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Ain’t it a bitch when you’re excited for a workout one day, yet it goes horribly? The weights that you normally rep-out on any other day are pinning you down on this certain day. Nothing else quite smacks the ego like a poor workout does. What explains an unprovoked drop in performance in the weight room? Well, if you’ve got the flu or injured one of your joints, it’s pretty self-explanatory. Barring an injury or illness, there are a few reasons why your workout went down the drain. Last Night’s Sleep Was Nothing to Brag About I’ve observed many people stumble into the gym after staying up really late (or for the entire night) and still successfully push through a workout. I’ve observed just as many do the same thing, but fail to complete their workout. They just gas out immediately, and that’s it. Bad workout: 1, lifter: 0. It’s logical. Sleep provides you with recovery from the previous day and energy for the following day. In fact, less time until exhaustion as well as increased perceived effort is correlated with sleep deprivation (Van Helder et. al). Failing to sleep well the night before isn’t a guarantee for poor performance, but it’s a bet you’re taking against yourself. You Drank Like a Fish, Ate Like Crap, or Are Dehydrated If you stayed up all night drinking, I think it’s safe to say you’re not going to be impressive in the gym the next day. Let’s say you drank quite a bit of alcohol earlier in the night and went to bed at a reasonable time. Should you still worry about your workout performance being effected? Depending on the amount of alcohol consumed, your “full night of sleep” may very well have been not so restorative and energizing. It appears that heavy alcohol-consumption decreases sleep quality (Carole et. al) (Roehrs, et. al). Now, I’ve got no evidence for this, but I believe eating a big greasy, unhealthy meal the night before can cause a bad workout, as well. I’ve experienced it a number of times. After getting some chicken fingers and mozzarella sticks, bad things happen in the gym for me. You’d think an excess of food would fuel the following workout! It’s difficult to explain, but my guess that despite this excess food, the quality (or lack of) I consume can make or break a workout. Broscience, yo. Now, dehydration is another obvious no-no for gym performance. If you wake up, urinate dark yellow liquid, and head straight to the gym, expect a bad workout. Dehydration negatively affects all aspects of fitness without fail (Judelson et. al). Your Head’s Not in the Game The mind is a powerful entity. Mere thoughts can influence the body to perform incredible things. Take the placebo-effect, for example. Simply taking a sugar pill but falsely believing it is medicine can cause someone to experience positive medicinal effects. If that is possible through the power of thinking, it doesn’t seem so far-fetched that mental state can affect physical performance. We’re all aware of the “home court advantage”. You’ve got two rival sports teams facing off at one-or-the-other’s home court/field/stadium/whatever. Despite the physical location of the game having no direct effect on a player’s skill or performance, playing home is still considered an advantage. It’s 100% mental, yet one study found did find an advantage for teams playing at home in college basketball (Harville et. al). So what if you’re not having a good day? Maybe you broke up with you significant other or someone at work put you down. Should you be afraid of having a bad workout (and further ruining your day)? Well, we’ve all seen and heard of athletes/lifters/etc. performing like crap while “not having a good day”. I have a difficult time arguing that mental state has no effect on physical performance. Doing Your Best to Avoid Bad Workouts Life happens. Occasionally, we cannot avoid the inevitable and suffer the consequences afterwards. Plenty of people don’t plan on getting piss drunk, binging on fast food, having insomnia, or feeling like a sad panda. We can’t always prevent these events that are pretty negative to our health and performance. Sometimes, avoiding a bad workout is the last thing on our minds. Yet, some people do amazingly well at keeping their performance to the max and avoiding bad workouts. Look at professional athletes. These folks train day-in and day-out, and are the best of the best. They surely can’t afford a bad workout. No way. How do they do it? Well, they do everything they can to keep their bodies as tuned up as possible. This includes: sleeping 9+ hours every night, eating only the best quality foods, not partying or staying out late, avoiding excess booze/drugs/vices, and separating themselves from anything or anyone that may screw with their mental state. Granted, these guys and gals make physical performance their careers. It would be very impractical for a lay-person to mimic this lifestyle. The takeaway is, however, that you and others can probably improve your lifestyle to prevent bad workouts and mishaps. Some ups and downs in the gym may not mean much to you, but take a look again at the potential causes for a bad workout. All of these are associated with an unhealthy lifestyle. Poor diet, poor sleep, stress – why would you want these things in your life anyway? In Conclusion People will experience bad workouts from time-to-time. Poor sleep, poor diet/hydration, excessive alcohol (and other vices), and a poor mental state can screw up your physical performance. If physical performance isn’t a top priority for you, consider the fact that these “causes” may also negatively affect your health in general. References: 1. Van Helder, T., and M. W. Radomski. “Sleep deprivation and the effect on exercise performance.” Sports Medicine 7.4 (1989): 235-247. 2. Carole, White, et al. “Alcohol increases sleep apnea and oxygen desaturation in asymptomatic men.” The American journal of medicine 71.2 (1981): 240-245. 3. Roehrs, Timothy, and Thomas Roth. “Sleep, sleepiness, and alcohol use.” Alcohol research and Health 25.2 (2001): 101-109. 4. Judelson, Daniel A., et al. “Hydration and muscular performance.” Sports Medicine 37.10 (2007): 907-921. 5. Harville, David A., and Michael H. Smith. “The home-court advantage: How large is it, and does it vary from team to team?.” The American Statistician 48.1 (1994): 22-28.	{ "pile_set_name": "OpenWebText2" }
value? (a) w (b) q (c) 4 a Let j = 423.5 + -427.333. Let m = j + -0.067. Let n = m - 0.1. Which is the third smallest value? (a) -5 (b) n (c) 0 c Let j = 8 - -1. Let h be j/1510/2. What is the third biggest value in -5, h, 1? -5 Let f be (-1 - 0)/(6/30). Let s = 0.3 + -0.4. Let i be (4/15)/((-2)/(-5)). Which is the second smallest value? (a) i (b) s (c) f b Let s = 5.4 + -5. Let y = 11 - 11.3. Which is the third smallest value? (a) s (b) -3 (c) y a Let k be 1/2 + 146/(-90). Let x = 9/10 + k. Which is the third smallest value? (a) 2/5 (b) x (c) -0.2 a Let m = -31.46 - -31. Let v = m + -0.04. Let q = 16 - 11. Which is the second smallest value? (a) v (b) 2 (c) q b Let r = -147 + 139.3. Let b = 8 + r. What is the biggest value in -2/3, b, -1? b Let l(a) = -a3 + 3a*2 - a - 1. Let n be l(2). Suppose -3 = -w - 0. Let j be ((-4)/2)/(w/n). What is the second biggest value in -1, j, 0? j Let q be (-3)/3(-1)/(-4). Let m = 299/56 + -45/8. Which is the third biggest value? (a) 3/5 (b) q (c) m c Suppose 0q + q = 0. Suppose 4t - 47 = -5m, -t - 4 = -qm - 4m. Let p be ((-6)/t)/(42/(-16)). What is the biggest value in -2, p, 0.4? 0.4 Let r = 6.67 + 0.33. Let u = r + -7.3. Let p(a) = -a3 - 7a*2 - 8a - 9. Let m be p(-6). What is the second biggest value in m, 2/3, u? 2/3 Suppose -12 = 5n - 7. Let y = 4 - 7. Let w(j) = -j3 + 4j*2 - 5j + 2. Let x be w(3). Which is the third biggest value? (a) y (b) n (c) x c Suppose -2v - 2 = -8. Let x = 8209/21 + -391. Which is the third smallest value? (a) -2 (b) v (c) x b Let x = 0.09 + -0.29. Which is the second biggest value? (a) -0.1 (b) x (c) -3 b Let h be -283/(-60) - (3 + -1). What is the second biggest value in h, 0, 0.5? 0 Let a = 10 + -6. Let n = -66 + 71. What is the third smallest value in 2, n, a? n Let m = -0.05 + 0.25. Let p = 0.1 + m. What is the second biggest value in -3, p, 3? p Let o = 0.76 + -0.36. What is the third biggest value in -1.1, -1, o? -1.1 Let w = -3.5 - 0. Let z = 3 + w. Let s = 0.5 + z. What is the second biggest value in -2, 0.2, s? s Let f = 0.6 + -1. Let i = 7 - 8. What is the second smallest value in f, i, -3? i Let x = 34 - 103/3. Let d = 116 + -121. Which is the biggest value? (a) x (b) -2 (c) d a Let j = 3 + -3.1. Suppose 0h + 25 = -5h, 0 = -x + 5h + 29. Which is the third smallest value? (a) 3 (b) j (c) x c Let i be 70(-6)/453. Let k be -2 - 7/(i/6). What is the third biggest value in 0.3, -1/4, k? k Let o be 9/12(-24)/(-45). What is the smallest value in -0.2, o, 0.1? -0.2 Let w be 1 - 1 - 20/(-16). Let p = 5/24 - -1/8. Which is the biggest value? (a) p (b) w (c) -4 b Let u = 14/33 - 1/11. Let g = 2 - 0. Let j be g1 - 7/3. Which is the third biggest value? (a) u (b) j (c) -1/2 c Let y = 0.34 + -0.74. What is the third biggest value in 7, 0.1, y, -2? y Let z = -6.6 - -7. What is the third biggest value in -4, z, 1/5? -4 Let z = 673.97 + -670. Let r = z + 0.03. Which is the smallest value? (a) 5 (b) -4 (c) r b Let s = -323.91 - -346. Let o = -19 + s. Let p = -0.09 + o. What is the biggest value in p, -3, 0.3? p Let z = -5.6 - -5.8. Which is the third biggest value? (a) -0.7 (b) z (c) -0.2 a Let g = -0.22 - -0.22. Which is the biggest value? (a) 3 (b) 1 (c) g a Suppose -7 = -5t + 18. Suppose -8 - 12 = -tz. Which is the biggest value? (a) z (b) -0.5 (c) -4 a Let k = -8 - -10. Let j be (57/30 + -2)k. Which is the biggest value? (a) 0 (b) 0.2 (c) j b Let d = -0.15 - -0.47. Let o = -0.02 + d. Let q = o + -0.2. Which is the biggest value? (a) -2 (b) q (c) -0.2 b Let r = -0.6 + -1.8. Let f = r - -2. What is the third smallest value in f, 1/9, -0.02? 1/9 Let p = 0.03 - 0.13. What is the third smallest value in 0, 0.1, p? 0.1 Let u be 0 + 1 - 224. Let v be (1 + u)/(5 + -4). Let q be 3/15 + v/(-20). Which is the second smallest value? (a) -2 (b) -1 (c) q b Suppose 3q + 0q + 4m = -29, 4q = -m - 17. Let p be -493/51 + -3 + 6. Which is the smallest value? (a) q (b) p (c) 0.4 a Let l be ((-45)/(-1))/(2 + 0). Let k = l - 22. Let f be ((-1)/2)/(2 + -1). What is the third biggest value in k, 3, f? f Let s = -0.07 - -0.57. Which is the third smallest value? (a) s (b) 6 (c) 3 b Let a be (-316)/(-198) + -2 + 4/18. What is the third smallest value in -16, a, -3? a Let t = -37.2 + 31. Let f = 6 + t. Suppose -6u = -4u + 2. Which is the biggest value? (a) f (b) -3/5 (c) u a Let d(r) = -2 + 3 + 3r3 - 3r*2 - 4r*3 + 9r*2. Let g be d(6). Which is the second biggest value? (a) 0 (b) g (c) 0.4 c Let u = 12 - 8. Suppose -3c + 8 = -1. Suppose -4m + 11 - c = 3y, 4y - 4m + 36 = 0. What is the third smallest value in -5, u, y? u Let g(c) = c*2 - 3c - 4. Let p be g(3). Let b = p - -1. Let i(h) = h - 9. Let l be i(5). What is the third biggest value in -1/10, b, l? l Let i = -76 - -381/5. Let j = -587/176358 + -2/4641. Let v = j - -543/2926. What is the biggest value in v, -4, i? i Let z = -6.06 - -6. Let d = z + 0.06. Which is the second biggest value? (a) d (b) -0.2 (c) 0.4 a Let i = 40 + -40.4. Which is the third biggest value? (a) -0.5 (b) -63/5 (c) i b Let i = 16.4 + -11. Let y = -5 + i. Suppose 24 = -4z + 2w - 6w, 0 = 2z + w + 10. Which is the biggest value? (a) y (b) z (c) -2 a Let h = -77.7 + 78. What is the fourth biggest value in 0.5, h, -1/5, -9/4? -9/4 Let x be -1 + ((-7)/(-9) - 0). Let j = 4.24 - 4. Let r = j - 0.04. Which is the third smallest value? (a) x (b) r (c) 1/3 c Let j be (111 - 0 - 0) + 1. Let o be 12/42 - 74/j. What is the second biggest value in -0.1, o, 2/11? -0.1 Let h = -1.93 - 0.07. Let z = h - -1.9. Which is the second biggest value? (a) z (b) 1/3 (c) 0 c Let q = -0.04 - 0. Let g = 1.25 - -1.79. Let a = q + g. What is the second biggest value in -3, a, 4? a Let d = -1/2 - -3/14. Let s = 18.88 - 19. Let w = s + -4.88. What is the smallest value in d, 4, w? w Let h = 2.7 + -2. Let i = -953/3 + 319. What is the third smallest value in i, h, -2/11? i Let q = 0.04 - 0.04. Let z = q + -0.2. Let l = 0.02 + 0.28. Which is the biggest value? (a) -1/7 (b) z (c) l c Let b = -169/2 + 83. What is the smallest value in 0.3, 3, -1, b? b Let j = -2.7 - -6.7. What is the second smallest value in 10, 2/5, j? j Let f(i) = i - 5. Let v be f(8). Let u = 19 - 9. Suppose 4g - u = 9g. Which is the biggest value? (a) -1 (b) v (c) g b Let x(s) = -s*2 - s + 1. Let l be x(1). Let v be (-4)/12 - (-21)/9. Let q be 1/(v + 4 + -3). Which is the third biggest value? (a) 2/9 (b) q (c) l c Let b = -12.8 - -19.1. Let s = 6 - b. What is the smallest value in 2, -3, s? -3 Let s = 557078 - 8352808/15. Let r = s - 224. Let f = -8 - -5. Which is the second biggest value? (a) f (b) r (c) 0 c Let v be 0 + 1 - (-20)/(-15). What is the smallest value in 0.2, 8, v? v Suppose -4u + 15 + 1 = 0. Suppose 4t + 6 = -14. Which is the third smallest value? (a) t (b) 0 (c) u c Let f = -0.08 - -0.38. Let c = f - -0.1. Let w be -7 - 1/(-2)6. What is the biggest value in c, 2/9, w? c Let m be 42/5 - 4/10. Let t(z) = z*3 - 5z*2 - 24z - 4. Let u be t(8). What is the third smallest value in u, -0.5, m? m Let g = 21 + -21.2. Let r be (-24)/14 - 6/(-3). Which is the third biggest value? (a) r (b) 4 (c) g c Let m = 5 - 6. What is the biggest value in m, 1, 0.5? 1 Let r = 6.9 - 7. Let k = 0.05 - -0.25. What is the smallest value in k, -0.2, r? -0.2 Let r = 1.52 + -1.5. Which is the smallest value? (a) 3 (b) r (c) -3 c Let v be (-2)/5 + (-1)/10. Suppose 2d + 60 - 10 = 0. Let n = 227/9 + d. Which is the third biggest value? (a) 2 (b) v (c) n b Let u = 2 + -2. What is the second smallest value in -1, 3, u? u Let l be (-45)/(-20) + 1/(-4). Let y(j) = j + 4. Let t be y(-5). Which is the third smallest value? (a) l (b) -2/5 (c) t a Let t = -5/7 - -3/7. Which is the biggest value? (a) -0.4 (b) t (c) -7 b Suppose -5 + 4 = z, -4d - 2*z = 18. Let g = 35028/3515 + -184/19. Let q = g + -3/37. Which is the biggest value? (a) -3 (b) d (c) q c Let m = 0 + 17. Let g = m + -16.5. What is the smallest value in -4/5, 2, g? -4/5 Let w = 164 + -1806/11. Which is the third smallest value? (a) 0 (b) w (c) -3 a Let y be ((-2)/3)/((-10)/6). Let h = 206 + -210. What is the biggest	{ "pile_set_name": "DM Mathematics" }
Stillbirths and rate of neonatal deaths in 76,761 postterm pregnancies in Sweden, 1982-1991: a register study. To study stillbirths and neonatal mortality in the postterm period. Register study of information obtained from the Swedish Medical Birth Registry (MBR), National Board of Health and Welfare, Stockholm. Singleton pregnancies with deliveries occurring between 1982 and 1991 were selected involving 914,702 women (of whom 76,761 had a postterm pregnancy continuing beyond the 42nd week of amenorrhea). All 2,043 records of dead infants were scrutinized before analysis of neonatal deaths. Stratification was made for year of birth, maternal age, and parity. Generally, the rates of stillbirths and neonatal deaths were low. The stillbirth rate was highest for primiparas at 38 completed weeks (2.72%), lowest at 40 weeks (1.23%), then increasing to 2.26% in the postterm period. The difference vs. multiparas was significant from 41 weeks onwards. Neonatal mortality was increased at 41 completed weeks for primiparas, but for multiparas it changed significantly first in the postterm period. The OR for a primipara to have an intrauterine death increased from 1.50 at 41 weeks (1.0 at 40 weeks) to 1.79 at 42 weeks and beyond. The OR for multiparas showed no sign of increase as gestation progressed. The results of this study indicate an increased risk of stillbirth with gestational age for primiparas but not for multiparas. The neonatal death rate was increased for both primiparas and multiparas (after 42 completed weeks).	{ "pile_set_name": "PubMed Abstracts" }
2017 Charming Double Coat German Shepherd Grooming Dog Images site heartily releases you all a blog post of Double Coat German Shepherd . This writing of 2017 Charming Double Coat German Shepherd Grooming is published by Willis Gleichner on October, 20 2016. If you all want to see a great amount articles regarding to Double Coat German Shepherd , you all may willingly click cielosereno.net, and do not forget to note our writing because http://www.cielosereno.net site posts articles regarding to Double Coat German Shepherd every day. If you like the image of 2017 Charming Double Coat German Shepherd Grooming, please don’t forget to help this site to give it to your friends on Google Plus, Facebook, and Twitter.	{ "pile_set_name": "Pile-CC" }
Q: Project rotation matrix to closest rotation matrix on a specific plain I have a rotation matrix created by some values of roll, pitch, yaw and I'm looking for the value yaw2 s.t the rotation matrix created by [0, 0, yaw2] is closest to the roration matrix created by [roll, pitch, yaw]. I think It can be rephrased as projecting the rotation matrix to the horizontal plane. I'm defining my rotation matrix as Ryaw X Rpitch X Rroll, but does the answer change if I reverse the order? A: Here is my best guess as to what you are asking. Typically if yaw, pitch, and roll are given by a vector of the form $\left [ \alpha \;\; \beta \;\; \gamma \right ]^T$ then the corresponding rotation matrices associated to this representation are given by: $$ R_z(\alpha) \;\; =\;\; \left [ \begin{array}{ccc} \cos \alpha & - \sin \alpha & 0 \\ \sin\alpha & \cos\alpha & 0 \\ 0 & 0& 1 \\ \end{array} \right ] \hspace{2pc} R_y(\beta) \;\; =\;\; \left [ \begin{array}{ccc} \cos \beta & 0 & -\sin \beta \\ 0 & 1 & 0 \\ \sin \beta & 0 & \cos \beta \\ \end{array} \right ] \hspace{2pc} R_x(\gamma) \;\; =\;\; \left [ \begin{array}{ccc} 1 & 0 & 0 \\ 0 & \cos\gamma & - \sin \gamma \\ 0 & \sin \gamma & \cos \gamma \\ \end{array} \right ] $$ and a rotation matrix in $SO(3)$ can be represented by $R(\alpha,\beta, \gamma) = R_z(\alpha)R_y(\beta)R_x(\gamma)$. I have a rotation matrix created by some values of roll, pitch, yaw and I'm looking for the value yaw2 s.t the rotation matrix created by [0, 0, yaw2] is closest to the roration matrix created by [roll, pitch, yaw]. What I believe you're asking here is to find some matrix of the form $R_z(\eta)$ which closest represents the matrix $R(\alpha,\beta,\gamma)$ given above. The way we can do this depends on what you mean by "closest". This often has to do with how you measure distance between rotation matrices. How you want to measure the distance is up to you, but you have a couple of options at your disposal: \begin{eqnarray} \text{Euclidean Norm}: && d(R_z(\eta), R(\alpha, \beta, \gamma)) \;\; =\;\; \left\| \left\| R_z(\eta) - R(\alpha,\beta,\gamma) \right\| \right\|_F \\ \text{Left-Invariant Norm}: && d(R_z(\eta), R(\alpha,\beta,\gamma)) \;\; =\;\; \left \| \left \| \text{Log}\left ( R(\alpha,\beta,\gamma)^TR_z(\eta) \right )\right \| \right \|_F \\ \end{eqnarray} If you are to take this approach, my best advice would be to perform some sort of gradient descent procedure, particularly using geodesics. I think It can be rephrased as projecting the rotation matrix to the horizontal plane. If instead you want to interpret this problem simply in terms of projection, then you have to be careful in exactly how you do this. You may be tempted to simply pick a Euclidean basis (i.e. $\hat{x}$ and $\hat{y}$ for your $xy$-plane) and then express your vector components under the rotation $R$ as follows: \begin{eqnarray} R\hat{x} & = & a_x \hat{x} + a_y\hat{y} + a_z\hat{z} \\ R\hat{y} & = & b_x \hat{x} + b_y\hat{y} + b_z\hat{z}. \end{eqnarray} It would be an incorrect choice to construct the following matrix: $$ R_z \;\; =\;\; \left[ \begin{array}{ccc} a_x & a_y & 0 \\ b_x & b_y & 0 \\ 0 & 0 & 1 \\ \end{array} \right ]. $$ The reason why here is that the columns of the above matrix are not guaranteed to be orthogonal, let alone of unit norm. The above matrix might also be strangely dubious in the case where we have particular types of rotations (for instance, imagine if $R = R_x(\gamma)$ for any $\gamma$). Instead what I would recommend would be to use the exponential and logarithmic maps for matrix Lie groups. Compute the matrix $\Omega = \log(R)$ (in Matlab this would be the function logm). This essentially linearizes rotation matrix $R$ and gives you a matrix of the form: $$ \Omega \;\; =\;\; \left [ \begin{array}{ccc} 0 & \alpha & -\beta \\ -\alpha & 0 & \gamma \\ \beta & -\gamma & 0 \\ \end{array} \right ]. $$ This matrix will essentially contain all of the yaw, pitch, roll data that you need. Because this space is linear (set of skew-symmetric matrices) project to your yaw component here: $$ P_\alpha(\Omega) \;\; =\;\; \left [ \begin{array}{ccc} 0 & \alpha & 0 \\ -\alpha & 0 & 0 \\ 0 & 0 & 0 \\ \end{array} \right ] $$ and now use the exponential map (in Matlab this is expm) and compute: $$ R_z \;\; =\;\; \text{Exp}(P_\alpha (\text{Log}(R))). $$ I'm defining my rotation matrix as Ryaw X Rpitch X Rroll, but does the answer change if I reverse the order? Yes it does. These matrices do NOT commute. If you change their order, you change the rotation that's being represented. A: After thinking and researching the problem further, the solution is to project the perpendicular vector. e.g when the Yaw is the only rotation that is not zero, the up vector remains pointing at (0,0,1), regardless of the yaw value. When taking the full rotation matrix, calculate the direction of the "up vector" by rotating it using the rotation matrix, and then find the rotation matrix that will rotate this new up vector back to (0, 0, 1). This is a common and easy problem, easiest using quaternions. The multiplication of the original rotation matrix, with the new rotation matrix to align the up-vector back to its position will generate the rotation matrix. the last step is to extract the yaw value, this is easy as the rotation matrix is constructed only using sin,cos of the yaw	{ "pile_set_name": "StackExchange" }
It is well known to use battens in roof construction. Battens are generally metal strips or bars which are used to secure or hold down materials upon building roofs. In constructing roofs, one or more flexible cover membranes, such, as for example, thermoplastic or elastomeric sheets, are placed over a rigid substrate so as to form a part of the roof structure. The flexible membranes serve to seal the roof structure against liquid penetration and also may serve to provide an insulating effect. Such membranes are secured in place by means of batten strips or bars which are placed at spaced intervals over the flexible membrane. Headed fasteners, such as, for example, screws or nails, are then passed downwardly through the batten strips or pre-punched holes therein and the flexible membranes so as to secure the battens and membranes to the roof substrate. The batten strips should be of such nature as to permit a pointed mechanical fastener to pass therethrough without destroying the hold-down effectiveness of the batten bar. Under certain conditions wind can uplift the membrane causing it to pull, upwardly away and thereby, in turn, causing the batten strip to rip or tear about the fastener with the headed fasteners thereby passing through the batten strip so as to no longer secure either the batten strip or the membrane to the roof substrate. The batten bars, to be satisfactory, must exhibit high pull-through resistance, that is, good tear or split resistance at points where pointed mechanical fasteners penetrate the bars. Batten bars can also be used in accordance with this invention to secure a layer or layers of insulation to a roof substrate or upon vertical building walls. They also can be used to secure flashing upon buildings and in other fastening applications where strips or bars are employed. For example, "batten strips" can be used as termination bars in order to secure membranes to the edges of vertical parapet walls to rough structure along the periphery of the roof. Thus, as used herein the term "batten strip" is not limited to roof battens but includes fastening means in building construction applications where strips or bars are useful in fastening building members. Roofing batten bars should not unduly curl, kink or distort when penetrated by means of a fastener. Metal batten bars made of sheet metal have been used, but such bars are relatively heavy constituting a relatively dead weight upon the building roof and can be difficult to penetrate by means of a threaded mechanical fastener unless pre-drilled openings are provided therein. Metal bars are also known to corrode and diminish the soundness of the roof structure. Aluminum batten bars have also been used, but are more expensive and unless quite thick are subject to curling, kinking or distortion when penetrated by means of a threaded fastener. Wood battens decay. Plastic batten strips have also been proposed. U.S. Pat. No. 4,718,211 discloses batten bars of a particular configuration made having plastic. Likewise, U.S. Pat. No. 4,445,306 discloses an elongated fastening bar made of plastic which has a flat batten surface and a convex top surface. The batten strips and fastening bars disclosed in these patents have a thickness at one point of approximately 1/4 inch and have pre-drilled holes therein so as to receive the fasteners.	{ "pile_set_name": "USPTO Backgrounds" }
The drug war on the U.S.-Mexican border has never been deadlier. As cartels rule by fear and violence, they begin to traffic terrorists across the border. In order to stem this tide, federal agent Matt Graver re-teams with the unconventional Alejandro in hopes of making a difference. -- Chris Kavan	{ "pile_set_name": "Pile-CC" }
Q: Manually specify constraints in Xcode 4 interfacebuilder/storyboard This seems like a really basic question, but I can't find the answer to it. When I add elements to a scene in my storyboard, or drag them around or resize them, Xcode automatically adds and removes constraints to describe their sizing and positioning. Now, once Xcode has created a constraint of a particular type - say, a height constraint - I know that I can modify its attributes - Relation, Constant and Priority in the case of the height constraint - via the attributes inspector. What I can't figure out is how to manually add or remove constraints of a given type rather than relying on Xcode's magic to do so for me. For example, in my current scenario, I have a ViewController that contains a toolbar and a table view. Now, I know exactly what constraints I want to use to describe the vertical positioning and sizing of those two views: The top of the toolbar has Vertical Space 0 from the top of the screen The toolbar has a fixed height The bottom of the table view has Vertical Space 0 from the bottom of the screen The top of the table view has Vertical Space 0 from the bottom of the toolbar This way the table view's height will adjust appropriately to the screen size. However, Xcode, in its wisdom, has decided that this isn't what I want, and has instead inflicted the following constraints on me (which it doesn't seem to want to change no matter how much I randomly drag stuff around and pray): The top of the toolbar has Vertical Space 0 from the top of the screen The bottom of the toolbar has Vertical Space 526 from the bottom of the screen The table view has Vertical Space 0 from the bottom of the screen The table view has a fixed height of 526 As a result, everything goes wrong when I try viewing my ViewController on a smaller screen, or in a container: Not being able to just manually set my own constraints when I know exactly what I need is frustrating. How can I explicitly delete the bullshit constraints that Xcode has automatically created and manually add my own instead? A: The problem when working with constraints in IB/storyboard is that Xcode will never allow you to have ambiguous constraints. Ever. Including when you are in the process if editing them. So whenever you may want to edit multiple constraints, Xcode may decide to automatically add some to prevent a disallowed state. This can be painful to work with. What I have found kind of works is adding bogus constraints on all four edges while I am setting other constraints. This - hopefully - keeps IB in check and prevents it from adding completely dumb stuff. You can add constraints from the top menu. Click the object and then Editor from the to menu. You can add constraints with the Align and Pin submenus (which then can be edited later on). Note: not all constraints can be added in IB. Aspect ratio for example can only be done in code. PS. Xcode will only allow you to delete constraints that are redundant, i.e that are not going to leave an ambiguous state. So in order to delete the "b****t" constraints, you have to first add enough others to create an allowed state.	{ "pile_set_name": "StackExchange" }
Login using You can login by using one of your existing accounts. We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. Repeated noise exposure induces inflammation and cellular adaptations in the peripheral and central auditory system resulting in pathophysiology of hearing loss. In this study, we analyzed the mechanisms by which noise-induced inflammatory-related events in the cochlea activate glial-mediated cellular responses in the cochlear nucleus (CN), the first relay station of the auditory pathway. The auditory function, glial activation, modifications in gene expression and protein levels of inflammatory mediators and ultrastructural changes in glial-neuronal interactions were assessed in rats exposed to broadband noise (0.5–32 kHz, 118 dB SPL) for 4 h/day during 4 consecutive days to induce long-lasting hearing damage. Noise-exposed rats developed a permanent threshold shift which was associated with hair cell loss and reactive glia. Noise-induced microglial activation peaked in the cochlea between 1 and 10D post-lesion; their activation in the CN was more prolonged reaching maximum levels at 30D post-exposure. RT-PCR analyses of inflammatory-related genes expression in the cochlea demonstrated significant increases in the mRNA expression levels of pro- and anti-inflammatory cytokines, inducible nitric oxide synthase, intercellular adhesion molecule and tissue inhibitor of metalloproteinase-1 at 1 and 10D post-exposure. In noise-exposed cochleae, interleukin-1β (IL-1β), and tumor necrosis factor α (TNF-α) were upregulated by reactive microglia, fibrocytes, and neurons at all time points examined. In the CN, however, neurons were the sole source of these cytokines. These observations suggest that noise exposure causes peripheral and central inflammatory reactions in which TNF-α and IL-1β are implicated in regulating the initiation and progression of noise-induced hearing loss. In this study, adult Wistar rats were exposed to broadband noise (0.5–32 kHz, 118 dB SPL) for 4 h/day during 4 consecutive days to induce permanent auditory damage. The spatiotemporal expression profile and activation of glial cells as well as the gene expression profile of proinflammatory cytokines, cell adhesion molecules, neurotoxic mediators, and metalloproteinases were assessed in the inflamed cochlea. Specifically, the sources of the inflammatory mediators, TNFα, and IL-1β, which are crucial in triggering inflammatory gene cascades and modulating neuronal function in injured tissue, were evaluated in the noise-exposed cochlea and in the anteroventral cochlear nucleus (AVCN). In addition, glial-neuronal interactions were evaluated in the CN using electron microscopy. These results suggest that following noise overexposure there is a complex interplay between peripheral and central signaling events involving glial cell responses and release of newly synthesized neuroactive molecules such as TNFα and IL-1β, which might be essential to restore glial-neuronal signaling. Materials and Methods Animals Adult Wistar rats (n = 48; 3 months, female, Charles River Laboratories, Barcelona, Spain) were maintained on a 12 h light/dark cycle with food and water ad libitum at the Universidad of Castilla-La Mancha Animal house (Albacete, Spain). The procedures involving the use and care of the animals were approved by the corresponding Institutional Animal Care and Use Committee (Permit Number: PR-2013-02-03). These protocols were in accordance with the guidelines of the European Communities Council (Directive 2010/63/EU) and current national legislation (R.D. 53/2013; Law 32/2007). Auditory Function Evaluation Auditory Brainstem Responses (ABR) ABR testing was conducted as described elsewhere (Alvarado et al., 2012). Only animal subjects that exhibited a normal hearing function were included in this study. Testing took place in a sound-attenuating, electrically shielded booth (EYMASA/INCOTRON S.L., Barcelona, Spain) placed inside a sound-attenuating room. Rats were anesthetized with isoflurane (1 L/min O2 flow rate) at 4% for induction and 1.5–2% for maintenance and during recordings, their temperature was monitored with a rectal probe and maintained at 37.5 ± 1°C using a non-electrical heating pad. Subdermal needle electrodes (Rochester Electro-Medical, Tampa, FL, USA) were positioned at the vertex (non-inverting) and in the right (inverting) and the left (ground) mastoids. Sound stimulation and recordings were performed using a BioSig System III (Tucker-Davis Technologies, Alachua, FL, USA). The acoustic stimuli were pure tone bursts sounds (5 ms rise/fall time without a plateau with a cos2 envelope delivered at 20/s) at seven different frequencies (0.5, 1, 2, 4, 8, 16, and 32 kHz). The sounds were generated digitally by the SigGenRP software (Tucker-Davis Technologies, Alachua, FL, USA) and the RX6 Piranha Multifunction Processor (Tucker-Davis Technologies, Alachua, FL, USA), and were delivered into the right ear using an EDC1 electrostatic speaker driver (Tucker-Davis Technologies) through an EC-1 electrostatic speaker (Tucker-Davis Technologies). Calibration was performed prior to the experiments using SigCal software (Tucker-Davis Technologies) and an ER-10B+ low noise microphone system (Etymotic Research Inc., Elk, Groove, IL, USA). Evoked responses were filtered (0.3–3.0 kHz), averaged (500 waveforms) stored for offline analysis. The ABR recordings were evaluated the day before sound stimulation and at the end of each survival time. Noise Exposure Protocol This noise stimulation paradigm consisted of exposure to broadband noise at 118 dB SPL, for 4 h a day during 4 consecutive days. The sound was delivered inside of a methacrylate reverberating chamber with 60 × 70 × 40 (length × width × height) cm with tilted and non-parallel walls with the purpose to avoid standing waves and ensure a more homogeneous sound field. The chamber was placed into a double wall sound-attenuating booth located inside a sound-attenuating room. During the procedure, animals were awake, move freely around the chamber and had access to water. Noise-exposed rats of each group were either perfused or sacrificed at 1 (1D), 10 (10D), and 30 (30D) days post-exposure (PE). Cochlear Whole-Mount Surface Preparations The right cochleae from the same rats were processed for whole-mount surface preparations (Melgar-Rojas et al., 2015). After cochlear decalcification, the sensory epitheliums were collected, and microdissected into individual turns that were incubated for 24 h at 4°C in prestin antibody (Supplementary Table 1) diluted in PBS-Tx (0.2%). After several rinses in PBS-Tx (0.2%), each organ of Corti was incubated in donkey anti-goat conjugated to Alexa 594 secondary antibody for 2 h, rinsed in PBS, mounted on glass slides, counterstained with DAPI nuclear staining and coverslipped. Immunofluorescence was examined with a laser scanning confocal microscope (LSM 710; Zeiss, Germany) with excitation laser lines at 405 and 594 nm. Z-stack series of 3–5 μm thickness were acquired as images of 1024 × 1024 pixels recorded at intervals of 0.5 μm with a 40X Plan Apo oil-immersion objective (1.4 NA). Quantification of Surviving OHC Cells were counted in segments of ~250 μm in length each along the basilar membrane by using the public domain image analysis software Scion Image for Windows (version beta 4.0.2; developed by Scion Corp). Dark spots and/or the phalangeal scars of supporting cells in the spaces previously occupied by OHC were used as criteria to assess sensory cell loss (Hu and Henderson, 1997; Minami et al., 2007; Fetoni et al., 2013). The results were expressed as percentage of remaining OHC compared to control condition, over the length of the basilar membrane (Viberg and Canlon, 2004; Fetoni et al., 2013). Image acquisition was performed with a laser scanning confocal microscope (LSM 710; Zeiss, Germany). By using the ZEN 2009 Light Edition software (Zeiss, Germany), the images of each dye were captured sequentially with a 40X Plan Apo oil-immersion objective (1.4 NA), merged and saved as TIFF files. Cochlear Dissection, RNA Extraction, and cDNA Synthesis Tissue collection from control (n = 4) and experimental animals (n = 12), RNA extraction and cDNA synthesis were performed as previously described (Melgar-Rojas et al., 2015). Briefly, the whole cochlea was dissected from the temporal bone of euthanized animals, quickly frozen in dry ice and stored at −80°C. Total RNA was extracted from frozen samples by following the TRIzol (Invitrogen) standard protocol and purity. Integrity and concentration of each RNA sample was measured by electrophotometric (Nanodrop ND-1000, Thermo Scientific) and electrophoretic methods (agarose gels). The synthesis of single-strand cDNAs was performed by using the RevertAid First Strand cDNA Synthesis Kit (Thermo Scientific) from 1 μg of RNA. The reactions were carried out in a DNA Engine® Peltier Thermal Cycler (BioRad) and in a final volume of 20 μl. Reaction conditions were as previously published (Melgar-Rojas et al., 2015). After the reaction, cDNAs were diluted 1:10 in sterile H2O MilliQ. RT-qPCRs were performed using specific primer pairs for amplifying transcripts of genes of interest (GOIs) that were designed using the Primer3 Plus software (http://www.bioinformatics.nl/cgi–bin/primer3plus/primer3plus.cgi/; Supplementary Table 2). Gene specificities were tested by BLAST analysis (NCBI) and every primer was matched against its genomic sequence (Ensembl Data Base) to check its genomic location and to avoid false-positive amplification in the case of genomic DNA contamination. The RT-qPCR amplification was performed in a One Step Plus Real-Time PCR System machine (Applied Biosystems) using Fast SYBR Green Master Mix (Applied Biosystems) as dye reagent. The reaction mix per well-consisted of 2.8 μl of sterile H2O MilliQ, 0.1 μl of forward and reverse primer (final concentration of 100 nM), 5 μl of Fast SYBR Green Master Mix and 2 μl of 10-fold diluted cDNA. The RT-qPCR program and the melting curve generation were carried out as previously described (Melgar-Rojas et al., 2015) and confirmed that the primers amplified only one specific PCR product. The amplification efficiencies (E-values) and correlation coefficients (R2-values) of each primer pair were obtained also as previously reported (Melgar-Rojas et al., 2015; Supplementary Table 2). Specifically, E-values were calculated by the following formula: Efficiency (%) = [–1 + 10(– 1/slope)] × 100. All the RT-qPCR plates included non-template controls (NTC) which generated Cq > 35. The experiments were performed technically in triplicate and biologically in quadruplicate. Quantification of expression (fold change) from the Cq data was calculate using Step One Software v2.3 (Applied Biosystems) and following the ΔΔCq method (Schmittgen and Livak, 2008). Briefly, the expression level of GOIs were first normalized to the average level (the geometric mean as recommended in Vandesompele et al., 2002) of Hprt1 and Tbp which were the most stably expressed along time in the rat cochlea in response to noise exposure. After obtaining the ΔCq, the ΔΔCq of each GOI was calculated as: ΔCq (noise-exposed group) −ΔCq (control group). Relative expression (fold change) was calculated as: 2−ΔΔCq. All RT-qPCR experiments were compliant with the MIQE guidelines (Bustin et al., 2009). CN Immunohistochemistry Brains obtained from the same animals used for cochlear histology were removed from the cranium, and sucrose-cryoprotected for 48 h. Frozen sections 40 μm thick were cut on a sliding microtome in the coronal plane. The immunohistochemistry procedure followed was the same as indicated earlier for cochlear sections excepting that CN sections were also incubated with GFAP primary antibody (Supplementary Table 1). To evaluate the specificity of the immunohistochemistry detection system the following sets of control experiments were assessed: (1) omission of the primary antibody by replacement with TBS-BSA; (2) omission of secondary antibodies; and (3) omission of ABC reagent. Under these conditions, no immunostaining was detected. Boundaries between CN subdivisions were defined in accordance with previous studies in rats describing the distribution and cytoarchitecture of auditory neurons in these cellular domains (Mugnaini et al., 1980; Cant and Benson, 2003). Double Immunofluorescence Labeling Adjacent sections from these same animals were used for double-labeling studies. Both cochlear and CN sections were rinsed several times in 0.2% TBS-Tx and blocked for 1 h in the same buffer solution containing 10% normal goat serum. Cochlear sections were incubated overnight in a solution containing either Iba1 or TNF-α/Iba1, or IL-1β-/Iba1 or calretinin (CR)/Iba1 primary antibodies. Meanwhile, brain sections were double-labeled with either TNF-α-/Iba1, or TNF-α/glial fibrillary acidic protein (GFAP) or IL-1β/Iba1 or IL-1β/GFAP or triple-labeled with NeuN/Iba1/GFAP primary antibodies (Supplementary Table 1). After several rinses in TBS-Tx 0.2%, sections were incubated in the corresponding cocktail of fluorescently labeled secondary antibodies [1:200, donkey anti-goat conjugated to Alexa 488 and donkey anti-rabbit conjugated to Alexa 594 for TNF-α/Iba1, IL-1β-/Iba1, calretinin (CR)/Iba1, and goat anti-rabbit conjugated to Alexa 488 and goat anti-mouse conjugated to Alexa 594 for NeuN/GFAP; Molecular Probes, Eugene, OR, USA] for 2h at room temperature and coverslipped with DAPI. Fluorescent sections were examined with confocal microscopy (Zeiss LSM710 multichannel laser scanning confocal imaging system). Data Analysis Quantification of the Immunostaining Iba1 immunostaining was examined using a 40× objective on a Nikon Eclipse 80i photomicroscope (Nikon Instruments Europe B.V.) and images were captured using a DXM 1200C digital camera (Nikon Instruments Europe B.V.) that was attached to the microscope. The color images of each field were digitized, and the resultant 8-bit red channel images, containing a grayscale of pixel intensities from 0 (white) to 255 (black), were used for analysis. In the cochlea, the analysis was performed on equally spaced (80 μm apart) mid-modiolar sections. Two microscopic 60× fields (dorsal and ventral) per section were sampled in the spiral ganglion and the spiral ligament. In the AVCN, the immunostaining was measured on equally spaced (160 μm apart) coronal sections. For each section, three microscopic 60× fields (dorsal, middle, and ventral) extending through the rostrocaudal dimension of the nucleus were selected, photographed and analyzed. As described elsewhere (Fuentes-Santamaría et al., 2003, 2005, 2007a,b; Alvarado et al., 2004, 2009a), the immunostaining was evaluated by using the public domain image analysis software Scion Image for Windows (version beta 4.0.2; developed by Scion Corp). For suitable comparisons of the staining across samples, a macro was used to process and analyze the captured images (Alvarado et al., 2004). Then, the images were normalized, the threshold level was set at two SD above the mean gray level of the field, and the immunostained elements above this threshold were identified as labeled. Immunostained Indexes and Percentage of Variation of the Immunostaining For quantitative analysis of the immunostaining, the following indexes were calculated: (1) the mean gray level of the immunostaining, which was used as an indirect indicator of protein levels within cells and (2) the percentage of variation of the immunostaining, which was calculated by using an enhancement index, according to the following formula (Meredith and Stein, 1983; Alvarado et al., 2007a,b, 2009b, 2016). % of variation=[(IEC - IUC)/(IUC)]×100 Where IEC and IUC represent the mean gray level in the noise-exposed and unexposed conditions; respectively. Quantification of Glial-Neuronal Interactions For quantification of presumptive interactions among neurons, astrocytes, and microglia, four sections (43672.47 μm2) from five animals were selected from each group. For each section, three microscopic fields extending through the rostrocaudal dimension of the nucleus were sampled using a 40X objective. The colocalization area (NeuN/Iba1 or NeuN/GFAP) was estimated from representative z- stack confocal microscopy images by using the public domain image analysis software Scion Image for Windows (version beta 4.0.2; developed by Scion Corp), as previously described (Fuentes-Santamaria et al., 2008). The immunostained profiles above the threshold were identified and the resultant images were converted into binary. To determine the degree of colocalization, the binary images corresponding to a given antibody were pseudocolored (green for Iba1 or red for GFAP) and then merged with the other pseudocolored image (blue for NeuN). The resultant image was used to quantified the overlapped area (putative region of interaction). The percentage of variation was calculated as above mentioned: % of variation=[(AEC - AUC)/(AUC)]×100 Where AEC and AUC represent the immunostained colocalized area in the noise-exposed and unexposed conditions, respectively. Pre-embedding Electron Microscopy After intracardial perfusion with 0.9% saline wash followed by a fixative solution of 4% paraformaldehyde and 0.5% glutaraldehyde (0.1 M PB, pH 7.3), unexposed (n = 3) and noise-exposed (n = 9) brains were removed, and cut at 70 μm on a vibratome. After several rinses in PBS-Tx (0.2%), transverse sections were processed for Iba1 or GFAP immunohistochemistry as previously described with the exception that no detergent was used in any step after the initial permeabilization. Peroxidase activity was visualized with a nickel-intensified DAB reaction in buffer solution to produce a black reaction product. CN sections were postfixed with osmium tetraoxide (1% in 0.1 M PB) for 1 h, block-stained with 1% uranyl acetate for 30 min, dehydrated in graded series of ethanol and embedded in Durcupan (Fluka) resin (Fuentes-Santamaría et al., 2014). Ultrathin sections (~75 nm) in the silver-gold range were cut on an ultramicrotome (Reichert Ultracut E, Leica, Austria), collected on 200-mesh copper grids and examined with a Jeol-1010 electron microscope. Preparation of Figures and Statistical Analysis Photoshop (Adobe v5.5) and Canvas (Deneba v6.0) software packages were used to adjust the size, brightness and contrast of the images for the preparation of figures. All data are expressed as means ± SEM. The measurements of the ABRs parameters were performed at 80 dB SPL unless otherwise indicated. One-way analysis of variance (ANOVA) with Scheffé post-hoc analysis as necessary was used for comparisons between groups. A p < 0.05 was considered statistically significant. Results Physiological Assessment of Noise-Induced Cochlear Damage To determine hearing dysfunction following exposure to a high level of noise, ABR recordings were conducted in noise-exposed rats at 1, 10, and 30D post-exposure. When compared to unexposed rats which had a distinctive pattern of 4–5 waves after the stimulus onset (Figure 1A), the recordings in exposed rats showed an almost complete elimination of the waves at all frequencies and time points evaluated (Figures 1B–D). Regarding the absolute hearing threshold in experimental rats, they were higher than in unexposed animals and very similar across frequencies (Figure 1E). The mean thresholds in noise-exposed animals were above 75 dB SPL while in unexposed rats the average thresholds were higher at the lowest frequencies, reduced at medium frequencies and augmented again at the highest frequencies (Figure 1E). At all post-exposure time points evaluated, the threshold shift ranged from 32 to 42 dB and showed no sign of recovery between day 1 and 30 following the exposure, indicating that experimental animals had permanent hearing loss at all frequencies in response to repeated noise exposure (Figure 1F). FIGURE 1 Figure 1. Line graphs showing ABR recordings (A–D) in control (n = 12) and noise-exposed (n = 36) rats at 80 dB SPL for frequencies between 0.5 and 32 kHz. When compared to the ABR pattern of unexposed rats (A), noise exposure (118 dB SPL) for 4 h/day during 4 consecutive days resulted in an almost complete absence of the typical ABR waves at all frequencies and time points assessed following the exposure (B–D). Progression of the auditory thresholds (E,F) indicated that noise-exposed rats at all survival times had higher values than those observed in unexposed animals (E). The threshold shift values fluctuated between 32 and 42 dB (F). Recordings in (A–D) are represented at 80 dB SPL. Histological Assessment of Noise-Induced Cochlear Damage Loss of OHC and Upregulation of Prestin Evidence of OHC damage was assessed by determining the percentage of cell loss and the expression of prestin protein, which is highly sensitive to noise overstimulation and essential for OHC electromotility (Figure 2). When compared to unexposed rats (Figure 2A), there was a high percentage of surviving OHC at 1D post-exposure (Figure 2B; Supplementary Table 3) which was concomitant with a significant increase in prestin staining in the basolateral membrane of OHC (Figures 2E,F; Supplementary Table 4). At later time points after overstimulation, OHC integrity in the first and second rows was mostly compromised, as the proportion of missing OHC (asterisks in Figure 2C; Supplementary Table 3) and prestin levels in the surviving ones progressively increased over time (Supplementary Table 4). On day 30 post-trauma, the majority of prestin-stained OHC were disrupted and/or degraded in all rows indicating a widespread cell damage, consistent with severe cochlear dysfunction (Figures 2G,H; Supplementary Table 4). Note that a few hair cells with swollen nuclei were evident (yellow arrow in Figure 2G). Quantification of the percentage of surviving OHC following noise-exposure demonstrated that cell death was mostly localized in the middle and basal cochlear turns at all survival times after the exposure (Supplementary Table 3). In the apical turn, however, the cell death was only observed at the longest time point studied (Supplementary Table 3). Upregulation of prestin levels in OHC in noise-exposed rats was confirmed by quantifying the mean gray level intensities of the immunostaining (Figure 2I; Supplementary Table 4). The percentage of variation of the immunostaining indicated that these increases ranged from 15.21 to 51.23% (Figure 2J). FIGURE 2 Figure 2. Surface preparation images illustrating double-labeling of prestin (red) and DAPI (blue) in the middle cochlear turn in control (A) and noise-exposed (B–H) rats. The survival of OHC was significantly decreased with longer time points post-exposure. Loss of OHC are indicated by yellow asterisks. Arrows in (E,G) indicate disrupted OHC stained with prestin protein. The yellow arrow in (G) indicates a swollen nucleus. Quantification of the mean gray levels indicated noise-induced increases in prestin staining when compared to control cochleae (I). The percentage of variation of the immunostaining in noise-exposed (n = 5 for each group) animals relative to control (n = 5) is shown in (J). The time of sacrifice following exposure (PE) is indicated in the upper left of each image. Significant differences in prestin immunostaining among animal groups (I) are indicated by asterisks (p < 0.05; p < 0.01, *p < 0.001). Scale bars: 20 μm in (D,H). Effects of Noise Exposure on MLC in the Cochlea As microglial cells are very sensitive indicators of alterations in tissue homeostasis and the main contributors to post-lesion adaptive immune responses, their temporal expression and activation in the cochlea were investigated following repetitive sound stimulation by using Iba1, a macrophage/microglia-specific calcium-binding protein. Iba1 mRNA in the cochlea had a maximum expression peak between 1 and 10D post-exposure as compared to the control condition (Figure 3A). On day 30, mRNA levels were still significantly elevated above control values (Figure 3A). Iba1-immunostaining was evaluated in different cochlear structures which are known to be vulnerable to permanent damage caused by noise (Figure 3B). FIGURE 3 Figure 3. Iba1 mRNA expression and protein levels in the cochlea of control and noise-exposed rats. mRNA levels in the noise-exposed cochleae were elevated at all time points post-exposure (A). The time course of MLC activation was examined in noise-vulnerable cochlear regions including the spiral ganglion (B1), the spiral limbus and cochlear nerve (B2), and the spiral ligament (B3) at 1, 10, and 30D post-exposure. As compared to control rats (C–G), noise produced increases in MLC activation were observable on day 1, when cells had larger cell bodies and thickened and shortened processes (H–L). Although these cells remained active by 10D post-exposure (M–Q), with longer time points (30D) Iba1-stained cells recovered their ramified appearance (R–V). Confocal images showing close appositions between microglia (green) and SGN (red) are indicated by arrows in (E,J,O,T;n = 5 for each group). Significant differences in Iba1 mRNA levels among control and noise-exposed animals (A) are indicated by asterisks (p < 0.05; p < 0.01, p < 0.001). Scale bars: 200 μm in (B); 50 μm in (R); 10 μm in (S4,V) and 25 μm in (T). Spiral Ganglion In unexposed rats, scarce Iba1-stained cells with small cell bodies and ramified long processes were distributed among SGN (Figures 3C–E). On day 1 following noise-exposure, reactive MLC were enlarged and intensely stained with thick or no processes that were closely associated with SGN (Figures 3H–J). Note that these microglial cells had an amoeboid phenotype that resemble active macrophages (Figures 3I1–I3). With longer time points post-lesion, the response of microglial activation diminished progressively as reflected by cells with smaller somata and highly branched processes (Figures 3M–O,R–T) when compared to the control condition (Figures 3C–E). In noise-exposed animals, the frequency of SGN-glial contacts decreased over time as did the degree of microglial activation and number of activated microglial cells. In this regard, early activity-dependent increases in CR levels within SGN were correlated with increased microglial activation. These interactions are indicated by arrows in Figures 3E,J,O,T. On days 1 and 10 post-exposure, CR levels were upregulated (Figures 3J,O) in comparison with longer time points (Figure 3T) and unexposed (Figure 3E) animals. Iba1 upregulation within the SG was confirmed by significant increases in the mean gray level of the immunostaining that ranged from 56.12 to 42.88% (Supplementary Table 5). Spiral Limbus and Cochlear Nerve Similar to what occurs in the SG, there were significant increases in the intensity of Iba1-immunostaining in the SLB and cochlear nerve following noise exposure (Figures 3K,L,P,Q,U,V) when compared to unexposed (Figures 3F,G) rats. At the earliest time point post-exposure, MLC in the cochlear nerve were higher in number and had phenotypic features that resembled that of activated microglia (Figure 3L). This cellular response gradually decreased over time (Figure 3Q) and cells recovered their resting phenotype (Figure 3V). Spiral Ligament In the control condition, Iba-immunostaining was located mostly in the dorsolateral part of the SL, which corresponds to type I fibrocytes region (Figures 4A–D). On day 1, noise-exposure triggered a microglial activation response characterized by an increased number of microglial cells, which were intensely stained, hypertrophic, and with widened short processes (arrows in Figures 4E–H). Immunostaining remained elevated on day 10 (Figures 4I–L) but this enhanced activated phenotype decreased in intensity as function of time (Figures 4M–P). At all time points evaluated, activated microglial cells extended to the area where type IV fibrocytes were distributed (Figures 4E–P). The quantification of Iba1 immunostaining and the percentage of its variation in the SL confirmed the significant increases in the mean gray level (Supplementary Table 5). In the stria vascularis, blood flow modifications were reflected as a decrease in the diameter of blood vessels at earlier time points after noise-stimulation (yellow arrows in Figures 4H,L) and partial recovery on day 30 (yellow arrows in Figures 4P) when compared to the control condition (yellow arrows in Figures 4D). Microglial cells attached to blood vessel are indicated by asterisks in Figure 4. FIGURE 4 Figure 4. Digital images showing Iba1-immunostaining in the spiral ligament of control (n = 5) and noise-exposed (n = 5 for each group) rats. When compared to the control condition (A–C), Iba1-immunostaining at all time points post-exposure evaluated was markedly increase in MLC located in type I and IV fibrocytes regions (white arrows in E–G,I–K,M–O). Particularly on day 1, cells were darkly stained and had expanded cell bodies and thickened processes (arrows in F,G). Asterisks indicate the association of MLC with blood vessels. Yellow arrows in (H,L) point to noise-decreases in blood vessels diameter at 1 and 10D after the exposure in comparison to 30D post-exposure (arrows in P) and control (arrows in D) rats. Scale bars: 100 μm in M; 20 μm in O; and 25 μm in (P). Noise-Induced Upregulation in the Expression Levels of Cytokines, Adhesion Molecules, Tissue Inhibitor of Metalloproteinases, and iNOS To evaluate the inflammatory status in noise-exposed cochleae, the mRNA expression levels of pro-inflammatory cytokines (TNF-α, IL-1β, and TGF-β), intercellular adhesion molecule-1 (ICAM-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and inducible NO synthase (iNOS) were analyzed by RT-qPCR. The analysis showed that all the inflammatory cytokines and inflammatory factors evaluated were upregulated by 1D and 10D post-stimulation and slowly decreased at longer time points when compared to the control condition (Figure 5; Supplementary Table 6). While the upregulation of TGF-β, iNOS, and ICAM-1 expression peaked at the earliest time point evaluated (Figures 5C–E,G; Supplementary Table 6), that of TNF-α and IL-1β augmented on day 10 after the exposure (Figures 5A,B,G; Supplementary Table 6). Particularly, TIMP-1 expression was transiently upregulated by 1D post-exposure as it decreased markedly on day 10 to remain significantly elevated over control levels on day 30 (Figures 5F,H; Supplementary Table 6). FIGURE 5 Figure 5. Quantitative RT-qPCR analyses of inflammatory-related genes expression in the noise-exposed cochlea (n = 4 for each group). Significant elevations in the mRNA expression levels of TNF-α (A), IL-1β (B), TGF-β (C), iNOS(D), and ICAM-1(E) were detected after noise-exposure at all time points evaluated. TIMP-1 expression levels (F) were increased transiently on day 1 and quickly downregulated at longer time points post-exposure but without reaching normal levels. The overlapping distribution of genes expressed in response to noise exposure is shown in (G) while the particular progression of TIMP-1 expression is shown in (H). Significant differences among animal groups are indicated by asterisks (p < 0.05; p < 0.01, *p < 0.001). TNF-α and IL-1β-Expressing Cells in the Noise-Exposed Cochlea At the protein level, significant increases in TNF-α (Figure 6) and IL-1β (Figure 7) staining were predominantly observed in the SG and the SL from noise-exposed rats when compared to unexposed rats. Immunohistochemically analysis of these tissues on day 1 and 10 post-exposure revealed an increased synthesis of these proinflammatory cytokines by neurons (green in Figures 6, 7) and activated MLC (red in Figures 6, 7) in the SG (arrows in Figures 6D–I, 7D–I). Although these increases in the SG were still present by 30D post-lesion, they were evident mostly in MLC and barely detectable in neurons (Figures 6J–L, 7J–O). In the noise-exposed SL, the sources of these cytokines were fibrocytes (yellow arrows in Figures 6, 7) and activated MLC (Figures 6Q,T,W,Z, 7T,W,Z,Z3,Z6). Although the majority of reactive MLC produced TNF-α or IL-1β in the SG and in the SL (white arrows in Figures 6, 7), many TNF-α and IL-1β-expressing fibrocytes did not colocalize with Iba1 (yellow arrows in Figures 6, 7). Note that cytokine levels in the control condition were very low in both the SG (Figures 6A–C, 7A–C) and SL (Figures 6M–O, 7P–R). FIGURE 6 Figure 6. Confocal images depicting the colocalization between TNF-α (green) and the microglial marker, Iba1 (red), in the SG (A–L), and SL (M–Z1) in control (n = 5) and noise-exposed (n = 5 for each group) rats. In the SG, TNF-α producing cells in response to noise-exposure were neurons (D,G,J) and MLC (E,H,K) while in the SL, TNF-α protein was synthesized by MLC (Q,T,W,Z) and fibrocytes (yellow arrows in P,S,V,Y). White arrows point to double-stained cells in the SG and SL. Scale bars: 10 μm in (K,Z). FIGURE 7 Figure 7. Confocal images depicting the colocalization between IL-1β (green) and Iba1 (red) in the SG (A–O) and SL (P–Z7) in control (n = 5) and noise-exposed (n = 5 for each group) rats. In the SG, IL-1β producing cells in response to noise-exposure were neurons (D,G,J,M) and MLC (E,H,K,N) while in the SL, IL-1β producing cell types were MLC (T,W,Z,Z3,Z6) and fibrocytes (yellow arrows in S,V,Y,Z2,Z5). White arrows point to double-stained cells in the SG and SL. Scale bars: 10 μm in (N,Z). Effects of Noise Exposure on Microglia in the AVCN To determine how central auditory neurons respond to cochlear inflammation and subsequent sensorineural hearing loss, the contribution of microglia to maintain functional integrity, and prevent further damage was investigated in the CN. In unexposed rats, microglial cells were faintly stained and had multipolar and bipolar morphologies with long dynamic processes, which were indicative of the resting form (Figures 8A,B), as previously described (Fuentes-Santamaría et al., 2012, 2014). High-noise exposure led to progressive microglial activation and proliferation in the AVCN (Figure 8). Between 1D and 10D post-exposure, microglial cells turned into an alerted state characterized by larger cell bodies and cytoplasmic processes that were shorter and thicker (Figures 8C–F) when compared to unexposed rats (Figures 8A,B). On day 30, there was a heterogeneous population of microglia in which some of them had a bushy-like morphology characterized by enlarged cell bodies and thickened processes (Figure 8G and arrows in Figure 8H) which were suggestive of increased activation state when compared to earlier time points (Figures 8C–F) and unexposed (Figures 8A,B) rats. Upregulation of Iba1-inmunostaining at all time points evaluated was corroborated by significant increases in the mean gray levels of Iba1 in comparison with unexposed rats (Supplementary Table 7). To provide additional details of microglial phenotype following noise-exposure, the ultrastructural modifications of these cells were also evaluated (Figure 9). In the unexposed condition, proximal and distal microglial processes were frequently seen contacting multiple neuropil-associated elements (Figures 9A,B). Between 1 and 10D post-lesion, microglia was preferentially contacting presumptive lesioned axons and terminals (Figures 9C–E). On day 30, a few microglial cells had a very reactive phenotype characterized by enlarged cell bodies with multiple inclusions (small asterisks in Figure 9F) and remnants of engulfed membrane fragments (large asterisk in Figure 9F) in the cytoplasm, presumably from degenerating terminals. Note cell-cell direct interactions between irregular appearance microglia (Mg in Figure 9F), auditory terminals (T1 and T2 in Figure 9F) and astrocytic (As in Figure 9F) processes, suggesting noise-induced microglial remodeling of compromised synaptic connections. FIGURE 8 Figure 8. Digital images showing the time course of glial activation in the AVCN in control (n = 5) and noise-exposed (n = 5 for each group) rats. Microglial (A–H) and astroglial (I–L) activation responses increased progressively over time reaching maximum levels on day 30 post-exposure (H,L). Microglia are indicated by arrows in (A–H) while appositions between cochlear nucleus neurons (red) and astrocytes (green) are designated by arrows in (I–L). The inset in (A) shows the location of the AVCN, and the square box indicates the approximate locations of the fields represented in (A–L). Scale bars: 50 μm in (A; inset); 100 μm in (E); 50 μm in (F,L; inset); and 40 μm in (I). FIGURE 9 Figure 9. Ultrastructure of microglia (A–F) and astrocytes (G,H) in the AVCN in control (n = 4) and noise-exposed (n = 4 for each group) rats. In the control condition, microglial processes spread through the neuropil contacting multiple cellular elements (A). Between 1 and 10D post-exposure (C–E), dynamic microglia quickly associated with nearby elements preferentially axons and terminals in the vicinity. On day 30, a few microglial cells transformed into a phagocytic phenotype in which inclusion bodies (small asterisks) and engulfed material (large asterisk) were observed (F). Note that this microglial cell was in close association with terminals, axons, dendrites and astrocytic processes. When compared to the control condition (G), reactive astrocytic processes (P1–P4) on day 10 juxtaposed synapses (asterisks in H) and axons and terminals in the adjacent neuropil. As, astrocyte; Ax, Axon; D, D1-D5, dendrites; Mg, microglia, P1–P6, microglial/astroglial processes; T1–T6, terminals. Scale bars: 1 μm in (A,H); 2 μm in (B,D–G); 5 μm in (C). Effects of Noise Exposure on Astrocytes in the AVCN Given the role of astrocytes in the generation of trophic signals that stimulate recovery of auditory function, their temporal expression pattern in the CN was also assessed in response to noise overstimulation. In unexposed rats, astrocytes had a highly ramified appearance, and were distributed through the nucleus contacting other structural elements of the neuropil (arrows and asterisks in Figures 8I, 9G). Following noise stimulation, along with an astrocytes proliferation response that was more persistent with longer time points after the exposure, there was an increased occurrence of appositions between glia and AVCN neurons (arrows and asterisks in Figures 8J–L, 9H). Upregulation of GFAP-immunostaining was confirmed by quantifying the mean gray levels in noise-exposed and unexposed (Supplementary Table 7) rats. Note that synaptic terminals showing signs of degeneration (T1–T3 in Figure 9H) are making synaptic contacts (asterisks) with a dendrite (D2 in Figure 9H). One of the astrocytic processes (P4 in Figure 9H) is in close apposition with one of these terminals (T2 in Figure 9H). Interactions among