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PMC1868949_F1_10936.jpg | What is the main focus of this visual representation? | Phenotype of conditional Sp8 mutants. (a, b) WMISH of Sp8 in E8.5 and E9.5 embryos. Sp8 is strongly expressed in the anterior neural ridge and in the forebrain neuroepithelium at E8.5 (a). At E9.5, Sp8 expression covers the putative forebrain vesicle (b). (c) Foxg1-Cre activity, visualized by X-Gal staining, is evident throughout the telencephalon at E10.5. (d) Cre recombination ablates Sp8 expression in the telencephalon and olfactory placode of cKO at E10.5. (e, f") Histological (nissl stained) coronal sections at E18.5. (e', f') Mutant brains miss the septum and reveal a reduced size of the telencephalon. (e', e") Callosal fibers do not cross the midline and form probst bundles unilaterally. (g, g') On (nissl stained) sagittal sections, a strongly reduced cortical diameter is characteristic for cKO at E18.5. With 15% penetrance, cKO brains show an enhanced phenotype, highlighted by the complete absence of midline derivates. These mutants were termed 'cKO no midline' (e", f"). cKO and 'cKO no midline' only differ at rostral levels of the forebrain. In 'cKO no midline' specimens, a delamination of the cortex from the basal telencephalon is apparent medially, as a visible hole (asterisk in e"). Caudally in the brain, the difference between low and high penetrance of the phenotypes is not significant (f', f"). AC, anterior commissure; ANR, anterior neural ridge; CC, corpus callosum; CP, cortical plate; CTX, cortex; DI, diencephalon; FB, forebrain; HC, hippocampus; IZ, intermediate zone; LGE, lateral ganglionic eminence; MB, midbrain; MZ, marginal zone; OP, olfactory placode; PB, probst bundles; POA, preoptic area; SE, septum; SP, subplate; SVZ, subventricular zone; TH, thalamus; VZ, ventricular zone. |
PMC1868949_F1_10940.jpg | What does this image primarily show? | Phenotype of conditional Sp8 mutants. (a, b) WMISH of Sp8 in E8.5 and E9.5 embryos. Sp8 is strongly expressed in the anterior neural ridge and in the forebrain neuroepithelium at E8.5 (a). At E9.5, Sp8 expression covers the putative forebrain vesicle (b). (c) Foxg1-Cre activity, visualized by X-Gal staining, is evident throughout the telencephalon at E10.5. (d) Cre recombination ablates Sp8 expression in the telencephalon and olfactory placode of cKO at E10.5. (e, f") Histological (nissl stained) coronal sections at E18.5. (e', f') Mutant brains miss the septum and reveal a reduced size of the telencephalon. (e', e") Callosal fibers do not cross the midline and form probst bundles unilaterally. (g, g') On (nissl stained) sagittal sections, a strongly reduced cortical diameter is characteristic for cKO at E18.5. With 15% penetrance, cKO brains show an enhanced phenotype, highlighted by the complete absence of midline derivates. These mutants were termed 'cKO no midline' (e", f"). cKO and 'cKO no midline' only differ at rostral levels of the forebrain. In 'cKO no midline' specimens, a delamination of the cortex from the basal telencephalon is apparent medially, as a visible hole (asterisk in e"). Caudally in the brain, the difference between low and high penetrance of the phenotypes is not significant (f', f"). AC, anterior commissure; ANR, anterior neural ridge; CC, corpus callosum; CP, cortical plate; CTX, cortex; DI, diencephalon; FB, forebrain; HC, hippocampus; IZ, intermediate zone; LGE, lateral ganglionic eminence; MB, midbrain; MZ, marginal zone; OP, olfactory placode; PB, probst bundles; POA, preoptic area; SE, septum; SP, subplate; SVZ, subventricular zone; TH, thalamus; VZ, ventricular zone. |
PMC1868954_ppat-0030072-g006_10948.jpg | What is the principal component of this image? | Epitope Mapping of JS1 and JS2 Binding SitesShows the location in the three-dimensional model of P. falciparum MSP119 of residues in the first epidermal growth factor domain, which on mutation affect binding by JS1 or JS2. Mutation of Cys28 shown in red completely ablated binding of both mAbs (12.10 and 12.8) and JS1 or JS2. Mutation of the partnering Cys12, also shown in red, while ablating binding by the murine mAbs, had no effect on the binding by JS1 or JS2. Arg20 and Asn33 in salmon had intermediate effects on binding as determined by SPR analysis when mutated to more neutral or negatively charged side-chains (see Table 1). Three further substitutions at Lys40, Lys29, and Asn39 seen in brown had minor effects on binding when the interaction was studied by ELISA. The model of P. falciparum MSP119 was generated by PyMol using atomic coordinates available from NCBI under accession number PDB: 1CEJ. |
PMC1868954_ppat-0030072-g006_10947.jpg | What is the principal component of this image? | Epitope Mapping of JS1 and JS2 Binding SitesShows the location in the three-dimensional model of P. falciparum MSP119 of residues in the first epidermal growth factor domain, which on mutation affect binding by JS1 or JS2. Mutation of Cys28 shown in red completely ablated binding of both mAbs (12.10 and 12.8) and JS1 or JS2. Mutation of the partnering Cys12, also shown in red, while ablating binding by the murine mAbs, had no effect on the binding by JS1 or JS2. Arg20 and Asn33 in salmon had intermediate effects on binding as determined by SPR analysis when mutated to more neutral or negatively charged side-chains (see Table 1). Three further substitutions at Lys40, Lys29, and Asn39 seen in brown had minor effects on binding when the interaction was studied by ELISA. The model of P. falciparum MSP119 was generated by PyMol using atomic coordinates available from NCBI under accession number PDB: 1CEJ. |
PMC1871568_F1_10950.jpg | What object or scene is depicted here? | (Papanicolaou stain, × 200): Type AB thymoma. FNA smear shows elongate neoplastic epithelial cells with oval or spindle pale nuclei and inconspicuous nucleoli. |
PMC1871568_F1_10949.jpg | Describe the main subject of this image. | (Papanicolaou stain, × 200): Type AB thymoma. FNA smear shows elongate neoplastic epithelial cells with oval or spindle pale nuclei and inconspicuous nucleoli. |
PMC1871568_F2_10951.jpg | What is shown in this image? | (Papanicolaou stain, × 600): Type AB thymoma. FNA smear shows neoplastic epithelial cells with dispersed chromatin and small nucleoli, and background lymphocytes. |
PMC1871599_F3_10952.jpg | What is the principal component of this image? | Microscopic appearance of the duodenal GIST demonstrating epithelioid and spindle cells (H&E; magnification, ×10). |
PMC1871599_F4_10953.jpg | What is the dominant medical problem in this image? | GIST cells stained positive for CD117(c-KIT) (magnification, × 20). |
PMC1871612_pone-0000488-g003_10956.jpg | What is the core subject represented in this visual? | CWP release from ESVs is Bax specific.A) ESVs in encysting Bax-expressing cells treated with the membrane-permeable Bax-inhibiting peptide Ku70 are at least partially protected. Note the co-localization of Bax (green) with (partially intact) ESVs and significantly less cytoplasmic or nucleoplasmic CWP signal than in untreated cells (compare with FIG. 2C).16-May B) Deletion of the Bax C-terminus uncouples Bax targeting to ESV membranes and CWP release. BaxΔ22 lacks the C-terminal 22 amino acids of Bax and localizes to membranes of intact ESV. C, D) Electron micrographs of representative cells expressing Bax or BaxΔ22 at four hours post induction. C) Encysting trophozoite from the population expressing BaxΔ22 showing numerous ESVs with electron dense material (arrowheads). ESV and general compartment morphology are indistinguishable from wild type cells (not shown). Enlarged region shows an individual ESV. Peripheral vesicles underlying the plasma membrane are clearly visible. D) ESVs or organelle remnants are not present in surviving cell expressing Bax. Nuclei, and parts of the microtubule structures of the anterior flagella and significantly enlarged PVs are visible. N, nuclei. Scale bars: 2 µm. |
PMC1871612_pone-0000488-g003_10955.jpg | What stands out most in this visual? | CWP release from ESVs is Bax specific.A) ESVs in encysting Bax-expressing cells treated with the membrane-permeable Bax-inhibiting peptide Ku70 are at least partially protected. Note the co-localization of Bax (green) with (partially intact) ESVs and significantly less cytoplasmic or nucleoplasmic CWP signal than in untreated cells (compare with FIG. 2C).16-May B) Deletion of the Bax C-terminus uncouples Bax targeting to ESV membranes and CWP release. BaxΔ22 lacks the C-terminal 22 amino acids of Bax and localizes to membranes of intact ESV. C, D) Electron micrographs of representative cells expressing Bax or BaxΔ22 at four hours post induction. C) Encysting trophozoite from the population expressing BaxΔ22 showing numerous ESVs with electron dense material (arrowheads). ESV and general compartment morphology are indistinguishable from wild type cells (not shown). Enlarged region shows an individual ESV. Peripheral vesicles underlying the plasma membrane are clearly visible. D) ESVs or organelle remnants are not present in surviving cell expressing Bax. Nuclei, and parts of the microtubule structures of the anterior flagella and significantly enlarged PVs are visible. N, nuclei. Scale bars: 2 µm. |
PMC1871612_pone-0000488-g003_10954.jpg | What is the core subject represented in this visual? | CWP release from ESVs is Bax specific.A) ESVs in encysting Bax-expressing cells treated with the membrane-permeable Bax-inhibiting peptide Ku70 are at least partially protected. Note the co-localization of Bax (green) with (partially intact) ESVs and significantly less cytoplasmic or nucleoplasmic CWP signal than in untreated cells (compare with FIG. 2C).16-May B) Deletion of the Bax C-terminus uncouples Bax targeting to ESV membranes and CWP release. BaxΔ22 lacks the C-terminal 22 amino acids of Bax and localizes to membranes of intact ESV. C, D) Electron micrographs of representative cells expressing Bax or BaxΔ22 at four hours post induction. C) Encysting trophozoite from the population expressing BaxΔ22 showing numerous ESVs with electron dense material (arrowheads). ESV and general compartment morphology are indistinguishable from wild type cells (not shown). Enlarged region shows an individual ESV. Peripheral vesicles underlying the plasma membrane are clearly visible. D) ESVs or organelle remnants are not present in surviving cell expressing Bax. Nuclei, and parts of the microtubule structures of the anterior flagella and significantly enlarged PVs are visible. N, nuclei. Scale bars: 2 µm. |
