics have been proven to be effective in combating _Clostridium difficile_ (also called _C. difficile_ and _C. diff_ )—a potentially deadly infection—especially its recurrence. This bacterial infection, formerly found mainly in older populations, causes diarrhea and inflammation of the colon and is increasing in younger people.
Fecal microbiota transplant is a procedure where fecal matter (stool) is collected from a healthy donor and transplanted into the affected patient, usually during a colonoscopy. The theory is to replace "good" bacteria that has been killed or suppressed by _C. difficile_ overrunning the colon. The transplant is essentially repopulating a disturbed microbiota and—while still classified as experimental—appears extremely effective for this life-threatening condition. There are now capsules of stool extract available, and hopefully the research on the use of specific bacteria will make this therapy more palatable.
Using one kind of "natural" bacteria to combat another is well studied in this condition, and the offending pathogen is well known. This practice cannot be automatically translated to the treatment of other conditions. Researchers do not yet know which strains to select for specific physical and clinical conditions, the effect of different doses, or the effect on mechanisms or function.
Patients have reported weight gain and mood changes after receiving stool from overweight and/or "unhappy" donors. While this feedback may be anecdotal, there is some research linking changes in the microbiome and weight gain. (See chapter 9, "The Microbiome.")
The Downside—Quality Control
A 2015 study at the Center tested 22 probiotic products purchased commercially and examined them for gluten. About 30 percent of them had some form of gluten that was not listed on the label. As a result, we feel that supplement labels claiming a product is gluten-free cannot currently be trusted.
This in some ways reconfirms a previous study we did showing that patients with celiac disease who regularly took supplements had more symptoms than those who did not take supplements. Interestingly, they also reported a higher quality of life. This may attest to the placebo effect of supplements—they make people better because we expect them to. The "action" would appear to be more brain than gut.
It is unclear whether the levels of gluten found in the probiotics tested posed a risk to people with celiac disease, but the results reflect the underlying problem of supplement oversight, regulation, labeling, and testing.
Are the Products Viable?
Over-the-counter pills may not be a viable source of live bacteria. The probiotics in food (yogurts and acidified milks in cold storage) are usually produced with stricter control and contain viable amounts if stored properly and consumed before the expiration date.
Like other supplements, probiotics are produced and labeled with little oversight from the FDA or other agencies that guard consumer health interests. **The consumer is currently not buying the carefully regulated probiotic mixtures used in research studies.**
Reading Labels—"Doctor Recommended"?
_"You see what you expect to see, Severus."_
—ALBUS DUMBLEDORE IN J. K. ROWLING'S _HARRY POTTER AND THE DEATHLY HALLOWS_
Unethical marketing claims abound in supplement advertisements. Word-of-mouth endorsements coupled with aggressive advertising on every form of traditional and social media have fueled the supplement boom. Great examples are the products marketed as digesting gluten—a claim that is blatantly false. The pharmaceutical industry is currently developing and testing enzymes that _will_ digest the toxic fragments of gluten that cause celiac disease, but none of the currently available products do this. (See chapter 30, "Nondietary Therapies.")
The brain-gut connection is quite clear: We want to believe the claims, and some people actually feel better on supplements. This may be a placebo effect, but that has not been well studied. Unfortunately, supplements make many people sick from trying to correct conditions they never had.
Until we understand the composition, diversity, function, metabolic capacity, and plasticity of the microbial communities within us, attempting to manipulate them will continue to be somewhat hit-or-miss.
A Word of Advice
Real estate agents always advise: location, location, location. The microbes that inhabit the mouth are different from those found in the stomach, the small intestine, and the large intestine. Therefore, if microbes are to be studied in terms of their communication with the brain and body, researchers must first determine which bacteria and which gut area to target in any given therapy.
By inserting one type of bacteria to knock out another, what else is being destroyed or affected? The human gastrointestinal tract is a bacterial ecosystem with a genetic makeup almost 100 times the size of the human genome. We are therefore an amalgam of both our human genes and microbial "selves." And the interaction of the two is largely unexplored territory. Probiotics are an exciting area of research but should be ingested with great caution.
_There are 3 billion base pairs of nucleotides in the human genome engaged in a vast and complex dance that makes us who we are. We need to be awfully careful when we start to change the choreography, especially given our current lack of precision. When you try to move one dancer with a bulldozer, you're pretty darn certain to scoop up more than one Rockette._
—DR. SHARON MOALEM, _SURVIVAL OF THE SICKEST_
Summary
Supplements are overused and understudied regarding their effectiveness and safety. It is an industry that advertises heavily but lacks thorough regulatory oversight and quality control. Heavy metals, banned animal, pharmaceutical, and plant products, steroids, untested ingredients, and prescription medications are found in various supplements.
While prescription drugs must be proven safe and effective before they are marketed, probiotics and other dietary supplements do not need to pass that test. Every year contents are withdrawn because of toxicity—after the fact. One case report of a death in a child due to contamination with a fungus is enough to dampen enthusiasm.
As a 2014 news item from Columbia University noted: "This year marks the 20th anniversary of the passage of one of the most skillful pieces of legislation ever to undermine the health of Americans: the Dietary Supplement Health and Educational Act of 1994. The result was to remove from regulation by the Food and Drug Administration any substances labeled as a dietary supplement." It is time to take a hard look at the various vitamin, mineral, and probiotics bottles in your "medicine" cabinet and on your kitchen counter. Be well advised that you may be flushing money—quite literally—down the toilet and, more important, jeopardizing your health. Too many people are taking supplements and probiotics while removing the foods that naturally contain these vitamins and minerals from their diets.
While some dietary and medical supplementation is useful, much of it simply reflects media trends that we can enhance and increase our health with a fix-it pill. It is as enticing as it is unrealistic.
**Natural does not mean safe.**
A Word on Testing—What Do Antibodies Tell Us?
_Test first, then you treat right._
—NORTH AMERICAN SOCIETY FOR THE STUDY OF CELIAC DISEASE
Many people complain that they are "simply lab results" to their doctors. But these tests are often the most effective way of finding—as well as ruling out—serious conditions and avoiding complications. Rushing to self-diagnose gastrointestinal distress can mask a serious condition or prolong symptoms that can be cured if recognized and treated medically. Lab tests cannot resolve every issue, and they can lead to false conclusions, but they can quickly pinpoint and/or eliminate the causes of many GI complaints.
Since the GI tract is difficult to see without invasive procedures, various blood and breath tests can explain why some people do not respond to a gluten-free diet, why a drug may not cure a symptom—or cause others—and help to identify actual vitamin and mineral deficiencies. They enabled us to diagnose Carol's drug-induced hepatitis before it caused serious complications and permanent liver damage. (See chapter 5, "Supplements and Probiotics.")
Diagnostic tests for specific conditions are described in the following chapters, but it is important for anyone suffering from GI symptoms that they feel are caused by or related to gluten to understand the basic tests used to facilitate a diagnosis. What you see and feel may be the tip of a hidden iceberg, and a gluten-free diet may not help you avoid the impact of a collision.
Rule Out Celiac Disease
If you are suffering from symptoms that include:
• chronic diarrhea or constipation
• gas/bloating
• anemia
• vomiting
• canker sores
• weight loss
• failure to thrive (in children)
• vitamin deficiencies
• lactose intolerance
• behavioral issues
• brain fog
• neuropathies
and/or celiac disease has been diagnosed in a family member, you should be tested for celiac disease _before_ starting a gluten-free diet. Once you are on the diet, testing becomes more difficult to interpret, can be inaccurate, and may require a gluten challenge that brings a return of unwanted symptoms.
The blood and endoscopic tests for celiac disease are detailed in chapter 17. These are the definitive tests to determine if someone is mounting an autoimmune reaction to gluten that is destroying the lining of their small intestine and interfering with digestion.
Get Basic Standard of Care Tests
If you have continuing GI symptoms, it is important to know if your gut/body is inflamed, if you are anemic, and to measure specific vitamins and minerals to assess for the presence and severity of malabsorption. These tests also help your doctor to determine what part(s) of the intestine are involved and the degree of damage.
Tests include:
• **Erythrocyte sedimentation rate and C-reactive protein** —reveals the degree of inflammation in the body; they are not specific for any particular condition or organ.
• **Ferritin** —a parameter of iron stores, inflammation, or deficiency due to malabsorption or chronic blood loss. High values reflect excessive iron stores, as in hemochromatosis, a genetic disorder of excessive iron absorption that is associated with celiac disease.
• **Folic acid** —a parameter of disease of the upper small intestine, where it is absorbed. A deficiency or low levels are common in celiac disease and rare in Crohn's disease, which is predominantly in the ileum or lower small intestine.
• **B12** —a parameter of lower small intestinal disease or stomach issues such as bacterial overgrowth or chronic gastritis.
• **Vitamin D** —necessary for calcium absorption (in turn, necessary for bone formation and muscle contraction). Vitamin D is formed in the skin from sun exposure that can be impeded by sunblock and lack of outdoor activity. Dietary deficiency is also common.
• **Parathyroid hormone** —the parathyroid monitors and manages calcium metabolism. With calcium deficiency, the hormone increases to retain calcium and maintain blood levels to ensure cardiac, blood, and muscle function.
• **Stool testing** —important in GI issues to look for blood and, with diarrhea, to look for infections.
If there are neurological issues, vitamins E, B1, B2, and B6 as well as copper levels should be measured. If there are skin rashes or taste issues, zinc should be measured.
Use Breath Tests to Further Narrow the Diagnosis
Breath tests are used to diagnose a number of conditions that produce GI symptoms, including fructose and lactose intolerance, bacterial overgrowth, and intestinal transit time. It is important to exclude these conditions in patients with irritable bowel syndrome (IBS) and celiac disease with persistent symptoms.
The sugars and carbohydrates we eat are normally digested and absorbed in the small intestine. But when they are mal-absorbed, they get into the colon, where they are fermented by the bacteria that live there. The bacteria dine happily on them, producing gas, water, and the painful symptoms known to those suffering from IBS. This also produces the hydrogen and/or methane gas that are a normal by-product of carbohydrate digestion. These gases are absorbed into the bloodstream and eliminated through the lungs in the breath.
Patients drink different sugars (sucrose, glucose, lactulose, fructose), and their breath is measured every half hour with special analyzers in order to measure the "peaks" of hydrogen and to determine if and how rapidly you are absorbing or mal-absorbing sugars. If lactose and fructose are digested and absorbed in the small intestine, you normally will not produce excess hydrogen.
Therefore, an increase in hydrogen indicates specific intestinal problems. With rapid transit, hydrogen is produced soon after the sugar is ingested; with bacterial overgrowth, hydrogen levels peak twice—once when digested by bacteria not normally found in the small intestine and later by the bacteria in the colon.
Breath tests are a simple and safe method of measuring alterations in digestion that create symptoms, but they have limitations. Some people have colon bacteria that produce methane gas instead of hydrogen, while others produce both. Patterns of release vary from patient to patient—some people have slower but normal transit time. Other conditions may produce malabsorption of carbohydrates, such as pancreatic insufficiency and celiac disease.
Breath tests can be particularly helpful for people with IBS told to go on the FODMAP diet. They can help to eliminate specific problem carbohydrates prior to starting a very restrictive diet. If you can isolate the main carbohydrate problem you can eliminate many weeks of trial and error. The tests should be part of a gastroenterologist's armamentarium but are often not widely available or utilized.
Test for Vitamin and Mineral Deficiencies
My husband does not eat anything that is orange, green, or yellow—otherwise known as vegetables. He'll eat tomatoes because I told him they were fruit.
(TESS, 29)
Many people take vitamin and mineral supplements because they make them feel healthier. Others use them to supplement a restrictive diet. Several websites and TV personalities suggest easy ways to determine if you are deficient in specific vitamins. One "analysis" includes standing on your right foot for three seconds without losing your balance (to diagnose a B12 deficiency), or pressing your thumb into your breastbone to see if this causes discomfort (to diagnose a vitamin D deficiency). This "testing" ranges from useless to preposterous. It is more likely to uncover a balance disorder and/or leave a black-and-blue mark from pressing too hard.
If you feel that your diet does not contain sufficient amounts of everything your body needs, have your doctor run blood tests for essential vitamins and minerals.
While there are many people in the world suffering from malnutrition and serious vitamin deficiencies, they are rarely the people buying supplements in health food stores. People with malabsorption conditions—celiac disease, inflammatory bowel disease, protein allergies, intestinal damage, etc.—need to be monitored and, if necessary, supplemented, but a balanced diet of fresh ingredients is usually adequate to supply what the body requires.
For better or worse, our diets contain a surplus of fortified foods that usually make up for the nutrients removed during the processing that extends shelf life. An overuse of many vitamins can lead to toxicity, drug interactions, and other serious problems.
What Do Antibodies to Gluten Really Mean?
_When the right thing can only be measured poorly, it tends to cause the wrong thing to be measured well. And it is often much worse to have a good measurement of the wrong thing, especially when it is so often the case that the wrong thing will, in fact, be used as an indicator of [what is] right._
—JOHN TUKEY, PROMINENT STATISTICIAN
In the following chapters—notably those in Part V, which examine several psychiatric and neurological conditions—we refer to "antigliadin antibodies" that are found in the bloodstream of people with these disorders. While not part of current standard-of-care testing, they are the focus of many research studies on gut-brain interactions, and therefore a quick primer on immunoglobulins is in order.
What Do Antibodies Do?
Antibodies (also known as immunoglobulins) are a critical component of the immune system. They can do many things:
• Recognize and bind to a target and inactivate or destroy it
• Attract other cells when they do bind
• Set in motion a number of immune functions
• Initiate a cascade of other chemicals
• Cross-link other molecules
Antibodies are designed to recognize and neutralize toxins in the body by inactivating bacteria and viral products. They may also inappropriately recognize and react with specific "self" proteins. So, developed by nature to fight infection, they then fight us. The by-product is autoimmunity.
Antibodies to gluten (antigliadin antibodies or AGA) are targeting gliadin, the protein portion of gluten. They are markers that indicate an abnormal immune system response to gluten in people with celiac disease but are not specific for the disease. They have, however, been seen in the blood of some patients with autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), schizophrenia, and cerebral palsy. These are _not_ celiac antibodies, and the significance of this immune response has not yet been explained.
Immunoglobulin Primer
Antibodies/immunoglobulins (Ig) are classified by their specific features, structure, targets, and locations. Important to our discussion are:
**IgA** —antibodies that are found throughout the GI tract and other body surfaces that are exposed to the environment and foreign substances. They deal with surface and mucosal immunity and are seen in celiac disease.
**IgE** —antibodies that circulate in the bloodstream and trigger the immediate immune response in an allergic reaction. They are present in much smaller quantities than the other major classes. Allergies are IgE mediated: When IgE antibodies bind to pollen, venom, dander, or food antigens they cause the release of histamines that trigger symptoms such as swollen airways and other reactions found in food allergies.
**IgG** —the most common in the body, they fight bacterial and viral infections. They are the only antibodies that can cross the placenta. They are also seen in food sensitivities.
Both IgA and IgG antibodies recognize and react to gluten. IgG antigliadin antibodies are found in some people with autism spectrum disorder, ADHD, schizophrenia, and cerebral palsy. IgG antigliadin antibodies are also found in the bloodstream of healthy people.
If some patients with psychiatric and neurological conditions have antigliadin antibodies, they may be the best candidates to benefit from a gluten-free diet. However, we do not know if the antibodies develop due to an intestinal issue or are the result of the neuropsychiatric condition influencing intestinal function. Also, the gut-brain axis may be bidirectional.
The presence of antigliadin antibodies must be shown to have a direct effect on function to be considered significant. At this point, the direct effect on neural function of antigliadin antibodies is still being debated. If it is possible to eliminate these antibodies through a strict gluten-free diet, it may have important therapeutic implications, though this has not been demonstrated. It is still unclear if these antigliadin antibodies are cause, effect, or simply innocent bystanders.
"Nonsense on Stilts" Testing
Tennis superstar Novak Djokovic was supposedly diagnosed by a doctor who was a family friend by putting a slice of bread on his stomach and holding up his arm as the doctor pushed against it.* While Djokovic felt it was "madness," he noticed a difference in his ability to resist the pressure. This form of kinesiology is not reliable or accepted testing. As writer Alex Gazzola noted, "I cannot help but wonder how a top athlete can come to be convinced of this stuff. 'What matters is that you are open-minded' is Djokovic's take. Yes—but not so open-minded that your brains fall out." A gluten-free diet has apparently changed Djokovic's game and life, but his diagnostic journey is not a medical testing game changer.
Summary
Issues need to be isolated if they are to be properly diagnosed and a patient is to find treatment and relief. Because the gastrointestinal symptoms of different disorders mimic one another, it is intuitively easy to point a finger at the wrong food or event as a trigger. Diarrhea and pain can be caused by a bacterial infection, a virus, food poisoning, carbohydrate intolerance, lactose intolerance, celiac disease, or acute pancreatitis, as well as a long list of other multisystem disorders.
Test first, test right, and treat right.
PART II
What Is Going On in the Gut
(The Science Basics)
_Nature uses only the longest threads to weave her patterns, so that each small piece of her fabric reveals the organization of the entire tapestry._
—RICHARD FEYNMAN, PHYSICIST
There is a game called "telephone" in which one person starts a message that is whispered from one participant to another until the last person in the game announces the final message and the person who started the game states the original. Usually, the message announced by the final person is totally different and only bizarrely connected to the original. It is a game that shows how small misconceptions can make a huge difference, how errors accumulate.
What goes on in your gut is a bit like the game telephone. Foods, drugs, and supplements interact with many participants in the digestive process, and a crossed signal, misinterpreted message, or inflamed surface changes the effect of that food or drug into a cascade of unexpected problems for the body. The original intent is often lost in the translation.
The gut is a complex and intricate system composed of different organs, glands, enzymes, secretions, cells, and nerves as well as trillions of bacteria, viruses, fungi, and yeast that compose the microbiome. It also has its very own "second brain." There are many places for communications to go awry when every element is getting and sending whispered messages.
The Normal Gut and Digestion
_The human body is a machine which winds its own springs._
—JULIEN OFFROY DE LA METTRIE, 18TH-CENTURY PHYSICIAN AND PHILOSOPHER
_I don't digest things with my mind._
—MARILYN MONROE
In many ways, the digestive system is an extension of the environment—a long tube, open at both ends, that is designed to supply the body with all the nutrients and fluids it needs to function. And everything we consume—food, liquids, drugs, supplements, Play-Doh—ultimately affects the entire body as it travels through the tract.
Digestion is an amazingly effective and efficient process. The concept is simple, the design and execution quite remarkable and, as scientists are discovering, intriguingly complex. There is a constant interaction of organs, muscles, nerves, hormones, enzymes, microbes, and blood vessels, every one doing tasks that monitor, regulate, and control the job of nourishing the body. As you will see, our gut goes well beyond simply processing the food we eat. It engages in a constant conversation with other parts of the body. And the volume is often deafening.
Problems in the digestive tract are one of the most common reasons people seek medical help—or self-medicate with restrictive diets, over-the-counter remedies, supplements, and/or pre- and probiotics. The list is long, and the discomfort and inconvenience of gastrointestinal distress a source of pain as well as embarrassment.
To understand what goes wrong, and the real basis of GI problems, it is important to understand first how digestion actually occurs. It is an essential foundation for comprehending how what we ingest affects both body and brain, and why going gluten-free or lactose-free or carbohydrate-free works for some and not for others. And why we were not meant to simply eliminate one category of nutrients without ample cause.
I spend a great deal of time on the toilet. In fact, I do some of my best work in the bathroom.
(ED, 44, CROHN'S DISEASE)
The Gastrointestinal Tract
Since nothing we eat can be used by the body in its ingested form, digestion is a combination of mechanical and chemical processes that tear food apart, grind it down, shake it vigorously, and create a soupy mix that is propelled through the entire length of the digestive tract (the gut), where it is ultimately absorbed and anything unusable is eliminated.
Food enters the mouth, where it is chewed into smaller pieces and enzymes begin digestion. It then travels through the pharynx, esophagus, stomach, small intestine (the duodenum, jejunum, and ileum), and large intestine (colon), and nondigestible products exit from the anus. Throughout the GI tract are organs and glands—salivary glands, pancreas, liver, and gallbladder—that secrete the enzymes and fluids needed to break down and digest food.
Diagram 1
THE DIGESTIVE TRACT
The digestive system is intimately joined to:
• the circulatory system, which supplies nutrients to the organs and other tissues throughout the body
• the enteric (intrinsic) and autonomic (automatic) nervous systems, which control enzyme release and contractions of the gut, and report back to the brain
• the muscles of the digestive system, which provide coordinated motility (movement) to help digest and move/squeeze food through the long tract
• the hormones that regulate movement as well as the secretions that stimulate and/or inhibit the activities of digestion
While there is enormous capacity and redundancy built into the digestive system, if one section malfunctions, it almost necessarily affects another, and there are numerous places for things to go wrong.
Digestion
Digestion is actually a three-part process:
1. **Digestion** —the breakdown of food products into smaller components that can be absorbed.
2. **Absorption** —the passage of food products that have been broken down into the intestinal wall.
3. **Transport** —the transfer of food from the intestinal wall to the rest of the body.
It consists of two basic activities:
• the **mechanical** chewing and mixing of food in the mouth and stomach and propulsion by the intestinal muscle, called _peristalsis._ This muscular component is a crucial aspect of digestion since contractions of the smooth muscle both propel and mix the chyme (the liquid product of the broken-down food) as it travels down the digestive tract. Without peristalsis, there would be no digestion. When we discuss a lack of motility in various GI conditions, it means that peristalsis is affected.
• the **chemical** breakdown of food by secretions and enzymes throughout the digestive tract. This starts with saliva in the mouth and is completed by microbes in the colon.
Digestion actually begins before the food even enters your mouth. When you see, think about, or smell food, the _vagus nerve_ transmits a chemical message from your brain to release saliva in the mouth, increase stomach movement, and release gastric acid in the stomach. You begin to salivate, and the stomach "rumbles" at the very anticipation of food.
_The Mouth_
Digestion starts in the mouth as chewing tears, grinds, and crushes the food into smaller pieces. Saliva is secreted by glands under and around the tongue to lubricate and start to dissolve the food. Saliva contains enzymes that begin the digestion of fats and carbohydrates and acts as a glue to hold the food together as it travels toward the stomach.
The nervous system lends a hand to this process by inhibiting as well as stimulating the release of saliva. This is why we often get a "dry mouth" when fearful, and salivate at the thought or smell of food when hungry.
We swallow the ball or _bolus_ of chewed food and saliva that is transported down our esophagus. While the skeletal muscles at work in the mouth and throat are voluntary—we consciously move our jaws and swallow—smooth muscles that function involuntarily then take over in the esophagus. This is where peristalsis begins and moves the food into the stomach, where the action really begins.
_The Stomach_
The stomach is a big muscular bag that holds the chewed food, mixes it with gastric juices, and starts many of the chemical processes of digestion. The muscle movements of the stomach act like a Cuisinart—chopping, blending, and mixing the ball of food into a soupy puree called _chyme._
The main chemical ingredient in the stomach is hydrochloric (gastric) acid, a highly corrosive substance that both breaks down the food and converts the stomach into a disinfecting tank, killing bacteria and toxins in the food we have eaten. Gastric acid is an essential line of defense in the body's monitoring of dangerous substances entering it from the outside. The stomach also releases _pepsin_ , an enzyme that digests protein.
The walls of the stomach are composed of several layers of tissue—a structure found throughout the rest of the GI tract—that contain numerous mucous glands able to secrete mucus into the tract to lubricate the lining and protect it from friction and the acid bath of the chyme. The breakdown of this mucus coating is one of the causes of ulcers.
The communication system in the stomach also sends hormonal messages to the other digestive organs that food has arrived. This stimulates the secretion of pancreatic juices and bile from the liver that will further break down the chyme once it moves into the small intestine.
One-Way Street
Food is only meant to travel _down_ the GI tract—a street sign that is often ignored. The sphincters (ring-like muscles) connecting the esophagus to the stomach and the stomach to the small intestine are one-way valves. Occasionally, chyme refluxes or backs up into the esophageal area—a condition known as GERD, gastroesophageal reflux disease. The corrosive effect of gastric acid is well known to people who experience its effect on their less-well-protected esophagus. (See chapter 8, "The Gut in Disease.")
When the chyme is sufficiently liquefied, muscle/peristaltic contractions gradually push it into the upper part of the small intestine, the duodenum. The stomach empties in a slow and controlled way so as not to overwhelm all the mechanisms of digestion in the small intestine. Everything is released according to particle size.
As the small intestine fills with chyme, it signals the stomach to decrease its activity and slow down the emptying process. This is one reason a large or fatty meal stays with you. It lingers in the stomach until the small intestine is ready to process it.
The arrival of chyme in the small intestine triggers the release of a cascade of secretions. The small intestine, pancreas, liver, and gallbladder all deliver digestive enzymes and fluids that break down the food into components small enough to be absorbed. Alkaline mucus with a high concentration of bicarbonate is secreted to neutralize the gastric acid in the chyme.
All of these actions are regulated by both the nervous system and gastrointestinal hormones and called into action only when needed by the digestive system.
Most of these activities occur without any conscious awareness or control. In this sense, it is truly a "second brain" in your gut.
_The Pancreas_
A carrot-shaped gland that has a dual function in digestion and metabolism, the pancreas is both an endocrine gland—producing insulin, which enables the digestion and absorption of carbohydrates—and an exocrine gland—producing enzymes such as trypsin, which breaks down proteins; _amylase_ , which breaks down starches; and _lipase_ , which breaks down fats. When the pancreas becomes inflamed or diseased (e.g., pancreatitis), these enzymes are not secreted, and as a result carbohydrate, protein, and fat digestion is impaired.
_The Liver_
The liver is the energy-processing center of the body. It is the first stop for nutrients absorbed from the intestine. Its many functions include metabolizing, storing, and transporting nutrients to the body, producing chemicals necessary for digestion, and breaking down drugs and alcohol.
The liver stores glucose, iron, and vitamins A, B12, and D, sending out the nutrients and substances digested from the food to the cells of the body as they are needed. It also secretes bile, a fluid that increases the solubility of fats, enabling them to pass through the intestinal wall into the bloodstream. Bile is made in the liver and stored in the gallbladder until needed, and delivered to the small intestine when fatty foods arrive and stimulate its release through contraction of the gallbladder.
_The Small Intestine_
The small intestine, which is actually the longest part of the GI tract, is designed to complete digestion and much of the absorption of nutrients. It is approximately 22 feet long in adults and consists of three parts:
• the duodenum (the first segment)
• jejunum (the second segment)
• ileum (the third segment, or distal small intestine)
All three segments have similar anatomy, but each has a specialized job, digesting and absorbing specific nutrients.
Slow waves of peristalsis push chyme from the stomach through the duodenum toward the jejunum. It actually takes several hours for an entire meal to travel the entire length of the small intestine to enable absorption to occur through the lining or mucosal wall of the intestine.
This lining has a unique structure that possesses a much larger surface area than the midsection of the body in which it is contained. (See Diagram 2.) This lining, the _mucosa_ , consists of folds that increase its surface area. The folds are in turn covered with tiny fingerlike projections, or _villi_ , that contain the cells that absorb nutrients and again expand the surface area. (See Diagram 3.)
The surface of each villus has a "brush" border consisting of _microvilli_ or tiny hairs that increase the absorptive surface of the small intestine yet again. The brush border also secretes enzymes that are necessary for the digestion of specific food components.
If you were to flatten out the intestinal mucosa—all the villi, microvilli, and crypts that lie between the villi—the "small" intestine actually has a surface area about the size of a football field that is totally dedicated to absorbing food! This enormous capacity ensures that the intestine can sustain a fair amount of assault and/or damage and still feed the body.
Diagram 2
A CROSS SECTION OF THE INTESTINAL WALL
Diagram 3
Inflammatory cells normally inhabit the mucosa to protect the small intestine against toxins and bacteria. Since the food supply entering the GI tract is not sterile and may contain toxic substances, these white blood cells are another line of defense. This results in a state of constant, controlled inflammation in the mucosa.
_The Villi_
The villi are the workhorses of the intestine. They are the final intestinal link between your dinner plate and your bloodstream. This is where celiac disease does its primary damage and where other gluten and food-related disorders affect the body's ability to properly absorb nutrients.
The villi play a crucial role by:
• dramatically increasing the surface area of the small intestine to allow the absorption of food
• releasing enzymes that continue and complete the breakdown/digestion of food
• absorbing the products of digestion and transporting them into the bloodstream for distribution throughout the body
• acting as a barrier that blocks bacteria, parasites, and toxins from entering the body
Each villus is an independent but intimately related part of the assembly line. It is important to understand that the final stages of digestion, absorption, and transport of nutrients occurs _through—_ not between—these tiny, fingerlike projections. When there is inflammation, and a breakdown of the lining of the intestine, the bowel may become permeable, often termed "leaky."
There are _millions_ of microscopic villi in each section of the small intestine. Because of its enormous capacity to absorb, parts of it can be damaged with no obvious manifestations or symptoms. But when large sections of the lining are inflamed or destroyed, absorption, enzyme release, transport of nutrients to the body, and the defensive ability of the small intestine is compromised.
Absorption
Once the food components are sufficiently digested (broken down), they are absorbed by different parts of the small intestine.
This is why disease of or infection in one section of the small intestine is often revealed by the malabsorption of specific nutrients. Iron deficiency and metabolic bone disease (e.g., osteoporosis or osteopenia) occur when disease involves the _proximal intestine_ , the first two segments of the small intestine. Fat and sugars are absorbed throughout the intestine. Therefore, when one part is diseased, another can compensate and absorb these vital nutrients.
Unless there is a disease process at work, absorption works efficiently and steadily until every usable nutrient in the chyme is absorbed. Nutrients that the body does not need for energy and efficient cellular function are stored for later use—primarily as body fat.
Transport
Once the intestinal wall absorbs the fully digested food, it is transported into the bloodstream and made available to cells throughout the body. Carbohydrates, protein, and fat are transported across the epithelial cell membranes by different mechanisms, with some foods requiring specialized chemical "porters" that literally bind to the components and carry them across the cells of the villi.
_Carbohydrates_
Carbohydrates supply the body with the fuel it requires for immediate and long-term muscle function and energy. Complex carbohydrates (starches) are usually broken into simple carbs (sugars) in the small intestine. The simple sugars are usually readily transported across the villi into the bloodstream. But some sugars such as lactose or fructose are not absorbed by some people and arrive in the large intestine (colon) mostly undigested. It is these carbohydrates that are thought to cause many of the symptoms of IBS, and their digestive results are often mistaken for gluten intolerance.
_Proteins_
Proteins are large and complex molecules that are an essential part of every cell, organ, and body system. They are made up of hundreds of amino acids bound together in chemical chains that must be broken down to be used by the body. This is done by enzymes secreted by the pancreas and from the _brush border_ (microvilli), which split these chains into smaller and smaller molecules and amino acids that can then be absorbed.
The Problem Protein
Protein is not just found in meat, fish, eggs, and cheese; it is an essential part of many foods. It is the protein portion of wheat—both the gluten and nongluten parts—that gives the small intestine of many people the most trouble. For those with celiac disease, the troublemaker is _gliadin_ , the protein portion of wheat and several other grains. It contains one fraction that is not readily digested. So despite all the grinding, churning, mixing, and battering of digestion, some proteins remain intact. Gluten is a major culprit in this scenario.
But scientists are learning that for those with IBS and other gluten sensitivities, it may be the _nongluten_ portion of wheat contributing to the problem. (See chapter 11, "Gluten and Nongluten Grains.")
_Fat_
Fat is one of the major building blocks of the body. It provides long-term energy stores and needed cholesterol. While many people take statins to lower their cholesterol, it is the main component of cell membranes and is needed to maintain the integrity of every cell in the body and to make many hormones.
_Mineral and Vitamin Digestion_
Specific minerals and vitamins are crucial to body growth, function, and metabolism. Even minor deficiencies disrupt body chemistry.
Vitamins are either water or fat _soluble_. Water-soluble vitamins, the B family and C, move across the watery chyme quite easily either on their own or assisted by special carriers. Fat-soluble vitamins must be _emulsified_ to make the trip. Sodium (salt), calcium, iron, water, potassium, and other trace minerals are readily absorbed in different parts of the small intestine, but if the villi are damaged, minerals and vitamins cannot be absorbed.
_The Colon (Large Intestine)_
Whatever is left of the chyme in the small intestine is then pushed by peristalsis into the colon or large intestine. For many people, this is the part of the digestive tract where painful problems occur.
The digestive process that starts in the mouth culminates in the colon, which is about 6 feet long, shorter than the "small" intestine.
The colon is home to a huge population of bacteria (the microbiota) that have colonized your intestine throughout your lifetime. They feast on everything the small intestine has discarded and digest much of the unused fiber in our diet through fermentation—the bacterial version of chemical conversion. This reduces the chyme into feces and releases folic acid and vitamins B1, B2, B6, B12, and K (the clotting vitamin).
In fact, while the main function of the colon is the absorption of water, approximately 98 percent of the fluids entering from the small intestine—as well as a small but significant percentage of our calories—is actually absorbed in the large intestine. It is the fermentation process that produces carbon dioxide and methane gas, which often translates into flatulence (gas).
As the food is pushed through the colon, the fecal matter becomes more and more concentrated and then stored until it is eliminated through the rectum. The longer it takes to expel feces, the more water is absorbed, making the stool harder and, in turn, more difficult to expel. Diets high in fiber (raw fruits and vegetables, high-fiber cereals) or supplemented with drugstore fiber (e.g., Metamucil or FiberCon) create more fecal bulk that goes largely unabsorbed and creates larger stools.
One of the amazing abilities of the digestive system is its ability to function silently and independently of our brain. We do not need to think about how our food will be digested. The small intestine and much of the colon is controlled by involuntary muscles that work automatically. It is only when things go wrong that we become aware of digestion.
But our brains and extrinsic nerves (facilitated by stress, prunes, and opportunity) play a role in affecting gut muscles. When fecal residue reaches the rectum, we get a signal: We know when there is gas and when there is stool there that needs to be eliminated.
Summary
The digestive system is a wonderfully meshed machine that turns the food we eat into nutrients that support the functions and systems of the body. When all of the interconnected enzymes and secretions, glands and organs, nerve fibers and hormones, muscles and microbes enter and exit as scripted, the play runs smoothly. When any one of these actors is delayed, missing, or becomes overly temperamental, the entire production falters, and sometimes the show cannot go on.
The Gut in Disease
When she was good,
She was very good indeed,
But when she was bad she was horrid.
—HENRY WADSWORTH LONGFELLOW,
"THERE WAS A LITTLE GIRL"
Abdominal pain is one of the most common reasons people see a doctor and one of the most difficult symptoms to diagnose. With several notable exceptions (such as a heart attack), most of the pain is caused by problems in the digestive tract. Yet the stages of digestion are so intricately interrelated that disturbances in any one of them—muscles or nerve impulses not working or overworking, enzyme deficiencies, swallowing disorders, infections, reactions to foods or drugs—can result in symptoms and syndromes.
Your digestive system may be falling through the bathroom floor for a number of reasons, but most of the disruptions are not caused by gluten or specific foods. Although randomly eliminating certain foods or drugs may alleviate some symptoms, it is important to _isolate the problem_ before you can treat or cure it.
In fact, the underlying conditions that create many of the symptoms attributed to gluten are often diagnosable and treatable without restricting any particular food(s), including gluten. And due to the serious nature of some conditions, it is not just unwise but actually dangerous to ignore them or treat them with diet alone.
Symptoms of GI Disease and Distress
The GI tract is expert in ridding itself of unwanted food and toxins and in letting its "host" know when it is in trouble or simply unhappy. At this point the normally silent workings of digestion raise the volume.
Pain
_The truth is rarely pure and never simple._
—OSCAR WILDE
Pain is what drives most people to both the emergency room and the doctor. It is a clear signal of distress, but it is also a complex phenomenon that must be assessed in terms of its location, severity, and duration. Pain is physical—nerves and muscles being pressured, stretched, overstimulated. It is emotional—perceived differently from one individual to another and affected by ongoing or past pain. It is sociocultural—some people are taught to "bear up," and others receive sympathy through expression. Therefore both the triggers of pain and its perception are stimulated and inhibited by many interacting factors that differ from time to time. Some people have bloating and gas pain that they find "like a claw," while others are hardly bothered by it.
The perception of pain in the gut requires perception in the brain.
Nausea and Vomiting
Vomiting is one of the most useful defense mechanisms within the gut. It helps to expel undesirable food from the stomach, including poisons and microbial toxins. It can be triggered by overeating, a reaction to medication, infection, smells or sights, a brain injury, a heart attack, migraines, motion sickness, pregnancy, and other conditions. It is often experienced as a prelude to taking SATs, going onstage in your first major starring role, or meeting your future in-laws.
Vomiting is also a common symptom of gluten ingestion in a usually well-controlled celiac patient.
Diarrhea and Constipation
Most of my meals are very short-term rentals.
(BOB, 49)
I go about once, maybe twice a week. I get my money's worth at a restaurant—the memory and the food linger on.
(SYD, 61)
The word _diarrhea_ comes from the ancient Greek meaning "flow through," which characterizes the excessive, frequent, mostly liquid bowel movements of this condition. It can be caused by infections, food poisoning, parasites, medications, lactose intolerance, nerves, fructose, artificial sweeteners, surgery, and a number of digestive disorders. It can be caused by celiac disease and eliminated by a gluten-free diet. Other causes require different treatments.
Patients usually associate diarrhea with large quantities of watery stool. However, physicians define the term as more frequent and/or looser stools. When we ask "Do you have diarrhea?" and the answer is "No, just multiple softer stools," we will write in the chart: "Patient has diarrhea."
Constipation, another common digestive disorder, occurs when bowel movements are less frequent and usually hard. While it is difficult to categorize "normal" for this otherwise normal function, some people go two to three times a day, others that many times a week or month. As explained in the previous chapter, the role of the colon is to absorb water from the stools to keep the body from becoming dehydrated and depleted of necessary minerals. But when feces remain in the large intestine, the water is absorbed out of it, sometimes making it hard and difficult to pass.
Constipation can be caused by reduced intestinal motility (movement) that creates increased storage time, a lack of fiber in the diet, disrupted diet schedules, stress, "holding it in," medications (especially narcotics with codeine), irritable bowel syndrome, and other medical conditions.
People on a strict gluten-free diet often eliminate a fair amount of fiber from their diet in the process and need to replace it to avoid becoming constipated.
Putting Order in the Disorders
The following is a brief description of medically treatable intestinal disorders that all produce symptoms when they attack the 30-foot-long gastrointestinal tract. These can range from cramping and distention to gas, vomiting, diarrhea or constipation, fever, headache, fatigue, and malabsorption (leading to vitamin/mineral deficiencies and neuropathies). These illnesses create similar symptoms, but the diagnoses are as numerous as the tract is long.
Inflammatory Conditions
Inflammation can cause symptoms and signs that are the end product of many different conditions. (See also chapter 15, "Inflammation.")
_Inflammatory Bowel Disease_
Inflammatory bowel disease (IBD) is the main inflammatory disease of the GI tract. It is a classification that includes Crohn's disease, ulcerative colitis, collagenous colitis, and lymphocytic colitis. It is diagnosable by radiological imaging and biopsy of the small intestine or colon, and treatable mainly with drugs.
IBD is a serious and potentially life-threatening condition. (For more and evolving information on diet in IBD, see chapter 20.)
_Drug-Induced Inflammation_
Drugs are an increasingly recognized cause of GI inflammation and distress. Prescribed to treat one condition, they may create another in the process. It is not uncommon for a label to instruct you to "take with food" to prevent stomach upset.
My doctor prescribed four Advil three times a day for my shoulder pain. Two weeks later I had stomach pain and an ulcer. I should have known better.
(DICK, 70)
A striking example of drug-induced inflammation is familiar to many taking NSAIDs (nonsteroidal anti-inflammatories) or aspirin for arthritis and/or joint pain. Repeated use can inflame the GI tract. Benicar (olmesartan), a drug used to control blood pressure, can cause celiac-like villous atrophy and severe inflammation with associated symptoms, stomach pain, and diarrhea. (See chapter 13, "Drugs.")
We are taking an increasing number of pills to treat everything from pain to fatigue, itching to constipation, weight loss to hair growth. The list of pharmaceuticals used to treat disease today fills 3,250 pages of the _Physicians' Desk Reference_. Each drug has paragraphs of side effects, many of them GI related. The 1,100-page _Handbook of Nonprescription Drugs_ published by the American Pharmacists Association is recommended as an "interactive approach to self-care." Again, the number of GI side effects is extensive.
All of these drugs must be absorbed by the GI tract, where they regularly cause significant side effects in the form of inflammation. **Beware of the long-term consequences with any "quick fix."**
(For more, see "Antibiotics" in chapter 9, "The Microbiome," and chapter 13, "Drugs.")
Autoimmune Conditions
There are a number of autoimmune diseases that cause inflammation and disrupt the intestinal tract.
_Celiac Disease_
Celiac disease is a multisystem disorder where the main target of injury is the small intestine. It inflames and destroys the villi of the small intestine, causing symptoms that are seen throughout the body. (See chapter 17.)
_Diabetes_
Diabetes attacks the islet cells of the pancreas, creating a lack or deficiency of the hormone insulin that is needed to metabolize glucose, a critical fuel for body function. Type 1, _insulin-dependent diabetes mellitus_ (IDDM), destroys the pancreatic islets, requiring permanent insulin injections or an insulin pump. Type 2, _non-insulin-dependent diabetes mellitus_ (NIDDM), is not an autoimmune condition, and insulin production is unstable, not absent. (See chapter 23.)
_Scleroderma_
The word _scleroderma_ comes from the Greek _sclero,_ meaning "hard," and _derma,_ meaning "skin." While hardening and tightening of the skin is one of the most visible manifestations of the disease, the symptoms vary greatly, as do the parts of the body affected. The severity of scleroderma depends on the target as well as the extent of the hardening and tightening.
In people with systemic scleroderma, tissue in the esophagus and gastrointestinal tract (stomach and bowels) can become hard and fibrous, causing them to function less efficiently and affecting digestion. In addition to acid reflux and difficulty swallowing, resulting from damage to the esophagus, some people with scleroderma may also have problems absorbing nutrients if their intestinal muscles lose motility and food is not moving efficiently through the intestines. They can also suffer from diarrhea alternating with constipation. Lack of motility may also contribute to _small intestine bacterial overgrowth_ (SIBO).
Since the symptoms of scleroderma are very similar to other autoimmune and GI disorders, it can be mistaken for another condition (GERD or IBS), misdiagnosed, or missed.
Infective Conditions
Infections of the gut ( _gastroenteritis_ ) cause inflammation that disrupts function. Infection is the direct invasion, and inflammation is the reaction. The most common causes of gastroenteritis are:
• Viral infections: rotavirus, Norwalk agent.
• Bacterial infections. These include salmonella, E. coli, yersinia, and shigella. Most of these bacteria are found in food and contaminated water.
• Parasites. These include giardia and cryptosporidia (microscopic parasites found in contaminated water and via human transmission through food and contact) and helminths (flatworms, ringworms, and roundworms that contaminate food, water, and feces).
While most cases of gastroenteritis recover spontaneously or require treatment with antibiotics, antimicrobials, and antiparasitics, many people continue to have intestinal inflammation and symptoms long after the "bugs" are gone. **And the infection can trigger another GI disease.** There are many people who develop symptoms of celiac disease, IBS, and IBD after bouts of traveler's dysentery, parasites, or another bacterial infection. (See Chapters 17 and for discussions of post-infective celiac disease and IBS.)
Malignant Conditions
GI cancers can occur anywhere in the GI tract from the mouth to the anus, as well as the GI organs (gallbladder, pancreas, liver), and symptoms relate to the location of the malignancy. Colon cancer, the most common GI cancer, is silent until it obstructs or bleeds. Stomach and pancreatic cancer are also silent until they progress to a stage where they impair function, causing symptoms.
At this point, there are links between conditions such as celiac disease, as well as IBD, to an increased incidence of some intestinal cancers and lymphoma. In the absence of celiac disease, no direct link has been made between gluten and malignancy.
Functional Conditions
[IBS] interferes with your life. What is so upsetting is that it is hard to control. I try to eat very plain food in a restaurant. Occasionally you feel great and think: _When is the shoe going to drop?_
(LAURA, 73)
A diseased gut can look normal but not function properly. Functional gastrointestinal disorders (FGIDs), including IBS, are among the most common chronic diseases seen in the general public and affect from 20 to 30 percent of the population at any given time.
They include IBS, gastroparesis, SIBO, GERD, swallowing disorders, and muscle or nervous system problems causing lack of motility or altered function.
_Irritable Bowel Syndrome_
IBS is a diagnosis of exclusion when symptoms cannot be explained through blood and biopsy/pathology tests or damage to the anatomy of the gut. It is diagnosed by strict criteria. (See chapter 19.)
_Gastroparesis_
Gastroparesis is a condition where the stomach muscles are not working properly, affecting its ability to empty so that food literally sits there. The backup of food not being propelled down the GI tract into the small intestine can lead to the characteristic feeling of fullness before finishing a meal, occasional overgrowth of bacteria in the small intestine, the hardening of undigested food in the stomach (which can obstruct its passage into the small intestine), and blood sugar fluctuations. Gastroparesis may contribute to or aggravate GERD, especially at night.
The causes of gastroparesis are not fully known, but uncontrolled diabetes, damage to the nerves in the stomach or even the vagus nerve (which regulates chemical levels in the digestive system that signal the stomach to empty), scleroderma, and certain drugs such as opiates may cause or contribute to the condition. It has also been proposed that damage to the nerves controlling involuntary functions—such as stomach emptying—occurs.
The management of gastroparesis is primarily dietary, with medications prescribed when necessary. Patients are directed to avoid foods that delay gastric emptying, such as fatty foods, red meat, and high-fiber foods. Small, more frequent meals and soft and/or liquid foods also improve emptying.
Gastroparesis is common in celiac disease and may improve with a gluten-free diet.
_Small Intestinal Bacterial Overgrowth_
The entire GI tract is lined with bacteria. (See chapter 9, "The Microbiome.") The number as well as the composition of these bacteria differs from the small intestine to the colon, with the majority of our microbiota in the large intestine. SIBO occurs when bacteria that are normally found in the colon flourish in the small intestine.
It can occur when gut motility (movement) is impaired and bacteria linger in the small intestine and multiply, or when the small intestine is obstructed and food cannot move along. Diverticula (small sacs protruding from the intestinal wall) can also allow bacteria to accumulate and multiply within them.
Like many of the functional conditions of the GI tract, SIBO can cause flatulence, bloating, constipation, diarrhea, and pain. When SIBO is severe or goes undiagnosed, bacteria can interfere with digestion and cause vitamin and mineral deficiencies and weight loss. The resulting inflammation can also produce fatigue. **SIBO is a condition that is often mistaken for gluten sensitivity or intolerance.**
It can be diagnosed with a hydrogen breath test (see chapter 6, "Testing") or sampling of intestinal fluid.
SIBO is treated with antibiotics and probiotics or a combination of both. While most doctors will not keep patients on repeated courses of antibiotics due to long-term side effects, many do not have the same reluctance to recommend prolonged probiotic use. (See chapter 5, "Supplements and Probiotics.") Long-term studies comparing antibiotics, probiotics, and combinations of antibiotics and probiotics are needed.
_Gastroesophageal Reflux Disease_
I always had this very dramatic cough. In the winter I would get these scary coughs that were so deep, that wouldn't stop and wouldn't go away. About eight years ago, we were on vacation, and I went to a doctor and they put me on antibiotics, but the cough wouldn't go away. When I came back I went to a pulmonologist. He started doing breathing tests on me and then said I had asthma. So he put me on all types of asthma meds. It didn't really do very much, and I just didn't question it. I'm one who doesn't like to question authority.
Fortunately, I had a doctor friend who said, "I really wish you'd see someone else, because I think it has something to do with your esophagus, your vocal cords." I finally got to a doctor who deals with the nose down to the stomach, very unusual. She gave me all kinds of tests and diagnosed me as having silent reflux. I don't feel it. When I had reflux I coughed. Coughing was the only symptom. No sore throat.
She put me on a very, very restrictive food program for six months, and when it didn't help, she recommended a fundoplication [surgery that strengthens the valve between the stomach and the esophagus so acid does not back up]. So that was really amazingly helpful.
After a couple of years I started coughing again. So, I went on medication and on a very low pH diet again. I was on the diet more than a year, and it helped solve the issue.
I call it the "elevator syndrome." Someone says, "You should see someone for your chest," and you get on the elevator and you get off on the floor with all the chest doctors and they diagnose you with a chest issue. But if you'd gotten off two floors down and happen to go to a gastroenterologist, they might give you a diagnosis based on a stomach or gut issue. It all depends on the floor you get off on.
(LYNDSEY, 61)
GERD occurs when stomach acid or the contents of the stomach flow back into the esophagus. The reflux (meaning to return or flow back) irritates the lining of the esophagus, causing burning, chest pain, cough, hoarseness, a sore throat, or _globus_ (the sensation of a lump in the throat). Anyone who has ever suffered from GERD will tell you that the sour liquid filled with stomach acid seriously irritates the unprotected lining of the throat.
GERD can be caused by a number of physical, dietary, and lifestyle issues. They include a weakness in the sphincter that closes the esophageal opening (food is only supposed to go down the GI tract, not back up), a _hiatal hernia,_ and certain foods. Pregnancy and obesity may also contribute to the problem.
GERD is treated with changes to diet, eating times (eating right before lying down to sleep can make the transit of food downward from the stomach more difficult), weight loss, and other lifestyle changes. Various over-the-counter (OTC) and prescription drugs are also recommended for some patients. The amount of shelf space devoted to OTC remedies for reflux testifies to the prevalence of the condition.
The GERD diet does not usually restrict gluten, but patients with celiac disease can also suffer from the condition. Of those people who are tested for GERD we have found about 10 percent are diagnosed with celiac disease. For these patients, the gluten-free diet relieves the symptoms, and they are able to stop taking prescribed medications. Reflux can therefore be a manifestation of celiac disease.
_Pregnancy Disruptions_
_I think I burped my baby out_.
(RIANNE, 35)
Many women have jokingly referred to pregnancy as a nine-month series of GI disruptions. In fact, much of the GI tract and its related organs are rearranged and compressed as the fetus grows. This can alter bowel, digestive, and urinary function, causing reflux, gastroparesis, nausea, gas, and bloating. Most of these are triggered by hormonal changes, but some may be a function of the increased pressure on the GI tract. Problems are compounded because women cannot take the usual medications to treat these conditions.
Pregnancy can also make a pre-existing GI condition worse—studies have documented an increased flare-up of IBD in the first trimester of pregnancy and postpartum. (For more, see chapter 9, "The Microbiome.")
Infiltrative Conditions
Diseases such as ulcers and _collagenous sprue_ cause lesions or scars that penetrate the mucosal lining of the GI tract. While ulcers are neither caused by gluten ingestion nor cured by its removal from the diet, collagenous sprue does have an interesting relation to gluten.
_Ulcers_
Peptic ulcers are defects in the surface layer or mucous lining of the GI tract. They occur mainly in the stomach and the duodenum but can appear anywhere. Occasionally they may be deep and extend through the entire bowel wall, perforating the bowel.
The stomach and duodenum come into constant contact with gastric acid and enzymes, yet are not usually damaged by acid resulting in ulcers. It used to be believed that ulcers were a result of stress or acid and exacerbated by certain foods (e.g., alcohol, caffeine, tobacco, excess roughage, rich and fatty foods). However, Drs. Barry Marshall and J. Robin Warren won the Nobel Prize for their "remarkable and unexpected discovery" that ulceration of the stomach or duodenum—peptic ulcer disease—is the result of an infection of the stomach caused by _Helicobacter pylori_. Smoking and the overuse of NSAIDs (ibuprofen, naproxen, Aleve) and aspirin are the only other known causes of peptic ulcers. Ulcers lower in the GI tract are not acid or _H. pylori_ related.
Interestingly, some studies show that older adults are more likely to develop ulcers, and this may in fact be a result of their increased use of aspirin and NSAIDs to control arthritis pain.
Fortunately, peptic ulcers are relatively easy to treat with antibiotics and other drugs, such as proton pump inhibitors, which reduce the amount of acid produced by the stomach. Because of the danger of bleeding and the resulting anemia and/or stomach cancer, ulcers should be diagnosed and monitored by your doctor.
_Collagenous Sprue_
Collagenous sprue is a lesion within the small intestine that occurs in those with villous atrophy. It is so named because of a band of collagen (scar tissue) that forms right under the epithelial cells lining the intestine. Its symptoms mimic many other GI diseases, and it is typically associated with severe malabsorption and diarrhea. It can be caused by any kind of sprue—tropical, celiac, or drug-induced.
Celiac disease that does not normalize on a gluten-free diet is often called "refractory sprue" (type 1 and type 2) and can develop into collagenous sprue. This is treated with a combination of a gluten-free diet, steroids, or other immunosuppressants.
Miscellaneous Disorders of the Normal Gut
_Lactose Intolerance_
Lactose intolerance is caused by a lack of the enzyme ( _lactase_ ) that digests lactose, the sugar found in milk and milk products. There are two types of lactose intolerance—primary, which is genetic, and secondary, which is caused by the destruction of the microvilli of the small intestine that produce lactase (see chapter 7, "The Normal Gut and Digestion"). Secondary lactose intolerance occurs in celiac disease and many other conditions when inflammation "sears" and destroys the microvilli. It usually resolves when the underlying condition is treated and cured.
When undigested lactose arrives in the colon and is fermented by the bacteria—which thrive on this sugar—it then causes the bloating, gas, and diarrhea common to sufferers of lactose intolerance.
Genetic lactose intolerance is treated by the avoidance of milk products and the use of lactase supplements when ice cream and pizza beckon. Secondary lactose intolerance is treated by the resolution of the underlying condition causing the villous atrophy.
Summary
• A diseased gut sends signals in the form of symptoms, and interpreting them can be confusing. Symptoms are complex, and the same symptoms can underlie different problems with different treatments.
• Symptoms can evolve. Bacterial and parasitic infections in the GI tract can trigger other conditions. This is often the reason that symptoms do not resolve but progress into another problem.
• GI problems fall into four basic categories. They can be caused by inflammatory conditions, malignancies, functional, and/or infiltrative issues. Putting yourself on a gluten-free diet will not necessarily resolve the underlying problem and may delay a proper diagnosis and cure.
• Do not give in to the temptation to self-diagnose and blame the food you eat for GI symptoms.
• It is critical to isolate, test, and then treat.
The Microbiome
_Exploring the unknown requires tolerating uncertainty._
—BRIAN GREENE, THEORETICAL PHYSICIST
_If you don't like bacteria, you're on the wrong planet. This is the planet of the bacteria._
—CRAIG VENTER, BIOTECHNOLOGIST, BIOCHEMIST, AND GENETICIST
The human body is home to trillions of tiny organisms that vastly outnumber the cells in the body and affect our overall health. In fact, there are approximately 10 trillion cells in the human body and 100 trillion living microorganisms. These are the bacteria, viruses, fungi, and yeast that compose the microbiota.* They line all the surfaces of the body and live in the GI tract from mouth to anus as well as the skin, nose, teeth, and ears, and the male and female sexual organs.
The human body is their home, and they have evolved distinct "personalities" amenable to their particular living arrangements. There is even seasonal variability in our skin microbiota. But it is in the gut that most of them exist and flourish. Some thrive in the acidity of the stomach, others in the dark and wet large intestine. Microbiota are integral to the digestive process and the constant internal dialogue between the immune, metabolic, and nervous systems. They play a crucial role in human development and health, and are routinely affected by everything we put in our mouths.
They are a fulcrum of metabolism, releasing nutrients from foods that would be otherwise indigestible, and making B vitamins and vitamin K. They create a constant state of inflammation and immune regulation so that we do not identify all proteins as foreign and can also tolerate food products. In fact, the microbiome trains our immune system very early in life. They are part of the "tasting" system that samples foreign proteins and pathogens entering the gut, determining if they are safe or harmful, and then instructing the immune system.
These various organisms are often referred to as commensal bacteria, which derives from the Latin _com_ (in association) and _mensal_ (at the table or meal). We quite literally "eat at the same table" with our microbiotic family since the food we eat is their main source of energy. And everything we ingest plays a role in dictating which will thrive and which will perish.
Researchers now know that the relationship we have with our microbiome can best be described as one of _amphibiosis_ —as Martin Blaser, M.D., explains in his book _Missing Microbes_*—it is symbiotic (mutually dependent) or parasitic depending on context. Our microbiome works with and against us at any given time—and often simultaneously.
Everyone's microbiome is his or her own personal jar of multicolored jelly beans that gets shaken and rearranged, eaten, and replaced regularly. There are shifts in both the diversity and the pattern of each individual's bacterial makeup over time as well as within different cultures around the world.
Disruption in the microbiome is known as _dysbiosis_ ( _dys_ —abnormal, impaired; _biosis_ —mode of life), an imbalance in the microbiota, and this has different effects on the body and our health. There is the possibility that the manipulation of the microbiome may be a link between risk factors and development of many disorders ranging from diabetes to obesity. Intestinal dysbiosis has been associated with celiac disease, but whether the alterations in the microbiome are cause or consequence of the disease is unknown.
It is also possible that a specific genetic makeup may influence the composition of the first gut colonizers and could contribute to determining your risk for certain diseases. This is being studied in a number of neurological conditions and mood disorders as well as the gut.
Diet can also alter the composition of your flora and fauna. People on a vegan or vegetarian or very restricted diet can change the composition of their fecal microbiota. Yet there is no scientific proof as to the effect of this alteration and whether the microbiota returns to their "normal" once the diet changes. The diet can affect the composition, but not permanently. (Unless it is your permanent diet.)
We are currently studying the effects of a gluten-free diet on both celiac and gluten-sensitive volunteers to determine if it can change their microbiome.
The hot topic for scientists today is what this all means—the creation, growth, composition, mechanisms, and roles of the microbiome. Currently, almost any disease process that is looked at may be associated with alterations in the microbiome, and we may be applying "treatments" where they are unnecessary and/or harmful. There are many unanswered questions surrounding the rush to manipulate the microbiome with probiotics and a daily infusion of yogurt.
Where Does the Microbiome Come From?
_You can choose your friends, but not your relatives._
—ANONYMOUS
Our microbiota come to us both vertically and horizontally—that is, from our genes and constantly from our environment. We initially acquire our microbiome from our mother, but every child is also a product of the parental genes.
Bacteria line the birth canal and are introduced into the baby during childbirth. Exposure continues through suckling, licking, touching, and kissing the baby. Long before blenders, Beech-Nut, and Gerber, parents used to chew baby's food, and even now, mothers often use their saliva to wipe a smear of dirt from a child's mouth or face. The antibodies that are transferred from mother to child across the placenta and through breast-feeding are protective against infections and possibly dietary antigens. Everyone and everything a baby touches or consumes also feeds its microbiome. By the age of 3, the child's microbiome resembles that of an adult and stabilizes.
The adult microbiome continues to incorporate this horizontal and vertical input that changes as we age through the drugs we take; the food, vitamins, and supplements we ingest; the people we kiss and touch; the places we travel to; and the diseases we acquire. This ever-evolving, dynamic, and complex ecosystem differs not only from individual to individual but in the same person over time. Microbiota also differ from country to country depending on what you eat and where you live, and differ when you are sick.
More important, our microbiome has its own genetic component that is 100 times more complex than the human genome.
The 21st-Century Microbiome
The contemporary Western world has evolved—now we are all washing our hands, giving birth to babies in hospitals and not on the kitchen table, sterilizing baby bottles and nipples, and maintaining a level of cleanliness not seen either in our earlier human history or even in other parts of the world. And it is becoming clear that this emphasis on cleanliness has repercussions. (See chapter 3, "The Hygiene Hypothesis.") We are also taking various antibiotics—"drugs that kill bugs"—that change the composition of our microbiome.
While there is no one "healthy" microbiome, there is little doubt that 21st-century life has—and is—altering our intestinal ecosystem with ramifications for our health. When the microbiome is disrupted it upsets the entire body—slowly or rapidly depending on the degree of dysbiosis. While the active microorganisms within us may offer new keys to GI health and repair, we first must try to ascertain what comes first—the disease or the dysbiosis. That is, do changes in the microbiome initiate a disease, or are they a result of it? Quite possibly, they coexist in an elaborate dance where genes, germs, and environment take turns leading.
Why Is It Important?
_If we knew what it was we were doing, it would not be called research, would it?_
—ALBERT EINSTEIN
Since the microbiome is extremely diverse, even in healthy people, and most diseases have various subtypes and manifestations, it is very difficult to pinpoint a direct cause-and-effect relation between the microbiome and specific diseases. This complex and unpredictable system thrives because of its ability to respond so rapidly to change. We must attempt to decode the dialogue between the microbiome and the immune system of the body before we can understand its messages.
The following are a number of factors that scientists have isolated as affecting the microbiome. Keep in mind that the consequences of these changes are unclear.
Pregnancy and the Microbiome
While some bacteria may enter the child via the placenta in utero, the bulk of the newborn's microbiome is colonized during birth when the microbes in the mother's vagina populate the child's body. Thus, there is a biological cost to an elective Caesarean section (as opposed to an emergency C-section when the child has already descended into the birth canal) for the newborn. As Martin Blaser, M.D., notes in _Missing Microbes,_ the "founding populations of microbes found on C-section infants are not those selected by hundreds of thousands of years of human evolution or even longer." He asks, "What if those first microbial residents provide signals that critically interact with cells in the rapidly developing baby's body?" Studies have shown a connection between C-section babies, obesity, and celiac disease, as well as other disorders. Yet other studies have questioned the link.
There are interesting links between the colonization of the infant microbiome and various diseases and disorders, but the effect of genetics and infant environment leave much unanswered. We often hear remarks like "stomach issues run in our family." Certain diseases—e.g., celiac disease, Crohn's disease—have a genetic basis but also environmental triggers. This raises the intriguing issue of whether the mother's dysbiosis is passed genetically, acquired later or during pregnancy, and what effect, if any, it has on the newborn.
The jury is still out on this.
Antibiotics and the Microbiome
If we have coevolved with our microbiome, what happens when we take multiple courses of antibiotics that kill bacteria—both good and bad, either permanently or only at times—rearranging our intestinal flora or impacting our immune systems? Does that impact give certain conditions a chance to flourish or occur?
The average child in the U.S. has taken between three and four courses of antibiotics before his/her third birthday, when a child's microbiome is still plastic. In 2013, a nationwide study showed that half of all children in many Western countries receive antibiotics at least once a year. Allergies, celiac disease, autoimmune diseases, obesity, and autism diagnoses have mushroomed in the past decade. Some scientists believe antibiotics may be responsible for the rise in these and other conditions because of their effect on the microbiome and the resonating effect this has on the immune system.
Antibiotics also have a direct effect on the gut that can be easily demonstrated. Bacteria in the colon make vitamin K, which helps to clot our blood and stop excessive bleeding (see chapter 7, "Digestion"). But if you are taking antibiotics that kill the bacteria making vitamin K and you are also taking a blood thinner, such as Coumadin, you can get massively high levels of anticoagulation. This can be a huge problem.
Most of the many species of microorganisms in the digestive tract are helpful under normal circumstances. But when something upsets the balance of these organisms, an otherwise harmless bacteria can grow out of control and create huge problems. An example of this is a bacterium called _Clostridium difficile,_ or _C. diff_. When illness and/or different drugs wipe out competing bacteria, this usually benign organism overgrows the compromised intestine, releases toxins that attack the lining of the intestines, and causes severe colitis and diarrhea and occasionally death.
The disturbance of normal healthy bacteria by antibiotics, acid suppression and age may provide _C. difficile_ an opportunity to overrun the intestinal microbiome. It is carried in feces and acquired from contaminated surfaces including hands and equipment. In a healthy person's gut, it is contained by other thriving bacteria. Outbreaks therefore are often found in settings with compromised patients, such as hospitals and nursing homes. (See "Bugs as Drugs" later in this chapter and in chapter 30.)
It is clear that a disturbed microbiome reduces the body's ability to respond to and tolerate the many things we ingest.
Microbiome and Food Allergies
There has been a large rise in childhood food allergies over the past decades. Research from animal studies indicates that a microbiome diminished and/or changed by antibiotics may be a factor in this increase in allergic and immune responses.
In a recent study, mice given antibiotics early in life were far more susceptible to peanut sensitization, a model of human peanut allergy. When the mice were fed a solution containing _Clostridia,_ a common gut bacterium, the sensitization disappeared. When given _Bacteroides,_ another kind of common and healthy bacteria, the same effect was not found. The researchers determined that _Clostridia_ helped to "maintain the integrity of the [intestinal] barrier," which kept peanut proteins that can cause allergic reactions out of the bloodstream. While these researchers have concluded that it may be possible to manipulate the microbiota as allergy therapy, all of this needs testing in humans.
This and other research "opens up new territory," Blaser says. It "extends the frontier of how the microbiome is involved" in immune responses and the roles played by specific bacteria.
Research studies suggest that factors that alter the microbiome increase the risk of developing celiac disease. Most of the risk factors for celiac disease—elective Caesarean, gastrointestinal infections, antibiotic or proton pump inhibitor use—could also be interpreted as modulators of the microbiome. Some studies show that children with a genetic risk for celiac disease have different microbiota compared to other children.
Obesity and the Microbiome
There are several "nonintuitive" disruptions to the microbiome that are attracting scientific interest, such as obesity theories. Researchers have found more diversity in the microbiome of leaner people. This has raised the question of whether antibiotics contribute to the development of obesity, since they kill bacteria. Several hypotheses are suggesting manipulating the microbiome to treat obesity and metabolic disorders.
There are a number of mechanisms by which intestinal bacteria may promote obesity. Some studies demonstrate that certain bacteria improve the absorption of nutrients in the small intestine—possibly promoting weight gain.
Other studies point a finger at the ability of microbes to increase inflammation. Since intestinal inflammation has been seen as a condition preceding obesity and metabolic disease, and this can be altered by dietary changes of the gut microbiota, it is possible that dietary intervention can be designed to combat these disorders.
Finally, the levels of certain families of bacteria differ in obese and lean people, which lends support to the theory of a microbial link in obesity. But it is still unknown whether people are genetically prone to lower levels of specific classes of bacteria, making them prone to obesity.
In mouse studies, microbiota from obese patients transferred obesity to the mice, leading to the assumption that microbiota can be causative and transmissible.
We have learned from farmers that giving antibiotics to farm animals makes them grow fatter and faster. With studies showing that antibiotics change the microbiota, we must question the antibiotics that are now in our meat and our milk and the consequences of this approach on us and our children.
It is important to know that these theories are controversial, but it is clear that what we ingest plays a major role in the composition of the microbiota and therefore its function. Dietary strategies targeting the microbes in our gut may be a possible tool to control metabolic disorders and obesity. Research trials using diets, probiotics, prebiotics, or a combination are in very early stages. We need to understand the complex interactions between our genes, our germs, and everything we ingest before a treatment strategy can be determined.
Autism Spectrum Disorder and the Microbiome
It has been hypothesized that changes in the gut microbiota play a role in the development of autism. We will explore some of the proposed mechanisms linking such changes to neurological development, immune function, and behavior in chapter 26, "Autism."
The Microbiome and the Brain—Can Bacteria Change Behavior?
The link between our microbiota and our brains is another part of the new frontier. It has been studied mainly in mice, with intriguing results. Through them scientists have shown that microbiota are not only important to healthy metabolism and brain function, but that the gut-brain communication pathways include the enteric nervous system (see chapter 10, "The 'Second Brain'"), and that the development of gut microbiota may influence the wiring of circuits that affect stress and impact mood and behavior. Many of these studies involve germ-free mice with controlled introduction of antibiotics, bacteria, and foods. Caution is required since the mouse intestinal tract is not a substitute for the human. But researchers have "humanized" mice by inserting human genes associated with different diseases into them, and this is an opportunity to study the relationship between specific genes and diseases as well as the effect of drugs and dysbiosis in various conditions.
Many people consider chocolate and coffee the ultimate "mood foods"—capable of calming frazzled nerves and restoring energy. These foods actually contain chemicals that stimulate the brain. Researchers in Canada are now examining the influence of food on the composition and activity of our intestinal bacteria and whether this can influence brain function and mood. They have shown that specific probiotic mixtures can restore normal feeding behavior in mice whose patterns had become distorted after a stomach infection. These researchers are now investigating a specific probiotic for IBS and its effect on GI as well as psychiatric symptoms. They caution that the mouse research attempting to alter behavior by modifying bacteria in the gut cannot be translated to humans at this point.
Bugs as Drugs
Before the discovery and routine use of antibiotics in the 20th century, elixirs and tinctures of herbs and plants as well as actual bugs were routinely used to treat infections and various illnesses. The line between food, plants, worms, and medicine was thin. Today, antimicrobials—which include antibacterials, antivirals, antifungals, and antiparasitics—target every organism in our microbiotic ecosystem. Unfortunately, designed for adaptation and experienced over millions of years in survival techniques, bacteria and viruses have developed resistance to many of these drugs and found ways to elude them.
Because antimicrobial resistance is now a major health issue, researchers are using bacteria, "bugs," and viruses themselves to fight disease. They are also using the ability to decode the genome to find new treatments to circumvent the growing crisis of drug resistance. Maggots, leeches, and herbal remedies are making a comeback as well.
Fecal transplants have recently been approved as therapy for resistant and recurrent _C. difficile_ infection, and are under investigation for a host of other conditions. Stool, frequently from a relative or other healthy donor, is examined for different pathogens, mixed with a saline solution, and introduced into the patient's intestines via enemas or during a colonoscopy and/or upper endoscopy. The intent is to replace the "good bacteria" that has been killed by illness, drugs, or the _C. difficile_ in order to restore the missing flora and suppress the _C. diff_ that has overrun the intestines.
One researcher noted that "the intestinal flora is a promising new frontier for scientists and health care professionals alike." The question is not only whether the newly introduced outsider will stay but what effect he will have on the neighborhood.
How Constant Is the Microbiome?
If you alter the microbiome by changing your diet or taking pro- or prebiotics, what are the short- and long-term effects? This is a key question and the focus of most of the current research. Studies have shown that if you give antibiotics to a very young child, the microbiota will permanently change. When they are given later, the composition returns to what it was. But science is not at a point in its understanding of the microbiome to know what the short- and/or long-term effects are of these changes.
There is also the question of the safety of probiotics. Under what conditions are they made, and where? Are they viable? Can you trust the label? The recent death of a child due to contaminated probiotics is unacceptable. (See chapter 5, "Supplements and Probiotics.")
Summary
• The intestinal microbiome is an immense ecosystem within our body. It orchestrates and maintains stability in the digestive and immune systems by constantly responding to what we ingest and changes in external conditions.
• The microbiome is populated both vertically, i.e., genetically and from our mother during birth, and horizontally, by everything we eat, touch, and breathe. Its composition is therefore continually changing and rearranging.
• It is active in metabolism by helping to digest food that is otherwise indigestible and releasing vitamins and minerals.
• Everyone's microbiome is different and varies in any individual over time and circumstances. It changes with age, diet, and disease.
• The microbiome is instrumental in controlling inflammation in the gut—in effect, turning the gas up or down. Our ability to react to pathogens and intestinal disease depends on this microbiotic hand on the intestinal "oven."
• Chronic inflammation and/or dysbiosis can bring about a series of events that lead to altered bowel function, intestinal diseases such as IBS, and, it is hypothesized, various autoimmune diseases including IBD, celiac disease, autism spectrum disorder, type 1 diabetes, and obesity.
• If bacteria in the gut strays from its usual home, it can cause both systemic as well as gut diseases.
• Sometimes "good" bacteria is killed off by antibiotics or other drugs, and "bad" bacteria overruns the system, creating dysbiosis, or disruptions in the microbiota.
• It may be possible to modify the intestinal microbiota by diet, prebiotics, probiotics, or fecal transplant of donor stool. But little is known about the best types of interventions, the degree of resistance to a particular therapy, or the long-term effect of any therapy.
• Food and drugs, such as antibiotics, affect and alter the microorganisms in the gut. Conversely, it is also possible that any one person's microbiota may also affect the response to certain foods (such as gluten) and the efficacy or toxicity of drugs he or she takes. This requires more research on both genes and germs to determine the role of each microbial species.
• The microbiome is the new frontier in GI health. While it appears to offer tantalizing answers to many things affecting the body, the truth is proving to be as elusive as the many microscopic organisms eating at our table.
The "Second Brain" in the Gut
_. . . who wears his wit in his belly, and his guts in his head . . ._
—SHAKESPEARE, _TROILUS AND CRESSIDA_
_In every body, the brain is king. Its writ is law. At the top of the bowel, the rule of the king is acknowledged, but as one descends deeper and deeper into the depths of the gut, the rule of the king weakens. A new order emerges: that of the second brain._
—MICHAEL D. GERSHON, M.D., _THE SECOND BRAIN_
_The belly rules the mind._
—SPANISH PROVERB
Digestion has evolved over millions of years into a highly efficient workhorse that enables us to digest food without conscious thought—freeing us for evolutionally desirable activities like hunting, mating, and escaping danger and the modern equivalents of working, shopping, and texting. It is only when this system raises itself to the level of consciousness and sends SOS messages—cramps, diarrhea, heartburn—that we become consciously aware of its workings.
The independent nature of our gut and the interactions between the brain and the gut have been well known for many centuries. They are an important aspect of normal GI function and to the way we think and feel. Treating GI symptoms requires an understanding and appreciation of our "second brain."
I feel as if I have two brains—one in my gut and one in my head.
(GLEN, 50)
My gut was always sensitive to emotional things. When I was in a stressful situation I would get diarrhea. Something terrible would happen, and that would be the trigger.
(CARLA, 40, IBS)
Nervous System 101
In simplest terms, the nervous system consists of two main branches that work together to control all bodily functions. It is divided into the central nervous system (CNS), consisting of the brain and spinal cord, and the peripheral nervous system (PNS), which sends nerve fibers to and from the brain and spinal cord to the rest of the body. The CNS is the "top dog," and the PNS carries out orders and reports back with constant updates on bodily status. The autonomic nervous system (ANS) is a branch of the PNS and controls functions in the body that work independently of conscious control and awareness, e.g., sweating, heartbeat, and digestion.
The enteric nervous system (ENS) is the intrinsic (located within) division of the ANS that governs the functions of the gut—it does not need constant orders from the brain/spinal cord to function, although it reports back and stays in constant communication with the central nervous system. If you take a piece of bowel and isolate it, it has movement. It contracts automatically because there are local nervous connections within it to the intestinal muscles that act independently.
Thus, while all of the nervous system is interconnected and constantly engaged in cross-talk, the enteric nervous system is a "second brain" in the body.
The Enteric Nervous System
There are 100 million nerve cells in the small intestine, roughly equivalent to the number in the spinal cord. It is the largest and most complex division of the PNS and ANS, and consists of numerous different types of neurons. They monitor and control both the "automatic" aspects of digestion—which require no conscious thought to function—and the very real functional and nervous conditions it is involved in.
There are different types of nerve cells embedded within the walls of the GI tract, and each has anatomical features that reflect the cells' functions. An explanation of these different cells is beyond the scope of this book, but it is important to know that they have control over the stimulation and/or inhibition of motor activities and secretions in the bowel.
You might think of the ENS as an integrated circuit board—the "motherboard" of the system—that is involved in all aspects of intestinal function. It integrates GI motility/movement, the exchange of fluids across the mucosal surface of the intestine, blood flow, and the secretion of gut hormones. The ENS controls, coordinates, and impacts food regulation, digestion, and absorption as well as the development and perception of symptoms through its many sensory mechanisms. It is an integral and crucial component of the nervous system but capable of self-government as well as rebellion.
It acts independently, can learn and respond to emotions, and "remembers" in order to produce "gut" feelings.
I had the most outrageous pain in my lower abdomen—a take-your-breath-away, knifelike pain.
(MARION, 68)
I have an iron-man belly; nothing I eat or do affects it!
(MARSHAL, 65)
While the ENS normally runs silent and deep like a submarine, when it is altered in disease, it "surfaces," breaks radio silence, and rapidly expresses its distress. It is also capable of shooting ballistic pain missiles. This comes as no surprise to the 30 percent of all patients who visit doctors yearly for GI complaints. They have no trouble understanding that the ENS is also a sensory organ. But its "senses" are multilayered.
The GI Tract as Sensory Organ
In order to protect itself from the outside world, the GI tract must be able to mount appropriate defenses against pathogens and other harmful substances. At the same time, it must be open and permeable to nutrients. It integrates these two responses by a multifaceted detection system that senses the outside environment and then reacts appropriately. It identifies friend from foe and acts on that knowledge. It can reject foods through objectionable taste, vomiting, diarrhea, or any combination of these symptoms. This occurs through a very complex system of nerve and immune cells that line the tract and trigger responses such as nausea, vomiting, and pain. Vomiting and diarrhea can be rapid responses if toxic substances are ingested in sufficient quantities.
But the sensors can malfunction and initiate reactions that are responsible for many digestive problems—as many people with IBS will attest. As Michael Gershon, M.D. (an expert in the growing field of neurogastroenterology), notes in his book _The Second Brain,_ "Few things are more distressing than an inefficient gut with feeling. And, since the enteric nervous system can function on its own, it must be considered possible that the brain in the bowel may have its own psychoneuroses."
Many of the patients we interviewed complain that doctors tell them "It's all in your head" and prescribe a psychotropic. Their response to that is a vigorous "I am not depressed!" But it is becoming increasingly clear that many of these drugs are actually "gut-otropics"—therapies aimed at the "second brain" in the gut. A reversal in thinking on this subject may be an important answer to treating functional bowel disease.
While our understanding of the integrated responses of the gut to the sensory information it receives is growing, it is only in the early stages of developing therapeutic agents and dietary approaches that target specific gut receptors. One such receptor, serotonin, is receiving increased attention as both "sword and shield." If we can "sculpt" the ENS, we may be able to block the responses that lead to malfunctions in the GI tract and echo throughout the body.
The Molecular Busybody
Nerves act by releasing neurotransmitters, molecules that stimulate or inhibit a target receptor. These nervous impulses, like electrical transmission, release a host of different chemicals that initiate the "on" or "off" switch. One of the key chemicals in this scenario is serotonin.
What Is a Brain Chemical Doing in the Gut?
Serotonin was always considered a brain chemical—a neurotransmitter—mainly because it is targeted as a therapy for depression. But, in fact, 95 percent of the serotonin in your body can be found in your gut.
Serotonin is much more than a mood elevator. It has multiple functions—it is a "busybody" because its nose is into everything and everybody's business, and in particular it does this in the GI tract.
Serotonin has a number of important functions:
• It is critical in development, a growth factor.
• It is a hormone that moves from the gut into the bloodstream and regulates bone development.
• It regulates movement in the intestines. In other words, _too little_ serotonin can contribute to constipation (or slow transit time). _Too much_ serotonin can contribute to diarrhea (or fast transit time).
• It is a defensive molecule. The cells making serotonin have sensors that can detect bacteria. This causes serotonin to be released and can activate the immune system and start inflammation. This serves to warn the body of infection. If this malfunctions, it can lead to unwanted inflammation. But in reality, these antithetical functions are actually synergistic and, as Dr. Gershon notes, "allow the gut to have its inflammation and survive it too."
• It is a paracrine hormone (acting only in the vicinity of the gland secreting it) that stimulates peristalsis, movement in the gut that propels food down the GI tract.
• It is a neurotransmitter in the ENS involved in many nerve functions.
The role of serotonin in the GI tract is an emerging area of study. It may have a central role in GI function and the development of disease. It is important to gastrointestinal motility, intestinal neurogenesis, mucosal growth/maintenance, intestinal inflammation, and bone growth. Serotonin receptors are being actively studied as therapeutic targets to treat IBS, obesity, and type 2 diabetes, and as a potential sculptor of the ENS. Its true role has yet to be determined.
Can We Train or "Sculpt" the ENS?
Altering the activities of serotonin is being actively studied to produce long-lasting changes in the ENS. Since IBS and other GI conditions often begin in childhood, it is hoped that by "sculpting" the development of neurons, the pathways for and development of various psychological or infectious/inflammatory reactions could be influenced.
Work on the ENS has many diagnostic and study challenges, since it is difficult to test intestinal nervous tissue. Most of the current studies are on mice, many with human gene mutations.
Serotonin has become part of the arsenal of antidepressants such as tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) that are effective in the treatment of both _affective_ (mood) and GI disorders. These drugs treat the active part of the gut that talks to the brain quieting the GI tract and the pain. It also quiets the part of the brain making the gut upset.
When taking serotonin, you are treating the "second brain" in the gut.
_It's not "all in your head"—a great deal is in your gut._
—MICHAEL GERSHON, M.D.
Summary
• The gut has a mind of its own—the enteric nervous system. The ENS is one of the most intriguing parts of the brain-gut complex and involved in and/or responsible for many of the symptoms of GI disease and malfunction.
• The ENS is an efficient computing center that sends nerve, immunological, and hormonal messages throughout the GI tract and cross-talk to other parts of the body.
• The receptors in the gut think, feel, and stimulate responses and/or inhibit them—often simultaneously. They are the targets of much research. Training or "sculpting" them may enable scientists to prevent as well as treat GI malfunction and conditions.
• When we evaluate and treat GI conditions, we must also acknowledge and treat this ruler of "the lower kingdom."
PART III
The Fingers on the Trigger
_Trust those who seek the truth but doubt those who say they have found it._
—ANDRÉ GIDE, NOBEL LAUREATE IN LITERATURE
_We cannot solve our problems with the same thinking we used when we created them._
—ALBERT EINSTEIN
What is really causing your symptoms?
It usually takes more than one insult to result in a disease. While the connection between cause and effect may appear clear-cut—"I eat gluten and get symptoms"—the link may not be that straightforward. There are many triggers of symptoms that are attributed solely to gluten or grains that come from very different sources. The following chapters explain not only some of the newest research into the reasons for both GI and systemic disorders, but also explore the intriguing and nonintuitive links between what we ingest and experience with our GI and mental health.
Some come from left field, such as a drug for blood pressure that inflames the intestine and mimics celiac disease. Others are found in foods that create similar symptoms—the nongluten proteins in wheat, dietary carbohydrates that create bloating. A few are genetic, and, increasingly, research is examining inflammation itself as a potential source of both gut and brain issues.
Finally there is the "double hit," when one condition triggers another—a diagnosis often missed when the initial condition is supposedly successfully treated before the second one occurs. Links are now being identified between parasitic or bacterial infections that predispose to a compromised gut that then becomes sensitive or intolerant to specific foods; childhood abuse, trauma, and alcohol abuse have been identified as triggers of intestinal diseases later in life.
While we all like clear directions—"make a left, follow this road, and in 500 feet you are at your destination"—symptoms come from signals that loop through a jungle of interconnections within the 30-foot-long GI tract.
The following chapters will give you a scientific guidance system to help navigate the maze and reveal what may be triggering your symptoms.
Gluten and Nongluten Grains
_An editor is someone who separates the wheat from the chaff and then prints the chaff._
—ADLAI E. STEVENSON
In the past number of years the media has accused gluten of aggravated assault and bodily harm. Yet it is increasingly clear that there are many other proteins in wheat besides gluten that may be causing the same set of symptoms blamed solely on gluten. These nongluten proteins are being studied as an additional toxic component of wheat that may be a distinct culprit in celiac disease and other gluten-related disorders.
Which is to say that beneath the chaff, there is more than gluten in the wheat.
Gluten and Nongluten Proteins
_Gluten_ is a term that is used to describe the 70 different "storage" proteins of wheat. Often referred to as gliadins and glutenins in articles or studies, they are the bulk of the protein content. The many enzymes at work in the digestive tract do not easily digest these complex proteins. In people with celiac disease, the partially digested gliadin fragments cross the mucosal lining of the intestine and provoke an immune response. But _many_ people are unable to digest gluten well, and this also triggers a response within the GI tract, causing GI symptoms.
Nongluten proteins make up about 25 percent of the proteins in wheat and are often grouped as albumins or globulins. Several of these nongluten proteins—notably, amylase trypsin inhibitors—may be additional fingers on the trigger.
Wheat Amylase Trypsin Inhibitors
Amylase trypsin inhibitors (ATIs) are part of a family of nutritional proteins found in wheat and related grains that serve a protective function by inhibiting specific enzymes in bacteria and by increasing the plant's resistance to certain pests and parasites. Recent attempts to breed pest-resistant—and therefore high-yielding—wheat have led to a drastic increase of ATI content.
Nongluten proteins were once considered nontoxic for those with celiac disease, but recent studies disprove that assumption. People with celiac disease make antibodies to some of these proteins, such as ATIs, which have recently been incriminated as possibly contributing to the development of the disease. While ATIs do not explain the upsurge in cases of celiac disease, they may contribute to the development of gluten sensitivity. ATIs may be part of a group of nongluten molecules that drive intestinal inflammation.
This family of molecules has also been identified as allergens. They are responsible for wheat allergy and/or baker's asthma. Researchers have therefore focused on these nongluten proteins as possible mediators not only in celiac disease but other GI and nonintestinal inflammatory conditions.
_Importance of ATIs in Celiac Disease_
The role of nongluten proteins as a trigger of the immune response in celiac disease is a key question since current tests as well as therapies are directed against gluten. The suggestion that ATIs may be toxic may help to identify new targets for both diagnosis and treatment.
The role and significance of nongluten proteins in the development not only of celiac disease but other inflammatory conditions in the gut and body is an important avenue of current and future research. Research into the main nongluten proteins that may cause an immune response—including serpins, purinins, amylase/protease inhibitors, globulins, and farinins—may eventually target additional dietary troublemakers and treatment options.
Oats
I feel empty if I don't start the day with my bowl of steel-cut oats.
(MIMI, 37)
Oatmeal porridge? Even the thought of eating that mush . . .
(CARL, 43)
A bowl of steaming oatmeal has long been advertised as "the perfect way to start the day." Some would disagree. Because of the health benefits of oats—they contain many vitamins as well as fiber—they are also often made into cookies and added to crisp toppings and meat loaves. As a star player in the high-fiber arsenal, oats are praised for their ability to fight cholesterol, help prevent heart disease, lower blood sugar, and help prevent type 2 diabetes. They are also listed as a robust antioxidant.
Because of these many advantages, oats have been studied and accepted as a well-tolerated alternative to wheat for children and adults with celiac disease.
Oats have found their way to our "fingers on the trigger" list because a new study has found a molecular explanation for why some people with celiac disease and others with gluten sensitivities may not be as tolerant of oats as once believed. The inflammation that results may be the source of GI symptoms that are not initiated by but blamed on gluten.
The protein in oats are avenins, which are not thought to cause a reaction in the majority of people with celiac disease. Celiac disease involves a reaction to glutenins (the protein portion of wheat), _hordeins_ (barley), and secalins (rye). But antibodies to avenins have been documented in some people with celiac disease.
One possible reason for this enhanced response to oat protein may be a general elevation of food antibodies in an already inflamed intestine. When the gut is inflamed, the normal protective barrier of the intestine (the _epithelium_ ) can become damaged, and pathogens can travel through and between it and initiate an antibody response. (See chapter 16, "Intestinal Permeability.")
There are a number of other reasons that oats may cause GI symptoms. While oats are safe for most people with celiac disease and gluten sensitivities, cross-contamination during milling and processing can still occur. It is also important to note that because of oats' high fiber content, some people who add oats to their regular diet encounter bloating, gas, and indigestion. This is generally more a result of the sudden addition of so much fiber and usually gradually disappears when your intestines adjust to the change. This is very common for anyone adding any type of fiber to his or her diet—it must be gradual!
We continue to recommend monitoring and follow-up of people with celiac disease and gluten sensitivities who regularly ingest oats as part of their diet to ensure that there is no sensitivity or antibody reaction to this nongluten grain.
Summary
• Your body can develop an immune response to a number of proteins besides gluten in different grains. This immune response does not necessarily mean that these proteins are toxic.
• If other proteins in wheat are involved in the development of celiac disease, they may play a role in its treatment.
• The antibody response triggered by nongluten grains needs to be investigated further. We do not know if they are innocent bystanders, part of a general immune response in the gut of people with celiac disease, or if they may in fact have potential as biomarkers for other gluten-related disorders.
Carbohydrates and FODMAPs
_Carbohydrates, from the Latin carbo, which means "yummy," and hydrates, which means "cinnamon bun," are not something I can eliminate or even drastically cut back on._
—CELIA RIVENBARK
Most of the energy we need to move and live is provided by the carbohydrates we eat. They are the most readily digested form of fuel for the body—for most people. For others, carbohydrates often trigger the most gastric symptoms.
Taken in excess—mainly in processed and manufactured foods sweetened with them—they also fuel weight gain. In some people certain carbs also fuel a rapid race to the bathroom to deal with diarrhea and flatulence. For them, carbohydrates are not just fingers on the trigger but a heavy foot on the intestinal gas pedal.
What Exactly Are Carbohydrates?
All carbohydrates are sugars (saccharides) found in grains, fibers, fruit, vegetables, plants, roots, and nuts. Manufacturers also add them in a condensed form (e.g., dextrose, corn syrups/fructose, malt, glucose) to sweeten processed products from breads to soft drinks, canned goods to yogurts, cereals to soups. Catering to the human cravings for sugar, salt, and fat—necessary for body function and survival—the food industry has added sugars to so many products it is difficult to avoid them in the supermarket.
All carbohydrates are classified according to the complexity of their makeup.
• **Monosaccharides** ( _mono,_ "one"; _saccharide,_ "sugar") are the simplest sugars, such as glucose and fructose. Glucose is found in fruits, corn, corn syrup, honey, and some roots; fructose is found together with glucose in honey and fruit. It is commonly used to sweeten products in the form of high-fructose corn syrup.
• **Disaccharides** are two sugars joined together and usually contain glucose. Sucrose is glucose and fructose; lactose is glucose and galactose. Sucrose is table sugar and found in fruits, vegetables, honey, sugar cane, sugar beets, maple, and corn syrup. Lactose is the main sugar found in milk and can be broken down only by lactase.
• **Polyols** (sorbitol, mannitol, and xylitol) are the alcohol forms of some sugars. They are poorly absorbed, if at all, from the GI tract and inhibit a rapid rise in blood sugar, which is why they are often found in products designed for diabetics. While they are found in fruits and plants, they are also manufactured and usually added to sweeten "sugarless" products. People who chew sugarless gum consume a great deal of polyols. Because they are not fully absorbed by the body, they can be a potent cause of diarrhea and bloating.
• **Oligosaccharides** ( _oligo,_ "a few") contain several sugars and are the fructans and galactans. They are found in plants including wheat, some vegetables (e.g., onions and the onion family, garlic and asparagus), and legumes (e.g., beans, lentils).
• **Polysaccharides** ( _poly,_ "many") are the most complex carbohydrates and are starches, dextrin, glycogen, and cellulose. Starches and dextrin are most easily digested and found in plants. Glycogen is the main storage form of glucose in the body. Cellulose is largely indigestible.
Although it is possible to live on a low-carbohydrate diet, carbohydrates are the main source of energy for the brain and for maintaining function in nerve tissue and metabolizing fat. They are also the major food for the trillions of microbiota living in our gut. In this role, carbs have come under attack as a cause of obesity and implicated in various GI conditions such as irritable bowel syndrome.
While most of the sugars in the diet used to be consumed in the form of fruits, grains, vegetables, and table sugar—cooked into homemade baked goods—we now consume most of our carbohydrates from commercially prepared food to which sweeteners have been added.
The Problem with Carbohydrates
After I've eaten an apple or almost any other fruit, I can take a running start out of my driveway and take off without need of a car.
(HARRIET, 33)
As we saw in chapter 7, most of the food we eat is broken down and absorbed in the small intestine. But some sugars and insoluble fiber do not digest easily and arrive in the large intestine (colon) mostly undigested. The wall-to-wall bacteria lining the colon (see chapter 9, "The Microbiome") dine happily on the undigested fiber and sugars presented to them by our diet. This process is called fermentation and produces a great deal of gas and liquid that builds up in the large intestine. The result can be pain and bloating and changes in gut motility (movement). This in turn causes it to empty too quickly (diarrhea) or too slowly (constipation). Recently, researchers have identified a group of sugars/carbohydrates that appear to underlie many of the common symptoms seen by gastroenterologists. They are identified under a new classification: FODMAPs.
FODMAP is the acronym for:
**F** ermentable
**O** ligosaccharides
**D** isaccharides
**M** onosaccharides
**A** nd
**P** olyols
The FODMAP diet plan is based on avoiding the particular sugars for those people whose symptoms are triggered by them. It essentially removes the food supply for the bacteria in the colon that are creating the liquid, gas, and bloating. In particular, it is effective for quite a number of people with IBS, though not all experts in the IBS field agree with its curative abilities. The diet is individualized to each patient—some are only intolerant to fructose, others a combination of FODMAPs.
Nevertheless, it can be very restrictive as FODMAPs are the basis of a good deal of our foods. There are a number of breath tests (see chapter 6, "Testing") that can immediately diagnose intolerance to a specific sugar and enable patients to include or exclude them from their diet.
The low-FODMAP diet targets and eliminates specific carbohydrates—and is not intended as a cure but simply to control symptoms.
Wheat is an oligosaccharide (a fructan) and a FODMAP. Since many gluten-free products are also low in FODMAPs, people without celiac disease who go gluten-free are also eliminating many FODMAPs. Researchers have shown that the lowered FODMAP content, not the elimination of wheat per se, may be the reason symptoms resolve. This has raised the interesting question of whether people suffering from what is termed _gluten sensitivity_ or _intolerance_ actually have problems with the digestion of FODMAPs rather than with gluten.
People with celiac disease can also be intolerant to a number of FODMAPs and may need to eliminate them to fully resolve the symptoms.
The low-FODMAP diet removes many favorite and commonly consumed foods such as milk, garlic, onions, apples, and wheat and can lead to a reduction in fiber and calcium intake. Working with a knowledgeable dietitian ensures the patient is guided through the diet's many nuances, educated not only on appropriate low-FODMAP foods but encouraged to eat a well-balanced, varied, and nutrient-rich diet. When a patient is willing to embark on an elimination diet, they should be given the best opportunity to succeed with the diet plan. The dietitian plays a key role in successful implementation of the low-FODMAP diet education.
—KATE SCARLATA, R.D., L.D.N.
On a FODMAP program, you may also be eliminating a number of vitamin-, calcium-, and fiber-rich foods from your diet. For this reason the diet is best undertaken under the care of a registered dietitian or knowledgeable nutritionist. We will typically advise a strict low-FODMAP diet for several weeks. If it is going to work, it works quickly. Then foods can be reintroduced, because most patients do not have to avoid all FODMAPs.
A low-FODMAP diet is associated with a reduced abundance of bacteria in the colon, while a higher-FODMAP diet showed evidence of stimulation of the growth of bacterial groups with assumed health benefits. In other words, the low-FODMAP diet alters the diversity and reduces the abundance of the microbiome. The significance and health implications of this finding may lead to caution about reducing FODMAP intake for asymptomatic people or even symptomatic people for an extended period of time. More research is needed on the health benefits/drawbacks of any restrictive diet.
Things You Need to Know—It's Not All about Carbs
Bloating, diarrhea, and constipation are very common and can be caused by a number of things, including bacterial overgrowth, lactose intolerance, fructose intolerance, celiac disease, or IBS. Therapies are specific for each condition, and any one symptom can have an entirely different underlying cause.
Drugs
_For every action, there is an equal and opposite reaction._
—ISAAC NEWTON
Pharmaceuticals to me are as much part of the problem as part of the solution. There's a whole world of things out there. Hidden danger.
(NED, 52)
Most of us ingest an array of drugs to fight disease, aid digestion, control cholesterol and high blood pressure, replace hormones, dull pain, loosen joints, dry acne, grow hair, and elevate mood—to name just a few. While some drugs, such as laxatives, antidiarrheals, and antacids, are meant to affect the GI tract, others have side effects that can seriously alter GI function and impact the body. These drugs include proton pump inhibitors (PPIs) used to control stomach acid, aspirin and other nonsteroidal anti-inflammatories (NSAIDs), immunosuppressants, Benicar (a commonly prescribed antihypertensive), and antibiotics.
Like a seesaw, drugs intended to treat and cure one condition shift intestinal balances and can initiate another. Sometimes this very side effect can be helpful in treating another condition. For example, cholestyramine, a cholesterol-lowering drug, has a constipating effect and is used to treat diarrhea.
Other side effects are subtle, long-term, and obvious only after years of using the drug.
While the benefits of a pharmaceutical drug usually outweigh its potential side effects, an educated patient can better approach and manage GI reactions and ramifications. All of the drugs in this chapter work on and within the normal workings of the GI tract. Some appear to alter the intestinal microbiome, but the meaning of these alterations is still unclear.
It must be reiterated that many drugs have GI side effects. The following drugs stand out for their ability to alter GI function and trigger problems that are often misdiagnosed.
Proton Pump Inhibitors
Proton pump inhibitors (PPIs) are a class of drug that inhibit the amount of acid that your stomach produces. They are used to treat the symptoms of _gastroesophageal reflux disease_ (GERD) as well as other conditions caused by excess stomach acid, such as erosive esophagitis (damage to the esophagus by stomach acid), and ulcers. While PPIs are a blockbuster market for the pharmaceutical industry, most studies demonstrate that they are often used inappropriately.
Stomach acid and PPIs are both two-edged swords—they are beneficial as well as potentially harmful. On one hand, the microbiota of the stomach— _H. pylori_ is the dominant microorganism—are comfortable in and accustomed to their unique acidic environment. But _H. pylori_ and an acidic environment can encourage the formation of gastric and peptic ulcers.
While PPIs effectively reduce acid, they do not act on the _H. pylori_ that causes many ulcers. This bacteria lives under the thick mucous layer of the stomach and is difficult to eliminate. Treatment usually consists of a multidrug regimen including different antibiotics and antibacterials, as well as a PPI (which is necessary for the antibiotics to work).
The greatest clinical benefit of PPIs is to treat GERD. They are so effective that people with GERD may neglect the lifestyle changes that may be all that is needed to prevent GERD symptoms. (See chapter 8.)
But while PPIs efficiently lower stomach acid, they often disrupt the protective effect of the acid from the bacteria we ingest with our food, and increase the risk of _gastroenteritis,_ traveler's diarrhea, and _C. difficile_ infection. Available both with and without a prescription, drugs such as Prilosec, Nexium, and Prevacid are overused to treat excess stomach acid and, in the process, suppress its natural antibacterial effect. Once stomach acidity is lowered, the effect reverberates down the digestive tract, changing the balance of bacteria into the small intestine.
We have conducted studies on the effects of PPIs, and several interesting findings have emerged. Most important, we found that exposure to PPIs was strongly associated with a subsequent diagnosis of celiac disease. This was found mainly in younger individuals who were exposed to both PPIs and _H2RAs_ (histamine 2 receptor antagonists, a drug that reduces the amount of acid produced in the stomach, using a different mechanism than a PPI). While the mechanism by which acid suppression affects the development of celiac disease is unknown, it raises many intriguing questions about the connection of celiac disease to an altered microbiome.
PPIs are given to help eradicate _H. pylori,_ prevent and cure ulcers, and treat GERD. However, the long-term use of PPIs also increases the risk of several systemic and GI conditions, including increased risk of fracture, increased pneumonia, low magnesium levels, vitamin B12 malabsorption, and increased kidney disease.
They are a finger on many triggers.
Drugs That Mimic Celiac Disease
Olmesartan
Recently, a patient came into the Center with diarrhea and dehydration severe enough to cause kidney failure and requiring dialysis. The symptoms mimicked an acute and critical form of celiac disease but were, in fact, caused by Benicar (olmesartan), a drug given to lower blood pressure.
Olmesartan can cause intestinal problems that appear to be celiac disease. It is part of a class of drugs called angiotensin II receptor blockers (ARBs). Angiotensin II is a very potent chemical that causes the muscles that surround blood vessels to contract and the vessels to narrow. When blood vessels narrow, the pressure inside increases, creating high blood pressure. ARBs block angiotensin II, allowing the blood vessel to dilate and reducing the pressure. This is a very popular class of antihypertensive medication.
While the GI effect of Benicar is rare, it is a potentially life-threatening situation that should be investigated in anyone taking the drug. It can cause damage to the villi of the small intestine, diarrhea, malnutrition, dehydration, and weight loss. These celiac-like symptoms usually improve dramatically once the drug is stopped.
Immunosuppressants
Also called antirejection drugs, immunosuppressants reduce the strength of the body's immune system, which results in an increased risk of infection and malignancy. All patients receiving an organ transplant take them so that the body will not attack the new organ as "foreign" and reject it.
They are also used to suppress the immune system in autoimmune diseases such as lupus or rheumatoid arthritis, where the body inappropriately attacks its own tissue, or in severe cases of refractory or unresponsive celiac disease and other inflammatory bowel diseases (e.g., Crohn's, ulcerative colitis) to control the intestinal inflammation. With control, the inflammation is dampened, and the gut's powerful ability to respond to pathogens is also inhibited.
Immunosuppressants are classified into four basic categories that include azathioprine (Imuran), cyclosporine, monoclonal antibodies, and corticosteroids (prednisone). Many transplant patients and those suffering from severe IBD take a combination of them.
Immunosuppressants can stop the crippling effect of many autoimmune diseases but can also cause injury in the upper GI tract.
Nonsteroidal Anti-Inflammatories
Nonsteroidal anti-inflammatories (NSAIDs) are the mainstay of OTC treatment for aches and pains of all kinds. This grouping includes aspirin, ibuprofen (Advil, Motrin, Nuprin), naproxen (Aleve), and ketoprofen (Actron, Orudis). They are also prescribed in stronger form by doctors when needed for more acute pain. Many people take "an aspirin a day" to guard against blood clots. For others with arthritis and sports injuries, NSAIDs are part of their daily regimen.
The most common side effects of NSAIDs are GI problems. Since aspirin is absorbed directly into the bloodstream from the stomach, it does most of its damage there. Serious side effects include bleeding, peptic and esophageal ulcers, or perforation.
Some aspirin tablets are available enteric-coated so that they are carried farther down the GI tract, where they are absorbed and supposedly do less damage. But this can cause changes in intestinal permeability. So, while aspirin saves lives by reducing cardiac events, it can be toxic to the epithelial lining of the gut, causing intestinal ulcers or _strictures._
Many athletes take NSAIDs to prevent anticipated exercise-induced pain. But these drugs also may have a potentially hazardous effect on the GI mucosa during strenuous physical exercise. A small study recently showed that ibuprofen aggravated exercise-induced small intestinal injury and can cause gut barrier dysfunction in healthy individuals. The study concluded that NSAIDs consumed by athletes are not harmless and their use should be discouraged.
NSAIDs should not be used regularly unless under the guidance of a physician.
Opiates
Opiates (prescription painkillers derived from opium) slow down the motility (movement) of the GI tract. This can cause delays down the entire length of the gut and constipation. It can also result in nausea, a feeling of fullness after even a small meal, and bloating.
Antibiotics
_Science never solves a problem without creating 10 more._
—GEORGE BERNARD SHAW
Antibiotics are a class of drugs designed to kill or disarm bacteria. They have played a large role in saving lives and changing the average lifespan of people from 49 years in 1900 to more than 78 years today.
Some antibiotics are created to target specific bacteria; others are "broad spectrum" and destroy a range of bacteria. Although they are often taken inappropriately for viral infections such as colds and flu, they do not kill viruses.
But we have paid a price for their use—and overuse. There is a growing array of "superbugs" that are outsmarting our antibiotics. And of particular importance to what is going on in the gut, they often upset the balance of microbiota in the GI tract by destroying "good" as well as "bad" bacteria. Much research is now being conducted on the short- and long-term effects of antibiotics on both body and brain. And the microscope is on the microbiome.
Antibiotics, Allergies, and Obesity Theories
When my daughter was working in the ER, she got TB (tuberculosis). It took something like 12 weeks rather than the usual six for her sputum to test negative. There were pockets of the TB bacteria hidden in little cavities in her lungs, buried in deep, as I understand it. Her daughter has so many allergies—one pediatrician said when my granddaughter was six months old, "this child is an immunological disaster"—and she thinks they are related to all the antibiotics she took during that time.
(MARY, 67)
The prenatal exchange of antibiotics between mother and child may affect the colonization of bacteria in the newborn's gut. Researchers are examining the potential for an association with obesity (the mechanisms are unclear), allergies, and the early use of antibiotics.
There appears to be more diversity in the microbiome of leaner people. This has led to several hypotheses:
• Bacteria could use up calories.
• Antibiotics may cause obesity since they kill bacteria.
• Bacteria could affect the metabolic processes in the body.
• People with less microbiotic diversity are more likely to have a risk for type 2 diabetes, heart disease, and cancer as well as insulin resistance.
It should be noted that these theories are controversial.
Antibiotics and Animals
It has been shown that—for reasons not fully understood—some antibiotics help cattle grow faster, gain more weight, and get more from the feed they ingest. While the prolonged use of antibiotics in cattle and other "food" animals is under scrutiny for the potential side effects to humans eating these animal products, the alteration of bacteria through the use of antibiotics in these animals and the resulting weight gain give evidence to some mechanism related to an altered microbiome. (See chapter 9, "The Microbiome.")
The use of antibiotics on the farm has resulted in antibiotics in our food supply. While the effects are not known, they may be important. The FDA has been studying this issue, and more regulation and research is required to address this potential public health problem.
My uncle died of a kidney infection in 1928 at the age of 30. If he had been born 10 or 15 years later, after penicillin was discovered and in use, he would have lived to raise his infant son.
(ROBERT, 75)
It must not be forgotten that antibiotics save lives. They fight lethal infections and keep serious infections from becoming lethal. They are first-line therapy for many deadly infections that are now curable. But they are also misused—when prescribed for minor colds, sore throats, coughs, and infections that turn out to be viral. Patients often take part of a prescription and stop when they "feel better," leaving bacteria behind that becomes resistant to that antibiotic. Or, alternatively, they are taken for too long.
Unexpected Side Effects
A friend of mine was getting extremely tired. It turned out that the pharmacist had filled his prescription for his cholesterol-lowering drugs with Valium, which he was taking every day. They were both blue pills!
(PAUL, 66)
Some people have individual sensitivities to drugs that can cause a so-called side effect to take center stage. Unfortunately, prescriptions can also be misfilled with a similar-looking pill. Prescription refills should be examined closely to ensure that you are taking the right medicine.
Summary
• Drugs are a major cause of GI symptoms—because of their actions as well as your reactions to them.
• The side effects of many drugs are focused on their first point of contact in the body: the GI tract. The effects then ripple through other parts of the body.
• Older adults who take multiple pill regimens need to be particularly diligent of side effects—many of the pills interact with others.
• When we talk about the mouth, gut, and brain, this includes _everything_ we ingest. When asked by a doctor, "What medications or drugs are you taking?" remember to include OTC products even if they are labeled "natural."
• Drugs are self- and doctor prescribed. They cure symptoms and diseases but can often cause others. Before you blame the food you are eating for your symptoms, examine the drugs you ingest.
**For every action, there is a reaction.**
The Double Hit Theory
_The game is played away from the ball._
—ANONYMOUS
Diseases are caused by many interacting factors—more is usually involved than exposure to a virus, germ, or food. For example, when someone sneezes in a crowded room, some people will catch that person's cold; others will not. And while most people eat gluten, very few develop celiac disease. Even for people who are sensitive to the grain, gluten alone may be harmless until the body experiences a "double hit," causing a more active reaction to this protein.
The double hit theory explores the relationship between specific infections, illnesses, and conditions that are not caused by gluten yet open the door to a second "hit" or "insult" that creates celiac disease, gluten intolerance, or even diseases of the brain.*
Lighting the Fuse in the Gut
There are a number of GI conditions that occur after a double hit.
Traveler's Diarrhea
When I was living in South Africa I got giardia. And basically it went undiagnosed. They couldn't figure out what was going on. And they kept giving me antibiotics for treatment. I was terribly nauseated, had skin rashes, bouts of diarrhea. After that I was sick all the time.
Back home, I went to see gastroenterologists, who told me that I had gastritis and my gut was irritated—but that there was nothing really wrong with me. The gastroenterologist actually said to my mom after the appointment that he thought the symptoms were in my head. My mom told him that she had seen how sick I was, and it did not seem credible to her that a healthy 21-year-old wanted to be sick all the time.
It was only when I finally went to see another doctor, who looked at all of my symptoms together—including the rashes, allergies, etc.—that I was diagnosed with a significant parasitic infection and candida.
The healing process from that took a while. (I was dewormed, took probiotics, put on a restrictive diet that included taking me off gluten.) And I started feeling a lot better. Now? Sometimes I still get stomachaches. My tolerance for not feeling great is pretty good. Your baseline is different when you've been so sick.
(JUNE, 32)
Traveler's diarrhea or "turista" is a common complaint of people who leave home and develop gastroenteritis during their trip. For others, parasitic friends also return home with them, requiring numerous courses of drug therapy to erase.
This is a common story after travel to an exotic locale. Caused by different organisms, these GI infections upset normal GI function, possibly disrupt the microbiome, often require rounds of antibiotics or antiparasitics that can in themselves create symptoms, and may set off a chain reaction that results in another GI condition. For those people whose symptoms persist, some will then develop IBD, celiac disease, IBS, or food sensitivities.
But viruses, bacteria, and parasites also attack at home with similar results.
Fooling the Immune System—Gluten and Rotavirus
According to the CDC, rotavirus is the most common cause of childhood diarrhea throughout the world. It produces prolonged diarrhea and is common in preschool children. The CDC studies note that almost every child in the U.S. has had at least one rotavirus infection by the age of 3. The virus attacks the lining of the small intestine, causing inflammation and loss of fluids and _electrolytes_. Once exposed to rotavirus, the immune system "remembers" it.
Evidence that it is a risk factor for celiac disease comes from studies showing that children with celiac disease have a greater number of rotavirus antibodies than those without it. While the mechanisms behind this are not fully understood, one theory is that rotavirus sets up perfect conditions for a double hit because it cross-reacts with gluten through something called "molecular mimicry." Another theory is that gluten disrupts the mucosal barrier, allowing gluten to be recognized as foreign.
Gluten is similar in structure to other proteins in our body as well as some viruses, namely rotavirus. Therefore, when susceptible individuals eat gluten after having the viral infection, the body's immune system attacks the gluten molecule, thinking it is being besieged by rotavirus again. In other words, part of a molecule of one protein resembles a part of a molecule of a totally different protein. The initial infection primes the immune system's "memory" to react—a double hit that creates a sensitivity to gluten.
Lighting the Fuse in the Brain
Toxoplasmosis and Gluten Antibodies
An exposure to _toxoplasmosis_ —a parasitic disease that is found in more than 60 million people in the U.S. but usually kept in check by a healthy immune system—may be connected to an immune response to gluten in sensitive people that occurs well after the initial infection.*
Toxoplasmosis is the world's most common parasite. Most people with a healthy immune system never develop symptoms—or will have mild, flu-like ones—but it can lead to serious complications in infants born to infected mothers or people with a weakened immune system.
Research has also indicated a direct relationship between infection with this parasite and the development of schizophrenia in people who develop antibodies to gluten. For these people, this immune reaction is recognized as part of the pathology for psychiatric disorders such as schizophrenia, bipolar disorder, and perhaps autism.
This would support a gastrointestinal basis through which a double hit—toxoplasmosis and sensitivity to dietary gluten—might activate certain brain disorders. It is still unclear whether gliadin antibodies are helping initiate the disease, are a product of it, or are markers for other processes contributing to or causing the problems. (For more, see chapter 27, "Schizophrenia.")
Alcohol Ataxia
Similarly, studies have shown that prolonged and excessive alcohol intake can trigger ataxias in the brain and antigliadin antibodies—although it is unclear if this is the only factor responsible for the "insult" to the cerebellum, the part of the brain affected.
Ataxia (from the Greek _a,_ "without" and _taxis,_ "order") creates problems with balance, movement, and coordination. It can affect limbs, body, speech, and eye movements. There are many causes and manifestations of the condition, and the association with gluten in combination with alcohol, is an intriguing part of the "double hit."
Alcohol is a common cause of ataxia. A recent study examined patients with alcohol-related cerebellar ataxia to determine whether alcohol also created sensitivity to gluten in susceptible people. Researchers found that antigliadin antibodies were significantly higher in these patients and that the genes associated with celiac disease (HLA-DQ2/-DQ8) were more than double that of the healthy population. They concluded that alcohol-related cerebellar degeneration might, in genetically susceptible individuals, induce sensitization to gluten. This may result from a primary cerebellar insult, but a more systemic effect is also possible. The sensitization may be initiated by the insult to the brain, or other systemic effects. And the duration and amount of alcohol may not be the only factors responsible for the insult to the brain. (For more, see the discussion on gluten ataxia in chapter 22, "Neuropathy.")
Abuse, Trauma, and GI Illness
A history of abuse and trauma has multiple effects on gastrointestinal symptoms and disorders. Dr. Douglas Drossman, an expert who has studied these conditions for the past few decades, noted, "the prevalence of abuse history is greater among those who have more severe symptoms. The pathophysiological features [functional changes associated with or resulting from disease or injury] that explain this association relate to stress-mediated brain-gut dysfunction."
The mechanisms behind this double hit appear to be stress-initiated changes in immune function in the gut due to an impaired ability of the central nervous system to suppress certain stimuli and signals. Insult leads to injury that cascades into ongoing GI disorders. Or the stress may alter nerve cell connections in the brain that lead to GI-related symptoms or the patient's perception of them.
While victims of abuse and those of trauma (including war veterans) are usually seen in a psychiatric context, Drossman explains that it is important that "gastroenterologists and other health care providers . . . understand when to inquire about an abuse history and what to do with that information."
Abuse history is common in GI practice and more prevalent in patients with more severe symptoms. We have similarly shown that people with persistent symptoms after the diagnosis of celiac disease have an increased history of abuse and other psychological factors.
