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PMC1539001_F3_6486.jpg | What stands out most in this visual? | lin-3 mosaic analyis. (A) lin-3 mosaic animal at L4 stage with normal vulval development. Anchor cell labeled with arrowhead; bar indicates vulva. (B) Same lin-3 mosaic animal viewed under epifluoresence. The anchor cell has an intense spot of fluorescence, and thus the transgenic array (lin-3(+) + lacO + pPD118-33). The vulval descendants do not have the intense spot of fluorescence, and thus lack the transgenic array. (C) lin-3 mosaic animal at L4 stage with no Pn.px cells adopting vulval fate. Anchor cell labeled with arrowhead. Pn.px cell progeny labeled with arrows. (D) Same lin-3 mosaic animal viewed under epifluoresence. The anchor cell does not have the intense spot of fluorescence, and thus lacks the transgenic array (lin-3(+) + lacO + pPD118-33). The Pn.px cells do have the intense spot of fluorescence, and thus have the transgenic array. (E) lin-3 mosaic animal at L4 stage with multivulva phenotype. Anchor cell labeled with arrowhead; bar indicates vulva. (F) Same lin-3 mosaic animal viewed under epifluoresence. The anchor cell has an intense spot of fluorescence, and thus the transgenic array. The vulval descendants do not have the intense spot of fluorescence, and thus lack the transgenic array. |
PMC1539001_F3_6484.jpg | What is the main focus of this visual representation? | lin-3 mosaic analyis. (A) lin-3 mosaic animal at L4 stage with normal vulval development. Anchor cell labeled with arrowhead; bar indicates vulva. (B) Same lin-3 mosaic animal viewed under epifluoresence. The anchor cell has an intense spot of fluorescence, and thus the transgenic array (lin-3(+) + lacO + pPD118-33). The vulval descendants do not have the intense spot of fluorescence, and thus lack the transgenic array. (C) lin-3 mosaic animal at L4 stage with no Pn.px cells adopting vulval fate. Anchor cell labeled with arrowhead. Pn.px cell progeny labeled with arrows. (D) Same lin-3 mosaic animal viewed under epifluoresence. The anchor cell does not have the intense spot of fluorescence, and thus lacks the transgenic array (lin-3(+) + lacO + pPD118-33). The Pn.px cells do have the intense spot of fluorescence, and thus have the transgenic array. (E) lin-3 mosaic animal at L4 stage with multivulva phenotype. Anchor cell labeled with arrowhead; bar indicates vulva. (F) Same lin-3 mosaic animal viewed under epifluoresence. The anchor cell has an intense spot of fluorescence, and thus the transgenic array. The vulval descendants do not have the intense spot of fluorescence, and thus lack the transgenic array. |
PMC1540412_F5_6488.jpg | What key item or scene is captured in this photo? | Immunohistochemistry of thoracic aortas. Thoracic aortas were excised from rats and exposed to (B, C) or not exposed to (A) 100 μM H2O2 in vitro for 16 hours. Tissue sections were immunostained with rabbit polyclonal anti-FasL antibody, and immunoreactants were visualized with a substrate solution of 3-amino-9-ethylcarbazole. Cell nuclei were counterstained with a hemtoxylin solution. Exposure of thoracic aortas to 100 μM H2O2 increased expression of FasL on the aortic endothelium (B). Arrows point to positive FasL staining (red color in the original photomicrograph). Replacement of anti-FasL antibody with non-immune rabbit IgG resulted in negative staining (C). Photographs are representative of immunostaining of three thoracic aorta specimens Original magnification, 200×. |
PMC1540412_F5_6489.jpg | What is the central feature of this picture? | Immunohistochemistry of thoracic aortas. Thoracic aortas were excised from rats and exposed to (B, C) or not exposed to (A) 100 μM H2O2 in vitro for 16 hours. Tissue sections were immunostained with rabbit polyclonal anti-FasL antibody, and immunoreactants were visualized with a substrate solution of 3-amino-9-ethylcarbazole. Cell nuclei were counterstained with a hemtoxylin solution. Exposure of thoracic aortas to 100 μM H2O2 increased expression of FasL on the aortic endothelium (B). Arrows point to positive FasL staining (red color in the original photomicrograph). Replacement of anti-FasL antibody with non-immune rabbit IgG resulted in negative staining (C). Photographs are representative of immunostaining of three thoracic aorta specimens Original magnification, 200×. |
PMC1540432_F1_6491.jpg | What is shown in this image? | a) Prostate biopsy showing well differentiated adenocarcinoma of the prostate prior to neoadjuvant antiandrogen therapy (H&E staining). b) GSTP1 promoter methylation analysis of the tumor displaying both methylated (M, 92-base pairs (bp) product, blue fluorescence; tumor DNA) and unmethylated (UN, 99-bp product, green fluorescence) GSTP1 promoter sequences. |
PMC1540432_F1_6490.jpg | What is the principal component of this image? | a) Prostate biopsy showing well differentiated adenocarcinoma of the prostate prior to neoadjuvant antiandrogen therapy (H&E staining). b) GSTP1 promoter methylation analysis of the tumor displaying both methylated (M, 92-base pairs (bp) product, blue fluorescence; tumor DNA) and unmethylated (UN, 99-bp product, green fluorescence) GSTP1 promoter sequences. |
PMC1540436_F3_6499.jpg | What is being portrayed in this visual content? | Attenuated neuronal cell death in the injured hemisphere of factor B gene-deficient mice 24 hours after closed head injury. Coronal cryosections of the left (injured) hemisphere of wild-type (fB+/+, panels A-E) and factor B knockout mice (fB-/-, panels F-J) were analyzed by immunohistochemistry with a specific antibody to the neuronal marker NeuN (A, B, F, G) or by TUNEL-histochemistry of adjacent sections (D, E, I, J). The overall cellular morphology of the TUNEL sections is revealed by DAPI nuclear stain (C, H). The panels B, E, G, J represent a 4-fold magnification of the respective panels A, D, F, I. The evident destruction of the cortical tissue in brain-injured wild-type mice (upper panels) appears to be structurally preserved in fB-/- mice (bottom panels). The data shown here are highly reproducible in all tissue sections and animals assessed. Original magnifications: 100× (A, C, D, F, H, I), 400× (B, E, G, J). |
PMC1540436_F3_6496.jpg | What is shown in this image? | Attenuated neuronal cell death in the injured hemisphere of factor B gene-deficient mice 24 hours after closed head injury. Coronal cryosections of the left (injured) hemisphere of wild-type (fB+/+, panels A-E) and factor B knockout mice (fB-/-, panels F-J) were analyzed by immunohistochemistry with a specific antibody to the neuronal marker NeuN (A, B, F, G) or by TUNEL-histochemistry of adjacent sections (D, E, I, J). The overall cellular morphology of the TUNEL sections is revealed by DAPI nuclear stain (C, H). The panels B, E, G, J represent a 4-fold magnification of the respective panels A, D, F, I. The evident destruction of the cortical tissue in brain-injured wild-type mice (upper panels) appears to be structurally preserved in fB-/- mice (bottom panels). The data shown here are highly reproducible in all tissue sections and animals assessed. Original magnifications: 100× (A, C, D, F, H, I), 400× (B, E, G, J). |
PMC1540436_F3_6501.jpg | What is the main focus of this visual representation? | Attenuated neuronal cell death in the injured hemisphere of factor B gene-deficient mice 24 hours after closed head injury. Coronal cryosections of the left (injured) hemisphere of wild-type (fB+/+, panels A-E) and factor B knockout mice (fB-/-, panels F-J) were analyzed by immunohistochemistry with a specific antibody to the neuronal marker NeuN (A, B, F, G) or by TUNEL-histochemistry of adjacent sections (D, E, I, J). The overall cellular morphology of the TUNEL sections is revealed by DAPI nuclear stain (C, H). The panels B, E, G, J represent a 4-fold magnification of the respective panels A, D, F, I. The evident destruction of the cortical tissue in brain-injured wild-type mice (upper panels) appears to be structurally preserved in fB-/- mice (bottom panels). The data shown here are highly reproducible in all tissue sections and animals assessed. Original magnifications: 100× (A, C, D, F, H, I), 400× (B, E, G, J). |