PMC1871612_pone-0000488-g003_10958.jpg | What is the core subject represented in this visual? | CWP release from ESVs is Bax specific.A) ESVs in encysting Bax-expressing cells treated with the membrane-permeable Bax-inhibiting peptide Ku70 are at least partially protected. Note the co-localization of Bax (green) with (partially intact) ESVs and significantly less cytoplasmic or nucleoplasmic CWP signal than in untreated cells (compare with FIG. 2C).16-May B) Deletion of the Bax C-terminus uncouples Bax targeting to ESV membranes and CWP release. BaxΔ22 lacks the C-terminal 22 amino acids of Bax and localizes to membranes of intact ESV. C, D) Electron micrographs of representative cells expressing Bax or BaxΔ22 at four hours post induction. C) Encysting trophozoite from the population expressing BaxΔ22 showing numerous ESVs with electron dense material (arrowheads). ESV and general compartment morphology are indistinguishable from wild type cells (not shown). Enlarged region shows an individual ESV. Peripheral vesicles underlying the plasma membrane are clearly visible. D) ESVs or organelle remnants are not present in surviving cell expressing Bax. Nuclei, and parts of the microtubule structures of the anterior flagella and significantly enlarged PVs are visible. N, nuclei. Scale bars: 2 µm. |
PMC1872018_F1_10962.jpg | What is the central feature of this picture? | Histological section of mammary tissue of rats, showing normal cellular architecture (Normal Control, group A). Magnification, H & E × 40. |
PMC1872018_F2_10964.jpg | What can you see in this picture? | Histological section of mammary tissue of rats, showing marked proliferation of ductal epithelial lining with hyperchromatic enlarged nuclei (DMBA Control, group B) (marked with arrows). Magnification, H & E × 40. |
PMC1872018_F3_10963.jpg | What can you see in this picture? | Histological section of mammary tissue of rats, showing almost normal cellular architecture with no signs of proliferation (DMBA + Maxepa Treatment, group C). Magnification, H & E × 40. |
PMC1872018_F6_10965.jpg | What is the focal point of this photograph? | Representative immunohistochemistry photomicrograph of BrdU-labeling of rat mammary tissue [DMBA Control (group B)]. Arrows (→) indicate BrdU-labelled brown-stained cells. Magnification, × 40. |
PMC1872018_F7_10966.jpg | What is shown in this image? | Representative immunohistochemistry photomicrograph of BrdU-labeling of rat mammary tissue [DMBA + Maxepa-treated group (group C)]. Arrows (→) indicate BrdU-labelled brown-stained cells. Magnification, × 40. |
PMC1872018_F9_10968.jpg | What is being portrayed in this visual content? | Immunolocalization of p53 in the mammary tissue of rats [DMBA + Maxepa-treated group (group C)] with anti-sheep p53 antibody (1:200) and AEC. Arrows (→) indicate p53 immuno-positive cells in mammary tissue of rats. Magnification, × 40. |
PMC1872031_F6_10974.jpg | What is the main focus of this visual representation? | 1. Giant cell tumor like picture of giant cell reparative granuloma [MGG; ×400]. 2. Giant cell reparative granuloma: histological picture showing giant cells lying in loose stroma. [H&E ×200]. 3. CT scan of giant cell reparative granuloma showing a mass in right maxillary sinus with extension into the adjacent areas. |
PMC1872031_F6_10975.jpg | What is the principal component of this image? | 1. Giant cell tumor like picture of giant cell reparative granuloma [MGG; ×400]. 2. Giant cell reparative granuloma: histological picture showing giant cells lying in loose stroma. [H&E ×200]. 3. CT scan of giant cell reparative granuloma showing a mass in right maxillary sinus with extension into the adjacent areas. |
PMC1872031_F8_10970.jpg | What is the core subject represented in this visual? | 1. Photograph of a patient showing swelling over left shoulder: later diagnosed as Hemangiopericytoma. 2. X-ray showing lesion involving the left clavicle. 3. Smear showing malignant round cells radiating from vessels. [MGG ×400]. 4. Histological section of the same case showing monomorphic round cells radiating from cells [H&E × 200]. |
PMC1872035_pbio-0050144-g001_10976.jpg | What is the main focus of this visual representation? | Electron Micrographs of H. neapolitanus Carboxysomes(A) A thin-section electron micrograph of H. neapolitanus cells with carboxysomes inside. In one of the cells shown, arrows highlight the visible carboxysomes.(B) A negatively stained image of intact carboxysomes isolated from H. neapolitanus. The features visualized arise from the distribution of stain around proteins forming the shell as well as around the RuBisCO molecules that fill the carboxysome interior. Scale bars indicate 100 nm. |
PMC1872035_pbio-0050144-g001_10977.jpg | What stands out most in this visual? | Electron Micrographs of H. neapolitanus Carboxysomes(A) A thin-section electron micrograph of H. neapolitanus cells with carboxysomes inside. In one of the cells shown, arrows highlight the visible carboxysomes.(B) A negatively stained image of intact carboxysomes isolated from H. neapolitanus. The features visualized arise from the distribution of stain around proteins forming the shell as well as around the RuBisCO molecules that fill the carboxysome interior. Scale bars indicate 100 nm. |
PMC1876224_F3_10980.jpg | What object or scene is depicted here? | Drosophila growth cones and the (potential) factors regulating their cytoskeletal dynamics. (a) Growth cones of aCC (arrows) and RP2 motorneurons (double chevrons; cell bodies named) in two consecutive segments of the trunk of a Drosophila embryo, stained with a cell-specifically expressed membrane marker. (b,b') Cultured Drosophila growth cone stained for microtubules (green) and filamentous actin (magenta); some filopodia lack microtubules (curved arrows), whereas others are deeply invaded (arrow heads indicate microtubule tips). (c) Schematic representation of the cytoskeletal organisation in Drosophila growth cones as extrapolated from work on growth cones in other species (detailed in the section 'Principal structure and function of growth cones'): veil-like lamellipodia (black arrowhead) contain mesh-like networks of actin filaments (randomly oriented red lines), whereas pointed filopodia (white arrowhead) contain bundled actin filaments (parallel red lines); microtubules (blue lines) are bundled in the axon, but single splayed microtubules extend into the periphery of the growth cone (curved white arrows indicate splayed microtubule tips), reaching into filopodia, as was similarly reported for growth cones of other species or migrating cells [63,330]. (d) Details of the boxed area in (c); circled numbers correlate with the numbers in Table 1 and represent the following molecular activities: 1, actin filament nucleation by Arp2/3 (which subsequently stays with the pointed ends); 2, actin filament nucleation and elongation by formins (which stay with barbed ends); 3, actin monomer binding; 4, barbed-end capping; 5, pointed end-depolymerisation/severing; 6, actin filament bundling; 7, retrograde flow of actin cytoskeleton; 8, microtubule plus end binding; 9, microtubule stabilising; 10, actin-microtubule linkage. Black straight arrows indicate growth of actin filaments or microtubules, grey straight arrows shrinkage, black curved arrows addition of actin monomers, grey curved arrows removal of actin monomers or filamentous fragments, hatched arrows indicate direction of retrograde actin flow, and the grey dashed curved double arrow linkage of actin and microtubules. (e) Current view of the effectors downstream of the Slit receptor Robo mediating repulsion from the midline of the ventral nerve cord. Robo (top right) habours five immunoglobulin domains (half elipses) and three fibronectin type III domains (blue boxes) extracellularly, and four conserved cytoplasmic (CC) domains (light to dark green) intracellularly. Robo induces growth cone repulsion by controlling cytoskeletal dynamics via either Abelson kinase (Abl) and Enabled (Ena), or Rac activity. Ena binds at CC2 and acts most likely through Chickadee/Profilin on actin dynamics. Abl binding to Robo at CC3 influences actin dynamics via Capulet and microtubule dynamics via the +TIP protein Chromosome Bows (Chb/Orbit/MAST). Simultaneously, Abl phosphorylates CC1 to antagonise Robo function. The regulation of Rac activity through Robo occurs through CC2/3 recruitment of the SH3-SH2 adaptor molecule Dreadlocks (Dock) which, in turn, activates Rac through both Pak and the GEF Sos. In parallel, active Robo can influence Rac activity via the binding of RhoGAP93B (vilse/CrGAP) to CC2, but it remains unclear whether RhoGAP93B is positively or negatively regulated by Robo. Paradoxically, both decrease and increase of Rac activation levels can cause midline crossing, suggesting that: Rac might influence other effectors to cause repulsion; a precise Rac activation level is required to mediate Slit-induced repulsion; or a sequential modification of Rac in response to Robo activation has to occur, such as an initial role to prevent extension towards the source of the repellent and another role to encourage extension away from the Slit source. Calmodulin and GEF64C have additionally been identified as modifiers of Robo activity, although it is not clear yet how they influence Robo signalling (calmodulin possibly through Chic). |