_Effects of War Trauma on IBS Development_
The federal government commissioned a report by the Institute of Medicine (now known as the National Academy of Medicine) on the impact that deployment in a war zone could have on the mental and physical health of war veterans who served in the Gulf War. The review found sufficient evidence for an association with several specific psychiatric disorders (including PTSD and generalized anxiety disorder), substance abuse, and functional GI disorders such as IBS and functional dyspepsia.
Since more than 50 percent of deployed soldiers in the study acquired acute gastroenteritis, the review concluded that "deployed vets experiencing war trauma who are also exposed to gastroenteritis are at greater risk to later develop IBS."
While knowledge is growing about the role of abuse and trauma in gastrointestinal illness, the reasons for this association are not known. But stress-related brain-gut mechanisms are beginning to be clarified. This is a double hit that highlights the many complex aspects of the brain-gut axis.
Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections
The acronym PANDAS describes a subset of children with obsessive compulsive disorder (OCD) and/or tic disorders whose symptoms appear to be related to a streptococcus infection. It is an evolving and controversial concept originated in the late 1990s. The proposed mechanism behind this double hit states that the body produces antibodies that attack the streptococcal infection, which cross-react with proteins in the brain that mimic the streptococcal proteins. Repeated strep infections continuously damage the brain, resulting in a chronic psychiatric disorder.
Some researchers feel that the available evidence does not convincingly support the relationship between streptococcal infections and chronic tic disorders. And the autoimmune origin of PANDAS is still being evaluated. A recent study of a group of children and adolescents with PANDAS that looked for other autoimmune conditions—including thyroid function abnormalities and celiac disease antibodies—did not find any statistical difference with a healthy control population.
At this point, we will cautiously note the potential for streptococcal infections to trigger a double hit on the body, initiating a reaction in/on the brain. But PANDAS does not involve gluten, nor will removing gluten from the diet effect any behavioral change.
The Hormone Hit: Pregnancy
Pregnancy is a time of tremendous hormone variation and is also a stress on the digestive system. In order to feed the developing fetus, the mother's blood sugar levels are higher than normal. Usually, the body makes more insulin to metabolize the increased glucose in the bloodstream, but if it cannot, blood sugar levels rise, and this can result in gestational diabetes. Women with gestational diabetes are at a greatly increased risk of developing type 2 diabetes.
Pregnancy is often the tipping point for a diagnosis of celiac disease. It may or may not be the double hit that stimulates a more active form of the disease.
Food for Thought
Developing an immune response to gluten after a history of toxoplasmosis, alcohol abuse, trauma, and certain infections may be the tip of the double hit iceberg. These various conditions cause a level of gastrointestinal or systemic damage or dysfunction that can compromise and weaken it. Then an additional insult triggers another condition in the gut-brain axis.
Is the double hit involved in the increased incidence of celiac disease and gluten sensitivities? The amount of alcohol consumption, prevalence of toxoplasmosis, and/or intestinal infections has not necessarily increased in the past few decades, but perhaps the use of antibiotics, antifungals, and other drug therapies to treat these various conditions has. And they may be agents of change that open the door to further insult. There may be other environmental "hits" that we have not identified.
The connections between what goes through our digestive tract—food, pathogens, alcohol, drugs—and its effect on our body and brain often play out in more than one act(ion).
What is the take-away lesson? Symptoms and disorders often appear in one place but originate someplace else.
The champion hockey player Wayne Gretzky was once asked why he was so successful. He replied, "I skate to where the puck is going to be, not where it has been."
Inflammation
_Heat not a furnace for your foe so hot that it do singe yourself._
—WILLIAM SHAKESPEARE
I often feel as if my belly is on fire.
(SUSAN, 25)
Inflammation defends and destroys.
The gut exists in a constant state of low-grade, controlled inflammation. This is provided by the very active immune system found within the internal lining of the small intestine, which samples and monitors everything going through. All of the bacteria, viruses, fungi, pathogens, foods, and other substances we ingest are usually controlled this way. But the internal furnace that protects us from our foes often singes its host.
When things go wrong in the gut, the result is impaired GI function and disease. But you also have inflammation that can affect a specific area of the gut or travel throughout the body. This can contribute to abnormal function in other organs, migraines, peripheral neuropathies, and fatigue. The impact of this fire is being actively studied as a potential trigger for many different conditions that affect the brain as well as the gut and body.
What Is Inflammation?
Inflammation is many different things.
Viewed under a microscope, it is an explosion of cells that should not be there. While it can be seen this way, it appears as symptoms that we feel, such as fever, coughs, and chills due to infection, or swollen joints in conditions such as arthritis or fatigue.
It is possible to assess inflammation in the body through changes in the blood that can be measured, most commonly in an elevated white cell count. There are other commonly used inflammatory markers, such as _C-reactive protein_ and _erythrocyte sedimentation rate_. But other cellular markers that are released during inflammation and permeate organs—e.g., _cytokines_ —are not usually tested for or seen. This is the inflammation that signals the brain to induce a sickness response that includes increased pain and a negative affect (facial and body expression). It is one reason we crawl into bed with a bad flu. The brain and body are working together to heal themselves through rest and sleep.
What Causes the Transition from Low to High Heat?
Inflammation is a final product that can be triggered by many factors and conditions:
• Drugs—aspirin or NSAIDs that break down the intestinal barrier and result in ulceration and inflammation (ironically, these drugs are also used to lower fevers and reduce inflammation in conditions like arthritis)
• Infections
• Autoimmune conditions
• Immune dysregulation—an aberrant response to bacteria
• Toxins (ingesting a corrosive such as lye or drugs in excess such as Tylenol)
• Allergies
In turn, inflammation may contribute to functional issues affecting the hormonal, nervous, or immune systems.
Inflammation in the Gut
A chronic state of inflammation is necessary for the immune system to police the huge surface area of the gut. This is a challenge not only in terms of its vast microscopic area but because this 30-foot-long pipe is open to the world on both ends. Foreign substances are constantly washing through it.
Everything is held in check by cells of the immune system. The microbiome may also be part of the overall protective apparatus. We evolved with these organisms, and they provide a chronic stimulation for the immune system that is protective.
The immune system functions through a complex interaction of innate (born with) and adaptive mechanisms. These two branches of the system "know" to attack certain pathogens, "learn" to attack others—and "mislearn" in autoimmune diseases, where they inappropriately attack the body itself. In other words, they "recognize" the self as something foreign.
The Key Players
Many cells play a role in balancing the inflammatory response of the immune system in the gut and regulating the "temperature" of the GI burner. Of special importance in this very complex system—which is only outlined here—are cytokines, T-cells, and _dendritic cells_. These cells are cited in most articles about celiac disease and autoimmune disorders and offer a fascinating look at how the body "cross talks."
Cytokines are molecular messengers that respond to infection and trigger inflammation. They are chemical "switches" that turn different immune cells on and off. There are a variety of cytokines, such as interleukins, interferons, and growth factors. An explosion of cytokines can be destructive—they are instrumental in starting the cascade of cells that turn inflammatory heat to "high" and cause damage to intestinal villi as well as in different parts of the body. Drugs that block cytokines—cytokine antagonists, like infliximab—are used to treat several chronic inflammatory diseases.
_T-cells_ are a type of white blood cell that circulates around our body, scanning for infections and abnormalities. There are "killer" T-cells and "helper" T-cells. The first type hunts down and destroys cells that have been invaded by "foreign" material such as viruses, bacteria, or cancer. The second type helps to orchestrate both innate and adaptive immunity. They are capable of "remembering" any germ once they encounter it, and they will destroy them if they encounter them again.
Sometimes T-cell responses are inappropriate—they "recognize" cells of the body (self) as foreign and destroy them. This leads to many autoimmune diseases, including celiac disease, type 1 diabetes, multiple sclerosis, and rheumatoid arthritis. They are also responsible for the rejection of a transplanted organ—"recognizing" it as foreign. A lack of T-cells—as seen in HIV/AIDS—can be fatal, as the body is unable to defend itself against infection.
Special dendritic cells in the lining of the mucosa also monitor the contents of the intestine, both to suppress inflammatory reactions against food and to protect against invading pathogens. These messenger cells monitor the "talk" between our innate and adaptive immune system and play a role in allergic food reactions and autoimmune disease.
The development of the microbiome in early childhood may also drive the development of our intestinal immune function and allow us to tolerate the foreign proteins in foods and organisms. The potential mechanisms behind the cross talk between the microbiome, the intestine, and the immune system is under intense study.
Essentially, the digestive tract and its contents engage in a constant immune cross-talk with cells that maintain a protective inflammation. When we ingest something that is perceived as a threat, these cells turn up the heat.
Systemic Inflammation—Gut to Brain?
There is increasing interest in how—and whether—inflammation alters behavior and thought. The fatigue, pain, and withdrawal experienced during acute illness and infection makes evolutionary sense; they enable the body to fight the infection, heal wounds, and conserve energy. It is believed these reactions are a result of inflammation-generated signals to the brain.
However, if these states are prolonged, pain, fatigue, and withdrawal become depression. In conditions such as IBS, chronic inflammation appears to cause the transition from one set of symptoms into depression and chronic pain, but the mechanisms behind this are unclear.
Inflammation is also being actively studied in different neurological conditions such as autism. (See chapter 26.) Because brain tissue cannot be biopsied, researchers examine cerebrospinal fluid and use imaging tests such as PET scans to measure inflammatory markers in this arena.
There is also intriguing work on mice injected with human DNA that shows serotonin may be a possible mediator of inflammation in the brain. This opens the potential for serotonin drugs to help tame GI conditions. (See chapter 10, "The 'Second Brain' in the Gut.")
In disorders such as schizophrenia and autism spectrum disorder (ASD), systemic inflammation may also include the gut. In this scenario, systemic inflammation could lead to an abnormal immune response to different foods and, in turn, to an increased antibody response to gluten. It may include a breakdown of the intestinal barrier.
Some of the antigliadin antibodies formed in the gut in celiac disease are also found in conditions such as schizophrenia and ASD. These antibodies are not the precise ones found in celiac disease but are nonspecific antigliadin antibodies. It is unclear which is the horse and which is the cart—do the antibodies develop because of a primary gut problem and contribute to the brain problem? Or is the arrow going in the other direction, i.e., altered brain signals affect gut function?
Anti-Inflammation Diets
It is very exciting to think that you can alter inflammation by changing what you eat. Celiac disease is an amazing example of this—withdraw gluten from the diet and you can reverse a devastating autoimmune disease. However, there is little scientific evidence that changing one's diet can similarly affect other diseases.
But since the microbiome is instrumental in controlling inflammation in the gut, some of the so-called anti-inflammation diets may be altering the microbiome—which is what is actually affecting inflammation. While changing the diet can affect the composition of the microbiome—conceivably making it more or less healthy—this has not been translated into any scientifically proven therapeutic diets as yet.
One important exception may be the effect of extreme changes in diet on the inflammation in some patients with IBD. There is evidence from the 1970s that an elemental diet, devoid of fiber and whole food groups and consisting of predigested food components, may control inflammation in some patients. However, current versions of anti-inflammatory diets are little more than "healthy" diets rich in fiber, minerals, and vitamins.
Summary
We understand a great deal about the gut when there is destructive inflammation in conditions such as celiac disease and IBD. Here we can measure and identify inflammation. There are many unknowns regarding systemic inflammation involving the brain.
**More research is needed! Anti-inflammatory diets, supplements, and claims are running way ahead of the science.**
Intestinal Permeability—"Leaky Gut"
_Science is the father of knowledge, but opinion breeds ignorance._
—HIPPOCRATES
The so-called leaky gut has gotten a lot of press recently as the trigger for numerous diseases—as well as a potential target for therapies to treat them. It is a term that has been popularized in the alternative medicine literature.
What exactly is leaky gut? Despite popular articles on the subject, there is very little agreement—or good scientific research—about the subject.
Before we can treat it, we need to understand what causes it, what it may trigger, what this really means for our intestinal health, and, what, if any, effect diet has on it.
First, it is important to understand a few terms.
Intestinal Barrier vs. Intestinal Permeability
The intestinal barrier is the huge mucosal surface of the GI tract that protects the body from the billions of bacteria, microorganisms, toxins, and food components that wash through it daily. It functions as a barrier between the external environment and the closely regulated internal environment of the body and is crucial to our health. Conversely, this barrier must open and absorb essential fluids and nutrients to feed the body.
These opposing goals are achieved by a normal functional state described as intestinal permeability (IP). It is the gatekeeper of the intestinal tract.
This permeability allows the body to "sample" intestinal proteins and present them to the immune system, and allows small molecules to pass through the lining of the intestine. Its mechanism is complex, but it is essentially composed of epithelial cells held together by "tight junctions." Layers of water, mucous, and bacteria (microbiota) are additional barriers protecting the epithelial cells. Many factors can alter intestinal permeability, including infection, bacteria, drugs, alteration in the immune system, and stress.
When IP is altered, the result is often referred to as a "leaky gut." **But IP is a constantly changing and normal physical phenomenon.** Many circumstances and conditions cause the tight junctions that line the GI tract to become slightly porous. It occurs in healthy people—during strenuous exercise, stress, and/or the ingestion of medications, alcohol, aspirin or other NSAIDs—as well as in anyone with intestinal disease.
However, there are various degrees of IP, and we know that it is increased in almost any GI disorder and may contribute to other disease states. In fact, IP is often increased in relatives of people with GI disorders who don't have any manifestation of disease—indicating a possible genetic component.
Tests for Intestinal Permeability
There are various tests to measure IP, the most common being the measurement of two nondigestible sugar molecules—lactulose and mannitol. Mannitol is a small sugar molecule and is absorbed easily through the intestinal barrier. Lactulose is larger and more complex and gets taken up only partially—unless the barrier is more permeable.
The degree of IP or malabsorption is reflected in the levels of the two sugars recovered in a urine sample collected over the following hours. Because IP is so naturally variable and affected by multiple physiological causes—alcohol, pregnancy, exercise, drugs—the test must be done in a highly controlled setting. There is controversy about the timing as well as the reliability of these collections.
Altered Intestinal Permeability
As we noted, a number of factors can compromise the integrity of the intestinal barrier—the lining of the GI tract. This includes:
• Intestinal infection and inflammation
• Allergenic foods
• Toxic chemicals
• Drugs
• Lifestyle factors (intense exercise, trauma, stress)
• NSAIDs, including aspirin
Disruption of the intestinal barrier also disrupts—and is disrupted by—the microbiota living throughout the GI tract. When the intestinal barrier is inappropriately breached, it allows substances into the body that it cannot absorb and/or neutralize. The resulting inflammatory reaction causes a cascade of problems that may result in diseases, including inflammatory bowel diseases and celiac disease. Recently, obesity, fatty liver, and metabolic diseases have also been implicated.
Inflammation and Intestinal Permeability
More important, the pathways for unwanted substances into the body are both _through_ and _between_ the epithelial cell barrier. This is an important point in understanding the so-called leaky gut. The intestinal barrier absorbs nutrients and fluids _through_ the cells of the epithelium (see chapter 7, "The Normal Gut and Digestion"). But proteins can move _through_ an inflamed cell as well as _between_ the tight junctions opened by inflammation.
In order to treat celiac disease, it is necessary to stop all the gluten from crossing the intestinal barrier. This affects the celiac disease treatments designed to "close the tight junctions" and stop gluten from entering the body. These treatments do not address the gluten entering through the epithelial cells. (See chapter 30, "Nondietary Therapies.")
The Microbiome and Intestinal Permeability
The microbiome is involved in the development and maintenance of the intestinal immune system. Several diseases have been linked to changes in the populations of microbiota that, in turn, alter barrier function.
For example, it is thought that a high-fat diet causes alterations in gut microbiota and increased gut permeability. This may allow the transfer of bacterial products from the GI tract into the body and cause inflammatory reactions that trigger metabolic diseases such as insulin resistance, type 2 diabetes, and cardiovascular diseases. Since the liver is the first site where toxins get through the GI tract, an altered IP may contribute to a fatty liver. It is thought that nonalcoholic fatty liver disease may be a manifestation of altered IP.
Therefore it is tempting to speculate that modifying the intestinal microbiota and the cellular "gates" of the GI tract with drugs, food components, or probiotic bacteria might offer approaches for future therapy of intestinal barrier-related diseases. But the science has not as yet justified the hypothesis.
Autism and IP
A study was recently conducted to determine the occurrence of damage to the gut mucosa in a small group of autistic children with no known intestinal disorders. Using the lactulose/mannitol recovery tests, 43 percent of them showed altered intestinal permeability (versus none of the controls). The researchers speculated that altered IP could represent "a possible mechanism for the increased passage through the gut mucosa of peptides derived from foods, with subsequent behavioral abnormalities." Because of the difficulty in assessing "normal" intestinal permeability as well as the meaning of an altered one, these types of studies require much more extensive research to draw any conclusions about the effect of altered IP on the development of autism.
Summary
• _Leaky gut_ is not a scientific term. It is a popularized and somewhat inaccurate name for a normal physiological function—namely, changes in intestinal permeability, which is a feature of intestinal barrier function.
• The realization that the barrier is so important raises the questions of what can disrupt it and how we can improve gut barrier functions—and what role altering gut microbiota may play.
• Gluten is the known dietary cause for increased IP in people with celiac disease and some with diarrhea-prominent IBS, but not in any other condition.
• There are currently no drugs, probiotics, or diet that have been scientifically proven to improve a so-called leaky gut or to treat it. One drug, larazotide, does appear to tighten the intercellular junctions. Its role in various disease states is being studied.
• This area may be a valuable new target for disease prevention and therapy. We need good scientific research, not pseudoscience hypotheses, to explain potentially important concepts like IP.
PART IV
Putting Order in the Disorders
Most of the advice that I've gotten from doctors is: "Whatever works for you, even if it doesn't work." Sort of "just deal with it." One said: "Well, do the best you can. If it's really bad I'll give you an antibiotic." So I tried a gluten-free diet, and that seems to help. Most of the time.
(ELLIE, 28)
As long as your blood tests are good—that's it. As far as he [the doctor] was concerned I wasn't sick. How I felt? Must be nerves . . .
(LYNN, 48)
_A decade ago celiac disease was considered extremely rare outside Europe and, therefore, was almost completely ignored by health care professionals. In only 10 years, key milestones have moved celiac disease from obscurity into the popular spotlight worldwide. Now we are observing another interesting phenomenon that is generating great confusion among health care professionals. **The number of individuals embracing a gluten-free diet (GFD) appears much higher than the projected number of celiac disease patients, fueling a global market of gluten-free products.**_
—THE OSLO DEFINITIONS FOR COELIAC DISEASE AND RELATED TERMS*
Many people suffering from unexplained symptoms go from doctor to doctor, specialist to nutritionist, Internet blog to magazine article, and back again. When test results fail to uncover a disease or recognizable condition, patients are often sent on their way. And so, they seek out answers on their own. Many are convinced that gluten plays a major role as the solution to or cause of every unexplained symptom from which they suffer.
The actual picture is more complex. Our bodies are filled with feedback loops. To understand one signal or symptom is not enough to grasp either its message or its part in the whole. The conversations between the gut, the brain, and the microbiome are like a party line shared by multiple subscribers. And researchers are listening in with increasing interest.
The following section puts some order in disorders that affect the gut and the gut-brain axis, and explains where the gluten-free diet works and where it does not.
Keep in mind: Your gut has a limited number of ways to tell you it is suffering. Thus, many of the symptoms of one condition resemble others.
Celiac Disease
Being on a GF diet is fine now. But it was like drinking out of a fire hose the first few months: completely overwhelming.
(DIANA, 49)
I can talk forever about making sure the restaurant doesn't put croutons on your salad and preparing menus and all that kind of stuff, but that's way down on the list of really major concerns. I don't think that's the hardest part. I'm much more concerned about the risk of autoimmune diseases with celiac. About my daughter getting lupus or scleroderma.
(MARY, 67)
For those with celiac disease, gluten-free exuberance has created a wonderful array of "safe" products that are readily available at grocery stores as well as online and in health food stores. People now have "gluten intolerance," "gluten sensitivity," "gluten allergy," and plain old "glutenitis." These conditions are different from celiac disease, their autoimmune-driven cousin.
What Is Celiac Disease?
Celiac disease is a multisystem autoimmune disorder whose main target of injury is the small intestine. It is caused by an inappropriate immune reaction to gluten, the protein in wheat, rye, and barley, and occurs in 1 to 2 percent of the population worldwide. Most doctors now understand that a patient's migraine headaches, infertility, peripheral neuropathies, and/or blistering skin (among other conditions) may, in fact, be manifestations of this chameleon-like condition.
The digestive tract is a complex and highly efficient system designed to deal with the outside world going through it. To accomplish this, a series of defenses have been built into the GI system. These include:
• an intact lining of cells protecting the border from mouth to anus
• gastric acid that destroys pathogens in the stomach
• the microbiota that "taste" content, determine its status, then sculpt and continually signal the immune system
• immune cells underneath the mucosa that "learn" which parts of what we ingest are friendly and send antibodies to destroy what they perceive as foe
• the enteric nervous system or "second brain" in the gut, which silently regulates and coordinates the stages of digestion to maintain order while engaging in constant cross talk with a network of neurons outside of the tract
• a low level of controlled inflammation that immediately seals off an infected area
When the immune system senses a serious infection or foreign invader, the normally controlled inflammatory process revs up. In people with celiac disease, undigested gluten comes both through and between the mucosal cells lining the tract. It is inappropriately perceived as an invader by the immune cells, who call for the troops (a cascade of white blood cells producing inflammatory cytokines), thereby creating even more inflammation in order to destroy the perceived pathogen. After repeated assaults, the inflammation destroys the surrounding tissue and causes the villi to atrophy and eventually flatten, losing their ability to absorb nutrients. Without the epithelial cell barrier, our immune system begins to make more antibodies to food proteins.
Essentially, the firemen put out the fire, leaving a burned-out building. The small intestine, the main site of nutrient absorption, is damaged and/or partially destroyed, which can create vitamin and mineral deficiencies and diarrhea. The ongoing inflammation also creates fatigue and many other related symptoms.
The Gut in Flames
The inflammatory response resembles a battlefield with different troops racing to the scene, releasing their chemical weapons and leaving behind collateral damage and debris. If there is not much damage, the body repairs itself. This occurs when we eat spoiled food or get a stomach "bug." The body responds by putting in more inflammation, the problem is dealt with, and the inflammation subsides.
In people with celiac disease, the gliadin molecule gets into the intestinal lining and continually stimulates the inflammatory response. The inflammation will remain high and cause continual damage until the offending toxin is removed.
The intestine will not recover until you interrupt the vicious cycle by taking gluten out of the diet permanently. This allows the inflammation to subside and normal intestinal appearance to return. With the regrowth of the villi, function can return. Until then, the digestive system creates symptoms that reflect the level of damage to the body—it begins to ask or yell for help.
In some cases, the progress of the reaction is gradual; in others it's rapid and dramatic. Symptoms may also wax and wane over a long period of time. While we know the dietary trigger—gluten—we still do not know why only a small percentage of people who are genetically predisposed develop an active form of celiac disease and why it occurs at varying times in their lives.
Symptoms and Complications
There are four major categories of symptoms and complications in celiac disease.
1. **"Classic" celiac disease**
My dad at the age of 83 lost a lot of weight. He went from 160 pounds to 90-some. The physicians couldn't figure it out. I was on the phone with his doctor and asked if he checked for celiac disease. He said, "Two-year-olds get celiac disease, not someone his age." I asked: "Would you get a biopsy and check for it?" My dad had celiac disease and he recovered, but he never got all his weight back—which was a good thing. He said, "Living with this disease is not so bad. Whenever I get overweight and want to lose a few pounds, I eat a bagel."
(MICHAEL GERSHON, M.D.)
This category describes mild to severe symptoms that predominantly involve the GI tract. The severity of symptoms is related to the amount of intestinal damage and involves GI disturbances including diarrhea, cramps, bloating, lactose intolerance, increased reflux, and dyspepsia.
2. **"Silent" celiac disease**
I had numerous pregnancy losses, I had elevated liver enzymes, anemia, I had numbness in my hands, and saw numerous doctors who never connected the dots. After I was diagnosed, we had both of my daughters tested. I have a 17- and a 14-year-old. I could have sworn it was the 17-year-old—she had all of the symptoms . . . It was the 14-year-old, who had no symptoms.
The GI who did her procedure was so excited when he met me after the procedure—her intestines were scalloped and so damaged that he hadn't seen anything like that for a while. He couldn't contain his medical excitement. It was sort of like a _Saturday Night Live_ sketch.
(DARA, 42)
While GI problems were once considered to be the major manifestation of celiac disease, the more remote effects of malabsorption are now the most common symptoms seen by doctors. These include:
• **Vitamin and mineral deficiencies.** Vitamins and minerals are absorbed in specific sections of the small intestine: vitamin B12 in the ileum; iron and much of our calcium, fat-soluble vitamins, and folic acid in the proximal portion of the small intestine (where celiac disease does much of its damage).
• **Anemia.** The most common cause of anemia in women is menstrual blood loss. In men, it is blood loss through injury or an intestinal problem. People suffering from persistent anemia, especially iron-deficiency anemia, where other underlying medical conditions have been ruled out, should ask their doctors about testing for celiac disease.
• **Fatigue.** Fatigue can be caused by malnutrition and malabsorption of nutrients, inflammation, iron deficiency, vitamin deficiency, other autoimmune disorders, and/or depression. Chronic fatigue should be considered as a symptom of celiac disease. (See chapter 25.)
• **Osteoporosis.** Osteoporosis is a "silent" condition because most people do not know they have thin bones until one of them breaks. Low bone density and osteoporosis are common in patients with celiac disease. Low blood calcium levels are a specific marker for the condition.
• **Neuropathies.** Small-fiber neuropathies and some ataxias are associated with celiac disease. Neuropathies are also associated with inflammation. Many resolve on a gluten-free diet. (See chapter 22.)
3. **Systemic inflammation and autoimmune diseases**
While malabsorption underlies many of the symptoms of celiac disease, the inflammatory process itself is now understood to be a major factor in the development of symptoms. Inflammation, mainly through the increased levels of circulating cytokines, makes people feel unwell.
It is well documented that autoimmune diseases tend to "travel in packs." That is, if you develop one, you are more likely to develop another. It is believed that this is most likely due to a genetic predisposition. Approximately 8 to 10 percent of all type 1 diabetics have celiac disease, and the number may be higher as more patients are diagnosed. Among the celiac disease patients we see, 30 percent have at least one associated autoimmune disorder, compared to 3 percent of the general population.
People with one diagnosed autoimmune disease and unexplained symptoms should explore the possible link with celiac disease.
4. **Malignancies**
People with celiac disease have a twofold greater chance to develop a malignancy than the general population. The malignancies that occur at an increased rate include non-Hodgkin's lymphoma as the main culprit. However, esophageal carcinoma, small intestinal adenocarcinoma, and melanoma are also seen. A gluten-free diet appears to reduce the risk of developing these malignancies to that of the general population after five years of compliance—with the exception of non-Hodgkin's lymphoma, which appears to be associated with a villous atrophy that fails to heal.
Celiac disease was once called "the great pretender." Its many symptoms and manifestations can masquerade as many other illnesses. This is also the reason it is often missed—patients are labeled with another disease that "sticks," and treated for that condition. They continue to eat gluten and remain sick despite treatment.
What Causes Celiac Disease?
We need to rethink the way people get celiac disease. We know that it is a combination of gluten, genes, and environmental factors—but isolating the trigger remains elusive. While we have identified a number of environmental factors that appear to activate or trigger an active form of the condition, no one factor is present in all cases. This is a puzzle that still has many missing pieces.
While the response to gluten in people with celiac disease—and its manifestations and consequences—have been extensively documented in our book _Celiac Disease: A Hidden Epidemic_ , the newest areas of scientific study are focused on the underlying mechanisms initiating and driving the immune reaction.
Gluten
You have to be eating gluten to develop celiac disease. It is the only environmental trigger for an autoimmune disease that has been definitively identified. None of us digest gluten completely since it is a large, complex protein that remains mainly resistant to our normal intestinal enzymes. We know that the gliadin protein—the alcohol-soluble portion of gluten—gets into the lining of the intestine in certain individuals and sets off the inflammatory cascade that causes the disease.
Genes
There is a definite genetic influence that is demonstrated by the prevalence of celiac disease in families and in identical twins, but not all of the genes have been conclusively identified. The two specific genes that have been recognized so far are part of the HLA (human leukocyte antigens) class II DQ genes. The HLA genes are the "sentries" of the immune system. They patrol the immune system and identify "self"—belonging to the body—from "nonself"—a foreign substance. We all have slightly different versions of these proteins inherited from our parents. These are the genes that are used to determine organ transplant suitability.
Ninety-five percent of patients with celiac disease have HLA-DQ2, and most of the remaining 5 percent have HLA-DQ8.* In simple terms, specific genetically driven immune cells with these HLA "sentries" are primed to react to gliadin.
While it is absolutely necessary to have either HLA-DQ2 or -DQ8 or the separate components of these genes, they are not sufficient to _cause_ celiac disease. They increase the risk in the general population, but different genes have been identified in other populations. More than 40 other genes are seen more often in celiac disease patients than in unaffected people, but we believe that we have identified only about 50 percent of the genetic influences.
Therefore, in order to get celiac disease, you have to have gliadin, and you have to have HLA-DQ2 or -DQ8. Simple enough, but 30 percent of the general population have HLA-DQ2 or -DQ8 lymphocytes yet only about 1 percent get celiac disease. And since not all identical twins and a large percentage in a given family do not have celiac disease, there are obviously other factors at play. There is increasing interest in _epigenetics_ —the modification of genes by other, typically environmental factors that may in turn be inherited. These factors have as yet to be studied in celiac disease. (See chapter 33, "Food for Thought.")
The answer is not just gluten and genes.
Environmental Factors
There is convincing evidence that celiac disease has increased over the past 50 years—not just the rate of diagnosis that lags behind the actual prevalence of the disorder. But why? The presence of the necessary genetic variants has not changed, nor has the type or amount of wheat that is ingested by most people who eat wheat. Therefore other environmental factors must be contributing to this growing percentage of cases.
_Infant Feeding Practices_
Up until recently, researchers thought that infant feeding practices affected the onset of the disease. However, it will be hard for anyone to continue to recommend the introduction of gluten—specifically at the age of four to six months—since a recent extensive population study did not find that exposure to gluten at this age decreased the risk of celiac disease. Neither did delaying gluten exposure until a child was 12 months old protect him/her from getting celiac disease. This study was a 10-year, multicountry study conducted in Europe, prompted by the Swedish celiac disease epidemic study of 2001.
The researchers also did not find any evidence that breast-feeding, the duration of breast-feeding, or the introduction of gluten during breast-feeding influenced later development of celiac disease. Although we recognize the overall importance of breast-feeding for child health, breast-feeding does not appear to protect against celiac disease in children. While these European guidelines still appear in the popular press, the recommendation needs to be changed.
_Infections_
Infections—both in adults and children—may play a role in the development of celiac disease. When the lining of the intestine is disrupted by an infection, some larger molecules such as gliadin can get through the intestinal barrier and set off the immune reaction. Rotavirus infection in childhood and _campylobacter_ infection in adulthood (a common food-borne illness from raw or undercooked poultry) both increase the risk of celiac disease. (See chapter 14, "The Double Hit Theory.") Interestingly, infection with _H. pylori_ appears to be protective against the disease.
Drugs/Antibiotics/Proton Pump Inhibitors
Drugs and antibiotics can damage the intestinal lining, making it more permeable and more susceptible to food antigens. Just having an altered pH may alter the digestion of gluten. Medications also upset the delicate balance of our microbiome, and that may be a precipitating factor.
Aspirin and Other NSAIDs
Many people are taking enteric-coated aspirin that dissolves in the small intestine instead of the stomach. This transfers the damage from the stomach—where it can cause ulcers and bleeding—to the small intestine. It alters intestinal permeability and may increase the risk of other diseases such as CD. Other NSAIDs, widely available over the counter and used extensively for pain control, also disrupt the intestinal barrier and may play a role in the development of altered intestinal permeability and concurrent disease.
The Microbiome
As we discussed in chapter 9, "The Microbiome," there are many factors that influence the colonization of the microbiota in our gut, including birth mode, antibiotic use, diet, and early environment. Since exposure to microbes "educates" and helps shape the immune system, the initial flora that colonize the GI tract may have important consequences in a child's tolerance to food antigens. While there are no studies that demonstrate a direct relation between a disrupted microbiome and CD, it has been proposed that some microbiota may influence the immune response to gliadin in genetically predisposed individuals. In other words, alterations in the composition of intestinal flora may play a role in the loss of tolerance to gluten. This may be of particular importance during the first few years of life, when the immune system is maturing and being "educated."
Since it has been hypothesized that the intestinal microbiota is somehow involved in celiac disease, probiotics are appearing as an interesting enhancement in the dietetic management of the disease. We do not currently advise them because of the total lack of supporting evidence and regulatory oversight. (See chapter 5, "Supplements and Probiotics.")
_Testing Gluten and the Microbiome_
We are currently conducting a study to determine the effect of gluten on the microbiota of people with and without celiac disease. Using a gluten challenge, and testing skin and stool microbiota, we hope to have specific answers to its effect. We know that simple dietary modulation may alter the microbiome. What we do not know is whether this is beneficial, neutral, or harmful.
The composition of the microbiome and its role in immunity and celiac disease is an exciting new area of exploration and may be an important piece of the celiac disease puzzle.
An Allergic Component?
Recent studies have shown an increase in eosinophils (white blood cells that control mechanisms associated with allergies) in patients with active celiac disease. They subside on a gluten-free diet, suggesting that there may be an allergic component to the immune response in celiac disease. (See chapter 21, "Eosinophilic Esophagitis.")
_Smoking_
There are studies that suggest smoking may be protective for celiac disease, and others where this is not confirmed. There are many chemicals in cigarettes besides nicotine, but nicotine patches have been used as "drug" therapy in conditions such as severe ulcerative colitis. While the mechanisms of action are still not completely understood, the therapeutic effect of nicotine appears to dampen inflammation and the immune response. Nevertheless, this does not change the very negative effect of smoking on overall health.
Vital Wheat Gluten
Another factor that has so far received little attention is vital wheat gluten. Processed from wheat flour, this form of gluten is increasingly used in the preparation of baked goods and processed foods. It was investigated in a European multicenter study, and although that study showed negative results, the role of vital gluten needs to be explored further.* (For more, see chapter 31, "Eating Healthy.")
Stress, Life Events, and Trauma
I had a very successful but stressful career. I've always taken things emotionally home with me. I believe there has to be some trigger [for celiac disease]; maybe it's age or something else, but I think that it's stress. I was going through a very stressful period at work, the politics, a boss dying. That's when things really got bad.
(NED, 60)
Many patients pinpoint a stressful occurrence as the "triggering" event for their celiac disease diagnosis. A recent study showed that life events may favor the clinical appearance of celiac disease or accelerate its diagnosis.
Stress can be both physical and emotional. While biological stress seems to contribute to the improper functioning of immune cells, the "second brain" in the gut may also play a role in signaling the immune system during emotional stress.
Stress may also affect the protective responses in the gut and create an improper discrimination between pathogens and our microbiota. But to date, only animal models have shown that stress alters the microbiota.
Trauma and pregnancy may also be factors contributing to GI conditions, including celiac disease. (See chapter 14.)
The Mismatch Theory
The mismatch theory lies at the core of evolutionary biology/medicine, a field that applies evolutionary practices to health and illness. It suggests that we are developing illnesses that were previously rare because our bodies possess features preserved by natural selection and designed for survival in a given environment that is unlike the modern environments we have now created and live in. These environmental changes have altered how the body functions.
_Put simply, mismatches are caused by stimuli that are too much, too little, or too new._
—DANIEL E. LIEBERMAN, _THE STORY OF THE HUMAN BODY_
This theory has been narrowed into a hypothesis that we are eating a food (wheat) that we were not designed or evolved to eat. A number of anthropologists, archaeologists, and molecular biologists have countered this hypothesis based on the so-called Paleo diet:
_Our bodies have adapted over time to different circumstances, including to cooking and to modern agriculture, and this process is always ongoing. There is no pristine virtue in what our ancestors ate in Palaeolithic times, and in any case our bodies have already undergone significant changes since that time. Life, especially human life, is never perfectly matched to one kind of eating. It is always evolving as the food sources change._
—DIMITRA PAPAGIANNI, PH.D., AND MICHAEL MORSE, PH.D., COAUTHORS OF _THE NEANDERTHALS REDISCOVERED_
Ninety-eight percent of the worldwide population that regularly eats gluten does not get celiac disease. If you factor in other related gluten sensitivities and intolerances, 70 percent of this population has no GI distress from the grain at all.
_Tomatoes, peppers, squash, potatoes, avocados, pecans, cashews, and blueberries are all New World crops, and have only been on the dinner table of African and Eurasian populations for probably 10 generations of their evolutionary history. Europeans have been eating grain for the last 10,000 years; we've been eating sweet potatoes for less than 500. Yet the human body has seemingly adapted perfectly well to yams, let alone pineapple and sunflower seeds._
—DR. KARL FENST, BIOARCHAEOLOGIST
_Temporary Gluten Autoimmunity—a Confounding Factor_
Adding mystery to the puzzle are the children and adults with celiac disease antibodies that go away when they continue on a regular diet. While we feel that this is a rare event, it has been seen in children involved in long-term studies. It is one reason that asymptomatic children tested during a screening should have a second blood test prior to subjecting the child to an endoscopy.
Although this is rarely seen in adults, we did a study on a baker who had positive blood results for celiac disease but a negative biopsy, and whose blood tests normalized on a regular diet after a period of time. It does not appear to occur in patients who have abnormal biopsies.
What does it mean? It means that the switch can go on and then it can go off. But it is very risky to assume that celiac disease has "gone away" since being able to "tolerate" gluten is not a reliable test of whether celiac disease has gone away.
The long-term effects of positive blood tests that switch to negative remain unclear, and these patients should be followed into adulthood. Perhaps we should call these people "potential celiacs."
The danger rests in people who focus on the word _temporary_ and go back on a regular diet, only to suffer complications from the continued inflammatory reaction in their GI tract. There are patients in their 50s who were diagnosed with celiac disease as babies, whose parents were told it had gone away, and who ate gluten without symptoms for 40 years—and then developed intestinal cancer.
Management—Diagnosis and Treatment
There have been several advances in the diagnosis of celiac disease in the past few years. Some of the issues of the past, such as variation in lab and pathology interpretation, still lead to incorrect diagnoses.
The panel of tests available for celiac disease includes all of the following. While there are no tests that are 100 percent specific and sensitive for celiac disease, some of the following are extremely accurate.
Diagnostic Tests
1. **IgA tissue transglutaminase (tTG):** tTG is the enzyme that converts gliadin into a more toxic molecule. We consider this one test the "gold standard" blood test. It may be combined with the deamidated gliadin peptide (DGP) to increase the number of diagnoses.
2. **IgA endomysial antibodies (EMA):** This test adds specificity to the diagnosis. (This means that there are no other conditions that can cause a positive result.) It is an expensive test that is read manually by an expert technician. It has been advocated to replace the biopsy in the new European diagnostic pathways for children. (See opposite.)
3. **Total IgA:** This test is not done routinely, as it is unclear whether it is cost-effective. While it is helpful in finding people who are IgA deficient, that is a small group. ( **IgG tissue transglutaminase** is used to diagnose celiac disease in IgA-deficient individuals. There is no role when IgA is normal.)
4. **IgA deamidated gliadin peptide (DGP):** The deamidated gliadin peptide test has been developed recently and replaced the antigliadin antibody (AGA) test, which is no longer available. The test looks for specific antibodies that have developed in response to gliadin (the protein portion of gluten). The DGP may not be as valuable as the tissue transglutaminase test, but it is part of the panel that we recommend for celiac disease screening. This test may be positive in some patients with celiac disease who have negative IgA tTG tests.
_Biopsy Results_
If blood tests are positive, the diagnosis is confirmed with a biopsy. None of the blood tests are either 100 percent sensitive or specific for celiac disease, which is why we still recommend a biopsy as the ultimate gold standard for diagnosis.
Biopsy is pathologist dependent, and not all pathologists are expert at interpreting small intestinal biopsies nor use a standardized terminology for grading the changes in celiac disease. The Marsh score is one such form. If there is a question about the result, the biopsy can always be reviewed by a different pathologist.
False Negatives/False Positives
False negatives: You can have celiac disease and still have negative blood tests, and you can have negative blood tests and develop celiac disease later in life. If you are not eating a lot of gluten, you can have celiac disease with negative antibodies.
**A Word on Sensitivity and Specificity**
Testing criteria are based on the sensitivity and specificity of the test. These terms are often used in the medical literature, so it is important to understand their meaning.
**Specificity:** If a test is 100 percent specific, it means there is nothing else, no other medical condition that can cause the positive result.
**Sensitivity:** If a test is 100 percent sensitive, it means that everyone with the disease has a positive test.
However, no test is 100 percent. Blood tests are designed to have cut-offs that will include most people with the disease. However, they will include some as positive who do not have the disease if they fall in this range, and miss others who do not.
European Pediatric Guidelines
There are pediatric guidelines in Europe that suggest that you can diagnose celiac disease without a biopsy. They are not accepted in the United States. They were created in response to parents reluctant to subject children to a biopsy that is usually conducted under general anesthesia. If used, they require very strict guidelines that need to be adhered to.
The European guidelines require **all** of the following conditions:
The child **must be symptomatic** and then have:
1. A positive tTG more than 10 times the upper level of normal
2. A second blood test for EMA that is positive and that _must_ be taken on a separate occasion
3. Presence of genetic markers.
The second blood draw guards against temporary gluten autoimmunity and may account for "false positive" antibody tests. When these criteria are met, a presumptive diagnosis can be made and a gluten-free diet started.
There are pros and cons to these guidelines. On one hand, you diagnose most cases of celiac disease. It eliminates an invasive endoscopy and biopsy, as well as the concern about general anesthesia, which has been suggested as a contributing factor to some cognitive impairment in the very young. However, this has not been conclusively demonstrated. Conversely, the guidelines must be adhered to strictly, and some doctors do not do a separate blood draw, which may not catch children who are asymptomatic. Without an endoscopy, other conditions that occur with celiac disease may be missed. And some children with positive blood tests may not have celiac disease.
We favor being very certain because as the child becomes an adolescent, then an adult, he or she or their adult physician may not believe the diagnosis.
One patient who had been diagnosed with celiac disease as a child by his pediatrician discovered as a young adult that he did not have it. His anger toward his parents when he found out that the childhood diagnosis—done without a biopsy—was not correct remains troubling.
Gene Testing
In any one individual there are multiple factors in addition to genetic makeup that will lead to celiac disease, and they are different for each person. Having the gene(s)—specifically HLA-DQ2 and -DQ8—merely means that you are at risk. However, you must have these specific genes to have celiac disease.
HLAs are human leukocyte antigens, the proteins found on the surface of almost every cell in the body. They are the sentries that patrol the immune system identifying other cells as "self" or "nonself"—a foreign body. These are the genes that must "match" to determine compatibility for an organ transplant.
**People should not have a genetic test unless they understand the significance of the test.** It is not a determinant of celiac disease and cannot be used to diagnose it. Its value is in a negative result because this excludes the possibility of having the disease. If you have been correctly diagnosed with celiac disease you do not need a gene test.
Approximately 30 percent of people in the U.S. have these HLA-DQ2 and -DQ8 genes, and only 1 percent have celiac disease. It is necessary but not sufficient for development of celiac disease.
Gene testing should be conducted and interpreted by doctors who understand its significance. Home testing, because of the potential for misinterpretation, is not recommended. The presence of these genes is not a reason to commence a gluten-free diet.
The role of genetic testing is to:
• Determine which family members to screen for celiac disease. There is no point in testing family members in an "at risk" family without the genes.
• Diagnose patients in whom antibody and biopsy results appear incongruent.
Point-of-Care/Finger-Prick Testing
Point-of-care testing involves technology that gives an immediate result. These tests can be performed in a doctor's office or purchased commercially without any medical personnel input.
There is a great deal of precedence for point-of-care testing—notably in pregnancy, strep, and HIV kits. Such a test has been developed for celiac disease and currently approved for use in Canada as an OTC product. Because interpretation is particularly important in celiac disease, confirmation with an endoscopy is still necessary. The test is marketed and used in Canada to track a gluten-free diet.
Fecal Testing
Currently, fecal stool tests for celiac/gluten antibodies are neither specific nor sensitive enough to be used as a diagnostic tool. Some labs offer them, but there are _no_ rigorous scientific studies proving their validity, efficacy, or usefulness. They have no role in the diagnosis of gluten-related disorders.
Treatment
The current treatment for celiac disease is a lifelong gluten-free diet, though nondietary pharmaceutical treatments are being developed to eliminate the toxic effect of gluten on the intestines of susceptible people. The exact role of these adjunctive therapies remains to be seen, but most will not replace a gluten-free diet. (See chapter 30, "Nondietary Therapies.")
Patients often opt out of further treatment once they are diagnosed and on a gluten-free diet, but the management of celiac disease should not stop at the end of your fork. Celiac disease is a chronic condition like diabetes or high blood pressure and should be monitored with yearly visits to a physician specifically for the celiac disease, to prevent long-term complications.
L-Carnitine
There is a study showing that L-carnitine is effective in the treatment of some types of fatigue found in celiac disease. Supplementation can be very helpful in patients with fatigue and low levels of L-carnitine in their blood. (See chapter 5, "Supplements.")
L-carnitine is an amino acid (a building block for proteins) that is produced by the body and is a natural component of the diet. If tests show that you are deficient in this metabolite and cannot correct this through diet, you should take supplements under a doctor's instruction. It is not a cure-all for the fatigue found in celiac disease.
Summary
• Incidences of celiac disease appears to have increased over the past 50 years. While some risk factors have been pinpointed, others remain to be uncovered.
• Despite intensive research in the past decade, the mechanisms behind celiac disease remain a challenge, and it is still underdiagnosed.
• The variability of age at the onset of symptoms is still puzzling, as well as the variability of the symptoms themselves.
• While many of the environmental factors may be related, they are not necessarily causal. An infection, drug, or life event may uncover the underlying condition rather than trigger it. This is of particular interest as scientists investigate the role of the microbiome in diseases such as celiac disease. While alterations in the small intestine microbial composition have been associated with active celiac disease, there have been no studies demonstrating a causative effect to these changes.
• We continue to search for the "switch"—the genetic/epigenetic, environmental, infective, or physiological button—that causes someone to go from tolerating gluten to not tolerating gluten, so that we can prevent it.
We have come a long way, but many intriguing puzzle pieces are still missing.
Gluten Sensitivity—the New Kid on the Block
I became gluten-free in 2003 because I was feeling really awful most of the time. I was distended and bloated; my [throat] was always burning. A friend suggested I stop eating bread, and within three days, I noticed a huge difference. I haven't had real bread since then. When I eat it I feel terrible. Instead, I eat a variety of gluten-free grains like rice, corn, and quinoa.
(INGRID, 64)
Nonceliac gluten sensitivity (NCGS) is a new, emerging entity that encompasses a diverse group of conditions that all appear to improve when gluten is removed from the diet. It is unclear how long it has been around, but patients have been aware of it for years. In 2011 a consensus conference established the definition of NCGS within the framework of other gluten-related disorders in the medical community.
It is, without doubt, a popular name in the consumer press. While there are some people with gluten-sensitive symptoms, it is currently a self-diagnosis since **there is no definitive test to confirm its presence.** It is a common diagnosis by nontraditional medical practitioners.
However, the number of patients who have neither celiac disease nor a wheat allergy, but appear to derive benefit from a gluten-free diet, has increased substantially.
What Is NCGS?
NCGS is defined as a reduction in symptoms after eliminating gluten-containing products from the diet and a recurrence of symptoms when gluten is re-introduced in people without celiac disease and a wheat allergy. People with NCGS do not have the small intestinal damage or develop the antibodies (tissue transglutaminase, tTG) found in celiac disease. While it is important that celiac disease is ruled out in these patients, it is worth noting that most people with gluten sensitivity have not been tested for celiac disease or other possible causes of their symptoms.
It is the "youngest" member of the family of gluten-related disorders and is characterized by a great variability in symptoms and clinical history. Most patients report both GI and non-GI symptoms (especially fatigue or "foggy brain") that improve on a gluten-free diet.
The gastrointestinal symptoms are similar to symptoms of irritable bowel syndrome and include bloating, gas, diarrhea, constipation, abdominal pain, and nausea.
The extra-intestinal symptoms include lack of well-being, tiredness, headache, foggy mind, numbness, and joint or muscle pain.
The rapid disappearance of symptoms on a gluten-free diet and their recurrence after gluten reintroduction are also characteristic of the condition.
After a thorough medical evaluation, we find that many PWAGs (people who avoid wheat and gluten) have a variety of other conditions such as lactose or fructose intolerance, bacterial overgrowth, or microscopic colitis and once those are diagnosed and treated they are able to eat gluten again symptom-free. **Thus, a self-diagnosis of NCGS may mask other conditions**. It is also unclear whether another component of wheat is causing symptoms in these people. (See the following section.)
Patients often identify other foods that cause symptoms—50 percent of NCGS/PWAGs seen at the Center are avoiding dairy, soy, or corn as well as wheat.
What Causes NCGS?
Nongluten Components of Wheat?
While NCGS appears to be directly related to an adverse food-related reaction, recent studies suggested that gluten may not be the only trigger, and that different proteins found in wheat (e.g., ATIs) are likely to play a relevant role in this condition.
New studies have shown that a diet low in FODMAPs results in improved symptoms in some patients with self-reported NCGS, supporting the hypothesis of a major role of FODMAPs compared to gluten.
Other possible causes of symptoms in NCGS are wheat amylase trypsin inhibitors (ATIs), other proteins found in wheat and related grains. (See chapter 11, "Gluten and Nongluten Grains.")
Because it is unclear which components of wheat-based products are responsible for an individual's symptoms, it may be premature to assign all of the blame to gluten. This is why we and others prefer to call these individuals PWAGs, as the term better encompasses the possible underlying dietary culprits.
Genes?
Although celiac disease is characterized by a strong genetic association—about 95 percent of patients carry HLA-DQ2, and the remaining 5 percent carry HLA-DQ8—only about 50 percent of patients with NCGS carry HLA-DQ2 and/or HLA-DQ8. Nevertheless, this percentage is slightly higher than the general population (30 percent). This serves to further emphasize the need for patients to be assessed prior to going gluten-free. This is especially important as we learn the pitfalls and hazards of a gluten-free diet. (See chapter 4.)
As the cost of DNA sequencing lowers, it will be interesting to characterize the genetic profile of different subgroups of patients with NCGS.
Management of NCGS
Diagnosis
As noted earlier, there is currently no diagnostic test for NCGS. It is often a diagnosis of exclusion—patients do not have specific celiac disease markers or intestinal damage (villous atrophy), nor do they have high blood levels of IgE indicating a wheat allergy.
An intestinal biopsy sample should always be obtained from patients with suspected NCGS while they are eating gluten to exclude the presence of villous atrophy, the hallmark of CD. About 60 percent of NCGS patients have normal intestinal mucosa.
Some interesting results are starting to appear in regard to the antibodies found in patients with NCGS. Various studies have found IgG anti-gliadin antibodies in a large percentage of patients with NCGS. As explained fully in chapter 6, antigliadin antibodies are targeting gliadin, the protein portion of gluten. While these antibodies are found in celiac disease, these are not the specific IgA antibodies found in celiac disease.
Interestingly, after patients with NCGS started a gluten-free diet, the IgG levels returned to normal in almost all of them. Strict compliance and a good response to a gluten-free diet, with significant improvement in symptoms, were significantly related to the disappearance of IgG antigliadin levels in these patients.
Still, IgG antigliadin cannot be considered a reliable biomarker of NCGS because it is also found in people with many other disorders, including autoimmune diseases, autism spectrum disorder, and ADHD, as well as in healthy subjects. (For more, see part V, "The Brain-Gut-Gluten Connection.") These antibody tests are only available right now in a research setting.
Treatment
It is important to avoid self-diagnosis. If you think you have NCGS you should be tested for celiac disease as well as bacterial overgrowth, microscopic colitis, and other food intolerances and perform a trial of the FODMAP diet before starting—or continuing—a gluten-free diet. A full medical history regarding drugs (both OTC and prescription) should also be taken. NSAIDs and other drugs have been associated with similar symptoms in patients.
A self-diagnosis of NCGS can mask other serious conditions that can affect your long-term health.
Summary
• Patients suffering from NCGS are a diverse group, composed of several subgroups, each characterized by a different clinical history, and, probably, clinical course.
• None of us fully digest gluten the way we digest other proteins such as those in meat, but only 1 percent of people develop an autoimmune response. It is possible that the group with NCGS is a middle group that does not get the full immune response characterized by celiac disease, but develops a greater response than someone with some gas or burps. There may also be a group of NCGS patients who develop villous atrophy in the future.
• A diagnosis of NCGS can only be made by excluding celiac disease and a wheat allergy.
• It is important therefore that we look at ways of better classifying patients with NCGS. An accurate diagnostic test would certainly provide the best way of doing this. Gliadin antibodies and HLA DQ2/DQ8 genes are more prevalent in NCGS patients than the general population, and it may be that they play a role in delineating NCGS patients in the future, but as yet they cannot be used in diagnosis.
• We need to examine what is triggering symptoms—is it the gliadin proteins, nongliadin gluten parts in grains, gluten contaminants, other wheat constituents such as amylase trypsin inhibitor (ATIs), or only carbohydrates (lactose or fructose) in the diet?
• Future research should aim to identify the biomarkers for a diagnosis of NCGS diagnosis and better define the different NCGS subgroups.
In the past few years, NCGS has become increasingly recognized, and researchers are just beginning to define this entity.
Irritable Bowel Syndrome
Let me put it this way: IBS makes me feel as if someone is "fracking" my gut. Massive pressure is injected, enormous amounts of natural gas is forced to the surface, and the effect on the environment is undesirable to lots of people.
(GENE, 55)
Irritable bowel syndrome (IBS) interrupts a life. The symptoms are unpredictable, the pain can be crippling, and patients echo the challenges of airplane travel, family occasions, disrupted meetings, and the psychological burdens they carry.
What Is IBS?
IBS is a functional bowel disorder—which is to say that symptoms are caused by changes in how the gastrointestinal tract works. The GI tract continues to look normal—it appears undamaged—but creates symptoms. It is one of the most common disorders diagnosed by doctors and affects as many as 5 to 20 percent of people worldwide. It occurs more often in women and affects children as well as adults. Symptoms range from diarrhea to constipation—and can yo-yo between both—as well as abdominal discomfort or extreme pain, bloating, and gas. While the symptoms are common, it is unclear why they have such an intense impact on some people and not others.
Some people complain of daily distress while others have intermittent symptoms that may not occur for weeks or months. A decreased quality of life is well documented. While some studies show that only a minority of people who suffer seek out medical care, other patients go to numerous doctors and undergo endoscopies, colonoscopies, X-rays, scans, blood tests, and biopsies—the results of most of which are normal, confounding both patient and physician.
IBS is usually classified into four categories that also determine the type of treatment used for symptoms. These are:
1. **IBS with constipation (IBS-C)—** mainly hard or lumpy stool
2. **IBS with diarrhea (IBS-D)—** mainly loose or watery stools
3. **Mixed IBS (IBS-M)—** a combination of hard and watery stools
4. **Unsubtyped IBS (IBS-U)—** insufficient criteria to meet any of the other categories
It is not uncommon for patients to switch subtypes over time. There are also conditions that resemble IBS. These include functional constipation, diarrhea, and bloating syndromes.
How Is It Diagnosed?
Irritable bowel syndrome is diagnosed through a combination of the Rome III criteria, a physical exam, and tests to diagnose or rule out other conditions with similar symptoms. These include IBD (e.g., colitis, Crohn's disease), celiac disease, ulcers, SIBO, food allergies and intolerances, pancreatic insufficiency, microscopic colitis, or a chronic GI infection or parasite. It is essentially a diagnosis of exclusion.
Nothing in my life is predictable—I never know if I can get through a concert or a phone call without rushing to the bathroom.
(JANET, 70)
The Rome III Criteria
The Rome III criteria require that patients have had recurrent abdominal pain or discomfort at least three days per month in the last three months, associated with two or more of the following:
• Relieved by defecation
• Onset associated with a change in stool frequency
• Onset associated with a change in stool appearance
They must also have symptoms to support the diagnosis, which include:
• Abnormal stool frequency (greater than three bowel movements per day or less than three bowel movements per week)
• Abnormal stool form (lump/hard or loose/watery stool)
• Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation)
• Passage of mucus
• Bloating or feeling of abdominal distension
Patients with IBS also report fatigue, a "noisy" abdomen (borborygmi), and depression. IBS can also occur along with other conditions including IBD and celiac disease. Symptoms that include fever, weight loss, or blood in the stool demand a prompt clinical evaluation.
Few clinicians correctly label patients according to the Rome Criteria. Thirty percent of the patients we have diagnosed with celiac disease had a previous misdiagnosis of IBS.
There is considerable interest in the development of biomarkers for IBS. Several blood tests are promising, but the biomarkers tested overlap with and are elevated in other conditions, especially celiac disease. Thus, blood tests are not as sensitive for a diagnosis of IBS.
What's normal for you may not be normal for everyone else. I can't wear certain clothes because my belly blows up when I eat. That's my normal.
(CASSIE, 51)
Unfortunately, patients with IBS usually present with GI complaints for which their doctor can find no organic cause. This has led to diagnoses of psychiatric disorders, hypochondria, and "hysteria." It also forced many patients to ignore symptoms and regard them as a normal part of life. With our growing understanding of the "second brain" in the gut and gut-brain interactions, this perspective has begun to change.
What Causes IBS?
IBS is an extremely prevalent but poorly understood condition—its symptoms distinct, its causes more elusive. They appear to be a complex construction of:
• Genes (people often say that "bad stomachs run in my family")
• Diet and food sensitivity
• The microbiome—a makeup uncharacteristic of gut bacteria from that of healthy individuals
• Infections and/or with antibiotic therapy causing a "double hit"
• An abnormality of bile salt metabolism
• Altered GI motility (how the GI tract deals with and eliminates its contents)
• Brain-gut signaling problems (including a hyperreactivity to stress or psychosocial factors)
Right now, even the puzzle pieces keep changing shape in this complex and challenging condition.
Genes
IBS tends to "run in the family." It is common to hear comments such as "My mother had stomach issues, I've got belly issues, and my daughter pops antacids." While no specific genes have as yet been definitively identified, interesting studies regarding polymorphisms (anomalies) in genes that encode gut serotonin have been implicated.
Studies examining the environment and social learning suggest that the reinforcement of illness behavior in a family can contribute to the heightened awareness of GI symptoms.
Diet and Food Sensitivity
Many patients feel that certain foods trigger their symptoms. In particular, milk and dairy products, spicy or fatty foods, gluten, high-fiber vegetables and grains (cabbage, beans), caffeine, and fried foods. While many doctors recommend taking fat and caffeine out of the diet and increasing fiber, this has not been a satisfactory solution for most people. The low-FODMAP diet has been successful for some people.
It is still unclear to what extent diet causes the symptoms of IBS.
The Microbiome
The intestinal flora of IBS patients has been shown to differ from that of healthy controls, but the meaning of this is unclear since microbiota differ in many illnesses as well as between individuals.
Several studies have examined the role of the gut microbiota in IBS through manipulation with probiotics, antibiotics, fecal transplants, and germ-free animals. They have shown a relation between the microbiota and symptoms such as pain and bowel habits. Other studies are looking at the effect of stress on the intestinal microbiota. It continues to be an area of important research into possible therapeutic interventions for IBS.
Post-Infective IBS
She was treated for parasites and we assumed she had knocked it out but wasn't well. Then she went to Central America and got amoebas and got treated. But she still wasn't feeling fantastic. One doctor told her it was all in her head. I was furious at this doctor. I don't think anybody wants to be sick. If you're sick, you're sick. If you're sick enough to complain about it, it's real.
(ENID, 62)
A considerable number of cases of IBS are diagnosed following a GI infection. Patients get traveler's diarrhea, giardia (parasite infection), or campylobacter (food poisoning) and are never the same. (See chapter 14, "The Double Hit Theory.")
There are also cases of IBS following a diagnosis of inflammatory bowel disease (IBD). Illnesses such as IBD can cause more liquid to remain in the bowel, increasing the load of water that arrives in the large intestine and causing diarrhea. Excessive amounts of liquids in the bowel can also cause it to swell, and a red and inflamed gut can slow down the movement of the intestinal muscles, causing constipation. We also see many people with a diagnosis of celiac disease who respond well to a gluten-free diet and then appear to develop post-celiac IBS.
Brain-Gut Signal Problems
I remember sitting in morning assembly in grade school just filled with pain.
(ANNIE, 24)
It is said that IBS is "all in the head." Some is—the perception of pain is in the head—but the mechanism is in the gut.
Signals between the brain and the gut control how the intestines work. It is believed that disturbances in the neuroendocrine system that controls the motility (movement), secretions, and sensation within the gut may play a role in the development of IBS.
People with IBS have GI motor problems—i.e., slow or fast motility—that create spasms or sudden strong muscle contractions that can cause pain. And people with IBS have a lower pain threshold for the bowel stretching caused by gas or stool, leading to the hypothesis that their brain may process pain signals from the gut differently.
The "Gate" Theory of IBS
The Gate-Control Theory of pain perception suggests that the spinal cord contains a type of "gate" that opens and closes to allow or block pain signals traveling to the brain where they are interpreted and perceived.
It is proposed that people with IBS have gates that open more readily, and that the interpretation and perception of pain is amplified when they are experiencing psychological stress or distress. Pain is also a highly personal experience and difficult to measure. It can be influenced by expectations and augmented by psychological distress and strong emotions.
A maladaptive stress response may also contribute to the initiation, persistence, and severity of symptoms. Patients with IBS have a hyperreactivity or sensitivity to psychosocial factors such as a dramatic increase in bowel contraction in response to stress (e.g., final exams, presentations at work) or eating.
Psychological problems such as anxiety, depression, and PTSD are more common in people with IBS, although the link is unclear. GI disorders including IBS are often found in people who have reported past physical or sexual abuse. In a study we did of patients with celiac disease and persistent symptoms despite a strict gluten-free diet, a previous history of abuse (physical, emotional, or sexual) was shown to be the predominant driving factor of their symptoms.
Irritable bowel syndrome can be considered an example of the disruption of the complex relationships between the gut and the brain, and a better understanding of these alterations might provide new, targeted therapies. It is often addressed with psychological treatments, antidepressants, or both.
How Is IBS Treated?
We need to stop putting Band-Aids on symptoms and address the real problems behind common symptoms—such as bloating.
(FRAN, 69)
IBS is very difficult to treat. Most of the current medical options are limited to silencing symptoms but the more researchers uncover about the underlying causes of IBS, the more hope there is for drug therapies to treat them.
In addition, any one symptom can have a number of other diagnoses. Symptoms must be taken seriously even if the physician doesn't understand their mechanism of action.
Medications
The current arsenal for IBS medications includes:
• Laxatives for constipation
• Antidiarrheals to decrease the frequency of bowel movements
• Bile salt absorptive agents
• Antispasmodics to treat abdominal cramping and pain
• Antidepressants/psychotropics to treat pain and brain-gut dysfunction
The prescribing of antidepressants for IBS often elicits a response from patients of "You think this is all in my head!" or "I'm not depressed!" In fact, although antidepressants were developed to treat depression, they are also effective as analgesics, i.e., drugs that reduce pain. They block pain messages between the brain and the GI tract and reduce visceral hypersensitivity (within the inner organs). A recent study noted, "Much like treating diabetes with the insulin that is missing, antidepressants may help recover the brain's ability to respond to pain signals properly." Different categories of psychotropics also help treat diarrhea and constipation.
Antidepressants are often effective in treating IBS symptoms—we consider them "gut-otropics."
Serotonin
Serotonin, among its many activities, plays a major role in regulating peristalsis in the intestines as well as relaying sensory information to the brain. As noted in chapter 10 ("The 'Second Brain'"), mouse studies have demonstrated that _too little_ serotonin can contribute to constipation, and _too much_ can contribute to diarrhea. Studies are under way assessing abnormalities in serotonin transporters (SERT) as treatment in IBS. In addition, selective serotonin reuptake inhibitors (SSRIs) are a form of medication frequently prescribed for IBS.
Dietary Restriction
The majority of patients on a gluten-free diet have IBS and find the diet relieves some symptoms. What is unclear, however, is what aspects of wheat are causing their symptoms, whether this translates into an understanding or good treatment of the condition, and if it is an effective approach. It is clear that some people with diarrhea-predominant IBS (IBS-D) are wheat sensitive, and a trial of wheat or gluten restriction—after celiac disease has been excluded—is not unreasonable.
People with IBS often find relief with other types of dietary intervention such as lactose or fructose restriction. The low-FODMAP diet targets various carbohydrates (sugars) that are fermented in the colon by bacteria and create the gas and bloating characteristic of IBS. It is considered a miracle by some, and not truly effective by others.
Before commencing a strict FODMAP diet we would test for fructose intolerance. Fructose is a major component of the FODMAPs and, if positive, the avoidance of fructose-containing foods may be all that is required rather than the more restrictive FODMAP diet.
Probiotics
Probiotics are being studied as adjunctive therapy in treating IBS. To date, the studies have given researchers interesting observations, but the actual role of altered gut bacteria on the symptoms of IBS is unproven.
Supplements like probiotics are a largely unregulated market. Many contain unlabeled ingredients that may be harmful. (See chapter 5, "Supplements.") We suggest caution when taking various probiotics for IBS. Studies are often performed with products from specific manufacturers that may not be the same as those available over the counter.
Therapies for Mental Health Problems
Because cognitive processes play an important role in the top-down regulation of the body, various psychological treatments have been used to reduce pain and GI symptoms. This may include relaxation therapy or cognitive behavioral therapy to help modify the pain "gates" and stress responses in IBS.
Summary
• IBS is an extremely prevalent but poorly understood gastrointestinal disorder. While the gut can look normal, the disease is much more subtle pathologically.
• What we do understand is that it can interrupt everyday life with symptoms that are very real but whose causes are elusive.
• People with IBS appear to produce more gas in their GI tracts, eliminate it less effectively (promoting distension), and are more highly sensitized to the pain this causes. They also suffer from bouts of diarrhea and/or constipation—both often yo-yoing—triggered by a variety of environmental as well as physiological factors.
• Researchers are currently studying drugs that target diarrhea-predominant or constipation-predominant IBS.
• IBS is a condition that is often treated with dietary restrictions that may simply be a Band-Aid. As the science progresses, better therapies will become available. It is an area of intense research.
Inflammatory Bowel Disease
Most mornings I have a bout or two of diarrhea, and sometimes it wakes me up at night. And it's liquid, just like a faucet. I can tell you, it ain't no fun.
(GORDON, 52)
Inflammatory bowel disease (IBD) is the medical term for a digestive tract on fire. And the inflammation in all or parts of the GI tract can ulcerate and/or scar the intestines causing the pain, diarrhea, bleeding, and weight loss common to the condition. The disease may be mild and restricted to a localized area, or severe enough to require immunosuppressant drugs, _parenteral (intravenous) nutrition,_ or surgery.
While there is no one typical diet for people with IBD, dietary advice and management are of great importance to patients with the disease. Advice from the Internet or alternative medical practitioners is not a substitute for the role played by registered dietitians in the management of disease activity, symptoms, and general nutrition.
What Is IBD?
My life revolves around it.
(BILL, 40)
IBD is the umbrella term for Crohn's disease, which may occur anywhere in the GI tract, and ulcerative colitis, which is limited to the colon. It is characterized by a recurring or chronically active inflammation originating in the intestines, but manifestations also occur outside of the tract. Some patients are classified as having intermediate colitis when it is not clear if they have Crohn's or colitis.
Colitis
Colitis is an inflammation of the colon. It may be mild, moderate, or severe, and is categorized by its causes. This includes infective (bacterial or viral), vascular (caused by a diminished blood supply to the colon), and immune based. The symptoms of colitis include diarrhea, cramping and pain, bleeding or bloody stools, _tenesmus_ (the constant urge to have a bowel movement or sensation of incomplete evacuation), fever, fatigue, and other signs of inflammation.
Because some of these symptoms are also seen in IBS, celiac disease, and a number of other conditions, they are often confused, or mask a proper diagnosis.
Crohn's Disease
Crohn's disease can affect the entire GI tract—from the mouth to the anus—not just the colon. The symptoms are similar to other inflammatory bowel diseases, but abdominal pain is usually more prominent and bleeding less prominent than in ulcerative colitis.
It is important that you seek medical help if the diarrhea is persistent or you become dehydrated. Fever and blood in the stool are alarm symptoms that require an aggressive diagnostic approach.
What Causes IBD?
Stress and diet were once believed to initiate IBD, but it is now understood that they only aggravate the symptoms. Because inflammation can be ascertained through tests, we understand a lot about the gut itself in diseases like IBD, but uncovering its causes has proven more difficult.
IBD is a complex disease that appears to occur due to a combination of:
• genes
• an inappropriate immune response in the gut triggers inflammation
• the microbiome
• environmental factors
Recent studies are beginning to connect some of the dots.
Genes
Genes appear to be a factor, as the condition is found in clusters in some families. Ten to 20 percent of people with IBD have a family history of the disease. Thus, the genetic influence on microbial content in the gut is also thought to play a role.
Immune Responses
One theory regarding the development of IBD involves an inappropriate immune response within the gut that creates inflammation. It is thought that this response is triggered by a disturbed tolerance to antigens (toxins, bacteria) found in the _lumen_. And most of these antigens are derived from the intestinal microbiota.
The Microbiome
The colonization of the intestine by microbes in early life is the main stimulus that matures the immune system in babies. (See chapter 9, "The Microbiome.") This is an active and fluid process that depends on genetic and environmental factors.
Scientists are beginning to explore the possibility that the composition of our intestinal microbiota could contribute to inflammatory conditions in the gut. In people whose microbiota respond inappropriately to what is going through the digestive tract, the normal low-grade inflammation that keeps us safe from pathogens goes into overdrive and starts to damage and/or destroy the mucosal lining. There may be a similar genetic/microbiotic/environmental storm at work in celiac disease.
Studies on the microbiotic makeup of patients with IBD are being conducted. One study showed that people with IBD had 30 to 50 percent reduced biodiversity in _Firmicutes_ and _Bacteroidetes,_ two of the major classes of bacteria populating the gut. The Firmicutes family includes many "friendly" bacteria that are essential for digestion and balance in the body and others such as _Streptococcus_ and _Clostridium_ that cause infections when they overgrow.
Further evidence of the role of gut flora in the cause of inflammatory bowel disease is that affected individuals are more likely to have been prescribed antibiotics in the two- to five-year period before their diagnosis than unaffected individuals. The microbiome can be altered by environmental factors such as food or oral medications—antibiotics, iron preparations—but no direct link to specific diseases has been proven.
Future studies are necessary to determine the meaning of the complex interactions between our gut and our microbiota and the respective role each plays in inflammatory diseases such as IBD.
Environmental Factors
A number of environmental factors have been implicated in IBD. They include:
• **Geography:** The disease has concentrations in certain parts of the U.S. and the world
• **Smoking:** For unknown reasons smokers are at lower risk of developing ulcerative colitis while Crohn's disease is more common among smokers.
• **Medications:** Antibiotics and NSAIDs may aggravate symptoms rather than cause them, yet they have been implicated in the condition.
The Western diet—with its low-fiber, high-fat, and high-sugar content—has been implicated in the development of IBD, but there is little evidence to back up this supposition. Advice about anti-inflammatory, Paleo, low-carb, specific carbohydrate, or gluten-free diets abounds. However, they have not been studied and may place unnecessary nutritional burdens on patients with IBD.
Liquid diets have been studied in the dietary manipulation of Crohn's disease with some interesting results regarding the relation of food to the causes of IBD. The exclusive or partial enteral nutrition diets replace foods with predigested liquid. Gluten, animal fat, and dairy products are among the restricted items on these diets. The response to these dietary therapies in terms of remission rates is high—equivalent to the response to steroid therapy, a mainstay of treatment for IBD. While the mechanism remains unclear, it has moved from the concept of "bowel rest" to hypotheses about the effects on the intestinal microbiome, intestinal barrier repair, and the immune system. The dramatic response rate to the lack of specific foods and the presence of predigested dietary components highlight the role of food or specific components of food in the genesis—and possible treatment—of this disease.
How Is IBD Diagnosed?
They went in from the top and they went in from the bottom. The doctor showed me a picture—which meant little to me—of these fissures and said, "This is abnormal."
(GORDON, 52)
IBD is diagnosed through a variety of tests that may include endoscopy and/or colonoscopy with biopsy, blood and stool tests, and X-rays or scans in order to determine if the GI tract is inflamed and injured, as well as the extent and location of the damage. A patient history of symptoms and frequency and what environmental or dietary factors affect them is also taken.
How Is IBD Treated?
Treatment for IBD will depend on whether a patient has Crohn's disease or some form of colitis. It is usually some combination of medications to reduce inflammation, induce healing, and relieve symptoms, and/or surgery.
Diet
Dietary advice is essential in IBD. Since the inflammation of the GI tract can cause the malabsorption of essential vitamins and minerals leading to malnutrition, these deficiencies must be addressed. Nutrient deficiencies including vitamin B12, iron, vitamin D, and folic acid can be measured and treated when necessary.
After bouts of diarrhea, it is also important for patients to replenish lost water.
There are restriction diets used to control symptoms, and they vary with a patient's diagnosis, food intolerances, and other conditions that may occur simultaneously. Up to one-third of patients continue to have symptoms in the absence of inflammatory disease activity. This may be post–IBD irritable bowel syndrome, or a functional disorder caused by a fructose or FODMAP sensitivity that needs to be determined.
Lactose intolerance is common in ulcerative colitis, so avoiding milk products will alleviate symptoms for these people. Reducing fiber or specific foods that trigger symptoms often helps people who have flares or strictures.
Celiac Disease, Gluten, and IBD
My colitis improved since I started a gluten-free diet! Do I have celiac disease?
(WAYNE, 50)
On one hand, celiac disease and IBD can occur together, but the improvement may coincide with a remission in the IBD, since the disease is subject to spontaneous flares and remissions. In addition, the improvement of symptoms on a gluten-free diet may be due to the reduction of other carbohydrates. All of this highlights the need to be tested for celiac disease before starting a gluten-free diet.
Celiac disease does occur more commonly in IBD patients than in the general population. It is important to note that people can have two diseases and/or other food intolerances.
Summary
• IBD is a complex group of conditions that inflame and ulcerate the bowel. It requires an accurate medical diagnosis and dietary treatment.
• If you do go on an elimination diet, seek the help of a registered dietitian. There is evidence that a significant number of IBD patients are reducing gluten. Whether this alleviates symptoms is unclear, as is the effectiveness of the currently popular "anti-inflammatory" diets. There is no evidence that either diet actually reduces the inflammatory response causing the disease in the gut.
• It is especially important to remember that the symptoms of IBD overlap with those of other conditions and food intolerances.
• This is an area where isolating the issue, testing, and only then treating is particularly relevant.
Eosinophilic Esophagitis
_A good listener is a good talker with a sore throat._
—KATHERINE WHITEHORN
_Eosinophilic esophagitis (EoE)_ is an emerging food-related disorder. It is a specific type of inflammation of the esophagus that may cause food to become stuck in this muscular tube that connects the mouth to the stomach. It is seen in children as well as adults. Unlike other GI conditions such as celiac disease or IBS, it affects men more than women.
People often minimize symptoms, feeling that they will go away, are caused by eating too quickly, or are something the individual can live with. Children with the condition are often told that they are not chewing their food well or are eating too quickly. A lack of awareness of the condition in the medical community means that symptoms are often overlooked or misdiagnosed.
What Is EoE?
EoE is an inflammation of the esophagus characterized by dysfunction in the esophagus and the presence of eosinophils (white blood cells associated with allergies) in the mucosal tissue lining the esophagus. Patients typically complain of food "sticking" in the throat, although this symptom is not always present.
Other symptoms include:
• difficulty or pain with swallowing
• food becoming lodged within the esophagus
• refusal to eat or failure to thrive in children
• vomiting with meals
• heartburn
EoE may also coexist with other GI conditions, including celiac disease. Celiac disease and EoE are both associated with an aberrant immune response to food antigens and the different studies have demonstrated an association between the two. This is interesting, as the nature of the immune response is different in the two conditions. But both require endoscopy for diagnosis.
What Causes EoE?
There are two types of EoE. The main cause is an allergic immune response to specific foods. Because some people respond to intensive treatment for gastrointestinal reflux disease (GERD), we are aware that reflux may cause EoE. Esophagitis—an inflammation of the esophagus—is also caused by a number of other mechanisms including infections (viral and fungal) and radiation therapy. This is different from a diagnosis of EoE.
Food Allergy
The leading theory about the cause of eosinophilic esophagitis is that it represents a food allergy. The hallmark is the presence of a large number of eosinophils, a white blood cell associated with other allergic conditions, in the wall of the esophagus. Studies using elimination diets have shown a reversal of the esophagitis and disappearance of the eosinophils confirming this mechanism.
GERD
Some patients suffering from EoE have GERD, which is much more common, and will see symptoms resolved with medications, typically proton pump inhibitors (PPIs). (See chapter 8, "The Gut in Disease.") After a diagnosis of EoE, a trial of high-dose PPIs is often undertaken to assess if that will resolve symptoms and normalize biopsy results.
Interestingly, the pathological features of EoE due to GERD are similar to that of EoE caused by a food allergy. Pathologists examining biopsies of patients with GERD sometimes find "nests" of eosinophils.
Diagnosis of EoE
The diagnosis of eosinophilic esophagitis is done during an endoscopy. Biopsies then confirm the presence of a great number of eosinophils.
The tests for food allergies in EoE are not considered reliable. These include blood tests for IgE antibodies to specific foods and skin or patch tests. The most reliable tests are elimination diets in which people are advised to go on an exclusion diet eliminating the eight major food groups known to cause allergic reactions (dairy, soy, peanuts, tree nuts, eggs, wheat, fish, and shellfish). Different categories are then added back one by one until the offending food is found.
Often multiple endoscopies are performed to assess the effect of withdrawal, and foods are reintroduced based on the findings.
Treatment
The treatment for EoE depends on the age of the patient and the severity of symptoms. Swallowed steroids are the mainstay of treatment for symptom relief. Inhalers of the type used in the treatment of asthma are prescribed, with patients instructed to swallow, not inhale, the drug.
Patients with a markedly narrow esophagus may require stretching or dilation. This is done with some apprehension, however, as in some cases this can rupture the esophagus.
Summary
EoE is a disease that has become more prevalent in the past decade. It is primarily a food-related sensitivity.
Like celiac disease, other allergies, and autoimmune conditions, it is on the rise. This raises the intriguing question—what are the environmental triggers responsible for this remarkable change in medicine in the past few decades?
Neuropathy
_Science is wonderfully equipped to answer the question "How?" but it gets terribly confused when you ask the question "Why?"_
—ERWIN CHARGAFF
I found out about peripheral neuropathy because I'm old-fashioned. You see, I still write checks. I couldn't hold the pen to sign my name. And when I did, it didn't look like my signature. My kids told me it was time to switch to online banking, but I figured it was time to see a doctor.
(LILA, 59)
The nervous system and brain are perhaps the most complex and elusive parts of the human body. Nerve fibers run to, from, and through every inch of our frame—we are, quite literally, a bundle of nerves. Compounding this is the "second brain" in our gut that has a mind and plenty of "nerve" of its own. (See chapter 10.)
The nervous system is the regulator and monitor of every organ and system in the body and is intimately involved in our perception of the world. It is at once the wise and benign sovereign of all movement, coordination, and sensation, and the devil-like source of all pain.
Recently there have been claims that gluten is destroying our brains—a dangerously simplistic approach to an intricate system that is difficult to visualize and whose mechanisms are still largely unknown. While science has a good grasp of how the nervous system functions, the mechanisms behind and treatment of its malfunctions currently offer more questions than answers.
Gluten may actually play a role in nervous system malfunctions such as the neuropathies and ataxias suffered by some, but removing it from your diet is not a cure and may not even be an effective treatment.
What Is a Neuropathy?
The word _neuropathy_ ( _neuro,_ "nervous system"; _pathy,_ "disease of") encompasses all the nerves in the body. This includes:
• autonomic nerves (that control involuntary or unconscious nerves)
• motor nerves (that control movement of limbs, etc.)
• sensory nerves (that transmit various information about hot, cold, pain, position)
A person's symptoms depend on the type of neuropathy and the type of nerves affected. Our focus will be on the peripheral neuropathies and ataxia that appear to be related to gluten.
Peripheral Neuropathy
Try holding chopsticks when your fingers are numb.
(RITA, 36)
Peripheral neuropathies are a general term to explain an alteration of normal sensation occurring usually in the hands, feet, and face. They create _paresthesia_ (a burning or tingling), as well as numbness, cramps, restless legs, and especially pain in the hands and feet, and sometimes other parts of the body.
Most people have experienced paresthesia—a feeling of pins and needles—at some time in their lives. When you sit with crossed legs for too long, a leg may fall asleep. This occurs because sustained pressure is placed on a nerve; the leg "wakes up" once the pressure is relieved. The paresthesia may be mild or severe enough to interfere with normal function and activities.
Chronic _neuropathies_ are often a symptom of an underlying neurological disease or traumatic nerve damage. While diabetes is the most common cause of neuropathy, other medical conditions can also lead to the problem; these include vitamin or mineral deficiencies, Lyme disease, inflammation, trauma, excessive alcohol intake, Guillain-Barré syndrome, infections, pressure on nerves (computer use or sports related), celiac disease, and various pharmaceuticals.
Diabetic Neuropathy
Most cases of neuropathy are found in people who have type 1 diabetes, though it also occurs in type 2 diabetics. Diabetic neuropathy is a micro-vascular (involving small blood vessels) complication of the disease. Elevated levels of blood sugar in people with diabetes can, over time, injure the walls of the tiny blood vessels that supply nerves. Since one consequence of the nerve damage can be an inability to feel pain, problems can go unnoticed until digits are badly injured, especially in the legs. In the U.S., 50 to 70 percent of people with diabetes have some form of diabetic neuropathy. A diabetic patient's neuropathy often affects the gut (autonomic neuropathy), causing _gastroparesis._
Autoimmune Disease and Neuropathy
Neuropathies are common in various other autoimmune diseases. The neuropathies found in celiac disease appear to be related to vitamin deficiencies, inflammation, and/or autoimmune factors. Symptoms consistent with neuropathy are common when people are diagnosed, and often disappear on a gluten-free diet. We routinely test patients with celiac disease and neuropathy for vitamin deficiencies.
People with nonceliac gluten sensitivity (NCGS) may also feel that these symptoms resolve when gluten is removed. Yet some patients on a gluten-free diet develop peripheral neuropathies at a later date. This may be due to the development of a new autoimmune disease or as a result of the gluten-free diet itself—a heavy-metal toxicity (lead, mercury, arsenic) or a B vitamin deficiency. (See chapter 4, "Perils of a Gluten-Free Diet.")
Ataxia
When I went to an ataxia patient meeting, I wasn't prepared for what I saw. I encountered many people who struggled with or were unable to perform daily tasks that we take for granted, like walking, cutting their steak, or having a glass of water.
(ARMIN ALAEDINI, PH.D., BIOCHEMIST AND IMMUNOLOGIST)
Ataxia creates problems with balance, movement, and coordination. It describes a lack of muscle control during voluntary movements, such as walking or picking up objects. Ataxia can affect movement, speech, eye movement, and swallowing. It is also associated with degenerative diseases of the central nervous system. Persistent ataxia usually results from damage to your cerebellum—the part of your brain that controls muscle coordination. It is also seen in people with neuropathies because of an altered perception of the position of their limbs.
Many conditions can cause ataxia, including alcohol abuse, stroke, tumor, cerebral palsy, and multiple sclerosis. Inherited defective genes also can cause ataxia. About 40 percent of ataxias are genetic, but 60 percent are idiopathic (of unknown origin). In various studies, 9 to 15 percent of patients with idiopathic ataxia have celiac disease. In fact, some researchers believe that as many as 40 percent of the cases of idiopathic ataxia are gluten related.
Gluten Ataxia
Gluten ataxia (GA) is defined as an ataxia where other underlying causes cannot be ascertained and antigliadin antibodies are present. It is associated with cerebellar atrophy, where cells in the area of the brain controlling coordination and balance deteriorate and die. Some research indicates that GA may be immune mediated and part of the spectrum of gluten sensitivity, but this is open to question.
In a UK study, 40 percent of sporadic ataxia patients were positive for IgG antibodies to gluten. But the meaning of the presence of antigliadin antibodies in these patients is not fully understood. These are nonceliac antibodies also found in a percentage of people with a number of conditions, including ADHD and autism. The presence of these antibodies must be shown to have a direct effect on function to be considered significant.
At this point, the direct pathological effect on neural function of antigliadin antibodies is still being debated. If it is possible to eliminate these antibodies through a strict gluten-free diet, it may have important therapeutic implications, though this has not been demonstrated. (See chapter 6, "Testing—What Do Antibodies Tell Us?")
Researchers in Finland and England have studied the brains of people with gluten ataxia and found deposits of gluten antibodies around blood vessels in their brains. These investigators also found antibodies in the brain to transglutaminase 6 (TG6), a form of TG2, the enzyme that reacts with gliadin and sets off the reaction that triggers celiac disease. They feel these individuals develop antibodies to TG6 in an immune response to gluten. These results need to be duplicated by other researchers before the development of a test for GA will be commercially available.
Nevertheless, it is an intriguing finding that may uncover one of the few treatable causes of idiopathic sporadic ataxia.
There is also interest in the potential for an individual's immune response to gluten to cross-react with certain proteins found in the brain such as _synapsin I_. Synapsin I is a complex protein that does many things in the body, especially in the nervous system. In simple terms, it can act as a "shuttle" that helps in the transmission of nerve signals. As Armin Alaedini, a biochemist and immunologist at Columbia University, explains, "We have shown that antibodies to gliadin can cross-react and bind to the synapsin I protein. This does not necessarily mean that such cross-reactivity will cause neurologic disease but if the antibodies can access and bind to the protein, they may interfere with its functions or create a harmful inflammatory response against nerve tissue."
These findings open a window into the potential effect of the immune response to gluten on the nervous system. This may lead to an understanding of the mechanisms beneath the neurological symptoms found in gluten sensitivity; and the role that antibodies to gliadin may play in modifying cellular signaling within the nervous system.
How Is Neuropathy Diagnosed?
Peripheral neuropathies are diagnosed by a physical examination and patient history, as well as _nerve conduction studies_ (EMG) and laboratory tests. The small-fiber neuropathies associated with celiac disease are not the larger nerves tested in EMG. Therefore these EMG studies will be normal in people with celiac disease who have a peripheral neuropathy. Instead, we perform a skin biopsy that is stained to highlight the small nerve fibers. The diagnosis is made when the small nerve fibers are seen to be absent or reduced.
Ataxias are diagnosed based on a person's medical history, family history, and a complete neurological evaluation, including an MRI scan of the brain to determine if there is damage. Various blood tests may be performed to rule out other possible disorders that may present similar symptoms. Genetic testing is also available to determine if the ataxia is inherited.
Vitamin deficiencies (E, B12, B1, B2, and B6) and copper deficiency need to be excluded, as well as vitamin B6 toxicity.
How Is Neuropathy Treated?
The appropriate treatment for neuropathy depends on accurate diagnosis of the underlying cause. And since this is often unclear, most treatments focus on symptom relief.
For peripheral neuropathies, therapies such as electrical nerve stimulation, physical therapy, surgery to release compressed nerves, and various medications can resolve symptoms for many. Drugs such as IV gamma globulin and NSAIDs can be helpful. Frequently, SSRIs are prescribed.
There is conflicting data on the effect of a gluten-free diet. Putting the majority of the blame on gluten is a mistake, and even in people with celiac disease, a gluten-free diet does not always resolve symptoms. Some people see a complete reversal of symptoms, others find the symptoms are less severe, and some develop peripheral neuropathies while on a gluten-free diet. Others improve through nutritional supplementation because they are mal-absorbing the B vitamins, minerals, or other trace elements.
Summary
• Neuropathy is the result of a number of underlying medical conditions. It often exists without a clear cause—what doctors classify as idiopathic, of unknown origin.
• Peripheral neuropathies are fairly common. Everyone, at some point in his or her life, will probably have some type of neurological symptom. They are associated with a number of diseases and lifestyles. Recently, the science of ergonomics developed, to prevent musculoskeletal disorders in the workplace—which often includes paresthesia of the hands, wrists, back, and arms from computer use.
• Ataxia is a rare disease but disrupts function for those with the condition. It can be mild—occasional loss of balance—or paralyzing. In the absence of celiac disease, the presence of antigliadin antibodies indicates a gluten connection in some people.
• The cross-reaction of gluten with proteins in the brain is being studied in various neurological conditions. At this point, the mechanisms behind various neurological complications in gluten-related disorders are not clear.
• While gluten may be a cause of both neuropathy and ataxia, numerous other conditions need to be excluded before adopting a gluten-free diet.
Nevertheless, studies linking gluten to various neuropathies provide a tantalizing link between the gut and the brain.
Diabetes
You always have diabetes. Every moment you have diabetes. It's either something you're consciously thinking of, or it's there and you're going to have to think about it. _Is my blood sugar high, is it low? When do I have to eat? Or should I eat?_
Being on an insulin pump has made an enormous difference in that, but the potential for something getting out of control is there.
(ART, 67)
In the U.S. today, there are approximately 21 million people who have been diagnosed with diabetes. About 1.25 million of them have type 1 or insulin-dependent diabetes mellitus (IDDM). In the UK, approximately 3.2 million people have diabetes and the number is estimated by Diabetes UK to rise to 5 million by 2025. Studies show that about 10 percent of this group will also develop celiac disease. However, the role that gluten may play in the development of IDDM is a new and intriguing finding in the search for the mechanisms leading to this disease and the search for a cure.
There is a recognized association between celiac disease and type 1 or IDDM. The same association does not exist with type 2. Many clinics screen diabetic children for celiac disease, although the symptoms are often silent or go unrecognized. In fact, many doctors and clinics view the "double diagnosis" as a huge burden and will not test unless pushed by parents or the development of symptoms. This may not be a wise choice.
What Is Diabetes?
In the middle of final exams during my senior year in college, I started to have strange physical symptoms. I was experiencing extreme thirst and very frequent urination, always getting up in the middle of the night to go to the bathroom. Initially, my friends and I joked about it—"What the hell is this?" In response to the thirst, I would—in retrospect, absurdly—drink a bunch of sugared soda to quench my thirst, and then go to the bathroom even more. And it finally reached a point where I said, "I better go and do something about this." I went to the university medical clinic and was diagnosed with what is now called type 1 diabetes. That was forty-seven years ago.
(ART, 67)
Diabetes mellitus (from the Greek for "go through" and "sweet") describes a lack or deficiency of insulin, a hormone that enables the body to metabolize and use glucose (sugar). Glucose is a fuel that is critical for muscle, brain, and body function. Unable to enter the cells, it accumulates in the blood until it gets to the kidneys, where fluid is drawn from the body in order to excrete the excess sugar, which then spills into the urine. This causes the thirst and frequent glucose-filled urination Art describes, and a recognized symptom of the disease.
If the diabetes is not corrected, the body becomes starved for energy and begins drawing on fat and protein stores, leading to weight loss and muscle wasting. This emergency process releases fatty acids (in the form of ketones) into the bloodstream, which can lead to coma or death.
**There are two types of diabetes.**
**Type 1** , or insulin-dependent diabetes mellitus (IDDM), formerly referred to as juvenile-onset diabetes, is an autoimmune disorder that occurs mainly in younger people, but can occur in adults. The immune system attacks and destroys the pancreatic islets where the insulin-producing cells reside, setting off the sequence of events described above. When insulin is no longer produced by the body, it must be permanently replaced by injections/pump.
**Type 2** , or non-insulin-dependent diabetes mellitus (NIDDM), so-called adult onset diabetes, appears to start as an insulin resistance, a condition in which the insulin produced is less effective in controlling blood glucose. Type 2 diabetes is not an autoimmune condition, and insulin production is unstable, not absent. The condition appears to have a genetic or family association and occurs more commonly in people with obesity and older age. However, it is increasingly being seen in overweight children whose cells cannot handle the amount of carbohydrates they are consuming.
Type 2 diabetics can often control their condition through diet alone or with oral (non-insulin) medications. Some will also require insulin shots to control blood glucose levels.
A third type, _gestational diabetes_ , occurs during pregnancy and is usually temporary. The mother's body does not respond to insulin, and the condition can normally be controlled with diet alone. The condition usually resolves itself once the baby is born.
What Causes Diabetes?
The destruction of the islet cells of the pancreas, which produce insulin, in IDDM appears to be caused by several factors. While the precise trigger is not clear, it is believed to include an autoimmune reaction, infections that attack the islet cells, and other environmental factors that initiate the autoimmune process. The possible role of the microbiome is also of emerging interest.
Is Gluten a Trigger in IDDM?
Celiac disease is 5 to 7 percent more common in people with IDDM than in the general population. It is not more common in people with NIDDM.
There is evidence that patients diagnosed with celiac disease later in life have a higher rate of IDDM than patients diagnosed at a younger age. This indicates that a longer exposure to gluten increases the risk of developing IDDM in susceptible individuals.
Furthermore, two large human studies established an association between an early infant diet containing gluten and the development of autoantibodies (antibodies against "self") against the islet cells.
Several animal studies have documented that the development of IDDM is influenced by diet. While a gluten-free diet largely prevented the onset of diabetes in one study of mice specially bred with a susceptibility to develop IDDM, the mechanisms underlying the influence of gluten on the incidence of IDDM in humans are not fully understood.
Some studies have shown that gluten creates an inflammatory response affecting the microbiota. It raises the feasibility of early dietary interventions for IDDM and the need to determine if and how dietary intervention can affect immune regulation and disease development.
Diabetes and the Microbiome
The microbiome plays an important role in shaping immune responses in the gut as well as in the development of autoimmunity. A growing number of human studies demonstrate differences in the microbiome of people with IDDM versus controls. This supports the idea that alterations in the microbiome precede the onset of IDDM. Since the microbiome is sculpted and remodeled extensively in the first few years of life, there may be a window of opportunity to modify risk factors in children who have markers of anti-islet autoimmunity.
Studies are looking to find the mechanism(s), timeline, and possible therapeutic options to prevent the disease by altering the microbiome.
The Dual Diagnosis
As mentioned earlier, approximately 10 percent of all diabetics have a double diagnosis of celiac disease and IDDM. The link to gluten exposure as a potential triggering factor of the autoimmune reaction gives further validity to the need to test children with IDDM for celiac disease.
This raises the question of whether all children with IDDM should be routinely screened. A recent study showed tremendous variability on this question, as well as in the guidelines of different authoritative groups regarding which tests to use and the timing and frequency of those tests.
The Pros for Screening
There are several well-defined links between celiac disease and diabetes. Both are associated with similar _HLA (human leukocyte antigen) genes_. They are both autoimmune diseases where autoantibodies are present in children. Having one autoimmune disease increases the risk of getting another.
Those who advocate routine screening emphasize that patients with IDDM may have no symptoms or silent symptoms that are only recognized retrospectively. In addition, there are complications of untreated celiac disease, and it is better to pick up the potential subtle changes that might affect learning and achievement.
Symptoms to look for include:
• GI complaints, common in both diseases, should not be overlooked; mild symptoms such as bloating are often recognized retrospectively
• growth issues (failure to thrive)
• delayed puberty
• anemia
• fatigue
• iron deficiency
• dental enamel defects
• hypoglycemia and a reduction in insulin requirements, or "ping-ponging" when food is not being absorbed
• vitamin/mineral deficiencies
• elevated liver enzymes
Interestingly, in a recent study in the _Diabetes Educator,_ 49 percent of the respondents to a screening test reported that their patients improved with a gluten-free diet despite not being aware of symptoms prior to the diagnosis of celiac disease. It is unclear what percentage of physicians test for celiac disease in diabetic patients.
The Cons
Some argue against routine screening, claiming that it can affect quality of life, and that the outcome of subclinical celiac disease in diabetes is not fully investigated. Evidence is inconclusive as to whether the benefits of screening and potentially treating asymptomatic individuals outweigh the harms of managing a population already burdened with a serious illness.
Nevertheless, we recommend testing people with IDDM for celiac disease because of the high prevalence and the potential benefits of treatment with a gluten-free diet. This includes control of symptoms, stabilization of diabetes, and prevention of complications associated with celiac disease.
Recent population-based studies following patients with both IDDM and celiac disease for nearly 40 years showed a significantly higher mortality for these people than those who just had celiac disease. This implies that undiagnosed celiac disease is not a benign condition and needs to be diagnosed and treated. The explanation for the increased risk of death included:
• persistent low-grade inflammation due to disease activity
• poor adherence to the gluten-free diet
• difficulty following a gluten-free diet and insulin therapy
This study also highlights the need for excellence in both the care of the diabetes and of the celiac disease.
Treating the Double Diagnosis—Glucose and Gluten
A lot of these children are on the pump for a few years, are well managed and coping, and then [are] told "you have to be gluten-free." They did not necessarily feel bad to begin with, are already "different," and don't want to be gluten-free. Some manage it really well, and others don't. My goal is to encourage them to consider being gluten-free and to do so in a healthy way.
(SUZANNE SIMPSON, R.D.)
Our daughter was diagnosed with type 1 diabetes when she turned 4 and celiac disease two weeks afterward. From our perspective the celiac is more difficult to deal with. There's not much that she can't eat in relation to type 1 as long as we prepare and plan ahead, and cover her with the right amount of insulin. In terms of celiac disease, she needs to be totally gluten-free, and we're finding that a huge challenge.
(RAY, 38)
Most people with IDDM receive the diabetes diagnosis first and they develop the skills, knowledge, and how-to to manage the diabetes and blood sugar and insulin. And then they get diagnosed with celiac disease and many say it is harder having celiac disease than diabetes. On one hand, this may be due to having mastered the care of their diabetes—you can adjust your insulin to compensate for the candy bar you want—but with celiac disease you cannot just "take something" if you want to eat gluten or think you have inadvertently eaten it. It also means rethinking glucose in terms of its high presence in gluten-free foods.
Treating people with type 1 diabetes and celiac disease involves mind as well as matter. Balancing diet, lifestyle, and compliance is like walking an emotional and physical tightrope and can be difficult. Many do not have gastrointestinal symptoms, so the motivation to be gluten-free is not high.
The hardest part is not getting a break—it is sort of a double whammy of having to think about your food from two different perspectives. You have two conditions and you have to think about them all the time.
(SUZANNE SIMPSON, R.D.)
_Carbohydrates from Two Perspectives_
Dietary management in diabetes is based on controlling blood sugar levels. It is a combination of food, exercise/lifestyle, and insulin. When you look at food as a diabetic, you are looking primarily at the carbohydrates, since insulin regulation is based on the amount of carbohydrates in the food and your blood sugar levels at that particular moment.
When you have celiac disease, you are also focused on food—specifically gluten. And gluten-free foods are usually much higher in starch/carbohydrates, lower in fiber than their wheat-based counterparts, and have a different impact on blood sugar. The glycemic response to many gluten-free foods varies from patient to patient, but tends to be higher and faster. It is also important to be aware of the inadequacies of a gluten-free diet. (See chapter 4, "Pitfalls and Perils of a Gluten-Free Diet.")
The balance of food, insulin, and level of activity takes on an added dimension that must be learned and integrated into a lifestyle. This can be particularly hard on adolescents who live—and tend to enjoy—more spontaneous and unpredictable lives. Planning often means "let's go!"
The biggest thing for me is that I'm concerned that she's losing a bit of her childhood in a way, being forced to think about things a 4-year-old wouldn't have to face. I wonder how that's going to affect her. It seems that there's sort of a loss of innocence I feel bad about.
(RAY, 38)
Children and adolescents with a double diagnosis must buy into their own care. This may require the assistance not only of parents, but dietitians they trust and support groups that offer peer assistance. A sharing support system of family and friends is essential.
Despite the psychological burdens of a dual glucose- and gluten-restricted diet, the price paid for noncompliance is very high. Patients must learn to embrace a "live with" rather than "life without" lifestyle.
Summary
• The role(s) of gluten in the development of IDDM via its effect on autoimmune and inflammatory processes and the microbiome are being actively studied. They may offer an exciting pathway to block the development of IDDM.
• Is there a "switch" at play? If so, is there a time frame for turning it off or ensuring that it is not turned on?
• A gluten-free diet will not cure someone already diagnosed with type 1 diabetes or reverse any of its complications. Studies indicate that antigliadin antibodies do disappear on a gluten-free diet, and this may have a positive effect on those with a dual diagnosis, especially children.
Wheat and Other Food Allergies
In Candy Land there are a few things that can happen to you when you get to jump across the board. One is getting a lollipop and one is getting a peppermint candy and one is getting a peanut. And [my granddaughter] drew the peanut, and she said, "Eek! I can't have peanuts, get it away from me." I told her that her playing piece could jump on that square but that she wouldn't really eat it. We don't put the whole Candy Land away just because it has a peanut.
(MARY, 67)
Food allergies are a potentially lethal cousin of a food intolerance or sensitivity. While many people avoid wheat because it makes them bloated, gassy, or fatigued, others must avoid wheat because it makes their throats swell and breathing increasingly difficult and sometimes impossible.
Food allergies are one of the most common medical disorders and affect up to 15 million Americans and more than 17 million in Europe. A study by the CDC showed that food allergies increased by about 50 percent between 1997 and 2011. The upsurge in allergies is part of the medical puzzle surrounding our unexpected and increasing reactions to various foods.
What Are Food Allergies?
Food allergies are caused when your immune system sees an otherwise harmless food or substance as an invader (allergen). It releases antibodies, specifically IgE antibodies, to neutralize the perceived threat. These are different from the IgA and IgG antibodies seen in food intolerances and sensitivities. (See chapter 6, "Antibodies.") The first encounter is usually benign and simply sensitizes that person to the food. But when the IgE antibodies "see" that antigen again, they trigger the release of chemicals such as _histamines_ , causing the symptoms that characterize an allergic reaction. This may include swelling, itching, hives, asthma, vomiting, diarrhea, respiratory distress, and shock. The reactions range from mild—itchy skin or mouth—to severe _anaphylaxis_ , which can be life threatening.
IgE allergic reactions are immediate, usually occurring within seconds or up to several hours, and involve the whole body. They are different from the delayed sensitivity described in previous chapters. Allergens can be to different foods, drugs, insect bites and stings, as well as pollens, mold spores, animal dander, and dust mites.
They directly affect a person's quality of life and require extreme vigilance when eating out or traveling. Most children will outgrow allergies to eggs, dairy, wheat, and soy, possibly because of the immune system's response to the food. Allergies to peanuts, seafood, and tree nuts are rarely lost.
Specific Food-Induced Allergies
There was one kiwi slice on top of the fruit salad, so I thought I'd just dig underneath. That was hospital trip number one.
(GEORGE, 19)
There are eight categories of major food allergens (the so-called Big 8)—milk, eggs, fish, shellfish, tree nuts, peanuts, wheat, and soybeans. The USA Food Allergen Labeling Act requires that they must be listed on all processed food labels. These foods account for about 90 percent of all food allergies, but people can also be allergic to various seeds, legumes (including peanuts and soybeans), fruits, corn, vegetables, and various herbs and spices.
Allergies also occur in conjunction with other conditions, such as asthma, and in certain professions, i.e., baker's asthma.
Allergic Asthma
Allergies and asthma can occur together. Asthma is a lung disease that causes the airways to become inflamed and narrowed. It occurs often in childhood and its causes are unclear, but appear to have both genetic and environmental origins. For many people, it is connected to an allergic reaction to a specific food or substance. Over 50 percent of people suffering from asthma have allergic asthma. While many of these reactions are directed against dust, pollen, and airborne substances, several are food related.
Children who have food allergies as well as asthma are at an increased risk for a more severe reaction to both. The relationship between the two does not appear to be causal. It is crucial that patients are educated about avoiding the offending food(s) and the emergency use of asthma and allergy medications in the event of a reaction.
Baker's Asthma
Baker's asthma is the most common cause of occupational asthma, and annual incidences of the disease range between 1 and 10 cases per 1,000 bakery workers. The main agents that cause baker's asthma are cereal flours (wheat, rye, and barley) and enzymes. Baker's asthma is IgE mediated and can affect anyone working in a bakery, confectionery, flour miller, and/or food processing facility.
Wheat-Dependent Exercise-Induced Anaphylaxis
Wheat-dependent exercise-induced anaphylaxis (WDEIA) is a rare disorder where exercise that occurs after ingesting an allergen triggers anaphylaxis. This can occur even though the exercise and allergen exposure are tolerated independently of each other. It is one clinical form of IgE-mediated allergy to wheat. Wheat is not the only food associated with food-exercise-induced anaphylaxis—it was first described with celery!
Eosinophilic Esophagitis
Eosinophilic esophagitis is an allergic reaction to food that causes swelling of the tissue in the esophagus. (For a fuller description, see chapter 21, "Eosinophilic Esophagitis.")
What Causes Food Allergies?
When my granddaughter was a few weeks old, they noticed blood in her diaper. So the pediatrician said, "Let's test her." She was being breast-fed, and they told [my daughter] to stop eating dairy. So my daughter went on a dairy-free diet. But the baby continued to have lots and lots of stomach cramps.
When she was 6 months old, they went to an allergy clinic and were told that under one she was too young for the blood tests for allergies to be meaningful at all, but that they'd do a blood test anyway. And the allergies to a number of things showed up in the super-high zone.
She was allergic to salmon, nuts, eggs, and dairy. She's now three and a half and goes every six months to the clinic. And it got more complicated. Now it's sesame seeds, tree nuts, and peanuts as well as dairy and eggs and most fish.
Fortunately she's never choked and turned blue. But her reaction to surface contact is high. When she was at a wedding with her parents and someone spilled a cup of coffee with milk in it on her leg, she got hives all over her body because of the teaspoon of milk in the coffee. She got hives from playgroup where some of the babies were drinking milk out of a bottle. Maybe it got on their hands [and then they] touched hers, or [it was on] a common surface.
She has to be watched all the time.
(MARY, 67)
Food allergies are caused by an inappropriate response of the immune system to an otherwise harmless substance. The trigger of this response appears to involve a combination of genetic and environmental factors. It is also unclear why food allergies are being diagnosed at such an increased rate. The increased use of antibiotics and their effect on the makeup of the microbiome has been implicated. Others blame processed foods and/or the emphasis on "clean" living—the hygiene hypothesis. This last theory is based on the premise that exposure is not a bad thing and allows the immune system to develop a more complete tolerance to foreign proteins. (See chapter 3, "The Hygiene Hypothesis.")
Some people believe that a mother's eating habits during pregnancy also play a role but this has not been scientifically proven. A mother's antibodies are protective and can cross the placenta during pregnancy and even during breast-feeding. But their direct effect as a protective mechanism in the gut is being questioned. For example, it was believed that starting gluten exposure in an infant during breast-feeding was protective against celiac disease, but this was disproved in a recent large study.
How Food Allergies Are Diagnosed
Currently, diagnosis relies on the presence of IgE antibodies in the blood. Yet the detection of specific IgE antibodies in blood tests and skin-prick tests are neither completely accurate nor reliable indicators of allergy. Therefore a careful medical history, and for some a food challenge, in addition to lab tests is recommended for diagnosis. Most panels for food allergies test for the "Big 8" major allergens. Elimination diets that take all potential allergens out of the diet for six weeks and then reintroduce them, one by one, are also utilized.
Treating Food Allergies
The management of food allergies requires the avoidance of the food(s) causing the reaction, and an appropriate and rapid response to the allergic reaction. Many patients carry an EpiPen (injected epinephrine to treat anaphylaxis) and/or Benadryl tablets in case of an unexpected exposure.
Studies and trials are under way to increase tolerance to various food allergens utilizing oral immunotherapy. Vaccines, Chinese herbal medicines, and anti-IgE antibodies are also being studied. The effectiveness of these therapies varies among different food antigens, and their long-term safety is also unclear. Other treatments involving sublingual (under the tongue) and epicutaneous (delivered through the skin) immunotherapy are being studied. At this point, their benefits and safety have not been fully demonstrated.
Many childhood food allergies resolve with age, and some people develop food allergies as adults.
Summary
• Food allergies are common and can be fatal. They cause an immediate immune reaction to the offending allergen. They are IgE mediated and different from the IgA- and IgG-mediated reactions associated with celiac disease and gluten sensitivity.
• The "hygiene hypothesis," which is based on the premise that early exposure to germs, infections, and foods is not necessarily a bad thing, has developed as one intriguing reason behind the increase in allergies. It is thought that exposure enables the immune system to develop tolerance and helps prevent allergies and some autoimmune diseases.
• Another intriguing hypothesis connects the increased use of antibiotics, especially in children, to disruptions or imbalances in the microbiome ( _dysbiosis_ ) that in turn may account for some of the increase in childhood allergies.
• Allergies are another piece of the emerging food-gut-microbiome picture.
Fibromyalgia and Chronic Fatigue Syndrome
_The greatest evil is physical pain._
—ST. AUGUSTINE
My auto accident at sixteen was the initial onset of my extreme fatigue and fogginess. But throughout college, the fatigue got worse and I started getting different joint and soft tissue pain. But because I was an active person, I would just brush it off.
When I was in my twenties, [my husband and I] lived in Germany, and when I was in elevations—like in the mountains—I would have trouble walking. And having babies was very difficult—my pregnancies were all very hard. I had a lot of pain in my shoulders and lower back.
In my thirties, I started thinking, _There has to be more to this,_ and I started looking for answers. I started swimming and having massages, and started to try sensible eating, but nobody really knew why I was still so tired and had all these pains. The fatigue never dissipated.
(ANN, 71)
Fibromyalgia and chronic fatigue syndrome (also referred to as myalgic encephalomyelitis) are two diseases that have resisted neat medical categories—neurologic, rheumatic, and psychological—but cause fatigue and pain that can disrupt a life. Many people suffering with them believe that various exclusion diets are helpful, but others find them of little or no help. This has not kept alternative medicine practitioners from prescribing supplements and various diets—including a gluten-free diet—to treat the pain and fatigue people report.
Fibromyalgia
Fibromyalgia has been described as a problem with "volume control." The word _fibromyalgia_ comes from the Latin _fibro_ ("fibrous tissue") and the Greek _myo_ (muscle) and _algia_ (pain). It is characterized by chronic pain throughout the body, joint stiffness, and/or extremely tender musculoskeletal "trigger" points. The symptoms also include fatigue, problems sleeping, cognitive dysfunction, and mood and memory issues.
What Causes Fibromyalgia?
The causes of fibromyalgia are unknown, but there are probably a number of factors involved. The perceived pain appears to be related to biological, psychological, and sociological factors, as well as alterations or inflammation in the nervous system and its transmitters. Like Ann, many people associate the onset of fibromyalgia with a physically or emotionally stressful or traumatic event, repetitive injuries, or an illness. For others, fibromyalgia seems to occur spontaneously.
Many researchers are examining other causes, including problems with how the central nervous system processes pain. This syncs with the belief that fibromyalgia may be a condition of "central nervous system hypersensitivity" resulting in an amplified response to pain and stimuli. The problem has been in identifying the trigger of this sensitivity.
Researchers studying idiopathic (of unknown origin) pain disorders such as IBS and fibromyalgia believe that psychological distress and strong emotions play an important role in promoting the symptoms.
Some scientists speculate that there may be a genetic link in the way people process painful stimuli. Several genes that occur more commonly in fibromyalgia patients have already been identified.
How Is Fibromyalgia Diagnosed?
Since pain and fatigue are symptoms that occur in many other conditions, all of these must be ruled out before a diagnosis of fibromyalgia can be reached. Patients typically visit a number of doctors before getting a diagnosis, since standard laboratory tests often fail to reveal a physiological reason for the pain. Because there is no generally accepted, objective test for fibromyalgia, some doctors unfortunately may conclude that a patient's pain is not real, or they may tell the patient that little can be done.
A diagnosis can be made based on criteria established by the American College of Rheumatology that includes:
• tenderness in more than 19 pain locations
• six self-reported symptoms including difficulty sleeping, fatigue, poor cognition, headache, depression, and abdominal pain
• a history of widespread pain lasting more than three months
It is important that other conditions whose symptoms mimic fibromyalgia be ruled out. These include celiac disease, Lyme disease, arthritis, chronic fatigue syndrome, hypothyroidism, irritable bowel syndrome, lupus, and polymyalgia rheumatica. Some scientists have proposed that a percentage of patients with fibromyalgia suffer from underlying gluten sensitivity. Many symptoms of the two conditions are similar.
Conversely, some patients are given a diagnosis of fibromyalgia without proper lab testing, and are later found to have a treatable condition such as celiac disease.
How Is Fibromyalgia Treated?
I went to doctors who offered drugs and operations. I became addicted to painkillers and Valium because that's all they had to offer me. Fortunately, I had my own business—I had a job and a family—so I had a reason to keep going . . . I kept pursuing different avenues.
But I never got the connections to what I was eating until much, much later. In addition to the pain and fatigue, I've had irritable bowel syndrome for the past 15 years. Certain foods would make everything spasm. I constantly read and researched and tried things because my doctors didn't have answers.
In my 50s I started seeing some of the patterns but didn't know what to do with all the information. I was working hard on my diet but was given a lot of different ones. I knew that yeast was a problem in my body, and then I removed sugar and it seemed to be better. The white flour came later. I'm off dairy, gluten, sugar.
I found that diet and rest and exercise were the three things that kept me feeling better. I find that I'm in the water just about every day doing water aerobics classes, so I'm using the buoyancy of the water to help me. Going to a gym with a regular trainer and yoga got way too painful for me.