CN Neurons and Glia Following Noise-Exposure To further evaluate noise-induced alterations in neuronal-glial communication, the spatial relationship among microglia, neurons, and astrocytes was also examined by confocal and electron microscopy (Figures 10, 11). On day 1, microglial cells had shorter and thicker processes that came into close proximity with auditory neurons and astrocytes (arrows in Figures 10B,E,F) when compared to the unexposed condition (arrows in Figure 10A). By 10 and 30D post-exposure, there was a higher incidence of microglial contacts with other cellular elements (arrows in Figures 10C,D,G) including astrocytes (As, large asterisks in Figures 11A,B), axons (Ax, Figures 11A,B), synaptic terminals (T, Figures 11A,B), and dendrites (D, Figures 11A,B). Around the peak of glial maximum expression (day 30), the occurrence of glial-synapse contacts increased substantially (Figures 11B,B1). Note as irregular microglial appearance cell bodies were often juxtaposed with synapse-associated elements (pre- and post-synaptic elements and perisynaptic astrocyte). These glial direct interactions with synapses are suggestive of noise-induced microglial remodeling of synaptic connections. Note the close association between glial cells and blood capillaries (Figures 11B,B1). Quantitative analysis of these presumptive interactions revealed an increase in the colocalized area of both neurons and microglia and neurons and astrocytes at all time points post-exposure (Supplementary Table 8). This increase ranged from 30.84 to 92.73% for NeuN/Iba1 staining, and from 12.78 to 37.24% for NeuN/GFAP staining (Supplementary Table 8). FIGURE 10 Figure 10. Interactions between glia and neurons in the AVCN in control (A;n = 5) and noise-exposed (n = 5 for each group) rats (B–G). Microglial processes (green) and astrocytes (red) made multiple contacts simultaneously with cochlear nucleus neurons (blue) which increase in occurrence with longer time points post-exposure. Appositions between glial elements and neurons are indicated by arrows. Scale bars: 25 μm in (D); 20 μm in (F,G). FIGURE 11 Figure 11. Ultrastructural interactions among microglia, astrocytes and neurons in the AVCN are regulated by noise (n = 4 for each group). In response to noise-exposure, reactive microglial processes came into close proximity with astrocytes, terminals, and synapse-associated elements at all time points evaluated (A,B). Note that the perivascular microglial cell in (B,B1) is in close contact with an astrocyte (large asterisk) and is wrapping around a dendrite making synapses with multiple terminals (small asterisks). Although interactions among microglia, astrocytes and neuronal elements were observed at all time points post-exposure (A–A3), they increased in frequency particularly on day 30 (B,B1). Appositions between microglia and astrocytes are indicated by large asterisks while the small asterisks in (B1) point to synapses. Higher magnification images of (A,B) are represented in (A1–A3, B1); respectively. As, astrocyte; Ax, axon; D1–D3, dendrites; Mg, microglia, P1–P2, microglial processes; T1–T3, terminals. Scale bars: 5 μm in (A, B1); 2.5 μm in (A3; it also applies to A1,A2); 2 μm in (B). TNF-α and IL-1β-Expressing Cells in the Noise-Exposed CN In the AVCN, TNF-α (Figures 12, 13), and IL-1β (Figures 14, 15) levels were increased within neurons at 1 (asterisks in Figures 12G, 13D, 14D, 15D) and 10D (asterisks in Figures 12J, 13G, 14G, 15G) post-lesion although they diminished progressively by day 30 (asterisks in Figures 12M,P, 13J, 14J, 15J) post-exposure. The absence of colocalization between TNF-α and microglia (arrows in Figure 12), TNF-α and astrocytes (arrows in Figure 13), IL-1β and microglia (arrows in Figure 14), and IL-1β and astrocytes (arrows in Figure 15) at any of the time points evaluated indicated that neurons were the only cell type overexpressing proinflammatory cytokines in the AVCN after noise-exposure. FIGURE 12 Figure 12. Confocal images depicting the lack of colocalization between TNF-α and Iba1 in control (A–F) and noise-exposed (G–R) AVCN. Note that TNF-α (red) was only expressed by auditory neurons (asterisks) and not by activated microglia (green) at all time points post-exposure (n = 5 for each group). Asterisks indicate TNF-α-containing neurons while arrows point to microglia. Scale bar: 25 μm in (R). FIGURE 13 Figure 13. Confocal images depicting the lack of colocalization between TNF-α and the astroglial marker, GFAP, in control (A–C) and noise-exposed (D–L) AVCN. TNF-α (green) neither colocalized with GFAP (red) at any of the time points analyzed (n = 5 for each group). Asterisks indicate TNF-α-containing neurons while arrows point to astrocytes. Scale bar: 25 μm in (L). FIGURE 14 Figure 14. Absence of colocalization between IL-1β and Iba1 in the AVCN in control rats (A–C) and following noise-exposure (D–L). Microglial (green) production of IL-1β (red) was not observed at any of the time points post-exposure (n = 5 for each group). Cochlear nucleus neurons were the sole source of this cytokine. Asterisks indicate TNF-α-containing neurons while arrows point to microglia. Scale bar: 25 μm in (L). FIGURE 15 Figure 15. Absence of colocalization between IL-1β and GFAP in the AVCN in control rats (A–C) and following noise-exposure (D–L). Astroglial (red) production of IL-1β (green) was not observed at any of the time points post-exposure (n = 5 for each group). IL-1β was primarily synthesized by cochlear nucleus neurons after the exposure. Asterisks indicate TNF-α-containing neurons while arrows point to astrocytes. Scale bar: 25 μm in (L). Discussion Although the underlying mechanisms responsible for cochlear damage resulting from noise exposure have been extensively studied through the literature, much less attention has been given to the way that these noise-induced peripheral modifications translate into central changes. In this study, we have investigated the contribution of glial cells in regulating inflammation and resolution at peripheral and central levels in response to repetitive high-level noise exposure. Our results indicate that following such high intensity noise exposure there is a permanent hearing threshold shift of about 40 dB, which occurs concomitantly with OHC loss, prestin upregulation, and microglial activation in the cochlear structures most vulnerable to the lesion. Gene and protein expression levels of Iba1 in the SL and the SG were upregulated at 1 and 10D post-exposure and declined to basal levels at the longest time point (30D) assessed. A peripheral inflammatory response characterized by excessive synthesis of TNF-α, IL-1β, TGF-β, iNOS, and ICAM-1 was also observed on days 1 and 10 after noise exposure. Interestingly TIMP-1 expression peaked transiently at 1D post-lesion and quickly decreased between 10 and 30 days post-exposure. In the noise-exposed CN, microglial and astroglial responses were much more protracted reaching a maximum peak on day 30 which was associated with a significant increase in glial-neuronal interactions. These findings suggest that neurons, fibrocytes, and microglia represent the major cellular sources of TNF-α and IL-1β release in response to noise overexposure and highlight the fundamental role of these cytokines in the pathogenesis of noise-induced hearing loss. Although the degree of damage on auditory function and structure depends on several factors such as noise properties (i.e., intensity, duration, and frequency), individual vulnerability to noise and survival time after the exposure, there is abundant evidence that noise overexposure leads to increases in auditory thresholds and morphological alterations in the inner ear (Syka and Popelár, 1980; Saunders et al., 1991; Bohne and Harding, 2000; Nordmann et al., 2000; Le Prell et al., 2003, 2007; Park et al., 2013; Chen et al., 2014; Sanz et al., 2015). While the initiating events associated with noise-induced pathology are thought to be direct mechanical damage, a metabolic stress associated with formation of excessive free radicals, or some combination of both, previous studies have demonstrated that noise-induced sensorineural hearing loss may depend on damage to a number of different cochlear cells, such as hair cells and their stereocilia, fibrocytes in the SL and the SLB, the SGN and the stria vascularis (Hu et al., 2000; Ou et al., 2000; Wang et al., 2002; Hirose and Liberman, 2003; Melgar-Rojas et al., 2015). In CBA/J mice, a single 30 min exposure to swept-sine noise (9–13 kHz at 120 dB) or 2 h exposure to broadband noise (2–20 kHz at 106 dB) result in loss of OHC in the basal and middle cochlear regions along with a permanent threshold shift (Chen et al., 2012; Sanz et al., 2015). Similarly, continuous noise exposure in rats (10 kHz at 100 dB) for 1 h during 10 consecutive days leads to ABR thresholds elevations, OHC loss in the intermediate and basal turns, stereocilia damage and alterations in the integrity of SGN (Fetoni et al., 2013, 2015). In the current study, adult Wistar rats were exposed to broadband noise (0.5–32 kHz, 118 dB SPL) for 4 h/day during 4 consecutive days to induce permanent auditory damage. Although this noise exposure paradigm is different from the one used in the aforementioned studies, as its uses a wider frequency range, its impact on auditory thresholds and cochlear cell types agrees with previous observations. Our findings also demonstrate that OHC loss and dysfunction occurs concomitantly with upregulation in prestin levels in the lateral wall of surviving noise-exposed hair cells at all time points post-exposure. Consistent with this view, elevated prestin protein and gene expression in residual OHC has been reported in noise-exposed rodents and proposed as a compensatory mechanism by which hearing loss can be partially recovered after insult (Chen, 2006; Mazurek et al., 2007; Xia et al., 2013; Parham, 2015). The inner ear has its specialized resident immune system in which mainly phagocytic cells are involved in initiating and/or modulating inflammation in response to noise trauma (Abi-Hachem et al., 2010; Tan et al., 2013; Okano, 2014). During normal cochlear function, resident MLC serve fundamental roles as active sensors that detect minimal homeostatic disturbances (Lang et al., 2006; Okano et al., 2008; Sato et al., 2008). It has been reported previously that noise-induced damage to the cochlea triggers an inflammatory response that consists of early MLC activation and rapid synthesis and release of inflammatory mediators whose interplay facilitate migration of immune cells from the blood stream to the cochlea (Hirose et al., 2005; Fujioka et al., 2006; Tornabene et al., 2006; Miyao et al., 2008). In this regard, previous studies using CD45 as a leukocyte marker have demonstrated that the recruitment of circulating bone marrow-derived white blood cells takes place mainly in the SL which is considered a highly vulnerable structure to noise and a vascularized cellular system that may facilitate immune cells extravasation following noise-overstimulation (Hirose et al., 2005; Tornabene et al., 2006; Miyao et al., 2008). Our results demonstrate noise-induced MLC activation in the SL and also in the SG, the SLB and the cochlear nerve as early as 1D post-lesion, when microglia increase in number and exhibit a hypertrophic phenotype when compared to unexposed rats. These Iba1-stained cells were amoeboid or rounded in appearance resembling mature macrophages and were in close association with presumptive injured cochlear cells. This activation state remained elevated on day 10 and declined on day 30 to reach a near resting level. Although it is uncertain whether early activated phagocytes represent an activation and proliferation of a population of immune cells normally residing in the cochlea or an invasion of immune cells from the vasculature in response to injury, there is evidence of leucocytes infiltration to the SL between 2 and 4 days following noise exposure but not to the SG (Fujioka et al., 2006; Tornabene et al., 2006). Thus, at least for the SG, the observed cochlear phagocytes by 1D post-exposure were likely tissue resident cells. Our results agree with previous studies in which the authors by using additional monocyte/macrophage markers such us F4/80, CD68, and CX3CR1 reported a crucial role for cochlear MLC in regulating compromised auditory function (Hirose et al., 2005; Tornabene et al., 2006). However, in the current study we have observed a much higher degree of MLC activation than previously reported, particularly in the SL and the SG which correlates with a more extensive noise-induced tissue damage. iNOS is a stress-induced neurotoxic molecule associated with a variety of pathophysiological disorders (Brown, 2007; Charriaut-Marlangue et al., 2013). Excessive levels of this mediator are linked to inflammatory processes which involve cytokine overproduction and infiltration of immune cells (Moncada and Bolaños, 2006; Pannu and Singh, 2006). Supporting this view, our observations reveal elevated levels of iNOS mRNA on days 1 and 10 following noise-exposure that progressively declined, reaching basal levels by day 30. Noise also induced a parallel increase in TGF-β cochlear gene expression. These early TGF-β elevations have been linked to regulation of the inflammatory response as this cytokine inhibits the production of proinflammatory cytokines and chemokines and induces adhesion molecules and matrix metalloproteinases that contribute to leukocytes activation (Li et al., 2006; Worthington et al., 2012). Moreover, the blockade of this anti-inflammatory cytokine by using specific inhibitors (P17 and P144) before or immediately after noise damage significantly ameliorates the inflammatory state and protects the cochlea from noise-induced hearing loss (Murillo-Cuesta et al., 2015). Concomitantly with the observed noise-induced upregulation in TNF-α, IL-1β, TGF-β, iNOS, and ICAM-1 mRNA expression, our results demonstrate a rapid and transient increase in TIMP-1 levels on day 1 and a remarkable decline with time. This increased expression is consistent with previous data reporting upregulation of TIM-1 gene expression at 2 h and 1 day after noise-exposure. At the protein level, TIMP-1 immunostaining was located in sensory cells with advanced nuclear condensation indicating that this endogenous matrix metalloproteinases inhibitor may modulate apoptosis in response to acoustic trauma (Hu et al., 2012). Along with a noise-induced peripheral inflammatory response, we have reported a long-lasting response of reactive microglia and astrocytes in the AVCN that reached maximum levels on day 30 post-exposure. These results are agreement with a previous study in the CN demonstrating microglial activation in response to acoustic trauma (Baizer et al., 2015). In this latter study, the authors demonstrated that when rats were exposed to narrowband noise (bandwidth 100 Hz, 12 kHz, 126 SPL) for 2 h, OX6-immnostained cells distributed in both the dorsal and ventral subdivisions of the CN at 30 and 60 days and 6 months after the exposure. Such reactive cells have been proposed to act as scavengers, removing axonal debris. The involvement of glial-related mechanisms in stabilizing the activity of CN networks following cochlear damage has been investigated by others (Lurie and Rubel, 1994; de Waele et al., 1996; Campos-Torres et al., 1999; Fuentes-Santamaría et al., 2012, 2013, 2014; Fredrich et al., 2013; Janz and Illing, 2014). In this regard, the CN is a highly plastic structure whose neurons, in response to a permanent threshold shift, adapt easily to the changing conditions by modifying their cellular properties. Elevations in spontaneous firing rates in VCN neurons have been observed immediately after noise trauma (Gröschel et al., 2014). This increased neuronal excitability may reflect an increase in cochlear peripheral activity that induces elevations in glutamate release at synapses between the SG and the CN (Gröschel et al., 2014). In support of this hypothesis, it has been suggested that glial activation regulates neuronal activity and synaptic strength by limiting excessive glutamate release and/or uptake (Patel et al., 2003). It is important to note that cochlear damage along with the increased neuronal activity in subcortical structures, such as the CN, have been causally associated with the auditory phantom sensation (tinnitus) that frequently occurs following intense noise exposure (Zacharek et al., 2002; Eggermont and Roberts, 2004; Lobarinas et al., 2008; Zheng et al., 2012; Rüttiger et al., 2013; Chen et al., 2014). Thus, considering that glial-related mechanisms are involved in the stabilization of CN activity after noise-induced cochlear damage, it might be expected that they would contribute to the pathogenesis, maintenance and/or regulation of noise-induced tinnitus. Consistent with these observations, our data demonstrate an increased number of interactions among CN neurons, microglia and astrocytes at all time points after the exposure. However, more studies will be needed to explore whether glial cells could represent a possible pharmacological target to treat this auditory perceptual disorder (Zacharek et al., 2002; Zheng et al., 2012). One of the most noteworthy findings of this work is the fact that, TNF-α and IL-1β-producing cells in the SL and the SG were microglia, fibrocytes, and neurons, as opposed to the AVCN where solely neurons and not glial cells seemed to be responsible for the abnormal upregulation of TNF-α and IL-1β after noise trauma. Compelling evidence suggests that endangered neurons in the CN respond to modifications and/or deprivation of afferent activity by delivering signals that lead to phenotypic remodeling of nearby microglial and astrocytes which rapidly act to reduce tissue damage (Fuentes-Santamaría et al., 2012, 2013). In this regard, neuron-to-glia signaling is fundamental for glial activation, cytokines overproduction and neuronal excitability following irreversible cochlear damage. These observations together with our confocal and electron microscopy data indicate a reciprocal interaction among neurons, microglia and astrocytes that may facility activity-dependent release of secreted factors to maintain system homeostasis. TNF-α and IL-1β are multifunctional cytokines that, in addition to their essential role in the normal development of auditory function, regulate synaptic plasticity in response to microglia-mediated inflammation (Guo et al., 2007; Riazi et al., 2015). Thus, the fact that neurons themselves upregulate TNF-α and IL-1β levels in response to noise-exposure may represent an activity-dependent central mechanism to regulate glutamatergic transmission and maintain a stable level of excitability in the CN. Conclusions In summary, our results together with previous observations suggest a complex interplay among different cytokine-producing cells in the noise-exposed auditory system (i.e., neurons, glia, fibrocytes, and infiltrating macrophages). Collectively, this plethora of different cell types orchestrate a sequence of rapidly occurring cellular events that modulate the initiation/progression of cochlear inflammation in the pathogenesis of noise-induced hearing loss. Also, our data suggest a primary role of TNF-α and IL1β signaling in the noise-exposed peripheral and central auditory system. Author Contributions All authors had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: VF and JA. Acquisition of data: VF, JA, PM, and MG. Statistical analysis and interpretation of data: VF and JA. Drafting of the manuscript: VF and JA. Critical revision of the manuscript for important intellectual content: JA, VF, JM, and JJ. Funding This study was supported by Programa I3 del Ministerio de Ciencia e Innovación (I320101590 to VF and I320101589 to JA), PROHEARING project of the 7th Framework Programme (FP7-HEALTH-2012-INNOVATON 304925 to JJ). Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.	{ "pile_set_name": "Pile-CC" }
Live Hillary Clinton and Donald Trump both campaign in Florida on Tuesday after the state was hit by Hurricane Matthew.	{ "pile_set_name": "OpenWebText2" }
Chinese consumers will soon be able to buy New Zealand chilled meat in supermarkets, adding value to this country's exports. New Zealand stands to add hundreds of millions of dollars to the value of its red meat exports to China, now that agreement has been reached over allowing chilled meat into the market. In 2015 New Zealand exported $1.55 billion worth of red meat products to China, composed of $631 million of sheepmeat and $550m of beef. The remainder was "co-products" such as offal and intestines. At present all of the meat is in frozen form, most of it ready cut in New Zealand. Prime Minister John Key said the two countries had agreed to the protocols relating to chilled meat, and the first shipments would be only a matter of a month or so away. READ MORE: * Chinese tourists to reach 1m, Key says * Key chalks up small win in push for free-trade upgrade * China's bargaining chip in talks * Security, trade, agriculture on Key's Beijing agenda * Key yet to get FTA assurance * The China FTA: What to know * NZ open to Chinese investment, John Key says Australia recently stole a march on New Zealand when it was given permission to export chilled meat on a trial basis. However with the latest agreement New Zealand may have leapfrogged Australia, depending on the protocols, said Sirma Karapeeva from the Meat Industry Association. If the protocols were not for a trial, then it was a better deal. "At the moment Australia has a small trial of shipments based on a handful of export premises, and we've taken that as a proxy for what it might mean for New Zealand," Karapeeva said. It was hard to be accurate about the figures as the Australian exporters were cagey about their commercial contracts. As an indication, in February New Zealand exported 5476 tonnes of chilled sheepmeat to the United Kingdom for $55m. Frozen sheepmeat exports to China of 18,251 tonnes for the same month were worth $69.6m. The chilled meat segment in China is a growing one, both with retail ready packs in supermarkets or high end restaurants. One of the factors militating against chilled meat has been concern over the logistics of keeping it safe. Primary Industries Minister Nathan Guy welcomed the breakthrough. "We've got very strong air links, we've filling the planes with tourists coming down to New Zealand, coming back there's the opportunity for us to put chilled meat in the back of the plane," Guy said. Also this week the Ministry for Primary Industries and the China Certification and Accreditation Administration co-signed a new Halal Arrangement, under which China will recognise New Zealand's halal regulation and certification regime for halal goods exported to China. "This is a major step forward for New Zealand's halal meat producers, and it marks the first time China has recognised another county's halal regulatory and certification systems," Guy said. He said China was New Zealand's number one market for halal certified meat. In the 12 months to September 2015, about 77,672 tonnes of halal certified meat was exported to China, representing 33 per cent of New Zealand's total halal certified exports. There are 23 million Muslims in China, and it is a growing population. Guy also co-signed an arrangement with China's Minister of Agriculture, Han Changfu, for New Zealand and China to develop an Agricultural Growth Partnership (AGP). This is a public-private partnership that will use New Zealand expertise in research and training in areas such as agricultural policy exchange, dairy farmer training, livestock technology, animal health and disease control.	{ "pile_set_name": "OpenWebText2" }
Q: list files with first char within specific range I need to list all files that have first char within a specific range. If I use Powershell I can do this with gci [a-c]* How can I do it from command line? A: You may use the following command: dir /b \| findstr /R "^[a-c].*"	{ "pile_set_name": "StackExchange" }
As Mr. Eyman’s detailed and at times long-winded new book, “John Wayne,” makes very clear, the man Duke Morrison — born in 1907 with the unlikely name Marion Robert Morrison in the small town of Winterset, Iowa — was not synonymous with the John Wayne character he created on screen. “In Wayne’s own mind,” Mr. Eyman writes, “he was Duke Morrison. John Wayne was to him what the Tramp was to Charlie Chaplin — a character that overlapped his own personality, but not to the point of subsuming it.” Image John Wayne in the movie “The Big Trail,” from 1930, from a photograph included in the biography by Scott Eyman. A conscientious and tireless student, Duke started out as an extra and prop man, and spent a decade before his breakthrough role as the Ringo Kid in John Ford’s “Stagecoach” (1939), toiling away in B pictures, made in three, six or 10 days. During those years, he honed his craft and put together the pieces of a screen character — his distinctive start-and-stop phrasing; his low, slow growl of a voice; his graceful, rolling walk. It was a character that drew upon his easy charm and faith in self-reliance, but it was also modeled, he once said, on “the kind of man I’d liked to have been.” Mr. Eyman says the screen persona that Wayne devised for himself — of a man who was at once an outsider and an authority figure — helped transform an awkward, insecure boy into “the emphatic representation” of an “American masculinity” that was sure enough of itself to encompass a certain melancholy and vulnerability beneath the steadiness and self-assurance. This story of John Wayne’s invention of himself has been told many times before. “The Searchers: The Making of an American Legend,” Glenn Frankel’s succinct and powerful 2013 book about John Ford’s masterwork, discussed how the young Wayne studied the western star Harry Carey’s slow, soulful manner, and the lessons he learned from the accomplished stuntman Yakima Canutt, a former rodeo star. (“I studied him for many weeks, the way he walked and talked and rode a horse and pulled a gun.”) And Mr. Wills’s 1997 book, “John Wayne’s America,” which was less a biography than an extended essay about the dynamics of celebrity, also covered much of this same ground. Mr. Eyman’s book aims to be far more comprehensive than those earlier works; at times, it feels too comprehensive, doggedly chronicling more forgettable Wayne movies and offering tedious asides about the financing of various films. The author also spends an awful lot of space on issues that have been debated for decades (like the relationship between Wayne’s conservative politics and his choice of movies) without shedding new light on them.	{ "pile_set_name": "OpenWebText2" }
El Salvador: the debate on abortion law reform is officially open This year is the first time that this Central American country has openly debated abortion, forcing even conservative media organisations to cover the issue in editorials and primetime news programmes since abortion was made completely illegal almost 20 years ago. “This is an historic moment. There’s been a qualitative shift – it’s not just women’s groups speaking out. Abortion has become a priority topic for a range of groups. It… feels like change. Politicians must make amends for the damage done to thousands of women … there is no going back,” said Sara García, a campaigner with the Agrupación Ciudadana por la Depenalización de Aborto. In February 2017, CEDAW published its recommendations to the El Salvador government that it should decriminalise abortion at least in certain circumstances, and should expedite the adoption of the draft law tabled by the FMLN on four grounds to that effect. During CEDAW’s deliberations, the Agrupación, the Center for Reproductive Rights and the law firm Debevoise & Plimpton LLP submitted an expert report detailing how the extreme hostility exercised under the existing law put the lives and health of Salvadoran women at grave risk. In March, the Foundation for the Study of the Implementation of the Law (FESPAD), together with the Association of Women Lawyers (AMA), created a Forum for dialogue between Salvadoran and international jurists on the subject of decriminalisation of abortion, which called on the Members of the El Salvador Parliament to legislate for the health and lives of women, girls and adolescents by approving the proposals tabled earlier this year to decriminalise abortion on four grounds. The Forum, entitled Constitutional Guarantees, addressed the collision of rights between pregnant women and the developing child they are carrying, and the gulf between the country’s national legislation and international conventions on reproductive rights that currently exists. “The termination of pregnancy should be permitted in cases in which the pregnancy threatens the life of the pregnant woman, or when the fetus is unviable due to fetal anomalies,” said Ricardo Iglesias, Salvadoran constitutional expert. He held that while some rights from the moment of conception are recognised, these rights are not absolute, and they do not take precedence over other rights, including those of the pregnant woman. On 20 March, the Committee on Legislation and Constitutional Issues of the Legislative Assembly held a consultation on the two pending bills to reform Article 133 of the Penal Code in relation to abortion, the one a bill to increase the criminal penalties for abortion, tabled by Deputy Ricardo Velázquez Parker of the ARENA party, the other a bill to decriminalise abortion on four grounds, tabled by Lorena Peña of the FMLN. The FMLN bill would allow abortion in cases of risk to the life or health of the pregnant woman, fetal anomaly incompatible with life, pregnancies resulting from rape or trafficking, and for girls and adolescents who would have to face motherhood imposed by sexual abuse. “In regard to these two initiatives, we believe in and we support the amendment tabled by Lorena Peña, as it is a step forward on the issue and would provide pregnant women with the right to have an abortion on these four grounds,” said Abraham Abrego, Director of FESPAD. Although he acknowledged that these grounds are still limited, it is an improvement on the current situation and would give the necessary legal security to both women and abortion providers in high-risk cases. The Agrupación also reported on 21 March 2017 that María Teresa Rivera, 34, the most recent women among Las 17 to be released from prison in 2016, after serving four and a half years of a 40-year sentence on charges of aggravated homicide, was granted asylum by the government of Sweden for herself and her 11-year-old son. Then, on 24 March, they reported that two representatives of the US Congress, Debbie Wasserman Schultz and Norma J Torres, delivered a letter signed by 21 members of Congress, including the senior member of the Foreign Affairs Committee of the House of Representatives, Eliot Engel, to the President of El Salvador, Salvador Sánchez Cerén, and the President of the Salvadoran Congress, Guillermo Gallegos Navarrete. The letter asked them also to support the efforts to decriminalise abortion on four grounds. In the letter, these members of the US Congress expressed their opposition to the total ban on abortion in El Salvador and called on President Sánchez Cerén to work with civil society and the Salvadoran Congress to advance the FMLN amendments. The letter also emphasises that while the decriminalization of abortion on the four grounds is not sufficient to guarantee access to all reproductive health services for Salvadoran women, it does represent a significant improvement and brings El Salvador closer to complying with international human rights standards.	{ "pile_set_name": "Pile-CC" }
Power grid to energize Bangladesh and digitize Bhutan-India Bangladesh has abundant international Internet bandwidth while Bhutan generates surplus electricity. Newly appointed Bhutan’s Ambassador to Dhaka, Pema Choden, has expressed interest in importing surplus bandwidth from Bangladesh. In that meeting, the State Minister for Foreign Affairs M Shahriar Alam also showed interest in Bhutan’s plentiful electricity to meet the growing energy demand of Bangladesh. Both the neighbors are now poised to be the friend in mutual needs. Bangladesh currently consumes only 40Gbps of its 200Gbps capacity of the SEA-ME-WE 4 submarine cable. Landlocked Bhutan primarily relies on India and secondarily on China for global connectivity (click on the thumbnail of China Mobile map above). The Himalayan kingdom pays a lot to reach the nearest IP-transit hubs at Mumbai and Kunming. Dollars per Mbps per kilometer per month keeps the wholesale prices of IP-transit exorbitant across the developing Asia. Landlocked Bhutan is one of the worst victims. It will cost her far lesser if the intended 24 Gbps of IP-Transit bandwidth is forked from Dhaka. Infrastructure is the critical component of connectivity between Bangladesh and Bhutan. The ADB-funded cross-border optical fiber terrestrial network under South Asia Subregional Economic Cooperation (SASEC) Information Highway Project is being considered to link both the countries. This network is intended to loop Bangladesh, Bhutan, India and Nepal. Capacity of SASEC network remains undisclosed while its quality is to be tested in future. Details of the construction and management agreement (C&MA) are also yet to be made public. Identical initiative of ADB in Southeast Asia has not achieved its objectives. Therefore, Bangladesh and Bhutan should explore a viable alternative. The power transmission grid, which would link Bangladesh with Bhutan, can be the best option to simultaneously energize and digitize both the countries. The Bhutan-Bangladesh power grid, inherently fitted with optical ground ware (OPGW), will traverse across Assam. This infrastructure will bring power to Bangladesh and it will simultaneously carry the IP-Transit bandwidth back to Bhutan. This solution will also add significant resilience to the proposed terrestrial cross-border optical fiber link that Bangladesh will deploy across her eastern border to serve the neighboring states of India. The Bhutan-Bangladesh power grid will act as the second supply line to the currently negotiated IP-Transit deal for northeast India. Therefore, India also greatly benefits from the right of way it grants to proposed power transmission deal between Bangladesh and Bhutan. That is the beauty of regional cooperation. Political goodwill is, however, the fundamental prerequisite to rip extraordinary benefits out of such very ordinary engineering scheme.	{ "pile_set_name": "Pile-CC" }
+ 20i + 43. Calculate r(22). -1 Let q(y) = -2y*2 + 14y - 28. What is q(2)? -8 Let h(r) = 7r + 30. Give h(-4). 2 Let g(z) = z - 14. Give g(0). -14 Let d(s) = s2 + 14s + 5. Determine d(-12). -19 Let g(w) = w*3 + 10w*2 + 4w + 45. Determine g(-10). 5 Let r(i) = 6i3 + 5i*2 + 8i - 2. What is r(-3)? -143 Let v(l) = -l*3 - 15l*2 - 16l - 28. Determine v(-14). 0 Let u(s) = 9s - 10. What is u(-6)? -64 Let z(k) = -k2 - 2k + 4. Determine z(-5). -11 Let i(h) = -2h3 + 10h*2 + 10. Calculate i(5). 10 Let m(v) = -3v + 32. Determine m(13). -7 Let a(j) = -j*2 - 17j + 37. Determine a(-19). -1 Let n(a) = -10a + 13. Calculate n(2). -7 Let f(r) = r3 + 9r*2 + 13r - 6. Give f(-7). 1 Let k(s) = -s*3 + 8s*2 - 9s - 7. Give k(7). -21 Let n(a) = a*3 + 10a*2 + 9a + 9. Determine n(-9). 9 Let m(i) = -2i2 - 2i + 2. What is m(4)? -38 Let t(f) = -f*3 - 17f*2 + 39f + 28. Give t(-19). 9 Let g(x) = -x3 - x2 + 3x + 1. What is g(3)? -26 Let g(v) = -v2 - 8v + 2. Determine g(-9). -7 Let k(r) = 5r - 24. Determine k(4). -4 Let d(x) = -x2 + 2. Calculate d(-3). -7 Let o(w) = 2w*3 + 32w2 - w + 13. Determine o(-16). 29 Let u(f) = -f2 + f + 62. Determine u(8). 6 Let s(f) = 13f + 101. Determine s(-8). -3 Let g(f) = f2 + f - 5. Give g(-3). 1 Let y(k) = -k2 - 4k + 4. What is y(-4)? 4 Let v(l) = 57l + 331. Give v(-6). -11 Let s(o) = -2o*3 + 14o*2 + 17o - 7. What is s(8)? 1 Let t(l) = -l + 1. What is t(2)? -1 Let t(k) = -9k2 - 21k - 20. What is t(-1)? -8 Let r(o) = 10o + 99. Determine r(-10). -1 Let v(d) = 2d*3 + 7d*2 + 12d + 64. Calculate v(-4). 0 Let q(p) = -19p - 104. What is q(-4)? -28 Let w(f) = -f3 + 4f*2 - 3f + 8. Determine w(4). -4 Let b(i) = -i*3 - 24i*2 + 17i + 8. Give b(-25). 208 Let s(g) = -g3 - g2 + g - 18. What is s(0)? -18 Let m(l) = l*2 + 12l + 21. Give m(-11). 10 Let g(q) = q*2 + 11q - 5. What is g(-10)? -15 Let t(z) = 2z + 5. Calculate t(-8). -11 Let o(g) = -4g*2 - 10g - 1. Calculate o(-4). -25 Let c(g) = g*3 - 4g*2 - 2g + 6. What is c(5)? 21 Let r(t) = -t2 - t + 10. What is r(3)? -2 Let k(d) = d3 + 11d2 - 5d + 4. Give k(-11). 59 Let m(v) = v*3 + 3v*2 + 2v + 3. Determine m(-2). 3 Let a(o) = o*3 + 12o*2 + 8o + 269. What is a(-13)? -4 Let s(k) = -k3 - k2 + k - 6. Determine s(0). -6 Let w(v) = v*3 - 8v*2 - 11v + 10. What is w(9)? -8 Let u(k) = k*2 + 2k - 221. What is u(14)? 3 Let x(r) = -5r3 + r2 - r. Determine x(1). -5 Let v(s) = 5s + 2. Determine v(-8). -38 Let y(h) = 6h3 + 4h*2 + 2h. Determine y(-2). -36 Let k(t) = t*2 + 6t - 16. Determine k(-8). 0 Let v(k) = 7k - 21. Determine v(-2). -35 Let w(l) = l2 - 8l - 14. Calculate w(10). 6 Let z(h) = -3h - 4. Give z(7). -25 Let y(z) = z3 + 13z*2 - 2z - 16. Determine y(-13). 10 Let u(v) = -27v - 247. Determine u(-9). -4 Let d(r) = -r2 + 18r - 6. What is d(11)? 71 Let r(l) = -l*2 + 14l + 5. What is r(14)? 5 Let c(s) = 9s - 42. What is c(9)? 39 Let m(p) = -8p - 3. Calculate m(-9). 69 Let p(w) = w*3 - 2w*2 - 8w - 1. Calculate p(4). -1 Let p(a) = -a*3 - 15a*2 - 28a - 7. What is p(-13)? 19 Let d(n) = n*3 + 4n*2 + 3n + 1. Determine d(-3). 1 Let m(q) = -3q2 + 59q - 46. Give m(19). -8 Let f(b) = -b*3 + 9b*2 - 3b - 15. Determine f(8). 25 Let d(w) = 38w + 13. Give d(-5). -177 Let v(i) = -4i*2 + 2i - 3. Determine v(3). -33 Let a(c) = c*2 + 7c - 10. Calculate a(-10). 20 Let t(k) = -2k3 + 7k*2 + 3k - 16. What is t(6)? -178 Let u(q) = 131q - 1. Determine u(1). 130 Let x(p) = p3 - 15p*2 + 5p + 22. Calculate x(15). 97 Let k(j) = j*2 - 6j - 1. Give k(7). 6 Let p(b) = -b2 + b - 5. Calculate p(2). -7 Let n(c) = -c3 + 9c2 + c - 1. What is n(9)? 8 Let p(j) = -j2 - 29j - 23. Give p(-27). 31 Let o(z) = z*3 - 7z*2 + 6z - 10. What is o(6)? -10 Let o(r) = 8r3 - r2 + 5r - 3. Give o(1). 9 Let v(z) = -z*2 + 16z - 6. What is v(18)? -42 Let m(v) = -6v - 84. Calculate m(-17). 18 Let k(t) = t3 + 12t*2 + 14t + 9. What is k(-11)? -24 Let w(j) = j*3 - 25j*2 + 24j - 34. Give w(24). -34 Let j(q) = q*2 + 12q - 20. What is j(-14)? 8 Let h(w) = w - 22. Give h(12). -10 Let b(c) = -c*2 + 9c - 6. Give b(7). 8 Let k(r) = -r + 16. Calculate k(6). 10 Let o(v) = v*3 - 5v*2 + 2v - 1. Give o(5). 9 Let h(w) = -w3 - w2 + 1. What is h(-2)? 5 Let i(v) = 6v + 1. Calculate i(1). 7 Let h(d) = 2d*2 + 55d + 94. Give h(-26). 16 Let p(u) = -27u. Determine p(1). -27 Let o(n) = -n3 - 12n*2 - 3n - 13. Give o(-12). 23 Let p(q) = q*2 + 9q - 20. Calculate p(8). 116 Let f(p) = -3p + 10. What is f(2)? 4 Let q(k) = 2k*3 - 3k2 - k + 3. Determine q(2). 5 Let h(b) = -b2 + 6b + 9. What is h(6)? 9 Let x(o) = 2o*3 - 2o*2 - o + 3. Determine x(2). 9 Let t(w) = -2w*3 - 2w*2 - 4w - 3. What is t(-2)? 13 Let y(t) = t*3 + 13t*2 + 27t + 13. What is y(-11)? -42 Let k(m) = 16m - 83. Calculate k(5). -3 Let r(z) = -57z + 210. What is r(4)? -18 Let z(w) = w*3 - 3w*2 + 4w - 2. What is z(2)? 2 Let m(k) = k*3 + 10k*2 - 9k + 2. Calculate m(-11). -20 Let q(n) = -n*3 + 2n + 1. What is q(-2)? 5 Let m(h) = -h*2 - 3h. Determine m(-3). 0 Let g(h) = -h*3 + 6h2 + 3. Give g(6). 3 Let h(r) = r2 - 3r - 1. Determine h(3). -1 Let a(z) = -17z - 2. Calculate a(-1). 15 Let r(l) = l*3 + 20l*2 + 18l - 15. What is r(-19)? 4 Let c(t) = 6t + 127. Determine c(-12). 55 Let j(y) = -3y*2 + 50y - 20. Determine j(16). 12 Let s(o) = -2o2 - 5o - 8. Calculate s(-5). -33 Let z(f) = f*2 - 20f + 35. What is z(15)? -40 Let u(n) = 2n3 - n2 + 2. Calculate u(1). 3 Let k(o) = -o2 + 2o + 73. What is k(10)? -7 Let y(p) = p*3 - 6p*2 - 11p - 1. Determine y(8). 39 Let b(p) = -p*3 + 12p*2 - 15p. Determine b(10). 50 Let z(i) = -i*2 + 5i - 4. Give z(5). -4 Let b(w) = -4w + 35. Give b(0). 35 Let q(v) = 11v - 240. Calculate q(22). 2 Let h(t) = -t*3 - 9t*2 + 7t - 6. What is h(-10)? 24 Let r(c) = 29c + 1. Determine r(1). 30 Let h(n) = -9n. Give h(17). -153 Let x(s) = -3s - 24. What is x(-11)? 9 Let z(m) = m2 + 4m - 14. Give z(-6). -2 Let j(z) = z + 20. Calculate j(-16). 4 Let r(c) = -20c + 98. Determine r(5). -2 Let w(f) = -8f3 - f2 + f - 1. Calculate w(1). -9 Let s(q) = q*2 + 10q + 17. Calculate s(-8). 1 Let u(h) = 3h3 - 22h*2 + 7h - 20. Calculate u(7). -20 Let o(y) = y*2 + 3y - 15. Determine o(-8). 25 Let u(p) = -p*3 - 10p*2 - 12p + 24. Calculate u(-8). -8 Let j(y) = 2y + 35. Calculate j(-18). -1 Let h(i) = -3i - 92. What is h(28)? -176 Let r(g) = 10g + 43. Calculate r(-5). -7 Let s(g) = -40g2 - g. Determine s(-1). -39 Let i(d) = d2 + 2d - 7. Calculate i(-6). 17 Let s(x) = 10x*2 + 72x + 5. Give s(-7). -9 Let t(x) = 20x - 164. Determine t(7). -24 Let o(y) = -7y - 417. Determine o(-59). -4 Let s(o) = 15o + 12. Give s(1). 27 Let g(v) = -10v + 172. Calculate g(17). 2 Let t(r) = -r*3 - 4r2 + r - 1. Determine t(-4). -5 Let p(i) = -i2 - 23i - 110. Give p(-15). 10 Let z(q) = -q2 + 12q - 12. Give z(10). 8 Let y(a) = -a*2 - 8a - 4. Give y(-7). 3 Let s(p) = -26p - 160. Calculate s(-6). -4 Let z(h) = h2 - 11h + 13. Determine z(10). 3 Let t(c) = -160c + 808. Calculate t(5). 8 Let u(y) = -2y + 16. Determine u(9). -2 Let z(v) = 4v + 31. Calculate z(-8). -1 Let a(h) = -131h*3 + 3h + 3. Calculate a(-1). 131 Let d(s) = 4s + 20. Give d(-5). 0 Let g(u) = 16u - 44. What is g(2)? -12 Let n(g) = g*2 - 10g - 10. Calculate n(10). -10 Let p(f) = -60f3 + 2f*2 + 2f + 1. Calculate p(-1). 61 Let t(d) = d*2 + 6d - 6. Give t(1). 1 Let s(l) = l*3 + 57l*2 - 56l + 111. Give s(-58). -5 Let b(l) = -l - 9. Determine b(-16). 7 Let k(l) = 13l + 6. Calculate k(-2). -20 Let p(q) = -3q + 52. Determine p(20). -8 Let t(b) = -b*3 - 10b*2 - 11b - 1. Calculate t(-8). -41 Let w(a) = -3a - 13. Determine w(-6). 5 Let c(k) = -k3 - 11k*2 + 4k + 9. Give c(-11). -35 Let d(y) = -6y + 13. What is d(5)? -17 Let r(m) = -m3 + 7m*2 + 8m + 7. Give r(8). 7 Let c(d) = -d + 6. Determine c(-7). 13 Let s(v) = -13v. Determine s(3). -39 Let s(z) = -10z - 2. Calculate s(-1). 8 Let u(r) = -r*2 - 4r - 11. Calculate u(-2). -7 Let m(c) = c*3 - 6c*2 + 6c - 13. Give m(6). 23 Let w(k) = -k**2	{ "pile_set_name": "DM Mathematics" }
The pol gene of the human immunodeficiency virus (HIV) encodes three viral enzymes, reverse transcriptase, protease and integrase, which are critical for the replication of HIV. This project focused on the discovery of inhibitors of one of these viral enzymes, HIV reverse transcriptase (HIV RT). The broad objectives are to contribute to the chemistry and biochemistry of conceptually new nucleosides and nucleotides with useful therapeutic potential against the infectivity of HIV. These novel compounds, with stereochemically defined surrogate carbohydrate components, that are regioisomeric with the natural nucleosides and nucleotides, are referred to as isonucleosides and isonucleotides. A compelling rationale for this investigation comes from the discovery in this project of a potently anti-HIV active compound, (S,S)-isodideoxyadenosine [(S,S)-isoddA}. IsoddA 5'-triphosphate is a powerful inhibitor of HIV RT (KI 16 nM). This renewal proposal seeks to expand successful work of the current project to include cyclic monophosphate (MP) pro-drugs (cyclo Sal MPs) and hydrolytically stable phosphonyl derivatives in order to deliver the MPs or their isosteres directly inside the cell. In addition, new classes of isonucleosides with multiple supporting rationaleS for anti-HIV activity are proposed. The synthetic work will involve the development of approaches to the novel, chiral isodideoxynucleosides and their purification and complete characterization by magnetic resonance, mass spectral, and X-ray methods. Collaborative antiviral studies on the target compounds and pro-drug forms will be carried out against HIV-1 and HIV-2, including drug-resistant HIV isolates. Data on inhibition of the cytopathic effect of HIV, on inhibition of HIV RT, on inhibition of proviral DNA synthesis, on inhibition of the expression of HIV-1 p-24 Gag protein, on host cell cytotoxicicty including inhibition of cellular DNA polymerases alphaepsilon beta and gamma, and on therapeutic indexes will be determined and analyzed. Cellular combination drug studies, particularly those having the potential for synergistic inhibition of HIV infectivity, are also planned.	{ "pile_set_name": "NIH ExPorter" }
An electrophysiological study on the effects of Pa-1G (a phospholipase A(2)) from the venom of king brown snake, Pseudechis australis, on neuromuscular function. The effects of Pa-1G, a phospholipase A(2) (PLA(2)) from the venom of the Australian king brown snake (Pseudechis australis) were determined on the release of acetylcholine, muscle resting membrane potential and motor nerve terminal action potential at mouse neuromuscular junction. Intracellular recording from endplate regions of mouse triangularis sterni nerve-muscle preparations revealed that Pa-1G (800 nM) significantly reduced the amplitude of endplate potentials within 10 min exposure. The quantal content of endplate potentials was decreased to 58+/-6% of control after 30 min exposure to 800 nM Pa-1G. The toxin also caused a partial depolarisation of mouse muscle fibres within 60 min exposure. Extracellular recording of action potentials at motor nerve terminals showed that Pa-1G reduced the waveforms associated with both sodium and potassium conductances. To investigate whether this was a direct or indirect effect of the toxin on these ionic currents, whole cell patch clamp experiments were performed using human neuroblastoma (SK-N-SH) cells and B82 mouse fibroblasts stably transfected with rKv1.2. Patch clamp recording experiments confirmed that potassium currents sensitive to alpha-dendrotoxin recorded from B82 cells and sodium currents in SK-N-SH cells were not affected by the toxin. Since neither facilitation of acetylcholine release at mouse neuromuscular junction nor depression of potassium currents in B82 cells has been observed, the apparent blockade of potassium currents at mouse motor nerve endings induced by the toxin is unlikely to be due to a selective block of potassium channels.	{ "pile_set_name": "PubMed Abstracts" }
Q: Z values way too large compared to x and y in reconstruction I reconstruct x,y,z from disparity using triangulation formula .My problem is that x,y, and z values are in very different orders .For eg order of x is like 0.001 and similar for y but z is in the order of 10 .Because of this I see a straight line instead of seeing a face .Is there any way I could apply some transform preserving the structure of face but getting a better reconstruction. EDITED: here is a sample L image and the disparity map ( normalized to 0-255 for visualization not the true values).My point of giving this is to show that disparity comes out fairly decently. A: Assuming that you are solving for the fundamental matrix using point correspondences between the left and right images, this is the expected result. Because the fundamental matrix is rank-deficient, it is only defined up to a scale factor. If you define everything in terms of pixel units, there is no way to reconstruct the scene in real-world units. Solving this requires an additional piece of information: the relationship between a pair of corresponding points in a three-dimensional coordinate frame. For a stereo system, this is most often the baseline, the distance between the left and right camera centers.	{ "pile_set_name": "StackExchange" }
NCCN Clinical Practice Guidelines Prostate Cancer Early Detection, Version 2.2015. Prostate cancer represents a spectrum of disease that ranges from nonaggressive, slow-growing disease that may not require treatment to aggressive, fast-growing disease that does. The NCCN Guidelines for Prostate Cancer Early Detection provide a set of sequential recommendations detailing a screening and evaluation strategy for maximizing the detection of prostate cancer that is potentially curable and that, if left undetected, represents a risk to the patient. The guidelines were developed for healthy men who have elected to participate in the early detection of prostate cancer, and they focus on minimizing unnecessary procedures and limiting the detection of indolent disease.	{ "pile_set_name": "PubMed Abstracts" }
Channing Tatum's Gambit Movie Gets a Production Start Date Channing Tatum is a matter of months away from beginning production on Gambit. According to Omega Underground, Gambit begins filming in New Orleans on March 19th. Tatum stars as Remy LeBeau, the mutant thief called Gambit. Gore Verbinski will direct the film. The plot will reportedly finds Gambit leading a motley mutant crew on a dangerous heist. Tatum has spoken before about why it is he loves Gambit so much. "There wasn't a comic store, but the cartoon was on TV and he was this cool Cajun guy," Tatum said. "And he was the easiest person to play as a kid because you could just unscrew the broom handle, get a pack of cards and wrap a bandana around your head. We had a lot of fun throwing cards and trying to take our friends' eyes out across the living room. "He is just cool, man. He is one of the few superheroes that has an actual culture to him. He doesn't talk like a vanilla American. He is from a specific geo-location, New Orleans, which is a really specific thing." Chris Claremont and Jim Lee created Gambit. The character first appeared in 1990. Many fans were first exposed to Gambit through the 1990s X-Men: Animated Series. The mutant has the ability to charge objects with kinetic energy, causing them to explode. Though he joined the X-Men, Gambit remained a scoundrel. This and his ill-fated romance with Rogue made him an instant hit with fans. Gambit currently has a 3.49 out of 5 ComicBook.com User Anticipation Rating. That makes it the 21st-most-anticipated upcoming coming book movie among ComicBook.com user. Let us know how excited you are about Gambit by giving the movie your own personal ComicBook.com User Rating below. Gambit opens in theaters on February 14, 2019. Other upcoming X-Men movies include The New Mutants on April 13th, the untitled Deadpool sequel on June 1st, and X-Men: Dark Phoenix on November 2nd. Disclosure: ComicBook is owned by CBS Interactive, a division of ViacomCBS.	{ "pile_set_name": "OpenWebText2" }
Q: async_network_io issues with BIDS This is related to my previous question drastically different runtimes in BIDS and the SSRS Web Portal. I am struggling with refreshing some reports in BIDS because they run forever. I have now noticed that when I refresh the report in BIDS the query will experience ASYNC_NETWORK_IO waits. (also CXPACKET but I understand that's more an effect than a cause) The post Need help with ASYNC_NETWORK_IO seems to indicate SQL Server is waiting on the client, which I assume in this case is BIDS on my desktop. If it can be identified from this snippet of information, where is the problem here? Is it my desktop and its lack of oomph? Could it be the network? Is my report doing too many calculations on the report-side? Where else should I look? How can I fix it? I will add that oftentimes the data never full returns. Instead I receive the following (redundant) error message: An error occurred during local report processing. An error has occurred during report processing. Exception of type 'System.OutOfMemoryException' was thrown. A: We actually ran into a similar issue at StackOverflow and Kyle blogged about it: http://blog.serverfault.com/2011/03/16/views-of-the-same-problem-network-admin-dba-and-developer/ The problem can be a number of things: Queries bringing back too much data (like select * from a wide table with a lot of XML or binary fields) Client-side apps processing data row by row instead of pulling it all into memory and then doing whatever work necessary Underpowered app server hardware (or in your case, client machines) that are paging to disk or churning on CPU. I see this a lot on over-committed virtual machines. To tune it, start by looking at Perfmon counters on your own machine. My tutorial on it is at http://www.BrentOzar.com/go/perfmon, and it includes a list of counters to gather, how to analyze 'em, and how to interpret your bottleneck.	{ "pile_set_name": "StackExchange" }
Catheters are thin tubes utilized for insertion into the vessels of a body to perform a variety of medical procedures, including draining fluids, administering fluids, measuring internal body pressures, angioplasty procedures, delivery and deployment of stents or other prostheses (e.g. heart valve prostheses), and other such procedures. The catheters are often made of highly flexible material, capable of following the path of an artery or vein until the target area is reached and the medical procedure is begun. It is, however, difficult to know the exact location of a catheter within use in the body during a medical procedure. In some procedures, to achieve proper placement within the vessel, a physician must know the exact location of the distal end of the catheter within in the body. Fluoroscopy can be used to determine the location of a catheter within the body. Fluoroscopy is an imaging technique that utilizes a stream of X-rays to generate a series of images of the internal features of a body on a screen. The images are continuously updated in a way that resembles a real-time video. However, catheters are often made from materials that are not easily seen via fluoroscopy. Therefore, radiopaque marker bands are often added to catheters at critical locations, such as a distal end of the catheter or the location of a stent within the catheter. In another example, radiopaque material may embedded within the polymers of the catheter. In yet another example, radiopaque ink may be applied to an exterior surface of the catheter. In many procedures, multiple catheters and other devices may be simultaneously present in the body of the patient. Therefore, while radiopaque markers enable a treating clinician to view a particular area of a catheter, the clinician may not be able to distinguish one particular catheter from other catheters or devices in the body. Additionally, information such as the catheter brand, size of a balloon or stent, batch number, etc. are of importance to prevent or eliminate the chances that one catheter or medical tool is mistaken for another. Accordingly, there exists a need for a catheter with an identifier that can be seen under fluoroscopy and can provide certain information regarding the catheter.	{ "pile_set_name": "USPTO Backgrounds" }
Q: What are the differences between the spirit of God and spirit of Man? First, I thought that the spirit Christians get from God is the same as the spirit of God. Recently, I heard a sermon that asserted they are different, but gave no more details. Which verses describe this in the Bible? When we get the Holy Spirit are we getting the spirit of God? A: It helps to first know what the word "Spirit" actually means, which is more of a question for the Hermeneutics site. I do see you've been asking questions about the meaning of the word there, so I'll include a brief bit here as introduction. From http://www.pickle-publishing.com/papers/soul-and-spirit.htm In the New Testament the word for "spirit" is pneuma. Pneuma is translated the following ways: ghost 2 Ghost (with Holy) 90 life 1 spirit 151 Spirit 137 spiritual gift 1 spiritually 1 wind 1 The entire article is very long, but it does a good job of illustrating how a simple word can be interpreted different ways based on the context of the verse. The word "Spirit" can carry the more religious/supernatural connotation associated with the word today, or it can simply mean "life" or "the breath of life". Quite commonly it is used as a literary form of personification: One brief thought before we look at the verses: There are some verses that seem to use "soul" and "spirit" in ways that harmonize with the common concept of the nature of man. How can this be? Is the Bible contradicting itself? Here is one suggestion: It was commonplace for the Bible writers to take parts of man’s being and personify them, give them attributes they did not in actuality possess. Perhaps sometimes they personified the "soul" and "spirit" as well. The most familiar example of a part of a person being personified is the heart. The heart, simply an organ that pumps blood, is said to have qualities that the mind does have, but that the heart definitely does not have. Another example which is not so familiar is the personification of the kidneys, called the "reins" (Ps. 7:9; 16:7; 26:2; 73:21; Prov. 23:16; Jer. 11:20; 12:2; 17:10; 20:12; Rev. 2:23). The kidneys seem to have been made the seat of the affections and emotions. Another example is the use of the words for "bowels" (Ps. 40:8 (translated "heart"); Cant. 5:4; Is. 16:11; 63:15; Jer. 4:19; 31:20; Lam. 1:20; 2:11; Luke 1:78 (translated "tender"); 2 Cor 7:15 (translated "inward affection"); Php. 2:1; Col. 3:12; Phm. 1:7, 20; 1 Jn. 3:17). In the light of these scriptures, the possibility that the Bible writers also occasionally personify the "soul" and "spirit" should be considered. In other words, the "soul" and the "spirit" may in some verses be given qualities that they do not in actuality possess. The article shows the various verses in which the word "Spirit" is used. I'll include just a few: "And the LORD God formed man of the dust of the ground, and breathed into his nostrils the breath (neshamah, pnoe) of life; and man became a living soul" (Gen. 2:7). [God put the "spirit" into Adam's nose.] "And, behold, I, even I, do bring a flood of waters upon the earth, to destroy all flesh, wherein is the breath (ruach, pneuma) of life, from under heaven; and every thing that is in the earth shall die" (Gen. 6:17). [Animals have the "spirit" in them too.] "All the while my breath (neshamah, pnoe) is in me, and the spirit (ruach, pneuma) of God is in my nostrils" (Job 27:3). [The "spirit" lives in the nose.] "The Spirit (neshamah, pnoe) of God hath made me, and the breath (ruach, pneuma) of the Almighty hath given me life" (Job 33:4). [God's "spirit" gives us life.] I'm assuming your question deals with verses like the last two shown above. In the context, and general meaning. Job 27:3 has been translates several ways by scholars, in the various versions of the Bible. Examples: GOD'S WORD® Translation (©1995) 'As long as there is one breath [left] in me and God's breath fills my nostrils, American King James Version All the while my breath is in me, and the spirit of God is in my nostrils; Both of these clearly indicate that the Spirit of God is distinct from the breath of life (spirit of man). It indicates that man has a spirit in him, given to him by God, not that the spirit in him is the same spirit that God possesses. The spirit that God gives may be from God, but the connotation of the word "spirit" when it comes to man is simply life itself. We each have our own life - our own spirit - our own ?breath that gives us life" that is certainly a gift from God, but is not the same as God's spirit. It's also completely different than the Holy Spirit, which is the third person of God in the Trinity and, according to most traditions, indwells us at the point of, and remains in us after salvation.	{ "pile_set_name": "StackExchange" }
Co-written by Beth Dakin and Mihnea-Vlad Ovidenie CSS Regions is an exciting technology that makes it easier than ever to create rich, magazine-like layouts within web content. Regions have been under development in WebKit for a while now, and we’re delighted to tell you that they are available for use in Safari on iOS 7, Safari 7 on Mavericks, and Safari 6.1 on Mountain Lion. Magazine-like Layout So I wrote this little article for my personal blog: That’s cool and all, but wouldn’t it be so much cooler if it had a more interesting layout like this? So fab! Without regions, achieving a layout like this is a pain. You have to figure out exactly which parts of the article can fit into each box and then hard-code the article content into the appropriate boxes. And after all that work, the design will get totally messed up if the user changes the font size! The layout looks cool, but doing it this way is a lot of work, and it isn’t even a little bit flexible. Regions make achieving this layout as easy as pie. They allow authors to indicate that some sections of content are intended to define an overall layout template for a portion of the document and that other sections of markup represent the content that is intended to fill that template. The semantically-related content that will flow through the template is called a “named flow.” In our example above, the named flow is the text of my article. Once it has been named, the named flow is distributed into disjointed containers called regions, which can be positioned in any way to achieve the desired layout. Our simple example only scratches the surface of what you can do with regions. We’ll get to more sophisticated applications later, but first let’s take a closer look at the code. What is a Named Flow? A named flow is a collection of HTML elements extracted from the document’s normal flow and displayed separately. Any HTML element can be part of a named flow. When an element is collected in a named flow, all of its children are collected with it. You identify a collection of HTML elements as a named flow by using the CSS property -webkit-flow-into . In our example, the named flow will be the elements that contain the text of our article: < style > #flow-content { -webkit-flow-into: pizza-manifesto; } </ style > < div id = "flow-content" > < h1 > Pizza is amazing </ h1 > … </ div > Our example only has one, but a document can have any number of named flows, each with its own name. Flowing Into Regions A region is a block-level element that displays content from a named flow instead of its own content. Regions can have any size and can be positioned anywhere in the document. They are not required to be siblings or to be positioned next to each other in the layout. A region consumes content from a single named flow. Most of the time, to achieve an interesting layout, there will be more than one region associated with a named flow, and when that is the case those regions form a region chain. When content from a named flow does not fit into a region, the content simply flows into the next region in the chain. Making an element a region is as easy as adding the -webkit-flow-from CSS property. In our example, the regions are the elements that form the layout template for the document’s overall design: < style > .region { -webkit-flow-from: pizza-manifesto; } </ style > < div class = "region" id = "region-1" > </ div > < img src = "pizza.jpg" width = "512" height = "342" > < div class = "region" id = "region-2" > </ div > < div class = "region" id = "region-3" > </ div > < div class = "region" id = "region-4" > </ div > < div class = "region" id = "region-5" > </ div > Take a look at the code for the actual document to see the code for the regions side-by-side with the code for the named flow. One key thing to remember about regions is that they are only visual containers. Region elements do not become the DOM parents of the elements flowed inside them; they only establish the bounding boxes that visually constrain the flow content. Advanced Regions Features One cool feature in the CSS Regions specification is region styling. With region styling, a designer can style the content based on which region it ends up flowing through. For example, if you wanted to change the color of the text displayed in the second region of the article flow, you could do so with region styling: @-webkit-region #region-2 { p { color : green ; } } The extra styles are dynamically applied behind the scenes whenever the layout of the article content in the regions changes. So for example, if the user resizes the browser window and different pieces of content end up flowing through the styled region, the content will update dynamically. At this time, you can only style regions with the CSS properties color and background-color , but we intend to progressively add support for more properties, so stay tuned! In the meantime, check out this version of our article that uses region styling. There is also a whole object model available for interacting with regions and named flows from within JavaScript. The proposed API will make it even easier to create fluid designs that adapt to layout changes. For example, authors can use the API to determine whether or not there are enough regions to display the content from the named flow. Handy stuff! Dreaming with Regions CSS regions are powerful, and when they are combined with other advanced CSS features like shapes, filters, flexible boxes, transforms, and media queries, incredibly sophisticated designs can emerge. Back in February, during a CSS regions pattern rodeo hosted by CodePen, Tyler Fry and Joshua Hibbert created some awesome regions demos. Tyler won the contest with his reading carousel made out of regions and transforms, and Joshua created an exploding book, featuring a nice hover effect when opening the book. The Adobe WebPlatform team has created some very compelling demos with regions in partnership with National Geographic. Check out this article that seamlessly integrates text and photographs to create a flexible design. Adobe has also created a demo that is so cutting edge you will need to download a WebKit Nightly to view it properly. This beautiful prototype uses regions, so the article content breaks up automatically across the different containers, and if font size or window size changes, or if the user zooms in, everything reflows automatically. Check out the source code here! We are so excited about regions as a technology and excited that they are already available for use in shipping browsers. We plan to continue to refine our implementation in WebKit and to add additional features, so be sure to check back for improvements.	{ "pile_set_name": "OpenWebText2" }
House dust mite-induced airway changes in hu-SCID mice. SCID (severe combined immunodeficiency) mice reconstituted with peripheral blood mononuclear cells (PBMC) from Dermatophagoides pteronissynus (Dpt)-sensitive patients and exposed to Dpt aerosol (allergic hu-SCID mice) develop human IgE and pulmonary inflammation. The present study investigated concomitant changes in airway hyperresponsiveness (AHR). No significant difference in baseline airway responsiveness was seen between nonreconstituted SCID mice exposed or not to Dpt aerosol at Day 35. Allergic hu-SCID mice developed AHR (provocative dose of carbachol causing a 50% increase in lung resistance [PD(50) RL] = 96.33 +/- 16.88 microg/kg) compared with nonallergic hu-SCID mice (PD(50) RL = 242.03 +/- 37.84 microg/kg) and nonreconstituted SCID mice (PD(50) RL = 297.60 +/- 45. 60 microg/kg) exposed to Dpt aerosol. An inverse correlation was observed between PD(50) RL (Day 35) and total human IgE at Day 7 (r = -0.58) and Day 15 (r = -0.64). However, no correlation existed between PD(50) RL and human cell number in the lungs of allergic hu-SCID mice. Moreover, despite the absence of eosinophils, the bronchoalveolar lavage fluid (BALF) of allergic hu-SCID mice had more human interleukin-5 (IL-5) (3.28 +/- 0.40 pg/ml, n = 13) than nonallergic hu-SCID mice (< 0.5 pg/ml) which inversely correlated with the PD(50) RL (r = -0.61). No tumor necrosis factor-alpha (TNF-alpha), IL-6, or IL-4 was detected. These observations indicate that humanized allergic hu-SCID mice may develop AHR after exposure to the relevant allergen, suggesting that this model may improve our understanding of AHR, one characteristic feature of allergic asthma.	{ "pile_set_name": "PubMed Abstracts" }
