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PMC1764718_pone-0000156-g006_8333.jpg | What is the focal point of this photograph? | Good survival of F3.VEGF human neural stem cells pre-labeled with adeno-LacZ (β-gal) was found in hemorrhage core or lesion border of experimental ICH mouse brain 8 weeks post-transplantation. A large number of LacZ+ F3.VEGF human neural stem cells were found to migrate to contralateral side of hemisphere via corpus callosum (A). Higher magnification of migrating F3.VEGF cells is also shown (B–D). LacZ+ F3.VEGF cells differentiate into neurons as shown by β-gal+/NF-L+ (E–G), β-gal+NF-H+ (H–J) and β-gal/MAP2 (K–M) and also into astrocytes as demonstrated by β-gal+/GFAP+ staining (N–P). Bar indicates 50 µm. |
PMC1764718_pone-0000156-g006_8326.jpg | What is the main focus of this visual representation? | Good survival of F3.VEGF human neural stem cells pre-labeled with adeno-LacZ (β-gal) was found in hemorrhage core or lesion border of experimental ICH mouse brain 8 weeks post-transplantation. A large number of LacZ+ F3.VEGF human neural stem cells were found to migrate to contralateral side of hemisphere via corpus callosum (A). Higher magnification of migrating F3.VEGF cells is also shown (B–D). LacZ+ F3.VEGF cells differentiate into neurons as shown by β-gal+/NF-L+ (E–G), β-gal+NF-H+ (H–J) and β-gal/MAP2 (K–M) and also into astrocytes as demonstrated by β-gal+/GFAP+ staining (N–P). Bar indicates 50 µm. |
PMC1764718_pone-0000156-g006_8336.jpg | What stands out most in this visual? | Good survival of F3.VEGF human neural stem cells pre-labeled with adeno-LacZ (β-gal) was found in hemorrhage core or lesion border of experimental ICH mouse brain 8 weeks post-transplantation. A large number of LacZ+ F3.VEGF human neural stem cells were found to migrate to contralateral side of hemisphere via corpus callosum (A). Higher magnification of migrating F3.VEGF cells is also shown (B–D). LacZ+ F3.VEGF cells differentiate into neurons as shown by β-gal+/NF-L+ (E–G), β-gal+NF-H+ (H–J) and β-gal/MAP2 (K–M) and also into astrocytes as demonstrated by β-gal+/GFAP+ staining (N–P). Bar indicates 50 µm. |
PMC1764718_pone-0000156-g006_8327.jpg | What is the core subject represented in this visual? | Good survival of F3.VEGF human neural stem cells pre-labeled with adeno-LacZ (β-gal) was found in hemorrhage core or lesion border of experimental ICH mouse brain 8 weeks post-transplantation. A large number of LacZ+ F3.VEGF human neural stem cells were found to migrate to contralateral side of hemisphere via corpus callosum (A). Higher magnification of migrating F3.VEGF cells is also shown (B–D). LacZ+ F3.VEGF cells differentiate into neurons as shown by β-gal+/NF-L+ (E–G), β-gal+NF-H+ (H–J) and β-gal/MAP2 (K–M) and also into astrocytes as demonstrated by β-gal+/GFAP+ staining (N–P). Bar indicates 50 µm. |
PMC1764718_pone-0000156-g006_8330.jpg | What key item or scene is captured in this photo? | Good survival of F3.VEGF human neural stem cells pre-labeled with adeno-LacZ (β-gal) was found in hemorrhage core or lesion border of experimental ICH mouse brain 8 weeks post-transplantation. A large number of LacZ+ F3.VEGF human neural stem cells were found to migrate to contralateral side of hemisphere via corpus callosum (A). Higher magnification of migrating F3.VEGF cells is also shown (B–D). LacZ+ F3.VEGF cells differentiate into neurons as shown by β-gal+/NF-L+ (E–G), β-gal+NF-H+ (H–J) and β-gal/MAP2 (K–M) and also into astrocytes as demonstrated by β-gal+/GFAP+ staining (N–P). Bar indicates 50 µm. |
PMC1764718_pone-0000156-g006_8338.jpg | What is the core subject represented in this visual? | Good survival of F3.VEGF human neural stem cells pre-labeled with adeno-LacZ (β-gal) was found in hemorrhage core or lesion border of experimental ICH mouse brain 8 weeks post-transplantation. A large number of LacZ+ F3.VEGF human neural stem cells were found to migrate to contralateral side of hemisphere via corpus callosum (A). Higher magnification of migrating F3.VEGF cells is also shown (B–D). LacZ+ F3.VEGF cells differentiate into neurons as shown by β-gal+/NF-L+ (E–G), β-gal+NF-H+ (H–J) and β-gal/MAP2 (K–M) and also into astrocytes as demonstrated by β-gal+/GFAP+ staining (N–P). Bar indicates 50 µm. |
PMC1764722_F4_8342.jpg | What key item or scene is captured in this photo? | 4a shows a tortuous small fistula between the proximal right coronary artery and the pulmonary trunk, which has been closed with controlled-release coils (4b). Figure 4c shows a tortuous fistula between the left anterior descending coronary artery and the pulmonary trunk in the same patient, which has been closed also with controlled-release coils (4d). |
PMC1764722_F4_8343.jpg | What is the dominant medical problem in this image? | 4a shows a tortuous small fistula between the proximal right coronary artery and the pulmonary trunk, which has been closed with controlled-release coils (4b). Figure 4c shows a tortuous fistula between the left anterior descending coronary artery and the pulmonary trunk in the same patient, which has been closed also with controlled-release coils (4d). |