For years I've also done massage therapy and gone to support groups. Two other things are very helpful: aromatherapy and essential oils. I use those for pain instead of pills. I've never taken aspirin or anything for pain since the time I was addicted to pain pills.
(ANN, 71)
Fibromyalgia treatment is based on symptom control, which varies since every patient has a different level of physical and/or psychosocial distress. Many patients use a multifaceted approach that includes health care professionals, physical therapy, fitness training, cognitive behavioral therapy, acupuncture, and relaxation training. Most important, the patient must play an active role. The aim is the improvement of quality of life.
The FDA has approved several medications for the treatment of fibromyalgia but a recent study recommended that treatment for fibromyalgia using pharmaceuticals start "slow and low."
Doctors also treat fibromyalgia with a variety of other medications developed and approved for other purposes. Analgesics such as NSAIDs have been used to ease pain but are not effective at eradicating it. Antidepressants are also used to modulate pain.
Various dietary interventions have been investigated in fibromyalgia, and the findings were variable, ranging from negative to significantly effective.
Today I don't think of myself as sick—and I think that also has had a tremendous effect. Am I symptom free? No, but I get in the pool or take a nap or ride my bike (I got a tricycle) or meditate—I know how to make myself feel better. The water has been a godsend. Exercise of the right kind is terribly important.
I think if I didn't have the inner strength and positive outlook through the years, I would have been a shut-in.
(ANN, 71)
Chronic Fatigue Syndrome
Chronic fatigue syndrome (CFS) is a condition that causes marked long-term tiredness (fatigue), headaches, difficulty concentrating, sleep disturbances, and other symptoms that are not caused by any other known medical condition. The core symptoms are a sustained depletion of energy after minimal activity and profound ongoing fatigue.
Many experts and patients prefer the term _myalgic encephalomyelitis (ME),_ meaning "brain and spinal cord inflammation with muscle pain," or ME/CFS, because it underscores a physical basis for the condition. Although some research has suggested that inflammation of the central nervous system is involved, its role is not proven, and muscle pain is not as prominent as other features.
What Causes CFS?
Several factors have been suggested in the development of CFS, including genetic, viral, immunological, neuroendocrine, and psychological. While the exact causes of CFS are unknown, it appears to be triggered by a variety of factors in people who have an underlying predisposition. Some suggest that it may be part of a double hit—after a viral infection that initiates an inflammatory response—but there is little scientific evidence to support this theory.
A recent study showed that there are changing levels of cytokines (molecules that stimulate or inhibit immune cells) in the blood samples of people with ME/CFS, indicating some kind of inflammatory and/or disease process at work. These biomarkers also indicate that people are not imagining or "making up" their symptoms. The role of these markers in the initiation or aggravation of the syndrome is under study.
How Is CFS Diagnosed?
There are currently no diagnostic lab tests or criteria that can confirm the diagnosis. It is made based on a pattern of symptoms and, more important, by excluding other conditions and diseases with similar symptoms.
The diagnosis is made after symptoms have persisted for at least three to four months and other conditions have been ruled out.
How Is CFS Treated?
Like fibromyalgia, CFS is treated by symptom control. This may include drugs, dietary changes, exercise routines, and cognitive therapy under professional guidance and medical supervision. Severe symptoms may require the support of a specialist in the condition.
Patients often feel that dietary manipulation can help to ease the fatigue—removing sugar, gluten, dairy, and/or other foods. Whether this is because of an underlying sensitivity to specific foods is unclear.
Before removing gluten from your diet, it is important to test first to make sure that you do not have celiac disease. After a period on a gluten-free diet, it may be impossible to diagnose this underlying condition without a gluten challenge, which requires adding gluten back to your diet.
Some patients with ME/CFS have low L-carnitine levels (see "Carnitine Supplements" in chapter 17, "Celiac Disease") and may benefit from supplements to improve their fatigue.
Are Fibromyalgia, Chronic Fatigue Syndrome, and Nonceliac Gluten Sensitivity Related?
Fatigue, brain fog, and joint and muscle pain are common symptoms in people who diagnose themselves as gluten sensitive. It is very possible that we are going to find gluten sensitivity in certain people with chronic fatigue syndrome and fibromyalgia.
We are currently analyzing blood samples to determine if they contain antibodies to gluten (antigliadin antibodies). As discussed before, the meaning of these antibodies is unclear—they do not indicate celiac disease but do indicate some type of immune response to dietary gluten. A gluten-free diet may help these specific patients. The antibodies may also be part of an inflammatory reaction that may yield a biomarker for these conditions.
Since the symptoms mimic those of celiac disease, it is possible that some people with fibromyalgia and chronic fatigue syndrome have an immune response to gluten that is similar to those with various neurological and psychiatric syndromes seen in celiac disease. This raises many interesting questions regarding the role of gluten in various neuromuscular conditions.
Summary
• Fibromyalgia and chronic fatigue syndrome are painful, stressful, and often debilitating conditions that are difficult to diagnose and treat. Most treatments aim to turn down the volume of the pain and eliminate or ease the level of fatigue.
• Because of the lack of clear-cut medical guidelines and specific biomarkers in patients with these conditions, many medical doctors dismiss the symptoms or prescribe painkillers. Unable to get direction from their doctors and seeking a diagnosis, patients are vulnerable to practitioners who subject them to expensive tests not covered by insurance and arduous therapies for the wrong condition. Others recommend expensive supplements and restricted diets. The diets appear to help some—if only to feel temporarily better—but the cost of most of the supplements is high and the benefits are low. Some supplements are dangerous and cause more harm than good.
• If taking control of your diet initiates a greater involvement in taking control of your body and the condition itself, the psychological benefit outweighs the effect of the food elimination.
PART V
The Brain-Gut-Gluten Connection
_The human brain has 100 billion neurons, each neuron connected to 10 thousand other neurons. Sitting on your shoulders is the most complicated object in the known universe._
—MICHIO KAKU
_If the body be feeble, the mind will not be strong._
—THOMAS JEFFERSON
Recent books and articles have called gluten the "silent killer" of the brain, claiming that whole grains cause dementia, autism, headaches, depression, anxiety, ADHD, and more. The scientific truth is that _reading and believing_ this about grains probably fogs more brain cells than eating them will.
Our brains do exist in intimate interaction with our gut, where our "second brain" and our microbiome reside. But the direction of this interaction and who is in charge of which function is unclear. In fact, gut-microbiome-brain interactions offer insights into brain function in both health and disease. Whether this will have direct therapeutic results or prove to be only a small piece in a much larger brain-gut puzzle remains to be revealed. There are many more questions than scientific answers for this particular puzzle.
Brain study is in its infancy—we are still "orienteering." This is an activity where people are given a map and a compass, and navigate from point to point in unfamiliar territory to find something. Similarly, medical researchers are navigating a diverse and usually unfamiliar terrain to determine how, why, and if foods are the culprit in a number of psychiatric and neurological conditions.
Despite the many books and articles trumpeting clear connections, it is currently way too early to make scientific claims for specific or functional links between brain function, our microbiota, and gluten. What we do know is that intriguing pathways have been identified and that researchers are actively exploring them.
Autism Spectrum Disorders and ADHD
_If we want to solve a problem that we have never solved before, we must leave the door to the unknown ajar._
—RICHARD P. FEYNMAN
According to various studies, gluten-free and/or casein-free diets are used by between 15 and 38 percent of parents for children on the autism spectrum. While the diets are increasingly popular, the theories and findings that are portrayed in the popular press, on websites, and in books appear to be more firmly established than the science behind them.
When you first get a diagnosis, what you want is a way out, you want hope, you want treatment. So you're drawn to the promise of something.
(DONNA, 42)
Parents are looking for treatments to do something, and specific foods are an appealing answer. There is a misconception that gluten is exacerbating or causing the symptoms of autism. So some parents immediately put their children on a gluten-free and/or casein-free diet in hopes that it will "cure" them.
Autism Spectrum Disorder
Autism spectrum disorder (ASD) is a disorder of neural development. It is characterized by impaired social communication and restrictive and repetitive behaviors. Many children have language and physical difficulties as well.*
There is no one clear cause of ASD, but contributing risk factors include:
• genes—ASD runs in families. If one sibling is diagnosed, a second sibling will have a 15 to 20 percent chance of developing the condition.
• sex—Males are four times more likely to have ASD.
• other environmental and/or biological factors
Ultimately, the odds are low that specific environmental insults such as paternal age or maternal infection that have been the focus of recent studies will influence the outcome. Other risk factors for autism are being studied. For example, researchers are looking at the effect of alterations in a young child's microbiome to see the impact on the development of autism. (See "ASD and the Microbiome.")
Symptoms of ASD emerge during early childhood and are typically diagnosed between 2 and 4 years of age. Diagnosis is done by a clinician based on behavioral observation and reports from parents.
There are currently no biomarkers or medical tests to diagnose ASD. Some genes have been implicated in the development of the disorder, but genes alone do not determine the onset of the condition.
Typical treatments include behavioral, speech, and physical therapies. There are currently no pharmaceutical treatments but research is being conducted on possible targets and drugs.
((Mommy, My Tummy Hurts))
[Our son] has chronic constipation and takes Miralax on a daily basis—it keeps things under control and his behavior under control as well.
Before we figured out what to use, he went for two to three days or more without a movement. You could see that he was upset—he wants to do it, and when he fails he gets upset and does more self-stimulation. You can't get his attention—he's in a zone. He won't engage in normal activities if he's very constipated.
(MARTY, 45)
Gastrointestinal complaints and conditions are among the most common medical issues associated with ASD. Diarrhea, constipation, and GERD are often reported. This may be a direct effect of certain behaviors ("holding it in" may result in constipation), or the GI complaint may affect their behavior as well as their physical well-being.
Many nonverbal children who cannot simply say that their tummies hurt express distress in other ways. A child in pain may withdraw or engage in self-injurious behavior (i.e., bite him- or herself) or have a tantrum in order to get attention so that someone will come to help. This does not mean that all children who display disruptive behaviors are masking GI symptoms; and GI issues are not seen as a singular problem in ASD—a subset of neurotypical children also have GI issues—but GI symptoms may be an extra barrier to ameliorate symptoms and affect treatment.
One recent study by Pat Levitt, Ph.D., a neuroscientist and professor at USC, showed that parents were aware of the existence but not necessarily the nature of a GI disorder in their child. And that a large portion of children in the study with GI disorders and ASD lacked "expressive language" and showed increased social impairment compared to those children with ASD who did not have GI issues. The study noted that this "novel finding . . . warrants further study." It was unclear whether the GI medical issues affected the child's ability to respond to treatment or whether the lack of expressive language itself contributed to constipation by "limiting appropriate toileting behavior."
Individuals with GI issues and ASD need to be diagnosed and treated by a gastroenterologist in order to isolate and properly treat their symptoms.
Visiting the Gastroenterologist
Taking a child with ASD to the doctor can pose a challenge. Many children are sensitive to new environments, and the doctor's office has a variety of unknowns including smells, sounds, and unfamiliar people. Preparing a child with ASD for some of the unknowns—what the situation will look like and what will happen—can help to reduce anxiety and agitation.
Autism Speaks, a nonprofit organization dedicated to research and information for the ASD community, has a comprehensive Parent's Guide to medical appointments and blood work. Links can be found in Appendix B, "Resources."
Why a Gluten-Free and/or Casein-Free Diet?
The role of gluten in the development, progress, and treatment of ASD is complex and under intense scrutiny in different settings. It is possible that the presence of IgG antigliadin antibodies may indicate a subset of children who may benefit from a gluten-free diet. (See chapter 6, "What Do Antibodies Tell Us?")
Studies have shown that there are increased food antibodies (IgG antigliadin antibodies and anticasein antibodies) in a subset of children with autism who have GI symptoms. These are nonceliac antibodies. While this suggests a gut-brain interaction, we do not know the direction of this interaction (i.e., is the brain affecting gut permeability or vice versa?). The presence of antibodies has to be shown to have a direct effect on brain function or dysfunction if it is to have scientific significance as a causative factor. Nevertheless, this immune response may help to identify novel biomarkers of ASD and offer new insights into the disease mechanisms for some of those with ASD.
A study of children with attention deficit hyperactivity disorder (ADHD) also showed that a subset had IgG antigliadin antibodies, but their significance is similarly unknown. Some experts feel that tests for antigliadin antibodies and the specific celiac antibodies should be part of the diagnostic process for these children to rule out celiac disease and to determine a possible sensitivity to gluten. The causes of ADHD are not known, but genes and environmental factors (maternal smoking and alcohol use, lead exposure, brain trauma) may contribute to symptoms. The roles of sugar and food additives have been studied with mixed scientific results. Some parents report that a sugar-free, gluten-free diet has improved hyperactive behaviors. Scientific studies have not objectively shown that elimination diets are effective in treating the symptoms of ADHD. It is fairly common that children with ASD may have symptoms of ADHD.
Several rationales are suggested to explain the presence of antibodies to gluten and casein in some people with ASD.
• The "leaky gut" theory suggests that impaired intestinal permeability allows harmful peptides, including gluten and casein, to diffuse into the body, where they create an immune response in the form of antibodies. (See chapter 16, "Intestinal Permeability.")
• Gluten may trigger an inflammatory response in the gut of some children, which may react with the central nervous system.
• A study found a significantly higher IgG antibody response to casein and gluten in patients with ASD in comparison to neurotypical individuals, perhaps an indication of systemic inflammation that could include the gut.
• It is possible that altered intestinal permeability is a secondary effect that results from disturbed brain function (see the discussion on cerebral palsy in chapter 27, "Schizophrenia"), neither causing nor contributing to the brain dysfunction.
The exact significance of the presence of IgG antigliadin antibodies in this subset of people with ASD is unclear. Nevertheless, these individuals do appear to have more GI symptoms.
Most of the research studies following the effectiveness of gluten-free and/or casein-free diets in ASD have been shown to be too small to be statistically valid and/or flawed. Many rely on the reports of a parent or caregiver and may be influenced by the caregiver's desire for a positive outcome.
For the 1 percent of children with ASD who also have celiac disease, a gluten-free diet may have a dramatic effect on outcome. For those with nonspecific IgG antibodies to gluten, it may be helpful in alleviating symptoms, though this has not been demonstrated. For many others, isolating other causes for GI symptoms may be the most helpful way to resolve them.
Unfortunately, parents often receive conflicting advice about dietary interventions. While food and the GI tract are very clear issues for many individuals with autism, the science underlying the complex brain-gut puzzle is not.
When the twins got their diagnosis, it was a weeklong assessment that involved seeing a lot of specialists of different disciplines. And one of them was a psychiatrist. He was actually one of the most helpful, but at the end he wanted us to cut the boys off dairy completely for three months—he said it was just to see if it had an effect on their behavior. And he gave us forms to fill out for every day describing their behavior.
This was incredibly daunting, to say the least, having just received the autism diagnosis. And when we discussed this with the developmental pediatrician who was in essence the lead of the whole process, she actually rolled her eyes, and she said, "You're going through enough—no reason you have to do that. They need their dairy."
So, literally from the day of the diagnosis, we had two doctors telling us opposite things. To me the most daunting thing was that having gotten the diagnosis, there was no clear guidance as to what was real and what was not real.
Our disposition from the beginning, because of our experience with the two specialists, was to doubt dietary interventions.
(MARTY, 45)
Pitfalls of a Gluten-free Diet for People with ASD
There are many feeding issues in children with ASD. They are more "picky" eaters than those in the general population, perhaps a manifestation of restricted and repetitive behaviors that are a hallmark of the disorder. A gluten-free diet is often low in fiber and essential nutrients, and this may only compound the problem. Recent studies on the presence of heavy metals in people on a gluten-free diet raise possible neurological complications that need to be studied further. (See chapter 4, "Pitfalls and Perils of a Gluten-Free Diet.")
[My son's] teachers sometimes use food rewards when something requires a very high motivation, like during the first stages of toilet training. Now they use an activity they like. In most schools I had to send them the edible rewards. So you have that control over it.
(DONNA, 42)
A restrictive diet is also difficult to enforce—children with ASD often see many different therapists and clinicians in the course of a typical school day (speech, art, movement therapy). Often, each group uses food as a reward to enforce desired behaviors. If that reward is a cookie or cracker with gluten, it may trump efforts to keep to a gluten-free diet. Thus parents may be seeing results that relate more to therapy than to diet.
Feeding my son is incredibly hard work.
(SALLY, 36)
For some children with ASD, feeding and/or eating takes on a life of its own. A preference for specific foods—yellow or red, mushy or crunchy, spicy or bland—and sensory sensitivity can limit diets and create behavioral issues as well as malnutrition.
A gluten-free diet is a popular consideration for this population, but has not been demonstrated to alter the disorder state. It may also be extremely difficult to enforce, adding additional stress to family meals.
ASD and the Microbiome
It has been hypothesized that changes in the gut microbiome play a role in the development of ASD. These studies are further complicated by the fact that individuals with autism frequently receive medication with antibiotics, are often on special diets, are highly dietary selective, and/or have repetitive dietary behaviors, all of which may alter their microbiota. Thus, it is difficult to establish whether the changes are causative or simply a consequence of the disease or its treatment.
Since it is difficult to study the human gut at a molecular level, some researchers have studied the influence of the microbiota on brain development and function in ASD on specially bred mice. These studies have established a link between the microbiota and autism-like behaviors, but not the underlying mechanisms. That is, it is not clear whether alterations in the gut microbiota are causing autism symptoms.
Some studies indicate that the serotonin system is involved in the development of GI symptoms in ASD. (See "The Molecular Busybody" in chapter 10, "The 'Second Brain'.") These studies involve mice with a genetic mutation from humans with ASD affecting GI and serotonin function. The mouse does not have autism but genetic permutations and features that are similar to humans with ASD. This research has provided information about the relationships between diet and the microbiome in a specific subset of people with ASD. While mice are not, as a recent article noted, "little humans with tails," they open a window into the relationship between diet, the microbiome, and GI complaints.
What Does It All Mean?
Although the links are currently unclear, it is possible that breakthrough autism treatments may start in the GI tract. Researchers are studying whether GI symptoms are a manifestation of the neurodevelopmental disorder that could be a clue to its physical and biochemical development. An article in _Autism Speaks_ notes, "Studies that improve our understanding of these brain-gut connections are laying a pathway to innovations in treatment."
It is increasingly frustrating for the parents and caretakers of individuals with ASD to continually hear "it's unclear" and "we don't know what will work or what this means." What is clear is the importance of correctly testing for, diagnosing, and treating GI disorders in this population. _Anyone_ in pain or suffering from GI distress will have difficulty focusing on mental tasks. This can have distinct repercussions on the many interventions used to treat ASD.
Summary
• The use of gluten-free and/or casein-free diets in people with ASD is controversial. Scientific studies have not proven objective changes in behaviors for children on these diets.
• Parents should be aware of the serious pitfalls of a gluten-free diet before implementing one for their child. They are adding nutritional as well as food choice limitations to a population already burdened by restrictions.
• The presence of antibodies to gluten in a subset of children with ASD is an intriguing finding and may point to a group of people who might benefit from a gluten-free diet. But these antibodies must be studied further to determine when they develop and how this relates to the child's development. We must be careful not to confuse association with cause.
• Gastrointestinal dysfunction may provide a window to better understand both autism and the brain in autism. It is a bidirectional avenue that may hold answers even in those without GI disorders. Potentially it could mean that a drug targeting the intestines might help neuropsychiatric conditions.
Schizophrenia—Revisiting "Bread Madness"
_Science is like a love affair with nature; an elusive, tantalizing mistress. It has all the turbulence, twists and turns of romantic love, but that's part of the game._
—VILAYANUR S. RAMACHANDRAN
The evidence for a connection between disturbances in the GI tract and psychiatric illness has been accumulating for many years. Our growing understanding of how the brain, the microbiome, and the enteric nervous system—the "second brain" in the gut—interact has uncovered intriguing associations between what we ingest and behavior. But as we must consistently note in this section focusing on the brain, there is a big difference between association and cause.
Bread Madness
The association of bread with madness dates back to the Middle Ages, when rye was susceptible to ergot, a fungus containing chemicals that resemble LSD. When eaten, it caused convulsions, pain, and a type of "madness" called St. Anthony's Fire, or ergot poisoning. The symptoms became associated with "bewitching" and may have accounted for some of the accusations behind the Salem Witch Trials. The "madness" symptoms were then attached to schizophrenia. In the 1920s, the "intestinal intoxication" theory of schizophrenia was popular. Papers in the 1960s referred to schizophrenia as "bread madness."
This lingering belief has been replaced—at least in the scientific community—with an understanding that while the specific causes of schizophrenia are unknown, contributing factors appear to include a genetic predisposition interacting with complex environmental and neurotransmitter disturbances. But intriguing connections to gluten remain.
They exist in the similarity of genes for schizophrenia and certain genes found in other autoimmune disorders such as celiac disease. An infectious "insult"—exposure to the parasite _Toxoplasma gondii_ —is a known risk factor for the development of schizophrenia, presumably through a direct effect of the parasite on brain and behavior. This may also be part of a "double hit" where an infection with toxoplasmosis combined with an immune response to gluten in susceptible individuals can result in schizophrenia. (Also see chapter 14, "The Double Hit Theory.") Dr. Robert Yolken, an investigator from Johns Hopkins University, has provided evidence supporting this theory.
Some researchers hypothesize that an alteration of gut permeability may be the initial step causing both schizophrenia and celiac disease, sharing similar pathways of altered gut permeability. In this scenario, the gut of genetically susceptible people may lose its capacity to block toxins and psychosis-causing substances may enter the body, thus causing the development of various psychiatric conditions.
The microbiome may also play a part, since manipulation of the microbiota in germ-free animals has created behavioral as well as biochemical and molecular changes.
The Presence of Anti-gliadin Antibodies—The Horse or the Cart?
Studies show that some patients with schizophrenia have _IgG antigliadin antibodies_. These antibodies are also associated with neurologic and psychiatric manifestation (ataxia, peripheral neuropathies, brain fog) but without the GI symptoms seen in celiac disease. (See "What Do Antibodies to Gluten Really Mean?" in chapter 6, "Testing.")
It has been proposed that the IgG antigliadin antibodies seen in these patients reflect an increased sensitivity or immunological response to gliadin. This does not appear to affect the GI tract, but it has been suggested that the antibodies cross-react with parts of the central nervous system or specific proteins in the brain.
While it is hoped that a resolution of antibodies would improve symptoms in schizophrenia, studies with gluten-free diets have had mixed results. None of these studies, however, have focused on those most likely to respond—those with antigliadin antibodies. It is clear that the gut-brain interaction goes both ways. What is not clear is whether gluten sensitivity is the result of, or contributes to, the development or progression of this disease.
The effect of these antibodies on function cannot be proven as yet. They may very well be a good measure of the wrong thing.
Cerebral Palsy
Cerebral palsy (CP) results from "insults" to different areas of the developing nervous system and causes a varying severity of symptoms. The management of these symptoms is the goal of treatment, and children with severe spasticity often suffer from problems with swallowing, reflux, and delayed stomach emptying. This can lead to malnutrition.
An increased level of IgG antibodies to gliadin as well as other food components has also been found in some patients with cerebral palsy. The clinical implications of their presence in this condition are unclear. They do, however, indicate that the gut-brain interaction is bidirectional—CP is primarily a brain problem, yet there are increased food antibodies.
In one interesting study, positive IgG antigliadin antibodies to gliadin were found in children with CP who had lower weight, height, and BMI compared to healthy children. A number of possible reasons were suggested, focusing on an effect on the gut that was not recognized, an inflammation of the gut mucosa, or intestinal permeability leading to an immune response in the body.
While some parents put children with cerebral palsy on a gluten-free and/or casein-free diet, the pitfalls of the diet should be taken into account in children whose nutritional status may be at risk. (See chapter 4, "Pitfalls and Perils of a Gluten-Free Diet.") The benefits of the diet at this point appear to be very controversial and may be harmful for children already suffering from malnutrition.
Summary
Various neuropsychological conditions highlight the complex brain-gut connection. Clearly more research is needed to determine if IgG antigliadin antibodies and other food antibodies are a marker of blood-brain barrier disruption and contribute to brain dysfunction. If so, it would provide an impetus for examining the effect of a gluten-free diet in a subset of patients who have antibodies to gluten.
This is an exciting field of research that may help provide evidence that links disrupted pathways outside of the brain to the development of certain brain disorders.
Brain Fog—Neurology or Meteorology?
After only one month on a [gluten-free] diet, I felt as if a veil had been lifted from my brain.
(ROZ, 58)
"Brain fog" is one of the most common symptoms mentioned by people with gluten-related disorders. It is not an acknowledged medical term but a definition that originated with patients. It is described as mental confusion, a lack of clarity or focus, and forgetfulness.
The mechanisms causing these symptoms are unclear, but the same symptoms can be caused by a number of factors including lack of sleep, various neurological disorders, stress, early stages of dementia, diabetes (fluctuating glucose levels can affect brain function), chemotherapy (aka "chemo fog"), anesthesia, acute illnesses, and the side effects of various medications.
While the various tests to measure cognition and depression contain limitations, different instruments are used to measure attention, concentration, orientation, short- and long-term memory, praxis (the ability to learn and retain new information), speed of processing, language, and executive function. The results would indicate that brain fog is very real in a subset of patients with celiac disease.
Brain fog is also considered a classic aspect of chronic fatigue syndrome and fibromyalgia, and is often accompanied by disorientation and difficulty in finding words.
In an intriguing new study, Peter Gibson, M.D., of Monash University in Australia looked at the cognitive function of people newly diagnosed with celiac disease. He found that the cognitive performance of one group of patients on a strict gluten-free diet showed a definite improvement that paralleled the healing in their gut. He concluded that "suboptimal levels of cognition in untreated celiac disease may affect the performance of everyday tasks."
Before going on a gluten-free diet, the subjects had a level of impairment similar to people with a blood alcohol level equal to the upper legal limit for driving in Australia. It is also the equivalent of severe jet lag. This meant that someone with untreated celiac disease might be at risk for impaired performance at work or while driving. In fact, a Swedish study found that asymptomatic young adults in whom celiac disease was discovered by screening had fewer university degrees and managerial positions compared to subjects in an age-matched control group.
Using five different research instruments and questionnaires, Gibson's group assessed subtle cognitive impairment, the recall of words, fine motor movements, and the reconstruction of complex situations. The study showed that all were impaired and improved at six and twelve months on the diet. This correlated with improved blood tests and biopsy results. The results suggest that there is a real impairment of cognitive function related to disease activity. That said, the mechanisms underlying these symptoms are not clear, and the results could be different for different individuals. More studies are needed to replicate these findings.
What Causes Brain Fog?
There are a number of theories on the development of brain fog in gluten-related disorders.
Inflammation
Many cellular markers are released during inflammation that permeate organs and signal the brain to induce a "sickness response." This includes symptoms such as fatigue, depression, lack of motivation, and lack of mental clarity that often clears up along with the disease. Most people experience this crawl-into-bed response when sick with the flu. In conditions such as irritable bowel syndrome, chronic inflammation provokes a transition from this type of sickness response into depression and chronic pain.
Cytokines (molecules that signal the inflammatory response) are one such marker released in response to infections, illness, and stress. The brain has cytokine receptors, and these cells may bind to neurons and affect signaling. If levels of these cells persist in the body they may cause a disruption of perception.
Several studies offer insights into the complex relationship between inflammatory processes and neurological function. Studies show that antibodies to gluten do bind to nervous tissue in humans and animals. In celiac disease specifically, we know that antigliadin antibodies can bind to proteins in neurological tissue. While it is unclear whether binding interferes with the function of the tissue, studies suggest that it does.
It is also possible that inflammation in the gut disrupts the microbiota that in turn affects the gut-brain pathway.
Gluten
When someone has an immune response to gluten, there is an increase in inflammatory mediators (e.g., cytokines) that might interfere with the blood-brain barrier or disrupt various hormones and enzymes. These disruptions may cause depression, cognitive impairment, or brain fog in some individuals.
Nutrient Deficiencies
There is a fair amount of evidence showing that vitamin deficiencies affect the nervous system. Patients with untreated celiac disease or other intestinal malabsorption conditions may have vitamin and mineral deficiencies affecting cognitive function and/or causing neurological deficits.
Gut Microbiota
The gut-brain-microbiome axis appears to plays a role in influencing brain development, mood, and behavior. In a similar vein, an unhealthy diet has recently been highlighted as a risk factor for depression.
Our gut microbiota interacts bi-directionally with environmental factors such as diet and stress, and this may eventually be a target for interventions to treat mental conditions. Studies of this are in very early stages, and no direct link to brain fog has been suggested.
Stress and Anxiety Due to Illness or Trauma
An illness itself may play a major role in initiating brain fog. Sickness can alter one's ability to function, and subtle cognitive functions like memory are more vulnerable to stress and anxiety.
Poor stress resilience and an exaggerated inflammatory response to environmental stress is characteristic of people who have undergone trauma in their early lives. This in turn may affect cognition and well-being. (For more, see chapter 29, "The Stress of Holding Back.")
Summary
• Any physical illness, whether acute or chronic, is usually accompanied by numerous psychological symptoms that may include fatigue, depression, an increased sensitivity to pain, and lack of motivation, appetite, and sociability. They are part of what is called a "sickness response," and most disappear with the disease.
• Brain fog may be a symptom or part of a sickness response in those with an immune or inflammatory response to gluten. The mechanisms underlying the condition are unclear, but the brain fog is real.
• If your illness is chronic, your sickness response may be as well. This might require pharmaceuticals to treat both the physical as well as psychological symptoms.
• Brain fog may be another piece of the conversation between the brain, the gut, and our microbiome. This puzzle is still missing many pieces, which scientists may be able to identify as targets for treatment in the future. At this point, a gluten-free diet clears the fog for some people with celiac disease, but should not be considered the dietary answer to treating brain fog in others.
The Stress of Holding Back
_"Stressed" is "desserts" spelled backward._
—ANONYMOUS
College on a strict gluten-free diet is way harder than I expected. It's definitely not easy to balance schoolwork and also worry about food all the time! A lot of people here in California are on the gluten-free diet for the fad, which undermines the severity of celiac disease and cross-contamination and everything. It was a huge struggle. In college I've been more resentful of the disease than any time before. Social life is isolating, dealing with my own food. I often have to go back to my room to get something to eat, and that takes away that spontaneity that makes college so fun. I feel like I'm missing out. That's the most difficult [thing]. I constantly have to be vigilant. At home it's so nice to know that everything is safe—it's a lot more relaxing.
(ALEXIS, 20)
Is it a gluten-free diet—not the gluten—that is stressing your brain circuits and causing a literal brain drain?
Stress is defined as a physical, mental, or emotional factor that causes bodily or mental tension. There is good stress that keeps us alert and involved, and bad stress that takes a mental and physical toll. People who are always on alert when eating or living with a chronic illness have constant stress—a condition that loads the part of the brain responsible for executive function, tapping its resources and making it less effective. This eventually produces wear and tear on the entire body—referred to as "allostatic load" in the medical literature. This "load" is triggered by various chemicals and hormones released in response to stress, and can determine our patterns of emotional response and resiliency to events that can extend far beyond the dinner table.
The Evolutionary Perspective
Stress responses benefit animals in the wild and may have given our prehistoric ancestors a survival advantage in avoiding predators. Daniel Lieberman, an evolutionary biologist and professor at Harvard University, puts it most succinctly in noting that animals on the Serengeti do two things most of the day: "They eat and they worry."
These survival skills are not required when seeking food in the supermarket, but we now worry about gluten, fat, and carbohydrates rather than large predators—an evolutionary shift of focus that is affecting our brains and health in unexpected ways.
I feel nervous whenever I'm on a date. Afraid he won't like me because I ask the waiter so many questions. Makes me a neurotic mess, I guess.
(JOAN, 28)
While it is a highly subjective phenomenon that is difficult to measure, it is becoming increasingly clear that the stress of "holding back," of monitoring, measuring, and thinking about what we eat at every meal and in every social setting, has many silent and cumulative effects. Beyond the fight-or-flight response that characterizes acute stress, when food and eating become chronic concerns of everyday life, the stress can affect thought, mental performance, and the responses of numerous organs.
The Burden of Restrictive Dieting
Having a gluten-free home is expensive but manageable; the problem comes with outings, vacations and trips, and trying to go to restaurants. And it seems like school is much more prepared and willing to deal with peanut allergies and that sort of thing.
(RAY, 38)
For people with chronic illnesses such as celiac disease, IBS, IBD, type 1 diabetes, or a food allergy, stress comes in navigating a school cafeteria, counting carbs, always reading labels, carrying an EpiPen, ordering in a restaurant, and constantly being vigilant.
In a recent study, people with celiac disease perceived the treatment burden of the diagnosis as a heavier one than end-stage renal failure (a fatal condition in which the options are dialysis several times a week or a kidney transplant). Many come to an entirely gluten-free event and remark, "It was the first time I remember being so totally relaxed at a party—I never worried about what I was putting in my mouth." Others with IBS sometimes eat nothing at an event in fear of not reaching the bathroom in time. Like individuals with a food allergy, they are on perpetual alert, a stressful state of constant vigilance, where food is involved.
What Your Brain Gains and Loses on a Diet of Chronic Stress
The brain is the main organ in the body that determines what we perceive as stressful and how we will react and adapt to it. It is also a target of the stress, and this can have lasting effects on it. And there are enormous differences in how each individual responds. When stress becomes a destructive element in someone's life, it is important to take steps to address the consequences. Sometimes it is a silent pressure that only shows its face after much damage is done.
Stress "loads" the prefrontal cortex, the part of our brain where executive function is centered. This function involves a number of abilities that affect your capacity to organize and manipulate different types of information and behaviors. It comes into play during decisions that involve planning, decision-making, abstract thinking, troubleshooting, initiating or inhibiting responses and/or temptations, and processing sensory information. It may actually play a role in the brain fog that many patients report. (See chapter 28, "Brain Fog.")
Stress can also affect impulse control because it elevates _glucocorticoid_ levels, sometimes for extended periods of time. These steroid hormones regulate the body's need for energy. One of the glucocorticoids, cortisol, causes the body to crave food—many people say they "eat when stressed."
In teenagers, the prefrontal cortex is not yet fully developed—one reason many have poor impulse control in general. But impulse control is a complex phenomenon that is intertwined with other "reward" systems in the brain that are developing during adolescence. The combination of immature systems often results in poor choices within this age group that makes dietary and health constraints harder to follow.
There is also an increased sensitivity to pain that is often found in people suffering from chronic stress. This, however, is a two-way street. Not only is it possible that social distress may sensitize individuals to physical pain, enhanced pain may lead to greater perception of social distress. Researchers note that these two processes seem to be moving together and possibly influencing each other.
Adjusting to a Restricted Diet
_A crust eaten in peace is better than a banquet partaken in anxiety._
—AESOP
There are many reasons a restricted diet is difficult, including the necessary change in habits, social and cultural constraints and stigma, and loss of control (of impulses and the ability to find "safe" food). Your adjustment will then depend on your personality and how you respond to the change. People who need to be in control can become extremely frustrated. While some psychologists recommend trying out "other ways to be in the world," this is not always easily achieved.
What is it like to be the grandmother of a child with celiac disease? It's more a question of being the mother-in-law of the mother of the child with celiac disease.
(LUCY, 65)
The timing and delivery of the diagnosis can affect the difficulty in dealing with the condition. When diagnosis comes during adolescence—a sensitive developmental period—the perceived negative effects are often more severe than during early childhood, when the condition is integrated into identity and habit more readily.
My doctor said, "You have celiac disease. Go on a gluten-free diet, and I'll see you in six months." That's when we got really frustrated and really lost. My doctor sent me home without any guidance.
(ALEXIS, 20)
Patients who receive excellent dietary counseling and guidance at the time of diagnosis are more accepting of the diagnosis and restrictions than those left to fend for themselves on the Internet.
Identity Threats
It's interesting to watch my granddaughter develop her self-identity. Who she is is someone who cannot play with a child who has peanut butter on his hands. Who she is is someone who can never go into an ice cream store and eat regular ice cream. It's incorporated into her identity.
(MARY, 67)
In a recent book on how stereotypes affect us, the social psychologist Claude M. Steele discusses how stereotype threats have a real effect on people.* And people on a very restricted diet are often marginalized and/or made to feel an outsider to the food at parties, galas, business meals, school trips, and many restaurants. Some schools even refuse to take children with food allergies or intolerances on class trips where they cannot readily accommodate dietary restrictions that might cause a health issue.
Steele analyzed the effect when identity threats become chronic and are an ongoing experience in some area of one's life. His studies suggest that the long-term stress of dealing with threats to identity may undermine not only a person's happiness, but also contribute to health issues.
Fortunately, as Bruce McEwan, a neuroscientist and professor at Rockefeller University, emphasizes, "The good news is that interventions can prevent the negative effects of stress on the brain and body."
I kept a gluten-free kitchen even when my daughter went off to college. This way she can relax completely and feel safe when she comes home.
(AMY, 49)
Navigating Through the Stress of Holding Back
There are several steps you can take to improve your stress levels and your perception of stress.
1. **Rewrite the Script**
You hear, "It's not fair, I don't get to eat what the other kids are eating." It actually is fair. It would be unfair for me to give my son what the other kids are getting. What we can try to do is make things equivalent. So if they're getting a dessert, you might not get the same dessert, but you'll get the dessert that's good for you. That's fair.
We don't all get the same things out of life, but we can make them the equivalent.
(KEIRA, 43)
2. **Eat a Healthy Diet, Get Physical Activity, and Sleep**
Stress depletes the body—a balanced diet of fresh food, exercise, and sufficient hours of rest feed and restore it. Sleep deprivation also triggers hormones that stimulate hunger—studies have found that people who sleep less are more likely to be overweight.
3. **Get Social Support**
Eating is very personal, and many people feel it does not require outside intervention and interference. But people with chronic illnesses and allergies fare best when supported by medical professionals who understand the science behind their conditions. The support of family and friends can reduce the "solitary" burden and make social occasions easier to navigate. For example, celiac disease meet-ups have become increasingly popular in some cities and offer the exchange of restaurant and product suggestions that encourage compliance and comfort with the diagnosis, and grow social resilience through shared participation in a diagnosis and treatment.
4. **Try Different "Mind Practices"**
If compliance is difficult and causing medical issues, cognitive behavioral therapy (CBT) has been shown to be very effective in improving attitude and approach. Many patients with chronic fatigue syndrome, fibromyalgia, and IBS report that meditation and mindfulness also decrease painful symptoms and improve their quality of life.
You may need to set up a mental road map that differs from the patterns and routes you have been taking.
5. **Reward Yourself**
We all crave a treat or comfort food every so often and want to be rewarded for good behavior on a diet. People on a weight-loss diet are wisely counseled not to eat an entire piece of chocolate cake. When you _must_ have one, take a few bites. This is where the advice to those on a gluten-free diet to find substitutes for their favorite foods—pizza, chocolate brownies, beer, mac and cheese, etc.—cannot be emphasized enough.
There is a difference between rewarding yourself with a safe food and cheating.
6. **Seek Out Medical Professionals to Help Manage Your Disease**
Keeping your disease and symptoms well managed will lower your stress levels. Far too many people who are prescribed a gluten-free diet are not advised to see a dietitian or feel they are expert and vigilant enough to teach their children and handle the diet on their own. Yet we have heard children admit to cheating on the diet when their parents were not present. Dropping off the diet is frequent at times of stress and transition—changing schools, entering college, a first or new job—and having direct access to a dietitian can make these transitions easier.
7. **Use Pharmaceutical Agents If Necessary**
There are a number of drugs used to control stress, including antidepressants, beta blockers, sleeping pills, and other agents for relief from inflammation and pain. All have strengths, limitations, and side effects that must be measured and balanced with your underlying condition as well as your level of stress.
Directing your energy toward the management and control of personal perception and behaviors can help the brain respond more flexibly to stress. As Professor McEwan states, "Motivation and decision making and perseverance are all functions of the brain!"
Holding back can create stress that eventually colors an individual's perception of food, family, friends, and lifestyle. Being aware of its impact on your brain and body can affect your long-term health and well-being.
PART VI
Navigating a Gluten-Free Life
_Minds are like parachutes, they only function when open._
—THOMAS DEWAR
_Things should be made as simple as possible—but not simpler._
—ALBERT EINSTEIN
The first five sections of this book put gluten and the gastrointestinal tract under the microscope. They examined the public perceptions—and misconceptions—about the grain, its role in different diseases and conditions, its effect on the GI tract and possibly the brain, and how a gluten-free diet and lifestyle can affect your stress level and resilience.
We also explored how everything we ingest affects the GI tract and why other foods, drugs, and toxins create the symptoms often attributed to gluten.
But the complete picture cannot be drawn without a closer inspection of the pharmaceutical drugs being developed to assist those on a gluten-free diet as well as the myths, hidden ingredients, food guidelines, and future directions for those trying to navigate a healthy and symptom-free life.
Nondietary Therapies—the Drug Pipeline
_I can resist everything except temptation._
—OSCAR WILDE
It is difficult to follow a strict, lifelong diet of any type, but that is currently the only safe and effective treatment for those with celiac disease. Patients need and want a nondietary form of therapy for several reasons:
• Temptation, the desire to eat "some" gluten if symptoms are not severe, can make compliance a real problem, especially if there are no immediate symptoms when the gluten is ingested.
• Products, even those labeled "gluten-free," can be contaminated.
• A small percentage of patients do not respond to the diet, and an even greater number (estimated at 30 to 70 percent) do not heal completely.
• Patients with minimal symptoms prior to diagnosis may become more sensitive to gluten after a period on a gluten-free diet.
Various studies underscore the extent of these issues. One study of patients in the UK showed that 70 percent either intentionally and/or inadvertently ingested gluten. It is also hard to avoid gluten even in products marked "gluten-free." While there are only a few good studies, those that exist indicate that a few breakfast cereals marked as gluten-free contained amounts of gluten greater than the minimal amount allowed by law to carry that label. Gluten has also been found in various supplements, an unregulated industry where the "gluten-free" label currently is questionable.
A nondietary answer therefore holds tremendous appeal and has a long history in other GI conditions. Lactase pills, for example, have made having an ice cream cone or slice of pizza possible for those with lactose intolerance. And antacids are a staple in most households. They do not replace the need to avoid dairy or highly fatty foods for these individuals, but treat a dietary "mistake" or indiscretion. Severe IBD can be put into total symptomatic and histological remission.
All this has led to the development of some very promising and exciting alternative and/or complementary approaches to a gluten-free diet. Since more is known about the development of celiac disease than any other autoimmune disease, researchers have tracked the pathways through which the partially degraded and toxic fragment of gluten gets into the lining of the intestine and interacts with the immune system. It is these very pathways that are the target of various therapies.
While there is currently **_no_** product on the market that prevents, halts, or reduces the harmful effect of gluten on people with celiac disease, the following show the most promise at the moment. The potential therapies block, bind, or degrade the toxic components of gluten. **Except for the vaccine, they all currently work _in conjunction with_ a gluten-free diet.**
I'm the kind who, if you can take a pill for it, it's perfect. I'm ready when the pill is ready.
(CHERRY, 35)
I'm leery of untested things in general. I'd be scared of trying the new therapies until they've been on the market for a few years.
(NED, 52)
Helping Digest or Degrade Gluten
The gluten protein is not completely digested in the small intestine by the proteases (enzymes that break down proteins) in our GI tract. But a number of different proteases that do digest gluten exist in nature. They are referred to often as glutenases and can come from various sources.* They exist in some grains—including, ironically, barley—and in bacteria and fungi. These sources are being harnessed to be manufactured in commercial quantities with special qualities. They can also be specifically engineered in the laboratory. They need to be able to act fast and completely in the very acidic environment of the stomach, while the stomach is mixing and dissolving ingested food, and before it leaves to enter the small intestine. This is a very promising therapy.
Studies have demonstrated that some glutenase enzyme preparations can effectively digest gluten in the acidic environment of the stomach. ALV003, manufactured in the U.S. from barley and bacteria, and AN-PEP, manufactured in the Netherlands from fungi, appear effective. However, placebo-controlled studies in patients with celiac disease did not meet the planned primary end points of the studies. This emphasizes the difficulty in conducting placebo-controlled studies in those with celiac disease. A promising, potent engineered enzyme (Kuma030) is being studied by investigators at the University of Washington.
While other glutenases from various sources including mouth bacteria, stool bacteria, and probiotics have been detected, none have been commercially developed at this time.
It must be reiterated that there are currently many available OTC glutenases marketed as dietary supplements that have _not_ been evaluated by the FDA and are _not_ effective in degrading or digesting gluten in the stomach despite claims to the contrary. We recommend that patients with celiac disease specifically avoid using these products, as they could be harmful.
Inhibiting Intestinal Permeability
Larazotide Acetate
Another drug with FDA Fast Track designation, Larazotide, has a strategy based on keeping the toxic gliadin peptides from entering the intestinal lining, where they trigger the immune response. It essentially shuts the gate that lets the toxic peptides in.
Larazotide works on the "tight junctions" holding the cells together and may also be working on other components of the transport mechanisms between cells. Gluten is also transported _through_ the epithelial cells, and Larazotide would not block this entry. (See chapter 16, "Intestinal Permeability.")
Phase II clinical trials have shown it to be effective and generally well tolerated in improving symptoms of celiac disease more than a gluten-free diet alone. To date, the studies have not included biopsies to assess mucosal injury, but they would be necessary for FDA approval and will be necessary end points in definitive trials.
Binding Gluten with Polymers to Safely Escort It from the GI Tract
BioLineRx Ltd.'s BL-7010
Distinct from therapies that degrade gluten, this approach uses polymers that act in the intestinal tract (the _lumen_ ). The polymers are being developed with the ability and properties necessary to target and bind gliadin and prevent digestion and absorption. It would then be "escorted" out of the GI tract and excreted in stool. Studies in experimental animals show that BL-7010 does do this. In the U.S., it has not yet progressed to clinical trials in humans, where it must be proven safe. There is concern that it can also block/bind with vitamins and minerals and prevent their absorption. This is an attractive form of therapy, since physicians prescribe a similar class of drugs to treat high cholesterol and diarrhea.
Vaccine to Induce Tolerance to Gluten
ImmusanT's Nexvax2
Nexvax2 is an injectable vaccine that is designed to induce immune tolerance to gluten. It is designed to work like an allergy shot—exposing the immune system in a controlled way. It is assumed that the vaccine will induce tolerance by acting on the T-cells, which serve as a go-between in the immune system, and create a protective T-cell response.
ImmusanT has identified three of the most potent peptides causing the immune reaction in people with HLA-DQ2–associated celiac disease. This accounts for approximately 90 percent of people with celiac disease. The vaccine will not work for patients who have the -DQ8 genes.
It has been tested in Phase I trials in Australia and shown to be safe and tolerable. It must now move to trials to test its effectiveness in protecting the intestine from gluten damage. This treatment would involve patients continuing to eat gluten and require regular injections—similar to someone receiving allergy shots.
If proven safe and effective, a vaccination strategy might be even more attractive than other novel treatments.
Other Potential Therapies
Blocking Tissue Transglutaminase
Tissue transglutaminase (tTG Inhibitor) is the enzyme that changes gluten into a toxic molecule for people with celiac disease. Therefore, inhibiting its action has been suggested as an effective therapeutic approach for celiac disease. Since tTG is also an essential enzyme used by the body for wound binding and other binding activities, it poses a high risk if the therapy blocks tTG in any other organ or interacts and/or disturbs other metabolic or biological pathways.
Studies on this approach are still preclinical (not conducted in humans).
Modifying Wheat
It has been proposed that modifying wheat strains to remove the peptides causing the immune reaction—without removing the baking quality of the wheat—might be an option for people with celiac disease seeking to replace gluten-containing bread.
There are many challenges in the process of the modification of gluten contents in the wheat varieties. Modifying the protein contents may lead to a loss of or decrease in baking characteristics; all the peptides in wheat that causes an immune reaction are still not known; the potential for contamination of genetically modified grains with the wild strains during cultivation, pollination, harvesting, and processing is possible; commercial wheat is cheap and any future genetically engineered wheat would increase in cost in an already price-inflated gluten-free market.
An alternative approach is to detoxify gluten by using bacteria-derived peptidases during food processing that would "digest" the wheat peptides. This is the process by which sourdough bread is made and would have to be carried through to totally eliminate gluten. A study confirmed that this resulted in bread that was not toxic to individuals with celiac disease (although the product resembled a biscuit more than a bread).
Bugs as Drugs—Hookworms
Our early contact with bacteria and toxins trains our immune systems. Based on the theory that as we have lost the chronic immune stimulation that came with all the infections mankind evolved with, parasites, including hookworms, are being ingested to stimulate the immune system in a protective way. This is a telling example of how much we need "bugs," and an exciting area of research. This approach has been used in Crohn's disease and asthma—using different kinds of parasites—and has been applied to celiac disease. The hookworms get in through the skin and travel to the intestinal tract via the bloodstream. They grow in the gut and exert an immune response.
One study showed no benefit, and another done recently did not reduce the severity of symptoms or prevent intestinal deterioration. But the parasitic infection did suppress some inflammatory responses, suggesting that further studies should be done.
Hookworms can cause anemia, and we do not recommend trying this approach at home—although they are often obtained unwittingly while on vacation in developing countries, where they are widespread.
Oral Passive Antibody Therapy
This approach has been considered for some time. The theory is that some animals can be immunized and produce antibodies to gluten. These antibodies can then be produced in sufficient quantities and administered to bind to gluten in the intestine. There are two proposed sources—one developed from the colostrum of cow's milk, and recently an antibody to gluten developed in hens' eggs. Individuals with an egg allergy could not take the latter product.
While the press releases of each new potential product attract much attention, there is a great deal of work to get a drug to market. It is an expensive and time-consuming project, and many products never make it to the shelf.
Probiotics
Probiotics are an exciting form of potential therapy. It is possible that they can be genetically enriched with drugs and then ingested into the small intestine, where they would release the potential drug at a needed site and act locally. However, much research needs to be done on this mode of therapy. Probiotics would have to move from the category of dietary supplement to that of a drug and thus undergo the rigorous safety and efficacy studies required for drugs to be sold in the U.S.
Over-the-Counter Drugs Currently Available
There are currently _no_ products available over the counter that can fully degrade or digest gluten and block the effects it has on those with celiac disease, despite some manufacturers' claims to the contrary. Various OTC supplements are actively marketed in carefully worded advertisements that make claims about digesting gluten, healing the gut, and reducing inflammation. Manufacturers state in very fine print at the bottom of labels and websites that the supplements are not intended to cure or treat disease. And they advise people to take their products without the rigid testing for effectiveness and safety required by the FDA.
These products contain a variety of enzymes that can partially digest gluten in test tubes. However, studies by Dr. Frits Koning in the Netherlands have shown that they cannot digest gluten in the acidic environment of the stomach. In addition, they do not digest the toxic peptides that are resistant to the usual digestive enzymes. These different OTC supplements may also pose a health risk to anyone with undiagnosed celiac disease who believes they can "safely" eat gluten—all the while allowing it to silently inflame their intestines. We recommend that patients with celiac disease specifically avoid using these products as they could be harmful.
Most people with celiac disease and other GI disorders are careful about the foods they put in their mouth. They should be equally concerned—or even more careful—about OTC supplements they ingest.
FDA Approval
The development of therapies for celiac disease must follow a specific line negotiated by the drug companies with the FDA. Because celiac disease has specific tissue and biochemical abnormalities, it allows for the development of end points that must be satisfied prior to approval. These end points are agreed to prior to placebo-controlled studies. For celiac disease, therapies must prove to be effective in reducing inflammation and/or intestinal damage as well as symptoms. Most important, any drug must make people feel better. This needs to be determined in placebo-controlled randomized studies.
The FDA now also mandates that companies developing drugs develop a plan for studying the drug in children.
Once a drug is on the market, physicians can prescribe the medication for "off label" use to treat other conditions. It is anticipated that gluten-sensitive people may want these medications once they are available, especially if they are very sensitive to small amounts of gluten, as that is the target of the therapy. However, we hope to know more about gluten sensitivity and be able to target the cause—which may not be gluten, the gliadin fraction of wheat.
The Hazard of Taking a Pill
The widespread prescribing of statins (cholesterol-inhibiting drugs) has erroneously convinced some people that they can take a pill in the morning and then have a cheese omelet for lunch, "bread their butter," and then eat fried and creamed foods for dinner. They think, "The pill will take care of it." Statins can be "oversaturated" and essentially unable to take care of the cholesterol load ingested.
That is one of the real moral hazards of the new drugs being developed. Currently, they are not able to replace a gluten-free diet but do augment it and cover contamination or an occasional exposure. They are able to degrade small amounts of gluten, not a sandwich, pizza slices, or a piece of cake. People may take the medication and then feel it relieves them of the need to stay on a gluten-free diet. Or the medication may enable them to feel better when they eat out, all the while (unwittingly?) ingesting more gluten than the drug can handle. The patient then gets a low-grade chronic exposure to gluten for many years, feels good, does not get celiac-specific checkups, and develops a lymphoma in 10 years.
We will not find out how bad that may be for many people for decades, especially those who are asymptomatic—they can eat gluten and continue to have an immune inflammatory response and/or get the disease.
When choosing new treatment strategies, one must consider the possible risks versus benefits of the treatments against a gluten-free diet, which we know is safe, effectively eliminates the problem protein, and saves lives.
Questions Arise: Is the Drug Suitable for Me?
It is unclear if the drugs will work for everyone taking them. Some people might not respond and may not realize it. Other diseases or therapies could impact the delivery or efficacy of any of the potential therapies. For example, the enzymes that work in the stomach are dependent on an acidic environment—individuals cannot swallow acid blockers all the time and still have them work, and some people do not make acid at all (a condition known as hypochlorhydria).
Summary
There is a real need to continue to seek out and develop an alternative therapy to a gluten-free diet. Ideally, this will be a therapy that will not simply help with the diet by dealing with minor contamination, but that will allow people to eat a regular diet containing gluten.
Patients with celiac disease and most clinicians treating the patients will want to be convinced that any new drug for celiac disease is able to prevent the development of the gluten-induced damage to the lining of the small intestine, and ensure that patients live a long and symptom-free life.
The pipeline is built, but is not as yet pumping effective and safe treatments.
Eating Healthy
_Don't eat anything your great-grandmother wouldn't recognize as food._
—MICHAEL POLLAN
_High-tech tomatoes. Mysterious milk. Supersquash. Are we supposed to eat this stuff? Or is it going to eat us?_
—ANITA MANNING
Gluten is the most recent dietary sensation. But it is too often not a healthy one. Navigating your way to this particular table can be a dietary obstacle course.
The markets are filled with hidden gluten and, in gluten-free products, some ingredients that, for certain people, are possibly worse than gluten. There are also products and food manufacturing processes that may be contributing to the recent growth in celiac disease as well as other autoimmune conditions.
It is time to move the dialogue away from gluten alone and include everything else on your plate. We need to explore what is being done to gluten-free products to make them taste and look like the "real thing."
We may, in fact, be eating ourselves sick.
Emulsifiers, Binders, and Enhancers
In the Western world, most people who do not live on farms—growing and eating only what they produce—eat a diet of food that is processed to guard against spoilage, ensure longevity, and promote its taste and appeal. This includes everything from pasteurization (guarding against harmful bacteria) to supplementation with chemicals, vitamins, and minerals that put back what processing takes out—plus a list of sweeteners, salt, flavorings, and binders to make products more appealing to the perceived wants of the consumer.
Emulsifiers
_They were like oil and water._
—PROVERBIAL PHRASE
Emulsifiers are a common additive used to stabilize food. For example, if you add oil to water and vigorously shake it, the oil will disperse throughout the water. Left to sit, the oil and water will separate. When you add an emulsifier, the oil stays dispersed and a stable emulsion is formed. Mustard will accomplish this for the oil and vinegar in a salad dressing; bile salts accomplish this in the intestine. They enable fats to be spread through the liquid contents of the intestine and be digested and absorbed into the body. Chemicals are used in food processing to hold products together.
Emulsions are found throughout the food industry. They are used in baking to form and maintain the volume and texture of biscuits and breads, and to improve the structure of crumbs in cakes. They are also in dairy products, confectionery items like chocolates and toffees, meats, margarine, and spreads (e.g., peanut butter).
A new study suggests that emulsifiers may be linked to metabolic syndrome and IBD. The study, reported in the academic journal _Nature,_ showed that mice fed relatively low concentrations of two commonly used emulsifiers had low-grade inflammation and obesity/metabolic syndrome. The emulsifiers also promoted colitis in mice predisposed to this disorder. The researchers tested different species of bacteria in the mouse GI tract and hypothesized that a disruption of the microbiota encouraged the issues. While the scientists acknowledged that "excess caloric consumption was still a predominant factor driving the metabolic syndrome epidemic," the study pointed toward elements like emulsifiers in food as a potential promoter of low-grade intestinal inflammation.
If emulsifiers encourage inflammation in the gut, which in turn increases intestinal permeability ("leaky gut"), it would potentially enable food antigens and bacteria to move into the body from the intestinal tract, and might promote any number of allergies and conditions in predisposed people. More studies will need to be done to test this theory.
Food "Glue"
Another product used to enhance the texture and quality of food products is an enzyme called microbial transglutaminase (MTGase). It is a food "glue" that modifies proteins to improve the appearance, hardness, and shelf life of meat, the hardness of fish products, the quality and texture of milk and dairy products, the consistency and elasticity of candy, and the texture and volume of foods in commercially baked goods. If the label reads "added enzymes," those enzymes are more than likely MTGase.
Human tissue transglutaminase has long been recognized as the auto-antigen of celiac disease—the enzyme that reacts with gliadin and sets off the reaction that triggers celiac disease. But transglutaminases are found throughout nature in mammal tissue, invertebrates, plants, and microbial cells. MTGase is the biological glue used in food products and some medicine. In fact, our diets may contain large amounts of MTGase, raising the question of its relation to the rise in incidences of celiac disease.
The key question is whether MTGase added to food increases the risk to those susceptible to celiac disease or nonceliac gluten sensitivity, or whether it can cause disease by itself in these individuals. While it is considered to be generally safe for the majority of people because it is approved as a natural product, several studies have led to the hypothesis that the industrial use of MTGase is a new environmental enhancer of celiac disease and may have negative effects on the gluten-sensitive population.
It does this in two ways. It may create toxic gluten peptides capable of producing an immune response prior to ingestion; and/or once eaten, these peptides may increase toxicity in the intestine and initiate celiac disease in susceptible individuals.
MTGase is also used on gluten-free ingredients (e.g., soy) in gluten-free products. Thus a product labeled "gluten-free" but containing soy that has been cross-linked using MTGase creates an additional layer of confusion. Gluten-free foods frequently and inevitably contain small amounts of gluten, and these small amounts of contaminants would become more toxic to people with celiac disease due to MTGase action.
The scientists studying MTGase concluded that "If future research substantiates this hypothesis, the findings will affect food product labeling, food additive policies of the food industry, and consumer health education."
It is something to think about when you reach for processed products in the market. Because MTGase is not a food, it is not required to be listed on food labels.
Vital Gluten
For those who are focused solely on the gluten in their food, it is available in industrial-strength form.
Vital gluten is a powdered form of the protein portion of wheat with the starch washed out. It is sold alongside many flours and advertised as a "natural," "high-protein" baking product that improves the texture and elasticity of dough. One manufacturer advertises it as something that "can easily put the home bread baker on a par with the professionals." It is not a flour but powdered gluten.
Vital wheat gluten is the main ingredient in seitan, a food product used in vegetarian cooking and often referred to as "wheat meat." Wheat gluten is also used as a source of protein and in pet foods as a binder. Wheat gluten from China, adulterated by melamine, was blamed as the cause of pet food recalls in 2007. It also can hold other food products together, e.g., mushroom or vegetarian burgers.
It is unclear what effect a vegetarian or vegan diet high in vital wheat gluten might have on someone with a genetic susceptibility to celiac disease. Researchers are examining this issue.
Are You Eating Products or Food?
While nondairy milk may be of value for individuals who are lactose intolerant or dedicated to a vegan diet, it is not a food. Milk is a natural product of lactation, not of an electric blender or manufacturing plant. Juices that claim to have "fresh from the orange" taste often do not have fresh-from-the-orange ingredients.
Labels are required to list all ingredients in descending order by amount. If the first ingredient is water, then there is more water in the product than anything else. If we break down the label on soy or almond milk, both consist mainly of water that is sweetened and supplemented with calcium, vitamins, and thickening agents.
Both soy and almond milk usually contain carrageenan (highly processed seaweed), added to create a creamy texture—and implicated in inflammation and GI problems.
All these labels boast "natural" vitamins. Vitamins are found in all of the foods we eat—that is the natural form. Added vitamins are manufactured (calcium carbonate, D2, vitamin-synthetic vitamin A) and often lack the cofactors (the other food and/or vitamins) necessary for them to be properly absorbed by the body.
Adding back vitamins after the fact ignores the issue of synergy: how nutrients work naturally as opposed to when they are isolated. A 2011 study on broccoli at the Linus Pauling Institute illustrates this point. The researchers found that giving subjects fresh broccoli florets led them to absorb and metabolize seven times more of the anticancer compounds known as glucosinolates, present in broccoli and other cruciferous vegetables (Brussels sprouts, collard greens, kale) than when glucosinolates were given in straight capsule form. The researchers hypothesized that this might be because the fresh broccoli contained other compounds that helped people's bodies put the broccoli's anticancer chemicals to use.
There is a certain amount of irony in the instructions to take vitamins and certain minerals (i.e., calcium) with food for proper digestion and bodily effectiveness. Supplementation is also ironically praiseworthy as it returns to the food supply all the natural vitamins and minerals food processing and our diets have taken out.
**Everyone on a gluten-free diet should try to eat and drink less processed food. Your symptoms may be coming from ingredients that sound natural but are actually intestinal irritants.**
Where Is Gluten Hiding?
Gluten is found not only in products made with wheat, rye, and barley, but as an ingredient to modify texture, facilitate water or fat retention, and help bind products, from soups and meats to ready-to-eat meals, etc. It is also used as a filler in drug and supplement capsules.
In accordance with the FDA labeling law passed in 2013, any food labeled gluten-free must contain "less than 20mg/kg gluten" (less than 20 parts per million). The ruling further specifies that any "foods specially processed to reduce gluten content" or "very low gluten" must comply with levels between 20 and 100 mg/kg.
This is a controversial area, as there are different tests used by manufacturers to determine gluten content, and testing batches in food products varies. Since the labeling process is voluntary, there is no government-regulated testing to confirm labeling in the U.S. as there is in Canada. A few studies have shown contamination of gluten-free foods and medications/supplements, even in those made of inherently gluten-free grains.
Cross-Contamination
Cross-contamination can occur at any level of food production. While this problem is mainly directed to people with celiac disease who require a truly gluten-free product to maintain their health, there are few guarantees in place.
A number of so-called gluten-free flours and grains actually have tested for unsafe levels of contamination. Many home cooks can find the source of digestive problems related to gluten within their stock of gluten-free ingredients. Manufacturers may also receive batches of contaminated grains while making products in a dedicated facility. Unless they do regular on-site testing using validated assays, this can be an issue.
While various experts have studied the contamination of oats with wheat and barley, it is not the only grain that can be contaminated. Other grains that are naturally gluten-free, like millet, have been shown to be frequently contaminated by wheat.
To guarantee that a grain is gluten-free, it needs to be either grown and processed in dedicated fields and facilities, or, alternatively, tested to be free of gluten. All grains except for rice also have to be labeled "gluten-free" because of contamination studies.
Bulk Bins
Contamination can occur when food is displayed in open bins in the market. Suzanne Simpson, R.D., warns patients not to buy from bulk bins with a scoop. Scoops "travel" and can find themselves in the raisin bin having started the morning in another nearby bin containing a product with gluten. She also warns patients to beware of websites selling nuts, flours, and mixes that must be carefully monitored to be safe.
Reading Labels
We came up with a system. If the label has more than three different things that you cannot pronounce, then it's not really good for you.
(OWEN, 12)
If you are trying to be gluten-free, you need to read labels to avoid gluten. But many foods require no stamp of approval, as they are naturally gluten-free. Water is at the top of the list, yet there are actually water bottles labeled "gluten-free" and selling at a premium—"because you can never be too sure." Labeling rules now allow water as well as other products to be labeled gluten-free even though they may be just that by nature. The only thing that this label likely ensures is that you are paying more money unnecessarily.
The foods that require a gluten-free label are anything made from or with flours: cereals, pastas, breads, cookies, cakes, pretzels, rice cakes, crackers, pizza, breaded and frozen items, etc. Soups, mixes, and all-in-one products with packets of flavorings (e.g., rice pilaf mixes) should also be scrutinized carefully.
While there are many forms of hidden gluten, if a product contains wheat in any of its forms, it must be listed on the label. Barley is not part of the labeling law and must be identified in its various forms (malt) and uses (beer).
Reading labels is important and not difficult once certain words are ruled out. For example, malt is made from barley, but when it is the first four letters in a long word such as _maltodextrin_ or _maltitol_ it is safe. Yeast as an ingredient is fine, but brewer's yeast is not.
If a product is made in a facility that processes other products with wheat—and is not labeled gluten-free—it may be contaminated. If it is labeled gluten-free, it is most likely safe.
Eating Healthy
_"A gluten-free diet is the only treatment for gluten-related disorders—but in all honesty being just gluten-free is not enough. We need to think of our diet as part of our overall healthy lifestyle. We need to get back to basics and make sure that our diet is nourishing both our health and well-being."_
—ANNE R. LEE, ED.D., R.D.N., L.D.
CELIAC DISEASE CENTER AT COLUMBIA UNIVERSITY MEDICAL CENTER
The newest population studies—examining large numbers of people over an extended period of time—show that people eating a _high_ gluten diet had a lower risk of both type 2 diabetes and heart disease. This is linked to the high fiber and nutrients found in a wheat-based diet and underlines the importance of making your gluten-free diet equally rich in fiber and nutrients from different gluten-free sources to ensure your long-term health.
Despite the many roadblocks, the road to a healthy gluten-free diet can be found by focusing on what you _can_ eat, not on what you cannot.
• Eat a _balanced_ and _varied_ diet that is high in naturally gluten-free whole foods.
• Eat plenty of fresh fruits, vegetables, beans, nuts, and legumes.
• Limit processed and packaged gluten-free products as much as possible. If you use these products, choose those with a variety of gluten-free whole grains and few ingredients.
• Aim for low fat, low sugar, low salt.
• Add more whole grains such as quinoa, amaranth, buckwheat, millet, lentils, chick peas, and gluten-free oats that are gluten-free and high in fiber in place of rice, corn, or potatoes.
• Add these grains to soups, stews, and salads to increase their fiber, B vitamins, and protein.
• Eat raw and "crunchy, cooked" vegetables as well as beans and foods with skin to get as much soluble fiber as possible.
• Eat plenty of protein from various sources (fish, lean meat and poultry, dairy, eggs, beans, seeds, and nuts).
• Snack smart—nibble fresh fruit and vegetables, trail mix with nuts, seeds, and dried fruit; multigrain chips and crackers with seeds, nuts, and a source of at least 2 grams of fiber.
• Avoid processed products with long ingredient lists (they usually contain excessive chemical additives).
• Bake with flours made from gluten-free grains, nuts, and beans such chickpea, almond, quinoa, sorghum, and teff instead of simply using rice or corn flour.
• Read labels and shop smart.
**A healthy diet is not accomplished on a 7- or 14-day plan. It is a long-term commitment to changing habits, eating differently, and turning these guidelines into actions.**
A Note on Adding Fiber
A gluten-free diet doesn't mean living on rice, corn, and potatoes. I use as little of those ingredients as possible in my baking and daily diet. Instead, I rely on the great gluten-free whole grains and flours like buckwheat, quinoa, oats, amaranth, sorghum, chickpea, and teff. You only have to look at their nutritional profiles to see that each one is a powerhouse of nutrients, fiber, and protein.
—BETH HILLSON, FOOD EDITOR AND AUTHOR
All grains, fruits, and vegetables contain fiber, whether gluten-free or not. Quinoa, oats, and lentils are especially high in fiber, and unless you're accustomed to it the fiber by itself can cause gas and bloating. Whenever a patient has a flare of symptoms and says that they are "trying to eat really healthy," it often means they have increased their fiber and have not tolerated the rapid increase. Their problem may also be an intolerance to fructose or other FODMAPs.
If you are trying to eat healthier and add grains, fresh fruit, and vegetables rapidly, be careful not to confuse the possible ensuing bloating with a return of symptoms.
Summary
• A healthy gluten-free diet is one of variety and filled with naturally gluten-free "food" rather than "products" made from ingredients grown in a lab and compiled in a manufacturing plant.
• Substitute wisely—adding too many sugar- and fat-filled gluten-free cakes, cookies, and snacks will add pleasure, but also pounds. Eating gluten-free and eating healthy are not synonymous.
• Be smart when reading labels. "Natural" does not mean healthy.
• Diversify your diet—try new grains, vegetables, and fruits.
• Removing gluten from your diet may be a lifesaver, a symptom reliever, or a road to continuing medical issues. Make these guidelines the first steps to a healthier life.
Myths and Misconceptions
_Fables should be taught as fables, myths as myths, and miracles as poetic fantasies. To teach superstitions as truths is a most terrible thing._
—HYPATIA
Myths are widely held ideas that are false. But studies show that the more you tell people they are wrong, the more they believe their deeply held ideas. The following myths are a combination of "the usual suspects"—myths about gluten that absolutely refuse to die—and some interesting new misconceptions and questions that surround gluten.
**_Gluten causes dementia and Alzheimer's._**
No, it does not. These two conditions are not related to gluten. Some of the symptoms of the "brain fog" that many patients describe can be confused for the early stages of these conditions, but brain fog is a discrete entity.
**_Gluten causes "brain fog," and a gluten-free diet can boost brainpower and improve mental focus._**
Although brain fog is a poorly defined medical condition, it is frequently reported by patients. A medical term that encompasses this may well be "mild cognitive impairment." In recently diagnosed patients with celiac disease, studies show brain fog is common, but it improves with a gluten-free diet (and with the healing of the small intestine). There are no studies involving people with gluten sensitivity, nor is there any concrete science that indicates gluten causes brain fog in the general population.
There have also been no scientific studies that have shown that eliminating gluten from your diet (again, in the general population—and not those with celiac disease or a gluten-related issue) can boost your brainpower, improve mental focus, or prevent a decline in memory. (See chapter 28 for a more detailed discussion.)
Also, one could make an argument that thinking your focus is better makes it so—part of the placebo effect. And stomach issues in general, such as gas, bloating, and pain can decrease one's ability to concentrate. A feeling of fatigue or sleepiness after a meal may well be normal and related to hormones produced in the intestine. There are many studies that are exploring a brain-gut interaction but there is much that is unknown and several hypotheses that need to be explored before these claims can be substantiated.
**_Eating gluten makes you fat._**
Eating more calories than you can burn off during your daily activities will add pounds to your body. A diet that contains grains will not, in itself, make you fat. The amount you eat will determine your weight.
Gluten-free baked goods and snacks contain high amounts of sugar and fat to enhance their taste and hold them together. On a gluten-free diet, patients often gain weight when they substitute these gluten-free foods for their wheat-based counterparts.
**_A gluten-free diet is healthier._**
Unless you have a specific food allergy or intolerance, or a disease requiring food restrictions, a diverse diet—one that includes meat-based foods, dairy, fats, fresh fruits, vegetables, and whole grains that are high in fiber—is the healthiest. (See chapter 31, "Eating Healthy.")
**_Everyone should try eating gluten-free for a week._**
While a week of gluten-free eating is generally harmless, the majority of people have nothing to gain. You are also removing a great deal of fiber, vitamins, and minerals from your diet and need to replace them with plenty of fruits, vegetables, and other grains. Studies have also confirmed that a trial gluten-free diet is not a test for celiac disease.
The fact that something is harmless does not mean it is good for you. This is an adjunct to the concept that something labeled "natural" is therefore harmless. All plants are natural, but many are highly toxic.
**_Is gluten sensitivity common?_**
Since medical science does not know how to define or test for gluten sensitivity, it is unclear how prevalent it may be. A recent double-blind study showed that only about 30 percent of people who believed they were "gluten sensitive" actually had adverse reactions when fed gluten. The condition is real, but it is not believed to be as widespread as some experts report. There are many other causes of GI symptoms that people blame on gluten alone.
**_Is there a gene test for gluten sensitivity?_**
There is no genetic link to nonceliac gluten sensitivity and therefore no gene test that is meaningful.
**_Can you diagnose celiac disease with just a blood test?_**
Blood tests are the first step used to determine if someone has celiac disease. If they are positive, the next steps are an endoscopy and biopsy. The results of a biopsy are still the gold standard for diagnosis.
There are strict guidelines followed by some physicians in Europe that use only blood tests to diagnosis children, but this standard has not been accepted in the U.S.
A complete listing of tests for celiac disease, as well as a fuller discussion of this issue, can be found in chapters 6 and .
**_Does corn raise celiac antibody levels?_**
Corn is not harmful for the majority of people with celiac disease. But some individuals have corn allergies or sensitivities as a separate issue. So you can have celiac disease _and_ IgE antibodies (allergy based) to corn. Eating corn will not increase your antibodies to gluten.
**_Can gluten pass through the skin?_**
Gliadin is not absorbed through the skin, but it can enter the GI tract through the more porous mucous membranes of the nose and mouth. Therefore, lipstick can be a source of gluten. You can also breathe it in.
The skin barrier is designed to keep the outside world out—but if your skin is broken or damaged, gluten can get through. But it will not cause dermatitis herpetiformis (the skin manifestation of celiac disease).
Gluten can worsen hives, canker sores, psoriasis, and eczema in some people. There are also numerous ingredients in lotions and shampoos that can cause skin irritation and inflammation, which may then be blamed on gluten in the product.
**_What does it mean when antibodies to different foods are found in the stool?_**
Very little. We do not know how commonly antibodies to foods occur in those with no symptoms. Stool tests are not a reliable test for allergies or celiac disease.
**_Does having celiac disease mean that my immune system is depressed or suppressed?_**
No, it is just the opposite—it is more active. The gluten-free diet removes the trigger activating the immune system and causing the inflammation.
This is one reason that people with undiagnosed but active celiac disease are more likely to develop a second autoimmune condition: their immune systems are overactive, and can turn against the body.
There are, however, specific instances in which the immune system can be compromised—people with active celiac disease have impaired spleen function. The mechanism of this is not clear. Since pneumococcal and meningococcal bacteria require normal spleen function to be cleared by humans, it is recommended that individuals with celiac disease receive a pneumococcal vaccination.
There is evidence that those with celiac disease who fail to follow a gluten-free diet are at greater risk of developing more autoimmune diseases than those who do adhere to it. It is another reason that people with celiac disease are well advised to follow a strict gluten-free diet.
**_Over-the-counter (OTC) enzymes containing DPP4 "digest" gluten._**
There are currently _no_ OTC products that are able to digest the toxic fractions of gluten. Most of the "enzymes" found in these products (DPP4, amylase) are already found in the intestinal tract, where they are not able to break down the complex gliadin protein. Many people do not realize that they are paying money for OTC products containing ingredients claiming to digest gluten that are already present in the body and unable to do the job.
**_You can outgrow celiac disease._**
Celiac disease is an autoimmune condition that cannot be outgrown. Some people do not have overt symptoms after eating gluten and may think this means they have outgrown it. But even without symptoms, the grain may be silently inflaming their intestines and causing an autoimmune reaction throughout the body that will manifest in more serious disease years later. (This topic is discussed in more detail in chapter 17.)
**_Genetically modified wheat is causing the rise in celiac disease and gluten-related disorders today._**
Wheat today has been genetically modified by regular cultivation practices of crossbreeding to produce species with a higher yield that contain more protein and carbohydrates than the strains of wild grains found 10,000 years ago. The various species of wheat available today each contain different flavors, qualities, and uses (bread, pasta, cakes, etc.). In addition, some flours are fortified with "vital wheat gluten" to enhance their baking properties. This may contribute to increasing the gluten content of wheat products and the development of celiac disease. (See chapter 17, "Celiac Disease.")
Nevertheless, the modification of wheat cannot explain the rise in gluten-related disorders and celiac disease. In fact, it has been scientifically linked to many more environmental factors beyond wheat itself. These include the rise in antibiotic and other drug use—both OTC and prescription—that may alter the intestinal balance of microbiota living there, the hygiene hypothesis (see chapter 3, "Picky Eaters"), and possibly the change in diet to more processed food that is chemically enriched, preserved and pasteurized (see chapter 4, "Pitfalls and Perils of a Gluten-Free Diet") and other individual genetic, age, health, and lifestyle factors.
Researchers have been examining wheat species for the past two decades to try to isolate cultivars (specifically bred strains) of wheat that may be less and/or nontoxic to people with celiac disease and gluten sensitivity. In addition, there are attempts to genetically modify wheat in the laboratory (GMO wheat). At this point in time, it is unclear if any of these genetically modified wheat species that lack the toxic aspects of gluten can compete with regular wheat in terms of taste, baking and cooking qualities, and yield. But stay tuned.
Thus, wheat modification is neither cause nor _currently_ a cure for gluten-related disorders.
**_Glyphosates are contributing to the dramatic increase in celiac disease._**
Glyphosate is the active ingredient in the herbicide Roundup. It is an herbicide whose extensive use has led to an increase in weeds resistant to the product. This has become a serious problem for farmers, and therefore other products were developed to handle these weeds, leading the EPA to place restrictions on the levels of these herbicides allowable in water.
One paper became the banner for the antiglyphosate movement when it stated that glyphosate was a key contributor to the obesity and autism epidemics in the U.S., as well as to Alzheimer's disease, Parkinson's disease, infertility, depression, cancer, and celiac disease.
A number of scientists at Monsanto, the maker of Roundup, found the paper to be "a collection of unrelated data points that drew conclusion from observations that were incorrect or poorly established." In fact, the study was a collection of assertions that were not backed up by the observations cited. But the disapproval then went well beyond the Monsanto review of the paper when numerous other scientists and science writers joined the debate.
They saw "bad science becoming truth online" and posted an article "When Media Uncritically Cover Pseudoscience." One writer called "this kind of alarmism unethical and irresponsible."
While it is becoming increasingly apparent that the many chemicals we put in our food—to grow, enlarge, and/or bind it, in addition to those to make it taste better (especially the "low-fat" varieties)—may be harming us in unknown ways, association is not cause. Whether glyphosate is toxic to more than weeds is scientifically questionable. And whether it somehow epigenetically affects the genome is intriguing, but also unproven.
**_Can you drink coffee if you have celiac disease?_**
Regular and decaffeinated coffee are gluten-free. Flavored coffees and coffee drinks may contain gluten—check the label, especially for sweeteners with malt. Instant, ground, or whole-bean coffee should be gluten-free, but again, check the label. Flavoring can add ingredients that are not gluten-free.
**_The only vodka that is safe to drink, i.e., gluten-free, is made from potatoes._**
All distilled spirits are safe for people with celiac disease to drink. The gliadin molecule is removed during distillation. If "distillate" is added back or flavorings are added that are not distilled and contain gluten, these vodkas would not be safe to drink.
Fermented alcohols made of grain, such as beer, are not gluten-free, as the fermentation process does not remove the gluten.
And saving the best for last:
**_I read it on the Internet (so it must be true)._**
Medical misinformation is widely available on the Internet and in the popular press. If you search hard enough, you will eventually find a "doctor" or post to tell you what you want to hear.
If you are searching the web, make sure you look into the background of the person writing the piece. This holds true for any book or article you read. The ability to use buzzwords and medical terms does not mean someone is an expert on the subject or capable of giving you good advice. Many articles and so-called "medical" sites that are not affiliated with major medical centers are way ahead of the science and often misleading. If someone claims to be an expert, check them out on PubMed. This is where scientific articles and true expertise reside.
If you are looking for answers to your symptoms, you should make an appointment with a medical doctor.
Food for Thought
Stories Matter: Different Roads to a Healthy Life
I had horrible stomach problems my entire life and no one could tell me what was wrong. I had horrible diarrhea and a lot of vomiting, and no one knew what that was from. People gave me various diagnoses, from milk allergies to "neurotic and stressed out," that kind of stuff. No one ever could say what was wrong.
I was at my OB-GYN and she said, "You're really deficient in iron and a lot of other things—you should go to a gastroenterologist and be tested for celiac disease." So I did and he said, "It's very unlikely: you don't look like someone who would have celiac disease." So I went to another doctor who did a blood test and found [high] antibodies, then did an endoscopy and found pretty severe damage. I was diagnosed with celiac disease almost 10 years ago.
In the beginning I was a lot more paranoid and nervous about it—I didn't want to go to restaurants at all and made everything for myself. I would scrutinize labels and was incredibly restrictive. And there was also so much less out there.
Now I feel more comfortable. Restaurants are more educated about it. But if I am exposed to anything with gluten, my reaction is much, much worse. I have horrible, unbearable headaches for days that nothing can help.
The only time it's stressful is when I'm going to a business lunch or something honoring someone and there are 500 people. I'm never sure if I'll show up at a large function and there'll be nothing to eat. Sometimes I would eat before and not say anything.
I think now people don't take it as seriously as before because of all the new fads with dieting. Now when I say to people, "I can't eat gluten," there's some eye-rolling—like, "Oh, she's one of those women who has weird food fixations." Which is kind of annoying because it trivializes the disease and how serious it is.
The hardest part is having a child who doesn't have celiac disease. He spreads crumbs with gluten everywhere, puts his hand in my mouth. That has been a challenge and has made me sick a few times.
In the great scheme of things, it's not that bad. I'd only advise people to be very careful about the diet. I would tell them how much better I felt once I was diagnosed.
(ANNABELLE, 33)
I went on a gluten-free diet at the suggestion of my gastroenterologist. I have what they call idiopathic irritable bowel syndrome—which means they can't figure out what's causing my symptoms, but I've got a litany of them. My mom also had a terrible digestive system; she always had indigestion.
I get constipated for two to three days, and my colon fills and presses on my bladder. So I have to urinate frequently. When you have to hold that much fecal matter, your back hurts. I couldn't get comfortable until I had a bowel movement. But I was constipated and couldn't go. So I took medicine to poop and got diarrhea and took medicine to stop. The doctor said, "You've got to stop taking all these drugs to go and stop." And when it finally moves through the last part there is _major_ discomfort getting it out.
And the gas—I can literally see my belly blow up. I get bloated for two to three days and look like I'm four months pregnant. It's not gas that I can eliminate—it just sits there; it's this grumble. I also have something where the vaginal wall is falling—I think it's called pelvic floor dysfunction—which adds to these symptoms. My gynecologist suggested that I eat more fiber and change my diet.
My internist knew all the issues and suggested I change my diet by cutting back on carbs. I finally went on a gluten-free diet when my gastroenterologist said that gluten or something might be causing an issue in my digestion system and I should try the gluten-free diet and see if that helped. He tested me for celiac disease, and that was negative. He also put me on Linzess to loosen the fecal matter—after I had tried every other pill on the market so the insurance company would allow it.
I don't go crazy about the diet—I do not have to worry if I've had something with gluten so some may be in my diet. I read labels and understand hidden gluten. I don't eat packaged things and have never been a big bread eater anyway. I'm always happy with potatoes; I've never met one I didn't like.
This combination of things has made a difference. I don't have terrible gas pains and bloating and the difficulty of having fecal matter move through my body. There's no weight loss, none of that. I cook and I bake. What I've learned in my 53 years—everything in moderation.
I think it has made a big difference. Everyone comes to it from a different perspective. And this works for me.
(CASSIE, 53)
The reason I went on a gluten-free diet? I have Graves' disease [hyperthyroidism]. I had a terribly bad reaction—pounding heart, my hair fell out. I've been on and off different levels of methimazole [to control symptoms], but you can't take that forever. The flares, which were quite severe, responded to the drug the first two times. The third flare was mild, but I still needed medicine. After that episode, I asked my doctor: "Could diet play a part in this?" She said no.
But I believe, I really do believe, that being on a gluten-free diet helps to control these symptoms—these racing thyroid levels. Looking back, I do associate eating barley and pizza with an awful lot of bloating. I have not been able to digest barley for years. I get quite a sore belly. But I've never been tested for celiac disease. After the third episode I went gluten-free, and I've been symptom free for the past two to three years. And just in general I think I feel better.
(MAURI, 62)
For everyone calling me anorexic—I have a gluten and lactose allergy. It's not about weight; it's about health. Gluten is crapppp anyway!
—MILEY CYRUS, ON TWITTER
Everyone comes to a gluten-free diet with his or her own story—celiac disease, gastrointestinal and/or neurological symptoms, psychiatric conditions, or simply interest in the latest dietary "cure." People who avoid wheat and gluten are often seen as an aggregate, but they are in fact a diverse group of individuals who must find different roads to a healthy life.
There is rarely one simple solution—such as eliminating grains or gluten—no matter how appealing that may be, and not every symptom can be readily resolved. It is possible that some of the answers may lie at the very core of our individuality—in our genes and the ecosystem of microbiota living in our guts, or how each of our brains perceive and react to illness.
What Is Making Us Sick—Gluten or Genetics Gone Awry?
Our individuality begins with our genome and, also important, how each of us reacts to our environments. There is a great deal of variety between the responses of people to the same environmental risk, which implies that genetic susceptibility may play a big role in certain diseases. Celiac disease requires specific genes, as do autoimmune conditions such as type 1 diabetes, other common diseases such as hypertension, or congenital conditions such as cleft palate.
Our genes/DNA are an instruction manual for every cell in the body—they send directions for cells to be skin or bone, hair to be red or black or brown, the cholesterol produced in your liver to be high or low. They are the underlying source code for body function—and perhaps its disrepair.
A key question is whether certain genes that originally evolved as a protective measure to fight infections, i.e., involved in survival, are now putting people at risk for other conditions. While the original function has become obsolete, the gene remains and is now reacting to the current environment. New genetic research is expanding our knowledge of why so many more people have celiac disease and a host of related autoimmune disorders. And the environment may also be rewriting the DNA instruction manual.
Epigenetics
_Epigenetics_ is a term coined in 1942 to describe alterations in the expression or behavior of a gene caused by environmental factors. These changes do not affect the underlying DNA, but exist "on top of" ( _epi,_ Greek) the genetic inheritance.
If the DNA instruction manual arrives at the cell with directions in Chinese, and the cell can only read English, the gene would be silenced, unable to read the instructions. And if the manual contained faulty instructions, the cell's behavior would be altered accordingly.
In this way the epigenetic environmental changes do not affect the DNA of the gene but only how it behaves and may be altering how the body responds. If the environment can modify gene expression through epigenetic mechanisms, it may contribute to autoimmune disease in a genetically predisposed person. It has been proven that epigenetic dysregulation plays a role in cancer, and researchers are exploring the effect it may have on diet-related chronic diseases such as type 2 diabetes, obesity, cardiovascular disease, and perhaps celiac disease.
The influence of environment is particularly important during our development and may induce permanent changes in bodily structure, gene expression, and disease risk. If someone becomes sensitized to foods during early development, the effect may last into adulthood.
Or Is It Genes and Germs?
If humans are a composite of microbial and human cells, the human genetic landscape becomes an aggregate of the genes in the human genome and the microbiome—a blend of human and microbial traits. Understanding this immense diversity and the factors affecting it is one of the main goals of a new initiative—the Human Microbiome Project (HMP). The HMP is looking to identify and characterize the microorganisms found in both healthy and diseased humans.
Because the microbiome is populated vertically (genetically) as well as horizontally (by the environment) it may be that our genes determine the composition of our microbiome, thereby predisposing it to disease susceptibility.
Many studies are now showing that changes in the composition of our microbiome correlate with various disease states, raising the possibility that manipulating our bacterial friends and foes may be a way to treat disease.
It may be possible that the newest keys to health will not be an alteration in our diets, but in the bacteria that feeds on it.
How Great Is the Placebo Effect?
Responding to a gluten-free diet does not indicate gluten sensitivity. The response could be a placebo or nocebo effect.
The placebo effect ( _placebo_ is Latin for "I shall please") is a well-studied and well-known phenomenon in which a dummy treatment or therapy creates a beneficial response simply because the person taking it feels that it will help. In various studies, sugar pills often produce the same result as actual drugs.
While the exact psychological and neurological explanation of why inactive placebos work as well as the active drug in different trials is still unclear, various hypotheses (pills reduce anxiety, modulate expectations, raise self-awareness and attention) have been suggested. This has also been studied in alternative medicine, where rituals may act as a placebo.
_Nocebo_ (Latin for "I shall harm") is a substance or therapy that creates a harmful effect. The responses are a result of the patient's perception of how the substance will affect him or her. A nocebo creates the perception that a substance will be harmful, and these negative expectations can create an actual symptom. In one study of lactose intolerance, people were told they were receiving lactose but were in fact receiving a glucose pill. A large percentage of people with lactose intolerance (44 percent) and without (26 percent) complained of GI symptoms. Often, when doctors tell patients of the side effects of a drug or therapy—which they are ethically required to do—there is an increased likelihood that the patient will experience the side effect. People anticipating the negative effects of gluten can actually feel symptoms. The placebo and nocebo responses are another reason the FDA requires double-blind studies in which both the patient and the researcher are not aware of who is getting the active drug.
The mind is a powerful tool. Believing something is bad or good for you can make it so. Studies on the actual versus believed effects of gluten on various groups show this to be the case, perhaps contributing to the "glutenitis" surge reported in the media.
Gluten Realities
_We have stopped natural selection from purifying the species because deep in our heart of hearts, we are all terrified that we won't make the cut._
—MOXIE MEZCAL, WRITER
A gluten-free diet is many things.
It is a miracle treatment if you have celiac disease.
It is a myth if you think that eliminating gluten it is a healthy or effective weight-loss diet, or that it causes every brain or gut condition in the medical textbooks.
It is a menace if you eat the many gluten-free foods and supplements that contain heavy metals and potentially dangerous binders and emulsions.
Natural selection has given way to antibiotics, stents, and statins, and a focus on pills and potions that supposedly give us a biological advantage. We all want answers and our "connected world" promises that they are all readily available, but many of the substances we ingest to outwit Mother Nature may not be the clever strategies we think them to be.
With any new therapy there is often a great wave of enthusiasm that settles down to an appropriate level. To be of proven value any medical treatment needs time. The FODMAP diet is a good example of this. Irritable bowel syndrome is so difficult to manage in many patients that the early reports of great success with this diet caused a lot of enthusiastic support. Current studies showing a much lower rate of resolved symptoms are dampening that enthusiasm. But as with any therapy, the FODMAP diet will find its place as placebo-controlled studies on it are done.
The results of another large study on the effect of breast-feeding and the early introduction of gluten as a means of controlling celiac disease has recently been shown to be incorrect. This changes a decade of advice to patients. Again, it required a placebo-controlled study!
Isolate, Test First, Treat Right
There is a great deal of talk about "personalized medicine." This has various meanings that include matching treatment/drugs to a patient's genes (or those of a tumor or cell) as well as their characteristics, needs, and preferences. We look at personalized medicine as the basis of good doctoring—helping each patient navigate his or her own road to health. Gluten has a place in medical treatment—but it must be part of an individual story. Gluten is simply not causing the many conditions it is blamed for—nor can it treat and cure them. Test first—before going on a gluten-free diet.
As scientists uncover the mysteries of our brains, guts, and microbiota, new treatments and solutions will be found, and some old remedies will undoubtedly regain importance or fall by the wayside. Gluten will eventually find its scientific place.
_You cannot put the same shoe on every foot._
—PUBLILIUS SYRUS
Acknowledgments
This book evolved over the past few years, nurtured by the interdisciplinary environment that research into celiac disease and the overall effect of gluten on the body requires. We would like to thank everyone we have worked and collaborated with over the past number of years, but some deserve a special mention for providing the energy and focus needed to explore this topic.
My colleagues in the Celiac Center, Drs. Alaedini, Bhagat, Krisndreddy, Lebwohl, Lewis, and Reilly continue to inspire me. I would like to thank Cynthia Beckman, Director of Developmet at the Celiac Disease Center, for guiding the center, helping patients, and supporting all the activities that have kept the center functioning Also, I thank my family—Marise and my beautiful daughters, Alanya and Isabella—for their support. In addition, the patients and friends of the Celiac Disease Center at Columbia University, upon whom we depend so much for supporting all our activities.
—Peter Green, M.D.
This book found shape and inspiration in each and every narrative shared with me over the past few years by family, students, patients, and friends. I am particularly indebted to those friends who brainstormed titles that nurtured the writing process as well as the writer. And very special thanks to my daughter, Rebecca Jones, Ph.D., whose understanding of the social brain was fundamental to clearing up misconceptions about gluten's role on and in the brain. And always, my family, especially David, deserves the deepest thanks for their endless patience and humor as gut disorders became the main topic of conversation at dinner.
—Rory Jones, M.S.
Finally, we both want to express special thanks to:
Our editor, Jennifer Civiletto, who patiently, tirelessly, and ferociously championed this book from its conceptual infancy, and expertly guided it with a steady hand to completion; Faith Hamlin, our agent, who knew that gluten was ready for its close-up and shepherded us as well as the book into print. Last, we both want to thank the many patients and friends who so generously gave us their time, insights, and opinions—and openly shared personal and often difficult stories about gluten and gluten-related disorders. We remain impressed by their resilience and desire to help others by sharing their medical journeys. This book is for you, and for the many people still making the journey to diagnosis.
APPENDIX A
Diets Through the Ages
Diets have been practiced since the beginning of time—not always by choice.
**Approximately 150,000 BC—The Neanderthal (aka Paleo) Diet**
Lacking an abundance of food, Neanderthals ate whatever they could hunt or forage. Luck meant a mammoth or small deer, but their protein was limited and they had periods of near starvation. Despite the "paleofantasy" of the raw food diet, Neanderthals ate both cooked and raw meats as well as foraged tubers, plants, wild grains, and fruits.
**Approximately 10,000 BC—Agriculture Arrives**
Cultivated grains were added to the diet during the agricultural revolution, but wild grains were part of the early human diet before that.
**Ancient Greeks and Romans—The Original Mediterranean Diet**
_Mens sana in corpore sana_ —a healthy mind in a healthy body.
The Ancient Greeks and Romans left records of weight loss diets. Prescriptions for weight loss included vomiting, purgation (enema or laxative), worry, hard beds, heat, vigorous exercise, and eating sour and harsh things. Sour foods were often tainted or bad, which circled back to vomiting . . .
Pliny the Elder based his dietary advice on wine. To gain weight, drink wine with meals; to lose it, avoid wine with meals.
**Middle Ages—Anti-Sin Diets**
Some of the first diets came from the religious crusades against sin. Gluttony was one of the seven deadly sins, and hermits and monks seeking to cleanse mind and body ate a normal diet for five days and fasted for two.
Saint Catherine of Siena denied herself food as part of the spiritual denial of self.
People in the Middle Ages were also known to binge and purge in order to eat more at a meal. Now this is called bulimia.
**Circa 1829—Vegetarian Diet**
Sylvester Graham, an ordained preacher and dietary reformer, created the first vegetarian diet. Consisting mainly of fruits, vegetables, whole wheat, and high-fiber foods, limited amounts of milk products and eggs, and no meat or spices, the diet was believed to prevent "impure thought and in turn . . . stop masturbation," which Graham believed to cause blindness and early death. Graham is known more for the cracker named after him, a staple of the diet.
**Circa 1850s—The First Low-Carb Diet**
William Harvey treated English undertaker William Banting for obesity. Based on a diabetes management regime he had learned about in Paris, Harvey advised Banting to cut down on sugars and starches. This appears to be the first low-carb diet.
**Circa Late 1800s—The Chew and/or Spit Diet**
William Gladstone, Britain's prime minister, advised that food must be chewed 32 times before swallowed. The theory was based on the principle that the chewing could lessen one's appetite, which would lead to weight loss. By the turn of the 20th century, Horace Fletcher advocated the "chew and spit" diet, which recommended chewing food until all the "goodness" was extracted and then spitting the rest out. Now this is called an eating disorder.
**Early 1900s—The Tapeworm Diet**
Although later credited to opera singer Maria Callas, the tapeworm diet involves swallowing a parasite-packed pill (or live parasites). Side effects include weight gain (those worms are hungry), pain, nausea, malnutrition, vitamin deficiencies, diarrhea, and weakness. Tapeworms can grow up to 30 feet.
**1918—The Calorie Goes Mainstream**
Wilbur Atwater, an American chemist, discovered the energy provided by food and its caloric value in the late 1880s. It was not until 1918 that the concept went mainstream, when Dr. Lulu Hunt Peters wrote a bestseller that outlined the first methods of counting calories as a method to lose weight. Dr. Peters outlined 100-calorie portions of different foods and espoused counting calories to regulate weight.
**1925—The Cigarette Diet**
Lucky Strike cigarettes introduce the "Reach for a Lucky instead of a sweet" campaign, which promoted nicotine's ability to suppress appetite.
**1930s—The Grapefruit Diet**
This diet required eating grapefruit with every meal. It claimed that grapefruit had fat-burning enzymes or properties. It was normally consumed with high-fat foods. It was not until many decades later that the harmful effect of grapefruit interacting with numerous drugs came to light.
**1950s—The Cabbage Soup Diet**
This quick weight loss diet was based on consuming as much cabbage soup as you want every day with a limited amount of other foods. Most of the weight lost on this radical short-term diet is water. It created a great deal of interest and flatulence.
**Circa 1960—Macrobiotic Arrives**
The Zen or macrobiotic diet is a grain-heavy approach credited to Christoph Wilhelm Hufeland, a German doctor, and Sagen Ishizuka, a Japanese military doctor. The Japanese-style diet varies from the Western one, but both rely on whole grains, especially rice, vegetables, beans, legumes, and naturally processed foods. Fish and seafood, seeds and nuts, and fruits and beverages are allowed several times a week. Highly processed and refined foods are avoided, as are most animal products.
**1963—Weight Watchers**
Weight Watchers, founded by Jean Nidetch, is based on restricting consumption to approximately 1,000 calories per day until an optimal weight is achieved, but all foods are allowed. The group offers meetings, support material, and tracking tools to allow "members" to track their personal calorie deficits and stay on course. Dieters are given social support as well as dietary advice.
**1970s and 1980s—Drugs and Appetite Suppressants**
The appetite suppressant pill Dexatrim goes on the market. It is one of the first in a series of such drugs to come to market. Side effects such as stroke and heart attacks caused many of them to be removed from shelves.
**1977—Liquid Diets Arrive**
SlimFast becomes the first in a long line of "liquid" dietary staples. It advocates having a shake for breakfast and lunch, and then a sensible dinner. It is a grandparent of the "juicing" diet.
**1978—Dieting in Scarsdale**
Herman Tarnower, M.D., publishes _The Complete Scarsdale Medical Diet_. It is a high-protein, low-carb diet.
**1979—Pritikin: Fat Is Out**
The Pritikin Diet answers the trend of the high-protein, low-carb diets with a high-fiber, very-low-fat diet. Fat is your enemy.
**1981—Back to Hollywood: Food Is Out**
The Beverly Hills Diet recommends eating nothing but fruit for the first 10 days.
**1985—Peas at Noon, Hamburgers at Night**
Harvey and Marilyn Diamond publish _Fit for Life,_ which prohibits complex carbs and protein from being eaten during the same meal.
**1992—Atkins: Fat Is Back**
Robert C. Atkins, M.D., publishes _Dr. Atkins' New Diet Revolution_ , a high-protein, low-carb plan. Fat is your friend.
**1995—Zone: Balance Is Back**
The Zone Diet, which calls for a specific ratio of carbs, fat, and protein at each meal, ushered in the 40-30-30 ratio of carbs, fat, and protein.
**1996—Blood Types Are In**
_Eat Right for Your Type_ by Peter J. D'Adamo paired diets with blood type.
**2000—Macrobiotic Is Back**
The Macrobiotic Diet is popularized by celebrities who prefer the restrictive Japanese plan based on whole grains and veggies.
**2003—South Beach: "White Foods" Are Out**
Miami doctor Arthur Agatston, M.D., publishes _The South Beach Diet_ , seen as a more moderate version of Atkins. "White foods" (carbs) are off the menu.
**2010—Paleo Is Back as Fantasy**
_The Paleo Diet, The Paleo Solution,_ and _The Primal Blueprint_ books urge people to get in touch with their inner meat lover, ignoring the archeological evidence that early man also ate plants, vegetables, grains, and fruit.
**Circa 2010—Gluten Is Out**
With the rise in awareness of celiac disease and the popularity of _Wheat Belly, Grain Brain,_ and Miley Cyrus, gluten has become the target of much hype and bad publicity.
**Today—Take Your Pick**
Raw food diet
Vegan—forgoing all animal products
Vegetarian
Anti-inflammatory diet of Dr. Andrew Weil
Low-FODMAP
Master Cleanse (lemonade diet)
Juicing diet
Gluten-free diet
Atkins
Weight Watchers
The Whole30
Orthorexia
**Bottom Line: What goes around, comes around.**
APPENDIX B
Resources
There are numerous resources available for people interested in more information on specific medical conditions. Any medical information obtained via national foundations, support groups, and/or professional groups should be used only for informational purposes. We are not endorsing its use for diagnostic or treatment purposes, which can only be obtained through appropriate medical and professional consultation.
The following listings contain contact information that is accurate at time of publication. Website addresses and links may change.
General Information
**National Digestive Diseases Information Clearinghouse (NDDIC)**
A service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health
http://digestive.niddk.nih.gov/index.htm
**United States National Library of Medicine**
A service of the U.S. National Library of Medicine and the National Institutes of Health. Links to PubMed and MedlinePlus
www.nlm.nih.gov
www.nlm.nih.gov/medlineplus
**Gluten Free Watchdog**
A site that makes information on state-of-the-art testing of products for gluten available to the consumer
www.glutenfreewatchdog.org
Books
There are several medical, dietary, and lifestyle books that deal with different aspects of the gluten-free diet as well as the different conditions associated with its ingestion. This brief list contains publications mentioned in the text and others that provide background on the issues discussed.
Blaser, Martin J. _Missing Microbes._ New York: Henry Holt & Co., 2014.
Case, Shelley RD, R.D. _Gluten Free: The Definitive Resource Guide._ Regina, Saskatchewan, Canada: Case Nutrition Consulting, Inc., 2016.
Gershon, Michael D. _The Second Brain_. New York: HarperCollins, 1998.
Hillson, Beth. _Gluten-Free Makeovers_. Boston: Da Capo Lifelong Books, 2011.
Lieberman, Daniel E. _The Story of the Human Body_. New York: Pantheon Books, 2013.
Papagianni, Dimitra, and Michael A. Morse. _The Neanderthals Rediscovered._ London: Thames and Hudson Ltd., 2013.
Roberts, Annalise. _Gluten Free Baking Classics_. Surrey: Agate, 2008.
Scarlata, Kate. _The Complete Idiot's Guide to Eating Well with IBS (Idiot's_ _Guides)._ New York: Penguin Group, 2010.
Support Groups
There are a number of support groups for disease-specific information and advice. Several focus on gluten-related issues.
**Celiac Disease Foundation**
Patient and physician education, advocacy and research
www.celiac.org
**Gluten Intolerance Group**
www.gluten.org
**Beyond Celiac (formerly National Foundation for Celiac Awareness)**
www.celiaccentral.org
**American Diabetes Association**
www.diabetes.org
**Autism Science Foundation**
www.autismsciencefoundation.org
**Autism Speaks**
www.autismspeaks.org
APPENDIX C
Arsenic and Mercury Guidelines
The Environmental Protection Agency (EPA) and FDA have limits on the amount of arsenic in drinking water (tap and bottled) of 10 micrograms per liter. The EPA in the past set a reference dose for inorganic arsenic exposure of .3 micrograms per kilogram of body weight per day. Rice-based foods may contain inorganic arsenic. Arsenic in rice appears to be very bioavailable.
**To reduce arsenic in your diet:**
• Cook rice in large amounts of water and discard the water after cooking.
• Choose white rice instead of brown rice. Arsenic is concentrated in the outer layer of rice, which is removed to make white rice.
• If you eat flour-based gluten-free foods, limit your rice intake (most gluten-free flour-based foods will contain varying amounts of rice flour).
• Choose corn, soybean, or quinoa pasta (gluten-free) instead of pastas made from rice. Some gluten-free pastas contain a mix of grains.
• Choose crackers made from corn, tapioca, or buckwheat instead of rice.
• Choose snacks made without rice—popcorn, cheese, hummus, yogurt, etc.
• Check the arsenic content of your water.
• Do not use rice bran (it has been tested and found to have high levels of arsenic).
• Limit products sweetened with rice syrup.
• Choose gluten-free cereals, pitas, and tortillas that do not contain rice.
• Choose quinoa and other gluten-free grains (millet, buckwheat, teff) instead of rice.
**To reduce mercury in your diet:**
• Avoid tilefish, shark, swordfish, and king mackerel.
• Limit consumption of white (albacore) tuna to 6 ounces a week.
• Choose lower-mercury fish, including shrimp, pollack, salmon, canned light tuna, tilapia, catfish, and cod.
• When eating fish caught from local streams, rivers, and lakes, follow fish advisories from local authorities. If advice isn't available, limit your total intake of such fish to 6 ounces a week and 1 to 3 ounces for children.
• Limit your rice intake. Mercury is another heavy metal that can be leached from ground water.
APPENDIX D
Label Guidelines for Eating Gluten-Free
**The following ingredients must be avoided by those with celiac disease:**
• Wheat (in all its forms, including kamut, semolina, spelt/farro, triticale, bulgur, durum, einkorn, emmer, farina, atta/chapati flour)
• Oats (unless labeled gluten-free)
• Rye
• Barley (malt)
• Brewer's yeast
**These additives in FDA-regulated foods are generally safe for those with celiac disease:**
• Artificial color and flavor
• Baking powder
• Baking soda
• Caramel color
• Citric acid
• Dextrin
• Hydrolyzed soy protein
• Maltodextrin
• Modified food starch
• Mono- and diglycerides
• Monosodium glutamate
• Natural and artificial color and flavor
• Soy, soy protein
• Soy lecithin
• Vanilla, vanilla extract
• Vinegar (no malt vinegar)
• Whey
**In USDA foods not labeled gluten-free, check for the following ingredients (and contact the manufacturer if necessary to confirm the product is gluten-free):**
• Dextrin
• Starch, modified food starch
APPENDIX E
Scientific Articles and Studies
There are several celiac disease experts in most countries who publish in scientifically reputable journals on a variety of topics related to gluten, and their articles can be found on PubMed. The following is a listing of some of the more recent research on the topic.
Most of Dr. Green's articles are available through the website of the Celiac Disease Center at Columbia, www.celiacdiseasecenter.columbia.edu.
An abstract or summary of the following articles is also available on www.ncbi.nlm.nih.gov/pubmed.
Extraintestinal Manifestations of Coeliac Disease. Leffler DA, Green PH, Fasano A. _Nat Rev Gastroenterol Hepatol_. 2015 Aug 11.
Gluten Introduction, Breastfeeding, and Celiac Disease: Back to the Drawing Board. Lebwohl B, Murray JA, Verdú EF, Crowe SE, Dennis M, Fasano A, Green PH, Guandalini S, Khosla C. _Am J Gastroenterol_. 2015 Aug 11.
Attitudes Toward Genetic Testing for Celiac Disease. Roy A, Pallai M, Lebwohl B, Taylor AK, Green PH. _J Genet Couns_. 2015 Aug 2.
Protein Tyrosine Phosphatase PTPRS Is an Inhibitory Receptor on Human and Murine Plasmacytoid Dendritic Cells. Bunin A, Sisirak V, Ghosh HS, Grajkowska LT, Hou ZE, Miron M, Yang C, Ceribelli M, Uetani N, Chaperot L, Plumas J, Hendriks W, Tremblay ML, Häcker H, Staudt LM, Green PH, Bhagat G, Reizis B. _Immunity_. 2015 Aug 18;43(2):277–88.
Coeliac Disease: The Association Between Quality of Life and Social Support Network Participation. Lee AR, Wolf R, Contento I, Verdeli H, Green PH. _J Hum Nutr Diet_. 2015 Jul 21.
Cardiovascular Disease in Patients with Coeliac Disease: A Systematic Review and Meta-Analysis. Emilsson L, Lebwohl B, Sundström J, Ludvigsson JF. _Dig Liver Dis_. 2015 Jun 16.
Celiac Crisis in a 64-Year-Old Woman: An Unusual Cause of Severe Diarrhea, Acidosis, and Malabsorption. Mrad RA, Ghaddara HA, Green PH, El-Majzoub N, Barada KA. _ACG Case Rep J_. 2015 Jan 16;2(2):95–7.
Trends in Celiac Disease Research. Ciaccio EJ, Bhagat G, Lewis SK, Green PH. _Comput Biol Med_. 2015 Jun 5.
Blockers of Angiotensin Other Than Olmesartan in Patients with Villous Atrophy: A Nationwide Case-Control Study. Mårild K, Lebwohl B, Green PH, Murray JA, Ludvigsson JF. _Mayo Clin Proc_. 2015 Jun;90(6):730–7.
Distinct and Synergistic Contributions of Epithelial Stress and Adaptive Immunity to Functions of Intraepithelial Killer Cells and Active Celiac Disease. Setty M, Discepolo V, Abadie V, Kamhawi S, Mayassi T, Kent A, Ciszewski C, Maglio M, Kistner E, Bhagat G, Semrad C, Kupfer SS, Green PH, Guandalini S, Troncone R, Murray JA, Turner JR, Jabri B. _Gastroenterology_. 2015 May 19.
Suggestions for Automatic Quantitation of Endoscopic Image Analysis to Improve Detection of Small Intestinal Pathology in Celiac Disease Patients. Ciaccio EJ, Bhagat G, Lewis SK, Green PH. _Comput Biol Med_. 2015 Apr 24.
The Coeliac Stomach: Gastritis in Patients with Coeliac Disease. Lebwohl B, Green PH, Genta RM. _Aliment Pharmacol Ther_. 2015 Jul;42(2):180–7.
Risk of Neuropathy Among 28,232 Patients with Biopsy-Verified Celiac Disease. Thawani SP, Brannagan TH 3rd, Lebwohl B, Green PH, Ludvigsson JF. _JAMA Neurol_. 2015 Jul 1;72(7):806–11.
Celiac Disease. Green PH, Lebwohl B, Greywoode R. _J Allergy Clin Immunol_. 2015 May;135(5):1099–106.
Clinical Manifestations of Celiac Disease. Green PH, Krishnareddy S, Lebwohl B. _Dig Dis_. 2015;33(2):137–40.
Celiac Disease and the Forgotten 10%: The "Silent Minority." Lebwohl B. _Dig Dis Sci_. 2015 Jun;60(6):1517–8.
Abnormal Skeletal Strength and Microarchitecture in Women with Celiac Disease. Stein EM, Rogers H, Leib A, McMahon DJ, Young P, Nishiyama K, Guo XE, Lewis S, Green PH, Shane E. _J Clin Endocrinol Metab_. 2015 Jun;100(6):2347–53.
Cost Effectiveness of Routine Duodenal Biopsy Analysis for Celiac Disease During Endoscopy for Gastroesophageal Reflux. Yang JJ, Thanataveerat A, Green PH, Lebwohl B. _Clin Gastroenterol Hepatol_. 2015 Aug;13(8):1437–43.
Exploring the Strange New World of Non-Celiac Gluten Sensitivity. Lebwohl B, Leffler DA. _Clin Gastroenterol Hepatol_. 2015 Sep;13(9):1613–5.
Quantitative Image Analysis of Celiac Disease. Ciaccio EJ, Bhagat G, Lewis SK, Green PH. _World J Gastroenterol_. 2015 Mar 7;21(9):2577–81.
Increased Risk of Esophageal Eosinophilia and Eosinophilic Esophagitis in Patients with Active Celiac Disease on Biopsy. Jensen ET, Eluri S, Lebwohl B, Genta RM, Dellon ES. _Clin Gastroenterol Hepatol_. 2015 Aug;13(8):1426–31.
Larazotide Acetate for Persistent Symptoms of Celiac Disease Despite a Gluten-Free Diet: A Randomized Controlled Trial. Leffler DA, Kelly CP, Green PH, Fedorak RN, DiMarino A, Perrow W, Rasmussen H, Wang C, Bercik P, Bachir NM, Murray JA. _Gastroenterology_. 2015 Jun;148(7):1311–9.
Endoscopic Biopsy Technique in the Diagnosis of Celiac Disease: One Bite or Two? Latorre M, Lagana SM, Freedberg DE, Lewis SK, Lebwohl B, Bhagat G, Green PH. _Gastrointest Endosc_. 2015 May;81(5):1228–33.
Mucosal Healing and the Risk of Ischemic Heart Disease or Atrial Fibrillation in Patients with Celiac Disease; a Population-Based Study. Lebwohl B, Emilsson L, Fröbert O, Einstein AJ, Green PH, Ludvigsson JF. _PLoS One_. 2015 Jan 30;10(1):e0117529.
Increased Risk of Non-Alcoholic Fatty Liver Disease After Diagnosis of Celiac Disease. Reilly NR, Lebwohl B, Hultcrantz R, Green PH, Ludvigsson JF. _J Hepatol_. 2015 Jun;62(6):1405–11.
Mucosal Healing in Patients with Celiac Disease and Outcomes of Pregnancy: A Nationwide Population-Based Study. Lebwohl B, Stephansson O, Green PH, Ludvigsson JF. _Clin Gastroenterol Hepatol_. 2015 Jun;13(6):1111–7.
The Impact of Proton Pump Inhibitors on the Human Gastrointestinal Microbiome. Freedberg DE, Lebwohl B, Abrams JA. _Clin Lab Med_. 2014 Dec;34(4):771–85.
Seroprevalence of Celiac Disease Among United Arab Emirates Healthy Adult Nationals: A Gender Disparity. Abu-Zeid YA, Jasem WS, Lebwohl B, Green PH, ElGhazali G. _World J Gastroenterol_. 2014 Nov 14;20(42):15830–6.