PMC1540436_F3_6500.jpg | What is the core subject represented in this visual? | Attenuated neuronal cell death in the injured hemisphere of factor B gene-deficient mice 24 hours after closed head injury. Coronal cryosections of the left (injured) hemisphere of wild-type (fB+/+, panels A-E) and factor B knockout mice (fB-/-, panels F-J) were analyzed by immunohistochemistry with a specific antibody to the neuronal marker NeuN (A, B, F, G) or by TUNEL-histochemistry of adjacent sections (D, E, I, J). The overall cellular morphology of the TUNEL sections is revealed by DAPI nuclear stain (C, H). The panels B, E, G, J represent a 4-fold magnification of the respective panels A, D, F, I. The evident destruction of the cortical tissue in brain-injured wild-type mice (upper panels) appears to be structurally preserved in fB-/- mice (bottom panels). The data shown here are highly reproducible in all tissue sections and animals assessed. Original magnifications: 100× (A, C, D, F, H, I), 400× (B, E, G, J). |
PMC1540436_F3_6497.jpg | What object or scene is depicted here? | Attenuated neuronal cell death in the injured hemisphere of factor B gene-deficient mice 24 hours after closed head injury. Coronal cryosections of the left (injured) hemisphere of wild-type (fB+/+, panels A-E) and factor B knockout mice (fB-/-, panels F-J) were analyzed by immunohistochemistry with a specific antibody to the neuronal marker NeuN (A, B, F, G) or by TUNEL-histochemistry of adjacent sections (D, E, I, J). The overall cellular morphology of the TUNEL sections is revealed by DAPI nuclear stain (C, H). The panels B, E, G, J represent a 4-fold magnification of the respective panels A, D, F, I. The evident destruction of the cortical tissue in brain-injured wild-type mice (upper panels) appears to be structurally preserved in fB-/- mice (bottom panels). The data shown here are highly reproducible in all tissue sections and animals assessed. Original magnifications: 100× (A, C, D, F, H, I), 400× (B, E, G, J). |
PMC1540436_F3_6492.jpg | What is the core subject represented in this visual? | Attenuated neuronal cell death in the injured hemisphere of factor B gene-deficient mice 24 hours after closed head injury. Coronal cryosections of the left (injured) hemisphere of wild-type (fB+/+, panels A-E) and factor B knockout mice (fB-/-, panels F-J) were analyzed by immunohistochemistry with a specific antibody to the neuronal marker NeuN (A, B, F, G) or by TUNEL-histochemistry of adjacent sections (D, E, I, J). The overall cellular morphology of the TUNEL sections is revealed by DAPI nuclear stain (C, H). The panels B, E, G, J represent a 4-fold magnification of the respective panels A, D, F, I. The evident destruction of the cortical tissue in brain-injured wild-type mice (upper panels) appears to be structurally preserved in fB-/- mice (bottom panels). The data shown here are highly reproducible in all tissue sections and animals assessed. Original magnifications: 100× (A, C, D, F, H, I), 400× (B, E, G, J). |
PMC1540436_F3_6493.jpg | What can you see in this picture? | Attenuated neuronal cell death in the injured hemisphere of factor B gene-deficient mice 24 hours after closed head injury. Coronal cryosections of the left (injured) hemisphere of wild-type (fB+/+, panels A-E) and factor B knockout mice (fB-/-, panels F-J) were analyzed by immunohistochemistry with a specific antibody to the neuronal marker NeuN (A, B, F, G) or by TUNEL-histochemistry of adjacent sections (D, E, I, J). The overall cellular morphology of the TUNEL sections is revealed by DAPI nuclear stain (C, H). The panels B, E, G, J represent a 4-fold magnification of the respective panels A, D, F, I. The evident destruction of the cortical tissue in brain-injured wild-type mice (upper panels) appears to be structurally preserved in fB-/- mice (bottom panels). The data shown here are highly reproducible in all tissue sections and animals assessed. Original magnifications: 100× (A, C, D, F, H, I), 400× (B, E, G, J). |
PMC1540436_F3_6495.jpg | What stands out most in this visual? | Attenuated neuronal cell death in the injured hemisphere of factor B gene-deficient mice 24 hours after closed head injury. Coronal cryosections of the left (injured) hemisphere of wild-type (fB+/+, panels A-E) and factor B knockout mice (fB-/-, panels F-J) were analyzed by immunohistochemistry with a specific antibody to the neuronal marker NeuN (A, B, F, G) or by TUNEL-histochemistry of adjacent sections (D, E, I, J). The overall cellular morphology of the TUNEL sections is revealed by DAPI nuclear stain (C, H). The panels B, E, G, J represent a 4-fold magnification of the respective panels A, D, F, I. The evident destruction of the cortical tissue in brain-injured wild-type mice (upper panels) appears to be structurally preserved in fB-/- mice (bottom panels). The data shown here are highly reproducible in all tissue sections and animals assessed. Original magnifications: 100× (A, C, D, F, H, I), 400× (B, E, G, J). |
PMC1540708_pbio-0040271-g006_6513.jpg | What's the most prominent thing you notice in this picture? | ProSAP2 Lost from Dendritic Spine Heads Is Incorporated into PSDs of Adjacent SpinesA dendritic segment expressing both CFP (A) and PA-GFP:ProSAP2 (B). At time t = 0, PA-GFP:ProSAP2 within the region enclosed in rectangles was photoactivated by selective illumination at 405 nm. With time from photoactivation, fluorescence at tips of remote spines increased, whereas spine head fluorescence within the photoactivated region diminished. The contrast in (B) was enhanced linearly to emphasize fluorescence changes in remote spines, resulting in the apparent saturation at photoactivated spines. Spatial relationships between spines and PA-GFP:ProSAP2 puncta before and 29 min after photoactivation are shown in (C) and (D), respectively. In these images, PA-GFP:ProSAP2 fluorescence data were overlaid onto the CFP images after rendering the latter with the “emboss” filter of Adobe Photoshop. Note that PA-GFP:ProSAP2 fluorescence is restricted to spine heads, with little fluorescence observed in spine necks or the dendrite shaft. This distribution indicates that the PA-GFP:ProSAP2 that migrated to adjacent spines had become integrated into the PSD at these sites. Bar, 10 μm. Quantification of fluorescence changes at photoactivated (E) and neighboring spine heads (F) reveals a gradual decrease of fluorescence in the photoactivation region concomitant with fluorescence increases at nearby spines, most prominent at spines nearest to the photoactivation site. Values are normalized to prephotoactivation fluorescence levels. |
PMC1540708_pbio-0040271-g006_6519.jpg | What is the focal point of this photograph? | ProSAP2 Lost from Dendritic Spine Heads Is Incorporated into PSDs of Adjacent SpinesA dendritic segment expressing both CFP (A) and PA-GFP:ProSAP2 (B). At time t = 0, PA-GFP:ProSAP2 within the region enclosed in rectangles was photoactivated by selective illumination at 405 nm. With time from photoactivation, fluorescence at tips of remote spines increased, whereas spine head fluorescence within the photoactivated region diminished. The contrast in (B) was enhanced linearly to emphasize fluorescence changes in remote spines, resulting in the apparent saturation at photoactivated spines. Spatial relationships between spines and PA-GFP:ProSAP2 puncta before and 29 min after photoactivation are shown in (C) and (D), respectively. In these images, PA-GFP:ProSAP2 fluorescence data were overlaid onto the CFP images after rendering the latter with the “emboss” filter of Adobe Photoshop. Note that PA-GFP:ProSAP2 fluorescence is restricted to spine heads, with little fluorescence observed in spine necks or the dendrite shaft. This distribution indicates that the PA-GFP:ProSAP2 that migrated to adjacent spines had become integrated into the PSD at these sites. Bar, 10 μm. Quantification of fluorescence changes at photoactivated (E) and neighboring spine heads (F) reveals a gradual decrease of fluorescence in the photoactivation region concomitant with fluorescence increases at nearby spines, most prominent at spines nearest to the photoactivation site. Values are normalized to prephotoactivation fluorescence levels. |