PMC1764722_F4_8344.jpg | What is the central feature of this picture? | 4a shows a tortuous small fistula between the proximal right coronary artery and the pulmonary trunk, which has been closed with controlled-release coils (4b). Figure 4c shows a tortuous fistula between the left anterior descending coronary artery and the pulmonary trunk in the same patient, which has been closed also with controlled-release coils (4d). |
PMC1764722_F4_8345.jpg | What object or scene is depicted here? | 4a shows a tortuous small fistula between the proximal right coronary artery and the pulmonary trunk, which has been closed with controlled-release coils (4b). Figure 4c shows a tortuous fistula between the left anterior descending coronary artery and the pulmonary trunk in the same patient, which has been closed also with controlled-release coils (4d). |
PMC1764728_F5_8349.jpg | What is the main focus of this visual representation? | COX-2 and NeuN double stains 24 hours and one week after tMCAo. The COX-2 IHC was developed with nickel-enhanced DAB (black), whereas NeuN was visualized with NovaRed® (brownish red). The images 5A and 5B are obtained from a pilot study where the animal was euthanized 24 hours after tMCAo. 5A visualizes a relatively small neocortical infarct in the right hemisphere. The box delineates a part of the ischemic border zone that is shown at forty times magnification in 5B. The penumbra contains large swollen neurons that express the membrane-bound COX-2 enzyme. In the infarct core the neurons tend to be small and star-shaped due to irreversible neuronal death. 5C and 5E are from a saline-treated animal one week after tMCAo. Forty times magnifications of the boxes are shown in 5D and 5F. The neurons in the border zone on Day 8 after ischemic injury showed a perinuclear expression pattern of the COX-2 enzyme (5D). COX-2+ neurons can be found in areas like the neocortex, piriform cortex and the DG of the hippocampus under normal conditions. 5F shows COX-2 expressed in dendrites of neurons in the molecular cell layer of the DG. The scale bar in 5A is 5 mm, whereas the scale bars in 5B, 5D and 5F equals 50 μm. |
PMC1764728_F5_8348.jpg | Can you identify the primary element in this image? | COX-2 and NeuN double stains 24 hours and one week after tMCAo. The COX-2 IHC was developed with nickel-enhanced DAB (black), whereas NeuN was visualized with NovaRed® (brownish red). The images 5A and 5B are obtained from a pilot study where the animal was euthanized 24 hours after tMCAo. 5A visualizes a relatively small neocortical infarct in the right hemisphere. The box delineates a part of the ischemic border zone that is shown at forty times magnification in 5B. The penumbra contains large swollen neurons that express the membrane-bound COX-2 enzyme. In the infarct core the neurons tend to be small and star-shaped due to irreversible neuronal death. 5C and 5E are from a saline-treated animal one week after tMCAo. Forty times magnifications of the boxes are shown in 5D and 5F. The neurons in the border zone on Day 8 after ischemic injury showed a perinuclear expression pattern of the COX-2 enzyme (5D). COX-2+ neurons can be found in areas like the neocortex, piriform cortex and the DG of the hippocampus under normal conditions. 5F shows COX-2 expressed in dendrites of neurons in the molecular cell layer of the DG. The scale bar in 5A is 5 mm, whereas the scale bars in 5B, 5D and 5F equals 50 μm. |
PMC1764728_F5_8351.jpg | What can you see in this picture? | COX-2 and NeuN double stains 24 hours and one week after tMCAo. The COX-2 IHC was developed with nickel-enhanced DAB (black), whereas NeuN was visualized with NovaRed® (brownish red). The images 5A and 5B are obtained from a pilot study where the animal was euthanized 24 hours after tMCAo. 5A visualizes a relatively small neocortical infarct in the right hemisphere. The box delineates a part of the ischemic border zone that is shown at forty times magnification in 5B. The penumbra contains large swollen neurons that express the membrane-bound COX-2 enzyme. In the infarct core the neurons tend to be small and star-shaped due to irreversible neuronal death. 5C and 5E are from a saline-treated animal one week after tMCAo. Forty times magnifications of the boxes are shown in 5D and 5F. The neurons in the border zone on Day 8 after ischemic injury showed a perinuclear expression pattern of the COX-2 enzyme (5D). COX-2+ neurons can be found in areas like the neocortex, piriform cortex and the DG of the hippocampus under normal conditions. 5F shows COX-2 expressed in dendrites of neurons in the molecular cell layer of the DG. The scale bar in 5A is 5 mm, whereas the scale bars in 5B, 5D and 5F equals 50 μm. |
PMC1764728_F5_8346.jpg | What is the core subject represented in this visual? | COX-2 and NeuN double stains 24 hours and one week after tMCAo. The COX-2 IHC was developed with nickel-enhanced DAB (black), whereas NeuN was visualized with NovaRed® (brownish red). The images 5A and 5B are obtained from a pilot study where the animal was euthanized 24 hours after tMCAo. 5A visualizes a relatively small neocortical infarct in the right hemisphere. The box delineates a part of the ischemic border zone that is shown at forty times magnification in 5B. The penumbra contains large swollen neurons that express the membrane-bound COX-2 enzyme. In the infarct core the neurons tend to be small and star-shaped due to irreversible neuronal death. 5C and 5E are from a saline-treated animal one week after tMCAo. Forty times magnifications of the boxes are shown in 5D and 5F. The neurons in the border zone on Day 8 after ischemic injury showed a perinuclear expression pattern of the COX-2 enzyme (5D). COX-2+ neurons can be found in areas like the neocortex, piriform cortex and the DG of the hippocampus under normal conditions. 5F shows COX-2 expressed in dendrites of neurons in the molecular cell layer of the DG. The scale bar in 5A is 5 mm, whereas the scale bars in 5B, 5D and 5F equals 50 μm. |