Assessing Bowel Preparation Quality Using the Mean Number of Adenomas Per Colonoscopy. Hillyer GC, Lebwohl B, Rosenberg RM, Neugut AI, Wolf R, Basch CH, Mata J, Hernandez E, Corley DA, Shea S, Basch CE. _Therap Adv Gastroenterol_. 2014 Nov;7(6):238–46.
Sprue-Like Histology in Patients with Abdominal Pain Taking Olmesartan Compared with Other Angiotensin Receptor Blockers. Lagana SM, Braunstein ED, Arguelles-Grande C, Bhagat G, Green PH, Lebwohl B. _J Clin Pathol_. 2015 Jan;68(1):29–32.
Specific Nongluten Proteins of Wheat Are Novel Target Antigens in Celiac Disease Humoral Response. Huebener S, Tanaka CK, Uhde M, Zone JJ, Vensel WH, Kasarda DD, Beams L, Briani C, Green PH, Altenbach SB, Alaedini A. _J Proeome Res_. 2015 Jan 2;14(1):503–11.
Editorial: Sprue-Like Enteropathy Due to Olmesartan and Other Angiotensin Receptor Blockers—the Plot Thickens. Lebwohl B, Ludvigsson JF. _Aliment Pharmacol Ther_. 2014 Nov;40(10):1245–6.
Editorial: Mucosal Healing and Adherence to the Gluten-Free Diet in Coeliac Disease. Lebwohl B, Ludvigsson JF. _Aliment Pharmacol Ther_. 2014 Nov;40(10):1241–2.
The Missing Environmental Factor in Celiac Disease. Ludvigsson JF, Green PH. _N Engl J Med_. 2014 Oct 2;371(14):1341–3.
Use of Basis Images for Detection and Classification of Celiac Disease. Ciaccio EJ, Tennyson CA, Bhagat G, Lewis SK, Green PH. _Biomed Mater Eng_. 2014;24(6):1913–23.
Methods to Quantitate Videocapsule Endoscopy Images in Celiac Disease. Ciaccio EJ, Tennyson CA, Bhagat G, Lewis SK, Green PH. _Biomed Mater Eng_. 2014;24(6):1895–911.
Risk of Celiac Disease According to HLA Haplotype and Country. Lebwohl B, Green P. _N Engl J Med_. 2014 Sep 11;371(11):1073–4.
Dietary Supplement Use in Patients with Celiac Disease in the United States. Nazareth S, Lebwohl B, Tennyson CA, Simpson S, Greenlee H, Green PH. _J Clin Gastroenterol_. 2015 Aug;49(7):577–81.
Rates of Suboptimal Preparation for Colonoscopy Differ Markedly Between Providers: Impact on Adenoma Detection Rates. Mahadev S, Green PH, Lebwohl B. _J Clin Gastroenterol_. 2014 Aug 20.
Editorial: "Brain Fog" and Coeliac Disease—Evidence for Its Existence. Lebwohl B, Ludvigsson JF. _Aliment Pharmacol Ther_. 2014 Sep;40(5):565.
Olmesartan, Other Antihypertensives, and Chronic Diarrhea Among Patients Undergoing Endoscopic Procedures: A Case-Control Study. Greywoode R, Braunstein ED, Arguelles-Grande C, Green PH, Lebwohl B. _Mayo Clin Proc_. 2014 Sep;89(9):1239–43.
Isotretinoin Use and Celiac Disease: A Population-Based Cross-Sectional Study. Lebwohl B, Sundström A, Jabri B, Kupfer SS, Green PH, Ludvigsson JF. _Am J Clin Dermatol_. 2014 Dec;15(6):537–42.
Genome-Wide Association Study of Celiac Disease In North America Confirms FRMD4B as New Celiac Locus. Garner C, Ahn R, Ding YC, Steele L, Stoven S, Green PH, Fasano A, Murray JA, Neuhausen SL. _PLoS One_. 2014 Jul 7;9(7):e101428.
Diagnosis and Management of Adult Coeliac Disease: Guidelines from the British Society of Gastroenterology. Ludvigsson JF, Bai JC, Biagi F, Card TR, Ciacci C, Ciclitira PJ, Green PH, Hadjivassiliou M, Holdoway A, van Heel DA, Kaukinen K, Leffler DA, Leonard JN, Lundin KE, McGough N, Davidson M, Murray JA, Swift GL, Coeliac Disease Guidelines Development Group; British Society of Gastroenterology. Walker MM, Zingone F, Sanders DS; BSG _Gut_. 2014 Aug;63(8):1210–28.
How Often Do Hematologists Consider Celiac Disease in Iron-Deficiency Anemia? Results of a National Survey. Smukalla S, Lebwohl B, Mears JG, Leslie LA, Green PH. _Clin Adv Hematol Oncol_. 2014 Feb;12(2):100–5.
Development and Validation of a Clinical Prediction Score (the SCOPE Score) to Predict Sedation Outcomes in Patients Undergoing Endoscopic Procedures. Braunstein ED, Rosenberg R, Gress F, Green PH, Lebwohl B. _Aliment Pharmacol Ther_. 2014 Jul;40(1):72–82.
Utilizing HDL Levels to Improve Detection of Celiac Disease in Patients with Iron Deficiency Anemia. Abu Daya H, Lebwohl B, Smukalla S, Lewis SK, Green PH. _Am J Gastroenterol_. 2014 May;109(5):769–70.
Risk of Cutaneous Malignant Melanoma in Patients with Celiac Disease: A Population-Based Study. Lebwohl B, Eriksson H, Hansson J, Green PH, Ludvigsson JF. _J Am Acad Dermatol_. 2014 Aug;71(2):245–8.
Issues Associated with the Emergence of Coeliac Disease in the Asia–Pacific Region: A Working Party Report of the World Gastroenterology Organization and the Asian Pacific Association of Gastroenterology. Makharia GK, Mulder CJ, Goh KL, Ahuja V, Bai JC, Catassi C, Green PH, Gupta SD, Lundin KE, Ramakrishna BS, Rawat R, Sharma H, Sood A, Watanabe C, Gibson PR; World Gastroenterology Organization-Asia Pacific Association of Gastroenterology Working Party on Celiac Disease. _J Gastroenterol Hepatol_. 2014 Apr;29(4):666–77.
Lack of Serologic Evidence to Link IgA Nephropathy with Celiac Disease or Immune Reactivity to Gluten. Moeller S, Canetta PA, Taylor AK, Arguelles-Grande C, Snyder H, Green PH, Kiryluk K, Alaedini A. _PLoS One_. 2014 Apr 14;9(4):e94677.
No Association Between Biopsy-Verified Celiac Disease and Subsequent Amyotrophic Lateral Sclerosis—a Population-Based Cohort Study. Ludvigsson JF, Mariosa D, Lebwohl B, Fang F. _Eur J Neurol_. 2014 Jul;21(7):976–82.
Re: "Decreased Risk of Celiac Diseasei Patients with Helicobacter Pylori Colonization." The Authors Reply. Lebwohl B, Blaser MJ, Ludvigsson JF, Green PH, Rundle A, Sonnenberg A, Genta RM. _Am J Epidemiol_. 2014 May 15;179(10):1275–6.
Characteristics Associated with Suboptimal Bowel Preparation Prior to Colonoscopy: Results of a National Survey. Basch CH, Hillyer GC, Basch CE, Lebwohl B, Neugut AI. _Int J Prev Med_. 2014 Feb;5(2):233–7.
Prediction of Celiac Disease at Endoscopy. Barada K, Habib RH, Malli A, Hashash JG, Halawi H, Maasri K, Tawil A, Mourad F, Sharara AI, Soweid A, Sukkarieh I, Chakhachiro Z, Jabbour M, Fasano A, Santora D, Arguelles C, Murray JA, Green PH. _Endoscopy_. 2014 Feb;46(2):110–9.
Celiac Disease Is Diagnosed Less Frequently in Young Adult Males. Dixit R, Lebwohl B, Ludvigsson JF, Lewis SK, Rizkalla-Reilly N, Green PH. _Dig Dis Sci_. 2014 Jul;59(7):1509–12.
Persistent Mucosal Damage and Risk of Fracture in Celiac Disease. Lebwohl B, Michaëlsson K, Green PH, Ludvigsson JF. _J Clin Endocrinol Metab_. 2014 Feb;99(2):609–16.
Predictors of Persistent Villous Atrophy in Coeliac Disease: A Population-Based Study. Lebwohl B, Murray JA, Rubio-Tapia A, Green PH, Ludvigsson JF. _Aliment Pharmacol Ther_. 2014 Mar;39(5):488–95.
Characteristics of Patients Who Avoid Wheat and/or Gluten in the Absence of Celiac Disease. Tavakkoli A, Lewis SK, Tennyson CA, Lebwohl B, Green PH. _Dig Dis Sci_. 2014 Jun;59(6):1255–61.
_Dermatitis herpetiformis:_ Clinical Presentations Are Independent of Manifestations of Celiac Disease. Krishnareddy S, Lewis SK, Green PH. _Am J Clin Dermatol_. 2014 Feb;15(1):51–6.
The Unfolding Story of Celiac Disease Risk Factors. Lebwohl B, Ludvigsson JF, Green PH. _Clin Gastroenterol Hepatol_. 2014 Apr;12(4):632–5.
Screening Colonoscopy Bowel Preparation: Experience in an Urban Minority Population. Basch CH, Basch CE, Wolf RL, Zybert P, Lebwohl B, Shmukler C, Neugut AI, Shea S. _Therap Adv Gastroenterol_. 2013 Nov;6(6):442–6.
Decreased Risk of Celiac Disease in Patients with _Helicobacter pylori_ Colonization. Lebwohl B, Blaser MJ, Ludvigsson JF, Green PH, Rundle A, Sonnenberg A, Genta RM. _Am J Epidemiol_. 2013 Dec 15;178(12):1721–30.
Lack of Association Between Autism and Anti-GM1 Ganglioside Antibody. Moeller S, Lau NM, Green PH, Hellberg D, Higgins JJ, Rajadhyaksha AM, Alaedini A. _Neurology_. 2013 Oct 29;81(18):1640–1.
Use of Proton Pump Inhibitors and Subsequent Risk of Celiac Disease. Lebwohl B, Spechler SJ, Wang TC, Green PH, Ludvigsson JF. _Dig Liver Dis_. 2014 Jan;46(1):36–40.
Interest in Medical Therapy for Celiac Disease. Tennyson CA, Simpson S, Lebwohl B, Lewis S, Green PH. _Therap Adv Gastroenterol_. 2013 Sep;6(5):358–64.
Mucosal Healing and Risk For Lymphoproliferative Malignancy in Celiac Disease: A Population-Based Cohort Study. Lebwohl B, Granath F, Ekbom A, Smedby KE, Murray JA, Neugut AI, Green PH, Ludvigsson JF. _Ann Intern Med_. 2013 Aug 6;159(3):169–75.
Antibiotic Exposure and the Development of Coeliac Disease: A Nationwide Case-Control Study. Mårild K, Ye W, Lebwohl B, Green PH, Blaser MJ, Card T, Ludvigsson JF. _BMC Gastroenterol_. 2013 Jul 8;13:109.
Prevalence of Gluten-Free Diet Adherence Among Individuals Without Celiac Disease in the USA: Results from the Continuous National Health and Nutrition Examination Survey 2009–2010. DiGiacomo DV, Tennyson CA, Green PH, Demmer RT. _Scand J Gastroenterol_. 2013 Aug;48(8):921–5.
Markers of Celiac Disease and Gluten Sensitivity in Children with Autism. Lau NM, Green PH, Taylor AK, Hellberg D, Ajamian M, Tan CZ, Kosofsky BE, Higgins JJ, Rajadhyaksha AM, Alaedini A. _PLoS One_. 2013 Jun 18;8(6):e66155.
Post-Colonoscopy Recommendations after Inadequate Bowel Preparation: All in the Timing. Lebwohl B, Neugut AI. _Dig Dis Sci_. 2013 Aug;58(8):2135–7.
Celiac Disease Patients Presenting with Anemia Have More Severe Disease Than Those Presenting with Diarrhea. Abu Daya H, Lebwohl B, Lewis SK, Green PH. _Clin Gastroenterol Hepatol_. 2013 Nov;11(11):1472–7.
Men with Celiac Disease Are Shorter Than Their Peers in the General Population. Sonti R, Lebwohl B, Lewis SK, Abu Daya H, Klavan H, Aguilar K, Green PH. _Eur J Gastroenterol Hepatol_. 2013 Sep;25(9):1033–7.
Development and Validation of a Celiac Disease Quality of Life Instrument for North American Children. Jordan NE, Li Y, Magrini D, Simpson S, Reilly NR, Defelice AR, Sockolow R, Green PH. _J Pediatr Gastroenterol Nutr_. 2013 Oct;57(4):477–86.
Is Dietitian Use Associated with Celiac Disease Outcomes? Mahadev S, Simpson S, Lebwohl B, Lewis SK, Tennyson CA, Green PH. _Nutrients_. 2013 May 15;5(5):1585–94.
Celiac Disease in Patients with Type 1 Diabetes: Screening and Diagnostic Practices. Simpson SM, Ciaccio EJ, Case S, Jaffe N, Mahadov S, Lebwohl B, Green PH. _Diabetes Educ_. 2013 Jul-Aug;39(4):532–40.
Gastrointestinal Dysfunction in Autism: Parental Report, Clinical Evaluation, and Associated Factors. Gorrindo P, Williams KC, Lee EB, Walker LS, McGrew SG, Levitt P. _Autism Res._ 2012 Apr;5(2):101–8.
Rigid-Compulsive Behaviors Are Associated with Mixed Bowel Symptoms in Autism Spectrum Disorder. Peters B, Williams KC, Gorrindo P, Rosenberg D, Lee EB, Levitt P, Veenstra-VanderWeele J. _J Autism Dev Disord._ 2014 Jun;44(6).
Cognitive Impairment in Coeliac Disease Improves on a Gluten-Free Diet and Correlates with Histological and Serological Indices of Disease Severity. Lichtwark IT, Newnham ED, Robinson SR, Shepherd SJ, Hosking P, Gibson PR, Yelland GW. _Aliment Pharmacol Ther._ 2014 Jul;40(2):160–70.
Effects of a Gluten-Free Diet on Gut Microbiota and Immune Function in Healthy Adult Human Subjects. De Palma, Giada; Nadal, Inmaculada; Collado, Maria Carmen; Sanz, Yolanda. _The British Journal of Nutrition._ 102.8 (Oct 28, 2009): 1154–60.
Gluten Contamination of Commercial Oat Products in the United States. Trisha Thompson, M.S., R.D. _N Engl J Med._ 2004; 351:2021–2.
A Nationwide Population-Based Study on the Risk of Coma, Ketoacidosis and Hypoglycemia in Patients with Celiac Disease and Type 1 Diabetes. Kurien M, Mollazadegan K, Sanders DS, Ludvigsson JF. _Acta Diabetol._ 2015 Dec;52(6):1167–74.
Editorial: Adherence in Coeliac Disease—Those That Can Will and Those That Can't Won't (and Need Support)! Kurien M, Sanders DS. _Aliment Pharmacol Ther._ 2015 Oct;42(7):934–5.
Cost and Availability of Gluten-Free Food in the UK: In Store and Online. Burden M, Mooney PD, Blanshard RJ, White WL, Cambray-Deakin DR, Sanders DS. _Postgrad Med J_. 2015 Nov;91(1081):622–6.
Noncoeliac Gluten Sensitivity: A Diagnostic Dilemma. Branchi F, Aziz I, Conte D, Sanders DS. _Curr Opin Clin Nutr Metab Care_. 2015 Sep;18(5):508–14.
The Spectrum of Noncoeliac Gluten Sensitivity. Aziz I, Hadjivassiliou M, Sanders DS. _Nat Rev Gastroenterol Hepatol_. 2015 Sep;12(9):516–26.
Gastro-Oesophageal Reflux Symptoms and Coeliac Disease: No Role for Routine Duodenal Biopsy. Mooney PD, Evans KE, Kurien M, Hopper AD, Sanders DS. _Eur J Gastroenterol Hepatol._ 2015 Jun;27(6):692–7.
Support for Patients with Celiac Disease: A Literature Review. Ludvigsson JF, Card T, Ciclitira PJ, Swift GL, Nasr I, Sanders DS, Ciacci C. _United European Gastroenterol J._ 2015 Apr;3(2):146–59.
Psychological Morbidity of Celiac Disease: A Review of the Literature. Zingone F, Swift GL, Card TR, Sanders DS, Ludvigsson JF, Bai JC. _United European Gastroenterol J_. 2015 Apr;3(2):136–45.
The Gluten-Free Diet and Its Current Application in Coeliac Disease and _Dermatitis herpetiformis_. Ciacci C, Ciclitira P, Hadjivassiliou M, Kaukinen K, Ludvigsson JF, McGough N, Sanders DS, Woodward J, Leonard JN, Swift GL. _United European Gastroenterol_ J. 2015 Apr;3(2):121–35.
Screening for Celiac Disease in the General Population and in High-Risk Groups. Ludvigsson JF, Card TR, Kaukinen K, Bai J, Zingone F, Sanders DS, Murray JA. _United European Gastroenterol J_. 2015 Apr;3(2):106–20.
Small-Bowel Capsule Endoscopy and Device-Assisted Enteroscopy for Diagnosis and Treatment of Small-Bowel Disorders: European Society of Gastrointestinal Endoscopy (ESGE) Clinical Guideline. Pennazio M, Spada C, Eliakim R, Keuchel M, May A, Mulder CJ, Rondonotti E, Adler SN, Albert J, Baltes P, Barbaro F, Cellier C, Charton JP, Delvaux M, Despott EJ, Domagk D, Klein A, McAlindon M, Rosa B, Rowse G, Sanders DS, Saurin JC, Sidhu R, Dumonceau JM, Hassan C, Gralnek IM. _Endoscopy_. 2015 Apr;47(4):352–76.
Prevalence of Idiopathic Bile Acid Diarrhea Among Patients with Diarrhea-Predominant Irritable Bowel Syndrome Based on Rome III Criteria. Aziz I, Mumtaz S, Bholah H, Chowdhury FU, Sanders DS, Ford AC. High _Clin Gastroenterol Hepatol_. 2015 Sep;13(9):1650–5.e2.
Systematic Review: Noncoeliac Gluten Sensitivity. Molina-Infante J, Santolaria S, Sanders DS, Fernández-Bañares F. _Aliment Pharmacol Ther_. 2015 May;41(9):807–20.
A Study Evaluating the Bidirectional Relationship Between Inflammatory Bowel Disease and Self-Reported Non-Celiac Gluten Sensitivity. Aziz I, Branchi F, Pearson K, Priest J, Sanders DS. _Inflamm Bowel Dis._ 2015 Apr;21(4):847–53.
The Rise and Fall of Gluten! Aziz I, Branchi F, Sanders DS. _Proc Nutr Soc._ 2015 Aug;74(3):221–6.
Editorial: Is a Histological Diagnosis Mandatory for Adult Patients with Suspected Coeliac Disease? Kurien M, Mooney PD, Sanders DS. _Aliment Pharmacol Ther_. 2015 Jan;41(1):146–7.
A No Biopsy Strategy for Adult Patients with Suspected Coeliac Disease: Making the World Gluten-Free. Kurien M, Ludvigsson JF, Sanders DS; authors of the BSG guidelines. _Gut._ 2015 Jun;64(6):1003–4.
Support for Patients with Celiac Disease: A Literature Review. Ludvigsson JF, Card T, Ciclitira PJ, Swift GL, Nasr I, Sanders DS, Ciacci C. _United European Gastroenterol J._ 2015 Apr;3(2):146–59.
Gastrointestinal Effects of Eating Quinoa ( _Chenopodium quinoa Willd_.) in Celiac Patients. Zevallos VF, Herencia LI, Chang F, Donnelly S, Ellis HJ, Ciclitira PJ. _Am J Gastroenterol_. 2014 Feb;109(2):270–8.
Evaluation of the Safety of Ancient Strains of Wheat in Coeliac Disease Reveals Heterogeneous Small Intestinal T Cell Responses Suggestive of Coeliac Toxicity. Šuligoj T, Gregorini A, Colomba M, Ellis HJ, Ciclitira PJ. _Clin Nutr._ 2013 Dec;32(6):1043–9.
Celiac Disease: Management of Persistent Symptoms in Patients on a Gluten-Free Diet. Dewar DH, Donnelly SC, McLaughlin SD, Johnson MW, Ellis HJ, Ciclitira PJ. _World J Gastroenterol,_ 2012 Mar 28;18(12):1348–56.
Pharmacotherapy and Management Strategies for Coeliac Disease. Donnelly SC, Ellis HJ, Ciclitira PJ. _Expert Opin Pharmacother_. 2011 Aug;12(11):1731–44.
Electrochemical Immunosensor for Detection of Celiac Disease Toxic Gliadin in Foodstuff. Nassef HM, Bermudo Redondo MC, Ciclitira PJ, Ellis HJ, Fragoso A, O'Sullivan CK. _Anal Chem._ 2008 Dec 1;80(23):9265–71.
Glossary
**Affective disorders—** Those disorders relating to moods, feelings, and/or attitudes.
**Alleles** —The different forms of a given gene.
**Amylase** —An enzyme secreted by the salivary glands and pancreas that breaks down starches (carbohydrates) into simple sugars.
**Anaphylaxis** —A sudden, severe systemic allergic reaction to a substance that causes inflammation in various parts of the body. Symptoms can be mild or potentially life threatening. It can affect the skin, blood pressure, breathing, and digestion.
**Antibody** —Antibodies are proteins secreted by cells of the immune system. They are found in the bloodstream and body tissues and protect the body from various foreign substances and infections. (See also _Immunoglobulin_.)
**Antigen** —Any foreign material that causes your immune system to produce antibodies against it.
**Antigliadin antibodies (AGA)** —A food antibody that targets the protein found in wheat.
**Ataxia** —A balance disturbance that affects motor control and coordination. It can affect limbs, body, speech, and eye movements and is also associated with degenerative diseases of the central nervous system.
**Atherosclerosis** —A hardening of the arteries due to the buildup of plaque, cholesterol, and other substances in artery walls
**Bacteroides—** A phylum of bacterium found in the GI tract and part of our microbiota.
**Barrett's esophagus** —An abnormality of the lining of the lower esophagus due to chronic reflux, considered premalignant.
**Bifidobacteria** —One of the dominant microbial populations of the intestinal tract.
**Bile duct** —The duct that connects the liver to the small intestine and enables bile to be released into the center of the duodenum.
**Bile** —A liver secretion that aids in the digestion of fats.
**Bolus** —A lump or mass. Used in two different contexts: A bolus of partially digested food is propelled from the stomach into the duodenum. Also as in a bolus of insulin that is the extra dose of short-acting insulin taken by a diabetic before a meal or snack to control or cover the glucose in the food.
**Brush border** —The microvilli or tiny "hairs" covering the villi of the small intestine that increase the absorptive area of the small intestine, and secrete specific enzymes that aid in digestion. When the microvilli are flattened or destroyed, both of these functions are impaired or halted.
**Cerebral calcification** —A calcium deposit in the brain.
**Chyme** —A soupy solution formed in the stomach consisting of food, gastric juices, enzymes, and saliva.
**_Clostridium difficile (C. difficile_ or _C. diff_ )**—A bacterium found in the intestines. This is regarded as one of the superbugs.
**Coeliac disease** —A spelling of celiac disease commonly used outside the U.S.
**Collagenous sprue** —A lesion within the small intestine in which inflammatory cells lay down a thickened band of fibrous tissue. It can occur in any type of villous atrophy including celiac disease and intestinal inflammatory disease caused by the drug olmesartan.
**Colon** —The lower end of the digestive tract.
**Cytokines** —Protein "messengers" produced by inflammatory cells to respond to infections, which increase the inflammatory response. They are released by cells to affect the behavior of other cells.
**Dementia** —Disorientation and/or impairment of mental processes caused by disease, old age, trauma, stroke, or unknown factors. The definition of Alzheimer's dementia is different from that of dementia.
**Dendric cells** —A highly specialized white blood cell found in the skin, mucosa, and lymph tissues that initiates an immune response.
**Dermatitis herpetiformis (DH)** —An extremely itchy, blistering skin condition that is caused by IgA deposits in the layers of the skin. If you have a definitive diagnosis of DH, you have celiac disease.
**Diverticula** —Small sacs protruding from the intestinal wall that can occur anywhere in the GI tract. Most often encountered in the colon.
**Dysbiosis** —An imbalance or disruption, e.g., of the intestinal microbiota.
**Dysphagia** —Difficulty swallowing.
**Electrolytes** —Minerals in your blood and other body fluids that carry an electric charge. Electrolytes affect the amount of water in your body, the acidity of your blood (pH), your muscle function, and other important processes.
**Emulsification** —The process through which fats are broken into small particles with a surface area that can unite or bind with water in order to pass through the intestinal wall. An emulsifying agent such as phospholipids keeps the droplets from reforming back into larger drops. This is the main function of bile.
**Endoscopy** —A minimally invasive procedure during which a small tube with a built-in camera is introduced into the body either through the mouth, colon, or airway. It can be used to take pictures or take tissue samples (biopsies), remove foreign bodies, and perform other therapeutic maneuvers.
**Enteropathy** —Any inflammatory disease of the small intestine characterized by villous atrophy.
**Eosinophilic esophagitis (EOE)** —An inflammation of the esophagus that causes food to "stick" and trouble swallowing.
**Eosinophils** —A type of white blood cell often present in immune reactions and allergies.
**Epithelium** —A grouping of cells that make up most of the surfaces of the body and line the GI tract.
**Erythrocyte sedimentation rate (ESR)** —A blood test to determine levels of inflammation in the body.
**Etiology** —The origins and causes of a disease.
**Firmicutes** —A phylum of bacteria found in the GI tract and part of our microbiota, includes other classes of bacteria such as _Lactobacillus, Streptococcus,_ and _Clostridium._
**FODMAPs—** Fermentable oligosaccharides, disaccharides, monosaccharides, and polyols. The carbohydrates found in many plants, vegetables, and fruits.
**Fumonisin** —A mycotoxin or environmental toxin that is produced by various fungi and molds. It occurs in the field or during storage, mainly in corn.
**Gastric acid** —The highly effective—and highly corrosive—acid that helps to digest the food in the stomach. It is also protective against infections.
**Gastroenteritis** —Inflammation of the digestive tract by food or pathogens, resulting in gastrointestinal symptoms.
**Gastroparesis** —Delayed emptying of the stomach. May be caused by decreased intestinal motility due to diabetes, scleroderma, or celiac disease.
**GERD** —Gastroesophageal reflux disease.
**Gestational diabetes** —A type of diabetes that occurs during pregnancy and usually resolves once the baby is born.
**GI** —Gastrointestinal.
**Gliadin** —The alcohol-soluble fraction of gluten found in wheat; the most studied portion in celiac disease, but not necessarily the only toxic fraction in grains.
**Globus** —The sensation of a lump in the throat, a common symptom of GERD or anxiety.
**Glucocorticoid** —A class of steroid hormones secreted by the adrenal glands in response to signals from the brain. They mobilize and replenish energy stores.
**Gluten** —The storage protein of wheat. Essentially, the portion of wheat flour that makes it "sticky." The gluten fraction that is most studied in celiac disease is called gliadin, but there are other proteins that chemically resemble gliadin in rye (secalins) and barley (hordeins). These proteins are not strictly glutens, but are generally included in the term.
**Hiatal hernia** —A condition where part of the stomach pushes through the diaphragm into the chest cavity. It is due to an enlargement of the opening in the diaphragm through which the esophagus passes.
**Histamine receptor type 2 (H2RA) inhibitors** —An acid reducer for healing ulcers and GERD; available in prescription and nonprescription form, e.g., Tagamet, Zantac, Pepcid.
**Histamines** —Substances released into tissues and the bloodstream that produce the symptoms of allergy including inflammation, itching, swelling, etc.
**Homeostasis** —Regulation of metabolic functions so that their processes remain stable and constant.
**Hordeins** —See _Gluten_.
**Human leukocyte antigens (HLA)** —Proteins that sit on the surface of white blood cells that play an important role in the immune system by reacting with foreign substances. These proteins are genetically determined, and every person receives one set from each parent.
**Hyperglycemia** —High blood glucose levels commonly seen in diabetics who do not have enough, or any, insulin that is required to metabolize the glucose for use by the body. Usually apparent after a meal.
**Hypoglycemia** —Low blood glucose levels commonly observed when too much insulin is administered, or too little food eaten to cover the insulin given.
**Ileitis** —An inflammation of the ileum.
**Immunoglobulin (Ig)** —Proteins secreted by specific white blood cells protecting the body against bacteria and viruses.
**Immunoglobulin A (IgA)** —The antibodies secreted by plasma cells into the lining of the GI tract, tissues, and bloodstream that act locally in the lining or on the surface to disinfect our ingested food. Other classes of immunoglobulins include IgE, IgM, IgD and IgE.
**Inflammatory bowel disease (IBD)** —Chronic inflammation of the digestive tract of unclear cause. Includes both ulcerative colitis and Crohn's disease.
**Inflammatory markers** —Tests used to measure the levels of inflammation in the body; e.g., C-reactive protein (CRP), Erythrocyte sedimentation rate (ESR).
**Insulin-dependent diabetes mellitus (IDDM)** —Also known as type 1 diabetes or juvenile-onset diabetes. Characterized by the decreased or total absence of insulin.
**Irritable bowel syndrome (IBS)** —Any persistent condition with diarrhea and/or constipation, gas, and abdominal pain that is not explained by other known diseases. There are strict criteria—the Rome criteria—that define the functional bowel disorders that include IBS, dyspepsia, functional bloating, and constipation.
**Lactase** —The enzyme secreted by the brush border of the small intestine that digests milk products. It is available commercially to treat lactase deficiency.
**Lactose intolerance** —A condition where lactase is not produced by the small intestine. Secondary lactose intolerance can occur when the brush border of the small intestine is damaged or destroyed and unable to produce the enzyme.
**Lactulose** —A nonmetabolized sugar.
**Lipase(s)** —The group of enzymes that break down fats into smaller and smaller components so they are able to be absorbed by the body. It is mainly secreted by the pancreas, but also by salivary glands (lingual lipase) that starts to digest fats in the stomach.
**Lumen—** The central, hollow portion of the digestive tube that is the site for the majority of digestive action.
**Lupus or systemic lupus erythematosus (SLE)—** An autoimmune disease in which the immune system attacks the various tissues within the body, leading to organ damage and dysfunction.
**Mannitol** —A nonmetabolized sugar.
**Microbial antigen** —Antigens are proteins that sit on the surface of a pathogen (any bacteria, virus, etc., that can cause disease) and causes the body to mount an immune response. The immune system produces antibodies that destroy the pathogen.
**Microscopic colitis** —An autoimmune inflammatory condition in the colon that may be associated with celiac disease. It is characterized by diarrhea, but no infection, and can vary in severity. It is diagnosed by biopsy.
**Microvilli** —The tiny hairlike projections lining each villus that further increase its absorptive potential.
**Mucosa** —The surface or superficial lining of the wall of the intestine. The mucosa consists of the epithelial (single) cell layer, the lamina propria, and a muscle layer.
**Nerve conduction studies** —Tests for nerve damage in which signals are run through nerve paths to determine if the nerve is functioning properly (i.e., conducting the signal and eliciting an appropriate response).
**Neuropathy** —A condition caused by the inflammation of nerves, resulting in altered sensation, weakness, or an array of other symptoms.
**Olmesartan** —A blood pressure medication that can cause a severe sprue-like disease. Patients may be told they have refractory celiac disease.
**Orthorexia nervosa** —A food disorder where people eliminate one food after another in the belief that the foods are "unhealthy," to the point of malnutrition.
**Parathyroid hormone (PTH)** —The hormone responsible for maintaining normal levels of calcium in the bloodstream. PTH increases the resorption of bone, causing calcium to be released into the bloodstream and the kidneys to retain calcium in the body. It also stimulates the activation of vitamin D that increases the intestinal absorption of calcium.
**Parenteral nutrition (PN)** —Feeding a person intravenously, bypassing the usual process of eating and digestion. The person receives nutrients such as glucose, amino acids, lipids, and added vitamins and dietary minerals.
**Paresthesia** —A burning, tingling, or prickling sensation that is usually felt in different parts of the body. The sensation is usually described as tingling or numbness, skin crawling, or itching.
**Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)** —A subset of children with obsessive compulsive disorder (OCD) and/or tic disorders whose symptoms appear to be related to a streptococcus infection.
**Pepsin** —An enzyme secreted by the stomach that breaks down proteins. Part of a category of enzymes that break down protein.
**Peptidases** —A group of enzymes, such as pepsin, that breaks down proteins into smaller amino acid units.
**Peptide bonds** —The molecular bond that binds two amino acids.
**Peripheral neuropathies** —Numbness and/or tingling in the hands, face, and feet because of damaged peripheral nerves.
**Peristalsis** —The undulating contraction of the wall of the digestive tract that moves food down the digestive tube.
**Proton pump inhibitors (PPIs)** —A group of drugs whose main action is a pronounced and long-lasting reduction of gastric acid production.
**Proximal intestine** —The upper portion of the small intestine that includes the duodenum and the upper jejunum.
**Rhinitis** —Inflammation of the nasal membranes characterized by sneezing, nasal congestion, itching, and runny nose. Seasonal allergy.
**Rotavirus** —The most common cause of severe diarrhea among infants and young children.
**Salivary glands** —The mucous glands in and around the mouth that supply saliva to aid in swallowing and digestion.
**Scleroderma** —The thickening and scarring of certain tissues. It may involve skin, intestine, lungs or kidneys, and the heart. The effects depend on the organ involved.
**Selective serotonin reuptake inhibitors (SSRIs) or serotonin-specific reuptake inhibitors** —A class of drugs that block a receptor that reabsorbs serotonin, making more of it chemically available. Serotonin messaging is known to influence mood and pain perception.
**Serologies** —Blood tests. Serum (blood) is drawn and analyzed. Physicians can request specific panels (tests).
**Serotonin (5-hydroxytryptamine [5-HT])** —A biological base that functions as a neurotransmitter in the body.
**Small intestine bacterial overgrowth (SIBO)** —A disease characterized by an increase in the small intestine of bacteria that normally inhabit the colon. The bacteria cause poor fat and carbohydrate (sugar) absorption. The bacteria also use vitamin B12 for their own growth, causing B12 deficiency in the body.
**Soluble** —Able to dissolve in water. (See _Emulsification._ )
**Sphincter** —A muscle that acts as a break or valve. The esophageal and pyloric sphincter muscles control the entrance of food into the stomach and its exit into the duodenum, respectively. Spasms and/or malfunctions of these sphincters can be extremely painful and cause digestive problems.
**Spruce** —A tree.
**Sprue** —A syndrome in which there is an inflammatory disease of the intestines with villous atrophy that results in malabsorption (enteropathy). Celiac disease was formerly called celiac sprue in the U.S. It is currently used to define enteropathies such as tropical sprue, olmesartan enteropathy, and undefined sprue.
**Stricture** —An abnormal narrowing of a bodily passage (as from inflammation, cancer, or the formation of scar tissue).
**Sucrase** —Enzyme that breaks down sugars into glucose.
**Synapsin** —A protein found in the brain that regulates neurotransmitter release.
**T-cells** —A type of white blood cell that has various roles in the immune system, such as identifying specific foreign substances in the body; activating and deactivating other immune cells. A category of T-cells (CD4+ cells) plays a role in celiac disease.
**Tenesmus** —The feeling that more stool is there when, in fact, the feces are liquid and have been fully voided. A common condition in acute diarrhea.
**Tissue transglutaminase (tTG)** —An enzyme found in every tissue of the body that joins proteins together. It reacts with gliadin, setting off the chain of reactions that destroys the villi of the small intestine in celiac disease.
**Toxoplasmosis** —A parasitic disease caused by _Toxoplasma gondii_ that occurs through infected meat; ingesting water, soil, or food that has come in contact with infected animal fecal matter (commonly household cats); or through transmission from an infected mother to her fetus during pregnancy.
**tTG** —See _Tissue transglutaminase_.
**Type 1 Diabetes (IDDM)** —See _Insulin-dependent diabetes mellitus_.
**Type 2 Diabetes (NIDDM)** —A condition where the pancreas cannot make enough insulin or does not use insulin properly (insulin resistance). Glucose builds up in the blood instead of being metabolized into the cells of the body.
**Vagus nerve** —A nerve that extends from the brain stem to the gut and commands unconscious body processes such as digestion.
**Villi** —Small projections lining the wall of the small intestine that greatly increase its absorptive power; they are lined with epithelial cells covered in microvilli that absorb nutrients.
**Villus atrophy** —The inflammation and eventual flattening (loss) of the villi of the small intestine resulting in a decreased surface for absorption.
Index
The pagination of this electronic edition does not match the edition from which it was created. To locate a specific entry, please use your e-book reader's search tools.
abdominal pain, 75
absorption, 64, 71
abuse, 137–38
AGA. _See_ antigliadin antibodies
alcohol ataxia, 136–37
allergic asthma, 225
alternative medicine, 8
ALV003, 273
Alzheimer's disease, 293
amphibiosis, 91
amylase trypsin inhibitors (ATIs), 114
in celiac disease, 115
anabolic steroids, 37
anaphylaxis, 224
anemia, 159
angiotensin II receptor blockers (ARBs), 127
animals, 130–31
anorexia nervosa, 19
antibiotics, 227
animals and, 130–31
food allergies and, 129–30
obesity and, 129–30
resistance to, 8
antibodies. _See also_ antigliadin antibodies
endomysial, 171
to gluten, 54–55
monoclonal, 127
role of, 55
transfer of, 93
antidepressants, 190–91
antigliadin antibodies (AGA), 55, 146, 246
schizophrenia and, 253
anti-inflammation diets, 146–47
antimicrobial resistance, 100
anxiety, 258
ARBs. _See_ angiotensin II receptor blockers
aromatase inhibitors, 37
arsenic, 26–27
ASD. _See_ autism spectrum disorder
aspirin, 128
celiac disease and, 164
ataxia, 10, 209
alcohol, 136–37
gluten, 210–11
athleticism, 16–17
ATIs. _See_ amylase trypsin inhibitors
Atkins diet, 16
attention deficit hyperactivity disorder, 55, 245
autism spectrum disorder (ASD), xiii, 55, 145, 242
gluten-free diet and, 244–47
intestinal permeability and, 151–52
microbiome and, 99, 248–49
autoimmune diseases, 9, 21–22
gastrointestinal, 80–81
avenins, 116
azathioprine, 127
Bacteroides, 97, 197
baker's asthma, 225
Benicar, 127
biological markers, 7
BL-7010, 275
Blaset, Martin, 91, 95, 97
bolus, 65
brain fog, xiii, 255–56, 293–94
anxiety and, 258
gluten and, 257–58
inflammation and, 257
microbiome and, 258
nutrient deficiencies and, 258
stress and, 258
brain-gut connection, 46, 239–40
in IBS, 188–89
breath tests, 52–53
brush border, 72
bulk bins, 289
calcium, 25–26
carbohydrates, 16
definition, 118–20
in gluten-free foods, 29
IDDM and, 221–22
problems with, 120–23
transport of, 71–72
casein-free diet, 244–47
CBT. _See_ cognitive behavioral therapy
celiac disease, 2, 9, 25, 80, 295–97
anemia in, 159
aspirin and, 164
ATIs in, 115
biopsy, 170
classic, 158
complications, 158–61
definition, 153, 155–57
diagnosis, 169–71
drugs mimicking, 126–29
environmental factors, 163–64
false test results, 171
fatigue in, 159
fecal testing, 174–75
finger-prick testing, 174
genetics and, 12, 161–62, 173–74
gluten and, 161
gluten-free diet and, 13
IBD and, 200
IDDM and, 220–21
infant feeding and, 163
infections and, 163–64
inflammation in, 157
L-carnitine in, 175
malignancies in, 160–61
microbiome and, 164–65
mineral deficiencies in, 159
mismatch theory, 167–69
neuropathies in, 159
NSAIDs and, 164
osteoporosis in, 159
pediatric guidelines, 172–73
point-of-care testing, 174
proton pump inhibitors and, 164
ruling out, 50
silent, 158–59
smoking and, 166
stress and, 166–67
symptoms, 158–61
systemic inflammation in, 160
testing sensitivity and specificity, 171–72
trauma and, 166–67
treatment, 169–71
central nervous system (CNS), 105
cerebral palsy, 253–54
chronic fatigue syndrome (CFS), 234
causes, 235
diagnosis of, 236–37
treatment, 236
chyme, 66, 73
cleanliness, 93–94
_Clostridium difficile_ , 44–45, 96, 97, 100–101, 126
CNS. _See_ central nervous system
coffee, 299
cognitive behavioral therapy (CBT), 266
colitis, 195
collagenous sprue, 88
colon, 73–74
Columbia University, 48
constipation, 77–78
corn fungi, 27–28
corticosteroids, 127
C-reactive protein, 51
Crohn's disease, 195–96. _See also_ inflammatory bowel disease
cross-contamination, 31, 288
C-section, 95
cyclosporine, 127
cytokines, 142, 144
deamidated gliadin peptide (DGP), 170
dendritic cells, 144
Dewar, Thomas, 269
DGP. _See_ deamidated gliadin peptide
diabetes, 80, 214. _See also_ insulin-dependent diabetes mellitus; non-insulin-dependent diabetes mellitus
causes of, 216
definition, 215–16
microbiome and, 217–18
diabetic neuropathy, 208
diarrhea, 77–78
digestion, 61
chemical processes in, 64
evolution of, 104
liver in, 67–68
mechanical processes in, 64
of minerals, 73
mouth in, 65–66
pancreas in, 67
phases of, 64
small intestine in, 68–70
stomach in, 65–66
villi in, 68, 70–71
of vitamins, 73
disaccharides, 119
Djokovic, Novak, 57
doctors
avoiding, 8–9
financial issues and, 10–11
as listeners, 9
specialists, 10
double hit, 112, 133
Drossman, Douglas, 137
drug-induced inflammation, 79–80
dysbiosis, 91–92
eating disorders, 19
electrolytes, 135
EMA. _See_ endomysial antibodies
emulsifiers, 283–84
endomysial antibodies (EMA), 171
enteric nervous system (ENS), 105–7, 109–10
environmental factors, 22–23
eosinophilic esophagitis (EoE), 202, 226
causes of, 203
definition, 203
diagnosis of, 204–5
food allergies and, 203
GERD and, 204
treatment, 205
epigenetics, 162, 305–6
EpiPen, 228
erythrocyte sedimentation rate, 51
fat, 72–73
fatigue, 159
chronic, 234–37
fat-soluble vitamins, 73
FDA. _See_ Food and Drug Administration
fecal transplants, 44–45 ferritin, 51
fiber, 26, 291–92
fibromyalgia
causes of, 231–32
diagnosis of, 232
treatment, 233–34
financial issues, 10–11
finger-prick testing, 174
fluoxetine, 37
FODMAPs, xiii, 15, 32, 53, 308
definition, 121
elimination of, 121–22
intolerance, 122
folic acid, 51
food allergies, 9, 224–25
antibiotics and, 129–30
causes of, 226–27
diagnosis of, 228
EoE and, 204
microbiome and, 97
treatment, 228
Food and Drug Administration (FDA), 27, 279–80
food glue, xiv, 284–85
food intolerance, 9
alternative tests for, 7
doctors on, 4–5
fructose intolerance, 14
gastroenteritis, 81–82, 126
gastroenterologist, 244
gastroesophageal reflux disease (GERD), 66, 84–85, 125–26
EoE and, 204
gastrointestinal disease
abuse as cause, 137–38
autoimmune, 80–81
causes of, 111
constipation in, 77–78
diarrhea in, 77–78
functional, 82–86
infective, 81–82
infiltrative, 87–88
inflammatory conditions, 78–80
malignant, 82
miscellaneous disorders, 88
nausea in, 76–77
pain in, 76
pregnancy disruptions, 86
symptoms, 76–78
trauma as cause, 137–38
vomiting in, 76–77
gastrointestinal (GI) tract, xii–xiii
inflammation in, 141, 143
neurological symptoms and, 10
as sensory organ, 107–8
serotonin in, 108–9
systems joined with, 62–64
gastroparesis, 14, 83, 208
Gazzola, Alex, 57
genetics
celiac disease and, 12, 161–62, 173–74
epigenetics, 162, 305–6
gluten and, 305
of IBD, 196
IBS and, 187
NCGS, 179
GERD. _See_ gastroesophageal reflux disease
Gershon, Michael, 107, 110
gestational diabetes, 216
giardia, 134
Gibson, Peter, 256
ginseng, 41
GI tract. _See_ gastrointestinal tract
gliadin, 13, 72. _See also_ antigliadin antibodies
glucocorticoids, 263
gluten, ix
alcoholic ataxia and, 136–37
antibodies to, 54–55
ataxia, 210–11
brain fog and, 257–58
celiac disease and, 161
definition, 13
digestive aids for, 273–74
genetics and, 305
hiding, 287–88
IDDM and, 217
microbiome and, 165
myths about, xi–xii
proteins, 113–16
rotavirus and, 135–36
toxoplasmosis and, 136
vaccine for tolerance of, 275–76
vital wheat, 166
gluten-free diet, 308
assessment of, 33
athleticism and, 16–17
autism spectrum disorder and, 244–47
celiac disease and, 13
doctor dismissal of, 4–5
energy and, 16
healthiness of, 290–91, 294
heavy metals in, 26–28
incorrect diagnosis and, 30–31
irritable bowel syndrome and, 14
microbiome and, 15–16
NCGS, 13–14
nutrition in, 25–26
pitfalls, 247–48
placebos and, 14
popularity of, x
stories, 301–4
success of, 13–15
weight loss and, 16, 29
gluten-free foods
additives in, 25, 282
carbohydrates in, 29
cost of, 29–30
labeling, 31–32
gluten sensitivity. _See also_ nonceliac gluten sensitivity
biological markers for, 7
erroneous testing for, 57
rates of, 295
testing, 177–78
glyphosates, 298
Groopman, Jerome, 5, 10
gut. _See_ gastrointestinal tract
_H2RAs_ , 126
heavy metals, 26–28
Helicobacter pylori, 87, 125
hepatitis, 35
herbal remedies, 34–36
hiatal hernia, 86
Hippocrates, xi
HLA-DQ typing, 12, 162, 173–74
HMP. _See_ Human Microbiome Project
holistic medicine, xi
hookworms, 277
hormones, 139–40
Human Microbiome Project (HMP), 306
hygiene hypothesis, 21–22, 227
IBD. _See_ inflammatory bowel disease
IBS. _See_ irritable bowel syndrome
IDDM. _See_ insulin-dependent diabetes mellitus
identity, 264–65
IgA, 55, 169–71
IgE, 56
IgG, 56, 170–71, 246
antigliadin, 180
immune system
environmental factors, 22–23
in IBD, 196–97
microbiome in, 91
rotavirus and gluten in, 135–36
immunoglobulin primer, 55–56
immunosuppressants, 127–28
immunotherapy, 228
ImmusanT, 275–76
impulse control, 263
infant feeding, 163
inflammation, 98
brain fog and, 257
in celiac disease, 157
cell responses in, 143–45
definition, 142
in GI tract, 141, 143
heat changes in, 142–43
intestinal permeability and, 150–51
systemic, 145–46, 160
inflammatory bowel disease (IBD), 30, 78–79, 194
causes of, 196–99
celiac disease and, 200
definition, 195
diagnosis of, 199
diet for, 199–200
environmental factors, 198–99
genetics of, 196–99
immune responses in, 196–97
microbiome in, 197–98
smoking and, 198
treatment of, 199–200
insects, 100–101
insulin-dependent diabetes mellitus (IDDM), 80, 215–16
carbohydrates and, 221–22
celiac disease and, 220–21
gluten and, 217
screening, 218–20
intestinal permeability
alterations in, 150
autism and, 151–52
inflammation and, 150–51
inhibition of, 274
microbiome and, 151
tests for, 148–49
intestinal wall, _69_
irritable bowel syndrome (IBS), 10, 30, 83, 138
brain-gut signal problems in, 188–89
causes of, 186–89
classifications, 184
definition, 183–84
diet for, 187, 191–92
gate theory, 189–90
genetics, 187
gluten-free diet and, 14
medication for, 190–91
mental health and, 192
microbiome and, 187–88
post-infective, 188
probiotics for, 192
Rome III criteria, 185–86
serotonin for, 191
lactase, 88, 272
Lactobacillus, 43
lactose intolerance, 14, 88, 200
larazotide, 274
L-carnitine, 39–40, 236
in celiac disease, 175
leaky gut, 149, 245, 284
Levitt, Pat, 243–44
liquid diets, 198–99
liver, 67–68
Lubbock, John, 4
Marshall, Barry, 87
McEwan, Bruce, 265
mental health, 192
microbial transglutaminase (MTGase), 284–85
microbiome
antibiotics and, 95–97
autism and, 99, 248–49
brain and, 99
brain fog and, 258
celiac disease and, 164–65
consistency of, 101
diabetes and, 217–18
diet and, 92
diversity, 32
food allergies and, 97
gluten and, 165
gluten-free diet and, 15–16
healthy, 42–43
IBD and, 197–98
IBS and, 187–88
in immune system, 91
importance of, 94
intestinal permeability and, 151
obesity and, 98
origin of, 92–93
pregnancy and, 95
self and, 47
in twenty-first century, 93–94
microscopic colitis, 14, 30
minerals, 73. _See also_ vitamin and mineral deficiencies
supplements, 38–39
mismatch theory, 167–69
_Missing Microbes_ (Blaset), 91, 95
monoclonal antibodies, 127
monosaccharides, 119
MTGase. _See_ microbial transglutaminase
mycotoxins, 28
National Eating Disorders Association, 19
National Health Service (NHS), 19
National Institutes of Health (NIH), 6
nausea, 76–77
NCGS. _See_ nonceliac gluten sensitivity
neuropathies
in celiac disease, 159
definition, 207
diabetic, 208
diagnosis of, 211–12
peripheral, 207–8
treatment, 212
Nexvax2, 275–76
NHS. _See_ National Health Service
NIDDM. _See_ non-insulin-dependent diabetes mellitus
NIH. _See_ National Institutes of Health
nocebo, 307
nonceliac gluten sensitivity (NCGS), 7, 236–37
causes of, 179
definition, 178
diagnosis of, 180
genetics and, 179
gluten-free diet and, 13–14
management, 180
self-diagnosis, 178
nongluten proteins, 113–16
non-insulin-dependent diabetes mellitus (NIDDM), 80, 216
nonsteroidal anti-inflammatories (NSAIDs), 79, 128
celiac disease and, 164
oats, 115–16
obesity, 294
antibiotics and, 129–30
microbiome and, 98
oligosaccharides, 119
olmesartan, 126–27
opiates, 129
orthorexia nervosa
definition, 19–20
diagnosis of, 20–21
osteoporosis, 159
over-the-counter (OTC) drugs, 3, 46, 278–79, 297
Paleo diet, 167–68
pancreas, 67
PANDAS, 139
parathyroid hormone, 51
parenteral nutrition, 194
pepsin, 65
peripheral nervous system (PNS), 105
peripheral neuropathies, 207–8
phenolphthalein, 37
placebos, 307
gluten-free diet and, 14
PNS. _See_ peripheral nervous system
point-of-care testing, 174
polyols, 119
polysaccharides, 120
post-infective IBS, 188
prefrontal cortex, 263
pregnancy
gastrointestinal disease and, 86
microbiome and, 95
probiotics, 42–43, 101, 278
caution with, 47
gluten and, 44
or IBS, 192
quality control of, 45
viability of, 46
proteins, 72
proton pump inhibitors, 125–26
celiac disease and, 164
PWAGs, 12, 178
rice, 26–27
Rome III criteria, 185–86
rotavirus, 135–36
schizophrenia, xiii, 251–52
antigliadin antibodies and, 253
scleroderma, 80
Second Brain, The (Gershon), 107
self-diagnosis, 4–7, 299–300
serotonin
functions of, 108–9
in GI tract, 108–9
for IBS, 191
SIBO. _See_ small intestinal bacterial overgrowth
sibutramine, 37
side effects, 131
sildenafil, 37
silent celiac disease, 158–59
small intestinal bacterial overgrowth (SIBO), 12–14, 30, 81, 83–84
small intestine, 68–70
smoking
celiac disease and, 166
IBD and, 198
statins, 280–81
St. John's wort, 36, 40
stool testing, 52, 296
celiac disease, 174–75
Strachan, David, 22
streptococcal infections, 139
stress, xiii, 260–61
brain fog, 258
celiac disease and, 166–67
navigating, 265–67
restrictive dieting and, 262–63
sugars, 52
supplements
for age 50 and up, 41–42
drug interactions, 40–41
labels, 46
mineral, 38–39
natural, 8
vitamin, 38–39
synapsin I, 211
systemic inflammation, 145–46
in celiac disease, 160
T-cells, 144
temporary gluten autoimmunity, 168–69
TG6. _See_ transglutaminase 6
tissue transglutaminase (tTG), 169–71
blocking, 276
toxoplasmosis, 252
gluten and, 136
transglutaminase 6 (TG6), 210
transport, 64
of carbohydrates, 71–72
of fat, 72–73
of proteins, 72
trauma
celiac disease and, 166–67
gastrointestinal disease caused by, 137–38
traveler's diarrhea, 126, 134–35
tTG. _See_ tissue transglutaminase
ulcers, 87
vaccines, 275–76
vertigo, 1
villi, 68, 70–71
vital wheat gluten, 166, 285–86
vitamin and mineral deficiencies
brain fog and, 258
in celiac disease, 159
testing for, 39, 53–54
vitamins
B6, 39
B12, 51
B complex, 25–26
C, 41
D, 38, 51
digestion of, 73
fat-soluble, 73
fortification, 287
K, 41, 97
supplements, 38–39
water-soluble, 73
vomiting, 76–77
Warren, Robin J., 87
water-soluble vitamins, 73
WDEIA. _See_ wheat-dependent exercise-induced anaphylaxis
weight loss, 16, 29
wheat
fortification of, 25
modification of, 276–77, 297
wheat-dependent exercise-induced anaphylaxis (WDEIA), 226
World Health Organization (WHO), 18–19
## P.S. Insights, Interviews & More . . .*
About the Authors
* * *
More about Dr. Peter H. R. Green and Rory Jones, M.S.
About the Book
* * *
The Inspiration Behind _Gluten Exposed_
A Conversation with Dr. Green and Rory Jones
Read On
* * *
What's Happening at the Celiac Disease Center at Columbia University Medical Center
Also by Dr. Green and Rory Jones: _Celiac Disease: A Hidden Epidemic_?
Health Quiz: Should You Get Tested for Celiac Disease?
## About the Authors
**More about Dr. Peter H. R. Green and Rory Jones, M.S.**
**PETER H. R. GREEN, M.D**., is the director of the Celiac Disease Center at Columbia University. He is the Ivan and Phyllis Seidenberg Professor of Medicine at the College of Physicians and Surgeons, Columbia University, and attending physician at the Columbia University Medical Center (New York–Presbyterian Hospital). Celiac disease has been his focus for the last twenty-five years, with equal concentration on patient care and research.
Dr. Green received his medical degree from the University of Sydney, Australia. After completing his residency and gastrointestinal fellowship in Sydney he became a research fellow at Harvard Medical School and in the Gastroenterology Department at the Beth Israel Hospital in Boston.
He is a fellow of the Royal Australasian College of Physicians and the American College of Gastroenterology as well as a member of the American Gastroenterologic Association and American Society of Gastrointestinal Endoscopy.
**RORY JONES, M.S**., is a writer and adjunct professor of Narrative Medicine at Barnard College of Columbia University. She has done extensive work on health and medical topics, including educational programs for both adults and children. She specializes in "translating" scientific information for a consumer audience. Diagnosed with celiac disease in 1998, she has researched and written about it and the gluten-free diet for medical as well as consumer publications.
She is also an award-winning educational film and TV writer and producer specializing in creating programs for hard-to-reach audiences as well as younger children and their adults.
Jones has a B.A. from Smith College and an M.S. from Columbia University.
Discover great authors, exclusive offers, and more at hc.com.
## About the Book
**The Inspiration Behind _Gluten Exposed_**
This book evolved from two converging trends that occurred within and outside of the celiac disease community. First, gluten-free became the new fad diet. Books like _Grain Brain_ and _Wheat Belly_ tended to treat gluten as the "one-cause-fits-all" villain.
Gluten-free foods proliferated, restaurants became familiar with the concept, and eventually self-diagnosis became all too common. Information from the Internet and various nonmedical "professionals" replaced science about gluten's real effect on the body and what a healthy gluten-free diet consists of.
Secondly, the neuropsychological symptoms of people with celiac disease and other conditions became more publicized and studied (depression, anxiety, eating disorders, neuropathies, autism, etc.). Research into the brain-gut relationship started to unearth real connections that were fascinating and important to explore.
On both fronts, pseudoscience became the norm—it was time to insert a scientific reality check and give this pendulum a push in the opposite direction. To let people know the pitfalls and long-term effects of a gluten-free diet, the supplements they were taking to bolster the diet, which gets left out of most articles about the subject; and important new links that can have a dramatic effect on someone's brain as well as their belly.
**A Conversation with Dr. Green and Rory Jones**
**_Q: How did gluten become the "root of all evil" when it comes to gastrointestinal issues?_**
**A:** Sound bites from the Internet and media; the inclination for most people to only read headlines and the first paragraph of an article (the reality of the piece occurring toward the end); books composed to sell the author rather than scientific truth; the public's desire for an easy answer to tough medical and weight issues (give me a pill).
Food elimination has become first-line treatment for many patients prior to seeing a doctor, where they end up when symptoms continue or worsen.
**_Q: What are some of the issues that can arise when people unnecessarily remove gluten from their diets?_**
**A:** Excluding gluten from your diet removes many of the nutrients that keep you out of the doctor's office, not in it. Let's start with the vitamin and mineral deficiencies; loss of fiber and variety in the diet; weight gain if gluten-free foods are substituted; increased arsenic in the diet (rice is a staple of many gluten-free foods and contains higher levels than the U.S. Food and Drug Administration now considers prudent, especially for children); and social stress. So, whether someone is following a gluten-free diet because they've been diagnosed with celiac disease or they're choosing to adopt the diet for personal reasons, it's critical that people read the book to be sure they're eating a healthy, varied diet that won't leave them nutritionally deficient.
And then there are recent studies showing that a gluten-free diet can _increase the risk of developing type 2 diabetes_. A long-term Harvard study shows that there may be a link between low gluten consumption and diabetes risk. Avoiding foods such as cereals, bread, and pasta may be doing you more harm than good unless you have celiac disease or are truly gluten intolerant. And even then, you have to know how to add back what you are eliminating nutritionally and eat a smart gluten-free diet to stay healthy.
Another population-based study is also showing _that people who consume high levels of gluten have less heart disease._ This is related to the importance of whole grains to heart health.
These studies raise serious concerns for people who do not have celiac disease or a medically diagnosed gluten sensitivity and decide to eliminate gluten because they think it is healthier, and underline the real importance of substituting healthy grains in a gluten-free diet. See chapter 31, "[Healthy Eating."]
**_Q. All the vitamins, iron, and minerals necessary for a healthy diet are abundant in meat, fish, poultry, and dairy products. Why should someone on a gluten-free diet suffer from these deficiencies?_**
**A:** They shouldn't.
But a recent study showed that people who are gluten-free are more apt to avoid other food groups. In addition, people on a gluten-free diet may be vegetarian, vegan, lactose intolerant, or avoid cheese and meat because of high cholesterol. They are therefore on an especially restrictive diet that can lead to serious nutritional deficiencies.
**_Q: What is your concern with people using supplements and probiotics?_**
**A:** Too many people are consuming pills (supplements and probiotics) while removing the foods that naturally contain these vitamins and minerals from their diets. Many don't realize that supplements are overused and understudied regarding their effectiveness and safety. Every year products are withdrawn because of toxicity—after the fact. One death because of contamination or toxicity is too many.
**_Q: What are some of the top illnesses or conditions that are often mistaken for a gluten intolerance?_**
**A:** Lactose intolerance, small intestine bacterial overgrowth, microscopic colitis, fructose intolerance. Many people eliminate gluten from their diet to cure bloating and stomach pain—and find temporary relief—only to have the symptoms recur after the initial "honeymoon" period. They then find out they are actually FODMAP sensitive, which is a reaction to the complex carbohydrates/sugars in gluten as well as other foods, especially garlic, onions, and certain fruits. See chapter 12, "[Carbohydrates and FODMAPs."]
**_Q: So many people report feeling healthier once they stop eating gluten. Can going gluten-free be that problematic if it makes so many people feel healthier?_**
**A:** It is hard to determine what "feeling better" consists of. A placebo effect with a new diet that you want to work? Thinking so can make it so. Many people say the same thing about removing red meat and sugar.
Wheat is not an easy protein to digest and causes bloating in many people—less bloat equals feeling better. If that's the case, then a modified gluten-free diet is great. Very few of these people are truly gluten-free nor need to be. They fall into the third "face of gluten," where reducing its input can make a difference.
**_Q: What is gluten's role in our nutrition? Does it serve any positive purposes?_**
**A:** Wheat is a healthy grain loaded with vitamins, minerals, and fiber. It's just not for people with celiac disease. As studies show, it may protect against developing type 2 diabetes and heart disease.
**_Q: If someone thinks they might have a gluten intolerance, what should they do instead of immediately cutting out gluten?_**
**A:** Go to a medical doctor and get tested for celiac disease and various carbohydrate intolerances [fructose, lactose, etc.], as well as other conditions related to their symptoms.
**_Q: Do you think the gluten-free craze is here to stay?_**
**A:** I think that gluten-free is here to stay; the "craze" is not. Like paleo and Whole 30, it is too restricted for most people to follow for an extended period of time. For those without celiac disease, it will become modified or incorporated into the next new dieting fad which may be an old one; see Appendix A, "[Diets Through the Ages"].
**_Q: Given the popularity of gluten-free diets, why do so many cases of celiac disease still go undiagnosed?_**
**A:** Many people with celiac disease are asymptomatic—one study showed 60 percent of children and 41 percent of adults were asymptomatic at diagnosis. For those who do show symptoms, they're often perceived as a dietary issue which most people feel they can treat and control themselves. There's also a lot of self-diagnosis from Internet and naturopathic sources. And once they're on a gluten-free diet, people with actual celiac disease feel better, which leads them to think, Why see a doctor if I'm now fine?
**_Q: Why is a gluten-free diet stressful?_**
**A:** Denying ourselves causes a specific effect on our brain. Anyone who has tried to lose weight can attest to this.
Yet, any type of restrictive eating or lifestyle change requires a constant focus on limiting certain cravings and/or behaviors. This causes an "alert response" that stresses certain parts of the brain that control performance and thought.
For people with celiac disease or a medically diagnosed gluten sensitivity, we recommend different ways to navigate the issue. See chapter 29, "[The Stress of Holding Back."]
For those who have other reasons for choosing a gluten-free lifestyle for themselves and/or their children, we ask: Should a healthy five-year-old or teenager have to worry about everything they are putting in their mouths?
The younger generation is more conscious of food and what they are eating. If we can instill thoughtful choices in our children it will be better in the long term. But we've forgotten some of the basics: the best diet is a balanced diet.
**_Q: What is the harm in using the gluten-free diet for children with Autism Spectrum Disorder (ASD)?_**
**A:** At this point in time the studies do not support the use of the diet for most children with ASD. But that does not mean that larger, well designed, and controlled studies will not identify a specific subgroup of children with ASD who would benefit most from a dietary intervention with a gluten-free regimen. As we explain in the book see chapter 26, "[Autism Spectrum Disorders and ADHD"], some subgroups of children may in fact be more sensitive to dietary input than others. A key objective is finding ways to recognize these children See [chapter 6 on current testing].
_Importantly, for those parents who do choose to undertake a gluten-free regimen, it is extremely important that they understand not only the lifestyle changes that the diet imposes, but the nutritional issues involved so that they keep their children well nourished._ The gluten-free diet is low in fiber, B vitamins, and iron. Given the role of folate (vitamin B9) in brain development, this is only one example of a potential pitfall of the diet.
As we note, the gluten-free diet gives with one hand and often takes with the other.
**_Q: Why can't people do their own_ research—the Internet has multiple "expert" sources?**
**A:** Unfortunately, "doing your own research" has resulted in many people coming to doctors with nutritional deficiencies as well as more complicated and advanced medical conditions.
Reading labels is an easily learned skill—but it is not enough to guarantee a healthy gluten-free existence.
**_Q: What new information will people learn from the revised edition of_ Celiac Disease _?_**
**A:** The book discusses advances in testing and treatments, as well as the most up-to-date understanding of the disease's causes (notably the changes in breast-feeding and early gluten introduction guidelines). The book also provides an updated/expanded list of gluten-free manufacturers, national and international support groups, and publications and resources.
## Read On
**What's Happening at the Celiac Disease Center at Columbia University Medical Center**
In addition to patient care for adults and children, the center specializes in clinical research, with current and future studies focusing on the many health, nutritional, and lifestyle issues affecting people on a gluten-free diet. These include:
• Analyzing how patients use the Nima sensor in managing the gluten-free diet (The Nima sensor is a portable device that allows people to test a food sample for gluten levels.)
• Examining the relation of the quality of life of adults and children with celiac disease and their degree of adherence to a gluten-free diet
• Establishing a tool to determine the degree of dietary adherence in people with celiac disease on a gluten-free diet
• Studying the beliefs and food avoidance patterns of people with celiac disease and gluten sensitivity
• Exploring the role of the microbiome in people with celiac disease and gluten sensitivity
• Developing a rapid test for the diagnosis of celiac disease in people already on a gluten-free diet
• Studying the effect of the gluten-free diet on the general health of individuals
• Researching the role of gastrointestinal infections in people with celiac disease
• Identifying the prevalence and significance of psychological disorders/diagnoses in patients with celiac disease
• Investigating trends in celiac disease research funding compared to inflammatory bowel disease
**Also by Dr. Green and Rory Jones:**
**_Celiac Disease: A Hidden Epidemic_** is _the_ authoritative guide on how this serious autoimmune disorder is properly diagnosed, treated, and managed. It is an essential and comprehensive resource for the countless people who seek relief from debilitating symptoms.
**This revised and updated edition includes:**
• The latest medical research on celiac disease, gluten intolerance, and gluten sensitivity
• New guidelines on testing, and the most recent scientific research toward a cure
• The most up-to-date understanding of the disease's causes (notably the changes in breast-feeding and early gluten introduction guidelines)
• An entire section on coping with the psychological aspects of living with a chronic illness and following a gluten-free diet
• An updated/expanded list of gluten-free manufacturers, national and international support groups, and publications and resources
**Health Quiz: Should You Get Tested for Celiac Disease?**
**SECTION 1: SYMPTOMS**
Check each of the symptoms that you have experienced at least once a week during the past three months:
___ Bloating
___ Gas and/or stomach cramping
___ Diarrhea or runny stools
___ Constipation
___ Joint pain
___ Numbness or tingling in your extremities
___ Itchy skin lesions
___ Constant unexplained fatigue
___ Frequent headaches or migraines
**SECTION II: DIAGNOSES**
Check if you have had or been diagnosed with any of the following:
___ Irritable bowel syndrome
___ Eczema or unexplained contact dermatitis
___ Fibromyalgia
___ Chronic fatigue syndrome
___ Nervous stomach (non-ulcer dyspepsia)
**SECTION III: ASSOCIATED ILLNESSES**
Check if you have any of the following:
___ Lactose intolerance
___ Osteopenia and/or osteoporosis
___ Autoimmune disorders
___ Thyroid disease (hypo/hyper)
___ Diabetes mellitus (type 1)
___ Sjögren's syndrome
___ Chronic liver disease
___ An immediate family member with an autoimmune condition
___ Peripheral neuropathy
___ Non-Hodgkin's lymphoma
___ Small intestinal cancer
___ Psychiatric disorders or depression
___ Anemia (iron deficiency)
___ Infertility
**SCORING:**
If you have checked one or more lines in _either_ Section I or II and have _any_ of the illnesses in Section III (especially males or women under forty-five with osteopenia and/or osteoporosis), you should consider testing for celiac disease. If you have checks in all three sections, you and your doctor(s) should explore a diagnosis of celiac disease.
All of the symptoms in Section I, all of the diagnoses in Section II, and all of the associated illnesses in Section III are intimately related to celiac disease. One in every 100 people in the United States is affected by celiac disease—and 85 percent of them are undiagnosed!
Discover great authors, exclusive offers, and more at hc.com.
Praise for _Gluten Exposed_
"There's a lot of confusion surrounding gluten—whether eliminating it can help you lose weight, clear brain fog, cure stomach issues, and more. The brilliant and renowned Dr. Peter Green and science writer Rory Jones have cut through the confusion to provide evidence-based answers and advice you can trust. In _Gluten Exposed,_ they sort through all the science to create a comprehensive guide on the subject. If you are considering going gluten-free, you should definitely read this book first."
—Joy Bauer, M.S., R.D.N, nutritionist for NBC's _Today_ show, founder of Nourish Snacks, and bestselling author of _From Junk Food to Joy Food_
"Years ago, Dr. Peter Green was the pioneer who revealed the prevalence of celiac disease and the life-saving value of a gluten-free diet for its victims. In _Gluten Exposed,_ he uncovers the hype that now misleads so many to go gluten-free for all the wrong reasons. This urgently needed, highly accessible, solidly science-based book is a must-read for people who care about their health."
—Walter Mischel, professor of psychology, Columbia University, and author of _The Marshmallow Test: Mastering Self-Control_
" _Gluten Exposed_ will hopefully put the brakes on the worldwide epidemic of using a gluten-free diet for just about everything that 'ails ya.' Peter Green and Rory Jones provide a masterful in-depth summary of the pitfalls and dangers of gluten-free diets in nonceliac individuals, and at the same time describe openings for more research where it may be helpful outside of celiac disease. _Gluten Exposed_ reviews a totality of gluten and celiac-related science that will enrich health care professionals and the health-minded community."
—Richard J. Deckelbaum, M.D., F.R.C.P. (C), Division of Pediatric
Gastroenterology, Hepatology, and Nutrition, and Director,
Institute of Human Nutrition, Columbia University Medical Center
"[ _Gluten Exposed_ ] is a model for how to communicate science to the public, an antidote to the breathless hype and simplistic headlines that too often dominate popular scientific discourse. . . . The book offers expert, up-to-date summaries of the scientific consensus (or lack thereof) on gluten, grains, the gut, the microbiome, and theories about how these come together in healthy and unhealthy people."
—Slate
"Written with keen intelligence and a kind heart, _Gluten Exposed_ illuminates what is known and not known, what is believed and what is doubted, what is claimed and what is disputed. This is an essential book for those seeking not only information but also wisdom about a most important and misunderstood condition."
—Jerome Groopman, M.D., Recanati Professor, Harvard Medical School, and coauthor with Dr. Pamela Hartzband of _Your Medical Mind: How to Decide What Is Right for You_
"Serious and comprehensive."
— _Publishers Weekly_
"In _Gluten Exposed,_ Dr. Peter Green, a leader in the care of patients with celiac disease, and science writer Rory Jones explain the illness and how ordinary people can optimize their health. This is a very useful book, and fully digestible!"
—Martin J. Blaser, M.D., Director, NYU Human Microbiome Program, and author of _Missing Microbes_
"The demonization of gluten has resulted in claims and counterclaims; profit-making by celebrities, pseudoscientists, and the food industry; and general confusion, even in the scientific community. _Gluten Exposed_ provides simple and digestible understanding in this perplexing debate, helping those with an open mind to better understand the issues and make reasoned, personal decisions about their health. It will contribute significantly to community understanding of the issues around gluten and more."
—Peter Gibson, M.D., Director of Gastroenterology at the Alfred Hospital and Monash University
"Dr. Peter Green is my gluten-free medical go-to. I am constantly learning and benefiting from his passion and pursuit, and we all benefit from his commitment to research when it comes to celiac disease and autoimmune connections."
—Elisabeth Hasselbeck, bestselling author of _The G-Free Diet_ and _Deliciously G-Free_ and creator and founder of NoGii—gluten-free solutions for the entire family
" _Gluten Exposed_ provides detailed but easy-to-read explanations of the science behind celiac disease, gluten sensitivity, and the relevance of gluten to a host of other conditions, from autism and 'brain fog' to diabetes and fibromyalgia. Dr. Green's deep clinical experience comes through on every page. The book provides sensible advice to all who are concerned about the impact of gluten on their bodies. Green and Jones aren't shy about pointing out common myths and misconceptions about gluten, and letting the reader know what is merely speculation rather than fact. The chapter on autism is a case in point. If you're curious about all the hype around gluten, read _Gluten Exposed_."
—Paul Wang, M.D., senior vice president, Autism Speaks
Also by Peter H. R. Green, M.D., And Rory Jones, M.S.
_Celiac Disease: A Hidden Epidemic_
## Copyright
This book contains advice and information relating to health care. It should be used to supplement rather than replace the advice of your doctor or another trained health professional. If you know or suspect you have a health problem, it is recommended that you seek your physician's advice before embarking on any medical program or treatment. All efforts have been made to assure the accuracy of the information contained in this book as of the date of publication. This publisher and the author disclaim liability for any medical outcomes that may occur as a result of applying the methods suggested in this book.
P.S.™ is a trademark of HarperCollins Publishers.
GLUTEN EXPOSED. Copyright © 2016 by Peter H. R. Green, M.D., and Rory Jones, M.S. All rights reserved under International and Pan-American Copyright Conventions. By payment of the required fees, you have been granted the nonexclusive, nontransferable right to access and read the text of this e-book on-screen. No part of this text may be reproduced, transmitted, downloaded, decompiled, reverse-engineered, or stored in or introduced into any information storage and retrieval system, in any form or by any means, whether electronic or mechanical, now known or hereafter invented, without the express written permission of HarperCollins e-books.
Chapter 7 appeared in a different form in _Celiac Disease: A Hidden Epidemic_ (first ed.) by Peter H. R. Green, M.D., and Rory Jones, published by William Morrow, 2006.
A hardcover edition of this book was published in 2016 by William Morrow, an imprint of HarperCollins Publishers.
FIRST WILLIAM MORROW PAPERBACK EDITION PUBLISHED 2017.
_Illustrations by Thom Graves_
_Cover design by Ariana Grabec-Dingman_
* * *
The Library of Congress has catalogued the hardcover edition as follows:
Names: Green, Peter H. R., author. | Jones, Rory, author.
Title: Gluten exposed : the science behind the hype and how to navigate to a healthy, symptom-free life / Peter H.R. Green, M.D. and Rory Jones, M.S.
Description: First edition. | New York, NY : William Morrow, an imprint of HarperCollinsPublishers, [2016] | Includes index.
Identifiers: LCCN 2016001185 (print) | LCCN 2016003081 (ebook) | ISBN 9780062394286 (hardback) | ISBN 9780062394293 (e-book)
Subjects: LCSH: Gluten—Health aspects—Popular works. | Gluten-free diet—Popular works. | Celiac disease—Popular works. | Self-care, Health—Popular works. | BISAC: HEALTH & FITNESS / Diets. | HEALTH & FITNESS / Nutrition. | HEALTH & FITNESS / Diseases / General.
Classification: LCC RC862.C44 G744 2016 (print) | LCC RC862.C44 (ebook) | DDC
616.3/99—dc23
LC record available at http://lccn.loc.gov/2016001185
* * *
ISBN 978-0-06-256155-8 (pbk.)
EPUB Edition August 2017 ISBN 978-0-06-239429-3
## About the Publisher
**Australia**
HarperCollins Publishers Australia Pty. Ltd.
Level 13, 201 Elizabeth Street
Sydney, NSW 2000, Australia
www.harpercollins.com.au
**Canada**
HarperCollins Canada
2 Bloor Street East - 20th Floor
Toronto, ON M4W 1A8, Canada
www.harpercollins.ca
**New Zealand**
HarperCollins Publishers New Zealand
Unit D1, 63 Apollo Drive
Rosedale 0632
Auckland, New Zealand
www.harpercollins.co.nz
**United Kingdom**
HarperCollins Publishers Ltd.
1 London Bridge Street
London SE1 9GF, UK
www.harpercollins.co.uk
**United States**
HarperCollins Publishers Inc.
195 Broadway
New York, NY 10007
www.harpercollins.com
* In order to preserve patient confidentiality we have used first names or pseudonyms throughout.
* Throughout the book we italicize less-familiar words and terms when they first appear and provide a more complete definition in the glossary at the back of the book.
* Or the "nocebo" effect, where believing something will harm you actually causes an adverse reaction to it.
* Reported in an article in the _Wall Street Journal_.
* The term _microbiota_ encompasses the trillions of microbes living in and on the human body; the term _microbiome_ technically means the collective genome of the microbiota. They are often used interchangeably.
* _Missing Microbes,_ Martin J. Blaser, M.D., Henry Holt and Co., 2014, p. 99.
* It is a cousin of the "two-hit" hypothesis of Alfred Knudson, which explained the relationship between the hereditary and nonhereditary, or sporadic, forms of one type of cancer.
* Centers for Disease Control.
* A multidisciplinary task force of 16 physicians from seven countries. Published in _Gut_ in 2013.
* These are "nicknames" for HLA-DQ2 (encoded by alleles DQA1*05 and DQB1*02) and -DQ8 (encoded by DQB1*0302 and DQA1*03).
* Of note: The amount of gluten administered to the children in the study was very low (about 2 to 3 percent of the amount of gluten in a slice of bread).
* The classification of Asperger's syndrome is no longer included in the latest revision of the _Diagnostic and Statistical Manual of Mental Disorders (DSM-V)_ , which is used by professionals as the standard criteria by which to diagnose mental disorders. Children with these symptoms are considered to have high-functioning ASD.
* Claude M. Steele, _Whistling Vivaldi_ (New York: W.W. Norton & Co., 2010).
* The suffix "–ase" is used to form the names of enzymes: lactase breaks down lactose, lipase breaks down lipids or fats, etc.
|
{
"redpajama_set_name": "RedPajamaBook"
}
| 3,284
|
Q: itemfulfillment: sublist item field inventorydetail is not a subrecord field I want to do a bin itemfulfillment in netsuite.
But I can't get an example that works. When I run the below code I am receiving this error:
Sublist item field inventorydetail is not a subrecord field
I need to know what is the correct subrecord name to create an itemfulfillment
Thanks!
var sales_internalid = '2465'; //saleorderid
var einternalid = '110'; //employeeid
var winternalid = '1'; //washsoueid
var sinternalid = '6'; //itemid
var quantity = 1;
var displayname ='iphone';
var shipgroup = 1;
var salesOrder= nlapiCreateRecord('salesorder', sales_internalid, {recordmode: 'dynamic'});
var obj = nlapiTransformRecord('salesorder', sales_internalid, 'itemfulfillment');
obj.selectLineItem('item',1);
obj.setCurrentLineItemValue('item', 'item', sinternalid );
obj.setCurrentLineItemValue('item', 'location', winternalid );
obj.setCurrentLineItemValue('item', 'quantity', 1);
var subrecord= obj.editCurrentLineItemSubrecord('item', 'inventorydetail');
subrecord.selectLineItem('inventoryassignment', 1);
subrecord.selectNewLineItem('inventoryassignment');
subrecord.setCurrentLineItemValue('inventoryassignment', 'inventorynumber', '1');
subrecord.setCurrentLineItemValue('inventoryassignment', 'quantity', '1');
subrecord.commitLineItem('inventoryassignment');
subrecord.commit();
obj.commitLineItem('item');
var fulfillmentOrderId = nlapiSubmitRecord(itemFulfillment, true);
A: I had this same issue when doing my first Inventory Transfer via code for a client. Turns out the Bin Number field is only a subrecord when the feature "Advanced Bin Management" is enabled. If the account you are working in is setup to just "Use Bins" then the Bin Number field on the line items of transactions is set via its text value. Example is in SS 2.0 but I believe it gets the point across:
newRec = nsRecord.create({
type: nsRecord.Type.INVENTORY_ADJUSTMENT,
isDynamic: true
});
// In dynamic mode must set the subsidiary first.
newRec.setValue({
fieldId: bodyFields.subsidiary,
value: locSub[datain.Location]
});
newRec.setValue({
fieldId: bodyFields.adjustment_Location,
value: datain.Location
});
newRec.setValue({
fieldId: bodyFields.date,
value: date
});
newRec.selectNewLine({
sublistId: columnFields.type
});
newRec.setCurrentSublistValue({
sublistId: columnFields.type,
fieldId: columnFields.item,
value: datain.Item
});
newRec.setCurrentSublistValue({
sublistId: columnFields.type,
fieldId: columnFields.adjust_Qty,
value: datain.Quantity.toString()
});
if (parseFloat(datain.Quantity) > 0) { // If qty is positive must set the Est Unit Cost.
itemVals = nsSearch.lookupFields({
type: nsSearch.Type.ITEM,
id: datain.Item,
columns: fields
});
cost = itemVals.averagecost || itemVals.lastpurchaseprice;
newRec.setCurrentSublistValue({
sublistId: columnFields.type,
fieldId: columnFields.est_Unit_Cost,
value: cost
});
}
//
// Format for binnumbers field is 'ValueText(qty)\rValueText(qty)\rValueText(qty)
// the only exception is in cases of negative qty
//
binText = datain.Bin ? datain.Bin + '(' + datain.Quantity + ')' : '';
newRec.setCurrentSublistValue({
sublistId: columnFields.type,
fieldId: columnFields.bin_Numbers,
value: binText
});
newRec.commitLine({
sublistId: columnFields.type
});
invRecResult.invRecId = newRec.save({
enableSourcing: true,
ignoreMandatoryFields: true
});
|
{
"redpajama_set_name": "RedPajamaStackExchange"
}
| 8,552
|
{"url":"https:\/\/learn.careers360.com\/ncert\/question-the-inner-diameter-of-a-circular-well-is-3-point-5-m-it-is-10-m-deep-find-i-its-inner-curved-surface-area\/","text":"# Q : 7\u00a0\u00a0\u00a0\u00a0The inner diameter of a circular well is $\\small 3.5\\hspace{1mm}m$. It is $\\small 10\\hspace{1mm}m$\u00a0deep. Find\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0(i) its inner curved surface area.\n\nGiven,\n\nThe inner diameter of the circular well =\u00a0\u00a0$d = \\small 3.5\\hspace{1mm}m$\n\nDepth of the well =\u00a0$h = 10\\ m$\n\nWe know,\n\nThe curved surface area of a cylinder =\u00a0$2\\pi rh$\n\n$\\therefore$\u00a0The curved surface area of the well =\u00a0$2\\times\\frac{22}{7}\\times\\frac{3.5}{2}\\times10$\n\n$\\\\ = 44 \\times 0.25 \\times 10 \\\\ = 110\\ m^2$\n\nTherefore, the inner curved surface area of the circular well is $110\\ m^2$\n\n## Related Chapters\n\n### Preparation Products\n\n##### JEE Main Rank Booster 2021\n\nThis course will help student to be better prepared and study in the right direction for JEE Main..\n\n\u20b9 13999\/- \u20b9 9999\/-\n##### Rank Booster NEET 2021\n\nThis course will help student to be better prepared and study in the right direction for NEET..\n\n\u20b9 13999\/- \u20b9 9999\/-\n##### Knockout JEE Main April 2021 (Easy Installments)\n\nAn exhaustive E-learning program for the complete preparation of JEE Main..\n\n\u20b9 4999\/-\n##### Knockout NEET May 2021\n\nAn exhaustive E-learning program for the complete preparation of NEET..\n\n\u20b9 22999\/- \u20b9 14999\/-","date":"2020-10-20 00:37:52","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 0, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 0, \"img_math\": 0, \"codecogs_latex\": 9, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.7737120985984802, \"perplexity\": 7381.789441787106}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2020-45\/segments\/1603107867463.6\/warc\/CC-MAIN-20201019232613-20201020022613-00222.warc.gz\"}"}
| null | null |
package com.ebay.myriad.executor;
import com.google.gson.Gson;
import org.apache.mesos.Executor;
import org.apache.mesos.ExecutorDriver;
import org.apache.mesos.MesosExecutorDriver;
import org.apache.mesos.Protos.ExecutorInfo;
import org.apache.mesos.Protos.FrameworkInfo;
import org.apache.mesos.Protos.SlaveInfo;
import org.apache.mesos.Protos.Status;
import org.apache.mesos.Protos.TaskID;
import org.apache.mesos.Protos.TaskInfo;
import org.apache.mesos.Protos.TaskState;
import org.apache.mesos.Protos.TaskStatus;
import org.slf4j.Logger;
import org.slf4j.LoggerFactory;
import java.io.File;
import java.io.IOException;
import java.nio.charset.Charset;
import java.nio.file.Paths;
import java.util.Map;
/**
* Myriad's Executor
*/
public class MyriadExecutor implements Executor {
private static final Logger LOGGER = LoggerFactory.getLogger(MyriadExecutor.class);
public static final String ENV_YARN_NODEMANAGER_OPTS = "YARN_NODEMANAGER_OPTS";
/**
* YARN container executor class.
*/
public static final String KEY_YARN_NM_CONTAINER_EXECUTOR_CLASS = "yarn.nodemanager.container-executor.class";
// TODO (mohit): Should it be configurable ?
public static final String VAL_YARN_NM_CONTAINER_EXECUTOR_CLASS = "org.apache.hadoop.yarn.server.nodemanager.LinuxContainerExecutor";
public static final String DEFAULT_YARN_NM_CONTAINER_EXECUTOR_CLASS = "org.apache.hadoop.yarn.server.nodemanager.DefaultContainerExecutor";
/**
* YARN class to help handle LCE resources
*/
public static final String KEY_YARN_NM_LCE_RH_CLASS = "yarn.nodemanager.linux-container-executor.resources-handler.class";
// TODO (mohit): Should it be configurable ?
public static final String VAL_YARN_NM_LCE_RH_CLASS = "org.apache.hadoop.yarn.server.nodemanager.util.CgroupsLCEResourcesHandler";
public static final String KEY_YARN_NM_LCE_CGROUPS_HIERARCHY = "yarn.nodemanager.linux-container-executor.cgroups.hierarchy";
public static final String KEY_YARN_NM_LCE_CGROUPS_MOUNT = "yarn.nodemanager.linux-container-executor.cgroups.mount";
public static final String KEY_YARN_NM_LCE_CGROUPS_MOUNT_PATH = "yarn.nodemanager.linux-container-executor.cgroups.mount-path";
public static final String KEY_YARN_NM_LCE_GROUP = "yarn.nodemanager.linux-container-executor.group";
public static final String KEY_YARN_NM_LCE_PATH = "yarn.nodemanager.linux-container-executor.path";
public static final String KEY_YARN_HOME = "yarn.home";
public static final String KEY_NM_RESOURCE_CPU_VCORES = "nodemanager.resource.cpu-vcores";
public static final String KEY_NM_RESOURCE_MEM_MB = "nodemanager.resource.memory-mb";
public static final String KEY_NM_ADDRESS = "myriad.yarn.nodemanager.address";
public static final String KEY_NM_LOCALIZER_ADDRESS = "myriad.yarn.nodemanager.localizer.address";
public static final String KEY_NM_WEBAPP_ADDRESS = "myriad.yarn.nodemanager.webapp.address";
public static final String KEY_NM_SHUFFLE_PORT = "myriad.mapreduce.shuffle.port";
/**
* Allot 10% more memory to account for JVM overhead.
*/
public static final double JVM_OVERHEAD = 0.1;
/**
* Default -Xmx for executor JVM.
*/
public static final double DEFAULT_JVM_MAX_MEMORY_MB = 256;
/**
* Default cpus for executor JVM.
*/
public static final double DEFAULT_CPUS = 0.2;
public static final Gson GSON = new Gson();
private static final String PROPERTY_FORMAT = "-D%s=%s ";
private SlaveInfo slaveInfo;
private Process process;
public static void main(String[] args) throws Exception {
LOGGER.info("Starting MyriadExecutor...");
MesosExecutorDriver driver = new MesosExecutorDriver(new MyriadExecutor());
System.exit(driver.run() == Status.DRIVER_STOPPED ? 0 : 1);
}
@Override
public void registered(ExecutorDriver driver,
ExecutorInfo executorInfo,
FrameworkInfo frameworkInfo,
SlaveInfo slaveInfo) {
LOGGER.debug("Registered ", executorInfo, " for framework ", frameworkInfo, " on mesos slave ", slaveInfo);
this.slaveInfo = slaveInfo;
}
@Override
public void reregistered(ExecutorDriver driver, SlaveInfo slaveInfo) {
LOGGER.debug("ReRegistered");
}
@Override
public void disconnected(ExecutorDriver driver) {
LOGGER.info("Disconnected");
}
@Override
public void launchTask(final ExecutorDriver driver, final TaskInfo task) {
new Thread(new Runnable() {
public void run() {
TaskStatus.Builder statusBuilder = TaskStatus.newBuilder()
.setTaskId(task.getTaskId());
try {
NMTaskConfig taskConfig = GSON.fromJson(task.getData().toStringUtf8(), NMTaskConfig.class);
LOGGER.info("TaskConfig: ", taskConfig);
ProcessBuilder processBuilder = buildProcessBuilder(task, taskConfig);
MyriadExecutor.this.process = processBuilder.start();
int waitFor = MyriadExecutor.this.process.waitFor();
if (waitFor == 0) {
statusBuilder.setState(TaskState.TASK_FINISHED);
} else {
statusBuilder.setState(TaskState.TASK_FAILED);
}
} catch (InterruptedException | IOException e) {
LOGGER.error("launchTask", e);
statusBuilder.setState(TaskState.TASK_FAILED);
} catch (RuntimeException e) {
LOGGER.error("launchTask", e);
statusBuilder.setState(TaskState.TASK_FAILED);
throw e;
} finally {
driver.sendStatusUpdate(statusBuilder.build());
}
}
}).start();
TaskStatus status = TaskStatus.newBuilder()
.setTaskId(task.getTaskId())
.setState(TaskState.TASK_RUNNING)
.build();
driver.sendStatusUpdate(status);
}
private ProcessBuilder buildProcessBuilder(TaskInfo task, NMTaskConfig taskConfig) {
ProcessBuilder processBuilder = new ProcessBuilder("bash", "-c", "$YARN_HOME/bin/yarn nodemanager");
Map<String, String> environment = processBuilder.environment();
Map<String, String> yarnEnvironmentMap = taskConfig.getYarnEnvironment();
if (yarnEnvironmentMap != null) {
for (Map.Entry<String, String> yarnEnvironment : yarnEnvironmentMap.entrySet()) {
environment.put(yarnEnvironment.getKey(), yarnEnvironment.getValue());
}
}
String envNMOptions = getNMOpts(taskConfig);
LOGGER.info(ENV_YARN_NODEMANAGER_OPTS, ": ", envNMOptions);
if (environment.containsKey(ENV_YARN_NODEMANAGER_OPTS)) {
String existingOpts = environment.get(ENV_YARN_NODEMANAGER_OPTS);
environment.put(ENV_YARN_NODEMANAGER_OPTS, existingOpts + " " + envNMOptions);
} else {
environment.put(ENV_YARN_NODEMANAGER_OPTS, envNMOptions);
}
processBuilder.redirectOutput(ProcessBuilder.Redirect.INHERIT);
processBuilder.redirectError(ProcessBuilder.Redirect.INHERIT);
return processBuilder;
}
private void makeWritable(String path) {
File file = new File(path);
if (!file.setWritable(true, false)) {
LOGGER.error(path, " is not writable");
}
}
private String getNMOpts(NMTaskConfig taskConfig) {
String envNMOptions = "";
// If cgroups are enabled then configure
if (taskConfig.getCgroups()) {
envNMOptions += String.format(PROPERTY_FORMAT, KEY_YARN_NM_CONTAINER_EXECUTOR_CLASS, VAL_YARN_NM_CONTAINER_EXECUTOR_CLASS);
envNMOptions += String.format(PROPERTY_FORMAT, KEY_YARN_NM_LCE_RH_CLASS, VAL_YARN_NM_LCE_RH_CLASS);
String containerId = getContainerId();
makeWritable("/sys/fs/cgroup/cpu/mesos/" + containerId);
// TODO: Configure hierarchy
envNMOptions += String.format(PROPERTY_FORMAT, KEY_YARN_NM_LCE_CGROUPS_HIERARCHY, "mesos/" + containerId);
envNMOptions += String.format(PROPERTY_FORMAT, KEY_YARN_NM_LCE_CGROUPS_MOUNT, "true");
// TODO: Make it configurable
envNMOptions += String.format(PROPERTY_FORMAT, KEY_YARN_NM_LCE_CGROUPS_MOUNT_PATH, "/sys/fs/cgroup");
envNMOptions += String.format(PROPERTY_FORMAT, KEY_YARN_NM_LCE_GROUP, "root");
envNMOptions += String.format(PROPERTY_FORMAT, KEY_YARN_HOME, taskConfig.getYarnEnvironment().get("YARN_HOME"));
} else {
// Otherwise configure to use Default
envNMOptions += String.format(PROPERTY_FORMAT, KEY_YARN_NM_CONTAINER_EXECUTOR_CLASS, DEFAULT_YARN_NM_CONTAINER_EXECUTOR_CLASS);
}
envNMOptions += String.format(PROPERTY_FORMAT, KEY_NM_RESOURCE_CPU_VCORES, taskConfig.getAdvertisableCpus() + "");
envNMOptions += String.format(PROPERTY_FORMAT, KEY_NM_RESOURCE_MEM_MB, taskConfig.getAdvertisableMem() + "");
envNMOptions += String.format(PROPERTY_FORMAT, KEY_NM_ADDRESS, "0.0.0.0:" + taskConfig.getRpcPort().toString() + "");
envNMOptions += String.format(PROPERTY_FORMAT, KEY_NM_LOCALIZER_ADDRESS, "0.0.0.0:" + taskConfig.getLocalizerPort().toString() + "");
envNMOptions += String.format(PROPERTY_FORMAT, KEY_NM_WEBAPP_ADDRESS, "0.0.0.0:" + taskConfig.gettWebAppHttpPort().toString() + "");
envNMOptions += String.format(PROPERTY_FORMAT, KEY_NM_SHUFFLE_PORT, taskConfig.getShufflePort().toString() + "");
return envNMOptions;
}
public String getContainerId() {
String cwd = Paths.get(".").toAbsolutePath().normalize().toString();
String[] split = cwd.split("/");
return split[split.length - 1];
}
@Override
public void killTask(ExecutorDriver driver, TaskID taskId) {
LOGGER.debug("KillTask received for taskId: " + taskId.getValue());
this.process.destroy();
TaskStatus status = TaskStatus.newBuilder()
.setTaskId(taskId)
.setState(TaskState.TASK_KILLED)
.build();
driver.sendStatusUpdate(status);
}
@Override
public void frameworkMessage(ExecutorDriver driver, byte[] data) {
LOGGER.info("Framework message received: ", new String(data, Charset.defaultCharset()));
}
@Override
public void shutdown(ExecutorDriver driver) {
LOGGER.debug("Shutdown");
}
@Override
public void error(ExecutorDriver driver, String message) {
LOGGER.error("Error message: " + message);
}
}
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 3,666
|
is a Japanese race car driver. Hirate has won the Super GT series twice.
Career
Hirate began karting in 1999 when he was 13. After winning the All Japan Junior Kart Championship, coming third and fifth in the All Japan Kart Championship and coming third in the FIA Oceania Championship, he moved on to Formula Toyota, where he raced for the Tom's Spirit team and came second with four wins to his name.
In 2003, he moved to Formula Renault, at the Prema Power team. In his two-year spell here he won 7 races and came second in the 2004 season. In 2004 he also raced for Prema Power's Formula Three Euroseries team twice, and in 2005 made the decision to race here. After coming twelfth for Team Rosberg, he was made a Toyota F1 test driver in 2006 and came third in the Formula Three Euroseries. In 2007 he continued as a Toyota test driver and also drove for GP2 team Trident Racing.
Hirate returned to Japan in 2008, where he competed in both Formula Nippon and Super GT. He finished fourth in the 2008 Formula Nippon season and fifth in 2009, both times driving for Team Impul.
Racing record
Career summary
* Season still in progress.
Complete GP2 Series results
(key) (Races in bold indicate pole position) (Races in italics indicate fastest lap)
Complete Formula Nippon/Super Formula results
(key) (Races in bold indicate pole position) (Races in italics indicate fastest lap)
Complete Super GT results
‡ Half points awarded as less than 75% of race distance was completed.
* Season still in progress.
References
External links
Kohei Hirate official website
Living people
1986 births
People from Komaki, Aichi
Japanese racing drivers
GP2 Series drivers
Formula Nippon drivers
Super GT drivers
Formula 3 Euro Series drivers
Italian Formula Renault 2.0 drivers
Formula Renault Eurocup drivers
German Formula Renault 2.0 drivers
Dutch Formula Renault 2.0 drivers
Asian Formula Renault Challenge drivers
Super Formula drivers
Prema Powerteam drivers
Team Rosberg drivers
Manor Motorsport drivers
Trident Racing drivers
Nismo drivers
Kondō Racing drivers
B-Max Racing drivers
|
{
"redpajama_set_name": "RedPajamaWikipedia"
}
| 9,889
|
\section{Introduction}
Antineutrinos were detected for the first time in 1956 by Clyde Cowan and Fred Reines by recording the transmutation of a free proton by particles born in nuclear reactors\,\cite{reines53}. This detection confirmed the existence of the neutrino and marked the advent of experimental neutrino physics. For decades, neutrino research has been an active and fruitful pursuit in the fields of particle physics, astrophysics, and cosmology. Neutrino experimental physics provided a glimpse into some of the most obscured astrophysical phenomena in the universe. The confirmed neutrino and/or antineutrino sources include the Sun\,\cite{Cleveland:1998nv}, nuclear reactors, particle accelerators\,\cite{K2K:2002icj}, the Earth\,\cite{Araki:2005qa,Borexino:2013tnm}, atmosphere\,\cite{Reines:1965qk}, and core-collapse supernovae\,\cite{Kamiokande-II:1987idp, Bionta:1987qt}. Moreover, the quantum mechanical phenomenon, known as neutrino oscillation, is our first observation beyond the Standard Model\,\cite{nobel_2015}, and it possibly holds the key to the explanation of the matter-dominated universe\,\cite{Bilenky:1978nj}. Since the neutrino discovery, reactor antineutrinos have continued to make huge contributions to studies of neutrino properties, including the measurement of neutrino oscillation parameters, neutrino mass ordering, and even the possibility of "sterile" neutrino flavors\,\cite{STEREO:2019ztb, PROSPECT:2020sxr}. Antineutrinos have also enabled a new interdisciplinary field of neutrino geoscience. Geoneutrinos are the only direct probe of radiogenic heat in the depths of the Earth, particularly the mantle, and can help discriminate between different geological models of Earth's formation and evolution. The number of electron flavour antineutrinos emitted in the radioactive decays of heat-producing elements (HPEs) with lifetimes compatible with the age of the Earth, such as \ce{^232Th}, \ce{^235U}, \ce{^238U}, and \ce{^40K}, is directly proportional to the HPE abundances and Earth's radiogenic heat.
Borexino (Italy) and KamLAND (Japan) are the only two experiments to have observed geoneutrinos. The most recent measurements of geoneutrinos are $52.6^{+9.4}_{-8.6}$ (stat)$^{+2.7}_{-2.1}$ (sys) in Borexino\,\cite{Geo_Borexino} and $164^{+28}_{-25}$ in KamLAND\,\cite{Geo_KamLand,KamLAND_preliminary},
corresponding to 18\% and 17\% precision. Expanding these measurements with higher statistics and to the other parts of the world will allow us to have a better understanding of radioactive elements abundances in the crust and mantle. SNO+\,\cite{snoplus} (Canada) and JUNO\,\cite{juno_2022} (China) will attempt geoneutrino measurements as part of their physics program in the near future. Of special interest is the concept of placing a neutrino detector on the seafloor as the oceanic crust is much thinner than the continental one, hence mantle contributions would dominate the measured geoneutrino flux. With the original idea developed for Hanohano\,\cite{hanohano} to be placed at the oceanic floor near Hawaii, more recently, a collaboration in Japan reinvigorated this idea with the Ocean Bottom Detector (OBD)\,\cite{snowmass-OBD}. Other proposed experiments that hope to measure geoneutrinos are Jinping\,\cite{Jinping} in China, and the \textsc{Theia}{} multipurpose detector\,\cite{theia_wp}. The latter is the focus of this paper. \textsc{Theia}{} is a proposed large-scale scintillation-based neutrino detector that will deploy new target media, photon detectors, readout techniques and reconstruction algorithms to help discriminate between Cherenkov and scintillation signals.
The considered detector design consists of a cylindrical tank viewed by inward-looking photomultipliers (PMTs) and filled with water-based liquid scintillator (WbLS)\,\cite{wbls}, a mixture of water and an organic oil-based scintillator, combined using surfactants.
This novel target allows for the combination of directional sensitivity from the Cherenkov signal, with the low energy threshold and good resolution from the scintillation. Hence, \textsc{Theia}{} has a broad physics program ranging from low energy solar to high energy accelerator neutrinos\,\cite{theia_wp}.
\begin{figure}[!htb]
\centering
\resizebox{0.49\textwidth}{!}{
\includegraphics{figures/Theia-25kT.png}
}
\caption{
A sketch of \textsc{Theia}{}-25 location and a box-shape detector outline.
The maximum space available in terms of fiducial volume is shown.
}
\label{fig:Theia-25kT}
\end{figure}
%
In this paper, we consider a \textsc{Theia}{} design that would fit in a cavern the size and shape of those intended for the Deep Underground Neutrino Experiment (DUNE) at Sanford Underground Research Facility (SURF), which we call \textsc{Theia}{}-25.
Figure~\ref{fig:Theia-25kT} shows a sketch of the available space on-site and a proposed design for \textsc{Theia}{}-25, a letterbox detector of dimensions $\SI{70}{\meter}\times\SI{20}{\meter}\times\SI{18}{\meter}$.
We explore the sensitivity of \textsc{Theia}{}-25 towards geoneutrinos based on simulations of a one-year data-taking equivalent. \textsc{Theia}{}'s first high statistics geoneutrino measurement in North America will be complementary to measurements in Asia and in Europe. A combined analysis, with contributions from experiments across the globe, is critical for understanding the contributions of the crust and mantle. \textsc{Theia}{}'s good energy resolution also offers the potential to extract the \ce{Th}/\ce{U} mass ratio from a spectral fit. We also estimate the sensitivity of \textsc{Theia}{} at SURF towards the antineutrinos originating at nuclear reactors at baseline of more than 700 km.
In Section~\ref{sec:sig_bkg}, we give a short overview of the antineutrino sources, the advantages of their detection, as well as the assumptions on the main background sources. We proceed by describing the full Monte Carlo simulations we have performed in Section~\ref{sec:mc}, including all the inputs. Section~\ref{sec:analysis} presents the analysis methods, while Section~\ref{sec:results} focuses on the results.
\section{Signals and Backgrounds}
\label{sec:sig_bkg}
\subsection{Antineutrino signals}
The main natural antineutrino sources expected at \textsc{Theia}{}-25 at SURF are radioactive elements in the crust and mantle of the Earth. Geoneutrinos are electron flavour antineutrinos emitted inside the Earth, in the radioactive decays of HPEs with lifetimes comparable with the age of the Earth (\SI[exponent-product=\ensuremath{\cdot}]{4.54e9}{\year}):
\ce{^232Th} ($T_{1/2} = \SI[exponent-product=\ensuremath{\cdot}]{1.40e10}{\year}$),
\ce{^238U} ($T_{1/2} = \SI[exponent-product=\ensuremath{\cdot}]{4.47e9}{\year}$),
\ce{^235U} ($T_{1/2} = \SI[exponent-product=\ensuremath{\cdot}]{7.04e8}{\year}$),
and \ce{^40K} ($T_{1/2} = \SI[exponent-product=\ensuremath{\cdot}]{1.25e9}{\year}$)\,\cite{IAEA}:
\begin{align}
\ce{^238U} \rightarrow& \, \ce{^206Pb} + 8\alpha + 8 e^{-} + 6 \bar{\nu}_e + \SI{51.7}{\mega\electronvolt} \nonumber\\
\ce{^235U} \rightarrow& \, \ce{^207Pb} + 7\alpha + 4 e^{-} + 4 \bar{\nu}_e + \SI{46.4}{\mega\electronvolt} \nonumber\\
\ce{^232Th} \rightarrow& \, \ce{^208Pb} + 6\alpha + 4 e^{-} + 4 \bar{\nu}_e + \SI{42.7}{\mega\electronvolt} \nonumber \\
\ce{^40K} \rightarrow& \, \ce{^40Ca} + e^{-} + \bar{\nu}_e + \SI{1.31}{\mega\electronvolt}~\mathrm{(89.3\%)} \nonumber\\
\ce{^40K} + e^{-} \rightarrow& \, \ce{^40Ar} + \nu _{e} + \SI{1.505}{\mega\electronvolt}~\mathrm{(10.7\%)}. \nonumber
\end{align}
Geoneutrino measurements can shed light on abundances and distributions of radioactive elements inside the Earth beyond the reach of direct measurements by sampling. In each decay, the emitted radiogenic heat is in a well-known ratio to the number of emitted geoneutrinos, providing a way to directly assess the Earth's heat budget\,\cite{Fiorentini:2007te}.
In addition to neutrinos produced from within the Earth, nuclear power plants produce abundant antineutrinos and are the strongest man-made source. Many nuclei, produced in the fission process of nuclear fuel, decay through $\beta$-processes with the consequent emission of electron antineutrinos with the energy up to \SI{10}{\mega\electronvolt}.
Antineutrinos can be detected via the inverse beta decay (IBD) reaction:
%
\begin{equation}
\bar{\nu}_{e} + p \rightarrow e^{+} + n,
\label{feq:ibd_int}
\end{equation}
%
in which the free protons of hydrogen nuclei act as the target.
IBD is a charge-current interaction that proceeds only for electron flavoured antineutrinos.
Since the combined mass of the neutron and positron is greater than the mass of the proton, the IBD interaction has a kinematic threshold of \SI{1.806}{\mega\electronvolt}.
A positron and a neutron are emitted as reaction products in this process.
The positron promptly comes to rest and annihilates emitting two 511\,keV $\gamma$-rays from para-positronium and three $\gamma$-rays from ortho-positronium decays, yielding a ``prompt'' signal, with a visible energy $E_\text{vis}$, which is directly correlated with the incident antineutrino energy $E_{\bar{\nu}_e}$:
%
\begin{equation}
E_\text{vis} \sim E_{\bar{\nu}_e} - \SI{0.784}{\mega\electronvolt}.
\label{eq:Epro}
\end{equation}
%
The offset results mostly from the difference between the \SI{1.806}{\mega\electronvolt}, absorbed from $E_{\bar{\nu}_e}$ in order to make the IBD kinematically possible, and the \SI{1.022}{\mega\electronvolt} energy released during the positron annihilation.
The emitted neutron initially retains information about the ${\bar{\nu}_e}$ direction.
However, the neutron is detected only indirectly, after it is thermalized and captured, mostly on a proton.
Such a capture leads to an emission of a \SI{2.22}{\mega\electronvolt} $\gamma$-ray, which interacts typically through several Compton scatterings and is detected in a delayed signal.
\subsection{Overview of background sources}
The time and spatial coincidence between prompt and delayed signals offer a clean topology for $\bar{\nu}_e$ IBD interactions, which strongly suppresses backgrounds.
Nevertheless, there are some non-antineutrino backgrounds that can imitate the IBD signature.
The rates of these backgrounds depend on the selection cuts applied to the search of prompt and delayed event coincidences. Assuming the same neutron capture time in WbLS as in water of $\tau_\text{n}=\SI{202}{\micro\second}$\,\cite{SNO:2020bdq}, an upper-bound for the time search of correlated events for IBD pairs candidates of $\Delta\text{t}_\text{cut}\equiv\SI{1}{\milli\second}$ is defined, corresponding to $5\tau_\text{n}$. However, the final selection cuts on the space and time correlation have been optimized and will be discussed in Section~\ref{subs:box}. Backgrounds mimicking the IBD interaction can be divided into two categories: 1) two independent sources produce prompt- and delayed-like events, 2) a sole physical process produces both the prompt and delayed events correlated in space and time.
We will refer to these categories as accidental and correlated backgrounds, respectively.
In the following, we give a brief overview of the backgrounds that can potentially contribute to the antineutrino search and classify them into those that require Monte Carlo simulations and those that can be safely neglected for this study.
\paragraph{Accidentals}
Radioactive impurities inside the PMTs glass bulb or dissolved in the WbLS are the primary sources of accidental background.
The cleaner the PMT glass and target material, the less is the probability of accidental coincidence to satisfy the search for prompt and delayed event pairs.
All these contributions were simulated and are discussed in Section~\ref{subsec:acc}.
\paragraph{Correlated from cosmogenic backgrounds}
A high-energy cosmic muon can produce a copious amount of activated radioisotopes while knocking off nuclei along its path.
Whilst in most cases these muons are easily recognizable as they leave a very clear signature inside the detector losing about \SI{2}{\mega\electronvolt\per\centi\meter}, the spallation products can be missed, creating an IBD-like signal from their subsequent decay.
Short-lived radioisotopes can be significantly suppressed by using a time veto cut.
However, long-lived radioisotopes can create a coincidental background long after the muon has been detected.
A previous study using data from Super-Kamiokande and FLUKA simulations evaluated the amount of radioisotopes spallation products from the muon track in water \cite{Li:2014sea}.
Assuming the same yield in WbLS, the expected spallation production rates inside \textsc{Theia}{}-25 are evaluated using Equation~\ref{eq:spallation-rates}:
%
\begin{eqnarray}
\phi_i &=& Y_i B_i P_i(\mu_\text{cut}) \cdot \Phi_\mu \label{eq:spallation-rates} \\
&=& Y_i B_i \exp{\left(-\ln{2}\,\frac{\mu_\text{cut}}{T_{{1/2}_i}}\right)} \cdot \int\limits_\theta \phi_\mu \mathcal{A} l_\mu \mathrm{d}\theta, \nonumber
\end{eqnarray}
%
where $Y_i$ is the yield of radioisotope $i$ taken from Reference\,\cite{Li:2014sea}, $B_i$ is the branching ratio for the considered decay, $P_i$ is the probability of the isotope with half-life $T_{{1/2}_i}$ to survive the muon veto cut $\mu_\text{cut}$, and $\Phi_\mu$ is the product of the muon flux and its path length inside the detector, integrated over all directions. The term $\Phi_\mu$ does not depend on the radioisotope $i$ and can be calculated with the average path length of all muons inside \textsc{Theia}{}-25 $\bar{l}_\mu$, assuming an overall angular distribution of cosmic muons to be $\propto\cos^n\theta_Z$\,\cite{Shukla:2016nio}, the coverage area above \textsc{Theia}{}-25 $\mathcal{A}$, and the integrated muon flux, measured previously at SURF to be $\phi_{\mu} = \SI{5.31e-9}{\mu\per\second\per\centi\square\meter}$\,\cite{Muon_flux_Majorana}.
Spallation products of interest can be divided into two categories: ($\beta^-$, n) emitters creating a correlated background, and $\beta^\pm$ emitters which can decay in coincidence with another spallation product from the same muon, creating a background that is fundamentally accidental but somewhat correlated in time and space. Tables~\ref{tab:spallation_rates} and~\ref{tab:spallation_single_rates} show the summary of the ($\beta^-$, n) and $\beta^\pm$ longest-lived radioisotopes of interest.
\begin{table}[!htb]
\caption{Summary of ($\beta^-$, n) emitters spallation products of interest inside \textsc{Theia}-25 and expected rates inside the whole volume before and after a \SI{1}{\second} muon veto cut.}
\centering
\begin{tabular}{p{0.8cm}p{0.8cm}p{0.8cm}p{1.2cm}p{1.2cm}p{1.4cm}}
\hline\noalign{\smallskip}
Isotope& $T_{1/2}$ & $B_i$ & $Y_i$ [$10^{-7}$ & $\phi_i$ & $\phi_\text{veto}$\\
& \SI{}{[\second]} & & \,\SI{}{\per\mu\per\gram\cdot\centi\square\meter}] & [\SI{}{\evts\per\year}] & [\SI{}{\evts\per\year}] \\
\noalign{\smallskip}\hline\noalign{\smallskip}
\ce{^{17}N} & 4.173 & 1 & 0.59 & 317 & 269\\
\ce{^{16}C} & 0.747 & 1 & 0.02 & 10.8 & 4.25\\
\ce{^{9}Li} & 0.178 & 0.51 & 1.90 & 520 & 9.6\\
\ce{^{8}He} & 0.119 & 0.16 & 0.23 & 19.78 & 0.06\\
\noalign{\smallskip}\hline
\end{tabular}
\label{tab:spallation_rates}
\end{table}
A dedicated study to evaluate the impact of a muon veto cut on the spallation rates has been performed.
For correlated backgrounds, the contribution of \ce{^{9}Li} and \ce{^{8}He} can be strongly suppressed by setting a \SI{1}{\second} muon veto cut.
Its impact on the rates is by comparing the values in the last two columns of Table~\ref{tab:spallation_rates}.