PMC1876224_F3_10981.jpg | What is the central feature of this picture? | Drosophila growth cones and the (potential) factors regulating their cytoskeletal dynamics. (a) Growth cones of aCC (arrows) and RP2 motorneurons (double chevrons; cell bodies named) in two consecutive segments of the trunk of a Drosophila embryo, stained with a cell-specifically expressed membrane marker. (b,b') Cultured Drosophila growth cone stained for microtubules (green) and filamentous actin (magenta); some filopodia lack microtubules (curved arrows), whereas others are deeply invaded (arrow heads indicate microtubule tips). (c) Schematic representation of the cytoskeletal organisation in Drosophila growth cones as extrapolated from work on growth cones in other species (detailed in the section 'Principal structure and function of growth cones'): veil-like lamellipodia (black arrowhead) contain mesh-like networks of actin filaments (randomly oriented red lines), whereas pointed filopodia (white arrowhead) contain bundled actin filaments (parallel red lines); microtubules (blue lines) are bundled in the axon, but single splayed microtubules extend into the periphery of the growth cone (curved white arrows indicate splayed microtubule tips), reaching into filopodia, as was similarly reported for growth cones of other species or migrating cells [63,330]. (d) Details of the boxed area in (c); circled numbers correlate with the numbers in Table 1 and represent the following molecular activities: 1, actin filament nucleation by Arp2/3 (which subsequently stays with the pointed ends); 2, actin filament nucleation and elongation by formins (which stay with barbed ends); 3, actin monomer binding; 4, barbed-end capping; 5, pointed end-depolymerisation/severing; 6, actin filament bundling; 7, retrograde flow of actin cytoskeleton; 8, microtubule plus end binding; 9, microtubule stabilising; 10, actin-microtubule linkage. Black straight arrows indicate growth of actin filaments or microtubules, grey straight arrows shrinkage, black curved arrows addition of actin monomers, grey curved arrows removal of actin monomers or filamentous fragments, hatched arrows indicate direction of retrograde actin flow, and the grey dashed curved double arrow linkage of actin and microtubules. (e) Current view of the effectors downstream of the Slit receptor Robo mediating repulsion from the midline of the ventral nerve cord. Robo (top right) habours five immunoglobulin domains (half elipses) and three fibronectin type III domains (blue boxes) extracellularly, and four conserved cytoplasmic (CC) domains (light to dark green) intracellularly. Robo induces growth cone repulsion by controlling cytoskeletal dynamics via either Abelson kinase (Abl) and Enabled (Ena), or Rac activity. Ena binds at CC2 and acts most likely through Chickadee/Profilin on actin dynamics. Abl binding to Robo at CC3 influences actin dynamics via Capulet and microtubule dynamics via the +TIP protein Chromosome Bows (Chb/Orbit/MAST). Simultaneously, Abl phosphorylates CC1 to antagonise Robo function. The regulation of Rac activity through Robo occurs through CC2/3 recruitment of the SH3-SH2 adaptor molecule Dreadlocks (Dock) which, in turn, activates Rac through both Pak and the GEF Sos. In parallel, active Robo can influence Rac activity via the binding of RhoGAP93B (vilse/CrGAP) to CC2, but it remains unclear whether RhoGAP93B is positively or negatively regulated by Robo. Paradoxically, both decrease and increase of Rac activation levels can cause midline crossing, suggesting that: Rac might influence other effectors to cause repulsion; a precise Rac activation level is required to mediate Slit-induced repulsion; or a sequential modification of Rac in response to Robo activation has to occur, such as an initial role to prevent extension towards the source of the repellent and another role to encourage extension away from the Slit source. Calmodulin and GEF64C have additionally been identified as modifiers of Robo activity, although it is not clear yet how they influence Robo signalling (calmodulin possibly through Chic). |
PMC1876234_F3_10986.jpg | What is being portrayed in this visual content? | The histopathological examination of the resected recurrent colostomy site specimen showing well-differentiated adenocarcinoma (40×). |
PMC1876237_F1_10991.jpg | What can you see in this picture? | In situ hybridization analysis of muskelin transcripts in the developing mouse embryo. (A) Schematic representation of muskelin. Individual protein domains are indicated. L: LisH domain; H: LisH homology domain (also known as CTLH for: C-terminal to LisH domain). The probes used for in situ hybridization are indicated with black bars. (B) Micrographs of X-ray films showing whole embryo sagittal sections from embryonic stages E12.5, E14.5 and E16.5. Data obtained with probe 1 are shown in representation for similar results with probes 2–4. The sense control displays a parallel experiment using sense RNAs as probe. (C) E12.5 coronal section through a posterior region at the midbrain level using probe 5 (a). High expression levels of muskelin mRNA were observed in the subventricular zone of the cortex, and the amygdala as well as in the neuroepithelium of the thalamus and hypothalamus. High magnification of a coronal section through the eye (b) at E12.5 showing the presence of muskelin transcripts in the lens vesicle, the neural retina and the retinal pigmented epithelium. Weak signal was detected in the optic nerve. (c) Coronal section through the spinal cord, showing muskelin mRNA expression in the ependymal and ventral mantle layers and in the DRG. Key: A, amygdala; ChP, choroid plexus; Cx, cortex; DRG, dorsal root ganglia; HTh, hypothalamus; LVS, lens vesicle; MB, midbrain; MO, medulla oblongata; NR, neural retina; ON, optic nerve; Ps, pons; RPE, retinal pigmented epithelium; SC, spinal cord; Th, thalamus. Scale bars: (B) 1 mm each, (C) (a) 1 mm, (b) and (c) 500 nm. |
PMC1876237_F1_10987.jpg | What is the core subject represented in this visual? | In situ hybridization analysis of muskelin transcripts in the developing mouse embryo. (A) Schematic representation of muskelin. Individual protein domains are indicated. L: LisH domain; H: LisH homology domain (also known as CTLH for: C-terminal to LisH domain). The probes used for in situ hybridization are indicated with black bars. (B) Micrographs of X-ray films showing whole embryo sagittal sections from embryonic stages E12.5, E14.5 and E16.5. Data obtained with probe 1 are shown in representation for similar results with probes 2–4. The sense control displays a parallel experiment using sense RNAs as probe. (C) E12.5 coronal section through a posterior region at the midbrain level using probe 5 (a). High expression levels of muskelin mRNA were observed in the subventricular zone of the cortex, and the amygdala as well as in the neuroepithelium of the thalamus and hypothalamus. High magnification of a coronal section through the eye (b) at E12.5 showing the presence of muskelin transcripts in the lens vesicle, the neural retina and the retinal pigmented epithelium. Weak signal was detected in the optic nerve. (c) Coronal section through the spinal cord, showing muskelin mRNA expression in the ependymal and ventral mantle layers and in the DRG. Key: A, amygdala; ChP, choroid plexus; Cx, cortex; DRG, dorsal root ganglia; HTh, hypothalamus; LVS, lens vesicle; MB, midbrain; MO, medulla oblongata; NR, neural retina; ON, optic nerve; Ps, pons; RPE, retinal pigmented epithelium; SC, spinal cord; Th, thalamus. Scale bars: (B) 1 mm each, (C) (a) 1 mm, (b) and (c) 500 nm. |
PMC1876237_F1_10993.jpg | What's the most prominent thing you notice in this picture? | In situ hybridization analysis of muskelin transcripts in the developing mouse embryo. (A) Schematic representation of muskelin. Individual protein domains are indicated. L: LisH domain; H: LisH homology domain (also known as CTLH for: C-terminal to LisH domain). The probes used for in situ hybridization are indicated with black bars. (B) Micrographs of X-ray films showing whole embryo sagittal sections from embryonic stages E12.5, E14.5 and E16.5. Data obtained with probe 1 are shown in representation for similar results with probes 2–4. The sense control displays a parallel experiment using sense RNAs as probe. (C) E12.5 coronal section through a posterior region at the midbrain level using probe 5 (a). High expression levels of muskelin mRNA were observed in the subventricular zone of the cortex, and the amygdala as well as in the neuroepithelium of the thalamus and hypothalamus. High magnification of a coronal section through the eye (b) at E12.5 showing the presence of muskelin transcripts in the lens vesicle, the neural retina and the retinal pigmented epithelium. Weak signal was detected in the optic nerve. (c) Coronal section through the spinal cord, showing muskelin mRNA expression in the ependymal and ventral mantle layers and in the DRG. Key: A, amygdala; ChP, choroid plexus; Cx, cortex; DRG, dorsal root ganglia; HTh, hypothalamus; LVS, lens vesicle; MB, midbrain; MO, medulla oblongata; NR, neural retina; ON, optic nerve; Ps, pons; RPE, retinal pigmented epithelium; SC, spinal cord; Th, thalamus. Scale bars: (B) 1 mm each, (C) (a) 1 mm, (b) and (c) 500 nm. |