PMC1764728_F5_8347.jpg | What is the principal component of this image? | COX-2 and NeuN double stains 24 hours and one week after tMCAo. The COX-2 IHC was developed with nickel-enhanced DAB (black), whereas NeuN was visualized with NovaRed® (brownish red). The images 5A and 5B are obtained from a pilot study where the animal was euthanized 24 hours after tMCAo. 5A visualizes a relatively small neocortical infarct in the right hemisphere. The box delineates a part of the ischemic border zone that is shown at forty times magnification in 5B. The penumbra contains large swollen neurons that express the membrane-bound COX-2 enzyme. In the infarct core the neurons tend to be small and star-shaped due to irreversible neuronal death. 5C and 5E are from a saline-treated animal one week after tMCAo. Forty times magnifications of the boxes are shown in 5D and 5F. The neurons in the border zone on Day 8 after ischemic injury showed a perinuclear expression pattern of the COX-2 enzyme (5D). COX-2+ neurons can be found in areas like the neocortex, piriform cortex and the DG of the hippocampus under normal conditions. 5F shows COX-2 expressed in dendrites of neurons in the molecular cell layer of the DG. The scale bar in 5A is 5 mm, whereas the scale bars in 5B, 5D and 5F equals 50 μm. |
PMC1764728_F5_8350.jpg | What object or scene is depicted here? | COX-2 and NeuN double stains 24 hours and one week after tMCAo. The COX-2 IHC was developed with nickel-enhanced DAB (black), whereas NeuN was visualized with NovaRed® (brownish red). The images 5A and 5B are obtained from a pilot study where the animal was euthanized 24 hours after tMCAo. 5A visualizes a relatively small neocortical infarct in the right hemisphere. The box delineates a part of the ischemic border zone that is shown at forty times magnification in 5B. The penumbra contains large swollen neurons that express the membrane-bound COX-2 enzyme. In the infarct core the neurons tend to be small and star-shaped due to irreversible neuronal death. 5C and 5E are from a saline-treated animal one week after tMCAo. Forty times magnifications of the boxes are shown in 5D and 5F. The neurons in the border zone on Day 8 after ischemic injury showed a perinuclear expression pattern of the COX-2 enzyme (5D). COX-2+ neurons can be found in areas like the neocortex, piriform cortex and the DG of the hippocampus under normal conditions. 5F shows COX-2 expressed in dendrites of neurons in the molecular cell layer of the DG. The scale bar in 5A is 5 mm, whereas the scale bars in 5B, 5D and 5F equals 50 μm. |
PMC1764728_F9_8358.jpg | What is the central feature of this picture? | BrdU, ED-1 and NeuN stains one week after tMCAo. 9A to 9F show the IHC for BrdU and ED-1. BrdU was developed with nickel-enhanced DAB (black), whereas the activated microglia marker ED-1 was visualized with NovaRed® (brownish red). 9A shows a representative example of a tMCAo animal one week after surgery. Four and forty time magnifications of the boxes in 9A and 9B are shown in 9B and 9C, respectively. The BrdU+ cells are typically found in clusters in the subgranular cell layer in DG. Our counting procedure started with delineating the DG. Hereafter, the BrdU+ cells in the whole DG were counted at forty times magnification (9C). We generally observed a very scarce ED-1 expression in the DG unless the hippocampus was directly affected by ischemic injury. 9D to 9I show an example of ischemia affecting the right hippocampus. The boxed area in 9D is shown at higher magnification in 9E. Activated microglia was abundantly seen in a part of the CA-1 and the whole DG. 9F shows a forty time magnification of the box in 9E. Clearly, activated microglia had an intimate relation to an increasing number of BrdU+ cells. Panel 9G to 9I show NeuN IHC developed with nickel-enhanced DAB. 9G and 9H correspond to 9D and 9E. The boxed area in 9H of the CA-1 is shown at forty time magnification in 9I. Note the ischemic degeneration of this part of the CA-1. The scale bar in 9A is 5 mm. In 9B the scale bar represents 300 mm, and in 9E and 9H 1 mm. The scale bars in 9C, 9F and 9I equals 50 μm. |