This time cut will result in a dead-time of the experiment of 6.7\%, which is applied to the signal and other background rates.
\begin{table}[!htb]
\caption{Most abundant single emitting $\beta$ products of spallation after a \SI{1}{\second} muon veto cut.}
\centering
\begin{tabular}{llllll}
\hline\noalign{\smallskip}
Isotope & Decay & $T_{1/2}$ \SI{}{[\second]} & $B_i$ & {$Y_i$} & $\phi_\text{veto}$ \SI{}{[\hertz]}\\
\noalign{\smallskip}\hline\noalign{\smallskip}
\ce{^{16}N} & $\beta^-$ & 7.13 & 0.94 & 18 & \SI{1.85e-4}{} \\
\ce{^{8}Li} & $\beta^-$ & 0.838 & 1 & 13 & \SI{6.85e-5}{} \\
\ce{^{8}B} & $\beta^+$ & 0.77 & 1 & 5.8 & \SI{2.84e-5}{} \\
\ce{^{9}Li} & $\beta^-$ & 0.178 & 0.49 & 1.9 & \SI{2.28e-7}{} \\
\noalign{\smallskip}\hline
\end{tabular}
\label{tab:spallation_single_rates}
\end{table}
The probability that a radioisotope decays within a specific time interval $\Delta\text{t}$ is $P = \exp{\left(-\Delta\text{t}\ln{2}/T_{1/2}\right)}$.
Taking into account all combinations of decays between isotopes from Table~\ref{tab:spallation_single_rates}, the resulting expected number of coincidence is estimated to be less than \SI{9e-4}{} events per year for $\Delta\text{t}=\Delta\text{t}_\text{cut}\equiv\SI{1}{\milli\second}$.
Therefore, from all the spallation products of cosmogenic muons only the leading contribution of \ce{^{17}N} is considered.
The details of the simulation are discussed in Section~\ref{subsec:cor}.
\paragraph{Correlated from fast neutrons}
A fast neutron (with an energy $\geq\SI{1}{\mega\electronvolt}$) interaction on a WbLS nucleus can imitate the IBD signature by producing a proton recoil, falsely identified as a prompt signal, and subsequently being thermalized and captured on a hydrogen hence producing a correlated delayed signal.
This recoil proton from neutron elastic scattering can produce measurable ionization, described by the empirical Birk's law\,\cite{Birks:1951boa}, which is an empirical formula for the light yield per path length as a function of energy loss per path length for an ionizing particle.
Birk's constant, $k_B$, which characterizes this process, has not yet been measured in WbLS at the \SI{}{\mega\electronvolt} scale, but can be interpolated from measurement at BNL with a high-energy proton beam\,\cite{Bignell:2015oqa}.
These fast neutrons are also a spallation product of high-energy cosmogenic muons passing through matter.
Therefore their rates are estimated using the same parent cosmogenic muon flux as in the previous section.
The characteristic fast neutron thermalization time constant during which a proton recoil may create a prompt signal is \SI{5.3}{\micro\second} \cite{fn_thermalization}, and afterwards the neutron capture time is taken as $\tau_\text{n}=\SI{202}{\micro\second}$.
Using the previously set muon veto cut of \SI{1}{\second}, the identification of the parent muon will strongly suppress all fast neutrons produced inside \textsc{Theia}{}-25.
Therefore all fast neutrons produced by visible muons are not considered throughout this analysis.
However, muons missing the detector may produce fast neutrons in the surrounding rock, and these can reach \textsc{Theia}{}-25 inner volume.
A previous study\,\cite{fast_neutrons_PhysRevD.73.053004} provides a parametrization of the expected fast neutron flux produced along the cosmic muons track at various underground laboratories ($\phi_n=\SI{5.39e-10}{\centi\meter^{-2}\second}^{-1}$ at SURF), the neutron multiplicity ($m_n=7.02$) and mean energy ($\langle E_n \rangle = \SI{98}{\mega\electronvolt}$), together with the fraction of neutrons detected with respect to the distance of the muon track.
Typically, the neutron flux is attenuated by about two orders of magnitude at distances larger than \SI{3.5}{\meter} from the muon track; however, as much as 10\% remain at distances from 2 to \SI{2.5}{\meter}\,\cite{fast_neutrons_PhysRevD.73.053004}.
Integrating from \textsc{Theia}{}-25 edges, the muon-induced neutron flux in the rocks surrounding the detector yields a rate:
%
\begin{equation}
m_n \phi_n \int\limits_0^\infty (2x(L+H)+4x^2)e^{-x}\mathrm{d}x = \SI[exponent-product=\ensuremath{\cdot}]{6.70e-3}{n\per\second},
\end{equation}
%
with $L=\SI{70}{\meter}$ \textsc{Theia}{}-25 length, $H=\SI{18}{\meter}$ \textsc{Theia}{}-25 width, and $x$ the distance from \textsc{Theia}{}-25 edges.
Therefore the fast neutrons contribution to the correlated background is considered, and its simulation is discussed in Section~\ref{subsec:fastn}.
\paragraph{Correlated from atmospheric neutrino neutral current interaction}
Atmospheric neutrinos can interact by neutral current quasielastic nucleon knock-out (NCQE) process on \ce{^{16}O}:
%
\begin{eqnarray}
\nu + \ce{^{16}O} &\rightarrow& \nu + n + \ce{^{15}O^*} \label{eq:NCQE} \\
\nu + \ce{^{16}O} &\rightarrow& \nu + p + \ce{^{15}N^*}.
\end{eqnarray}
%
This interaction becomes dominant for $E_\nu \geq \SI{200}{\mega\electronvolt}$ until \SI{1}{\giga\electronvolt} when neutral current inelastic process without nucleon knock-out, $\nu + \ce{^{16}O} \rightarrow \nu + \ce{^{16}O^*}$, overtake\,\cite{PhysRevLett.108.052505}.
The process shown in Equation~\ref{eq:NCQE} is a background to a low energy antineutrino search through IBD, because the excited \ce{^{15}O^*} will immediately decay into \ce{^{15}O} emitting $\gamma$-rays from nuclear de-excitation.
Reference~\cite{PhysRevLett.108.052505} provides a theoretical treatment of the probabilities of occurrences of different excited states, summarized in Table~\ref{tab:O15}.
The $(p_{1/2})^{-1}$ is the ground state of \ce{^{15}O} and therefore does not emit $\gamma$-ray.
The $(p_{3/2})^{-1}$ almost always emits one $\gamma$-ray with \SI{6.18}{\mega\electronvolt} energy.
The higher energy states $(s_{1/2})^{-1}$ and everything higher, referred to simply as ``others'', have a large branching ratio to nucleons or alpha particles, which can lead to secondary $\gamma$-rays emissions.
At the moment, there is neither data nor a theoretical prediction of $\gamma$-ray emission for the higher energy states covered by others.
Further detailed descriptions on the treatment of these states are given in References~\cite{PhysRevLett.108.052505,Folomeshkin:1976vj}.
%
\begin{table}[!htb]
\caption{Probabilities of \ce{^{15}O^*} state occurrences \cite{PhysRevLett.108.052505}. }
\centering
\begin{tabular}{lll}
\hline\noalign{\smallskip}
\ce{^{15}O^*} state & $P$ & $\gamma$ [\SI{}{\mega\electronvolt}] \\
\noalign{\smallskip}\hline\noalign{\smallskip}
$(p_{1/2})^{-1}$ & 0.158 & -- \\
$(p_{3/2})^{-1}$ & 0.3515 & \SI{6.18}{\mega\electronvolt}\\
$(s_{1/2})^{-1}$ & 0.1055 & $>$ \SI{8}{\mega\electronvolt} \\
others & 0.385 & \\
\noalign{\smallskip}\hline
\end{tabular}
\label{tab:O15}
\end{table}
%
The number of atmospheric NCQE interactions can be estimated by taking the convolution of the atmospheric neutrino flux with the electron and muon neutrino neutral-current cross-section.
The atmospheric neutrino flux at SURF is estimated from the modified ``DPMJET-III'' model\,\cite{Honda:2006qj}.
The oscillation probability is calculated with the Osc3++ framework\,\cite{Super-Kamiokande:2019gzr}.
Since atmospheric neutrinos generally experience a varying matter profile, and hence electron density changes as they travel through the Earth, they experience a variety of matter effects\,\cite{Wolfenstein:1977ue}. The calculation of oscillation probability in this analysis takes such variation on matter density into consideration, with a simplified version of the preliminary reference Earth model (PREM)\,\cite{Super-Kamiokande:2017yvm}.
NCQE cross-sections tables are taken from the NEUT framework\,\cite{Hayato:2009zz}.
For NCQE interactions the nominal nucleon momentum distribution is based on the Benhar spectral function\,\cite{Ankowski:2011ei,Benhar:2005dj}. The expected atmospheric neutrino rate is given by:
%
\begin{eqnarray}
N = \mathcal{N}_{n\ce{^{16}O}} \times
\int\limits_{\SI{200}{\mega\electronvolt}}^{\SI{1}{\giga\electronvolt}}
\int\limits_{0^\circ}^{90^\circ}
\phi(E_\nu, \theta) P(E_\nu, \theta) \times \nonumber\\
\sigma_\text{NCQE}(E_\nu)
\text{d}E_\nu \text{d}\theta\nonumber,
\end{eqnarray}
%
\noindent with $E_\nu$ the neutrino energy, $\theta$ the zenith angle, $\mathcal{N}_{n\ce{^{16}O}}$ the number of neutron target available, $\phi(E_\nu, \theta) P(E_\nu, \theta)$ the neutrino oscillated flux, and $\sigma_\text{NCQE}(E_\nu)$ the neutrino-oxygen neutral-current quasi-elastic (NCQE) cross-section.
After integration, the expected atmospheric neutrino NCQE rate is $\phi_{{\text{atm}}}=\SI{3.25e-06}{\hertz}$.
The expected rate of excited $(p_{3/2})^{-1}$ \ce{^{15}O^*} rate will be the product of $\phi_{{\text{atm}}}$ with the respective branching ratio, yielding \SI{1.14e-6}{\hertz} or 36.0 events per year.
Only the dominant contribution from the $(p_{3/2})^{-1}$ \ce{^{15}O^*} excited state is simulated and discussed in Section~\ref{subsec:NCQE}.
\paragraph{(${\alpha}$, n) background}
Energetic ${\alpha}$ particles, generated in $\ce{Po}$ decays along the $\ce{U}$ and $\ce{Th}$ chains, as well as an out-of equilibrium \ce{^210Po}, can produce neutrons and imitate IBDs. The processes of $\ce{^18O}(\alpha,n)\ce{^21Ne^*}$ and its equivalent with \ce{^17O}, produce neutrons.
As \ce{^21Ne^*} decays by neutron emission, each reaction of this kind produces two neutrons, with one being mistaken for a positron prompt signal and second one satisfying the delayed event criteria.
Moreover, in addition to neutron produced during ${\alpha}$ interaction on \ce{^13C},
\begin{equation}
\ce{^13C} +\alpha \longrightarrow \: \ce{^16O}^* + n,
\end{equation}
there are three possibilities for the generation of the event that can imitate an IBD prompt event\,\cite{Geo_Borexino}:
\begin{itemize}
\item $\gamma$-emission with energy of \SI{6.13}{\mega\electronvolt} or \SI{6.05}{\mega\electronvolt}, as a result of \ce{^16O^*} de-excitation;
\item recoil proton appearing after the scattering of the fast neutron on proton;
\item \SI{4.4}{\mega\electronvolt} $\gamma$-ray that is a product of the two-stage process: First, \ce{^12C} is excited into \ce{^12C^*} in an inelastic scattering off a fast neutron.
Then, \ce{^12C^*} transits to the ground state, accompanied by the $\gamma$ emission:
%
\begin{align}
n + \: ^{12}\text{C} &\longrightarrow \: ^{12}\text{C}^* + n, \\
^{12}\text{C}^* &\longrightarrow \: ^{12}\text{C} + \gamma \: (4.4\,\text{MeV}).
\label{eq:inelastic_scattering}
\end{align}
\end{itemize}
%
Probabilities of all above-mentioned (${\alpha}$, n) processes in 3\% WbLS target material have been calculated using the NeuCBOT\,\cite{NeuCBOT} software. We assume SNO cleanliness level for water\,\cite{SNO_water} (see Section~\ref{subsec:acc}), Borexino Phase-I cleanliness level for LS\,\cite{Geo_Borexino} with natural abundances of \ce{^17O}, \ce{^18O}, and \ce{^13C}.
The total expected (${\alpha}$, n) interaction rates are 2.16 on \ce{^13C}, 1.80 on \ce{^17O}, and 15.2 on \ce{^18O} events per year. Only the dominant contribution from $\ce{^18O}(\alpha,n)\ce{^21Ne^*}$ is simulated and discussed in Section~\ref{subsec:AlphaN}.
\section{Monte Carlo simulation}
\label{sec:mc}
\subsection{Detector configuration}
The detector configuration is modeled as a right cylinder with \SI{18}{\meter} diameter and \SI{70}{\meter} height.
Even though a letterbox \textsc{Theia}{}-25 detector would be deployed at SURF as shown in Figure~\ref{fig:Theia-25kT}, the right cylinder geometry was chosen as it was readily available within the simulation framework.
Furthermore, the reconstruction algorithm described in Section~\ref{subs:recon} had been previously set up to work with this right cylinder geometry.
Since this analysis relies on a volume fiducialization to optimize the signal over background ratio, edge effects that could affect event reconstruction at the letterbox's corners can be neglected, the reconstruction behaving similarly between both geometries far from the edges.
The expected target volume of this configuration would be \SI{17.8}{\kilo\tonne} (corresponding to \num{11.9e32} free protons).
Facing inwards arranged against the inner wall of the cylinder are located 79432 10" Hamamatsu R7081-100 PMTs, with 34\% quantum efficiency (QE) and \SI{1.5}{\nano\second} transit time spread (TTS).
A \SI{3}{\kilo\hertz} dark rate is assumed for this PMT model operating at a nominal gain.
This number of PMTs corresponds to an effective coverage of the detector walls and caps at 90\%, which is the highest photo-coverage achievable (in terms of packing capacity).
Lower coverage can be studied by scaling the number of PMT hits prior to the event reconstruction.
Simulation of the neutrino interactions and radioactive decays is performed using the Geant4-based\,\cite{geant4} RAT-PAC{} framework\,\cite{ratpac}.
Cherenkov photon production is handled by the default Geant4 model, G4Cerenkov.
Rayleigh scattering is implemented by the module developed by the SNO+ collaboration\,\cite{snoplus_private}.
GLG4Scint model handles the generation of scintillation light, as well as photon absorption and reemission. The inputs to the optical model used in the simulation are primarily based on data and bench-top measurements.
We chose 3\% WbLS (3\% liquid scintillator, 97\% water) with the light yield of 502 photons/MeV as the baseline target material to simulate. The light yield, the scintillation emission spectrum and time profile were interpolated from the 1\%, 5\%, 10\% WbLS measurements from \cite{chess_wbls} and \cite{drew_wbls}. Preliminary results show that absorption lengths are long and scattering is the dominant mode of light loss.
Due to no published measurements available for the absorption length in this material, the model as described in\,\cite{PhysRevD.103.052004} was used in the simulation. The implemented scattering length was measured at BNL\,\cite{bnl_private}.
\subsection{Signal simulation}
A dedicated generator inside the RAT-PAC{} software uses the positron energy spectrum as input to generate IBD pairs.
The positron spectrum is calculated from the expected antineutrino flux at SURF, available through the geoneutrino.org web app\,\cite{Dye:2015bsw}, uses decay spectra from \cite{Enomoto_Geo_Flux} and parameterized IBD cross section from \cite{Strumia:2003zx}.
Figure~\ref{fig:input_spectra} shows the antineutrino energy spectra used, with the (\ce{Th}/\ce{U}) ratio fixed to $4.24$.
For the reactor neutrinos spectrum, the nominal thermal power and the monthly load factors originate from the power reactor information system (PRIS), developed and maintained by the International Atomic Energy Agency (IAEA)\,\cite{PhysRevD.91.065002, ferrara_reactors}.
The given spectra already consider the neutrino oscillation effects, with the values of oscillation parameters taken from NuFit v5.0, specifically the global analysis excluding the Super-Kamiokande atmospheric neutrino data\,\cite{Esteban:2020cvm}.
%
\begin{figure}[!htb]
\centering
\resizebox{0.49\textwidth}{!}{
\includegraphics{figures/antineutrinos.pdf}
}
\caption{The expected rate of antineutrino interactions at SURF, as the function of antineutrino energies. 1 NIU (Neutrino Interaction Unit) = 1 IBD interaction/$10^{32}$ targets/year. Source: geoneutrinos.org \cite{Dye:2015bsw}}
\label{fig:input_spectra}
\end{figure}
%
IBD interactions are generated throughout the total WbLS volume available in \textsc{Theia}{}-25.
The number of expected IBD interactions from reactor and geoneutrinos can be found in Table~\ref{tab:SURF_rates}.
We also show the geoneutrino signal breakdown in crust and mantle contributions, expected at SURF.
\begin{table}[!htb]
\caption{Antineutrino interaction rates in one year in the full \textsc{Theia}{}-25\,kT volume.}
\centering
\begin{tabular}{ccccc}
\hline\noalign{\smallskip}
\multirow{4}{*}{Interactions [\SI{}{\evts\per\year}]}& \multicolumn{2}{c}{$R_\text{rea}$} & \multicolumn{2}{c}{$R_\text{geo}$} \\
& \multicolumn{2}{c}{384.7} & \multicolumn{2}{c}{551.4} \\ \cline{4-5}
& \multicolumn{2}{c}{} & $R_\text{crust}$ & $R_\text{mantle}$ \\
& \multicolumn{2}{c}{} & 441.8 & 109.6 \\
\noalign{\smallskip}\hline
\end{tabular}
\label{tab:SURF_rates}
\end{table}
\subsection{Background simulation}
\paragraph{Accidentals}
\label{subsec:acc}
The accidental coincidence rate is estimated from the R7081-100 PMT glass activity measurements by the WATCHMAN collaboration\,\cite{watchman_private} and the \ce{U}- and \ce{Th}-chain
backgrounds in the target material to be at the level of SNO water\,\cite{SNO_water}.
Table~\ref{tab:accidentals_rates} presents the concentration and the activity of each isotope used in the simulations, along with the calculated decay rate.
The PMT glass mass is taken as \SI{1400}{\gram}.
\begin{table}[!htb]
\caption{Assumed isotope concentrations, based on the R7081-100 PMT glass activity measurements by the WATCHMAN collaboration \cite{watchman_private} and the SNO cleanliness level water activity \cite{SNO_water}, followed by the corresponding expected rates inside the full \textsc{Theia}{}-25 volume.}
\centering
\begin{tabular}{llll}
\hline\noalign{\smallskip}
& Concentration & Activity & Rates \\
& & [\SI{}{\becquerel\per\gram}] & [\SI{}{\hertz}]\\
\noalign{\smallskip}\hline\noalign{\smallskip}
PMT \ce{^{238}U} & 0.043 [ppm] & \SI{1.24e4}{} & \SI{60.8e3}{} \\
PMT \ce{^{232}Th} & 0.134 [ppm] & \SI{1.45e3}{} & \SI{22.1e3}{} \\
PMT \ce{^{40}K} & 0.004212 [ppm] & \SI{2.59e5}{} & \SI{124.3e3}{} \\
Water \ce{^{238}U} & \SI{6.6e-15}{[\gram/\gram]} & \SI{1.24e4}{} & \SI{1.46}{} \\
Water \ce{^{232}Th} & \SI{8.8e-16}{[\gram/\gram]} & \SI{1.45e3}{} & \SI{2.27e-2}{} \\
\noalign{\smallskip}\hline
\end{tabular}
\label{tab:accidentals_rates}
\end{table}
A custom decay chain generator within RAT-PAC{} is used in order to simulate the spectra for these radioisotopes, starting from \ce{^{214}Bi} and \ce{^{208}Tl} for \ce{^{238}U} and \ce{^{232}Th} respectively. In the following, we will refer to these events with \ce{^{214}Bi} and \ce{^{208}Tl} designations.
The \ce{^234Pa} contribution for \ce{^{238}U} and \ce{^228Ac}, \ce{^212Bi} for \ce{^{232}Th} are ignored since their lower rates would have a negligible impact on the expected rates.
The $\beta$ spectrum of \ce{^{40}K} is used directly.
About $\mathcal{O}(10^6)$ events are simulated for each contribution. Contributions to the accidentals rate from any other single backgrounds can be safely neglected.
\paragraph{Correlated from cosmogenic backgrounds}
\label{subsec:cor}
The \ce{^{17}N} $\beta$ spectrum is simulated using RAT-PAC{}.
The delayed neutron is simulated separately as a \SI{2.22}{\mega\electronvolt} $\gamma$-ray, and both events are reassembled as a correlated background during the creation of the dataset described at Section~\ref{sec:datasets}.
About $\mathcal{O}(10^5)$ \ce{^{17}N} $\beta$ and \SI{2.22}{\mega\electronvolt} $\gamma$-ray events are simulated.
\paragraph{Correlated from fast neutrons}
\label{subsec:fastn}
Birk's constant for WbLS 3\% has been extrapolated from Reference~\cite{Bignell:2015oqa} to be \SI{0.43}{\milli\meter\per\mega\electronvolt}.
The fast neutron energy spectrum is taken as an exponential law with a mean value of $\langle E_n \rangle = \SI{98}{\mega\electronvolt}$ \cite{fast_neutrons_PhysRevD.73.053004} and simulated inside RAT-PAC{} at the edges of \textsc{Theia}{}-25.
About $\mathcal{O}(10^5)$ fast neutrons are simulated.
\paragraph{Correlated from atmospheric NCQE interaction}
\label{subsec:NCQE}
The $(p_{3/2})^{-1}$ deexcitation state of \ce{^15O^*} is simulated using RAT-PAC{} as a \SI{6.18}{\mega\electronvolt} $\gamma$-ray.
The delayed neutron is simulated separately as a \SI{2.22}{\mega\electronvolt} $\gamma$-ray, and both events are reassembled as a correlated background during the creation of the dataset described at Section~\ref{sec:datasets}.
About $\mathcal{O}(10^5)$ \SI{6.18}{\mega\electronvolt} $\gamma$-rays from \ce{^15O^*} and \SI{2.22}{\mega\electronvolt} $\gamma$-rays are simulated.
\paragraph{(${\alpha}$, n) background}
\label{subsec:AlphaN}
The $\ce{^18O}(\alpha,n)\ce{^21Ne^*}$ interaction is simulated using RAT-PAC{} as two successive \SI{2.22}{\mega\electronvolt} $\gamma$-rays.
Both events are reassembled as a correlated background during the creation of the dataset described at Section~\ref{sec:datasets}.
About $\mathcal{O}(10^5)$ \SI{2.22}{\mega\electronvolt} $\gamma$-rays are simulated.
\section{Analysis}
\label{sec:analysis}
\subsection{Methodology for analysis}
In order to obtain the sensitivity of the \textsc{Theia}{}-25 detector to antineutrinos, the following analysis steps were implemented:
\begin{enumerate}
\item Reconstruction of the event vertex position based on the PMT hit times.
\item Creation of merged dataset using an iterative procedure to prune background and select candidate IBD pairs from all signal and background events.
\item Optimization of Region-of-Interest (ROI) to increase signal-to-background ratio for a given antineutrino signal.
\item Sensitivity analysis based on the creation and spectral fit of one-year data equivalent toy experiments.
\end{enumerate}
\subsection{Reconstruction}
\label{subs:recon}
A dedicated code was developed to reconstruct event vertex positions based on the time-of-flight. We build the binned distribution of the PMT hits residuals, i.e., the difference between the PMT hit times $T_\text{Hit}$ and the time traveled by photons from the vertex interaction to the PMT position $\vec x_\text{Hit}$:
%
\begin{equation}
T_\text{Res}^i = \int\limits_\text{i}^\text{i+1}
\sum_\text{Hit} T_\text{Hit}-T_\text{est} - \frac{ \vec x_\text{Hit} - \vec x_\text{est} }{ c_\text{water} } ~\mathrm{dt}.
\end{equation}
The fit works by performing a maximum negative log-likelihood (NLL) search of the estimated vertex time $T_\text{est}$ and position $\vec x_\text{est}$ from a probability density function (PDF), created from a simulation of \SI{5}{\mega\electronvolt} electrons at the center of the detector.
A seeding algorithm is based on multilateration -- similar to the GPS location algorithm -- of all PMT hits. Solving the set of time-of-flight equations, we create a cloud of vertices eligible as hypotheses. This procedure yields $\mathcal{O}(10^3)$ seeds to reconstruct.
Figure~\ref{fig:reconstruction} shows the performance of positrons reconstruction from IBD interactions simulated throughout the whole \textsc{Theia}{}-25 volume.
For positrons from geoneutrino interactions vertex resolutions of ($58.0\pm0.3)\,\SI{}{\centi\meter}$ perpendicular to the cylinder axis and ($32.8\pm0.2)\,\SI{}{\centi\meter}$ parallel to the cylinder axis are achieved, while for reactor antineutrinos overall resolutions of ($34.3\pm0.2)\,\SI{}{\centi\meter}$ perpendicular to the cylinder axis and ($26.6\pm0.1)\,\SI{}{\centi\meter}$ parallel to the cylinder axis are obtained.
Moreover, we have mapped the energy resolution of the positrons between \SI{0.5}{\mega\electronvolt} and \SI{4}{\mega\electronvolt} generated throughout the whole detector volume.
As shown in Figure~\ref{fig:Energy_resolution}, the obtained energy resolution can be approximated as ${14\%}/{\sqrt{E}}$ for this particular choice of target material and detector configuration.
\begin{figure*}[!hbt]
\centering
\resizebox{0.99\textwidth}{!}{
\includegraphics{figures/New_Vtx_Geonu.png}
\includegraphics{figures/New_Vtx_Rea.png}
}
\caption{Reconstruction performance with respect to positron true position, for geo- (left) and reactor $\overline{\nu}_e$ (right), integrated throughout the whole detector and energy spectrum.}
\label{fig:reconstruction}
\end{figure*}
\begin{figure}[!hbt]
\centering
\resizebox{0.49\textwidth}{!}{
\includegraphics{figures/Energy_resolution.png}
}
\caption{Energy reconstruction resolution for positrons generated throughout the whole detector volume between \SI{0.5}{\mega\electronvolt} to \SI{4}{\mega\electronvolt}.}
\label{fig:Energy_resolution}
\end{figure}
\subsection{Event pruning and pairs dataset creation}
\label{sec:datasets}
The search for candidate pairs in the simulated data is dealt with by creating a single merged dataset of all signal and background contributions, which intersperses events in time in order to mimic data from the detector.
This allows a full study of accidentals, including all correlations, as well as true coincidence backgrounds.
The events are merged thanks to an iterative process.
For each component $B_i$, an interval $\Delta\text{t}(B_i)$ is calculated:
%
\begin{equation}
\Delta\text{t}(B_i) = \frac{-\ln(1-u)}{\phi(B_i)},
\end{equation}
%
\noindent where $u$ is a random number generated from a uniform distribution between ]0, 1[ and $\phi(B_i)$ is the rate associated with component $B_i$.
The shortest $\Delta\text{t}(B_i)$ is selected as the next event to be merged, and the time of the event is added to a previous point in time, starting at $t_0$:
%
\begin{equation}
t_{i+1} = t_i + \min_i{\left(\Delta\text{t}(B_i)\right)}.
\end{equation}
%
\noindent The procedure is iterated until $t_i =$ 1 year.
Special care is taken for some correlated backgrounds that do not have a dedicated Geant4 generator implemented in RAT-PAC{}, and were simulated in two stages: first, the equivalent prompt signal, and then the \SI{2.22}{\mega\electronvolt} $\gamma$-ray from the neutron capture on hydrogen.
To ensure the spatial correlation between the two events, both the equivalent prompt signal and \SI{2.22}{\mega\electronvolt} $\gamma$-ray were simulated at the center of the detector.
This spatial correlation is preserved during the merging procedure, when the prompt and delayed events pair are placed together at a random position within the detector volume.
Lastly, each prompt event is assigned a corresponding delayed event with $\Delta\text{t}$ according to the neutron capture time, randomly sampling an exponential distribution $\exp{-\Delta\text{t}/\tau_{\text{n}}}$.
%
\begin{figure*}[!htb]
\centering
\resizebox{0.99\textwidth}{!}{
\includegraphics{figures/n400.png}
\includegraphics{figures/dwall.png}
\includegraphics{figures/chi2.png}
}
\caption{PMT (in red) and signal (in blue) event distributions of the characteristic parameters used in the BDT training: $n_{400}$ energy estimator (left), $d_\text{wall}$ distance of the reconstructed event from the closest wall (middle), and $\chi^2$ of the reconstruction fit (right).
}
\label{fig:BDT_features}
\end{figure*}
%
\paragraph*{}
The high fission rates of radioisotopes contained in the PMT glass (see Table~\ref{tab:accidentals_rates}) will yield about $\mathcal{O}(10^5\SI{}{\hertz})$ background events during this iterative process.
Hence, extra steps are needed to prune the number of IBD candidates before saving the merged dataset to disk and performing the subsequent analysis steps.
First, a cut on $\Delta\text{t}(B_i)\geq\SI{1}{\milli\second}$ discards events separated by more than $5\tau_n$.
Second, a cut $\Delta\text{R}\geq\SI{3}{\meter}$ between the distance of two consecutive events,
%
\begin{equation}
\Delta\text{R} = \vec{\mathbf{v}}_{B_{i+1}} - \vec{\mathbf{v}}_{B_{i}},
\end{equation}
%
discards events unlikely to originate from a single source.
Even considering the finite reconstruction resolution of the detector (see Figure~\ref{fig:reconstruction}) and the neutron displacement during its thermalization, it is expected that the prompt and delayed events of a true IBD interaction are contained within $\Delta\text{R}$.
Nevertheless, both $\Delta\text{t}$ and $\Delta\text{R}$ cuts do not yield enough suppression for the PMT accidental backgrounds.
Therefore, $\Delta\text{t}$ and $\Delta\text{R}$ cuts are complemented with an additional cut from a Boosted Decision Tree (BDT) in order to distinguish PMT radioisotope decays from the geo- and reactor antineutrinos prompt signal.
A dedicated study has been performed to evaluate which features have the most powerful handle to discriminate this background from the signal.
Figure~\ref{fig:BDT_features} shows three suitable parameters: an energy estimator of the event, $n_{400}$, which is the number of PMT hits in a \SI{400}{\nano\second} window after the trigger time; the shortest distance from a detector wall to the reconstructed vertex $d_\text{wall}$; and the Goodness-of-Fit $\chi^2$ of the reconstructed vertex, taken as the NLL of the hit time residuals distribution.
A good fit from a radioisotope PMT $\gamma$-ray event would have a low NLL and be close to a detector wall, whereas a bad fit would have higher NLL and be further away from the wall.
Signal events are distributed throughout the detector and a good reconstruction algorithm should yield no dependency between NLL and the true signal position at first order.
Furthermore, it is expected that the fit quality must depend on the number of hits detected.
As the number of hits $n_{400}$ can also be used to estimate the energy of the event, adding this feature to the BDT provides an additional handle from the $d_\text{wall}$ and $\chi^2$, which both depend on the reconstructed vertex position.
%
%
The training of the BDT is performed, using CERN's ROOT library TMVA\,\cite{Hocker:2007ht}, against the hypothesis of being a signal, either a geo- or a reactor prompt event, or a $\gamma$-ray emitted by a \ce{^{214}Bi}, \ce{^{208}Tl} or \ce{^{40}K}. The following inputs are used:
%
\begin{itemize}
\item a total of \num{10000} PMT fission events for each decay chain, \ce{^{214}Bi}, \ce{^{208}Tl} and \ce{^{40}K};
\item a total of \num{10000} IBD interaction events for geo- and reactor antineutrinos. Only the prompt signal is used in the training;
\item an additional \num{10000} \ce{^{214}Bi} and \ce{^{208}Tl} decay chains, corresponding to radioisotopes dissolved in water, are used as a control sample.
Since these \ce{^{214}Bi} and \ce{^{208}Tl} decay chains are similar to the PMTs events, but distributed uniformly throughout the detector, they can indicate if the BDT parameters are over-fitting the event classification.
\end{itemize}
The BDT yields a weight $w_i$ representing a score under each background hypothesis to originate from radioisotope $i$: a signal event would tend to have a weight of 1, whereas a background-like event would tend towards -1.
Figure~\ref{fig:BDT_results} shows the weight for each background hypothesis, for all PMT $\gamma$-ray events and prompt signals from geo- and reactor antineutrinos.
%
\begin{figure*}[!htb]
\centering
\resizebox{0.99\textwidth}{!}{
\includegraphics{figures/cls_pmt_bi214.png}
\includegraphics{figures/cls_pmt_tl208.png}
\includegraphics{figures/cls_pmt_k40.png}
}
\caption{BDT discriminant variable distributions for PMTs (in red) and signal (in blue) in case of \ce{^{214}Bi} $\gamma$-ray hypothesis (left), \ce{^{208}Tl} $\gamma$-ray hypothesis (middle), and \ce{^{40}K} $\gamma$-ray hypothesis (right).
}
\label{fig:BDT_results}
\end{figure*}
%
Using these weights, a BDT cut has been chosen to discriminate most background while preserving as much signal as possible:
%
\begin{equation}
\tau_{\text{BDT}} \equiv \min{\left( w_{\ce{^{214}Bi}}, w_{\ce{^{208}Tl}}, w_{\ce{^{40}K}} \right)} \geq 0.999.
\end{equation}
%
Table~\ref{tab:eff_rates} shows the summary of each contribution at all the analysis stages: the post-BDT singles rates of each background used for creation of the merged dataset, contributions to the merged dataset pairs, which satisfy pre-optimized coincidence cuts ($\Delta\text{t}=\SI{1}{\milli\second}$ and $\Delta\text{R}=\SI{3}{\meter}$), and contributions of each component in the Region-of-Interest (ROI), optimized for geo- and reactor neutrinos signal, described in the following section.
%
\begin{table}[!htb]
\centering
\caption{
The summary of all background and signal contributions at different analysis stages: the post-BDT singles rates of each background used for the creation of the merged dataset, contributions to the merged dataset pairs, which satisfy pre-optimized selection cuts ($\Delta\text{t}=\SI{1}{\milli\second}$ and $\Delta\text{R}=\SI{3}{\meter}$), and contributions of each component in the Region-of-Interest (ROI), optimized for geo- and reactor neutrinos signal, described in the following section.
}
\label{tab:eff_rates}
\begin{tabular}{
>{\raggedright}p{1.7cm}
>{\raggedright}p{1.8cm}
>{\raggedright}p{1.9cm}
l}
& Post-BDT & Pair cand. & Pair cand. \\
& singles rate & post-merging & in ROI \\
& [\SI{}{\hertz}] & [\SI{}{\evts\per\year}] & [\SI{}{\evts\per\year}] \\
\hline \noalign{\smallskip}
PMT \ce{^{214}Bi} & \SI{4.24}{} & \num{6.80e4} & 24.0 \\
PMT \ce{^{208}Tl} & \SI{3.10}{} & \num{4.68e4} & 13.6 \\
PMT \ce{^{40}K} & \SI{1.47}{} & \num{2.41e4} & 11.6 \\
Water \ce{^{214}Bi} & \SI{8.18e-1}{} & \num{1.21e4} & 32.9 \\
Water \ce{^{208}Tl} & \SI{1.59e-2}{} & \num{0.21e4} & 0.78 \\
\hline\noalign{\smallskip}
Cosmogenic & \SI{5.78e-6}{} & 182 & 84.0 \\
Atmospheric & \SI{1.13e-6}{} & 35.6 & 30.3 \\
Fast n & \SI{4.48e-4}{} & 1411 & 69.6\\
$\ce{^18O}(\alpha,n)$ & \SI{4.58e-7}{} & 14.5 & 12.8\\
\hline\noalign{\smallskip}
\hline\noalign{\smallskip}
Reactor & \SI{7.61e-6}{} & 240 & 166 \\
Geoneutrinos & \SI{9.36e-6}{} & 295 & 221 \\
\end{tabular}
\end{table}
Using all three cuts $\Delta\text{t}$, $\Delta\text{R}$ and $\tau_{\text{BDT}}$, a suppression factor on the order of $10^{-5}$ is achieved for accidental backgrounds, whereas 54\% of geo- and 63\% of reactor antineutrinos are preserved.
Additional studies based on a simpler analysis show that a similar order of magnitude in suppression factors can be achieved with an optimized two-dimensional cut on $d_\text{wall}$ and $\chi^2$, supporting the conclusions from this more sophisticated study.
\subsection{Box analysis}
\label{subs:box}
\begin{table*}[!htb]
\centering
\caption{Results of ROI optimization in the phase space of selection cuts necessary for antineutrino candidates selection.}
\label{tab:optimization}
\begin{tabular}{llllllllll
\hline\noalign{\smallskip}
Signal & $\text{E}_\text{prompt}$ & $\text{E}_\text{delay}$ & $z$ & $\rho$ & $\Delta\text{t}$ & $\Delta\text{R}$ & S & B & ${S}/{\sqrt{S+B}}$ \\
definition & range [n$_{400}$] & range [n$_{400}$] & [\SI{}{\meter}] & [\SI{}{\meter}] & [\SI{}{\micro\second}] & [\SI{}{\meter}] & [\SI{}{\evts\per\year}] & [\SI{}{\evts\per\year}] & \\
\noalign{\smallskip}\hline\noalign{\smallskip}
Geoneutrinos & (200, 550) & (400,600) & 31 & 7 & 700 & 1.4 & 221 & 169 & 11.2\\
Reactor & (500, 1200) & (400,600) & 31 & 7 & 700 & 1.4 & 124 & 189 & 7.02\\
Geo + reactor & (200, 1200) & (400,600) & 31 & 7 & 700 & 1.4 & 387 & 280 & 15.0\\
\noalign{\smallskip}\hline
\end{tabular}
\end{table*}
We perform a box optimization of selection cuts in eight dimensions: prompt and delayed energy thresholds and upper limits (expressed in $n_{400}$), $\rho$ ($\perp$ cylinder axis) and $z$ ($\parallel$ cylinder axis) to define a fiducial volume in 2-D, and $\Delta\text{t}$ and $\Delta\text{R}$.
We optimize a ROI to maximize the signal-to-background ratio, specifically $S/\sqrt{S+B}$ for three cases:
\begin{enumerate}
\item when geoneutrinos are considered signal, and everything else including reactor antineutrinos are background;
\item when reactor antineutrinos are considered signal, and everything else including geoneutrinos are counted towards background;
\item both geo- and reactor neutrinos are signal, and the rest is background.
\end{enumerate}
The results of this optimization are summarized in Table~\ref{tab:optimization}.
A high signal-to-background ratio is achieved with the box analysis within one year for all three studied scenarios.
The selection cuts in $\Delta\text{t}$, $\Delta\text{R}$, delayed energy range, and fiducial volume have converged to the same values for all three scenarios, and only the prompt energy range is dependent on the target signal.
Comparing the values in the third and fourth columns in Table~\ref{tab:eff_rates} shows the impact of the optimized selection cuts on the number of pair candidates. Dedicated studies have been performed to study the impact of applying the BDT cut to the spatial and energy distributions of the events in the ROI. No significant change in the spectral shapes has been observed with varying degrees of BDT threshold, allowing us to use pre-BDT energy spectra as the PDFs for the spectral likelihood fit.
Using the box analysis, we obtain a signal-to-background ratio $S/\sqrt{S+B}$ of 7.02 for reactor signal, 11.2 for geoneutrinos, and 15.0 for the summed antineutrino signal after one year of data taking. These significances do not include any systematic uncertainties on the individual contributions.
\subsection{Sensitivity analysis}
\label{subs:sensi}
The box analysis allows us to extract the rates $\lambda_i$ of each signal and background inside the optimized cuts.
We then create a toy experiment by randomly sampling events from PDF of each spectrum, assuming Poisson fluctuations for all the rates, and perform the likelihood fit.
Figure~\ref{fig:stacked_PDFs} depicts the stacked spectra of all the PDFs scaled in correspondence with the expected rates in the ROI optimized for geo and reactor combined signal.
\begin{figure}[!htb]
\resizebox{0.49\textwidth}{!}{
\includegraphics{figures/merged.pdf}
}
\caption{
Stacked PDF spectra of all signal and background contributions in the ROI optimized for geo and reactor combined signal.
}
\label{fig:stacked_PDFs}
\end{figure}
%
In the following section, the sensitivity of two analyses is presented: first, the simultaneous extraction of the geo- and reactor signals; second, the simultaneous extraction of the \ce{Th} and \ce{U} contributions to the geoneutrino signal.
A 2-D spectral fit is performed using a grid search on target signals $(S_\text{geo}, S_\text{rea})$ or $(S_\text{Th}, S_\text{U})$.
For each couple of $S_i$ tested, a binned histogram is created by scaling each component of the PDF spectra.
Then a negative log-likelihood test against the toy experiment is performed while marginalizing on each background component $\lambda_B$.
The marginalization is computed between $\lambda_B\pm10\sqrt{\lambda_B}$ (or $[0, \lambda_B+10\sqrt{\lambda_B}]$ to ensure that all rates are positives), using the extended Newton-Cotes formulas, or trapezoidal rule\,\cite{press2002numerical}.
We extract an average negative log-likelihood for each couple of $S_i$ tested distributed from a $\chi^2$ law with two degrees of freedom from which we can extract the sensitivity of each analysis.
The minimum value corresponds to our best fit.
To evaluate the sensitivity of this procedure, \num{1000} toy experiments are generated, each corresponding to one year of data taking.
\section{Results}
\label{sec:results}
Figure~\ref{fig:SignificanceNGeo} shows the simultaneous extraction of the number of geo- and reactor antineutrinos.
The best fit values of 1000 toy experiments are $218^{+28}_{-20}$ and $170^{+24}_{-20}$ for geo- and reactor neutrinos, respectively.
The contours on Figure~\ref{fig:SignificanceNGeo} correspond to the $[1\sigma, 8\sigma]$ confidence levels.
The no-signal hypothesis for both geo- and reactor neutrinos is rejected at more than $8\sigma$ in a year.
The extracted number of geoneutrinos using $(\ce{Th}/\ce{U})_\text{SURF}=4.24$ in one year corresponds to $S_\text{geo} = 45.9^{+5.9}_{-4.2}$\,NIU, and assuming the prediction of the crust signal at SURF\,\cite{Huang2013}, we estimate the mantle signal to be $S_\text{mantle} = 8.8^{+1.2}_{-0.8}$\,NIU.
%
\begin{figure}[!htb]
\resizebox{0.49\textwidth}{!}{
\includegraphics{figures/Geo_vs_Rea.png}
}
\caption{
2-D confidence level of the geoneutrino versus reactor antineutrinos flux after one year of data taking, estimated with \num{1000} toy experiments.
The confidence level are drawn for $[1\sigma, 8\sigma]$.
The individual projection for each contribution at the best fit position is also shown with the statistical significance as dashed line.
}
\label{fig:SignificanceNGeo}
\end{figure}
The precision of the fitting procedure has been evaluated using the the relative difference between the best fit value and the true value.
Figure~\ref{fig:Flux_precision} shows this difference for each experiment on the example of geoneutrinos.
A Gaussian fit is applied to check that the fitting procedure does not introduce any systematic shifts (less than 0.004) and to extract the standard deviation $\sigma_\text{flux}$ quantifying the uncertainty on the antineutrino interactions in a one year experiment.
The standard deviation values from the fits are $\sigma_\text{flux}^\text{geo} = (6.72\pm0.01)\%$ for geoneutrinos and $\sigma_\text{flux}^\text{rea} = (8.55\pm0.01)\%$ for reactors.
%
\begin{figure}[!htb]
\resizebox{0.49\textwidth}{!}{
\includegraphics{figures/geo_norm.pdf}
}
\caption{The relative difference between the best fit value and the true value of the number of geoneutrinos, obtained with \num{1000} toy experiments.}
\label{fig:Flux_precision}
\end{figure}
Using the selection cuts optimized for the geoneutrino signal only (see Table~\ref{tab:optimization}), we performed a spectral fit to extract individual contributions of \ce{U} and \ce{Th} geoneutrino fluxes.
Marginalizing on all backgrounds, including reactor antineutrinos, we extract the best fit and confidence level contours between $[1\sigma, 8\sigma]$, as represented in Figure~\ref{fig:exFitThU}.
$N_{\ce{U}}$ null hypothesis can be rejected with more than 5$\sigma$ confidence level within one year, while $N_{\ce{Th}}$ null hypothesis can be rejected at 2$\sigma$.
The $N_{\ce{Th}}/N_{\ce{U}}$ ratio is proportional to (\ce{Th}/\ce{U}) mass ratio\,\cite{PhysRevD.82.093006}, and hence is an important parameter for comparison with geological models.
For a one year exposure in \textsc{Theia}{}-25, we obtain $N_{\ce{Th}}/N_{\ce{U}} = 0.22^{+0.13}_{-0.11}$, which corresponds to \ce{Th}/\ce{U} mass ratio of $4.3^{+2.6}_{-2.2}$. For comparison, the only preliminary measurement of (\ce{Th}/\ce{U}) mass ratio with geoneutrinos is $4.1^{+5.5}_{-2.0}$, performed by the KamLAND collaboration\,\cite{KamLAND_preliminary}.
From our sensitivity studies, we expect to discard the null hypothesis of (\ce{Th}/\ce{U}) mass ratio with $3\sigma$ confidence level with three years of data, and the uncertainty of this measurement to be reduced to 15\% with ten years of data taking.
\begin{figure}[!htb]
\resizebox{0.49\textwidth}{!}{
\includegraphics{figures/U_vs_Th.png}
}
\caption{
2-D confidence level of the number of \ce{Th} versus \ce{U} antineutrinos detected after one year of data taking, estimated with \num{1000} toy experiments.
The confidence level are drawn for $[1\sigma, 8\sigma]$.
The individual projections for each contribution at the best-fit value are also shown with the statistical significance as dashed lines.
}
\label{fig:exFitThU}
\end{figure}
Finally, considering the extracted number of individual U and Th contributions, corresponding detection efficiencies, and S(Th)/S(U) for crust and mantle from\,\cite{Huang2013}, we obtain $S_\text{mantle} = 9.2^{+2.0}_{-1.6}$\,NIU with one-year data.
\section{Conclusions}
Up to date, only two experiments in the world, Borexino and KamLAND, have observed a combined total of 216.6 geoneutrinos in the span of 12 years and 14 years, correspondingly. As presented above, \textsc{Theia}{}-25 will coincidentally observe the same number of geoneutrinos within just one year of data-taking. For this analysis, we considered one of the possible designs for the \textsc{Theia}{} detector, a 25-ktonne detector filled with WbLS placed at SURF. \textsc{Theia}{}-25 will provide the first high-statistics measurement of geoneutrinos in North America: $218^{+28}_{-20}$ events per year. Due to variations of the crust thickness, the geoneutrino flux measurements at different geographical locations will help separate a much less position-dependent mantle contribution \cite{SMIRNOV2019103712}.
The geoneutrino measurement in \textsc{Theia}{}-25 after one year of data taking assuming $(\ce{Th}/\ce{U})=4.24$ corresponds to $S_\text{geo} = 45.9^{+5.9}_{-4.2}$\,NIU.
Assuming the crust contribution from \cite{Huang2013}, the estimated mantle signal is $S_\text{mantle} = 8.8^{+1.2}_{-0.8}$\,NIU.
Furthermore, \textsc{Theia}{}-25 will extract the Th and U geo-neutrino signals and have sensitivity towards the (\ce{Th}/\ce{U}) ratio, discarding the null-hypothesis for the first time with three years of data-taking and achieving 15\% precision within ten years. A global assessment of the (\ce{Th}/\ce{U}) mass ratio of the primitive mantle could give insight into the Earth's early evolution and its differentiation. (\ce{Th}/\ce{U}) concentration in the outermost Earth's crust can be sampled directly, but determining these concentrations in the mantle can be done only with the geoneutrino flux measurements. Moreover, while we discuss sensitivity in \textsc{Theia}{}-25 in this paper, in further studies, we plan to explore the potential improvements in sensitivity with higher antineutrino statistics achievable in \textsc{Theia}{}-100, as well as with extracting the directional information of IBD interactions and applying it to the antineutrino search.
The two existing measurements confirm the general validity of different geological models predicting the Th and U abundances in the Earth. With \textsc{Theia}{} and other large experiments providing new precise measurements, we will enter a new era of geoneutrino measurements informing geoscience.
\section{Acknowledgements}
This work was performed under the auspices of the U.S. Department of Energy by Lawrence Berkeley National Laboratory under Contract DE-AC02-05CH11231. The project was funded by the U.S. Department of Energy, National Nuclear Security Administration, Office of Defense Nuclear Nonproliferation Research and Development (DNN R\&D). We also thank Tanner Kaptanoglu for detailed review of the manuscript and insightful suggestions.
\printbibliography
\end{document}
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Ain't Them Bodies Saints
Bob Muldoon (Casey Affleck) and Ruth Guthrie (Rooney Mara), an impassioned young outlaw couple on an extended crime spree, are finally apprehended by lawmen after a shootout in the Texas hills. Although Ruth wounds a local...
Bob Muldoon (Casey Affleck) and Ruth Guthrie (Rooney Mara), an impassioned young outlaw couple on an extended crime spree, are finally apprehended by lawmen after a shootout in the Texas hills. Although Ruth wounds a local officer, Bob takes the blame. But four years later, Bob escapes from prison and sets out to find Ruth and their daughter, born during his incarceration.
Set against the backdrop of 1970's Texas Hill Country, director David Lowery paints a poetic picture, evoking the mythology of westerns and saturating the dramatic space with an aching sense of loss.
Winner of the Cinematography Award, the Indian Paintbrush Producer's Award and Nominated for the Grand Jury Prize in the Dramatic Category at the Sundance Film Festival.
"A slow, banjo-string-tight thriller...BODIES get under your skin and stays there." - Cath Clarke, Time Out
Ben Foster, Casey Affleck, Charles Baker, Keith Carradine, Rami Malek, Rooney Mara
Roadshow Films
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Le terme Panzergrenadier désigne, à partir de 1942, l'infanterie spéciale des forces armées allemandes (Heer, Waffen-SS, et Luftwaffe) chargée d'accompagner les chars de combat. De nos jours, le terme est toujours employé au sein de la Bundeswehr (les forces armées allemandes), mais aussi dans la Bundesheer autrichienne et l'Armée suisse, pour désigner l'infanterie mécanisée des bataillon de chars.
Wehrmacht (1935-1945)
Organisation du Troisième Reich
À l'époque du Troisième Reich, la Panzerwaffe avec ses Panzerdivisionen a été le fer de lance de l'armée allemande, la Wehrmacht (composée d'une armée de terre, la Heer, d'une aviation, la Luftwaffe, et d'une marine, la Kriegsmarine), ce qui lui a permis de remporter de nombreuses victoires dans les premières années du conflit mondial, rapides et décisives, ce qui fut dénommé le Blitzkrieg. La Panzerdivision (en abrégé, PzDiv) était composée d'un régiment blindé (à l'origine de deux régiments), mais aussi de régiments d'infanterie, d'artillerie et de diverses troupes (transmissions, génie), plus des services, qui permettaient une efficacité d'action entre les diverses armes (arme blindée, infanterie, artillerie, etc.) employées.
Seconde Guerre mondiale
Création
Auparavant, les régiments chargés de ce rôle au sein des panzerdivisions, étaient appelés Schützen-Regimenten (en allemand, littéralement : « régiments de tireurs fantassins »).
La décision d'Adolf Hitler de renommer tous les régiments d'infanterie, en régiment de grenadiers, pour rendre hommage au roi prussien Frédéric II, entraîna le renommage des et des en régiments de (). À la suite de cette évolution, les anciennes divisions d'infanterie motorisée (Infanterie Division (mot)) devinrent, elles, des divisions de (Panzergrenadier-Division ou PzGrD en abrégé), gagnant au passage un soutien blindé sous la forme d'un bataillon de chars.
Du fait d'un manque chronique de chars, dans la plupart des , le bataillon de chars fut remplacé par un bataillon de canons d'assaut de type Sturmgeschütz III ou IV.
En 1944, une Panzerdivision comprenait normalement un régiment de chars à deux bataillons (un de chars Panther et un de chars Panzer IV) plus un bataillon de canons d'assaut et un bataillon de chasseur de chars ainsi que deux régiments de à deux bataillons chacun.
Équipement et armement durant la Seconde Guerre mondiale
Pour remplir leur mission, les Panzergrenadiers bénéficiaient de moyens de transport organiques.
Une partie d'entre eux combattaient à bord de semi-chenillés comme le SdKfz 250 ou le SdKfz 251, il était essentiellement destiné à équiper les Panzerdivisions et les unités de (Panzergrenadieren-Panzergrenadiers) et partageait de nombreux éléments mécaniques avec le SdKfz 7. Leurs unités prenant le qualificatif de gepanzert (littéralement cuirassés), et d'autres faute de moyens devaient se contenter de camions, et étaient qualifiés de motorisiert (motorisés).
Sur les 226 bataillons de Panzergrenadiers affectés à la Heer, Waffen-SS ou Luftwaffe en 1943, seuls 26, soit un peu plus de 10 %, étaient équipés de véhicules semi-chenillés.
Ils étaient souvent armés de façon nettement plus puissante que l'infanterie conventionnelle, équipés de nombreuses mitrailleuses MG34 ou MG42, et d'une dotation supérieure en pistolets-mitrailleurs de type MP40.
Vers la fin de la guerre, ils furent parmi les premières unités à recevoir des fusils d'assaut Sturmgewehr 44.
Au niveau de leur uniforme, ils se distinguaient par le passepoil de leurs pattes d'épaule de couleur vert pré, qu'ils avaient repris aux troupes motocyclistes, à ne pas confondre avec le vert clair des chasseurs de montagne.
Les Panzergrenadier division
Dans la Heer (Wehrmacht)
3. Panzergrenadier-Division
10. Panzergrenadier-Division
14. Panzergrenadier-Division
15. Panzergrenadier-Division
16. Panzergrenadier-Division
18. Panzergrenadier-Division
20. Panzergrenadier-Division
25. Panzergrenadier-Division
29. Panzergrenadier-Division
Panzergrenadier-Division Feldherrnhalle
90. Panzergrenadier-Division
Ces divisions de panzergrenadiers, furent formées par la transformation des divisions motorisées correspondantes.
la Panzergrenadier-Division Großdeutschland fut, formée par l'accroissement d'effectif du régiment de même nom.
: la division est renommée « Panzergrenadier-Division Großdeutschland ».
Panzergrenadier-Division Brandenburg
Panzergrenadier-Division Kurmark
Panzerdivision Feldherrnhalle 1 (division d'infanterie motorisée)
Dans la Luftwaffe
Fallschirm Panzergrenadier Division 2 Hermann Göring
Dans la Waffen-SS
division SS « Polizei »
division SS Nordland
division SS Reichsführer SS
division SS Götz von Berlichingen
division SS Horst Wessel,
Panzergrenadierdivision de volontaires SS Nederland (23. SS-Freiwilligen-Panzergrenadier-Division Nederland).
À noter que toutes les divisions blindées (Panzerdivisionen) de la Waffen SS reçurent initialement l'appellation de Panzergrenadier-Division lors de leur transformation (, , et blindées) ou de leur formation initiale (, et blindées) et ne prirent l'appellation de Panzerdivision qu'en .
Ainsi, par exemple, les 1re division SS Leibstandarte SS Adolf Hitler, 2e division SS Das Reich et 3e division SS Totenkopf, qui étaient en 1942 des divisions d'infanterie motorisées furent retirées du front de l'Est dans le courant de l'année et transformées en Panzergrenadierdivisionen, dotées d'un bataillon de char. Mais elles reçurent une deuxième bataillon de char ainsi qu'une compagnie lourde de chars Tigres au cours de cette transformation et, lors qu'elles retournèrent au front en pour être engagées dans la troisième bataille de Kharkov au sein du SS-Panzerkorps, elles étaient en fait des divisions blindées, même si elles conservèrent l'appellation de Panzergrenadierdivisionen pendant la majeure partie de l'année, y compris durant la bataille de Koursk.
Ce fut également le cas de la 5e division SS Wiking transformée de division d'infanterie motorisées en Panzergrenadier-Division en 1942 puis redésignée Panzer-Division en ou des 9e division SS Hohenstaufen, division SS Frundsberg, 12e division SS Hitlerjugend, formées en 1943 comme Panzergrenadierdivisionen puis redésignées Panzerdivisionen fin 1943.
Durant l'après-guerre et la guerre froide, L'Allemagne, l'Autriche et la Suisse dotèrent leurs armées d'unités de Panzergrenadiers.
Au
Heer (Bundeswehr)
Budget de la défense 2019
En 2019, (Wehrbeauftragter des deutschen Bundestages) le budget de la défense avoisine les 43,2 milliards d'euros. La part du budget de la défense dans le budget fédéral en 2019 est de 12,1%. Des mesures d'investissement sont prévues pour environ 9,9 milliards d'euros.
Organigramme 2020
Selon leur taille et le rôle, les brigades peuvent être commandées soit par un Brigadegeneral ou un colonel. Contrairement à d'autres armées européennes, telles celles des Pays-Bas voisins ou de la France, les régiments n'ont pas une forme commune d'organisation et sont donc rares dans l'Armée allemande. Les bataillons sont directement subordonnés aux brigades ou divisions de troupes divisionnaires.
à Leipzig
« État libre de Sax » à Frankenberg
« Poméranie occidentale » à Neubrandenbourg
À la suite de la réorganisation de la Heer à partir de 2002, le nombre de bataillons de Panzergrenadier a été réduit. Une brigade blindée de la Eingreifkräfte (forces d'intervention) comprendra un bataillon de Panzergrenadier, tandis que les Brigades mécanisées de la Stabilisierungskräfte (forces de stabilisation) comprendra deux bataillons Panzergrenadier.
Un bataillon Panzergrenadier type est constituée d'un état-major, de trois compagnies de combat, et d'une compagnie d'entraînement.
À partir de la réorganisation de 2002, l'armée allemande a huit bataillons actifs de Panzergrenadier en service :
Bataillons de Eingreifkräfte (forces d'intervention):
Panzergrenadierbataillon 33, (Neustadt am Rübenberge),
, (Augustdorf),
Bataillons de Stabilisierungskräfte (forces de stabilisation) :
Panzergrenadierbataillon 112, (Regen),
Panzergrenadierbataillon 122, (Oberviechtach), Panzerbrigade 12
Panzergrenadierbataillon 391, (Bad Salzungen), Panzergrenadierbrigade 37
Panzergrenadierbataillon 371, (Marienberg), Panzergrenadierbrigade 37
Panzergrenadierbataillon 401, (Hagenow), Panzergrenadierbrigade 41
Panzergrenadierbataillon 411, (Viereck), Panzergrenadierbrigade 41
De plus, en 2008, deux bataillons de Panzergrenadier inactifs seront reformés:
Panzergrenadierbataillon 908, (Viereck), Panzergrenadierbrigade 41, avec comme unité de logistique et de maintenance : Panzergrenadierbataillon 411
Panzergrenadierbataillon 909, (Marienberg), Panzergrenadierbrigade 37, avec comme unité de logistique et de maintenance : Panzergrenadierbataillon 371
Matériels
Le Boxer, véhicule blindé de combat d'infanterie à 8 roues motrices. Équipage : 3 + 8 passagers.
Le Schützenpanzer (SPz) Marder, véhicule de combat d'infanterie chenillé. Équipage : 3 (pilote, tireur et chef d'engin) + 7 soldats (6 sur le modèle A2).
Le Puma est un véhicule de combat d'infanterie chenillé. Équipage : 3 + 6 fantassins.
Autriche
La Bundesheer (Österreichisches Bundesheer) comporte deux bataillons de Panzergrenadiers.
La brigade de panzer grenadier forme la brigade lourde de l'armée fédérale. Dans la fédération, les forces mécanisées de l'armée fédérale sont résumées. L'association de la brigade est destinée aux opérations robustes à la maison et à l'étranger et est cruciale pour la préservation de la capacité dans la défense militaire conventionnelle.
Le brigadier , nouveau commandant de la brigade Panzer Grenadier, le , la cérémonie de passation du commandement du colonel de l'état-major général Stefan Fuchs au brigadier-capitaine Siegward Schier a eu lieu à la base aérienne de Vogler à Hörsching, près du District de Linz-Land.
Brigade Panzer Grenadier
Panzer Grenadier Bataillon 13
Panzer Grenadier Bataillon 35
Suisse
Les grenadiers de chars sont des unités militaires d'infanterie blindée mécanisée incorporées dans des troupes blindées ; ce corps est l'infanterie des troupes blindées de l'armée suisse. Leur formation comprend une instruction adaptée à leur fonction au sein des troupes blindées en plus de leur formation d'infanterie.
Les missions qui leur sont attribuées comprennent la défense des blindés, le nettoyage de poches de résistance, la fixation ou cassure d'un front, l'infiltration/exfiltration et les combats urbains. Un accent particulier lors de l'entraînement est mis sur la lutte antichar, le combat de localité et le combat à mains nues et avec armes tranchantes.
Brigade mécanisée 1 () / ex-brigade Panzer 11)
Le Brigadier Serge Pignat. Est responsable de l'état de préparation de base de ses états-majors et de ses forces et relève du commandant des forces terrestres. Le commandant de la brigade mécanisée 1 est chargé de former sa brigade à la planification et à la réalisation d'opérations de défense contre les attaques militaires et aux opérations de soutien aux affaires civiles en Suisse.
Brigade mécanisée 4 ()
Le Brigadier A. Kohli. Commandant de la brigade mécanisée 4, est une formation qui se compose essentiellement de militaires germanophones.
()
Le Brigadier Gregor Metzler, est le commandant de la brigade mécanisée 11. L'unité mécanisée comprend environ , sous-officiers et officiers.
Avec les chars de combat Leopard 2, les grenadiers de chars sont les troupes offensives des troupes blindée de l'armée suisse. Il s'agit de formations de choc et d'attaque ayant pour but de percer le front ennemi.
Ils opèrent en tête des formations mécanisées aussi bien sur un terrain découvert qu'en milieu urbain afin de faciliter le passage des troupes blindées. Équipés de lance-roquettes Panzerfaust 3, les grenadiers de chars peuvent détruire les unités blindées ennemies. Les autres armes sont le SIG-550, le lance-grenades additionnel (LGA), les TIFLU (tireur au fusil d'assaut à lunette), et les LMG 05 (FN Minimi). Comme l'indique leur nom, les grenadiers de chars se déplacent à l'intérieur de véhicule de combat d'infanterie. Il s'agit, depuis les années 2000, du Combat Vehicle 90 (CV9030), appelé localement char gren 2000 ou Spz 2000, qui donne une bonne mobilité tactique en zone confinée et permet un déploiement rapide des grenadiers directement à l'emplacement de la mission.
La version grenadier de ce véhicule transporte 11 hommes (1 conducteur, 1 pointeur-tireur, 1 commandant de char et 8 grenadiers embarqués). Les trois premières fonctions sont accomplies par des militaires formés au maniement du Char gren 2000, les "équipages" ou "besatze" , tandis que les 8 militaires débarqués sont des unités d'infanterie d'élite, les "combats" ou encore "débarqués". Cette séparation dans les fonctions s'effectuent déjà lors du recrutement et les deux unités ne travaillent ensemble qu'à partir de la fin de leur école de recrue et essentiellement durant les cours de répétition.
Décorations
1939/1945
Parmi les unités de ses différentes PzGrD, nombres d'individus reçurent pour bravoure et fait-d'arme ses décorations.
L'Oberst Walter Gorn de la Panzergrenadier-Regiment 10 a obtenu le la croix de fer avec feuilles de chêne et glaives ().
L'Oberleutnant Adelbert Schulz du Pz.Rgt. 25 de la Panzerdivision a obtenu le la croix de fer avec feuilles de chêne et glaives ().
Le , Walter Fries en tant que Generalleutnant et commandant de la 29. Panzergrenadier-Division reçoit la croix de chevalier de la croix de fer avec feuilles de chêne et glaives (87).
Le , le Generalleutnant Ernst-Günther Baade commandant de la 90. Panzergrenadier-Division « Adiatisches Küstenland » reçoit la croix de chevalier de la croix de fer avec feuilles de chêne et glaives (111).
Le , le Generalleutnant Dietrich von Müller de la Panzerdivision reçoit la croix de chevalier de la croix de fer avec feuilles de chêne et glaives (134).
De nos jours
La croix d'honneur de la Bundeswehr pour bravoure est la première récompense de valorisation explicite de l' histoire des forces armées allemandes. Elle a été créée le .
.
Feldwebel ()
Feldwebel ()
[...]
Stabsfeldwebel Stefan Weinmüller ()
Oberfeldwebel Norman Reichow ()
Oberstleutnant Jared Sembritzki ()
Hauptfeldwebel Jürgen Wölf ()
Oberstabsgefreiter Jan Bauer ()
Notes et références
Bibliographie
: Témoignage des deux années passées par l'auteur, alors adolescent, sur le front de l'Est pendant la Seconde Guerre mondiale.
Articles connexes
Infographie
Liens externes
De la Crimée, à la Syrie en passant par le Donbass, la 18ème brigade indépendante de fusiliers motorisés a été de tous les derniers engagements de l'armée russe.
La 3e division d'infanterie motorisée en 1940.
Unité militaire allemande
Unité militaire autrichienne
Unité militaire suisse
Histoire militaire de l'Allemagne
Glossaire militaire
Unité de la Wehrmacht
Division de la Wehrmacht
Division de grenadiers de la Wehrmacht
Unité militaire allemande de la Seconde Guerre mondiale
Décoration militaire du Troisième Reich
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| 8,384
|
{"url":"http:\/\/icpc.njust.edu.cn\/Problem\/Hdu\/1165\/","text":"# Eddy's research II\n\nTime Limit: 4000\/2000 MS (Java\/Others)\n\nMemory Limit: 65536\/32768 K (Java\/Others)\n\n## Description\n\nAs is known, Ackermann function plays an important role in the sphere of theoretical computer science. However, in the other hand, the dramatic fast increasing pace of the function caused the value of Ackermann function hard to calcuate.\n\nAckermann function can be defined recursively as follows:\n\nNow Eddy Gives you two numbers: m and n, your task is to compute the value of A(m,n) .This is so easy problem,If you slove this problem,you will receive a prize(Eddy will invite you to hdu restaurant to have supper).\n\n## Input\n\nEach line of the input will have two integers, namely m, n, where 0 < m < =3.\nNote that when m<3, n can be any integer less than 1000000, while m=3, the value of n is restricted within 24.\nInput is terminated by end of file.\n\n## Output\n\nFor each value of m,n, print out the value of A(m,n).\n\n## Sample Input\n\n1 3\n2 4\n\n## Sample Output\n\n5\n11\n\nJGShining","date":"2020-02-20 18:51:10","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 0, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 1, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.5566133856773376, \"perplexity\": 2503.059123413481}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2020-10\/segments\/1581875145260.40\/warc\/CC-MAIN-20200220162309-20200220192309-00546.warc.gz\"}"}
| null | null |
{"url":"https:\/\/brilliant.org\/problems\/looks-big-but-easy\/","text":"# A number theory problem by Kushal Bose\n\nFind the number of ordered pairs of $(x,y)$, where $x,y \\in \\mathbb{N} \\leq 100$ and such that\n\n$\\large 5 \\mid 3^x+3^y$\n\n\u00d7","date":"2021-07-27 01:54:25","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 3, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 0, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 0, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.8175432682037354, \"perplexity\": 1036.6711719761347}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2021-31\/segments\/1627046152168.38\/warc\/CC-MAIN-20210727010203-20210727040203-00354.warc.gz\"}"}
| null | null |
package org.apache.hadoop.hdfs.server.namenode;
import org.apache.hadoop.conf.Configuration;
import org.apache.hadoop.hdfs.MiniDFSCluster;
import org.junit.Test;
import javax.management.MBeanAttributeInfo;
import javax.management.MBeanInfo;
import javax.management.MBeanServer;
import javax.management.ObjectName;
import java.lang.management.ManagementFactory;
import java.util.HashSet;
import java.util.Set;
import org.apache.commons.logging.Log;
import org.apache.commons.logging.LogFactory;
import static org.junit.Assert.*;
/**
* Class for testing {@link NameNodeMXBean} implementation
*/
public class TestFSNamesystemMBean {
public static final Log LOG = LogFactory.getLog(TestFSNamesystemMBean.class);
/**
* MBeanClient tries to access FSNamesystem/FSNamesystemState/NameNodeInfo
* JMX properties. If it can access all the properties, the test is
* considered successful.
*/
private static class MBeanClient extends Thread {
private boolean succeeded = false;
@Override
public void run() {
try {
MBeanServer mbs = ManagementFactory.getPlatformMBeanServer();
// Metrics that belong to "FSNamesystem", these are metrics that
// come from hadoop metrics framework for the class FSNamesystem.
ObjectName mxbeanNamefsn = new ObjectName(
"Hadoop:service=NameNode,name=FSNamesystem");
// Metrics that belong to "FSNamesystemState".
// These are metrics that FSNamesystem registers directly with MBeanServer.
ObjectName mxbeanNameFsns = new ObjectName(
"Hadoop:service=NameNode,name=FSNamesystemState");
// Metrics that belong to "NameNodeInfo".
// These are metrics that FSNamesystem registers directly with MBeanServer.
ObjectName mxbeanNameNni = new ObjectName(
"Hadoop:service=NameNode,name=NameNodeInfo");
final Set<ObjectName> mbeans = new HashSet<ObjectName>();
mbeans.add(mxbeanNamefsn);
mbeans.add(mxbeanNameFsns);
mbeans.add(mxbeanNameNni);
for(ObjectName mbean : mbeans) {
MBeanInfo attributes = mbs.getMBeanInfo(mbean);
for (MBeanAttributeInfo attributeInfo : attributes.getAttributes()) {
mbs.getAttribute(mbean, attributeInfo.getName());
}
}
succeeded = true;
} catch (Exception e) {
LOG.error(e,e);
}
}
}
@Test
public void test() throws Exception {
Configuration conf = new Configuration();
MiniDFSCluster cluster = null;
try {
cluster = new MiniDFSCluster.Builder(conf).build();
cluster.waitActive();
FSNamesystem fsn = cluster.getNameNode().namesystem;
MBeanServer mbs = ManagementFactory.getPlatformMBeanServer();
ObjectName mxbeanName = new ObjectName(
"Hadoop:service=NameNode,name=FSNamesystemState");
Object pendingDeletionBlocks = mbs.getAttribute(mxbeanName,
"PendingDeletionBlocks");
assertNotNull(pendingDeletionBlocks);
assertTrue(pendingDeletionBlocks instanceof Long);
} finally {
if (cluster != null) {
cluster.shutdown();
}
}
}
// The test makes sure JMX request can be processed even if namesystem's
// writeLock is owned by another thread.
@Test
public void testWithFSNamesystemWriteLock() throws Exception {
Configuration conf = new Configuration();
MiniDFSCluster cluster = null;
FSNamesystem fsn = null;
try {
cluster = new MiniDFSCluster.Builder(conf).build();
cluster.waitActive();
fsn = cluster.getNameNode().namesystem;
MBeanClient client = new MBeanClient();
client.start();
client.join(20000);
assertTrue("JMX calls are blocked when FSNamesystem's writerlock" +
"is owned by another thread", client.succeeded);
client.interrupt();
} finally {
if (cluster != null) {
cluster.shutdown();
}
}
}
}
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 3,071
|
Cited as one of the nation's most outstanding 1985 engineering achievements.
The earth and rock fill moved to construct the dams and other project facilities, if piled up, would create a mountain 1,000 feet high.
Enough concrete was poured to build 200 miles of interstate highway.
The station consists of two large reservoirs. When demand is low, water is pumped from the lower reservoir to the upper one.
When demand is high, valves permit water to run through the tunnels to the lower reservoir at a rate as high as 13.5 million gallons per minute, turning six turbine generators.
The water level in the 265-acre upper reservoir can fluctuate as much as 106 feet when the unit is operated.
The station occupies a relatively small amount of land, minimizing adverse effect on the environment. Flows to Back Creek and Little Back Creek, are supplemented by storage from the station reservoirs. This significantly improves stream flow during periods of drought and enhances the environment for fish and other aquatic life.
The Bath County Pumped Storage Station Recreation Area is open to the public. Opened in 1989, it has facilities for fishing, non-power boating, picnicking, swimming, hiking and camping. There are two ponds (27 and 45 acres).
|
{
"redpajama_set_name": "RedPajamaC4"
}
| 7,306
|
Marc Christoffer Axengren, född 16 maj 1992, är en svensk fotbollsspelare som spelar för Gällstads FK.
Karriär
Axengren började spela fotboll i Gällstads FK. Inför säsongen 2010 gick han till Annelunds IF. Mellan 2011 och 2015 spelade Axengren för Norrby IF.
I januari 2016 värvades Axengren av Husqvarna FF, där han skrev på ett tvåårskontrakt. I januari 2018 återvände Axengren till Norrby IF, där han skrev på ett tvåårskontrakt. Den 2 april 2018 gjorde Axengren sin Superettan-debut i en 2–2-match mot IK Frej.
I december 2018 värvades Axengren av division 2-klubben Dalstorps IF, där han skrev på ett tvåårskontrakt. I januari 2021 återvände Axengren till moderklubben Gällstads FK.
Karriärstatistik
Källor
Marc Axengren på fotbolltransfers.com
Noter
Svenska fotbollsspelare
Spelare i Norrby IF
Spelare i Husqvarna FF
Spelare i Superettan
Spelare i Division 1 i fotboll för herrar
Födda 1992
Levande personer
Män
|
{
"redpajama_set_name": "RedPajamaWikipedia"
}
| 9,701
|
<?php
declare(strict_types=1);
namespace K911\UriBuilder\Exception;
use RuntimeException;
class UriBuilderException extends RuntimeException implements UriBuilderExceptionInterface
{
}
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 7,672
|
{"url":"https:\/\/www.kuniga.me\/blog\/2015\/02\/20\/revisiting-python-basic-types.html","text":"Revisiting Python: Basic Types\n\nkuniga.me > NP-Incompleteness > Revisiting Python: Basic Types\n\n# Revisiting Python: Basic Types\n\n20 Feb 2015\n\nI\u2019ve been using Python for quite a while now, but always on pet projects, small scripts, programming contests and I feel that my knowledge didn\u2019t really improve much. I had a chance to work on a Python project and realized there are many basic things I don\u2019t know.\n\nEvery time I dedicate some time to learn and write about some subject, I feel like my knowledge about it improves a lot. Thus, I decided to revisit some Python concepts and write a series of posts about things I didn\u2019t know in Python 2.7. The first of our posts will be the Built-in types.\n\n### Booleans Types\n\nBoolean types can take True and False as values. Falsy values include False, 0, empty sequences (string, list, dictionary) and any class that implements __len__() and returns 0.\n\nLogical operators. many languages use && and ||. In Python it is and and or, and it works the same way (short-circuiting).\n\nNegation is also more verbose: not instead of !. Other logical operators test whether an element belongs to a sequence\/container or if a string is a substring of another, in.\n\nNote that it can be composed with the not operator for better readability. Another operator is the is operator (similar to triple equal in PHP or Javascript). It\u2019s the same as the == operator for basic types, but for other types, it only returns True if they point to the same object:\n\nThis operator can also be combined with the not operator.\n\nComparison operators. It\u2019s the same as in most languages. In Python, they work with custom classes if these classes implement the following methods: __lt__(), __le__(), __gt__(), __ge__(), the __cmp__().\n\n### Numeric Types\n\nNumeric types can be one of the following: int (plain integer), float (floating point numbers), long (long integers) and complex. int\u2019s are like C++\u2019s long, 32 bits of precision. float\u2019s are equivalent to C++\u2019s double, usually 64 bits, 53 bits for mantisse, 10 bits for exponents and 1 bit for sinal. long\u2019s have unlimited precision. complex is a pair of floats (named real and imag).\n\nMath operations. Most operators are the same as other languages. The different ones include \/\/, which performs floored quotient, for comparison\n\nNote that if both values are integers, the division is integer. divmod() is also interesting. It\u2019s basically divmod(a, b) = (a \/\/ b, a % b).\n\nBitwise operators works as in C++.\n\nNumeric types are classes too, and implement numbers.Integral. We can invoke methods on variables, but not on literals:\n\n### Iterator Types\n\nPython supports a concept of iteration over containers. Classes that implement the __iter__() and next() methods are of type iterator. The next() method should return the current value and proceed to the next value, using raise StopIteration when the end is reached.\n\nWe can implement our own (x)range function as an example:\n\n### Sequence Types\n\nThe types that fall in this family of type are str, unicode, list, tuple, bytearray, buffer, xrange.\n\nStrings. is a list of characters, which themselves are 8-bits encoded ascii values (strings have some overhead besides the characters [1]). Strings literals can be written in single or double quotes.\n\nFormatting strings: It accepts a syntax similar to sprintf from C. One interesting form is passing an dictionary of values and naming the patterns by the key name:\n\nThere also an alternative formatting using the .format() method. A discussion can be read here.\n\nUnicode strings. Python uses UTF-8 encoding for unicode. Literals of this type can be created by prefixing the value with an u, for example u'abc'.\n\nTuples. are shallowly \u201cimmutable\u201d containers. Their contents can\u2019t be changed, but the objects their elements point to might be. It can be used without parenthesis and can be used in the LHS to unwrap values. For example:\n\nHere, (1, 2) and (a, b) are tuples. It has bracket access, for example\n\nTuples are hashable if all its elements are hashable. This allows using tuples in sets or dictionary keys.\n\nLists. are mutable sequences. They\u2019re indexed from 0 to length-1 and access out of this range throws an exception. The + operator can be used to concatenate lists. Conveniently, the * operator where the first operator is a list and second operant is an integer N, creates N shallow copies of the list (this works for tuples too).\n\nAccess to lists can be made using ranges, in which case it returns another list, for example\n\nWe must be careful in making copies of arrays where the elements are references to objects (for example other lists). In the example below, it\u2019s likely not doing what we would want:\n\nXranges. The existence of the xrange type is justified by the xrange() function. The python docs explain it well:\n\nThis function is very similar to range(), but returns an xrange object instead of a list. This is an opaque sequence type which yields the same values as the corresponding list, without actually storing them all simultaneously. The advantage of xrange() over range() is minimal (since xrange() still has to create the values when asked for them) except when a very large range is used on a memory-starved machine or when all of the range\u2019s elements are never used (such as when the loop is usually terminated with break).\n\nBytearrays. are essentially mutable strings.\n\nBuffer. is intended for memory-efficient manipulation of a large arrays, which otherwise would cause a copy. Guido van Rossum describes an example [2]:\n\nIt was created with the desire to avoid an expensive memory-copy operation when reading or writing large arrays. For example, if you have an array object containing several millions of double precision floating point numbers, and you want to dump it to a file, you might prefer to do the I\/O directly from the array\u2019s memory buffer rather than first copying it to a string.\n\nThis Stack Overflow question also discusses the subject.\n\n### Set types\n\nSet and Frozenset. The main difference between these two is that set is mutable while frozenset is immutable. These structures are implemented using a hash table, so all elements in a set\/frozenset must be hashable. A type is hashable if it implements __hash()__ (which shouldn\u2019t change during its lifetime) and either __eq()__ or __cmp()__. Since frozenset is immutable and all its elements are hashable, frozenset itself is hashable.\n\nIn Python 2.7, sets can be constructed by a shorthand {'foo', 'bar'}.\n\n### Map types\n\nDictionaries are associative arrays. They\u2019re called dict in Python code. Dictionary keys must be hashable.\n\nWe can get a dictionary\u2019s keys and values by .keys() and .values() respectively. The .items() method returns an array of pairs, each containing key and value. These methods all return copies, so if we assign .keys() to a variable and make changes to the dictionary, the changes won\u2019t get reflected in the list assigned to the variable.\n\nTo get references instead of copies, we can use the .viewkeys(), .viewvalues() and .viewitems() methods, which are read-only references.\n\n### File Objects\n\nReturned by the open() function. It\u2019s used for file manipulation operations.\n\n### Memory View\n\nIt was introduced in Python 2.7 and is a replacement for the buffer type.\n\n### Context Manager Types\n\nAny user defined class that implements __enter()__ and __exit()__ has a context manager type. These types are useful for abstracting a specific try\/finally pattern. More specifically, imagine we have the following pseudo-code:\n\nIf we do \u201cset things up\u201d and \u201ctear things down\u201d in many places and only change \u201cdo something\u201d, we can abstract those in a class implementing a context manager type:\n\nThis post from Effbot as a very clear explanation.\n\n### Conclusion\n\nIn this post we covered the basic types from the Python environment. We were able to learn about some interesting features even from basic types like booleans and numeric. We also covered some more exoteric types like buffer and xrange. We got some exposure to other features like context manager.\n\nIn the next post in the series we\u2019ll talk about functions.\n\n### References\n\n\u2022 [1] Theano - Python Memory Management\n\u2022 [2] Python-Dev - The buffer interface\n\u2022 [3] Python Docs - Built-in Types","date":"2021-02-27 16:15:28","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 0, \"mathjax_display_tex\": 0, \"mathjax_asciimath\": 1, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.3087780475616455, \"perplexity\": 2602.566331252668}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2021-10\/segments\/1614178358976.37\/warc\/CC-MAIN-20210227144626-20210227174626-00032.warc.gz\"}"}
| null | null |
(function e(t,n,r){function s(o,u){if(!n[o]){if(!t[o]){var a=typeof require=="function"&&require;if(!u&&a)return a(o,!0);if(i)return i(o,!0);throw new Error("Cannot find module '"+o+"'")}var f=n[o]={exports:{}};t[o][0].call(f.exports,function(e){var n=t[o][1][e];return s(n?n:e)},f,f.exports,e,t,n,r)}return n[o].exports}var i=typeof require=="function"&&require;for(var o=0;o<r.length;o++)s(r[o]);return s})({1:[function(require,module,exports){
/** @jsx React.DOM */
var CrewBattlePlayer = React.createClass({displayName: "CrewBattlePlayer",
render: function() {
return (
React.createElement("td", {className: "player"}, this.props.player)
);
}
});
var CrewBattleStocks = React.createClass({displayName: "CrewBattleStocks",
render: function() {
return (
React.createElement("td", {className: "stocks"}, this.props.stocks)
);
}
});
var CrewBattleRowList = React.createClass({displayName: "CrewBattleRowList",
render: function() {
var crewRows = this.props.data.map(function(row) {
return (
React.createElement(CrewBattleRow, {data: row})
)
});
return (
React.createElement("table", {className: "table"},
React.createElement("tbody", null,
crewRows
)
)
);
}
});
var CrewBattleRow = React.createClass({displayName: "CrewBattleRow",
render: function() {
return (
React.createElement("tr", {className: "crewRow"},
React.createElement(CrewBattlePlayer, {player: this.props.data.player1.name}),
React.createElement(CrewBattleStocks, {stocks: this.props.data.player1.stocks}),
React.createElement(CrewBattleStocks, {stocks: this.props.data.player2.stocks}),
React.createElement(CrewBattlePlayer, {player: this.props.data.player2.name})
)
);
}
});
var CrewBattleRowForm = React.createClass({displayName: "CrewBattleRowForm",
handleSubmit: function(e) {
e.preventDefault();
var p1 = this.refs.p1.getDOMNode().value.trim();
var p1stocks = this.refs.p1stocks.getDOMNode().value.trim();
var p2 = this.refs.p2.getDOMNode().value.trim();
var p2stocks = this.refs.p2stocks.getDOMNode().value.trim();
if (!p1 || !p2 || !p1stocks || !p2stocks) {
return;
}
this.props.onRowSubmit({
player1: {
name: p1,
stocks: p1stocks
},
player2: {
name: p2,
stocks: p2stocks
}
});
this.refs.p1.getDOMNode().value = '';
this.refs.p2.getDOMNode().value = '';
this.refs.p1stocks.getDOMNode().value = '';
this.refs.p2stocks.getDOMNode().value = '';
return;
},
render: function() {
return (
React.createElement("form", {className: "crewRowForm", onSubmit: this.handleSubmit},
React.createElement("input", {type: "text", placeholder: "Player 1", ref: "p1"}),
React.createElement("input", {type: "text", placeholder: "P1 stocks", ref: "p1stocks"}),
React.createElement("input", {type: "text", placeholder: "P2 stocks", ref: "p2stocks"}),
React.createElement("input", {type: "text", placeholder: "Player 2", ref: "p2"}),
React.createElement("input", {type: "submit", value: "Submit"})
)
);
}
});
var CrewBattle = React.createClass({displayName: "CrewBattle",
getInitialState: function() {
return {data: []};
},
updateRows: function(rowdata) {
var curData = this.state.data;
var newData = curData.concat([rowdata]);
this.setState({data: newData});
},
render: function() {
return (
React.createElement("div", null,
React.createElement(CrewBattleRowList, {data: this.state.data}),
React.createElement(CrewBattleRowForm, {onRowSubmit: this.updateRows})
)
);
}
});
React.render(
React.createElement(CrewBattle, null),
document.getElementById('content')
);
},{}]},{},[1])
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 3,071
|
Q: Swift Combine - Accessing separate lists of publishers I have two lists of URLs that return some links to images.
The lists are passed into a future like
static func loadRecentEpisodeImagesFuture(request: [URL]) -> AnyPublisher<[RecentEpisodeImages], Never> {
return Future { promise in
print(request)
networkAPI.recentEpisodeImages(url: request)
.sink(receiveCompletion: { _ in },
receiveValue: { recentEpisodeImages in
promise(.success(recentEpisodeImages))
})
.store(in: &recentImagesSubscription)
}
.eraseToAnyPublisher()
}
Which calls:
/// Get a list of image sizes associated with a featured episode .
func featuredEpisodeImages(featuredUrl: [URL]) -> AnyPublisher<[FeaturedEpisodeImages], Error> {
let featuredEpisodesImages = featuredUrl.map { (featuredUrl) -> AnyPublisher<FeaturedEpisodeImages, Error> in
return URLSession.shared
.dataTaskPublisher(for: featuredUrl)
.map(\.data)
.decode(type: FeaturedEpisodeImages.self, decoder: decoder)
.receive(on: networkApiQueue)
.catch { _ in Empty<FeaturedEpisodeImages, Error>() }
.print("###Featured###")
.eraseToAnyPublisher()
}
return Publishers.MergeMany(featuredEpisodesImages).collect().eraseToAnyPublisher()
}
/// Get a list of image sizes associated with a recent episode .
func recentEpisodeImages(recentUrl: [URL]) -> AnyPublisher<[RecentEpisodeImages], Error> {
let recentEpisodesImages = recentUrl.map { (recentUrl) -> AnyPublisher<RecentEpisodeImages, Error> in
return URLSession.shared
.dataTaskPublisher(for: recentUrl)
.map(\.data)
.decode(type: RecentEpisodeImages.self, decoder: decoder)
.receive(on: networkApiQueue)
.catch { _ in Empty<RecentEpisodeImages, Error>() }
.print("###Recent###")
.eraseToAnyPublisher()
}
return Publishers.MergeMany(recentEpisodesImages).collect().eraseToAnyPublisher()
}
and is attached to the app state:
/// Takes an action and returns a future mapped to another action.
static func recentEpisodeImages(action: RequestRecentEpisodeImages) -> AnyPublisher<Action, Never> {
return loadRecentEpisodeImagesFuture(request: action.request)
.receive(on: networkApiQueue)
.map({ images in ResponseRecentEpisodeImages(response: images) })
.replaceError(with: RequestFailed())
.eraseToAnyPublisher()
}
It seems that:
return Publishers.MergeMany(recentEpisodes).collect().eraseToAnyPublisher()
doesn't give me a reliable downstream value as whichever response finishes last overwrites the earlier response.
I am able to log the responses of both series of requests. Both are processing the correct arrays and returning the proper json.
I would like something like:
return recentEpisodeImages
but currently this gives me the error
Cannot convert return expression of type '[AnyPublisher<RecentEpisodeImages, Error>]' to return type 'AnyPublisher<[RecentEpisodeImages], Error>'
How can I collect the values of the inner publisher and return them as
AnyPublisher<[RecentEpisodeImages], Error>
A: Presuming that the question is how to turn an array of URLs into an array of what you get when you download and process the data from those URLs, the answer is: turn the array into a sequence publisher, process each URL by way of flatMap, and collect the result.
Here, for instance, is how to turn an array of URLs representing images into an array of the actual images (not identically what you're trying to do, but probably pretty close):
func publisherOfArrayOfImages(urls:[URL]) -> AnyPublisher<[UIImage],Error> {
urls.publisher
.flatMap { (url:URL) -> AnyPublisher<UIImage,Error> in
return URLSession.shared.dataTaskPublisher(for: url)
.compactMap { UIImage(data: $0.0) }
.mapError { $0 as Error }
.eraseToAnyPublisher()
}.collect().eraseToAnyPublisher()
}
And here's how to test it:
let urls = [
URL(string:"http://www.apeth.com/pep/moe.jpg")!,
URL(string:"http://www.apeth.com/pep/manny.jpg")!,
URL(string:"http://www.apeth.com/pep/jack.jpg")!,
]
let pub = publisherOfArrayOfImages(urls:urls)
pub.sink { print($0) }
receiveValue: { print($0) }
.store(in: &storage)
You'll see that what pops out the bottom of the pipeline is an array of three images, corresponding to the array of three URLs we started with.
(Note, please, that the order of the resulting array is random. We fetched the images asynchronously, so the results arrive back at our machine in whatever order they please. There are ways around that problem, but it is not what you asked about.)
|
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| 8,013
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Keegan Messing (born January 23, 1992) is a Canadian-American figure skater. Representing Canada, he has competed at two Winter Olympic Games in 2018 and 2022. He has also appeared at three World Championships, placing as high as sixth. He is the 2023 Four Continents silver medalist, 2021 CS Golden Spin of Zagreb champion, a two-time Nebelhorn Trophy champion (2018 and 2022), and a two-time Grand Prix medalist. At the national level, he is a two time Canadian national (2022 and 2023) champion.
Previously, representing the United States, he was the two-time International Cup of Nice champion (2011, 2012) and the 2012 Nebelhorn Trophy bronze medalist. He placed fourth at the 2010 World Junior Championships.
Personal life
Keegan Messing was born on January 23, 1992, in Girdwood, Anchorage, Alaska, USA. He has two brothers, Paxon and Tanner; Paxon was killed in a motorcycle accident at age 26, in 2019. Keegan holds dual U.S. and Canadian citizenship; his mother was born in Edmonton, Alberta, Canada, and he is a great-great-grandson of Manzo Nagano, the first Japanese person to officially immigrate to Canada. His father is a firefighter.
In October 2018, he became engaged to his girlfriend Lane Hodson. Messing and Hodson married in the summer of 2019. Their son Wyatt was born in July 2021. Their second child, a daughter, was born in January 2023.
Career
Early career
Messing started skating at age 3 after watching the 1994 Winter Olympics in Lillehammer. Naming Elvis Stojko as his biggest influence, Messing said: "Watching him skate made me want to skate". In addition to singles, Messing formerly competed in pair skating with Ellie Gottstein.
Anne Durham coached Messing from 1995 to 1999. He is now coached by Ralph Burghardt in Anchorage, Alaska.
Messing won the junior silver medal at the 2009 U.S. Championships. The following season, he made his senior national debut, finishing ninth. He finished eighth at the 2011 U.S. Nationals.
Messing won the 2011 Coupe de Nice after placing first in the short program and fourth in the free. He then placed seventh at the 2012 U.S. Nationals, which would be his highest placement as an American senior. He won the bronze medal at the 2012 Nebelhorn Trophy, and repeated as the victor at the 2012 Coupe de Nice.
At the 2013 U.S. Nationals, Messing placed sixteenth, followed by a twelfth-place finish the following year.
In July 2014, Messing said that he would begin competing for Canada. In the 2014–15 season, he won bronze at the Skate Canada Challenge and qualified for the 2015 Canadian Championships. He placed fifth at Nationals, representing a club in Sherwood Park, Alberta.
In the 2015–16 season, Messing placed fifth at the 2015 CS Ondrej Nepela Trophy and eleventh at the 2015 Skate Canada International, his senior Grand Prix debut. He went on to place sixth at the 2016 Canadian Championships.
The 2016–17 season saw Messing compete at two Challenger events, placing fourth at the 2016 CS Autumn Classic International and winning a bronze medal at the 2016 CS Golden Spin of Zagreb. He again placed fifth at the 2017 Canadian Championships.
2017–2018 season: Olympic and Worlds debut
Messing began the Olympic season at the 2017 CS Autumn Classic International, where he won the bronze medal behind Javier Fernandez and Yuzuru Hanyu. Competing on the Grand Prix circuit, he placed eighth at the 2017 Skate Canada International and fifth at the 2017 NHK Trophy.
Competing at the 2018 Canadian Championships that would decide the nation's delegation to the 2018 Winter Olympics, Messing placed third in both the short program and free skate, winning the silver medal behind Patrick Chan. Messing was named along with Chan to the Olympic team, as well as to the 2018 World Championships team alongside national bronze medallist Nam Nguyen.
Competing at the 2018 Winter Olympics in PyeongChang, South Korea, Messing finished twelfth overall. At his World Championships debut, Messing placed sixth in the short program with a new personal best score, qualifying for the final flight of the free skate. Messing placed eleventh in the free skate following errors for an eighth-place finish overall.
2018–2019 season: Challenger gold, Grand Prix silver
Beginning the season at the 2018 CS Nebelhorn Trophy, Messing placed first in both segments to win the gold medal, his first international win while representing Canada.
Competing on the Grand Prix, Messing placed first in the short program at the 2018 Skate Canada International, following mistakes by presumed frontrunner Shoma Uno. He then placed second in the free skate, behind Uno, to win the silver medal overall, his first Grand Prix medal. At the 2018 Rostelecom Cup, he placed fifth, having placed seventh in the short program and sixth in the free program. He was initially named as the first alternate to the Grand Prix Final and was subsequently called up following the withdrawal of Yuzuru Hanyu due to injury.
At the Final, Messing underrotated two jumps in the short program, placing sixth. He moved up to fifth place in the free skate, despite falling on a triple Axel and doubling a planned quadruple toe loop. Messing landed the quad Lutz in competition for the first time, the second Canadian skater to do so after Stephen Gogolev.
At the 2019 Canadian Championships, Messing was considered a favourite going in but struggled in both programs. In the short program, he placed second behind Gogolev, despite falling on his opening quad attempt. The free skate was also a challenge, and he dropped to third place, winning the bronze medal behind Nguyen and Gogolev. He was named to the Canadian teams for the Four Continents and World Championships.
At the 2019 Four Continents Championships, Messing placed fifth in the short program after rough landings on his triple Axel and triple Lutz jumps. He then placed third in the free program with a personal best score, winning a small bronze medal and placing fourth overall. At the 2019 World Championships, Messing placed fifteenth after two error-riddled programs. The placements of Messing and Nguyen meant that Canada would have only one men's berth at the 2020 World Championships. Messing concluded the season at the 2019 World Team Trophy, where he placed sixth overall among the twelve men, including a fourth-place free skate that featured only one error.
2019–2020 season
Messing selected "Perfect" as his short program music for the season in commemoration of his marriage, the song having been the first dance at his wedding. His first competition of the season was the 2019 CS Autumn Classic International, where he won the bronze medal with third-place finishes in both segments. Messing held the Japanese flag in aid of the event's winner, Yuzuru Hanyu, during the medal ceremony and was praised in the media for an example of good sportsmanship.
Messing's younger brother Paxon was killed in a road accident days after the Autumn Classic. Messing opted to compete on the Grand Prix a few weeks later. Messing placed third in the short program at 2019 Skate America, fractions of a point behind Dmitri Aliev, and set a new personal best. He struggled in the free skate, placing eighth and dropping to fourth place overall. Messing performed a tribute to Paxon at the Skate America gala, saying it felt like "a last goodbye." At his second Grand Prix, the 2019 Cup of China, he was fifth in the short program after falling on his quad toe loop and performing only a double Axel instead of a triple. He was third in the free skate and finished fourth overall.
Making only an error on his final triple Lutz, Messing placed first in the short program at the 2020 Canadian Championships. He struggled in the free skate, falling on both his attempted quad jumps and making a number of other errors, and dropped to third place overall behind Roman Sadovsky and Nguyen. Skate Canada assigned all three podium finishers to compete at the 2020 Four Continents Championships, declining for the time being to fill Canada's one berth at the 2020 World Championships.
At Four Continents, Messing placed fourth in the short program with a clean program, which he cited as especially meaningful given his six-month wedding anniversary. He struggled in the free skate, making several jump errors that dropped him to eighth place overall, with Nguyen, the highest-finishing Canadian skater, at sixth.
2020–2021 season: Pandemic
The onset of the coronavirus pandemic disrupted Messing's normal plans, including touring and spending time in Canada with choreographers and the national team. He was assigned to the 2020 Skate America event on the Grand Prix circuit, following the decision of the ISU to base assignments largely on training location. Following the cancellation of the 2020 Skate Canada International event due to the pandemic and teammate Stephen Gogolev's withdrawal from Skate America, Messing was the only Canadian skater remaining with a Grand Prix assignment that year. Messing placed third in the short program despite putting a hand down on his open quadruple jump and stumbling in his footwork. Delivering a strong free skate with only two minor jump errors, he won the bronze medal, his second Grand Prix medal, which he dedicated to his fellow Canadian skaters who were unable to compete on the Grand Prix.
Due to the difficulty of hosting in-person events, the 2021 Canadian Championships were cancelled. Messing also did not participate in the 2021 Skate Canada Challenge, a virtual qualifying competition.
On February 25, Messing was announced as Canada's lone men's entry to the 2021 World Championships in Stockholm. The stakes for his performance were high, as this was the primary qualifier for the 2022 Winter Olympics in Beijing and the only means for a country to earn more than one berth per discipline, which Messing would later call "quite a heavy burden." Messing placed fifth in the short program with a clean skate. In the free skate, he made only two errors at the end of the program, stepping out of a triple Axel and doubling a planned triple flip. He was sixth in that segment and placed sixth overall. His performance guaranteed Canada one men's entry to the Olympics and the opportunity to qualify for a second one at the 2021 Nebelhorn Trophy.
2021–2022 season: National title and Beijing Olympics
In celebration of the birth of his son Wyatt, Messing selected "Home" by Phillip Phillips for his free program music.
Messing made his season debut at the 2021 CS Finlandia Trophy, where he placed first in the short program. He struggled in the free skate, placing seventh in that segment, and dropped to fourth overall. Despite this, he called the event "a great stepping stone for the rest of the season." On the Grand Prix at the 2021 Skate Canada International, he placed third in the short program but again struggled in the free skate and dropped to fifth overall. He was sixth at his second event, the 2021 Internationaux de France, producing his best free skate score of the season to date. Assessing his performance, Messing said that he "had slow start to the season as it's taken me time to figure things out. After Skate Canada, we decided to work on the long program and have a better strategy. It's still not perfect, but I feel like we are on the right track now."
Journeying from Alaska to Ottawa for the 2022 Canadian Championships in the midst of restrictions prompted by the Omicron variant, Messing's skates were initially lost in transit. He initially attempted to practice with a new pair of skates but had his original skates arrive in time for the beginning of competition on Friday. He placed first in the short program despite singling his triple Axel. Messing also won the free skate despite a few jump errors, finally winning the Canadian national title. He was named to his second Canadian Olympic team and indicated that he had not yet decided whether it would be his final year of competitive skating.
Messing was originally scheduled to travel to Beijing with the bulk of the Canadian figure skating delegation. However, on February 1, it was reported that he had been unable to fly to China at that point due to the need to produce two negative PCR tests and that, as a result, his expected participation in the team event was especially in jeopardy. Messing was eventually cleared to fly to travel to China via Montreal and Milan, arriving on Monday, a day in advance of the men's event. Five hours after arriving, he attended a practice session. His travails received significant media coverage. In the short program, Messing landed all his jumps successfully but lost his balance at multiple points during the step sequence, earning a score of 93.24 points to finish ninth in the segment. He extolled the importance of "keeping the happy-go-lucky attitude. To hop on Olympic ice and to put out a performance I can be happy with, it means a lot." Tenth in the free skate, with his main error being tripling a planned quad toe loop, Messing finished eleventh overall. He said he had hoped to remain in the top ten, but that "it wasn't in the cards, but at the same time, I can still leave here happy. This is still a program I can be proud of." He announced afterward that he intended to compete for one more season, hoping to attend the next edition of the World Team Trophy.
Messing concluded his season at the 2022 World Championships, in a men's field considerably more open than usual due to the absences of Nathan Chen and Yuzuru Hanyu and the International Skating Union banning all Russian athletes due to their country's invasion of Ukraine. He was ninth in the short program but dropped to fourteenth after a rough free skate.
2022–2023 season
Beginning the season at the 2022 CS Nebelhorn Trophy, Messing was third after the short program, where he performed poorly. A strong free skate carried him to the gold medal, and he noted afterward that it had been "a constant battle to overcome the nerves. In the short program, the nerves won. In the free skate, I was able to conquer them and put out a solid performance." He also shared the Fritz Geiger Trophy with the rest of the Canadian delegation as the top country in the competition.
Messing commenced his planned final Grand Prix at the 2022 Skate Canada International. After a quad toe loop fall in the short program, he was fourth in that segment. He was third in the free skate but narrowly remained fourth overall, 0.31 points behind the bronze medalist Matteo Rizzo. Messing said afterward that he "couldn't have asked for a better skate" in the free and that he was "not skating for a medal but for myself this year." In his final Grand Prix appearance at the 2022 Grand Prix of Espoo, he finished fourth in the short program but dropped to eighth after a twelfth-place free program.
The 2023 Canadian Championships coincided with the due date for Messing's second child, but he opted to travel with his parents to compete there. He placed first in the short program by over eight points. He was second in the free skate after a number of jump errors at the beginning of his program, but remained first overall and won his second consecutive Canadian title. He departed immediately after the medal presentations, not staying for the gala the following day. Messing called the experience "such a joyous, sad, emotional whirlwind that I could not have ended on a better note. I could hang up my skates right now and just be happy forever." He subsequently was able to return to Girdwood in time for the birth of his daughter.
Despite falling on his open quad attempt in the short program of the 2023 Four Continents Championships, Messing placed second in the segment with a season-high international score of 86.70, winning a silver small medal. He was 5.20 points back of segment leader Kao Miura of Japan, and only 0.06 ahead of third-place American Jimmy Ma. In the free skate, Messing was the penultimate skater, and produced a clean program, receiving a new personal best score in free (188.87) and overall (275.57), and a standing ovation from the crowd. He finished segment overall in the segment, narrowly behind Miura, and won the silver medal. On winning his first ISU championship medal, Messing remarked that "it took me 28 years of skating to get here."
Programs
Competitive highlights
GP: Grand Prix; CS: Challenger Series; JGP: Junior Grand Prix
For Canada
For the United States
Detailed results
Small medals for short and free programs awarded only at ISU Championships. Current personal bests in bold. Historical ISU personal bests in italics.
Senior career
References
External links
Keegan Messing at U.S. Figure Skating
1992 births
Living people
Sportspeople from Anchorage, Alaska
Figure skaters from Edmonton
Canadian male single skaters
American male single skaters
Canadian sportspeople of Japanese descent
American people of Canadian descent
American sportspeople of Japanese descent
Figure skaters at the 2018 Winter Olympics
Olympic figure skaters of Canada
Figure skaters at the 2022 Winter Olympics
Four Continents Figure Skating Championships medalists
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{"url":"https:\/\/www.physicsforums.com\/threads\/short-distance-divergences-in-thermal-states.323581\/","text":"# Short distance divergences in thermal states\n\n1. Jul 6, 2009\n\n### DrFaustus\n\nA question for the more theoretically oriented forum users... but please feel free to suggest an answer to the puzzle anyways.\n\nIn the book of selected works by Glimm & Jaffe, on page 4 (they discuss the massive scalar interacting filed in 1+1 dimension and give an overview of the divergences that occur in QFT), one finds the following:\n\n\"[...] In a similar but less obvious fashion, the ultraviolet divergences are forced by the invariance of the theory under Lorentz rotations.\"\n\n(The \"less obvious\" refers to the \"infinite volume\" divergences that arise because of translation invariance of the theory, i.e. momentum conservation)\n\nAnd I'd be fine with accepting that without actually seeing the \"less obvious\" reasons. What is puzzling me are really the claims one finds essentially in all the treatments on field theory at finite temperature (like LeBellac's book) that ultraviolet divergences at finite temperature are of the same nature as in the vacuum. But finite temperature (KMS) states are NOT Lorentz invariant. There is a preferred frame, the one in which you cannot \"feel any temperature flow\".\n\nHow is that possible? The two statements seem to be in contradiction...\n\n2. Jul 6, 2009\n\n### ytuab\n\n(This is my personal opinion. OK?)\n\nI think the basic problem exists in the \"quantum mechanics(QM)\".\n\nIn QM, we can not image the motion of the particle concretely (spin of the electron, uncertainty principle, the zero orbital angular momentum of S orbital.....).\n\nSo QM had to get away into \" the world of numerical formulas and symbols\" from this real world.\n\nIn this real world, we can easily use the relativistic theory for each particle's motion.\nBut in \"the world of numerical formulas\" like QM, it is much more difficult (we must restrict the formulas, and divergent problems (infinite bare charge and mass , infinite momentum and energy...) will occur).\n\nIf we use the nonrelativistic theory, we must give up the relativistic mass change and the spin-orbital interaction (of Dirac equation). (Of course we can use the nonrelativistic theory for approximation.)\n\nTo avoid such problems, we must go back to the real (classical mechanical) world (like Bohr model .....).\n\nLast edited: Jul 6, 2009\n3. Jul 7, 2009\n\n### DrFaustus\n\nytuab -> I think I see your point, but unfortunately does not solve my doubts. The thing is that the problem I'm facing is, basically, of a purely mathematical\/constructive nature. In other words, if insisting in constructing Lorentz invariant theories yields ultraviolet divergences, how comes that when the symmetry is somehow broken, the ultraviolet problem is not solved? Mind you, it need not have any physical interpretation. Think of it as a purely mathematical problem if you wish. That is, I define certain objects and some relations between them and verify a property (\"ultraviolet divergence\") and then want to see where is this coming from. And encounter the above \"contradiction\"...\n\n4. Jul 7, 2009\n\n### ytuab\n\nI'm sorry to speak my personal opinion, (but I believe the classical mechanical model like Bohr model, which you probably think strange.)\n\nPlease explain more about \"how comes that when the symmetry is somehow broken, the ultraviolet problem is not solved?\"\n\nI think when the symmetry (Lorentz invariance) is broken, the ultraviolet problem will be solved.\nIn Lorentz invariant theory,(like QED), in the vacuum, there are infinite \"virtual\" photons and particles (which have every momentum and energy (including infinite momentum and energy) at any condition (even at finite temperature)).\n(photons and particles are interacted)\n\nThe ultraviolet divergent problems are caused by the infinite momentum and energy of them (the virtual process).\nSo the bare charge and mass of the electron are infinite to cancel it (by using the renormalization theory).\n\nIn QFT (nonrelativistic theory), we treat the actually-existing particles(their total number may be infinite), and the vacuum polarization is not occurred.\nso there is a natural cutoff (there is a upper and lower limit of momentum and energy of the particles).\n\n(I'm sorry if I misunderstand your question.)\n\nLast edited: Jul 7, 2009\n5. Jul 8, 2009\n\n### Bob_for_short\n\nMaybe you can find some answers in \"Independent research\" forum\n\n6. Jul 9, 2009\n\n### DrFaustus\n\nytuab ->\nWhat I mean is simply that if there is a logical implication \"Lorentz symmetry $$\\Longleftrightarrow$$ ultraviolet divergences\" then if I remove the assumption, the consequences should also fall. Unless the implication is not equivalent to the assumption and Lorentz symmetry is only sufficient for ultraviolet divergences to arise.\n\nWhich is precisely what I'm puzzled about. That is, I'm trying to make sense of the statment from my first post.\n\nbob -> I appreciate your effort to solve the many problems of QFT, but as I'm still a PhD student trying to work my way to my degree, I'm not sure an unconventional view on the subject would in any way help me.\n\n7. Jul 9, 2009\n\n### ytuab\n\nMay I ask you one more question?\n\nYou said \"finite temperature (KMS) states are NOT Lorentz invariant\". What do you mean by that?\n\nI think there is no relation between temperature and Lorentz invariant theory(QED).\nWhen I care about the temperature, this is nonrelativistic theory.\n\nAs I said, In Lorentz invariant theory, \"the vacuum polarization\" is occurred.\nThe vacuum polarization means that infinite \"virtual\" photons and particles which have infinite momentum and energy are occurred in the vacuum even at finite temperature (the temperature is not relevant in Lorentz invariant theory.)\n\nThe temperature has the relation with the actually-existing (not virtual) particles.\n\nLast edited: Jul 9, 2009\n8. Jul 9, 2009\n\n### Bob_for_short\n\nI showed that divergences appear due to too bad initial approximation - strongly and permanently interacting (bound!) particles (electrons and photons) are initially considered as decoupled.\n\nTaking some essential part of their interaction into account in the initial approximation improves the perturbative series behaviour. Electron interacting with the quantized EMF has a smeared charge (a natural cut-off in coordinate and in the momentum spaces), so no divergences appear.\n\nFinite temperature is not different from zero temperature case since it signifies the initial and final photon state have non-zero populations. In QED there is no limitations or particularities about that. In fact, the correct QED approach takes the initial and final non-zero photon state populations automatically - in the inclusive picture that is the only picture to make sense.\n\nLast edited: Jul 9, 2009\n9. Jul 9, 2009\n\n### Naty1\n\nAu contraire!!!,\n\nAs if Copernicus, Einstein, Planck, de Broglie, Witten, 'T Hooft, Susskind to name a few, solved problems \"conventionally\"...good grief, man, don't use that as any criteria!!!!!\n\nThat may be the most \"fantastical\" (yes, I know not a real word) comment I have seen in this forum so far!!!\n\n10. Jul 9, 2009\n\n### malawi_glenn\n\nAre you a professor and know how one does science?\n\n11. Jul 9, 2009\n\n### Bob_for_short\n\nMy approach is not unconventional or fantastic. It is clear and practical.\n\nYou asked a fundamental question, not resolved so far. What did you expect as an answer?\n\nI answer with certainty because I am very well aware of this problem.\n\nLast edited: Jul 9, 2009\n12. Jul 9, 2009\n\n### DrFaustus\n\nI'll try to be as clear as possible. The reason for my wanting a conventional answer is very simple. Actually very pragmatic. Since I want to get a PhD recognized in the \"conventional physics\" comunity, I better understand conventional physcs damn well before going on to consider alternative explanations and speculations. (And this is coming from someone who doesn't mind at all new and alternative ideas.) Trust me, the examination commitee will not appreciate unconventional explanations that openly contradict the established knowledge. And just by the way, it is \"established knowledge\" for a reason.\n\nNaty1 -> By what you say I will assume you are not too familiar with the works of the people you mentioned and the state of physics at the time they were or are working. I can assure you that except for Einstein, DeBroglie and probably Copernicus, the others have been solving problems in a pretty conventional way. Brilliantly, but conventional science neverthelss. (And I'm still not sure what does Susskind have to do with the likes of Planck, Einstein, Witten... ) But I'm pretty pleased of having made your day with the most fantastical post on here.\n\nBob -> I will have a look at your work, but more out of curiosity than as the answer I'm looking for as I have two remarks on what you said. One, the fact that I or you don't know how the above puzzle is resolved in a conventional scientific way does not mean it has not been resolved or that it has no solution at all. I'm pretty sure both Glimm or Jaffe would know how to answer. Two, you mention photons and electrons and hence QED. In whatever approach you might want, but you're still talking about one specific model. My question, on the other hand is not tied to a specific model. It is supposed to be a feature of QFT in general. And incidentally comes from a discussion of scalar quantum fields with polynomial interaction in 2D. So it's not even tied to the dimensionality where the theory is formulated. If your work can be extended so to include every possible quantum field, regardless of the type or the dimension in which you formulate the theory, then it is a valid alternative and I'm sure it can be published. If it's model dependent, then you'll have to expand your results to really claim a novel perspective on old problems.\n\nytuab -> Finite temperature states (any physical state in thermal equilibrium) are not Lorentz invariant in the sense that there exists a preferred reference frame. Consider a huge box of gas at constant temperature. The preferred frame is the one in which you don't feel any \"flow of warm gas\" in your face. Also, if you want to describe an extremly hot gas for which the particles are relativistic, then you'll have to tackle field theory at finite temperature. So it's defeinitely not something intrinsically non relativistic. And finally, if you have not done so, please read my reply to bob_for_short. I'm NOT asking a question specifically in the case of QED. The claim is supposed to hold for any QFT model. Like $$\\varphi^4$$, for instance.\n\n13. Jul 9, 2009\n\n### ytuab\n\nEDIT: I'm very sorry. You are speaking 1+1 dimension? I'm misundestanding. Please tell me in 1+1 dimension, does the ultraviolet divergence occur? Is it as same as 4 dimension ? I'm speakin in 4D as follows,\n\n------------------------------------------------------------------------------------------------\nI think ultraviolet divergence (Lorentz invariant theory) is caused by the vacuum polarization.\n\nOf course this world is at finite temperature, but Lorentz invariant.\nI didn't say \"extremely hot gas\" means Lorentz invariant. (\"extremely hot energy\" is caused by the \"virtual\" vacuum).\n\nBut when the ultraviolet divergence is solved using the renormalization theory, in this actual vacuum(observable), the temperature is finite.\n\nAnd also in $$\\varphi^4$$ (Lorentz invariant theory), the ultraviolet divergence is caused by the infinite momentum and energy. And when we use the renormalization theory, the temperature becomes finite and it keeps Lorentz invariant.\n(the virtual process)\n\nLast edited: Jul 10, 2009\n14. Jul 10, 2009\n\n### Bob_for_short\n\nThe very first time the electron charge smearing was considered in T. Welton's publication in Phys. Rev. 1948, and I refer to it since he made a lot of good estimations.\n\nCurrently the UV divergences are removed with renormalizations, and Glimm or Jaffe know it. Just their explanation is too wrong.\n\nThe problem is not in QED but in how QED and other theories are constructed - the field interaction is a product of fields involved that contain the self-action. Quantization of any QFT is similar to QED so everything in them is alike, not model-specific.\n\nI just wanted you to know that sometimes a theory can be reformulated so that no divergences appear at all.\n\nLast edited: Jul 10, 2009","date":"2017-08-22 17:27:55","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 0, \"mathjax_display_tex\": 1, \"mathjax_asciimath\": 0, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 0, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.7942809462547302, \"perplexity\": 1011.9328945022952}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 20, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2017-34\/segments\/1502886112533.84\/warc\/CC-MAIN-20170822162608-20170822182608-00482.warc.gz\"}"}
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Produced by Dianna Adair, Paul Clark and the Online
Distributed Proofreading Team at http://www.pgdp.net (This
file was produced from images generously made available
by The Internet Archive)
Transcriber's Note:
Every effort has been made to replicate this text as faithfully as
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THE DEACON
AN ORIGINAL COMEDY DRAMA IN FIVE ACTS
BY
HORACE C. DALE
AUTHOR'S EDITION, WITH THE CAST OF THE CHARACTERS,
SYNOPSIS OF INCIDENTS, TIME OF REPRESENTATION, DESCRIPTION
OF THE COSTUMES, SCENE AND PROPERTY
PLOTS, SIDES OF ENTRANCE AND EXIT, RELATIVE
POSITIONS OF THE PERFORMERS, EXPLANATION
OF THE STAGE DIRECTIONS, AND ALL OF
THE STAGE BUSINESS.