Tuesday, August 28, 2007 Pick Up... Here are some snapshots of Emma's first pick up from school. I mostly took video when I went to pick her up, so I only got 4 shots with the camera. She was clearly getting tired of all the fuss, and I had to make room for all the other flashing cameras and their respective parents. Anyway, here are a couple of cute ones... Proudly displaying her first bit of art work from school and standing next to her backpack hook. Notice that she's not looking at the camera at all! At this point, I'd already taken about 15 minutes of video of her reaction when I came to pick her up, and she was DONE with cameras. I think her words were something like, "C'mon mom! I'm thirsty. We gotta' go get me somethin' to drink! No more pictures, puuuhhlleeeeeeease." I should mention that when Emma first saw me walk in her classroom, she came running over saying, "I made somethin' for you mommy!" which is when I was handed her art work from the day. As soon as we walked in the door at home, she announced, "We're gonna' put it on the 'fridgerador', right?!?" "Of course baby. I would be honored." I happened to get a few shots of her in action while I was there as well. These were taken when we dropped her off, and as you can see, there was no love lost when it was time to leave mommy and daddy and get on with the day. She jumped right in with two feet and never looked back. That's my girl! The teacher had set out some toys on the rug so the kids would feel welcome and ready to have fun. Emma didn't miss a beat on that one. Miss Marie then asked her to come sit down and paint her ladybug which, if you look back at the "fridgerador" pictures, you'll see displayed directly above the handprints art work. The blonde woman in the front is Emma's teacher Miss Keri, and Emma absolutely LOVES her! She's been talking about her all day. All in all, she had a great first day at school and is in bed as I type, singing a newly memorized song about monkeys swinging in a tree teasing Mr. Alligator, saying, "Can't get me." I'm sure you can guess how it ends.	{ "pile_set_name": "Pile-CC" }
In a recent interview with ReactMag.com rapper Dirty South talked about what it’s like coming up as an MC in the birthplace of Country music — Meridian, Mississippi. Dirty South spoke about everything from the flag controversy, to how quickly Hip-Hop is growing in a place that normally evokes thoughts of people like Jimmy Rodgers. Read more.	{ "pile_set_name": "Pile-CC" }
/* deko3d Example 03: Cube This example shows how to draw a basic rotating cube. New concepts in this example: - Setting up and using a depth buffer - Setting up uniform buffers - Basic 3D maths, including projection matrices - Updating uniforms with a dynamic command buffer - Adjusting resolution dynamically by recreating resources (720p handheld/1080p docked) ** - Depth buffer discard after a barrier / // Sample Framework headers #include "SampleFramework/CApplication.h" #include "SampleFramework/CMemPool.h" #include "SampleFramework/CShader.h" #include "SampleFramework/CCmdMemRing.h" // C++ standard library headers #include <array> #include <optional> // GLM headers #define GLM_FORCE_DEFAULT_ALIGNED_GENTYPES // Enforces GLSL std140/std430 alignment rules for glm types #define GLM_FORCE_INTRINSICS // Enables usage of SIMD CPU instructions (requiring the above as well) #include <glm/vec3.hpp> #include <glm/vec4.hpp> #include <glm/mat4x4.hpp> #include <glm/gtc/matrix_transform.hpp> namespace { struct Vertex { float position[3]; float color[3]; }; constexpr std::array VertexAttribState = { DkVtxAttribState{ 0, 0, offsetof(Vertex, position), DkVtxAttribSize_3x32, DkVtxAttribType_Float, 0 }, DkVtxAttribState{ 0, 0, offsetof(Vertex, color), DkVtxAttribSize_3x32, DkVtxAttribType_Float, 0 }, }; constexpr std::array VertexBufferState = { DkVtxBufferState{ sizeof(Vertex), 0 }, }; constexpr std::array CubeVertexData = { // +X face Vertex{ { +1.0f, +1.0f, +1.0f }, { 1.0f, 0.0f, 0.0f } }, Vertex{ { +1.0f, -1.0f, +1.0f }, { 0.0f, 1.0f, 0.0f } }, Vertex{ { +1.0f, -1.0f, -1.0f }, { 0.0f, 0.0f, 1.0f } }, Vertex{ { +1.0f, +1.0f, -1.0f }, { 1.0f, 1.0f, 0.0f } }, // -X face Vertex{ { -1.0f, +1.0f, -1.0f }, { 1.0f, 0.0f, 0.0f } }, Vertex{ { -1.0f, -1.0f, -1.0f }, { 0.0f, 1.0f, 0.0f } }, Vertex{ { -1.0f, -1.0f, +1.0f }, { 0.0f, 0.0f, 1.0f } }, Vertex{ { -1.0f, +1.0f, +1.0f }, { 1.0f, 1.0f, 0.0f } }, // +Y face Vertex{ { -1.0f, +1.0f, -1.0f }, { 1.0f, 0.0f, 0.0f } }, Vertex{ { -1.0f, +1.0f, +1.0f }, { 0.0f, 1.0f, 0.0f } }, Vertex{ { +1.0f, +1.0f, +1.0f }, { 0.0f, 0.0f, 1.0f } }, Vertex{ { +1.0f, +1.0f, -1.0f }, { 1.0f, 1.0f, 0.0f } }, // -Y face Vertex{ { -1.0f, -1.0f, +1.0f }, { 1.0f, 0.0f, 0.0f } }, Vertex{ { -1.0f, -1.0f, -1.0f }, { 0.0f, 1.0f, 0.0f } }, Vertex{ { +1.0f, -1.0f, -1.0f }, { 0.0f, 0.0f, 1.0f } }, Vertex{ { +1.0f, -1.0f, +1.0f }, { 1.0f, 1.0f, 0.0f } }, // +Z face Vertex{ { -1.0f, +1.0f, +1.0f }, { 1.0f, 0.0f, 0.0f } }, Vertex{ { -1.0f, -1.0f, +1.0f }, { 0.0f, 1.0f, 0.0f } }, Vertex{ { +1.0f, -1.0f, +1.0f }, { 0.0f, 0.0f, 1.0f } }, Vertex{ { +1.0f, +1.0f, +1.0f }, { 1.0f, 1.0f, 0.0f } }, // -Z face Vertex{ { +1.0f, +1.0f, -1.0f }, { 1.0f, 0.0f, 0.0f } }, Vertex{ { +1.0f, -1.0f, -1.0f }, { 0.0f, 1.0f, 0.0f } }, Vertex{ { -1.0f, -1.0f, -1.0f }, { 0.0f, 0.0f, 1.0f } }, Vertex{ { -1.0f, +1.0f, -1.0f }, { 1.0f, 1.0f, 0.0f } }, }; struct Transformation { glm::mat4 mdlvMtx; glm::mat4 projMtx; }; inline float fractf(float x) { return x - floorf(x); } } class CExample03 final : public CApplication { static constexpr unsigned NumFramebuffers = 2; static constexpr unsigned StaticCmdSize = 0x10000; static constexpr unsigned DynamicCmdSize = 0x10000; dk::UniqueDevice device; dk::UniqueQueue queue; std::optional<CMemPool> pool_images; std::optional<CMemPool> pool_code; std::optional<CMemPool> pool_data; dk::UniqueCmdBuf cmdbuf; dk::UniqueCmdBuf dyncmd; CCmdMemRing<NumFramebuffers> dynmem; CShader vertexShader; CShader fragmentShader; Transformation transformState; CMemPool::Handle transformUniformBuffer; CMemPool::Handle vertexBuffer; uint32_t framebufferWidth; uint32_t framebufferHeight; CMemPool::Handle depthBuffer_mem; CMemPool::Handle framebuffers_mem[NumFramebuffers]; dk::Image depthBuffer; dk::Image framebuffers[NumFramebuffers]; DkCmdList framebuffer_cmdlists[NumFramebuffers]; dk::UniqueSwapchain swapchain; DkCmdList render_cmdlist; public: CExample03() { // Create the deko3d device device = dk::DeviceMaker{}.create(); // Create the main queue queue = dk::QueueMaker{device}.setFlags(DkQueueFlags_Graphics).create(); // Create the memory pools pool_images.emplace(device, DkMemBlockFlags_GpuCached \| DkMemBlockFlags_Image, 1610241024); pool_code.emplace(device, DkMemBlockFlags_CpuUncached \| DkMemBlockFlags_GpuCached \| DkMemBlockFlags_Code, 1281024); pool_data.emplace(device, DkMemBlockFlags_CpuUncached \| DkMemBlockFlags_GpuCached, 110241024); // Create the static command buffer and feed it freshly allocated memory cmdbuf = dk::CmdBufMaker{device}.create(); CMemPool::Handle cmdmem = pool_data->allocate(StaticCmdSize); cmdbuf.addMemory(cmdmem.getMemBlock(), cmdmem.getOffset(), cmdmem.getSize()); // Create the dynamic command buffer and allocate memory for it dyncmd = dk::CmdBufMaker{device}.create(); dynmem.allocate(pool_data, DynamicCmdSize); // Load the shaders vertexShader.load(pool_code, "romfs:/shaders/transform_vsh.dksh"); fragmentShader.load(pool_code, "romfs:/shaders/color_fsh.dksh"); // Create the transformation uniform buffer transformUniformBuffer = pool_data->allocate(sizeof(transformState), DK_UNIFORM_BUF_ALIGNMENT); // Load the vertex buffer vertexBuffer = pool_data->allocate(sizeof(CubeVertexData), alignof(Vertex)); memcpy(vertexBuffer.getCpuAddr(), CubeVertexData.data(), vertexBuffer.getSize()); } ~CExample03() { // Destroy the framebuffer resources destroyFramebufferResources(); // Destroy the vertex buffer (not strictly needed in this case) vertexBuffer.destroy(); // Destroy the uniform buffer (not strictly needed in this case) transformUniformBuffer.destroy(); } void createFramebufferResources() { // Create layout for the depth buffer dk::ImageLayout layout_depthbuffer; dk::ImageLayoutMaker{device} .setFlags(DkImageFlags_UsageRender \| DkImageFlags_HwCompression) .setFormat(DkImageFormat_Z24S8) .setDimensions(framebufferWidth, framebufferHeight) .initialize(layout_depthbuffer); // Create the depth buffer depthBuffer_mem = pool_images->allocate(layout_depthbuffer.getSize(), layout_depthbuffer.getAlignment()); depthBuffer.initialize(layout_depthbuffer, depthBuffer_mem.getMemBlock(), depthBuffer_mem.getOffset()); // Create layout for the framebuffers dk::ImageLayout layout_framebuffer; dk::ImageLayoutMaker{device} .setFlags(DkImageFlags_UsageRender \| DkImageFlags_UsagePresent \| DkImageFlags_HwCompression) .setFormat(DkImageFormat_RGBA8_Unorm) .setDimensions(framebufferWidth, framebufferHeight) .initialize(layout_framebuffer); // Create the framebuffers std::array<DkImage const, NumFramebuffers> fb_array; uint64_t fb_size = layout_framebuffer.getSize(); uint32_t fb_align = layout_framebuffer.getAlignment(); for (unsigned i = 0; i < NumFramebuffers; i ++) { // Allocate a framebuffer framebuffers_mem[i] = pool_images->allocate(fb_size, fb_align); framebuffers[i].initialize(layout_framebuffer, framebuffers_mem[i].getMemBlock(), framebuffers_mem[i].getOffset()); // Generate a command list that binds it dk::ImageView colorTarget{ framebuffers[i] }, depthTarget{ depthBuffer }; cmdbuf.bindRenderTargets(&colorTarget, &depthTarget); framebuffer_cmdlists[i] = cmdbuf.finishList(); // Fill in the array for use later by the swapchain creation code fb_array[i] = &framebuffers[i]; } // Create the swapchain using the framebuffers swapchain = dk::SwapchainMaker{device, nwindowGetDefault(), fb_array}.create(); // Generate the main rendering cmdlist recordStaticCommands(); // Initialize the projection matrix transformState.projMtx = glm::perspectiveRH_ZO( glm::radians(40.0f), float(framebufferWidth)/float(framebufferHeight), 0.01f, 1000.0f); } void destroyFramebufferResources() { // Return early if we have nothing to destroy if (!swapchain) return; // Make sure the queue is idle before destroying anything queue.waitIdle(); // Clear the static cmdbuf, destroying the static cmdlists in the process cmdbuf.clear(); // Destroy the swapchain swapchain.destroy(); // Destroy the framebuffers for (unsigned i = 0; i < NumFramebuffers; i ++) framebuffers_mem[i].destroy(); // Destroy the depth buffer depthBuffer_mem.destroy(); } void recordStaticCommands() { // Initialize state structs with deko3d defaults dk::RasterizerState rasterizerState; dk::ColorState colorState; dk::ColorWriteState colorWriteState; dk::DepthStencilState depthStencilState; // Configure viewport and scissor cmdbuf.setViewports(0, { { 0.0f, 0.0f, (float)framebufferWidth, (float)framebufferHeight, 0.0f, 1.0f } }); cmdbuf.setScissors(0, { { 0, 0, framebufferWidth, framebufferHeight } }); // Clear the color and depth buffers cmdbuf.clearColor(0, DkColorMask_RGBA, 0.0f, 0.0f, 0.0f, 0.0f); cmdbuf.clearDepthStencil(true, 1.0f, 0xFF, 0); // Bind state required for drawing the cube cmdbuf.bindShaders(DkStageFlag_GraphicsMask, { vertexShader, fragmentShader }); cmdbuf.bindUniformBuffer(DkStage_Vertex, 0, transformUniformBuffer.getGpuAddr(), transformUniformBuffer.getSize()); cmdbuf.bindRasterizerState(rasterizerState); cmdbuf.bindColorState(colorState); cmdbuf.bindColorWriteState(colorWriteState); cmdbuf.bindDepthStencilState(depthStencilState); cmdbuf.bindVtxBuffer(0, vertexBuffer.getGpuAddr(), vertexBuffer.getSize()); cmdbuf.bindVtxAttribState(VertexAttribState); cmdbuf.bindVtxBufferState(VertexBufferState); // Draw the cube cmdbuf.draw(DkPrimitive_Quads, CubeVertexData.size(), 1, 0, 0); // Fragment barrier, to make sure we finish previous work before discarding the depth buffer cmdbuf.barrier(DkBarrier_Fragments, 0); // Discard the depth buffer since we don't need it anymore cmdbuf.discardDepthStencil(); // Finish off this command list render_cmdlist = cmdbuf.finishList(); } void render() { // Begin generating the dynamic command list, for commands that need to be sent only this frame specifically dynmem.begin(dyncmd); // Update the uniform buffer with the new transformation state (this data gets inlined in the command list) dyncmd.pushConstants( transformUniformBuffer.getGpuAddr(), transformUniformBuffer.getSize(), 0, sizeof(transformState), &transformState); // Finish off the dynamic command list, and submit it to the queue queue.submitCommands(dynmem.end(dyncmd)); // Acquire a framebuffer from the swapchain (and wait for it to be available) int slot = queue.acquireImage(swapchain); // Run the command list that attaches said framebuffer to the queue queue.submitCommands(framebuffer_cmdlists[slot]); // Run the main rendering command list queue.submitCommands(render_cmdlist); // Now that we are done rendering, present it to the screen queue.presentImage(swapchain, slot); } void onOperationMode(AppletOperationMode mode) override { // Destroy the framebuffer resources destroyFramebufferResources(); // Choose framebuffer size chooseFramebufferSize(framebufferWidth, framebufferHeight, mode); // Recreate the framebuffers and its associated resources createFramebufferResources(); } bool onFrame(u64 ns) override { hidScanInput(); u64 kDown = hidKeysDown(CONTROLLER_P1_AUTO); if (kDown & KEY_PLUS) return false; float time = ns / 1000000000.0; // double precision division; followed by implicit cast to single precision float tau = glm::two_pi<float>(); float period1 = fractf(time/8.0f); float period2 = fractf(time/4.0f); // Generate the model-view matrix for this frame // Keep in mind that GLM transformation functions multiply to the right, so essentially we have: // mdlvMtx = Translate * RotateX * RotateY * Scale // This means that the Scale operation is applied first, then RotateY, and so on. transformState.mdlvMtx = glm::mat4{1.0f}; transformState.mdlvMtx = glm::translate(transformState.mdlvMtx, glm::vec3{0.0f, 0.0f, -3.0f}); transformState.mdlvMtx = glm::rotate(transformState.mdlvMtx, sinf(period2 * tau) * tau / 8.0f, glm::vec3{1.0f, 0.0f, 0.0f}); transformState.mdlvMtx = glm::rotate(transformState.mdlvMtx, -period1 * tau, glm::vec3{0.0f, 1.0f, 0.0f}); transformState.mdlvMtx = glm::scale(transformState.mdlvMtx, glm::vec3{0.5f}); render(); return true; } }; void Example03(void) { CExample03 app; app.run(); }	{ "pile_set_name": "Github" }
Back to physics and LTC Hooke’s Law is what’s in play folks. From historical price set ups, the longer the stretch, the stronger the break out and I have emphasized that enough times. So maybe you should look at buying NEM, IOTA and Monero especially if it closes above that double top as trend resumes. Let’s have a look at other alt coin charts NEM IS BACK IN LINE As the week nears to an end, NEM is finally getting some traction and from yesterday’s analysis, all we need is a close above the 50% Fibonacci retracement. With higher highs, it is most likely and that is what we are waiting today. In line with this expectation, I recommend buyers to get in at the close of this candlestick. LUMENS DIPS TOWARDS MIDDLE BB IS ANOTHER BUYING OPPORTUNITY As long as XLM candlesticks continue to print, we remain buyers. At the moment, we have a minor spinning tops formation along the 38.2% Fibonacci retracement level and two things can happen. One, buyers may continue pushing prices higher-and that is what I think might happen or there might be a correction to the 50% retracement level and the middle BB. Of course, given the set-up that is ideal for “buy on dips” strategy and should offer a wonderful opportunity to profit with minimum risk for swingers. TRADE THE BREAK OUT AND BUY IOTA Now that we have a break out above the minor resistance trend line, we may as well as buy. Now, if prices correct, our first support will be the middle BB and below it, IOTA bulls should look to place their stops and account safety net. CLOSE ABOVE MONERO DOUBLE TOPS IS IMPORTANT FOR TREND CONTINUATION A simple Fibonacci retracement from last week’s high lows shows that prices reversed from around last week’s highs. Regardless of the current Monero higher highs, it would have been ideal if buyers jumped in from the main break out-now support line at 0.025 BTC. However, that has not been the case so we trade as per the trend. Of course from previous analysis, Monero is playing within a break out and the moment prices close above the double tops, then well, those who didn’t snatch Monero at a discount should load up. LTC HOOKE’S LAW I had to check twice to see if my chart was loading right. Yes, it was and LTC is still in a squeeeeeeezzzze!! The longer it gets the better and stronger the break out. It’s like the Hooke’s law in physics, the longer you stretch that rubber band the snap back will be more powerful and painful if you are on the receiving end. I’m net long and I recommend longs now with stops below 0.017 BTC. All charts courtesy of Trading View	{ "pile_set_name": "OpenWebText2" }
Mỹ Đức, An Giang Mỹ Đức is a rural commune (xã) and village of the Châu Phú District of An Giang Province, Vietnam. Category:Communes of An Giang Province Category:Populated places in An Giang Province	{ "pile_set_name": "Wikipedia (en)" }
Enid, Oklahoma Enid ( ) is the ninth-largest city in the U.S. state of Oklahoma. It is the county seat of Garfield County. As of the 2010 census, the population was 49,379. Enid was founded during the opening of the Cherokee Outlet in the Land Run of 1893, and is named after Enid, a character in Alfred, Lord Tennyson's Idylls of the King. In 1991, the Oklahoma state legislature designated Enid the "purple martin capital of Oklahoma." Enid holds the nickname of "Queen Wheat City" and "Wheat Capital" of Oklahoma and the United States for its immense grain storage capacity, and has the third-largest grain storage capacity in the world. History In summer 1889, M.A. Low, a Rock Island official, visited the local railroad station then under construction, and inquired about its name. At that time, it was called Skeleton. Disliking the original name, he renamed the station Enid after a character in Alfred Lord Tennyson's Idylls of the King. However, a more fanciful story of how the town received its name is popular. According to that tale, in the days following the land run, some enterprising settlers decided to set up a chuckwagon and cook for their fellow pioneers, hanging a sign that read "DINE". Some other, more free-spirited settlers, turned that sign backward to read, of course, "ENID". The name stuck. During the opening of the Cherokee Outlet in the Land Run of 1893, Enid was the location of a land office which is now preserved in its Humphrey Heritage Village, part of the Cherokee Strip Regional Heritage Center. Enid, the rail station, (now North Enid, Oklahoma) was the original town site endorsed by the government. It was platted by the surveyor W. D. Twichell, then of Amarillo, Texas. The Enid-Pond Creek Railroad War ensued when the Department of the Interior moved the government site 3 mi (5 km) south of the station prior to the land run, which was then called South Enid. During the run, due to the Rock Island's refusal to stop, people leaped from the trains to stake their claim in the government-endorsed site. By the afternoon of the run, Enid's population was estimated at 12,000 people located in the Enid's town plat. Enid's original plat in 1893 was 6 blocks wide by 11 blocks long consisting of the town square on the northwest end, West Hill (Jefferson) school on the southwest end, Government Springs Park in the middle southern section, and East Hill (Garfield) school on the far northeast corner. A year later, the population was estimated at 4,410, growing to 10,087 by 1907, the year of Oklahoma statehood. The town's early history was captured in Cherokee Strip: A Tale of an Oklahoma Boyhood by Pulitzer Prize-winning author Marquis James, who recounts his boyhood in Enid. He writes of the early town: Enid experienced a "golden age" following the discovery of oil in the region in the 1910s and continuing until World War II. Enid's economy boomed as a result of the growing oil, wheat, and rail industries, and its population grew steadily throughout the early 20th century in conjunction with a period of substantial architectural development and land expansion. Enid's downtown had the construction of several buildings including the Broadway Tower, Garfield County Courthouse, and Enid Masonic Temple. In conjunction with the oil boom, oilmen such as T. T. Eason, H. H. Champlin, and Charles E. Knox built homes in the area. Residential additions during this period include Kenwood, Waverley, Weatherly, East Hill, Kinser Heights, Buena Vista, and McKinley. Union Equity, Continental, Pillsbury, General Mills, and other grain companies operated mills and grain elevators in the area, creating what is now the Enid Terminal Grain Elevators Historic District, and earning Enid the titles of "Wheat Capital of Oklahoma", "Queen Wheat City of Oklahoma," and "Wheat Capital of the United States" Geography Located in Northwestern Oklahoma, Enid sits at the eastern edge of the Great Plains. It is located at (36.400583, -97.880784), north of Oklahoma City. According to the United States Census Bureau, the city has a total area of , of which is land and (0.12%) is covered by water. Climate Enid's weather conditions are characterized by hot summers, cold, often snowy winters, and thunderstorms in the spring, which can produce tornadoes. The greatest one-day precipitation total by an official rain gauge in Oklahoma was in Enid when fell on October 11, 1973. Temperatures can fall below in the winter, and reach above in the summer. The highest recorded temperature was in 1936, and the lowest recorded temperature was in 1905. On average, the warmest month is July, January is the coolest month, and the maximum average precipitation occurs in June. An ice storm struck Northwest Oklahoma in late January 2002. The storm caused over $100 million of damage, initially leaving some 255,000 residences and businesses without power. A week later, 39,000 Oklahoma residents were still without power. Enid, with its population of 47,000, was entirely without electricity for days. The Oklahoma Association of Electric Cooperatives reported over 31,000 electrical poles were destroyed across the state. The American Red Cross set up a shelter at Northern Oklahoma College. Some other notable storms in Enid's history include: March 16, 1965, an F4 tornado away from the city center injured seven people and caused between $50,000 and $500,000 in damages. October 11–13, 1973, Oklahoma's greatest urban rainfall on record occurred. Known as the "Enid flood", an intense thunderstorm was centered over Enid with rainfall accumulations between 15 and 20 inches within a area. About fell in three hours. Enid received , forcing residents to cut holes in rooftops to reach safety. Nine people died. May 2, 1979, an F4 tornado away from the Enid city center killed one person, injured 25 people and caused between $500,000 and $5,000,000 in damages. April 25, 2009, an EF-2 tornado damaged the Chisholm Trail Expo Center. No one was injured or killed. Demographics As of the 2010 census, 49,379 people, 19,726 households and 12,590 families resided in the city. The population density was 670 per square mile (260/km2). The racial makeup of the city was 81.6% White, 3.6% African American, 2.3% Native American, 1.1% Asian, 2.2% Pacific Islander, 5.4% from other races, and 2.84% from two or more races. The population of Hispanic or Latino Americans more than doubled between 2000 and 2010, up from 4.74% in 2000 to 10.3% in 2010. Of the 19,726 households, 28.6% had children under the age of 18 living with them, 47% were married couples living together, 11.9% had a female householder with no husband present, and 36.2% were not families. Households with individuals living alone accounted for 30.5% of households and 26.6% of households consisted of individuals 65 years of age or older living by themselves. The average household size was 2.41 and the average family size was 3.0. The median age of the population was 36. Enid has been predominantly a Republican stronghold since its days as part of Oklahoma Territory, owing to the influence of settlers from neighboring Kansas. Several politicians have called Enid home, including Oklahoma Territory's last governor Frank Frantz; U.S. Representative Page Belcher; US Congressman and former Enid mayor, Milton C. Garber; Oklahoma Lieutenant Governor Todd Lamb; U.S. Representative George H. Wilson; and James Yancy Callahan, the only non-Republican territorial congressional delegate. Of the people in Enid, 61.9% claim affiliation with a religious congregation; 9.4% are Catholic, 39.2% are Protestant, 1.1% are Latter Day Saints and 12.2% are another Christian denomination. By 1987, there were 90 churches of 27 different denominations of Christianity. Enid's Phillips University, although formally affiliated with the Disciples of Christ, was a product of religious collaboration between followers of the Disciples of Christ, Presbyterian Church, and Judaism. Although Phillips University has closed, Enid still has a number of private Christian schools, including St. Paul's Lutheran School. Enid is home to several Protestant churches including pentacostal Iglesia Cristiana El Shaddai (Hispanic) founded in 2001, four Lutheran congregations, Immanuel, founded in 1899, Trinity, founded in 1901, St. Paul, founded in 1909, and Redeemer, founded in 1934, and two Catholic congregations, St. Francis Xavier, founded in 1893, and St. Gregory, founded in 1971. St. Francis Xavier's Bishop Theophile Meerschaert was responsible for founding Calvary Catholic Cemetery in 1898. Enid is the home of two Masonic Lodges, the Enid Lodge #80 and the Garfield Lodge #501. The Enid Lodge has many Jewish members. Historically, Enid was home to a small Jewish congregation called Emanuel, which met at the Loewen Hotel, founded by Al Loewen, a local merchant who also served on the committee to create Phillips University. The Enid Cemetery also has a Jewish section where many of early Enid's Jewish merchants are interred, including the founders of Kaufman's Style Shop, Herzberg's Department Store, Newman Mercantile, and Meibergen and Godschalk, Enid's first clothing store. Currently, no synagogues or mosques are in Enid. Economy When Enid participated in the City Beautiful movement in the 1920s, Frank Iddings wrote the city song, "Enid, The City Beautiful". "You're right in the center where the best wheat grows and you've got your share of the oil that flows," his lyrics read. These were the early staples of the Enid economy. Enid's economy saw oil booms and agricultural growth in the first half of the 20th century. The Great Depression, however, caused both of these staples to lose value, and many businesses in Enid closed. However, Enid recovered, prospering and growing in population until a second wave of bad economic times hit in the 1980s, when competition with the local mall and economic factors led Enid's downtown area to suffer. Since 1994, Enid's Main Street program has worked to refurbish historic buildings, boost the local economy, and initiate local events such as first Friday concerts and holiday celebrations on the town square. Companies with corporate headquarters in Enid: AdvancePierre Foods (prepared food products, primarily for institutional customers) Atwood Distributing, LP (farming supplies, hardware, pet supplies) Johnston Enterprises Inc. (grain processing, storage, and transportation; founded 1893) GEFCO, George E. Failing Company (manufacturer of portable drilling rigs for oil, gas, water wells, and other applications; founded 1931) STECO (manufacturer of transfer and dump trailers) Pumpstar (manufacturer of concrete pumping equipment) Groendyke Transport (tank truck fleet operator; bulk liquid transport) Companies with operations in Enid: The Koch Industries plant produces 10 percent of the anhydrous ammonia in the United States, a primary ingredient in fertilizer. Arctic Slope Regional Corporation provides base operations services at nearby Vance Air Force Base. Vertex provides aircraft maintenance services at nearby Vance Air Force Base. Historical companies in Enid: Champlin Oil: The company was founded in 1916 by H.H. Champlin and grew to operate service stations in 20 different states by 1944. In 1984, after a series of different owners, American Petrofina closed the operation. What remains is the H. H. Champlin Mansion, which is one of many Enid sites listed on the National Register of Historic Places. Geronimo Motor Company. Arts and culture Enid is home to the annual Tri-State Music Festival which was started in 1932 by Russell L. Wiley, who was Phillips University band director from 1928 to 1934. From 1933 to 1936, Edwin Franko Goldman headlined the festival. The festival takes place each spring in Enid. In the summertime, Enid's Gaslight Theatre hosts a production of Shakespeare in the Park, as well as year-round theater productions. The Enid Symphony Orchestra was formed in 1905 and is the oldest symphony in the state, performing year-round in the Enid Symphony Center. Enid's Chautauqua in the Park takes place each summer in Government Springs Park, providing five nights of educational performances by scholars portraying prominent historical figures. The Chautauqua program was brought to Enid in 1907 by the Enid Circle Jewish Chautauqua and is now produced by the Greater Enid Arts and Humanities Council. Enid's Cherokee Strip Regional Heritage Center preserves the local history of the Land Run of 1893, Phillips University, and Garfield County. The museum originated as the Museum of the Cherokee Strip in the 1970s, and reopened on April 1, 2011. Enid also commemorates its land run history each September by hosting the Cherokee Strip Days and Parade. The Humphrey Heritage Village next to the museum offers visitors a chance to see the original Enid land office and other historical buildings. Visitors to Enid's Railroad Museum of Oklahoma, located in the former Santa Fe Railway Depot, can see railroad memorabilia, explore historical trains, and watch model railroads in action. The Midgley Museum is operated by the Enid Masonic Lodge #80 and features the rock collection of the Midgley family. Leonardo's Discovery Warehouse, located in the former Alton Mercantile building in downtown Enid, is an arts and sciences museum, which features Adventure Quest, an outdoor science-themed playground. Simpson's Old Time Museum is a Western-themed museum by local filmmakers Rick and Larry Simpson. The pair closed their downtown business, Simpsons Mercantile, in 2006 to convert the building into a movie set and museum. George's Antique Auto Museum features the sole existing Geronimo car, once manufactured in Enid. The Leona Mitchell Southern Heights Heritage Center and Museum records the history and culture of African Americans and Native Americans, featuring exhibits on Enid's former black schools (George Washington Carver and Booker T. Washington), and opera star Leona Mitchell. Enid also has a number of locations listed on the National Register of Historic Places. Sports Enid has produced several athletes, including NFL football players Todd Franz, Steve Fuller, Ken Mendenhall, John Ward, Jeff Zimmerman, Jim Riley, and the CFL's Kody Bliss. Brothers Brent Price and Mark Price became NBA players, and Don Haskins is a Hall of Fame basketball coach. USSF soccer player Andrew Hoxie, Major League Baseball pitchers, Ray Hayward and Lou Kretlow, Olympian and runner, Chris McCubbins, and Stacy Prammanasudh, an LPGA golfer, all were born or lived in Enid. Baseball The Enid Harvesters (active from 1920 to 1924) were named as the 20th-best minor league farm team ever by Minor League Baseball. They had a 104–27 record in the 1922 season. The Harvesters, along with their earlier counterparts the Railroaders, were members of the Western Association. During the 1951 season, the team was an affiliate of the Houston Buffaloes, and were known as the "Enid Buffaloes" to match. The Enid Majors youth baseball team won the American Legion Baseball World Series in 2005. Several Enid teams played in the National Baseball Congress championships, winning the championship in 1945 by the Army Air Field (runners up in 1943 and 1944), in 1940 and 1941 by the Champlins, and in 1937 by the Eason Oilers (runners up in 1938). Phillips University baseball teams, coached by Enid native Joe Record, went to the NAIA World Series three times during his tenure as head coach (1952–1981). Record was the NAIA Coach of the Year in 1973, and was inducted into the NAIA Hall of Fame in 1975. The Northern Oklahoma College Enid Jets baseball team were conference champions in 2002, 2003, 2005 and 2018. They were Region II champions in 2002, 2004, 2018, and runners up in 2009. They were Southwest District Champions in 2002 and also received third place in the NJCAA World Series in that 2002 and 2018. Basketball The Oklahoma Storm USBL franchise called Enid home. Through their eight years in Enid (2000–2007 seasons), they won their division more than once and the USBL Championship in 2002. Football The Enid High School Plainsmen have won six state football championships (1919, 1942, 1964, 1965, 1966, and 1983). They went to the Oklahoma State Championship football game in 2006 and lost to the Jenks Trojans. The Phillips University football teams, coached by John Maulbetsch, beat the University of Oklahoma and University of Texas football teams and lost only one game in the 1918 and 1919 seasons. When Phillips defeated Texas 10–0 in Austin, Texas, in October 1919, the Longhorns had not lost a game since 1917. The newest football team in Enid is the Enid Enforcers, a semiprofessional/minor-league team playing in the Central Football League. Their first season of play was in the spring of 2008. Made up of players from Enid and the surrounding areas, the team has achieved national ranking status three times, amassing a CFL League Championship in 2012, two Northern Division Championships, and 47 league All-star players, while helping numerous young men gain college athletic scholarships and boasting a 40-13 record in just five years. Education Enid has several institutions of education and is served by two school districts: Enid Public Schools and Chisholm Public Schools. Pioneer-Pleasant Vale Schools's elementary school, often referred to as Pleasant Vale Elementary. The Cimarron Montessori School and Summerhill Childrens House are the city's two Montessori style schools. Several private Christian schools representing a variety of denominations are also located in Enid: Bethel Bible Academy, Emmanuel Christian School, Enid Adventist School, Hillsdale Christian School, Saint Joseph Catholic School, and Saint Paul's Lutheran School. Enid High School, Chisholm High School, and Oklahoma Bible Academy are the city's largest secondary education schools. Autry Technology Center serves as the city's only vocational education institution, Northern Oklahoma College as its community college, and Northwestern Oklahoma State University (NWOSU) provides bachelor and graduate level education. Enid was formerly home to Phillips University, which closed in 1998. The Public Library of Enid and Garfield County, established in 1899, also serves as an educational resource for the community. Enid was once home to a Carnegie library, which opened in 1910. After years of funding shortages, the building was condemned in 1957, and the library's current modernist building was opened in 1964. Media The Enid News & Eagle is the city's daily newspaper. Historically, the city had 28 newspapers. The Enid Eagle began publication on September 22, 1893. The Enid Daily Wave (later the Enid Morning News) began on December 11, 1893. In February 1923, the papers were combined to form the Enid Publishing Company. Enid has two local television stations: Public-access television station, PEGASYS, which broadcasts locally produced programming on cable channels 11 and 12, and a community bulletin board on channel 19. UHF channel 32, KXOK-LD, which currently is a Retro TV affiliate. Historically, Enid was home to television station KGEO, an ABC affiliate from July 2, 1954 to 1958 when it moved its transmitter to Oklahoma City, Oklahoma. The station is now KOCO-TV. KQOB 96.9 FM broadcasts in a classic hits format. Stations KNID 107.1 FM and KOFM 103.1 FM specialize in country music. KAMG 92.1 FM, KKRD 91.1 FM, KLGB-LP 94.3 FM, and K226BR 93.1 FM are devoted to religious content. KCRC 1390 AM broadcast sports games. KGWA 960 AM and KZLS 1640 AM is a talk radio station, and KXLS 95.7 FM plays various musical genres. Infrastructure Healthcare Enid has a number of medical clinics and two hospitals. INTEGRIS Bass Baptist Health Center has 207 beds throughout its three facilities. Bass is the oldest hospital in Enid, founded in 1910, and incorporated in 1914 as Enid General Hospital and Training School for Nurses. St. Mary's Regional Medical Center, a 245-bed facility with 127 licensed professionals, was established in 1915 as Enid Springs Sanatorium. Both Enid hospitals are affiliated with the Oklahoma Hospital Association, and their CEOs are FACHE certified. Clinics include the Garfield County Health Department, and Veterans Affairs Clinic. Vance Air Force Base Clinic is operated by the 71st Medical Group which consists of the 71st Medical Operations and Support Squadrons. Transportation The main highways serving the City of Enid are U.S. Highway 81 Van Buren and U.S. Highway 412 Owen K. Garriott. U.S. Highway 64 runs west down Garriott and U.S. Highway 60 runs east. Both of these highways join together with highway 81 in North Enid, Oklahoma. State Highway 45 also runs through North Enid on Carrier Road. Railroad development in Garfield County began four years prior to the land opening, and Enid became a central hub within the county, with rail systems running in ten directions. Historical railroads included Enid and Tonkawa Railway, Enid and Anadarko Railway, Blackwell, Enid and Southwestern Railway, Enid Central Railway and the Denver, Enid and Gulf Railroad. Enid's railroad history is displayed at the Railroad Museum of Oklahoma which is housed in the former Santa Fe railroad Depot. The Rock Island Depot is listed on the National Register of Historic Places. Active railroad operations in Enid are Farmrail (FMRC) / Grainbelt Corporation (GNBC), BNSF Railway, and Union Pacific Railroad (UP). In the past Atchison, Topeka & Santa (ATSF), Burlington Northern (BN), Chicago, Rock Island & Pacific (CRIP), Missouri-Kansas-Texas (MKT), North Central Oklahoma and Saint Louis San Francisco "Frisco" (SLSF) connected Enid to the rest of Oklahoma by rail. From 1907 to 1929, Enid also had its own streetcar system, operated by Enid City Railway. The street cars were later replaced by buses, following a declaration by the Enid government that made streetcars illegal. Since 1984, the Transit, operated by Enid Public Transportation, has been in operation, providing on-demand shuttle services. The Transit also offers service to Oklahoma City's Will Rogers Airport, Greyhound Bus Service, and Amtrak Train Station. Airports Enid Woodring Regional Airport (KWDG) (1167 feet above mean sea level) is located four miles (6 km) southeast of Enid at 36 degrees 22.75 north latitude and 97 degrees 47.47 west longitude. This Class D facility has a primary runway and a 3149 secondary runway. There is no scheduled air service. Vance Air Force Base (KEND) (1,307 feet above mean sea level) is located four miles (6 km) south of the city at 36 degrees 20.21 north latitude and 97 degrees 54.59 west longitude. It was founded in 1941 on land leased by the city of Enid to the United States Army Air Forces, now the United States Air Force. Vance also uses the KWDG facility for military training flights. Since its establishment the base, named after Lt. Col Leon Robert Vance, Jr., has been a major employer in the area. Utilities Enid's electricity is provided by Oklahoma Gas & Electric and natural gas by Oklahoma Natural Gas Company. The City of Enid provides water, wastewater, and trash collection services. Internet, television, and telephone providers include Suddenlink Communications, Pioneer Telephone, and AT&T. Notable people Enid's Frank Frantz was the seventh and final Oklahoma Territorial Governor. Enid has been home to several successful entrepreneurs from oilman Herbert Champlin to casino owner, Sam Boyd, founder of the Boyd Gaming Corporation. The arts have also flourished among Enid natives, from Native American painter Paladine Roye to Pulitzer Prize winning author Marquis James. Two Oklahoma State Poets Laureate, Bess Truitt and Carol Hamilton, grew up in Enid. Poets Quraysh Ali Lansana, J. Quinn Brisben, Louis Jenkins, and D.L. Lang also once called Enid home. Actors Richard Erdman, Glenda Farrell, Lynn Herring, and Thad Luckinbill were all born in Enid, as was Emmy Award winning director, Sharron Miller. Many musicians have called Enid home, jazz great Sam Rivers, jazz pianist Pat Moran McCoy, folk singer and banjoist Karen Dalton, fingerstyle guitarist Michael Hedges and opera singer Leona Mitchell, with the last two having streets in Enid bearing their names. Mitchell's brother, Hulon Mitchell Jr (Yahweh Ben Yahweh) was the founder of the religious group, Nation of Yahweh. Attorney Stephen Jones defended Timothy McVeigh after the Oklahoma City bombing. A number of military heroes have also come from Enid, including former US Army Special Forces operator Bo Gritz, Medal of Honor recipient Harold Kiner, and Pearl Harbor hero USAF General Kenneth M. Taylor. Enid has a history of aviation professionals from aviation pioneer Clyde Cessna, founder of the Cessna Aircraft Company, to Irving Woodring, one of the Army's Three Musketeers of Aviation. Cessna's pioneering flights earned him the nickname the "Birdman of Enid". One of Enid's main streets is named after Astronaut Owen K. Garriott, and Enid's air force base is named for Medal of Honor recipient Leon Vance. Mark Kelly, bass player of the Christian rock band Petra calls Enid home. Former White House photojournalist David Scott Holloway, recipient of the Getty Grant and photographer for Anthony Bourdain: Parts Unknown on CNN was born in Enid, attending Longfellow Jr. High School, before his family moved near Waukomis where he attended Pioneer Pleasantvale High School. Even some fictional characters hold Enid as their home town, including Paul and Amanda Kirby (portrayed by William Macy and Téa Leoni) in Jurassic Park III, Maggie Gyllenhaal's character, journalist Jean Craddock, in Crazy Heart, and in The Rifleman, Lucas McCain and his son Mark lived in Enid, Oklahoma before settling in North Fork, New Mexico Territory. Some even claim two figures from the Abraham Lincoln assassination lived and died in Enid. In 1901, Osborn H. Oldroyd wrote The Assassination of Abraham Lincoln Flight, Pursuit (sic), Capture, and Punishment of the Conspirators which claimed that Sgt. Boston Corbett, the man who killed John Wilkes Booth in Virginia, resided in Enid, employed as a medicine salesman. Local legend holds that Corbett is buried in one of the unmarked graves in the Enid Cemetery. In 1907, Finis L. Bates wrote The Escape and Suicide of John Wilkes Booth. The book claimed that David E. George, a tenant at the Grand Avenue Hotel who committed suicide by poison in 1903, was actually John Wilkes Booth. After sitting for years in Penniman's Funeral Home, George's mummified body later toured the carnival circuit. The 1937 short film The Man in the Barn by Jacques Tourneur revisits the story of David E. George as Booth. In popular culture In 2019, the Oklahoma State Chamber of Commerce ranked Enid as "The best Oklahoma city in which to live." Enid was ranked the 28th best place in the US to raise a family in a 1998 Reader's Digest poll. and in the March 2004 issue of Inc. listed as one of the top 25 small cities in the US for doing business. Good Morning America listed Enid as one of its top five up and coming areas in a January 2006 episode. Hollywood has come to Enid, shooting scenes from Dillinger in front of the Mark Price Arena and the Grand Saloon, the 1955 short film Holiday for Bands features Enid's Tri-State Music Festival, and portions of the film The Killer Inside Me were filmed in Enid's downtown square. According to television, Enid has been the site of hauntings and exorcisms as Ghost Lab featured Enid as part of an investigation of sites claimed to be haunted by John Wilkes Booth, and A Current Affair in a segment on expensive religious exorcisms. Enid has been the subject of songs, such as the song "Greeted in Enid" by Hank Williams, Jr. from his 1995 album Hog Wild, which tells the story of a woman he met in Enid. It has been the subject of ridicule, by comedian Bill Hicks who used to make fun of this town in his act, including a routine on a man named Elmer Dinkley, most likely fictional. Enid is also mentioned in passing in a few popular novels and films. In chapter 12 of The Grapes of Wrath, Enid is one of the towns that feeds into Route 66 from the north via Route 64. The movie Twister (1996) references the city just before the chasers leave Aunt Meg's house to chase the "Hailstorm Hill" Tornado. The storm warning on the television broadcast states that the latest warning has been issued "for Garfield County, including the city of Enid". (Subtitles may be needed to find this out.) In the 1995 novel, Left Behind by Tim LaHaye and Jerry B. Jenkins, primary character Chloe Steele Williams returns home from California by a flight that lands in Enid to make connections. The Enid Woodring Regional Airport was the only operable airport in the area during the 48 hours after the "vanishings". In Stephen King's 2011 novel, 11/22/63, the main character Jake Epping mails a questionnaire to Enid, Oklahoma, to acquire a bachelor's degree after traveling back to 1958. In Harry Turtledove's 2016 baseball-themed fantasy novel, The House of Daniel, the early scenes take place in Enid. In the television series Night Court, Bull goes on a game show and one of the contestants is a computer programmer from Enid. In Jurassic Park III, Paul Kirby mentions that his business is located in Enid, Oklahoma. At the end of the movie, as the survivors look out at a flock of Pteranodons flying free, Alan Grant muses they must be looking for new nesting grounds. Amanda Kirby mutters in response "I dare them to nest in Enid, Oklahoma!" During World War II, two Victory Ships from Kaiser's Richmond, California shipyard were named after Enid and Phillips University, the SS Enid Victory and the SS Phillips Victory. In 1999, astronomer Tom Stafford of Oklahoma, named an asteroid after Enid. In the CBS series The Big Bang Theory, character Sheldon Cooper contemplates moving to Enid because of its "low crime rate" and "high speed internet" service, but decides against it because the city lacks a model railroad store.'. In fact, contrary to Sheldon's claim, Enid hosts the Railroad Museum of Oklahoma. Sister city Kollo, Niger was declared as Enid's sister city on August 1, 2010 by Mayor John Criner. References Further reading James, Marquis. Cherokee Strip: A Tale of an Oklahoma Boyhood Viking Press, 1945. Marshall, Frank Hamilton. Phillips University's first fifty years (October 9, 1906 – October 9, 1956) Phillips University, 1957. Rockwell, Stella, ed., Garfield County, Oklahoma, 1907–1982, Vol. I & II, Garfield Historical Society, Josten's Publishing Company, Topeka, Kansas. 1982. Klemme, Michael. Celebrating Enid!, 2010. McIntyre, Glen V. Images of America: Enid:1893–1945, Arcadia Publishing, 2012 External links Tourism information Category:Cities in Garfield County, Oklahoma Category:Cities in Oklahoma Category:County seats in Oklahoma Category:Micropolitan areas of Oklahoma	{ "pile_set_name": "Wikipedia (en)" }
--- title: "Illusion of the eye" excerpt: "PaperFaces portrait of @robhampson drawn with Paper for iOS on an iPad." image: path: &image /assets/images/paperfaces-robhampson-twitter.jpg feature: *image thumbnail: /assets/images/paperfaces-robhampson-twitter-150.jpg categories: [paperfaces] tags: [portrait, illustration, Paper for iOS, black and white] last_modified_at: 2017-01-17T14:33:25-05:00 --- PaperFaces portrait of [@robhampson](https://twitter.com/robhampson). {% include_cached boilerplate/paperfaces-2.md %} {% figure caption:"Work in progress screen captures Made with Paper." class:"gallery-3-col" %} [![Work in process screenshot](/assets/images/paperfaces-robhampson-process-1-600.jpg)](/assets/images/paperfaces-robhampson-process-1-lg.jpg) [![Work in process screenshot](/assets/images/paperfaces-robhampson-process-2-600.jpg)](/assets/images/paperfaces-robhampson-process-2-lg.jpg) [![Work in process screenshot](/assets/images/paperfaces-robhampson-process-3-600.jpg)](/assets/images/paperfaces-robhampson-process-3-lg.jpg) [![Work in process screenshot](/assets/images/paperfaces-robhampson-process-4-600.jpg)](/assets/images/paperfaces-robhampson-process-4-lg.jpg) [![Work in process screenshot](/assets/images/paperfaces-robhampson-process-5-600.jpg)](/assets/images/paperfaces-robhampson-process-5-lg.jpg) [![Work in process screenshot](/assets/images/paperfaces-robhampson-process-5-600.jpg)](/assets/images/paperfaces-robhampson-process-5-lg.jpg) [![Work in process screenshot](/assets/images/paperfaces-robhampson-process-6-600.jpg)](/assets/images/paperfaces-robhampson-process-6-lg.jpg) {% endfigure %}	{ "pile_set_name": "Github" }
Radio Bío Bío tuvo acceso exclusivo a los mensajes incluidos en la denuncia del fiscal Sergio Moya en contra de su superior, Emiliano Arias. En este caso aparecieron antecedentes que incluyen diálogos, por la aplicación WhatsApp, registrados en 2017, entre Andrés Chadwick y el alcalde de Rancagua, Eduardo Soto, quien será formalizado el próximo mes por malversación de caudales públicos. A esta información, y otros datos, accedió el fiscal nacional, Jorge Abbott, para abrir una indagatoria penal a Arias a cargo del fiscal del caso Pacogate, Eugenio Campos. Por dos horas se prolongó el consejo extraordinario de fiscales convocado por el fiscal nacional para resolver la apertura de una causa penal por las denuncias que hizo Moya, en contra de su superior, el fiscal regional de O’Higgins, Emiliano Arias. Tras la cita, donde los fiscales debieron dejar fuera del auditorio sus respectivos teléfonos móviles, se designó al fiscal de Magallanes, Eugenio Campos, para dilucidar esta denuncia por presunto tráfico de influencias, violación de secreto y obstrucción a la investigación. La indagatoria penal se suma al sumario administrativo por estos mismos hechos que llevará el fiscal regional de Antofagasta, Alberto Ayala, quien tiene un plazo de cinco días, pero prorrogables según sus necesidades. La vocera del Ministerio Público Nacional, Marta Herrera, quien además es la jefa de la Unidad Anti Corrupción, al ser consultada si el Consejo de Fiscales tuvo acceso a los antecedentes que presentó Moya, contestó afirmativamente y calificó de graves los hechos. Entre estos antecedentes, a los que tuvo acceso en exclusiva Bío Bío La Radio en fuentes de la Fiscalía Nacional, aparecen los diálogos por WhatsApp entre Andrés Chadwick, registrados en abril de 2017, con el alcalde de Rancagua, Eduardo Soto, quien será formalizado por malversación de caudales públicos el próximo 24 de mayo, a raíz de las irregularidades en el Teatro Municipal de esa ciudad. A continuación los mensajes Chadwick: Sería bueno un apoyo al fiscal (Arias). Es muy injusto lo que ha hecho la fiscalía nacional al sancionarlo por investigar incendios. Un twitter tuyo sería un muy buen respaldo. Soto: Ok. Chadwick: tú bien? Soto: Esperando qué sucede Chadwick: mejor cara? Soto: Creo que sí. Ojalá no se enrede lo del teatro. Chadwick. Dios quiera. Soto: cualquier cosa te comento. Después, en junio 2017, están los mensajes entre el alcalde de Rancagua y su abogado Luis Hermosilla: Soto: respecto al teatro regional alguna novedad? Hermosilla: si vamos a declarar en próxima fecha y después archivar. Seis meses después, el alcalde le escribe a su abogado: Soto: Me acaba de escribir Emiliano En otra conversación, el edil le contesta a Hermosilla: Soto: Está disponible, Andrés lo conoce y eficiente cien por ciento. Consultada la vocera de la fiscalía nacional si la causa del teatro Municipal de Rancagua estaba a cargo de Arias, Marta Herrera aclaró que es Moya el responsable de la indagatoria. En la entrevista con nuestra emisora, el viernes recién pasado, el fiscal Moya detalló la denuncia contra su superior por el caso del teatro Municipal de Rancagua. El persecutor relató que el miércoles 15 de noviembre de 2017, antes de las elecciones presidenciales, Arias lo citó a su despacho donde se encontraba el abogado defensor del edil. Según Moya, su jefe le pidió que estuviera “atento a los requerimientos del abogado”. Al otro día, el jueves, Moya allanó las oficinas del alcalde Soto, donde incautó su teléfono móvil, una tablet y un computador. El viernes 17 de noviembre, según este relato, Arias le ordena devolver las especies a lo que Moya se niega. Marta Herrera, además, aclaró que el fiscal Arias se mantiene plenamente en sus funciones y con todas sus causas, entre las que se cuenta la investigación por los delitos de connotación sexual cometidos presuntamente por sacerdotes de la Iglesia Católica.	{ "pile_set_name": "OpenWebText2" }
Exploring the emotion of hate through the Cronulla race riot that occurred on a Sydney beach in Australia in December 2005, this article’s principle concern is to interrogate the pleasure and the pain of hate, by asking what is happening to us when we hate? Analysing hate as an emotional response to and a soothing strategy for dealing with human alienation, it suggests that crucial to understanding hate is a grasp on the ontological entanglement of self, otherness and hate. Viewing hate through this lens it is possible to become attentive to the ways in which hate is mobilised by and for social institutions such as masculinity and nationalism and enacted as racial hate.	{ "pile_set_name": "OpenWebText2" }
Amnesty International says Qatar is failing to act fast enough to improve conditions for migrant workers building its World Cup soccer stadiums. But critics says it's only when sponsors like Coca-Cola and VISA speak up that soccer's governing body, FIFA, pays attention. President Barack Obama spent more than an hour talking about the gender pay gap during a town hall recently, but he didn’t mention the group that faces some of the worst workplace discrimination: transgender people.	{ "pile_set_name": "Pile-CC" }
Q: What is the right xpath/css to use to get each paragraph text in a single string? First I create a HtmlResponse And read it using scrapy: from scrapy.http import HtmlResponse from scrapy.selector import Selector body = """ <div class="a"> <p> text1<br> text2 </p> </div> <div class="a"> <p> text3 </p> </div> """ response = HtmlResponse(url='http://example.com/', body=body) sel = Selector(response) Now, I would like to extract text from this html But I get a list with 2 elements. This is what I have so far tried: sel.xpath('//div[@class="a"]/p/text()').extract() # [u'\n text1', u' text2\n ', u'\n text3\n '] As you note I get 3 text elements for 2 paragraphs? How can I do to get only 2 text elements? [u'text1 text2',u'text3'] Note that I prefer not to use BeautifulSoup since performance is a requirement here. A: With CSS selectors (including Scrapy's ::text extension): >>> from scrapy.http import HtmlResponse >>> from scrapy.selector import Selector >>> >>> body = """ ... <div class="a"> ... <p> ... text1<br> text2 ... </p> ... </div> ... <div class="a"> ... <p> ... text3 ... </p> ... </div> ... """ >>> response = HtmlResponse(url='http://example.com/', body=body) >>> sel = Selector(response) >>> [u''.join(paragraph.css('::text').extract()).strip() for paragraph in sel.css('div.a > p')] [u'text1 text2', u'text3'] >>>	{ "pile_set_name": "StackExchange" }
At ACGHK 2019, Siliconera sat in on a game introduction session for Final Fantasy VII Remake with producer Yoshinori Kitase. During the introduction session, we were able to get a full look at the entire Bombing Mission opening sequence right up to before the boss shown off at E3 via a prerecorded gameplay video. Kitase first started off wit an introduction to the game, mentioning that the game, despite being a remake, still follows the Final Fantasy series tenets of innovation, challenging the limits of what they can make, and giving the player a fun experience. He also emphasized that the game is being developed by a mixture of original staff and new blood who grew up on the original game. Lots of international staff are also involved in the game. While we’ve seen snippets of the opening section of the game here and there, yesterday was the first time we’ve seen the thing in full. While the general structure of the area has been faithfully recreated, there are new areas that are original to the remake, as the team has taken care to create new architecture to flesh out the Mako reactor area in between where loading screens would be in the original game. During the first area, Cloud also showed off his moves in the new ARP-style combat, which consists of action combat, and Wait Mode where everything is immensely slowed down so the player can use abilities and magic. The sword abilities are also able to be activated via a shortcut with L1 for those good with action games, said Kitase. Meanwhile, Cloud had two modes of combat to switch between – Operator and Punisher mode. Operator Mode focuses on quick slashes, while Punisher mode heavily slows down Cloud as he takes a different stance, in exchange for higher damage. One thing that really did pop to me was how the remake has expanded on the early cast of Cloud, Barrett, Biggs, Wedge, and Jessie. When they first get off the train, Barrett is much more hostile and distrusting of Cloud than in the original, saying that one misstep and he’ll shoot Cloud down. Meanwhile, Jessie is much more exasperated at how loud and distrusting Barrett is being. While Cloud splits from the rest of the crew mid-way to not get caught, he rejoins them when they begin opening the doors to reach the reactor, and the game went into a cutscene. While Biggs is skeptical of Cloud’s abilities, Wedge is more friendly and shoots Cloud a thumbs-up that Cloud clearly has no idea how to respond to. These parts really help flesh out the relationships between the crew in ways that weren’t achieved in the original. The elevator sequence with Cloud, Barrett, and Jessie is also expanded upon. While waiting for the elevator to arrive, Jessie notes that Tifa was adamant on recommending Cloud for the job, and asks what Cloud’s relationship with Tifa is. Cloud is clearly struggling to come up with an appropriate reply, but is saved by the arrival of the elevator. Inside, Barrett gives his spiel about the world dying from Mako overconsumption, but goes full ham and mentions that he can hear the world crying for help, to which Cloud snarks that Barrett should go see a doctor. These moments of levity help lighten the tense mood, and also harkens back to Cloud’s depiction in the original game, where he wasn’t without a sense of humor. Leaving the elevator, Barrett finally joins the party, and Kitase explained how his long-range gatling is easily used by holding down Square, and suitable for long-range enemies Cloud can’t reach. Conveniently, there were a couple of cameras Barrett could use as target practice, and we watched as the video showed off character swapping and commanding other characters to take actions. Finally, Cloud and Barrett reached the ladders leading to the bottom of the reactor, which leads to the scorpion boss we’ve seen since E3. While undoubtedly this first chapter is only a small part of the full game, I could appreciate how it expanded upon the cast established in the original. With the first game completely set in Midgar, I’m looking forward to seeing what other nuances will be added to the interactions between the cast. Final Fantasy VII Remake will come to the PlayStation 4 on March 3, 2020.	{ "pile_set_name": "OpenWebText2" }
It is impossible to resolve the Syrian conflict without Russia, German Foreign Minister Heiko Maas said at a meeting with his Russian counterpart Sergey Lavrov on Thursday. “I would like to point out that it is impossible to resolve the Syria issue without Russia,” he said. “Germany realizes its responsibility for what goes on in Europe and in German-Russian relations, this is what we will particularly talk about today. The prerequisite for dialogue between Germany and Russia, as well as between Europe and Russia, is that we do everything possible to listen to arguments concerning issues we disagree on, look to the future and search for ways to resolve serious issues the world has been facing. In this regard everyone can make their contribution, for instance as far as Syria goes,” Maas added. In addition, the German top diplomat said that ahead of Thursday’s talks, he had paid tribute to those killed during the Great Patriotic War laying a wreath at the Tomb of the Unknown Soldier in the Alexander Garden outside the Moscow Kremlin.	{ "pile_set_name": "OpenWebText2" }
Currently researching a new restoration project; an H-mod racer, similar to the Mercury "H-bomb". (But slightly bigger ) We believe the project car to be a "La Boa", which is mentioned in the "Vintage American Road Racing Cars 1950-1969".According to that book, engine option for the Mk. 1 is a Coventry Climax, and the Mk. 2/3 are Climax, Saab, Lotus twin-cam, Porsche.The car is currently setup to run a Mercury outboard, similar to the H-Bomb pictured above, RWD, chain drive. A BMW 700 motor came up as a possible option, which would be similar in execution to the Shirdlu shown here at BAT when it came up for auction. BMW 700 drivetrains, however, aren't readily available and I've already reached out to Mr. Selbert to inquire as to availability. There aren't many, it seems. A Porsche/VW powerplant could be a possibility, but, the fan shroud would likely require modifying the rear bodywork. That's also a pretty big lump to have hanging out behind the driver, and as the car is really quite small, would probably be detrimental to any kind of cornering ability. So, I would be interested in other forum members' thoughts on the matter. The easiest option would be to retain the Mercury, but I'd like to have a complete picture of what is available/possible during the research phase. Perhaps there's some H-mod/DSR historians who could provide a bit more insight than I can immediately gather on the world wide web. On that note, I think I found an old (6+ years) thread with Peter Krause on it, if he's watching perhaps he could chime in? Excellent point Stefan - only entertaining options on behalf of the car's owner, and partly due to a current lack of knowledge of the period equipment on my behalf. I don't know that the Mercury was the original motor for this car, but if that is the case, then retaining it would be correct. What would you consider to be most appropriate in this case? I suppose a more precise identification of the actual car will help, once I know that, I will follow up. What is the thing in the last picture of the rear suspension that looks like it needs to be replaced by a coil over? It looks like it has a rubber bushing in the middle. Also, where does the rod that attaches to the top link of the rear upright (hub carrier) go? I don't mean the radius rod or the anti-roll bar but the black rod that goes through the hole in the chassis member. I assume in this pic the half shaft is missing. Rick - thanks for the links! I've seen them, but I keep losing the bookmarks so now, I know where to find them! Mack - not certain on either point; we only spent a short while with the car, and will be investigating further soon. The halfshafts are missing. The uprights are place holders, and it's likely the case that a lot of the suspension is the same. I think this was very much a work in progress, or yet to be started, when the current owner purchased it. Sorry to leave you hanging. Hope to have some more details in the next week or so. Finding a relative of this chassis, if one exists, is going to be important me thinks. Excellent point Stefan - only entertaining options on behalf of the car's owner, and partly due to a current lack of knowledge of the period equipment on my behalf. I don't know that the Mercury was the original motor for this car, but if that is the case, then retaining it would be correct. What would you consider to be most appropriate in this case? I suppose a more precise identification of the actual car will help, once I know that, I will follow up. Neat car!The Mercury certainly could have been the original motor, as the H-Bomb proves such a configuration did exist in-period. I don't necessarily believe that every racecar needs to be returned to its original configuration. Rather, I would choose the car's most "significant" configuration as a point to aim for. Not knowing more of the car's history, the Mercury seems to be the simple and logical choice. If you later learn that the car originally had a Crosley or SAAB or something else in it... Then there's a decision to be made. If you are struggling with a lack of information, there is a YahooGroup for HMod. https://groups.yahoo.com/neo/groups/HMOD/I'm a member. There are a lot of members actually, though only a few are active at posting. Still, if you send photos and want to identify something, SOMEONE there will probably recognize it. HMod was the "tinkerer" class in the 50's-60's. No other class allowed for so much variation and invention, especially at such a low cost of entry. You could race everything from a near-stock production car, to a wildly modified production car, to a modified racecar, to a pure 100% homebuilt. Accordingly, "mystery" H-Mods show up all the time. If you are struggling with a lack of information, there is a YahooGroup for HMod. https://groups.yahoo.com/neo/groups/HMOD/I'm a member. There are a lot of members actually, though only a few are active at posting. Still, if you send photos and want to identify something, SOMEONE there will probably recognize it. HMod was the "tinkerer" class in the 50's-60's. No other class allowed for so much variation and invention, especially at such a low cost of entry. You could race everything from a near-stock production car, to a wildly modified production car, to a modified racecar, to a pure 100% homebuilt. Accordingly, "mystery" H-Mods show up all the time. Excellent - thanks for the link to the HMod group, that should provide for a great resource. It does seem that the Mercury would be the obvious choice, pending something else turns up. So, I think best to do some homework, and then see what best suits the needs and parts availability. From what I've been reading, it does seem like there was wild variation and innovation taking place during that time - really an interesting class to be researching. This should allow for a serviceable and period appropriate solution. OK - something of a revelation. I was close, in my googling, when trying to track down the car, but the owner passed along some information that got me the correct search terms. I was just a page or two away on the following site. Who is online Users browsing this forum: No registered users and 2 guests You cannot post new topics in this forumYou cannot reply to topics in this forumYou cannot edit your posts in this forumYou cannot delete your posts in this forumYou cannot post attachments in this forum	{ "pile_set_name": "Pile-CC" }