PMC1764728_F9_8360.jpg | What is the principal component of this image? | BrdU, ED-1 and NeuN stains one week after tMCAo. 9A to 9F show the IHC for BrdU and ED-1. BrdU was developed with nickel-enhanced DAB (black), whereas the activated microglia marker ED-1 was visualized with NovaRed® (brownish red). 9A shows a representative example of a tMCAo animal one week after surgery. Four and forty time magnifications of the boxes in 9A and 9B are shown in 9B and 9C, respectively. The BrdU+ cells are typically found in clusters in the subgranular cell layer in DG. Our counting procedure started with delineating the DG. Hereafter, the BrdU+ cells in the whole DG were counted at forty times magnification (9C). We generally observed a very scarce ED-1 expression in the DG unless the hippocampus was directly affected by ischemic injury. 9D to 9I show an example of ischemia affecting the right hippocampus. The boxed area in 9D is shown at higher magnification in 9E. Activated microglia was abundantly seen in a part of the CA-1 and the whole DG. 9F shows a forty time magnification of the box in 9E. Clearly, activated microglia had an intimate relation to an increasing number of BrdU+ cells. Panel 9G to 9I show NeuN IHC developed with nickel-enhanced DAB. 9G and 9H correspond to 9D and 9E. The boxed area in 9H of the CA-1 is shown at forty time magnification in 9I. Note the ischemic degeneration of this part of the CA-1. The scale bar in 9A is 5 mm. In 9B the scale bar represents 300 mm, and in 9E and 9H 1 mm. The scale bars in 9C, 9F and 9I equals 50 μm. |
PMC1764728_F9_8356.jpg | What is the main focus of this visual representation? | BrdU, ED-1 and NeuN stains one week after tMCAo. 9A to 9F show the IHC for BrdU and ED-1. BrdU was developed with nickel-enhanced DAB (black), whereas the activated microglia marker ED-1 was visualized with NovaRed® (brownish red). 9A shows a representative example of a tMCAo animal one week after surgery. Four and forty time magnifications of the boxes in 9A and 9B are shown in 9B and 9C, respectively. The BrdU+ cells are typically found in clusters in the subgranular cell layer in DG. Our counting procedure started with delineating the DG. Hereafter, the BrdU+ cells in the whole DG were counted at forty times magnification (9C). We generally observed a very scarce ED-1 expression in the DG unless the hippocampus was directly affected by ischemic injury. 9D to 9I show an example of ischemia affecting the right hippocampus. The boxed area in 9D is shown at higher magnification in 9E. Activated microglia was abundantly seen in a part of the CA-1 and the whole DG. 9F shows a forty time magnification of the box in 9E. Clearly, activated microglia had an intimate relation to an increasing number of BrdU+ cells. Panel 9G to 9I show NeuN IHC developed with nickel-enhanced DAB. 9G and 9H correspond to 9D and 9E. The boxed area in 9H of the CA-1 is shown at forty time magnification in 9I. Note the ischemic degeneration of this part of the CA-1. The scale bar in 9A is 5 mm. In 9B the scale bar represents 300 mm, and in 9E and 9H 1 mm. The scale bars in 9C, 9F and 9I equals 50 μm. |
PMC1764728_F9_8352.jpg | What is the focal point of this photograph? | BrdU, ED-1 and NeuN stains one week after tMCAo. 9A to 9F show the IHC for BrdU and ED-1. BrdU was developed with nickel-enhanced DAB (black), whereas the activated microglia marker ED-1 was visualized with NovaRed® (brownish red). 9A shows a representative example of a tMCAo animal one week after surgery. Four and forty time magnifications of the boxes in 9A and 9B are shown in 9B and 9C, respectively. The BrdU+ cells are typically found in clusters in the subgranular cell layer in DG. Our counting procedure started with delineating the DG. Hereafter, the BrdU+ cells in the whole DG were counted at forty times magnification (9C). We generally observed a very scarce ED-1 expression in the DG unless the hippocampus was directly affected by ischemic injury. 9D to 9I show an example of ischemia affecting the right hippocampus. The boxed area in 9D is shown at higher magnification in 9E. Activated microglia was abundantly seen in a part of the CA-1 and the whole DG. 9F shows a forty time magnification of the box in 9E. Clearly, activated microglia had an intimate relation to an increasing number of BrdU+ cells. Panel 9G to 9I show NeuN IHC developed with nickel-enhanced DAB. 9G and 9H correspond to 9D and 9E. The boxed area in 9H of the CA-1 is shown at forty time magnification in 9I. Note the ischemic degeneration of this part of the CA-1. The scale bar in 9A is 5 mm. In 9B the scale bar represents 300 mm, and in 9E and 9H 1 mm. The scale bars in 9C, 9F and 9I equals 50 μm. |
PMC1764728_F9_8355.jpg | What is the main focus of this visual representation? | BrdU, ED-1 and NeuN stains one week after tMCAo. 9A to 9F show the IHC for BrdU and ED-1. BrdU was developed with nickel-enhanced DAB (black), whereas the activated microglia marker ED-1 was visualized with NovaRed® (brownish red). 9A shows a representative example of a tMCAo animal one week after surgery. Four and forty time magnifications of the boxes in 9A and 9B are shown in 9B and 9C, respectively. The BrdU+ cells are typically found in clusters in the subgranular cell layer in DG. Our counting procedure started with delineating the DG. Hereafter, the BrdU+ cells in the whole DG were counted at forty times magnification (9C). We generally observed a very scarce ED-1 expression in the DG unless the hippocampus was directly affected by ischemic injury. 9D to 9I show an example of ischemia affecting the right hippocampus. The boxed area in 9D is shown at higher magnification in 9E. Activated microglia was abundantly seen in a part of the CA-1 and the whole DG. 9F shows a forty time magnification of the box in 9E. Clearly, activated microglia had an intimate relation to an increasing number of BrdU+ cells. Panel 9G to 9I show NeuN IHC developed with nickel-enhanced DAB. 9G and 9H correspond to 9D and 9E. The boxed area in 9H of the CA-1 is shown at forty time magnification in 9I. Note the ischemic degeneration of this part of the CA-1. The scale bar in 9A is 5 mm. In 9B the scale bar represents 300 mm, and in 9E and 9H 1 mm. The scale bars in 9C, 9F and 9I equals 50 μm. |