PMC1876237_F1_10990.jpg | What's the most prominent thing you notice in this picture? | In situ hybridization analysis of muskelin transcripts in the developing mouse embryo. (A) Schematic representation of muskelin. Individual protein domains are indicated. L: LisH domain; H: LisH homology domain (also known as CTLH for: C-terminal to LisH domain). The probes used for in situ hybridization are indicated with black bars. (B) Micrographs of X-ray films showing whole embryo sagittal sections from embryonic stages E12.5, E14.5 and E16.5. Data obtained with probe 1 are shown in representation for similar results with probes 2–4. The sense control displays a parallel experiment using sense RNAs as probe. (C) E12.5 coronal section through a posterior region at the midbrain level using probe 5 (a). High expression levels of muskelin mRNA were observed in the subventricular zone of the cortex, and the amygdala as well as in the neuroepithelium of the thalamus and hypothalamus. High magnification of a coronal section through the eye (b) at E12.5 showing the presence of muskelin transcripts in the lens vesicle, the neural retina and the retinal pigmented epithelium. Weak signal was detected in the optic nerve. (c) Coronal section through the spinal cord, showing muskelin mRNA expression in the ependymal and ventral mantle layers and in the DRG. Key: A, amygdala; ChP, choroid plexus; Cx, cortex; DRG, dorsal root ganglia; HTh, hypothalamus; LVS, lens vesicle; MB, midbrain; MO, medulla oblongata; NR, neural retina; ON, optic nerve; Ps, pons; RPE, retinal pigmented epithelium; SC, spinal cord; Th, thalamus. Scale bars: (B) 1 mm each, (C) (a) 1 mm, (b) and (c) 500 nm. |
PMC1876237_F1_10989.jpg | What can you see in this picture? | In situ hybridization analysis of muskelin transcripts in the developing mouse embryo. (A) Schematic representation of muskelin. Individual protein domains are indicated. L: LisH domain; H: LisH homology domain (also known as CTLH for: C-terminal to LisH domain). The probes used for in situ hybridization are indicated with black bars. (B) Micrographs of X-ray films showing whole embryo sagittal sections from embryonic stages E12.5, E14.5 and E16.5. Data obtained with probe 1 are shown in representation for similar results with probes 2–4. The sense control displays a parallel experiment using sense RNAs as probe. (C) E12.5 coronal section through a posterior region at the midbrain level using probe 5 (a). High expression levels of muskelin mRNA were observed in the subventricular zone of the cortex, and the amygdala as well as in the neuroepithelium of the thalamus and hypothalamus. High magnification of a coronal section through the eye (b) at E12.5 showing the presence of muskelin transcripts in the lens vesicle, the neural retina and the retinal pigmented epithelium. Weak signal was detected in the optic nerve. (c) Coronal section through the spinal cord, showing muskelin mRNA expression in the ependymal and ventral mantle layers and in the DRG. Key: A, amygdala; ChP, choroid plexus; Cx, cortex; DRG, dorsal root ganglia; HTh, hypothalamus; LVS, lens vesicle; MB, midbrain; MO, medulla oblongata; NR, neural retina; ON, optic nerve; Ps, pons; RPE, retinal pigmented epithelium; SC, spinal cord; Th, thalamus. Scale bars: (B) 1 mm each, (C) (a) 1 mm, (b) and (c) 500 nm. |
PMC1876237_F1_10992.jpg | What is being portrayed in this visual content? | In situ hybridization analysis of muskelin transcripts in the developing mouse embryo. (A) Schematic representation of muskelin. Individual protein domains are indicated. L: LisH domain; H: LisH homology domain (also known as CTLH for: C-terminal to LisH domain). The probes used for in situ hybridization are indicated with black bars. (B) Micrographs of X-ray films showing whole embryo sagittal sections from embryonic stages E12.5, E14.5 and E16.5. Data obtained with probe 1 are shown in representation for similar results with probes 2–4. The sense control displays a parallel experiment using sense RNAs as probe. (C) E12.5 coronal section through a posterior region at the midbrain level using probe 5 (a). High expression levels of muskelin mRNA were observed in the subventricular zone of the cortex, and the amygdala as well as in the neuroepithelium of the thalamus and hypothalamus. High magnification of a coronal section through the eye (b) at E12.5 showing the presence of muskelin transcripts in the lens vesicle, the neural retina and the retinal pigmented epithelium. Weak signal was detected in the optic nerve. (c) Coronal section through the spinal cord, showing muskelin mRNA expression in the ependymal and ventral mantle layers and in the DRG. Key: A, amygdala; ChP, choroid plexus; Cx, cortex; DRG, dorsal root ganglia; HTh, hypothalamus; LVS, lens vesicle; MB, midbrain; MO, medulla oblongata; NR, neural retina; ON, optic nerve; Ps, pons; RPE, retinal pigmented epithelium; SC, spinal cord; Th, thalamus. Scale bars: (B) 1 mm each, (C) (a) 1 mm, (b) and (c) 500 nm. |
PMC1876244_F6_11000.jpg | What key item or scene is captured in this photo? | Internalization of Au-AbVF and Au alone by primary CLL-B cells after 1 h incubation. 6a) nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6b) higher magnification image of 6a; 6c and 6d) showing the internalized particles in different endocytic compartments. Figure 6e to 6h show the internalization of Au nanoparticles alone by primary CLL-B cells after 1 h incubation. 6e) Nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6f) higher magnification image of 6e; 6f) showing the internalized particles in multivesicular bodies; and 6g) higher magnification image of 6f. |
PMC1876244_F6_11001.jpg | What is being portrayed in this visual content? | Internalization of Au-AbVF and Au alone by primary CLL-B cells after 1 h incubation. 6a) nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6b) higher magnification image of 6a; 6c and 6d) showing the internalized particles in different endocytic compartments. Figure 6e to 6h show the internalization of Au nanoparticles alone by primary CLL-B cells after 1 h incubation. 6e) Nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6f) higher magnification image of 6e; 6f) showing the internalized particles in multivesicular bodies; and 6g) higher magnification image of 6f. |
PMC1876244_F6_11002.jpg | What does this image primarily show? | Internalization of Au-AbVF and Au alone by primary CLL-B cells after 1 h incubation. 6a) nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6b) higher magnification image of 6a; 6c and 6d) showing the internalized particles in different endocytic compartments. Figure 6e to 6h show the internalization of Au nanoparticles alone by primary CLL-B cells after 1 h incubation. 6e) Nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6f) higher magnification image of 6e; 6f) showing the internalized particles in multivesicular bodies; and 6g) higher magnification image of 6f. |
PMC1876244_F6_10998.jpg | What key item or scene is captured in this photo? | Internalization of Au-AbVF and Au alone by primary CLL-B cells after 1 h incubation. 6a) nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6b) higher magnification image of 6a; 6c and 6d) showing the internalized particles in different endocytic compartments. Figure 6e to 6h show the internalization of Au nanoparticles alone by primary CLL-B cells after 1 h incubation. 6e) Nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6f) higher magnification image of 6e; 6f) showing the internalized particles in multivesicular bodies; and 6g) higher magnification image of 6f. |
PMC1876244_F6_10999.jpg | What is the central feature of this picture? | Internalization of Au-AbVF and Au alone by primary CLL-B cells after 1 h incubation. 6a) nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6b) higher magnification image of 6a; 6c and 6d) showing the internalized particles in different endocytic compartments. Figure 6e to 6h show the internalization of Au nanoparticles alone by primary CLL-B cells after 1 h incubation. 6e) Nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6f) higher magnification image of 6e; 6f) showing the internalized particles in multivesicular bodies; and 6g) higher magnification image of 6f. |
PMC1876244_F6_10997.jpg | What is the principal component of this image? | Internalization of Au-AbVF and Au alone by primary CLL-B cells after 1 h incubation. 6a) nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6b) higher magnification image of 6a; 6c and 6d) showing the internalized particles in different endocytic compartments. Figure 6e to 6h show the internalization of Au nanoparticles alone by primary CLL-B cells after 1 h incubation. 6e) Nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6f) higher magnification image of 6e; 6f) showing the internalized particles in multivesicular bodies; and 6g) higher magnification image of 6f. |
PMC1876244_F6_10995.jpg | What stands out most in this visual? | Internalization of Au-AbVF and Au alone by primary CLL-B cells after 1 h incubation. 6a) nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6b) higher magnification image of 6a; 6c and 6d) showing the internalized particles in different endocytic compartments. Figure 6e to 6h show the internalization of Au nanoparticles alone by primary CLL-B cells after 1 h incubation. 6e) Nanoparticles were seen at the cell periphery (within uncoated tubules and vacuoles); 6f) higher magnification image of 6e; 6f) showing the internalized particles in multivesicular bodies; and 6g) higher magnification image of 6f. |
PMC1876258_pone-0000493-g002_11005.jpg | What is shown in this image? | The Golgi shows no asymmetry in distribution during the first cell cycle.(A–C) Even distribution of Golgi structures in a wild-type telophase embryo. The Golgi is visualized using two markers: (A) YFP::ManS, a fusion of YFP and the Golgi resident mannosidase F58H1.1 and (B) anti-CASP/Y54F10AM.4b staining. CASP is an integral Golgi membrane protein [17]. Arrowheads in (A), (B), and (C) (the merged image) show colocalization of puncta with the two markers. Central focal planes are shown. (D) even distribution of Golgi structures in a projection of 12 focal planes of YFP::ManS in a wild-type anaphase stage embryo. |