PMC1540708_pbio-0040271-g006_6510.jpg | What is the core subject represented in this visual? | ProSAP2 Lost from Dendritic Spine Heads Is Incorporated into PSDs of Adjacent SpinesA dendritic segment expressing both CFP (A) and PA-GFP:ProSAP2 (B). At time t = 0, PA-GFP:ProSAP2 within the region enclosed in rectangles was photoactivated by selective illumination at 405 nm. With time from photoactivation, fluorescence at tips of remote spines increased, whereas spine head fluorescence within the photoactivated region diminished. The contrast in (B) was enhanced linearly to emphasize fluorescence changes in remote spines, resulting in the apparent saturation at photoactivated spines. Spatial relationships between spines and PA-GFP:ProSAP2 puncta before and 29 min after photoactivation are shown in (C) and (D), respectively. In these images, PA-GFP:ProSAP2 fluorescence data were overlaid onto the CFP images after rendering the latter with the “emboss” filter of Adobe Photoshop. Note that PA-GFP:ProSAP2 fluorescence is restricted to spine heads, with little fluorescence observed in spine necks or the dendrite shaft. This distribution indicates that the PA-GFP:ProSAP2 that migrated to adjacent spines had become integrated into the PSD at these sites. Bar, 10 μm. Quantification of fluorescence changes at photoactivated (E) and neighboring spine heads (F) reveals a gradual decrease of fluorescence in the photoactivation region concomitant with fluorescence increases at nearby spines, most prominent at spines nearest to the photoactivation site. Values are normalized to prephotoactivation fluorescence levels. |
PMC1540708_pbio-0040271-g006_6512.jpg | What is the central feature of this picture? | ProSAP2 Lost from Dendritic Spine Heads Is Incorporated into PSDs of Adjacent SpinesA dendritic segment expressing both CFP (A) and PA-GFP:ProSAP2 (B). At time t = 0, PA-GFP:ProSAP2 within the region enclosed in rectangles was photoactivated by selective illumination at 405 nm. With time from photoactivation, fluorescence at tips of remote spines increased, whereas spine head fluorescence within the photoactivated region diminished. The contrast in (B) was enhanced linearly to emphasize fluorescence changes in remote spines, resulting in the apparent saturation at photoactivated spines. Spatial relationships between spines and PA-GFP:ProSAP2 puncta before and 29 min after photoactivation are shown in (C) and (D), respectively. In these images, PA-GFP:ProSAP2 fluorescence data were overlaid onto the CFP images after rendering the latter with the “emboss” filter of Adobe Photoshop. Note that PA-GFP:ProSAP2 fluorescence is restricted to spine heads, with little fluorescence observed in spine necks or the dendrite shaft. This distribution indicates that the PA-GFP:ProSAP2 that migrated to adjacent spines had become integrated into the PSD at these sites. Bar, 10 μm. Quantification of fluorescence changes at photoactivated (E) and neighboring spine heads (F) reveals a gradual decrease of fluorescence in the photoactivation region concomitant with fluorescence increases at nearby spines, most prominent at spines nearest to the photoactivation site. Values are normalized to prephotoactivation fluorescence levels. |
PMC1540708_pbio-0040271-g006_6514.jpg | What object or scene is depicted here? | ProSAP2 Lost from Dendritic Spine Heads Is Incorporated into PSDs of Adjacent SpinesA dendritic segment expressing both CFP (A) and PA-GFP:ProSAP2 (B). At time t = 0, PA-GFP:ProSAP2 within the region enclosed in rectangles was photoactivated by selective illumination at 405 nm. With time from photoactivation, fluorescence at tips of remote spines increased, whereas spine head fluorescence within the photoactivated region diminished. The contrast in (B) was enhanced linearly to emphasize fluorescence changes in remote spines, resulting in the apparent saturation at photoactivated spines. Spatial relationships between spines and PA-GFP:ProSAP2 puncta before and 29 min after photoactivation are shown in (C) and (D), respectively. In these images, PA-GFP:ProSAP2 fluorescence data were overlaid onto the CFP images after rendering the latter with the “emboss” filter of Adobe Photoshop. Note that PA-GFP:ProSAP2 fluorescence is restricted to spine heads, with little fluorescence observed in spine necks or the dendrite shaft. This distribution indicates that the PA-GFP:ProSAP2 that migrated to adjacent spines had become integrated into the PSD at these sites. Bar, 10 μm. Quantification of fluorescence changes at photoactivated (E) and neighboring spine heads (F) reveals a gradual decrease of fluorescence in the photoactivation region concomitant with fluorescence increases at nearby spines, most prominent at spines nearest to the photoactivation site. Values are normalized to prephotoactivation fluorescence levels. |
PMC1540708_pbio-0040271-g006_6518.jpg | What's the most prominent thing you notice in this picture? | ProSAP2 Lost from Dendritic Spine Heads Is Incorporated into PSDs of Adjacent SpinesA dendritic segment expressing both CFP (A) and PA-GFP:ProSAP2 (B). At time t = 0, PA-GFP:ProSAP2 within the region enclosed in rectangles was photoactivated by selective illumination at 405 nm. With time from photoactivation, fluorescence at tips of remote spines increased, whereas spine head fluorescence within the photoactivated region diminished. The contrast in (B) was enhanced linearly to emphasize fluorescence changes in remote spines, resulting in the apparent saturation at photoactivated spines. Spatial relationships between spines and PA-GFP:ProSAP2 puncta before and 29 min after photoactivation are shown in (C) and (D), respectively. In these images, PA-GFP:ProSAP2 fluorescence data were overlaid onto the CFP images after rendering the latter with the “emboss” filter of Adobe Photoshop. Note that PA-GFP:ProSAP2 fluorescence is restricted to spine heads, with little fluorescence observed in spine necks or the dendrite shaft. This distribution indicates that the PA-GFP:ProSAP2 that migrated to adjacent spines had become integrated into the PSD at these sites. Bar, 10 μm. Quantification of fluorescence changes at photoactivated (E) and neighboring spine heads (F) reveals a gradual decrease of fluorescence in the photoactivation region concomitant with fluorescence increases at nearby spines, most prominent at spines nearest to the photoactivation site. Values are normalized to prephotoactivation fluorescence levels. |
PMC1540708_pbio-0040271-g006_6515.jpg | What is the central feature of this picture? | ProSAP2 Lost from Dendritic Spine Heads Is Incorporated into PSDs of Adjacent SpinesA dendritic segment expressing both CFP (A) and PA-GFP:ProSAP2 (B). At time t = 0, PA-GFP:ProSAP2 within the region enclosed in rectangles was photoactivated by selective illumination at 405 nm. With time from photoactivation, fluorescence at tips of remote spines increased, whereas spine head fluorescence within the photoactivated region diminished. The contrast in (B) was enhanced linearly to emphasize fluorescence changes in remote spines, resulting in the apparent saturation at photoactivated spines. Spatial relationships between spines and PA-GFP:ProSAP2 puncta before and 29 min after photoactivation are shown in (C) and (D), respectively. In these images, PA-GFP:ProSAP2 fluorescence data were overlaid onto the CFP images after rendering the latter with the “emboss” filter of Adobe Photoshop. Note that PA-GFP:ProSAP2 fluorescence is restricted to spine heads, with little fluorescence observed in spine necks or the dendrite shaft. This distribution indicates that the PA-GFP:ProSAP2 that migrated to adjacent spines had become integrated into the PSD at these sites. Bar, 10 μm. Quantification of fluorescence changes at photoactivated (E) and neighboring spine heads (F) reveals a gradual decrease of fluorescence in the photoactivation region concomitant with fluorescence increases at nearby spines, most prominent at spines nearest to the photoactivation site. Values are normalized to prephotoactivation fluorescence levels. |