Philosopher Jonathan Kaplan recently published an article called Race, IQ, and the search for statistical signals associated with so-called “X”-factors: environments, racism, and the “hereditarian hypothesis,” which can be downloaded here. His thesis is that the black-white IQ gap could plausibly be due to racism and what he calls racialized environments. He presents simulations in support of this argument. He also argues that “given the actual state of the world there is no way to generate any reasonably strong evidence in favor of the hereditarian hypothesis.” I have written a detailed critique of his claims. In short, he is wrong. Here’s the abstract of my article: Jonathan Michael Kaplan recently published a challenge to the hereditarian account of the IQ gap between whites and blacks in the United States (Kaplan, 2014). He argues that racism and “racialized environments” constitute race-specific “X-factors” that could plausibly cause the gap, using simulations to support this contention. I show that Kaplan’s model suffers from vagueness and implausibilities that render it an unpromising approach to explaining the gap, while his simulations are misspecified and provide no support for his model. I describe the proper methodology for testing for X-factors, and conclude that Kaplan’s X-factors would almost certainly already have been discovered if they did in fact exist. I also argue that the hereditarian position is well-supported, and, importantly, is amenable to a definitive empirical test. The PDF is available at Open Differential Psychology. You can also read the article below the cut. The Elusive X-Factor: A Critique of J. M. Kaplan’s Model of Race and IQ Contents 1. Introduction 2. Background 3. Kaplan’s model 3.1. How racist is America? 3.1.1. Crime facts versus crime fiction 3.1.2. Race and policing 3.1.3. Labor market discrimination 3.1.4. Housing discrimination 3.2. Disparate treatment or disparate individuals? 3.3. The missing mechanisms 4. The nature of the IQ gap 5. Kaplan’s simulations 5.1. Unimportance of variance differences 5.2. Abilities and tests 5.2.1. Measurement invariance 5.2.2. Stereotype threat 5.2.3. Flynn effect 5.2.4. Rowe and colleagues’ findings 5.3. Can X-factors influence g? 6. Non-cognitive differences between blacks and whites 7. How to test HM 8. Discussion References 1. Introduction The hereditarian model (henceforth, HM) of the IQ gap between whites and blacks in the United States holds that the gap is mainly caused by genetic differences between the two races (Jensen, 1998; Rushton & Jensen, 2005). Kaplan (2014) challenges this view, arguing that racism and “racialized environments” are “X-factors” that can explain the gap. He presents simulations in support of this argument. He also claims that given the present state of science, there is no conceivable way to test HM. I will show that Kaplan’s attack on HM is not convincing. My argument consists of four parts. First, I will show that Kaplan’s suggested explanation of the black-white gap is theoretically too vague and underdeveloped to be regarded as a serious model. Second, I will show that even if Kaplan’s model were to be considered as plausible, his simulations do not provide any support for it, or any evidence against HM. This is due to the fact that Kaplan ignores basic psychometric principles and most of the facts pertinent to any explanation of the gap. I will describe the proper method that could be used to search for X-factors. Third, I will argue that Kaplan’s model predicts that there are large racial differences in various non-cognitive traits, whereas such differences do not in fact exist. Lastly, I will show that, contra Kaplan, HM is a fully testable scientific model. Before describing and dissecting Kaplan’s arguments, I will discuss the theoretical and conceptual background of the dispute. 2. Background Arthur Jensen (1998, pp. 447–458; see also Sesardic, 2005, pp. 138–142) noted that there are two different models of environmental causation that could, in principle, explain the observed white-black IQ gap of about one standard deviation (15 IQ points): 1) According to the “variable environments” or VE model, all environmental factors influencing IQ are common to the black and white populations, but vary so that some factors are more frequent and others less frequent in one race versus the other. There are thus no factors unique to either race, but the black IQ disadvantage is caused by their having been exposed to more negative factors and/or fewer positive ones. The black distribution of environmental effects is shifted into the negative direction, with the average black growing up in a “cognitive environment” similar to that experienced only by disadvantaged whites. 2) The X-factor model is based on the idea that there are race-specific environmental factors that affect only one race. This is typically conceptualized as there being cognitively detrimental factors that affect all blacks and no whites. Thus the black IQ mean is lower than the white one because American society singles out all blacks for very specific IQ-sapping experiences. Jensen gave the name X-factor to the unknown non-genetic variable (or set of variables) that would affect the IQs of blacks but not whites. If the VE model were true, it would mean that the environmental circumstances of the average black must be similar to those of the most deprived few percent of whites. The logic behind this calculation is the following. IQ has a high heritability within populations, perhaps as much as 80 percent in adults. If we assume that the genetic component does not cause racial differences, then the black-white gap must be entirely due to the environmental component, which accounts for as little as 20 percent of IQ variation. Environmental influences on IQ can be thought of as a unidimensional scale along which black and white individuals are distributed. Given that the total environmental effect on a given individual’s IQ can be conceptualized as the sum of a number of more or less independent negative and positive factors, the distributions of the total environmental effects must be roughly normal. If the environmental influence on IQ variation is only 20 percent, then, for the VE model to hold, the mean of the distribution of environmental effects for blacks would have to be about 2.2 standard deviations lower than the mean for whites on the same scale of total environmental effects. [1] This would entail that the average black is exposed to a worse cognitive environment than about 99 percent of whites. Even if we assume that heritability is lower, say, 50 percent, the cognitive environment of the average black must be worse than that of about 92 percent of whites. However, when black-white differences in the environmental factors that have traditionally been thought of as causes of the IQ gap have been investigated, it has been found that the differences are much too small to explain the gap. For example, differences in parental socioeconomic status can account for about one third of the gap (Herrnstein & Murray, 1994, p. 286), while according to Card & Rothstein (2007) residential segregation can explain about 25 percent of the SAT score gap (which is similar in size to the IQ gap). Similarly, Currie (2005) estimated that racial differences in health conditions explain at most 25 percent of the IQ gap in children. [2] Phillips et al. (1998) found that even after controlling for more than 30 variables related the economic, educational, cognitive, emotional, and health characteristics of parents and grandparents, about a third of the verbal IQ gap in children remained unexplained. The reason why it is very difficult to account for the gap in terms of environmental differences is that, firstly, they are usually not that strongly associated with IQ, and that, secondly, white and black distributions on those environmental variables overlap much more than what is expected on the basis of the VE model. However, the problems of the VE model go much deeper. Eric Turkheimer has crystallized the results of many decades of behavioral genetic research into three “laws” (Turkheimer, 2000). They represent empirical generalizations of the causes of human behavioral differences. The first law states that all behavioral traits are heritable, while according to the second law familial resemblance in behavioral traits is mainly due to shared genetic rather than shared environmental influences. The third law states that the non-shared or within-family environment is an important source of behavioral differences. These laws apply to IQ, too, particularly after childhood as the heritability of IQ increases and shared environmental influences subside. [3] It is important to understand that it follows from Turkheimer’s laws that proposed environmental effects on IQ are also expected to be confounded by genetic influences. Accordingly, behavioral genetic research indicates that “environmental” factors, such as measures of family environment, child rearing style, and peer relations, are under substantial genetic control (Plomin et al., 1994; Rowe et al., 1998; Kendler & Baker, 2007; Vinkhuyzen et al., 2010). Environments are not randomly distributed across the population, and an individual’s likelihood of encountering a specific environment may depend, in part, on his or her genotype or that of his or her parents, giving rise to spurious relationships between environmental factors and individual traits. “Partialing out” the influence of an “environmental” factor therefore typically also removes some of the genetic differences between individuals. Notably, the association between children’s IQ and parental socioeconomic status appears to be mostly due to the influence of the same genes on both variables (Trzaskowski et al., 2014). Therefore, the reported correlations between IQ and environmental factors purporting to explain (some of) the IQ gap are, at best, overestimates of the true causal effects. Moreover, it is clear that the shared family environment is not a major cause of IQ differences within races, whereas the proposed environmental causes of the gap are generally shared between family members. Environmental influences on IQ are overwhelmingly non-shared (i.e., non-familial) in character, and few of them have been identified (Turkheimer & Waldron, 2000). Much of the “missing” non-shared influence on IQ may be developmental noise (Kan et al., 2010) that affects both races more or less equally, and therefore cannot contribute to the gap. Simply put, it is not possible to explain the black-white IQ gap in terms of specific environmental differences because behavioral genetic studies indicate that very little of the IQ variation within races can be attributed to any identifiable environmental causes. While blacks grow up in environments that are in many respects inferior to those of whites, on the average, the distributions of environmental effects on IQ cannot be shown to greatly differ between races, which means that there is no credible evidence in favor of the VE model. If there were an IQ-sapping environmental factor that harms all blacks but leaves whites intact, it could potentially explain the IQ gap even if VE-type factors cannot do so. The problem is, as Jensen pointed out, that it is difficult to come up with plausible candidates for such an X-factor. Any environmental influence on black IQ that one might think of would affect many whites, too. Significantly, the black IQ disadvantage is found across all regions, social classes, and generations; wherever one looks, blacks appear to suffer from a similarly sized IQ deficiency compared to white peers. This means that the putative X-factor must have very little variance, inflicting an almost constant 15 IQ point deficit on virtually all blacks. One might think that racism against blacks would be a perfect candidate for an X-factor, but a moment’s reflection suggests that that racism much more closely resembles a VE-factor. More than thirty years ago, James Flynn articulated the inadequacy of racism as an X-factor in this way: “Racism is not some magic force that operates without a chain of causality. Racism harms people because of its effects and when we list those effects, lack of confidence, low self-image, emasculation of the male, the welfare mother home, poverty, it seems absurd to claim that any one of them does not vary significantly within both black and white America.” (Flynn, 1980, p. 60) The conceptual implausibility of the X-factor model and the empirical inadequacy of the VE model lend credence to the hereditarian explanation. 3. Kaplan’s model Kaplan rejects the argument that racism is not a promising X-factor. He thinks that the effects of racism on black IQ are not exhausted by the fact that racism may cause poverty, low self-esteem, or other VE-type effects. Instead, he suggests that the everyday experiences of just about all blacks, while superficially similar to those of many whites, are in fact infused by racism and are therefore qualitatively different in ways that affect IQ. He gives the following specific examples of the potential influence of racism or “racialized environments” on IQ: 1) Black criminals are overrepresented in television news, which means that the experience of black and white children viewing the same tv programming is different. 2) Blacks are more likely than whites to be stopped by the police for questioning. 3) Blacks who go into retail establishments are more likely to be suspected of theft or treated rudely by clerks. 4) Blacks face discrimination in the labor market. 5) Landlords, real estate agents, and other “gatekeepers” discriminate against blacks to keep them out of certain neighborhoods. Kaplan suggests that such racialized environmental X-factors are prevalent in America, and that there are large numbers of them. He agrees that it is not plausible that their effect would be exactly the same on all blacks, but argues that if it is assumed that there are a number of uncorrelated X-factors, each with at most moderate variability, they would be very difficult to detect in a statistical analysis of test scores. He suggests that different classes of blacks are affected by different X-factors, but that all are affected to the same degree, causing a similarly sized IQ deficit in them regardless of class background and other VE-type circumstances. According to this model, the racism encountered by, for example, “young Black men in poor urban centers” is different in its outward character but not in its IQ-sapping effects from that encountered by “young Black women attending an elite university.” Kaplan’s model is depicted in Figure 1. Figure 1. Kaplan’s X-factor model. Various environmental X-factors negatively influence observed black IQs, but have no influence on observed white IQs._______________________________________ 3.1. How racist is America? While Kaplan appears to view the above list as clear-cut evidence of the pervasive influence of racism in American society, a closer look reveals that the evidence is ambiguous at best. The racial disparities discussed by Kaplan cannot be used as proof of racial bias or animus unless blacks are treated differently from non-blacks who behave the same way, and he offers no evidence that this is the case. I will next show how these examples of “racialized environments” can be plausibly interpreted in alternative, non-racial terms. 3.1.1. Crime facts versus crime fiction Black criminals are generally overrepresented in television news coverage in relation to the black share of the population as a whole. However, there is little evidence of their being overrepresented in relation to the black share of the perpetrators of crime (Gilliam et al., 1996; Dixon & Linz, 2000; Chiricos & Eschholz, 2002). The fact that black offenders are disproportionately portrayed in crime news can be regarded simply as a reflection of the great overrepresentation of black individuals in the ranks of criminals. A better test of racial bias in television—and also more pertinent to Kaplan’s concerns about children’s television viewing—is the portrayal of race in fictional crime shows. Unlike news programs, such shows are not constrained by verisimilitude, which means that gross racial biases in the portrayal of crime are possible. However, studies have consistently found that compared to real-life crime statistics, blacks are underrepresented among criminal offenders in crime dramas, while whites are greatly overrepresented (Potter et al., 1995; Eschholz, 2002; Eschholz et al., 2004; Deutsch & Cavendar, 2008; Case, 2013). For example, 75 percent of the violent offenders and suspects in the 2000–01 season of Law & Order were white, whereas in the late 1990s only 13 percent of real-life violent crime suspects were white in New York City where the show was set. For black offenders and suspects, the proportions were 14 percent in the fictional world of Law & Order versus 51 percent in real life. (Eschholz et al., 2004, Table 1.) 3.1.2. Race and policing Coviello & Persico (2013) found that while the New York City Police Department’s “stop-and-frisk” program led to blacks being stopped much more often than whites, the stops of whites were somewhat less “productive” in terms of arrests, which could be interpreted as evidence of a police bias against whites. To take another example, Worden et al. (2012) investigated vehicular stops made by the police in Syracuse, New York, over a period of four years, and found that African Americans were not more likely to be stopped during daylight than after dark when the police suffer an impaired ability to detect motorists’ race. This suggests that the greater propensity of black motorists to be stopped was not due to racial bias. From these examples it is clear that racial disparities in encounters with the police do not constitute prima facie evidence of racial bias. Even if the police never relied on the (generally reasonably accurate) racial stereotypes about criminal offending, racial disparities in police scrutiny would arise because blacks are more likely than whites to engage in suspicious and illegal activities. The same inevitably applies to private security guards singling out seemingly disproportionate numbers of blacks for scrutiny. More generally, the observed black-white differences in crime rates are predictable from black-white differences in IQ and aggressiveness (Beaver et al., 2013), and victim surveys indicate that the high arrest and conviction rates of blacks reflect their genuinely high rates of offending (New Century Foundation, 2005). The common belief that a racially biased criminal justice system underlies the high black crime rate is difficult to reconcile with these findings. 3.1.3. Labor market discrimination Racial discrimination in the labor market is another area where Kaplan jumps to unsupported conclusions. He cites experimental audit studies where employers were found to prefer white job applicants to black ones with identical qualifications, arguing that this proves racial discrimination to be pervasive. However, Heckman (1998) has identified many severe limitations in this research. First, the experimental designs of such studies are based on dubious and untestable assumptions. Second, even if the experiments do identify genuine discrimination, the typical study reports only small differences between races, explaining very little of the existing racial disparities in the labor market. Third, the effect of racial discrimination on labor market outcomes is ultimately not determined by discriminatory employers but by those that actually employ blacks. In a typical audit study, white and black “auditors” with matching (fictitious) credentials apply to low-skill, entry level positions, with the consequence that the studies have very poor ecological validity with respect to the labor market as a whole. The auditors sometimes exist only on paper, but experiments where actual persons are sent to job interviews are neither randomized (race cannot be assigned to individuals) nor double-blind (the auditors know the purpose of the study), which compromises any attempt to make causal inferences. The auditors can never be matched on all the variables that different employers may find important. It is often quite reasonable to regard white applicants as more qualified than ostensibly similar blacks. For example, the average IQ gap between black and white applicants to low-complexity jobs is 0.86 standard deviations, favoring whites (Roth et al., 2001), something that audit studies do not adjust for. Such racial differences may assume a greater-than-usual importance in the decision-making of the audited employers because many other characteristics that normally show racial differences in the applicant population have been experimentally equalized. In recruitment to cognitively more complex occupations, a rational employer would similarly expect a white graduate from a selective college to be smarter and more diligent than a black graduate from a similarly prestigious school, given the widespread use of racial preferences in college admissions. [4] A basic problem with many claims of group discrimination in modern, free labor markets is that they are based on the assumption that employers voluntarily leave money on the table. If the labor of some group were systematically undervalued by discriminatory employers, then surely some rational employers would step in and make a large profit on the basis of this market inefficiency. This would increase the demand on the labor of the discriminated-against group, driving up its wages. Widespread and significant labor market discrimination can continue only if there are legal or social norms that enforce discrimination even at a substantial economic cost to employers, but, as discussed below, such norms in today’s America encourage or mandate discrimination in favor of blacks. Significantly, the measured job performance of black employees is inferior to that of whites working in similar occupations (Roth et al., 2003), whereas the discrimination thesis predicts the opposite. There is no evidence that the labor of black employees is undervalued in today’s America. Racial differences in labor market outcomes are clearly driven by “pre-market” factors, such as differences in education and IQ. When blacks and whites are equated on even a limited set of relevant pre-market factors, differences in their labor market outcomes are greatly attenuated or eliminated (Johnson & Neal, 1998; Carneiro et al., 2005). Indeed, the black-white income gap is often reversed after such equating (Johnson & Neal, 1998; Nyborg & Jensen, 2001; Heckman et al., 2006), which may signal the presence of discrimination in favor of blacks. While it is difficult to establish whether anti-black discrimination plays any significant role in the labor market outcomes of today’s blacks, pro-black discrimination must play such a role, considering that it is something that is openly, legally, and widely practised in the name of “affirmative action”, “diversity”, and so on. For example, more than 60 percent of private sector workplaces in the US had affirmative action plans as of 2002 (Kalev et al., 2006), while federal and state agencies are bound by numerous rules concerning racial diversity in their hiring and contracting (e.g., Office of Federal Contract Compliance Programs, 2002). In fact, the disparate impact doctrine entails that many employers must in practice discriminate in favor of blacks so as to avoid legal repercussions (Wax, 2011). When one recognizes the fact that differences in skills and human capital are the primary reason for racial disparities in labor market outcomes, while also appreciating the prevalence of preferential treatment for blacks, it is apparent that Kaplan’s case for employment discrimination as a differentiating factor between whites and blacks is not credible. 3.1.4. Housing discrimination Finally, Kaplan mentions housing discrimination by landlords, real estate agents, and others. Even this paradigmatic example of racial discrimination turns out to be ambiguous when examined more carefully. While the practices mentioned by Kaplan may contribute to residential segregation by race, it is not clear that racial animus drives the ostensibly discriminatory practices. The reasons why one would want to control who gets to move into a neighborhood include such interlinked considerations as preserving property values, keeping crime levels down, and maintaining the quality of local public schools. In the presence of imperfect information, a rational actor interested in preserving a prosperous neighborhood would prefer whites to blacks as home buyers and tenants considering that the presence of blacks is statistically associated with many or all of the negative indicators for neighborhood value. Blacks may therefore end up being disproportionately turned down even when there is no racist intent. Considering that housing discrimination by race is illegal and thus a risky course of action, it is unclear if blacks are truly discriminated in the housing market when one compares them to objectively similar whites. To establish that a pair of black and white individuals are really comparable in all their relevant characteristics, it is not sufficient to match them on just a few variables. A good illustration of this is the fact that black and white borrowers with the same credit scores and current incomes are not equally creditworthy in terms of the probability of loan default. Blacks consistently default more often than whites after adjusting for such factors as payment and credit history and income (Ferguson & Peters, 1995; Laderman & Reid, 2008; Anacker et al., 2012). When one appreciates the fact that the distributions of many important personal characteristics are different in the black and white populations, with the means of the black distributions located lower than the means of the white distributions, it is easy to understand why black individuals are not truly as creditworthy as ostensibly similar whites, on the average. For example, as a result of the different income distributions of blacks and whites, the expected future income of a white individual is higher than that of a black individual who has the same income in a particular year (Sanandaji, 2009). Over time, the characteristics of individuals tend to regress toward population averages which differ between races. When deciding on who gets to rent or buy in a given neighborhood, it is not just the characteristics of a particular individual that may influence the decision. The way in which the family members of a prospective renter or buyer are perceived may also have an impact. Racial differences in the distributions of various psychological traits mean that the relatives of even highly accomplished black individuals tend to be inferior in many of their personal characteristics when compared to the relatives of seemingly similar whites. For example, the average levels of cognitive ability and academic achievement of upper-middle class black children do not resemble those of white children of the same social class but rather those of lower class whites (Herrnstein & Murray, 1994, p. 288; “Why Family Income”, 2008). The economic, social, and physical decay of many urban areas in the wake of swelling black populations and white flight was a defining feature of American race relations in the 20th century. Seen against this historical background, it is difficult to argue that whites’ (and other non-blacks’) concerns about the character of their black neighbors are irrational. 3.2. Disparate treatment or disparate individuals? The fact that blacks face adversities with disproportionate frequency is consistent with the racism explanation, but it is not the only possible explanation. Controlling for black-white differences in what can be plausibly interpreted as causally prior variables shows that many, if not all, of the outcome differences that Kaplan attributes to racism can be parsimoniously explained in non-racial terms. The same would in all likelihood apply to any further examples of racialized environments that he could come up with. After adjusting for relevant covariates, it is in fact not infrequently the case that whites rather than blacks appear to be targets of discrimination. Interestingly, while Kaplan thinks that the available research justifies very expansive claims about the prevalence and effects of racism in contemporary America, he expresses great scepticism about the results of human behavioral genetics. He claims that given the non-feasibility of experimental manipulations, it is “fiendishly difficult” to make any accurate estimates of the influence of genes and environments in humans. [5] I think Kaplan greatly underestimates the power of behavioral genetic research designs. While behavioral genetics is not properly experimental, it relies on the convergence of results from different natural experiment paradigms (e.g., twin, adoption, and GCTA designs) increasingly applied to many large and representative population samples from around the world. This, together with the field’s robust basis in both quantitative evolutionary theory and the results of non-human breeding studies, enables stronger causal inferences than are possible in almost any other area of social or behavioral science. In contrast, the research on racial discrimination cited by Kaplan relies on simple correlational analyses and single-blind quasi-experiments suffering from poor ecological validity and omitted variable bias. The causal interpretations Kaplan gives to these studies immediately crumble under even very simple robustness checks, as detailed in previous sections. Nevertheless, Kaplan thinks that not only is it not “fiendishly difficult” to make causal inferences about the influence of racism in the absence of experimental manipulations, it is positively easy: in his conception, a zero-order correlation between race and a negative outcome, or a quasi-experiment that is in all respects pitifully rudimentary compared to those routinely conducted in behavioral genetics enables one to draw far-ranging conclusions about the effects of racism in America. Kaplan’s epistemological double standard cannot be explained away by the fact that he only briefly and cursorily reviews research on racism in America. The studies he cites appear to be quite representative in terms of study designs that are prevalent in this area of research (cf., Pager & Shepherd, 2008). Kaplan’s sweeping condemnation of American society as imbued by anti-black racism is premature. Of course, he is not alone in making this error—the conviction that racism has great explanatory power is widespread in certain sections of American society despite the distinct weaknesses of the evidence behind this conviction. The individual differences approach reflected in HM presents a necessary corrective to such beliefs about racism: psychological differences within and between races explain many outcome differences, indicating that accusations of racism against various institutions are often misplaced. Only after a thorough appraisal of the origins and significance of racial differences in socially valued traits can racism be allotted its proper role in understanding American society. Uncovering the etiology of the black-white IQ gap is particularly important, given IQ’s pervasive importance in modern society (Gottfredson, 2002). 3.3. The missing mechanisms The very existence of the “racialized environments” proposed by Kaplan is doubtful, but even if we accepted that potential X-factors of this type exist (or at least are perceived to exist by most blacks), Kaplan’s model would still be highly inadequate. This is because he does not offer any reason to believe that such factors would influence cognitive ability (of all traits). Why would a security guard’s suspicious gaze at a store, a police officer’s gratuitous stop-and-frisk search, or a suspicion that a CV or an offer to purchase a house was overlooked because of racial bias cause an individual’s IQ to plummet? [6] Kaplan does not present even a hypothesized mechanism of how this could happen, let alone any evidence that it actually happens. Notably, he claims that his X-factors are very heterogeneous, with each section of the black community being affected to the same degree by partly different sets of X-factors. Thus we are to believe that there are numerous different X-factors that depress IQ scores in the same way, yet we know nothing about the actual mechanisms behind any of them. We do not even know if these X-factors are supposed to decrease IQ in a permanent manner (say, each stop-and-frisk lowers an individual’s IQ by 0.5 points for the rest of his or her life), or only temporarily (a black murderer on tv makes the viewer somewhat less intelligent for the next two weeks). Nor does Kaplan’s model suggest any explanation for the familiality of the black decifit, that is, the fact that the IQs of black individuals are predictable from the IQs of their relatives with the same accuracy that obtains for white individuals (Jensen, 1998, pp. 447, 467–471). This familiality suggests that X-factors would have to be tightly linked to family background, while from Kaplan’s description they appear to be much more randomly distributed. Another problem is that Kaplan’s model assumes experiences of racism to be ubiquitous, whereas only 1.7 percent of today’s black adults report that they are frequently treated poorly because of their race. A slightly higher proportion of whites, 2.3 percent, report often receiving such treatment. [7] Kaplan brings up stereotype threat (Steele & Aronson, 1995) as an example of a subtle environmental influence that can have a large effect on IQ scores, arguing that his X-factors could be similar in nature. However, stereotype threat is based on a causal theory of how anxiety about confirming a stereotype about intelligence hampers performance on intelligence tests. There is thus a direct and immediate link, supported by experimental evidence, between poor test performance and the proposed causal factor—something that certainly cannot be said of any of Kaplan’s far-fetched propositions. Furthermore, if Kaplan’s X-factors were real, their influence on IQ would have to be, for reasons discussed later in this article, far more subtle than that of stereotype threat. Kaplan’s X-factor model must be seen as a casual speculation rather than a well thought-out challenge to HM. It suffers from so many implausibilities and lacunae that it cannot provide a credible explanation of the black-white IQ gap. Nevertheless, the fundamentally vague and impressionistic (if not downright fantastical) character of the model will be disregarded in the following sections because it is instructive to examine why the simulations that Kaplan presents in support of his claims in fact provide no such support. 4. The nature of the IQ gap Before discussing Kaplan’s simulations, a consideration of certain facts about the black-white gap is in order. While Kaplan seems to conceive of HM exclusively in terms of VE-factors and X-factors, this particular argument is in fact just one piece in the body of evidence supporting HM. There are equally or more interesting arguments that Kaplan completely ignores. One of the most important discoveries made by Arthur Jensen in his research on the black-white IQ gap was the finding that its magnitude is not invariant across different tests but tracks their g loadings, or correlations with the latent general factor of intelligence. He devised the method of correlated vectors (MCV) to assess the strength of this association. In MCV analyses, a vector of g loadings from a test battery is correlated with a vector of the values of some other variable, such as the black-white gap on different tests. The MCV tests if the other variable’s association with test scores is driven by g or by other sources of variance that are orthogonal to g. Psychometrically, these other sources represent non-g factor variances, test specificities, and measurement error, but except for measurement error (which can be partialed out) the MCV usually cannot specify the nature of the non-g variance. If the MCV correlation is large and positive, it indicates that the association between test scores and the other variable is primarily due to g. Conversely, a large negative MCV correlation indicates that the association is driven by non-g sources of variance. If the MCV correlation is close to zero, the association between test scores and the other variable usually reflects some complex combination of influences that may involve both g and non-g components. In practice, MCV analyses are often subject to false positives and false negatives, and meta-analytic aggregation of MCV results is required for reliable inferences. In a meta-analysis of 149 tests from 15 test batteries, Jensen found an average correlation of 0.63 between the magnitudes of black-white gaps and g loadings (Jensen, 1998, pp. 377–378). [8] What this means is that the better a measure of the g factor a given cognitive test is, the greater the black-white gap on it usually is. The significance of this Jensen effect, as the positive MCV correlations between g loadings and other variables are called, is that such effects are otherwise only found for strongly genetically influenced biological variables. [9] Specifically, the g loadings and heritability coefficients of tests have been found to be intercorrelated moderately to highly in many studies (te Nijenhuis et al., 2014b; Rushton & Jensen, 2010). Jensen effects have also been detected for correlations between test performance and inbreeding depression, heterosis, and head size (Jensen, 1998, p. 419), the last being a highly heritable characteristic (Smit et al., 2010) robustly associated with IQ (Rushton & Ankney, 2009). In contrast, strong “anti-Jensen effects”, or negative MCV correlations between g loadings and other variables, have been reported for the environmentality coefficients of cognitive ability tests, that is, the complements of heritability coefficients (Rushton & Jensen, 2010); for the effects of retesting or practice on test performance (te Nijenhuis et al., 2007); and for the test score gains induced by the Head Start compensatory education programs (te Nijenhuis et al., 2014a). Similarly, the observed increases in the cognitive test scores of many populations across much of the last 100 years (the Flynn effect) are correlated at –0.38 with the g loadings of the tests (te Nijenhuis and van der Flier, 2013). [10] Notably, Flynn et al. (2014) found in a meta-analysis that “biological-environmental” effects, such as iodine deficiency and traumatic brain injury, have a strong negative influence on cognitive test performance, but that this effect is unrelated to g loadings (MCV correlation ~0). If the black-white IQ gap reflected environmental rather than genetic disparities, it would constitute a very unusual Jensen effect. Research on Jensen effects indicates that g is mainly a genetic phenomenon, and that variables that are positively associated with g are biological variables that share genetic influences with g. This is underscored by the finding that the kinds of environmental effects, such as brain injuries, that directly affect the neurobiological substrate of cognition do not cause g-linked cognitive changes. The principally genetic nature of g has also been supported in multivariate behavioral genetic analyses where genetic influences on different cognitive abilities have been found to be largely common rather than ability-specific (Plomin & Spinath, 2004; Trzaskowski et al., 2013b; see also Panizzon et al., 2014 where it was found that genetic correlations between different tests and abilities can be best explained in terms of a hierarchical g factor model). Kaplan does not consider the g-saturated nature of black-white cognitive differences at all, despite this finding’s centrality to the debate. What this means is that his proposed explanation of the gap cannot account for the pattern of cognitive differences that is actually observed. It also means that his simulations, discussed in more detail below, are misspecified and, for this reason alone, do not provide evidence for or against any realistic model of racial differences. It should be noted that one cannot nullify the importance of Jensen effects by simply denying the reality of the g factor as a source of cognitive differences. Regardless of the nature of g, environmental variables are differentially associated with g loadings than genetically saturated variables, and the black-white gap resembles genetic variables in this respect. Any alternative, non-g theory of intelligence must be capable of explaining why we see these consistent patterns of correlations between g factor loadings and other variables. 5. Kaplan’s simulations Kaplan presents a series of simulations of the effects of his hypothesized racialized environments on the IQs of blacks. He claims that the simulations show that such effects would generally not be statistically detectable in any study with a realistic sample size. He concludes that racism against blacks is therefore a promising explanation of the IQ gap, and that HM is not viable. Unfortunately, Kaplan’s simulations are psychometrically so flawed that they cannot provide evidence in favor of his model or against HM. The flaws can be summarized in the following three points: 1) The test for the equality of variances which Kaplan uses to test for the presence of X-factors cannot be used for that purpose. 2) There are well-established ways to model intelligence differences and methods that can be used to search for X-factors in the framework of such models, but Kaplan ignores them. 3) The simulations disregard the empirically observed pattern of correlations between g loadings and black-white cognitive differences. I will next discuss these three points in some detail. 5.1. Unimportance of variance differences Kaplan uses Levene’s test for the equality of variances to investigate whether his simulated X-factors inflate IQ variances to a statistically significant extent. He finds that given realistic sample sizes, the increases in variances are not generally statistically significant. He regards this as the main finding of his study, and concludes that X-factors are therefore not generally detectable. This conclusion is completely unwarranted. Given the abundance of data on black-white IQ differences, one could easily conduct a powerful meta-analysis of variance differences. For example, a 2001 meta-analysis of racial differences in general cognitive ability (Roth et al., 2001) had sample sizes in the millions, enabling very accurate estimation of population parameters. If the variances of black IQ scores were slightly but consistently higher than those of whites, a meta-analysis would show it with a high degree of statistical reliability. As it happens, the variances of IQ scores in blacks are typically smaller than those of whites. Jensen (1998, p. 353) found that black standard deviations are usually in the range of 11–14 IQ points, with a mean of 12, compared to the white standard deviation of 15 points. [11] This indicates that the outputs of Kaplan’s simulations do not even approximate actual IQ data. One of the peculiarities of his article is that he does not examine variance differences in any real-life data sets. However, a more important reason why Kaplan’s simulation results do not support his conclusions is that differences in IQ variances could be due to other causes besides X-factors. Specifically, one group could be inherently more variable than another group on a given phenotype. For example, the pigmentation of hair and eyes varies in Europeans much more than in black Africans, reflecting the fact that the genetic mutations causing this phenotypic diversity in Europeans arose, or at least became selectively advantageous, long after the evolutionary divergence of African and non-African lineages. Given that there is no a priori reason to expect different populations to have exactly the same “natural” IQ variances, Levene’s test, which assesses deviations from a null difference, cannot provide any useful evidence for or against the existence of environmental X-factors. The proper way to test for X-factors is discussed next. 5.2. Abilities and tests The predominant view among psychometricians and the one that is adopted in this article is that individual differences in intelligence can be conceptualized in terms of a factor hierarchy with a third-level general factor (g), second-level broad ability factors, and first-level test-specific variation (Deary, 2012). Higher-level sources of variation exert a causal influence on the lower levels of the hierarchy. Observed test scores, whether they be full- or subscale scores, subtest scores, or item scores, are regarded as reflections of the latent abilities that underlie performance on all cognitive tasks. [12] The distinction between abilities and test scores is completely ignored by Kaplan. His simulated X-factors directly influence observed, full scale IQ scores (see Figure 1 above). However, full scale IQ scores are typically composites of scores on different tests. The fact that any causal influence on test performance is almost inevitably differentially associated with different tests and abilities offers rich possibilities for testing for group differences in causal processes. There are standard methods for doing such analyses. In contrast, Kaplan’s simulations are based on manipulating single test scores, are focused on uninformative variance differences, and are not grounded in any realistic model of intelligence. This means that they tell us nothing about how difficult or easy it is to detect X-factors. 5.2.1. Measurement invariance A proper test of Kaplan’s model would involve the specification of a causal model for test score differences where X-factors would influence observed test scores in blacks alongside underlying abilities, whereas in whites only the underlying abilities (and unique variances) would influence test performance. [13] The plausibility of such a model could then be investigated through an analysis of measurement invariance in the framework of multiple-group confirmatory factor analysis. The analysis would examine whether simulated variance-covariance matrices and mean structures produced by the X-factor model could be statistically distinguished from those produced by the same model without X-factors. The X-factor-free white model and the black X-factor model are depicted in Figures 2a and 2b, respectively. [14] Figure 2a. Model for white test scores. The squares represent different cognitive tests, while the ellipses are latent ability constructs that, except for g, are unspecified here but could represent verbal, fluid, and spatial abilities, and short-term memory, for example. Residual variances are not shown but are assumed to be uncorrelated. The letters a–g are selected factor loadings. Figure 2b. X-factor model for black test scores. Various X-factors, conceptualized as latent variables, influence test scores alongside ability constructs. Residual variances are not shown but are assumed to be uncorrelated. The letters a–i are selected factor loadings._________________________________________ The test for measurement invariance that could be performed on the simulated variances, covariances, and means produced by the white and black models would essentially be a test of whether it is statistically plausible that the black test scores that were actually produced by the X-factor model could as well have been produced by the white model. Assuming that the white model shows an adequate fit to the data generated by the X-factor model in a single-group confirmatory factor analysis (if it does not, the X-factors have already been detected and the analysis can end), we can proceed to a multiple-group analysis, in which the following four conditions are examined (Brown, 2006, pp. 269–270): 1) Equal form. Across the two groups, the number of latent factors must be the same, and the same tests must load on the same factors. This condition will necessarily be true if the white model fits the data produced by the X-factor model in a single-group analysis, but the equal form condition of the multiple-group analysis serves as a baseline model for the next step of the analysis. 2) Equal factor loadings. The loadings (or regression slopes) of the tests on the factors must be equal across groups, that is, a change in the level of a factor must be associated with similarly-sized changes in the levels of the associated tests in both groups. [15] 3) Equal intercepts. When the tests are regressed on their respective factors, the intercepts must be equal across groups. This guarantees that any differences in the means of the tests can be attributed to differences in the means of the factors. If the intercepts are unequal, it indicates that group differences in test means are not due to group differences in the underlying abilities. 4) Equal residuals. The magnitudes of the residual (unique) variances of the tests must be equal across groups. This ensures that any variance differences in the tests can be attributed to the latent factors. [16] The plausibility of these four conditions is tested by sequentially introducing additional cross-group equality constraints on the model and examining whether the fit of the model deteriorates. If all the relevant parameters can be constrained to be equal across groups without a significant deterioration in model fit (compared to if the parameters were freely estimated for both groups), then strict measurement invariance holds across groups. [17] Strict invariance indicates that test score differences between groups can be fully attributed to the same underlying abilities that cause differences within groups (Lubke et al., 2003). It is easy to see how Kaplan’s X-factors could violate measurement invariance. For example, in terms of factor loadings a–i shown in Figures 2a and 2b, the model-implied correlation between tests #4 and #5, calculated using path tracing rules, is abcd in the white model and abcd + hi in the black model. [18] Because the measurement invariance model assumes that the black data can be explained using the parameters of the white model, the only way to account for the increased correlation (i.e., the term hi) between tests #4 and #5 in blacks is to make one or more of the factor loadings a–d larger. This jeopardizes measurement invariance because equal loadings across groups is one of its requirements. Constraining the loadings to values between the optimal white and black ones may well lead only to a non-significant deterioration in model fit if just a few loadings are modestly affected. But as the X-factors introduce a large number of new dependencies between tests, many loadings will be affected, some strongly, making factor loading invariance difficult to achieve. Another example of how X-factors can violate measurement invariance concerns the invariance model’s assumption that group differences in the means of the tests can be explained by group differences in the means of the latent factors. This necessitates that test score gaps be collinear with factor loadings that are constrained to be equal across groups, that is, the size of group differences on different tests must be consistent with the size of the group-invariant factor loadings of those tests (Wicherts & Dolan, 2010). For example, the size of the black-white gaps on tests #5, #6, #7, and #8 in Figures 2a and 2b must be fully predictable from the size of the factor loadings d, e, f, and g. This is tested by constraining the intercepts of the tests to be equal across groups, and examining whether the requirement to reproduce the mean differences in the tests from factor means leads to a deterioration in model fit compared to a model without this constraint. From Figure 2b it is apparent that multiple X-factors exert negative influences on the means of the tests in blacks in a way that is completely unrelated to the loadings of the tests on the ability factors. Therefore, X-factors tend to change the pattern of black-white gaps on different tests so that the gaps are no longer predictable from ability factor loadings, leading to non-invariant intercepts across groups. If the tests for measurement invariance showed (across many iterations) that the black and white models of intelligence produce significantly different variance-covariance matrices and mean structures, this would indicate that the invariance tests successfully detect the existence of X-factors. If, on the other hand, there were no significant differences between the black and white matrices and mean structures, we would conclude that the method is not sensitive enough to detect X-factors. Unfortunately, Kaplan’s model is psychometrically very underdeveloped, providing no information on how his X-factors would influence performance on different kinds of tests. Why is the black-white gap greatly attenuated on tests of short-term memory and perceptual speed, while it is particularly large on tests of general knowledge and abstract reasoning? Kaplan provides no explanation. Jensen explained such findings by reference to the varying g-loadings of cognitive tests, showing that controlling for the influence of g eliminates the vast majority of cognitive differences between the two races. [19] Given the lack of information on how Kaplan’s X-factors would influence different tests, it is not currently possible to analyze if they could be detected using the procedure just described. It has been repeatedly shown that black-white differences on IQ test batteries satisfy the requirements of measurement invariance (Dolan, 2000; Dolan & Hamaker, 2001; Lubke et al., 2003; Trundt, 2013). This indicates that the same latent abilities that explain test score differences within each race also explain the observed interracial IQ gap. The fact that statistical signals of race-specific X-factors are not empirically observed in the literature on IQ measurement invariance strongly suggests that Kaplan’s model is a non-starter. He could, of course, aver that his X-factors are so subtle that they would not violate measurement invariance, but he has not tested this claim and it cannot presently be tested given the sketchy nature of his model. 5.2.2. Stereotype threat However, we can get a good idea of whether a properly specified X-factor model would pass a test of measurement invariance by examining whether environmental factors known to influence test scores pass this test. In particular, Kaplan identifies stereotype threat (Steele & Aronson, 1995) as an influence analogous to his X-factors. Wicherts et al. (2005) found that the presence of experimentally induced stereotype threat led to measurement non-invariance between the experimental and control groups. The non-invariance was easy to detect in a multiple-group confirmatory factor analysis even when sample sizes were modest (N<100). As Sackett et al. (2004) point out, when stereotype threat was absent in the control condition of Steele and Aronson’s study, the IQs of the black and white college students participating in the experiment were what one would have expected them to be on the basis of their prior SAT scores. This indicates that rather than causing the black-white IQ gap, stereotype threat widens a pre-existing gap that is persistently observed regardless of social context. Stereotype threat appears to be no more than yet another curiosity of the psychological laboratory without real-world implications (Lee, 2009). Given the assumed similarity of stereotype threat and Kaplan’s X-factors, we would expect the latter to cause measurement non-invariance, too, something that has not been observed in analyses of white and black test scores in non-experimental settings. This strongly suggests that Kaplan’s X-factors are non-existent. 5.2.3. Flynn effect Kaplan believes that the Flynn effect presents another environmental influence supporting his thesis. He claims that there is “no evidence of an increase in overall variance, nor in the association with other variables, associated with the increase in IQ scores within particularly populations over time.” It is true that the Flynn effect is not associated with increased test score variances, underlining the inadequacy of Kaplan’s variance difference tests as a way to discover environmental influences. However, it is not true that more appropriate methods fail to detect the Flynn effect. When tests of measurement invariance, described above, and analogous differential item functioning tests have been applied to IQ data from different age cohorts, it has consistently been found that measurement invariance between cohorts is untenable (Wicherts et al., 2004; Beaujean & Osterlind, 2008; Must et al., 2009; Wai & Putallaz, 2011; Shiu et al., 2013; Pietschnig et al., 2013; Fox & Mitchum, 2013, 2014; Beaujean & Sheng, 2014). As Wicherts et al. (2004) point out, the fact that black-white IQ differences are associated with measurement invariance while the Flynn effect is not indicates that the two phenomena are separate, and that one of them does not tell us anything about the other. Consistently with this finding, Ang et al. (2010) found that the magnitude of the Flynn effect does not differ between races. The environmental improvements underlying the Flynn effect have reached blacks and whites equally, suggesting that the environmental factors influencing cognitive development are highly similar in the two races. Contrary to what Kaplan believes, the Flynn effect is easy to identify with standard psychometric methods and ordinary sample sizes. If he wants to maintain that his racial X-factors would not be detectable with the same methods, he must modify his thesis and argue that the influence of his X-factors is uniquely subtle and completely different in character from known environmental influences such as the Flynn effect. 5.2.4. Rowe and colleagues’ findings One of the principal targets of Kaplan’s article are two studies by David Rowe and colleagues (1994, 1995). These studies investigated variance-covariance and correlation matrices of “environmental” influences (e.g., quality of child’s home environment, mother’s education, and parents’ school involvement) and outcome variables (e.g., IQ, self-esteem, and delinquency) across different races and ethnic groups. This study design where the equality of matrices is directly compared represents a model-free analogue to the model-based analyses of measurement invariance discussed above (although mean vectors were not examined by Rowe et al.). While the model-based analyses examine the statistical structure of individual differences in IQ test performance, Rowe and colleagues extended the same logic to an analysis of a wide range of variables beyond tests. Both methods rely on the insight that the effects of X-factors will not be limited to a specific variable, but rather will ramify across a whole network of related variables, reorganizing their mutual relations in a way that can be detected with statistical techniques. X-factors are expected to cause differences especially in the covariances (or correlations) of observed variables across groups. Kaplan’s model assumes that “racialized environments” simultaneously reduce IQ and make the environmental circumstances of blacks worse, which should show up as increases in the covariances between IQ and measured environmental factors. Similarly, one would expect Kaplan’s X-factors, if they exist, to negatively influence not only the IQs of black children, but also their self-esteem and aspirations, increasing the associations between these variables. In contrast, there is no way to say if the variance of IQ scores, which is the only statistic that Kaplan is interested in, should be lower, the same, or higher in blacks due to the influence of X-factors, given that we do not know what the variance would be without the putative influence of the X-factors. Rowe and colleagues found the many matrices of environmental and outcome variables that they analyzed to be statistically indistinguishable across groups. Therefore, there appear to be no group-specific sources of developmental differences, or X-factors. This corroborates the consistent finding of measurement invariance between races in confirmatory factor analyses of IQ batteries. Group differences in the mean level of IQ can be attributed to differences in developmental antecedents that are common to all groups. Therefore, black individuals tend to have low IQ scores for the very same reasons that (a smaller proportion of) white individuals have low IQ scores. These reasons plausibly include genetic differences, but if group differences are to be explained in completely non-genetic terms, then the causes must be VE-type factors: the IQ-decreasing environments experienced by most blacks have to be similar to those experienced only by disadvantaged whites. However, as discussed above, the available empirical evidence argues strongly against the existence of such VE-factors. The task of the non-hereditarian is further complicated by the fact that genetic and environmental factors show differential associations with different cognitive ability parameters, and black IQ deficits closely resemble genetic influences in this respect. 5.3. Can X-factors influence g? The prospect of Kaplan’s X-factors not being detected in an analysis of measurement invariance is very poor. This is because they present an influence on test scores that is orthogonal to the influence exerted by latent factors, whereas black-white cognitive differences can in fact be attributed to latent factors. In particular, black-white differences on cognitive tests are positively correlated with the g loadings of the tests, and can be mostly explained by a racial difference in the mean level of g. Kaplan’s model cannot account for the observed pattern of g-linked differences. However, there is a theoretical possibility of X-factors causing g-linked black-white gaps and not violating measurement invariance. That would happen if the X-factors directly influenced g, with their effect on observed test scores fully mediated by latent abilities. This would ensure that the X-factor-induced racial gaps could be attributed to the latent abilities (i.e., measurement invariance), and that the gaps would be correlated with g loadings (because X-factors would explain some of the variance in g). A model like this is depicted in Figure 3. Figure 3. A model where X-factors influence g directly and test scores indirectly. Residual variances are not shown._____________________________________ Is it plausible that X-factors would exclusively and directly influence g? As discussed earlier, it has consistently been found that environmental influences on test performance are negatively or not at all associated with g loadings, whereas genetic influences are associated strongly and positively with g loadings. Unless the nature of the racial X-factors is completely unique in the domain of environmental influences, they would not cause g-linked gaps. Furthermore, as we have seen, the environmental factors that Kaplan offers as analogues to his X-factors do not cause test score gaps that can be attributed to latent abilities—this is true of both the stable, trait-like gaps associated with the Flynn effect, and the ephemeral, state-like gaps associated with stereotype threat. While g is overwhelmingly a genetic phenomenon, there are nevertheless some non-genetic influences on it. For example, Panizzon et al. (2014) found that in a large sample of middle-aged male twins the heritability of the latent g factor was 86 percent, with 14 percent accounted for by the non-shared environment. Could X-factors be included in that 14 percent? As discussed above, no environmental factors directly affecting g have been identified, suggesting that environmental influences on g may not have anything to do with aspects of the social environment but rather that they may consist of random, noise-like influences affecting individual development regardless of external circumstances (Kan et al., 2010). Kaplan posits that there is a large number of environmental X-factors, many of them affecting only certain subgroups of blacks, so to assume that all these X-factors would have the same, laser-like focus on g, completely unlike how all known environmental factors influence test scores, makes this model so implausible as to leave it devoid of interest. 