PMC1876258_pone-0000493-g002_11004.jpg | What is the focal point of this photograph? | The Golgi shows no asymmetry in distribution during the first cell cycle.(A–C) Even distribution of Golgi structures in a wild-type telophase embryo. The Golgi is visualized using two markers: (A) YFP::ManS, a fusion of YFP and the Golgi resident mannosidase F58H1.1 and (B) anti-CASP/Y54F10AM.4b staining. CASP is an integral Golgi membrane protein [17]. Arrowheads in (A), (B), and (C) (the merged image) show colocalization of puncta with the two markers. Central focal planes are shown. (D) even distribution of Golgi structures in a projection of 12 focal planes of YFP::ManS in a wild-type anaphase stage embryo. |
PMC1876258_pone-0000493-g002_11003.jpg | What can you see in this picture? | The Golgi shows no asymmetry in distribution during the first cell cycle.(A–C) Even distribution of Golgi structures in a wild-type telophase embryo. The Golgi is visualized using two markers: (A) YFP::ManS, a fusion of YFP and the Golgi resident mannosidase F58H1.1 and (B) anti-CASP/Y54F10AM.4b staining. CASP is an integral Golgi membrane protein [17]. Arrowheads in (A), (B), and (C) (the merged image) show colocalization of puncta with the two markers. Central focal planes are shown. (D) even distribution of Golgi structures in a projection of 12 focal planes of YFP::ManS in a wild-type anaphase stage embryo. |
PMC1876258_pone-0000493-g002_11006.jpg | What is the main focus of this visual representation? | The Golgi shows no asymmetry in distribution during the first cell cycle.(A–C) Even distribution of Golgi structures in a wild-type telophase embryo. The Golgi is visualized using two markers: (A) YFP::ManS, a fusion of YFP and the Golgi resident mannosidase F58H1.1 and (B) anti-CASP/Y54F10AM.4b staining. CASP is an integral Golgi membrane protein [17]. Arrowheads in (A), (B), and (C) (the merged image) show colocalization of puncta with the two markers. Central focal planes are shown. (D) even distribution of Golgi structures in a projection of 12 focal planes of YFP::ManS in a wild-type anaphase stage embryo. |
PMC1876259_pone-0000496-g001_11012.jpg | What can you see in this picture? | Images showing primary and secondary micro concavities at scanning electron and confocal microscopy.(A) Primary micro concavity (arrow) of the PLGA surface at SEM. Cells can be completely contained within a primary concavity, due to its dimensions. (Calibration Bar = 10 µm); (B) SEM analysis of primary concavity dimensions (Calibration Bar = 10 µm); (C) SEM analysis of secondary concavity dimensions (Calibration Bar = 10 µm); (D) The interaction between the concave surface, showing primary (white arrow) and secondary (red arrows) micro-concavities at the confocal microscope (in green a cell within a concavity). The intimate adherence of a cell to the polymer surface and its nuclear polarity are clearly observable. The image was been obtained superimposing dark field with light field confocal microscopy (Calibration Bar = 10 µm); (E) Confocal image showing primary (outlined in red) and secondary (outlined in blue) micro-concavities and spider-shaped cellular elongations (Calibration Bar = 10 µm); (F) A gingival fibroblast not showing cellular alterations or nuclear polarity at the confocal microscope (Calibration Bar = 10 µm). |
PMC1876259_pone-0000496-g001_11009.jpg | What's the most prominent thing you notice in this picture? | Images showing primary and secondary micro concavities at scanning electron and confocal microscopy.(A) Primary micro concavity (arrow) of the PLGA surface at SEM. Cells can be completely contained within a primary concavity, due to its dimensions. (Calibration Bar = 10 µm); (B) SEM analysis of primary concavity dimensions (Calibration Bar = 10 µm); (C) SEM analysis of secondary concavity dimensions (Calibration Bar = 10 µm); (D) The interaction between the concave surface, showing primary (white arrow) and secondary (red arrows) micro-concavities at the confocal microscope (in green a cell within a concavity). The intimate adherence of a cell to the polymer surface and its nuclear polarity are clearly observable. The image was been obtained superimposing dark field with light field confocal microscopy (Calibration Bar = 10 µm); (E) Confocal image showing primary (outlined in red) and secondary (outlined in blue) micro-concavities and spider-shaped cellular elongations (Calibration Bar = 10 µm); (F) A gingival fibroblast not showing cellular alterations or nuclear polarity at the confocal microscope (Calibration Bar = 10 µm). |
PMC1876259_pone-0000496-g001_11008.jpg | What is the focal point of this photograph? | Images showing primary and secondary micro concavities at scanning electron and confocal microscopy.(A) Primary micro concavity (arrow) of the PLGA surface at SEM. Cells can be completely contained within a primary concavity, due to its dimensions. (Calibration Bar = 10 µm); (B) SEM analysis of primary concavity dimensions (Calibration Bar = 10 µm); (C) SEM analysis of secondary concavity dimensions (Calibration Bar = 10 µm); (D) The interaction between the concave surface, showing primary (white arrow) and secondary (red arrows) micro-concavities at the confocal microscope (in green a cell within a concavity). The intimate adherence of a cell to the polymer surface and its nuclear polarity are clearly observable. The image was been obtained superimposing dark field with light field confocal microscopy (Calibration Bar = 10 µm); (E) Confocal image showing primary (outlined in red) and secondary (outlined in blue) micro-concavities and spider-shaped cellular elongations (Calibration Bar = 10 µm); (F) A gingival fibroblast not showing cellular alterations or nuclear polarity at the confocal microscope (Calibration Bar = 10 µm). |
PMC1876259_pone-0000496-g001_11007.jpg | What is shown in this image? | Images showing primary and secondary micro concavities at scanning electron and confocal microscopy.(A) Primary micro concavity (arrow) of the PLGA surface at SEM. Cells can be completely contained within a primary concavity, due to its dimensions. (Calibration Bar = 10 µm); (B) SEM analysis of primary concavity dimensions (Calibration Bar = 10 µm); (C) SEM analysis of secondary concavity dimensions (Calibration Bar = 10 µm); (D) The interaction between the concave surface, showing primary (white arrow) and secondary (red arrows) micro-concavities at the confocal microscope (in green a cell within a concavity). The intimate adherence of a cell to the polymer surface and its nuclear polarity are clearly observable. The image was been obtained superimposing dark field with light field confocal microscopy (Calibration Bar = 10 µm); (E) Confocal image showing primary (outlined in red) and secondary (outlined in blue) micro-concavities and spider-shaped cellular elongations (Calibration Bar = 10 µm); (F) A gingival fibroblast not showing cellular alterations or nuclear polarity at the confocal microscope (Calibration Bar = 10 µm). |
PMC1876259_pone-0000496-g001_11010.jpg | What does this image primarily show? | Images showing primary and secondary micro concavities at scanning electron and confocal microscopy.(A) Primary micro concavity (arrow) of the PLGA surface at SEM. Cells can be completely contained within a primary concavity, due to its dimensions. (Calibration Bar = 10 µm); (B) SEM analysis of primary concavity dimensions (Calibration Bar = 10 µm); (C) SEM analysis of secondary concavity dimensions (Calibration Bar = 10 µm); (D) The interaction between the concave surface, showing primary (white arrow) and secondary (red arrows) micro-concavities at the confocal microscope (in green a cell within a concavity). The intimate adherence of a cell to the polymer surface and its nuclear polarity are clearly observable. The image was been obtained superimposing dark field with light field confocal microscopy (Calibration Bar = 10 µm); (E) Confocal image showing primary (outlined in red) and secondary (outlined in blue) micro-concavities and spider-shaped cellular elongations (Calibration Bar = 10 µm); (F) A gingival fibroblast not showing cellular alterations or nuclear polarity at the confocal microscope (Calibration Bar = 10 µm). |
PMC1876262_pone-0000498-g001_11015.jpg | What's the most prominent thing you notice in this picture? | Effect of αB crystallin peptides on microtubule assembly.Samples containing tubulin and αB crystallin peptides or control molecules were excited at λ = 355 nm and the fluorescence emission of DAPI bound to assembled microtubules was recorded at λ = 460 nm. The fluorescence of the sample containing tubulin alone increased rapidly to a maximum value at 45 minutes of incubation at 37°C. The ST (N-terminus) and DR (β3) peptides had no effect on total microtubule assembly, the FI (loop) peptide inhibited microtubule assembly, while the LT (β8) and ER (C-terminus) peptides promoted microtubule assembly. The positive control, Paclitaxel, accelerated microtubule assembly, while the negative control, CaCl2, inhibited microtubule assembly which was consistent with previous reports [59], [60]. |
PMC1876459_F1_11016.jpg | Describe the main subject of this image. | Preoperative CT scan showing pelvic mass; Contrast enhanced CT scan showing lobulated mass lesion in pelvis compressing anterior wall of sigmoid colon and located posteriosuperior to the urinary bladder. |