PMC1540708_pbio-0040271-g008_6507.jpg | What object or scene is depicted here? | Incorporation Rates of ProSAP2 from Somatic Sources into Remote PSDs(A) Composite image of a neuron expressing CFP and PA-GFP:ProSAP2. Only CFP fluorescence is shown here.(B) PA-GFP:ProSAP2 fluorescence for same region as in (A). At time t = 0, PA-GFP:ProSAP2 within the cell body was photoactivated by selective illumination of the soma at 405 nm. With time, photoactivated PA-GFP:ProSAP2 migrated to PSDs along the dendrites, initially to proximal PSDs and later to more distal ones. During the time-lapse session, recurrent, low-level photoactivation of the soma was performed, to maintain a constant level of somatic, photoactivated PA-GFP:ProSAP2.(C) Quantification of fluorescence changes at the soma.(D) Quantification of fluorescence changes at PSDs, grouped according to distance from the soma. Fluorescence data for each PSD were normalized to prephotoactivation fluorescence levels for the same PSD. Bar, 20 μm. |
PMC1540708_pbio-0040271-g008_6503.jpg | What stands out most in this visual? | Incorporation Rates of ProSAP2 from Somatic Sources into Remote PSDs(A) Composite image of a neuron expressing CFP and PA-GFP:ProSAP2. Only CFP fluorescence is shown here.(B) PA-GFP:ProSAP2 fluorescence for same region as in (A). At time t = 0, PA-GFP:ProSAP2 within the cell body was photoactivated by selective illumination of the soma at 405 nm. With time, photoactivated PA-GFP:ProSAP2 migrated to PSDs along the dendrites, initially to proximal PSDs and later to more distal ones. During the time-lapse session, recurrent, low-level photoactivation of the soma was performed, to maintain a constant level of somatic, photoactivated PA-GFP:ProSAP2.(C) Quantification of fluorescence changes at the soma.(D) Quantification of fluorescence changes at PSDs, grouped according to distance from the soma. Fluorescence data for each PSD were normalized to prephotoactivation fluorescence levels for the same PSD. Bar, 20 μm. |
PMC1540708_pbio-0040271-g008_6505.jpg | Describe the main subject of this image. | Incorporation Rates of ProSAP2 from Somatic Sources into Remote PSDs(A) Composite image of a neuron expressing CFP and PA-GFP:ProSAP2. Only CFP fluorescence is shown here.(B) PA-GFP:ProSAP2 fluorescence for same region as in (A). At time t = 0, PA-GFP:ProSAP2 within the cell body was photoactivated by selective illumination of the soma at 405 nm. With time, photoactivated PA-GFP:ProSAP2 migrated to PSDs along the dendrites, initially to proximal PSDs and later to more distal ones. During the time-lapse session, recurrent, low-level photoactivation of the soma was performed, to maintain a constant level of somatic, photoactivated PA-GFP:ProSAP2.(C) Quantification of fluorescence changes at the soma.(D) Quantification of fluorescence changes at PSDs, grouped according to distance from the soma. Fluorescence data for each PSD were normalized to prephotoactivation fluorescence levels for the same PSD. Bar, 20 μm. |
PMC1540709_pbio-0040272-g002_6534.jpg | What can you see in this picture? | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1540709_pbio-0040272-g002_6527.jpg | What's the most prominent thing you notice in this picture? | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1540709_pbio-0040272-g002_6522.jpg | What is the main focus of this visual representation? | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1540709_pbio-0040272-g002_6528.jpg | What is the focal point of this photograph? | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1540709_pbio-0040272-g002_6532.jpg | What is shown in this image? | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1540709_pbio-0040272-g002_6529.jpg | What stands out most in this visual? | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1540709_pbio-0040272-g002_6526.jpg | What is the core subject represented in this visual? | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1540709_pbio-0040272-g002_6537.jpg | What is the core subject represented in this visual? | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1540709_pbio-0040272-g002_6523.jpg | Describe the main subject of this image. | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1540709_pbio-0040272-g002_6531.jpg | What object or scene is depicted here? | The Translation of the Xenopus Homeobox Xotx5b, Xvsx1, and Xotx2 mRNAs Parallels the Generation of Photoreceptors and Bipolar CellsIn situ hybridization of Xotx2, Xotx5b, and Xvsx1 mRNAs (Fast Red detection) compared to immunostaining of the corresponding proteins (green detection) on serial 10-μm sections of embryonic retinas at st. 34 (mid-neurogenesis), st. 37 (late-neurogenesis), and st. 42 (mature embryonic retina). Schematics show the retinal cell types present at the corresponding times of analysis (see also Figure S2). Dashed lines border the entire thickness of neural retinas (st. 34–37), or indicate the boundaries between different cell layers (st. 42, magnification of central retinal aspect); GCL: ganglion cell layer, INL: inner nuclear layer, ONL: outer nuclear layer. |
PMC1543629_F1_6539.jpg | What is the dominant medical problem in this image? | MRI sagital scan showing mass extending into the mediastinum and right pleural cavity. This scan shows clearly the anatomical relationship between the tumour and one of the vessels of the aorto-coronary by-pass. |
PMC1543629_F2_6538.jpg | What object or scene is depicted here? | MRI transverse scan showing mass extension and anatomical relationship between the tumour and the tree grafts at level of ascending aorta. |
PMC1543641_F6_6549.jpg | What is the dominant medical problem in this image? | Stage 25 was the only stage when all plexins and neuropilins were expressed in the spinal cord. The most prominent mRNA levels were found for plexinAs. They were all detectable in dorsolateral commissural interneurons (arrowheads) and in motor neurons (open arrowheads). Expression of plexinA2 was restricted to some scattered cells in the ventral horn, but absent from lateral areas. Only subpopulations of motor neurons expressed plexinD1, npn-1, and npn-2. PlexinB1, B2, and C1 were found in all motor neurons although at low levels (open arrowheads). Panels A and B are higher magnifications of the sections hybridized with plexinA1 and npn-1, respectively, in comparison to Isl1 (C) and MNR2 (D) staining in adjacent sections. The expression domains of plexinA1, A4, and npn-2 are more similar to the domains expressing Isl1, whereas those for plexinA2, D1, and npn-1 overlap with the more medial motor neurons expressing MNR2. Floor-plate expression was still found for plexinA1 (lateral floor-plate cells only), A2, B1, and C1 (open arrows). The presence of plexinA1, A2, A4, B1, npn-1, and npn-2 in DRGs is indicated by asterisks. Bar 200 μm. |
PMC1543641_F6_6543.jpg | Describe the main subject of this image. | Stage 25 was the only stage when all plexins and neuropilins were expressed in the spinal cord. The most prominent mRNA levels were found for plexinAs. They were all detectable in dorsolateral commissural interneurons (arrowheads) and in motor neurons (open arrowheads). Expression of plexinA2 was restricted to some scattered cells in the ventral horn, but absent from lateral areas. Only subpopulations of motor neurons expressed plexinD1, npn-1, and npn-2. PlexinB1, B2, and C1 were found in all motor neurons although at low levels (open arrowheads). Panels A and B are higher magnifications of the sections hybridized with plexinA1 and npn-1, respectively, in comparison to Isl1 (C) and MNR2 (D) staining in adjacent sections. The expression domains of plexinA1, A4, and npn-2 are more similar to the domains expressing Isl1, whereas those for plexinA2, D1, and npn-1 overlap with the more medial motor neurons expressing MNR2. Floor-plate expression was still found for plexinA1 (lateral floor-plate cells only), A2, B1, and C1 (open arrows). The presence of plexinA1, A2, A4, B1, npn-1, and npn-2 in DRGs is indicated by asterisks. Bar 200 μm. |
PMC1543641_F6_6548.jpg | What is the main focus of this visual representation? | Stage 25 was the only stage when all plexins and neuropilins were expressed in the spinal cord. The most prominent mRNA levels were found for plexinAs. They were all detectable in dorsolateral commissural interneurons (arrowheads) and in motor neurons (open arrowheads). Expression of plexinA2 was restricted to some scattered cells in the ventral horn, but absent from lateral areas. Only subpopulations of motor neurons expressed plexinD1, npn-1, and npn-2. PlexinB1, B2, and C1 were found in all motor neurons although at low levels (open arrowheads). Panels A and B are higher magnifications of the sections hybridized with plexinA1 and npn-1, respectively, in comparison to Isl1 (C) and MNR2 (D) staining in adjacent sections. The expression domains of plexinA1, A4, and npn-2 are more similar to the domains expressing Isl1, whereas those for plexinA2, D1, and npn-1 overlap with the more medial motor neurons expressing MNR2. Floor-plate expression was still found for plexinA1 (lateral floor-plate cells only), A2, B1, and C1 (open arrows). The presence of plexinA1, A2, A4, B1, npn-1, and npn-2 in DRGs is indicated by asterisks. Bar 200 μm. |