PMC1764728_F9_8357.jpg | What can you see in this picture? | BrdU, ED-1 and NeuN stains one week after tMCAo. 9A to 9F show the IHC for BrdU and ED-1. BrdU was developed with nickel-enhanced DAB (black), whereas the activated microglia marker ED-1 was visualized with NovaRed® (brownish red). 9A shows a representative example of a tMCAo animal one week after surgery. Four and forty time magnifications of the boxes in 9A and 9B are shown in 9B and 9C, respectively. The BrdU+ cells are typically found in clusters in the subgranular cell layer in DG. Our counting procedure started with delineating the DG. Hereafter, the BrdU+ cells in the whole DG were counted at forty times magnification (9C). We generally observed a very scarce ED-1 expression in the DG unless the hippocampus was directly affected by ischemic injury. 9D to 9I show an example of ischemia affecting the right hippocampus. The boxed area in 9D is shown at higher magnification in 9E. Activated microglia was abundantly seen in a part of the CA-1 and the whole DG. 9F shows a forty time magnification of the box in 9E. Clearly, activated microglia had an intimate relation to an increasing number of BrdU+ cells. Panel 9G to 9I show NeuN IHC developed with nickel-enhanced DAB. 9G and 9H correspond to 9D and 9E. The boxed area in 9H of the CA-1 is shown at forty time magnification in 9I. Note the ischemic degeneration of this part of the CA-1. The scale bar in 9A is 5 mm. In 9B the scale bar represents 300 mm, and in 9E and 9H 1 mm. The scale bars in 9C, 9F and 9I equals 50 μm. |
PMC1764729_F4_8371.jpg | What is the core subject represented in this visual? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8369.jpg | What is the principal component of this image? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8379.jpg | What is shown in this image? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8364.jpg | What is the core subject represented in this visual? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8368.jpg | What does this image primarily show? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8375.jpg | What object or scene is depicted here? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8378.jpg | Can you identify the primary element in this image? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8372.jpg | What stands out most in this visual? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8366.jpg | What stands out most in this visual? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8376.jpg | What is the central feature of this picture? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8365.jpg | What is the central feature of this picture? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8377.jpg | What object or scene is depicted here? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F4_8374.jpg | Can you identify the primary element in this image? | Repression of Tbx2 and Tbx5 expression by exogenous Noggin. (A) Post-culture embryo showing Tbx5 expression in the non-treated dorsal optic cup. (B) Contralateral Noggin-treated eye, showing absence of Tbx5 expression in the optic cup. (C) Post-culture embryo showing Tbx2 expression in the non-treated dorsal optic cup. (D) Contralateral Noggin-treated eye showing a reduced Tbx2 expression domain. Tbx5 expression (E, F) and Tbx2 expression (G, H) are not altered in non-operated and BSA-treated eyes respectively of post-culture embryos. A'-H' show higher magnifications of eyes in A-H. Arrows indicate boundaries of gene expression domains. Implanted beads are marked by asterisks. (I-P) Serial transverse vibratome sections through the optic cup showing altered morphology after Noggin treatment, with the dorsal-most sections in upper panels. (I-L) Post-culture non-treated eye showing invagination of the presumptive neural retina (P-NR) in the ventral optic cup. (M-P) Contralateral Noggin-treated eye showing dorsal extension of the optic stalk region as compared to the non-treated eye. (Q) Schematic representation of normal Tbx2 and Tbx5 expression domains in a lateral view of the optic cup, and the dorsal shift of the expression domains induced by exogenous Noggin. Scale bars: A-H, 0.5 mm; I-P, 0.1 mm. Abbreviations; MN, mandibular process of the first branchial arch; MX, maxillary process of the first branchial arch; N, nasal process; P-NR, presumptive neural retina; OS, optic stalk. |
PMC1764729_F6_8361.jpg | What is the focal point of this photograph? | Effect of BMP4 treatment on eye size and shape. (A) Retinal volume in BMP4-treated and contralateral BSA-treated eyes estimated from four post-culture embryos and represented by bar charts as mean ± 1 S.D. p = 0.033 by the paired t-test indicates a significant reduction in retinal volume in BMP4-treated eyes. (B, C) Coronal sections of control (B) and contralateral BMP4-treated (C) eyes stained with H&E and showing a reduction in eye size and retinal thickness upon BMP4-treatment. Scale bars: 0.05 mm. |