PMC1876502_ppat-0030066-g002_11023.jpg | What is shown in this image? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1876502_ppat-0030066-g002_11021.jpg | What is the focal point of this photograph? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1876502_ppat-0030066-g002_11024.jpg | What is the core subject represented in this visual? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1876502_ppat-0030066-g002_11019.jpg | What is the dominant medical problem in this image? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1876502_ppat-0030066-g002_11025.jpg | What is the principal component of this image? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1876502_ppat-0030066-g002_11020.jpg | What is the main focus of this visual representation? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1876502_ppat-0030066-g002_11028.jpg | What can you see in this picture? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1876502_ppat-0030066-g002_11022.jpg | What object or scene is depicted here? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1876502_ppat-0030066-g002_11018.jpg | Can you identify the primary element in this image? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1876502_ppat-0030066-g002_11027.jpg | What is being portrayed in this visual content? | Location of PrPSc within the Skin of Hamsters Orally Infected with Scrapie(A–H) Topographical localisation of PrPSc in sections of skin samples from the snout (A and B) and the forelimb (G and H); (A and G) PET blots, (B and H) H&E staining. PrPSc was detected in free nerve endings of the subepidermal plexus on the border of the epidermis to the dermis ([A], [B], [G], and [H], arrows), in fibres of the subepidermal, the deep cutaneous and the subcutaneous plexus, in circular and longitudinal fibres of the follicular neural network of the hair ([A], [B], and [G], arrowheads), in the hair follicle isthmus ([G]; rhombus), and in small intradermal striated fibres of mimic muscles ([A and B], asterisks).(C–F) Visualisation of PrPSc and nerve fibres in the neural network of hair follicles by fluorescence microscopy (skin sample from the abdomen). Co-localisation of PrPSc (C) with nerve fibres labelled by using an anti–S-100 protein antibody against Schwann cells (D). (E) Merged figure from micrographs (C and D). (F) Adjacent section to (C), stained with H&E.(I–K) Visualisation of PrPSc and nerve fibres in the cutaneous plexus by fluorescence microscopy (skin sample form the snout). Co-localisation of PrPSc (I) with nerve fibres labelled by using the anti-neurofilament antibody SMI 31 (J). (K) Merged figure from micrographs (I and J).(L) Adjacent section to (I), stained with H&E. The box indicates the region used for the immunofluorescence stainings in (I–K).(M and N) Control skin samples from the forelimb of a hamster perorally mock-challenged with normal hamster brain homogenate; PET blot (M) and fluorescence microscopy for PrP and neurofilament (N).Scale bars = 200 μm for (B, F, H, and M), 50 μm for (K and L), and 25μm for (N). Same scale bars as displayed in (B), (F), (H), and (K) apply to (A), (C–E), (G), and (I and J), respectively. |
PMC1877082_F1_11044.jpg | Describe the main subject of this image. | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11043.jpg | What's the most prominent thing you notice in this picture? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11054.jpg | What is the focal point of this photograph? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11046.jpg | What does this image primarily show? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11045.jpg | What key item or scene is captured in this photo? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11052.jpg | What is the central feature of this picture? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11051.jpg | What is the main focus of this visual representation? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11049.jpg | What is being portrayed in this visual content? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11053.jpg | What is shown in this image? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11050.jpg | What is being portrayed in this visual content? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F1_11047.jpg | What object or scene is depicted here? | Rybp localization during prenatal mouse ocular development. (A-H) Sagittal sections were immunostained for Rybp (brown) and counterstained lightly with hematoxylin (purple) at E10.5 (A), E11.5 (B) and E16.5 (C-H). Higher-magnification of areas stained with the Rybp antibody indicated in (C) are shown in panels D-G. (I-L) Panels show the gradual increase of Rybp expression in the developing neural retina at E10.5 (I), E11.5 (J), E13.5 (K) and E18.5 (L). C; cornea, E; embryonic, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, NR; neuroretina, ON; optic nerve, PM; periocular mesenchyme, SE; surface ectoderm, OC; optic cup. Magnifications: A (×460); B(×320); C(×250); D(×800); E-H(×400); I(×630); J(×460), K(×320); L(×250). |
PMC1877082_F2_11029.jpg | What is shown in this image? | Rybp localization in the postnatal mouse eye. Sagittal sections of the eye at the level of the optic nerve at P2.0 (A, C, E, G, and H), and P21 (B, D, and F) were immunostained for Rybp. Shown are the retina (A, B), lens (C, D) cornea (E, F), connectiva (G) and optic nerve (H). C; cornea, Ep; corneal epithelium, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, LE; lens epithelium, ON; optic nerve, PLF primary lens fiber cells, T; transitional zone P; postnatal day. Magnification: (320×) |
PMC1877082_F2_11036.jpg | What's the most prominent thing you notice in this picture? | Rybp localization in the postnatal mouse eye. Sagittal sections of the eye at the level of the optic nerve at P2.0 (A, C, E, G, and H), and P21 (B, D, and F) were immunostained for Rybp. Shown are the retina (A, B), lens (C, D) cornea (E, F), connectiva (G) and optic nerve (H). C; cornea, Ep; corneal epithelium, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, LE; lens epithelium, ON; optic nerve, PLF primary lens fiber cells, T; transitional zone P; postnatal day. Magnification: (320×) |
PMC1877082_F2_11031.jpg | Can you identify the primary element in this image? | Rybp localization in the postnatal mouse eye. Sagittal sections of the eye at the level of the optic nerve at P2.0 (A, C, E, G, and H), and P21 (B, D, and F) were immunostained for Rybp. Shown are the retina (A, B), lens (C, D) cornea (E, F), connectiva (G) and optic nerve (H). C; cornea, Ep; corneal epithelium, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, LE; lens epithelium, ON; optic nerve, PLF primary lens fiber cells, T; transitional zone P; postnatal day. Magnification: (320×) |
PMC1877082_F2_11035.jpg | What is shown in this image? | Rybp localization in the postnatal mouse eye. Sagittal sections of the eye at the level of the optic nerve at P2.0 (A, C, E, G, and H), and P21 (B, D, and F) were immunostained for Rybp. Shown are the retina (A, B), lens (C, D) cornea (E, F), connectiva (G) and optic nerve (H). C; cornea, Ep; corneal epithelium, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, LE; lens epithelium, ON; optic nerve, PLF primary lens fiber cells, T; transitional zone P; postnatal day. Magnification: (320×) |
PMC1877082_F2_11030.jpg | What can you see in this picture? | Rybp localization in the postnatal mouse eye. Sagittal sections of the eye at the level of the optic nerve at P2.0 (A, C, E, G, and H), and P21 (B, D, and F) were immunostained for Rybp. Shown are the retina (A, B), lens (C, D) cornea (E, F), connectiva (G) and optic nerve (H). C; cornea, Ep; corneal epithelium, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, LE; lens epithelium, ON; optic nerve, PLF primary lens fiber cells, T; transitional zone P; postnatal day. Magnification: (320×) |
PMC1877082_F2_11032.jpg | What is the dominant medical problem in this image? | Rybp localization in the postnatal mouse eye. Sagittal sections of the eye at the level of the optic nerve at P2.0 (A, C, E, G, and H), and P21 (B, D, and F) were immunostained for Rybp. Shown are the retina (A, B), lens (C, D) cornea (E, F), connectiva (G) and optic nerve (H). C; cornea, Ep; corneal epithelium, GCL; ganglion cell layer, INL; inner nuclear layer, L; lens, LE; lens epithelium, ON; optic nerve, PLF primary lens fiber cells, T; transitional zone P; postnatal day. Magnification: (320×) |
PMC1877082_F3_11040.jpg | What is shown in this image? | Retinal coloboma in Rybp+/- mouse embryo. (A-B) Hematoxylin and eosin- stained coronal sections of normal (A) and Rybp heterozygous null (B) eyes at E14.5. The neuroretina of the mutant eye is thickened and fails to close leading to the formation of coloboma (B; arrowhead). (C-D) Immunolocalization of Pax6 in wild type (C) and mutant (D) eyes. Pax6 is normally expressed in the ventral side of neuroretina. In the mutant eyes it shows broader expression in the retina and it is also more posteriorly positioned in the transition zone of the lens (C compare to D). (E-F) Immunolocalization of Pax2 in wild type (E) and mutant (F) eyes. L; lens, NR; neuroretina, ON; optic nerve, V; ventral, T; transitional zone. HE; hematoxylin and eosin. Magnifications: A-D(×320); E-F(×460) |
PMC1877082_F3_11042.jpg | What is the central feature of this picture? | Retinal coloboma in Rybp+/- mouse embryo. (A-B) Hematoxylin and eosin- stained coronal sections of normal (A) and Rybp heterozygous null (B) eyes at E14.5. The neuroretina of the mutant eye is thickened and fails to close leading to the formation of coloboma (B; arrowhead). (C-D) Immunolocalization of Pax6 in wild type (C) and mutant (D) eyes. Pax6 is normally expressed in the ventral side of neuroretina. In the mutant eyes it shows broader expression in the retina and it is also more posteriorly positioned in the transition zone of the lens (C compare to D). (E-F) Immunolocalization of Pax2 in wild type (E) and mutant (F) eyes. L; lens, NR; neuroretina, ON; optic nerve, V; ventral, T; transitional zone. HE; hematoxylin and eosin. Magnifications: A-D(×320); E-F(×460) |
PMC1877082_F3_11038.jpg | Can you identify the primary element in this image? | Retinal coloboma in Rybp+/- mouse embryo. (A-B) Hematoxylin and eosin- stained coronal sections of normal (A) and Rybp heterozygous null (B) eyes at E14.5. The neuroretina of the mutant eye is thickened and fails to close leading to the formation of coloboma (B; arrowhead). (C-D) Immunolocalization of Pax6 in wild type (C) and mutant (D) eyes. Pax6 is normally expressed in the ventral side of neuroretina. In the mutant eyes it shows broader expression in the retina and it is also more posteriorly positioned in the transition zone of the lens (C compare to D). (E-F) Immunolocalization of Pax2 in wild type (E) and mutant (F) eyes. L; lens, NR; neuroretina, ON; optic nerve, V; ventral, T; transitional zone. HE; hematoxylin and eosin. Magnifications: A-D(×320); E-F(×460) |