PMC1543641_F6_6541.jpg | What stands out most in this visual? | Stage 25 was the only stage when all plexins and neuropilins were expressed in the spinal cord. The most prominent mRNA levels were found for plexinAs. They were all detectable in dorsolateral commissural interneurons (arrowheads) and in motor neurons (open arrowheads). Expression of plexinA2 was restricted to some scattered cells in the ventral horn, but absent from lateral areas. Only subpopulations of motor neurons expressed plexinD1, npn-1, and npn-2. PlexinB1, B2, and C1 were found in all motor neurons although at low levels (open arrowheads). Panels A and B are higher magnifications of the sections hybridized with plexinA1 and npn-1, respectively, in comparison to Isl1 (C) and MNR2 (D) staining in adjacent sections. The expression domains of plexinA1, A4, and npn-2 are more similar to the domains expressing Isl1, whereas those for plexinA2, D1, and npn-1 overlap with the more medial motor neurons expressing MNR2. Floor-plate expression was still found for plexinA1 (lateral floor-plate cells only), A2, B1, and C1 (open arrows). The presence of plexinA1, A2, A4, B1, npn-1, and npn-2 in DRGs is indicated by asterisks. Bar 200 μm. |
PMC1543641_F6_6545.jpg | What is the central feature of this picture? | Stage 25 was the only stage when all plexins and neuropilins were expressed in the spinal cord. The most prominent mRNA levels were found for plexinAs. They were all detectable in dorsolateral commissural interneurons (arrowheads) and in motor neurons (open arrowheads). Expression of plexinA2 was restricted to some scattered cells in the ventral horn, but absent from lateral areas. Only subpopulations of motor neurons expressed plexinD1, npn-1, and npn-2. PlexinB1, B2, and C1 were found in all motor neurons although at low levels (open arrowheads). Panels A and B are higher magnifications of the sections hybridized with plexinA1 and npn-1, respectively, in comparison to Isl1 (C) and MNR2 (D) staining in adjacent sections. The expression domains of plexinA1, A4, and npn-2 are more similar to the domains expressing Isl1, whereas those for plexinA2, D1, and npn-1 overlap with the more medial motor neurons expressing MNR2. Floor-plate expression was still found for plexinA1 (lateral floor-plate cells only), A2, B1, and C1 (open arrows). The presence of plexinA1, A2, A4, B1, npn-1, and npn-2 in DRGs is indicated by asterisks. Bar 200 μm. |
PMC1543641_F6_6550.jpg | Can you identify the primary element in this image? | Stage 25 was the only stage when all plexins and neuropilins were expressed in the spinal cord. The most prominent mRNA levels were found for plexinAs. They were all detectable in dorsolateral commissural interneurons (arrowheads) and in motor neurons (open arrowheads). Expression of plexinA2 was restricted to some scattered cells in the ventral horn, but absent from lateral areas. Only subpopulations of motor neurons expressed plexinD1, npn-1, and npn-2. PlexinB1, B2, and C1 were found in all motor neurons although at low levels (open arrowheads). Panels A and B are higher magnifications of the sections hybridized with plexinA1 and npn-1, respectively, in comparison to Isl1 (C) and MNR2 (D) staining in adjacent sections. The expression domains of plexinA1, A4, and npn-2 are more similar to the domains expressing Isl1, whereas those for plexinA2, D1, and npn-1 overlap with the more medial motor neurons expressing MNR2. Floor-plate expression was still found for plexinA1 (lateral floor-plate cells only), A2, B1, and C1 (open arrows). The presence of plexinA1, A2, A4, B1, npn-1, and npn-2 in DRGs is indicated by asterisks. Bar 200 μm. |
PMC1543641_F6_6547.jpg | What object or scene is depicted here? | Stage 25 was the only stage when all plexins and neuropilins were expressed in the spinal cord. The most prominent mRNA levels were found for plexinAs. They were all detectable in dorsolateral commissural interneurons (arrowheads) and in motor neurons (open arrowheads). Expression of plexinA2 was restricted to some scattered cells in the ventral horn, but absent from lateral areas. Only subpopulations of motor neurons expressed plexinD1, npn-1, and npn-2. PlexinB1, B2, and C1 were found in all motor neurons although at low levels (open arrowheads). Panels A and B are higher magnifications of the sections hybridized with plexinA1 and npn-1, respectively, in comparison to Isl1 (C) and MNR2 (D) staining in adjacent sections. The expression domains of plexinA1, A4, and npn-2 are more similar to the domains expressing Isl1, whereas those for plexinA2, D1, and npn-1 overlap with the more medial motor neurons expressing MNR2. Floor-plate expression was still found for plexinA1 (lateral floor-plate cells only), A2, B1, and C1 (open arrows). The presence of plexinA1, A2, A4, B1, npn-1, and npn-2 in DRGs is indicated by asterisks. Bar 200 μm. |
PMC1543641_F6_6542.jpg | What key item or scene is captured in this photo? | Stage 25 was the only stage when all plexins and neuropilins were expressed in the spinal cord. The most prominent mRNA levels were found for plexinAs. They were all detectable in dorsolateral commissural interneurons (arrowheads) and in motor neurons (open arrowheads). Expression of plexinA2 was restricted to some scattered cells in the ventral horn, but absent from lateral areas. Only subpopulations of motor neurons expressed plexinD1, npn-1, and npn-2. PlexinB1, B2, and C1 were found in all motor neurons although at low levels (open arrowheads). Panels A and B are higher magnifications of the sections hybridized with plexinA1 and npn-1, respectively, in comparison to Isl1 (C) and MNR2 (D) staining in adjacent sections. The expression domains of plexinA1, A4, and npn-2 are more similar to the domains expressing Isl1, whereas those for plexinA2, D1, and npn-1 overlap with the more medial motor neurons expressing MNR2. Floor-plate expression was still found for plexinA1 (lateral floor-plate cells only), A2, B1, and C1 (open arrows). The presence of plexinA1, A2, A4, B1, npn-1, and npn-2 in DRGs is indicated by asterisks. Bar 200 μm. |
PMC1543641_F6_6551.jpg | What is the principal component of this image? | Stage 25 was the only stage when all plexins and neuropilins were expressed in the spinal cord. The most prominent mRNA levels were found for plexinAs. They were all detectable in dorsolateral commissural interneurons (arrowheads) and in motor neurons (open arrowheads). Expression of plexinA2 was restricted to some scattered cells in the ventral horn, but absent from lateral areas. Only subpopulations of motor neurons expressed plexinD1, npn-1, and npn-2. PlexinB1, B2, and C1 were found in all motor neurons although at low levels (open arrowheads). Panels A and B are higher magnifications of the sections hybridized with plexinA1 and npn-1, respectively, in comparison to Isl1 (C) and MNR2 (D) staining in adjacent sections. The expression domains of plexinA1, A4, and npn-2 are more similar to the domains expressing Isl1, whereas those for plexinA2, D1, and npn-1 overlap with the more medial motor neurons expressing MNR2. Floor-plate expression was still found for plexinA1 (lateral floor-plate cells only), A2, B1, and C1 (open arrows). The presence of plexinA1, A2, A4, B1, npn-1, and npn-2 in DRGs is indicated by asterisks. Bar 200 μm. |
PMC1543641_F9_6552.jpg | What is the dominant medical problem in this image? | Expression of plexins and neuropilins in late stages of spinal cord development. At stage 40, the latest stage we analyzed, plexin expression still changed. The most prominent change was found for plexinB1, which was now restricted to the white matter (arrow; high magnification shown in A). Strong expression in the dorsal spinal cord was still found for plexinA2, C1, and npn-1 (arrowhead). Few positive motor neurons were still found for plexinA1, A2, npn-1, and npn-2 (open arrowheads). DRGs maintained expression of plexinA4, C1, and npn-1 (asterisk). Single scattered cells were still expressing plexinA1 and A2. Panels A – C show high magnifications of a section processed by in situ hybridization to detect plexinB1 (A). Adjacent sections were stained with antibodies recognizing the oligodendrocyte marker O4 (B) and the astrocyte marker GFAP (C). Bar 500 μm for in situ hybridizations of plexins and neuropilins and 200 μm for panels A-C. |