PMC1764729_F6_8362.jpg | Can you identify the primary element in this image? | Effect of BMP4 treatment on eye size and shape. (A) Retinal volume in BMP4-treated and contralateral BSA-treated eyes estimated from four post-culture embryos and represented by bar charts as mean ± 1 S.D. p = 0.033 by the paired t-test indicates a significant reduction in retinal volume in BMP4-treated eyes. (B, C) Coronal sections of control (B) and contralateral BMP4-treated (C) eyes stained with H&E and showing a reduction in eye size and retinal thickness upon BMP4-treatment. Scale bars: 0.05 mm. |
PMC1764747_F2_8388.jpg | What is the principal component of this image? | GFP fluorescence of bovine theca cells infected with adenoviral vectors expressing NR5A1. Bovine theca cells were infected with adenoviral vectors expressing wild-type or mutant NR5A1 and stimulated or not (control) with 2 μg/ml insulin and 10 μM forskolin (Insulin/Forskolin). The scale bar represents 20 μm. |
PMC1764747_F2_8384.jpg | What is the core subject represented in this visual? | GFP fluorescence of bovine theca cells infected with adenoviral vectors expressing NR5A1. Bovine theca cells were infected with adenoviral vectors expressing wild-type or mutant NR5A1 and stimulated or not (control) with 2 μg/ml insulin and 10 μM forskolin (Insulin/Forskolin). The scale bar represents 20 μm. |
PMC1764747_F2_8382.jpg | What key item or scene is captured in this photo? | GFP fluorescence of bovine theca cells infected with adenoviral vectors expressing NR5A1. Bovine theca cells were infected with adenoviral vectors expressing wild-type or mutant NR5A1 and stimulated or not (control) with 2 μg/ml insulin and 10 μM forskolin (Insulin/Forskolin). The scale bar represents 20 μm. |
PMC1764747_F2_8387.jpg | What object or scene is depicted here? | GFP fluorescence of bovine theca cells infected with adenoviral vectors expressing NR5A1. Bovine theca cells were infected with adenoviral vectors expressing wild-type or mutant NR5A1 and stimulated or not (control) with 2 μg/ml insulin and 10 μM forskolin (Insulin/Forskolin). The scale bar represents 20 μm. |
PMC1764747_F2_8386.jpg | What is the main focus of this visual representation? | GFP fluorescence of bovine theca cells infected with adenoviral vectors expressing NR5A1. Bovine theca cells were infected with adenoviral vectors expressing wild-type or mutant NR5A1 and stimulated or not (control) with 2 μg/ml insulin and 10 μM forskolin (Insulin/Forskolin). The scale bar represents 20 μm. |
PMC1764747_F2_8385.jpg | What is the main focus of this visual representation? | GFP fluorescence of bovine theca cells infected with adenoviral vectors expressing NR5A1. Bovine theca cells were infected with adenoviral vectors expressing wild-type or mutant NR5A1 and stimulated or not (control) with 2 μg/ml insulin and 10 μM forskolin (Insulin/Forskolin). The scale bar represents 20 μm. |
PMC1764747_F2_8381.jpg | What is the core subject represented in this visual? | GFP fluorescence of bovine theca cells infected with adenoviral vectors expressing NR5A1. Bovine theca cells were infected with adenoviral vectors expressing wild-type or mutant NR5A1 and stimulated or not (control) with 2 μg/ml insulin and 10 μM forskolin (Insulin/Forskolin). The scale bar represents 20 μm. |
PMC1764752_F3_8393.jpg | What can you see in this picture? | (A) On the left, hemi-brain from individual III-1 of family 476 diagnosed with FTD showing marked frontal and anterior temporal lobe atrophy. On the right, a coronal slice showing severely dilated lateral ventricles with narrowed gyri and widened sulci; (B) ubiquitin-positive, tau-negative inclusions in the superficial laminae of the middle frontal gyrus (arrow, scale bar = 10 nm); (C) high power photomicrograph of a neuronal cytoplasmic inclusion; (D) high power photomicrograph of a dystrophic neurite in the neuropil; (E) high power photomicrograph of a neuronal intranuclear inclusion (C -E, bar = 5 nm); (F) Ubiquitin-positive cytoplasmic inclusions in motor neurons of the lower medulla-spinal cord (arrow, bar = 50 nm); (G) higher power photomicrograph of a neuron containing a cluster of Bunina body-like inclusions; (H) higher power photomicrograph of a loosely aggregated cytoplasmic inclusion (G & H, ubiquitin immunohistocemistry, bar = 5 nm). |
PMC1764752_F3_8396.jpg | What object or scene is depicted here? | (A) On the left, hemi-brain from individual III-1 of family 476 diagnosed with FTD showing marked frontal and anterior temporal lobe atrophy. On the right, a coronal slice showing severely dilated lateral ventricles with narrowed gyri and widened sulci; (B) ubiquitin-positive, tau-negative inclusions in the superficial laminae of the middle frontal gyrus (arrow, scale bar = 10 nm); (C) high power photomicrograph of a neuronal cytoplasmic inclusion; (D) high power photomicrograph of a dystrophic neurite in the neuropil; (E) high power photomicrograph of a neuronal intranuclear inclusion (C -E, bar = 5 nm); (F) Ubiquitin-positive cytoplasmic inclusions in motor neurons of the lower medulla-spinal cord (arrow, bar = 50 nm); (G) higher power photomicrograph of a neuron containing a cluster of Bunina body-like inclusions; (H) higher power photomicrograph of a loosely aggregated cytoplasmic inclusion (G & H, ubiquitin immunohistocemistry, bar = 5 nm). |