Copyright, 1892, by Horace C. Dale. All rights reserved.
[Illustration]
NEW YORK
HAROLD ROORBACH
PUBLISHER
[Illustration]
NOTE.--The acting rights of this play are expressly reserved by the
author. Theatrical Managers wishing to produce it should apply to the
author in care of the publisher. Amateur representation may be made
without such application and without charge.
THE DEACON.
CAST OF CHARACTERS.
_Grand Opera House,
Reading, Pa.,
Dec. 16th and 17th, 1886._
{_Mrs. Thornton's brother-in-law,}
DEACON THORNTON, {with a passion for lemonade } William Ward.
{with a stick in it_, }
GEORGE GRAEF, _Mrs. Thornton's nephew_, Geo. W. Endy.
GEORGE DARRAH, _alias Matt Wheeler_, Jas. I. Foos.
JAMES READ, _a friend of Darrah's_, H. C. Lewis.
PEDRO, _an organ grinder_, Sam'l Bechtel.
PARSON BROWNLOW, W. H. Wilson.
PETE, _Mrs. Thornton's servant_, H. W. Button.
BILLY, _the Deacon's boy_, Sam'l Wolfskell.
MRS. THORNTON, Agnes Jameson.
HELEN, _her daughter_, Claribel Lewis.
MISS AMELIA FAWCETT, _Mrs. Thornton's maiden sister_, Minnie Riffert.
MRS. DARRAH, _George Darrah's wife_, Ida Radcliffe.
NELLIE, _her child_, Lizzie Rivers.
DAISY, _Mrs. Thornton's servant_, Annie C. Fisher.
Violinist, Policeman, Villagers, etc., by the Company.
TIME OF REPRESENTATION.--TWO HOURS AND A HALF.
TIME, the present. LOCALITY, Eastville, Va.
NOTE.--Officer, in Act I, Pedro and Parson Brownlow can be doubled and
played by Read. Officer in Act IV, by Violinist.
SYNOPSIS OF INCIDENTS.
Act I. Scene, Eastville Hotel garden. The Robbery.--Pete delivers
an invitation.--"By golly, he's mad already."--Meeting of Graef and
Wheeler.--"I'm no coward; I'll either live down the stigma attached
to it, or die in the attempt."--A promised reward.--The Deacon's
arrival.--"I'm a gentleman, sir."--"Be sure to put a little stick in
it."--The Deacon gets hilarious.--Pete imposes upon Billy.--The Deacon
is sick.--"Oh, my head, my head!"--Triumph No. 1.--Curtain.
Act II. Scene, Mrs. Thornton's sitting-room. Pete promotes himself.--"I
spruced up to do de honors ob de 'casion."--Miss Amelia is anxious
about her dear little pet.--"Ze dog or ze money."--"Horrid men, but
dear doggy woggy."--The Deacon's reception.--The Deacon makes a
mistake.--"Everything lovely admires me."--"Were you and Bill married by
candle light?"--"Deacon, you are drunk!"--Miss Amelia prescribes for the
Deacon.--Triumph No. 2.--Curtain.
Act III. _Scene 1._ A street. Mother and child.--"Mamma, will we never
reach papa's house?"--The meeting of husband and wife.--"What, you
here!"--Accused of many bitter things.--Left in the streets.
_Scene 2._ George Graef's lodgings. Graef meditates.--The finding of
the diamonds.--Meeting of Graef and Mrs. Darrah.--"Minnie, is this
you?"--"Welcome little coz."--The photo.--"Yes, alas, too well!"
_Scene 3._ A street. Pete has a dream and persuades Billy to accompany
him on an expedition.
_Scene 4._ A wood. The treasure hunters.--"Oh, Lor', I'm dead!"--"Let's
go home and get the mules."--The treasure is found.--Caught by the
spirits.--Tableau. Curtain.
Act IV.--Scene, Mrs. Thornton's sitting-room. Daisy shows Pete what
she would do.--Miss Amelia's heart is in a flutter.--"I know I'll
refuse him."--Pete at his old tricks.--"Then kiss me."--Consternation.
--Pete continues his tricks.--"'Tis he, by Jerusalem!"--The Deacon
taken by surprise.--More consternation.--"I was insulted by a <DW52>
woman."--Billy creates some excitement.--"Thank heaven, at last I enfold
thee!" Curtain.
Act V. Scene, Mrs. Thornton's sitting-room. The Deacon in clover.
An interruption.--"Hang the Parson!"--The interrupted marriage
ceremony.--"That man has a wife living."--"'Tis false!"--An
attack.--Pete to the rescue.--"No, it is a forgery."--The villain
foiled.--Arrest of George Darrah.--Reinstatement of Graef.--Refusal
of a hand.--The Deacon is obstinate.--"I can't help it, Minnie, I
mean it."--Mrs. Darrah and Nellie forgiven.--"Oh, Deacon, don't be so
silly."--The Deacon made happy. Curtain.
COSTUMES.
MRS. THORNTON.--Act II. Light tasteful morning dress, with head dress.
Act IV. House dress with apron. Act V. Elegant silk dress. Slightly
gray-mixed wig.
HELEN.--Act II. Street dress, with hat, gloves, etc. Act IV. House
dress and apron. Act V. Bridal dress with train, orange blossoms, veil,
gloves, etc.
MISS AMELIA.--Act II. Either a very plain or very flashy dress;
eyeglasses dangling from cord; regulation spinster curls, gray. Act IV.
Dress to suit taste. Act V. Elaborate get-up for the occasion.
MRS. DARRAH.--Acts III and V. Dark dress, bonnet, gloves, etc.
NELLIE.--Acts III and V. Dark dress to suit taste, hat, etc.
DAISY.--Act I. Tasteful maid's dress and hat. Act II. Same, minus hat.
Act IV, 1st entrance, same with dusting cap. 2nd, 3rd and 4th entrances,
same, with apron, minus cap.
DEACON.--Acts I, II and IV. Old-fashioned-cut pantaloons, dotted vest,
old-fashioned easy fitting coat; ditto shirt collar; broad brimmed,
light felt hat; square watch fob dangling from watch pocket; square
glass spectacles; white bald wig and white throat whiskers. Act V.
Old-fashioned dark cloth suit; rose on lapel of coat.
GEORGE GRAEF.--Acts I and III. Dark cutaway suit. Straw hat. Act V.
Prince Albert dress coat; light trousers. Dark dress wig and moustache.
GEO. DARRAH.--Acts I and III. Dark cutaway suit. Silk hat. Acts II and
V. Prince Albert dress coat and pants. Black dress wig and moustache
throughout.
BILLY.--Acts I, II and III. Long white stockings; light broad plaid
pants, cut short below the knees; pleated shirt waist; loose fitting
linen jacket; low-crowned, narrow-brimmed light hat. Act IV. Same with
night gown thrown over. Act V. Same, minus coat. Light flaxen fright
wig.
PETE.--Act I. Linen suit, straw hat. Act II. Black pants, white vest,
smoking jacket, low-cut patent leather shoes, white shirt, standing
collar, white tie and cuffs. Act III. Same as Act I, minus hat. Act IV,
1st entrance, same. 2nd entrance, see description; ditto, 3rd entrance;
4th entrance, same as 1st entrance. Curly <DW64> wig throughout.
PARSON BROWNLOW.--Ministerial suit, coat buttoned up to chin, long black
curly wig, black side whiskers and moustache.
PEDRO.--Make-up to represent organ-grinder.
VILLAGERS.--Modern costumes, straw hats.
FIDO.--Red flannel jacket, small straw hat with ribbon streamers. Collar
with light chain attached.
PROPERTY PLOT.
Act I.
Newspaper. Note for PETE. Green umbrella and pocket-book containing
check for DEACON. White powder for WHEELER. Pitcher of lemonade, salver,
1 empty glass and one filled with soda water. Carpet bag. Placard with
"Pinch me" on it for BILLY. Police star. Violin.
Act II.
Books and flowers. Cigar for PETE. Dog dressed to represent monkey.
Small hand organ for PEDRO. Pin for PETE. Purse and money for MRS.
THORNTON.
Act III.
Bank-note and pocket-book for WHEELER. Books and papers. Candle lighted.
Pitcher of water and glasses. Small pasteboard box for PETE. Photo
for MRS. DARRAH. Lighted lantern, spade and flask for PETE and BILLY.
Leaves. Small wooden box containing iron pot, covered with tan bark to
represent mound. Iron chains. Gun loaded. Bass drum for thunder. "Flash
box" for lightning. 3 sheets for "spooks." Red fire.
Act IV.
Dust pan and brush, broom and bits of paper. Linen suit, spectacles, wig
and whiskers, similar to DEACON'S, for PETE. Dress and wig, similar to
AMELIA'S, for PETE. Flour and dough for DAISY. Bandages for BILLY.
Act V.
Large butcher knife for PETE. Prayer-book for PARSON. Small pasteboard
box. Charm and note for GRAEF. Handcuffs for Officer. Large piece of
molasses cake for BILLY.
SCENE PLOT.
Act I.
SCENE.--Landscape in 4 G. Wicket fence crossing from R. 3 E. to L. 3 E.
with practicable gate C. Set house R. 2 E. with practicable door and
steps. Table and two chairs down L. C. Rustic settee up L. Green baize.
Lights up. Time, morning.
Act II.
SCENE.--Fancy chamber boxed in 3 G., backed with Landscape in 4 G.
Double door C. in flat, open and hung with curtains. Door L. 2 E. Tables
down R. and L. C. Sofa up L. Large rocking chair R. near 2 E. Chairs
around sides. Medallion carpet. Lights up. Time, morning.
Act III.
SCENE 1.--Street in 1 G. Practicable door R. C. in flat.
SCENE 2.--Cottage interior in 3 G. Table R. C., with chair. Chairs
around sides. Door L. 2 E.
SCENE 3.--Street in 1 G.
SCENE 4.--Woods in 4 G. Mound L. 3 E. Green baize down throughout Act.
Lights low. Time, night.
Acts IV and V.
SCENE.--Same as Act II.
STAGE DIRECTIONS.
The player is supposed to face the audience. R., means right; L.,
left; C., centre; R. C., right of centre; L. C., left of centre; D.
R. C. in F., door right of centre in flat or back scene; D. C., door
centre; 1 E., first entrance; 2 E., second entrance; R. U. E., right
upper entrance; L. U. E., left upper entrance; 1, 2, 3, or 4 G., first,
second, third or fourth grooves; UP, toward the back of the stage; DOWN,
toward the audience.
R. R.C. C. L.C. L.
[Illustration]
[Illustration]
THE DEACON.
ACT I.
Scene:--_Garden. Eastville Hotel. Set house R. 2 E., with
practicable door and steps. Wicket fence from R. 4 E. to L. 4 E.,
with practicable gate C. Rustic table and two chairs down L. C.
Rustic settees up R. C. and L. C. As curtain rises MATT WHEELER is
discovered seated at table L., with newspaper in hand, reading_.
=Wheeler.= (_reading_) Last evening a bold and daring robbery was
committed at the residence of Mrs. Thornton. While she was serving her
guests with refreshments, some one entered her dressing-room and removed
from her jewel-case diamonds valued at a fabulous price, leaving in
exchange perfect specimens of worthless glass imitations. Suspicion
points strongly to George Graef, her nephew, as the guilty party. He was
seen to enter Davis's pawn shop late last night, after the guests had
left his aunt's residence, and pawn something. One of the diamonds was
recovered this morning from Davis's store, but he professed ignorance
as to the name of the man who left it. Young Graef, though he strongly
denies committing the theft, was compelled to leave his aunt's residence
this morning. He has been very dissipated of late, drinking and gambling
to excess, and it is thought that financial embarrassment tempted him
to commit the crime. (_lays paper on table_) Poor fellow! What an
inglorious ending for what _might_ have been a brilliant career. _Gilded
youth_, like the rest of common humanity, when it enters the arena
against the sparkling cup, witty companions and fascinating games of
chance, must finally succumb.
Enter _PETE, L. U. E.; passes through gate_.
=Pete.= (_bowing_) Massa Wheeler, missus sends her best 'spects, an'
quests de delight ob yo'r pleasure to dinner, sah.
=Wheeler.= Requests the pleasure of my _company_, I suppose you mean.
=Pete.= Yes, sah, I 'spects dat's what she meant. (_aside_) One nebber
knows what dese wimmin folks mean by what dey says, no-how.
=Wheeler.= At what time do you dine?
=Pete.= (_looking at WHEELER a moment_) Sah?
=Wheeler.= At what time do you eat dinner?
=Pete.= When de rest git froo.
=Wheeler.= What time do the rest usually "get through?"
=Pete.= I dunno. (_laughs_) Guess when dey gits tired ob eatin'.
=Wheeler.= You impertinent black rascal! What do you mean by answering
me in that manner?
=Pete.= (_aside_) By golly, he's mad already! (_aloud_) Massa Wheeler,
yo' knows jest as well as I do dat I was not sassin' yo'. Yo' axes me
at what time I eats, an' I tole yo'. Yo' don't s'pose I eats wid de
_quality_ folks, does yo'?
=Wheeler.= I'd not be the least bit surprised if they were to allow you.
You have never been taught your true position, nor how to address a
gentleman.
=Pete.= I 'spects I knows how to 'dress dem when I meets 'em.
=Wheeler.= (_angrily_) What's that?
=Pete.= Massa Wheeler, it 'pears mighty queer dat yo' an' I can't talk
sociably for five minnits widout quarrelin'. I'se agwine to tell missus
dat de next time she wants a note sent to you, dat she will hab to seek
some oder 'vayance, for I won't take it, suah.
=Wheeler.= So Mrs. Thornton sent me a note, did she?
=Pete.= Ob course she did.
=Wheeler.= Where is it?
=Pete.= In my pocket.
=Wheeler.= Why did you not give it to me then, instead of attempting to
deliver her message verbally?
=Pete.= Kase yo' nebber axed me for it.
=Wheeler.= Give it to me this instant, you black imp. (_PETE gives note;
WHEELER hastily reads it_)
=Pete.= (_aside_) It's mighty plain what kind ob company he 'sociates
wid. 'Pears to me he's nebber learned how to 'dress gen'men, eider.
(_points to self_)
=Wheeler.= (_folding note_) Give my compliments to Mrs. Thornton and
tell her I shall be pleased to accept her kind invitation.
=Pete.= (_going_) Yes, sah. An' I'll gib her a message or two dat yo'
didn't send her.
=Wheeler.= (_angrily_) What's that? Off with you! I shall inform Mrs.
Thornton of your insolence as soon as I see her.
=Pete.= Don't worry yo'self. I'll see her 'fore yo' will. (_laughs and_
exit, _gate C. Goes L._)
=Wheeler.= (_angrily_) Confound that piece of ebony! He's enough to
irritate a saint. He's been petted by the whole household until he has
become worse than a spoiled child. Just wait--(_PETE re-appears softly
at gate C., and listens_) until Helen and I are married, and _I'm_ his
master. I'll teach that grinning jackanapes his true position. (_PETE
shakes his fist at WHEELER, and runs off L., smiling_) Why doesn't Daisy
come? I must regain possession of that charm and note, otherwise I may
have trouble in accounting for their presence wherever they may be. Hang
my carelessness!
Enter _GRAEF, R. U. E.; passes through gate and goes down C._
=Wheeler.= (_advances and playfully slaps GRAEF on left shoulder_)
Graef, old boy, how are you? I was just thinking about you, and
regretting that you had got yourself into trouble.
=Graef.= To what do you refer?
=Wheeler.= (_lightly_) To that little affair at your aunt's house last
night.
=Graef.= Then you have heard about it?
=Wheeler.= Why, of course.
=Graef.= From whom?
=Wheeler.= I saw a little account of it in this morning's issue
(_pointing to paper on table_) of the _Sun_.
=Graef.= (_surprised_) What! Has it already appeared in print? (_picks
up paper and reads to himself while WHEELER is talking_)
=Wheeler.= Yes, but you need not mind that. All you have to do is to
leave town for a few years. Go to some place where you are unknown,
carve out a name and fortune for yourself, return here _wealthy_, and
this trivial offence of yours will be condoned, at least, if you are not
made a hero of.
=Graef.= (_excitedly, pointing to passage in article_) That's not true.
I was not "compelled to leave my aunt's residence." I left of my own
free will. I could not remain there after I knew she thought I had
committed the deed.
=Wheeler.= (_soothingly_) Of course not; never mind that article, it's
not of much importance. No one believes sensational newspaper reports,
anyhow.
=Graef.= But that does me a gross injustice.
=Wheeler.= Oh, pshaw, that's nothing. Let it go, and forget all about
it. What do you intend doing with yourself now?
=Graef.= I intend to remain here, turn over a new leaf, make a man of
myself, and live down this disgrace.
=Wheeler.= (_coolly_) Better not.
=Graef.= Why?
=Wheeler.= Because you will not find it a comfortable existence. Persons
who know you well, like myself, would pay no attention to the charge
preferred against you, but----
=Graef.= Well?
=Wheeler.= There are plenty of others who would, and your daily life
would be beset by the harassing knowledge of being surrounded by those
who doubted your honesty.
=Graef.= Let them doubt me if they will. The peace and tranquility that
innocence imparts to me will more than over-balance that.
=Wheeler.= Have it as you will. But if you were to follow the advice
of a friend, you would do as I suggested, leave this town and that
instantly.
=Graef.= (_suspiciously_) You appear anxious to have me go.
=Wheeler.= Oh, no; not anxious in the sense you mean. I only wish to
save you and your friends unnecessary pain. If you are short of funds,
say so and I will advance you any reasonable sum you may require.
=Graef.= (_coldly_) Thank you. I did not come here to beg assistance. I
merely stopped to tell you that under existing circumstances you will
have to select some other groomsman; I cannot officiate.
=Wheeler.= I'm sorry, but as to selecting another, that's out of the
question. It's too late. If you remain in town I presume you will be
present at our marriage.
=Graef.= No, that's impossible! (_going_)
=Wheeler.= It's too bad, old boy; but keep up your spirits. You had
better think over my suggestion.
=Graef.= (_at gate_) Once for all, Wheeler, I tell you, I'll never do
it. I'm no coward. Here in this town I was born and raised, and _here_
I'll remain and redeem my character. I'll either live down the stigma
attached to it, or die in the attempt.
Exit _gate C., and goes off R._
=Wheeler.= (_with power_) Curse it! Foiled again! But go he must, or
I'll ruin him body and soul. I know his weaknesses, and I'll play upon
them until he accomplishes my purpose. (_bitterly_) Oh, to get even with
her father and relations has been my prayer for years. (_goes to table
L., and sits; picks up paper and pretends to read, but lays it aside as
soon as DAISY comes forward_)
Enter _DAISY L. U. E.; opens gate C. and comes down_.
=Wheeler.= Ah, Daisy, is that you?
=Daisy.= Yes, sir.
=Wheeler.= I thought you had forgotten the message I sent you.
=Daisy.= No, sir, but I could not come any earlier, and I can only stay
a moment now. We are very busy at home preparing for the Deacon's
arrival. You know Mrs. Thornton expects him to-day.
=Wheeler.= Yes, I was aware of it. How does Mrs. Thornton stand her
loss?
=Daisy.= Oh, she feels terribly about it, sir. She has forbidden Miss
Helen, Pete and all of us ever to mention the subject to her. Just to
think that Mr. George should be guilty of such a thing! But then I don't
believe he did do it!
=Wheeler.= (_affecting surprise_) Don't you? Well, I wish I could think
so, too. You know he has been very wild of late.
=Daisy.= I know he has; but Mr. George would never do a mean thing like
that.
=Wheeler.= (_doubtingly_) I don't know.
=Daisy.= (_warmly_) Well, I do. But I must be going. What did you wish
to see me about, sir?
=Wheeler.= Did you find a watch charm or note anywhere in your house
this morning?
=Daisy.= No, sir.
=Wheeler.= I lost them somewhere last night, and I'm pretty sure it was
in your house. They are of no use to anybody but me. I prize the charm
solely because it was a present from my mother, and the note accompanied
it. Now if you find them and return them to me as soon as you possibly
can, I'll make you a present of a ten-dollar bill.
=Daisy.= Oh, thank you, sir. I'll try my best to find them. Is that all?
I must hurry back home again.
=Wheeler.= Yes, I believe so.
=Daisy.= Be careful when you see Mrs. Thornton and don't say anything to
her about her loss or Mr. George. Good morning, sir.
=Wheeler.= All right, I won't. Good morning. (Exit _DAISY, gate C.; goes
L. WHEELER walks to door steps R. 2 E.; stops and faces audience_) If
her search proves successful, that will be the easiest ten dollars she
ever earned. But suppose it proves fruitless! What then? I should be
placed in a very unpleasant position. (_thinks_) Ah, well, it's time to
worry when trouble overtakes one. I've often been more sorely pressed
than I shall be by this little affair, and come out all right; and I
guess I can do it again if the emergency arises. (_turns quickly and
starts to enter house_).
Enter READ, R. U. E.
=Read.= (_at gate outside_) Hist, Matt, are you alone?
=Wheeler.= Yes.
=Read.= Then get ready, for the Deacon is coming.
=Wheeler.= (_off steps, near gate_) Where is he?
=Read.= Coming up the street, (_pointing R._) about a square off. We
missed the early stage, so there was no one to meet him. I directed him
here for information as to Mrs. Thornton's residence.
=Wheeler.= Did you ride over with him in the stage?
=Read.= Yes, there was no one in the stage with us except the Deacon's
boy, Billy.
=Wheeler.= (_disappointed_) Has he a boy with him? That's bad.
=Read.= Yes, a dull, ignorant, country lout. But he'll not interfere
with your plans, for I sent him around the square, and some of the boys
will be sure to detain him and have some fun with him.
=Wheeler.= Did you have any trouble in getting the Deacon to try your
lemonade?
=Read.= (_laughing_) Not a particle. He complained about the heat
and the jostling of the stage making him feel sick and giddy; so I
pulled out my flask, told him I was subject to just such attacks while
travelling, and that I always went prepared for such emergencies, etc.
After I assured him that the flask contained nothing but weak lemonade
and a harmless ingredient to give it its peculiar color, he nearly
emptied it for me.
=Wheeler.= Did you mix your lemonade according to my directions?
=Read.= Yes, and if he is not jolly blind drunk inside of a half hour,
then I don't know my man. His tongue was beginning to wag when I left
him. But I must be off, for the Deacon is nearly here. (_starts to go,
but stops near L. U. E. as WHEELER speaks_)
=Wheeler.= Read, stop a moment. Try and find Walters, and send him here
inside of an hour, will you?
=Read.= You forget that Walters has not returned from----
=Wheeler.= Hush! Confound it, that's true. It takes him an eternity to
do the simplest thing. Never mind, I'll attend to it myself. Get off
with you now, quick. (Exit _READ, L. U. E. WHEELER goes down C._) I'll
let the precious booty remain in its hiding place until I start on my
wedding tour, then I'll take it along with me. It's safe where it is.
(_crosses to chair L. of table_) First I must make the Deacon gloriously
drunk. Then ascertain if it be true that he intends to give Helen a
wedding present of a check for ten thousand dollars; and, finally, send
him to his sister-in-law's in a drunken condition. That will be triumph
No. 1. (_sits in chair_)
Enter _the DEACON R. U. E., with large umbrella hoisted,
fanning himself with bandanna handkerchief. Comes to gate, opens it
smiling, a picture of good humor; closes gate, shuts umbrella, and
approaches WHEELER._
=Deacon.= (_at WHEELER'S side, clears throat_) Are you the landlord of
this hotel?
=Wheeler.= (_pleasantly_) Well, no, not exactly.
=Deacon.= (_blandly_) Of course not. Excuse me. I knew you weren't the
moment I sot eyes on you. What did I understand you to say you were?
=Wheeler.= I'm a gentleman, sir.
=Deacon.= Yes, of course you are. That's just what I thought you were.
I'm a gentleman, too. You wouldn't believe it, would you? (_laughs and
clears throat_) I'm a _country_ gentleman. I live over in Rockford
county. Perhaps you have heard tell of me. I'm Deacon Thornton.
=Wheeler.= (_in joyful surprise_) Indeed! (_rises and shakes DEACON'S
hand warmly_) Why, Deacon, I'm _delighted_ to make your acquaintance,
sir. (_DEACON smiles and appears pleased_) Heard of you, sir? Why,
you are known the state over as being the wealthiest and most
liberal-hearted gentleman in Rockford county. Is it possible I have the
honor of shaking hands with so noted a gentleman as Deacon Thornton?
=Deacon.= (_appears slightly intoxicated_) None other, I assure you.
Excuse me, but may I rest a few moments in that chair? (_points to chair
L. of table_) I'll feel more sociable like.
=Wheeler.= Why, certainly, sir. (_goes to chair, takes out handkerchief
and dusts it off. Helps seat the DEACON in it_) You seem to be tired,
sir.
=Deacon.= Yes, I am, and warm, too. (_fans himself with hat_) You see,
I've come over here to attend my niece's wedding. (_abruptly_) Say, do
you know where Mrs. Thornton lives?
=Wheeler.= Oh, yes, I'm well acquainted with the family. (_takes seat
R._)
=Deacon.= That's good. I'll get you to show me her house presently.
(_WHEELER manifests a desire, by half rising, to show him immediately_)
Not now, sit still. I'm not rested yet. You see, I've never met Mrs.
Thornton. She's my sister-in-law. My brother Bill and I had a fall-out
when we were young, and never made up afterward. She's Bill's widow.
Helen's her daughter, my niece. She's going to be married day after
to-morrow. (_the DEACON talks rapidly_) Whew, but it's hot!
=Wheeler.= Yes, it is warm. (_rising_) Excuse me, but I never thought of
it. Perhaps your long ride in the sun has made you thirsty, too. Let me
get you some lemonade. It will refresh you.
=Deacon.= Well, yes, you may, if you will. (_WHEELER starts for door L.
2 E._) Be sure (_with a wink_) to put a little stick in it. (_rubbing
hands_) It gives it _tone_, you know.
=Wheeler.= Oh, yes, I understand. (_Winking and nodding head. DEACON
fans himself with hat, smiling and seeming well pleased. WHEELER, when
he reaches steps, pauses, half turning toward audience, takes a white
paper parcel from breast pocket and holding it up exclaims, aside_) And
I'll put something else in that will soon make your head swim.
Exit _through door_.
Enter _DAISY hastily, L. U. E.; passes through gate and goes down C._
=Daisy.= Oh, Mr. Wheeler, I forgot----(_perceives DEACON_) Oh!
=Deacon.= (_rising, appears a little unsteady. Gazes admiringly at
DAISY. Speaks to audience_) Blast my buttons! Ain't she a daisy?
=Daisy.= (_slightly advancing_) Did you speak to me, sir?
=Deacon.= (_confused_) No--yes,--that is--What's your name, my pretty
miss?
=Daisy.= Daisy Dean, sir.
=Deacon.= Are you married?
=Daisy.= No, sir.
=Deacon.= Wouldn't you like to be?
=Daisy.= (_demurely_) I--don't know, sir.
=Deacon.= (_to self_) I'll think the matter over. (_aloud, coaxingly_)
Won't you come and give me a kiss?
=Daisy.= (_looks at the DEACON a moment in amazement, then with
emphasis_) No, sir, I won't. (_turning quickly with toss of head, she
exits at gate, closes it, looks a moment at DEACON, who follows her
retreating form with open-mouthed astonishment, then quickly_ exits
_L. The DEACON gradually faces round to audience, with the look of
wonderment still suffusing countenance_)
=Deacon.= Well, it's plain she was not _particularly_ smitten with me.
(_resumes seat_)
Enter _WHEELER, door 2 E. L., with pitcher, one empty glass,
and another glass filled with soda-water. Goes to table and places
pitcher and empty glass upon it._
=Wheeler.= (_filling glass_) Here we are, with a drink like the nectar
the gods used to brew. (_handing DEACON glass_) I can recommend it, for
I helped to make it.
=Deacon.= You will not object if I take off my coat, will you! It's so
warm. (_removing coat. WHEELER takes it and hangs it over back of his
chair. DEACON empties glass_)
=Wheeler.= Certainly not; make yourself at home. (_Refills DEACON'S
glass, and continues so to do as fast as the DEACON empties it. Sits
and sips soda-water while talking. Invest this scene with as much
naturalness and life as possible_)
=Deacon.= As I told you, my brother Bill and I never made up after
our first quarrel, but I'm not going to allow that to stand against
his widow and daughter. No, sir. (_emphatically_) I intend to do the
handsome thing by Helen. She's going to marry a Mr. Wheeler. Perhaps you
know him? (_WHEELER shakes head_) No? I'm sorry, for folks say he's a
mighty fine gentleman, and rich, too. (_abruptly_) Do you know Amelia?
=Wheeler.= Mrs. Thornton's sister?
=Deacon.= (_eagerly_) Yes, do you know her?
=Wheeler.= Oh, yes, very well.
=Deacon.= (_rubbing hands_) Fine woman, isn't she?
=Wheeler.= Indeed, she is. I don't know a lady whose _opinion_ I respect
more.
=Deacon.= (_slightly hilarious_) Oh, she's bright!----
=Wheeler.= And so amiable?----
=Deacon.= (_joyously_) Ain't she kind----
=Wheeler.= Yes, I think her the perfect pattern of a saint.
=Deacon.= Oh, she's angelic, my boy, she's angelic. I'll tell you
something, if you'll keep it a secret. I'm in love with Amelia.
=Wheeler.= I'm not surprised at that, for I can't see how any body can
help loving her.
=Deacon.= Yes, sir, I'm clean gone; and I'll marry her, too, see if I
don't.
=Wheeler.= I hope that you may, with all my heart.
=Deacon.= Say, I think that you are the nicest fellow I ever met--I
do, indeed,--and you have got--to be my--groomsman. Don't say no--for
I'll--not--listen--to--it--(_head falls on folded arms resting on table.
Maudlin drunk_)
=Wheeler.= The drug is taking effect. (_takes DEACON'S coat from chair,
searches pockets, finds large pocket-book, takes check from it and
examines it_) Here it is, drawn up and signed. (_starts to put it in
his own pocket_) No, I won't, for it will soon be mine at any rate.
(_Replaces it and doubles up coat and lays it on table L. of DEACON_)
=Wheeler.= (_calls_) Deacon, Deacon. (_DEACON rouses up with a start,
brushes coat off L. upon floor with arm_) I must leave you now to attend
to some business. I will send some one to direct you to Mrs. Thornton's.
(_goes R. near door, DEACON protesting_)
Enter _POLICEMAN L. U. E.; passes through gate. WHEELER walks
down R. motioning POLICEMAN to follow. Stands R. 1 E._
=Deacon.= No, don't go. Don't. All right--I'll--get ready--(_slowly
rises, looks for coat. Does not notice WHEELER and POLICEMAN_)
Never had so glorious a time--before--(_places hand on head_)
Oh,--my--head! Where's--my--coat? (_sees it on floor. Bis. of
attempting to pick it up; finally falls in a heap beside it.
Picks it up and examines it_) Blast it, some--boy--been--fooling--with
it--turned it inside out. (_turns coat_) I've--had--another--
sun--stroke--wish--I--was--home--in--bed--I'm--sick--
=Wheeler.= (_to officer. Talks through scene_) If you detain that man
here for two hours, and then take him to Mrs. Thornton's residence, I
will make it well worth your trouble. Will you do it? (_OFFICER bows
head_) Very well; now go and assist him. (_OFFICER goes to DEACON, who
has coat turned inside out and one sleeve on. OFFICER tries to take it
off, but the DEACON protests and finally has his own way_) A pretty
plight for one's father-in-law to be in! Perhaps if he knew me he would
reconsider the opinion he expressed about me a moment ago. (_smiles_)
Enter BILLY L. U. E., _with large carpet-bag, half crying.
Talks as he comes to gate. PETE follows him and beckons L. as
though urging others to follow._
=Billy.= Now leave me alone. Dog-gone your ugly pictures! I didn't do
nuffin to amongst you. (_leans on gate. Faces R. C. PETE sneaks up and
pinches him. BILLY kicks and yells. Cries. OFFICER assisting DEACON to
feet, sees PETE_)
=Officer.= Leave that boy alone, you black rascal, or I'll arrest you.
=Pete.= Well, make him take in his sign, if he don't want de boys to hab
any fun wid him. You can't scare me, ole fiddle strings, I knows yo'.
(_OFFICER feints to start for him. PETE pulls off hat and runs off L. U.
E._)
=Deacon.= (_authoritatively_) Come here, Billy. (_BILLY opens gate and
goes down to DEACON, sniffling. DEACON looks steadily at him a moment_)
Enter _three lads and lassies R. U. E., with VIOLINIST.
WHEELER whistles to them softly as they reach gate and beckons for
them to enter. They come in; VIOLINIST goes up L. , the rest R.
WHEELER goes to them and makes a proposition, then exit door, R. 2
E._
=Deacon.= Billy, you're drunk! Now don't deny it. Aren't you ashamed of
yourself, for disgracing me? Now go to that seat (_pointing up L._) and
stay there until I'm ready to leave. (_BILLY goes to settee up L. and
sits. Has large placard on back with the words "PINCH ME" printed on
it_)
_One of the lads goes to the VIOLINIST and speaks to him, then returns
R. VIOLINIST starts playing "I Won't Go Home Till Morning." Villagers
form set and commence dancing. OFFICER urges DEACON to become his
partner. DEACON consents. Take position. After a few steps the DEACON
evinces great gusto. Commences singing, seizes one of the lassies,
shoves her partner into his position. Laddie becomes angry, shows
fight. Strikes the DEACON, who pulls up sleeves and starts for his
assailant. General confusion. OFFICER arrests Laddie and starts toward
gate with him. DEACON comes C., singing and dancing. As curtain falls,
he suddenly clasps hands to head, exclaiming:_
=Deacon.= Oh, my head, my head!
QUICK DROP.
ACT II.
=Scene.=--_MRS. THORNTON'S sitting-room. PETE is seated on
rocking-chair R., with left leg dangling over arm; has lighted
cigar in R. hand and occasionally draws it. Is rocking and softly
singing "Gospel Train," as curtain rises._
Enter _DAISY L. 2 E. PETE springs quickly to feet and hides
cigar under coat_.
=Pete.= Golly, but you scared me. I thought it was missus. (_resumes
former position, singing and smoking_)
=Daisy.= You can thank your lucky stars that you were mistaken. (_amazed
at PETE'S attire_) For goodness sake, what are you doing rigged out in
Mr. George's clothes?
=Pete.= Why, yo' know missus 'spects her brudder-in-law, de Deacon, dis
mawnin', an' some oder company fur dinner, an' as I'se de only male
pusson in dis house now, I spruced up to do de honors ob de 'casion.
=Daisy.= Honors of the occasion! Why, what do you mean?
=Pete.= When people hab parties an' 'ceptions don't dey always hab
somebody to do de 'ceivin'?
=Daisy.= Of course they do, but you are not such a great goose as to
suppose Mrs. Thornton will call upon a black booby like you to meet her
guests, are you?
=Pete.= (_rising hastily and assuming a threatening attitude_) Black
booby? Don't yo' say that again! (_contemptuously_) Niggahs always
better than poor white trash. I 'spose yo' think if yo' was a man missus
would call upon yo', but she'd nebber do dat while I was around, suah.
(_resumes seat_)
=Daisy.= (_soothingly_) There, there, Pete, I did not mean to hurt your
feelings, but you get on your "high horse" so often and make yourself so
ridiculous that one must say something to save you from being thrown and
badly injured.
=Pete.= Well, it's none ob yo'r bis'nis if dat hoss breaks my neck.
=Daisy.= Very well, then, Pete, we will drop the subject. Now, I want to
ask you something.
=Pete.= It am no use, fo' I'll not answer yo'.
=Daisy.= Yes, you will, for maybe there'll be some money in it for you.
=Pete.= (_eagerly_) What am it?
=Daisy.= Did you find a watch charm or a packet of letters anywhere in
the house this morning?
=Pete.= (_sulkily_) No, I didn't, and mighty little good would it do yo'
if I did. (_gently draws at cigar_)
=Daisy.= Mr. Wheeler lost a charm and some letters here last night, and
he told me this morning that he would give me ten dollars if I found and
returned them to him. Now, if you have found them I'll give you five
dollars for them.
=Pete.= (_straightening up in chair_) Let me see if I 'stand yo' right.
Mr. Wheeler lost a charm an' some letters?
=Daisy.= Yes.
=Pete.= An' he offered ten dollars to hab dem returned?
=Daisy.= Yes.
=Pete.= If I finds dem an' gibs dem to _yo'_ I'se to git five dollars?
=Daisy.= Yes.
=Pete.= An' if I gibs dem to _him_ I gits ten dollars!
=Daisy.= Oh, no; he did not say that. He only offered to give _me_ the
ten dollars. I offered you five for helping me find them.
=Pete.= (_looks at her a moment_) Oh, yes, I see. I'm sorry I can't help
yo'. I'm not such a booby as I look. No, I did not find dem letters.
(_pauses a moment_) But yo' needn't worry yo'self about looking for dem.
(_settles back in chair and gently draws cigar_)
=Daisy.= (_angrily_) You mean, horrid, black creature! I believe you
have found them and are going to try to get the whole ten dollars. Never
mind, I'll tell Mr. Wheeler not to give you a red cent.
=Pete.= (_indifferently_) I don't care if yo' do; yo'll be none de
better off anyhow.
=Miss Amelia.= (_off L._) Pete, Pete, where are you? (_PETE springs
quickly to feet, and hides cigar under coat with left hand. DAISY
crosses to R. of PETE_)
Enter MISS AMELIA L. 2 E.
=Miss A.= (_stops at L. C.; speaks authoritatively_) Pete, where is
Fido?
=Pete.= I 'clar to goodness, Miss 'Melia, I don't know.
=Miss A.= You do. You have done something to my dear little pet. I know
you have. (_notices smoke, elevates head, then looks at PETE_) Who has
been smoking in this room? (_removes her gaze from PETE, and looks
around room overhead. PETE catches DAISY by arm with right hand_)
=Pete.= (_aside_) Don't tell on me, an' I'll help yo' to find dem
letters. (_aloud_) I don't know, Miss 'Melia, guess it's de 'roma from
de gem'men's Herbana's ob last night you smell. I don't notice it, do
yo', Daisy? (_aside_) Say, no, quick, or I'm a gone goslin'. (_quickly
changes cigar to right hand, placing left fingers in mouth, and making a
wry face. Goes down R._)
=Miss A.= I wish, Daisy, you would have the rooms properly aired after
the horrid men leave. Now, Pete, I want you to go and bring Fido to me
this instant.
=Pete.= (_quickly changing from one foot to the other, shaking and
blowing his fingers, and keeping up his facial contortions_) I tole yo'
I didn't know whar he was. I ain't seen him since last night. (_aside_)
Blame de cigar.
=Miss A.= That's a falsehood, and you know it. (_notices PETE'S unrest_)
Why, what is the matter with you?
=Pete.= I stuck a pin clar froo my finger.
=Miss A.= You wicked boy, it serves you right for telling stories.
Enter _HELEN, L. 2 E., with FIDO._
=Helen.= Oh, Auntie, I found Fido down town in this terrible plight,
being dragged around by a nasty organ grinder. (_MISS A. springs forward
the instant she sees FIDO; tears the hat, jacket and collar off and
throws them on floor; gathers him in her arms_)
=Miss A.= Oh, you dear, abused darling! What a naughty wicked wretch of
a man he must have been to treat my poor doggy woggy so shamefully!
=Pete.= (_aside_) Horrid man, but dear doggy woggy!
=Helen.= The horrid wretch at first refused to let me have him, but a
policeman soon brought him to terms.
=Pete.= (_aside_) I hope dat police will break his neck! (_occasionally
shakes and looks at his fingers_)
=Helen.= He followed me into the house and insisted upon having either
the dog or the money he paid for him.
=Pete.= (_aside, grinning_) He needn't tackle dis child fo' de money,
fer he done spent it.
=Miss A.= (_angrily_) Pete, this is some of your work, and I'll see that
you are justly punished for it.
=Pete.= Miss 'Melia, I 'clar 'fore all de world, I nebber harmed a hair
ob dat dog. I 'spects Neff Jones done sold him, fo' I seed him only day
arter yesterday pintin' to him an' talkin' to some ob de boys. (_scuffle
heard off L. 2 E., and door pushed violently open_)
Enter _PEDRO, L. 2 E., followed by MRS. THORNTON._
PEDRO. (_enraged_) I'll have ze dog or ze money! (_MISS A., HELEN and
DAISY scream and retreat up R., and form a column; MISS A. back, with
FIDO in her arms, HELEN next and DAISY front. PETE looks scared and
slowly edges toward R. 1 E._)
=Mrs. Thornton.= (_sternly_) Pete, what is the meaning of this
disgraceful scene?
=Pete.= I dunno. (_PEDRO advances angrily toward PETE, who retreats to
extremity of stage_)
=Pedro.= Zer ze boy zat sold me ze dog.
=Pete.= Yo' say dat ag'in an' I'll bust yo'r jaw for yo'.
=Pedro.= Ze money--ze two dollars--I gave ze.
=Pete.= (_advancing_) Lebe dis house at once, or I'll break yo'r head.
(_picks up chair_)
=Mrs. T.= Put down that chair this instant, Pete. How dare you?
=Pete.= (_reluctantly drops chair_) He mustn't tell lies on me, den, or
I'll do it, suah.
=Pedro.= Ze money, ze money.
=Mrs. T.= (_taking purse from pocket, hands PEDRO money_) Now, be off
with you. (Exit _PEDRO L. 2 E., muttering to himself indistinctly. PETE
starts quickly across stage but is halted at C._)
=Mrs. T.= Where are you going, Pete?
=Pete.= To show him out. (_aside_) Wid de toe ob my boot.
=Mrs. T.= Never mind, remain where you are. Some of the other servants
can attend to him. Now, I wish you to know that my stock of patience is
about exhausted. You have tried me the past few months beyond endurance.
If you don't turn over a new leaf and behave yourself like other people,
I shall be obliged to transfer you to the care of someone who _can_
manage you. (_HELEN removes hat and gloves and gives them to DAISY who
exits L. 2 E._)
=Pete.= I guess I knows to who yo's 'ferrin' to, but he can't manage me.
(_aside_) An' he better not try, neider.
=Mrs. T.= To whom do you think I was referring?
=Pete.= Why, to dat Mr. Wheeler.
=Helen.= Oh, mamma, I met Mr. Wheeler this morning, and he said Pete
grossly insulted him in delivering the note you sent him just after
breakfast.
=Pete.= Dat's a whopper! (_aside_) He'll not git dem letters now.
=Mrs. T.= Pete?
=Pete.= Well, it ain't true, so it ain't.
=Mrs. T.= What did you say to him?
=Pete.= I didn't say nuffin'.
=Mrs. T.= What did you do to him, then?
=Pete.= I didn't _do_ nuffin', neider. I'll tell yo' all about it,
missus. Massa Wheeler sassed me in de fust place, called me a black
niggah, an' said he' kill me, an' a lot ob bad things. An' den I tole
him he was no gemman to talk like dat to a poor orphan cullud boy; den
he flared up an' frothed at de mouf, an' shook his fist at me, an' said
right dar in public dat when he married Miss Helen, dat he'd teach me my
true position.
=Miss T.= } How shocking!
=Miss A.= }
=Mrs. T.= (_indignantly_) Did he really say that right out in public?
=Pete.= He did dat, sartin'. (_aside_) He's got hisself in a hornet's
nest now, fo' suah. Let him blow on me ag'in.
=Helen.= Mamma, I don't believe a word of it.
=Pete.= Yo' don't eh? Yo' jest ax any ob dose fellers what was 'round,
an' see if dey don't tell yo' de same thing, an' justify me in keepin'
up de 'spectability ob our family.
=Helen.= It's untrue, mamma. Pete made up every word of that story.
=Mrs. T.= Helen, I cannot believe it possible that Mr. Wheeler would be
guilty of such indiscretion.
=Pete.= Dat's de way. Nobody b'lieves a word I say. I, too, is gittin'
tired ob dis lack ob confidence. Some of dese mornin's yo' folks will
wake up an' find dis child in de promised land.
=Helen.= Mamma, it's preposterous to entertain for one moment Pete's
account of Mr. Wheeler's conduct.
=Mrs. T.= I shall interrogate Mr. Wheeler privately, and ascertain from
him the truth of the matter. To be guilty of such baseness, I cannot
believe it.
=Miss A.= It's just like the horrid men. They are not to be trusted.
Ugh! But I detest them.
Re-enter _DAISY, followed by WHEELER._
=Daisy.= Mr. Wheeler. (_WHEELER bows; ladies return salutation_)
=Pete.= (_aside_) Guess I'd better be leabin'!
=Wheeler.= Mrs. Thornton, it is with the most profound pleasure that I
accept the invitation you so graciously extended to me this morning.
=Pete.= (_aside_) Listen to dat. He's puttin' dem on, now.
=Wheeler.= I trust my tardiness has not inconvenienced you. A business
affair detained me.
=Mrs. T.= Not in the least. My brother-in-law, whom I desired you to
meet, has not arrived yet. I cannot imagine what detained him. We
expected him by the early stage, but he did not come. I fear he will
disappoint us, for the last stage was due here over two hours ago.
(_Door bell off L. 2 E._) That must be he now.
=Miss A.= Oh, dear, the Deacon must not see me in this condition. (_to
WHEELER_) Please excuse me, I'll take Fido out and give the dear little
pet something to eat. He must be nearly famished.
=Helen.= (_to WHEELER_) Please excuse me, too, I have some duties to
attend to.
=Wheeler.= (_bowing_) Certainly. (Exeunt _MISS A. and HELEN, L. 2 E.
Door bell rings_)
=Mrs. T.= Pete, answer the bell.
=Pete.= Yes, missus. (_going_)
=Mrs. T.= (_noticing PETE'S appearance_) Why, what is the meaning of
your being arrayed in that attire? (_WHEELER smiles_)
=Daisy.= (_laughing_) He imagined he was to play the host this morning
and receive your guests. So he dressed himself up accordingly.
=Pete.= Mind your own bis'nis. Missus wasn't a talkin' to yo'.
=Mrs. T.= (_warningly_) Pete!
=Pete.= Well, make Daisy keep quiet. She's always meddlin' wid my
affairs. Some day I'll make her wish she'd never been born.
=Mrs. T.= (_firmly_) Just as soon as you answer the bell, go to your
room, change your clothing, and make yourself tidy. I want you to wait
on the table at dinner.
=Pete.= Wait on de table? (_DAISY'S face wears an irritating smile_)
=Mrs. T.= That's what I said.
=Pete.= (_in expostulating tone_) But dat's Daisy's work.
=Mrs. T.= No matter whose work it is, I wish you to do it.
=Pete.= (_to DAISY_) Dis is yo'r doin's. I'll pour a pitcher ob ice
water down yo'r back, see if I don't. I'll git eben wid yo'. (_aside_) I
won't wait on de table.
=Mrs. T.= What's that?
=Pete.= (_quickly_) I said Daisy would hab to help.
=Mrs. T.= Go instantly and do as I told you. (_Exit PETE L. 2 E.,
grumbling; slams door after him. WHEELER, half smiling, crosses R. and
sits. MRS. T. sits on sofa. DAISY remains standing just R. of door L. 2
E._) I declare I don't know what to do with that boy. He's growing worse
and worse. Oh, Mr. Wheeler, before I forget it, I wish to have a few
minutes' talk with you after dinner about Pete's conduct toward you this
morning.
=Wheeler.= Very well, madam, it will give me great pleasure to comply
with your request.
=Mrs. T.= I do hope that was brother ringing. Do you know, I feel no
little anxiety about this meeting.
=Wheeler.= I think your daughter told me that you never had met your
brother-in-law?
=Mrs. T.= No; William, my late husband, and he were not good friends.
It was the Deacon's fault. In his younger days he was too fond of the
wine cup, and when William attempted to warn him of its evils, he became
angry, alienated himself from my husband, and refused from that day on
to have any intercourse with him whatever.
=Wheeler.= I think I have heard it mentioned somewhere that he is still
a little too fond of the cup at times.
=Mrs. T.= Yes, I am sorry to say that the habit contracted in youth
still clings to him. That is usually the case. But it is only on very
rare occasions that he imbibes too much. I believe he is conscientious
and tries to do what is right. I do hope and pray that he will not
consider this a _rare_ occasion, and may remain sober during his stay
with us.
=Wheeler.= It is to be _sincerely_ hoped so.
=Mrs. T.= This visit of his is due entirely to the exertions of my
sister Amelia. She met him last year while visiting a friend of hers
residing in his neighborhood. A sort of mutual attachment sprang up
between them. Where it will end goodness only knows. I fear Amelia is
very much in love with him.
=Wheeler.= Indeed!
=Mrs. T.= Yes, hence my anxiety that our meeting may prove a pleasant
one.
=Wheeler.= The Deacon is not a bachelor, is he?
=Mrs. T.= Oh, no. He lost his wife some thirty years ago.
=Wheeler.= Has he no children?
=Mrs. T.= Only one daughter. But never refer to her in his presence.
He has disowned her. She married against his wishes, and a miserable
life she has led. The Deacon is very self-willed, stubborn and
self-opinionated, and will listen to no reason when it clashes against
his set views.
=Wheeler.= But, surely if one were to represent to him that his daughter
was suffering and needy, he would not refuse to aid her.
=Mrs. T.= He would, as sure as you are living. Oh, Mr. Wheeler, I know
the nobility of your character, how anxious you are to aid suffering
humanity; but let me beseech you, as you value Helen's peace of mind and
mine, _never_ refer to the Deacon's daughter in his presence unless you
desire to bring on a storm.
=Wheeler.= But----
=Mrs. T.= Hush, I hear him coming. (_MRS. T. and WHEELER rise_)
Enter _DEACON L. 2 E. Has a wearied look; still intoxicated;
vest unbuttoned, coat mussed up and full of wrinkles, cravat under
left ear; general condition "used up." He is followed by BILLY with
carpet-bag, PETE expostulating and trying to take it from him.
DAISY stands near door L. 2 E.; MRS. T. up C.; WHEELER R. 2 E.;
PETE goes down L. with BILLY; appears disgusted_.
=Deacon.= (_embracing and kissing DAISY_) My dear, dear sister. I'm
rejoiced to meet you.
=Mrs. T.= (_advancing quickly_) Brother, brother, what are you doing?
That is my servant.
=Deacon.= (_releasing Daisy_) Ah, I made a mistake. My eyesight is bad.
Excuse me. (_embraces MRS. T._) Tillie, I'm _de_lighted, most supremely
blest to enfold--(_quickly_) to have the pleasure of folding--meeting
you and calling you _sister_. I'm most inexpressibly happy! (_releases
her_) Yet as I compare you two, (_looking first at DAISY and then at
MRS. T._) I can't refrain from saying that I think _your_ eye for beauty
far superior to my brother's. So she's your servant, is she? (_looking
at DAISY admiringly_) She's a beauty! (_to DAISY who stands smiling_)
Come, and let me kiss you again.
=Mrs. T.= (_expostulating_) Brother, brother! (_to DAISY_) Daisy, leave
the room. (Exit _DAISY L. 2 E., left hand over mouth, giggling_)
=Deacon.= (_in injured tone_) Why, what has the poor girl done?
=Mrs. T.= Brother, my servants are not accustomed to have such liberties
taken with them. Permit me to introduce you to Mr. Wheeler, Helen's
affianced.
=Deacon.= (_shaking hands with WHEELER_) I'm _de_lighted, sir, to know
you will soon have the honor of becoming _my_ nephew. It's quite a
distinction, sir, and I hope you justly appreciate it. (_WHEELER bows
and returns to former position_).
=Pete.= (_to audience, pointing to BILLY disgustedly_) He's got wimmin's
stockings on. (_takes pin from coat, bends it schoolboy fashion,
balances it on hand, places it on seat of chair; goes to BILLY and in
pantomime asks him to be seated_).
=Wheeler.= (_aside_) He does not recognize me. So far my plans are
working admirably.
=Deacon.= (_to MRS. T.; appears unsteady, speaks confidentially_)
Tillie, Helen's got taste. She has an eye for beauty. (_looks at
WHEELER_) He's a fine looking fellow. (_looks at MRS. T._) Excuse me,
but were you and Bill married by candle light?
=Mrs. T.= Why, no; certainly not.
=Deacon.= Did he have all his senses?
=Mrs. T.= (_slightly irritated_) Of course he did. Why do you ask?
=Deacon.= (_perplexed_) I can't understand it.
=Mrs. T.= Can't understand what?
=Deacon.= (_looks at MRS. T. a moment, then speaks with emphasis_) How
in the name of wonders he came to marry _you_ and pass by that sweet,
lovely being you sent out of the room.
=Billy.= (_takes PETE'S proffered seat, but instantly springs up_) Oh!
=Mrs. T.= Why, what is the matter, Pete?
=Pete.= (_examining chair_) I dunno. I'se jest tryin' to find out.
(_picks up pin; conceals bent part, displaying point_) Daisy nebber
half dusted de chairs. Jest see, she left a pin on dat chair, an' it
stuck Billy. She nebber does her work right. (_lays his hand on BILLY'S
shoulder and consoles him_)
Re-enter HELEN, L. 2 E.
=Mrs. T.= Brother, this is my daughter Helen.
=Deacon.= (_looks at HELEN_) She inherits her beauty from Bill. Helen,
my dear, I'm _de_lighted to see you are so pretty. You will kiss your
old uncle, won't you? I knew you would. Everything lovely admires _me_.
Re-enter MISS AMELIA, L. 2 E.
=Mrs. T.= And here is my sister Amelia. But you need no introduction to
her.
=Deacon.= Bless me, no. Miss Amelia, I'm delighted, filled with
joy unspeakable to behold you again. (_advances quickly with arms
outstretched as though to embrace her. MISS. A. dodges him and crosses
R., MRS. T. following her and expostulating. The DEACON stops suddenly,
reels and clasps hand to head_) Oh, my head, my head!
=Miss A.= (_sharply_) Deacon, you're drunk.
=Mrs. T.= (_startled; expostulating_) Sister!
=Miss A.= Don't "sister" (_imitating MRS. T._) me! I can manage him. I
never saw the man yet I was afraid of.
=Pete.= (_aside, quickly_) Dat's so; cross-eyed, bow-legged, big,
little, great or small, dey's all de same to her. He's nebber been
created.
=Deacon.= (L.) Miss Amelia, I protest, I sincerely, most emphatically
protest against the injustice of your charge. I've had another
sunstroke. (_places hand upon brow_) My head, my head! I'm--sick--
deathly--sick! (_advances a step C., unsteadily_)
=Pete.= (_aside_) Yes, he's got de spirits yell infantum!
=Miss A.= You're beastly drunk. A pretty figure you must have cut,
staggering along the streets, disgracing our whole family. (_DEACON in
front of sofa, raises his hand deprecatingly_) Now, don't deny it; I'm
ashamed of you.
Re-enter _DAISY L. 2 E.; she stands near door._
=Miss A.= (_sharply_) Pete! (_PETE trembles and seems frightened_) Take
him to his room, give him a hot foot bath, apply mustard plasters to
both temples and back of his neck, drench him with strong soda water,
wrap him in woolen blankets----
=Deacon.= (_sinks to sofa with hopeless expression_) Oh, Lord, kill me
at once, and be done with it.
=Wheeler.= (_folds arms_) Triumph No. 2.
_DEACON on sofa; MRS. T. up C.; MISS A. R. 3 E.; HELEN L. 2
E.; DAISY L. 2 E.; WHEELER R. 2 E.; PETE and BILLY L. 1 E._
QUICK DROP.
ACT III.
Scene 1.--_A street in 1st Grooves. Practicable door R., in
flat. Soft music throughout scene. Time, night._
Enter _MRS. DARRAH and NELLIE, L. 1 E._
=Nellie.= (_complainingly_) Oh, Mamma, shall we never find papa's home?
=Mrs. D.= (_sadly_) I hope so darling, but you must be patient.
=Nellie.= I will, dear mamma. But I think papa was real mean to run away
and leave us.
=Mrs. D.= Hush, my child, that is naughty. You must remember that no
matter what papa does, you are still his little daughter, and must love
him and be good.
=Nellie.= I am good, and I try to love him. But I can never love him as
I love you.
=Mrs. D.= (_embraces NELLIE_) Heaven bless you, my darling. You are the
only treasure left me.
=Wheeler.= (_back of scene, near door_) You will attend to it, then?
=Mrs. D.= (_starts as though bewildered_) That voice! (_speaks to
herself. NELLIE walks to L. 1 E._)
=Wheeler.= (_within_) If you see to it in the morning that will answer.
=Mrs. D.= (_listens; takes a step nearer the door_) It is he, I cannot
be mistaken.
=Wheeler.= (_within_) All right, I must be off.
=Mrs. D.= He is coming out. Nellie, pet, (_NELLIE runs to her_) please
run down to the corner, (_points off R._) and see that no one comes this
way for a few moments. (Exit _NELLIE, R. 1 E., MRS. D. follows her until
she reaches L. C. behind door in flat where she remains standing_)
=Wheeler.= (_opening door slightly_) Good night. (_passes out and starts
toward L. 1 E._)
=Mrs. D.= (_slightly advancing_) George! Husband!
=Wheeler.= (_starts; turning quickly, recognizes MRS. D._) What! you
here?
=Mrs. D.= (_tremulously_) Yes, but why that frown? (_pleadingly_) Oh,
George, you are not sorry to see me, are you?
=Wheeler.= (_evasively_) What brought you here?
=Mrs. D.= The desire to find you--to be with my husband.
=Wheeler.= (_coldly_) Now that you have found him, what do you propose
doing?
=Mrs. D.= Staying with him and fulfilling my wifely vows.
=Wheeler.= (_vexed_) I thought we had parted never to meet again.
=Mrs. D.= (_astonished_) Why, George, what have I done to merit this
cruelty? What is the meaning of this? (_with pathos_) In Heaven's name,
speak! (_WHEELER hesitates_) Tell me, or my heart will break. (_places
hand affectionately upon WHEELER'S shoulder_)
=Wheeler.= (_removing her hand_) Upon your own head be the consequences
of your rash request. (_speaks vehemently_) You have destroyed every
vestige of manliness in my character; you have changed my nature and
caused me to become a gambler, a thief and a blackleg; with your artful
smile you cajoled me into marrying you; taught me to loathe myself, shun
society, and spurn my _true_ friends----
=Mrs. D.= George!
=Wheeler.= You drove me from home, by convincing me that I did not love
you, into scenes of revolting crime and iniquity; and now, after a lapse
of over two years--spent in the prostitution of the nobler traits of
my character, at the gaming table, in drinking revelries and in fast
society--just as the sun is beginning to shed its rays upon a pathway
leading to my reclamation, you--_you_, who have been the bane of my
life, cross it, and your fitful shadow hisses in my ear, "stop, or I'll
destroy you."
=Mrs. D.= George, let me beseech you to desist. What demon possesses you
thus to accuse me, who am innocent of ever having injured you by word,
thought or deed. Oh, George, I love you too dearly to believe that you
mean the bitter things you have just uttered.
=Wheeler.= But I do mean them. You alone are responsible for the hatred
I bear you.
=Mrs. D.= Hate me! I, who sacrificed home, friends, wealth, position and
parent for you! (_places hand upon shoulder_) Am I awake, or is this
some frightful hallucination? I cannot believe it. George, husband,
father of my child, in mercy's name recall your cruel words!
=Wheeler.= They are too true. I cannot.
=Mrs. D.= Then you no longer love me?
=Wheeler.= You force me to say it--I do not.
=Mrs. D.= Heaven help me then, and protect a discarded wife and
fatherless child.
=Wheeler.= Minnie, the sooner this harassing interview is over the
better it will be for both.
=Mrs. D.= Yes, no doubt of it. I came searching for my lost husband,
loving and trusting in him. I have found him, 'tis true, but false to
his marriage vows, and doubly false to the common ties of humanity.
=Wheeler.= Once more, Minnie, let me urge upon you to end this scene.
What are your plans for the future?
=Mrs. D.= I have none. The God of the fatherless must now direct my
steps. (_appears stupefied_)
=Wheeler.= Listen to me then. If you promise to leave this place and
never place foot in it again, I will deposit with McGrath, the banker, a
sum of money sufficient to support you and Nellie the remainder of your
lives.
=Mrs. D.= Then this is to be our last meeting as man and wife?
=Wheeler.= (_ill at ease_) It is----
=Mrs. D.= And thus you ignore your marriage vow to "love, honor and
protect" me?
=Wheeler.= If you are not satisfied, you have the courts to seek for
redress----
=Mrs. D.= In what manner?
=Wheeler.= By applying for a divorce.
=Mrs. D.= A divorce?
=Wheeler.= Yes.
=Mrs. D.= Then you _are_ in earnest?
=Wheeler.= Was never more so in my life. As a proof of it (_takes
pocket-book from pocket, and quickly selecting a couple of notes,
tenders them to MRS. D._) there is sufficient means to obtain shelter
for yourself this night, and to carry you back to your former home in
the morning.
=Mrs. D.= (_haughtily spurns it_) Keep your money! I'll never touch a
cent of your ill-gotten wealth. For two long years have I supported
myself and my child without assistance from you, and Heaven helping me,
I will continue to do so for the future.
=Wheeler.= Very well, let it be as you please. (_replaces money_) As you
have discarded my proffered help and refuse to allow me to aid you, it
is needless to prolong this interview. (_going_)
=Mrs. D.= (_pleadingly_) George, is there nothing I can do to regain
your affections?
=Wheeler.= Nothing.
=Mrs. D.= You disown me as your wife!
=Wheeler.= Merely wish to sever the bonds connecting us, and the sooner
you leave this place the better I'll be pleased.
=Mrs. D.= Your wishes shall be complied with. To-morrow will find me
once more in my humble cottage home awaiting the return of my reclaimed
husband.
=Wheeler.= Thank you. Good by. (Exit _WHEELER, hastily, L. 1 E. MRS. D.
does not notice his absence_)
=Mrs. D.= But, oh, what a life of wretchedness, misery and woe it will
be. (_notices that she is alone_) George, husband! (_goes to L. 1 E.,
quickly_) Gone! (_returns, stops near C., places hand upon brow_) Left
alone in the street, a discarded wife. It is more than I can bear.
Nellie--my child--come--(_falls fainting to stage_)
Re-enter _NELLIE, R. 1 E., running_.
=Nellie.= Here I am, mamma. Why, what is the matter? (_kneels, gently
shakes her, half crying_) Wake up! I believe she's dead. Mamma! Mamma!
speak--it's Nellie. (_whistling heard off L. 1 E._)
Enter _PETE L. 1 E. Stops whistling the instant he sees mother and
child._
=Pete.= (_speaks as he advances_) Did yo' eber see de like! Git on to
dat, will yo'? Why, what's de trouble, little one?
=Nellie.= Oh, please, sir, help me. Some one has killed my mamma.
(_tries to lift MRS. D._)
=Pete.= Some one kilt yo'r mammy? Let me see. (_stoops; MRS. D. moans
and moves slightly_) She's not dead. She's--she's--toppled over. (_MRS.
D. half rises on elbow_)
=Mrs. D.= Where am I?
=Pete.= Why here, mum. Yo' needn't be afeared. I'll took care ob yo'.
Does yo' feel better, mum?
=Mrs. D.= How came I here?
=Pete.= 'Deed, mum, I don't know. P'raps de little one can tell yo'.
=Mrs. D.= Nellie, you here?
=Nellie.= Yes, mamma, you called me and I came. Are you sick, dear
mamma?
=Mrs. D.= (_places hand upon brow_) No--yes--It all comes back to me
now. Oh, why did I not die--better death than this agony! I suppose I
must have fainted.
=Pete.= Shall I fetch de doctor fo' yo', mum?
=Mrs. D.= No, I feel better already. (_attempts to rise. PETE assists
her to feet. She reels slightly and places hand to head_) Oh, my head!
(_to PETE_) Please take me somewhere, so that I may obtain shelter and
rest. I am a stranger here.
=Pete.= All right, mum. Dar's a fust rate hotel jest around de corner.
(_points off R. 1 E._)
=Mrs. D.= (_quickly_) No, no; not there. I desire some quiet lodging
where my child and myself will not be subjected to the gaze of the
curious.
=Pete.= Well, den, mum, I knows jest de place fo' yo'. It's on one ob de
back streets. Dis way, it's not very far.
(Exit L. 1 E.)
=Mrs. D.= (_slowly following_) Come, Nellie, dear, we shall soon be able
to tell our sorrows to One who will comfort us.
(Exeunt L. 1 E.)
_Flats are drawn off disclosing_
=Scene 2.=--_A lodging room, plainly furnished. Door L. 2 E.;
table R. C., with pitcher and water glasses, candle, books, papers,
etc. Candle lighted. GRAEF discovered_.
=Graef.= (_seated, with right arm resting on table_) I suppose there is
nothing left for me to do, but lie low in this hiding place and await
further developments. It must be hard for a guilty party to have his
fellow men stigmatize him as a thief--but, oh, what are his feelings
to those of an innocent man's, particularly when one's own flesh and
blood prefer the charges. That was a bright idea of Pete's, bringing me
that note he found, for it will go a great way toward establishing my
innocence. Now, if he is only fortunate enough to obtain those diamonds,
and discover who it was that pawned one at Davis's shop, my innocence
will be proved, and the guilty party punished. I never gave Pete credit
for the acuteness he has displayed in this affair. (_knock_) That must
be he, now. Come in.
Enter PETE, L. 2 E.
=Pete.= Massa George, I found dem (_displaying box_) jest whar de note
said dey was--in de hollow ob dat big chestnut tree. (_hands box to
GEORGE_) But does yo' t'ink yo' ought to keep dem diamonds here? S'pose
de folks finds out yo' is hidin' here, an' gits out a search warrant,
an' comes here an' finds dem? Why, yo'd be a goner, suah.
=Graef.= Never fear, Pete, I'll take good care that they won't be
discovered. I can never thank you for what you have done for me.
=Pete.= Nebber mind de t'anks, Massa George. When yo's clared yo' name
ob all 'spicion, an' can look honest men in de face like de honest man
yo' is--den dat will be t'anks enough for me.
=Graef.= Did you find out who it was that pawned that diamond at
Davis's?
=Pete.= No, sar, but it 'pears to me dat we don't need dat ev'dence. We
can make out a cl'ar case widout dat.
=Graef.= (_musing_) Let me see. Helen's marriage takes place day after
to-morrow, does it not?
=Pete.= Yes, sar.
=Graef.= At ten o'clock?
=Pete.= Dat's de time a'pinted--if de groom does not come up wantin'.
=Graef.= Then you come to me here about eight o'clock in the morning.
I'll try to have all my plans arranged by that time. Now, you had better
leave me, for your absence may be observed.
=Pete.= By golly, Massa George, if I didn't done gone an' clar forgot
dat I left a lady an' her little gal standin' out dar on de landin'.
(_points L._)
=Graef.= A lady and child out there? Why, what do they want at this time
of night?
=Pete.= Shelter an' rest, dat's what dey said. I brought dem. Dey am
strangers. I found dem on de street, sick an' kinder faint-like. I
wanted dem to go to de hotel, but dey kicked an' said dey didn't want
folks starin' at 'em, so I brought 'em here to stay fo' de night. De
landlady is out, so I tole dem to wait out dar 'till I axes yo' if dey
might come in here an' stay until she comes home.
=Graef.= But, Pete, think of the risk I run.
=Pete.= (_quickly_) Oh, yo' needn't be 'fraid ob dem blowin'. Dey is
_quality_ folks.
=Graef.= (_laughing_) On your recommendation, Pete, they may be
admitted.
=Pete.= (_goes to the door and opens it_) Come in, mum.
Enter _MRS. D. and NELLIE._
=Pete.= Dis am Massa George. (_GEORGE bows_)
=Mrs. D.= Pardon me, sir, for presuming to intrude on your privacy, but
I am not well and could not stand upon ceremony.
=Graef.= Apologies are unnecessary, madam. I am only too happy to place
my humble room at your disposal. (_Places chair C. near table. MRS. D.
sits. PETE takes NELLIE'S hand and leads her up L. to chair. PETE stands
beside her. GRAEF goes to table, pours glass of water and returns to
MRS. D., offering it_) Permit me to offer you a glass of water, perhaps
it will do you good. I am sorry I have nothing more invigorating to
offer.
=Mrs. D.= Thank you, sir, you are very kind. (_drinks. In returning
glass looks up into GRAEF'S face, smiling faintly_) A cup of cold water
given in charity's name often becomes----
=Graef.= (_interrupting her, grasps her by shoulder and anxiously scans
her features_) Minnie, is this you?
=Mrs. D.= (_startled_) Yes, that is my name. But why do you ask?
=Graef.= (_eagerly_) Don't you know me?
=Mrs. D.= (_coldly, shrinking away from him_) No, sir, I think you are
mistaken in the person.
=Graef.= Why, I'm George Graef.
=Mrs. D.= (_joyously_) My cousin--the one who played with me in my
girlish days?
=Graef.= None other. (_they shake hands_) How happy I am to see you.
=Mrs. D.= Strange that I did not recognize you at first.
=Graef.= Stranger it is that I should be so blind; for you have changed
but little since I last saw you--some eight years ago.
=Pete.= By jiminy crickitees! She's some relation ob ours. I's so glad.
(_rubs hands gleefully_)
=Graef.= (_crosses to NELLIE_) And this is your little daughter?
Welcome, little coz. (_shakes hands; then retraces steps to MRS. D.'S
side_) But tell me, Minnie, what are you doing here? We had heard
nothing from you for over three years. (_PETE talks silently with
NELLIE, introducing any comicalities he deems necessary to amuse her,
so that they do not interfere with the dialogue. He completely absorbs
NELLIE'S attention_)
=Mrs. D.= I came here in search of my husband.
=Graef.= Your husband?
=Mrs. D.= Yes. You know father was bitterly opposed to our union, and
after George found out that he had disinherited me for marrying against
his wishes, he began to gamble and drink heavily. He swore to be
revenged upon every member of our family. Oh, what days and nights of
torture I was obliged to endure! Finally one evening over two years ago
he left me without a word of warning.
=Graef.= Why did you not inform us of his actions? We surely could have
been of assistance to you.
=Mrs. D.= I preferred bearing my sorrow and disgrace alone; besides I
needed no assistance, for the dowry settled upon me by my father when he
closed his doors upon me, was ample to support Nellie and myself.
=Graef.= Still, by our sympathy we might have alleviated your
sufferings, which must have been intense.
=Mrs. D.= They were--words fail to describe them. If I had been anything
but a loving faithful wife they would not have been so hard to bear.
(_weeps_)
=Graef.= (_consolingly_) There, never mind. I hope there are brighter
days in store for you. Are you aware that your father is in town?
=Mrs. D.= (_alarmed_) No. For mercy's sake don't let him see me. It
would kill me in my present condition to meet his gaze now, after the
fulfilment of his prophecy in regard to George.
=Graef.= I believe he never met your husband, did he?
=Mrs. D.= No, we were married away from home. But he _knew_ him by
reputation, and warned me against him. None of my relatives ever met
him. Where is my father?
=Graef.= At Auntie Thornton's. He came on to attend Helen's wedding. But
have no fear of seeing him, you are safe here.
=Mrs. D.= (_looking around room_) But, George, what are you doing here?
I thought you made Auntie's house your home.
=Graef.= (_confused_) Yes--I did once--but-- Some other time I'll tell
you my story. It would only distress you to hear it now. Tell me more
about your husband. Have you never met or heard anything about him since
he left you?
=Mrs. D.= Not until this evening.
=Graef.= (_surprised_) This evening! Why, what do you mean?
=Mrs. D.= That I both met him and heard him to-night!
=Graef.= Where did you meet him?
=Mrs. D.= On the street.
=Graef.= Impossible! For I know every creature in this town.
=Mrs. D.= Perhaps you do not know him by his right name. If you know
every creature in this town, tell me if you ever (_takes photograph from
pocket and hands it to GRAEF_) met a man who resembled that? He is my
husband.
=Graef.= (_takes photo; starts_) What! he your husband?
=Mrs. D.= He is. You know him then?
=Graef.= Yes, alas, too well!
=Pete.= Massa George, yo' sartinly will hab to 'scuse me now, fo' I must
be goin'. I hab a 'pintment wid Billy de Deacon's boy. I'se gwine to hab
more fun wid him to-night dan a bushel basket would hold. (_walks toward
the door, but stops when GEORGE speaks to him_)
=Graef.= Very well; don't forget _my_ appointment. But wait a moment.
(_walks across to him and hands him photo._) Do you know who that is?
=Pete.= (_laughs_) Yo' jest bet I does. But won't he look different
when he has his head shaved, eh? (_with a knowing wink._ Exits. _GRAEF
crosses over to MRS. D.'S side_)
=Mrs. D.= What did you mean a moment ago when you said you knew my
husband "too well?"
=Graef.= I cannot tell you now, the story is too long. How long do you
intend to remain with us?
=Mrs. D.= I return home in the morning.
=Graef.= (_quickly_) No, no; you must not. You _shall_ not.
=Mrs. D.= (_surprised_) Why not?
=Graef.= For several reasons. First you must hear _my_ story in the
morning. Then learn how well your husband is trying to keep his oath in
regard to injuring your relatives, and, lastly, you may be needed as a
witness against him. You are safe in this house and no one will know of
your presence.
=Mrs. D.= Why, what has he done?
=Graef.= You shall hear in the morning. Sufficient is it for you to know
he's the blackest-hearted villain that ever went unhung. Come, let us
find the landlady and see about lodgings for you. Come, Nellie.
_Close in to_
=Scene 3.=--_Street in 1st grooves._
Enter _PETE, L. 1 E., with lighted lantern, followed by BILLY carrying a
spade over left shoulder_.
=Pete.= Now, if yo's 'fraid, say so, an' I'll git one ob de boys to go
along.
=Billy.= I'm not a bit afeared. But it's so dark. Are you sure we'll get
any money?
=Pete.= Ob course. Didn't I tell yo' I dreamed last night whar dar was
more dan free hundred potsfull hid?
=Billy.= Yes, I know you did, but do you think the folks who own it will
let us have it?
=Pete.= We's not gwine to ax 'em. 'Spects dey's all dead, anyhow. Dar
won't be nuffin' to keep us from gittin' it, 'less de spirits put in dar
'pearance.
=Billy.= (_frightened, drops spade_) Spirits!
=Pete.= Yes, yo's not afraid ob dem, are yo'? I's often played wid dem
behind de kitchen door (_aside_) in mince-pie season.
=Billy.= Oh, no, I'm not afeared. (_trembles_)
=Pete.= What's yo' shakin' fo'?
=Billy.= I'm not very well.
=Pete.= Kind o' weak-like, eh?
=Billy.= (_doubtingly_) Yaas.
=Pete.= Want somet'ing to make yo' strong, does yo'? (_takes small flask
from breast pocket, drinks, then passes it to BILLY_) Try dat, it's
nervin'. (_aside_) Den if he sees somet'ing, dar'll be spirits widin an'
spirits widout. (_BILLY takes flask and drinks. PETE watches him, and as
the fluid disappears, grows uneasy_) Hole on, dar.
=Billy.= (_removing flask a moment, but tightening grasp_) That's what
I'm doing. (_hands flask back empty_)
=Pete.= Feel better, don't yo'?
=Billy.= Yaas.
=Pete.= I should t'ink so. (_places flask in pocket. Takes up lantern_)
Come on, now, we's no time to lose.
Exit, R. 1 E.
=Billy.= (_picking up spade_) I'm ready.
Exit, R. 1 E.
_Flats are drawn off disclosing_
=Scene 4.=--_Wood in 4th grooves._
Enter _PETE R. U. E., followed by BILLY._
=Billy.= Aren't we most there? (_peal of thunder_) I'm afeared it's a
going to rain.
=Pete.= What ob dat? Can't we 'ford to git wet to be independent de rest
ob our lives? (_looks round; places lantern up C._)
=Billy.= Do you know where we are?
=Pete.= Ob course I do. We's mighty nigh de place.
=Billy.= You don't say so! Kin you see it? (_alarmed_)
=Pete.= (_looking off L. 2 E._) Yes, I do. (_flash of lightning,
followed by loud clap of thunder_)
=Billy.= (_jumps and screams_) Oh!
=Pete.= What's de matter? Am yo' hurt?
=Billy.= (_trembling violently and confused_) No--yes--Oh, Pete, let's
go home.
=Pete.= Look dar! Dar! What's dat? (_points off L. 3 E. Lightning and
loud peal of thunder_)
=Billy.= Whar? (_looks off L. 3 E. Drops spade, screams and starts
running off R. 3 E. PETE catches him by coat tails. BILLY struggles
violently to release himself_)
=Pete.= (_coaxingly_) Don't leab me, Billy. Nuffin, will hurt yo'.
=Billy.= (_frantic with fear_) Let go of me. Let go of me! (_turns
on PETE and strikes him several blows rapidly. PETE falls and BILLY
stumbles over him. Practice this scene well_)
=Billy.= Oh, Lord, I'm dead--dead----
=Pete.= (_springing to feet and assuming a pugilistic attitude. A
thunder clap brings BILLY to feet, thoroughly frightened. Faces PETE who
advances upon him enraged_) What did yo' do dat fo', eh? Say? What did
yo' do dat fo'? (_dances in front of BILLY_)
=Billy.= (_backing_) Was that you?
=Pete.= Ob co'rse it were, an' I'se gwine ter lick yo' for it, too.
=Billy.= I thought it were a spirit. What did you see?
=Pete.= Why, de mound whar de money is hid. Yo's a big coward, an' I's a
great mind to knock de stuffin' out ob yo'. (_advances upon BILLY with
fists up_)
=Billy.= Don't Petey, please don't. I didn't hurt you. I'll not get
scared again. Whar's the money? (_picks up spade_)
=Pete.= (_mollified, pointing to L. 3 E._) Thar! an' if yo' don't git to
diggin' fo' it, I'll lam yo' so bad dat de Deacon won't know yo' when
yo' git home. (_BILLY starts toward mound, manifesting great fear. When
near it, a clap of thunder causes him to drop the spade again and shake
violently. PETE grabs him by the arm. BILLY again picks up spade. PETE
pushes him forward, talking as he does so_)
=Pete.= We'll be richer dan missus an' all her relations. I jus' bet dat
dar's more money in dat pile dan all de Deacon's mules kin pull.
=Billy.= (_hanging back_) Let's go home and get the mules, then.
=Pete.= No, yo' don't. If we git mor'n we kin tote, we'll jest 'phone
fer help. So go to work. (_thunder and lightning to continue throughout
scene, at intervals. BILLY throws earth off L. 3 E._) Dat's good. Now,
go at it right, shubble fast. (_BILLY strikes iron pot_) Now, yo' struck
it, suah. Work quick. (_the second time spade strikes pot, a rattling of
chains overhead is heard_) Hurry up, Billy, I'll go an' see if anybody
is coming. (_BILLY reaches down for pot. PETE starts toward R. 3 E.
As he reaches C. a gun is fired from R. 3 E. and PETE, with a groan,
falls with head toward L. As gun is fired chains fall to stage off L. 3
E. BILLY lifts large iron pot from earth as sound of gun is heard. He
sees PETE fall and, throwing hat off, he picks up pot with both hands
kicks spade aside, and, half bent, starts for R. 3 E. on a run. When
near entrance, he is met by figure enveloped in a sheet. Screaming with
fright he retraces his steps and is met at L. 3 E. by another figure.
Starting up C. a third figure arrests him. Screaming, he stands a moment
bewildered. Figures close in around him. Rushing to side of PETE, he
drops pot and falls to knees, clasps hands, eyes roll, fright wig stands
on end, lips work convulsively as in prayer. Red lights from both
sides._)
SLOW DROP.
ACT IV.
=Scene.=--_MRS. THORNTON'S sitting-room, same as Act II. As
curtain rises DAISY is discovered C. with broom in left hand,
pointing with right hand to small pile of bits of paper, dust,
etc., on floor. Dust pan on floor. PETE down C._
=Daisy.= Hold the dust pan! Don't you hear what I say?
=Pete.= (_indifferently_) Ob co'rse, I do. I'se not deaf.
=Daisy.= (_stamping foot_) Then do what I tell you. (_PETE makes
grimaces at her_) Don't you intend to do it?
=Pete.= No, do it yo'self. Yo'r not my boss.
=Daisy.= (_seizing dust pan and brushing paper, etc., into it
vigorously_) It's well for you I'm not!
=Pete.= (_tantalizingly_) What does yo' t'ink yo'd do, if yo' were?
=Daisy.= (_dropping dust pan_) What would I do? I'll show you! (_rushes
at him with broom upraised. Drives him around stage, repeatedly striking
him on head with broom until he reaches C. again_) Now, I hope you are
satisfied. If I had my way I'd give you a sound thrashing and send
you to bed to keep poor Billy company. (_going_) Ain't you ashamed of
yourself for playing that horrid joke upon him last night! You know you
hid that iron pot yourself and made him believe that you dreamed there
was money buried there. Never mind, sir. Some day you'll meet your match
and get paid back for all of your badness.
Exit, _door L._
=Pete.= (_laughing_) I wonder if dat gal thinks she hurt my head. I'd
butt ag'in a stone wall wid it all day for fifty cents. Poor Billy! He's
not feelin' well to-day. He ran against a tree las' night, an' bruised
hisself mighty bad. So he stayed abed. But he didn't blow on me. He
knowed better. Said he fell from a tree an' hurted hisself. I's takin'
his place an' lookin' after de Deacon's interests. De Deacon is takin' a
nap. I was to call him at 2 sharp. He had a 'ticular 'pintment wid Miss
'Melia. It must be nigh about dat time now. (_starts to go_) No, I won't
call him, eider. I'll let de ole man sleep while he can. (_footsteps,
L._) Oh, Lor', here comes Miss 'Melia now.
Exit, _C. door_
Enter _MISS AMELIA, L. 2 E.; goes down C. PETE re-appears at
door C. and listens_.
=Miss A.= I declare, my heart's all in a flutter. The Deacon has
requested a private interview. I know he is going to propose. I feel
it; I am sure of it; and, oh, dear, I know I'll refuse him. What shall
I do! (_PETE shakes finger at her in a knowing way and disappears_) The
dear man has eaten scarcely anything since he entered this house. He
sits at the table pretending to eat, but all the while he is looking at
me, and wondering if I love him. His eyes literally devour me with their
lustrous flame of love----
Enter _DAISY, L. 2 E. MISS AMELIA is startled._
=Daisy.= Miss Amelia, Mrs. Thornton would like to see you a moment in
the dining-room.
=Miss A.= Tell her she must excuse me. I'm engaged for the next half
hour.
=Daisy.= Yes, ma'am. (_going_)
=Miss A.= Daisy.
=Daisy.= Ma'am?
=Miss A.= (_affectedly_) How am I looking to-day?
=Daisy.= Most charmingly.
=Miss A.= Do you really think so?
=Daisy.= Indeed I do. To see you now, no one would suppose you were a
day over thirty. (_aside_) Horrid thing! She's fifty if she's a day.
=Miss A.= I fear you are a flatterer. Now, you don't think I'm too old
to marry, do you?
=Daisy.= Why, no ma'am. Lots of people get married who are much older
than you. (_aside_) And big fools they are, too.
=Miss A.= That will do, Daisy. You are a nice, well-behaved girl. So
sensible.
=Daisy.= Thank you, ma'am. (_going_)
=Miss A.= Daisy, stop a moment. If you see the Deacon enter this room,
please be sure and see that we are not disturbed for the next half hour,
and I'll make you a present of that handsome silk dress of mine I saw
you admiring yesterday. (_goes R._)
=Daisy.= Oh, thank you. (_aside_) Handsome silk dress! It's as ugly as
sin and as old as the hills. I wouldn't be seen in such a delapidated
affair. Ugh!
(Exit _hastily, L. 2 E._)
=Miss A.= I wonder what detains the Deacon. I'm sure it's after 2
o'clock. I do hope he'll come right to the point, for I know I can't
stand any long preamble. (_fidgety_) I do wish he would come. Hark!
I hear his footsteps now. (_Goes to sofa, sits R._) I'll pretend I'm
offended because he kept me waiting. Oh, dear, I know it's coming; I
feel frightfully nervous.
Re-enter _PETE backward, dressed in DEACON'S suit, with spectacles
on_.
=Miss A.= (_glances around as PETE enters_) It's he! (_bows head on
right arm of sofa and remains in that position; PETE advances slowly,
imitating the DEACON'S shuffling gait and clearing of throat. Takes seat
beside MISS AMELIA_)
=Pete.= Amelia, dearest! (_Coughs and makes wry face. Aside_) She's
skeered! (_aloud_) I guess yo' know fo' what I wanted to see yo'?
(_pause_) Yo' love me!
=Miss A.= (_in muffled astonishment_) Oh, Deacon, how----
=Pete.= Now, don't say yo' don't, fo' I know yo' do. (_archly_) I've
seen yo' castin' eyes at me on de sly. (_aside_) What shall I say next!
Oh, yes. (_clears throat; aloud_) Yo' can have me, I's willin'. (_aside,
disgustedly_) She don't know how to lub. (_aloud_) Does yo' doubt my
love fo' yo'? Go ask the dear little stars if I don't whisper yo'r name
to them every mornin' an' at noon. (_pause_) Does yo' still doubt me?
=Miss A.= No--no--only----
=Pete.= (_aside_) She's gittin' up courage. (_aloud_) Only what,
dearest? (_gradually edges to side of MISS A._) Don't be afraid to
speak, I'll not hurt yo'. Don't yo' lub me just a little wee bit?
=Miss A.= No--yes--I mean that----
=Pete.= (_tenderly_) Yo' mean that yo' will marry me if I'll wait a
little while! Oh, but you are a darling! (_places arm around MISS
A.'S shoulder and attempts to raise her head. MISS A. makes faint
resistance_) Look up, Birdie, and give me one little kiss to seal the
bargain. Just one.
=Miss A.= You are irresistible! (_gently inclines head toward PETE with
face averted. Gushingly_) Do you really and truly love me?
=Pete.= With all my heart!
=Miss A.= Then kiss me. (_turning quickly as in act of kissing,
sees PETE, but does not recognize him. Falling in corner of sofa,
she screams. PETE jumps up and quickly exits D. C._) Help! help!
murder--help!
Re-enter _DAISY, L. 2 E.; she has common apron on, sleeves
rolled up, hands covered with dough and arms bearing flour marks;
followed by MRS. THORNTON and HELEN, both wearing common aprons_.
=Daisy.= For goodness' sake, what is the matter?
=Miss A.= (_in hysterics_) Oh--oh--oh--I've been frightened nearly to
death. Oh, dear, oh!
=Mrs. T.= By whom?
=Miss A.= A tall <DW52> man. He sat down on the sofa beside me. Oh,
dear, I shall die, I know I shall. (_MRS. T. and HELEN approach and try
to quiet her. DAISY goes to D. C. and peers behind curtain_)
=Miss A.= He was dressed in one of the Deacon's suits.
=Mrs. T.= In my brother's clothes? Impossible!
=Miss A.= He was, I tell you. He escaped out of the balcony window.
(_points to D. C._)
=Daisy.= Oh! (_screaming, runs to group. All appear frightened, and
scream_)
=Helen.= Did you see him?
=Daisy.= No--but--I thought I did.
=Helen.= Auntie, I believe you fell asleep and had a bad dream.
=Miss A.= Asleep! I've not closed my eyes this blessed day. I saw him as
plainly as I see you. The ugly wretch! Oh, oh!
=Mrs. T.= Daisy, go and find Pete and send him for a policeman. This
matter must be investigated.
=Daisy.= Yes, ma'am.
(Exit, L. 2 E.)
=Helen.= (_going to door, L., listening_) I think I hear uncle moving
about his room. He'll soon be down and will help us search the house.
=Miss A.= Oh, for goodness' sake, help me to get away before he comes.
(_MRS. T. and HELEN assist her to rise, and start with her toward L. 2
E._)
=Miss A.= No, no, not that way. I might meet him. Take me out along
the balcony way. I'd rather meet that horrid <DW52> man again than
the Deacon in my present condition. Oh, dear, it was a terrible shock!
Terrible!
(Exeunt, D. C.)
Re-enter _PETE, L. 2 E., disguised as MISS A.; wears a similar wig
etc._
=Pete.= (_C., imitating MISS A.'S manner_) I declar', my heart's
flutterin' like all creation. I have a 'pintment wid de Deacon. I knows
he's gwine to ax me to marry him. Oh, dear, I shall faint! I knows I
shall, but I can't refuse him. (_takes seat on sofa_) Hark! I hear
footsteps. 'Tis he, by Jerusalem! I'll 'tend I'm mad wid him for not
comin' sooner. (_bows head on L. arm of sofa, conceals feet under dress,
pulls curls over side of face, and hides hands under chin_)
Enter _DEACON, L. 2 E., smiling blandly_.
=Deacon.= How lovely she appears. Still waiting for me. While I have
been sleeping, she, like the grand noble creature that she is, has been
patiently waiting my coming, no doubt considering each moment an hour.
What a beautiful picture the sentiment of love in woman presents! (_goes
to sofa, sits R._) Have I kept you waiting long, my darling? It was not
my fault. Pete forgot to call me. You'll forgive me, my love, won't you?
(_edging nearer_)
=Pete.= (_in muffled tone of voice_) I--I--don't know.
=Deacon.= Oh, yes, you will. I know you will. Amelia,--you will let me
call you by your beautiful first name, won't you?--ever since my wife
died, I've been looking for another angel to take her place. I have at
last found her. Can't you guess who it is? (_pause_) I mean you. Oh,
Amelia, I love you--love you dearly, tenderly, most devotedly. Do you
doubt me?
=Pete.= No--no--only----
=Deacon.= Only what, my love? (_draws close to PETE'S side_) Don't
be afraid to tell me. Hereafter I expect to help you bear all your
trials and sorrows. What a blissful abode of love our home will be.
(_tenderly_) You surely love me a little, don't you?
=Pete.= No,--yes--I mean that----
=Deacon.= (_placing arm around PETE_) Oh, you precious darling! You mean
that in time you may be able to love and marry me. I'm the happiest man
on earth. (_tries to pull PETE gently toward him. PETE resists faintly_)
Nothing is now wanting to make my earthly lot a foretaste of the bliss
of Paradise, but one little kiss from your sweet lips, and the coveted
honor of leading you to the altar. You won't refuse me the boon of one
kiss, will you, dear? (_attempts to raise PETE'S head_)
=Pete.= (_yielding_) Yo' are puffec'ly irresistible! (_rests head upon
the DEACON'S shoulder; keeps face well averted_) Do yo' really and truly
love me?
=Deacon.= (_warmly_) As truly as the sun shines.
=Pete.= Then kiss me. (_quickly turning, he throws both arms around the
DEACON'S neck and gives him a loud kiss. Springing to feet, he exits
quickly D. C._)
=Deacon.= (_rises bewildered_) Ah--oh--what--what's this? The huzzy!
(_takes handkerchief from breast pocket and wipes lips_) Ugh! The
infern--(_calls loudly_) Pete! Pete! Daisy! Pete! Where in the mischief
are they? Why don't they come! Pete! Pete! Pete! (_walks excitedly R._)
Re-enter _MRS. T., HELEN, MISS A., and DAISY, L. 2 E._
=Mrs. T.= Why, brother, what is the matter? Are you going mad?
=Deacon.= (_angrily_) No--yes--I am mad. Madam, what do you mean by
allowing your <DW52> cook the freedom of this house?
=Mrs. T.= (_in amazement_) Why, brother, I have no <DW52> cook.
=Deacon.= You have! Now, don't say again you haven't, for I know better.
If she ain't your cook, she fills some position in your house, which is
all the same.
=Helen.= Why, uncle, there's not a <DW52> woman in this house.
=Miss A.= Deacon, I fear you have been indulging again, and you promised
me so faithfully never to touch another drop. Oh, dear, the depravity of
mankind is distressing!
=Deacon.= Heaven preserve me! Hold your tongues, every one of you.
Don't you suppose I know a <DW52> woman when I see one! I've been most
infern--grossly insulted by one.
=Mrs. T.= Where?
=Deacon.= Why, in this room.
=Mrs. T.= }
=Helen.= } In this room?
=Miss A.= }
=Deacon.= Yes, in this room. Upon that very sofa. (_pointing to sofa_)
Only a moment ago there was a <DW52> woman sitting there arrayed in one
of Miss Amelia's dresses.
=Miss A.= In one of my dresses!
=Deacon.= Yes, and she looked just like you.
=Miss A.= (_in horror, raises her hands_) Like me!
=Deacon.= Like you, until she turned her face toward me. She escaped out
that window. (_pointing to D. C._)
=Miss A.= (_to MRS. T._) Sister, I believe this house is haunted!
=Mrs. T.= There certainly is something going on that I cannot
understand. (_to DAISY_) Did you send Pete for that policeman?
=Daisy.= No, ma'am, I could not find him.
=Helen.= That's just like him. He's never around when he's wanted.
=Miss A.= Sister, something must be done, or I'll not sleep in this
house to-night.
=Mrs. T.= (_to DAISY_) Go and see if Pete is anywhere around now, and if
you find him send him for an officer at once.
=Daisy.= Yes, ma'am.
(Exit, L. 2 E.)
=Mrs. T.= Brother, are you sure you saw a <DW52> woman?
=Deacon.= Didn't I tell you I did? Do you think I'm blind? Confound it!
(_wipes lips with handkerchief_) I saw her too plainly for comfort. I
wish I had her now. I'd wring her neck off. Blast her buttons!
=Miss A.= Deacon, I fear you are forgetting yourself.
=Mrs. T.= Brother! Brother!
=Deacon.= That's nothing, I feel like saying----
=Miss A.= (_quickly_) Don't! Please don't, Deacon.
Re-enter _PETE hurriedly, L. 2 E.; appears short of breath. Fans
himself with hand._
=Pete.= What's de mattah? (_to DEACON_) I heard yo' callin'. I was
out in de orchard pickin' some apples an' I run myself out of bref. I
t'ought de house was a-fire.
=Deacon.= Why didn't you call me when I told you to?
=Pete.= I did. I called yo' ag'in an' ag'in, an' yo' said, all right. I
t'ought yo' wus awake. 'Spect yo' must agone to sleep ag'in.
(_MRS. T., and HELEN cross R._)
=Mrs. T.= Pete, did you see a <DW52> man or woman pass out of that
window this afternoon?
=Pete.= (_in astonishment_) Why, no, missus. Dar was none passed out,
fo' I were jist over dar (_pointing_) in de orchard, right opposite de
window, an' nobody could pass out widout 'tractin' my 'tention. (_PETE
goes to D. C. and looks out. The DEACON crosses L. near MISS A._)
=Mrs. T.= It's very strange. I can't account for your vision, brother,
upon any other grounds, than that you were dreaming.
=Deacon.= (_angrily_) Then you think I didn't see a <DW52> woman at
all----
=Miss A.= And that my eye-sight failed me, too----
=Deacon.= And I'm telling a falsehood----
=Miss A.= And that I'm not to be believed? Oh, sister, sister! (_clasps
hands. Noise heard off L., as of some one crying. PETE crosses up
L. C._)
Re-enter _DAISY, hurriedly, L. C._
=Daisy.= (_angrily_) Pete, you horrid wretch, what did you mean by
putting that cat in poor Billy's room. You know how mortally afraid he
is of them.
=Pete.= I didn't put no cat in his room.
=Daisy.= You did, for he saw you open his door, and he's scared almost
out of his wits.
_The curtains at D. C. are pulled violently aside, and in rushes
BILLY._
=Billy.= (_screaming with fright_) Take him away! Take him away! (_goes
down C. Has left eye covered with cloth, left arm in sling, black patch
on right cheek and nose swollen. Has on night-shirt and long white
stockings. All the ladies scream. MRS. T. springs to support HELEN in
her arms; MISS AMELIA faints in the DEACON'S arms_)
_MRS. THORNTON and HELEN R.; DEACON and MISS AMELIA L.;
DAISY and PETE up C._
=Deacon.= Thank Heaven! At last I enfold thee!
SLOW DROP.
ACT V.
=Scene.=--_MRS. THORNTON'S sitting-room, same as Act IV. MISS
AMELIA seated on sofa, the DEACON beside her; PETE looks in upon
them from behind curtain C., grinning._
=Deacon.= In a short time, my love, Helen will be the happy bride of Mr.
Wheeler. Oh, that I could persuade you to become my blushing bride at
the same time. (_places arm around her, and looks at her fondly_)
=Miss A.= (_half-playfully_) I declare, Deacon, the more one sees of you
the more impressive your silliness becomes. The bare idea of a man of
your age desiring to marry, is simply ridiculous.
=Deacon.= Perhaps it is, my darling, but let me enjoy the happiness of
living over my youth again. I feel fifty years younger this morning than
I did last night before I obtained your consent to bless my declining
years with your sweet smile. But when we come to consider our age, and
the subject of marriage in connection with it, it certainly does appear
as though _both_ of us were silly geese.
=Miss A.= (_amazed and offended_) Sir!
=Deacon.= (_confused_) I beg your pardon. I did not mean to refer to
your age. I--I--meant my own. That was what I was thinking about.
(_tenderly_) As I look at you, you appear as fresh and bright as a lass
of sixteen.
=Miss A.= (_reassured, gushingly_) Oh, Deacon, I can't believe you mean
that.
=Deacon.= I do though.
=Pete.= (_at D. C._) Look out, de parson am coming! (_MISS A. and DEACON
start, then separate. PETE enters and goes R. At same instant_
Enter PARSON BROWNLOW, L. 2 E.
=Deacon.= (_rises, faces PETE, enraged_) How dare you enter my--our
presence unannounced! What do I care if the parson has come! (_MISS A.,
catching sight of PARSON B., who stands L. amazed, with uplifted hands,
tugs at the DEACON'S sleeve to attract his attention_) If a dozen of
them come, are they any better than any body else? If ever you enter my
presence again so abruptly, old as I am, I'll cane you within an inch of
your life.
=Miss A.= Deacon, Deacon, do be still. You are disgracing yourself and
mortifying me. Just look! There stands Parson Brownlow listening to
every word you say.
=Deacon.= Hang the Parson! I'll--(_sees the parson_) I beg your pardon,
sir, I was not aware of your presence. You must excuse my unseemly
passion. I have been greatly irritated by that black rascal standing
there. (_pointing to PETE_)
=Parson B.= What, Pete in trouble again! (_to PETE_) What have you been
doing now?
=Pete.= (_in injured tone_) I weren't doin' nuffin'. De Deacon dar was
a-spoonin', (_the DEACON frowns and starts for PETE, but is detained by
MISS A. catching him by the arm. PETE starts to run up R._) an' cause I
warned him of your approach to keep yo' from catchin' ob him, he got
mad.
=Miss A.= There, Pete, that's enough. (_to PARSON B._) It was a little
misunderstanding, that is all. (_DEACON manifests a desire to reach
PETE. To DEACON_) Deacon, do be still. I think I hear the bride and
groom coming.
Enter _MRS. THORNTON and guests, if any, R. 2 E. They take
places. =Mrs. T.= down L., guests up L. and R.; MISS AMELIA, DEACON
and PARSON cross R.; PARSON stands R. of MISS A.; PETE goes up R.
near curtain. Orchestra plays a wedding march. After a few bars
enter HELEN D. C., arrayed in bridal robes, leaning on the left arm
of WHEELER. Take positions directly in front of L. 2 E. door. PETE
makes a low salaam as they enter, but shakes fist at WHEELER as he
crosses to position. PARSON takes book from pocket, steps in front
of contracting parties, and proceeds with ceremony as music ceases.
PETE peeps out D. C._
=Parson.= (_reading from book_) We are gathered together here in the
presence of this company to join together this man and woman in the
holy bonds of matrimony. If any man can show just cause why they may
not lawfully be joined together, let him now speak, or else hereafter
forever hold his peace--(_during the delivery of this, PETE manifests
uneasiness and occasionally glances around at D. C. When GRAEF enters he
displays joy by rubbing hands gleefully_)
Enter _GRAEF D. C.; goes down C. Speaks as he comes forward._
=Graef.= One moment, Parson. I forbid this marriage.
=Wheeler.= On what grounds?
=Graef.= Aunt--Helen--you are being imposed upon!
=Wheeler.= (_angrily_) What is the meaning of this interference, sir?
=Graef.= (_to HELEN_) That man has a wife living.
=Wheeler.= 'Tis false! As false as he who makes the accusation. (_to
HELEN, angrily_) You will not allow yourself to be influenced by the
base charge of a common thief, will you?
=Graef.= Helen, I ask no one to believe my simple word. I have proof
amply sufficient to convince you of the truthfulness of my assertion.
(_to WHEELER_) Do you deny my charge?
=Wheeler.= I do, and challenge you to produce your proof.
Enter MRS. DARRAH, D. C.
=Graef.= (_to WHEELER_) It is here. Do you know this lady?
=Wheeler.= (_surprised_) Minnie!
=Graef.= You know her then?
=Wheeler.= You here?
=Mrs. T.= (_to GRAEF_) Who is that woman?
=Graef.= Uncle's daughter, (_the DEACON'S back is turned toward MRS.
D._) and your would-be son-in-law's wife.
=Mrs. T.= (_to WHEELER_) Is this true?
=Wheeler.= I cannot deny it. (_bows head. MRS. T. catches HELEN by arm
and supports her to sofa as MRS. D. speaks. PARSON B. closes book and
crosses to R. of MISS AMELIA_)
=Mrs. D=. Alas, it is too true! But I remain such only until the courts
sever our relation. (_goes to sofa and helps comfort HELEN, after
casting a longing glance at the DEACON who still stands with back toward
her_)
=Wheeler.= (_hisses through clenched teeth, to GRAEF_) So I have _you_
to thank for this humiliation, have I?
=Graef.= Yes, and it is a pleasure I have been anticipating for the past
two days.
=Wheeler.= Then you prepared this plan for my exposure?
=Graef.= I did.
=Wheeler.= Have you the effrontery to tell me to my teeth that you
deliberately prepared my downfall?
=Graef.= (_coolly_) I have.
=Wheeler.= Then, you miserable cur, I'll be revenged. (_rushes at GRAEF
who retreats a little. PETE draws huge butcher knife and runs to GRAEF'S
side_)
=Pete.= Pull on him, Massa George, pull on him, I'se wid yo'! (_holding
knife aloft dramatically. At sight of knife MISS AMELIA has slight
attack of hysterics, throws both arms around the DEACON'S neck and
chokes him. The DEACON struggles to release himself. PARSON B. stoops
behind MISS A. and tries to make her dress shield him. =Wheeler= stops
suddenly_)
Enter _OFFICER, L. 2 E.; approaches WHEELER softly_.
=Graef.= He's not worth the effort, Pete. Officer, arrest that man.
=Officer.= (_seizing WHEELER from behind_) George Darrah, I arrest
you for the crime of theft. (_WHEELER struggles. GRAEF helps OFFICER
handcuff him. The DEACON unloosens MISS A.'S arms, when her head falls
upon his right shoulder. The DEACON supports her drooping form by
placing his right arm around her waist. MRS. T. rises_)
=Wheeler.= What is the meaning of this indignity?
=Graef.= You will soon know. (_to MRS. T._) Aunt, there stands the
George Graef who stole your diamonds!
=Pete.= Say, Massa George, what do yo' think his picture will look like
now, arter it's took, eh? (_GRAEF smiles. PETE crosses to PARSON B.
and makes feint to stab him with knife. PARSON sinks almost to knees,
manifesting great fear. Aside_) He kin teach others how to die bravely,
but he skeers when deff comes nigh him.
=Mrs. T.= (_to GRAEF_) I don't understand you.
=Graef.= George Darrah, there, known to you as Mr. Wheeler, is the thief
you thought was myself. (_to WHEELER_) Do you require _proof_ to that
effect?
=Wheeler.= Yes, if you possess it.
=Graef.= (_taking watch charm from pocket_) Do you recognize that charm?
=Wheeler.= No, I never saw it before.
=Pete.= Dat's a whopper!
=Graef.= (_taking paper from pocket_) Perhaps you will deny also ever
having seen this note with your name attached to it. (_folds note so
that signature only is seen, and shows it to WHEELER_) Is that your
signature?
=Wheeler.= No, it's a forgery.
=Pete.= By crickitees! I'se not a circumstance to dat feller in lyin'.
=Graef.= Aunt, this charm and note were found by Pete just outside of
your dressing-room door the morning after the robbery. He, thinking they
might lead to a clue, brought them to me. From the contents of this note
I learned who committed the theft and where the diamonds were secreted.
=Wheeler.= Will you let me see that note?
=Graef.= With pleasure. (_walks to WHEELER, unfolds note and holds it up
for him to read, talking as he does so_) Pete visited the place where
the diamonds were hidden, and brought them to me. I will give them to
you in a moment. Are you through? (_to WHEELER. Takes small package from
pocket and hands it to MRS. T._) There they are.
=Wheeler.= Mrs. Thornton, that note is supposed to be written by me.
In it I am made to state the _hour_ I was to commit the robbery, and
the _place_ where I would hide the diamonds, so that my confederate
could find them. Now, do you think if _I_ planned the affair and had an
accomplice, I would be likely to write him a tell-tale note, and allow
it to fall into an interested party's hands to be used against me?
=Pete.= Did yo' eber hear de like?
=Mrs. T.= Well, hardly, but how do you account for the note explaining
where the diamonds were hidden?
=Wheeler.= That's plain enough to me. There stands the man (_looking at
GRAEF_) who _took_ the diamonds; there stands the man who _returned_
them, and _there_ is the man who wrote that note and trumped up this
charge to shield himself at my expense.
=Graef.= You infamous scoundrel! (_advances upon WHEELER_)
=Pete.= (_excitedly_) Pin him, Massa George. I'd nebber stand dat, suah!
=Mrs. T.= (_looks reproachfully at GRAEF_) Can it be possible!
=Graef.= Aunt, for heaven's sake, believe not that black-hearted
villain. In one moment I'll convince you of his guilt beyond question.
This morning, Davis the pawnbroker, came to my room of his own free
will, and told me that that man (_pointing to WHEELER_) was the one who
left one of your jewels at his shop, and that he was to pay Davis three
hundred dollars to keep that fact a secret. Is that sufficient for you?
=Pete.= (_aside_) Ob his own free will, did he? I guess I skeered ole
Davis nigh about to deff. I tole him we knew who gave him dat diamond
an' I was on my way to git an officer to 'rest him as a 'complice.
=Wheeler.= The lying scoundrel! I'll get even with him for that, and
with _you_ (_to GRAEF_) and you, (_to MRS. T._) and with all of you.
=Mrs. T.= Off with you. I no longer doubt your guilt. Officer, remove
him instantly from our presence. (exeunt _OFFICER and WHEELER, L. 2 E.
MRS. T. goes to GRAEF_) George, can you ever forgive me for my unjust
suspicions? I will do anything in my power to make retribution to you
for your sufferings.
=Graef.= Then extend to Minnie, there, your niece, a welcome worthy of
her. (_MRS. T. goes to sofa, grasps MRS. D.'S hand, takes seat beside
her and engages her in conversation. HELEN rises and approaches GRAEF_)
Innocence requires no retribution from those who suspect her.
=Helen.= Cousin, no one can ever be more grateful to you than I am for
the life of misery you have saved me from. What could have been that
_fiend's_ motive in trying to bring disgrace upon us all, baffles my
comprehension.
=Graef.= His desire to be revenged upon Minnie and all her relatives,
for the fancied insult he received in uncle's disinheriting her for
marrying contrary to his wishes, has been the motive that actuated him.
(_PARSON, MISS AMELIA and DEACON cross to GRAEF_)
=Parson.= (_shaking GRAEF'S hand_) Bless you, my son, bless you.
=Miss A.= George, you are a son worthy of your mother. I always said you
would yet make a man of yourself----
=Graef.= (_interrupting_) There, there! you are all showering your
thanks upon me and forgetting Pete, to whom most of the glory belongs.
=Pete.= Yo' just bet it does. I'se done my share ob keepin' up de
'spectability ob de family.
=Helen.= Yes, Pete, you have, and we are all very grateful to you for
it.
=Pete.= (_bowing_) T'ank yo'.
=Deacon.= (_advancing and extending hand_) George, my boy, you will at
least let me extend to you my hearty congratulations. You have acted
nobly.
=Graef.= (_refusing hand_) Excuse me uncle, but----
=Deacon.= Why! why! what's the matter? Refuse to shake hands with me?
Why--ah--I can't understand it.
=Graef.= Pardon me, uncle for my plainness of speech. But I'll never
shake hands with a father who has disowned his motherless child, until
he forgives her and acknowledges her as his own flesh and blood.
=Pete.= (_aside_) Dat's de noblest t'ing he ever said or done.
=Minnie.= (_rising_) George!
=Graef.= I can't help it, Minnie. I mean it. (_the DEACON turns back_)
=Pete.= Dat's right, Massa George, make him toe de scratch.
Enter NELLIE, D. C.
=Nellie.= Where's mamma? Oh, there you are! (_runs to her_)
=Graef.= (_approaches DEACON; lays hand upon his left shoulder_) Uncle,
your daughter and child await your forgiveness.
=Deacon.= (_doggedly_) I have no daughter!
=Pete.= Miss 'Melia, please come here a minnit. (_MISS A. goes to PETE,
who is down R._) Yo' tackle de Deacon, he'll refuse yo' nuffin'.
=Miss A.= Go long with you! (_returns to former position_)
=Parson.= Brother, the good book says, "Forgive, and we shall be
forgiven." (_MRS. D. and NELLIE approach DEACON and kneel at his L.
side_)
=Mrs. D.= Father, I ask your forgiveness, not for myself, but for this
innocent child's sake.
=Pete.= Now, go for him, Miss 'Melia, an' yo'll fotch him, suah.
=Deacon.= Rise, my child, for inhuman would be the man who could refuse
the pleadings of a kneeling child. You are forgiven. (_tenderly kisses
the brow of MRS. D. She and NELLIE rise_)
=Miss A.= Oh, Deacon, Deacon!
=Pete.= (_aside_) She's jealous!
=Miss A.= How noble you are.
=Pete.= (_elevating eyebrows and opening mouth_) Oh, dat's what she
means!
=Graef.= (_grasping the DEACON'S hand_) Now, uncle, I'll shake hands
with you and thank you, too, for the nobility of character you have
shown. Though there will be no marriage bells ringing in this house
to-day, yet I'm sure there will not be a happier gathering of loved ones
to be found in this wide, wide world.
=Pete.= But t'ink ob de good things we'll miss!
=Deacon.= (_gleefully_) Who says there will be no marriage-bells
sounding in this house to-day? Parson, step right down. (_motioning down
C. Enter BILLY, D. C., with huge piece of cake in hand, eating. His
disfigurements are slightly less than in Act 4. Stands up C._) Where are
you, Amelia, my love?
=Miss A.= Oh, Deacon, don't be so silly! (_holding back. All smile_)
=Deacon.= Come along, my love. Don't keep the Parson waiting, come
along. (_take positions down C. PETE runs to NELLIE and places her
beside MISS A., while he goes to DEACON'S side. MRS. T. and HELEN up L.;
GRAEF and MRS. D. up R.; BILLY up C., eating_)
=Pete.= Let de band play fo' we's all ready fo' de dance. (_PARSON opens
book and steps in front of MISS A. and the DEACON as the curtain falls_)
CURTAIN.
[Illustration]
SAVED FROM THE WRECK.
_A DRAMA IN THREE ACTS, BY THOMAS K. SERRANO._
PRICE, 15 CENTS.
Eight male, three female characters: Leading comedy, juvenile man,
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Two interior and one landscape scenes. Modern costumes. Time of playing,
two hours and a half. The scene of the action is laid on the New Jersey
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SYNOPSIS OF INCIDENTS.
ACT I. THE HOME OF THE LIGHT-HOUSE KEEPER.--An autumn afternoon.--The
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advice.--Married for money.--A golden chance.--The intercepted
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ACT II. SCENE AS BEFORE; time, night.--Dark clouds gathering.--Changing
the jackets.--Father and son.--On duty.--A struggle for fortune.--Loved
for himself.--The divided greenbacks.--The agreement.--An unhappy
life.--The detective's mistake.--Arrested.--Mistaken identity.--The
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_A COMEDY-DRAMA IN THREE ACTS, BY THOMAS K. SERRANO._
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Eight male, three female, and utility characters: Leading juvenile
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SYNOPSIS OF INCIDENTS.
ACT I. AT FORT LEE, ON THE HUDSON.--News from the war.--The
meeting.--The colonel's strange romance.--Departing for the war.--The
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the war.--TABLEAU.