PMC1543641_F9_6553.jpg | What object or scene is depicted here? | Expression of plexins and neuropilins in late stages of spinal cord development. At stage 40, the latest stage we analyzed, plexin expression still changed. The most prominent change was found for plexinB1, which was now restricted to the white matter (arrow; high magnification shown in A). Strong expression in the dorsal spinal cord was still found for plexinA2, C1, and npn-1 (arrowhead). Few positive motor neurons were still found for plexinA1, A2, npn-1, and npn-2 (open arrowheads). DRGs maintained expression of plexinA4, C1, and npn-1 (asterisk). Single scattered cells were still expressing plexinA1 and A2. Panels A – C show high magnifications of a section processed by in situ hybridization to detect plexinB1 (A). Adjacent sections were stained with antibodies recognizing the oligodendrocyte marker O4 (B) and the astrocyte marker GFAP (C). Bar 500 μm for in situ hybridizations of plexins and neuropilins and 200 μm for panels A-C. |
PMC1543641_F9_6556.jpg | What is the focal point of this photograph? | Expression of plexins and neuropilins in late stages of spinal cord development. At stage 40, the latest stage we analyzed, plexin expression still changed. The most prominent change was found for plexinB1, which was now restricted to the white matter (arrow; high magnification shown in A). Strong expression in the dorsal spinal cord was still found for plexinA2, C1, and npn-1 (arrowhead). Few positive motor neurons were still found for plexinA1, A2, npn-1, and npn-2 (open arrowheads). DRGs maintained expression of plexinA4, C1, and npn-1 (asterisk). Single scattered cells were still expressing plexinA1 and A2. Panels A – C show high magnifications of a section processed by in situ hybridization to detect plexinB1 (A). Adjacent sections were stained with antibodies recognizing the oligodendrocyte marker O4 (B) and the astrocyte marker GFAP (C). Bar 500 μm for in situ hybridizations of plexins and neuropilins and 200 μm for panels A-C. |
PMC1543641_F9_6558.jpg | What key item or scene is captured in this photo? | Expression of plexins and neuropilins in late stages of spinal cord development. At stage 40, the latest stage we analyzed, plexin expression still changed. The most prominent change was found for plexinB1, which was now restricted to the white matter (arrow; high magnification shown in A). Strong expression in the dorsal spinal cord was still found for plexinA2, C1, and npn-1 (arrowhead). Few positive motor neurons were still found for plexinA1, A2, npn-1, and npn-2 (open arrowheads). DRGs maintained expression of plexinA4, C1, and npn-1 (asterisk). Single scattered cells were still expressing plexinA1 and A2. Panels A – C show high magnifications of a section processed by in situ hybridization to detect plexinB1 (A). Adjacent sections were stained with antibodies recognizing the oligodendrocyte marker O4 (B) and the astrocyte marker GFAP (C). Bar 500 μm for in situ hybridizations of plexins and neuropilins and 200 μm for panels A-C. |
PMC1543641_F9_6559.jpg | Can you identify the primary element in this image? | Expression of plexins and neuropilins in late stages of spinal cord development. At stage 40, the latest stage we analyzed, plexin expression still changed. The most prominent change was found for plexinB1, which was now restricted to the white matter (arrow; high magnification shown in A). Strong expression in the dorsal spinal cord was still found for plexinA2, C1, and npn-1 (arrowhead). Few positive motor neurons were still found for plexinA1, A2, npn-1, and npn-2 (open arrowheads). DRGs maintained expression of plexinA4, C1, and npn-1 (asterisk). Single scattered cells were still expressing plexinA1 and A2. Panels A – C show high magnifications of a section processed by in situ hybridization to detect plexinB1 (A). Adjacent sections were stained with antibodies recognizing the oligodendrocyte marker O4 (B) and the astrocyte marker GFAP (C). Bar 500 μm for in situ hybridizations of plexins and neuropilins and 200 μm for panels A-C. |
PMC1543641_F9_6562.jpg | What is the main focus of this visual representation? | Expression of plexins and neuropilins in late stages of spinal cord development. At stage 40, the latest stage we analyzed, plexin expression still changed. The most prominent change was found for plexinB1, which was now restricted to the white matter (arrow; high magnification shown in A). Strong expression in the dorsal spinal cord was still found for plexinA2, C1, and npn-1 (arrowhead). Few positive motor neurons were still found for plexinA1, A2, npn-1, and npn-2 (open arrowheads). DRGs maintained expression of plexinA4, C1, and npn-1 (asterisk). Single scattered cells were still expressing plexinA1 and A2. Panels A – C show high magnifications of a section processed by in situ hybridization to detect plexinB1 (A). Adjacent sections were stained with antibodies recognizing the oligodendrocyte marker O4 (B) and the astrocyte marker GFAP (C). Bar 500 μm for in situ hybridizations of plexins and neuropilins and 200 μm for panels A-C. |
PMC1543641_F9_6561.jpg | What stands out most in this visual? | Expression of plexins and neuropilins in late stages of spinal cord development. At stage 40, the latest stage we analyzed, plexin expression still changed. The most prominent change was found for plexinB1, which was now restricted to the white matter (arrow; high magnification shown in A). Strong expression in the dorsal spinal cord was still found for plexinA2, C1, and npn-1 (arrowhead). Few positive motor neurons were still found for plexinA1, A2, npn-1, and npn-2 (open arrowheads). DRGs maintained expression of plexinA4, C1, and npn-1 (asterisk). Single scattered cells were still expressing plexinA1 and A2. Panels A – C show high magnifications of a section processed by in situ hybridization to detect plexinB1 (A). Adjacent sections were stained with antibodies recognizing the oligodendrocyte marker O4 (B) and the astrocyte marker GFAP (C). Bar 500 μm for in situ hybridizations of plexins and neuropilins and 200 μm for panels A-C. |
PMC1543641_F9_6560.jpg | What object or scene is depicted here? | Expression of plexins and neuropilins in late stages of spinal cord development. At stage 40, the latest stage we analyzed, plexin expression still changed. The most prominent change was found for plexinB1, which was now restricted to the white matter (arrow; high magnification shown in A). Strong expression in the dorsal spinal cord was still found for plexinA2, C1, and npn-1 (arrowhead). Few positive motor neurons were still found for plexinA1, A2, npn-1, and npn-2 (open arrowheads). DRGs maintained expression of plexinA4, C1, and npn-1 (asterisk). Single scattered cells were still expressing plexinA1 and A2. Panels A – C show high magnifications of a section processed by in situ hybridization to detect plexinB1 (A). Adjacent sections were stained with antibodies recognizing the oligodendrocyte marker O4 (B) and the astrocyte marker GFAP (C). Bar 500 μm for in situ hybridizations of plexins and neuropilins and 200 μm for panels A-C. |