PMC1764752_F3_8395.jpg | Describe the main subject of this image. | (A) On the left, hemi-brain from individual III-1 of family 476 diagnosed with FTD showing marked frontal and anterior temporal lobe atrophy. On the right, a coronal slice showing severely dilated lateral ventricles with narrowed gyri and widened sulci; (B) ubiquitin-positive, tau-negative inclusions in the superficial laminae of the middle frontal gyrus (arrow, scale bar = 10 nm); (C) high power photomicrograph of a neuronal cytoplasmic inclusion; (D) high power photomicrograph of a dystrophic neurite in the neuropil; (E) high power photomicrograph of a neuronal intranuclear inclusion (C -E, bar = 5 nm); (F) Ubiquitin-positive cytoplasmic inclusions in motor neurons of the lower medulla-spinal cord (arrow, bar = 50 nm); (G) higher power photomicrograph of a neuron containing a cluster of Bunina body-like inclusions; (H) higher power photomicrograph of a loosely aggregated cytoplasmic inclusion (G & H, ubiquitin immunohistocemistry, bar = 5 nm). |
PMC1764753_F1_8389.jpg | What does this image primarily show? | Examples of single 3-D MRI slices, showing delineation of in-slice volumes of total brain (left) and amygdala (right) [green] and the defined superior limit according to Watson et al. [14] [white] within MRreg. |
PMC1764753_F1_8390.jpg | What can you see in this picture? | Examples of single 3-D MRI slices, showing delineation of in-slice volumes of total brain (left) and amygdala (right) [green] and the defined superior limit according to Watson et al. [14] [white] within MRreg. |
PMC1764859_pone-0000166-g001_8398.jpg | What's the most prominent thing you notice in this picture? | Brain imaging of the rejection process in patient 3 and its reversion under treatment.Magnetic resonance imaging and metabolic activity using 18F-deoxyglucose before surgery (T0), during the rejection process (T1) and after 6 months of reinstated immunosuppressive treatment (T2) are shown separately (upper and middle panel, respectively), then co-registered (lower panel). The white arrow indicates the right striatum. The false colour scale shows levels of metabolic activities from lowest (min) to highest (max). |
PMC1764859_pone-0000166-g001_8397.jpg | What is the core subject represented in this visual? | Brain imaging of the rejection process in patient 3 and its reversion under treatment.Magnetic resonance imaging and metabolic activity using 18F-deoxyglucose before surgery (T0), during the rejection process (T1) and after 6 months of reinstated immunosuppressive treatment (T2) are shown separately (upper and middle panel, respectively), then co-registered (lower panel). The white arrow indicates the right striatum. The false colour scale shows levels of metabolic activities from lowest (min) to highest (max). |
PMC1764872_F1_8405.jpg | What is shown in this image? | Qualitative examples of GUS expression. Histochemical staining of the controls indicates that Adh/GUS was not expressed in these plants (a – b). An increase in magnetic field strength induces expression of the Adh/GUS transgene (e.g. 20 Tesla for 2.5 hours, c – d). The increased magnification of the plants shown in b and d (second row) provide closer inspection of GUS localization in the roots and leaves of these samples. The middle panel (e) provides a top-view of the five 21 day-old plants just prior to insertion into the bore of the magnet. The right hand panel (f) shows the plants from the side. |
PMC1764872_F1_8400.jpg | What is the dominant medical problem in this image? | Qualitative examples of GUS expression. Histochemical staining of the controls indicates that Adh/GUS was not expressed in these plants (a – b). An increase in magnetic field strength induces expression of the Adh/GUS transgene (e.g. 20 Tesla for 2.5 hours, c – d). The increased magnification of the plants shown in b and d (second row) provide closer inspection of GUS localization in the roots and leaves of these samples. The middle panel (e) provides a top-view of the five 21 day-old plants just prior to insertion into the bore of the magnet. The right hand panel (f) shows the plants from the side. |
PMC1764872_F1_8402.jpg | What is shown in this image? | Qualitative examples of GUS expression. Histochemical staining of the controls indicates that Adh/GUS was not expressed in these plants (a – b). An increase in magnetic field strength induces expression of the Adh/GUS transgene (e.g. 20 Tesla for 2.5 hours, c – d). The increased magnification of the plants shown in b and d (second row) provide closer inspection of GUS localization in the roots and leaves of these samples. The middle panel (e) provides a top-view of the five 21 day-old plants just prior to insertion into the bore of the magnet. The right hand panel (f) shows the plants from the side. |
PMC1764872_F1_8403.jpg | What is shown in this image? | Qualitative examples of GUS expression. Histochemical staining of the controls indicates that Adh/GUS was not expressed in these plants (a – b). An increase in magnetic field strength induces expression of the Adh/GUS transgene (e.g. 20 Tesla for 2.5 hours, c – d). The increased magnification of the plants shown in b and d (second row) provide closer inspection of GUS localization in the roots and leaves of these samples. The middle panel (e) provides a top-view of the five 21 day-old plants just prior to insertion into the bore of the magnet. The right hand panel (f) shows the plants from the side. |