ACT II. ON THE BATTLEFIELD.--An Irishman's philosophy.--Unconscious of
danger.--Spies in the camp.--The insult.--Risen from the ranks.--The
colonel's prejudice.--Letters from home.--The plot to ruin.--A token of
love.--True to him.--The plotters at work.--Breaking the seals.--The
meeting of husband and wife.--A forlorn hope.--Doomed as a spy.--A
struggle for lost honor.--A soldier's death.--TABLEAU.
ACT III. BEFORE RICHMOND.--The home of Mrs. De Mori.--The two
documents.--A little misunderstanding.--A deserted wife.--The
truth revealed.--Brought to light.--Mother and child.--Rowena's
sacrifice.--The American Eagle spreads his wings.--The spider's
web.--True to himself.--The reconciliation.--A long divided home
reunited.--The close of the war.--TABLEAU.
=> _Copies mailed, postpaid, to any address, on receipt of the annexed
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UNCLE TOM'S CABIN (NEW VERSION.)
_A MELODRAMA IN FIVE ACTS, BY CHAS. TOWNSEND._
PRICE, 15 CENTS.
Seven male, five female characters (some of the characters play two
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SYNOPSIS OF INCIDENTS: ACT I.--_Scene I._--The Shelby plantation in
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for Canada.--"I won't be taken--I'll die first."--Shelby and
Haley.--Uncle Tom and Harry must be sold.--The poor mother.--"Sell
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ACT III.--The angel child.--Tom and St. Clare.--Topsy's mischief.--Eva's
request.--The promise.--Pathetic scene.--Death of Eva.--St. Clare's
grief.--"For thou art gone forever."
ACT IV.--The lonely house.--Tom and St. Clare.--Topsy's
keepsake.--Deacon Perry and Aunt Ophelia.--Cute on deck.--A distant
relative.--The hungry visitor.--"Chuck full of emptiness."--Cute
and the Deacon.--A row.--A fight.--Topsy to the rescue.--St. Clare
wounded.--Death of St. Clare.--"Eva--Eva--I am coming."
ACT V.--Legree's plantation on the Red River.--Home again.--Uncle
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PRICE, 15 CENTS.
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SYNOPSIS OF INCIDENTS: ACT I.--Parkhurst & Manning's law office, New
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will destroyed.--A cunning plot.--Weaving the web.--The unseen
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ACT II.--Winter quarters.--Colonel Hastings and Sergeant Tim.--Moses.--A
message.--Tim on his dignity.--The arrival.--Playing soldier.--The
secret.--The promise.--Harry in danger.--Love and duty.--The promise
kept.--"Saved, at the loss of my own honor!"
ACT III.--Drawing-room at Falconer's.--Reading the news.--"Apply to
Judy!"--Louise's romance.--Important news.--Bertha's fears.--
Leamington's arrival.--Drawing the web.--Threatened.--Plotting.--
Harry and Bertha.--A fiendish lie.--Face to face.--"Do you know
him?"--Denounced.--"Your life shall be the penalty!"--Startling
tableau.
ACT IV.--At Uncle Toby's.--A wonderful climate.--An impudent rascal.--A
bit of history.--Woman's wit.--Toby Indignant.--A quarrel.--Uncle Toby's
evidence.--Leamington's last trump.--Good news.--Checkmated.--The
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=> _Copies mailed, postpaid, to any address, on receipt of the annexed
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TOWNSEND'S "AMATEUR THEATRICALS."
_A Practical Guide for Amateur Actors._
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HELMER'S
ACTOR'S MAKE-UP BOOK.
_A Practical and Systematic Guide to the Art of Making up for the
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CONTENTS.
Chapter I. THEATRICAL WIGS.--The Style and Form of Theatrical Wigs and
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Chapter II. THEATRICAL BEARDS.--How to fashion a Beard out of Crepe
Hair. How to make Beards of Wool. The growth of Beard simulated.
Chapter III. THE MAKE-UP.--A successful Character Mask, and how to make
it. Perspiration during performance, how removed.
Chapter IV. THE MAKE-UP BOX.--Grease Paints. Grease Paints in Sticks;
Flesh Cream; Face Powder; How to use Face Powder as a Liquid Cream;
The various shades of Face Powder. Water Cosmetique. Nose Putty. Court
Plaster. Cocoa Butter. Crepe Hair and Prepared Wool. Grenadine. Dorin's
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Bear's Grease. Eyebrow Pencils. Artist's Stomps. Powder Puffs. Hare's
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Chapter V. THE FEATURES AND THEIR TREATMENT.--The Eyes: Blindness. The
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apparently reduced in size. The Mouth and Lips: a juvenile mouth; an
old mouth; a sensuous mouth; a satirical mouth; a one-sided mouth;
a merry mouth; a sullen mouth. The Teeth. The Neck, Arms, Hands and
Finger-nails: Finger-nails lengthened. Wrinkles: Friendliness and
Sullenness indicated by wrinkles. Shading. A Starving Character. A Cut
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Chapter VI. TYPICAL CHARACTER MASKS.--The Make-up for Youth: Dimpled
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another method. Old Age. <DW64>s. Moors. Chinese. King Lear. Shylock.
Macbeth. Richelieu. Statuary. Clowns.
Chapter VII. SPECIAL HINTS TO LADIES.--The Make-up. Theatrical Wigs and
Hair Goods.
=> _Copies of the above will be mailed, post-paid, to any address, on
receipt of the annexed prices._ <=
HAROLD ROORBACH, Publisher, 9 Murray St., New York.
Transcriber's notes:
The following is a list of changes made to the original.
The first line is the original line, the second the corrected one.
author. Threatrical Managers wishing to produce it should apply to
author. Theatrical Managers wishing to produce it should apply to
JAMES REED, _a friend of Darrah's_, H. C. Lewis.
JAMES READ, _a friend of Darrah's_, H. C. Lewis.
and played by Reed. Officer in Act IV, by Violinist.
and played by Read. Officer in Act IV, by Violinist.
life would be beset by the harrassing knowledge of being surrounded
life would be beset by the harassing knowledge of being surrounded
I'll let the precious booty remain in it's hiding place until I
I'll let the precious booty remain in its hiding place until I
=Daisy.= Oh, Mr. Wheeler, I forgot----(_percieves DEACON_) Oh!
=Daisy.= Oh, Mr. Wheeler, I forgot----(_perceives DEACON_) Oh!
(_dicks up pin; conceals bent part, displaying point_) Daisy nebber
(_picks up pin; conceals bent part, displaying point_) Daisy nebber
=Graef.= (_interrrupting her, grasps her by shoulder and anxiously_
=Graef.= (_interrupting her, grasps her by shoulder and anxiously_
=Miss A.= I fear your are a flatterer. Now, you don't think I'm
=Miss A.= I fear you are a flatterer. Now, you don't think I'm
=Miss A.= That will do, Daisy. You are are a nice, well-behaved
=Miss A.= That will do, Daisy. You are a nice, well-behaved
this morning than I did last night before I obtained you consent
this morning than I did last night before I obtained your consent
=Officer.= (_seizing WHEELER from behind_) George Darrah, I ar-
=Officer.= (_seizing WHEELER from behind_) George Darrah, I arrest
End of the Project Gutenberg EBook of The Deacon, by Horace C. Dale
***
|
{
"redpajama_set_name": "RedPajamaBook"
}
| 1,684
|
\section{Introduction}
\label{sec:intro}
Reinforcement learning (RL) is a computational framework for modeling and automating goal-directed learning and sequential decision-making~\cite{Puterman1994,sutton2018reinforcement}. Unlike other learning approaches, namely supervised learning and unsupervised learning, RL emphasizes learning by an agent from direct interaction with its environment. RL is particularly suitable for settings that involve an agent who needs to learn a policy on what to do in different situations---how to map states to actions---to maximize a long-term utility.
The agent must explore different actions to discover actions yielding high reward; crucially, actions affect not only the immediately received reward but also the next state and, through that, all future rewards. These characteristics---actions having long-term consequences, delayed reward, and sequential decision-making under uncertainty---are the key features of RL.
So far, some of the most impressive applications of RL have been limited to game playing only~\cite{mnih2013playing,mnih2015human,silver2016mastering,silver2017mastering}. Given the centrality of sequential student-teacher interactions in education (ED), there has been a surge of interest in applying RL to improve the state-of-the-art technology for ED. There are several problem settings in ED where RL methodology is useful, including training instructional policies using RL methods and modeling a human student using RL.
While promising, it is typically very challenging to apply out-of-the-box RL methods to ED. Further, many problem settings in ED have unique challenges that make the current RL methods inapplicable. Some of the key challenges in ED include the following: (a) the lack of simulation-based-environments to train data-hungry RL methods, (b) the need for large (often unbounded) state space representations, (c) the limited observability of the environment's state (i.e., the student's knowledge), (d) significantly delayed and noisy outcome measures, and (e) concerns about the robustness, interpretability, and fairness of RL methods when applied to the critical domain of ED.
The goal of the RL4ED workshop has been to facilitate tighter connections between researchers and practitioners interested in the broad areas of RL and ED. The workshop focused on two thrusts:
\begin{itemize}[parsep=5pt, leftmargin=*,labelindent=0pt]
\item \textbf{RL\ensuremath{\rightarrow}ED}: Exploring how we can leverage recent advances in RL methods to improve the state-of-the-art technology for ED.
\item \textbf{ED\ensuremath{\rightarrow}RL}: Identifying unique challenges in ED that are beyond the current methodology, but can help nurture technical innovations and next breakthroughs in RL.
\end{itemize}
\section{Overview of the RL4ED@EDM'21 Workshop Activities}
\label{sec:workshop_summary}
\looseness-1In this section, we provide an overview of the RL4ED workshop organized at the EDM 2021 conference; full details are available on the \href{https://rl4ed.org/edm2021/}{workshop website}. The workshop was organized as an online event; we had over $120$ people register and over $60$ simultaneous attendees at the peak. The workshop was structured around invited talks, contributed papers, spotlight presentations, and two panels.
\subsection{Topics of Interests}
As mentioned above, the workshop focussed on two thrusts, each covering several topics of interest. These topics served as guidelines when selecting the speakers for invited talks and when selecting the contributed papers for spotlight presentations.
The topics in \textbf{RL\ensuremath{\rightarrow}ED} thrust focussed on leveraging recent advances in RL methods for ED problem settings, including: (i) survey papers summarizing recent advances in RL with applicability to ED; (ii) developing toolkits, datasets, and challenges for applying RL methods to ED; (iii) using RL for online evaluation and A/B testing of different intervention strategies in ED; and (iv) novel applications of RL for ED problem settings.
\looseness-1The topics in \textbf{ED\ensuremath{\rightarrow}RL} thrust focussed on unique challenges in ED problem settings for nurturing next breakthroughs in RL methods, including: (i) using pedagogical theories to narrow the policy space of RL methods; (ii) using RL framework as a computational model of students in open-ended domains; (iii) developing novel offline RL methods that can efficiently leverage historical student data; and (iv) combining statistical power of RL with symbolic reasoning to ensure the robustness for ED.
\subsection{Invited Talks and Panel Sessions}
We invited a set of people from academia and industry to cover various topics of interest and achieve a balance across different perspectives and disciplines. In total, the workshop had $7$ invited talks; each of these talks being about $25$ minutes long. The final list of speakers, along with their talk titles, is provided below:
\begin{enumerate} [label={[T\arabic*]}, parsep=2pt, leftmargin=*,labelindent=-4pt]
\item \href{https://people.epfl.ch/tanja.kaeser/?lang=en}{Tanja K{\"a}ser}; \textpapertitle{Modeling and Individualizing Learning in Open-Ended Learning Environments}.
%
\item \href{https://www.linkedin.com/in/simon-woodhead/}{Simon Woodhead}; \textpapertitle{Eedi and the NeurIPS 2020 Education Challenge Dataset}.
%
\item \href{https://jmhl.org/}{Jos{\'e} Miguel Hern{\'a}ndez Lobato}; \textpapertitle{Deconfounding Reinforcement Learning in Observational Settings}.
%
\item \href{https://people.engr.ncsu.edu/mchi/}{Min Chi}; \textpapertitle{The Impact of Pedagogical Policies on Student Learning - A Reinforcement Learning Approach}.
%
\item\href{https://cs.stanford.edu/people/ebrun/}{Emma Brunskill}; \textpapertitle{More Practical Reinforcement Learning Inspired by Challenges in Education and Other Societally-Focussed Applications}.
%
\item \href{https://psych.wisc.edu/staff/austerweil-joe/}{Joe Austerweil}; \textpapertitle{Is Reinforcement Just a Value to be Maximized?}.
%
\item \href{https://faculty.sites.uci.edu/doroudis/}{Shayan Doroudi}; \textpapertitle{Reinforcement Learning for Instructional Sequencing - Learning from Its Past to Meet the Challenges of the Future}.
\end{enumerate}
The video recordings of these invited talks are available on the workshop website. In addition to these invited talks, the speakers also participated in two separate panel discussions, each of $30$ minutes duration. The Q/A time after the talks and these panel sessions provided an ample opportunity for discussions among workshop participants.
\subsection{Contributed Papers and Spotlight Presentations}
Given the workshop's focus on community-building and networking, we experimented a bit in our call for papers and solicited submissions of two types. The first type, what we called the ``Research track'', includes papers reporting the results of ongoing or new research, which have not been published before. The second type, what we called the ``Encore track'', includes papers that have been recently published or accepted for publication in a conference or journal.
For the ``Research track'', we received $4$ submissions and accepted $3$ for the workshop. For the ``Encore track'', we sent invitations to authors with recently published that were relevant to the workshop and we received $6$ submissions in this track. In total, we had $9$ contributed papers covering various topics of interest for the workshop. These contributed papers were presented as spotlight presentations; each of these talks being about $8$ minutes long. In total, we had $10$ spotlight presentations, corresponding to these contributed papers and an additional invited presentation, listed below:
\begin{enumerate} [label={[S\arabic*]}, parsep=2pt, leftmargin=*,labelindent=-4pt]
\item\textpapertitle{Statistical Consequences of Dueling Bandits}. \\ (Research track; \cite{RL4ED_EDM2021_Saxena})
%
\item \textpapertitle{Capturing Student-Robot Interactions for a Data-Driven Educational Dialogue RL Environment}. \\ (Research track; \cite{RL4ED_EDM2021_Maidment})
%
\item \textpapertitle{Towards Transferrable Personalized Student Models in Educational Games}. \\ (Encore track; \cite{DBLP:conf/atal/SpauldingSPB21})
%
\item \textpapertitle{Extending Adaptive Spacing Heuristics to Multi-Skill Items}. \\ (Encore track; \cite{RL4ED_EDM2021_Choffin})
%
\item \textpapertitle{Getting Too Personal(ized): The Importance of Feature Choice in Online Adaptive Algorithms}. \\ (Encore track; \cite{DBLP:conf/edm/LiYSSWR20})
%
\item \textpapertitle{Approximately Optimal Teaching of Approximately Optimal Learners}. \\ (Encore track; \cite{DBLP:journals/tlt/WhitehillM18})
%
\item \textpapertitle{Learning Expert Models for Educationally Relevant Tasks using Reinforcement Learning}. \\ (Encore track; \cite{Maclellan_EDM2021})
%
\item \textpapertitle{Deep Reinforcement Learning to Simulate, Train, and Evaluate Instructional Sequencing Policies}. \\ (Research track; \cite{RL4ED_EDM2021_Subramanian})
%
\item \textpapertitle{Adaptively Scaffolding Cognitive Engagement with Batch Constrained Deep Q-Networks}. \\ (Encore track; \cite{DBLP:conf/aied/FahidRSGPL21})
%
\item \textpapertitle{Integrating Reinforcement Learning into the ASSISTments Platform}. \\ (Additional invited spotlight presentation)
\end{enumerate}
The video recordings of these spotlight presentations are available on the workshop website.
\section{Summary of the Main Research Directions in RL4ED}
\label{sec:research_directions}
In this section, we summarize the main research directions in the area of RL for ED.
\paragraph{RL methods for personalizing curriculum across tasks.} The most direct and well-studied application of RL for ED is to train an instructional policy for providing students with a personalized curriculum. In this problem setting, one trains an RL agent to induce an instructional policy in an intelligent tutoring system, and the human student is part of the ``environment'' as per RL terminology~\cite{sutton2018reinforcement}. For a given student, such an instructional policy maps the student's history of responses to the next task to maximize long-term learning gains. We refer the reader to \cite{doroudi2019s}, which provides an excellent survey on this topic; also, see invited talk [T7] from the authors of the survey. The latest research in this direction is also covered by the invited talk [T4], spotlights [S6] and [S8], as well as several recent works~\cite{DBLP:journals/cogsci/RaffertyBGS16,DBLP:conf/aied/SawyerRL17,DBLP:journals/tlt/WhitehillM18,DBLP:conf/edm/AusinABC19,zhou2019hierarchical,DBLP:conf/chi/BassenBSTPZGFM20}.
Despite being a natural application for RL, in practice, there are several challenges to train effective RL-based policies for ED domains in the real world; see \cite{doroudi2019s}. One of the major challenges is that the students' true knowledge state is not directly observable~\cite{DBLP:journals/cogsci/RaffertyBGS16,DBLP:journals/tlt/WhitehillM18} -- we need to use appropriate representations for mapping students' responses to a knowledge state. Another major challenge arises from the lack of simulation-based environments to train data-hungry RL methods. An RL agent typically requires millions of training episodes, and such training is generally done in a simulator for gaming domains; however, we do not have such realistic simulators or computational models of human students for ED domains. To tackle these challenges, an important research direction is to investigate how to effectively combine policies derived from RL methods and pedagogical theories, or using pedagogical theories to narrow the policy space of RL for ED problem settings. Another important research direction is developing novel offline RL methods that can efficiently leverage historical data; see invited talk [T5].
\paragraph{RL methods for providing hints, scaffolding, and quizzing.} Beyond curriculum across tasks, another important application of RL for ED is to train policies that can provide hints as feedback within a task. Especially for complex open-ended domains, such as block-based visual programming or high-school algebra, hints feedback and scaffolding play an important role in improving student engagement and learning gains~\cite{aleven2016instruction,DBLP:conf/lats/WilliamsKRMGLH16,DBLP:conf/lats/PatikornH20,DBLP:conf/lak/EricksonBMVH20}. In one of the early works, \cite{barnes2008toward} used Markov Decision Processes formalism for automatic generation of hints for logic proof tutoring using historical student data. In recent contemporary work, \cite{edm20-zero-shot} proposed an RL framework to train a hints policy for block-based visual programming tasks without relying on historical student data, thereby tackling the zero-shot challenge of providing hints in this domain. We also refer the reader to recent works of \cite{DBLP:conf/edm/JuCZ20,DBLP:conf/aied/FahidRSGPL21}
where RL methods are used for scaffolding and assisting at critical decision-making points; also see invited talk [T4] and spotlight [S9] from the authors of these papers. In a somewhat different problem setting, \cite{edm21-quizzing-policy} have investigated how an RL-based policy can be used for quizzing students to infer their knowledge state, tackling the challenge\#4 in Eedi's NeurIPS Education Challenge (see \cite{eedi,wang2020diagnostic} and invited talk [T2]).
These works are still in the early stages and showcase the potential of using RL-based policies for different problem settings beyond curriculum across tasks. In the coming years, we believe that RL methods can play a critical role in providing feedback to students for complex, open-ended tasks. An exciting direction of research here would be to train RL-based policies that can balance different objectives when providing hints -- completing the current task quickly with hints vs. maximizing the pedagogical value of hints in terms of the learner's knowledge gain (i.e., better performance in future tasks).
\paragraph{RL for adaptive experimentation and A/B testing in educational platforms.} In recent years, there is a growing interest in using RL methods for assessing different educational interventions in large-scale online platforms. In particular, a special family of RL methods, called multi-armed bandits (MAB), are used for adaptive experimentation in recent works -- each student is assigned to a version of the technology or a type of intervention (aka ``arm'' in MAB terminology), and the algorithm observes the student's learning outcome (the reward associated with the assigned ``arm''); each subsequent student is more likely to be assigned to a version of the technology that has been more effective for previous students, as the algorithm discovers what is effective~\cite{DBLP:conf/edm/LiuMBP14,DBLP:conf/chi/WilliamsRTALK18,DBLP:conf/aied/RaffertyYW18}. While the standard MAB algorithms do not allow per-student personalization, the contextual MAB algorithms can also account for student features and personalize the assignment to further improve learning gains. In recent work, \cite{DBLP:journals/tlt/WhitehillM18} investigated the effect of features used in contextual MAB algorithms and highlighted the trade-offs of personalization on learning gains (also, see spotlight [S5] from the authors of this paper). In another recent work, \cite{DBLP:conf/aied/Zavaleta-Bernuy21} conducted adaptive experiments as a case study of sending homework email reminders to students, and the paper reports various open issues that arise in conducting such experiments in real-world settings. We also refer the reader to several other recent works, including \cite{rafferty2019statistical,DBLP:conf/aied/MuiLD21} as well as spotlights [S1] and [S10]. In [S10], the authors discuss their ongoing effort to bring MAB-based adaptive experimentation to recommend and personalize the content students receive in the ASSISTments educational platform~\cite{ASSISTments}. Overall, RL for adaptive experimentation is a very promising area where we expect to see the deployment of RL-driven techniques in real-world educational platforms in the coming years. An important research direction in this area is to better understand the ethical implications of adaptive experiments, and design contextual MAB algorithms that can account for fairness and ensure educational equity across different groups.
\paragraph{RL framework to model a human student.} In contrast to using the RL agent for representing a teacher / tutoring system, one can take an orthogonal view and use the RL framework for modeling the students' learning or problem-solving process. In this setting, the human student is modeled as an RL agent, and the teacher represents the ``environment''; cf. the setting of training an instructional policy where the RL agent represents the teacher or tutoring system. This modeling framework is especially useful in open-ended learning domains where tasks are conceptual, open-ended, and sequential, including domains such as block-based visual programming and high-school algebra. Such an RL-based computational model of human students is useful for a variety of settings. For instance, one could use such a model to diagnose students' mistakes based on their attempted solutions and in designing more effective environment feedback (e.g., via appropriate interventions); see \cite{rafferty2020assessing,DBLP:conf/edm/YangZTAC20}. Furthermore, such a computational model could be used as simulated students to evaluate teaching algorithms or to train instructional policies. In the machine teaching research \cite{DBLP:journals/corr/abs-1801-05927}, a series of recent works have used RL-based agents as a student model to investigate the theoretical foundations of teaching for sequential decision-making tasks. For instance, \cite{DBLP:conf/nips/HaugTS18,DBLP:conf/nips/TschiatschekGHD19,DBLP:conf/ijcai/KamalarubanDCS19} studied the problem of curriculum design and optimizing demonstrations when the student is modeled as an imitation learning agent, and \cite{DBLP:conf/icml/RakhshaRD0S20} studied the problem of policy teaching and environment design when the student is modeled as an RL agent. A number of recent works and workshop activities focussed on this research direction, including \cite{mcilroy2020aligning,DBLP:conf/atal/SpauldingSPB21,Maclellan_EDM2021}, invited talks [T1] and [T6], and spotlights [S3] and [S7]. In the coming years, we believe that the RL framework to model a human student will continue to be an important research direction. One of the most important research questions is how to incorporate human-centered aspects of learning into an RL agent so that these agents are a better representation of human students. More concretely, it would be important to develop RL agents that can capture the capabilities of human learners, e.g., few-shot learning, deductive reasoning, and learning from different feedback types.
\paragraph{RL for educational content generation.} Another important research direction is to leverage RL methodology for educational content generation, such as generating new exercises, quizzes, or videos. Often referred to as procedural content generation (PCG), recent works have explored the applicability of RL for PCG in the context of generating different levels of Sokoban puzzles~\cite{khalifa2020pcgrl,kartal2016data} and racing games~\cite{gisslen2021adversarial}. In recent work, \cite{ahmed20synthesizing} used Monte Carlo Tree Search (MCTS) method combined with symbolic techniques to synthesize new tasks for block-based visual programming domain. These synthesized tasks could be useful in many different ways
in practical systems -- for instance, tutors can assign new practice tasks as homework or quizzes to students to check their knowledge, and students can automatically obtain new similar tasks after
they failed to solve a given task. Given the critical need to provide personalized and diverse educational content on online platforms, RL for educational content generation is an important research area that needs to be explored further.
\section{Conclusions}
\label{sec:conclusions}
RL for ED is an important application area for future work that may lead to practical improvements in education and to new advances in reinforcement learning. The talks and discussions at the EDM2021 workshop highlighted excitement in the community around the main areas covered in this document, and the diverse array of perspectives as well as panelist comments demonstrated the importance of drawing on ideas from multiple disciplines, including (but not limited to) the learning sciences, cognitive science, and machine learning. This need for multiple perspectives and the unique challenges raised by educational applications suggest the need for continued fostering of community in this area.
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A Trinity Church (Szentháromság-templom) a New York-i püspöki egyházmegye történelmi plébániatemploma, New York pénzügyi központjában a Broadway és a Wall Street kereszteződésénél, a Wall Street bejáratával szemben áll Lower Manhattanben. A Szentháromság-templom több mint 300 éven át jelentős szerepet játszott New York City történetében. Mind elhelyezkedése, mind alapítványai miatt is nevezetes. A jelenlegi, 1846-ban felépült templom sorrendben a harmadik, az első templomot angol királyi utasításra eredetileg 1697-ben az Anglikán Egyház számára emelték. A templomépület 1869-ig a város legmagasabb épületének számított. A következő évtizedekben körülötte megindult építkezések következtében a neogótikus, barna homokkőből épült templom már eltörpül a toronyházak között. Tornya 83 m magas. A templom tervezője Richard Upjohn, a XIX. század legnevesebb amerikai egyházi építészeinek egyike volt. A Trinity Church manhattani ingatlanvagyonával az Egyesült Államok leggazdagabb egyházközségei közé tartozik.
Története
Az első Szentháromság-templom
Az első, a Hudson folyó felé néző Szentháromság-templom épületét 1698-ban építették a Wall Streeten az Anglikán Közösség számára, első tiszteletese William Vesey volt, a közeli Vesey Street későbbi névadója lett. A földterület, melyen a templom felépült, eredetileg kert volt, majd temetkezési hely. 1705-ben Anna brit királynő adományával az egyházközséghez tartozó földbirtokot 215 acres (870 000 m2) területűre növelték. A templomépület az 1776-os, majdnem 400 épületet felégető New York-i tűzvészben elpusztult.
New York állam egyik 1784-ben megszavazott törvénye értelmében egyházuk továbbiakban már nem tartozott hűséggel az angol királynak. Whig patriótákat neveztek ki egyházi tisztségekre, így került 1784-től Samuel Provoost az egyházközség élére. Az Amerikai Egyesült Államok formálódó Episzkopális Egyháza 1787-ben Provoostot az újonnan alapított New York-i egyházmegye első püspökévé szentelte fel. Provoost a második templom 1790-ig történő felépítéséig a szertartásokat az egyházközséghez tartozó Szent Pál kápolnában tartotta.
A második Szentháromság-templom
A második Szentháromság-templom felépítése 1788-ban kezdődött, 1790-ben szentelték fel. A 200 láb magas, a Wall Street felé néző Szentháromság-templom politikailag is jelentős volt, G. Washington elnök, valamint kormányának tagjai gyakran vettek részt a szertartásokon.
A harmadik Szentháromság-templom
A harmadik, a jelenlegi Trinity Church építése 1839-ben kezdődött, 1846-ban lett kész. Ekkor New York legmagasabb épületeként neogótikus tornya, fölötte pedig az aranyozott kereszt uralta Lower Manhattan látképét. A templombelső színes üvegablakai az amerikai történelem kiemelkedő jeleneteit ábrázolják.
A Trinity Church az Egyesült Államok leggazdagabb egyházközségei közé tartozik. A terület, melyet Anna királynő a XVIII. század elején az egyházközségnek adományozott, felöleli a Broadwaytól nyugatra eső egész alsóvárosi részt. A Trinity tulajdonában levő telkeket északon a Christopher Street határolja, értékük csillagászati összegekben fejezhető ki.
A Trinity egyházközséghez tartoznak még a további New York-i kápolnák is: St. Augustine's, a St. Paul's, a St. Luke's, valamint a Governors Islandon levő St. Cornelius.
Szentháromság-templomkert
A Szentháromság-templomkertben az USA történelme számos nevezetes személyének sírhelye van. 1186 sírkő felirata közül 1018 még ma is olvasható. Itt nyugszik többek között William Bradford, a forradalmár újságíró az első Kongresszus hivatalos nyomdásza, Robert Fulton, a gőzhajó feltalálója (sírkövének reliefjét önarcképe nyomán készítették), Albert Gallatin városatya, Isaac Berryman kapitány, Hercules Mulligan, Washington elnök barátja és Francis Lewis, a Függetlenségi Nyilatkozat egyik aláírója, valamint Livingston polgármester.
A templomot körülvevő temetőben áll a bibliai figurákkal körülvett ún. Astor-kereszt. A kőkereszt tetején Mária ül gyermekével, a szobrok pedig a következők: Júda, Sém, Ádám, Éva, Ruth, Ábrahám, Jákob, Izsák, Énok, Dávid és Noé.
Ingatlan vagyon
Az 1780-as évektől Anna brit királynő 1705-ös 62 acres területű adományát az eredeti holland tulajdonosának leszármazottai perelték. A per alapja volt, hogy a hat örökösből csak öt adta át 1671-ben az angol koronának a birtokot. A hat évtized alatt indított perek mindegyikét elveszítették.
A plébánia egyik peres ügye során az egyházközség vagyonát 2011-ben körülbelül 2 milliárd dollárra értékelték, bár a Trinity Church az Anna királynő által adományozott földterület nagy részét ekkorra már eladta. A plébánia New York City egyik legnagyobb földtulajdonosa 14 acres területű manhattani ingatlanvagyonnal, beleértve 5,5 millió négyzetméternyi kereskedelmi területet is a Hudson Square-en. A plébániának az ingatlanvagyonából származó éves bevétele 2011-ben 158 millió dollár volt, a nettó jövedelme pedig 38 millió dollár, így valószínűleg a világ egyik leggazdagabb egyházközsége.
Galéria
Jegyzetek
További információk
Trinity Wall Street.org – Trinity Church hivatalos honlapja
Trinity Music Programs – Trinity Church zenei programjai a hivatalos honlapon
Trinity History – Trinity Church története
Trinity Real Estate – Trinity Church ingatlan holding hivatalos honlapja
Trinity sírkert és templomkert a hivatalos honlapon
Trinity Church digitális adatbázisa
Trinity Gift Shop – Trinity and St. Paul's Gift Shop
Trinity Preschool – Trinity Preschool
Manhattan
New York egyházi épületei
Neogótikus vallási építmények
Anglikán templomok
Wall Street
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4 hálószobás, 4 fürdőszobás eladó villa 695.00 m2 alapterületen. A telek mérete: 3500.00 m2. Ennek az ingatlannak a jellemzői: Riasztó rendszer, Medence, Terasz, Garázs, Kert, Tengerre Néző.
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Q: how to develop a widget for windows 7's start menu I want to develop a Google searcher for windows 7's start menu.
It means a widget for start menu to show Google search result for search pattern of start menu.
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#!/bin/bash
VERSION="0.4 [04 Feb 2016]"
BLOATALLOWDEFAULT=256
BLOATED=0
BACKSTEP=1
while getopts ":dhln:psvwz:" optname; do
case "$optname" in
"d") DEBUG="y";;
"h") HELP="y";;
"l") CHANGELOG="y";;
"n") BACKSTEP=$OPTARG;;
"p") USEPREVIOUS="y"; [[ $BACKSTEP -eq 1 ]] && BACKSTEP=2;;
"s") SAVE="y";;
"v") VERBOSE="y";;
"w") COLUMNS="9999";;
"z") DOLAST="$OPTARG";;
"?") echo "Unknown option $OPTARG"; exit 1;;
*) echo "Unknown error while processing options"; exit 1;;
esac
done
shift $(($OPTIND-1))
THIS=`basename $0`
COLUMNS=$(stty size 2>/dev/null||echo 80); COLUMNS=${COLUMNS##* }
[ -z "$QUIET" -o -n "$HELP" -o -n "$CHANGELOG" ] && echo -e "\n$THIS v$VERSION by Dominic (try -h for help)\n${THIS//?/=}\n"
if [ -n "$HELP" ]; then
echo -e "Checks for growth in size of rdiff-backup repositories at \
/home/*/[here] and /home/*/*/[here] since the last time $THIS was run. \
If the growth of any repository is greater in MiB than the value stored \
in the single-line file bloatwatch.daily in that repository's \
rdiff-backup-data subdirectory (default $BLOATALLOWDEFAULT) then a warning \
is shown and the program will exit with code >0.
$THIS is part of the TimeDicer Server software suite.
Usage:\t $THIS [options]
Options:
-h - show this help and quit
-l - show changelog and quit
-n [num] - compare repository sizes with sizes num backups ago (default: 1)
-p - instead of current repository sizes, bases for comparison are the sizes when $THIS was last run with -s; in this case the default -n option becomes 2
-s - save results
-v - verbose output
-z [name] - process any repositories with path containing text 'name' last
License: Copyright 2016 Dominic Raferd. Licensed under the Apache License, \
Version 2.0 (the \"License\"); you may not use this file except in compliance \
with the License. You may obtain a copy of the License at \
http://www.apache.org/licenses/LICENSE-2.0. Unless required by applicable \
law or agreed to in writing, software distributed under the License is \
distributed on an \"AS IS\" BASIS, WITHOUT WARRANTIES OR CONDITIONS OF ANY \
KIND, either express or implied. See the License for the specific language \
governing permissions and limitations under the License.
"|fold -sw $COLUMNS
fi
if [ -n "$CHANGELOG" ]; then
# changelog
[ -n "$HELP" ] && echo "Changelog:"
echo -e "\
0.4 [04 Feb 2016] - improve text output
0.3 [01 Feb 2016] - add -z option
0.2 [26 Jan 2016] - add -s, -p and -n options, change text output
0.1 [13 Jan 2016] - first version
"|fold -sw $COLUMNS
fi
[ -n "$HELP$CHANGELOG" ] && exit 0
[ -n "$DEBUG" ] && echo "Debug mode"
TMPF=$(mktemp)
[[ $(id -u) -eq 0 ]] || { echo "Must run as root or with sudo, sorry"; exit 1; }
[[ -n $VERBOSE ]] && echo -en "All sizes in Mebibytes\nObtaining locations of repositories in /home: "
find /home -mindepth 2 -maxdepth 4 -type d -name rdiff-backup-data|sed 's@/rdiff-backup-data$@@'|sort >$TMPF
[[ -n $DOLAST ]] && sed -i "/${DOLAST//\//\\/}"'/{H;d};${G;s/\n//}' $TMPF
[[ -n $VERBOSE ]] && echo "[OK]"
while read REPO; do
BFILE="$REPO/rdiff-backup-data/bloatwatch"
[[ ! -f $BFILE.log ]] && touch $BFILE.log
LOGLINETOT=$(<$BFILE.log wc -l)
if [[ -z $USEPREVIOUS ]]; then
SIZEM=$(du -sBM $REPO|awk -F "M" '{print $1}')
TIME_S=$(date +%s)
TIME_H=$(date +"%F %T")
elif [[ $LOGLINETOT -ge 1 ]]; then
# feed strings into read with <<<. feed documents with <<, feed commands with < <(...)
read SIZEM TIME_S TIME_H < <(tail -n1 $BFILE.log)
else
SIZEM=0
fi
if [[ $LOGLINETOT -ge $BACKSTEP ]]; then
PREV=( $(tail -n $BACKSTEP "$BFILE.log" | head -n1) )
GROWTH=$(($SIZEM-${PREV[0]}))
DAYS=$(( (($TIME_S-${PREV[1]}+10800)/86400) ))
[[ $DAYS -lt 1 ]] && DAYS=1
[[ $DAYS -eq 1 ]] && DAYTEXT="day" || DAYTEXT="days"
BLOATALLOW=$BLOATALLOWDEFAULT
[[ -s "$BFILE.daily" ]] && BLOATALLOW=$(cat "$BFILE.daily")
TEXT="$(printf "%+.0f" $GROWTH) in $DAYS $DAYTEXT, $SIZEM total, ${PREV[2]} ${PREV[3]} to $TIME_H - $REPO"
if [[ $(( $GROWTH/$DAYS )) -gt $BLOATALLOW ]]; then
echo "$TEXT >${BLOATALLOW}/day:[WARN]"; let BLOATED++
elif [[ -n $VERBOSE ]]; then
echo "$TEXT <${BLOATALLOW}/day:[OK]"
fi
elif [[ -n $VERBOSE ]]; then
echo " - no previous bloatwatch entry found: [OK]"
fi
[[ -n $SAVE && -z $USEPREVIOUS ]] && echo "$SIZEM $TIME_S $TIME_H" >>"$BFILE.log"
done <$TMPF
[[ -n $DEBUG ]] && echo "Retained temp file $TMPF" || rm $TMPF
[[ $BLOATED -gt 0 || -n $VERBOSE ]] && echo "$BLOATED repositories have grown alarmingly..."
exit $BLOATED
|
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The ABCs of Media and Children: Attention, Behavior, and Comprehension
Ellen A. Wartella, Alexis R. Lauricella, Leanne Beaudoin-Ryan, and Drew P. Cingel
This is an advance summary of a forthcoming article in the Oxford Research Encyclopedia of Communication. Please check back later for the full article. Children are and have been active media users for decades. Historically, the focus on children and media issues have centered on the concerns and consequences of media use, generally around violence. In the last 40 years, we have seen a shift to study children and media from a more holistic approach, to understand both the positive and negative relationships between children and media use. Further, the recognition of the very important developmental differences that exist between children of different ages and the use of grand developmental theories, including those by Piaget and Vygotsky, have supported the field's understanding of the unique ways in which children use media and the effects it has on their lives. Three important constructs related to a more complete understanding of children's media use are the ABCs (attention, behavior, and comprehension). The first construct, attention, focuses on the way in which children's attention to screen media develops, how factors related to parents and children can direct or influence attention to media, and how media may distract attention. The second construct is the behavioral effect of media use, including the relationship between media use and aggressive behavior, but importantly, the positive effect of prosocial media on children's behavior and moral development. Finally, the third construct is the important and dynamic relationship between media and comprehension and learning. Taken together, these constructs describe a wide range of experiences that occur within children's media use.
Absent Information in Integrative Environmental and Health Risk Communication
Jari Lyytimäki and Timo Assmuth
Communication is typically understood in terms of what is communicated. However, the importance of what is intentionally or unintentionally left out from the communication process is high in many fields, notably in communication about environmental and health risks. The question is not only about the absolute lack of information. The rapidly increasing amount and variability of available data require actors to identify, collect, and interpret relevant information and screen out irrelevant or misleading messages that may lead to unjustified scares or hopes and other unwanted consequences. The ideal of balanced, integrative, and careful risk communication can only rarely be seen in real-life risk communication, shaped by competition and interaction between actors emphasizing some risks, downplaying others, and leaving many kinds of information aside, as well as by personal factors such as emotions and values, prompting different types of responses. Consequently, risk communication is strongly influenced by the characteristics of the risks themselves, the kinds of knowledge on them and related uncertainties, and the psychological and sociocultural factors shaping the cognitive and emotive responses of those engaged in communication. The physical, economic, and cultural contexts also play a large role. The various roles and factors of absent information in integrative environmental and health risk communication are illustrated by two examples. First, health and environmental risks from chemicals represent an intensively studied and widely debated field that involves many types of absent information, ranging from purposeful nondisclosure aimed to guarantee public safety or commercial interests to genuinely unknown risks caused by long-term and cumulative effects of multiple chemicals. Second, light pollution represents an emerging environmental and health issue that has gained only limited public attention even though it is associated with a radical global environmental change that is very easy to observe. In both cases, integrative communication essentially involves a multidimensional comparison of risks, including the uncertainties and benefits associated with them, and the options available to reduce or avoid them. Public debate and reflection on the adequacy of risk information and on the needs and opportunities to gain and apply relevant information is a key issue of risk management. The notion of absent information underlines that even the most widely debated risk issues may fall into oblivion and re-emerge in an altered form or under different framings. A typology of types of absent information based on frameworks of risk communication can help one recognize its reasons, implications, and remediation.
A Case Study of Sesame Workshop's Cleaner, Happier, Healthier Intervention in Bangladesh, India, and Nigeria: Reporting on Exposure and Impact
Dina L. G. Borzekowski
The Cleaner, Happier, Healthier hygiene intervention was developed and tested in 2013, featuring the Sesame Workshop characters. Through broadcast television, four public service announcements (PSAs) addressed washing hands with soap, using a latrine, wearing sandals, and drinking clean water. The main audiences were young preschool children and their parents or guardians. Research occurred in Bangladesh, India, and Nigeria, exploring the reach and impact of these PSAs. Although low percentages, from well-drawn samples of extremely vulnerable populations in these countries, reported awareness and recall of these messages, such percentages can reflect large numbers of viewers. Considering data from the participating children, measures of knowledge and attitudes were associated with engaging in several of the behavioral outcomes. As well, awareness and recall of the PSA messages predicted "all the time" for several of the hygiene behaviors. In contrast, parents' reports of PSA awareness and recall were not associated with reports of children's hygiene behaviors. Conducting reach studies is extremely difficult, especially in developing countries and communities. Despite the challenges, this study is encouraging. Participants reported seeing the messages, and in several models, this "reach" predicted reports of hygiene and health behaviors. Lessons learned from this case study and research can offer valuable insight into the production of future health PSAs, especially with harder-to-reach populations.
A Case Study: Targeting the Stop.Think.Connect. Cybersecurity Campaign to University Campuses
Matthew W. Savage, Sarah E. Jones, Jenna E. Reno, and Shari Veil
University students, faculty, and staff are among those most vulnerable to cybersecurity risks due to their reliance on modern technologies, the nature of their online activities, and the open infrastructure of institutional networks. Furthermore, cyberbullying has emerged as a public health concern by the Centers for Disease Control and Prevention (CDC), which first warned of electronic aggression in 2008, or any type of harassment or bullying that occurs via email, chat, instant messaging, websites, blogs, or text messaging. Roberto and Eden emphasized the communicative nature of cyberbullying, defining it as the "deliberate and repeated misuse of communication technology by an individual or group to threaten or harm others" in 2010 (p. 201). In response to serious cybersecurity concerns and growing evidence of cyberbullying behavior, the national Stop.Think.Connect. (STC) campaign was developed to educate Americans on cybersecurity risks and equip citizens with tools for safe, respectful, and appropriate online behavior; however, it lacks targeted messaging for those on university campuses. Formative research is needed to ascertain the specific cybersecurity risks and challenges identified by those living and working on large university campuses. Research by Noar in 2006 demonstrates that formative evaluation leads to more successful campaigns. The process involves learning about target populations, discovering communicative determinants of behavior change, and testing message concepts. To that end, this case study is a first step in targeting STC campaign messages to university students, faculty, and staff. Specifically, we sought to identify the distinct cybersecurity needs faced by university students and personnel, their perceptions of the saliency of the problem, and potential motives for increasing their cybersecurity-enhancing behaviors. These activities are needed to implement the campaign on college campuses and to increase the likelihood of any future outcome evaluation efforts that yield evidence of campaign effectiveness. Currently, we are unaware of any outcome evaluation. Focus group methodology was conducted to examine the target audiences' knowledge, interests, needs, and attitudes regarding the management of cybersecurity threats. Additionally, practical recommendations for enhancing STC campaign implementation on university campuses were ascertained. Results emphasized key ways to improve the theoretical underpinnings of the campaign using the Integrated Behavioral Model (IBM). We identified how determinants of behavior change can be utilized to strengthen campaign messaging. Students displayed laissez-faire attitudes toward cybersecurity, while faculty and staff attitudes demonstrated a much higher level of concern. Social norms for personal cybersecurity action taking were notably low among students as well as faculty and staff. Students displayed limited personal agency in regards to enacting cybersecurity measures, while faculty and staff had greater knowledge of steps they could take, but little faith that these actions would be efficacious. Finally, thematic recommendations for implementing an effective cybersecurity campaign on a university campus were identified.
Accountability in Journalism
Susanne Fengler
In the past decade, academic and professional debates about media accountability have spread around the globe – but have done so in a fundamentally different framework. In many Western democracies, trust in media – along with trust in politics and trust in institutions – as eroded dramatically. Fundamental shifts regarding the patterns of media use and the structure of media and revenue markets have made media and journalism more exposed to criticism from various stakeholders, and more vulnerable to the strategic influence of national and international actors. While many "Western" media professionals have reacted to these challenges to its credibility by new initiatives to demonstrate accountability and transparency, policy makers in other countries even in the "Global North" have tightened their grip on independent media and gradually weakened the concept of self-control. At the same time, an ongoing democratization in many parts of the world, along with a de-regulation of media markets, has created a growing demand for self-regulation and media accountability in countries formerly characterized by rigid press control. Claude-Jean Bertrand defined the development and current structures of accountability in journalism as "any non-State means of making media responsible towards the public." Key aims of media accountability are "to improve the services of the media to the public; restore the prestige of media in the eyes of the population; diversely protect freedom of speech and press; obtain, for the profession, the autonomy that it needs to play its part in the expansion of democracy and the betterment of the fate of mankind." Journalists and news outlets have a wide array of responses to professional, public, and political criticisms via press councils, ombudsmen, media criticism, and digital forms of media accountability, while online and offline media accountability instruments have distinct traditions in different media systems and journalism cultures.
Acculturation and Intergroup Communication
Richard Y. Bourhis
Acculturation is the process of bidirectional change that occurs when two ethnolinguistic groups come in sustained contact with one another. Acculturation usually occurs between groups of unequal power, status, and demographic background. At stake for the unity of multilingual states are intergroup relations between language minorities and majorities that yield harmonious to conflictual outcomes. The Interactive Acculturation Model (IAM) is adapted to intergroup relations between language communities in four parts. The first part of the model provides an overview of the ethnolinguistic vitality framework accounting for the strength of minority/majority language communities as they struggle to gain the institutional support they need to develop as distinctive and thriving language communities. The second part of the IAM offers an analysis of the pluralist, civic, assimilationist, and exclusionist ideologies that underpin language policies regulating the co-existence of minority/majority language communities. The third part examines the acculturation orientations endorsed by majority and minority language group speakers. The fourth part of the IAM proposes that the interaction of majority and minority acculturation orientations yield intergroup communication outcomes that may range from harmonious, problematic, to conflictual. Taken together, the IAM model offers a conceptual tool for analyzing the fate of linguistic minorities as they seek to survive in the dominant majority group environments of post-modern globalizing states.
Accuracy in Journalism
Accuracy is a central norm in journalism and at the heart of the journalistic practice. As a norm, accuracy developed out of objectivity, and has therefore an Anglo-American origin. Nevertheless, the commitment to the rule of getting it right is shared among journalists across different journalistic cultures. The history of accuracy is closely related to other central concepts in journalism like truthfulness, factuality and credibility, because it raises epistemological questions of whether and how journalism is capable of depicting reality accurately, truthfully and based on fact. Accuracy plays a particularly important role with regard to the factuality of the journalistic discourse, as it forces journalists not only to ground their reporting on facts, but to check whether presented facts are true or not—which is reflected both in the description of the journalistic profession as the discipline of verification as well as the central relevance of accuracy for instruments of media self-regulation like press councils and codes of ethics. Accuracy is an important standard to determine the quality of the news reporting. In fact, many studies, most of them carried out Western democracies, have investigated the accuracy of journalistic reporting based on the number of errors that sources mentioned in the articles perceived. As journalism moved online and the immediacy of the news cycle requested a faster pace of publication, news outlets often adopted the strategy to publish first and to verify second, although research has shown that the accuracy of journalistic reporting and trustfulness are related. Especially in the current debate on disinformation, many online fact-checking and verification services have thus seen a global rise of attention and importance.
Active Involvement Interventions in Health and Risk Messaging
Kathryn Greene, Smita C. Banerjee, Anne E. Ray, and Michael L. Hecht
Results of national epidemiologic surveys indicate that substance use rates among adolescents remain relatively steady or even show slight declines; however, some substance use rates, such as electronic cigarettes, are actually rising. Thus, the need for efficacious drug prevention efforts in the United States remains high. Active Involvement (AI) interventions are a promising avenue for preventing and reducing adolescent substance use, and they create opportunities for adolescents to experience a core feature of engagement that is common to these interventions, such as producing videos, posters, or radio ads; or generating themes and images for messages such as posters. Existing interventions grounded in theories of Active Involvement include programs delivered face-to-face and via e-learning platforms. Narrative Engagement Theory and the Theory of Active Involvement guide the components of change in AI interventions. Youth develop message content during participation in Active Involvement interventions. Advanced analytic models can be applied to address new research questions related to the measure of components of AI interventions.
Actor-Network Theory and Journalism
Victor Wiard
Actor-network theory (ANT) is a sociological approach to the world that treats social phenomena as network effects. This approach focuses on the evolution of interactions within networks over time and is useful for studying situations of change, unsettled groups, and evolving practices such as current developments in the world of journalism. Journalism is a messy and complex social practice involving various actors, institutions, and technologies, some of which are in a state of crisis or are undergoing rapid change due to digitization. ANT has gained momentum in journalism studies among researchers analyzing journalists' relationships with the diverse agents they in contact with on a daily basis (e.g., technologies, institutions, audiences, other news producers) and the relationships between news production, circulation, and usage. ANT practitioners use a set of simple concepts referred to as an infra-language, which allows them to exchange ideas and compare interpretations while letting the actors they are studying develop their own range of concepts (i.e., to speak in their own words). These concepts include actants, actor networks, obligatory passage points, and translation. ANT also proposes a set of principles for researchers to follow. These include considering all entities as participants in a phenomenon (e.g., people can make other people do things, and objects, such as computers or institutions, can as well) and following actors as they trace associations with others. Therefore, journalism scholars who use this approach conduct qualitative studies focusing on the place of a particular technology within a network or situation by following who and what is involved and how entities connect. They collect data such as the content produced, direct observations of news production, or statements from interviews during or after the case is over. Using ANT, journalism scholars have extended their comprehension of news production by highlighting technology's role in journalistic networks. Although journalists naturalize technologies through daily use (e.g., search engines, content management systems, cell phones, cameras, email), these tools still influence journalistic practices and outputs. ANT practitioners also consider the diversity of agents participating in news production and circulation: professional journalists, politicians, activists, and diverse commercial and noncommercial organizations. If this diversity is becoming more active and connected in this networked environment, it seems that legacy media is still an obligatory passage point for anyone willing to bring information to the general public. Recent societal changes, such as the generalization of news consumption on smartphones and the rise of platform journalism on multiple apps, indicate that ANT may be useful in the collective endeavor to provide a clear picture of what journalism is and what it will become.
Adherence and Communication
Teresa L. Thompson and Kelly Haskard-Zolnierek
Patient adherence (sometimes referred to as patient compliance) is the extent to which a patient's health behavior corresponds with the agreed-upon recommendations of the healthcare provider. The term patient compliance is generally synonymous with adherence but suggests that the patient played a more passive role in the healthcare professional's prescription of treatment, whereas the term adherence suggests that the patient and healthcare professional have come to an agreement on the regimen through a collaborative, shared decision-making process. Another term related to the concept of adherence is persistence (i.e., taking a medication for the recommended duration). Some patients are purposefully or intentionally nonadherent, whereas others are unintentionally nonadherent due to forgetfulness or poor understanding of the regimen. Patients may be intentionally nonadherent because of a belief that the costs of the regimen outweigh the benefits, for example. Nonadherence behaviors in medication taking include never filling a prescription, taking too much or too little medication, or taking a medication at incorrect time intervals. Patient adherence is relevant not only in medication-taking behaviors, but also in health behaviors such as following a specific dietary regimen, maintaining an exercise program, attending follow-up appointments, getting recommended screenings or immunizations, and smoking cessation, among others. A number of factors predict patient adherence to treatment, but the relationship between provider-patient communication and adherence to treatment will be stressed. Focusing on recent research, the article examines the concept of patient adherence, describes how provider-patient communication can enhance patient adherence, explains what elements of communication are relevant for adherence, and illustrates how interventions to improve communication can improve adherence.
Advertisers as Agents for Change in Health and Risk Messaging
Michael Mackert and Marie Guadagno
Advertising as a field and industry often has a contentious relationship with both health communication and public health due to legitimate concerns about how advertising for certain products, such as alcohol and tobacco, could contribute to less-healthy decisions and behaviors. While acknowledging such concerns, advertisers and their approach to solving communication problems could also provide valuable lessons to those working in health communication. Indeed, advertising agencies are designed to develop creative and effective messages that change consumer behavior—and health communication practitioners and scholars aim to change population-level behavior as well. The perspective and approach of the account planner in the advertising agency—a role whose chief responsibility is to bring the consumer perspective into every step of the advertising development process and inspire effective and creative campaigns—would be particularly valuable to those working in health communication. It was account planning work that shifted traditional milk advertising from promoting it as a healthy drink to the iconic "got milk?" campaign, which positioned milk as a complement that makes other food better—an approach that drove positive sales after years of declining milk consumption. Yet many who work in health communication and public health often know little of how advertising agencies work or their internal processes that might be productively adopted. This lack of understanding can also lead to misperceptions of advertisers' work and intentions. As an example, one might assume dense medical language in prescription drug advertising is intended to add unnecessary complexity to the advertisements and obscure side effects; instead, advertising professionals who work on prescription drug advertising have often been trained on clear communication—but cannot fully utilize that training because of regulations that require medically accurate terminology that might not be comprehensible to most viewers. Improved understanding of how advertisers can act as agents of change, and increased dialogue between the fields of advertising and health communication, could contribute to improved health communication research, practice, and policy.
Advertising and Journalism
Corinna Lauerer
News is produced primarily to inform readers and viewers. However, audiences are charged only a fraction of the high production costs or not asked to pay at all. The reason is subsidy by advertising revenue. Since the beginning of professional journalism, news has been bundled with advertisements. This way, media companies can sell the attention of audiences attracted by journalistic content to advertising companies, which in return seek to attract consumers to their products and brands. Beyond distributing both simultaneously, advertising and journalism can intermingle, which causes ethical concerns. From a normative point of view, news and advertisements should be separated clearly in regard to the production process and the content itself. The separation of "church and state" or the "Chinese Wall" between the newsroom and the business side within a media company are commonly used metaphors used to express the ideal of separation. This principle aims to protect journalistic autonomy from economic influences such as advertising considerations. Nevertheless, advertising interests may influence journalism in different forms and to various degrees. They are regularly discussed as influence on journalistic selection of topics as well as writing style, and as the source of attempts to blend advertising and editorial content. Scholarly concerns are increasingly consumer oriented and less critical journalism, biased reporting on advertisers' brands or products, and the potential deception of audiences, for example, when hybrid forms of advertising such as native ads camouflage their commercial nature. The relationship between journalism and advertising has been treated as an orphan compared to the relationship to public relations or politics. However, the media organizations' struggles for sustainable business models in the 21st century fuel discussions in media economics and journalism studies about whether advertising is a blessing or curse to journalism. In a nutshell, the relationship between advertising and journalism is as long-standing as it is ambivalent (see "Evolution of the Relationship"). On the one hand, advertising revenue largely lays the financial foundation for prospering professional journalism (see "Funding Journalism"). On the other hand, this financial dependency causes potential threats to journalistic autonomy (see "Influencing Journalism").
Advertising and Persuasion
Kevin D. Thomas
This is an advance summary of a forthcoming article in the Oxford Research Encyclopedia of Communication. Please check back later for the full article. When discussing the relationship between advertising and persuasion the focus typically centers on the intended effects of advertising, which include increasing brand awareness, piquing brand interest, promoting brand use, and fostering brand loyalty. As such, the impact of advertising and persuasion is generally discussed in terms of market metrics. Did the advertising campaign lead to increased brand awareness, more favorable attitudes toward the brand, or increased consumer trial or retention? Structuring the relationship between advertising and persuasion in such a narrow fashion dismisses the broad array of unintended social effects associated with advertising, such as how race, gender, class, and sexuality are perceived and lived. While the goals of advertising explicitly exist within the realm of marketplace economics, its pervasive use of cultural symbols as a tool of persuasion squarely places it beyond the confines of mere business logic and in the domain of social learning. So while the messages communicated by advertisers are deliberately designed to impact how individuals relate to brands, those same messages also influence how individuals perceive themselves and relate to each other. Given the ways in which advertising serves as a marketing tool and socialization agent, the depth and breadth of its persuasive reach can only be understood when the intended and unintended effects of its output are examined in tandem.
Advice: Communicating to Support and Influence
Erina MacGeorge and Lyn Van Swol
Advice is a recommendation for action that includes both suggestions for behavior and ways of feeling and thinking about the problem. It is a ubiquitous phenomenon in personal and professional settings, and functions as a form of both social support and social influence. Advice often improves coping and decision-making outcomes but can also be perceived as intrusive, threaten recipient's sense of competence and autonomy, and damage relationships. Although advisors often have expertise that can benefit the recipient, advice recipients often discount and underutilize advice, to their disadvantage. Recipients are more likely to utilize advice from advisors they trust, who engender confidence, and who have more expertise or experience. They are also more likely to seek and use it when they have not thought of solutions independently. Recipients who are overconfident, have more expertise, or have more power than an advisor are much less likely to seek and utilize advice. When giving advice, advisors often consider different factors than they would if they were making decisions for themselves, resulting in advice that is more normative and less tailored to individual preferences. Advice can be delivered in a variety of ways, and this stylistic variation has consequences for recipient outcomes. For example, highly direct or blunt forms of advice underscore the advisor's implicit claim to status and often generate more negative evaluations of the advice and advisor. Advice message content also influences recipients' advice evaluation. Content that emphasizes efficacy of the action, feasibility, and limitations of the advice tends to improve evaluation and utilization of advice. This research is synthesized in advice response theory (ART), which indicates that advice outcomes are influenced by message content and style, interaction qualities, advisor characteristics, recipient traits, and features of the situation for which or in which advice is sought. Behaviors that co-occur with advice, such as argumentation, emotional support, and planning, also influence outcomes. The sequencing of advice in interaction also matters; the integrated model of advice (IMA) indicates that advice in supportive interactions is best placed after emotional support and problem analysis. The contexts in which advice are given influence the exchange and outcomes of advice. These include personal and professional relationships, in which relational cognitions and professional norms affect the process and outcomes of advising; groups and organizations, in which advising processes become complex due to the multiplicity of relationships, goals, and expectations; cultures, in which advice-seeking and advice-giving varies in perceived appropriateness; and digital environments, which are often valued for advice that is unobtainable elsewhere.
Advocacy Groups as Agents for Change in Health and Risk Messaging
Jen Ptacek, Kirstin N. Dolick, and Marifran Mattson
Advocacy can be defined as the systematic process set in motion by an individual or group of individuals to encourage, support, and empower others surrounding a topic in need of change. Individuals may become an advocacy group in support of an issue, such as health care, civil rights, environment, or labor. Advocacy groups often serve as mediators between vulnerable/underprivileged populations and policymakers or decision-makers. The Health Communication Advocacy Model (HCAM) is a tested advocacy model comprising five phases including assembling the team, formative research, message development, message implementation, and evaluation. HCAM also includes a correction loop allowing for revisions of campaign messages. The HCAM is an adaptable model that offers a perspective in which advocacy groups may be considered a dynamic framework for building successful campaigns. Once the advocacy group is established, members can agree upon goals and responsibilities and craft a position statement. The group can then develop messages to reach the intended target audience(s). Target audiences may include legislators, the population affected by the issue, and media organizations. When crafting messages, care should be taken to ensure messages are stimulating, motivational, culturally consistent, resource contingent, and without barriers. Advocacy groups may use a number of channels to send messages through, such as social media, rallies, press releases, and other media outlets. Overall, advocacy groups must address a variety of needs to effectively reach the target audiences and impact change.
Advocacy Journalism
Ingrid Bachmann Cáceres
A contested term with defenders and critics, advocacy journalism refers to a genre of journalism that combines reporting with a point of view. With roots as far as the origins of journalism itself, as a contemporary practice it can be found—to varying degrees—in all kinds of media outlets across the globe. Its key premise is that journalists participate in the mass-mediated public sphere and that their work deliberately and transparently stands for specific perspectives, with stories actively championing for certain ideas and values. While some authors have labeled advocacy as the binary opposite of objective (factual) reporting, in recent decades several journalism scholars and practitioners have argued that this is not the case, and that advocacy and informing are not necessarily mutually exclusive. At the core of this discussion are normative considerations of how journalism should be, the role of objectivity in news reporting, and professional models shaping news cultures and news content in different regions. Ethical concerns are also common arguments in this debate. Advocate journalists do not necessarily dismiss objectivity—although some do—and insist they adhere to professional standards nonetheless, since they still do journalism rather than propaganda. Promoters of advocacy also argue that having a situated viewpoint is more transparent, whereas critics argue against what they deem news reporting with an agenda or promoting an ideological campaign. More recently, advocacy journalism has been adopted—and adapted—by nongovernmental organizations and civic movements, which highlights the constant redefinitions of journalism practice outside of legacy media and traditional contexts.
A Fanonian Philosophy of Race
Armond Towns
Frantz Fanon was one of the most important voices in decolonial and black liberation struggles of the mid-20th century. Writing about race and colonialism in Martinique, France, and Algeria, he articulated the importance of blackness to Western frameworks of the human. The black studies scholarship influenced by Fanon has continued in a similar vein, arguing that much of modern, Western thought either does not discuss race at all or considers race as an add-on to the larger discussion of Western subjectivity. Alternatively, Fanon and his interlocutors argue that race is the central function of the larger fields of Western philosophy and science, even if race is not mentioned at all. To make this claim, they largely point toward two tendencies in Western thought. First, Fanon and his interlocutors often examine the centrality of time and space in modern Western philosophy. Indeed, much of Western philosophy and science has implicitly and explicitly examined time as a linear trajectory that is largely monopolized by the Western European and North American white male subject; alternatively, space has been theorized as the static and nondynamic measure of the Western subject's capacity to progress. Second, Fanon and his interlocutors also critically interrogate the related discussion of mutual recognition that is assumed in much of Western thought. As such, Western thinkers have often contended that, historically, the self recognizes itself in the other, and vice versa, and that self/other relationship is the basis for concepts of subjectivity. Yet, Fanon and his interlocutors have also pointed out that the lack of recognition of black people as human or as subjects has done little to foreclose whiteness as the position overrepresented as the human. Rather than recognition, white people have historically enacted racial violence against black bodies as a central mode through which to enter into humanity. As such, time and space and the lack of recognition as outlined by Fanon and his interlocutors suggest that nonwhite bodies have always provided a crisis for Western concepts of universality and subjecthood.
Affect in Critical Studies
Brian L. Ott
Affect has historically been conceptualized in one of two dominant ways. The first perspective, which has its roots in psychology and neuroscience, tends to view affect as an elemental state. This tradition is reflected in Silvan S. Tomkins's theory of primary affects and Antonio Damasio's theory of basic emotions. Recent extensions of this tradition include the work of Eve Kosofsky Sedgwick, Lisa Cartwright, and Teresa Brennan. The second perspective, which is typically associated with developments in philosophy and the humanities, treats affect as an intensive force. This tradition, whose most famous proponent is Gilles Deleuze, is evident in Brian Massumi's theory of autonomous affect and Nigel Thrift's non-representational theory. Recent extensions of this tradition tend to emphasize the importance of materiality, or what Jane Bennett has called "thing-power." A number of scholars working in communication and cultural studies have created a third, hybrid tradition that attempts to bridge or mediate the two dominant historical accounts. This third perspective includes Lawrence Grossberg's notion of affective investments, Christian Lundberg's Lacanian-inspired view of affect, Sara Ahmed's work on the sociality of emotion, and Gernot Böhme's theory of atmospheres.
Affection Exchange Theory
Kory Floyd and Benjamin E. Custer
Affectionate communication constitutes verbal behaviors (e.g., saying "I love you"), nonverbal gestures (e.g., hugging, handholding), and socially supportive behaviors (e.g., helping with a project) that humans employ to develop and maintain close relationships with others. In addition to its relational benefits, affectionate communication contributes to health and wellness for both senders and receivers. Affection exchange theory (AET) addresses the questions of why humans engage in affectionate communication and why diverse benefits are associated with such behaviors. A robust empirical literature supports AET's contention that both expressing and receiving affectionate behavior are associated with physical and mental health benefits. Despite these contributions, however, some compelling questions about affectionate communication remain to be addressed, and AET can provide a useful framework for doing so.
Agenda Setting and Journalism
Sebastián Valenzuela
People use the news media to learn about the world beyond their family, neighborhood, and workplace. As news consumers, we depend on what television, social media, websites, radio stations, and newspapers decide to inform us about. This is because all news media, whether through journalists or digital algorithms, select, process, and filter information to their users. Over time, the aspects that are prominent in the news media usually become prominent in public opinion. The ability of journalists to influence which issues, aspects of these issues, and persons related to these issues, are perceived as the most salient has come to be called the agenda-setting effect of journalism. First described by Maxwell McCombs and Donald Shaw in a seminal study conducted during the 1968 elections in the United States, agenda-setting theory has expanded to include several other aspects beyond the transfer of salience of issues from the media agenda to the public agenda. These aspects include: the influence of journalism on the attributes of issues and people that make news; the networks between the different elements in the media and public agendas; the determinants of the news media agenda; the psychological mechanisms that regulate agenda-setting effects; and the consequences of agenda setting on both citizens' and policymakers' attitudes and behaviors. As one of the most comprehensive and international theories of journalism studies available, agenda setting continues to evolve in the expanding digital media landscape.
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{"url":"https:\/\/electronics.stackexchange.com\/questions\/172550\/capacitor-and-inductor-power-factor","text":"# Capacitor and inductor power factor\n\nI need an explanation about the leading and lagging power factor at electron level.\n\nCase1:\nIn a inductor it has the lot of free electrons are ready to move when we applied a voltage(AC or DC). If we apply a alternating voltage to a inductor, a change in current with respect to time is passing through it. According to induction principle, a change in current produce a change in magnetic field. So that a change in magnetic field produce a induced emf. This emf opposes the change in current wich was supplied by a alternating potential and which was causes of that emf.\n\nHere My first question is for inductor: How the electron flow lags behind the supply voltage?\n\nCase2:\nFor a capacitor there is a dielectric medium between two plates. The dielectric medium itself has the randomly oriented dipoles. So that the net electrostatic force is zero. When we apply a potential between these two plates, the potential start to align the randomly oriented dipole's positive sides towards in which plate the electrons are accumulated and the negative sides of the dipole towards in which plate the electrons are pulled away.\n\nHere My question for capacitor is: How the electron flow (current) leads the voltage?\n(according to electrical laws potential only causes of electron flow. So without a potential the electron flow doesn't possible. How the electron flow leads the voltage in capacitor?)\n\n\u2022 Please consider using some proper formatting and consistent lower\/uppercase for future questions. I improved it a bit. \u2013\u00a0Rev1.0 May 27 '15 at 7:57\n\nFor an inductor, how does the electron flow (current) lag behind the supply voltage?\n\nIn an inductor which has no magnetic field already established, the application of electricity initially sees an open circuit (little current flow.) As the magnetic field builds, the current also builds, and it eventually behaves like a solid conductor (full current flow.) So the current lags the supply voltage due to the delay in establishing the magnetic field.\n\n(If you then instantly disconnect the inductor, the magnetic field will collapse in reverse as quickly as it can. With no resistance to slow it down, dv\/dt dictates that the voltage will go exponentially high. This is called \"inductive kickback\" and can be problematic, even dangerous.)\n\nFor a capacitor, how does the electron flow (current) lead the voltage?\n\nIn a discharged capacitor, the potential (electric field) between the two plates is nothing, so no current flows. Application of any electricity initially sees a short circuit (full current flow.) As the plates start charging up, the current decreases, and eventually behaves like an open circuit (little current flow.) So the current leads the supply voltage due to the delay in establishing the electric field.\n\n(If you then instantly disconnect the capacitor, the electric field remains static, like static electricity. It may remain there for years, ready to zap you, such as in older televisions and radios.)\n\nThe key similarity between the two is that it takes time for magnetic fields to build\/collapse and plates to charge\/discharge; this delay creates an imbalance between the voltage and current measured at each device... and we call the ratio of this \"Power Factor.\"\n\nLet's assume a sinusoidal voltage source.\n\nCase1:\n\nAt the start of the AC cycle there is a rapidly increasing voltage. This tries to push current through the coil. As the current rapidly increaces this creates a changing magnetic field. This creates an emf which opposes the very change in current (as you rightly said). This emf pushes electrons back in the opposite direction. This is what essentially leads to the lagging current.\n\n1. initially the change is voltage is maximum, this creates a large back emf and hence a large current is \"pussed back in the opposite direction\"\n\n2. As the voltage approaches its maximum the change in voltage is minimal and hence the back emf is minimal, and hence this backward current ceases to flow.\n\n3. Now the change in emf becomes negative and hence it pushes the electrons in the forward direction. Hence forwards currents start to flow\n\nIf you plot this you will see that a sinusoidal input leads to a lagging output because the voltage is proportional to the change in current.\n\n$$v_L=L\\frac{di}{dt}$$\n\nCase 2:\n\nSimilarly for a capacitor the current is proportional to the change in voltage. Therefore initially when the change in voltage is maximum the current passed around the circuit will be maximum. Now since the plates are saturated with charge adding more becomes difficult and the current flow decreases. As the voltage becomes maximum the current through the circuit becomes zero as the change in voltage is also zero.\n\n$$i_c=C\\frac{dv}{dt}$$\n\nThe electrons (or current) do not physically \"lag\" the voltage (in an inductor). This is because the voltage is proportional to derivative of current: $$U = -\\frac{di}{dt} \\times L$$\n\nPlease consider DC: the current does not change, so there is no voltage drop on the inductor terminals. If you have current that changes, but not in sinusoidal way, the voltage drop is proportional to the current. For example, if current applies to the formula $i(t) = 5 + 2 \\times t$ (in Amps), the voltage drop would be constant, 2 Volts (even if the current increases to infinity), multiplied by L.\n\nThe AC is just a special case which takes into account that a derivative of sin function is the cos function and vice versa (with or without the minus sign). If the current would be $i(t) = 5 + 2 \\times \\sin(\\omega\\times t)$ the voltage would be $v(t) = -L \\times \\frac{di}{dt} = -L \\times 2 \\times \\omega \\times \\cos(\\omega \\times t)$.\n\nBecause both voltage and current have the same frequency ($\\omega$), we can compare them (for example using complex numbers) and it looks like the current is behind the voltage (ie. it is lagging), but it only applies to ac.\n\nIn my opinion, when you use this method, it is not possible to understand the phenomenon on the electron level in other way you did. The complex numbers do not exists in real world, it is just a mathematical method of calculation, correct for this particular case only (ie. for sinusoidal alternating current). You explained correctly that currents makes the magnetic flux which then causes a voltage drop and this is all to be understood.\n\nIf you take any changing current and represent it with a Taylor series (see Fourier transform, Fourier series and relative articles), you may perform the calculations for any harmonic ($n \\times \\omega$, with n being consecutive integers), on its complex plane, however you can't merge planes for different harmonics.\n\nThe Fourier method also is a mathematical tool, but of course the inductor does not \"know\" it should calculate harmonics for every signal it reads.\n\nFor capacitor the same applies.\n\n(I don't know how to insert formulas, could anybody please edit my text?)\n\nPartial answer regarding the capacitor, maybe later I can add the inductor.\n\nInitially the capacitor is 'empty': the dielectric medium's dipoles are randomly (un)aligned. Now if you apply a sinusoidally alternating voltage to the plates, the plates need to be populated by electrons (and on the opposite side a lack thereof?).\n\nIn order to populate the plates with charge, per definition a current needs to flow. That is basically the transport of the charged particles to\/from the plates.\n\nIf you have a capacitor with capacity $$\\C\\$$, then for every volt across the plate you need to populate with $$\\Q=CV\\$$ charge. For a constantly increasing voltage, lets say $$\\\\frac{dU_C}{dt}\\$$, you constantly need to increase the amount of charge on plates in order for the voltage to rise constantly. For a rise in voltage $$\\\\frac{dU_C}{dt}\\$$ you need a flow of $$\\C\\frac{dU_C}{dt}\\$$ of charge to the plates. This is a DC current, say, $$\\I_C\\$$.\n\nNow, if you apply a changing, but not constantly increasing, voltage to the plates, the flow of charge will obey the same law: $$\\I_C(t)=C\\frac{dU_C}{dt}\\$$. Hence when you apply a sinusoidally alternating voltage $$\\U_C(t)=U.sin(\\omega t)\\$$, the current to the capacitor will be $$\\I_C(t)=CU\\frac{dsin(\\omega t)}{dt} = \\omega CUcos(\\omega t) \\$$, which is leading the voltage. This is understandable as the rise in voltage is the greatest at the start of the sinus, and thus the current must be the biggest at that moment. While at the top of the sinus the voltage doesn't change and therefore no charge is supplied to or removed from the capacitor; therefore the current then is zero (for a moment).","date":"2019-10-18 11:30:59","metadata":"{\"extraction_info\": {\"found_math\": true, \"script_math_tex\": 0, \"script_math_asciimath\": 0, \"math_annotations\": 0, \"math_alttext\": 0, \"mathml\": 0, \"mathjax_tag\": 0, \"mathjax_inline_tex\": 1, \"mathjax_display_tex\": 1, \"mathjax_asciimath\": 1, \"img_math\": 0, \"codecogs_latex\": 0, \"wp_latex\": 0, \"mimetex.cgi\": 0, \"\/images\/math\/codecogs\": 0, \"mathtex.cgi\": 0, \"katex\": 0, \"math-container\": 9, \"wp-katex-eq\": 0, \"align\": 0, \"equation\": 0, \"x-ck12\": 0, \"texerror\": 0, \"math_score\": 0.71526038646698, \"perplexity\": 550.6878988334647}, \"config\": {\"markdown_headings\": true, \"markdown_code\": true, \"boilerplate_config\": {\"ratio_threshold\": 0.18, \"absolute_threshold\": 10, \"end_threshold\": 15, \"enable\": true}, \"remove_buttons\": true, \"remove_image_figures\": true, \"remove_link_clusters\": true, \"table_config\": {\"min_rows\": 2, \"min_cols\": 3, \"format\": \"plain\"}, \"remove_chinese\": true, \"remove_edit_buttons\": true, \"extract_latex\": true}, \"warc_path\": \"s3:\/\/commoncrawl\/crawl-data\/CC-MAIN-2019-43\/segments\/1570986682037.37\/warc\/CC-MAIN-20191018104351-20191018131851-00376.warc.gz\"}"}
| null | null |
Am 1. Mai 1867 nahm die ungarische Postverwaltung ihren Betrieb auf. Sie umfasste die Gebiete Ungarn, Temeser Banat, Woiwodschaft Serbien sowie die sechs Konsularpostämter in der Moldau und Walachei (Bucarest, Giurgevo, Ibraila, Fokschan, Galatz und Plojestie). Kroatien-Slavonien und die Militärgrenze blieb bis zum 1. April 1868 unter österreichischer Postverwaltung.
Da sich die einer Herstellung neuen Briefmarkenausgabe verzögerte, wurden bis zum 1. Juni 1867 die Marken mit dem habsburgischen Doppeladler 1863/64 weiterhin in den Postämter verkauft. Diese sogenannten Provisorien, konnten bis zum 15. Juni 1867 in Ungarn verwendet werden.
Stephan Gorore, Königlich Ungarischer Minister für Ackerbau, Industrie und Handel beauftragte Mihály Gervay mit der Leitung des Postverwaltung, d. h. er wurde der Generaldirektor. Durch seine Persönlichkeit wurde die Entwicklung des unabhängigen ungarischen Postwesens maßgeblich beeinflusst. Diesen Position hatte er bis zu seiner im Jahre 1887 erfolgten Pensionierung inne. Das Gründungsdokument des Allgemeinen Postvereins von 1874 trägt seine Unterschrift. Er vertrat als Repräsentant der ungarischen Post auch bei den darauf folgenden Kongressen 1878 und 1885 deren Interessen.
Als am 1. September 1887 der königlich ungarische Handelsminister die, bisher getrennt arbeitenden, Post- und Telegraphendienste zusammengefasst hatte, mussten die Postwertzeichen auch die höheren Telegrammgebühren decken. Außerdem wurde die Fahrpost, bis dahin für Pakete und Wertbriefe zuständig, in die neue Poststruktur integriert.
Die Briefmarken
Die erste ungarische Briefmarkenausgabe
Die ersten von der selbständigen ungarischen Postverwaltung ausgegeben Briefmarken erschienen am 1. Juni 1867. Zunächst kamen die Werte von 2 Kr, 3 Kr, 5 Kr, 10 Kr und 15 Kr an die Postschalter. Die beiden Höchstwerte zu 25 Kr und 50 Kr wurden erst ab dem 1. September verkauft. Da die ungarischen Postämter in der Levante (Bucarest, Fokshan, Galatz, Giurgevo, Ibraila und Ploestie) die Briefgebühren in Soldi verrechneten, wurden dort die gleichen Nennwerte mit der entsprechenden Währungsbezeichnung verwendet. Der Termindruck bewegt den ungarischen Ministerrat 30. März 1867 von einer Ausgabe von Marken in einer eigenen Zeichnung zunächst abzusehen um, die unerwünschte Ausgabe mit dem habsburgischen Doppeladler zu ersetzen. Es wurde ein Entwurf akzeptiert, der das Bildnis des Kaisers ohne Kaiserkrone zeigte und eine Wertangabe kr, die sowohl dem ungarischen "krajczár" als auch dem österreichischen "Kreuzer" gerecht wurde. Somit kann eine Verwendung der Marken in Ungarn nur anhand der Stempel nachgewiesen werden.
Mit der ersten ungarischen Briefmarken-Ausgabe erschienen am 1. Juni 1867 auch Ganzsachenumschläge zu 3 Kr, 5 Kr, 10 Kr, 15 Kr und 25 Kr.
Die Franz-Josef-Ausgabe von 1871
Die ersten in Ungarn gedruckten Briefmarken wurde 1871 herausgegeben.
Die Herstellung der ersten komplett unter ungarischer Verantwortung konzipierten Marken sollte in den Räumen der königlich ungarischen Staatsdruckerei erfolgen, die 1868 im Regierungsviertel am Ferdinands Platz auf der Budaer Seite eingerichtet wurde. Das ungarische Finanzministerium gab gleichzeitig eine klare Vorgabe: die neuen Marken durften in der Herstellung nicht mehr kosten, als in der Wiener Staatsdruckerei, nämlich 4 Kr pro Bogen. Um die neuen Aufgaben bewältigen zu können, wurden neben zwei Zähnungsmaschinen von A. Gotthard (Wien) vor allem Schnelldruckpressen bei C. Alauzet in Paris und bei den Maschinenwerkstätten Bauer & Söhne in Würzburg bestellt. Letztere wurden laut einem Bericht an das Finanzministerium erst im Juli 1871 geliefert.
Neben der Schaffung der technischen Voraussetzungen musste auch ein neues Motiv für die neue Freimarkenserie festgelegt werden, wobei die Darstellung von Ferenc József (deutsch: Franz Joseph) bereits vorgegeben worden war. Nach verschiedenen Aussagen wurde das Rahmenmotiv von dem seit 1870 bei der k. und k. Staatsdruckerei in Buda angestellten János Unrein (1830–1882) entworfen. Es unterscheidet sich deutlich von den anderen vorgelegten Zeichnungen.
In der Postverordnung Nr. 4060/366 vom 26. April 1871 wurde die Ausgabe der neuen Marken zum 1. Mai angekündigt. Sie wurden im Steindruckverfahren hergestellt und hatten eine 9 ¼ : 9 ½ Linienzähnung, d. h. hier elf Zähnungslöcher an den senkrechten und neun an den waagerechten Seiten. Die Zähnungsnadeln saßen so unregelmäßig, dass jeder Marke anhand ihrer Zähnung eine Bogenposition zugeordnet werden kann. Die unterschiedlichen Farbtönungen lassen sich mit den verschiedenen Auflagen während der kurzen Druckperiode im ersten Halbjahr 1871 erklären. Bereits ab Ende Juni wurde die Produktion auf den Stichtiefdruck umgestellt.
Diese Marken haben kein Wasserzeichen.
Die Briefmuster-Ausgabe 1874–1900
Bereits 1873 beantragte das ungarische Handelsministerium die Zulassung einer neuen Briefmarkenserie, in der wie bei anderen Staaten das Wertzeichen deutlich erkennbar ist. Am 24. Mai 1874 unterschrieb Kaiser Franz-Josef einen entsprechenden Erlass (1874–4781 Handelsministerium), der es ermöglichte, dass die neuen Marken zu 2 kr, 3 kr, 5 kr und 10 kr ab dem 1. Oktober 1874 an die Postschalter kamen. Da der Bestand an 25 Kr Marken noch sehr hoch war, wurde der Wert zu 20 kr erst ab Mai 1876 verkauft. Das Markenbild wurde von Janos Lajos L'Hiver entworfen. Die Stahlstiche stammten von Ferenc Haske und die Grundschraffierungen von Emanuel Jung.Die Briefmusterausgabe wurde in der Zeit von 1874 bis 1881 auf wasserzeichenlosem Papier gedruckt. Es hatte eine Stärke von 0,07 bis 0,11 mm und wurde von verschiedenen österreichischen Herstellern und der ungarischen Papierfabrik in Nagyszlabos geliefert. Während der gesamten Herstellungszeit änderten sich die Zähnungen regelmäßig, da verschiedene Maschinen und Kämme dafür eingesetzt wurden.
Ab dem 1. Februar 1881 begann, ohne weitere amtliche Bekanntmachung, der Verkauf der bisherigen Freimarken mit dem Wasserzeichen. Das Papier wurde von der Papierfabriken in Nagyszabos und Fiume bezogen. Die Marken wurden ebenfalls am 30. September 1900 ungültig.
In die Verwendungszeit dieser Briefmusterausgabe fiel auch die Umstellung der Währungen in der k.u.k Monarchie. Nach dem Ausgleich von 1867 hatte Ungarn das Recht auf eine eigene Währung, Österreich und Ungarn kamen jedoch überein, die gemeinsame Währung beizubehalten. Nach Jahren langwieriger Verhandlungen gelang es im Jahre 1878, die Nationalbank in ein Institut zu überführen, an dem Österreich und Ungarn gleichermaßen beteiligt waren. Die "Oesterreichisch-ungarische Bank" sollte die Aufgaben einer Notenbank beider Reichshälften erfüllen. Zu den weitreichenden Währungsreformen, die es für die Oesterreichisch-ungarische Bank zu bewältigen galt, zählte der Übergang von der Silberwährung zum Goldstandard. Dies begann 1892 mit der Ausgabe neuer Münzen in Filler (=Heller) und Korona (Krone).
Die Turul-Ausgaben 1900–1916
Nach einer achtjährigen Übergangsfrist löste mit dem 1. Januar 1900 die "Gold-Korona" den "Silber-Forint" als gesetzliches Zahlungsmittel ab, wobei 1 Forint (100 Kr) in 2 Korona (200 Filler) umgerechnet wurden. Deshalb wurde auch die Ausgabe einer neuen Briefmarkenserie notwendig.
In der Zeit von 1892 bis 1900 machte die Postverwaltung Versuche mit verschiedenen Entwürfen. Am 1. Januar 1898 wurde ein offener Wettbewerb für eine passende Markenzeichnung ausgeschrieben. 56 Künstler nahmen daran teil und 166 Markenvorschläge wurden eingereicht. Von den siegreichen Entwürfen konnte keiner verwendet werden, weil die zu feinen Zeichnungen nicht ausgeführt werden konnten. Zwei Zeichnungen, die nicht prämiert waren, wurden ausgewählt, eine von J. Böhm, die den Turulvogel zeigte und die andere von Odön Tull mit einer Darstellung des Kaisers Franz Josef. Die unter den Sammlern geläufig als Turulausgabe bezeichnete Serie erschien in der ersten Auflage am 1. Januar 1900. Sie wurde im Buchdruck auf Wasserzeichenpapier gedruckt, wobei sich die Wasserzeichen bei den Neuauflagen von 1904, 1905/06, 1908, 1909 und 1913 jeweils änderten. Die Filler-Werte wurden in Bogen zu 400 Marken gedruckt, die dann in vier Schalterbögen zu je 100 geschnitten wurden. Die Korona-Werte wurden in Bogen zu 200 Stück hergestellt und dann in Schalterbogen zu je 100 geteilt.
Nachdem der Erste Weltkrieg endete, wurden Teile Ungarns mehrmals besetzt (von Frankreich (Arad), Rumänien (Debrecen, Temesvàr) und Serbien (Baranya, Temesvàr)), was jedes Mal in den betroffenen Gebieten neue Aufdrucke in das ungarische Postsystem brachte.
1919 wurde nach der Besetzung von Budapest durch die bolschewistischen Truppen der Restbestand der Briefmarken in der Hauptpost von Szegedin durch die nationale ungarische Regierung mit "MAGYAR NEMZETI KORMANY SZEGED, 1919", überdruckt. Ebenfalls wurden Briefmarken der Lokalausgabe Sopron (Ödenburg) 1956 mit Stempeln markiert.
Im frühen 20. Jahrhundert wurden auf den Briefmarken hauptsächlich der mythische Vogel "Turul" oder der ungarische Schutzheilige Stephan dargestellt. Über die Zeit gab es verschiedene Währungen, wie zum Beispiel Fillér, Korona, Forint oder Pengő. Heute ist der Forint die Hauptwährung und die Briefmarken sind mit Magyarország (ungar. für Ungarn) bedruckt. Ungarn ist berühmt für die Verwendung von Blattgold in seinen Briefmarken.
Die Schnitter- und Parlaments-Ausgaben 1916–1924
Ab 1. Oktober 1916 kamen neue Dauermarkenserien mit Schnitter- und Parlamentsmotiven zum Einsatz. In der Räterepublik wurden diese mit einem Aufdruck versehen. Es kamen auch weitere Sondermarken und Flugpostmarken zum Einsatz.
Weitere Ausgaben
1932 wurde die Briefmarkenserie Berühmte Ungarn herausgegeben und es erhöhte sich die Anzahl der Sonderbriefmarken.
Wasserzeichen
Die ungarischen Briefmarken zeichnen sich oftmals durch Wasserzeichen aus. Insgesamt sind laut Michel-Katalog 12 Wasserzeichen bekannt.
Fälschungen
Es gibt in allen Epochen von den ungarischen Marken und Stempeln Fälschungen.
Siehe auch
Magyar Posta
Literatur
Handwörterbuch des Postwesens. Hrsg. Bundespost, Frankfurt am Main 1953, S. 719 f.
Die Marken des Königreiches Ungarn bis 1900. M. Rhein, Naposta 2020.
Weblinks
Arbeitsgemeinschaft Ungarn e.V im Bund Deutscher Philatelisten
Einzelnachweise
Ungarn
Philatelie (Ungarn)
hu:Bélyeggyűjtés
|
{
"redpajama_set_name": "RedPajamaWikipedia"
}
| 1,253
|
Estremadura je povijesna regija na obali Atlantskog oceana u središnjem dijelu Portugala, gdje je smješten Lisabon, glavni grad. Većinom zauzima poluotok na zapadu estuarija rijeke Tajo.
Regiju Estremadura ne treba miješati sa španjolskom autonomnom zajednicom Ekstremadura, koja se na hrvatski također prevodi i kao Estremadura.
U svakom slučaju, naziv obiju regija dolazi od činjenice što su za vrijeme Rekonkviste (oslobođenja Pirenejskog poluotoka od Arapa) bile granice, ekstremi (španjolski extremo) kršćanskog teritorija.
Zemljopis Portugala
|
{
"redpajama_set_name": "RedPajamaWikipedia"
}
| 4,900
|
import os.path
import string
import pprint
import ast
# from FeedScrape.FeedDataParser import extractChapterVol
from tests.title_test_data import data as test_data
from WebMirror.OutputFilters.util.TitleParsers import TitleParser
def load_better_json(filepath):
'''
Load a json file, but allow shit necessary for sanity (like comments!)
'''
print("Loading file: '%s'" % filepath)
with open(filepath) as fp:
contin = fp.read()
return ast.literal_eval(contin)
def load_test_data(mismatch=True, only_mismatch=False):
ret = []
cdir = os.path.join(os.path.dirname(__file__), "title_data")
files = os.listdir(cdir)
files.sort()
for fn in files:
if fn.endswith(".pyson"):
fqp = os.path.join(cdir, fn)
if only_mismatch:
if "mismatch" in fn:
ret.extend(load_better_json(fqp))
elif mismatch:
ret.extend(load_better_json(fqp))
else:
if "mismatch" not in fn:
ret.extend(load_better_json(fqp))
print("Loaded %s test-cases!" % len(ret))
return ret
def create_data_file(prefix, outdir, bin_cont):
print("Bin for {} has {} items".format(prefix, len(bin_cont)))
bin_cont.sort(key=lambda x: x[0])
# p_str = ord(prefix) if len(prefix) == 1 and prefix not in string.ascii_lowercase+string.digits else prefix
mod_name = "'{}'_titles.pyson".format(prefix)
fpath = os.path.join(outdir, mod_name)
dat = pprint.pformat(bin_cont)
with open(fpath, "w") as fp:
fp.write("\n\n")
fp.write("# Titles for releases starting with the character '{}'".format(prefix))
fp.write("\n\n")
fp.write("[\n")
for item in bin_cont:
dat = pprint.pformat(item, width=99999999)
fp.write(" {},\n".format(dat))
fp.write("]\n\n")
return mod_name
def test():
dataset = []
for key, value in test_data:
if len(value) == 2:
e_chp, e_vol = value
dataset.append((key, (e_vol, e_chp, None, None)))
elif len(value) == 4:
e_vol, e_chp, e_frag, e_post = value
dataset.append((key, (e_vol, e_chp, e_frag, e_post)))
else:
print("Wat?", key, value)
print("Loaded {} item dataset".format(len(dataset)))
dataset.sort(key=lambda x: x[0])
bins = {}
for row in dataset:
prefix = row[0].lower()
if prefix:
prefix = prefix[0]
bins.setdefault(prefix, [])
bins[prefix].append(row)
print("Prefix bins: {}".format(len(bins)))
outdir = os.path.abspath(os.path.join(os.path.dirname(__file__), 'title_data'))
print("Output dir:", outdir)
small_bin = []
for key in list(bins.keys()):
if len(bins[key]) < 10:
dat = bins.pop(key)
small_bin.extend(dat)
bins['other'] = small_bin
print("Prefix bins after consolidation: {}".format(len(bins)))
mod_list = []
for prefix in bins.keys():
mod = create_data_file(prefix, outdir, bins[prefix])
mod_list.append(mod)
load_test_data()
if __name__ == "__main__":
test()
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 3,859
|
\section{Introduction}
\label{Introduction}
The defining challenge in biomedical Entity Linking (EL) is performing classification over a large number of entity labels with limited availability of labelled mention data, in a constantly evolving knowledge base. For instance, while the Unified Medical Language System (UMLS) knowledge base \cite{Bodenreider2004} contains millions of unique entity labels, the EL training data in the biomedical domain as a whole is notoriously scarce, particularly when compared to the general domain -- Wikipedia, for instance, is powerful as \emph{both} a Knowledge base and a source of matching entities and mentions. Furthermore, biomedical knowledge bases are evolving rapidly with new entities being added constantly. Given this knowledge base evolution and scarcity of training data it is crucial that biomedical entity linking systems can scale efficiently to large entity sets, and can discover or discern entities outside of the knowledge base and training data.
Recent methods in the general entity linking domain \cite{logeswaran-etal-2019-zero, wu-etal-2020-scalable} address the data issue with zero-shot entity linking systems that use entity descriptions to form entity representations and generalise to entities without mentions. A particularly powerful architecture was initially proposed by \citet{humeau2020polyencoders} and further improved by \citet{wu-etal-2020-scalable}. It consists of a two-stage approach: 1) candidate retrieval in a dense space performed by a \textit{bi-encoder} \cite{wu-etal-2020-scalable} which independently embeds the entity mention and its description, and 2) candidate ranking performed by a \textit{cross-encoder} which attends across both the mention and entity description \cite{logeswaran-etal-2019-zero}. In this work we focus on the former, which is traditionally optimised with the cross-entropy (CE) loss and aims to maximise the similarity between the entity mention and its description relative to the similarities of incorrect mention-description pairs. In practice, the large number of knowledge base entities necessitates the use of negative sampling to avoid the computational burden of comparing each mention to all of the entity descriptions. However, if the sampled distribution of negatives is not reflective of the model distribution, the performance may be poor. Recently, \citet{zhang-stratos-2021-understanding} showed that using hard negatives - the highest scoring incorrect examples - results in bias reduction through better approximation of the model distribution. Collecting hard negatives is computationally expensive, as it requires periodically performing inference and retrieving approximate nearest neighbours for each mention.
At the ranking stage, negative sampling is not required, as the number of candidates usually does not exceed 64. However, the state-of-the-art cross-encoder model used for ranking is very expensive to run, scaling quadratically with the input sequence length. This highlights the need for efficient and performant candidate retrieval models capable of disambiguating mentions without the need for the expensive ranking step.
In this paper, we propose and evaluate a novel loss for the candidate retrieval model, which breaks the dependency between the positive and negative pairs. Our contributions are: (1) a novel loss which significantly outperforms the benchmark cross-entropy loss on the candidate retrieval task when using random negatives, and performs competitively when using hard negatives. (2) We design and apply an adversarial regularization method, based on the Fast Gradient Sign Method \cite{goodfellow2014explaining}, which is designed to simulate hard negative samples without expensively mining them. (3) We construct a biomedical dataset for out of knowledge base detection evaluation using the MedMentions corpus and show that our model can robustly identify mentions that lack a corresponding entry in the knowledge base, while maintaining high performance on the retrieval task.
Our main testing ground is the biomedical entity linking dataset MedMentions \cite{Mohan2019}, which utilizes UMLS as its knowledge base. Additionally, to confirm that our method works also in the general, non-biomedical domain, we evaluate it on the Zero-Shot Entity Linking (ZESHEL) dataset proposed in \citet{logeswaran-etal-2019-zero}. We focus on the retrieval task with the recall@1 metric, because we are aiming to predict the entity directly without requiring the additional expensive ranking stage. Our results show that both the proposed loss and regularization improve performance, achieving state-of-the-art results on recall@1 and competitive performance on recall@64 on both datasets. Finally, we demonstrate that our model can robustly identify biomedical out of knowledge base entities, without requiring any changes to the training procedure.
\section{Related Work}
\label{Related Work}
\paragraph{Zero-Shot Entity Linking} There is a plethora of work on zero-shot entity linking methods leveraging the bi-encoder architecture \cite{wu-etal-2020-scalable} for candidate retrieval. These include novel scoring functions between the input and the label \cite{humeau2020polyencoders, luan-etal-2021-sparse, khattabzaharia}, cross-domain pretraining methods \cite{varma-etal-2021-cross-domain}, training and inference optimisation techniques \cite{Bhowmik2021FastAE} and effective entity representation methods \cite{ma-etal-2021-muver}. Our work instead focuses on optimising the candidate retriever's loss function.
The impact of hard negatives on the entity linking model performance has also been investigated \cite{Gillick2019, zhang-stratos-2021-understanding}. Notably, \citet{zhang-stratos-2021-understanding} develop analytical tools to explain the role of hard negatives and evaluate their model on the zero-shot entity linking task. We draw on this work, but move away from the CE loss towards a novel contrastive proxy-based loss.
Finally, there is a body of work on zero-shot entity linking in the biomedical domain using clustering \cite{angell-etal-2021-clustering, agarwal2021entity}. Our method does not consider the affinities between mentions directly and links them independently. Therefore, we do not study entity discovery.
An important aspect of biomedical entity linking systems is the detection of ``unlinkable'' mentions that lack a corresponding entry in the Knowledge Base - referred to as $\mathrm{NIL}$ detection. Methods for this task can be grouped into four main strategies \cite{shen2014entity, sevgili2020neural}: (1) label a mention as $\mathrm{NIL}$ when the corresponding candidate retriever does not return any candidate entities \cite{tsai2016cross}, (2) assign the $\mathrm{NIL}$ label to mentions whose corresponding top-ranked entity does not exceed some score threshold \cite{bunescu2006using, gottipati2011linking, lazic2015plato}, (3) train a classifier that predicts whether the top-ranked entity for a given mention is correct \cite{moreno2017combining}, (4) explicitly introduce a $\mathrm{NIL}$ class to the candidate ranking model \cite{kolitsas2018end}. A downside of the final approach is that knowledge of the $\mathrm{NIL}$ mention distribution is required at training time. In this work we tune a $\mathrm{NIL}$ score threshold (2) on a validation set. Detecting unlinkable mentions is particularly important in the biomedical domain, where the knowledge bases are rapidly evolving.
\paragraph{Proxy-based Losses} State-of-the-art entity linking models such as BLINK \cite{wu-etal-2020-scalable} leverage metric learning loss during training to make mentions similar to its assigned entity representations. Metric learning losses could be divided into two categories, pair-based and proxy-based losses \cite{Kim2020a}. Pair-based losses can leverage semantic relations between data points, here mentions. However, training them can be highly computationally expensive. On the other hand, proxy-based losses are significantly less computationally complex. This is done by establishing a proxy for each class and trying to increase the similarity between data points and its assigned proxies. Therefore, avoiding comparing the mentions to each other in favour of comparing the mentions to their proxies. We draw heavily on proxy-based losses \cite{Movshovitz-Attias2017a, Kim2020a} from metric learning by treating entity descriptions as the proxies. We establish a proxy for each entity, creating mention-proxy (i.e. entity) pairs, and optimise the model to embed the mention close to its assigned proxy. The loss proposed here is similar to the Proxy-NCA loss of \citet{Movshovitz-Attias2017a}. Our modification is the use of the Softplus function, similar to \citet{Kim2020a}, to avoid a vanishing gradient for the true mention-proxy pair.
\paragraph{Adversarial Regularization} Entity linking systems often rely on careful mining of hard negative examples to boost their performance \cite{Gillick2019, zhang-stratos-2021-understanding} at the expense of increased computational complexity. The model needs update hard negatives for each mention periodically. A potential alternative to hard negative mining is training on adversarial examples \cite{szegedy2013intriguing, goodfellow2014explaining} - synthetic data points designed to induce the model to making incorrect predictions, such that they are more challenging. Adversarial training can be seen as data augmentation and can help reduce overfitting. \citet{goodfellow2014explaining} introduced a simple method for generating adversarial examples, called Fast Gradient Sign Method (FGSM), which we build upon in this work. FGSM creates adversarial examples by applying small perturbations to the original inputs - often the word embeddings for NLP problems. FGSM has been used successfully as a regulariser in supervised and semi-supervised NLP tasks \cite{miyato2016adversarial, pan2021improved}. Here, we follow a similar approach and use FGSM to augment our training pairs with adversarial positive and negative examples.
\section{Task formulation}
\label{Task Formulation}
In the \textbf{Entity Linking task} we are provided with a list of documents $D \in \mathcal{D}$, where each document has a set of mentions $M_{D} = \{m_{1}, m_{2}, \dotsc, m_{N_D}\}$. The task is to link each mention $m_{i}$ to an entity $e_{i}$, where each entity belongs to the Knowledge Base (KB) $\mathcal{E}$. In this work we focus specifically on the problem of biomedical zero-shot entity linking. The setup for the zero-shot task is the same as for entity linking introduced above, except that the set of entities present in the test set is not present in the training set, i.e. $\mathcal{E}_{\mathrm{train}} \cap \mathcal{E}_{\mathrm{test}} = \emptyset$ with $\mathcal{E}_{\mathrm{train}} \cup \mathcal{E}_{\mathrm{test}} = \mathcal{E}$. We focus specifically on the \textbf{Candidate Retrieval} task, where the goal is given a mention $m_{i}$, reduce the pool of potential candidate entities from a KB to a smaller subset. Candidate retrieval is crucial for biomedical entity linking because of the large size of knowledge bases. In this work we use the bi-encoder architecture for candidate retrieval. Finally, in addition to the \textit{in-KB} entity linking task, where you only consider entities inside the KB, we also consider an \textbf{out of KB} scenario, where the task is to map mentions to the augmented set of labels $\mathcal{E} \cup \mathrm{NIL}$, with $\mathrm{NIL}$ indicating the absence of a corresponding KB entity.
\section{Methods}
\label{Methods}
\begin{figure}[ht!]
\centering
\includegraphics[width=\columnwidth]{graphics/illustration.pdf}
\caption{Overview of our proxy-based entity linking method. The mention and entity embeddings are encoded into a joint embedding space. During training, the magnitude of the gradients of the Proxy loss function with respect to the embedding coordinates is a function of the similarity between the mention and the entities (proxies). The gradients are represented by arrows whose widths indicate their magnitude. The $\mathrm{adv}$-labelled dotted arrows are the Fast Gradient Sign Method adversarial perturbations. The blue circle symbolizes the margin $\delta$.}
\label{illustrated_method}
\end{figure}
In this section, we review the categorical CE loss, used by current state-of-the-art models, in the context of entity linking \cite{wu-etal-2020-scalable, zhang-stratos-2021-understanding}. We then compare it to our proposed Proxy-based loss. Finally, we describe and motivate our regularization approach.
\subsection{Loss} \label{loss}
Given a set of data points corresponding to mention representations $m \in M$ and to a set of proxies corresponding to entities $e \in \mathcal{E}$, the categorical CE loss is defined as:
\begin{equation}\label{firstlce}
L_{\text{CE}}(m, P) := - \log\bigg(\frac{\exp(s(m, e^+))}{\sum_{e \in P} \exp(s(m, e))}\bigg),
\end{equation}
where $s$(·, ·) denotes a similarity function (e.g. cosine similarity or dot product), $e^{+}$ is the positive proxy for mention representation $m$, $P^{-}$ is a set of negative proxies used as negative samples, and $P = \{e^{+}\} \cup P^{-}$.
The gradient of the CE loss with respect to $s(m, e)$ is given by:
\begin{equation}\label{grad_ce}
\frac{\partial L_{\text{CE}}}{\partial s(m, e)} =
\begin{dcases}
-1 + \frac{\exp(s(m, e^+))}{\sum_{e \in P} \exp(s(m, e))} , & e = e^{+} \\
\frac{\exp(s(m, e^-))}{\sum_{e \in P} \exp(s(m, e))}, & e \in P^{-}
\end{dcases}
\end{equation}
In practice training is performed with negative sampling. If the negatives are sampled randomly, often the exponential term for the positive entity is much larger than that of the negative samples and the gradients vanish. When $ s(m, e^+) \gg s(m, e^-) \ \forall e^- \in P^{-}$ then $ \partial L_{\text{CE}}/{\partial s(m, e)} \rightarrow 0 $. This behaviour is desirable when training with the full distribution of negative pairs, but stifles learning in the noisier sampling setup. A common approach is the use of hard negatives \cite{Gillick2019, zhang-stratos-2021-understanding}, which increases performance over training with random negatives at the cost of increased computational complexity.
On the other hand, contrastive metric learning losses \cite{bromley1993, chopra2005, hadsell2006dimensionality} alleviate the vanishing gradients problem by decoupling the positive and negative loss terms. Proxy-based contrastive losses, such as Proxy-NCA \cite{Movshovitz-Attias2017a}, aim to increase the similarity between a data point $x$ and its assigned proxy $e^{+}$, while decreasing the similarity between $x$ and its negative proxies $e^{-} \in P^{-}$. As demonstrated in \cite{Kim2020a}, a downside of Proxy-NCA is that the scale of its gradient is constant for positive samples. This issue is alleviated by the Proxy Anchor loss \cite{Kim2020a}, whose gradient reflects the relative hardness of both positive and negative pairs, resulting in improved model performance.
Drawing inspiration from the proxy-based metric learning losses described above, we formulate our Proxy-based (Pb) candidate retrieval loss as follows:
\begin{equation}
\label{proxy_anchor_loss_eq}
\begin{split}
L_{\mathrm{Pb}}(m, P) = \log(1 + \exp(-\alpha(s(m, e^{+}) - \delta)) \\ + \log(1 + \sum_{e^{-} \in P^{-}}\exp(\alpha(s(m, e^{-}) + \delta)),
\end{split}
\end{equation}
where we use the same notation as in Eq.~\ref{firstlce}. In addition, $\alpha$ is a hyperparameter controlling how strongly positive and negative samples pull and push each other, and $\delta$ is a margin. If $\alpha$ and $\delta$ are large, the model will be strongly penalized for the positive pair being too far from each other, and conversely the negative pair for being too close to each other. If $\alpha$ and $\delta$ are small, the model will receive weaker feedback. The Softplus function, a smooth approximation of the $\mathrm{ReLU}$, introduces an additional margin beyond which the model stops penalising both positive and negative pairs, thus reducing overfitting. The gradient of our Proxy-based loss function is given by:
\begin{equation}\label{grad_sp}
\frac{\partial L_{\text{Pb}}}{\partial s(m, e)} =
\begin{dcases}
\frac{-\alpha \exp(-\alpha s^{+})}{1 + \exp(-\alpha s^{+})} , & e = e^{+} \\
\frac{\alpha \exp(\alpha s^{-})}{1 + \sum\limits_{e^{-} \in P^{-}} \exp(\alpha s{-})}, & e \in P^{-}
\end{dcases}
\end{equation}
where $s^{+} = s(m, e^+) - \delta $, $s^{-} = s(m, e^-) + \delta $. This gradient reflects the relative hardness of negative examples, decoupled from the positive pair, which makes it less sensitive to the choice of negative sampling scheme.
\subsection{Regularization}\label{sec:methods-reg}
Our regularization approach is based on a simple adversarial training technique, called \textit{Fast Gradient Sign Method} (FGSM) \cite{goodfellow2014explaining}. The idea of FGSM is to generate adversarial examples according to the following equation:
\begin{equation}
x_{\mathrm{adv}} = x + \epsilon * \sign(\nabla_{x} L(x, y))
\end{equation}
where $x$ is the original training example, $y$ its corresponding label, $L$ the loss function that is minimised during model training, and $\epsilon$ a small number defining the magnitude of the perturbation.
FGSM applies a small perturbation to the input example that should not change the label of the resulting example $x_{\mathrm{adv}}$. However, \citet{goodfellow2014explaining} demonstrated that even infinitesimal perturbations can cause drastic changes to the model output when carefully designed. This effect is due to the locally linear nature of neural networks in combination with the high dimensionality of their inputs. Moreover, it is the direction, rather than the magnitude, of the perturbation that matters the most. In FGSM the direction is determined by the gradient of the loss function with respect to the model input - $x$ is pushed in the direction of highest loss increase given its true label $y$.
In the context of entity linking task, we are interested in generating examples adversarial to the learned metric, in other words hard negative and hard positive examples for a given mention $m$. To this end, we applied the following perturbations to the entity encoder input embeddings $z = \inputembed(e)$:
\begin{align}
z_{\mathrm{adv}}^{-} &= z^{-} + \epsilon * \sign(\nabla_{z^{-}} s(m, e^{-})) \label{eq:adv-neg} \\
z_{\mathrm{adv}}^{+} &= z^{+} - \epsilon * \sign(\nabla_{z^{+}} s(m, e^{+})) \label{eq:adv-pos}
\end{align}
where $m$ is the anchor mention and $z^{-}, z^{+}$ are the encoder input embeddings of negative and positive entities $e^{-}, e^{+}$ correspondingly.
Given $N$ negative entities for a mention $m$, the generated adversarial entity embeddings $P_{\mathrm{adv}} = \{ z_{\mathrm{adv\_1}}^{-}, \ldots, z_{\mathrm{adv\_N}}^{-}, z_{\mathrm{adv}}^{+} \}$ are used as additional training examples, giving rise to an auxiliary loss term that encourages the model to be invariant to local adversarial perturbations. Thus, the final objective we are trying to minimise becomes:
\begin{equation}
L_{\mathrm{Pb}}(m, P) + \lambda L_{\mathrm{Pb}}(m, P_{\mathrm{adv}})
\end{equation}
where $\lambda$ is a hyperparameter controlling the relative contributions of the two losses.
\section{Experiments}
\label{Experiments}
\subsection{Datasets}
\paragraph{MedMentions} This is is a biomedical entity-linking dataset consisting of over 4,000 PubMed abstracts \cite{Mohan2019}. As recommended by the authors, we use the ST21PV subset, which has around 200,000 mentions in total. A large number of mentions in both the validation and test splits are zero-shot, meaning their ground truth label is not present in the training data. We do not carry out any additional preprocessing on the dataset. Finally, for the knowledge base (KB), we follow the framework in \citet{varma-etal-2021-cross-domain} and use the UMLS 2017AA version filtered by the types present in the ST21PV subset. The final KB includes approximately 2.36M entities.
To evaluate our models in the $\mathrm{NIL}$ detection setting, we have created a new dataset based on MedMentions. In this dataset, we have assigned mentions corresponding to 11 entity types a $\mathrm{NIL}$ label and removed them from the Knowledge Base. Details on the dataset statistics and removed entity types can be found in the Appendix.
\begin{table}[]
\resizebox{\columnwidth}{!}{%
\begin{tabular}{lcccccc}
\hline
& \multicolumn{3}{c}{\textbf{MedMentions}} & \multicolumn{3}{c}{\textbf{Zero-Shot EL}} \\
& \textbf{Train} & \textbf{Val} & \textbf{Test} & \textbf{Train} & \textbf{Val} & \textbf{Test} \\ \hline
Mentions & 120K & 40K & 40K & 49K & 10K & 10K \\
Entities & 19K & 8K & 8K & 333K & 90K & 70K \\
\% Entities seen & 100 & 57.5 & 57.5 & 100 & 0 & 0 \\ \hline
\end{tabular}%
}
\caption{Statistics of datasets used. "\% Entities seen" signifies the percentage of ground truth entities seen during training.}
\label{tab:dataset-stats}
\end{table}
\paragraph{Zero-Shot Entity Linking dataset} ZESHEL, a general domain dataset was constructed by \citet{logeswaran-etal-2019-zero} from Wikias\footnote{https://wikia.com}. It consists of 16 independent Wikias. The task is to link mentions in each document to a Wikia-specific entity dictionary with provided entity descriptions. The dataset is zero-shot, meaning there is no overlap in entities between training, validation and test sets.
\subsection{Input Representation and Model Architecture}
Similarly to \citet{wu-etal-2020-scalable, zhang-stratos-2021-understanding, varma-etal-2021-cross-domain} our candidate retriever is a bi-encoder consisting of two independent BERT transformers. We use the bi-encoder to encode a textual mention and an entity description independently then obtain a similarity score between them.
Namely, Given a mention and its surrounding context $\tau_{m}$ and an entity $\tau_{e}$, we obtain dense vector representations $\mathbf{y_{m}} = \red(T_{1}(\tau_{m}))$ and $\mathbf{y_{e}} = \red(T_{2}(\tau_{e}))$, where $T_{1}$ and $T_{2}$ are the two independent transformers of the bi-encoder and $\red(\cdot)$ is a function that reduces the output of a transformer into a single vector. We use a mean pooling operation for the function $\red(\cdot)$.
As in \citet{wu-etal-2020-scalable, zhang-stratos-2021-understanding, varma-etal-2021-cross-domain} we use the dot product to score the mention $\mathbf{y_{m}}$ against an entity vector $\mathbf{y_{e}}$ when using the CE loss. For our Proxy-based loss we use cosine similarity.
In this, work, we focus on entity linking by efficient candidate retrieval, but we also include the ranker results using the highest scoring candidate entities in the Appendix, where we also include more details on entity, mention and context modelling.
\subsection{Training \& Evaluation Details}
In all our experiments we used the transformer architecture \cite{vaswani2017} for the encoders. Namely, we used BERT \cite{devlin-etal-2019-bert}, initialised with appropriate pre-trained weights: SapBERT \cite{liu-etal-2021-self} for MedMentions and the uncased BERT-base \cite{devlin-etal-2019-bert} for ZESHEL. For FGSM regularization, we apply adversarial perturbations to the composite token embeddings (i.e. sum of word, position and segment embeddings) used as input to BERT. We apply our regularization to both Proxy-based and CE. For information on hyperparameter tuning please refer to the Appendix. We tune all of our experiments on the validation set and report results on the test set. Due to hardware limitations, the training was conducted on a single V100 GPU machine with 16 GB of GPU memory. The limited GPU capacity, in particular, memory, posed a challenge by constraining us to using a relatively low number of negatives when training a retriever.
\subsubsection{Candidate Retriever}
The retriever model is optimised with the Proxy-based loss (\ref{proxy_anchor_loss_eq}) and benchmark CE loss (\ref{firstlce}) for fair comparison. We evaluate the retriever on the micro-averaged recall@1 and recall@64 metrics, where in our setup recall@1 is equivalent to accuracy. Here we focus on the recall@1 metric, which is highly relevant for efficient candidate retrieval models that do not necessitate running an expensive cross-encoder for candidate ranking. We use two negative sampling techniques: (1) Random, where the negatives are sampled uniformly at random from all entities in the knowledge base, and (2) Mixed-p: p percent of the negatives are hard, the rest are random. This is motivated by the results shown in Zhang and Stratos (2021). We set
the p to 50\%.
\paragraph{Hard negative mining} Retrieving hard negatives requires running the model in the inference mode over the entire KB. Then, for each mention, the most similar (i.e. hard) negatives are sampled according to a scoring function. Here, we use FAISS \cite{johnson2019billion} for obtaining hard negatives given a mention and an index of entity embeddings from the KB.
Running a forward pass over the entire KB at regular intervals can be costly and time-consuming as the KB often amounts to millions of entities. Moreover, the computational complexity of retrieving hard negatives may grow exponentially depending on the scoring function. For example, the traditionally used scoring function also leveraged in this work, where the mention and entity are both represented with a single embedding requires $\mathcal{O}(me)$ approximate nearest neighbour searches, where $m$ and $e$ are the number of mentions and entities respectively. However, employing an alternative scoring function such as the \emph{sum-of-max} used in \citet{zhang-stratos-2021-understanding} which requires comparing a set of mention embeddings with a set of entity embeddings results in $\mathcal{O}(mexy)$ where $x$ and $y$ is the number of mention vector and entity vector embeddings. In \citet{zhang-stratos-2021-understanding} $x$ and $y$ are set to $128$, the number of maximum tokens in the mention and entity input sequence.