PMC1543659_F2_6575.jpg | What is the focal point of this photograph? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6569.jpg | Can you identify the primary element in this image? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6564.jpg | What can you see in this picture? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6567.jpg | What does this image primarily show? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6572.jpg | Can you identify the primary element in this image? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6577.jpg | What can you see in this picture? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6566.jpg | Can you identify the primary element in this image? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6578.jpg | What is the dominant medical problem in this image? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6571.jpg | What's the most prominent thing you notice in this picture? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6573.jpg | What is the dominant medical problem in this image? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6579.jpg | Describe the main subject of this image. | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6563.jpg | What is the core subject represented in this visual? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6576.jpg | What's the most prominent thing you notice in this picture? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6570.jpg | What is shown in this image? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6568.jpg | What is the focal point of this photograph? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6574.jpg | What can you see in this picture? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1543659_F2_6565.jpg | What is the dominant medical problem in this image? | Severe iris disease in double-congenic B6. Tyrp1b GpnmbR150X mice. Cohorts of B6.Tyrp1isa GpnmbR150X mice were aged and analyzed by slit-lamp examination; representative eyes of indicated ages are shown. Each row contains three images of the same eye. The left column shows broad-beam illumination. The middle column shows transillumination defects. The right column shows the relative dimensions of the anterior chamber. The degree of pigment dispersion and iris atrophy is remarkably similar in both timing and severity to that of D2 mice (see reference [19] for comparable image of D2 eyes). (A to C) Until 5 months, B6.Tyrp1bGpnmbR150X eyes were indistinguishable from wild-type, with a complex iris morphology, no transillumination, and anterior chambers of normal dimension with a closely juxtaposed cornea and iris. (D to F) By 6 months, all B6.Tyrp1b GpnmbR150X eyes exhibit a clear phenotype characterized by slight swelling of peripupillary tissue. This timing and phenotype closely resembles the initial stages of the D2 iris disease. (G to I) In 9-month-old eyes, the peripupillary region becomes notably atrophic, transillumination is obvious, and dispersed pigment is present on both the lens and cornea. Beyond this age, a steadily worsening course ensues, which at (J to L) 12 months, (M to O) 14 months, and (P to R) 18 months is characterized by increasing degrees of iris atrophy that include full-thickness iris holes, profound transillumination, pigment dispersion and frequent pigment accumulation on the lens and cornea, and changes to the dimensions of the anterior chamber. No sex-specific differences were evident in these phenotypes. This synopsis of disease progression involved >146 eyes aged 2–20+ months, with each of the cohorts described above involving groups of at least 14 eyes. |
PMC1544328_F9_6585.jpg | What is the core subject represented in this visual? | Immunofluorescence localisation of epitope tagged TcSOD A. Cells were induced as in Fig [8]. The parasites were fixed in paraformaldehyde and stained with mouse monoclonal anti-c-myc 9E10. Slides were examined on a Zeiss LSM 510 confocal microscope. The epitope tagged protein is shown as green fluorescence with the DNA stained red. Arrows indicate the strong staining of a structure adjacent to the kinetoplast (K). The nucleus is indicated (N). The white bar indicates 5 μm. The phase image is shown for comparison. Both images show cells in the process of dividing. |
PMC1544328_F9_6582.jpg | What object or scene is depicted here? | Immunofluorescence localisation of epitope tagged TcSOD A. Cells were induced as in Fig [8]. The parasites were fixed in paraformaldehyde and stained with mouse monoclonal anti-c-myc 9E10. Slides were examined on a Zeiss LSM 510 confocal microscope. The epitope tagged protein is shown as green fluorescence with the DNA stained red. Arrows indicate the strong staining of a structure adjacent to the kinetoplast (K). The nucleus is indicated (N). The white bar indicates 5 μm. The phase image is shown for comparison. Both images show cells in the process of dividing. |
PMC1544339_F3_6586.jpg | What is the principal component of this image? | Electron Tomographic image of a single square cell of H, walsbyi. In agreement with previous observations, gas vesicles (GV) recognized by their spindle shape are found at the borders of the cell. The large number of circular electron-dense bodies are most likely poly-3-hydroxy-butyric acid (PHB) polymers consistent with Nile-Blue staining patterns [4]. The genes encoding PHB biosynthesis proteins have been identified (image by H. Engelhardt). |
PMC1544348_F1_6587.jpg | What can you see in this picture? | Cytology of HTN. Papanicolaou stained fine-needle aspiration of hyalinizing trabecular neoplasm showing elongated tumor enveloped by or associated with acellular stroma. The tumor cells demonstrate nuclear features of papillary carcinoma (arrow and inset). |
PMC1550223_F7_6601.jpg | What is the main focus of this visual representation? | 3D CLSM reconstruction: the serial plan scanning imaging shows the complete micro-fracture of the apical screw. |
PMC1550223_F7_6597.jpg | What can you see in this picture? | 3D CLSM reconstruction: the serial plan scanning imaging shows the complete micro-fracture of the apical screw. |
PMC1550223_F7_6594.jpg | What stands out most in this visual? | 3D CLSM reconstruction: the serial plan scanning imaging shows the complete micro-fracture of the apical screw. |
PMC1550223_F7_6593.jpg | What is being portrayed in this visual content? | 3D CLSM reconstruction: the serial plan scanning imaging shows the complete micro-fracture of the apical screw. |
PMC1550223_F7_6596.jpg | What's the most prominent thing you notice in this picture? | 3D CLSM reconstruction: the serial plan scanning imaging shows the complete micro-fracture of the apical screw. |
PMC1550223_F7_6590.jpg | What can you see in this picture? | 3D CLSM reconstruction: the serial plan scanning imaging shows the complete micro-fracture of the apical screw. |
PMC1550223_F7_6598.jpg | What is the central feature of this picture? | 3D CLSM reconstruction: the serial plan scanning imaging shows the complete micro-fracture of the apical screw. |
PMC1550223_F7_6591.jpg | What is the principal component of this image? | 3D CLSM reconstruction: the serial plan scanning imaging shows the complete micro-fracture of the apical screw. |
PMC1550223_F7_6595.jpg | What is the core subject represented in this visual? | 3D CLSM reconstruction: the serial plan scanning imaging shows the complete micro-fracture of the apical screw. |
PMC1550228_F4_6602.jpg | What stands out most in this visual? | 3D reconstruction of the tidemark. This shows a composite photograph made by cutting around the cartilage prolongations on the individual photographs from Figure 3 and then overlaying them. |
PMC1550235_F4_6604.jpg | What key item or scene is captured in this photo? | mGlu2/3 expression in DRG neuronal cultures following the inhibition of the NF-κB transcriptional activity. (A-B) Immunocytochemical analysis of mGlu2/3 in mouse DRG cultures treated with vehicle or CAPE (2.5 μg/ml for 30 min) respectively. (C) Upper Panel: In-Cell western image for mGluR2/3 (green fluorescence) and MAP-2 (red fluorescence) in mouse DRG cultures in the absence or presence of CAPE (2.5 μg/ml for 30 min). Lower panel: Quantification of mGlu2/3 expression normalized to MAP-2 protein expression. Infrared fluorescence levels were measured 4 days after CAPE incubation. Results are expressed as the mean ± SEM of 6 different determinations. *p < 0.05, vs vehicle (Student's t test). |
PMC1550235_F4_6603.jpg | Can you identify the primary element in this image? | mGlu2/3 expression in DRG neuronal cultures following the inhibition of the NF-κB transcriptional activity. (A-B) Immunocytochemical analysis of mGlu2/3 in mouse DRG cultures treated with vehicle or CAPE (2.5 μg/ml for 30 min) respectively. (C) Upper Panel: In-Cell western image for mGluR2/3 (green fluorescence) and MAP-2 (red fluorescence) in mouse DRG cultures in the absence or presence of CAPE (2.5 μg/ml for 30 min). Lower panel: Quantification of mGlu2/3 expression normalized to MAP-2 protein expression. Infrared fluorescence levels were measured 4 days after CAPE incubation. Results are expressed as the mean ± SEM of 6 different determinations. *p < 0.05, vs vehicle (Student's t test). |