6. Non-cognitive differences between blacks and whites Kaplan’s model of the IQ gap presupposes that the daily lives of African Americans are saturated with racially motivated insults and humiliations that inflict serious psychological trauma on them. The nature of these negative experiences is such that one would expect them to have their most direct and most profound effects on non-cognitive rather than cognitive characteristics. If Kaplan had presented his model as an explanation of racial differences in the prevalence of some psychiatric disorder rather than in the mean level of IQ, it would have had some prior plausibility, given the well-established link between stressful life events and mental disorders (e.g., Hammen, 2005). “Racialized environments” would be expected to discourage blacks in their pursuits, lower their self-esteem, and lead to a high prevalence of mood disorders such as depression and social phobia among them. It is difficult to imagine why the emotional well-being, motivation, and self-concept of blacks would not suffer from the same experiences that supposedly greatly harm their cognitive abilities. Therefore, one would expect that if Kaplan’s model were correct, measures of relevant non-cognitive characteristics would show even larger white-black gaps than the ones seen on tests of cognitive ability. Table 1 lists variables related to emotional well-being, self-confidence, and optimism, broadly construed, with the gaps between whites and blacks on these variables reported in terms of Cohen’s d. The data are from various meta-analyses and large, nationally representative studies, as indicated in the table. They are coded in such a way that a positive (>0.00) gap always indicates that, on the average, blacks are better off on the particular variable than whites, while a negative (<0.00) gap indicates that whites are, on the average, better off. For example, the self-esteem gap of +0.19 means that blacks tend to have higher self-esteem, and the panic disorder gap of +0.28 means that the disorder is more common in whites, while the bipolar disorder gap of –0.10 indicates that this disorder is more common in blacks. For comparative purposes, the black-white IQ gap is also presented in the table. ___________ Two things are immediately evident from Table 1. Firstly, there are no racial differences in the non-cognitive variables that could be characterized as large or even medium-sized in terms of Cohen’s (1988) taxonomy of effect sizes. The differences are small to very small, providing a stark contrast to the IQ gap which stands at d = –1.10, representing a very large effect. Secondly, blacks appear to suffer from many psychiatric disorders somewhat less frequently than whites, and they generally have at least as optimistic and confident an outlook on life as whites. Several objections can be presented against these results. It is possible that due to lack of access to health care, blacks are underdiagnosed with respect to the disorders examined here. Similarly, the self-report measures used could reflect a greater tendency towards socially desirable responding in blacks, and black suicides may remain unidentified more often than white ones. However, the reported gaps generally favor blacks, and if the true effect sizes really had the opposite sign and were large, the bias in the measures used would have to be implausibly pervasive. For example, if the real gap in social phobia, obscured by underdiagnosis, were –1.10 (favoring whites), instead of the actually observed gap of 0.12 (favoring blacks), it would mean that the real lifetime prevalence of the disorder is more than 50 percent in blacks, compared to the observed prevalence of 10.8 percent, assuming that there is no underdiagnosis at all in whites whose observed lifetime prevalence is 12.6 percent. We can safely conclude that the basic pattern of results shown in Table 1 does not stem from measurement bias. Another objection might be that the levels of emotional well-being and self-esteem in blacks as compared to whites could be inherently higher (for genetic or cultural reasons), so that even very traumatic experiences would not altogether eliminate the black advantage. However, this explanation is entirely ad hoc and without evidentiary basis, and it is contrary to the tenor of Kaplan’s argument (so he would probably not endorse it). [20] An even less promising conjecture to explain the results in Table 1 is that racism has beneficial effects on blacks, making them strive more to prove themselves and providing protection against mental ailments, while simultaneously causing large cognitive and academic deficits in them. All in all, these results present a strong disconfirmation of Kaplan’s model, corroborating the psychometric evidence against the model presented in previous sections. The personal characteristics that one would expect to be most directly and potently affected by the kind of chronically racially biased society that Kaplan describes are in fact generally not affected at all. On the contrary, the data show African Americans to be at least as well-adjusted as whites. Black Americans appear to possess a great deal of confidence in their abilities and a very optimistic attitude to life, as exemplified by the fact that the educational and occupational aspirations of black adolescents and young adults are virtually identical to those of their white peers, in spite of the large white advantage in academic performance. [21] Kaplan’s portrayal of black Americans as psychologically traumatized victims of a racist society is bluntly contradicted by these findings. 7. How to test HM Kaplan argues that HM is not a testable scientific proposition. This claim is mistaken. As previously noted by Rowe (2005), Murray (2005), Rushton & Jensen (2005, p. 262), and Lee (2009), among others, one of the appealing features of HM is that there exists an experimentum crucis whose outcome could settle the issue once and for all. This natural experiment is fully feasible using current technology. The study design would exploit the fact that African Americans are an admixed population with a major West African and a smaller European element, while white Americans are almost exclusively descended from European immigrants (Lao et al., 2010). On the average, the ancestry of black Americans is approximately 80 percent African and 20 percent European, but, crucially, these percentages vary considerably across individuals—the standard deviation is about 12 percentage points (Bhatia et al., 2013). Modern genomic methods using ancestrally informative markers enable the accurate partition of an individual’s ancestry into African, European, and other ancestral components (Kosoy et al., 2009). Because genetic influence on IQ mostly reflects the additive effects of up to thousands of genes (Davies et al., 2011), HM predicts that there is a strongly positive and linear relation between IQ and the extent of white ancestry in African Americans. In other words, a greater amount of white admixture is assumed to bring with it a more advantageous mix of alleles influencing IQ. Therefore, one only needs to recruit a large, representative sample of black Americans and obtain from each of them a valid IQ score and a DNA-based estimate of European admixture. If HM is correct, there should be a strong correlation between white ancestry and IQ. To ensure that any possible association is not driven by correlations between ancestry and physical appearance, appropriate covariates (e.g., skin color) can be used in the analysis. The most direct and powerful way of ruling out the influence of confounding variables would be to use a sibling fixed effects design where IQ and ancestry are investigated within sibling pairs. This admixture design has been frequently used in biomedical research. The degree of African ancestry has been found to be associated with, for example, preterm birth (Tsai et al., 2011), osteoporosis (Chen et al., 2011), body mass index (Nassir et al., 2012), diabetes (Cheng et al., 2012), asthma (Flores et al., 2012), and hypertension (Kosoy et al., 2012). Of greater interest to the present discussion is the finding that African ancestry is negatively correlated with educational and occupational attainment and family income in black Americans (Cheng et al., 2012, Table S2). This finding greatly complicates theories that attribute the black-white IQ gap to social class differences. The feasibility of admixture analysis means, at the very least, that HM is falsifiable. If no correlation between IQ and ancestry were found in African Americans, HM would have to be rejected, and a redoubled effort at identifying environmental causes of racial differences could commence. In contrast, if white ancestry were found to be strongly associated with greater IQ, it would provide very powerful evidence in favor of HM, but I would expect that many committed anti-hereditarians would still not accept HM. Even so, a high correlation between ancestry and IQ would necessarily greatly constrain many proposed models of environmental causation. For example, Kaplan’s theory of racialized environments would have to be modified to accommodate the notion that the effects of racism on IQ are heavily moderated by largely cryptic differences in ancestry. Considering that few black Americans have knowledge of their precise ancestry, it would be very challenging to explain high IQ-ancestry correlations in purely social terms. Thus, contrary to Kaplan’s claim that “given the actual state of the world there is no way to generate any reasonably strong evidence in favor of the hereditarian hypothesis”, HM is an eminently testable scientific model. In contrast, the non-hereditarian explanation of the black-white IQ gap is essentially unfalsifiable because even in the face of overwhelming evidence in favor of HM, it is always possible to postulate that some exotic and imperceptible environmental influence is to blame for the gap. [22] 8. Discussion James Flynn has criticized researchers for assuming that racism is a magical ambient force rather than one whose possible effects are manifested through such ordinary mechanisms as poverty and poor self-esteem. Kaplan rejects this argument. Indeed, Kaplan’s racial X-factors resemble nothing so much as magic. He presents no evidence for the hypothesis that what he calls racialized environments have an effect on IQ, and his evidence for the very existence of these environments is very weak. Nevertheless, his model presupposes that such environments, no matter how heterogeneous, act like magic bullets, causing large, g-linked cognitive deficits in blacks from all backgrounds while miraculously bypassing all the brain systems that mediate emotional and motivational processes. Furthermore, the racial X-factors do all this in such a subtle way that no statistical signals of their presence can ever be observed, making racism a causal force completely unlike all known environmental influences on IQ scores. The essentially occult powers that Kaplan attributes to white racism take his arguments beyond the bounds of science. A fundamental flaw in Kaplan’s thesis is that of the many lines of evidence presented by hereditarians, he considers only one, Jensen’s binary of VE-factors and X-factors. Thinking that he has refuted this particular argument, Kaplan concludes that HM as a whole is untenable. However, HM consists of a large body of interlocking theoretical arguments and pieces of empirical evidence (not all of which have been explicitly considered in this article) which should not be investigated in isolation from each other. Postulating X-factors to explain the IQ gap is an empty exercise unless one shows that such factors fit the totality of evidence. Because Kaplan fails to consider all the relevant facts, his X-factor model could be correct only if a long list of assumptions that he leaves unstated and unexplored were correct. When those assumptions are spelled out, the model’s fatal flaws come into view. The fact that Kaplan’s proposed X-factors turn out to be very elusive upon closer inspection attests to the wisdom of Jensen’s argument about the non-existence of X-factors in general. Considering that Kaplan is an associate professor of philosophy, another lesson that might be drawn from his very confidently presented yet completely unsuccessful challenge to HM is that a philosophical education alone is without value in a scientific dispute. A good command of the theories, methods, and evidence pertinent to the particular area of research is necessary for making useful scientific contributions. Kaplan attacks HM on rather general grounds and appears to be largely ignorant of the extensive network of evidence that makes HM such a compelling model. In particular, the psychometric aspects of Kaplan’s model are so underdeveloped that it cannot be properly tested by simulation, but he nevertheless thinks that his simulations provide strong evidence against HM. If a properly elaborated version of Kaplan’s simulation model were put to test in a multiple-group confirmatory factor analysis framework, the chances of his X-factors going undetected would be very small. Kaplan is also oblivious to the fact that, perhaps uniquely among all the long-running disputes in social science, a definitive empirical resolution to the black-white IQ controversy is within the reach of contemporary science. The strong causal implications of DNA-based admixture studies have been frequently discussed in the literature, and the ability gap between blacks and whites is widely recognized as one of the most significant social problems in America (Jencks & Phillips, 1998; Paige & Witty, 2010; Giles, 2011). That there nevertheless has been no rush to use genomic methods to clarify the etiology of the gap testifies to the taboo nature of the hereditarian model. 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Q: call functions on events NodeJs actually i'm trying to call the function demandConnexion after an event, but it is working for me , it telles me that "this.demandeConnexion is not a function" . how can i get it to work ? help , this is the code : Serveur.prototype.demandConnexion = function(idZEP) { if (this.ZP.createZE(idZEP)) { console.log(' ==> socket : demande de creation ZE pour '+idZEP +' accepte'); } else { console.log(' ==> socket : demande de creation ZE pour '+idZEP +' refuse'); } }; Serveur.prototype.traitementSurConnection = function(socket) { // console.log('connexion'); console.log(' ==> socket connexion'); // traitement de l'evenement DEMANDE DE CONNEXION D'UNE ZE socket.on('connection', (function(idZEP) { this.demandConnexion(idZEP) console.log('good') })) A: It's because when the callback is called "this" isn't your "Serveur" instance. In your case try something like var that = this; socket.on('connection', (function(idZEP) { that.demandConnexion(idZEP) console.log('good') })) or socket.on('connection', this.demandConnexion.bind(this)); An other solution (the best in my opinion) would be to use the arrow functions to keep the same scope as the closure socket.on('connection', ()=>{ //here this refers to your Serveur (the enclosing scope) });	{ "pile_set_name": "StackExchange" }
Q: Tab-completion of shell patterns On my Debian servers I'm used to hitting Tab to "preview" the expansion of shell patterns: $ cp some<Tab> something somewhat have-some-cake $ cp some_ When the pattern expands to one entry, Tab replaces the pattern with the actual entry; otherwise it shows a list of matching entries. This is intuitive and useful because it's consistent with the regular "prefix" Tab completion. But my Ubuntu servers and desktops behave differently: even when it would expand to more than one entry, Tab replaces the pattern with the first entry. I have checked the usual suspects (/etc/bash.bashrc, /etc/inputrc, and the local versions) and I couldn't find any difference. Does anybody know which setting controls this behaviour? A: Contrary the other answer, this particular problem is probably a direct result of using bash-completion. The bash-completion package has several bugs (as noted in this U&L answer about a similar problem, for instance). If I comment out this section in my .bashrc: # enable programmable completion features (you don't need to enable # this, if it's already enabled in /etc/bash.bashrc and /etc/profile # sources /etc/bash.bashrc). if ! shopt -oq posix; then if [ -f /usr/share/bash-completion/bash_completion ]; then . /usr/share/bash-completion/bash_completion elif [ -f /etc/bash_completion ]; then . /etc/bash_completion fi fi and start a new instance of bash, then I get: $ echo o<tab><tab> foo food foo.sh $ echo o And then if I source the /usr/share/bash-completion/bash_completion script like it was in the .bashrc: $ . /usr/share/bash-completion/bash_completion $ echo foo The o was immediately autocompleted to foo without showing the other matches. I'm using 16.04, by the way. I don't know if this has been fixed in newer releases. $ dpkg-query --show --showformat='${Package} ${version}\n' bash bash-completion bash 4.3-14ubuntu1.2 bash-completion 1:2.1-4.2ubuntu1.1	{ "pile_set_name": "StackExchange" }
1. Introduction =============== Mucosal melanomas are a rare clinical entity, in the literature the incidence is described with 1% to 2% of all melanomas and 2 to 2.6 per 1,000,000 persons/year.^\[[@R1]--[@R3]\]^ Melanomas arising from mucosal surfaces have a different profile of risk factors (eg, no exposure to ultraviolet radiation) and other genetic mutations than cutaneous melanomas, especially KIT-mutations are more frequent in mucosal melanomas.^\[[@R4]\]^ Mucosal melanomas have a poor prognosis which is much worse than that of cutaneous melanomas.^\[[@R1]\]^ It remains uncertain whether the poorer prognosis is due to the usually more progressed disease at initial diagnosis or to the biologically more aggressive growth. Prognostic factors are not well established thus far.^\[[@R5]\]^ Therefore, we have retrospectively analyzed 75 patients with mucosal melanomas at different locations of the primary tumor in regard to their prognostic factors. Furthermore, we summarized our experiences using new immunologic and targeted therapies. 2. Patients und methods ======================= 2.1. Patients ------------- Patients of our Department including the years 1993 to 2015 with primary mucosal melanomas were recorded in a database, their history was regularly updated. The patients were divided in 3 groups in regard to the location of the primary tumor: head/neck, anorectal, and female genital tract (FGT). Since the American Joint Committee on Cancer-classification^\[[@R6]\]^ for cutaneous melanoma is not established for mucosal melanoma, we implemented 3 groups for a clinical tumor grading according to the Mucosal Melanoma Staging System published by Iversen and Robins^\[[@R7]\]^ in 1980 and proposed by Thoelke et al: I -- local tumor, II -- regional lymph node metastasis, and III -- distant metastasis.^\[[@R8],[@R9]\]^ The follow-up, adjuvant and palliative therapy, was done according to the recommendations for patients with cutaneous melanomas.^\[[@R10]\]^ One patient with a KIT Exon 11 L576P Mutation was treated with imatinib, this case has already been published as a case report.^\[[@R11]\]^ The median follow-up time was 32 months, with a minimum of 2 and a maximum of 231 months. Mutation analysis was performed partly in the context of scientific research,^\[[@R12]\]^ others within clinical trials and routine clinical treatment. Sixty-two patients were screened for KIT and 57 patients for BRAF-mutations by various methods: Sanger sequencing for the KIT-gene and on 5 patients for the BRAF-gene, further analysis of the BRAF-gene was performed via melting curve analysis for 29 and pyrosequencing for 23 patients. The ethics committee of the Hannover Medical School provided IRB approval for the retrospective data collection of melanoma patients (vote no. 1612--2012). 2.2. Statistical analysis ------------------------- The Programs Statistica 8 (Statsoft), GraphPad Prism version 5.01 for Windows, GraphPad Software, and EpiInfo 3.5.3 (Centers for Disease Control and Prevention) were used for the statistical analysis. The evaluation included the usual descriptive statistics (mean, median, and percentages) and survival analysis with the Kaplan--Meier estimate. The Log-Rank-test was used for the calculation of significance for the overall and relapse-free survival between the groups. The influence of various prognostic factors was tested on the basis of the Cox proportional hazard model. The initial group comparison (Table [1](#T1){ref-type="table"}) for nominal data was done with the Chi-square test or Fisher exact test, respectively, for the comparison of multiple groups with ordinal or metric data by use of the Kruskal--Wallis test. A P-value \< 0.05 was considered significant. ###### Characterization of the patients in regard to localization. ![](medi-96-e5753-g001) 3. Results ========== 3.1. Clinical parameters ------------------------ We identified 75 patients with mucosal melanomas, 32 melanomas were localized in the head/neck area, 24 melanomas were situated in the FGT, and 19 melanomas were diagnosed in the anorectal region, respectively (Table [1](#T1){ref-type="table"}). The median age at the time of 1st diagnosis was 66 years, with 57% female and 43% male patients. The overall higher percentage of females is due to patients with a melanoma in the FGT, tumors in the head/neck region occurred more often in males, whereas anorectal melanomas were evenly distributed between females and males (Table [1](#T1){ref-type="table"}). After initial diagnosis the total excision of the mucosal melanoma could be achieved in 64/75 patients (85%). Total lymphadenectomy of the regional lymph nodes was performed in 43/75 patients (57%), 20 of which had metastasis at time of initial diagnosis, 8 following a positive sentinel lymph node (SLN), and 15 as an elective procedure (Table [1](#T1){ref-type="table"}). A total of 34/75 patients received an adjuvant therapy. Adjuvant radiotherapy was applied in 20 patients, 17 of them with the primary tumor in the head/neck region, 2 with anorectal, and 1 with FGT tumors. Adjuvant interferon alpha with a dosage of 3 × 3 million units per week for 24 month was administered to 21 patients, 5 of them also had succeeding adjuvant radiotherapy. 3.2. Prognosis -------------- A recurrence of the disease was recorded in 48/61 (79%) of the patients where an initial complete excision had been realized. The median time until the 1st recurrence was 14 month (Table [1](#T1){ref-type="table"}). An initial local recurrence or in transit metastasis was recorded in 18/48 patients, regional lymph node metastasis in 8/48 patients, and distant metastasis in 22/48 patients. During follow-up 48/75 (64%) patients died of the melanoma, 1/75 (1.3%) patients of others causes. The median overall survival through all groups was 32 months (Table [1](#T1){ref-type="table"}). 3.3. Prognostic factors in the univariate analysis for the overall and recurrence-free survival ----------------------------------------------------------------------------------------------- The 5-year survival rate was 26.3%, 22.0% in the head/neck group, 10.6% anorectal, and 33.2% in the FGT group. Patients with the melanoma in the head/neck region and anorectal region displayed a significant worse overall survival than patients with melanomas in the FGT (P = 0.04, Table [2](#T2){ref-type="table"}, Fig. [1](#F1){ref-type="fig"}B). ###### Univariate analysis of the prognostic factors (log rank test). ![](medi-96-e5753-g002) ![Kaplan--Meier analysis of survival in regard to the location of the tumor (A and B), tumor grade at time of 1st diagnosis (C and D), age (E), and different time frames (F).](medi-96-e5753-g003){#F1} The probability for recurrence-free survival after 5 years was 13.8% overall 3 groups, 8.1% with mucosal melanoma in the head/neck region, and 23.8% in the FGT, a 5-year follow-up period was not reached for anorectal tumors (Fig. [1](#F1){ref-type="fig"}A). Again a significant advantage could be demonstrated for the group with melanomas in the FGT for the recurrence-free survival versus the patients with anorectal and head/neck tumors (P = 0.03, Table [2](#T2){ref-type="table"}). For patients under 60 years of age at the time of 1st diagnosis we saw a trend for an advantage in overall and recurrence-free survival (P = 0.06, Table [2](#T2){ref-type="table"}, Fig. [1](#F1){ref-type="fig"}E). Patients in disease stage I at the time of 1st diagnosis had significant advantage in terms of overall survival (P = 0.04, Fig. [1](#F1){ref-type="fig"}D, Table [2](#T2){ref-type="table"}) and a highly significant for the recurrence-free survival (P \< 0.001, Table [2](#T2){ref-type="table"}) in comparison with patients with stages II and III at the time of the initial diagnosis. In regard to gender no significance for overall and recurrence-free survival could be demonstrated. Because of the long period of observation we divided the patients in 3 groups, 1993 to 2005, 2006 to 2009, and 2010 to 2015, the comparison showed no significant difference between the groups for recurrence-free survival and overall survival (Fig. [1](#F1){ref-type="fig"}F). In the group of head/neck mucosal melanomas, in which the major part of the adjuvant radiation took place, a significant advantage (P = 0.02) toward the prevention of local recurrences was shown (Fig. [2](#F2){ref-type="fig"}). ![Impact of adjuvant radiation on the way of metastazation for 30 patients with mucosal melanoma in the head/neck region. (2 Patients with severe distant metastazation at the time of the initial diagnosis were not included).](medi-96-e5753-g004){#F2} As expected the multivariate analysis (Table [3](#T3){ref-type="table"}) showed a high statistical significance for the tumor-stage at time of the initial diagnosis in terms of recurrence-free survival (P \< 0.001). Also age younger than 60 was correlated with a significant recurrence-free survival benefit (P = 0.03). In contrast the localization of the primary did not reach any independent prognostic significance. ###### Multivariate analysis of the prognostic factors (Cox proportional hazard). ![](medi-96-e5753-g005) 3.4. KIT/BRAF mutations ----------------------- A molecular analysis of the KIT-gene was performed in 62 of the patients studied. A total of 7/62 (11.3%) of the patients had a KIT mutation, 5 in exon 11 (once each 579del, K550N, W557R, twice L576P), 1 in exon 13 (K642E), and 1 in exon 18 of the KIT-gene (I841V). The analysis for 36 patients was done in our own laboratory (exons 9, 11, 13, 17, and 18), 6 of them showed a KIT-mutation. These results were already described in detail.^\[[@R12]\]^ Within the TEAM-study (Tasigna Efficacy in Advanced Melanoma) the KIT-exons 9, 11, 13, and 17 were analyzed in 6 further patients, all 6 patients did not show a mutation. Another 20 analyses were done during routine diagnostics employing Sanger-Sequencing of the exons 9, 11, and 13, which revealed a K642E-mutation in 1 patient. In regard to localization of the primary tumor KIT-mutations were shown in 2/27 (7.4%) patients in the head/neck region, 2/16 (12.5%) anorectal, and 3/19 (15.8%) in the FGT. A BRAF V600E Mutation was demonstrated in 2/57 (3.5%) of the patients, one each in the anorectal and head/neck-group. 3.5. Targeted therapy and therapy with checkpoint inhibitors ------------------------------------------------------------ Four patients were treated with targeted therapies, patients 1 to 3 with imatinib due to a KIT-mutation in exon 11 or 13. Patient 1 achieved a short-term partial remission (PR), patient 2 a short-term stable disease (SD) (Table [4](#T4){ref-type="table"}). ###### Therapy with targeted therapies and checkpoint inhibitors. ![](medi-96-e5753-g006) Patient 4 (Table [4](#T4){ref-type="table"}) is a male patient with a metastasized anorectal melanoma harboring a BRAF mutation. Therapy with ipilimumab yielded in a PR for 6 month, subsequent vemurafenib-therapy resulted in a PR for another 5 month. Reexposition first with ipilimumab then with vemurafenib did not lead to any further tumor control. Besides these patients 6 other patients were treated with ipilimumab (Table [4](#T4){ref-type="table"}), one of those had an SD for 4.5 months. Seven patients received programmed disease-1 (PD-1)-checkpoint inhibitors (Table [4](#T4){ref-type="table"}), in 2 patients a PR lasting 366+ and 240+ days was achieved. 4. Discussion ============= Mucosal melanoma is disease of advanced age, among our patients the median age over all 3 groups was 66 years corresponding well to the spectrum described in the literature ranging from 60 to 75 years.^\[[@R8],[@R13]--[@R17]\]^ The gender distribution with 57% female patients was consistent with other observations and can be explained by the patients with melanoma in the FGT.^\[[@R15],[@R18]\]^ As described in the literature male patients suffered more often (69%) from mucosal melanomas in the head/neck region.^\[[@R16]\]^ Anorectal melanomas showed a fairly balanced gender distribution with 53% male patients in our study in contrast to the literature where mostly a higher ratio of male patients is described.^\[[@R16],[@R19]\]^ An SLN biopsy is particularly possible if lymph drainage into peripheral lymph stations is expected, for example, distal the linea dentata for anal melanomas^\[[@R20]\]^ or vulvar melanomas in the FGT.^\[[@R21]\]^ In individual cases SLN biopsy is described even for mucosal melanomas in the head/neck region.^\[[@R19]\]^ Contrary to cutaneous melanomas the SLN is not established as a prognostic factor in mucosal melanoma. For having a poor prognosis in respect of distant metastasis a complete regional lymph node dissection following a positive SLN is discussed controversially.^\[[@R20],[@R21]\]^ During follow-up 79% of the patients had a recurrence, especially mucosal melanomas in the head/neck region demonstrated a short recurrence-free survival time with a median of 10 months. In our study 64% of the patients died during follow-up, the 5-year survival rate was 26.3%, which is slightly lower than indicated in the literature with 5-year survival rates of 32.4%,^\[[@R22]\]^ 34%,^\[[@R15]\]^ and up to 55.8%.^\[[@R23]\]^ In line with expectations, the tumor-grade is an important prognostic factor as described in the literature.^\[[@R17],[@R22]\]^ In our study, the age with a threshold value of 60 years was an additional important prognostic factor. In the literature age is described as a prognostic factor for either mucosal melanomas^\[[@R14],[@R22]\]^ and skin melanomas.^\[[@R24]\]^ A better prognosis for tumors in the FGT became apparent in our univariate analysis but could not be confirmed in the multivariate analysis. Mehra et al^\[[@R23]\]^ could also show a better prognosis for vulvar melanomas in comparison to other localizations of the primary tumor. Local recurrence occurred notably in patients with the primary tumor in the head/neck region, which had not undergone adjuvant radiotherapy, among the adjuvant group the local tumor control was significantly better. Some studies already have shown that adjuvant radiation of mucosal melanomas in the head/neck region can reduce the risk of local recurrence from 33%--83% to 0%--56%.^\[[@R19]\]^ Another study could demonstrate that at least 54 Gray should be applied to have a positive effect.^\[[@R25]\]^ For KIT-mutations we could show a higher rate in mucosal melanomas in the FGT (15.8%) in comparison to the other 2 groups, head/neck (7.4%) and anorectal (12.5%). This is consistent with a recent publication that outlined the highest rate of KIT-mutations for vulvovaginal melanomas (35%) followed by anorectal melanomas (25%) and mucosal melanomas in the head/neck region (10%).^\[[@R26]\]^ In our patient collection, the treatment with imatinib showed 1 short-term SD and 1 short-term PR in 2 of 3 patients with KIT-mutations in exon 11 and 13, respectively (Table [4](#T4){ref-type="table"}). In the literature, several case series describe an objective response in 16% to 30% of the patients treated imatinib, the median time for recurrence-free survival was about 3 months, with major benefit for patients with mutations in exon 11 and 13.^\[[@R27]--[@R29]\]^ In a case series with 7 patients with mucosal melanomas and KIT-mutations in exon 11 or 13 sunitinib showed a response in 3 cases.^\[[@R30]\]^ A reason for the relative poor response to KIT-inhibitors could be a concurrent NRAS-mutation, which are described in patients with KIT-mutations.^\[[@R29]\]^ This results in activation of the pathway downstream of KIT, thus it is advisable to rule out NRAS-mutations before using a KIT-inhibitor. BRAF-mutations are described in mucosal melanoma. In our cohort 3.5% of the patients examined displayed a BRAF-mutation, in the literature the values differ from 3.6%,^\[[@R31]\]^ 6%^\[[@R32]\]^ up to 11.1%,^\[[@R33]\]^ and 16.5%.^\[[@R34]\]^ Little is published on the response of targeted therapies in BRAF positive patients with mucosal melanomas, the response in our patient suggests that this is possible. For the use of ipilimumab for the treatment of metastatic mucosal melanoma there are case studies mostly on pretreated patients. In a series of 30 patients (76% of which with the dosing of 3 mg/kg bodyweight, 24% with 10 mg per/kg) 1 patient responded with a complete remission, 1 patient with a PR, and 5 patients with an SD.^\[[@R35]\]^ In a series of 71 patients in the Italian "early access program" a response rate of 12.5% and a 36% rate of SD was observed.^\[[@R36]\]^ On the use of PD-1 inhibitors in mucosal melanomas there are individual case reports.^\[[@R37]--[@R39]\]^ A pooled analysis of mucosal melanomas in a variety of trials using nivolumab (n = 86), nivolumab plus ipilimumab (n = 35), or ipilimumab (n = 36) provided evidence for an effect of nivolumab in mucosal melanomas.^\[[@R40]\]^ The median progression-free survival and response rates were 2.96 months and 23.2% for nivolumab, 5.85 months and 37.2% for nivolumab plus ipilimumab, and 2.69 months and 8.3% for ipilimumab, respectively. This corresponds well with our data showing a long-lasting response in 2/7 patients treated with PD-1 inhibitors. 5. Conclusions ============== In our study, mucosal melanomas displayed a poor prognosis with metastasis often being already present at the time of initial diagnosis. We could confirm the recommendation for an adjuvant radiation of the primary tumor region on patients with head/neck mucosal melanomas in order to significantly lower the risk of local recurrence. In case of metastazation considered inoperable targeted therapies and immunotherapies with checkpoint inhibitors can be considered. PD-1 inhibitors or their combination with ipilimumab appear to show the highest response rates and longest progression-free survival. In case of a KIT mutation, additional analysis of NRAS is recommended before treating with a KIT-inhibitor. In the rare event of a BRAF V600 mutation, targeted therapy analogous to cutaneous melanomas is recommended. The limitations of this study are the small number of patients and the long period of patient acquisition, in particular the low number of patients with targeted and immunotherapy treatment. Therefore, no conclusions with regard to therapy standards can be achieved. Abbreviations: FGT = female genital tract, PD-1 = programmed disease-1, PR = partial remission, SD = stable disease, SLN = sentinel lymph node, SLNB = sentinel lymph node biopsy. The authors have no conflicts of interest to disclose.	{ "pile_set_name": "PubMed Central" }
Gaetano Pizza & Calzone At Gaetano Pizza & Calzone, we have got your food urges covered with delicious pizzas and calzones. We make tasty and specially made pizzas that are order able by the slice or whole. Also, grab a bite of our savory calzones. Order online for carryout today! You can find us on Independent Way and NY-312 just off of I-84 and a few minutes from Brewster Hill.	{ "pile_set_name": "Pile-CC" }
436 F.Supp. 234 (1977) In re Samuel J. FRIEDMAN, Receiver for Gilbert Steinhorn and Joyce Steinhorn, Bankrupts. SUPERIOR METAL MOULDING COMPANY, INC. v. Bernard and Elaine SHIPP. Civ. A. No. M-77-696. United States District Court, D. Maryland. August 1, 1977. 235 Michael J. Schwarz, Baltimore, Md., for appellant Superior Metal Moulding Co. Neil Warren Steinhorn, Baltimore, Md., for appellees Bernard & Elaine Shipp. MEMORANDUM JAMES R. MILLER, District Judge. This appeal under Bankruptcy Rule 810 raises a question of the quantum and quality of the evidence that the objector to a creditor's proof of claim must present in order to require the bankruptcy judge to weigh the evidence and make express findings of fact to support the allowance or disallowance of said claim. In this proceeding Elaine and Bernard Shipp, parents of the bankrupts, filed a proof of claim for $16,000 on an unsecured confessed judgment note dated April 30, 1975. Another unsecured creditor, Superior Metal Moulding Company, Inc., filed an objection to $11,000 of the claim, which it argued consisted, in actuality, of gifts made by the parents at important family milestones. At the hearing, before the bankruptcy judge, examination of the claimant, Mrs. Shipp, revealed that for many years prior to the eve of bankruptcy there had been no 236 note or other documentation for the $11,000, no agreement on interest, and no partial repayment. In addition, between the time of the inception of the alleged debt and the declaration of bankruptcy the bankrupts had submitted to bank loan departments three separate financial statements, none of which reported the $11,000 as a debt. Finally, the evidence disclosed that the transfers had been made at happy family times the grandson's bar mitzvah, the one room addition to the new house, and the opening of a new business. When the $11,000, which had allegedly been loaned to the bankrupts between 1965 and 1968, was finally made the subject, together with a $5,000 loan in 1974, of the $16,000 note on April 30, 1975, it was almost immediately reduced to judgment on May 28, 1975. A sheriff's return was filed showing service of the confessed judgment suit upon the bankrupts on June 4, 1975. On July 3, 1975, the bankrupts filed voluntary Petitions in Bankruptcy. Mrs. Shipp also testified, however, that repayment was expected by the parents, that repayment was promised by the children when business improved, that unpressured inquiries about repayment were made occasionally, and that the informal $11,000 "loans" were made prior to Mr. Shipp's retirement when the claimants were in a better financial position than now. From the evidence before the bankruptcy judge, conflicting inferences could be drawn, and different conclusions reached, depending largely upon the credibility of Mrs. Shipp. If the evidence had been weighed and a finding of fact made, the findings of the bankruptcy judge would be subject to change only if clearly erroneous. Bankruptcy Rule 810. From the record here, this court cannot ascertain whether such a finding was made. In his oral ruling, the bankruptcy judge said: "I don't think the evidence as produced here today is sufficient to overcome the presumption of the existence of a debt that arises by virtue of the filing of claim and the judgment and, therefore, the objection to the claim will be overruled." (Tr. 36) (Paper No. 69). The objector to the claim of the Shipps urges that the evidence presented by it was sufficient to compel the bankruptcy judge to make an express finding of fact on the validity of the debt and that excessive weight was given by the bankruptcy judge to the presumption created by a properly executed proof of claim. I Preliminarily, the objector urges that the proof of claim was not entitled to any evidentiary weight under Bankruptcy Rule 301(b) because it failed to state the consideration for the debt as required. See Bankruptcy Rule 301, Official Form 15; 3 Collier on Bankruptcy § 57.03[3.2] (1976 ed.). Although the proof of claim must present enough detail for the bankruptcy judge to make an informed decision, the objector's argument is mooted by the bankruptcy judge's decision to accept the claimant's oral testimony to compensate for the deficiencies. That decision was entirely within his discretion and is consistent with the expeditious administration of bankruptcy cases. In re Welborne, 266 F. 385, 386-387 (S.D.N.Y.1920); cf. Katchen v. Landy, 382 U.S. 323, 329, 86 S.Ct. 467, 15 L.Ed.2d 391 (1966); Gardner v. New Jersey, 329 U.S. 565, 573, 67 S.Ct. 467, 91 L.Ed. 504 (1947). Accordingly, for purposes of the appeal, this court will assume that the proof of claim was properly executed. II Bankruptcy Rule 301(b) provides that a "proof of claim executed and filed in accordance with these rules shall constitute prima facie evidence of the validity and amount of the claim."[1] 237 The term "prima facie evidence" or "prima facie case" has at least two separate, while related, meanings. On the one hand, it may mean evidence which is sufficient to shift the burden of producing evidence and which entitles the proponent to a favorable ruling if the opponent fails to produce evidence. The other meaning is that the proponent has produced enough evidence to go to the finder of fact and to permit a favorable ruling. See J. Wigmore, Evidence § 2494 (1940); McCormick on Evidence § 342, at 803 n.26 (Cleary ed. 1972). In bankruptcy, it is settled that a properly executed proof of claim is sufficient to shift the burden of producing evidence and to entitle the claimant to a share in the distribution of the bankrupt's estate unless an objector comes forward with evidence contradicting the claim. See Bankruptcy Act § 57(d), 11 U.S.C. § 93(d); Bankruptcy Rule 306(b)-(c); Whitney v. Dresser, 200 U.S. 532, 26 S.Ct. 316, 50 L.Ed. 584 (1906); 3 Collier on Bankruptcy § 57.14. While a properly executed claim does shift the burden of producing evidence to the objector, the burden of persuasion remains at all times with the claimant. See, e. g., Whitney v. Dresser, 200 U.S. at 535, 26 S.Ct. 316; In re Pringle Engineerings & Mfg., 164 F.2d 299 (6th Cir. 1947); In re Sabre Shipping Corp., 299 F.Supp. 97 (S.D.N.Y.1969). At no time does the objector assume the burden of disproving the claim. See 3 Collier § 57.18[5]. The nature and amount of evidence that must be presented by the objector has been described in two ways that diverge in expression and, at least here, in application. Under the first approach, the objector must present "some evidence" contradicting the proof of claim, whereupon the bankruptcy judge must weigh the evidence presented by the objector against the proof of claim, which itself retains some weight as evidence, e. g., Whitney v. Dresser, supra, and any evidence presented by the claimant. After weighing the evidence, the judge must make a finding of fact as to the validity and amount of the claim. See In re Hannevig, 10 F.2d 941, 942 (2d Cir. 1925) ("evidence contradicting [the proof of claim]"); In re Sabre Shipping Corp., 299 F.Supp. 97, 99 (S.D.N.Y.1969) ("contradictory evidence"); In re Bradley, 16 F.2d 301, 302 (S.D.N.Y.1926) ("some evidence contradicting it"); 3 Collier § 57.13, at 225 ("some evidence to the contrary"). Under the other approach, the objector must put on enough evidence to rebut or overcome the prima facie case created by the proof of claim; only then, after a preliminary victory over the presumptive validity of the debt as expressed in the proof of claim, does the objector's additional evidence in nature or amount require the bankruptcy judge to weigh the evidence and find the facts. See In re Estrada's Market, 222 F.Supp. 253, 255 (S.D.Cal.1963) ("evidence to rebut the . . . claim"); 3 Collier § 57.18[5], at 294 ("enough evidence to rebut the claimant's prima facie case"). Apparently this latter view was followed here where, despite the evidence produced by the objector, the bankruptcy judge concluded that the evidence was not "sufficient to overcome the presumption of the existence of a debt." This court concludes that the first approach is the better one to follow. To give the effect of a presumption to a proof of claim and thereby to require an objector to produce sufficient evidence to overcome the presumption is to give greater stature to the proof of claim than is warranted by Rule 301(b) which provides only that a proof of claim is prima facie evidence. To require an objector to produce enough evidence to rebut or overcome the so-called presumption would create a confusing additional step in administering claims against a bankrupt's estate. The Bankruptcy Rules anticipate (1) that an unobjected to proof of claim will be deemed allowed, Rule 306(b); (2) that, upon objection, a hearing will be held, evidence will be presented, and a finding of fact as to the validity and amount of the claim will be made by the bankruptcy 238 judge, see Rule 306(c); and (3) that upon appeal to the district court, the finding of fact may be changed only if clearly erroneous, Rule 810. In this scheme, there is no place for an intermediate ruling that there is not enough evidence to rebut the presumption created by the proof of claim. For these reasons and in accord with the the weight of authority above cited, this court holds that when an objector to a claim goes forward at the hearing with some evidence contradicting the claim, the objector's burden of going forward with the evidence is met. Then the bankruptcy judge must weigh the evidence presented by the objector against the proof of claim, see Whitney v. Dresser, supra, together with any evidence presented by the claimant, and he must make a finding of fact as to the validity and amount of the claim. III It is unclear whether the Order of the bankruptcy judge rested upon the required findings of fact relating to the validity and amount of the claim or instead reflected the use of an erroneous legal standard placing the burden upon the objector to disprove the claim or to overcome a non-existent presumption. The Order of December 21, 1976, denying the objection must be vacated and the case remanded. Upon remand the decision whether or not to reopen the evidence is within the discretion of the bankruptcy judge. If another appeal should be considered after findings of fact by the bankruptcy judge, counsel should bear in mind that the "issue whether the sums paid by [the parents] to the bankrupts were gifts or advancements, or loans is wholly a question of fact." In re German, 193 F.Supp. 948, 950 (S.D.Ill.1961) (emphasis added). This appeal must be remanded so that the finding of fact may be made and expressed. An Order will be entered. NOTES [1] The Federal Rules of Evidence, which apply in bankruptcy subject to specific provisions, see Bankruptcy Rule 917, do not define the effect of "prima facie evidence." F.R.Evid. 301 does govern the effect of a presumption in general in civil actions. To analogize a proof of claim to a complaint, an objection to an answer, and a summary hearing in bankruptcy to a civil trial might be possible, but it seems unnecessary in this case.	{ "pile_set_name": "FreeLaw" }
EM523L, a nonpeptide motilin agonist, stimulates gastric emptying and pancreatic polypeptide secretion. We investigated the efficacy and the mechanism of action of EM523L, a nonpeptide motilin agonist (motilide), on the stimulation of gastric emptying and on the release of gut peptides after ingestion of a solid meat in normal controls (n = 8) and in diabetic patients (n = 8) with signs of neuropathy. A dose of 2 mg EM523L was administered IV over 15 min just after ingestion of a solid meal (200 kcal Gastric emptying was measured by a radionuclide technique. EM523L accelerated gastric emptying and markedly augmented postprandial pancreatic polypeptide (PP) response in both normal control and diabetic patients. This may suggest the mediation of the Vagal-cholinergic pathway to accelerate gastric emptying. The present study offers a promising therapeutic potential of the motilide in gastrointestinal motility disorders like those observed in diabetics mellitus.	{ "pile_set_name": "PubMed Abstracts" }
Colleen Anderson I returned to school because I am interested in advancing my career in the project and facilities management field. I found that the bachelor’s degree in project management at Wentworth is well aligned with my career goals. Additionally, several of my colleagues at Liberty Mutual spoke highly of the school. How has the education you’ve received at Wentworth benefited you? I’ve been able to apply several of the concepts that I’ve learned in the classroom to my job. For instance, my statistics class has enhanced my reporting skills, which is a key task in my role. Please describe the in-class experience at Wentworth. My classmates and I share a common bond of being working adults that are balancing the demands of school, work, and family. Wentworth provides flexibility to meet these demands.	{ "pile_set_name": "Pile-CC" }
Conservation Wrangler Summit and Celebration Texan by Nature and our founder, Mrs. Laura Bush, are thrilled to host the first annual Conservation Wrangler Summit and Celebration. This important event brings together 300 Texas leaders to engage in a thought-provoking summit exploring the beneficial connection between conservation and business. The event culminates in a gourmet meal and celebration of this year’s Texan by Nature Conservation Wrangler projects. This exciting summit and celebration is made possible by the generous support of the Pine Foundation.	{ "pile_set_name": "Pile-CC" }
Funding information No funding information provided. A woman aged in her 80s presented at our hospital complaining of sudden‐onset abdominal and right hip pain. An abdominal ultrasound revealed protruded small intestine and fluid in the right groin area (Fig. [1A](#ams2547-fig-0001){ref-type="fig"}, asterisk). Computed tomography (CT) established the diagnosis of obturator hernia (Fig. [1B](#ams2547-fig-0001){ref-type="fig"}, asterisk). She underwent emergency intestinal resection and was discharged without complications 10 days after the surgery. ![An abdominal ultrasound image (A) and a computed tomography image (B) of the patient showed protruded small intestine and fluid in the right groin area (Asterisk), pectineus (dagger), and obturator internus muscle (double dagger).](AMS2-7-e547-g001){#ams2547-fig-0001} As the obturator foramen is located deep inside the body, it is difficult to palpate the protruded intestine. The obturator hernia is often misdiagnosed as hip osteoarthritis or hip fracture.[^1^](#ams2547-bib-0001){ref-type="ref"} Computed tomography is the gold standard for the diagnosis of the obturator hernia,[^2^](#ams2547-bib-0002){ref-type="ref"} however, it can be time‐consuming, and delaying diagnosis can cause intestinal necrosis. However, because obturator hernias are more common among thin elderly women whose pelvic floor muscles are atrophic, obturator foramen can be evaluated by ultrasound with high‐frequency, small‐part linear transducers.[^3^](#ams2547-bib-0003){ref-type="ref"} In this case, ultrasound could visualize the pectineus (Fig. [1](#ams2547-fig-0001){ref-type="fig"}, dagger) and the obturator internus muscle (Fig. [1](#ams2547-fig-0001){ref-type="fig"}, double dagger). Ultrasound can be easily carried out in an emergency room and is less invasive than CT. We can establish the diagnosis of obturator hernia faster than CT, and that leads to early intervention, such as surgery. Disclosure {#ams2547-sec-0002} ========== Approval of the research protocol: N/A. Informed consent: N/A. Registry and the registration no. of the study/trial: N/A. Animal studies: N/A. Conflict of interest: None.	{ "pile_set_name": "PubMed Central" }
Q: Connecting to Google via OAuth 2, "invalid_request" when requesting an access token There are several questions along these lines already on SE, but I've read everything I can find that seems relevant, and I'm still not quite there. I got an authentication code, so now I need to exchange it for an access token and a refresh token. However, Google returns the wonderfully non-specific error "invalid_request". Here's my code: private const string BaseAccessTokenUrl = "https://accounts.google.com/o/oauth2/token"; private const string ContentType = "application/x-www-form-urlencoded"; public static string GetRefreshToken(string clientId, string clientSecret, string authCode) { Dictionary<string, string> parameters = new Dictionary<string, string> { { "code", authCode }, { "client_id", clientId }, { "client_secret", clientSecret }, { "redirect_uri", "http://localhost" }, { "grant_type", "authorization_code" } }; string rawJson = WebUtilities.Post(BaseAccessTokenUrl, parameters, ContentType); return rawJson; // TODO: Parse out the actual refresh token } My Post() method URL-encodes the parameters keys and values and concatenates them: public static string Post(string uri, Dictionary<string, string> properties, string contentType = "application/x-www-form-urlencoded") { string content = String.Join("&", from kvp in properties select UrlEncode(kvp.Key) + "=" + UrlEncode(kvp.Value) ); return Post(uri, content); } The two-parameter Post() method just handles converting the content to bytes, adding content-length, etc., then returns the contents of the response even if it came as a WebException. I can include it if it's of any interest. The authorization code looks right, it's similar to others I've seen: 62 characters, and it starts with "4/". The client ID, secret, and redirect URL I've carefully copied from the Google API Console. The app is registered as an "Other" app, and I'm connecting from a Windows machine. Per this and this post, I've tried NOT URL-encoding, with no change. The OAuth Playground suggests that URL-encoding is correct. Per this post and this one, the properties are concatenated on a single line. Per this post, I've tried approval_prompt=force in the authorization request, but the new auth code did not work any better. Do auth codes expire? I'm using new codes within a few seconds, usually. Per the Google docs and this post, I'm using content-type "application/x-www-form-encoded". My authorization request is for scope "https://www.googleapis.com/auth/analytics.readonly". Per this post, there's no leading question mark in the parameters. There is a Google .NET OAuth library, but I was not able to get it working easily, and ~50,000 lines of code is more than I'd like to study if I have a choice. I prefer to write something clean from the ground up than to blindly copy over a bunch of libraries, cargo cult-style. A: Found it. The redirect_uri used to request tokens needs to match what was used when getting the authorization code. Here's my working code to get an auth code: private const string BaseAuthorizationUrl = "https://accounts.google.com/o/oauth2/auth"; public string GetAuthorizationUrl(string clientId, IEnumerable<string> scopes) { var parameters = new Dictionary<string, string> { { "response_type", "code" }, { "client_id", clientId }, { "redirect_uri", RedirectUrl }, { "scope", String.Join(" ", scopes) }, { "approval_prompt", "auto" } }; return WebUtilities.BuildUrl(BaseAuthorizationUrl, parameters); } ...here's my code to get an access token and a refresh token: private const string BaseAccessTokenUrl = "https://accounts.google.com/o/oauth2/token"; public void GetTokens(string clientId, string clientSecret, string authorizationCode, out string accessToken, out string refreshToken) { var parameters = new Dictionary<string, string> { { "code", authorizationCode }, { "redirect_uri", RedirectUrl }, // Must match that used when authorizing an app { "client_id", clientId }, { "scope", String.Empty }, { "client_secret", clientSecret }, { "grant_type", "authorization_code" } }; string rawJson = WebUtilities.Post(BaseAccessTokenUrl, parameters, "application/x-www-form-urlencoded"); dynamic parsedJson = JsonUtilities.DeserializeObject(rawJson); accessToken = parsedJson.access_token; refreshToken = parsedJson.refresh_token; } ...here's the code to get a fresh access token: public string GetAccessToken(string clientId, string clientSecret, string refreshToken) { var parameters = new Dictionary<string, string> { { "client_id", clientId }, { "client_secret", clientSecret }, { "refresh_token", refreshToken }, { "grant_type", "refresh_token" } }; string rawJson = WebUtilities.Post(BaseAccessTokenUrl, parameters, "application/x-www-form-urlencoded"); dynamic parsedJson = JsonUtilities.DeserializeObject(rawJson); return parsedJson.access_token; }	{ "pile_set_name": "StackExchange" }
Eugène Martin Eugène Martin (March 24, 1915 in Suresnes – October 12, 2006 in Aytre) was a racing driver from France. He participated in two Formula One World Championship Grands Prix, debuting on May 13, 1950. He scored no championship points. Martin is better known for his participation in several of the prewar grands prix. He won the first Grand Prix Aix les Bains Circuit du Lac in 1949 with a Jicey-BMW developed by Jean Caillas. In the 1950s he embarked on a brief career as an auto-maker, working at the Paris-based garage he owned with his father to produce the Martin-Spéciale. The car was exhibited at the 1952 Paris Motor Show but never progressed to series production. He was one of the last surviving drivers from that era until his death at a hospital near his home in La Rochelle in 2006. Complete Formula One World Championship results (key) References External links Profile at oldracingcars.com Category:French racing drivers Category:French Formula One drivers Category:Talbot Formula One drivers Category:1915 births Category:2006 deaths Category:24 Hours of Le Mans drivers Category:World Sportscar Championship drivers	{ "pile_set_name": "Wikipedia (en)" }
Ghibli Museum Videos: Explore the World of Studio Ghibli from Home Ghibli Museum in Mitaka, Tokyo is one of the most popular tourist sites in Japan, attracting tourists and anime fans across the world. One of notable features of Ghibli Museum is the photography restriction, which all visitors are strictly prohibited to take photos and videos inside the museum (you can take photos outside). This is in order to focus on the exhibits and keep the special memory inside the heart. Therefore, Ghibli Museum remains mysterious to those who have never been to the museum. Sadly, Ghibli Museum has been closed due to the prevention of spreading Coronavirus since late February 2020, however, the museum recently launched its official YouTube channel and started sharing exclusive videos of museum diaries. These videos give us an amazing opportunity to enjoy the museum and glance the interior in detail. Yes, you can now take a virtual tour to Ghibli Museum from your home. Currently, there are 4 videos uploaded on YouTube by the museum staff as of 11 May. The first video was posted on 14 April, introducing the entrance to the museum and the reception area. As you step into the building, you are greeted by colourful stained glass windows and the fresco painting on the ceiling with some Ghibli characters. The second video features the museum’s permanent exhibition “Where a Film is Born” followed by the third video “Night at the Museum”, sharing the night sight of the museum which visitors usually don’t get to see. The fourth video is “Cafe”, introducing the popular Straw Hat Cafe which serves dishes and drinks inspired by Studio Ghibli movies. The museum promises that there are more videos to come, so let’s wait and see, and make a further exploration of the museum from home! 【Latest Update】 Fifth and sixth videos were uploaded in mid May, featuring inside the ladies restroom and the main hall of the museum. Thankfully, Studio Ghibli has been sharing with us several contents to enjoy at home since the Coronavirus outbreak started. For example, the popular souvenir at the museum, the Ghibli Museum, Mitaka Cookies are usually sold only at the museum shop, but they are now available to purchase online. (Donguri Republic Sora no Ue Online Shop: https://www.donguri-sora.com/products/detail.php?product_id=8544) Also, Studio Ghibli offers free download of wallpapers for video chats. There are currently 20 different Ghibli movie themed background images available to download on the official website. (Studio Ghibli Official Website: http://www.ghibli.jp/info/013251/) Moreover, a producer and co-founder of Stidio Ghibli, Toshio Suzuki shows how to draw Totoro on a Youtube video. The video was shared by Nagoya City Board of Education as a part of the project to keep children active and smile while staying home during the Coronavirus pandemic. Toshio Suzuki is from Nagoya City and gives local kids some ideas how to spend a good time at home by lecturing how to draw Totoro step by step. We have introduced more contents to enjoy at home previously, so please check them out if you are self-quarantine due to the Coronavirus and looking for thing to do at home!	{ "pile_set_name": "Pile-CC" }
Unexpected rain during today’s Formula 1 test in Bahrain meant teams were unable to to run for several hours as they had not brought any suitable tyres. None of the 10 teams selected any intermediate or wet weather tyres for this week’s test. Bahrain typically sees around 10 millimetres of rainfall during April. However some rain fell before Sunday’s race and further rainfall occured on Tuesday during the test. With no suitable tyres to run on, teams stayed in their garages for several hours. “The rain was a bit of a surprise,” admitted Mercedes’ chief race engineer Andrew Shovlin. “It wasn’t forecast but ended up costing us four or five hours of our programme. “We selected the tyres for this test back in December and not expecting rain, we chose only dry tyres. So, once the track was properly wet we didn’t have any option but to wait for it to dry again.” “It was a very frustrating day for everyone here in Bahrain,” added Williams’ senior race engineer Dave Robson. “Conditions first thing this morning looked reasonable following the dust clouds yesterday and some overnight rain. “However, some further rain meant that little happened between mid-morning and early evening when conditions improved again. We were able to complete some aero testing early in the morning with George, concentrating on data gathering with the rake instrumentation. We then started a performance programme before the rain came.” The disruption to today’s running means the teams should have plenty of slick tyres available for tomorrow’s test, which is forecast to remain dry. When last year’s pre-season test at the Circuit de Catalunya was affected by snow several teams suggested moving more future tests to track in drier climates such as Bahrain. However they returned to the Spanish venue for this year’s pre-season test and all eight days were unaffected by wet weather. Don't miss anything new from RaceFans Follow RaceFans on social media: Advert \| Become a RaceFans supporter and go ad-free 2019 F1 season	{ "pile_set_name": "OpenWebText2" }
The value of bronchoalveolar lavage for discrimination between healthy and diseased individuals. Bronchoalveolar lavage (BAL) is standard diagnostic procedure. Procedural recommendations have been made by pneumological societies including normal values for interpretation of BAL cytology. These normal values derive from small studies in healthy volunteers and have never been analysed for their sensitivity and specificity. This study aims to analyse sensitivity and specificity of these normal values by assessing lavage cell composition in healthy and diseased individuals. More than 6000 BAL were retrospectively analysed for their cellular distribution including BALs of 250 healthy individuals. All BALs were obtained under similar conditions. Bronchoalveolar lavage cytology of healthy individuals mirrors data from previous studies with smoking being the most important manipulator of BAL cytology. Analyses of proposed normal values demonstrate specificity between 80% and 95%, whereas sensitivity ranges between 35% and 65%. Using different mathematical models, a value summing up the differences to ATS-proposed normal values of the cytological pattern was found to best discriminate between healthy and diseased individuals with a sensitivity of nearly 60% with a predefined specificity of 95%. In summary, our analysis confirmed prior results for healthy volunteers and enlarged these findings by analysing sensitivity and specificity of lavage results in an independent validation cohort of diseased individuals. Thereby, the study may influence the acceptance of BAL in the diagnostic workup of individuals with pulmonary diseases. Additionally, the study proposes a novel value that facilitates lavage interpretation and may therefore be useful in further studies.	{ "pile_set_name": "PubMed Abstracts" }
Asiana Airlines pilots involved in a deadly San Francisco plane crash earlier this year have told investigators that the failure of an automated speed-control system played a major role in the accident. The pilots said that the auto-throttles disconnected without warning before the twin-engine jet slowed dramatically and hit a sea wall near a runway at San Francisco’s international airport, the Wall Street Journal reported on Monday. This account differs from the safety board’s preliminary findings, which did not uncover any mechanical or electrical problems with the Boeing 777 prior to impact. Air safety officials previously said the pilots may have failed to activate the auto-throttle correctly, but Asiana maintenance logs detail a number of “uncommanded auto-throttle disconnects.” the pilot in command reads the gripe sheets before he signs for the aircraft. if this is a noted gripe, then the pilot should have been very aware of this issue and made the appropriate mental notes.....if not this responsible......he should have NEVER been in command of the aircraft... If you were on a highway and set the cruise control in your car to 60 mph and it disconnected by itself, would you allow your speed to slow by over 20%, to less than 48 mph without intervening manually by taking over operation of the throttle? And suppose you were a student driver with an instructor with you and another driver in the back seat? Would all three of you fail to notice that the speed was deteriorating until you got hit from behind? That is the equivalent of what happened here. Whether they set up the auto-throttle incorrectly or whether it malfunctioned is immaterial. As others have said, these guys had a responsibility to monitor their air-speed. It is perhaps the most critical variable during final approach. You can't set the auto-throttle and forget it. It certainly looks like these pilots were overly dependent on automation, trusted it too much, and failed to fly their airplane. Put it this way: let's assume the auto-throttle failed, which is highly questionable. But let's give them that. Do you think if Captain Sullenberger had been in command of this flight and the auto-throttle failed, we'd be discussing this? If you plan to blame the auto-throttle for your crashes, why have pilots on board at all? The flight crew is there to make decisions and take responsibility for the safe conduct of flight; had they done so this crash probably wouldn't have happened. Engaging autothrottle is not an excuse for neglecting to monitor airspeed. Strange, none of the other "uncommanded disconnects" resulted in the plane slamming into the ground. Really weak attempt to redirect blame.	{ "pile_set_name": "Pile-CC" }
FILE - In this July 15, 2014 file photo, Silicon Valley venture capitalist Tim Draper presents his drivers license for identification purposes to Heather Ditty, elections manager for the Sacramento County Registrar of Voters, as he turns in boxes of petitions for a ballot initiative that would ask voters to split California into six separate states in Sacramento, Calif. The court struck venture capitalist Draper's initiative from the ballot in July 2018 as part of a legal challenge in response to a lawsuit but didn't rule on the merits of the case. Draper says he's giving up on the effort after the state Supreme Court knocked it off the November 2018 ballot. (AP Photo/Rich Pedroncelli, File) FILE - In this July 15, 2014 file photo, Silicon Valley venture capitalist Tim Draper presents his drivers license for identification purposes to Heather Ditty, elections manager for the Sacramento County Registrar of Voters, as he turns in boxes of petitions for a ballot initiative that would ask voters to split California into six separate states in Sacramento, Calif. The court struck venture capitalist Draper's initiative from the ballot in July 2018 as part of a legal challenge in response to a lawsuit but didn't rule on the merits of the case. Draper says he's giving up on the effort after the state Supreme Court knocked it off the November 2018 ballot. (AP Photo/Rich Pedroncelli, File) SACRAMENTO, Calif. (AP) — The billionaire behind a measure to split California in three said he’s giving up on the effort to reimagine the nation’s most populous state after the state Supreme Court knocked it off the November ballot. “The political environment for radical change is right now,” venture capitalist Tim Draper wrote in a letter to the court dated Aug. 2 and made public by his opponents Thursday. “The removal of Proposition 9 from the November ballot has effectively put an end to this movement.” ADVERTISEMENT The court struck Draper’s measure in July in response to a lawsuit but didn’t rule on the merits of the case, allowing Draper the opportunity to fight to put it on future ballots. He’s not moving forward with the case. Draper spent more than $1.7 million to qualify his initiative for the ballot, which requires gathering hundreds of thousands of signatures. It’s not his first effort to break up California — his plan to split the state into six didn’t qualify for past ballots. He’s argued California has become ungovernable due to its size and diversity, politically and geographically. The latest plan would have divided California into three pieces. One would comprise the Bay Area, Silicon Valley, Sacramento and the rest of Northern California; the second would be a strip of land from Los Angeles to Monterey; and the third would include San Diego, the Central Valley and Orange County. The Planning and Conservation League sued to keep Draper’s initiative off the ballot, arguing that such a massive change to the state’s governance couldn’t be done through a ballot initiative. “At the end of the day, this was a billionaire’s massive and illegal use of the initiative process, and the court was correct in stopping this folly,” Carlyle Hall, an attorney who worked on the suit with the environmental group. Draper, meanwhile, said he had “no idea” if his initiative would have passed or if Congress would have given the necessary approval for the split but that the ballot measure would have spurred debate over government failings. “I wanted to let the voters debate, discuss and think about a different way forward — essentially a reboot. And, I wanted the political class to hear and witness the frustration of California’s voters with decades of inaction and decay,” he wrote. “I believed there was significant benefit to our democracy in that.”	{ "pile_set_name": "OpenWebText2" }