This highlights the computational cost of hard negative mining and underlines the need for both methods which can work effectively with random samples as well as more efficient hard negative mining strategies. In this work we propose a method for the former.
\paragraph{Biomedical Out of Knowledge Base Detection} For the biomedical $\mathrm{NIL}$ detection scenario training proceeds exactly as in the in-KB setting. We train models with the Proxy-based loss with different margins, and also a model with the CE loss. In each case, we use a validation set that includes $\mathrm{NIL}$ mentions to select an appropriate threshold for the retrieval model. Mentions whose corresponding top-ranked entity does not achieve this score are assigned the $\mathrm{NIL}$ label. We choose the threshold that maximises the F1 score for $\mathrm{NIL}$ entities in the validation set. We then apply this threshold to detect $\mathrm{NIL}$ mentions in the test set.
\begin{table}[ht!]
\resizebox{\columnwidth}{!}{%
\begin{tabular}{lccc}
\toprule
& \textbf{\# Neg.} & \textbf{recall@1} & \textbf{recall@64} \\ \cmidrule{1-4}
\citet{angell-etal-2021-clustering} & - & 50.8 & 85.3 \\
\citet{agarwal2021entity} & - & 72.3 & 95.6 \\
\citet{varma-etal-2021-cross-domain} & 100 & 71.7 & - \\ \cmidrule{1-4}
\multirow{3}{*}{{\textbf{PEL-CE}}} & 32 (mixed) & 72.1 & 95.5 \\
& 64 (mixed) & 72.1 & 95.6 \\
& 64 (random) & 55.7 & 94.0 \\ \cmidrule{2-4}
\multirow{3}{*}{{\textbf{PEL-Pb}}} & 32 (mixed) & 71.6 & 93.3 \\
& 64 (mixed) & \textbf{72.6} & 95.0 \\
& 64 (random) & 63.3 & \textbf{95.9} \\ \cmidrule{2-4}
\textbf{PEL-CE + FGSM} & 32 (mixed) & 72.3 & 95.5 \\
\textbf{PEL-Pb + FGSM} & 32 (mixed) & 72.4 & 93.7 \\
\bottomrule
\end{tabular}
}
\caption{Candidate retrieval results on the MedMentions dataset. CE and Pb refers to cross-entropy and proxy-based losses respectively. All experiments were run with mixed random and hard negatives ``(mixed)", or only ``(random)" negatives. The bold figures represent the best score for each recall metric. Note that FGSM PEL variants were only run with 32 negatives due to GPU memory constraints.}
\label{tab:medmentions-cand-gen}
\end{table}
\begin{table}[ht!]
\resizebox{\columnwidth}{!}{%
\begin{tabular}{lcccc}
\toprule
& \multicolumn{2}{c}{\textbf{Random}} & \multicolumn{2}{c}{\textbf{Mixed}} \\
& recall@1 & recall@64 & recall@1 & recall@64 \\ \cmidrule{1-5}
\citet{Wu2019}$^\dag$ & - & 81.80 & 46.5 & 84.8 \\
\citet{agarwal2021entity} & 38.6 & 84.0 & 50.4 & 85.1 \\
\citet{ma-etal-2021-muver} & 45.4 & \textbf{90.8} & - & - \\
\citet{zhang-stratos-2021-understanding} & - & 87.62 & - & \cellcolor[HTML]{EFEFEF} \textbf{89.6} \\ \cmidrule{1-5}
\textbf{PEL-CE} & 44.1 & 84.8 & 52.5 & 87.2 \\
\textbf{PEL-Pb} & 48.9 & 85.2 & 53.1 & 86.0 \\
\textbf{PEL-CE + FGSM} & 44.1 & 85.2 & 53.2 & 87.2 \\
\textbf{PEL-Pb + FGSM} & \textbf{49.7} & 85.6 & \cellcolor[HTML]{EFEFEF} \textbf{54.2} & 86.6 \\
\bottomrule
\end{tabular}
}
\caption{Candidate retrieval results on the ZESHEL dataset. CE and Pb refers to cross-entropy and proxy-based losses respectively. The negative to positive sample ratio for all PEL runs is 32. The bold figures represent the best score for each sampling strategy (random vs. mixed random and hard). The highlighted figure represents the best overall score across strategies. \dag we use the results reported in \citet{zhang-stratos-2021-understanding} for random negatives and \citet{ma-etal-2021-muver} for mixed negatives.
}
\label{tab:zeshel-cand-gen}
\end{table}
\section{Results}
\label{Results}
We present the results for candidate retrieval and benchmark our models against suitable methods. We name our method Proxy-based Entity Linking (PEL-Pb). We also report the results of a version of our model which uses the CE (PEL-CE) loss on all experiments for comparison.
\subsection{MedMentions}
Table \ref{tab:medmentions-cand-gen} shows that all approaches using bi-encoder transformer models strongly outperform the N-Gram TF-IDF proposed in \citet{angell-etal-2021-clustering} for recall@1 and also recall@64. We also observe the strong positive effect of including hard negatives during model training. The effect is particularly strong for the CE loss, where recall@1 increases by 17\% compared with training on random negatives. We believe that such difference is partly due to the large size of the KB MedMentions KB, amounting to 2.36M entities, which contributes to the importance of hard negative mining. For the Proxy-based loss, including hard negatives increases recall@1 by 9\%, achieving state-of-the-art performance of 72.6\%. Adding FGSM regularisation boosted performance, as can be seen from the experiments with 32 negatives (the largest number of negatives we could fit into GPU memory when applying FGSM). However, it did not exceed the performance of the unregularized model with 64 negative samples.
\begin{table}[h!]
\resizebox{\columnwidth}{!}{%
\begin{tabular}{lccccc}
\toprule
& \multicolumn{3}{c}{\textbf{$\mathrm{NIL}$}} & \multicolumn{2}{c}{\textbf{All classes incl. $\mathrm{NIL}$}} \\
& \textbf{auPR} & \textbf{Precision} & \textbf{Recall} & \textbf{Recall@1} & \textbf{Recall@64} \\ \cmidrule{1-6}
Pb (m=0) & 83.7 & 81.2 & 71.0 & \textbf{72.6} & \textbf{90.4} \\
Pb (m=0.01) & 84.4 & 81.6 & 71.5 & 72.5 & 90.2 \\
Pb (m=0.05) & 85.8 & 83.3 & 73.5 & 72.4 & 89.9 \\
Pb (m=0.1) & \textbf{87.6} & \textbf{85.2} & \textbf{79.2} & 69.4 & 85.7 \\
CE & 32.3 & 31.8 & 74.0 & 64.4 & 76.1 \\
\bottomrule
\end{tabular}
}
\caption{$\mathrm{NIL}$ detection results on the MedMentions dataset. auPR, precision and recall are reported exclusively for the $\mathrm{NIL}$ class, whereas micro-averaged recall@1 and recall@64 are reported for all classes including $\mathrm{NIL}$. Pb: Proxy-based with margin $m$, CE: Cross-Entropy.}
\label{tab:okb-results}
\end{table}
\begin{figure}[h!]
\centering
\includegraphics[width=\columnwidth]{graphics/okb_medmentions_test.pdf}
\caption{Precision Recall curves for $\mathrm{NIL}$ detection on the MedMentions dataset. Pb: Proxy-based with margin $m$, CE: Cross-Entropy.}
\label{fig:okb_medmentions}
\end{figure}
\paragraph{Biomedical Out of Knowledge Base detection} We also evaluated our proposed loss function on $\mathrm{NIL}$ detection. All models trained with the Proxy-based loss significantly outperform the CE-based model in terms of both precision and recall (Figure \ref{fig:okb_medmentions}). The CE loss does not encourage low scores in absolute value for negatives examples, but rather encourages scores that are lower than the scores of positive examples. As we can see from the results, CE training fails to assign low scores to $\mathrm{NIL}$ mentions, as these are out-of-distribution negatives and thus have not been compared to positive examples during model training. Our Proxy-based loss does not suffer from this issue, even with a margin of $0$. We believe that this is accomplished by the decoupling of the positive and negative loss terms, such that low \textit{absolute} score values are encouraged for negative examples.
Furthermore, the higher the Proxy-based margin the better the model's performance with respect to detecting $\mathrm{NIL}$ mentions. At the same time, Proxy-based models with lower margins perform better at the overall recall metrics (Figure \ref{fig:okb_medmentions}). These metrics are computed with respect to all classes including the $\mathrm{NIL}$ class. Given that the performance differences among models with different margins are minimal, a practitioner could choose how to set the margin considering the trade-off between $\mathrm{NIL}$ detection and overall model performance. To our knowledge, we are the first to propose a method for $\mathrm{NIL}$ detection using the bi-encoder architecture.
\subsection{Zero-Shot Entity Linking dataset}
Based on the candidate retrieval results in Table \ref{tab:zeshel-cand-gen}, we can conclude six key points.
(1) Proxy-based models (Pb) outperform their Cross-Entropy (CE) counterparts across all considered settings for recall@1. In particular, our Proxy-based model using hard negatives and FGSM regularization achieves state-of-the-art recall@1 on this dataset. This highlights the gain that we get by breaking the dependency between positive and negative pairs.
(2) Including hard negatives always boosts model performance. This is particularly evident on the recall@1 metric. The model trained with CE loss strongly depends on hard negatives, with recall@1 increasing by 8\% compared to training with random negatives. For the Proxy-based loss the increase is 4\%, as the model already performs competitively when trained with random negatives. This showcases the importance of hard negative sampling for the CE loss. Hard negatives provide the model with much more meaningful feedback and avoid the threat of vanishing gradients (Eq.~\ref{grad_ce}).
(3) The difference between Pb and CE models becomes much smaller for recall@64. Trivially, as \textit{k} increases, recall@\textit{k} for all models will converge towards 1. Additionally, as \textit{k} increases to above the number of hard negatives, the model's ability to distinguish the hard negatives from the positive will not be seen in the metric.
(4) CE models marginally outperform Pb models with hard negatives at recall@64. Hard negatives consistently have a larger impact on CE compared to Pb also at recall@64 (2), while the benefits of Pb have been nullified as discussed in (3).
(5) Alternative methods leveraging the CE loss and different model architectures such as MuVER \cite{ma-etal-2021-muver} and SOM \cite{zhang-stratos-2021-understanding} outperform the bi-encoder based approach at recall@64. However, both MuVER and SOM are more complex models tuned for achieving high recall@64, whereas the main focus of our approach is high recall@1 in the pursuit of avoiding the additional ranking stage. Pb outperforms the only single stage entity linking model \citet{agarwal2021entity} across the board.
(6) FGSM regularization boosts the results of both Proxy-based and CE models, demonstrating its promise as a general method for regularizing the retrieval model.
\section{Discussion and Future Work}
\label{Discussion and Future Work}
We have proposed and evaluated a novel proxy-based loss for biomedical candidate retrieval. Additionally, we have adopted an adversarial regularization technique designed to simulate hard negatives, and shown that both our loss and regularization boost performance on the recall@1 metric. We have also constructed a biomedical dataset for $\mathrm{NIL}$ detection and demonstrated that our candidate retrieval model can robustly identify biomedical $\mathrm{NIL}$ entities, while maintaining high overall performance. These are important advances towards closing the gap between the two-stage approach that include an expensive cross-encoder and a candidate retriever-only setup.
Notably, our work highlights the importance of hard negative sampling when optimising the candidate generator with the CE loss. Random negative sampling together with CE loss can result in the problem becoming trivial, for example the randomly sampled negative entity having a different type. However, accessing hard negative examples during model training can be challenging, particularly when the knowledge base is large and entity representations are frequently updated.
Considering this, we recommend to employ our Proxy-based loss for the candidate retrieval task in three different scenarios: (1) training with random negatives, (2) optimising for recall@1, (3) detecting $\mathrm{NIL}$ entities. Moreover, we also recommend leveraging FGSM regularisation in any setup and both retrieval and ranking tasks.
An interesting approach would be to attempt to approximate hard negatives without frequent updates of the entity representations. This could potentially be done by keeping the entity encoder frozen, or exploring alternative relatedness measures which does not require frequently running the model over the whole knowledge base. Finally, there is a plethora of work on proxy-based \cite{Movshovitz-Attias2017a, Kim2020a} and pair-based losses \cite{bromley1993, chopra2005, schroff2015, Dong_2018_ECCV}, usually discussed in the computer vision and metric learning literature. Improving the candidate retrieval is a crucial step towards high-performing and efficient entity linking systems that can be easily applied in real-world settings.
\section*{Limitations}
There are several limitations of our work. Firstly, we only demonstrate the advantages of our proposed method when computing hard negatives is computationally expensive, which is the case with large knowledge bases and expensive scoring methods. If computing hard negatives is not a bottleneck, one may use negative sampling with the baseline CE loss. However, biomedical knowledge bases typically contain a huge number of entities. Secondly, in our experiments we were limited to single GPU machines with at most 16GB of GPU memory. This prevented us from including more than 64 negatives samples in the standard setup and 32 negative samples when using FGSM regularization, which could potentially be benefit model performance. Thirdly, we acknowledge that some comparison to related work is missing, in particular, \citet{zhang-stratos-2021-understanding}. We were not able to reproduce the results cited in the paper using the publicly available code. Finally, our work is limited to proxy-based metric learning losses. More space could be devoted to the topic of how one could utilise metric learning more broadly for biomedical entity linking. We leave this for future work.
\section*{Ethics Statement}
The BERT-based models fine-tuned in this work and datasets are publicly available. We will also make our code as well as the biomedical out of knowledge base detection dataset publicly available.
The task of entity linking is often crucial for downstream applications, such as relation extraction, hence potential biases at the entity lining stage can have significant harmful downstream consequences. One source of such biases are the pre-trained language models fine-tuned in this work. There is a considerable body of work devoted to the topic of biases in language models. One way the entity linking systems can be particularly harmful is when they commit or propagate errors in the language models, knowledge bases, mention detection across certain populations such as races or genders. Because of the high ambiguity across biomedical mentions and entities in the knowledge base, it is important that the users investigate the output prediction of the entity linking system and often take is a suggestion, rather than gold standard. Finally, we highlight that linking the entity to its entry in the knowledge base and out of knowledge base detection can be analogous to surveillance and tracking in the computer vision domain, which comes with substantial ethical considerations.
\section*{Acknowledgements}
We thank Dane Corneil, Georgiana Neculae and Juha Iso-Sipil\"a for helpful feedbacks and the anonymous reviewers for constructive comments on the manuscript.
|
{
"redpajama_set_name": "RedPajamaArXiv"
}
| 1,732
|
use crate::util::errors::CargoResult;
use crate::util::paths;
use std::path::{Path, PathBuf};
/// Finds the root `Cargo.toml`.
pub fn find_root_manifest_for_wd(cwd: &Path) -> CargoResult<PathBuf> {
let file = "Cargo.toml";
for current in paths::ancestors(cwd) {
let manifest = current.join(file);
if manifest.exists() {
return Ok(manifest);
}
}
anyhow::bail!(
"could not find `{}` in `{}` or any parent directory",
file,
cwd.display()
)
}
/// Returns the path to the `file` in `pwd`, if it exists.
pub fn find_project_manifest_exact(pwd: &Path, file: &str) -> CargoResult<PathBuf> {
let manifest = pwd.join(file);
if manifest.exists() {
Ok(manifest)
} else {
anyhow::bail!("Could not find `{}` in `{}`", file, pwd.display())
}
}
|
{
"redpajama_set_name": "RedPajamaGithub"
}
| 5,180
|
A photography startup called Light launched a new camera called the L16. This new device is a multi-aperture computational camera that comes equipped with 16 individual lenses. The cool part is that despite having all of these individual lenses, the camera is as thin as a cell phone and significantly less bulky compared to DSLRs.
When a photo is captured, the Light L16 uses all 16 lenses to record the photo simultaneously at different focal lengths. This allows the device to capture more data in every shot. The L16 then turns all of the pictures into one single 52-megapixel image.
The L16 is based on Android OS and has built-in WiFi, allowing users to post their pictures to social media accounts right from the device! It comes with an integrated 35mm-150mm optical zoom and a 5″ touchscreen display.
If you were hoping to pick one of these up instead of buying a new DSLR- don't expect to save too much! The expense is still a hefty $1,699 to purchase one. This is comparable and maybe even more expensive than similar consumer entry-level cameras on the market.
|
{
"redpajama_set_name": "RedPajamaC4"
}
| 4,382
|
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Start work in an excellent Primary school in Wandsworth, London. This Primary school is looking for someone who is a positive, creative Key Stage 2 Teacher to start work in April 2017. This excelling school is known for its great academic success and is recognised for its personality and diversity. The school offers free parking on site and for those traveling by public transport the school is located 6 minutes away from the train station.
This Primary School is a charming characteristic place to work. The school upholds a tremendously supportive Senior Leadership team, which strives for success. This Primary School is known for its extraordinary support for SEN students and teaching approaches that offers extra support and adapts to the needs of these pupils. This 'Outstanding' school is known for its high-spirited community events such as their musicals, plays and charity events involving parents and the community.
You will be employed to teach a lovely Year 3 class which contains 30 mixed ability pupils. You will be one of a team of three Year 3 teachers who work together and will plan core subjects collectively, non-core subjects will require you to plan independently.
This Primary School is searching for someone positive, creative and fun. They are looking for a Year 3 Teacher Key Stage 2 (KS2) Teacher, who demonstrates good behaviour management skills. They are looking for someone who has a track record of raising attainment of all children, great humour, determined and determined to help the success of their pupils. The ideal candidate will have a minimum of 1 years of experience as a Year 3, Key Stage 2 (KS2) teacher and have excellent knowledge of the subject.
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|
{
"redpajama_set_name": "RedPajamaCommonCrawl"
}
| 5,034
|
Q: Checkbox issue on ios safari Issue Image
I am facing this issue only for ios safari. this checkbox working ok for other platforms.
I cant inspect to apply the styling.
On web safari its working fine as well.
A: I ran into a similar issue with a button. This line of code fixed it for me.
-webkit-appearance: none;
|
{
"redpajama_set_name": "RedPajamaStackExchange"
}
| 2,287
|
Q: не работает выбор через input и if При вводе(через input) 1 и 0 все ровно выдает 1
class FirstClass:
def FirstDef(self):
print('0 или 1:')
inpt = input()
if inpt == 0:
print('Hello, 0')
elif inpt != 1:
print('Hello, 1')
p = FirstClass()
p.FirstDef()
A: У тебя в elif inpt != 1, что можно перевести как - "Если inpt не равно 1."
Просто измени != на ==
UPD
Также возможно ещё проблема в типе получаемого значения
Попробуй inpt = int(input()). Это преобразует получаемое значение из input в целочисленный тип int
A: class FirstClass:
def FirstDef(self):
inpt = input('0 или 1:')
if inpt == '0':
print('Hello, 0')
elif inpt == '1':
print('Hello, 1')
A: input() по умолчанию будет считывать строку. Тут есть два пути:
*
*Преобразовать полученные данные в int: int(input())
*Сравнивать со строкой: if unpt == '1'
|
{
"redpajama_set_name": "RedPajamaStackExchange"
}
| 2,233
|
'Weird red sphere' filmed over South Carolina's Kiawah Island on Christmas Eve
© Debra Thomson, Kiawah Island Girl
Mark Pierce
The Charlotte Observer
A South Carolina woman says she filmed a possible UFO off South Carolina's Kiawah Island on Christmas Eve, and other witnesses are stepping forward on social media to report they saw the same "beautiful red sphere."
"I'm not a nut," wrote
Debra Thompson in a YouTube post with the video. "…I just wanted to know if anyone has had any experiences in the last few days…It really is quite amazing when you see one that seems to 'splat' out of another dimension and change into a round shape."
Kiawah Island is just off the South Carolina coast, about 25 miles south of Charleston.
Thompson says in the video that she spotted the object about 9:30 p.m. on Christmas Eve as she stood on the deck of her home. One five-minute video shows "an extraordinarily bright and beautiful" red ball as it bounces, stops, fades and then grows brighter.
"What the hell is that?…It looks like fire in the sky," Thompson says in the video. "That's so weird. It just seems like it's observing….I don't think it's some kid's toy and I know it's not an airplane."
TV station WCBD posted Thompson's video on Dec. 27 and reported four days later that the station had "received several emails from people who believe they may have also seen the mysterious object" in eastern South Carolina.
Even more people posted sightings on Facebook, including some who say they saw it in Ladson, North Myrtle Beach, Summerville and Edisto Beach, where someone told WCBD a room inside their home "lit up brighter than the full moon at about 6 a.m."
Thompson says she has also heard directly from witnesses, including one who "saw something strange in the sky last night while driving on the highway."
Some social media commenters have offered more down-to-earth ideas, guessing it was a drone, a Chinese lantern or a weather balloon.
Thompson has disputed those theories on YouTube and Facebook, saying the object was flying, "not floating."
"It was dead still that night and crystal clear," Thompson wrote Sunday. "There wasn't a sound outside except for some owls. Not even a breeze. This was very high in the sky and it intelligently moved."
The web site UFO-Hunters.com says UFOs have been reported at least twice before off Kiawah Island since 2009, including a 2012 instance in which the object was described as "a very red round light."
The Charleston Post & Courier reported on Dec. 31 that the sphere is "a phenomenon that turns up in the sky here every so often," including multiple reports in 2015.
Related Topics:fire in the skyred ball
'Furry animal' turns out to be clump of spiders
Mystery of the Blue Light in New York continues !! Another video with strange lights becomes viral
A Tesla electric car with an activated autopilot function recorded an invisible person who allegedly moved around the cemetery. Social network users jokingly noted in the comments that, most likely, this is some new function from Elon Musk, which allows you to see ghosts.
In the United States, a Tesla electric car with an activated autopilot function recorded an invisible person who allegedly moved through a cemetery.
The corresponding video was posted by Twitter user Ovidiu Maciuc.
The recording shows how a silhouette of a man appears on the monitor of an electric car, moving around the cemetery. After that, the driver raises the camera and starts filming the graveyard through the windshield, but there are no people there.
After some time, the "ghost" went in the opposite direction from Tesla and disappeared from the on-board computer screen.
Tesla collision avoidance system detecting an invisible human/entity at the cemetery. Excuse me but wtf @elonmusk ? pic.twitter.com/VcANAzH1uh
— Ovidiu Maciuc (@OMaciuc) January 12, 2021
Social network users jokingly noted in the comments that, most likely, this is some new function from Elon Musk, which allows you to see ghosts.
For many though, if you take into account the comments, the video seemed rather creepy. Some even tried to guess what the navigation system actually showed.
Some users thought the system could recognize ghosts. Others refuted this version and said that the reason for all this is an insufficiently accurate sensor, which was used for the equipment of the Tesla car.
Earlier it became known that Tesla electric cars in the near future may receive a new function with which they can talk with pedestrians. For this, American cars will be equipped with special external speakers.
In addition, Tesla cars in the future will receive the option to change the horn and sound of movement at low speeds to warn pedestrians. According to Elon Musk, among the sounds of movement there will be the sound of the clatter of a horse's hooves, and as a whistle – the bleating of a goat.
About two weeks ago, Tel Aviv residents noticed that the concrete surface outside their homes was heating up and steam was coming out of the ground. Tests showed that steam that reached 60 ° C (140 ° F) was water based.
The witness explains: "I was afraid that there was a power line in the area and asked a worker to dig out the ground with a shovel. Steam suddenly came out. I imagined it was probably a geyser. It seemed to me that this was a geological incident – also because there were no problems with electricity in the building. "
עוד אנשי מקצוע בשטח. אני מבין שכל גורמי התשתיות ובהם גם אנשי חברת החשמל במקום pic.twitter.com/2vCfqrVqnl
— Bar Peleg (@bar_peleg) January 1, 2021
Although the experts did not find any hazardous substances or any risk to the stability of buildings at the site, residents as well as kindergartens in the area were evacuated.
Officials described the heat source as "trapped energy" of unknown origin.
Work continues, steam is still rising and the ground is still hot. It is currently unclear what is causing the warming. Note the hole dug in the area. The area is still blocked.
Mysterious origins
City officials said they will "continue to monitor the temperature of the earth, which is expected to cool down for a long time, and will continue to investigate the causes of the unusual event."
Israel Electric Corporation has not found a connection between heat and power in the area.
חדשות מחמי גבירול: העבודות והמדידות נמשכות. האדים כנראה פסקו וגם האדמה מעט התקררה (שימו לבל לסרטון, במקום המדידה הזה 39.3 מעלות). כמה סברות ששמעתי על הסיבה מגורמים שעבדו בשטח: תשתית חשמל ישנה בעומק הקרקע (חברת חשמל שללו) או חומר אורגני שבמגע עם מי תהום התחמם
צילום @ilanrcohen1 pic.twitter.com/CDKtDxVdQF
The Israel Geological Survey confirmed the rise in temperature after testing ground and water temperature levels, but said it has not yet found an explanation.
Despite their best efforts, municipal officials, the fire department, Israel Electric Corporation and the Ministry of the Environment have yet to find a source of heat.
Meanwhile, the Tel Aviv municipality has informed dozens of evacuees that they can return to their homes. However, residents are not going to return until they receive a detailed account of the source of the mysterious event.
"They evacuated us because they were concerned about our safety, and now they are urging us to return without any convincing explanation. How can you be sure that there is no more danger? "
Photo by WILLIAM WEST - AFP VIA GETTY IMAGES
Some people in Chiayi, Taiwan took pictures of a large dark red moon hanging in the night sky on the first night of 2021 and uploaded them to Facebook. There are also people in Tainan who have photographed the rare "red moon". The weird scene has aroused heated discussions among netizens. Some people worry that an earthquake may occur, while others suspect that this is a precursor to the year of disaster in 2021?
Yesterday, on January 1 at about 8:00 in the evening, Chiayi residents shared a photo of "2021's first red moon" on Facebook. As you can see in the photo, the weather was quite good at that time. There was a clear big round moon in the night sky, but it was a dark red moon, which was very different from the usual moon.
Later, people in Kaohsiung and Tainan also posted photos of the red moon they had taken.
The weird and rare "big red moon" immediately attracted the attention of netizens. Some people think that such a sight is caused by air pollution, and some people think that the red moon is "extremely beautiful", but many people worry about whether it is a harbinger before the disaster ?
"Hope is not a harbinger of disaster~", "A harbinger of disaster in 2021???", "It looked uneasy", "After seeing the red moon, I hope everyone will be safe".
Some netizens worry that this is a pre- earthquake omen.
"Remember the red moon before the 921 earthquake (omen)", "earthquake precursors", "I feel that there will be an earthquake again recently", and "It seems that 2021 will be another year of bloody disaster."
The British clairvoyant Craig Hamilton-Parker published his prediction for 2021 on YouTube in December last year, stating that, as far as the world is concerned, 2021 will be a year full of social unrest, armed conflict and political changes. There will be difficult times right now until 2025.
He also predicted that the biggest worry is climate and earthquakes. A tsunami will occur near Japan. Large earthquakes will occur in the Himalayas, Iran and the Americas. There will also be problems such as floods, dams bursting, and huge icebergs obstructing shipping. Until 2025, the severity of environmental problems will gradually increase.
|
{
"redpajama_set_name": "RedPajamaCommonCrawl"
}
| 6,094
|
\section{Introduction}
\setcounter{equation}{0}
Solutions of long flexible polymer chains in confined geometries
such as thin films, porous media or mesoscopic particles dissolved
in the solution have been extensively studied during last years,
including experimental, numerical and theoretical investigations.
These investigations showed that polymer solutions and binary liquid
mixture in confined geometries gave rise to a new phenomena not
observed in the bulk. The confinement of critical fluctuations of
the order parameter in a binary liquid mixture leads to an effective
long-ranged forces between the confining walls or particles immersed
in fluid as it was predicted by \cite{FdeG78}. It is named critical
(or thermodynamic) Casimir force. Such fluctuation-induced forces
are omnipresent in the nature. For example, such forces arise from
the confinement of quantum fluctuations of the electromagnetic field
and due to the well known quantum-electrodynamic Casimir effect
\cite{C48}. In polymer solutions the reason for this depletion force
originates from the presence of depletion zones near the confining
walls or mesoscopic particles due to the additional amount of
entropic energy for polymers confined within the slit or between
colloidal particles. For entropic reasons the polymer chains avoid
the space between the walls or two close particles. This leads to an
unbalanced pressure from outside which pushes the two walls or two
colloidal particles towards each other. In the case of addition of
the polymer chains to the solvent of colloidal solution effective
attraction between particles leads to flocculation \cite{SHT80}.
Such solvent-mediated flocculation mechanism was observed
experimentally for silica spheres immersed in the binary liquid
mixture of water and 2,6-lutidine \cite{BE85,GKM92,KM95}. Improving
of the experimental technique allowed recently even measure with
high accuracy the depletion force between a wall and a single
colloidal particle \cite{OSO97,RBL98,VCLY98,HHGDB08}. It should be
mentioned, that the case of two parallel walls gives the possibility
via the Derjaguin approximation \cite{D34} to describe the case of
big colloidal spherical particle, whose radius $R$ is large than the
radius of gyration $R_{g}$ and the distance between particle and the
wall $L$. It indicates, that the investigation of the case of
polymer solutions confined to geometry of two parallel walls is
important not only for description of polymer solutions confined to
film geometry and porous media, but it is also interesting from the
point of view of investigation of behavior of big colloidal
particles in polymer solutions.
During long period the interaction between polymers and colloidal
particles has been modeled by approximating the polymer chains as
hard spheres \cite{AO54,AO58}. But, such approach does not give
possibility to describe correctly behavior of small colloidal
particles in polymer solution and for the case of colloidal particle
of the big size the difference between theoretical predictions and
experimental data are bigger than $10{\%}$. In accordance with this
more effective were approaches which took into account the chain
flexibility. For example, for the case of strongly overlapping
polymer chains as it has place for the case of semidilute solution,
the chain flexibility is taken into account via phenomenological
scaling theory \cite{JLdeG79,deGS79} or self-consistent field theory
\cite{O96}. In the case of dilute polymer solution different polymer
chains do not overlap and the behavior of such polymer solution can
be described by a single polymer chain using the model of random
walk (for an ideal chain at $\theta$-solvent) or self-avoiding walk
(the real polymer chain with excluded volume interaction). The last
case corresponds to the situation when solvent temperature is above
the $\theta$-point (good solvent) and polymer coils are less compact
than in the case of ideal chains. The remarkable progress in the
investigation of this task was achieved by \cite{E97,SHKD01} via
using of dimensionally regularized continuum version of the field
theory with minimal subtraction of poles in $\epsilon=4-d$, where
$d$ is dimensionality of the space. But, as it is easy to see
\cite{SHKD01}, still there are a lot of unsolved problems and the
question arises : "How to find the theory which allows to explain
experimental data in a better way?".
One of the methods, which up to our knowledge has not yet been applied to
this task is the massive field theory approach. This method, as it
was shown for the case of infinite \cite{Par80,Parisi},
semi-infinite \cite{DSh98} systems and specially for the case of
dilute polymer solutions in semi-infinite geometry \cite{U06} gives
better agreement with experimental data and results of the Monte
Carlo calculations. In accordance with this, the emphasis of the
present work is on the investigation of dilute polymer solution
confined to geometry of two parallel walls using the massive field
theory approach in fixed dimension $d=3$.
The most remarkable properties of fluctuation-induced forces is
their universality. They are independent of most microscopic details
and depend only on a few macroscopic properties such as the
adsorption properties of the confining walls or shape of the
particles. In accordance with this we used different combinations of
confining walls, i.e. we performed calculations for the case of two
repulsive walls, two inert walls and mixed case of one repulsive and
one inert wall. Besides, taking into account the Derjaguin
approximation \cite{D34} we obtained results for colloidal particles
of big radius near the wall and compare the obtained results with
experimental data\cite{RBL98}. In the case of two repulsive walls we
found good agreement of our results with results of Monte Carlo
simulations \cite{MB98,HG04}.
\section{The Model}
We shall assume that the solution of polymer chains is sufficiently
dilute, so that interchain interactions and overlapping between
different chains can be neglected, and it is sufficient to consider
the configurations of a single chain. Long flexible polymer chains in a good
solvent are perfectly described by a model of self-avoiding walks (SAW) on a regular
lattice \cite{CJ90}, \cite{Sh98}. Taking into account the
polymer-magnet analogy developed by \cite{deGennes}, their scaling
properties in the limit of an infinite number of steps $N$ may be
derived by a formal $n \to 0$ limit of the field theoretical
$\phi^4$ $O(n)$- vector model at its critical point. The average
square end-to- end distance, the number of configurations with one
end fixed and with both ends fixed at the distance $x=\sqrt{({\vec
x}_{A}-{\vec x}_{B})^{2}}$ exhibit the following asymptotic behavior
in the limit $N\to \infty$ \begin{equation} <R^2>\sim N^{2\nu},\quad\quad\quad
Z_{N}\sim q^{N}N^{\gamma-1},\quad\quad\quad Z_{N}(x)\sim
q^{N}N^{-(2-\alpha)},\label{RZ} \end{equation}
respectively. $\nu$, $\gamma$ and $\alpha$ are the universal
correlation length, susceptibility and specific heat critical
exponents for the $O(n)$ vector model in the limit $n\to 0$, $d$ is the space dimensionality, $q$
is a non universal fugacity. $1/N$ plays a role of a critical
parameter analogous to the reduced critical temperature in
magnetic systems.
In the case when the polymer solution is in contact with a
solid substrate, then the monomers interact with the
surface. At temperatures, $T<T_a$, the
attraction between the monomers and the surface leads to a critical adsorbed
state, where a finite fraction of the monomers is attached to the
wall and form $d-1$ dimensional structure. Deviation from the adsorption
threshold $(c\propto(T-T_a)/T_a)$ changes sign at the transition between the
adsorbed (so-named normal transition, $c<0$) and the nonadsorbed
state (ordinary transition, $c>0$) and it plays a role of a
second critical parameter. The adsorption threshold for long-flexible
infinite polymer chains, where $1/N\to 0$ and $c\to 0$ is a multicritical phenomenon.
The aim of the present investigations is to describe the behavior of
such dilute solution of long-flexible polymer chains confined to a
slit geometry of two parallel walls located at the distance $L$ one
from another in $z$- direction such that the surface of the bottom
wall is located at $z=0$ and the surface of the upper wall is
located at $z=L$. Each of the two surfaces of the system is
characterized by a certain surface enhancement constant $c_{i}$,
where $i=1,2$. The correspondent effective Landau-Ginzburg
Hamiltonian describing such system is:
\begin{eqnarray} {\cal H}_{||}[{\vec \phi}] &=&\int d^{d-1}r \int_{0}^{L} d
z\bigg\lbrace \frac{1}{2} \left( \nabla{\vec{\phi}} \right)^{2}
+\frac{1}{2} {\mu_{0}}^{2} {\vec{\phi}}^{2} +\frac{1}{4!} v_{0}
\left({\vec{\phi}}^2 \right)^{2}
\bigg\rbrace\nonumber\\
&+&\frac{c_{1_0}}{2} \int d^{d-1}r {\vec{\phi}}^{2}({\bf r},z=0)
+\frac{c_{2_0}}{2}\int d^{d-1}r {\vec{\phi}}^2({\bf r},z=L),
\label{hamiltonianslit}\end{eqnarray}
where ${\vec \phi}({\bf x})$ is an $n$-vector field with the
components $\phi_i(x)$, $i=1,...,n$ and ${\bf{x}}=({\bf r},z)$,
$\mu_0$ is the "bare mass", $v_0$ is the bare coupling constant
which characterizes the strength of the excluded volume interaction
(EVI). The surfaces introduce an anisotropy into the problem, and
directions parallel and perpendicular to the surfaces are no longer
equivalent. In accordance with the fact that we have to deal with
the slit geometry $({\bf x}=({\bf r},0\leq z\leq L))$, only parallel
to surfaces Fourier transforms in $d-1$ dimensions take place. The
interaction of the polymer chain with the walls is implemented by
the different boundary conditions. As it was mentioned above, we
consider the case of two repulsive walls (the Dirichlet-Dirichlet
boundary conditions) \begin{equation} c_{1}\to +{\infty},\quad c_{2}\to
+{\infty}\quad or\quad{\vec \phi}({\bf {r}},0)={\vec \phi}({\bf
{r}},L)=0\label{DD}, \end{equation}
two inert walls (the Neumann-Neumann boundary conditions)
\begin{equation} c_{1}=0,\quad c_{2}=0\quad or\quad\frac{\partial{\vec \phi}({\bf
{r}},z)}{\partial z}|_{z=0}=\frac{\partial{{\vec \phi}({\bf
{r}},z)}}{\partial z}|_{z=L}=0\label{NN},\end{equation}
and the mixed case of one repulsive and one
inert wall ( the Dirichlet-Neumann boundary conditions) \begin{equation} c_{1}\to
+{\infty},\quad c_{2}=0\quad or\quad {\vec \phi}({\bf {r}},0)=0,
\quad\frac{\partial{{\vec \phi}({\bf {r}},z)}}{\partial
z}|_{z=L}=0\label{DN}.\end{equation}
The requirement in Eq.(\ref{NN}) describing the inert character of
the walls corresponds to the fixed point of the so-named special
transition \cite{DD81,D86,DSh98} in field theoretical treatment.
In the present case the only relevant lengths are the average
end-to-end distance $\xi_R=\sqrt{<R^2>}\sim N^{\nu}$ and the
length $L$ -- the distance between two walls. The properties of the
system depend on the ratio $L/\xi_R$. It should be mentioned, that
the present field-theoretical approach is not able to describe the
dimensional crossover from $d$ to $d-1$-dimensional systems which arises for $L<<\xi_{R}$.
In this case the system is characterized by another
critical temperature (see, for example, on situation in magnetic or liquid thin films)
and moves to a new critical fixed point.
In accordance with this the present theory is valid for the case
$L>>\xi_{R}$. Nevertheless, we performed some assumptions, which
allowed us to describe the region $L<<\xi_{R}$.
The well-known arguments of the polymer-magnet analogy
\cite{deGennes,CJ90,Sh98,E93} assume the correspondence between the
partition function $Z_{\parallel} ({\bf x},{\bf x}')$ of polymer
chain with ends fixed at ${\bf x}$ and ${\bf x}'$ immersed in the
volume containing the two parallel walls and the two-point
correlation function $<{\vec\phi({\bf x})}{\vec{\phi}}({\bf x}')>$
in the field theoretical $\phi^4$ $O(n)$- vector model at the formal
limit $n\to 0$ in the restricted geometry:
\begin{equation} Z_{\parallel}({\bf x},{\bf x}';N,L,v_{0})={\cal
IL}_{\mu_{0}^2\to N}(<{\vec \phi}_1({\bf x}){\vec\phi}_1({\bf
x'})>|_{n=0})\label{critpoly} \end{equation}
Here the r.h.s. denotes the Inverse Laplace transform $\mu^2\to N$
of the two point correlation function for a system modelled via the
corresponding Landau-Ginzburg Hamiltonian in the limit, where the
number of components $n$ tends to zero. $N$ determines the number of
monomers of the polymer chain and represents only an auxiliary
parameter, the trace along the chain and fixes its {\it size}
globally. The most common parameter in polymer physics to denote the
size of a polymer chains which can be observable in experiments is
$R_g$ \cite{CJ90},\cite{Sh98},\cite{E93}):
\begin{equation}
R_g^2\,=\chi^2_d\frac{R_x^2}{2}\label{RxRg}, \end{equation} where $\chi_d$ is a
universal numerical prefactor which depends on the dimension $d$ of
the system. For an ideal polymer chains one has
$\chi^2_d=\frac{d}{3}$ and for three dimensional case $N$ equals
$R_{x}^2/2$. For the chains with EVI it could be obtained within a
perturbation expansion \cite{CJ90}.
The basic element in our calculations is the Gaussian two-point
correlation function (or the free propagator) $<{\vec \phi}_{i}({\bf
x}){\vec \phi}_{j}({\bf x}')>_{0} $ in the mixed ${\bf p}z$
representation of the form
\begin{eqnarray} {\tilde G}_{\parallel}({\bf
p},z,z';\mu_{0},c_{1_{0}},c_{2_{0}},L) = \frac{1}{2 \kappa_0}
((\kappa_0^2+\kappa_0(c_{1_{0}}+c_{2_{0}})+c_{1_{0}}c_{2_{0}})e^{\kappa_0
L}
&-&(\kappa_0^2-\kappa_0(c_{1_{0}}+c_{2_{0}})+c_{1_{0}}c_{2_{0}})e^{-\kappa_0
L})^{-1}\nonumber\\
((\kappa_0^2+\kappa_0(c_{1_{0}}+c_{2_{0}})+c_{1_{0}}c_{2_{0}})e^{\kappa_0(L-|z-z'|)}
&+&(\kappa_0^2
-\kappa_0(c_{1_{0}}+c_{2_{0}})+c_{1_{0}}c_{2_{0}})e^{-\kappa_0(L-|z-z'|)}\nonumber\\
+(\kappa_0^2+\kappa_0(c_{2_{0}}-c_{1_{0}})-c_{1_{0}}c_{2_{0}})e^{\kappa_0(L-z-z')}
&+&(\kappa_0^2-\kappa_0(c_{2_{0}}-c_{1_{0}})-c_{1_{0}}c_{2_{0}})e^{-\kappa_0(L-z-z')}),\nonumber\\
\label{g0slit} \end{eqnarray} with $\kappa_{0}=\sqrt{p^2+\mu^2_{0}}$, where
${\bf p}$ is $d-1$ dimensional moment. It should be mentioned, that
in the case $L\to\infty$ and $0\leq z,z'<<L$ (or $0<< z, z'\leq L$)
the free propagator (\ref{g0slit}) reproduces the free propagator of
the semi-infinite model (see \cite{DSh98}).
\section{Thermodynamical description}
We consider a dilute solution of long-flexible polymer chains with
the slit and allow of the polymer coils exchange between the slit
and a reservoir outside the slit. Thus the polymer solution in the
slit is in equilibrium contact with an equivalent solution in the
reservoir. We follow the thermodynamical description of the problem
as given in \cite{SHKD01}. The free energy of interaction between
the walls in such a grand canonical ensemble is defined as the
difference of the free energy of an ensemble where the wall
separation is fixed at finite distance $L$ and that where the walls
are separated on infinite distance one from another:
\begin{equation} \delta F = -k_B T \,{\cal N}\,\ln\left(\frac{{\cal Z}_{||}
(L)}{{\cal Z}_{\parallel}(L\to\infty)}\right)\,,\label{dF2}\end{equation}
where $\cal{N}$ is the total amount of polymers in the solution and $T$ is
the temperature. ${\cal Z}_{\parallel}(L)$ is the partition function
of a polymer chain located in volume $V$ containing the walls at a
distance $L$:
\begin{equation} {\cal Z}_{\parallel} (L)=\int_V\int_V\,d^dx\,d^dx'\,{\cal
Z}_{\parallel}({\bf x},{\bf x}')~,\label{outintZ}\end{equation}
with ${\cal Z}_{\parallel}({\bf x},{\bf x}')$ representing the
partition function of a single polymer chain in the slit with its
ends fixed at points ${\bf x}$ and ${\bf x}'$. For convenience we
can renormalise the partition functions ${\cal Z}_{\parallel}(L)$
and ${\cal Z}_{\parallel}(L\to\infty)$ on the partition function $Z$
of one polymer chain in the volume $V$ without the walls. The volume
of system $V$ can be divided into two independent subsystems $V_i$
and $V_o$ which correspond to the volume inside and outside the
slit, respectively. This gives possibility to split the term $\ln
(\frac{{\cal Z}_{\parallel}(L)}{\cal Z})$ into two parts \begin{equation}
\frac{1}{V}\int_{V_{o}}d^{d}x(\frac{\hat{\cal Z}_{o}(z)}{\hat{\cal
Z}_{b}}-1)+\frac{1}{V}\int_{V_{i}}d^{d}x(\frac{\hat{\cal
Z}_{i}(z)}{\hat{\cal Z}_{b}}-1),\label{VOVI} \end{equation} with ${\cal Z}=V
\hat{\cal Z}_{b}$, $\hat{\cal Z}_{b}=\int_{V}d^{d}x' {\cal
Z}_{b}({\bf x},{\bf x}')$ where ${\cal Z}_{b}({\bf x},{\bf x}')$ is
the partition function of one polymer chain in the unbounded
solution with fixed ends at ${\bf x}$ and ${\bf x}'$ and $\hat{\cal
Z}_{o,i}(z)=\int_{V_{o,i}}d^{d}x' {\cal Z}_{\parallel}({\bf x},{\bf
x}')$.
In the thermodynamical limit (as ${\cal N},V\to\infty$) the contribution
from the first term in (\ref{VOVI}) disappear and the reduced free energy of interaction $\delta f$ per
unit area $A=1$ of the confining walls may be written as:
\begin{eqnarray} \delta
f =\frac{\delta F}{n_p k_B T} = L
&-& \int_{V_i} d^dx \frac{{\hat{\cal Z}}_i (z)}{{\hat{\cal Z}}_b}\\
+\int_{V_{HS_{1}}}d^{d}x \left(\frac{{\hat{\cal
Z}}_{HS_1}(z)}{{\hat{\cal Z}}_b}-1\right)
&+&\int_{V_{HS_{2}}}d^{d}x\left(\frac{{\hat{\cal
Z}}_{HS_2}(z)}{{\hat{\cal Z}}_b}-1\right),\label{df}\end{eqnarray}
where $n_p = {\cal N}/V$ is the number density of the polymer chains
in the bulk solution and
\eq{ \label{oneendint2} {\hat{\cal
Z}}_{HS_i}(z) = \int_{V_{HS}} d^d x' {\cal Z}_{HS_i}({\bf x},{\bf
x'})\,, } with $i=1,2$ and ${\cal Z}_{HS_i}({\bf x},{\bf x'})$
denoting the corresponding partition functions for a polymer chain
in a half space with two fixed ends at points ${\bf x}$ and ${\bf
x'}$. The functions ${\hat{\cal Z}}_i (z)$ and ${\hat{\cal
Z}}_{HS_i} (z)$ depend only on the $z$-coordinates perpendicular to
the walls. The {\it reduced free energy of interaction} $\delta f$,
according to (\ref{df}), is a function of the dimension of a length
and dividing it by another relevant length scale (namely that for
the size of the chain in the bulk, e.g. $R_x$) yields a universal
dimensionless scaling function \eq{ \label{Theta} \Theta(y) =
~\frac{\delta f}{R_x}\,, } where $ y = L/R_x $ is a dimensionless
scaling variable. The resulting depletion force between the two
walls induced by the polymer solution is denoted as: \eq{
\label{Gamma} \Gamma(y) =~-\frac{d (\delta
f)}{dL}~=~-\frac{d\Theta(y)}{dy}~. \vspace*{0.5cm}}
The total grand canonical free energy $\Omega$ of the polymer
solution with the slit is: \eq{ \label{tdlimitgrandcan} \Omega =
-n_p\,k_b\,T\,A\,L\omega } with \eq{ \label{omega}
\omega\,=\frac{1}{L}\int_0^L\,dz\,\frac{\hat{\cal Z}_i(z)}{\hat{\cal
Z}_b}. } Taking into account (\ref{df}) and (\ref{tdlimitgrandcan})
we can write for unit surface area $A=1$: \begin{equation}
\frac{\Omega}{n_{p}k_{B}T}=f_b\,L\,+\,f_{s_1}\,+\,f_{s_2}\,+\,\delta
f\,,\label{decompgrandcan}\end{equation} with the reduced bulk free energy per
unit volume $ f_b =-1$ and the reduced surface free energy per unit
area \begin{equation}
f_{s_i}=\int_{V_{HS_{i}}}dz\left( 1-\frac{{\hat{\cal
Z}}_{HS_i}(z)}{{\hat{\cal Z}}_b}\right).\label{surfm}\end{equation}
Further for convenience we can introduce ${\cal X}$, the total
system susceptibility in the form
\begin{equation}
{\cal X} =\frac{1}{V}\int_{V}\int_{V}d^dx\,
d^dx'\,< {\vec\phi}_1({\bf x}){\vec\phi}_1({\bf x'})>.\label{chi}\end{equation}
This definition is consistent with the bulk susceptibility for the
unbounded space given as ${\cal X}_b=\frac{1}{m^2}$ to all orders of
perturbation theory
(e.g. \cite{Parisi}). $\hat{\cal Z}_b$ being the Inverse Laplace
transform of ${\cal X}_b$ and $\hat{\cal Z}_b=1$ to all orders as
well. Accordingly to (\ref{critpoly}) and (\ref{chi}) we can rewrite
(\ref{df}) in the form
\begin{equation} \delta f = {\cal IL}_{\mu^2\to R_x^2/2}\Big\lbrace\,L\, ({\cal
X}_b-{\cal
X}_{||})\,-\,\Upsilon_{1}\,-\,\Upsilon_{2}\Big\rbrace,\label{dfcrit}
\end{equation} where ${\cal X}_{||}$ denotes the total susceptibility for a
slit geometry and $\Upsilon_{i}$ with $i=1,2$ give two half-space
(HS) contributions such that $ f_{s_i}={\cal IL}_{\mu^2\to
R_x^2/2}\big\lbrace\Upsilon_{i}\big\rbrace\,$ (see Appendix A).
\section{Correlation functions and renormalization conditions}
Correlation functions which involve $N'$ fields $\phi({\bf{x}}_{i})$
at distinct points ${\bf{x}}_{i}(1\leq i \leq N')$ in the bulk,
$M_{1}$ fields $\phi_{1}({\bf{r}}_{j_{1}},z=0)\equiv
\phi_{s_{1}}({\bf{r}}_{j_{1}})$ at distinct points on the wall $z=0$
and $M_{2}$ fields $\phi_{2}({\bf{r}}_{j_{2}},z=L)\equiv
\phi_{s_{2}}({\bf{r}}_{j_{2}})$ at distinct points on the wall
$z=L$, and $I$ insertion of the bulk operator
$\frac{1}{2}\phi^{2}({\bf{X}}_{k})$ at points ${\bf{X}}_{k}$ with
$1\leq k \leq I$, $I_{1}$ insertions of the surface operator
$\frac{1}{2}\phi_{s_{1}}^{2}({\bf{R}}_{l_{1}})$ at points
${\bf{R}}_{l_{1}}$ with $1\leq l_{1} \leq I_{1}$ and $I_{2}$
insertions of the surface operator
$\frac{1}{2}\phi_{s_{2}}^{2}({\bf{R}}_{l_{2}})$ at points
${\bf{R}}_{l_{2}}$ with $1\leq l_{2} \leq I_{2}$, have the form
\cite{D86,DSh98}
\begin{eqnarray} G^{(N',M_{1},M_{2},I,I_{1},I_{2})}(\{{\bf x}_{i}\},\{{\bf
r}_{j_{1}}\},\{{\bf
r}_{j_{2}}\},\{{\bf{X}}_{k}\},\{{\bf{R}}_{l_{1}}\},\{{\bf{R}}_{l_{2}}\})&=&\nonumber\\
< \prod_{i=1}^{N'} \phi({\bf
x}_{i})\prod_{j_{1}=1}^{M_{1}}\phi_{s_{1}}({\bf
r}_{j_{1}})\prod_{j_{2}=1}^{M_{2}}\phi_{s_{2}}({\bf
r}_{j_{2}})\prod_{k=1}^{I}\frac{1}{2}\phi^{2}({\bf{X}}_{k})
\prod_{l_{1}=1}^{I_{1}}\frac{1}{2}\phi^{2}_{s_{1}}({\bf{R}}_{l_{1}})
\prod_{l_{2}=1}^{I_{2}}\frac{1}{2}\phi^{2}_{s_{2}}({\bf{R}}_{l_{2}})>~~.
\label{10} \end{eqnarray}
Here, the symbol $<...>$ denotes averaging with Hamiltonian
(\ref{hamiltonianslit}). The free propagator of a Gaussian chain in
slit geometry in the mixed ${\bf{p}},z$ representation has the form
(\ref{g0slit}), as was mentioned above.
Taking into account that surface fields
$\phi_{s_{i}}({\bf{r}}_{j_{i}})$ and surface operators
$\frac{1}{2}\phi_{s_{i}}^{2}({\bf{R}}_{i})$ with $i=1,2$ scale with
scaling dimensions that are different from those of their bulk
analogs $\phi({\bf{x}}_{j})$ and $\frac{1}{2}\phi^{2}({\bf{X}}_{j})$
(see \cite{DSh98}), the renormalized correlation functions involving
$N'$ bulk fields and $M_{1}$ surface fields on the wall $z=0$ and
$M_{2}$ surface fields on the wall $z=L$, $I$ bulk operators,
$I_{1}$ and $I_{2}$ surface operators can be written as \begin{eqnarray}
G_{R}^{(N',M_{1}M_{2},I,I_{1},I_{2})} ( ;
\mu,v,c_{1},c_{2},L)=&&\nonumber\\ Z_{\phi}^{-(N'+M_{1}+M_{2})/2}
Z_{1}^{-M_{1}/2}Z_{2}^{-M_{2}/2} Z_{\phi^2}^{I}
Z_{\phi_{s_{1}}^2}^{I_{1}}
Z_{\phi_{s_{2}}^2}^{I_{2}}G^{(N',M_{1},M_{2},I,I_{1},I_{2})} ( ;
\mu_{0},v_{0},c_{1_0},c_{2_0},L)&&,\label{12} \end{eqnarray} where $Z_{\phi}$,
$Z_{1}$, $Z_{2}$ and $Z_{\phi^2}$, $Z_{\phi_{s_{1}}^2}$,
$Z_{\phi_{s_{2}}^2}$ are correspondent UV-finite (for $d<4$)
renormalization factors. The typical bulk and surface short-distance
singularities of the correlation functions $G^{(N',M_{1},M_{2})}$
can be removed via mass shift $\mu_{0}^{2}=\mu^2+\delta \mu^2$ and
surface-enhancement shifts $c_{i_0}=c_{i}+\delta c_{i}$,
respectively \cite{DSh98}.
The renormalizations
of the mass $\mu$, coupling constant $v$ and the renormalization
factor $Z_{\phi}$ are defined by standard normalization conditions
of the infinite-volume theory \cite{Parisi,BGZ76,A84,Z89,ID89}. In
order to adsorb uv singularities located in the vicinity of the
surfaces, a surface-enhancement shifts $\delta c_{i}$ are required.
In this connection the new normalization conditions should be
introduced. It is obvious, that in the limit $L\to \infty$ we should
have
\begin{eqnarray} \lim_{L\to\infty}\left[{\tilde
G}^{(0,2,0)}_{R}({\bf
p};\mu,v,c_{1},c_{2},L)\vert_{p=0}\right]&=&\frac{1}{\mu+c_1},\nonumber\\
\lim_{L\to\infty}\left[{\tilde G}^{(0,0,2)}_{R}({\bf
p};\mu,v,c_{1},c_{2},L)\vert_{p=0}\right]&=&\frac{1}{\mu+c_2}.\label{ccond1semi}
\end{eqnarray} For the renormalization factors $Z_{i}$, $Z_{\phi_{s_{i}}^2}$
where $i=1,2$ we obtain, respectively
\begin{eqnarray} \lim_{L\to\infty}\left[\frac{\partial}{\partial p^2}{\tilde
G}^{(0,2,0)}_{R}({\bf p};\mu,v,
c_{1},c_{2},L)\big\vert_{p=0}\right]&=&
-\frac{1}{2\mu(\mu+c_1)^2},\nonumber\\
\lim_{L\to\infty}\left[\frac{\partial}{\partial p^2}{\tilde
G}^{(0,0,2)}_{R}({\bf
p};\mu,v,c_{1},c_{2},L)\big\vert_{p=0}\right]&=&
-\frac{1}{2\mu(\mu+c_2)^2},\label{Zsurfcondsemi} \end{eqnarray} and
\begin{eqnarray} \lim_{L\to\infty}\left[{\tilde G}^{(0,2,0;0,1,0)}_{R}({\bf
p},{\bf P};\mu,v,c_{1},c_{2},L)\big\vert_{p,P=0}\right]&=&
\frac{1}{(\mu+c_1)^2},\nonumber\\
\lim_{L\to\infty}\left[{\tilde G}^{(0,0,2;0,0,1)}_{R}({\bf p},{\bf
P};\mu,v,c_{1},c_{2},L)\big\vert_{p,P=0}\right]&=&
\frac{1}{(\mu+c_2)^2}. \label{Z2surfcondsemi} \end{eqnarray} In the limit
$L\to\infty$ all these conditions yield exactly the same shifts
$\delta c_i$ and renormalization factors as in the semi-infinite
case. It is intuitively clear that in the case of two inert walls or
mixed walls situated on big, but finite distance $L$ with $L\gtrsim
R_{g}$ such that the chain is still not deformed too much from its
original size in the bulk, the shift of $c_0^{sp}\to c^{sp}$ may
depend on the presence of the other surface and hence on the size of
the slit. So, in the case of $L\gtrsim R_{g}$ (or $\mu L\gtrsim 1$)
from (\ref{g0slit}) and (\ref{ccond1semi}) we obtain new conditions
\begin{eqnarray} \lim_{L\mu\gtrsim 1}\left[{\tilde G}^{(0,2,0)}_{R}({\bf
p};\mu,v, c_1,c_2,L)\vert_{p=0}\right]&=&
\frac{1}{\mu+c_1}\left(1+\frac{2\mu}{\mu+c_1}\frac{\mu-c_2}{\mu+c_2}\mathrm{e}^{-2\mu
L}+{\cal O}(\mathrm{e}^{-4\mu L})\right),\nonumber\\
\lim_{L\mu\gtrsim 1}\left[{\tilde G}^{(0,0,2)}_{R}({\bf p};\mu,v,
c_1,c_2,L)\vert_{p=0}\right]&=&
\frac{1}{\mu+c_2}\left(1+\frac{2\mu}{\mu+c_2}\frac{\mu-c_1}{\mu+c_1}\mathrm{e}^{-2\mu
L}+{\cal O}(\mathrm{e}^{-4\mu L})\right). \label{ccondslit} \end{eqnarray}
The above mentioned conditions (\ref{ccondslit}) give one-loop order
corrections to the respective surface-enhancement shifts $\delta
c_{i}$ of semi-infinite theory in the case of large, but finite wall
separation $L$ . In accordance with this for the case of mixed walls
we obtain \begin{equation} \delta c_{1}^{S-O}=\delta c_{1}+\Delta^{(S-O)}
\label{cslitso}\end{equation} with corrections of order ${\cal O}(e^{-2\mu L})$
\begin{equation}
\Delta^{(S-O)}\,=\,\frac{\mu}{4}\left(\frac{1}{\mu
L}+C_E+\,\ln8\,-\,3+\,\ln \mu L\,-\mathrm{e}^{4\mu L}{\rm Ei}(-4\mu
L)\right)\mathrm{e}^{-2\mu L}.\label{deltaos} \end{equation}
In the case when both walls are inert, the modified surface
enhancement shifts are \begin{equation} \delta c_{i}^{S-S}=\delta c_{i} +\Delta^
{(S-S)}\label{cslitss} \end{equation} with
\begin{equation}
\Delta^{(S-S)}=-\Delta^{(S-O)}\,-\,\mu\left(\ln2\,-\,\frac{1}{2}\right)\mathrm{e}^{-2\mu
L}.\label{deltass} \end{equation} The above mentioned corrections $\delta
c_{i}$ are UV singular for $d=3$ dimensions. They provide the
singular parts of the counterterms that cancel the UV singularities
of correspondent correlation functions by analogy as it took place
for semi-infinite systems (see \cite{DSh98}). The above mentioned
corrections $\Delta^{(S-O)}$ and $\Delta^{(S-S)}$ are finite in
$d\leq 4$ dimensions.
\section{Results for Gaussian Chains}
Let us consider at the beginning the Gaussian model for ideal
polymer chains ($v_0=0$). As mentioned above it corresponds to the
situation of a polymer chain under $\Theta$-solvent conditions.
For general case of arbitrary $c_1$ and $c_2$ on the confining walls
we obtain for the reduced free energy of interaction:
\begin{eqnarray} \delta f=-\,{\cal IL}_{\mu^2\to
R_x^2/2}\Bigg\lbrace\frac{1}{\mu^3}
\Big[(\mu+c_1)(\mu+c_2)\mathrm{e}^{\mu L}\,&-&\,(\mu-c_1)(\mu-c_2)\mathrm{e}^{-\mu L}\Big]^{-1}\times\nonumber\\
\Big\lbrace4\,c_1c_2-\left(\mu(c_1+c_2)+2\,c_1c_2\right)\mathrm{e}^{\mu L}+
\left(\mu(c_1+c_2)-2\,c_1c_2\right)\mathrm{e}^{-\mu L}\Big\rbrace
&+&\,\frac{1}{\mu^3}\left(\frac{c_1}{\mu+c_1}\,+\,\frac{c_2}{\mu+c_2}\right)\Bigg\rbrace.
\label{dfgauss}\end{eqnarray}
First, consider the case of the Dirichlet-Dirichlet (D-D) boundary conditions (\ref{DD}) on
the confining surfaces. Taking the limits $\frac{c_1}{m}\to
\infty,\frac{c_2}{m}\to \infty$ yields:
\begin{equation} {\Theta}^{D,D}(y)=-4y\,{\cal {IL}}_{\tau\to(2y^2)^{-1}}
\left(\frac{1}{\tau^{3/2}}\frac{1}{1+\mathrm{e}^{\sqrt{\tau}}}\right)\,,
\label{thoogauss}\end{equation} where $\tau=\mu^2L^2$ and $y=\frac{L}{R_x}$.
The result indicates that if both $c_i$ being positive, the
depletion interaction potential is negative and hence the walls
attract each other due to the depletion zones near repulsive walls.
The inverse Laplace transform can only be performed numerically (the
plot is shown in Figure \ref{fig:theta_gamma_oo}) or may be expanded
for asymptotic values of $\sqrt{\tau}$. The obtained results for
ideal polymer chains in slit of two repulsive walls are in agreement
with previous theoretical results obtained in Ref.\cite{SHKD01}.
But, it should be mentioned, that on plotting these functions the
authors of \cite{SHKD01} used a rescaled variable $\sqrt{2}R_x$,
which was not mentioned there.
Now we proceed to the case of two inert walls, what corresponds to
the Neumann-Neumann (N-N) boundary conditions (\ref{NN}).
For the free energy of interaction we obtain \begin{equation}
{\Theta}^{N,N}(y)~=~0. \end{equation} This corresponds to the fact that ideal
chains do not loose free energy inside the slit in comparison to the
free chains in unrestricted space. The entropy loss is fully
regained by the surface interactions provided by the two walls.
Taking the limits $\frac{c_1}{m}\to \infty, \,\frac{c_2}{m}\to 0$ in
accordance with (\ref{DN}) (the Dirichlet-Neumann (D-N) boundary
conditions) from (\ref{dfgauss}) we obtain: \begin{equation}
{\Theta}^{D,N}(y)=-\,2y\,\,{\cal IL}_{\tau\to(2y^2)^{-1}}
\left(\frac{1}{\tau^{3/2}}\frac{1}{1+e^{2\sqrt{\tau}}}\right).
\label{thosgauss}\end{equation}
This result can only be evaluated
numerically and is plotted in Figure \ref{fig:theta_gamma_os}. Lets
consider different
asymptotic regions of $y$.\\
{\bf Wide slits ($y>>1$):}\hfill\\[0.1cm]
In the case $\mu L>>1$ from (\ref{thoogauss}) we obtain for two
repulsive walls: \begin{equation} {\Theta}^{D,D}(y)\,{\approx}\,
4y\bigg[\,{\rm{erfc}}\left(\frac{y}{\sqrt{2}}\right)-
\frac{1}{y}\sqrt{\frac{2}{\pi}}\exp\left(-\frac{y^2}{2}\right)\bigg]-
8y\bigg[\,{\rm{erfc}}\left(\sqrt{2}\,y\right)-\frac{1}{y\,
\sqrt{2\pi}}\exp\left(-2y^2\right)\bigg].\label{thooexp}\end{equation} The
force (\ref{Gamma}) becomes \begin{equation} \Gamma^{D,D}(y)\,{\approx}\,-4\,{\rm
erfc} \left(\frac{y}{\sqrt{2}}\right)\,+\,8\,{\rm
erfc}\left(\sqrt{2}\,y\right).\label{gaooexp} \end{equation}
And for one repulsive and one inert wall we have:
\begin{equation} {\Theta}^{D,N}(y){\approx}4y\,
{\rm{erfc}}\left(\sqrt{2}\,y\right)\,-\,\frac{4}{\sqrt{2\pi}}\,
\exp\left(-2y^2\right),\label{thosexp}\end{equation} which implies \begin{equation}
\Gamma^{D,N}(y){\approx}-4\,{\rm{erfc}}\left(\sqrt{2}\,y\right).\label{gaosexp}
\end{equation} These approximating functions are presented on Figures
\ref{fig:theta_gamma_oo} and \ref{fig:theta_gamma_os}, respectively.
\smallskip\\
{\bf Narrow slits ($y\ll1$)}\\[0.1cm]
In the case of narrow slit $\mu L<<1$ the asymptotic solution for
(\ref{thoogauss}) reads: \begin{equation}
{\Theta}^{D,D}(y){\approx}\,-\frac{4}{\sqrt{2\pi}}\,+\,y\,.
\label{thoonarrow}\end{equation} and the force simply becomes
$\Gamma^{D,D}(y){\approx}-1$.
For the depletion interaction potential (\ref{thosgauss}) we get:
\eq{ \label{thetanarrowos}
{\Theta}^{D,N}(y){\approx}\,-\frac{2}{\sqrt{2\pi}}\,+\,y~. } For the
force we have again $\Gamma^{D,N}(y){\approx}-1$.
These results can be understood phenomenologically. In our units the
quantities ${\Theta}$ and ${\Gamma}$ are normalized to the overall
polymer density $n_p$. So, the above results simply indicate that
the force is entirely induced by the free chains surrounding the
slit or in other words by the full bulk osmotic pressure from the
outside of the slit. No chain has remained in the slit. It is
reasonable in the case of repulsive walls in the limit of narrow
slits. Unfortunately, the narrow slit regime is beyond the validity
of our approach in the presence of EVI, as mentioned above. But, the
above mentioned arguments can be used in order to obtain the leading
contributions to the depletion effect as $y\to 0$. We can state that
in the case of very narrow slits the chains would pay a very high
entropy to stay in the slit or even enter it. It is due to the fact
that the phase space containing all possible conformations is
essentially reduced by the squeezing confinement to a size
$\frac{d-1}{d}$\,times its original size (for an unconfined chain).
Therefore, the ratio of partition function of polymer chain in slit
and free chain partition function vanishes strongly as $y\to 0$,
which implies directly the function $\omega$ in (\ref{omega}).
Setting $\omega=0$ and using only the corresponding surface
contributions and the bulk contribution ($f_b=-1$) in
(\ref{decompgrandcan}) must lead to the same asymptotic limits in
the narrow slit regime.
The advantage of this procedure is that no expansion necessary and it
should be equally valid in the EVI-regime.
In Figures \ref{fig:theta_gamma_oo},\ref{fig:theta_gamma_os}
and \ref{fig:theta_gamma_ss} the depletion interaction
potential $\Theta(y)$ and depletion force $\Gamma(y)$ are plotted for all boundary
conditions. As expected, the results for mixed walls are located in
between the results of two inert walls and those of two repulsive
walls.
\section{Results for good solvent}
In good solvent the EVI between chain monomers play a crucial role
so that the polymer coils occupy the bigger volume and are less
compact than in the case of ideal polymer chains. The influence of
EVI on the depletion functions can be obtained in the framework of
the massive field theory approach in fixed dimensions $d=3$ up to
one-loop order expansion of the two-point correlation functions
$G^{(2,0,0)}$ restricted in slit geometry (\ref{hamiltonianslit}).
The bare total susceptibility ${\cal X}_{\parallel}^{bare}$
(see(\ref{dfcrit})) for the slit geometry in accordance with
(\ref{chi}),(\ref{omega}) and (\ref{10}) is : \begin{eqnarray} {\cal
X}^{bare}_{||}(\mu_0,v_0,\c{1},\c{2},L)=\frac{1}{L}
\int_0^L\int_0^Ldzdz'\bigg\lbrace\tilde{G}_{||}({\bf p}=0,z,z';\mu_0,\c{i},L)\nonumber\\
-\frac{n+2}{6}v_0\int_0^Ldz''\int_{\bf q}\tilde{G}_{||}({\bf
p}=0,z,z'';\mu_0,\c{i},L) \tilde{G}_{||}({\bf
q},z'',z'';\mu_0,\c{i},L) \tilde{G}_{||}({\bf
p}=0,z'',z';\mu_0,\c{i},L)\bigg\rbrace\,.\label{1Loop} \end{eqnarray} The two
HS contributions denoted by $\Upsilon_{i}$ (see (\ref{dfcrit}))can
be obtained in accordance with (\ref{surfm}) similarly to
(\ref{1Loop}) with the propagators of semi-infinite system. Some
details for the calculation of these quantities for zero-loop and
one-loop order for different surface critical points of interest
(ordinary, special) are presented in the Appendix A.
\subsection{Two repulsive walls}
Lets consider first the case of D-D boundary conditions (\ref{DD})
on each of the two surfaces. In this case no surface divergences
appear in the calculation of the correlation functions and any
surface renormalization is not necessary at all. Each surface term
($f_{s_i}\,,\,i=1,2$) contributes: \eq{ \label{surfO}
f^{D}_{s}\,=\,\sqrt{\frac{2}{\pi}}\left(\,1\,-
\,\frac{\ln\frac{9}{8}}{4}\right)\,R_x\,. } After performing the
standard mass and coupling constant renormalization and additive
subtraction at zero momentum all divergent terms disappear and the
corespondent function ${\cal X}_{||\,ren}^{D,D}$ can be obtained.
In order to be concise, we do not present here the complicated form
for ${\cal X}_{||\,ren}^{D,D}$ and just discuss the limiting cases
of wide and narrow slit regimes. \\
{\bf Wide slits ($y\gtrsim1$):}\hfill\\[0.1cm]
\begin{figure}[ht!]
\begin{center}
\includegraphics[width=8cm]{thetaoo_paper}\hspace*{0.3cm}
\includegraphics[width=8cm]{gammaoo_paper}
\caption{The functions $\Theta(y)$ and $\Gamma(y)$ for two repulsive
walls} \label{fig:theta_gamma_oo}
\end{center}
\end{figure}
The massive field-theory approach at fixed dimensions $d=3$ gives a
rather simple result in one-loop order than results obtained in \cite{SHKD01} with help of dimensionally
regularized field theory with minimal subtraction of poles in
$\epsilon$-expansion. It should be mentioned, that in \cite{SHKD01}
a wide slit approximation was carried out as well up to the first
non trivial order (apparently ${\cal O}\left(\mathrm{e}^{-\mu L}\right)$).
Therefore, we performed calculations up to the next order term
$\sim{\cal O}\left(\mathrm{e}^{-2\mu L}\right)$. The renormalized total
susceptibility for the slit geometry up to one-loop order in $d=3$
for polymer case $n\to 0$ in the wide slits regime $\mu L>>1$ is:
\begin{eqnarray} {\cal X}_{||\,ren}^{D,D} L {\approx}
\frac{L}{\mu^2}\,&-&\,\frac{1}{\mu^3}\left(2-\frac{\ln\frac{9}{8}}{2}\right)\,
+\,\frac{\mathrm{e}^{-\mu L}}{\mu^3}\left(4-\ln\frac{3}{2}\right)\nonumber\\
-\,\frac{\mathrm{e}^{-2\mu L}}{\mu^3}\bigg\lbrace\frac{9-C_E-2\,
\ln\frac{3}{2}}{2}\,-\,\frac{3}{2\mu L}\,-\,\frac{\ln(\mu L)}{2}
&+&\,\mathrm{e}^{\mu L}\,\Ei{-\mu L}\,-\,\mathrm{e}^{3\mu L}\,\Ei{-3\mu
L}\,+\,\frac{\mathrm{e}^{4\mu L}}{2}\,\Ei{-4\mu
L}\bigg\rbrace.\label{suscoo}\end{eqnarray} The exponential integral
functions, denoted by $\Ei{x}$, can be expanded for large, negative
arguments as well in accordance with (see e.g. \cite{Gradshteyn}):
$\mathrm{e}^{x}\,\Ei{-x}=\,-\,\frac{1}{x}\,+{\cal
O}\left(\frac{1}{x^2}\right)$. Thus, for the depletion interaction
potential we obtain: \begin{eqnarray} \Theta(y){\approx}
\left(4-\lne{\frac{3}{2}}\right)
\left[y\,{\rm{erfc}}\left(\frac{y}{\sqrt{2}}\right)-
\sqrt{\frac{2}{\pi}}\exp\left(\frac{y^2}{2}\right)\right]
-\frac{55}{48y}\,{\rm erfc}\left(\sqrt{2}\,y\right)\nonumber\\
-\,\left(\frac{163}{24}-\lne{\frac{3}{2}}-\frac{C_E}{2}\right)\,
\left[2\,y\,\,{\rm{erfc}}\left(\sqrt{2}\,\,y\right)-\,
\sqrt{\frac{2}{\pi}}\,\,\exp\left(-2y^2\right)\right]
-\,\frac{y}{4}\,\,{\cal IL}_{\tau\to\frac{1}{2y^2}}
\left(\frac{\lne{\tau}}{\tau^{3/2}}\,\mathrm{e}^{-2\sqrt{\tau}}\right)~.\label{thetaoo}
\end{eqnarray}
A comparison of the obtained results to the ideal chain results in a wide slit
regime (see Figure 1) shows that the EVI
reduces the depletion effects for two repulsive
walls.\smallskip\\
{\bf Narrow slits $(y\ll1)$:}\hfill\\[0.1cm]
Following the simple argument obtained from the discussion of the
exactly solvable ideal chain model the entire slit contribution
$\omega$ (\ref{omega}) to the reduced free energy of interaction
$\delta f$ in (\ref{decompgrandcan}) is simply set to zero and the
depletion effect is only calculated from the bulk and surface
contributions. In this limit the depletion potential becomes: \begin{equation}
\Theta(y){\approx}\,y\,-\,
\frac{2\,\sqrt{2}}{\sqrt{\pi}}\left(\,1\,-
\,\frac{\ln\frac{9}{8}}{4}\right)\,.\end{equation} and the force again is
unity. In Figure \ref{fig:theta_gamma_oo} one can follow how the two
regimes come to match in the crossover regime $y\approx1$. The
lowest order expansion in case of wide slits would not be able to
show this matching. With these two approximations we are in the
position to present a rather complete picture of the problem in
comparison to the approach given in \cite{SHKD01}.
\subsection{One repulsive / One inert wall}
This case has not been studied so far in any approach. Since we are
now dealing with an inert wall, the surface renormalization should
be taken into account. Again, the full result for the renormalized
total susceptibility in a slit system ${\cal X}_{||\,ren}$ has
complicated form and we discuss just limiting cases of wide and
narrow slits.
The surface contribution for a repulsive wall coincides with
(\ref{surfO}) and for inert wall we have:
\begin{equation}
f^{N}_{s}\,=\frac{2\ln2\,-\,1}{8}\sqrt{\frac{2}{\pi}}\,R_x\,\,.
\label{surfS}\end{equation}
{\bf Wide slits ($y\gtrsim1$):}\hfill\\[0.1cm]
For the total susceptibility up to ${\cal O}\left(\mathrm{e}^{-2\mu
L}\right)$ order we obtain: \begin{eqnarray} {\cal X}_{||\,ren}^{OS}\,L
{\approx}\frac{L}{\mu^2}\,-
\,\frac{1}{\mu^3}\left(1+\frac{2\,\ln\frac{4}{3}\,-\,\frac{1}{2}}{4}\right)\,
&+&\,\frac{\mathrm{e}^{-\mu L}}{\mu^3}\left(\frac{2\ln4\,-\,\ln3\,-\,1}{2}\right)\nonumber\\
+\,\frac{\mathrm{e}^{-2\mu
L}}{\mu^3}\bigg\lbrace\frac{31-2C_E}{8}-\frac{\ln3}{2}-
\frac{7\,\ln2}{4}-\frac{3}{4\mu L}-\frac{\ln(\mu L)}{4}
&+&\frac{\mathrm{e}^{\mu L}}{2}\,\Ei{-\mu L}\,+\,\frac{\mathrm{e}^{4\mu L}}{4}\,
\Ei{-4\mu L}\,-\,\frac{\mathrm{e}^{3\mu L}}{2}\,\Ei{-3\mu L}\bigg\rbrace.
\label{suscos}\end{eqnarray} In comparison to the result for ideal chains
(\ref{thosgauss}) where the lowest order term, contributing to the
total susceptibility in the wide slit limit is of order ${\cal
O}\left(\mathrm{e}^{-2\mu L}\right)$, now the additional term of order
${\cal O}(\mathrm{e}^{-\mu L})$ appears.
\begin{figure}[ht!]
\begin{center}
\includegraphics[width=8cm]{thetaos_paper}\hspace*{0.3cm}
\includegraphics[width=8cm]{gamma_os_paper}
\caption{The functions $\Theta(y)$ and $\Gamma(y)$ for one repulsive
and one inert wall with and without excluded volume interactions
(EVI)} \label{fig:theta_gamma_os}
\end{center}
\end{figure}
In this case the depletion interaction potential becomes :
\begin{eqnarray} \Theta(y){\approx}\frac{1}{2}
\left(\ln{\frac{16}{3}-1}\right)\left(y\,{\rm erfc}
\left(\frac{y}{\sqrt{2}}\right)- \sqrt{\frac{2}{\pi}}\,
\exp\left(-\frac{y^2}{2}\right)\right)+\frac{55}{96y}\,
{\rm erfc}\left(\sqrt{2}\,y\right)\nonumber\\
+ \frac{1}{4}\left(\frac{229}{12}-C_E-\lne{1152}\right)
\left(2y\,{\rm erfc}\left(\sqrt{2}\,y\right)-
\sqrt{\frac{2}{\pi}}\,\exp\left(-2y^2\right)\right)
+\frac{y}{8}\,{\cal IL}_{\tau\to\frac{1}{2y^2}}
\left(\frac{\ln{\tau}}{\tau^{3/2}}\,\mathrm{e}^{-2\sqrt{\tau}}\right).\label{thetaos}
\end{eqnarray} The Figure \ref{fig:theta_gamma_os} presents the depletion
interaction potential $\Theta(y)$ and the force $\Gamma(y)$. It
clearly indicates that in comparison to ideal chains the depletion
effect is stronger in the regime of wide slits.\hfill\smallskip\\
{\bf Narrow slits $(y'\ll1)$:}\hfill\\[0.1cm]
Following again the thermodynamic argument, $\omega$ is set to zero
and only bulk and surface contributions are taken into account in
(\ref{decompgrandcan}). One gets: \begin{equation} \Theta(y) {\approx}\,y\,-
\,\left(1+\frac{2\,\ln\frac{4}{3}\,-\,\frac{1}{2}}{4}\right)\sqrt{\frac{2}{\pi}}\,,\end{equation}
which is also slightly below the depletion potential in comparison
to the case of ideal chains (see Figure \ref{fig:theta_gamma_os}).
The depletion force is unity.\\
Both approximations for wide, as well as for
narrow slits suggest the depletion effect to be stronger in the case
of excluded volume interactions than for ideal polymer chains (see
Figure 2).
\subsection{Two inert walls}
In order to obtain the renormalized total susceptibility for a
system confined by two parallel inert walls we have to apply the
surface renormalization scheme suggested by \cite{DSh98} for both
surfaces at their surface critical point $\c{i}^{sp}$. Starting from
(\ref{1Loop}) we obtain for the renormalized total susceptibility:
\begin{equation} {\cal
X}_{||\,ren}^{SS}\,L=\frac{L}{\mu^2}\,-\,\frac{1}{2\mu^3}\,
\left(\ln2\,-\,\frac{1}{2}\,-\,\ln\left(1-\mathrm{e}^{-2\mu
L}\right)\right)\,.\label{suscss}\end{equation} The surface contribution has
already been presented in (\ref{surfS}). Lets consider the
asymptotic expansion for wide slits $\mu L>>1$. Taking into account
the surface (\ref{surfS}) and the bulk contributions, the result for
the depletion interaction potential becomes: \begin{equation}
\Theta(y){\approx}\frac{1}{\sqrt{2\pi}}\,\mathrm{e}^{-2y^2}\,- \,y\,{\rm
erfc}\left(\sqrt{2}\,y\right).\label{thetassdcsemi} \end{equation}
This function and its derivative for the force are plotted in Figure \ref{fig:theta_gamma_ss}.\\
\begin{figure}[ht!]
\begin{center}
\includegraphics[width=8cm]{theta_ss_paper}\hspace*{0.3cm}
\includegraphics[width=8cm]{gamma_ss_paper}
\caption{The functions $\Theta(y)$ and $\Gamma(y)$ for two inert
walls with and without excluded volume interactions (EVI). Here we
introduced notations: $\delta c_{semi}=\delta c_{i}$ and $\delta
c^{S-S}_{i}=\delta c_{slit}$ with $i=1,2$}
\label{fig:theta_gamma_ss}
\end{center}
\end{figure}
It is obvious that only the wide slit approximation can be applied
here since the usual argument for the narrow slit approximation is
no more valid and $\omega$ does not necessarily vanish.\\
Interestingly, the depletion force turns out to be positive and the
walls are repelled from each other. This means that the chains
rather like to stay in between the slit than leave it. This in turn
means that the chains gain enough energy from attractive
interactions on the walls, which forces them to exert their loss of
entropy (due to the confinement) onto the walls instead
of leaving the slit.\\
It is very instructive to have a more general look on the terms
appearing in the free energy of interaction. If now we take into
account the new normalization conditions for surface-enhancement
constants for slit geometry (see Eqs.(\ref{ccondslit})-
(\ref{deltass})), which assume that we have big, but finite wall
separation $L$, the $\delta f$ can be written as: \begin{equation} \delta
f=2\,\,{\cal{IL}}_{\mu^2\to \frac{R_x^2}{2}} \left(\frac{\delta
c_{i}^{S-S}-\delta c_{i}}{\mu^4}\right) \,-\,{\cal{IL}}_{\mu^2\to
\frac{R_x^2}{2}} \left(\frac{\ln\left(1-\mathrm{e}^{-2\mu
L}\right)}{2\mu^3}\right)\,. \label{dfssdcsemi}\end{equation} Here $\delta
c^{S-S}$ is the surface-enhancement constant shifts for slit
geometry which appears in the case of finite walls separation and
$\delta c_{i}$ is surface-enhancement constant shift in the case of
infinite walls separation. In the presented approach the same
renormalization of critical values $c_0^{sp}$ was used and equally
the same shifts to the renormalized values were obtained. So the
first term on the r.h.s. just disappeared on the assumption that the
surface-enhancement constant shift on one surface is not affected by
the presence of the second one.\\
In fact this assumption could be doubted and an additional shift
through the influence of the second wall (coupling effect between
the two walls) may appear. Since the interaction potential itself is
purely local, such a coupling effect can only be mediated through
the chain conformations. As a result the number density of monomers
near the walls might differ in comparison to a semi-infinite
constraint and also the shift of the critical point (due to excluded
volume interactions) can change. As already proposed in \cite{GrD08}
this in turn would require a different renormalization scheme for
the surface critical point, where this coupling effect is to be
taken into account. The results of calculations for a slightly
modified surface renormalization scheme which takes into account the
finite surface separation $L$ are introduced at the Appendix B and
are presented in Figure \ref{fig:theta_gamma_ss} as well.
\section{Comparison to Previous Work}
\subsection{Theoretical approach}
As was mentioned in the Introduction, the remarkable progress in the
investigation of the influence of EVI on the depletion interaction
and depletion force between two repulsive walls was achieved by
\cite{E97,SHKD01} via using of dimensionally regularized continuum
version of the field theory with minimal subtraction of poles in
$\epsilon=4-d$, where $d$ is dimensionality of the space. Figure
\ref{fig:compshkd} presents comparison of our results obtained in
the framework of massive field theory at fixed dimensions $d=3$ for
the case of two repulsive walls and results obtained in
\cite{SHKD01}.
\begin{figure}[ht!]
\begin{center}
\includegraphics[width=8cm]{theta_compSHKD_paper}\hspace*{0.3cm}
\includegraphics[width=8cm]{gamma_compSHKD_paper}
\caption{The functions $\Theta(y)$ and $\Gamma(y)$ for two repulsive
walls in comparison to \cite{SHKD01}} \label{fig:compshkd}
\end{center}
\end{figure}
The results obtained in the framework of both analytical methods are
in quantitative agreement. But, one notes that the reduction of the
depletion effect due to excluded volume interactions is less
stronger within the massive field approach as compared to an
$\epsilon$-expansion in one-loop order. It should be noted, that we
extended our results up to the next $e^{-2\mu L}$ order. This
allowed us to obtain good matching with approximating results in
narrow slit limit (see Figures 1,2 for $\theta(y)$).
\subsection{Simulations}
One of the possibilities to test reliability of the obtained
analytical results is to compare them to results obtained by Monte
Carlo simulations. In this section we compare our results with
results of MC calculations obtained by \cite{MB98} and \cite{HG04}
for a single polymer chain trapped inside a slit of two repulsive
walls, what corresponds to a canonical ensemble. The canonical free
energy can be obtained via a Legendre transform from the grand
canonical one in the thermodynamical limit ($N,V\to\infty$) in the
form:
\begin{equation}
F(N_{l})=\Omega[\mu(N_{l})]+\mu(N_{l})N_{l},\end{equation} with $\Omega$ from
(\ref{tdlimitgrandcan}).
Thus the reduced canonical force for a one polymer chain
$N_{l}=1$ can be written as its dimensionless counterpart: \begin{equation}
\frac{K\,L}{k_b\,T}\,=\,\frac{1}{\omega}\frac{d}{d\,L}\big(L\,\omega\big).\label{trapforce}
\end{equation}
It should be mentioned, that both Monte Carlo algorithms (see
\cite{MB98} and \cite{HG04}) differ very much from each other in the
range of analyzed slit widths and chain lengths of the simulated
polymers. In \cite{MB98} an off-lattice bead and spring model for
the self-avoiding polymer chain in $d=3$ dimensions trapped between
two parallel repulsive walls at distance $D$ has been studied by
Monte Carlo methods, using chain lengths up to $N\leq512$ (number of
monomers in the chain) and distances $D$ from $4$ to $32$ (in units
of the maximum spring extension). It was stated that the total force
$K$ exerted on the walls is repulsive and diverges for the case of
narrow slit as \begin{equation} \frac{K\,L}{k_b\,T}\sim
(\frac{L}{R_{g}})^{-1/\nu},\end{equation} where $R_{g}$ is the radius of
gyration of the polymer chain in unrestricted geometry.
In Ref. \cite{HG04} a lattice Monte Carlo algorithm on a regular
cubic lattice in three dimensions, with $D$ lattice units in
$z$-direction and impenetrable boundaries was applied. The other
directions obeyed periodic boundary conditions. The proposed MC
simulations \cite{HG04} are based on the analytical result obtained
by \cite{E97} for the scaling behavior of partition function for a
chain confined to a slit geometry of width $D$: \eq{
\label{slitlattice}
Z_N(D)\,\propto\,\left(\mu_{\infty}+aD^{-\frac{1}{\nu}}\right)^{-N}\,
\,N^{\gamma_2-1}\,\,D^{\frac{(\gamma_2-\gamma_3)}{\nu}}\,\,, } for
$N,D\to\infty$, but $D\ll N^{\nu}$, where $\mu_{\infty}$ is the
critical fugacity per monomer and $\gamma_d$ is the universal
exponent (see (\ref{RZ})) dependent on the space dimension $d$ and
the parameter $a$ is a universal amplitude. The critical fugacity
means the averaged inverse number of possible steps at each site. In
\cite{HG04} universal amplitudes and exponents for the partition
function of a chain trapped in the slit with respect to that of a
free chain have been obtained through analyzing the statistics for
different $D$ and number of chain monomers up to $N\leq80\,000$.
Also both cases of ideal chains (modeled as a simple random walk
(RW)) and chains with excluded volume interactions (modeled via
self-avoiding walks (SAW)) have been studied. In the case of an
ordinary random walk on a regular cubic lattice in three dimensions
one has obviously $\mu_{\infty}=\frac{1}{6}$ and $\gamma_{d=3}=1$.
In the case of a SAW on such a lattice it is clear that at least
$\mu_{\infty}\geq\frac{1}{5}$. From Eq. (\ref{slitlattice}) one may
obtain the force exerted onto the walls in units of $k_B\,T$ as:
\eq{ \tilde{K}\,=k_B\,T\,\frac{d}{dD}\,\ln\big(Z_N(D)\big)\,. } In
the limit ($D\ll N^{\nu}$, $N,D\to\infty$) $\tilde{K}$ becomes: \eq{
\tilde{K}\,=
\,k_B\,T\left(\frac{Na}{\nu\mu_{\infty}}\,D^{-1-\frac{1}{\nu}}\right)\,.
} One should note that all functions here are in terms of
dimensionless length scales, the number of lattice sites ($D$ and
$N$). In order to compare with our results it must be translated
into terms of $L$ and $R_g$. Apparently $L=uD$, with $u$ denoting
the lattice spacing, and the reduced, dimensionless force reads:
\eq{k=\frac{\tilde{K}\,D}{k_B\,T}\,=
\,\frac{a}{\nu_3\,\mu_{\infty}}\,\left(\frac{6}{\chi^2_d}\right)^{\frac{1}{2\nu_3}}\,
\left(\frac{L}{R_g}\right)^{-\frac{1}{\nu_3}}\,, } where we
take
into account the general relation (e.g. \cite{CJ90}): \eq{
R_g^2=\chi^2_3\frac{b^2\,N^{2\nu_3}}{6} } in $d=3$ dimensions.
Parameter $b$ denotes the (effective) segment length of the polymer
model under consideration. In the case of RW and SAW on a cubic
lattice one has simply $b=u$ because the segment length in these
models is naturally provided by the lattice parameter $u$. In
\cite{HG04} the universal amplitude $a$ for the case of ideal chains
\begin{figure}[ht!]
\begin{center}
\includegraphics[width=10cm]{MC_oo_paper}
\caption{Comparison of our theoretical results with Monte Carlo
simulations for a {\it trapped} chain between two repulsive walls}
\vspace*{0.2cm}\centering {\small The plots Ideal chain (exact) and
EVI (wide slit) represent the results of our calculations. MC - RW
and MC - SAW are due to the estimated asymptotic behaviour in the
narrow slit limit by \cite{HG04} for random walks and self avoiding
walks. MC - EVI are the results obtained by \cite{MB98}. }
\label{fig:comp_MC}
\end{center}
\end{figure}
was found as $a\approx0.2741$, which is very close to the exact
value, computed analytically in \cite{E97}, of $a=\frac{\pi^2}{36}$.
Taking into account that for ideal chain $\nu=0.5$, $\chi_d=1$ and
$\mu_{\infty}=\frac{1}{6}$ the force becomes: \eq{
\label{idealcanforce}
k_{id}\,=\,2\,\pi^2\,\left(\frac{L}{R_g}\right)^{-2}\,\,. } In
Figure \ref{fig:comp_MC} this asymptotic behaviour for narrow slits
is clearly recovered by our results for ideal chains, where the
narrow slit limit is valid. By contrast, for a SAW in Ref.
\cite{HG04} was suggested the value $a\approx0.448$. Taking into
account the values for $\nu\approx0.588$, $\chi_3\approx0.958$
\cite{CJ90} and $\mu_{\infty}\approx0.2135$ the reduced force can be
written as \eq{ \label{evicanforce}
k_{saw}\,\approx\,16.95\,\left(\frac{L}{R_g}\right)^{-1.7}\,\,. }
The result Eq.(\ref{evicanforce}) is presented in Figure
\ref{fig:comp_MC} in its regime of validity and compared to our
theoretical results for a trapped chain with EVI, which are valid
for the wide slit regime. As it easily can be see from Figure
\ref{fig:comp_MC}, the result (\ref{evicanforce}) very well fit to
our predictions in wide slit limit. Also, in Figure
\ref{fig:comp_MC} the results obtained by the authors of Ref.\
\cite{MB98} are plotted and one notes a qualitative agreement to our
predictions. One of the possible reason for the remaining deviations
with results of Ref. \cite{MB98} is that the chain in the MC
simulation is too short in order to compare with results of
field-theoretical calculations. It should be noted, that at the
moment no simulations concerning two inert walls or one inert/ one
repulsive wall exist.
\subsection{Experiment}
In Ref.\cite{RBL98} an experimental study of the depletion effect
between a spherical colloidal particle immersed in a dilute solution
of nonionic linear polymer chains and a wall of the container
through total internal reflection microscopy was analyzed. Using the
Derjaguin \cite{D34} approximation we could compare our theoretical
results with experimental data in the case when the radius of the
spherical colloid particle $R$ is much larger than radius of
gyration $R_{g}$ and the closest distance $a$ between particle and
the surface. The deviation of the experimental setup to the
presented theoretical approach connected with the fact that the {\it
second} wall is not plane but curved. Summing up the depletion
potential per volume unit for the case of two plane surfaces in the
margins of the curved volume allows to estimate the depletion
effects in the case of a sphere and a wall. In the experiment by
\cite{RBL98} the radius of gyration was measured as
$R_g=0.101\,\,\mu m$ and the colloidal particle was reported to have
a radius $R=1.5\,\,\mu m$. Straightforward application of the
Derjaguin \cite{D34} approximation yields: \begin{equation}
\frac{\phi_{depl}(a)}{n_p\,k_b\,T}\,=
\,2\,\pi\,R_x^2\int\limits_{\frac{a}{R_x}}^{\frac{a+R}{R_x}}
dy\,\big(R+a-R_xy\big)\,\Theta\big(y\big), \label{derjaguin} \end{equation}
with $a$ the minimal distance between the sphere and the wall. Since
in the range of $y$ the last two terms in the parenthesis are much
smaller in comparison to the first one we can assume that: \begin{equation}
\frac{\phi_{depl}(a)}{n_p\,k_b\,T}\,\approx
\,2\,\pi\,R\,R_x^2\int\limits_{\frac{a}{R_x}}^{\infty}
dy\,\Theta\big(y\big)~. \end{equation} The experimental data in comparison to
our theoretical prediction are plotted
\begin{figure}[ht!]
\begin{center}
\includegraphics[width=9cm]{comp_exp_paper}
\caption{Comparison of approximated theoretical results with
experimental observation, due to \cite{RBL98}} \label{fig:compexp}
\end{center}
\end{figure}
in Figure \ref{fig:compexp}. It should be mentioned, that our
results obtained in the framework of the massive field theory are
situated slightly closer to the experimental data than previous
theoretical results obtained in the framework of the dimensionally
regularized continuum version of the field theory with minimal
subtraction of poles in $\epsilon=4-d$ \cite{SHKD01}. Unfortunately,
this shift is not enough in order to obtain quantitative agreement
with experimental data. But, the obtained theoretical curves in
Figure \ref{fig:compexp} are in qualitative agreement with
experimental data. The quantitative discrepancy can be removed if we
use the radius of gyration as adjusting parameter by analogy as it
was done in \cite{SHKD01}. From another side this indicate about
importance of further theoretical investigations of depletion
interaction potential and depletion force in the crossover region
from wide to narrow slit.
\section{Conclusions}
Using the massive field theory approach directly at fixed dimensions
$d=3$ we calculated the depletion interaction potential and
depletion force between two repulsive, two inert and one repulsive
and one inert walls confining a dilute solution of long flexible
polymer chains. The obtained calculations for all cases of
polymer-surface interactions were performed for the ideal chain and
real polymer chain with excluded volume interactions in the wide
slit regime. Besides, we used some assumptions which allowed us to
estimate the depletion interaction potential in the region of narrow
slit. Our results are obtained up to the next $e^{-2\mu L}$ order in
comparison with results of $\epsilon$-expansion \cite{SHKD01}. Our
investigations include modification of renormalization scheme for
the case of two inert walls (or mixed walls) situated on big, but
finite distance $L$ with $L\gtrsim R_{g}$ such that the polymer
chain is still not deformed too much from its original size in the
bulk. The obtained results indicate that the reduction of the
depletion effect due to excluded volume interactions is less
stronger within the massive field theory approach as compared to the
dimensionally regularized continuum version of the field theory with
minimal subtraction of poles in $\epsilon=4-d$ \cite{SHKD01} in
one-loop order. We found very good agreement with Monte Carlo
simulation data \cite{HG04} and \cite{MB98} for the case of two
repulsive walls. Taking into account Derjaguin approximation we
obtained good qualitative agreement with experimental data
\cite{RBL98} for the depletion potential between a spherical
colloidal particle of big radius and repulsive wall. From comparison
of obtained theoretical results and experimental data we can see
that the results obtained in the framework of the massive field
theory are situated slightly closer to experimental data. But, this
shift is not enough in order to obtain good quantitative agreement
with experiment. Interesting fact is that even the taking into
account the excluded volume interaction between the monomers of the
polymer chain do not resolve completely this problem. One of the
possible ways to find a good agreement could be connected with
further theoretical investigation of crossover region from wide to
narrow slit.
\section*{Acknowledgments}
We gratefully acknowledge fruitful discussions with H.W. Diehl.
This work in part was supported by grant from the Alexander von Humboldt Foundation
(Z.U.).
\renewcommand{\theequation}{A1.\arabic{equation}}
\section*{Appendix A: The surface contributions}
\setcounter{equation}{0}
To calculate the function $\Upsilon$ defined in Eq.(\ref{dfcrit}),
we need the free propagator for a semi-infinite system confined by a
surface at $z=0$. This free full propagator has a form \cite{DSh98}:
\begin{equation} {\tilde G}^*_{ij\,HS}({\bf p},{\bf p'},z,z';\mu_0,c_0)=
(2\pi)^{d-1}\delta_{ij}\delta({\bf p}+{\bf p'}) {\tilde G}_{HS}({\bf
p},z,z',\mu_0,c_0)~, \label{semipropagator} \end{equation} with \ali{
\label{g0semi} {\tilde G}_{HS}({\bf
p},z,z',\mu_0,c_0):\,&=\frac{1}{2\k_0}
\left(\mathrm{e}^{-\k_0|z-z'|}+\frac{\k_0-c_0}{\k_0+c_0}\mathrm{e}^{-\k_0(z+z')}\right)~,\\[0.2cm]
&\hspace*{4cm}{\rm where}~~\k_0=\sqrt{p^2+\mu_0^2}~.\nonumber } In
the zero-loop order we have: \begin{equation}
\Upsilon_{i}=\frac{1}{\mu^3}\,\frac{c_i}{\mu+c_i}\,.
\label{0loopsemi}\end{equation} In one-loop order the calculation for Dirichlet
boundary conditions on the surface (or $\frac{c}{m}\to\infty$)
yields after renormalization in fixed dimensions $d=3$: \begin{equation}
\Upsilon^{D}=\frac{1}{\mu^3}\,\left(1-\frac{n+2}{n+8}\,\tilde{v}\,\ln\frac{9}{8}\right)\,.\label{1loopsemiD}\end{equation}
And for Neumann boundary conditions ($c=0$) after renormalization we
obtain: \begin{equation}
\Upsilon^{N}=\frac{\tilde{v}}{\mu^3}\,\left(\ln2-\frac{1}{2}\right)\frac{n+2}{n+8}\,,
\label{1loopsemiN}\end{equation} where we introduced rescaled renormalized
coupling constant $\tilde{v}$ in the form:
$\tilde{v}=\frac{(n+8)}{6}\frac{\Gamma({\epsilon/2})}{(4\pi)^{d/2}}
v$. The correspondent fixed point in one-loop order approximation is
$\tilde{v}^{*}=1$.
\renewcommand{\theequation}{A2.\arabic{equation}}
\section*{Appendix B: The case of finite slit separation for two inert walls}
\setcounter{equation}{0}
Taking into account the new $\delta c_i^{S-S}$ (see
Eq.(\ref{cslitss}) we can calculate $\delta f$ in accordance with
Eq.(\ref{dfssdcsemi}) for the case of big, but finite slit
separation $L$. We obtain: \begin{equation} \delta
f\,{\approx}\,\,{\cal{IL}}_{\mu^2\to
\frac{R_x^2}{2}}\left(\frac{~~2\,\,\Delta^{(S-S)}}{\mu^4}+\frac{\mathrm{e}^{-2\mu
L}}{2\mu^3}\right)\,. \end{equation} After substitution of $\Delta^{(S-S)}$
from (\ref{deltass}) the result for $\delta f$ is: \begin{equation} \delta
f\,{\approx}-\,{\cal{IL}}_{\mu^2\to
\frac{R_x^2}{2}}\left\lbrace\left( \frac{1}{\mu L}+C_E+7\ln2\,-6+\ln
\mu L\,-\mathrm{e}^{4\mu L}\,{\rm Ei}(-4\mu L)\right)\frac{\mathrm{e}^{-2\mu
L}}{2\mu^3}\right\rbrace. \end{equation} If we carry out the inverse Laplace
transform, the result for $\Theta(y)$ in the wide slit limit is:
\mli{ \Theta(y)\,{\approx}\,-\frac{C_E\,+\,7\ln2\,-7}{2}
\left(\sqrt{\frac{2}{\pi}}\,\mathrm{e}^{-2y^2}\,-\,2\,y\,{\rm
erfc}\left(\sqrt{2}\,\,y\right)\right)\, -\,\frac{1}{4\,y}\,{\rm
erfc}\left(\sqrt{2}\,\,y\right)\\-\,\frac{y}{4}\,\,{\cal{IL}}_{\tau\to
\frac{1}{2y^2}}\left(\frac{\mathrm{e}^{-2\sqrt{\tau}}}{\tau^{3/2}}\ln\tau\right)
\,+\,\frac{y}{2}\,\,{\cal{IL}}_{\tau\to
\frac{1}{2y^2}}\left(\frac{\mathrm{e}^{2\sqrt{\tau}}}{\tau^{3/2}}{\rm
Ei}\left(-4\sqrt{\tau}\right)\right)\,. } In contrast to
(\ref{thetassdcsemi}) this expression is indeed negative. Thus, if
we perform calculations for the depletion interaction potential and
the depletion force including big, but finite slit separation $L$ we
obtain, that force for the case of two inert walls change character
and becomes attractive. In Figure \ref{fig:theta_gamma_ss} the
depletion interaction potential and the depletion force obtained in
the framework of this alternative renormalization scheme with
$\delta c_{slit}$ are plotted in comparison to the results obtained
via the original renormalization using $\delta c_{semi}$. Here we
introduced for convenience the following notations: $\delta
c_{semi}=\delta c_{i}$ and $\delta c^{S-S}_{i}=\delta c_{slit}$ with
$i=1,2$.
|
{
"redpajama_set_name": "RedPajamaArXiv"
}
| 2,039
|
Franciaország
Monthureux-sur-Saône, település Franciaországban, Vosges megyében
Monthureux-le-Sec, település Franciaországban, Vosges megyében
|
{
"redpajama_set_name": "RedPajamaWikipedia"
}
| 2,129
|
Q: Closing a running program from a process How can I close a program from a child process?
For exanple:
import easygui
import multiprocessing
def func():
reply=easygui.buttonbox("start?",image="F:\project\phonber.png",choices=['yes','no'])
if reply=="yes":
exit_option()
if __name__=='__main__':
p=multiprocessing.Process(target=func,args=())
t=p.start()
while True:
None
Is there a way to execute the exit_option() ?
A: Your forgot to actually call the function:
import easygui
import multiprocessing
def func():
reply=easygui.buttonbox("start?",image="F:\project\phonber.png",choices=['yes','no'])
if reply=="yes":
exit_option()
func()
if __name__=='__main__':
p=multiprocessing.Process(target=func,args=())
t=p.start()
while True:
None
Then, to actually kill a running process there are, of course, many options. The most obvious ones being psutil its kill or terminate method, or os its kill method. Both as shown here.
|
{
"redpajama_set_name": "RedPajamaStackExchange"
}
| 9,764
|
Lucas Tire & Auto Care provides Excessive Smoke Diagnostic services to Chicago, IL, Evanston, IL, Park Ridge, IL, and other surrounding areas.
Why Should You Have Excessive Smoke Diagnostic Services Performed at Lucas Tire & Auto Care?
We proudly service the Excessive Smoke Diagnostic needs of customers in Chicago, IL, Evanston, IL, Park Ridge, IL, and surrounding areas.
|
{
"redpajama_set_name": "RedPajamaC4"
}
| 5,155
|
#racismstinks
"Can I join, I'm not black?" "Am I allowed?" "What will my family think?" "Am I welcomed?" These are questions that many people ask themselves when they hear about #RacismStinks. The short answer is: yes. Please join. We welcome you.
Read on to learn more about what we do.
Celebration of Reconciliation
This celebration has a two-fold purpose. First to highlight, applaud, and inspire the people who are doing the difficult work of racial reconciliation, and social justice, to keep going. The second is to write "our chapter", the chapter of healing to the story of Tulsa's Race Massacre of 1921. We pay respects to our history and honor the lives that were lost during the massacre that destroyed the most affluent African American community in the United States due to racism.
We host our annual 5k, "The Race Against Racism" or nick-named "The Skunk Run" along with our "Jr. Skunk Olympics" for the kids which consist of tug-o-war, soccer, and 20-yard dash. We have guest speakers and a local historian who gives the history of the 1921 Race Massacre, and the speaks to the resilience of the Greenwood Community. The Tulsa Police Department speaks on their efforts to heal Tulsa through community policing. Also in attendance are multiple agencies and organizations who are passionate about racial reconciliation in our city. These organizations give out information on how you can get involved in this important and great work!
The most important piece in this event is YOU, the community! Join us for Tulsa's unifying fun run to heal the racial divides in our city! By jogging this historic path together, we are symbolically stomping out racism with every step! Be a part of making #OneTulsa a reality!
Remember: It takes us all
Together We Will Change The World
Fight for Fatherhood
The Fight for Fatherhood initiative is to address and tackle the leading cause of the vast divide in foundational areas of human existence in America. These divides represent themselves in all racial disparity indicators across the board, racial disparities in employment for example. The 2018 Tulsa Equality Indicator Report states, "Unemployed individuals are those who are in the labor force but are not currently working." Black Tulsans (81.2) are almost two and a half times more likely to be unemployed compared to White Tulsans (34.3). Asians (61.5) and Native Americans (60.6) also have unemployment rates that are nearly twice that of Whites. Hispanic/Latinos have a similar rate of unemployment to Whites (39.0). We know unemployment leads to a host of other conditions that accompany the lack of finances. These disparities expose unsettling truths about the difference in living conditions amongst races of people who live so close together in one of the greatest countries on earth.
In his article in The Guardian author Kirk E. Harris states, "Research has established that father involvement improves a child's educational outcomes, confidence, minimizes counter-productive behavior and decreases early sexual activity and other dangerous risk-associated behaviors," (June 2018).
We combat this issue by providing these desperate fathers with access to resources necessary to become an active participant in their child/children's lives. This consists of legal support, emotional support, educational and constructive recreational options. By streamlining access to these services vital to rekindling and sustaining a healthy father/child relationship we wholeheartedly believe we will see a positive change to the Tulsa Equality Indicators Report.
Fight for Families
We are building a great program for the people highly effected by separation and breakdown of the family unit. This is sure to be one of our greatest programs.
HomeSafe 101
We host a monthly community training class on best safety practices for encounters with law enforcement. With the heightened climate of officer-involved shootings of unarmed black and brown people, racism has been heavily discussed as a motive. If in fact, an officer is racially biased, we wouldn't be able to tell. We're not out to change that officer's individual beliefs concerning minority people. We believe that we must challenge the systems that allow any racial biases to thrive. In the immediate instance of a situation where someone finds themselves encountered with a police officer, we feel that it's necessary to equip the individual with situational knowledge and safety recommendations. This is so they understand the legitimate fears police officers may have in those encounters, the potential dangers of the situation they face and the dangers that officers face along with the boundaries of the law. Our primary concern is not the immediate assertion of an individual's rights, but the preservation of life for all parties involved in the encounter to make it HomeSafe.
People Policing People
We also offer training to police departments for their officers called "People Policing People." We understand that the profession of policing can be a very dangerous profession. We also understand that there can be Acute Dissociative Experiences put in place by the brain as methods to protect ones moral-sanity during a critical incident. When an officer dissociates the human element from the being who is accused of committing a crime it is easier to pull the trigger in fear. We believe that infusing the human element into the interaction between law enforcement and potential detainee will lead to a safer interaction for not only the potential detainee but for the officer as well.
Are you interested in becoming a corporate sponsor or community partner? Send us a message.
crystal@racismstinks.org
© 2020 #racismstinks. Powered by Websites4Good.
|
{
"redpajama_set_name": "RedPajamaCommonCrawl"
}
| 8,942
|
Dans ses yeux
The secret in their eyes (Juan José Campanella, 2010)
The secret in their eyes is a striking movie, giving a lot of thoughts to the viewer. It tells the story of Benjamin Esposito who wants to solve an old criminal case which was opened 25 years ago: a woman was raped and murdered. This case has haunted Esposito, who decides to reopen it to find the culprit. Meanwhile, he has always been in love with Irene, an investigating judge who works with him, but can't confess his feelings.
The actors are really good and act well. Ricardo Darin and Soledad Villamil are convincing in their roles. Their presence is powerful in the screen. Esposito's friend, Sandoval , is also a great character, bringing a comic touch in the movie. The characters are quite complicated and believable.
The movie is really well-structured, with some flash-backs of the murder scene and of Esposito's love story. Moreover, the atmosphere is full of melancholy and memories of the past. Morales, the husband, is always thinking about what happened to his wife, and how it happened… He doesn't live in the present, making hypothesis on what could have happen if he had done something else. The movie also tackles several deep questions about the value of a crime and how it can be punished. According to Morales, the best way is to make the criminal live an "empty life". This is what he suffers in the end, being imprisoned in Morales' house who has never said a word since he locked Gomez up. The effects of such a story on people are also mentioned in the movie. In fact, not only the criminal is imprisoned, but also Morales, who tries to live with the weight of the past. He realizes that he is slowly forgetting the memories of his wife.
The final scene shows that the"prison" feeling is endured by the culprit, but also by Morales. The composition of the shot is really expressive: both characters are shown behind bars. We can also see the themes of failure and success. First, Esposito fails to solve the criminal case and can't find the suspect. And even if in the end, he knows the murderer, Gomez, is imprisoned in Morales' house, he still has the case on his mind. But also, he has never confessed his love to Irene until the very end of the movie. Moreover, he has trouble writing his novel and don't know how to begin it. But he finally managed to solve everything and the movie ends with a note of hope.
The subject of the look is also often present in the movie. Indeed, the way the murderer is looking at Morales' wife on the old pictures, and the analogy with Esposito and Irene pictures. This look finally allows the case to be solved. But also, the final scene relies also on the look of the three characters through the prison bars.
Concerning the movie direction, the way it is filmed is really academic and not original. The other criticism we can make is the very slow rhythm of the movie. The shots really stretch and last a long time.
However, the dialogues are really good and the scenario is interesting. Some shots are technically really good, such as the soccer field scene… and the camera-work is pretty much impressive, with a lot of sequence-shot.
The movie also offers an historic context of the ascent of the dictatorship in Argentina and shows the corruption of the juridical system at that time.
In the end, we can say that The Secret in their Eyes is a beautiful movie, emotionally involving the viewer. This movie is a good way to discover Latin-American cinema, with an interesting scenario which blends love, violence, humor and a criminal case.
La estrella del cine
farsamag.com.ar
Malgré son abord simple et décontracté, l'acteur argentin Ricardo Darin est la star du cinéma hispanophone. Après une longue carrière à la télévision dans des séries à l'eau de rose, il est révélé par le réalisateur Fabian Bielinsky dans le film El Aura , en 2005. En effet, c'est un fils d'acteur qui tourne depuis l'âge de cinq ans. Son père s'opposait à sa carrière d'acteur parce que, comédien lui-même, il a vu sa propre carrière détruite par l'arrivée de la télévision. Sous la dictature, il a contribué à l'entreprise d'anesthésie des consciences à travers la télévision, mais en 1982, il met son talent au service des combats associatifs dans un esprit démocratique pour défendre les valeurs démocratiques.
Texte mis en forme par Clément Le Chanu, à partir du travail réalisé en accompagnement sur l'article "Le parrain de Buesnos Aires" de Guillemette Odicino, Télérama 3343, 5 février 2014.
Ricardo Darìn, acteur de qualité
Ricardo Darin Copyright Jorge Bisbo
Bien qu'il soit une star du cinéma hispanophone, Ricardo Darìn est un homme modeste et simple. Né de parents acteurs, il tourne depuis son enfance. Après s'être spécialisé dans le feuilleton télévisuel et dans les petits rôles du cinéma argentin, il est propulsé dans sa carrière de star en 2005 avec le film El Aura. Son père, dont la carrière a été mise à mal pas la télévision, ne voulait pas que son fils soit comédien. Sous la dictature, Ricardo Darìn joue dans des séries de télévisions anesthésiantes, mais à partir de 1982 il entre dans le combat associatif. Il met son charisme au service des valeurs démocratiques en aidant les gens, en particulier les jeunes cinéastes. Et il ne cesse d'être engagé par de grands réalisateurs.
Texte mis en forme par Salim Amara, à partir du travail réalisé en accompagnement sur l'article "Le parrain de Buesnos Aires" de Guillemette Odicino, Télérama 3343, 5 février 2014.
La estrella del cine farsamag.com.ar Malgréson ab...
RicardoDarìn, acteur de qualité Ricardo Darin...
|
{
"redpajama_set_name": "RedPajamaCommonCrawl"
}
| 9,944
|
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