PMC1877082_F3_11041.jpg | What can you see in this picture? | Retinal coloboma in Rybp+/- mouse embryo. (A-B) Hematoxylin and eosin- stained coronal sections of normal (A) and Rybp heterozygous null (B) eyes at E14.5. The neuroretina of the mutant eye is thickened and fails to close leading to the formation of coloboma (B; arrowhead). (C-D) Immunolocalization of Pax6 in wild type (C) and mutant (D) eyes. Pax6 is normally expressed in the ventral side of neuroretina. In the mutant eyes it shows broader expression in the retina and it is also more posteriorly positioned in the transition zone of the lens (C compare to D). (E-F) Immunolocalization of Pax2 in wild type (E) and mutant (F) eyes. L; lens, NR; neuroretina, ON; optic nerve, V; ventral, T; transitional zone. HE; hematoxylin and eosin. Magnifications: A-D(×320); E-F(×460) |
PMC1877082_F3_11037.jpg | What is shown in this image? | Retinal coloboma in Rybp+/- mouse embryo. (A-B) Hematoxylin and eosin- stained coronal sections of normal (A) and Rybp heterozygous null (B) eyes at E14.5. The neuroretina of the mutant eye is thickened and fails to close leading to the formation of coloboma (B; arrowhead). (C-D) Immunolocalization of Pax6 in wild type (C) and mutant (D) eyes. Pax6 is normally expressed in the ventral side of neuroretina. In the mutant eyes it shows broader expression in the retina and it is also more posteriorly positioned in the transition zone of the lens (C compare to D). (E-F) Immunolocalization of Pax2 in wild type (E) and mutant (F) eyes. L; lens, NR; neuroretina, ON; optic nerve, V; ventral, T; transitional zone. HE; hematoxylin and eosin. Magnifications: A-D(×320); E-F(×460) |
PMC1877082_F4_11059.jpg | What does this image primarily show? | Progenitor cell fate is not changed in the mutant retinas of the Rybp heterozygous eyes. Wild type (A, C, E) and Rybp heterozygous null eyes exhibiting retinal coloboma (B, D, F) were stained with TUJ1 (A, B), NeuN (C, D) and Nestin (E, F) at E14.5. (A-B) TUJ1 staining, marking early neuronal cell types including ganglion cells of the retina, is comparable in the wildtype and mutant mice. (C-D) Similarly, NeuN, a postmitotic neural marker, shows no significant alteration in the mutant retinas. (E-F) The distribution of nestin, an intermediate filament marker for neural progenitor cells, is not affected in the mutant retinas. L; lens, NR; neuroretina, Magnifications: (×460) |
PMC1877082_F4_11056.jpg | What object or scene is depicted here? | Progenitor cell fate is not changed in the mutant retinas of the Rybp heterozygous eyes. Wild type (A, C, E) and Rybp heterozygous null eyes exhibiting retinal coloboma (B, D, F) were stained with TUJ1 (A, B), NeuN (C, D) and Nestin (E, F) at E14.5. (A-B) TUJ1 staining, marking early neuronal cell types including ganglion cells of the retina, is comparable in the wildtype and mutant mice. (C-D) Similarly, NeuN, a postmitotic neural marker, shows no significant alteration in the mutant retinas. (E-F) The distribution of nestin, an intermediate filament marker for neural progenitor cells, is not affected in the mutant retinas. L; lens, NR; neuroretina, Magnifications: (×460) |
PMC1877082_F4_11055.jpg | What is the core subject represented in this visual? | Progenitor cell fate is not changed in the mutant retinas of the Rybp heterozygous eyes. Wild type (A, C, E) and Rybp heterozygous null eyes exhibiting retinal coloboma (B, D, F) were stained with TUJ1 (A, B), NeuN (C, D) and Nestin (E, F) at E14.5. (A-B) TUJ1 staining, marking early neuronal cell types including ganglion cells of the retina, is comparable in the wildtype and mutant mice. (C-D) Similarly, NeuN, a postmitotic neural marker, shows no significant alteration in the mutant retinas. (E-F) The distribution of nestin, an intermediate filament marker for neural progenitor cells, is not affected in the mutant retinas. L; lens, NR; neuroretina, Magnifications: (×460) |
PMC1877082_F4_11060.jpg | What object or scene is depicted here? | Progenitor cell fate is not changed in the mutant retinas of the Rybp heterozygous eyes. Wild type (A, C, E) and Rybp heterozygous null eyes exhibiting retinal coloboma (B, D, F) were stained with TUJ1 (A, B), NeuN (C, D) and Nestin (E, F) at E14.5. (A-B) TUJ1 staining, marking early neuronal cell types including ganglion cells of the retina, is comparable in the wildtype and mutant mice. (C-D) Similarly, NeuN, a postmitotic neural marker, shows no significant alteration in the mutant retinas. (E-F) The distribution of nestin, an intermediate filament marker for neural progenitor cells, is not affected in the mutant retinas. L; lens, NR; neuroretina, Magnifications: (×460) |
PMC1877082_F4_11061.jpg | What can you see in this picture? | Progenitor cell fate is not changed in the mutant retinas of the Rybp heterozygous eyes. Wild type (A, C, E) and Rybp heterozygous null eyes exhibiting retinal coloboma (B, D, F) were stained with TUJ1 (A, B), NeuN (C, D) and Nestin (E, F) at E14.5. (A-B) TUJ1 staining, marking early neuronal cell types including ganglion cells of the retina, is comparable in the wildtype and mutant mice. (C-D) Similarly, NeuN, a postmitotic neural marker, shows no significant alteration in the mutant retinas. (E-F) The distribution of nestin, an intermediate filament marker for neural progenitor cells, is not affected in the mutant retinas. L; lens, NR; neuroretina, Magnifications: (×460) |
PMC1877082_F4_11057.jpg | What is the central feature of this picture? | Progenitor cell fate is not changed in the mutant retinas of the Rybp heterozygous eyes. Wild type (A, C, E) and Rybp heterozygous null eyes exhibiting retinal coloboma (B, D, F) were stained with TUJ1 (A, B), NeuN (C, D) and Nestin (E, F) at E14.5. (A-B) TUJ1 staining, marking early neuronal cell types including ganglion cells of the retina, is comparable in the wildtype and mutant mice. (C-D) Similarly, NeuN, a postmitotic neural marker, shows no significant alteration in the mutant retinas. (E-F) The distribution of nestin, an intermediate filament marker for neural progenitor cells, is not affected in the mutant retinas. L; lens, NR; neuroretina, Magnifications: (×460) |
PMC1877082_F7_11064.jpg | What is the dominant medical problem in this image? | Abnormal lens development in the lens-specific Rybp transgenic mice. (A-D) Histological appearance of wild type (A, C) and ROSA26-RYBP/EGFP; αA-crystallin/Cre transgenic (B, D) lenses at early postnatal (P2) development (A, B) and adulthood (3 month) (C, D). (A, C) Wild type eyes with normal morphology of the lens epithelium and fiber cells. (B, D) Transgenic eyes showing cortical inhomogeneity as a sign of developing cataract and impaired lens development (B). Lenses of adult transgenic mice (3 month) show progressed cataractous morphology (D). CA; cataract, L; lens, LE; lens epithelium, T; transitional zone, TG; transgenic, WT; wild type; P; postnatal. Magnification: A-B (×160); C-D (×250); E-F (×120) |
PMC1877082_F7_11063.jpg | What object or scene is depicted here? | Abnormal lens development in the lens-specific Rybp transgenic mice. (A-D) Histological appearance of wild type (A, C) and ROSA26-RYBP/EGFP; αA-crystallin/Cre transgenic (B, D) lenses at early postnatal (P2) development (A, B) and adulthood (3 month) (C, D). (A, C) Wild type eyes with normal morphology of the lens epithelium and fiber cells. (B, D) Transgenic eyes showing cortical inhomogeneity as a sign of developing cataract and impaired lens development (B). Lenses of adult transgenic mice (3 month) show progressed cataractous morphology (D). CA; cataract, L; lens, LE; lens epithelium, T; transitional zone, TG; transgenic, WT; wild type; P; postnatal. Magnification: A-B (×160); C-D (×250); E-F (×120) |
PMC1877083_F1_11086.jpg | Can you identify the primary element in this image? | EGFP expression within lysC::EGFP transgenic embryos and larvae. EGFP expression within 22 hpf (A), 36 hpf (B and C), 48 hpf (D-I), 5 dpf (J), 6 dpf (K-M) and 7 dpf (N and O) transgenic embryos/larvae. (A, B and D) Lateral views of developing head, anterior to left. (C, F-I, L and M) Lateral views of trunk/tail region, anterior to left. (E, J and N) Dorsal view of cranio-trunk region, anterior to left. (K) Ventral view of head region, anterior to left. (A-N and A'-N') Bright field and dark field views, respectively. Insets in A' and I' represent magnified views of A' and I', respectively. (G) Summed Z stacks through aggregates of EGFP-labeled cells within posterior ICM region (marked by box in F). (H) Magnified view of cells in G. (I and M) Microangiography using red fluorescent microspheres within 48 hpf and 6 dpf transgenic larvae, respectively. (I' and M') Images merged with EGFP expression. Arrow in I' denotes EGFP-labeled cell within caudal vascular plexus. Arrows in J' and N' denote expression within the pronephric glomerulus. (O) Summed Z stacks through mid-intestine of 7 dpf lysC::EGFP/I-FABP::RFP compound transgenic larva (anterior to left). Abbreviations: Lu, gut lumen. Scale bars: 200 μm in A-F and I-N; 10 μm in G and O; 5 μm in H. |
PMC1877083_F1_11083.jpg | What is shown in this image? | EGFP expression within lysC::EGFP transgenic embryos and larvae. EGFP expression within 22 hpf (A), 36 hpf (B and C), 48 hpf (D-I), 5 dpf (J), 6 dpf (K-M) and 7 dpf (N and O) transgenic embryos/larvae. (A, B and D) Lateral views of developing head, anterior to left. (C, F-I, L and M) Lateral views of trunk/tail region, anterior to left. (E, J and N) Dorsal view of cranio-trunk region, anterior to left. (K) Ventral view of head region, anterior to left. (A-N and A'-N') Bright field and dark field views, respectively. Insets in A' and I' represent magnified views of A' and I', respectively. (G) Summed Z stacks through aggregates of EGFP-labeled cells within posterior ICM region (marked by box in F). (H) Magnified view of cells in G. (I and M) Microangiography using red fluorescent microspheres within 48 hpf and 6 dpf transgenic larvae, respectively. (I' and M') Images merged with EGFP expression. Arrow in I' denotes EGFP-labeled cell within caudal vascular plexus. Arrows in J' and N' denote expression within the pronephric glomerulus. (O) Summed Z stacks through mid-intestine of 7 dpf lysC::EGFP/I-FABP::RFP compound transgenic larva (anterior to left). Abbreviations: Lu, gut lumen. Scale bars: 200 μm in A-F and I-N; 10 μm in G and O; 5 μm in H. |