Q: How to avoid or report targeting I have heard many reports of a user being watched by a specific person, and that person constantly downvoting all posts by that user, and adding comments to put them down, such as "How do you not know this" or "Have you ever used a computer before?", as well as other such verbiage. He reported the person several times but no action was taken for almost 8 months. Is there any expedited process to report and remove these people from commenting on questions? A: H‌i! I'm a moderator! Although that makes me one of a declining breed around here, there are a few of us who still exist. As a moderator, I do a variety of things to help make Stack Overflow a better place, including removing non-answers, closing off-topic questions, investigating vote fraud, investigating trolling/harassment. If you notice something going wrong on the site, and you want to bring it to a moderator's attention, you can do so by raising a flag. Flags are strictly confidential—the only people who will see them are moderators, and we're bound by a confidentiality agreement that prevents us from disclosing any details about flags or flaggers in public. This ensures that you can report something to us without any fear of retaliation. We consider and investigate every flag that is raised. We may not always act on them, but we do pay them careful attention. If you want us to look at something, or something is going on that makes you feel uncomfortable, please raise a flag to let us know. In most cases, what you'll be flagging is a post (question or answer) or comment. The former have a handy "flag" link underneath them, while the latter have a little flag comment in the left-hand margin. The UI explicitly supports flagging for these because content is the focus of this site, so most of what gets reported and addressed by moderators is content. We would prefer in every case that you report content, if possible, not users. For example, flag the abusive comment, not the user who left it. Sometimes, though, it's not possible. For example, you want to report a pattern of behavior by a particular user. That's okay, you are allowed to do that, and since flags are confidential, there's no way the user you're reporting will find out. To report a user, just flag one of their posts. Or one of your own posts. It really doesn't matter. Choose the "needs moderator attention" option, which gives you a text box to type into. Use that text box to explain what your concern is and provide as much evidence as possible—links to Q&A where you see evidence of harassment or targeting behavior, for example. It's okay if they're deleted: moderators can see deleted content. Either way, we'll investigate, and if we conclude that something untoward is happening, then we'll deal with it appropriately. We have the ability to see lots of different information (including, as I mentioned, deleted posts and comments), as well as to see histories of users' behavior, which allows us to judge patterns. When targeting becomes harassment, it is not appropriate here. It is a clear violation of the Code of Conduct even in its simplest form (be nice, and respect one another), so it would absolutely not be allowed. Now, of course, as Alexei mentions in his answer, you need to be discerning about what constitutes "targeting". If you're saying to yourself, why whenever I post a question about x86 assembly language does this fellow Peter Cordes show up and leave a comment or an answer—is he targeting me? Well, yeah, I guess you could kind of say that in a certain sense, but not really. He's targeting assembly language questions, because that's one of his major areas of expertise. If you ask an assembly language question on Stack Overflow, you're very likely to run into him. If you post an incorrect assembly language answer on Stack Overflow, you're very likely to get a downvote from him. It doesn't mean that he's targeting you, and it's only a problem if he, as you mention in the question, were to start leaving rude comments or otherwise harassing you. (I'm picking on Peter here because I know him. There are dozens or hundreds of equivalent examples in other tags. We call these "subject matter experts", and we're very thankful for their regular high-quality contributions.) Thankfully, moderators are smart enough to tell the difference between innocent, coincidental targeting and abusive behavior, and that's one of the things we'll investigate in response to a flag. In summary, if you want us to take a look at something that is bothering you or seems suspicious, please raise a flag to let us know and we'll be happy to do so. A: I expect "this user follows me" to happen very frequently as a person who multiple have questions on the same topic endup with relatively small group of answerers who see those questions. While it may look like answerers "follow you" it's most likely other way around. Like if you wake up 7am daily the Sun is out by that time - it's strange to blame the Sun for watching you... The best way I know (and seen used) to no be targeted by a single user is to post subsequent questions/groups of questions in different unrelated tags, preferably at very different time of the day. Most of the tags have relatively small set of people who answer/curate questions and each person would be most active at particular time of day. This leads to perceived "this @#$@#$ follows me" when one posts similarly styled questions on the same subject around the same time. The other things to consider - do not ask question that request continuation of your work. I.e. you assignment is "read multiple values for a list and print them in reverse order" then asking "how to read a value", "what is a list", "previous questions shown how to read a value how to put it in a list", "previous questions show how to add value, how to reverse it".... may look like lack of understanding of basic concepts as well as lack of effort to learn things. Some people can lash out when it happen. avoid any personal writing style that stands out while asking not-so-on-topic questions. While SO gets a lot of low/average quality of the question it is rare to see those questions asked with good quality of writing. Those stand out and likely trigger "I think I've seen something form that person... totally off-topic too... let me doublecheck all questions they asked" Note that if you see actually offensive/not kind comments - flag them appropriately. But I would not expect to see punishment for something "did you even read anything" type of comment on "how to declare variable in JavaScript" type of question... What is expected to happen is author of comment get notified of their undesired behavior and changes the behavior as result - this outcome is not really visible to the flagger by design. If behavior continues despite flags - bringing "why my specific question attracted unkind comments" may be a way to get help (assuming you believe the post is of good quality) or contact community managers via "contact us".	{ "pile_set_name": "StackExchange" }
Succinoglycan production by solid-state fermentation with Agrobacterium tumefaciens. Succinoglycan was produced by cultivating Agrobacterium tumefaciens on various solid substrates, including agar medium, spent malt grains, ivory nut shavings, and grated carrots, impregnated with a nutrient+ solution. Fermentations were performed on a laboratory scale, both under static conditions and with agitation, using bottles and a prototype horizontal bioreactor. Several fermentation parameters were examined and optimized, including carbon and nitrogen composition, water content and layer thickness of the substrate. The yields and rheological properties of the polymers obtained under different fermentation conditions were compared. The highest succinoglycan yield was achieved in static cultivation, reaching 42 g/l of impregnating solution, corresponding to 30 g/kg of wet substrate. The polymer production in the horizontal bioreactor was faster, but the final yield was lower (29 g/l of impregnating solution).	{ "pile_set_name": "PubMed Abstracts" }
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} .container .offset-by-eleven { padding-left: 528px; } .container .offset-by-twelve { padding-left: 576px; } .container .offset-by-thirteen { padding-left: 624px; } .container .offset-by-fourteen { padding-left: 672px; } .container .offset-by-fifteen { padding-left: 720px; } } / #Mobile (Portrait) ================================================== / / Note: Design for a width of 320px / @media only screen and (max-width: 767px) { .container { width: 300px; } .columns, .column { margin: 0; } .container .one.column, .container .two.columns, .container .three.columns, .container .four.columns, .container .five.columns, .container .six.columns, .container .seven.columns, .container .eight.columns, .container .nine.columns, .container .ten.columns, .container .eleven.columns, .container .twelve.columns, .container .thirteen.columns, .container .fourteen.columns, .container .fifteen.columns, .container .sixteen.columns, .container .one-third.column, .container .two-thirds.column { width: 300px; } / Offsets / .container .offset-by-one, .container .offset-by-two, .container .offset-by-three, .container .offset-by-four, .container .offset-by-five, .container .offset-by-six, .container .offset-by-seven, .container .offset-by-eight, .container .offset-by-nine, .container .offset-by-ten, .container .offset-by-eleven, .container .offset-by-twelve, .container .offset-by-thirteen, .container .offset-by-fourteen, .container .offset-by-fifteen { padding-left: 0; } } / #Mobile (Landscape) ================================================== / / Note: Design for a width of 480px / @media only screen and (min-width: 480px) and (max-width: 767px) { .container { width: 420px; } .columns, .column { margin: 0; } .container .one.column, .container .two.columns, .container .three.columns, .container .four.columns, .container .five.columns, .container .six.columns, .container .seven.columns, .container .eight.columns, .container .nine.columns, .container .ten.columns, .container .eleven.columns, .container .twelve.columns, .container .thirteen.columns, .container .fourteen.columns, .container .fifteen.columns, .container .sixteen.columns, .container .one-third.column, .container .two-thirds.column { width: 420px; } } / #Clearing ================================================== / / Self Clearing Goodness / .container:after { content: "\0020"; display: block; height: 0; clear: both; visibility: hidden; } / Use clearfix class on parent to clear nested columns, or wrap each row of columns in a <div class="row"> / .clearfix:before, .clearfix:after, .row:before, .row:after { content: '\0020'; display: block; overflow: hidden; visibility: hidden; width: 0; height: 0; } .row:after, .clearfix:after { clear: both; } .row, .clearfix { zoom: 1; } / You can also use a <br class="clear" /> to clear columns */ .clear { clear: both; display: block; overflow: hidden; visibility: hidden; width: 0; height: 0; }	{ "pile_set_name": "Github" }
Non-two-state thermal denaturation of ferricytochrome c at neutral and slightly acidic pH values. Thermal denaturation of ferricytochrome c (cyt c) has been methodically studied by absorbance, fluorescence, circular dichroism spectroscopy, viscosimetry and differential scanning calorimetry in pH range from pH 3.5 to 7.5. Thermal transitions have been monitored by intrinsic local probes of heme region such as absorbance at Soret, 620nm and 695nm bands and circular dichroism signals at 417nm. Global conformational changes were analyzed by circular dichroism signal at 222nm, fluorescence of the single tryptophan, reduced viscosity and differential scanning calorimetry. We show that cyt c thermal denaturation above pH ~5 can be described by an apparent two-step transition in which the heme iron stays in a low-spin state. The thermal denaturations of cyt c below pH ~5 proceed in one step to an unfolded highly compact form with a high-spin state of the heme iron. Cyt c conformational plasticity is discussed in regard to its physiological functions.	{ "pile_set_name": "PubMed Abstracts" }
Q: Oracle SQL How can I separate values from a column in two different columns? I want to code a query to return description of some concepts and their respective price but I want to make two different columns to categorise two diferentes items categories of values. Is it possible? SELECT b.descripcion CONCEPTO, a.cantidad, a.importe, c.descripcion FROM detalles_liquidaciones a JOIN conceptos b ON (a.codigo_concepto = b.codigo) JOIN tipos_conceptos c ON (b.codigo_tipo = c.codigo) WHERE a.numero_liquidacion = 13802 AND c.descripcion IN ('HABER', 'RETENCION', 'ANTICIPO'); Output Query I want to code something like this: Ideal query A: Could this work ? ( Perhaps there's a better solution, it feels a bit tricky... litterally "switching" ): SELECT Concepto , (CASE WHEN description LIKE 'HABER' THEN importe ELSE NULL END) haberes, (CASE WHEN description LIKE 'HABER' THEN cantidad ELSE NULL END) cantidad, (CASE WHEN description LIKE 'RETENCION' OR description LIKE 'ANTICIPO' THEN importe ELSE NULL END) retenciones FROM (SELECT b.descripcion concepto, a.cantidad, a.importe, c.descripcion FROM detalles_liquidaciones a JOIN conceptos b ON (a.codigo_concepto = b.codigo) JOIN tipos_conceptos c ON (b.codigo_tipo = c.codigo) WHERE a.numero_liquidacion = 13802 AND c.descripcion IN ('HABER', 'RETENCION', 'ANTICIPO'));	{ "pile_set_name": "StackExchange" }
Q: how to add UILabel within a UILabel? This question looks very usual.. but I had a problem yesterday, I have added a label in xib and created outlet for it, I want to have multiple lines, buttons inside that label, So I have decided to add new sub labels inside it... UILabel label; label = [[UILabel alloc] initWithFrame:initial_rect]; label.font = [UIFont systemFontOfSize:[UIFont smallSystemFontSize]]; label.text = sel_obj->start_time; label.backgroundColor = [UIColor whiteColor]; [xib_label addSubview:label] When I tried like that, it was not working, then I have added the same label in self.view it works fine.. So what do I need to do when I want to add a label within a label which was added using xib. Am I missing anything here.. thanks... A: I came across this situation long ago. Just FYI : I think the problem is the initial_rect, which is in the view's frame but out of the xib_label's frame. The frame of label is relative to xib_label, not self.view. You can try this : UILabel label; CGRect rect = (CGRect){0, 0, 10, 10}; label = [[UILabel alloc] initWithFrame:rect]; label.font = [UIFont systemFontOfSize:[UIFont smallSystemFontSize]]; label.text = sel_obj->start_time; label.backgroundColor = [UIColor redColor]; [xib_label addSubview:label]; Change the backgroundColor to red to see the label clearly. And if you want to show multiple lines in a label, you can : label.numberOfLines = 0;.	{ "pile_set_name": "StackExchange" }
Differences in synthesis of membrane proteins by leukemic cells from spleen and peripheral blood indicate distinct subsets of malignant cells in a patient with prolymphocytic leukemia. Morphological and biochemical differences were demonstrated between prolymphocytic leukemia cells obtained from the spleen and peripheral blood of one patient. Peripheral blood prolymphocytes had consistently smaller nuclear-cytoplasmic ratios than did splenic prolymphocytes. Percoll gradient-purified prolymphocytes from the spleen synthesized abundant amounts of some membrane proteins which were hardly expressed by peripheral blood prolymphocytes. Peripheral blood prolymphocytes did not change their expression of membrane proteins during three days in culture. These findings are consistent with the view that prolymphocytic leukemia cells from the spleen exist, on the average, at an earlier stage of differentiation than do circulating leukemic cells, and that peripheral blood leukemic cells are frozen at a specific phase of differentiation.	{ "pile_set_name": "PubMed Abstracts" }
Ask HN: Designing a Database - bgnm2000 I'm primarily a designer with a good amount of code experience (classes in school, messing around on my own etc.) I started to learn rails over the summer, and built one pretty messy app. That said, I'm gearing up to build my second app, this time around I've been thinking a lot about the database and how everything needs to connect etc. rather than doing it as I go.<p>So far I've drawn it on paper (looks like something out of MS Access) but I was wondering if there are any other recommended steps I should take before I start coding this all out (besides the usual flow charts etc.)?<p>Thanks!<p>-bgnm ====== tom_b Do you need your system to be transaction-oriented (think ATMs and banking) or analytic (for doing slice and dice reporting of data)? You'll do well to check out normalization for the first and understand star schemas for the second. It's awesome you are thinking about db design upfront, just think about what your data will be, how it will be used, and how you will want to move it around for your app. Don't discount not using a db at all (and I'm a db guy for work) - for one of my current projects, I'm simply dumping small data objects into individual JSON files. Easy to fetch with Ruby/Sinatra and easy for the GUI part of the app to play with (Javascript eats up JSON on that side). Not to discount Rails at all, but going with a minimal toolset like Ruby/Sinatra/Sequel might be just the ticket for you roll simple web apps really quickly. Heck, this forum uses flat files for storing submissions, comments, and user data. ~~~ bgnm2000 Thanks for the reply! I'd say the data is definitely going to be analytical - but some parts will be transaction oriented, if that makes sense (people will be able to pay for greater functionality). I don't think I know enough about flat file systems to code one up myself at this point either (not that I know enough about DB's - but enough to create something). Any good resources for understanding star schemas? ~~~ tom_b Sure, grab one of the data warehouse books from Kimball. Inmon is the other big data warehouse author out there, but I'm not as familiar with his texts. Kimball's stuff is an easy read and not platform focused in any way. If you are aiming to do business visualizations with the data, you might want to check out Stephen Few - he's written several books on business data visualization (think Tufte distilled for charts and dashboards). ------ fragmede Make sure you've read Wikipedia's article on normalizing databases. <http://en.wikipedia.org/wiki/Database_normalization> ~~~ pbhjpbhj If you understand such gems as: _[For 3NF ensuring that] Every non-prime attribute is non-transitively dependent on every key of the table_ Then that's the perfect reminder article. I did an undergrad course in db design covering db normalisation (years ago) and still found that page to be a bit dense. I'd look elsewhere for a primer. <http://www.databaseprimer.com/normalization.html> is a bit too simplified but makes it easy to understand what's happening. This [http://www.databasejournal.com/sqletc/article.php/1428511/Da...](http://www.databasejournal.com/sqletc/article.php/1428511/Database- Normalization.htm) appears to be a good overview using a realistic worked example db.	{ "pile_set_name": "HackerNews" }
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Q: pyftpdlib slow .read on file blocks entire mainloop Helllo, I am using a custom AbstractFS on pyftpdlib that maps files on a HTTP server to FTP. This files are returned by my implementation of open (of AbstractFS) which returns a httplib.HTTPResponse wrapped by the following class: class HTTPConnWrapper: def __init__(self, obj, filename): # make it more file obj like self.obj = obj self.closed = True self.name = filename.split(os.sep)[-1] def seek(self, arg): pass def read(self, bytes): #print 'read', bytes read = self.obj.read(100) #we DONT read var byes, but 100 bytes #print 'ok' return read The problem is that if a client is downloading files the entire server becommes sluggish. What can I do? Any ideas? PS: And why just monkey patching everything with evenetlet does'nt magically makes everything work? A: Ok, I posted a bug report on pyftpdlib: I wouldn't even know what to recommend exactly as it's a problem which is hard to resolve and there's no easy or standard way to deal with it. But I got a crazy solution to solve this problem without using pyftpdlib. rewrite everything using wsgidav (which uses the cherrypy wsgiserver, so its threaded) mount that WebDAV filesystem as native filesystem (net use on windows, mount.davfs on linux) serve this mounted filesystem with any ftp server that can handle blocking file systems	{ "pile_set_name": "StackExchange" }
" 7:30, Halsted!" " Nice one, loser!" " How many's that?" " 92 and counting." " We're supposed to get out today for a bit." " Step nine, making amends." "Can't wait." " Let's go." "Good morning." " He hit on me yesterday." "Nice one, douche bag!" " Hey, pick that up." " Hey!" "Hey!" " Come on!" " You're dead." " All right, tough guy." "You too." "Thank you." "There you go." "I need you to sit down." " What are you looking at, huh?" " Fuck..." "Get me out of this place, please." " I know it isn't easy, but taking that step towards reconciliation with the people most hurt by your addictions, that's the door to recovery." "Okay, we're gonna keep working at this." "This is mandatory policy now in all rehabilitation cent res." "Each and every one of you will be participating." "You're gonna be getting a day pass every day this week, so get out there and make good use of your time." "Remember, don't rush, all right?" "Every step is a good one..." " Okay, so, I have a proposition for you." " I don't think I want to hear this" " I stole them from my mom, and now you have to take them." "Come on, I went through so much trouble." " Okay." " I don't know how to" " Are you holding it?" " Yeah, I'm holding it." " So you put it..." " Hey, Charlotte." "No, hey, Char" " I don't want to talk to you, Kyle." " Charlotte, come on, I'm-I'm still your brother." " No, I don't want to talk to him..." " Well, well." "If it isn't one of our illustrious alumni." "If you and whatever drugs you're selling aren't off the school property in the next 30 seconds," "I'm going to call the police." "All third-floor staff to the nurses' station..." " Hey, Dad." "How you doing?" " What do you want?" " Are they-are they treating you all right?" "What the fuck do you want, you little prick?" "Huh?" "I told you I never wanted to see you again." "You get out of my sight." "Ten years because of you, you fuckin' dope fiend." "You fuckin' coward!" "If I see you again, I will fucking kill you!" "If you come back here, I'll fucking kill you!" "I swear, I'll kill you!" " Okay, so let's talk about today's adventures." "Kyle?" " Do I have to?" " Please." "I went to see my sister." " Okay, and how did that go?" " Not very well." " Can you elaborate?" " No." " Kyle" " He doesn't want to talk about it." " Talking is the only way to move forward." " Oh, fuck you and move forward!" "Fuck this whole place!" "None of this makes any fucking difference to us!" " Fuck, I hate Bob." " He's a cock." " He's a fuckin' idiot." "It's "make amends" day." "Good to see you." "Sorry about all that money I stole." " Yeah, sorry for ruining your life." "Oh, wait a minute, you ruined my life." " It's all fucking bullshit anyways." " Speaking of which." " Sonia..." "There's a call for you." " My dad just died." "¢Ü I wish that I had known ¢Ü" "¢Ü In that first minute we met ¢Ü" "¢Ü The unpayable debt ¢Ü" "¢Ü That I owed you ¢Ü" "¢Ü 'Cause you'd been abused by that bone that refused you ¢Ü" "¢Ü And you hired me to make up for that... ¢Ü" " Just after 11 :00 this morning, an unidentified man threw himself off the Mission City dam." "Authorities believe he died on impact, but crews are still dredging the reservoir to find his body." "In Mission City..." " Fuck..." "Let's go!" "7:30, Halsted!" " Nice one, loser!" " It's weird." " What?" "93, right?" " Yeah, should be 93, but... 92." " Let's go." "Good morning." " Nice one, douche bag!" " All right, funny guy, clean it up." " What?" " Right now." "Right now." " Shit..." " All of it." " Did you guys see that?" " Fuck you, Bob." " Get back here." " Dick." " Hey..." "Get back here!" " That was fucking weird." " Okay, so, I have a proposition for you." " I don't think I want to hear this proposition." " I stole them from my mom, and now you have to take them." "Come on, I went through so much trouble." " How did you steal this?" " I took it from her purse like I take everything, okay?" " I don't know how to" " Okay, just hold it." " Okay, okay, I'm holding it." " Okay, right?" " Yeah." " Now you have to put it to your lips like you're French." " Okay." " Okay." "You'll never get that!" " All third-floor staff to the nurses' station..." " Pick up the fuckin' phone." "What?" "Pick up the goddamn phone." "I told you I never wanted to see you again!" "You get outta my sight!" "10 years 'cause of you!" "You fuckin' dope fiend!" "You fuckin' coward!" "I see you again, I will fucking kill you!" "If you come back here, I'll fucking kill you!" "I swear, I'll kill you!" " Well, well." "If it isn't one of our illustrious alumni." "If you and whatever drugs you're selling are not off the school property in the next 30 seconds," "I'm calling the police." " Okay, so let's talk about today's adventures." "Kyle?" " Yeah?" " What did you do today?" " Uh..." "I went to see my sister." " And how did that go for you?" " Not very well." " Can you elaborate on that, please?" " No." " Halsted." "Halsted." "Kyle..." "Kyle..." " What the fuck is going on?" "How is this even possible?" "I mean..." "Wait..." "The storm." "Last night, the power went out, right?" "I was in the rec room and I-I touched the TV." "I got this shock." "That's the last thing I remember." " Same thing happened with me with my light." " Weeks?" " Who cares how it happened?" "The real question is, what are we gonna do with it?" " What were you doing last night?" " What were you doing?" " I was in the shower, okay?" "I got shocked, too." " Then what?" " I don't remember." " Me neither." " The same thing happened to all of us." " Fuck, I'm gonna get that call again." " Uh, Sonia, there's a call for you." " Exactly the same." " You all right?" " Shouldn't we be doing something?" "We just lived through the same day twice." "Are we just gonna sit here and waste it?" " Last night, on the news..." "There's-there's a jumper at the dam." "Let's go." "Let's do it." " What about curfew?" " Fuck curfew." " Shit, we gotta stop him." " No, it's..." "It's too late." " Couldn't sleep." " Me neither." "At least you went to see him." " I didn't." " I thought you went to the hospital." " I went to the hospital, but..." "I just couldn't go into his room." " What do you think'd happen if we just..." "Stayed in here all night?" " Trouble for sure." " Then I'm not leaving." " Why do you think this is happening to us?" " Sorry." " No, it's..." "It's okay." " 7:30, Halsted!" " Bob!" " What?" " What day is it?" "Last time I checked, it was Wednesday." " Look, we're gonna figure this out." " We're not gonna figure out shit, okay?" "We're gonna keep repeating the same day over and over again until we go completely out of our fucking minds." " Okay, but, look, we each had the same shock of electricity or whatever, right?" "So..." " So, what?" "So maybe that's something that we do?" " Okay, you go and electrocute yourself then, sister, but I'm gonna enjoy it while I got it." "God, what is that girl's problem?" "You know, if you think about it, it doesn't really matter what we do today." "Right?" "I mean, I could take a piss in group." "As a matter of fact, I could just piss on Bob." "Tomorrow, it'd be like it never happened." " Yeah." "I don't know, man." "I... just feel like we shouldn't mess with it, you know?" " What do you think we should do with it?" " I don't know." " Pull it out and put it back." ":" "What?" " The bottle of gin." "I can see it in your pants." "Pull it out and put it back!" " It's not in my pants." " What do you call that?" "Put it back!" "You know what, both of you, get the hell out of my store!" "Both of you, get out!" "Idiots!" " Feeling better?" " Oh, starting to." " What the fuck are you doing?" "What the fuck are you doing?" "Oh, no, dude." "We'd better pray tomorrow repeats." "Fuck!" "You're sick!" "Sick!" "Oh, Bobby..." "Whoa, Bob likes pussy." "Who am I?" "Who am I?" "Bob... loves... lady cock." " What the fuck?" " Oh, no..." "Nearly Legal." "Nearly Legal." "Fuck, look." "Oh, fuck." " All right, freeze, boys!" "Party's over." "Hands on your head." "Let's go, right now." "Hands on your head." "That's it." "Looks like you screwed up royally this time, eh, Weeks, huh?" "Just like the old man, huh?" "Hands behind your back." "Halsted." "Your mom posted bail." " See you this morning." " Well..." "Looks like no daddy coming for you, cowboy." " Breaking and entering?" "Vandalism?" "Your first day pass and that's what you do with it, huh?" "Well, you must be really proud of yourself." "You have any idea what that little exercise just cost me?" "Kyle..." " Just after 11:00 this morning, an unidentified man threw himself off the Mission City dam" " It's weird." "I was scared, but..." "At the same time, I felt... really alive." " What if it doesn't repeat?" "You're gonna have a criminal record on top of your drug history." "That's pretty awesome, Halsted." "7:30, Halsted!" " Hey, Bob?" "Bob..." "I hear there's been a few break-ins in the neighbourhood lately?" " What the hell are you talking about?" " Nothing." " Okay, come on, let's go." "Get your ass in gear." " Hello." " Well, hello." "Again." " Every time." " Let's go." " Bob, look in' slick." ":" "Morning." ":" "Nice one, douche bag." "So, what's on the program?" " Clean it up." "Right now." " You know," "I think our man, Bob, on his down time, he likes to just settle in with a little bit of Victoria gin." " Victoria gin?" " Yeah, yeah, a little bit of lubrication before he kicks off his shoes, and he thumbs through his favorite magazine..." "Nearly Legal!" "Right, Bob?" " I knew he was a pig." " Oh, not to worry, Logan." "I think you're a bit too old for him now." " Fuck you." " Well, fuck it, cowpokes, let's celebrate!" " Yeah." "Yeah!" " Three more!" "Here!" "Baby, baby, baby, baby..." " Woo!" " Are you gonna be able to pay for all this?" " Oh, you bet your sweet ass, girl." " All right, yeah, I'm gonna need you to settle up." " I apologize." "He hasn't gotten laid in a bit." " A very long time." "You want to help me out with that?" " Oh..." " I'm sorry, I'm sorry." "That there male and that there female are gonna pay for me." " I have no money." " Fuck sakes..." " I'm so sorry!" " Okay, thanks, partner, that was great!" "All right, uh, I'm gonna sing a little song to pay for some drinks." " Woo!" " Yeah, that's right, pal!" "And I'm gonna dedicate it to my two friends." "Y'all know who you are" " It's us!" "We're his friends!" "Oh, my darlin' oh, my darlin'" "Oh, my darlin'" "Oh, my darlin' Clementine" " Let him sing!" "Hey, let him sing!" "Oh, my darlin'" "Oh, my darlin'" "Oh, my darlin' Clementine..." " Where did you get this from?" " What was that noise?" "And?" " Oh, that is" "Mine stinks, dude." " Milady?" " Oh, shit." "Wow." " My friend." "One for you." " Oh, my G" "Are we really gonna do this?" " Tell me you haven't always wanted to knock off a liquor store?" " Are these things clean?" " What?" " Well, they jam if they're dirty, right?" ":" "We're not going to shoot anybody." "Okay, you know what, the only thing that my old man cares about more than his knife collection is his fucking gun collection." "So yeah, they're clean." "Let's do this, kiddies!" "Oink!" "Oink!" "Stick your hands up!" "It's a stick-up!" "Let's go!" " Try to touch my dick and I'll blow your fuckin' brains out!" "Go!" " Shit..." " Open the fuckin' register!" " Okay." " You think this is fuckin' funny?" "Hurry up!" "Get me a bag, fuck!" "Quick!" "Here..." " What the fuck?" " Shit, there's a car!" " What?" " There's a car, fuck!" "Hurry up!" " Let's go!" " Hurry!" " Let's go, come on!" "Let's go, let's go, let's go!" "Oh, my God, what the fuck?" " How much did we get?" " I don't know, man." "There's like 500 bucks here and 42 pennies." "I took it all, man." "I took it all." "Shit..." " Yo, Tiko, what's up, man?" " Well, if it isn't my favourite customer, man." "Long time, no show, bro." " Yeah, man." "Look, um..." "Michelle?" "Charlotte?" "Tiko, what the fuck, man?" "Tell me you didn't get my sister fuckin' high." " That's not all we did, G." " Hey..." " Charlotte!" " Easy!" "Fuck..." "Jesus..." "We good?" "Nobody in there wants to talk to you." "Okay, man?" "So just fuck off." " Fuck you." " Really?" " Yeah." " There's room for you." " Nice fuckin' sweatpants." " Don't worry, guys." "I know a guy that we can score from." "Welcome to my drug of choice, kiddies." " This shit always fuckin' scared me." " They say you're addicted the moment you take your first hit." "Only today..." "You get to be unaddicted again." "Here it comes." "Go, go, go, go, go." "¢Ü ...ain't gonna cure you ¢Ü" "¢Ü Honey time's just gonna hit on you ¢Ü" "¢Ü You got to ¢Ü" "¢Ü You got to go steal ahead ¢Ü" "¢Ü You got to go steal ahead ¢Ü" "¢Ü You got to You got to go steal ahead... ¢Ü" "Fuck me." "¢Ü You've got to You got to go steal ahead ¢Ü" "¢Ü Uh-huh... ¢Ü" "You know, your sister's little friend, she's pretty hot." " Yeah, she's also 15 fucking years old, dude." " Nearly Legal!" "I mean, she is fuckin' hot, though." "¢Ü Time's just gonna hit on you ¢Ü" "¢Ü I said ¢Ü" "¢Ü Six kinds of glue ¢Ü" "¢Ü Won't hold you ¢Ü" "¢Ü Won't hold you ¢Ü" "¢Ü Oh my oh ¢Ü" "¢Ü Oh my you've got to You got to you got to you got to... ¢Ü" "¢Ü Go steal ahead Go steal ahead... ¢Ü" " Hold the fuck on!" "What?" " Grab his legs." " Jesus..." "Fuck, he's heavy." " Fuck..." " God, Tiko..." " Get on your knees." "Get on your fuckin' knees!" " Okay, okay..." "We were just having some fun, man." "I didn't-I didn't" " Shut the fuck up!" " Okay, okay, okay... :" "Come on, man." " Pick that up." "What?" " Pick that up." " No, man." "Fuck you, man!" " Pick that up, you fuck!" " Fuck..." "I didn't touch your fucking sister, man!" " Pick it fucking up!" " Don't make me fucking do this, man." "Don't make me do it, man..." " Fuck." "Don't fucking cry, just fuckin' pick it up." ":" "No..." " Mm-h mm." "Now take a bite." "Take a bite, Tiko..." "Fuck you, man!" "I didn't touch your fucking sister, man!" "You're all going to fucking jail!" "Fuck you!" " All right, kiddies, let's go." " It's okay." "Woo!" " Time to up the ante!" "If you slip?" "Bang!" "Wake up in bed like it's a bad dream." " Yeah, that's assuming we have another repeat." " Hmm, if we don't..." "Make sure they bury me with my boots on." " Jesus..." " Hey, Mike, come on, man." " Shh..." "Kyle..." "You're gonna mess up my concentration." "Ah..." "Who's next?" "Huh?" " Hey..." " What?" " What are you doing?" "You're ripped out of your mind." "We still don't even know if we're gonna repeat." "We can't fuck around like this." " I'm okay." "It's okay." " Oh, who is this girl?" "There you go, girl." "Rip that pole." "Oh, one foot, one foot" " Fuck off, Weeks!" " Woo!" "I saw a smile!" " Stop it!" " I won't say another word" "No!" " Don't let go!" "Weeks!" "Weeks, help me!" "No!" " You're fuckin' dead!" "You're fucking dead, you fuck!" "Fuck you!" " See you this morning!" " Fuck you!" "You're fucking dead!" "7:30, Halsted." " You should get some hash browns before they're all gone." "Nice one, loser!" " Never realized how much I loved the hash browns." " Jesus..." " Yeah." "Only it took him three days to rise from the dead." " Good morning." " Okay, you died last night." "I saw you die." " What was it like?" "Do you... remember anything?" " I just remember right before, and then..." "It's blank." "You know, I've thought about suicide before, but..." "I mean, right in that moment, right before it happened," "I..." "Can't believe how bad I wanted to live." " We have to stop." "Right now." " What?" " If today hadn't repeated" " But it did repeat, and it looks like it's gonna keep on repeating." " Yeah, w-we're tempting fate." " We just gotta figure something out, okay?" "We gotta get out of this somehow." " You've got to be fucking kidding me." "This is a fucking gift." "We can do anything we want, anything." "It's your fuckin' loss." " Don't you think it's kind of weird that all this stuff happens on the same day your dad dies?" " My dad used to force himself on me." "And a-at first, I-I didn't know what to do." "I mean, I..." "I didn't even know what he was doing." "And as I got older," "I would fight back, but..." "Never seemed to stop it." "So, I mean, I-I don't know what..." "What, I'm supposed to give him some sort of peace of mind for that?" " Here we go." "No!" " No, no, no!" "Don't!" "Don't!" "No!" " Fuck off!" " No!" " You don't want to do this!" " Who are you?" " You don't want to do this." "Look at me." " Let go of me!" " You don't want to do this." " Please let me go, please let me go." ":" "Please..." "It's okay..." ":" "Please let me go..." " The news said it was a man, but..." "It was a girl." "Just a girl." " I know, she's, like, the same age as me." " Maybe that's what we're supposed to be doing." "You know, maybe we're supposed to be helping people." " She's still going to be there again tomorrow." " He grabbed me, and I tried, and I said stop, and he wouldn't, and I..." " Okay, we'll get you another jacket." " Copy that." "We'll bring her in for an assessment." "Get all the necessary tests." " What's going on?" " A girl got attacked." " I need a description." " I don't know what he looked like!" " Do you know who did this to you?" " Don't touch me!" " Can you give me a description?" " It was him." " What?" " It was him!" " Hey, hey!" " Just let me go..." "Don't touch me, okay?" " What the hell is the matter with you Kyle, huh?" " Kyle!" "Stop!" "Stop it!" " What the fuck?" " You raped her!" "You fucking raped her!" " I don't know what you're fucking talking about!" " Don't fucking lie to me!" "You raped a 15-year-old girl!" " Okay, first of all, she was 16, and I'm pretty sure that she was into it." " You fucking raped her!" " Tomorrow, it'll be like it never happened, Kyle!" " It doesn't make it okay." " So, what about holding up the liquor store, huh?" "Is that okay?" "What about kidnapping the dealer, sticking a gun in his face, making him eat cow shit?" "You were this close to blowing his fucking brains out, Kyle!" "Now you're on some fucking guilt trip, you're gonna tell me how I can act?" "I don't know why this is happening, but since it is, I'm gonna take advantage of it, okay?" "And you two better stay the fuck out of my way." " Why is this happening to us?" "7:30, Halsted!" " Bob!" " What do you want, Halsted?" " It's Wednesday, right?" " Last time I checked, yeah." " Nice one, loser!" " I can't believe that Charlotte was hanging out with Tiko." "No, I..." "I just never thought that she was" " She was what?" "Like you?" " I don't know." " Okay, so, I have a proposition for you." " I don't think I want to hear this proposition." " I stole them from my mom, and now you have to take them." "Come on, I went through so much trouble." " How did you steal this?" " I took them from her purse like I take everything." " Hey, Charlotte..." "Hey, uh..." "Look, do you want to, uh... just, um" " I don't want to talk to you." " Charlotte!" "Hey..." "Hi." "I'm Sonia." "Um..." "Look, I know you think your brother's an asshole, and you're probably right, but..." "It's just, if you would just let him talk to you for a minute, you would be doing me such a favour, okay?" "Because I am so tired of hearing him bitch about how shitty he's been to you, and how you'll never forgive him..." "Look, we're going to go get some Chinese food." "Why don't you guys come?" " Okay." " Okay." "We can fit in the truck, right?" " Uh, yeah." "Yeah." " Come in." "What colour?" " Blonde." " You're gonna go blond e?" " Yeah." " No..." "Did not know." "I mean, I love the blond e, but your hair..." "I mean, it goes so well with your eyes." "It's pretty." " Yeah, well, we already bought the pack, and we're doing it this weekend, so..." " Should be fun." " Oh, ho, ho!" "Well, well, well..." "If this just isn't too cute for prime time." "You girls want to get more fucked up than you've ever been in your squeaky little lives?" " Put it away, Weeks." " What, it's okay for you to smoke meth, but it's off limits for the rest of the family, is that it?" "If it isn't the friendly neighborhood dick!" " Say that again, Weeks." " How'd they ever let a gutless sack of shit like you become a cop anyways?" " Just keep talking." "Come on, Weeks, keep talking." "All right, you know what, that's not even remotely funny." "Look, you want to think very carefully about what you're doing right now." " Oh, I'm thinking, I'm thinking." "I'm all thunk out." " Mike" " Shut the fuck up, Kyle." "I'm gonna give you three seconds to get your ugly fat ass outta here." "One..." "Hand away from the gun, Gerald." "Hand away from the gun." "There you go, there you go." "Two..." "Fucking mess with me!" "Yeah, no daddy coming for you!" "Fuck off!" "You don't know what you're missing." " You guys okay?" "Hey..." "You okay?" "Charlotte, you okay?" "You all right?" "You okay?" "7:30, Halsted!" " What are you doing?" "What the fuck are you doing?" " Hey, everything that you're doing is gonna stay with you!" "It's gonna stay with all of us!" " No, Kyle!" "You do not want to do this, Kyle!" ":" "Kyle!" " You have to do this." " It's not gonna make any difference." "Nothing does." " You have to try." "You know, it's amazing..." "The things I could justify just to score, you know?" "Like, I'll take this from my mom, she'll never know it was gone, or... steal my sister's ATM card... siphon off some cash here and there." "What's a kid need with all that money, right?" "Then they..." "They trashed my house 'cause of the money I owed." "And..." "Beat the shit out of my little sister while I was five feet away... fucking blasted out of my mind." " I couldn't let anyone touch me for the longest time." " Come on, Mike..." "You haven't had anything to eat or drink all day." "Me and Sonia are worried about you, man." " Oh, you are, huh?" "The two of you, the thoughtful couple." "How nice." "God, she finally got to you, huh?" "Did she feed you the line..." "What was it?" "Uh... "I couldn't let anybody touch me for the longest time?"" "It's right before she grabs your cock, right?" "How was she for you?" "You know, I wasn't all that impressed, myself." "The biggest challenge is to find a nice place to fuck around here." "Where'd you do it?" "You didn't do it, did you?" "What's the matter, buddy?" "!" " Look!" "Mike!" "Just... stop, okay?" "Stop." "Let's just forget about this, okay?" "Let's just forget about all this shit..." "And just try again." "Let's try to figure this out." "There's got to be some kind of deeper meaning... to this." " I..." "I just took a piss in my pants." "There's got to be some deeper meaning in that, don't you think?" "See, look?" "I'll see you this morning!" " Are you tipsy yet?" " Maybe." "Aren't you supposed to be locked up somewhere?" " Charlotte, I need to talk to you." " I don't want to talk to you." " Charlotte..." " Fuck off." " I just thought if I could talk to her..." "If I could explain..." "Maybe there's just no point in me trying to explain the shit I did." " Kyle, she'll come around." " I don't know." "Are you, uh..." "Are you okay about earlier?" " Yeah." "I'm very okay." "Doesn't a part of you wonder if maybe he's right?" "I mean, if every good thing we do gets erased..." "Every bad thing we do gets erased..." "What does it really matter what we do?" " I guess..." "I just need for it to matter." "7:30 Halsted!" "Nice one, loser!" " Hey..." "Bob, where's Mike?" " What?" " Sonia?" "You know where they are?" "I don't know, Halsted, having a smoke?" "I don't know." " Drop the club." "Come on, Kyle, it's a fucking club." "Drop it." "You think you can decide how I spend my repeats?" "It's only fair that I return the favour." "Take the knife." "The knife on the table, take it." " What?" " Come on, Kyle." "Good." "Stand over there." " Mike, what" " Now..." "Cut his throat." " Mike, please don't do this." " Cut his throat, or I'll put a bullet in her leg." "I kid you not, Kyle." "I will put a hole in her leg the size of a fucking grapefruit." "Do it, or I'll put a bullet in her head!" " You're fucked!" " That's right, get angry!" "Get motherfucking feral!" "Cut his fucking throat!" "Welcome to the club, Kyle." " You're okay..." "Come on, come on." "All right..." " We'll have fun..." " I'm okay." "Come on, what's wrong?" "Come on..." " No, I'm okay." "I'm okay." " Fuck!" " Get the fuck up!" "Get up, you fucking piece of shit." " I knew you had it in you." "I'm gonna give you three seconds to get lost." " Fuck you." "See you this morning, Kyle." "7:30, Halsted!" " Do you want me to come up?" " No." "I'm fine." " You're gonna die tonight." "Don't ask me how I know, but it's true." "I've thought about what I wanted to say to you so many times." "I don't hate you anymore." "I don't, but I have to move on from this." "I have to, or else no thing's gonna change..." "For any of us." " What do you want?" "Are you in trouble?" " No, I..." "They let us out for a few hours." "Can I-can I come in?" "I really need to talk to Charlotte." " I-I really don't think it's a good idea." " Mom, I really need to talk to her." " Are you clean?" " Yeah, Mom." "Please let me talk to her." " Okay." " Residents are reeling tonight over the death of two local police officers in what's shaping up to be a double homicide." "The suspect is described as a Caucasian male in his early 20s..." " Charlotte?" " What are you doing here?" " I need to talk to you." " Get the fuck out of my room." " No." "Charlotte, no, I'm not going anywhere until you and I have talked, okay?" " We've got nothing to talk about." "Who's in the car?" "One of your addict friends?" " Her name's Sonia." "Yeah, I met her in rehab." "I've been thinking a lot lately..." "Just about..." "About what I did to you and to Mom." " I don't want to hear this, Kyle." " And I can't let another day pass without telling you..." "Without telling you how sorry I am." " Fine." "Are we through now?" " Thing is," "Charlotte, I see you going down the same path that I did, and" " You think I'm a fuck-up like you?" " No..." "No, that's not what I meant." " You don't have to watch over me." " But I..." "I do." "Charlotte..." "Charlotte, I do, 'Cause that's what big brothers do for their little sisters." "And I know you probably don't care right now, but..." "But from now on, I'm going to be there for you." "I'll be there for you when it counts, because..." "I love you." "And..." "And I'm gonna be your big brother." "7:30, Halsted!" " Sonia!" " Kyle?" " Drop it." "Drop it." "Good." "Now, I could tie you up all day, Kyle, let you wallow in your own piss, but that's not much fun." "So what we're gonna do is play a little game of hide-and-seek... with a twist." "If I find you..." "I'm gonna spend the rest of the day hurting you." "You've got one minute." "One minute." " You okay?" " Other door." "One..." " Come on!" " ...two... three... four... five... six... seven... eight... nine... ten..." "Come on, come on..." " One minute!" " There!" "There!" "This way!" "Yeah!" "Woo!" " Come on." "Come on..." " Come on out, kiddies, I ain't got all day." "Come on out!" " Come on." "Come on!" "Come on..." "Come on, come on..." "Go!" "Come on!" "Go!" " Are you guys having fun yet?" "You know, the last rehab place I went to..." "They had us act out horrible events from our past." "What do you say, Logan?" "You could be nine years old again." "I could play daddy!" "Or maybe Kyle could play daddy since he can't stop fucking you!" "What the fuck are you doing?" " Go." "Go!" "Go!" " Hey..." "Hey, kid!" "Hey, you all right?" " It doesn't snow today." "What day is it?" "I said, what day is it?" "!" "Oh, fuck..." " How are you doing?" " I'm fine." "I just got a tetanus shot and some stitches." "Where is he?" " No one's seen him." " We need you to come with us." " Get your fucking head down on the floor!" "If you two fucking move," "I will put a fucking bullet in your head, do you hear me?" "I'll fucking kill you." "I will fucking kill you." " Mom?" "I'm sorry." " Lieutenant, this is Kyle Halsted and Sonia Logan." " So I understand you've been brought up to speed?" " Yeah." " Most important thing is you keep him calm." "Gimme the phone, come on." "Hurry up!" "Hello?" " I have your friend right here." " Mike?" " Kyle." " Mike, man, y-you didn't know." "You thought the day was gonna repeat again, right?" "You thought you had a clean slate." "You didn't know." " You think a jury's gonna fuckin' believe that?" " Mike..." "We can fix this." "We got into this together, right?" "So we can fix it together." " You guys turned on me, man." "You should've let it go." "You should've let it run its course." "You should have had my back, Kyle!" "Mike..." "Please..." "Don't do this, man." "Don't take it out on them." "Please, man, don't do this to Charlotte." "Mike?" "Mike!" " Okay, we're going to have to go inside." " No, no, let me try again, I can" " Listen, this kid has killed two people already." "Come with me." "Hey, hey, hey!" " No, no, Kyle, don't!" " Stand down!" "Everybody, stand down!" " Mike?" " Kyle, you die now, you die for keeps." " Mike, I'm coming up, man." "Mike, you gotta let 'em go." " Nobody move." "Nobody fucking move!" "Stay still and shut up!" " Mike!" "That's my sister." "That's my baby sister and I'm not gonna let you hurt her, okay?" " I'm warning you, Kyle." "Stay where you are." " Mike..." "It's over." " Stop." " Just give me the gun." " Stop." " I was never gonna make amends with my old man." "I never was, and I never will." "It doesn't matter how many days repeat!" " Give me the gun." " That's the difference between you and me, right?" "Mike!" "Shh, shh..." "It's okay, it's okay..." "Shh, shh..." "Shh..." "Shh, it's okay." " You okay?" " Yeah." "¢Ü Where the doors are moaning ¢Ü" "¢Ü All day long ¢Ü" "¢Ü Where the stairs are leaning ¢Ü" "¢Ü Dusk till dawn ¢Ü" "¢Ü Where the windows ¢Ü" "¢Ü Are breathing in the light ¢Ü" "¢Ü Where the rooms are ¢Ü" "¢Ü A collection of our lives ¢Ü" "¢Ü Where the doors ¢Ü" "¢Ü Are moaning all day long ¢Ü" "¢Ü Where the stairs are leaning ¢Ü" "¢Ü Dusk till dawn ¢Ü" "¢Ü Where the windows ¢Ü" "¢Ü Are breathing in the light ¢Ü" "¢Ü Where the rooms are ¢Ü" "¢Ü A collection of our lives ¢Ü" "¢Ü This is a place ¢Ü" "¢Ü Where I don't feel alone ¢Ü" "¢Ü This is a place ¢Ü" "¢Ü That I call my home... ¢Ü" " Get up, Weeks." "Another day in paradise." "¢Ü Breakneck speed ¢Ü" "¢Ü Tying up your hands ¢Ü" "¢Ü 'Cause you're landing back on your feet ¢Ü" "¢Ü You know what I mean ¢Ü" "¢Ü Vowel change ¢Ü" "¢Ü I remember when our voices used to sound the same ¢Ü" "¢Ü Now we just translate ¢Ü" "¢Ü 'Cause I'm still amazed you made it out alive ¢Ü" "¢Ü After what you did ¢Ü" "¢Ü Born on your feet running ¢Ü" "¢Ü Forest fires underneath your bed ¢Ü" "¢Ü But it's good to be back ¢Ü" "¢Ü Good to be back Good to be back ¢Ü" "¢Ü Spell it out ¢Ü" "¢Ü I always skip the words ¢Ü" "¢Ü 'Cause all the pictures are so bright and loud ¢Ü" "¢Ü Better off than now ¢Ü" "¢Ü 'Cause I'm still amazed you made it out alive ¢Ü" "¢Ü After what you did ¢Ü" "¢Ü Born on your feet running ¢Ü" "¢Ü Forest fires underneath your bed ¢Ü" "¢Ü 'Cause it's good to be back ¢Ü" "¢Ü Good to be back ¢Ü" "¢Ü Super fun ¢Ü" "¢Ü At the movies drunk and young ¢Ü" "¢Ü Double knots that came undone ¢Ü" "¢Ü But the big bad years are gone ¢Ü" "¢Ü Yeah the big bad years are done ¢Ü" "¢Ü And gone away ¢Ü" "¢Ü I remember when our voices used to sound the exact same ¢Ü" "¢Ü Now we just translate ¢Ü" "¢Ü 'Cause I'm still amazed you made it out alive ¢Ü" "¢Ü After what you did ¢Ü" "¢Ü Born on your feet running ¢Ü" "¢Ü Forest fires underneath your bed ¢Ü" "¢Ü But it's good to be back ¢Ü" "¢Ü Good to be back Good to be back ¢Ü" "CNST, Montreal"	{ "pile_set_name": "OpenSubtitles" }
News If The World Lets Venezuela Fall, Democracy In The Region Will Fall With It June 12, 2017 If The World Lets Venezuela Fall, Democracy In The Region Will Fall With It CARACAS, Venezuela ― For the past two months, Venezuelans like myself have taken to the streets to exercise our constitutional right to peaceful protest against the most repressive regime in our nation’s history. While the unconstitutional and failed attempt by the Supreme Court to dissolve the Venezuelan National Assembly on March 29 sparked these protests, we have sustained them for so long because we know we are in the fight of our lives. We protest amidst an immense humanitarian crisis. Our failing economy has led to a scarcity of food and medicine, which has in turn led to an increase in the prevalence of malnutrition and other preventable diseases in the country. Our suffering is gravely compounded by the government’s despotic response to our cries for help. Since the start of the protests, there have been at least 60 deaths and about 1,000 people have been wounded, many a result of the indiscriminate violence used by the armed forces. Organizations on the ground have identified almost 3,000 arbitrary detentions, numerous reports of torture and some 303 political prisoners. One of those political prisoners is my husband, Leopoldo López, the opposition leader and a prisoner of conscience. Leopoldo has been in prison for over three years because he publicly challenged the regime by calling for peaceful protests as a way out of our suffering. Three years later, and the people of Venezuela still hear his call. He remains in jail because the Nicolás Maduro government fears him. The repression against us becomes more violent every day. Violence, as Mahatma Gandhi once roughly said, is the fear of the ideals of others, and the regime fears our ideals of peace and freedom. There already have been deaths due to tear gas thrown directly at crowds, and armed tanks have rolled over protesters. Now, facing a shortage of ammunitions, the regime has begun shooting buckshot. The government’s violence has only strengthened our resolve and increased the international support for our cause. But the Maduro regime is now taking illegal and unconstitutional action in an attempt to dismantle that support. When the governments of the region tried to hold President Maduro to account in the Organization of American States for his anti-democratic acts, he responded by choosing to begin the process for withdrawing Venezuela from the organization rather than face his international and legal commitments. When our people gathered signatures for a recall referendum, Maduro stopped it from happening. Now, when we have called for early elections, Maduro says he is going to rewrite the constitution to redistribute political representation in the country so that the voice of the majority will be silenced in favor of dictatorship. These acts isolate Maduro internationally and draw comparisons to some of the worst dictatorships in the region’s past. His control over the country is unsustainable, as is the overall crisis. We have arrived at the inevitable collapse of a failed model where power is corrupted and held in the hands of an elite few. This reality to which we are subjected is inhumane, and it does not correspond to the promises of the 21st century. We organize in defense of our fundamental rights. We have released our strategy very publicly, a strategy first stated by Leopoldo three years ago. Our method is non-violence, our terrain is the street and our purpose is all rights for all people. Venezuelans have resisted on the streets, and we will be there for as long as is necessary. But the international community should also recognize that we understand the need to identify constitutional means to usher in a democratic transition. To start, we have identified four demands for a path forward: the release of all political prisoners, the opening of a United Nations-led humanitarian channel, the immediate scheduling of general elections and the respect for the autonomy of the National Assembly. We are under immense pressure because what is at stake is not only the survival of Venezuelans, but the survival of democracy in the region as well. How is it possible that a nation with the resources of Venezuela cannot feed its citizens? That our children die of curable diseases for lack of basic medicines? That mothers do not know if their children will return home each day or succumb to the violence on the street? This is morally indefensible. We have arrived at the inevitable collapse of a failed model where power is corrupted and held in the hands of an elite few. And the sad truth is that a corrupt few benefit from this chaos, including the government officials who profit off of our misery on the black market and the narco-traffickers who often don’t faces any foreseeable consequences. But there are many who help prop up this regime who do not benefit from this situation ― and they are not happy. Those National Guard members under orders to shoot at us protesters fear that their family members and friends may be on the receiving ends of their bullets. They, too, have no way to properly feed their families and no hope if a family member gets sick. I have talked at length with Leopoldo about the need to build bridges with those factions of the government that want to detach from the dictator and his criminal actions. We know there are very few people who support this instability, which has generated a massive exodus of Venezuelans, skyrocketing rates of crime and rolling blackouts that have come to define life in this energy-rich country. This regime, whose highest officials are accused of drug trafficking, is a stain on the country and the continent. But this dark hour serves as an opportunity. With around 90 percent of Venezuelans expressing a desire for change in the country’s current situation, now is the time for us reconcile our differences and come together for the greater good of the country. Reconciliation will bring us peace, and our diversity of thought and background will make us a stronger nation. Venezuelans have shown that we have the commitment and the courage to rescue our democracy. Despite our differences, we are more united than ever. And we ask that the international community share our solidarity. As May drew to a close, foreign ministers of the OAS nations met to discuss Venezuela. They deferred taking action this week because they couldn’t come to a consensus on a way forward. While this was disappointing, the collapse of Venezuela is only going to accelerate as the humanitarian crisis grows and Maduro is forced to take more extreme measures to maintain his grip on power. When the foreign ministers meet again later this month, I trust that the OAS will take the necessary action, in line with the values enshrined in the Inter-American Democratic Charter, to stand on the right side of history.	{ "pile_set_name": "Pile-CC" }
Schedules and plans, as most cruisers know, are written in the sand at low tide. It doesn't take much wave action for them to wash away and require us to make new ones. We knew we wanted to make trips to PA and NC to see family. There was also this RV show taking place in Hershey PA (“America's Largest”). We wanted to take Orion for a trip up the bay. And we kept shopping for an RV online and elsewhere. So, we made a plan. First, the RV show. That's on the way to Allentown to visit Dave's Mom and sister. Then back to Hampton. Then to NC for a visit with Cathy's family that would coincide with our great-nephew's baptism. Back to Hampton, where we'd get Orion ready to go out on her trip. Sounds great. And we actually managed to get some of it done. Hershey RV show in Giant Center America's Largest RV Show We've been to dozens of boat shows and, in the last couple of years, a few RV shows. So what does the “Largest” RV show look like? It's held in Hershey PA at the Giant stadium where the Hershey Bears Hockey team plays. However, the RV's are not inside the stadium. They are on 21 acres of parking lot that surrounds the stadium. The stadium building is filled with vendors, and a few venues for seminars. We helped open up the show on a beautiful, crisp September morning, and were dragging ourselves out to the truck in the dark as it was closing down. By this time, our search had narrowed to a particular model of Fifth Wheel – a 25 ft Palomino Puma. Since this is considered very short for a fifth wheel, we didn't find any of this model at the show, but did manage to find one made by a different Forest River make, Flagstaff, that came pretty close. The unit at the show was loaded with extras we didn't really want, and we didn't find their price for a stripped down model too attractive. So, we'd keep shopping. The Tin Man ponders weighty matters in York PA In the meantime, we learned about fifth wheel hitches, and the unique problems we have in our short bed truck. We talked to vendors about roofs and how to replace one that is failing (one of the ways an RV can go bad quickly). There were seminars about traveling to Alaska and about maintaining your RV that we managed to squeeze in. Although maintaining our sailboat is a good foundation for maintaining the RV, there are some obvious differences. By the end of the day, we were on overload – armed with more information and also more questions. Do we buy a new one or a quality used one? Do we buy now or in the spring? Which hitch do we get? However, a week later, Dave stumbled across a new fifth wheel on Craigs List that was almost exactly what we were looking for – a 2015 Palomina Puma 253FBS. After some conversations with the dealer and lots of investigation on the internet, we managed to make a deal. We haven't seen it yet, but it's waiting for us to arrive in a couple of weeks. So, we're one step closer to becoming land cruisers – when we're not on the water. Jason with mom, dad and Pastor Mac Family North and South After leaving the RV show, we spent several days in Allentown (as planned), and discovered the financial paperwork had slowed to a trickle, allowing us to enjoy the time together with Dave's mom and sister a little more. By Sunday, we were making our way south again to Hampton. Or not. Before leaving to head north, Orion's refrigeration had stopped working. It needed a new compressor, which was on order and still delayed. So, we asked each other why go back to the boat. The repair couldn't be done until the compressor arrived. So, we decided to keep driving south and west toward Winston-Salem to visit with Cathy's mom. It didn't hurt that it took us by way of another RV dealer, of course. Carolyn honors the birthday girl Arriving in NC on Monday evening, we had almost a full week visit with Cathy's mom, which included some house projects and paperwork. Dave can now say that he has planted collards, which was yeoman's duty, since he is unlikely to want to eat any of their eventual harvest. And Cathy was able to sort through a few financial issues with her mom outside all of the hubbub of the large Christmas gathering. On Sunday, we joined the rest of the family for our great-nephew, Jason's, baptism in Raleigh. After the service we gathered for a festive lunch at Cathy's sister's new home in Raleigh. Grace and John had moved there in September, after having raised their family in Memphis, TN. It was a dual celebration of Jason's baptism and Grace's birthday the day before. As is typical at these things, there was no shortage of good food. And, of course, you would never know that Grace and John had moved in less than a month earlier. The new house was beautiful. After lunch, we made our way back to Hampton, arriving just before high tide and discovered to our dismay that the finger piers were already under water thanks to several days of rain, the super moon, and the persistent northeast winds. Rather than slosh through the water with our stuff, we took Steve up on a standing invitation to stay at his house. But by Monday afternoon, we were back on Orion. We just weren't going to stay there that long. Thursday afternoon would find her stripped of canvas, battened down for the storm as we headed out of town, pulling Jr behind us. Orion Jr says goodbye to Steve's yard, as the water rises. Rain, Rain, Go Away Seven foot tides. That was the early forecast when it was possible that Joaquin would track directly up the Bay. And it wasn't arriving until late Sunday / early Monday. Before then, we were going to have rain and lots of it. That, combined with gale force northeast wind would create coastal flooding by Friday afternoon that would start to rival hurricane Irene from 2011. Orion was likely to be fine. We just needed to strip the canvas and get our stuff off. But we couldn't stay on board unless we wanted to wade to shore. With that much water, the docks would be underwater for most of the day. Then there was Orion Jr which was sitting in Steve's backyard in Poquoson. With the forecasted tide levels, Jr's spot would likely be under water. That meant we had to find another place for her. Looking out of Steve's house toward Jr's parking spot by the trees Unfortunately, it was already too late to get the boats ready “before” the weather arrived. By Tuesday afternoon, it was already raining and wasn't supposed to stop for any significant stretch of time for the next week. That meant taking down canvas in the rain and stowing it wet down below. Fun. Then off to Steve's where we had to get Jr ready to move in the rain as well. Dave put air in all of the tires, while Cathy mopped up all the water down below. (We have had a significant leak that was related to our temporary hatch boards. Needless to say they are not being used anymore.) We put up the flags, replaced the straps with new ones that Cathy had made earlier in the summer. (Good thing.) Once everything was re-stowed down below and secured on deck, we hooked up and made our way to Jarratt and our daughter's house. A hundred miles inland would at least mean we were far enough away from the coastal flooding, if not from the endless rain. And her property gave us a few options for storing Jr. We were splitting our time between several boats during the time back in Hampton: Orion, Orion Jr, Bay Dreamer, and our friend Betty's boat, Kanoa. We managed to get a lot done in a relatively short time. As Rat says, there's “nothing half so much worth doing as simply messing about in boats”. Betty's new bimini Pulling out the sewing machine Our busy summer had caused Cathy to defer several sewing projects that she finally was able to catch up on. The biggest was to make a bimini for our friend, Betty's power boat. Before Cathy could pattern the bimini, we needed to repair a couple of mount points for the bimini frame. Dave managed to find a little starboard to provide the backing for one side mount, and we found the missing hardware for a good price at perfectfit.com. With a little epoxy to fill the old holes, the new mounts allowed us to open the existing bimini. Cathy used this to pattern the new bimini, which fit very well. This is her 3rd time making one, and each time she has learned more and made the building easier. The result looks pretty good, too. It also was a big help to have access to a house to work in (thanks to Sue and Steve), where she could leave the project laid out over the 3 days it took to complete. Back at Joy's, Steve had asked for a new pocket for Bay Dreamer's starboard locker, and while she was at it, Cathy re-stitched his dodger. Orion Jr has a new grill that needed a cover, and which now has one. The tiller handle box in need of repair Hardware and Software It was almost by accident that we realized as we were putting Jr away for the season that there was a BIG hole in the box that held the tiller extension handle locked in place. The plastic had simply become too brittle and failed. However, the folks at Forespar were great, sending us a replacement for free. It was an exact replacement, so the work involved was mostly cleaning up the old opening and ensuring it was caulked well when installing the new – a pretty easy install. Over on Bay Dreamer, Dave helped Steve investigate why his auto-pilot had stopped working. As supervisor, Dave got to send Steve down into the “hole” by the rudder to discover the rudder sensor had slipped out of place. He was also on hand to hellp install clips on Steve's azy jacks to make it easier to disconnect them when he wants to deploy his sun shade. We had an unfortunate “oops” when we were showing Orion to some prospective buyers. It appeared that one of the AIS cables that connects to the PC down below had failed. This connection is critical to ensuring the AIS at the helm works. Dave ordered a new one, and it was another pretty easy install. Once in place, the AIS on the PC at the helm was working as before. Last, but not least, Dave had to talk to the city of Hampton about a new boat licensing fee they were implementing. We had received some mail that requested feedback, but it was already late when we received it. The bottom line was that Florida hadn't told VA that we had moved Orion Jr and the portabote to Florida. Once Dave got VA DNR to confirm this, Hampton took them over their books. Tri-Service – Again On a cloudy morning, the first hint of fall after a long, hot summer, we fell in line behind the other sailboats making their way to annual Tri-Service Race, passing the aircraft carrier Eisenhower as we left the Hampton River. We were crewing this year on Bay Dreamer, with Steve as Captain and Linda as first mate. What a difference a year makes. Last year, we drifted backward toward the Monitor Merrimac Bridge Tunnel as the current overpowered the little wind to keep us from even making the start line. This year we had a good 15 knots of wind all around the course, finishing in only an hour and half, as we made the circuit off Fort Monroe, out to Thimble Shoals light and back. It was a lot of fun. The Tri-Service is a competition between the yacht clubs from the Navy, the Air Force and (what used to be) the Army at Old Point Comfort. The cup had been ours for several years, but was lost in 2014. With much fanfare, we won it back this year, as we hosted the post-race party. There were cheers from everyone, especially our commodore in getting the cup back. Tarun on Orion Parting Shots When we weren't working on boats, or crewing on boats, we had time to enjoy some dinners with friends and a few visits from Bonnie and Troy and the kids – even one where they arrived by boat after the Tri-Service race. We made it to Busch Gardens one final time for the season as well. But the biggest surprise was a visit from Tarun (a friend from our winter in Marathon) who stopped by Orion in Hampton as she was heading up to Williamsburg.	{ "pile_set_name": "Pile-CC" }