PMC1550235_F4_6606.jpg | What is the dominant medical problem in this image? | mGlu2/3 expression in DRG neuronal cultures following the inhibition of the NF-κB transcriptional activity. (A-B) Immunocytochemical analysis of mGlu2/3 in mouse DRG cultures treated with vehicle or CAPE (2.5 μg/ml for 30 min) respectively. (C) Upper Panel: In-Cell western image for mGluR2/3 (green fluorescence) and MAP-2 (red fluorescence) in mouse DRG cultures in the absence or presence of CAPE (2.5 μg/ml for 30 min). Lower panel: Quantification of mGlu2/3 expression normalized to MAP-2 protein expression. Infrared fluorescence levels were measured 4 days after CAPE incubation. Results are expressed as the mean ± SEM of 6 different determinations. *p < 0.05, vs vehicle (Student's t test). |
PMC1550242_F1_6607.jpg | What can you see in this picture? | ERα and ERβ immunofluorescence labelling of morphologically normal spermatozoa and spermatozoa carrying superfluous cytoplasm A: ERα red brilliant light (Texas-Red) in excess residual cytoplasm of immature spermatozoa. A1: ERα fluorescence in mid-piece regions of normal sperm. B: ERβ green intense light (FITC) in excess residual cytoplasm and tails of immature spermatozoa. B1: ERβ fluorescence in mid-piece regions and tails of normal sperm. Scale bars 5 μm. |
PMC1550242_F1_6610.jpg | What can you see in this picture? | ERα and ERβ immunofluorescence labelling of morphologically normal spermatozoa and spermatozoa carrying superfluous cytoplasm A: ERα red brilliant light (Texas-Red) in excess residual cytoplasm of immature spermatozoa. A1: ERα fluorescence in mid-piece regions of normal sperm. B: ERβ green intense light (FITC) in excess residual cytoplasm and tails of immature spermatozoa. B1: ERβ fluorescence in mid-piece regions and tails of normal sperm. Scale bars 5 μm. |
PMC1550242_F1_6608.jpg | What object or scene is depicted here? | ERα and ERβ immunofluorescence labelling of morphologically normal spermatozoa and spermatozoa carrying superfluous cytoplasm A: ERα red brilliant light (Texas-Red) in excess residual cytoplasm of immature spermatozoa. A1: ERα fluorescence in mid-piece regions of normal sperm. B: ERβ green intense light (FITC) in excess residual cytoplasm and tails of immature spermatozoa. B1: ERβ fluorescence in mid-piece regions and tails of normal sperm. Scale bars 5 μm. |
PMC1550242_F1_6609.jpg | What is shown in this image? | ERα and ERβ immunofluorescence labelling of morphologically normal spermatozoa and spermatozoa carrying superfluous cytoplasm A: ERα red brilliant light (Texas-Red) in excess residual cytoplasm of immature spermatozoa. A1: ERα fluorescence in mid-piece regions of normal sperm. B: ERβ green intense light (FITC) in excess residual cytoplasm and tails of immature spermatozoa. B1: ERβ fluorescence in mid-piece regions and tails of normal sperm. Scale bars 5 μm. |
PMC1550243_F10_6611.jpg | What can you see in this picture? | Multiple fluorescence 2PE imaging. 2PE multiple fluorescence image from a 16 μm cryostat section of mouse intestine stained with a combination of fluorescent stains (F-24631, Molecular Probes). Alexa Fluor 350 wheat germ agglutinin, a blue-fluorescent lectin, was used to stain the mucus of goblet cells. The filamentous actin prevalent in the brush border was stained with red-fluorescent Alexa Flu or 568 phalloidin. Finally, the nuclei were stained with SYTOX ® Green nucleic acid stain. Imaging has been performed at 780 nm, 100 x 1.4 NA Leica objective, using a Chameleon XR ultrafast Ti-Sapphire laser (Coherent Inc., USA) coupled at LAMBS-MicroScoBio with a Spectral Confocal Laser Scanning Microscope, Leica SP2-AOBS. |
PMC1550243_F11_6613.jpg | What key item or scene is captured in this photo? | 3D and 2D fluorescence projections. Pictorial representation of the 3D and 2D projections of multiple fluorescence from a marine sponge, Chondrilla nucula. The specimen has been loaded with Alexa 488 fluorescent molecules specific aminobutirric acid (GABA) emitting in green, DAPI for nuclear DNA for the blu component. Red signals are due to the autofluorescence from symbiontic bacteria contamination. Imaging has been perfomed using a Chameleon XR ultrafast Ti-Sapphire laser (Coherent Inc., USA) coupled at LAMBS-MicroScoBio with a Spectral Confocal Laser Scanning Microscope, Leica SP2-AOBS. (Sample availability and preparation, courtesy of Renata Manconi, University of Sassari, Roberto Pronzato and Lorenzo Gallus, University of Genoa). |
PMC1550268_ppat-0020085-g002_6651.jpg | What can you see in this picture? | Actin Filaments Form in the Nuclei of PRV-Infected Neurons(A) Confocal images are 2-D projections from five consecutive layers in an image stack, taken 0.5 μm apart. GFP-VP26 is visualized by direct fluorescence. Scale bar = 20 μm. An enlargement of one of the nuclei is shown for clarity. Scale bar for enlargement = 10 μm.(B) Quantitation of actin filament formation within nuclei (infected versus mock-infected neurons). |
PMC1550268_ppat-0020085-g002_6650.jpg | What can you see in this picture? | Actin Filaments Form in the Nuclei of PRV-Infected Neurons(A) Confocal images are 2-D projections from five consecutive layers in an image stack, taken 0.5 μm apart. GFP-VP26 is visualized by direct fluorescence. Scale bar = 20 μm. An enlargement of one of the nuclei is shown for clarity. Scale bar for enlargement = 10 μm.(B) Quantitation of actin filament formation within nuclei (infected versus mock-infected neurons). |
PMC1550268_ppat-0020085-g002_6652.jpg | Can you identify the primary element in this image? | Actin Filaments Form in the Nuclei of PRV-Infected Neurons(A) Confocal images are 2-D projections from five consecutive layers in an image stack, taken 0.5 μm apart. GFP-VP26 is visualized by direct fluorescence. Scale bar = 20 μm. An enlargement of one of the nuclei is shown for clarity. Scale bar for enlargement = 10 μm.(B) Quantitation of actin filament formation within nuclei (infected versus mock-infected neurons). |
PMC1550268_ppat-0020085-g002_6654.jpg | What does this image primarily show? | Actin Filaments Form in the Nuclei of PRV-Infected Neurons(A) Confocal images are 2-D projections from five consecutive layers in an image stack, taken 0.5 μm apart. GFP-VP26 is visualized by direct fluorescence. Scale bar = 20 μm. An enlargement of one of the nuclei is shown for clarity. Scale bar for enlargement = 10 μm.(B) Quantitation of actin filament formation within nuclei (infected versus mock-infected neurons). |
PMC1550268_ppat-0020085-g002_6648.jpg | What does this image primarily show? | Actin Filaments Form in the Nuclei of PRV-Infected Neurons(A) Confocal images are 2-D projections from five consecutive layers in an image stack, taken 0.5 μm apart. GFP-VP26 is visualized by direct fluorescence. Scale bar = 20 μm. An enlargement of one of the nuclei is shown for clarity. Scale bar for enlargement = 10 μm.(B) Quantitation of actin filament formation within nuclei (infected versus mock-infected neurons). |
PMC1550268_ppat-0020085-g002_6646.jpg | What is the dominant medical problem in this image? | Actin Filaments Form in the Nuclei of PRV-Infected Neurons(A) Confocal images are 2-D projections from five consecutive layers in an image stack, taken 0.5 μm apart. GFP-VP26 is visualized by direct fluorescence. Scale bar = 20 μm. An enlargement of one of the nuclei is shown for clarity. Scale bar for enlargement = 10 μm.(B) Quantitation of actin filament formation within nuclei (infected versus mock-infected neurons). |
PMC1550268_ppat-0020085-g003_6624.jpg | What is the central feature of this picture? | Polarity of Nuclear Actin Filaments Reflect the Overall Polarity of the CellNeurons were stained with AF568-phalloidin, anti-GM130 to stain the Golgi. GFP-VP26 is visualized by direct fluorescence. Each image is a 2-D projection from four consecutive layers in a confocal image stack, taken 0.5 μm apart. Scale bar = 20 μm. Top two rows show polarized SCG neurons with one axon. Bottom row shows a single SCG neuron with two axons emanating from opposite sides of the cell body. |
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