PMC1877083_F1_11089.jpg | What is the central feature of this picture? | EGFP expression within lysC::EGFP transgenic embryos and larvae. EGFP expression within 22 hpf (A), 36 hpf (B and C), 48 hpf (D-I), 5 dpf (J), 6 dpf (K-M) and 7 dpf (N and O) transgenic embryos/larvae. (A, B and D) Lateral views of developing head, anterior to left. (C, F-I, L and M) Lateral views of trunk/tail region, anterior to left. (E, J and N) Dorsal view of cranio-trunk region, anterior to left. (K) Ventral view of head region, anterior to left. (A-N and A'-N') Bright field and dark field views, respectively. Insets in A' and I' represent magnified views of A' and I', respectively. (G) Summed Z stacks through aggregates of EGFP-labeled cells within posterior ICM region (marked by box in F). (H) Magnified view of cells in G. (I and M) Microangiography using red fluorescent microspheres within 48 hpf and 6 dpf transgenic larvae, respectively. (I' and M') Images merged with EGFP expression. Arrow in I' denotes EGFP-labeled cell within caudal vascular plexus. Arrows in J' and N' denote expression within the pronephric glomerulus. (O) Summed Z stacks through mid-intestine of 7 dpf lysC::EGFP/I-FABP::RFP compound transgenic larva (anterior to left). Abbreviations: Lu, gut lumen. Scale bars: 200 μm in A-F and I-N; 10 μm in G and O; 5 μm in H. |
PMC1877083_F1_11085.jpg | What is the core subject represented in this visual? | EGFP expression within lysC::EGFP transgenic embryos and larvae. EGFP expression within 22 hpf (A), 36 hpf (B and C), 48 hpf (D-I), 5 dpf (J), 6 dpf (K-M) and 7 dpf (N and O) transgenic embryos/larvae. (A, B and D) Lateral views of developing head, anterior to left. (C, F-I, L and M) Lateral views of trunk/tail region, anterior to left. (E, J and N) Dorsal view of cranio-trunk region, anterior to left. (K) Ventral view of head region, anterior to left. (A-N and A'-N') Bright field and dark field views, respectively. Insets in A' and I' represent magnified views of A' and I', respectively. (G) Summed Z stacks through aggregates of EGFP-labeled cells within posterior ICM region (marked by box in F). (H) Magnified view of cells in G. (I and M) Microangiography using red fluorescent microspheres within 48 hpf and 6 dpf transgenic larvae, respectively. (I' and M') Images merged with EGFP expression. Arrow in I' denotes EGFP-labeled cell within caudal vascular plexus. Arrows in J' and N' denote expression within the pronephric glomerulus. (O) Summed Z stacks through mid-intestine of 7 dpf lysC::EGFP/I-FABP::RFP compound transgenic larva (anterior to left). Abbreviations: Lu, gut lumen. Scale bars: 200 μm in A-F and I-N; 10 μm in G and O; 5 μm in H. |
PMC1877083_F1_11087.jpg | What key item or scene is captured in this photo? | EGFP expression within lysC::EGFP transgenic embryos and larvae. EGFP expression within 22 hpf (A), 36 hpf (B and C), 48 hpf (D-I), 5 dpf (J), 6 dpf (K-M) and 7 dpf (N and O) transgenic embryos/larvae. (A, B and D) Lateral views of developing head, anterior to left. (C, F-I, L and M) Lateral views of trunk/tail region, anterior to left. (E, J and N) Dorsal view of cranio-trunk region, anterior to left. (K) Ventral view of head region, anterior to left. (A-N and A'-N') Bright field and dark field views, respectively. Insets in A' and I' represent magnified views of A' and I', respectively. (G) Summed Z stacks through aggregates of EGFP-labeled cells within posterior ICM region (marked by box in F). (H) Magnified view of cells in G. (I and M) Microangiography using red fluorescent microspheres within 48 hpf and 6 dpf transgenic larvae, respectively. (I' and M') Images merged with EGFP expression. Arrow in I' denotes EGFP-labeled cell within caudal vascular plexus. Arrows in J' and N' denote expression within the pronephric glomerulus. (O) Summed Z stacks through mid-intestine of 7 dpf lysC::EGFP/I-FABP::RFP compound transgenic larva (anterior to left). Abbreviations: Lu, gut lumen. Scale bars: 200 μm in A-F and I-N; 10 μm in G and O; 5 μm in H. |
PMC1877083_F1_11081.jpg | What is the core subject represented in this visual? | EGFP expression within lysC::EGFP transgenic embryos and larvae. EGFP expression within 22 hpf (A), 36 hpf (B and C), 48 hpf (D-I), 5 dpf (J), 6 dpf (K-M) and 7 dpf (N and O) transgenic embryos/larvae. (A, B and D) Lateral views of developing head, anterior to left. (C, F-I, L and M) Lateral views of trunk/tail region, anterior to left. (E, J and N) Dorsal view of cranio-trunk region, anterior to left. (K) Ventral view of head region, anterior to left. (A-N and A'-N') Bright field and dark field views, respectively. Insets in A' and I' represent magnified views of A' and I', respectively. (G) Summed Z stacks through aggregates of EGFP-labeled cells within posterior ICM region (marked by box in F). (H) Magnified view of cells in G. (I and M) Microangiography using red fluorescent microspheres within 48 hpf and 6 dpf transgenic larvae, respectively. (I' and M') Images merged with EGFP expression. Arrow in I' denotes EGFP-labeled cell within caudal vascular plexus. Arrows in J' and N' denote expression within the pronephric glomerulus. (O) Summed Z stacks through mid-intestine of 7 dpf lysC::EGFP/I-FABP::RFP compound transgenic larva (anterior to left). Abbreviations: Lu, gut lumen. Scale bars: 200 μm in A-F and I-N; 10 μm in G and O; 5 μm in H. |
PMC1877083_F1_11090.jpg | What is the dominant medical problem in this image? | EGFP expression within lysC::EGFP transgenic embryos and larvae. EGFP expression within 22 hpf (A), 36 hpf (B and C), 48 hpf (D-I), 5 dpf (J), 6 dpf (K-M) and 7 dpf (N and O) transgenic embryos/larvae. (A, B and D) Lateral views of developing head, anterior to left. (C, F-I, L and M) Lateral views of trunk/tail region, anterior to left. (E, J and N) Dorsal view of cranio-trunk region, anterior to left. (K) Ventral view of head region, anterior to left. (A-N and A'-N') Bright field and dark field views, respectively. Insets in A' and I' represent magnified views of A' and I', respectively. (G) Summed Z stacks through aggregates of EGFP-labeled cells within posterior ICM region (marked by box in F). (H) Magnified view of cells in G. (I and M) Microangiography using red fluorescent microspheres within 48 hpf and 6 dpf transgenic larvae, respectively. (I' and M') Images merged with EGFP expression. Arrow in I' denotes EGFP-labeled cell within caudal vascular plexus. Arrows in J' and N' denote expression within the pronephric glomerulus. (O) Summed Z stacks through mid-intestine of 7 dpf lysC::EGFP/I-FABP::RFP compound transgenic larva (anterior to left). Abbreviations: Lu, gut lumen. Scale bars: 200 μm in A-F and I-N; 10 μm in G and O; 5 μm in H. |
PMC1877083_F1_11082.jpg | What is the core subject represented in this visual? | EGFP expression within lysC::EGFP transgenic embryos and larvae. EGFP expression within 22 hpf (A), 36 hpf (B and C), 48 hpf (D-I), 5 dpf (J), 6 dpf (K-M) and 7 dpf (N and O) transgenic embryos/larvae. (A, B and D) Lateral views of developing head, anterior to left. (C, F-I, L and M) Lateral views of trunk/tail region, anterior to left. (E, J and N) Dorsal view of cranio-trunk region, anterior to left. (K) Ventral view of head region, anterior to left. (A-N and A'-N') Bright field and dark field views, respectively. Insets in A' and I' represent magnified views of A' and I', respectively. (G) Summed Z stacks through aggregates of EGFP-labeled cells within posterior ICM region (marked by box in F). (H) Magnified view of cells in G. (I and M) Microangiography using red fluorescent microspheres within 48 hpf and 6 dpf transgenic larvae, respectively. (I' and M') Images merged with EGFP expression. Arrow in I' denotes EGFP-labeled cell within caudal vascular plexus. Arrows in J' and N' denote expression within the pronephric glomerulus. (O) Summed Z stacks through mid-intestine of 7 dpf lysC::EGFP/I-FABP::RFP compound transgenic larva (anterior to left). Abbreviations: Lu, gut lumen. Scale bars: 200 μm in A-F and I-N; 10 μm in G and O; 5 μm in H. |
PMC1877083_F1_11076.jpg | What is the principal component of this image? | EGFP expression within lysC::EGFP transgenic embryos and larvae. EGFP expression within 22 hpf (A), 36 hpf (B and C), 48 hpf (D-I), 5 dpf (J), 6 dpf (K-M) and 7 dpf (N and O) transgenic embryos/larvae. (A, B and D) Lateral views of developing head, anterior to left. (C, F-I, L and M) Lateral views of trunk/tail region, anterior to left. (E, J and N) Dorsal view of cranio-trunk region, anterior to left. (K) Ventral view of head region, anterior to left. (A-N and A'-N') Bright field and dark field views, respectively. Insets in A' and I' represent magnified views of A' and I', respectively. (G) Summed Z stacks through aggregates of EGFP-labeled cells within posterior ICM region (marked by box in F). (H) Magnified view of cells in G. (I and M) Microangiography using red fluorescent microspheres within 48 hpf and 6 dpf transgenic larvae, respectively. (I' and M') Images merged with EGFP expression. Arrow in I' denotes EGFP-labeled cell within caudal vascular plexus. Arrows in J' and N' denote expression within the pronephric glomerulus. (O) Summed Z stacks through mid-intestine of 7 dpf lysC::EGFP/I-FABP::RFP compound transgenic larva (anterior to left). Abbreviations: Lu, gut lumen. Scale bars: 200 μm in A-F and I-N; 10 μm in G and O; 5 μm in H. |
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