I've problems with the handle pass. I ride at a cable park and until now I managed to do some handle passes but it is really difficult. I am trying over and over again but can't get a better result. There must be a point I am missing. For example the guy in this video can easily do the handle pass even by pulling the handle to his back just with one hand. My problem is I can't pull the handle to my back. The rope is always really tense and I don't have the power to pull the handle to my back. If I get away from the cable doing progressive edge (or If I pull the handle with both hands really strong) I create enough slack in the rope to do the handle pass but I only have time to do just one pass. I've seen guys doing surface 720 or over and it looks like they are doing the trick easily without wasting too much power to pull the handle, it looks like they can easily pull the handle to their back. P.S.: If I use the classic method and keep the handle near to my hip with both hands, as soon as I let go one hand to do the pass, I can't keep the handle close to my hip anymore and the handle goes back to the initial position which is far away from my hip. A good way to practice off the water that a good friend taught me is to get your handle. Hook up a bungee cord to it and put a gallon jug of water on the other end and use the momentum of swinging it around to get that muscle memory down. Hope I explained this good enough. But if you do it enough when your on the water it should just come natural. Make sure to practice passing it both ways. Basically just keep passing it around over and over using the weight and momentum to mimic the pull from the boat or cable. You talking about kicker spins like your other post? The guy in the video is a professional rider that rides all day every day. Those guys have built up amazing strength in their arms and backs. I wouldn't worry too much about it. But as I mentioned in the other thread, spinning at the cable is easier than behind the boat as you can initiate your spin earlier. So use that to your advantage and start pulling in as you are riding up the obstable. There is very little friction when you're on a ramp/kicker so you should be able to advance yourself relatively easily. Keeping your arms out on your approach will help so that you have some room to pull in on the handle. no expert as I am not there yet but it looks like me most riders have a good position before rotating. So much so that the handle is right on their hip and they just hold position and rotate around the handle rather than having put the handle.	{ "pile_set_name": "Pile-CC" }
Q: How can I duplicate the terminal/prompt in a file like using history + sink I know the sink command can divert the stdout to a file, but basically if I do this in the command window: library(data.table) a = 1; b = 2; a [1] 1 Only the last line [1] 1will be printed in the file. Is there a way my whole command window could be printed to a file like it is done with sink ? NOTE: I want it to be done each time I write something to avoid losing everything if R crashes, meaning I do not want to have to type printAllCommandToFile() for this to be done A: What about txtStart from the "TeachingDemos" package? See here. Sometimes, when introducing students to R, I've recommended it to help them remember what they did and what the results were, a situation somewhat like you describe. In my experience on a Linux machine, even if you close R without calling txtStop, the output is saved to whatever text file you had specified at the start of your session.	{ "pile_set_name": "StackExchange" }
Q: Estimating the $L^1$ norm of the Dirichlet kernel Suppose $D_N(x)=\frac{\cos\frac{x}{2}-\cos(N+\frac{1}{2})x}{\sin\frac{x}{2}}$. How to prove the inequality below$$\int_{-\pi}^\pi\|D_N(x)\|\text{d}x\leq c\log N$$ for some constant $c>0$ ? A: By recalling that $$D_n(x)=\sum_{k=-n}^n e^{ikx}=1+2\sum_{k=1}^n\cos(kx)=\frac{\sin\left(\left(n +1/2\right) x \right)}{\sin(x/2)}\tag{1}$$ it is not difficult to locate the stationary points of $D_n(x)$ in $(-\pi,\pi)$ and conclude that $$ \left\|D_N(x)\right\|\leq \min\left(2N+1,\frac{\pi}{\|x\|}\right)\tag{2}$$ from which: $$ \int_{-\pi}^{\pi}\|D_N(x)\|\,dx\leq \int_{-\frac{\pi}{2N+1}}^{\frac{\pi}{2N+1}}N\,dx+2\pi\int_{\frac{\pi}{2N+1}}^{\pi}\frac{dx}{x}\leq 10\log N\tag{3} $$ for any $N\geq 8$.	{ "pile_set_name": "StackExchange" }
:imagesdir: ../../../images [[sahi-controller]] ==== Sahi Controller [#git-edit-section] :page-path: docs/manual/testdefinition/advanced-topics/sahi-controller.adoc git-link:{page-path}{git-view} \| git-link:{page-path}{git-edit} TIP: Use the Sahi Controller to identify elements on the page to write and test Sahi methods! There are two ways to get Sahi instructions into your testcase `your-testcase.js`: * identify, copy & paste from the Sahi Controller * record by the Sahi Controller, copy & paste from the file, see <<sahi-recorder>> [[sahi-open-controller]] .Open the Sahi Controller Add to your testcase the following line, at position where you want to identify your HTML object: [source,js] ---- //.... your testcode env.sleep(9999); ---- Then start your test suite and the Sakuli test should appear and stop at that position for 9999 seconds. The "sleep" statement is a nice trick when writing long tests; wherever you put a 9999s sleep in, the test will execute until this position and wait. Think of it like a breakpoint when debugging a program. Now open the Sahi Controller (hold the `ALT` key on Windows or `CTRL + ALT` on Linux and doubleclick anywhere on the page) to open this window: image:tutorial_contoller.png[sahi_controller] [[sahi-controller-copy-paste]] .copy/paste code First, we want Sahi to check if there is for example the Sakuli Logo on the page. Hold the `CTRL` key and move the mouse pointer on the logo. Watch the Sahi Controller: it detects the HTML elements below the mouse pointer and generates the http://sahipro.com/docs/sahi-apis/accessor-apis.html#_image[accessor method for "image"] automatically: image:tutorial_logo_accessor.png[logo_accessor] Click on "Assert" to let Sahi autogenerate http://sahipro.com/docs/sahi-apis/assertions.html[assertion methods]: image:tutorial_assert2.png[assert] Just copy the second line (which checks the visibility of an element) into the clipboard and paste it into your testcase `your-testcase.js` before the `env.sleep(9999)` statement. Further, we want for example to assure that the contact form of the web page os displayed correctly. Move the mouse pointer down to the "Kontakt" link; Sahi should display the accessor `_image("Kontakt zu ConSol")` . This time use the "click" button on the controller . To execute a click; this also generates the complete http://sahipro.com/docs/sahi-apis/action-apis.html[browser action] statement . copy/paste also into the test case image:tutorial_click_action.png[click] In the end, Sahi should check that the appeared popup window contains the text "Schreiben Sie uns!". You guessed it - move the mouse pointer over this text and click the "Assert" button again. The fourth assertion is the right one, which we also paste into the test script: image:tutorial_contains_text.png[contains_text] Now remove the "sleep" statement from the script file; it should look now like that: [source,js] ---- _dynamicInclude($includeFolder); var testCase = new TestCase(60, 70); var env = new Environment() try{ //your code _assert(_isVisible(_image("sakuli.png"))); _click(_image("Kontakt zu conSol")); _assertContainsText("Schreiben Sie uns!", _heading3("Schreiben Sie uns!")); //env.sleep(9999); } catch (e) { testCase.handleException(e); } finally { testCase.saveResult(); } ---- TIP: Perhaps you want Sahi to highlight the items it is acting on: just use the `_highlight()` method from the http://sahipro.com/docs/sahi-apis/debug-helper-apis.html[debug helper API] to mark each element with a red border before accessing it: `_highlight(_image("sakuli.png"));`	{ "pile_set_name": "Github" }
Sony will shift its European headquarters from Britain to the Netherlands to avoid Brexit-related customs issues, but operations at its current UK company will remain unchanged, a company spokesman said Dutch officials are in contact with more than 250 companies about a possible post-Brexit move, the government said Wednesday, after Sony revealed it would shift its base to the Netherlands. The Dutch government will announce a final figure in February but "every new arrival of a business, big or small, is a success," Michiel Bakhuizen, a spokesman for the Netherlands Foreign Investment Agency, told AFP. Japanese electronics giant Sony is following Panasonic in moving its European headquarters across the North Sea to the Netherlands ahead of Britain's scheduled departure from the EU in March. While Prime Minister Mark Rutte said during a recent visit by Japanese premier Shinzo Abe that he "doesn't see Brexit as a business opportunity", the Netherlands has still pushed hard to win post-Brexit investment. Via the investment agency, the Dutch government is "in contact with more than 250 interested in an eventual move to the Netherlands because of Brexit", Bakhuizen said. "The number of businesses we are in contact with for a possible arrival is growing. At the start of 2017 it was 80, at the start of 2018 150, and now it's more than 250," he added. "This increase will continue and it's not strange, because there is great uncertainty at the moment in Britain. And if there is one thing that's bad for business, it's uncertainty." The spokesman said he would not comment on "individual" cases like Sony, but added that the Netherlands welcomed any such decision. "In mid-February we will announce the number of companies that have left the United Kingdom for the Netherlands because of Brexit," he added. Asked whether Abe's visit had helped with the Sony move, the spokesman said that "it's certain that these political and diplomatic moments help." However Rutte warned in a press conference with Abe that any extra investments would be offset by the overall "negative impact" of Brexit, particularly if Britain crashes out without a deal with the EU. Dutch officials said this week they are preparing for the "blue sea of uncertainty" that a no-deal Brexit would create. Dutch Foreign Minister Stef Blok told a parliamentary committee on Wednesday that "we have started early with our preparations, but of course it has become more intensive because of a possible no-deal Brexit."	{ "pile_set_name": "OpenWebText2" }
Charles Honoris Charles Honoris (born in Jakarta, ) is a member of the Indonesian House of Representatives from the Indonesian Democratic Party - Struggle (PDI-P). He was elected from the DKI Jakarta III (North Jakarta, West Jakarta and the Thousand Islands) electoral district with 96,842 votes. Currently he is serving at Commission I of the House of Representatives overseeing Defence, Foreign Affairs, Intelligence, Communications and Informations. He is married to Irene Bertina Irawan and resides in West Jakarta. Charles is the son of Indonesian businessman Luntungan Honoris Charles was educated in political science at the International Christian University in Japan. An active writer, he has written since his college days on issues related to politics, human rights and international relations published in several Indonesian national media. Charles Honoris is chairman of Taruna Merah Putih Jakarta chapter, a youth organization of the Indonesian Democratic Party - Struggle Education Sekolah Pelita Harapan primary school, Karawaci Indonesia, 1996 Sekolah Pelita Harapan secondary school, Karawaci Indonesia, 1999 Christ Church Grammar School, Australia, 2001 International Christian University, Tokyo, 2007, Family Charles is the fifth child of Luntungan Honoris, an Indonesian businessman who together with 8 other Indonesian entrepreneurs participated with Bill Gates in donating US 80 million dollars into Indonesia Health Fund Luntungan Honoris is listed as president commissioner of property company PT. Modernland Realty Tbk and member of the Board of Protective Harmony Family of South Sulawesi. Work Associate, Hanafiah Ponggawa & Partners 2007 - 2009 Direktur, PT. Foton Mobilindo, 2009 - Vice President, PT. Modernland Realty Tbk, 2012 - Elected as member of the House of Representatives (2014-2019) 'Charles Honoris' '' who is also Chairman of Taruna Merah Putih Jakarta chapter, a youth wing organization of PDI-P was elected as a member of the Indonesian House of Representatives during the elections held on 9 April 2014 for a five-year term. Charles received the most votes in his electoral district with 96,842 votes surpassing senior politicians such as Effendi Simbolon and Speaker of the House of Representatives Marzuki Alie from the (Democratic Party). Further reading The Jakarta Post It's time to be truthful about the past Mengenal Lebih Dekat pada website Charles Honoris Profil Caleg di BeritaSatu.com Berita tentang Charles Honoris di pemilu 2014 References Category:1984 births Category:Living people Category:Indonesian Democratic Party of Struggle politicians Category:Members of the People's Consultative Assembly	{ "pile_set_name": "Wikipedia (en)" }
// // Copyright © 2020 osy. All rights reserved. // // 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. // // Parts taken from iSH: https://github.com/ish-app/ish/blob/master/app/AppGroup.m // Created by Theodore Dubois on 2/28/20. // Licensed under GNU General Public License 3.0 #import <Foundation/Foundation.h> #include <dlfcn.h> #include <errno.h> #include <mach/mach.h> #include <mach-o/loader.h> #include <mach-o/getsect.h> #include <pthread.h> #include <stdio.h> #include <string.h> #include <sys/mman.h> #include <sys/sysctl.h> #include <TargetConditionals.h> #include <unistd.h> #include "UTMJailbreak.h" struct cs_blob_index { uint32_t type; uint32_t offset; }; struct cs_superblob { uint32_t magic; uint32_t length; uint32_t count; struct cs_blob_index index[]; }; struct cs_entitlements { uint32_t magic; uint32_t length; char entitlements[]; }; extern int csops(pid_t pid, unsigned int ops, void * useraddr, size_t usersize); extern boolean_t exc_server(mach_msg_header_t , mach_msg_header_t ); extern int ptrace(int request, pid_t pid, caddr_t addr, int data); #define CS_OPS_STATUS 0 /* return status / #define CS_DEBUGGED 0x10000000 / process is currently or has previously been debugged and allowed to run with invalid pages / #define PT_TRACE_ME 0 / child declares it's being traced / #define PT_SIGEXC 12 / signals as exceptions for current_proc / kern_return_t catch_exception_raise(mach_port_t exception_port, mach_port_t thread, mach_port_t task, exception_type_t exception, exception_data_t code, mach_msg_type_number_t code_count) { fprintf(stderr, "Caught exception %d (this should be EXC_SOFTWARE), with code 0x%x (this should be EXC_SOFT_SIGNAL) and subcode %d. Forcing suicide.", exception, code, code[1]); // _exit doesn't seem to work, but this does. ¯\_(ツ)_/¯ return KERN_FAILURE; } static void exception_handler(void argument) { mach_port_t port = (mach_port_t )argument; mach_msg_server(exc_server, 2048, port, 0); return NULL; } static bool am_i_being_debugged() { int flags; return !csops(getpid(), CS_OPS_STATUS, &flags, sizeof(flags)) && flags & CS_DEBUGGED; } static NSDictionary parse_entitlements(const void entitlements, size_t length) { char copy = malloc(length); memcpy(copy, entitlements, length); // strip out psychic paper entitlement hiding if (@available(iOS 13.5, )) { } else { static const char needle = "<!---><!-->"; char found = strnstr(copy, needle, length); if (found) { memset(found, ' ', strlen(needle)); } } NSData data = [NSData dataWithBytes:copy length:length]; free(copy); return [NSPropertyListSerialization propertyListWithData:data options:NSPropertyListImmutable format:nil error:nil]; } static NSDictionary app_entitlements(void) { // Inspired by codesign.c in Darwin sources for Security.framework // Find our mach-o header Dl_info dl_info; if (dladdr(app_entitlements, &dl_info) == 0) return nil; if (dl_info.dli_fbase == NULL) return nil; char base = dl_info.dli_fbase; struct mach_header_64 header = dl_info.dli_fbase; if (header->magic != MH_MAGIC_64) return nil; // Simulator executables have fake entitlements in the code signature. The real entitlements can be found in an __entitlements section. size_t entitlements_size; uint8_t entitlements_data = getsectiondata(header, "__TEXT", "__entitlements", &entitlements_size); if (entitlements_data != NULL) { NSData data = [NSData dataWithBytesNoCopy:entitlements_data length:entitlements_size freeWhenDone:NO]; return [NSPropertyListSerialization propertyListWithData:data options:NSPropertyListImmutable format:nil error:nil]; } // Find the LC_CODE_SIGNATURE struct load_command lc = (void ) (base + sizeof(header)); struct linkedit_data_command cs_lc = NULL; for (uint32_t i = 0; i < header->ncmds; i++) { if (lc->cmd == LC_CODE_SIGNATURE) { cs_lc = (void ) lc; break; } lc = (void ) ((char ) lc + lc->cmdsize); } if (cs_lc == NULL) return nil; // Read the code signature off disk, as it's apparently not loaded into memory NSFileHandle fileHandle = [NSFileHandle fileHandleForReadingFromURL:NSBundle.mainBundle.executableURL error:nil]; if (fileHandle == nil) return nil; [fileHandle seekToFileOffset:cs_lc->dataoff]; NSData csData = [fileHandle readDataOfLength:cs_lc->datasize]; [fileHandle closeFile]; const struct cs_superblob cs = csData.bytes; if (ntohl(cs->magic) != 0xfade0cc0) return nil; // Find the entitlements in the code signature for (uint32_t i = 0; i < ntohl(cs->count); i++) { struct cs_entitlements ents = (void ) ((char ) cs + ntohl(cs->index[i].offset)); if (ntohl(ents->magic) == 0xfade7171) { return parse_entitlements(ents->entitlements, ntohl(ents->length) - offsetof(struct cs_entitlements, entitlements)); } } return nil; } bool jb_has_jit_entitlement(void) { static NSDictionary entitlements = nil; if (!entitlements) { entitlements = app_entitlements(); } return [entitlements[@"dynamic-codesigning"] boolValue]; } bool jb_enable_ptrace_hack(void) { #if defined(NO_PTRACE_HACK) return false; #else bool debugged = am_i_being_debugged(); // Thanks to this comment: https://news.ycombinator.com/item?id=18431524 // We use this hack to allow mmap with PROT_EXEC (which usually requires the // dynamic-codesigning entitlement) by tricking the process into thinking // that Xcode is debugging it. We abuse the fact that JIT is needed to // debug the process. if (ptrace(PT_TRACE_ME, 0, NULL, 0) < 0) { return false; } // ptracing ourselves confuses the kernel and will cause bad things to // happen to the system (hangs…) if an exception or signal occurs. Setup // some "safety nets" so we can cause the process to exit in a somewhat sane // state. We only need to do this if the debugger isn't attached. (It'll do // this itself, and if we do it we'll interfere with its normal operation // anyways.) if (!debugged) { // First, ensure that signals are delivered as Mach software exceptions… ptrace(PT_SIGEXC, 0, NULL, 0); // …then ensure that this exception goes through our exception handler. // I think it's OK to just watch for EXC_SOFTWARE because the other // exceptions (e.g. EXC_BAD_ACCESS, EXC_BAD_INSTRUCTION, and friends) // will end up being delivered as signals anyways, and we can get them // once they're resent as a software exception. mach_port_t port = MACH_PORT_NULL; mach_port_allocate(mach_task_self(), MACH_PORT_RIGHT_RECEIVE, &port); mach_port_insert_right(mach_task_self(), port, port, MACH_MSG_TYPE_MAKE_SEND); task_set_exception_ports(mach_task_self(), EXC_MASK_SOFTWARE, port, EXCEPTION_DEFAULT, THREAD_STATE_NONE); pthread_t thread; pthread_create(&thread, NULL, exception_handler, (void *)&port); } return true; #endif }	{ "pile_set_name": "Github" }
Skinny Baked Mozzarella Sticks 14836 shares 421 4941 9474 Jump to Recipe Save It Saved! Hot baked mozzarella sticks – I can’t think of a more popular finger food for both kids and adults alike. My oldest daughter Karina LOVES them and these never disappoint! Skinny Baked Mozzarella Sticks Made lighter with part-skim mozzarella then coated with crispy seasoned breadcrumbs and baked (not fried!) until hot and golden. Serve them with my quick marinara sauce and you have yourself an appetizer everyone will love! This would go great along side Mini Burger Bites for a party! I’ve revived these from the archives as Super Bowl is approaching, these would be a great appetizer. Baking them as opposed to frying and using part skim cheese doesn’t effect how good these are. The cheese still melts, see for yourself! See here for more Super Bowl party food ideas. Of course, you’ll want to serve them hot right out of the oven, because like any cheese, as they cool they harden fast. It actually took me several attempts to get these perfect. I played around with different brands of light string cheese to see which yielded the best results. The winner was Sargento part-skim, low-sodium. Although it’s not the cheese with the least amount of fat compared to some other brands, it had the best flavor and wasn’t as salty as I found some brands to be. These are freezer friendly, in fact these MUST be frozen before you bake them or you will have one big cheesy mess in your oven so it’s best to make them at least a day ahead! The good news is you can bread them all ahead of time then place them on a tray with wax paper and freeze them until you are ready to bake. I then transfer them to ziplock bags, so any time I want to bake a few I just pop them in the oven! I serve them with my marinara sauce or dipping, enjoy! Print 4.84 from 6 votes Did you make this recipe? Leave a review » Skinny Baked Mozzarella Sticks Prep Time: 1 hr 15 mins Cook Time: 10 mins Total Time: 1 hr 25 mins Hot mozzarella sticks – I can't think of a more popular finger food for both kids and adults alike. My oldest daughter Karina LOVES them and these never disappoint! Made lighter with part-skim mozzarella then coated with crispy seasoned breadcrumbs and baked (not fried!) until hot and golden. Serve them with my quick marinara sauce and you have yourself an appetizer everyone will love! Ingredients 12 sticks part-skim , reduced sodium mozzarella string cheese (Sargento) , 1 large egg , beaten , 2 tbsp flour 5 tbsp Italian seasoned breadcrumbs , or GF breadcrumbs , 5 tbsp panko crumbs 2 tsp parmesan cheese 1 tbsp dried parsley olive oil cooking spray , I used my misto Save Instructions Cut cheese in half to give you 24 pieces. Place cheese in the freezer until cheese is frozen. In small bowl, whisk the egg. Place the flour on another small dish. In separate bowl, combine bread crumbs, panko, parmesan cheese and dried parsley. Dip the frozen sticks in flour, shaking off excess, then into the egg, then coat with the crumbs. Repeat this process with the remaining cheese placing them on a tray with wax paper. Place cheese back into the freezer at least 1 hour until ready to bake (this is a MUST or they will melt before the crumbs get golden). When ready to bake preheat oven to 400° F. Line a baking sheet with aluminum foil and lightly spray with oil. Place frozen cheese sticks on baking sheet. Spray the tops of the mozzarella sticks with a little more oil and bake in the bottom third of your oven until crisp, about 4 to 5 minutes. Turn and bake an additional 4 - 5 minutes watching them closely so they don't melt. * There will be extra crumbs and flour after breading, I've deducted them from the nutritional info. Nutrition Serving: 2 pieces , Calories: 87 kcal , Carbohydrates: 7 g , Protein: 7.5 g , Fat: 5 g , Saturated Fat: 0.5 g , Cholesterol: 21 mg , Sodium: 168.5 mg , Fiber: 0.2 g , Sugar: 0.2 g Blue Smart Points: 2 Green Smart Points: 3 Purple Smart Points: 2 Points +: 2 Keywords: baked mozzarella sticks, baked mozzarella sticks recipe, kids party food ideas, party appetizers, Skinny Baked Mozzarella Sticks Pin It To Save For Later!	{ "pile_set_name": "OpenWebText2" }
Q: Magento 2 - How to show tax and shipping costs in mini-cart pop up How to show tax and shipping costs in mini cart popup in Magento 2? A: To show additional stuff or costs in the minicart (like taxes or shipping costs), you need to understand where the data in the minicart comes from. The Customer Data Section Pool If you add a product to the cart, you can see in your inspector a XHR request is made to /customer/section/load with the arguments ?sections=cart,messages. This controller checks in the section pool (Magento\Customer\CustomerData\SectionPoolInterface) for objects that provide data for the required sections. This data is saved in the local storage of your browser and utilized in the minicart. This design pattern is called an Object Pool and they are used thoroughly in Magento 2. You can hook into this Object Pool very easily by adding the following to your modules' di.xml: <type name="Magento\Customer\CustomerData\SectionPoolInterface"> <arguments> <argument name="sectionSourceMap" xsi:type="array"> <item name="my-section" xsi:type="string">Vendor\Module\CustomerData\Something</item> </argument> </arguments> </type> As for the Something-class in this example: the only requirement is that it implements \Magento\Customer\CustomerData\SectionSourceInterface so it has the getSectionData()-method. This method should return an array with data that is added to the JSON object when you ask the controller to load it (for example: /customer/section/load?sections=my-section. Extending existing functionality Now as for your question the answer is even simpler: since you want to add some extra quote information (like taxes and shipping costs) you can simply use a plugin to hook into Magento\Checkout\CustomerData\Cart::getSectionData() to add your information to the data that is fetched when /customer/section/load?sections=cart is called. In your di.xml add: <type name="Magento\Checkout\CustomerData\Cart"> <plugin name="my_custom_stuff" type="Vendor\Module\Plugin\Magento\Checkout\CustomerData\Cart"/> </type> And in your plugin: /** * @param \Magento\Checkout\CustomerData\Cart $subject * @param array $result * @return array */ public function afterGetSectionData(\Magento\Checkout\CustomerData\Cart $subject, array $result) { $result['something'] = 'Stuff'; return $result; } Now what you do in your plugin is beyond the scope of this help, so you have to figure out on your own how to fetch the Tax and/or shipping costs at this point, but I'm pretty sure you'll figure that out. Implementing it in the Frontend Now we have a hook where we can add data from the backend to the frontend. Please note that this is only executed when the customer section data is loaded! or even better: as soon as you add a product to the cart. In other words: you won't have this data on the frontend without updating your cart first. Now, the data in our plugin is added to our cart-node in the JSON, and we can access this in the Magento_Checkout/js/view/checkout/minicart/subtotal/totals UI Component. This has a property called cart which is an observable that contains everything from our JSON response. This becomes very clear if you look at the template Magento_Checkout/minicart/subtotal/totals.html: <div class="amount"> <span data-bind="html: cart().subtotal"></span> </div> In this file, cart().subtotal reflects that cart.subtotal-item in the JSON data. Adding an extra rule to the minicart Now here comes the most important part (and probably the answer to your question): How can we show our extra data in the minicart? Well the minicart is made up of a bunch of UI Components tangled into each other, so without too much further explanation this is how you set it up. Add checkout_cart_sidebar_total_renderers.xml to your modules' frontend/layout-folder: <?xml version="1.0"?> <page xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:noNamespaceSchemaLocation="urn:magento:framework:View/Layout/etc/page_configuration.xsd"> <body> <referenceBlock name="minicart"> <arguments> <argument name="jsLayout" xsi:type="array"> <item name="components" xsi:type="array"> <item name="minicart_content" xsi:type="array"> <item name="children" xsi:type="array"> <item name="subtotal.container" xsi:type="array"> <item name="children" xsi:type="array"> <!-- Include stuff in MiniCart: --> <item name="stuff" xsi:type="array"> <item name="component" xsi:type="string">uiComponent</item> <item name="config" xsi:type="array"> <item name="template" xsi:type="string">Vendor_Module/checkout/minicart/stuff</item> </item> <item name="children" xsi:type="array"> <item name="subtotal.totals" xsi:type="array"> <item name="component" xsi:type="string">Magento_Checkout/js/view/checkout/minicart/subtotal/totals</item> <item name="config" xsi:type="array"> <item name="template" xsi:type="string">Vendor_Module/checkout/minicart/stuff/totals</item> </item> </item> </item> </item> </item> </item> </item> </item> </item> </argument> </arguments> </referenceBlock> </body> </page> And the template frontend/web/checkout/minicart/stuff.html: <div class="my-stuff"> <span class="label"> <!-- ko i18n: 'My Custom Stuff' --><!-- /ko --> </span> <!-- ko foreach: elems --> <!-- ko template: getTemplate() --><!-- /ko --> <!-- /ko --> </div> And the template frontend/web/checkout/minicart/stuff/totals.html: <div class="amount price-container"> <span class="price-wrapper" data-bind="html: cart().something"></span> </div> This should do the trick. Haven't tested this example, but it's taken from an implementation I did where I need to add the FPT, Shipping costs and Grand Total to the minicart and it worked like a charm! It's so easy! ;-)	{ "pile_set_name": "StackExchange" }
201 P.3d 940 (2009) 225 Or. App. 500 HERRERA-ORTIZ v. HOEFEL. Court of Appeals of Oregon. January 28, 2009. Affirmed without opinion.	{ "pile_set_name": "FreeLaw" }
--- abstract: 'The correlation-driven Mott transition is commonly characterized by a drop in resistivity across the insulator-metal phase boundary; yet, the complex permittivity provides a deeper insight into the microscopic nature. We investigate the frequency- and temperature-dependent dielectric response of the Mott insulator $\kappa$-(BEDT-TTF)$_{2}$Cu$_2$(CN)$_3$ when tuning from a quantum spin liquid into the Fermi-liquid state by applying external pressure and chemical substitution of the donor molecules. At low temperatures the coexistence region at the first-order transition leads to a strong enhancement of the quasi-static dielectric constant $\epsilon_1$ when the effective correlations are tuned through the critical value. Several dynamical regimes are identified around the Mott point and vividly mapped through pronounced permittivity crossovers. All experimental trends are captured by dynamical mean-field theory of the single-band Hubbard model supplemented by percolation theory.' author: - 'A. Pustogow' - 'R. Rösslhuber' - 'Y. Tan' - 'E. Uykur' - 'M. Wenzel' - 'A. Böhme' - 'A. Löhle' - 'R. Hübner' - 'Y. Saito' - 'A. Kawamoto' - 'J. A. Schlueter' - 'V. Dobrosavljević' - 'M. Dressel' date: - - - title: 'Low-Temperature Dielectric Anomalies at the Mott Insulator-Metal Transition' --- [^1] [^2] [^3] The insulator-metal transition (IMT) remains the main unresolved basic science problem of condensed-matter physics. Especially intriguing are those IMTs not associated with static symmetry changes, where conventional paradigms for phase transitions provide little guidance. Early examples of such behavior are found in certain disorder-driven IMTs [@Shklovskii1984]. In recent years, IMTs with no symmetry breaking were also identified around the Mott transition [@Imada1998], which bears close connection to exotic states of strongly-correlated electron matter such as superconductivity in the cuprates. From a theoretical point of view, the single-band Hubbard model is at present well understood [@Georges1996; @Vollhardt2012], and is found to be in excellent agreement with experiments [@Limelette2003; @Limelette2003a; @Hansmann2013; @Kagawa2005; @Kagawa2004; @Furukawa2015]. While commonly concealed by antiferromagnetism, recent development in the field of organic quantum spin liquids (QSL) enabled us to study the low-temperature Mott IMT in absence of magnetic order [@Kurosaki2005; @Shimizu2003; @Shimizu2016; @Itou2017; @Li2019; @Furukawa2018; @Pustogow2018], revealing finite-frequency precursors of the metal already on the insulating side [@Pustogow2018]. The Mott insulator and the correlated metal converge at the critical endpoint $T_{\rm crit}$ (Fig. \[fig:phase-diagram\]). The former is bounded by a quantum-critical region along the quantum Widom line (QWL) [@Terletska2011; @Vucicevic2013; @Furukawa2015; @Pustogow2018; @Dobrosavljevic1997]. On the metallic side, resistivity maxima at the “Brinkman-Rice” temperature $T_{\rm BR}$ signal the thermal destruction of resilient quasiparticles [@Radonjic2012; @Deng2013] and the crossover to semiconducting transport. Below $T_{\rm crit}$, the IMT is of first order and comprises an insulator-metal coexistence regime [@Georges1996; @Terletska2011; @Vucicevic2013]. It is currently debated whether electrodynamics is dominated by closing of the Mott gap or by spatial inhomogeneity, fueled by recent low-temperature transport studies [@Furukawa2018]. ![(a) Tuning the bandwidth $W$, for instance by chemical or physical pressure, transforms a Mott insulator to a correlated metal. Dynamical mean-field theory predicts a first-order transition with phase coexistence up to the critical endpoint [@Georges1996], and a quantum-critical regime associated with the quantum Widom line (QWL) above $T_{\rm crit}$ [@Vucicevic2013]. The metallic state is confined by the Brinkman-Rice temperature $T_{\rm BR}$, the coherent Fermi-liquid regime by $T_{\rm FL}$. When interactions $U$ are comparable to $W$, and $ T \gg T_{\rm crit}$, semiconducting behavior prevails; neither a gap nor a quasiparticle peak are stabilized. (b-d) Resistivity signatures of the crossovers.[]{data-label="fig:phase-diagram"}](phase-diagram38.pdf){width="0.8\columnwidth"} Phase coexistence around the first-order line ($T<T_{\rm crit}$) emerges from bistability of the insulating and metallic phases between closing of the Mott gap at $U_{c1}$ and demise of the metal at $U_{c2}$ [@Georges1996]. One generally expects hysteretic behaviors when tuning across a first-order transition. Seminal transport and susceptibility experiments indeed found a pronounced hysteresis in Mott insulators with a magnetically-ordered ground state [@Lefebvre2000; @Limelette2003; @Limelette2003a]. Unfortunately, analogue measurements with continuous pressure tuning are not feasible on QSL compounds, such as , due to the low temperatures ($T<20$ K) and high pressures ($p>1$ kbar) required to cross the first-order IMT. A more direct insight into the coexistence region was provided by spatially resolved optical spectroscopy [@Sasaki2004]. The most compelling results came from near-field optical experiments on vanadium oxides by Basov and collaborators [@Qazilbash2007; @Huffman2018; @McLeod2016] where a spatial separation of metallic and insulating regions upon heating could be visualized, in accord with x-ray studies [@Lupi2010; @Hansmann2013]; the range with hysteresis in $\rho(T)$ coincides with the observed phase coexistence. Although recent developments in cryogenic near-field instrumentation are rather promising [@McLeod2016; @Post2018; @Pustogow2018s], they fall short of covering the regime $T<T_{\rm crit} \approx 15$ K required here and do not allow for pressure tuning. For this reason, we suggest dielectric spectroscopy as novel bulk-sensitive method in order to reveal the coexistence regime, distinguish the individual phases and obtain a deeper understanding of the dynamics around the IMT. The complex conductivity $\sigma_1+{\rm i}\sigma_2$ not only reveals the closing of the Mott gap but yields insight into the growth of metallic regions and the formation of quasiparticles as correlation effects decrease. In this Letter we tackle the fundamental question whether the electrodynamic response around the Mott IMT is overwhelmed by the gradual decrease of the Mott-Hubbard gap within a homogeneous insulating phase, or whether the effects of phase coexistence dominate. Furthermore, is it possible to distinguish on the metallic side between the coherent (quasiparticle) low-$T$ regime and incoherent transport at high-$T$? To answer these questions, we present temperature- and frequency-dependent dielectric measurements on a genuine Mott compound that is bandwidth-tuned across its first-order IMT. In addition to hydrostatic pressure we developed a novel approach of chemically substituting the organic donor molecules. The experimental findings are complemented by dynamical mean-field theory (DMFT) calculations, incorporating spatial inhomogeneities in a hybrid approach. We conclude that electronic phase segregation plays a crucial role, leading to percolative phenomena due to the separation of insulating and metallic regions, also allowing clear and precise mapping of different dynamical regimes around the IMT. ![The dielectric conductivity and permittivity of were measured as a function of temperature and frequency for various applied (a-e) pressures and (f-j) chemical substitutions \[introduction of Se-containing BEDT-STF molecules illustrated in (h) and (k)\] that drive the system across the Mott transition. (a,f) Starting from the insulator, $\sigma_1(T)$ grows with increasing $p$ or $x$; a metallic phase is stabilized below $T_{\rm BR}$, in accord with dc transport [@Kurosaki2005; @Furukawa2015; @Furukawa2018]. (b,c,g,h) In the Mott-insulating state $\epsilon_1(T)$ exhibits relaxor-ferroelectric behavior similar to the parent compound [@Abdel-Jawad2010; @Pinteric2014]. Extrinsic high-temperature contributions are subtracted. (d,i) The strong enhancement of $\epsilon_1(T)$ at the transition is a hallmark of a percolative IMT, as sketched in (l-o). (e,j) When screening becomes dominant in the metal, $\epsilon_1$ turns negative; $\sigma_1$ exhibits Fermi-liquid behavior below $T_{\rm FL}$. []{data-label="fig:sigma-eps_T"}](Fig_2_44.pdf){width="1\columnwidth"} We have chosen single crystals for our investigations because this paradigmatic QSL candidate is well characterized by electric, optical and magnetic measurements [@Kurosaki2005; @Shimizu2003; @Kezsmarki2006; @Kanoda2011; @Zhou2017; @Furukawa2018; @Pustogow2018; @Culo2019]. Although the dimerized charge-transfer salt possesses a half-filled conduction band, strong electronic interaction $U \approx 250$ meV stabilizes a Mott-insulating state below the QWL ($T_{\rm QWL}\approx 185$ K at ambient pressure [@Pustogow2018; @Furukawa2015]). The effective correlation strength $U/W$ can be reduced by increasing the bandwidth $W$; for pressure $p > 1.4$ kbar the metallic state is reached at low temperatures [^4], with $T_{\rm crit} \approx 15$-20 K. In addition, we exploited a novel route of partially replacing the S atoms of the donor molecules by Se, where more extended orbitals lead to larger bandwidth \[see sketches in Fig. \[fig:sigma-eps\_T\](h,k)\]. The substitutional series ($0\leq x \leq 1$, abbreviated ) spans the interval ranging from a Mott insulator to a Fermi-liquid metal [^5]. Details on the sample characterization and experimental methods are given in Refs. . Here we focus on the out-of-plane dielectric response measured from $f=7$ kHz to 5 MHz down to $T=5$ K. Both physical pressure and STF-substitution allow us to monitor the permittivity while shifting the system across the first-order IMT. Fig. \[fig:sigma-eps\_T\] displays the temperature-dependent conductivity and permittivity data of when $p$ rises (a-e) and $x$ increases in (f-j). The insulating state ($p<1.4$ kbar, $x<0.1$), characterized by ${\rm d}\sigma_1/{\rm d}T>0$, generally features small positive $\epsilon_1\approx 10$. The relaxor-like response previously observed in the parent compound below 50 K has been subject of debate [@Abdel-Jawad2010; @Pinteric2014]. The metallic state ($p>3$ kbar, $x>0.2$) is defined by ${\rm d}\sigma_1/{\rm d}T<0$ and, concomitantly, $\epsilon_1<0$ that becomes very large at low $T$ as itinerant electrons increasingly screen [^6]. This onset of metallic transport identifies $T_{\rm BR}$ [@Radonjic2012]; while thermal fluctuations prevail at higher $T$, the quasiparticle bandwidth is the dominant energy scale for $T<T_{\rm BR}$. Below $T_{\rm FL}$ the resistivity $\rho(T)\propto T^2$ indicates the Fermi-liquid state. Right at the first-order IMT, however, the dielectric behavior appears rather surprising. When approaching the low-temperature phase boundary, $\epsilon_1$ rapidly increases by several orders of magnitude. This colossal permittivity enhancement is more pronounced in the quasi-static limit, $\epsilon_1\approx 10^5$ at $f=7.5$ kHz, and the peak value approximately follows a $f^{-1.5}$ dependence. The overall range in $T$ and $p$/$x$ of the divergency is robust and does not depend on the probing frequency; detailed analysis on the dynamic properties is given in [@Rosslhuber2019; @Saito2019]. In Fig. \[fig:sigma-eps\_p\_x\_DMFT\](a,b) the pressure evolution of $\sigma_1$ and $\epsilon_1$ is plotted for fixed $T$. At $T=10$ K, $\sigma_1(p)$ rises by six orders of magnitude in the narrow range of 1 kbar and $\Delta x = 0.1$. This behavior flattens to a gradual transition above 20 K, associated with the quantum-critical crossover at the QWL. The inflection point shifts to higher $p$, in accord with the positive slope of the phase boundary [@Pustogow2018] associated with the rising onset of metallicity at $T_{\rm BR}$. The series exhibits similar behavior \[Fig. \[fig:sigma-eps\_p\_x\_DMFT\](c,d)\]: around the critical concentration of $x\approx 0.12$ a drastic increase in $\sigma_1$ is observed at low $T$ that smears out as $T$ rises. The maximum in $\epsilon_1(x)$ is reached for $x=0.16$ but broadens rapidly upon heating. ![(a) The Mott IMT of $\kappa$-(BEDT-TTF)$_2$Cu$_2$(CN)$_3$ appears as a rapid increase of $\sigma_1(p)$ that smoothens at higher $T$; above $T_{\rm crit}$ a gradual crossover remains. (b) $\epsilon_1(p)$ exhibits a sharp peak below $T_{\rm crit}$. The results at $f=380$ kHz are plotted on a logarithmic scale. (c,d) Similar behavior is observed for chemical BEDT-STF substitution. (e,f) Fixed-temperature line cuts of our hybrid DMFT simulations (see text) as a function of correlation strength $U/W$ and $T/W$ [@Vucicevic2013; @Pustogow2018] resemble the experimental situation in minute detail, including the shift of the IMT with $T$. The lack of saturation of $\sigma_1(T\rightarrow 0)$ seen in DMFT modeling reflects the neglect of elastic (impurity) scattering in the metal (outside the coexistence region).[]{data-label="fig:sigma-eps_p_x_DMFT"}](Fig_3_41.pdf){width="1\columnwidth"} ![image](Fig_4_47small.pdf){width="90.00000%"} The Mott IMT is based on the idea that a reduction of electronic correlations, i.e. rise of $W/U$, gradually closes the Mott-Hubbard gap: a coherent charge response develops, causing a finite metallic conductivity. Pressure-dependent optical studies on several organic Mott insulators actually observe this behavior [@Faltermeier2007; @Merino2008; @Dumm2009; @Li2019]. It was pointed out [@Aebischer2001] that even in the case of certain second-order phase transitions, a continuously vanishing charge gap might induce an enhancement in $\epsilon_1$, perhaps leading to a divergence at low $T$. Probing the optical response at THz frequencies is actually a convenient method to monitor the gap contribution to the permittivity. From $p$ and $T$ sweeps across the Mott IMT of very different materials an increase by a factor of 10 is consistently reported [@Qazilbash2007; @Li2019]; in the case of we find it even smaller [@Saito2019]. Hence, the dielectric catastrophe of $\epsilon_1 \approx 10^5$ observed in our pressure and substitution-dependent dielectric experiments evidences an additional effect. Treating the fully-frustrated model at half filling, even at $T=0$ DMFT finds metallic and insulating solutions coexisting over an appreciable range of $U/W$ [@Georges1996]. This may result in a spatial segregation of these distinct electronic phases. Such a picture resembles composite materials, such as microemulsions, composites or percolating metal films [@vanDijk1986; @Clarkson1988a; @Clarkson1988b; @Pecharroman2000; @Nan2010; @Hovel2010]. Classical percolation is not a thermodynamic phase transition, but a statistical problem that has been studied theoretically for decades by analytical and numerical methods in all details; one of the key predictions is the divergency of $\epsilon_1$ when approaching the transition from either side, with characteristic scaling [@Dubrov1976; @Efros1976; @Bergman1977; @Bergman1978]. Over a large parameter range the dielectric properties are well described by the Maxwell-Garnett or Bruggeman effective medium approaches [@Choy2015]. To further substantiate this physical picture in quantitative details, we carried out theoretical modeling of the systems under study. We calculated $\epsilon_1+{\rm i}\epsilon_2$ using DMFT for a single-band Hubbard model, and obtained the respective responses for both the insulating and the metallic phase around the Mott point [@Vucicevic2013]. The DMFT phase diagram (Fig. \[fig:phase-diagram\]) also features an intermediate coexistence region below $ k_{B} T_{\rm crit} \approx 0.02 W$. In accord with the analysis of our experimental results, we assumed a smoothly varying metallic fraction $x$ within the phase coexistence region. To obtain the total dielectric response, we solved an appropriate electrical-network model representing such spatial inhomogeneity utilizing the standard effective-medium approximation (for details, see Ref. ). Our hybrid DMFT simulation yields excellent agreement with experiment – both pressure-tuning and chemical substitution – as illustrated in Fig. \[fig:sigma-eps\_p\_x\_DMFT\](e,f) and in the false-color plots in Fig. \[fig:contour-plots\]. We find that the colossal peak in $\epsilon_1$ is confined to the spatially inhomogeneous coexistence regime, exactly as observed in experiments. As correlation effects diminish, the dynamical conductivity (upper panels) increases from the Mott insulator to the Fermi liquid. The step in $\sigma_1$ and drop in $\epsilon_1$ appear abruptly in the model but more smoothly in experiment, most likely due to inhomogeneities which broaden the coexistence regime by providing nucleation seeds for the incipient phase. Note, the percolative transition region narrows for $T\rightarrow T_{\rm crit}$ and vanishes above that; the metallic fraction of the simulation is indicated in Fig. \[fig:contour-plots\](f). The inset of panel (f) clearly demonstrates that the colossal permittivity enhancement appears exclusively for a percolating mixture of metallic and insulating regions, and not for the pure phases. These results render the gap closing irrelevant for the electrodynamics at the low-temperature Mott IMT. While the transition is of first-order at half filling, doping [@Hebert2015] or disorder [@Gati2018; @Urai2019] effectively move $T_{\rm crit}\rightarrow 0$, eventually turning it into a true quantum-critical point. We further point out that the discussed mechanism of a percolative enhancement of $\epsilon_1$ may also apply to related organic compounds subject to first-order transitions. Similar dielectric anomalies in and were previously assigned to ferroelectricity [@Gati2018a] and multiferroicity [@Lunkenheimer2012], respectively. The former exhibits a peak in $\epsilon_1$ right at its charge-order IMT, where phase coexistence is evident [@Gati2018a; @Hassan2019]. The latter is located extremely close to the Mott IMT [@Limelette2003a], so the coexistence region is likely entered already at ambient pressure [^7]. While previous transport and optical studies [@Furukawa2015; @Pustogow2018] already provided hints favoring the DMFT scenario, they do not map out the predicted dynamical regimes, especially regarding a well-defined coexistence region at $T < T_{\rm crit}$. Our new dielectric data, however, reveal all phases in vivid detail and in remarkable agreement with the respective crossover lines obtained from dc transport. Indeed, we recognize the gapped Mott insulator by essentially constant $\epsilon_1$ (light red) bounded precisely by the QWL [@Vucicevic2013], while also below $T_{\rm BR}$ [@Radonjic2012; @Deng2013] the response clearly follows the dielectric behavior expected for a metal ($\epsilon_1 < 0$, blue). Most remarkably, these two crossover lines converge towards $T_{\rm crit}$, which marks the onset of the coexistence region, just as anticipated from Fig. \[fig:phase-diagram\]. The emergence of phase segregation is evidenced by the huge peak of $\epsilon_1$ in excellent agreement with our current DMFT-based modeling. The sharply defined boundaries of this dielectric anomaly imply that the corresponding inhomogeneities are [the consequence and not the cause]{} of phase separation, the latter resulting from strong correlation effects inherent to Mottness. Our findings leave little room for doubt that the DMFT scenario offers a rather accurate picture of the Mott IMT, in contrast to other theoretical viewpoints [@Senthil2008] which focus on the spin degrees of freedom in the QSL. This also confirms recent experimental and theoretical results [@Lee2016; @Pustogow2018spinons] suggesting that such gapless spin excitations, while dominant deep within the low-temperature Mott-insulating phase, are quickly damped away by the onset of charge fluctuations close to the IMT. We also demonstrated that the novel chemical method of partially substituting the organic donor molecules of the fully-frustrated Mott insulator by BEDT-STF yields similar bandwidth-tuning like physical pressure. By comparing the boundaries of the Mott state and the correlated metal (QWL, $T_{\rm BR}$, $T_{\rm FL}$) we find that 1 kbar is equivalent to $\Delta x \approx 0.06$. The pronounced divergency in $\epsilon_1$ evidences a spatial coexistence of metallic and insulating electronic phases around the first-order IMT that can be circumstantially described by percolation theory. Our results yield that the Mott gap has a minor effect on the dielectric properties while the effects of phase coexistence dominate. We appreciate discussions with S. Brown, B. Gompf and I. Voloshenko. We acknowledge support by the DFG via DR228/52-1. A.P. acknowledges support by the Alexander von Humboldt Foundation through the Feodor Lynen Fellowship. Work in Florida was supported by the NSF Grant No. 1822258, and the National High Magnetic Field Laboratory through the NSF Cooperative Agreement No. 1157490 and the State of Florida. E.U. receives support of the European Social Fund and the Ministry of Science Research and the Arts of Baden-Württemberg. J.A.S. acknowledges support from the Independent Research/Development program while serving at the National Science Foundation. A.P., R.R. and Y.T. contributed equally to this work. [67]{}ifxundefined \[1\][ ifx[\#1]{} ]{}ifnum \[1\][ \#1firstoftwo secondoftwo ]{}ifx \[1\][ \#1firstoftwo secondoftwo ]{}““\#1””@noop \[0\][secondoftwo]{}sanitize@url \[0\][‘\ 12‘\$12 ‘&12‘\#12‘12‘\_12‘%12]{}@startlink\[1\]@endlink\[0\]@bib@innerbibempty @noop []{} (, , ) [, ()](https://link.aps.org/doi/10.1103/RevModPhys.70.1039) [, ()](https://link.aps.org/doi/10.1103/RevModPhys.68.13) [, ()](\doibase 10.1002/andp.201100250) [, ()](http://science.sciencemag.org/content/302/5642/89.abstract) [, ()](https://link.aps.org/doi/10.1103/PhysRevLett.91.016401) [, ()](\doibase 10.1002/pssb.201248476) @noop [, ()]{} [, ()](\doibase 10.1103/PhysRevB.69.064511) @noop [, ()]{} [, ()](https://link.aps.org/doi/10.1103/PhysRevLett.95.177001) [, ()](https://link.aps.org/doi/10.1103/PhysRevLett.91.107001) [, ()](https://link.aps.org/doi/10.1103/PhysRevLett.117.107203) [, ()](http://advances.sciencemag.org/content/3/8/e1601594.abstract) [, ()](\doibase 10.1103/PhysRevB.99.115137) [, ()](\doibase 10.1038/s41467-017-02679-7) [, ()](\doibase 10.1038/s41563-018-0140-3) [, ()](https://link.aps.org/doi/10.1103/PhysRevLett.107.026401) [, ()](https://link.aps.org/doi/10.1103/PhysRevB.88.075143) [, ()](\doibase 10.1103/PhysRevLett.79.455) [, ()](https://link.aps.org/doi/10.1103/PhysRevB.85.085133) [, ()](https://link.aps.org/doi/10.1103/PhysRevLett.110.086401) @noop [, ()]{} [, ()](\doibase 10.1103/PhysRevLett.92.227001) [, ()](\doibase 10.1126/science.1150124) [, ()](\doibase 10.1103/PhysRevB.97.085146) [, ()](\doibase 10.1038/nphys3882) [, ()](\doibase 10.1038/ncomms1109) [, ()](\doibase 10.1038/s41567-018-0201-1) [, ()](\doibase 10.1126/sciadv.aau9123) [, ()](\doibase 10.1103/PhysRevB.82.125119) [, ()](https://link.aps.org/doi/10.1103/PhysRevB.90.195139) [, ()](https://link.aps.org/doi/10.1103/PhysRevB.74.201101) [, ()](\doibase 10.1146/annurev-conmatphys-062910-140521) [, ()](https://link.aps.org/doi/10.1103/RevModPhys.89.025003) [, ()](\doibase 10.1103/PhysRevB.99.045114) @noop [, ()](\doibase 10.1103/PhysRevB.98.205141) @noop [ ]{} [, ()](https://link.aps.org/doi/10.1103/PhysRevB.76.165113) [, ()](https://link.aps.org/doi/10.1103/PhysRevLett.100.086404) [, ()](https://link.aps.org/doi/10.1103/PhysRevB.79.195106) [, ()](\doibase 10.1103/PhysRevLett.86.468) [, ()](\doibase 10.1063/1.451588) [, ()](\doibase 10.1103/PhysRevA.37.2070) [, ()](\doibase 10.1103/PhysRevA.37.2079) [, ()](\doibase 10.1002/(SICI)1521-4095(200002)12:4<294::AID-ADMA294>3.0.CO;2-D) [, ()](\doibase 10.1146/annurev-matsci-070909-104529) [, ()](https://link.aps.org/doi/10.1103/PhysRevB.81.035402) @noop [, ()]{} @noop [, ()]{} [, ()](\doibase 10.1103/PhysRevLett.39.1222) [, ()](\doibase https://doi.org/10.1016/0370-1573(78)90009-1) @noop []{}, ed. (, , ) [**, ()](\doibase 10.1103/PhysRevB.92.195112) [, ()](\doibase 10.1103/PhysRevB.97.075115) [, ()](\doibase 10.1103/PhysRevB.99.245139) [, ()](\doibase 10.1103/PhysRevLett.120.247601) [, ()](http://dx.doi.org/10.1038/nmat3400 http://10.0.4.14/nmat3400 https://www.nature.com/articles/nmat3400{#}supplementary-information) @noop [ ]{} [, ()](https://link.aps.org/doi/10.1103/PhysRevB.78.045109) [, ()](https://link.aps.org/doi/10.1103/PhysRevLett.117.136601) [**, ()](\doibase 10.1103/PhysRevLett.121.056402) [^1]: authors contributed equally [^2]: authors contributed equally [^3]: authors contributed equally [^4]: The superconducting state at $T\approx 4$ K [@Kurosaki2005; @Furukawa2018] is below the temperature accessible to us here. [^5]: BEDT-TTF stands for bis-ethylene-dithio-tetrathiafulvalene. Substituting two of the inner sulfur atoms by selenium leads to bis-ethylenedithio-diselenium-dithiafulvalene, abbreviated BEDT-STF [@Saito2019]. [^6]: Comparison of the results in Fig. \[fig:sigma-eps\_T\](j) with optical data measured on the same substitution yields fair agreement of the metallic values $\epsilon_1 < 0$ [@Saito2019]. Technical details of the dielectric experiments can be found in Ref. [@Rosslhuber2019]. [^7]: While $\epsilon_1$ initially increases upon cooling in , it peaks at the antiferromagnetic transition and reduces at lower $T$. This could be a consequence of the metallic fraction first increasing as the insulator-metal phase boundary approaches the ambient-pressure position, but then reducing below $T_{\rm N}$ because of the negative slope of the boundary between antiferromagnet and metal which moves the IMT further away from $p=0$.	{ "pile_set_name": "ArXiv" }
Arctic reindeer really like these psychedelic mushrooms and give new meaning to Santa's flying reindeer. Fly Agaric is a hallucinogenic fungi found in the Arctic. It's been used for centuries by the native shamans during spiritual journeys and to induce visions, but they aren't the only ones who like to snack on these magic mushrooms. More videos from Wide Open Spaces: Fly Agaric is known to give psychedelic hallucinations to people, but it's unsure at this point if the same effect is felt in Arctic reindeer. It's interesting that one of the main effects the mushrooms produce is the feeling of flying, hence the name. Come Christmas we just happen to have an old man in a red suit who is pulled around by flying reindeer. Coincidence? I think not. Although the reindeer love Fly Agaric so much they even dig them out of the snow, don't go out looking for your own to eat. These red and white mushrooms are extremely poisonous and have been know to be fatal.	{ "pile_set_name": "Pile-CC" }
1. Introduction {#sec1-molecules-21-00911} =============== Agarwood is the dark resinous and aromatic wood from genus Aquilaria trees belonging to the family Thymelaeaceae \[[@B1-molecules-21-00911],[@B2-molecules-21-00911],[@B3-molecules-21-00911]\], and is created as a tree response to various form of injury, including natural injuries, such as lightning strikes, animal grazing, insect attacks or microbial invasion, or artificial injuries, such as cutting, nailing, holing, fire, chemical wounding, and deliberate fungal inoculation \[[@B3-molecules-21-00911],[@B4-molecules-21-00911],[@B5-molecules-21-00911]\]. Agarwood not only plays an important role in Traditional Chinese Medicine, but also has been used for centuries as incense in Buddhist, Hindu and Islamic ceremonies \[[@B1-molecules-21-00911],[@B2-molecules-21-00911],[@B3-molecules-21-00911]\]. Unfortunately, in natural forests, only 7%--10% of the agarwood trees contain resinous material, and wild agarwood is rare due to its exhaustive exploitation. Nowadays, agarwood in trade mostly comes from cultivated Aquilaria trees induced by artificial methods, of which the traditional artificial holing is the most common and popular one. As far as we know, nineteen accepted species have been reported up to date, growing from southeast Asia to the Malay Archipelago \[[@B1-molecules-21-00911],[@B2-molecules-21-00911]\]. However, only the heartwood of A. crassna, A. malaccensis, A. sinensis and A. filarial have been commercially exploited \[[@B1-molecules-21-00911]\]. 2-(2-Phenylethyl)chromone derivatives, of which about one hundred different structures have been reported, are considered to be one of the characteristic and most abundant constituents responsible for the quality of agarwood \[[@B1-molecules-21-00911],[@B3-molecules-21-00911],[@B4-molecules-21-00911],[@B6-molecules-21-00911],[@B7-molecules-21-00911],[@B8-molecules-21-00911],[@B9-molecules-21-00911]\]. These compounds were divided into four types according to the various chromone moiety skeletons, in which the benzyl moiety is the same. In these four types, both 2-(2-phenylethyl)chromones of the flidersia type (FTPECs) and 5,6,7,8-tetrahydro-2-(2-phenylethyl)chromones (THPECs) were widely distributed and accumulated most in agarwood, while only four 5,6-epoxy-2-(2-phenylethyl)chromones (EPECs) and three 5,6:7,8-diepoxy-2-(2-phenylethyl) chromones (DEPECs) with one or two epoxy substituents on the chromone moiety respectively, have been reported from 2005 to the present \[[@B7-molecules-21-00911],[@B10-molecules-21-00911],[@B11-molecules-21-00911]\]. Based on the above reports, 2-(2-phenylethyl)chromones were considered as the necessary diagnostic components to evaluate the quality of agarwood. Mei et al. summarized the MS characterization of the FTPECs, which was helpful for the analysis and characterization of FTPECs in agarwood by GC-MS \[[@B3-molecules-21-00911]\]. Xia et al. reported that 29 FTPECs were detected from agarwood by supercritical fluid chromatography in combination with mass spectrometry (SFC-MS) then obtained further detailed structural information by using tandem mass spectrometry (MS/MS) \[[@B12-molecules-21-00911]\]. Li et al. identified and quantified eight characteristic THPECs in Chinese eaglewood, and analyzed the MS fragmentation behavior of THPECs by HPLC/DAD/MS \[[@B13-molecules-21-00911]\]. Lancaster et al. detected diagnostic ions at m/z 319.118 (FTPECs) or 349.129 (FTPECs) and the occurrence of ten or more of the other target chromone ions by real time time-of-flight mass spectrometry (DART-TOFMS) to infer agarwood \[[@B5-molecules-21-00911]\]. Espinoza et al. analyzed the diagnostic chromones ions by using DART-TOFMS followed by discriminant analysis to differentiate wild agarwood from cultivated samples \[[@B2-molecules-21-00911]\]. However, the MS characterization of EPECs and DEPECs have not been reported yet. In this paper, the MS characterization and fragmentation behavior of EPECs and DEPECs was described, and the fragmentation regularity of mass spectra (MS) used to distinguish and identify the four different types of 2-(2-phenylethyl)chromones was concluded for the first time. Nowadays, artificial holing agarwood from A. crassna tree plays an extremely important role in the market. In this report, we detected and analyzed 2-(2-phenylethyl)chromones in three agarwood samples (from A. crassna) with different holing times by using HPLC/DAD/ESI/MS^2^, and revealed the variation of relative contents of different types of 2-(2-phenylethyl)chromones in agarwood after two, four and five years of artificial holing. This could be referenced for the variation of 2-(2-phenylethyl)chromones, also identification and quality evaluation of agarwood with different formation time. 2. Results and Discussion {#sec2-molecules-21-00911} ========================= 2.1. Characteristic Fragmentation Behavior of Reference Compounds *F1--F31* {#sec2dot1-molecules-21-00911} ----------------------------------------------------------------------------------- In this study, the different fragmentation behavior of four types of chromones according to their MS spectra was summarized by the reference compounds ([Table 1](#molecules-21-00911-t001){ref-type="table"} and [Figure 1](#molecules-21-00911-f001){ref-type="fig"}). The characteristic fragment ions produced by four types of chromones due to their structural difference on the basic skeleton of chromone moiety were used as the basis for identification. For THPECs (compounds F1--F4), the characteristic fragmentations were the loss of a molecule of H~2~O (\[M + H--18\]^+^) and a successive loss of another H~2~O molecule (\[M + H--18--18\]^+^) \[[@B13-molecules-21-00911]\]. For EPECs (compounds F5--F7), the characteristic fragmentations were loss of a molecule of H~2~O (\[M + H--18\]^+^), followed by loss of a molecule of CO (\[M + H--18--28\]^+^). For DEPECs F8--F10, the characteristic fragmentation was the loss of a molecule of CO (\[M + H--28\]^+^). For twenty-one FTPECs in the reference compounds, their characteristic fragmentations were benzyl ions and/or chromone moiety ions. In addition, the benzyl ions observed in the MS spectrum of these four types chromones were the same, and the typical ions included m/z 91 \[C~7~H~7~\]^+^, 107 \[C~7~H~6~ + OH\]^+^, 121 \[C~7~H~6~ + OCH~3~\]^+^, 137 \[C~7~H~5~ + OH + OCH~3~\]^+^, 151 \[C~7~H~5~ + 2OCH~3~\]^+^. [Figure 2](#molecules-21-00911-f002){ref-type="fig"} presents examples of the MS^2^ fragmentation behavior from each type of chromone. 2.2. The Method Deduced for Identification of Four Types of 2-(2-Phenylethyl)chromone Derivatives {#sec2dot2-molecules-21-00911} ------------------------------------------------------------------------------------------------- (1)The type of 2-(2-phenylethyl)chromone could be determined by the characteristic fragment ions as discussed above and listed in [Figure 3](#molecules-21-00911-f003){ref-type="fig"}. The present of the ions \[M + H--18\]^+^ and \[M + H--18--18\]^+^ was proposed to be THPECs. When both ions \[M + H--18\]^+^ and\[M + H--28\]^+^ were observed in the spectrum, EPECs was deduced. If only \[M + H--28\]^+^ was detected, it would be DEPECs. FTPECs only gave the peaks of benzyl ions and/or chromone moiety ions in the MS spectrum. It should be noticed that the \[M + H--18\]^+^ ion may appear as a pseudo-characteristic ion during identification, when the CH~2~-CH~2~ group between chromone moiety and phenyl moiety was substituted by a hydroxyl group (-OH) \[[@B1-molecules-21-00911]\].(2)The four types of 2-(2-phenylethyl)chromone derivatives in agarwood have different basic skeletons (the epoxy group was assigned as a part of the basic skeletons), but substituted with similar substituent groups (mainly hydroxyl, methoxyl group and/ or chlorine atom). The molecular weights of the basic skeletons of THPECs, EPECs, DEPECs and FTPECs were 254, 268, 282 and 250, respectively. Thus, the number of different substituents of the structure could be deduced by Formula (1), where "MW" meant the molecular weight, "a" meant the number of methoxy groups, "b" represented the number of hydroxyl groups, and "c" meant the number of chlorine atom. $${MW} - (30a + 16b + 34c) = \left\{ \begin{array}{l} {254~\left( {THPECs} \right)} \\ {268~\left( {EPECs} \right)} \\ {282~\left( {DEPECs} \right)} \\ {250~\left( {FTPECs} \right)} \\ \end{array} \right.$$(3)The four types of chromones presented the same characteristic benzyl ion, while it could not be observed in some compounds. The benzyl moiety without substituent group was 91 \[C~7~H~7~\]^+^, therefore, the number of hydroxyl and/or methoxyl groups substituted on the benzyl moiety could be deduced according to Formula (2), where "MW~bm~" means the molecular weight of benzyl ion, "a~bm~" means the number of methoxy groups on the benzyl moiety, "b~bm~" represents the number of hydroxyl groups on the benzyl moiety. For example, according to Formula (2), the hydroxyl- or methoxyl-substituted benzyl moiety provided characteristic ions at m/z 107 \[C~7~H~6~ + OH\]^+^, 121 \[C~7~H~6~ + OCH~3~\]^+^, 137 \[C~7~H~5~ + OH + OCH~3~\]^+^, 151 \[C~7~H~5~ + 2OCH~3~\]^+^:(4)Except for FTPECs, the fragment ion of the chromone moiety was rarely observed in the MS^2^ spectra of THPECs, EPECs and DEPECs, nevertheless the number of substituent groups of the chromone moiety could still be calculated by subtracting the number of substituents on the benzyl moiety deduced by Formula (2) from the number of substituents on the whole structure deduced by Formula (1).For FTPECs with hydroxyl-substituted benzyl moieties, according to \[[@B3-molecules-21-00911],[@B6-molecules-21-00911]\], if one of characteristic fragment ions at m/z 161 \[C~10~H~8~O~2~ + H\], 177 \[C~10~H~7~O~2~ + OH + H\], 191 \[C~10~H~7~O~2~ + OCH~3~ + H\], 193 \[C~10~H~6~O~2~ + 2OH + H\], 207 \[C~10~H~6~O~2~ + OCH~3~ + OH + H\], 221 \[C~10~H~6~O~2~ + 2OCH~3~ + H\] from different substituted chromone moieties was observed, a 4′/2′-OH substituent on the benzyl moiety was deduced. Otherwise, if none of them was observed, a hydroxyl group substituted at the 3′ position of the benzyl moiety was deduced, whether an ion of chromone moiety at m/z 160, 176, 190, 192, 206, 220 appeared or not. The above mentioned MS characterization has been confirmed by the FTPEC reference compounds in [Table 1](#molecules-21-00911-t001){ref-type="table"}. The observed fragment ions of the chromone moieties of F11, F15, F18, F22 and F24 with 4′/2′-OH on the benzyl moiety were m/z 177, 177, 161, 191 and 161, respectively, which were not observed for the F12, F17, F20, F23 and F27 with 3′-OH on the benzyl moiety, while only a fragment ion at m/z 220 of F17 was observed. These chromone moiety ions could be used to suggest the position of hydroxyl groups on the benzyl moieties.(5)Following the above procedure, a compound could be characterized as one of the four types of 2-(2-phenylethyl)chromones, as well as calculated the numbers of substituent groups of the chromone moiety and benzyl moiety. Furthermore, the position of substituent groups could be deduced sometimes. Besides, if more than one structure were suggested for a single peak, the comparison of retention time and MS spectra with reference compounds was performed. The compound was identified when the data were the same to the reference compound, otherwise, it might be a new compound. 2.3. Identification of 2-(2-Phenylethyl)chromones According to MS Characterization {#sec2dot3-molecules-21-00911} ---------------------------------------------------------------------------------- In the HPLC chromatograms of the ether extract of three agarwood samples (S1, S2, S3) detected at UV 254 nm, a total of fifty-six compounds (four types of chromones) were detected ([Figure 3](#molecules-21-00911-f003){ref-type="fig"}). By comparing their retention time and MS spectra with reference compounds, twenty-six of them were identified, and thirty compounds were tentative identified. The identified or characterized results of THPECs, EPECs and DEPECs were listed in [Table 2](#molecules-21-00911-t002){ref-type="table"}, and the retention time of THPECs, EPECs and DEPECs were in the range of 12\~30 min, 18\~34 min, 21\~43 min, respectively. The results of FTPECs were showed in [Table 3](#molecules-21-00911-t003){ref-type="table"}, and the retention time of FTPECs were in the range of 34\~80 min, except for compound 20 (26.1 min). ### 2.3.1. Structural Analysis of THPECs {#sec2dot3dot1-molecules-21-00911} Taking compounds 1 and 3 for example, the characteristic fragment ions at m/z 331(\[M + H--18\]^+^) and 313 (\[M + H--18--18\]^+^), indicated both were THPECs. The molecular weight (MW) of these two compounds were determined as 348 based on the protonated precursor ion at m/z 349. According to formula (1) (MW − (30a + 16b +34c) = 254), a, b and c were calculated as 1, 4 and 0, respectively, which meant compounds 1 and 3 had four hydroxyl and one methoxyl substituent groups on the whole compound. Furthermore, the benzyl ion at m/z 121 was found in compound 1, which meant one methoxy substitution occurred on its benzyl moiety according to Formula (2), thus, the other four hydroxyl substitutions occurred on its chromone moiety. Neither benzyl ion nor chromone moiety ions were observed in compound 3, thus the positions of substituent groups were uncertain. By searching the literature, we found six THPECs with the MW = 348 were reported, including four of them possessing one methoxy substitution occurring on the benzyl moiety, and four hydroxyl substitutions occurring on their chromone moiety, which matched the above deduced structural characterization of compound 1, so compound 1 was tentative identified as one of the four reported compounds. The positions of the substituent groups of compound 3 were uncertain, so it was tentative identified as one of the six reported compounds while different from compound 1. By comparing the retention time and MS spectra with the reference compounds, compound 1 was identified as F3, and further proved that the above identification method was reasonable. According to above method of identification, compounds 1--7 were deduced as THPECs. Except for compound 5 (m/z 317), the other six compounds, with \[M + H\]^+^ ions of m/z 319, 303, 367, 337, have been reported as THPECs. Compound 5 was identified as a new compound. ### 2.3.2. Structural Analysis of EPECs {#sec2dot3dot2-molecules-21-00911} Taking compounds 10 and 11 for example, according to the characteristic fragment ions of m/z 313 (\[M + H--18\]^+^) and 285 (\[M + H--18--28\]^+^), they were identified as EPECs. The protonated precursor ions at m/z 331 meant their molecular weight (MW) was 330. According to the Formula (1), a, b and c were calculated as 1, 2 and 0, respectively, which meant they had two hydroxyl and one methoxyl substitutions on the whole compound. The benzyl ion at m/z 121 indicated one methoxy substitution occurred on its benzyl moiety according to Formula (2), therefore, the two hydroxyl groups substitutions occurred on the chromone moiety. Subsequently, by literature searching, only one EPEC with MW = 330 was reported, which meant that one of them would be a new compound. By comparing the retention time and MS spectra with reference compound, compound 11 was identified as F6, which proved that the above identification method was feasible, and meanwhile compound 10 should be a new compound. By the same method, compounds 8--12 were deduced as EPECs. Except for compound 9 (which \[M + H\]^+^ ion is m/z 285), all the other compounds, which \[M + H\]^+^ ions were at m/z 347 or 301, have been reported. By comparing retention time and MS spectra with reference compounds, compounds 8 and 12 were identified as reference compounds F5 and F7, respectively. Compounds 9 and 10 were proposed to be new compounds as listed in [Table 2](#molecules-21-00911-t002){ref-type="table"}, because only four EPECs have been reported until now \[[@B7-molecules-21-00911],[@B14-molecules-21-00911]\]. ### 2.3.3. Structural Analysis of DEPECs {#sec2dot3dot3-molecules-21-00911} According to the above method of identification, compounds 13--19 were assigned as DEPECs. By comparing the retention time and MS spectra with the reference compounds, compounds 16, 18, and 19 were identified as the reference compounds F8\~F10, respectively. The other DEPECs were proposed to be new compounds, as only a total of three DEPECs (F8\~F10) have been reported until now \[[@B10-molecules-21-00911]\]. The results are shown in [Table 2](#molecules-21-00911-t002){ref-type="table"}. ### 2.3.4. Structural Analysis of FTPECs {#sec2dot3dot4-molecules-21-00911} Taking compounds 22\~24, 27 and 30 for example, only benzyl ions (m/z 137 and 121) and chromone moiety ion (m/z 177) were detected, leading to identification of these compounds as FTPECs. All of them showed protonated precursor ions at m/z 313, which meant their molecular weight (MW) was 312. According to Formula (1), the a, b and c values were calculated as 1, 2 and 0, respectively, which meant they have two hydroxyl and one methoxyl substituent group on the whole compound. Then, according to Formula (2), the benzyl ion at m/z 137 was found in compounds 22 and 23, which meant one methoxyl and one hydroxyl substitution occurred on their benzyl moiety, while the benzyl ion at m/z 121 was detected in compounds 24, 27 and 30, which meant one methoxy substitution occurred on their benzyl moiety. Consequently, one hydroxyl substitution occurred on the chromone moiety of compounds 22 and 23, and two hydroxyl substitutions occurred on the chromone moiety of compounds 24, 27 and 30. In particular a chromone moiety ion (m/z 177) was detected in compound 22, which indicated the hydroxyl group should be substituted at the 4′/2′ position of the benzyl moiety. Five FTPECs with MW = 312 have been traced from the literature, so the five FTPECs were tentatively identified as reported compounds. By comparing the retention time and MS spectra with reference compounds, compounds 22, 24 and 27 were identified as F12, F13 and F16, respectively, and the results proved that the above identification method was reasonable. According to the method of identification, compounds 20--56 were deduced as FTPECs ([Table 3](#molecules-21-00911-t003){ref-type="table"}), among which nineteen compounds were identified according to the reference compounds. Finally, fifty-six 2-(2-phenylethyl)chromone derivatives were identified or characterized from the three samples according to the fragmentation behavior and the comparison of retention time and MS spectra with reference compounds ([Table 1](#molecules-21-00911-t001){ref-type="table"}). A total of 37 (seven DEPECs, four EPECs, three THPECs and 23 FTPECs), 43 (five EPECs, five THPECs and 33 FTPECs), and 29 (one DEPEC, two EPECs, three THPECs and 23 FTPECs) 2-(2-phenylethyl)chromones were identified or characterized in S1, S2 and S3, respectively. The respective relative content of 2-(2-phenylethyl)chromone derivatives was 66.42%, 81.39% and 79.20% in S1, S2 and S3 ([Table 4](#molecules-21-00911-t004){ref-type="table"}). Based on the above data, it was found that the number and relative content of DEPECs (7/8.01%) from S1 was the highest among the three samples, while they were merely traces in S2 and S3 ([Table 4](#molecules-21-00911-t004){ref-type="table"}, [Figure 4](#molecules-21-00911-f004){ref-type="fig"}). The relative content of EPECs showed a downtrend from S1 to S3 (12.58%, 8.07% and 2.96%, respectively), while the relative content of THPECs and FTPECs showed an uptrend from S1 to S3 (1.58%/1.73%/2.47%, 44.25%/71.59%/73.56%, respectively). It was noticeable that both the total number and relative content of DEPECs, and EPECs decreased obviously (20.59%, 8.07% and 3.17%, respectively) from S1 to S3, and this was consistent with that observed in the HPLC chromatograms ([Figure 3](#molecules-21-00911-f003){ref-type="fig"}), in which the height of peaks for the DEPECs, EPECs (before 43 min) showed a remarkable decreasing trend. This finding was in agreement with the proposed biosynthetic pathways of the four types of chromones ([Figure 4](#molecules-21-00911-f004){ref-type="fig"}) \[[@B11-molecules-21-00911]\], which showed transformations among them during different agarwood formation time. DEPECs have been recognized as precursors, and only accumulated at the early stage of agarwood formation. Then, the next group was EPECs, where the low occurrence rate also suggested they were early intermediates during the agarwood formation. The following group was the highly oxidized THPECs, and the last presented group were FTPECs, both of which were widely distributed in agarwood. In total, twenty-one 2-(2-phenylethyl)chromones (two EPECs, two THPECs and 17 FTPECs) were detected in all three samples, while ten (six DEPECs, one THPEC and three FTPECs), twelve (one EPEC, three THPECs and eight FTPECs), and one (THPEC) 2-(2-phenylethyl)chromone were only found in S1, S2, and S3, respectively. Furthermore, we found that the relative content of six FTPECs, 6,8-dihydroxy-2-\[2-(4-methoxy)phenylethyl\]chromone, 6-methoxy-7-hydroxy-2-\[2-(4-methoxy)-phenylethyl\]chromone, 6-hydroxy-2-(2-phenylethyl)chromone, 6,7-dimethoxy-2-(2-phenylethyl) chromone, 2-\[2-(4-methoxy)phenylethyl\]chromone, and 2-(2-phenylethyl)chromone, which are reported as the main constituents of agarwood, showed a uptrend from S1 to S3. This finding suggested that the relative content of the six 2-(2-phenylethyl)chromones was the significant factor to evaluate the formation time of agarwood. 3. Experimental Section {#sec3-molecules-21-00911} ======================= 3.1. Chemicals and Materials {#sec3dot1-molecules-21-00911} ---------------------------- HPLC-grade acetonitrile (ACN) and methanol were supplied by Tedia (Fairfield, CR, USA). Chromatographic grade absolute formic acid was purchased from Roe Scientific Inc. (Shanxi, HPLC, China). Water was purified using a Milli-Q Plus185 system from Millipore (Milford, MA, USA). The times of artificial holing into the trunk of A. crassna tree were Aug of 2011 (S1), 2009 (S2) and 2008 (S3), respectively, so the agarwood formation times of S1--S3 were 2 years, 4 years and 5 years, respectively ([Figure 5](#molecules-21-00911-f005){ref-type="fig"}). The samples were collected by Dr. Haofu Dai from Guangnan Province of Vietnam at 14 August 2013. Voucher specimens were deposited at Institute of Tropical Bioscience and Biotechnology, Chinese Academy of Tropical Agricultural Sciences. Thirty-one references compounds were isolated and purified from agarwood in our previous work \[[@B11-molecules-21-00911],[@B14-molecules-21-00911],[@B15-molecules-21-00911],[@B16-molecules-21-00911],[@B17-molecules-21-00911]\]. Their structures were identified by spectroscopic methods (MS and NMR), and they are listed in [Table 1](#molecules-21-00911-t001){ref-type="table"} and [Figure 1](#molecules-21-00911-f001){ref-type="fig"}. The purity of each compound was determined to be higher than 97% by high-performance liquid chromatography (HPLC). 3.2. Preparation of Sample Solutions and Reference Compound Solutions {#sec3dot2-molecules-21-00911} --------------------------------------------------------------------- In this study, the crushed agarwood (100g, dry weight) was soaked in Et~2~O (3 × 200 mL) and extracted by ultrasonication (3 × 15 min). The Et~2~O extracts were filtered and evaporated to get brownish yellow oil. The yields of S1, S2 and S3 were 0.56%, 0.46%, and 2.08%, respectively. Then each extract oil sample was diluted to 1 mg/mL with methanol in a volumetric flask. The solution was filtered through 0.45 µm membranes and stored at 4 °C until use. Accurately weighed samples of thirty-one reference compounds were dissolved in methanol (1.0 mg/mL), respectively, and filtered through 0.45 µm membranes to get the standard solutions. All standard solutions were stored at 4 °C until use. 3.3. HPLC Chromatographic Condition {#sec3dot3-molecules-21-00911} ----------------------------------- A Dionex 3000 series HPLC instrument composed of a diode array detector, a vacuum degasser, a quaternary pump and an auto-sampler was used (Bruker Daltonics Inc., Bremen, HPLC/DAD/VD/QP/AS, Germany). The chromatographic separation was carried out on a Dionex-Acclaim 120 C~18~column (250 mm × 4.6 mm, 5 µm). The mobile phase consisted of acetonitrile (A) and water-acetic acid (99.5:0.5, v/v) (B). The gradient elution program was as follows: 25%--55% A in 0--60 min, 55%--80% A in 60--80 min, 80%--100% A in 80--90 min, and 100% A in 90--95 min. The flow rate was 0.4 mL/min, the column temperature was maintained at 26 °C, and the injection volume was 20 µL. The detection wavelength was set at 254 nm for all the tested compounds. 3.4. MS Spectrometry {#sec3dot4-molecules-21-00911} -------------------- MS experiments were performed using an electrospray ionization tandem mass spectrometry system (Amazon SL, Bruker Daltonics Inc., Bremen, Germany) mainly in positive-ion mode. Helium gas was used as the collision gas and high-purity nitrogen gas as the nebulizer and drying gas at flow rates of 0.4 L/min and 6.0 L/min, respectively. The ESI source conditions were as follows: capillary voltage, −4000 V (position); end plate voltage, −500 V (position); drying gas temperature of 250 °C; and nebulizer pressure 15 psi. Scan spectra from m/z 70 to 2200. All the mass data was processed using Bruker Compass Data Analysis 4.0 software (Bruker Daltonics: Germany, 2009). 4. Conclusions {#sec4-molecules-21-00911} ============== HPLC/ESI-MS/MS is a powerful tool to identify or characterize 2-(2-phenylethyl)chromone derivatives in agarwood. Thirty-one reference compounds including four types of chromones were analyzed by ESI-MS/MS, thus the characteristic fragmentation behavior of DEPECs and EPECs and the methods to distinguish the four types of chromones by their MS characteristic fragmentations were described for the first time, on the basis of the MS spectra of the thirty-one reference compounds. A total of fifty-six 2-(2-phenylethyl)chromone derivatives comprising seven DEPECs, five EPECs, seven THPECs and thirty-seven FTPECs were identified or characterized by their fragmentation pathways and characteristic fragment ions. It was found, with the increase of artificial holing time of agarwood (two years to five years), the total relative content of DEPECs and EPECs showed a downtrend, while the relative content of THPECs and FTPECs showed an increasing trend, which was consistent with the biosynthetic pathway of the formation of agarwood. The relative content of six FTPECs went upward from S1 to S3. This finding could be useful to distinguish agarwood samples with different formation times, and further studies on more agarwood samples with different formation times are needed to validate these conjectures. Supported by Special Fund for Agro-scientific Research in the Public Interest (201303117), Special Fund for The Young Talents's Science and Technology Project of Hainan Association for Science and Technology (HASI201628), Special Fund for Key Research Project of Hainan Province in 2016 (ZDYF2016210), and Major Technology Project of Hainan Province (ZDKJ2016004). Sample Availability: Not available. The list authors contributed to this work as follows: J.L. Yang performed the HPLC/MS/MS and prepared the manuscript. W.H. Dong, F.D. Kong and G. Liao contributed to the revision of this manuscript. G. Liao and W. Li provided the reference compounds, and J. Wang dealt with the picture. The whole research was performed based on the planning of H.F. Dai and W.L. Mei. All authors approved the final version of the manuscript. The authors declare no conflict of interest. ![The structure of reference compounds F1\~F31.](molecules-21-00911-g001){#molecules-21-00911-f001} ![MS^2^ fragmentation pathway of four types of chromones.](molecules-21-00911-g002){#molecules-21-00911-f002} ![Chromatograms of three agarwood samples (S1, S2, S3) at 254 nm.](molecules-21-00911-g003){#molecules-21-00911-f003} ![Biosynthetic progress of chromones and the varieties of the four types of chromones in S1 to S3.](molecules-21-00911-g004){#molecules-21-00911-f004} ![Pictures of the three batches of agarwood.](molecules-21-00911-g005){#molecules-21-00911-f005} molecules-21-00911-t001_Table 1 ###### Characterization of thirty-one reference compounds by HPLC/ESI-MS/MS. Type No. t~R~/min Fragment Ions (m/z) Name -------- --------- ---------- ----------------------- ------ ----- ----- ----- ----- ------------------------------------------------------------------------------------------------------------------------ THPECs F1 12.9 349 331 313 137 (5S\,6R\,7S\)-5,6,7-Trihydroxy-2-\[2-(3-hydroxy-4-methoxyphenyl)ethyl\]-5,6,7,8-tetrahydrochromone* F2 13.2 349 331 313 137 (5S\,6R\,7R\)-5,6,7-Trihydroxy-2-\[2-(3-hydroxy-4-methoxyphenyl)ethyl\]-5,6,7,8-tetrahydrochromone* F3 15.2 349 331 313 121 5α,6β,7α,8β-Tetrahydroxy-2-\[2-(4-methoxyphenyl)-ethyl\]-5,6,7,8-tetrahydrochromone F4 17.3 383 365 347 137 (5S\,6R\,7S\,8R\)-8-Chloro-5,6,7-trihydroxy-2-\[2-(3-hydroxy-4-methoxyphenyl)ethyl\]-5,6,7,8-tetrahydro-chromone EPECs F5 18.3 347 329 301 137 5,6-Edroxy-7,8-dihydroxy-2-\[2-(3-hydroxy-4-methoxy)phenylethyl\]-5,6,7,8-tetrahydrochromone F6 33.1 331 313 285 121 5,6-Edroxy-7,8-dihydroxy-2-\[2-(4-methoxy)phenyl-ethyl\]-5,6,7,8-tetrahydrochromone F7 33.8 301 283 255 91 5,6-Edroxy-7,8-dihydroxy-2-(2-phenylethyl)-5,6,7,8-tetrahydrochromone DEPECs F8 24.4 329 301 137 5,6:7,8-Diedroxy-2-\[2-(3-hydroxy-4-methoxy)phenyl-ethyl\]-5,6,7,8-tetrahydrochromone F9 42.6 313 285 121 Oxidoagarochromones B F10 43.5 283 255 91 Oxidoagarochromones A FTPECs F11 34.7 283 177 107 6-Hydroxy-2-\[2-(4-hydroxy)phenylethyl\]chromone F12 36.6 313 137 6-Hydroxy-2-\[2-(3-hydroxy-4-methoxy)phenylethyl\]-chromone F13 38.3 313 192 121 6,8-Dihydroxy-2-\[2-(4-methoxy)phenylethyl\]chromone F14 39.5 283 192 91 6,8-Dihydroxy-2-(2-phenylethyl)chromone F15 41.5 283 177 107 6-Hydroxy-2-\[2-(2-hydroxy)phenylethyl\]chromone F16 42.4 313 121 6,7-Dihydroxy-2-\[2-(4-methoxy)phenylethyl\]chromone F17 43.2 357 220 137 6,7-Dimethoxy-2-\[2-(3-hydroxy-4-methoxy)phenyl-ethyl\]chromone F18 47.5 297 161 137 2-\[2-(3-Methoxy-4-hydroxy)phenylethyl\]chromone F19 49.8 267 176 91 8-Hydroxy-2-(2-phenylethyl)chromone F20 50.4 296 137 2-\[2-(3-Hydroxy-4-methoxy)phenylethyl\]chromone F21 51.2 327 121 6-Methoxy-7-hydroxy-2-\[2-(4-methoxy)phenylethyl\]-chromone F22 52.3 327 191 137 6-Methoxy-2-\[2-(3-methoxy-4-hydroxy)phenylethyl\]-chromone F23 54.3 327 137 6-Methoxy-2-\[2-(3-hydroxy-4-methoxy)phenylethyl\]-chromone F24 55.2 267 161 107 2-\[2-(2-Hydroxy)phenylethyl\]chromone F25 56.5 297 121 6-Hydroxy-2-\[2-(4-methoxy)phenylethyl\]chromone F26 58.3 267 176 91 6-Hydroxy-2-(2-phenylethyl)chromone F27 59.1 343 137 5-Hydroxy-6-methoxy-2-\[2-(3-hydroxy-4-methoxy)-phenylethyl\]chromone F28 64.9 311 220 91 6,7-Dimethoxy-2-(2-phenylethyl)chromone F29 72.0 281 121 2-\[2-(4-Methoxy)phenylethyl\]chromone F30 73.8 251 160 91 2-(2-Phenylethyl)chromone F31 78.7 326 121 5-Hydroxy-6-methoxy-2-\[2-(4-methoxy)phenylethyl\]-chromone CM: chromone moiety; BM: benzyl moiety. molecules-21-00911-t002_Table 2 ###### The MS characterization and identified or characterized results of DEPECs, EPECs and THPECs from S1 to S3. No. t~R~ (min) \[M + H\]^+^ (m/z) (+)Fragment Ions (m/z) OCH~3~ OH Identification RFC RC (%) -------- ------------ ---------------------- -------------------------- -------- ----- ---------------- ----- -------- --- --------------------------------------------------------------------------------------------------------- --------- ------ ------ ------ THPECs 1 15.9 349 331 313 121 1 4 5α,6β,7α,8β-Tetrahydroxy-2-\[2-(4-methoxyphenyl)ethyl\]-5,6,7,8-tetrahydrochromone F3 0.51 2 16.0 319 301 283 4 (5S,6S,7R)-5,6,7-Trihydroxy-2-\[2-(2-hydroxyphenyl)-ethyl\]-5,6,7,8-tetrahydrochromone or isomers 0.15 3 16.7 349 331 313 1 4 Isomer of F3 0.50 4** 23.7 303 285 267 3 rel-(5R,6S,7R)-5,6,7-Trihydroxy-2-(2-phenylethyl)-5,6,7,8-tetrahydrochromone 0.09 5 24.2 317 299 281 121 1 2 New compound (two hydroxy on CM, one methoxy on BM) 0.08 6 29.4 367 349 331 121 1 3 rel-(5R,6S,7S,8R)-8-Chloro-5,6,7-trihydroxy-2-\[2-(4-methoxyphenyl)ethyl\]-5,6,7,8-tetrahydrochromone 0.65 0.65 1.16 7 30.1 337 319 301 3 (5S,6S,7S,8R)-8-Chloro-2-(2-phenylethyl)-5,6,7-trihydroxy-5,6,7,8-tetrahydrochromone or new compound 0.43 0.76 0.80 EPECs 8 18.5 347 329 301 137 1 3 5,6-Edroxy-7,8-dihydroxy-2-\[2-(3-hydroxy-4-methoxy)-phenylethyl\]-5,6,7,8-tetrahydrochromone F5 1.13 0.12 9 23.3 285 267 239 1 New compound (one hydroxy on CM) 0.09 10 25.0 331 313 285 121 1 2 New compound (isomer of F6) 0.94 0.15 11 33.0 331 313 285 121 1 2 5,6-Edroxy-7,8-dihydroxy-2-\[2-(4-methoxy)phenylethyl\]-5,6,7,8-tetrahydrochromone F6 7.25 4.95 2.11 12 33.7 301 283 255 2 5,6-Edroxy-7,8-dihydroxy-2-(2-phenylethyl)-5,6,7,8-tetrahydrochromone F7 3.26 2.76 0.85 DEPECs 13 21.8 329 301 137 1 1 New compound (isomer of F8) 1.00 14 23.0 329 301 193 137 1 1 New compound (isomer of F8) 0.50 15 23.3 329 301 137 1 1 New compound (isomer of F8) 0.28 16 24.2 329 301 137 1 1 5,6:7,8-Diedroxy-2-\[2-(3-hydroxy-4-methoxy)phenylethyl\]-5,6,7,8-tetrahydrochromone F8 0.47 17 24.6 329 301 137 1 1 New compound (isomer of F8) 0.02 18 42.0 313 285 121 1 Oxidoagarochromones B F9 4.85 19 42.9 283 255 Oxidoagarochromones A F10 0.89 0.21 CM: chromone moiety; BM: benzyl moiety; RFC: Reference compound; RC: Relative content. molecules-21-00911-t003_Table 3 ###### The MS characterization and identified or characterized results of FTPECs from S1 to S3 by HPLC/DAD/ESI/MS^2^. No. t~R~ (min) \[M + H\]^+^ (m/z) Fragment Ions (m/z) CM BM Identification RFC RC (%) -------- ------------ ---------------------- ----------------------- ----- ------ ---------------- ----- ----------- -------------------------------------------------------------------------------------------------------- --------- ------ ------ ------- 20 26.1 329 137 2 1 3′- 6,8-Dihydroxy-2-\[2-(3-hydroxy-4-methoxyl)phenylethyl\]-chromone 0.28 21 34.2 283 177 107 6- 4′- 6-Hydroxy-2-\[2-(4-hydroxy)phenylethyl\]chromone F11 8.6 0.03 22 35.0 313 177 137 1 1 4′or 2′- 6-Hydroxy-2-\[2-(3-methoxyl-4-hydroxy)phenylethyl\]-chromone 0.26 0.26 23 36.8 313 137 6- 4′- 3′- 6-Hydroxy-2-\[2-(3-hydroxy-4-methoxyl)phenylethyl\]-chromone F12 0.66 0.23 0.41 24 38.4 313 121 6,8- 4′- 6,8-Dihydroxy-2-\[2-(4-methoxy)phenylethyl\]chromone F13 0.66 0.87 2.32 25 39.5 283 192 91 6,8- 6,8-Dihydroxy-2-(2-phenylethyl)chromone F14 0.93 1.81 26 41.3 283 177 107 6- 2′- 6-Hydroxy-2-\[2-(2-hydroxy)phenylethyl\]chromone F15 0.05 27 42.7 313 121 6,7- 4′- 6,7-Dihydroxy-2-\[2-(4-methoxy)phenylethyl\]chromone F16 2.80 0.46 0.45 28 44.0 283 192 91 2 New compound (isomer of F14) 1.33 0.52 29 59.1 343 137 6- 5- 3′- 4′- 5-Hydroxy-6-methoxy-2-\[2-(3-methoxy-4-hydroxy)phenyl-ethyl\]chromone F27 1.18 30 66.3 313 121 2 1 5,8-Dihydroxy-2-\[2-(4-methoxy)phenylethyl\]chromone 1.82 31 68.5 283 192 91 2 5,8-Dihydroxy-2-(2-phenylethyl)chromone 0.78 32 43.1 357 220 137 6,7- 4′- 3′- 6,7-Dimethoxy-2-\[2-(3-hydroxy-4-methoxyl)phenylethyl\]-chromone F17 0.46 33 46.8 267 161 107 1 2-\[2-(4-Hydroxy)phenylethyl\]chromone 0.27 0.21 0.20 34 47.5 297 161 137 1 4′- 2-\[2-(3-Methoxy-4-hydroxy)phenylethyl\]chromone F18 0.22 35 48.5 297 191 107 1 2′ or 4′- 6-Methoxy-2-\[2-(4-hydroxy)phenylethyl\]chromone or new compound 0.16 36 49.2 267 176 91 8- 8-Hydroxy-2-(2-phenylethyl)chromone F19 0.78 1.16 37 50.3 297 121 1 1 6-Hydroxy-2-\[2-(4-methoxy)phenylethyl\]chromone or new compound 0.16 0.04 1.16 38 51.4 327 121 6- 7- 4′- 6-Methoxy-7-hydroxy-2-\[2-(4-methoxy)phenylethyl\]-chromone F20 1.27 1.57 2.55 39 52.3 327 191 137 6- 3′- 4′- 6-Methoxy-2-\[2-(3-methoxy-4-hydroxy)phenylethyl\]-chromone F22 2.88 0.85 1.88 40 53.0 297 206 1 1 6-Hydroxy-7-methoxy-2-(2-phenylethyl)chromone 1.74 2.32 41 54.3 327 137 6- 4′- 3′- 6-Methoxy-2-\[2-(3-hydroxy-4-methoxy)phenylethyl\]-chromone F23 5.43 2.06 1.98 42 54.9 267 161 107 2′- 2-\[2-(2-Hydroxy)phenylethyl\]chromone F24 1.06 43 55.8 297 121 1 1 6-Hydroxy-2-\[2-(4-methoxy)phenylethyl\]chromone or new compound F25 4.25 5.36 8.17 44 57.6 267 176 91 6- 6-Hydroxy-2-(2-phenylethyl)chromone F26 1.42 6.64 8.17 45 58.7 297 191 107 1 2′ or 4′- 6-Methoxy-2-\[2-(4-hydroxy)phenylethyl\]chromone or new compound 0.27 46 78.2 357 121 2 1 1 New compound (two methoxyls and one hydroxyl on CM, one methoxyl on BM) 1.00 47 78.7 327 121 6- 5- 4′- 5-Hydroxy-6-methoxy-2-\[2-(4-methoxy)phenylethyl\]-chromone F31 4.31 2.79 3.47 48 80.3 297 206 91 1 1 5-Hydroxy-6-methoxy-2-(2-phenylethyl)chromone 1.36 2.58 2.23 49 62.5 341 121 2 1 6,7-Dimethoxy-2-\[2-(4-methoxy)phenylethyl\]chromone 5.67 5.06 4.43 50 63.3 341 151 1 2 New compound (one methoxyl on CM, two methoxyls on BM) 1.28 0.51 51 64.8 311 220 91 6,7- 6,7-Dimethoxy-2-(2-phenylethyl)chromone F28 5.58 6.41 11.93 52 71.7 281 121 4′- 2-\[2-(4-Methoxy)phenylethyl\]chromone F29 0.62 0.98 1.18 53 73.2 281 190 91 1 6-Methoxy-2-(2-phenylethyl)chromone or new compound 0.17 54 73.4 251 160 91 2-(2-phenylethyl)chromone F30 0.17 1.05 1.52 55 74.7 311 121 1 1 6-Methoxy-2-\[2-(3-methoxy)phenylethyl\]chromone or 6-methoxy-2-\[2-(4-methoxy)phenylethyl\]chromone 4.89 6.59 56 76.3 281 190 91 1 6-Methoxy-2-(2-phenylethyl)chromone or new compound 2.28 10.6 9.34 CM: chromone moiety; BM: benzyl moiety; RFC: Reference compound; RC: Relative content.2.3.1. Structural Analysis of THPECs molecules-21-00911-t004_Table 4 ###### The statistical results of 2-(2-phenylethyl)chromone derivatives. N(RC/%) DEPECs EPECs Total (E) THPECs FTPECs Total (all) --------- ----------- ------------ ------------- ----------- ------------- ------------- S1 7 (8.01%) 4 (12.58%) 11 (20.59%) 3 (1.58%) 23 (44.25%) 37 (66.42%) S2 0 (0%) 5 (8.07%) 5 (8.07%) 5 (1.73%) 33 (71.59%) 43 (81.39%) S3 1 (0.21%) 2 (2.96%) 3 (3.17%) 3 (2.47%) 23 (73.56%) 29 (79.20%) N: number; RC: Relative content; E: DEPECs and EPECs.	{ "pile_set_name": "PubMed Central" }
Q: Drywall taping/floating steps if finish will be skim coating I am finishing up a master bath remodel which involved removing some walls, and creating new walls. I have: Hung new sheetrock for the new walls Patched the ceiling where the old walls were with drywall (~4.5" wide strips) Patched some gaps with hot mud Taped all the joints and covered with the first layer of all-purpose joint compound. The next step will be to sand down this first layer as prep for the subsequent layers, repeating until the joints 'disappear'. For the final finish, we have decided to skim coat as we like the way this worked and looked in our previous bathroom. My question is: Do I need to do the subsequent (2 or 3) layers of joint and screw-divot feathering if I intend to put 2 or 3 coats on for skimming? I have not skim-coated a wall before, and I just don't know how much of the surface topography I will be able to hide. Thanks! A: Read the datasheet for the compound you want to use to skim coat and see what's the maximum allowable depth for a layer. (For European products I'm familiar with it's about 2 or 3 mm.) Then you can decide what dimples need pre-covering and which can simply get covered in the skim coat. If you exceed the max depth you might get hairline cracks, but [in my experience] that only happens on larger areas, not screw-size... and you can fix it anyway by filling the crack(s) with the same compound, which usually takes less time than strictly following the prescribed layer depth. YMMV.	{ "pile_set_name": "StackExchange" }
Cotes, Leicestershire Cotes is a hamlet and very small civil parish near the town of Loughborough in Leicestershire, England.Cotes has a population of about 50. At the 2011 census the population remained less than 100 and was included in the civil parish of Burton on the Wolds. It lies on the River Soar, and Cotes Bridge provides the main bridging point in that area. The A60 Trunk Road goes over Cotes Bridge on its way out of Loughborough towards Nottingham. The B676, the only other significant nearby road, begins at the A60 just to the east of Cotes Bridge and goes off towards the village of Burton on the Wolds. The medieval village of Cotes was abandoned, possibly because of plague, although a hall remained at Cotes for some time. There was a minor battle at Cotes Bridge during the English Civil War. References External links Category:Hamlets in Leicestershire Category:Civil parishes in Leicestershire Category:Borough of Charnwood	{ "pile_set_name": "Wikipedia (en)" }
As the value and use of information continues to increase, individuals and businesses continually seek additional ways to process and store information. One option available to users of information is an information handling system. An information handling system generally processes, compiles, stores, and/or communicates information or data for business, personal, or other purposes, thereby allowing users to take advantage of the value of the information. Because technology and information handling needs and requirements vary between different users or applications, information handling systems may also vary with regard to the kind of information that is handled, how the information is handled, how much information is processed, stored, or communicated, and how quickly and efficiently the information may be processed, stored, or communicated. The variations in information handling systems allow for information handling systems to be general or configured for a specific user or specific use, including such uses as financial transaction processing, airline reservations, enterprise data storage, or global communications. In addition, information handling systems may include a variety of hardware and software components that may be configured to process, store, and communicate information and may include one or more computer systems, data storage systems, and networking systems. In conventional compute blade chassis designs, each compute blade has its own couple of local hard disk drives that are used for bootstrapping the operating system and/or local storage. These two local hard disk drives are typically mirrored using a host-based and/or an operating system-based RAID solution to provide fault tolerance. However, such a design impacts compute blade density, form factor, air flow, and thermal cooling, and, in addition, adds cost to the overall compute blade design. It is typical to include a minimum of two hard disk drives on each compute blade of the system. For example, assuming a compute blade configuration has ten compute blades, at least twenty local hard disk drives would be needed, a minimum of two per compute blade, to support the compute blade configuration.	{ "pile_set_name": "USPTO Backgrounds" }
South American marked gecko There are two species of gecko named South American marked gecko: Homonota horrida Homonota fasciata	{ "pile_set_name": "Wikipedia (en)" }
In vivo evaluation of a MR-guided 980nm laser interstitial thermal therapy system for ablations in porcine liver. To evaluate the use of a 980-nm diode laser for magnetic resonance-guided laser interstitial thermal therapy (MR-guided LITT) ablations in liver tissue in an in vivo porcine model. MR-guided guided LITT was performed on nine juvenile pigs placed under general anesthesia. Target ablation sites were selected in the left and right lobes of the liver. Laser applicators were placed in the liver using intermittent MR guidance. Up to four separate ablations were performed in each animal using a 15 or 30 W laser generator using one or two applicators. During the ablations, continuous MR-based temperature mapping (MR-thermal mapping), using a proton resonance frequency technique, was performed to monitor the size of the ablation in real-time. Extent of thermal tissue damage was continuously estimated based on Arrhenius model. Two-minute ablations were performed at each site. MR-thermal mapping of ablations within the posteroinferior liver were accomplished with continuous breathing at low tidal volume. In the mid right lobe of the liver, due to motion artefacts, MR-thermometry was performed intermittently during breath hold periods. In the left lobe of the liver, ablations were performed with ventilation using positive end expiratory pressure (PEEP) of 10 cm of water. Upon completion, MR imaging with gadolinium contrast was performed to assess the extent of treatment. Thermal lesions were subsequently measured using both, MR-thermal dose and MR gadolinium images, for comparison. Following the animal euthanasia, the liver was harvested and subjected to formalin fixation and paraffin embedding for histological examination. Between one and four focal liver ablations (total 24 ablations) were successfully performed in nine animals with either a 15 or 30 W laser generator. For the 15-W laser generator, the average single applicator ablation size was (2.0 ± 0.5) × (2.6 ± 0.4) cm(2) , as measured by magnetic resonance (MR) thermometry, or (1.7 ± 0.4) × (2.2 ± 0.6) cm(2) , as measured with gadolinium contrast, with the difference being not statistically significant. For the 30-W laser generator, the average single applicator ablation size was (2.4 ± 0.3) × (3.3 ± 0.5) cm(2) by MR thermometry and (2.1 ± 0.4) × (2.9 ± 0.3) cm(2) by gadolinium enhancement, with no statistically significant difference. Simultaneously activating two applicators with the 15 W generator demonstrated ablation sizes of (3.7 ± 0.9) × (3.2 ± 0.1) cm(2) using MR thermometry and (2.3 ± 0.6) × (2.4 ± 0.3) cm(2) with gadolinium contrast, while using two applicators in the 30-W laser generator, yielded (4.5 ± 0.6) × (3.9 ± 0.2) cm(2) using MR thermometry and (4.4 ± 1.1) × (3.6 ± 0.5) cm(2) with gadolinium contrast enhancement. In our experience, we found that liver ablations performed with a MR-guided 980-nm diode LITT system through the saline cooled catheter applicator could be performed throughout the liver. Additionally, liver ablations were safe and produced a clinically applicable ablation zone. These results suggest the 980-nm diode laser MR-guided LITT system could be effective in treatments of hepatic tumors.	{ "pile_set_name": "PubMed Abstracts" }
Q: How to get the value from JSON in JS I'm trying to get the "formatted_address" value from this JSON file. I'm new to this and found the documentation quite confusing. The code I have now is the following where the variable "location" is the url generated like the one above. $.getJSON(location, function( data ){ stad = data.results.formatted_address; console.log(stad); }); How would I achieve this? A: results is an array, so you need to access it as one. Given your example with only one item, you can access it directly by index: var stad = data.results[0].formatted_address; // = "'s-Hertogenbosch, Netherlands" If there were multiple items in the array you would need to loop through them: for (var i = 0; i < data.results.length; i++) { var stad = data.results[i].formatted_address; // do something with the value for each iteration here... }	{ "pile_set_name": "StackExchange" }
Erastus D. Telford Erastus Dalson Telford (April 23, 1874–December 4, 1936) was an American politician and lawyer. Telford was born near Salem, Illinois and graduated from Salem High School. He graduated from McKendree University and Georgetown University Law Center. He was admitted to the Illinois bar and practiced law in Salem. Teford served as the Salem city attorney. Telford served in the United States Army during World War I and was commissioned a major. Telford served in the Illinois Senate in 1911 and 1912 and from 1921 to 1929. He was a Republican. Teford died at Gliden Memorial Hospital in DeKalb, Illinois frpm an infection he suffered after fracturing his leg in an automobile accident near Vandalia, Illinois on October 25, 1936. Notes External links Category:1874 births Category:1936 deaths Category:People from Salem, Illinois Category:Military personnel from Illinois Category:McKendree University alumni Category:Georgetown University Law Center alumni Category:Illinois lawyers Category:Illinois Republicans Category:Illinois state senators Category:Road incident deaths in Illinois	{ "pile_set_name": "Wikipedia (en)" }
Q: How to append the string variables using stringWithFormat method in Objective-C I want to append the string into single varilable using stringWithFormat.I knew it in using stringByAppendingString. Please help me to append using stringWithFormat for the below code. NSString* curl = @"https://invoices?ticket="; curl = [curl stringByAppendingString:self.ticket]; curl = [curl stringByAppendingString:@"&apikey=bfc9c6ddeea9d75345cd"]; curl = [curl stringByReplacingOccurrencesOfString:@"\n" withString:@""]; Thank You, Madan Mohan. A: You can construct your curl string using -stringWithFormat: method: NSString apiKey = @"bfc9c6ddeea9d75345cd"; NSString curl = [NSString stringWithFormat:@"https://invoices?ticket=%@&apikey=%@", self.ticket, apiKey];	{ "pile_set_name": "StackExchange" }
Q: Recover files from a failed RAID 1 - How do I rsync if source file size is bigger I have 2 drives that were on a mirrored RAID. The server crashed (failed array) and there are no backups. The client was setup with Carbonite, but failed to renew their plan, which expired this past July. Now they're stuck with a down server and no backups. I pulled the drives, both of which appear when I connect them individually to my computer using a SATA to USB adapter. Both drives obviously have issues, but I've been able to recover most (almost all) of the files off of one of the drives. The recovery destination is a NAS in my office. Now, I would like to attempt a recovery from the second drive. I think it makes sense to ONLY overwrite the files on the destination NAS if the source (2nd hard drive) file size is bigger. My theory is that if files were corrupted on the first drive but not corrupted on the 2nd drive, they would be smaller (and vice-versa for good files on the 1st drive that are bad on the 2nd). Is this a stupid theory? Should I just stop acting like an idiot and create 2 separate directories for "disk 1" and "disk 2" and let the client sort it out? If my idea is sound, how would I go about this using rsync? I know how to use rsync in general, and I know how to use rsync if the file sizes are different or if the file timestamps are different, but I don't know how to do a conditional copy if (and only if) the source is bigger than the destination. A: I think it makes sense to ONLY overwrite the files on the destination NAS if the source (2nd hard drive) file size is bigger. File size would typically be the same; the filesystem tracks file size and corruption won't care about file length boundaries. Should I just stop acting like an idiot and create 2 separate directories for "disk 1" and "disk 2" and let the client sort it out? Best to leave data recovery to the professionals if you're not quite sure what you're doing. No article you read online or answer you'll get here will give you the background and experience needed to do a full and proper recovery. If the data is critical for your customer they need to pay up and get it professionally taken care of.	{ "pile_set_name": "StackExchange" }
t d = 64 + -69. Which is the closest to x? (a) 3/2 (b) -0.14 (c) d b Let r = -2882 - -2882.6. Which is the nearest to -4? (a) -2 (b) 1 (c) r a Suppose -9p = 3h - 10p - 1310, 4p = -2h + 850. Let i = h - 1306/3. Let s be 2/3(-3)/(-14). What is the closest to i in s, -0.2, -1/6? -0.2 Let j be (-338)/(-5)(-24 + 29). Let i = j + -333. Let c = 2.05 + -0.05. What is the nearest to i in 2/3, -5, c? c Let s be (-2)/((40/15)/(-4)) - 2. What is the nearest to -6 in s, -4, 0.1? -4 Let a = 139.061 + -139. Let d = 0.439 + a. Let v = 823/7 - 118. What is the nearest to -0.2 in d, 4, v? v Let m be (4824/300 - 4) + -12. What is the closest to 1/4 in m, -3/2, 0.2, -0.2? 0.2 Let j = -124/89 - -779/623. What is the closest to -3 in 16, -3, j, 3? -3 Let v = -8975 + 35899/4. Which is the closest to v? (a) 4 (b) 103 (c) -4 c Let h = 0.02 - 2.02. Let p = -0.407 + 41.407. What is the nearest to 0 in 3/7, p, h? 3/7 Let j be (-32)/20 - (0 + -2). Let k = 0.4 + -0.1. Let m = 4.81 - 5.31. Which is the closest to j? (a) k (b) -1 (c) m a Let o = 0.2941 + -0.1041. Which is the closest to -1/2? (a) 4/7 (b) o (c) -1/5 c Let h = -4585.06 + 4585. Which is the closest to -0.1? (a) h (b) -1/5 (c) 5 (d) -3/4 a Let f = 13707 - 68534/5. What is the closest to 0 in 1/11, -1/4, -2/1275, f? -2/1275 Let o = -656/741 + 54/247. Which is the nearest to -29? (a) -19 (b) -1 (c) o a Let d = -34 + 135/4. Let l = -466 - -549. Let z = l + -79. Which is the closest to -2/3? (a) -2/11 (b) d (c) z b Let v = 27.82 + 4.08. Let u = -32 + v. Which is the nearest to u? (a) -4 (b) -5/2 (c) 2/7 c Let l = -0.3 - -0.6. Let z = -1.527 - -0.527. What is the nearest to z in 2, 0.1, l? 0.1 Let m = -2965.763 - -2967. Let g = m + -1.337. Let q = -27 - -19. What is the closest to q in 2/3, -1, g? -1 Let v = 989.8 + -988.8. What is the closest to 9 in 4/3, -5, 4/5, v? 4/3 Suppose 73 = -p - 71. Let u = -149 - p. What is the nearest to 2/5 in u, 0.9, -2/7? 0.9 Let w = 0.1 + 2.9. Let t be (-4)/1023 - (-33)/(31977/(-532)). Which is the nearest to t? (a) -0.3 (b) w (c) -2 a Let a = 19.4 - 58.4. Let w = -42 - a. What is the closest to 0 in -16, w, 0.5? 0.5 Let v = -0.024 + -1.976. Let y = -5.842 + 10.842. Which is the closest to 0.1? (a) v (b) y (c) -10 (d) 2 d Suppose -30v - 9 - 51 = 0. What is the closest to -5/8 in -4/9, 3, 0.5, v? -4/9 Let r = -81 + 74. Which is the nearest to -4? (a) -9 (b) 2 (c) r (d) 1/2 c Let m = 3 + -3.22. Let a = 375.9648 - -0.0352. Let t = -376.4 + a. What is the closest to 1 in t, -1, m? m Suppose 0 = -290u + 304u - 28. What is the nearest to -2 in 3, 7/5, u, 1/5? 1/5 Let c = 264.02 - 263.02. What is the closest to -2 in 35.5, -2/9, 6, c? -2/9 Let o = -2.091 - 0.009. Let l = 66822.5 - 66823. Which is the closest to 0? (a) l (b) -0.2 (c) o b Suppose -2s = -10, 0 = -5n + 3n + s + 173. What is the closest to 1/3 in -5, -3/8, n, 0.5? 0.5 Let q be 265/20034-45 + (-4)/(-8). Suppose -m + 17 = 4w, 0 = 5m - 3m - w + 2. Which is the closest to m? (a) -5 (b) q (c) -1/5 (d) 1 d Let j(m) = -5m2 - 4m - 3. Let c be j(-1). Let h be 116/10155/2. What is the nearest to h in c, -3, 0.2, -5? 0.2 Suppose 3h - 12 = 0, -12 = 106r - 108r - 3h. Which is the closest to r? (a) 2 (b) -4 (c) 3/19 c Let m = 0.1092 - 111.1292. Let l = -111.99 + 0.99. Let i = m - l. Which is the nearest to -1? (a) i (b) 0.5 (c) 0.4 a Let v = -566 - -566.1. Let m = -30 - -30. Let t = 41 - 55. What is the closest to 0 in m, v, t? m Let k = 7110 - 7108. What is the nearest to 31 in -0.5, 1/4, k? k Let l = 0.3 + 0.2. Suppose t + 12t + 19t - 64 = 0. Let m = 3.961 + 0.039. Which is the nearest to -2? (a) m (b) t (c) l c Let f be 10/(-50) + -13 + 14. Which is the nearest to -1? (a) f (b) -54 (c) 2/15 c Let x be (-74)/(-185)(-2)/33/2. What is the closest to 0 in x, 4, -52/9? x Let w = 11 + -7. Let k = -2/6965 - 6961/13930. Let v = -0.5 + 0. Which is the nearest to k? (a) v (b) w (c) -9 a Let b = 25 - 24.8. Let t = 12309 - 12313. What is the closest to b in 3, 5, t, -2? -2 Let k = -717.2 - -717.2. Which is the closest to 0? (a) k (b) -1/6 (c) 1/4 (d) -2/255 a Let s = 51/31 + -499/341. Which is the nearest to 0? (a) -4 (b) -5.1 (c) s c Suppose 21 = s + 4c, 5c - 20 = -2s + 10. What is the closest to s in -0.9, -0.5, 2/15, -3/2? 2/15 Let n = -142 + 19. Let s = n - -117. Which is the closest to s? (a) -2/3 (b) -2 (c) -1 b Let h = 2068.8 + -2068.3. Which is the closest to 0? (a) h (b) 0.04 (c) 1.6 b Let u = 648 - 994. Let s = -348 - u. What is the closest to 0 in s, 3, 1/31? 1/31 Let w be (1 + 27/(-12))96/(-24). Which is the nearest to 0.1? (a) w (b) 2/23 (c) -1/8 b Suppose 0 = -3z - 5h - 5 - 7, -2z = -h - 5. Let i = 0.0066 + -356.0066. Let m = i - -357. Which is the nearest to m? (a) -0.5 (b) 15 (c) z c Let w = 170.198 - 170. Let z = 5.198 - w. Which is the closest to 0.1? (a) 4 (b) -4/3 (c) z b Let u = -11470 + 11470.2. Which is the nearest to 3? (a) -0.5 (b) u (c) 47 b Let u = -0.258 - -0.26. Let h = 4082 - 4082. Which is the closest to h? (a) u (b) -0.1 (c) 0.3 (d) 0 d Suppose -4o - 71 = t - 98, -5o - 5t = -45. What is the closest to -0.1 in 0.1, -4, -12, o? 0.1 Let d(y) = -2y + 88. Let i be d(-21). Let w be i/(-42) + 88/924. Which is the closest to -1/7? (a) w (b) -0.5 (c) -4 b Let p = 22.2 - 22. Let r be (-15)/(-40) + (-3)/12. What is the closest to 2/3 in 4, r, p? p Suppose 0 = 2x + 5s + 27 - 68, 5x = 4s + 86. Let k be (65/52 + -2)/(x/(-8)). What is the closest to -1/2 in k, -0.3, 0.112? -0.3 Let i be (-1)/(2/76)(-165)/(-66). Let z = 103 + i. Suppose -4m + z = -7m + 2d, 0 = -m - d - 6. Which is the closest to 1? (a) -0.03 (b) m (c) -5 a Let w = 0.14 - 0.24. Suppose -63 = -2r - 51. Suppose 0 = -rh - 15 - 9. Which is the closest to 1/2? (a) -8 (b) w (c) h b Let i be (-8)/(-42) - 2/6. Let l be ((-24675)/(-13160))/(135/12). What is the closest to -1 in -10, 1, l, i? i Let y = 0.9 - -2.1. Let a be (-1043)/(-447) + (-3)/(-6)10/(-15). What is the closest to -2 in y, a, -31? a Let r be ((-8)/6 - -1)/(-1). Let f = 81 + -61. Let q = 20 - f. What is the closest to q in r, 6, -1? r Let o = 6601 - 33007/5. Which is the nearest to o? (a) 6 (b) -597 (c) 1 (d) 3/4 d Let h = -45 + 40. Let f = 129.5 - 98. Let k = 31 - f. Which is the closest to 0? (a) k (b) h (c) 3 a Suppose 19h - 15h = -12. Let k be (-1 - (-27)/15)/(2/10). Let g = -6 + k. Which is the closest to 1/3? (a) 3 (b) h (c) g c Let d(f) = -6f - 25. Let q be d(-4). What is the closest to -2 in 0, -19, q, -2? -2 Let o = 1.84 - 5.84. Let z = -54/17 - -429/119. Which is the closest to 16? (a) z (b) 2/7 (c) o a Let h be ((-2)/10 + 1274/(-980))-3. Which is the closest to 3? (a) h (b) 13 (c) 5 (d) -0.2 a Let p = -18884.8 + 18885. What is the nearest to p in -4, -1/3, 1/6, -5? 1/6 Suppose 0 - 3 = -3i. Let q = 3707/3120 + 51/208. Let x = -11/6 + q. Which is the closest to -0.04? (a) x (b) 3 (c) i a Let q = 21.7 + -1.8. Let d = q - 21.9. What is the nearest to d in -4/3, 0, 0.3? -4/3 Suppose -t = -4t + 6, 4t = -5j + 23. Let l = -352 + 349. Which is the closest to -0.3? (a) 1/8 (b) j (c) l a Let m = 58 - 52. Let x be -5 + 8 - m - (-119)/3. Let p = -37 + x. What is the closest to p in 3, -4, -5? 3 Let w = -2 + 3. Let r be 51319/(-190) + (-2)/5. Let v = r + 269. What is the nearest to w in 1, 1/5, v? 1 Let g = -5617.9 + 5618. Which is the nearest to g? (a) -2/13 (b) -0.2 (c) -55 a Let q(u) = u3 - 14u*2 + 22u + 29. Let z be q(12). Which is the nearest to -6/23? (a) -0.4 (b) z (c) 2/13 a Let y = 3.586 + -3.486. What is the closest to y in -0.5, 2/13, -43? 2/13 Suppose 7x = -2k + 14, 2x - 95 = 5k - 247. Which is the nearest to 0? (a) 5 (b) -7 (c) k a Suppose 7m - 23m - 493 = -1565. Which is the closest to 0? (a) -2 (b) 1/7 (c) m (d) -3 b Let q = -1611 + 1610.5. Which is the closest to 1/2? (a) q (b) -1/4 (c) -3 (d) 0.5 d Let u = 468 + -443.1. Let l = u + -24.8. Let y be (3/(-18))/(1/(-3)). Which is the closest to l? (a) y (b) 2 (c) 0.06 c Let w = 4.55 - 4.35. Let y = 2/667 - -1985/5336. Let m = 0 - -0.02. Which is the nearest to w? (a) y (b) m (c) -4 a Let b = -1 - -6/5. Let j = 188 + -76. Let z = j - 110	{ "pile_set_name": "DM Mathematics" }
Monday, August 23, 2010 The One Tie You Need Whether you rock with a pared down wardrobe or are the kind of guy who likes to have 5 of everything, let me humbly recommend the one tie you absolutely need - a J. Press navy knit. Neckwear doesn't get any better. End of story. It's style for the ages - timeless, season-less, all occasions, etc. At 3" it's the perfect width and ties the perfect four-in-hand knot. The beauty of this tie is how squarely it falls into everyone's sweet spot. No matter what your personal aesthetic may be, this tie will not only transition in with no problem, but quickly become your go-to piece of neckwear. With this very post in mind, I made sure to head over to the J. Press store in NYC on Friday to check out their selection. After not finding a single navy knit I asked a salesman what the deal was. Apparently, early that morning a woman had come to J. Press and asked how many navy knits were currently in stock. After a salesman rounded up all 14 from both the floor and stockroom, the woman proceeded to buy every last one. She mentioned that her boyfriend only wore navy knits and that he got more compliments on his J. Press number than any other. $1,113 (before New York state sales tax) was spent and she left the store as quickly as she had come in. This post is obviously not for that guy - he already knows what's up. Anon @11:05- Uniqlo makes decent knits for the price, but you cannot compare them to J. Press' offerings in terms of quality or even style. The biggest issue for me, with most knit ties regardless of where they are from, is the width. Uniqlo's options, like 90% of knit ties on the market, are too skinny. 3" on up or bust...pause. The Press navy blue knit is nice but for my money I prefer the Paul Stuart. A bit more body and "scrunch." They're about 65 bucks in PS so maybe 15 bucks more expensive than Press but it's going to last a long time.	{ "pile_set_name": "Pile-CC" }
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Service is obtainable to household consumers only instead of accessible in all parts. †The data shoppers send and get each month will contribute to regular monthly data usage. Speeds and use allowances continue to be subject to vary. Better use will end in extra rates of $10, excluding taxes and fees, For each and every increment of around 50 added Gigabytes utilized. Terms & Conditions Geographic and service restrictions apply to AT&T U-verse® services. Call to see if you qualify. Fiber optics may utilize to all or Element of the community, based upon your locale. ? Residential Services and Rates differ for every site. By getting into your address, we are going to be capable to give you probably the most exact data for your house. Obtaining a Visa® pay as you go card is simple! Store the qualifying provides and observe three basic methods to redeem your card. This completes the era on the service along with the templates. 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Fiber optics could utilize to all or Section of the network, depending on your locale. EarthLink delivers more info you a lot of differing kinds and speeds of broadband Internet service. Fill out this way and we'll demonstrate you what is available at your area. 1Internet velocity promises stand for most community service capability speeds. Actual consumer speeds could fluctuate and so are not confirmed. Precise speeds change based on factors such as web site targeted traffic, articles company server ability, interior community administration things, and machine abilities and the use of other U-verse services. Your Social Safety selection just isn't demanded; nonetheless, we will require to check your credit rating history in an effort to process the purchase, and giving your Social Safety range tends to make this method faster. Other merchandise and firm names stated on the location can be logos of Individuals respective proprietors. 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Maxine writes concerning the highs and the lows of renovating her initially home, performing as an awesome inspiration to All those in the same placement. My intention before I started the training course was to set-up an Interior Design consultancy. For me To do that I actually needed to analyze and obtain experienced.	{ "pile_set_name": "Pile-CC" }
Wilson was great, but he missed a wide open Zach Miller twice in the end zone. Then he goes and over throws him again deep down the middle. If he makes that pass, this game never goes to OT. If he finds him in the end zone, this game never goes to OT. Wilson had a hell of a game, but Tate I think was better, and not just for the last TD catch. Every time that guy gets the ball, it directly correlates to points for us. Wilson was great, but he missed a wide open Zach Miller twice in the end zone. Then he goes and over throws him again deep down the middle. If he makes that pass, this game never goes to OT. If he finds him in the end zone, this game never goes to OT. Wilson had a hell of a game, but Tate I think was better, and not just for the last TD catch. Every time that guy gets the ball, it directly correlates to points for us. What game was I watching ? The one where if Miller catches a TD instead of us kicking a FG, we go up by 7 points instead of 3 at half. Last time I watched, the Bears got a ludicrous play at the end of the game to kick a 45 yard FG, not a TD. They would've needed a TD at the end, not a FG to tie. It's almost like saying the refs screwed us on the Edwards catch, or we would've won without OT. There never would've been that call without him missing Miller twice in the end zone before that. Yes, it's nitpicky, and Wilson made up for it, but I gave me game ball to Tate for his catches and YAC, and also his downfield blocking on many plays. While I'm being picky, Wilson also underthrew Edwards on that bomb. If he would've led him, that was money. But I still love me some Wilson. My game ball goes to Lovie Smith. Instead of kicking a field goal and going up two scores, he elects to go for it on 4th down. By NOT making the first down, the momentum swung to the Seahawks. I believe that the Seahawks took it to heart as disrespect in their ability. From that point on, the Bears offense had the ball for 2 minutes in the final 12 minutes of the first half. Russell was money too, leading the Seahawks on scoring drives of 94 and 49 yards, even more if the touchdown wasn't incorrectly reversed. Thank you Lovie for the disrespect you showed the Seahawks by passing up sure points, it woke the team up. Wilson was great, but he missed a wide open Zach Miller twice in the end zone. Then he goes and over throws him again deep down the middle. If he makes that pass, this game never goes to OT. If he finds him in the end zone, this game never goes to OT. Wilson had a hell of a game, but Tate I think was better, and not just for the last TD catch. Every time that guy gets the ball, it directly correlates to points for us. Wasn't Tate that made the last catch, it was seriously great Rice (blow to the head) to win in OT.Tate made the astonishing catch and run for the TD at the end of regulation time for the Seahawks OffenseBut I would have to give it to RW then Tate, then Rice, it took ALL of them to get the job done,,These guys are all taking control, and not worrying about the Defense making game breaking plays.Our ST's are damn great, so when they ALL get in the groove, these Seahawks will be pretty special. Golden tate is brilliant! One of my favorite players this year. I'm so glad all the chuckleheads that were calling for him to get the boot don't have anything to do with personnel decisions, cuz them guys is dumb.	{ "pile_set_name": "Pile-CC" }
Bryann Aguilar, CP24.com An 80-year-old woman has died in hospital after a three-vehicle collision in Vaughan Thursday afternoon. Emergency crews were called to the area of Weston and Rutherford roads just before 1:30 p.m. for reports of a crash. York Regional police said a blue Maserati and a black Hyundai collided and in the process, struck a third vehicle. York Region paramedics said they transported at least four people to a local hospital. Police said the woman, who is a resident of Vaughan and a passenger in the Tuscan, was pronounced dead in hospital. The driver of the Tuscan, an 83-year-old Vaughan man sustained serious injuries. The driver and passenger in the Maseratie suffered minor injuries. The cause of the collision has not been determined. Rutherford Road was closed between Weston Road and Highway 400 for the investigation but it has since reopened. Anyone with information about the incident is asked to contact police.	{ "pile_set_name": "OpenWebText2" }
Q: Why canvas is not working locally but working on TRYIT I Have build some code related to canvas but code is working on TRYIT but code is not working locally when i have copied all code to file and tried to run it . This is what this code is doing , it takes an image and set the width and height of canvas with respect to that image and draw a filled circle with text in it on that image(canvas). Here is code <head> <meta charset=utf-8 /> <title>Draw a circle</title> </head> <body onload="draw();"> <canvas id="circle"></canvas> </body> <script> var canvas = document.getElementById('circle'), context = canvas.getContext('2d'); function draw() { base_image = new Image(); base_image.src = 'http://sst-system.com/old/Planos/C21E34.JPG'; var canvas = document.getElementById('circle'); if (canvas.getContext) { base_image = new Image(); base_image.src = 'http://sst-system.com/old/Planos/C21E34.JPG'; var ctx = canvas.getContext('2d'); ctx.beginPath(); ctx.canvas.width = base_image.width; ctx.canvas.height = base_image.height; var X = 500; var Y = 229; var R = 6.4; ctx.font = "15px Arial bold"; ctx.beginPath(); ctx.arc(X, Y, R, 0, 2 * Math.PI, false); ctx.lineWidth = 12; ctx.strokeStyle = '#FF0000'; ctx.drawImage(base_image, 0, 0) ctx.stroke(); ctx.fillText("TT", X-9, Y+5); } } </script> There are no errors on console , but it shows these warnings in console : A: As @DBS mentioned, it was a speed thing. You weren't waiting for the image to load before working with it. The fix is to attach a listener to the load event of the image, either using image.addEventListener('load', () => { or the deprecated-but-still-works style of image.onload = () => {, which I have used below. The reason that it works in the TryIt example is that the image is cached by the browser from the second load onwards, so it is available immediately and you don't need to wait for it to load. I suspect that when you run it locally, if you have Devtools open, the cache is disabled due to an option in Devtools settings called "Disable cache (while DevTools is open)". So it will never be pulled from the cache, and thus never work. The following code works: <html> <head> <meta charset=utf-8 /> <title>Draw a circle</title> </head> <body onload="draw();"> <canvas id="circle"></canvas> </body> <script> var canvas = document.getElementById('circle'), context = canvas.getContext('2d'); function draw() { base_image = new Image(); base_image.src = 'http://sst-system.com/old/Planos/C21E34.JPG'; var canvas = document.getElementById('circle'); if (canvas.getContext) { base_image = new Image(); base_image.src = 'http://sst-system.com/old/Planos/C21E34.JPG'; // The key change: put the rest of the code inside the onload callback // to wait for the image to load before using it. base_image.onload = function() { var ctx = canvas.getContext('2d'); ctx.beginPath(); ctx.canvas.width = base_image.width; ctx.canvas.height = base_image.height; var X = 500; var Y = 229; var R = 6.4; ctx.font = "15px Arial bold"; ctx.beginPath(); ctx.arc(X, Y, R, 0, 2 * Math.PI, false); ctx.lineWidth = 12; ctx.strokeStyle = '#FF0000'; ctx.drawImage(base_image, 0, 0) ctx.stroke(); ctx.fillText("TT", X - 9, Y + 5); }; } } </script> </html>	{ "pile_set_name": "StackExchange" }
Club Crusoe ready to stun Cane Farm Iraq Thomas Former UWI T20 champions Club Crusoe will be counting on an experienced team to get past a weakened Cane Farm in the opening match of the 2018 edition which bowls off at 6.30pm tomorrow at the Sir Frank Worrel Grounds, UWI, St Augustine. This year’s tournament will be played in a knockout format from the opening day. Eight teams will feature this year with the first round of matches being virtual quarterfinals. Cane Farm won the tournament last year with an all-star line-up. Some of the national players that featured for Cane Farm in 2017 were Ravi Rampaul, Lendl Simmons, Denesh Ramdin, Imran Khan, Ewart Nicholson, Rayad Emrit and Evin Lewis. However, the Regional Four-Day tournament is currently taking place and a number of Cane Farm’s stars will not be competing in the UWI T20 tournament this year. Club Crusoe opening batsman Jason Persaud said the Tobago team may be in with a great chance to eliminate Cane Farm. “Last year they had a number of national players who would be occupied this year with the regional four-day (competition) playing for Trinidad and Tobago like Imran Khan, Ewart Nicholson, Denesh Ramdin – all these fellas played for them last year and they won’t be able to play this year.” Persaud said Club Crusoe, who won the 2015 UWI T20 tournament, have enough quality in their team to defeat Cane Farm and go all the way to the $35,000 first prize. “We have a couple of former national players in Nicholas Sookdeosingh; Atiba Allert, who is a former national fast bowler; we have Caldrac captain who is Tobago boy Ancil Nedd; we have this youngster from Tobago who just went to national trials, Iraq Thomas.” Persaud said Leron Lezama and Marcus Daniel are also part of the team this year. “The experience that we have, and most of these players would have played in the tournament before, so everybody is affiliated with the tournament. All of the guys that play in this Club Crusoe unit would have played some high division of cricket in Trinidad.”	{ "pile_set_name": "Pile-CC" }
Veranstaltungen des DIW Berlin/Events of DIW Berlin Britain is one of the most important partners of Germany in Europe, yet the upcoming referendum might force the UK out of the EU. Together with invited guests, we want to explore the historical and political aspects of the British-European relationship and discuss the future of Britain and Germany in the EU.	{ "pile_set_name": "Pile-CC" }

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