PMC1764872_F1_8401.jpg | What object or scene is depicted here? | Qualitative examples of GUS expression. Histochemical staining of the controls indicates that Adh/GUS was not expressed in these plants (a – b). An increase in magnetic field strength induces expression of the Adh/GUS transgene (e.g. 20 Tesla for 2.5 hours, c – d). The increased magnification of the plants shown in b and d (second row) provide closer inspection of GUS localization in the roots and leaves of these samples. The middle panel (e) provides a top-view of the five 21 day-old plants just prior to insertion into the bore of the magnet. The right hand panel (f) shows the plants from the side. |
PMC1764878_F3_8407.jpg | What object or scene is depicted here? | Facial appearances and panoramic radiophotographic findings of affected member II-9. |
PMC1764883_F2_8409.jpg | What key item or scene is captured in this photo? | High power view of metastatic lymph node cancer cells.(A) globular structures, in intracytoplasmic vacuoles (arrows), that are positive with alcian-PAS stain (B) (Alcian)(Original magnification: A and B 400X) |
PMC1764904_F1_8410.jpg | What is the main focus of this visual representation? | Axial contrast-enhanced CT scan at diagnosis (a) showing a heterogeneous mass encasing the stomach in the upper left quadrant, and diffuse multiple omental nodules; (b) axial contrast-enhanced CT scan after 8 cycles of pemetrexed showing a partial response with a significant shrinkage of the tumour mass and disappearance of the omental nodules. |
PMC1766346_F1_8413.jpg | What does this image primarily show? | A 3-D CT scan revealed the severity of the skull base penetrating injury. |
PMC1766349_F1_8415.jpg | What is the principal component of this image? | MRI heart. A. Sagittal. B. Coronal. RA = Right atrium, LA = Left atrium, LV = Left ventricle, SVC = Superior vena cava. The close proximity of the tumor to the right atrium and extension towards a thickened interatrial septum can be seen. |
PMC1766367_F3_8416.jpg | What does this image primarily show? | TEM of infected CEM cells. Control (A top panel, B, and C) or AdOx-treated HIV-1 infected CEM (A bottom panel, D E, and F) were thin sectioned and examined by TEM. A) Viewed at 100,000 × showing typical HIV-1 assembly structures. B and C) Viewed 100,000 × and 50,000 ×, respectively, show HIV-1 that are primarily ~100 nm in diameter. A large HIV particle (~150 nm) observed in control sections is indicated by an arrow in B. D) Viewed at 50,000 × shows many typical HIV-1 particles. Two larger virus particles with a diameter of ~150 to ~180 nm are depicted by the arrows. Large HIV-1 particles were present in all sections of AdOx treated cells and two more examples are shown in E and F (both at 100,000 ×). E depicts a particle which appears to contain two core structures. |
PMC1766367_F3_8420.jpg | What does this image primarily show? | TEM of infected CEM cells. Control (A top panel, B, and C) or AdOx-treated HIV-1 infected CEM (A bottom panel, D E, and F) were thin sectioned and examined by TEM. A) Viewed at 100,000 × showing typical HIV-1 assembly structures. B and C) Viewed 100,000 × and 50,000 ×, respectively, show HIV-1 that are primarily ~100 nm in diameter. A large HIV particle (~150 nm) observed in control sections is indicated by an arrow in B. D) Viewed at 50,000 × shows many typical HIV-1 particles. Two larger virus particles with a diameter of ~150 to ~180 nm are depicted by the arrows. Large HIV-1 particles were present in all sections of AdOx treated cells and two more examples are shown in E and F (both at 100,000 ×). E depicts a particle which appears to contain two core structures. |
PMC1766367_F3_8421.jpg | What is the principal component of this image? | TEM of infected CEM cells. Control (A top panel, B, and C) or AdOx-treated HIV-1 infected CEM (A bottom panel, D E, and F) were thin sectioned and examined by TEM. A) Viewed at 100,000 × showing typical HIV-1 assembly structures. B and C) Viewed 100,000 × and 50,000 ×, respectively, show HIV-1 that are primarily ~100 nm in diameter. A large HIV particle (~150 nm) observed in control sections is indicated by an arrow in B. D) Viewed at 50,000 × shows many typical HIV-1 particles. Two larger virus particles with a diameter of ~150 to ~180 nm are depicted by the arrows. Large HIV-1 particles were present in all sections of AdOx treated cells and two more examples are shown in E and F (both at 100,000 ×). E depicts a particle which appears to contain two core structures. |
PMC1766367_F3_8417.jpg | What is the central feature of this picture? | TEM of infected CEM cells. Control (A top panel, B, and C) or AdOx-treated HIV-1 infected CEM (A bottom panel, D E, and F) were thin sectioned and examined by TEM. A) Viewed at 100,000 × showing typical HIV-1 assembly structures. B and C) Viewed 100,000 × and 50,000 ×, respectively, show HIV-1 that are primarily ~100 nm in diameter. A large HIV particle (~150 nm) observed in control sections is indicated by an arrow in B. D) Viewed at 50,000 × shows many typical HIV-1 particles. Two larger virus particles with a diameter of ~150 to ~180 nm are depicted by the arrows. Large HIV-1 particles were present in all sections of AdOx treated cells and two more examples are shown in E and F (both at 100,000 ×). E depicts a particle which appears to contain two core structures. |
PMC1766367_F3_8418.jpg | What object or scene is depicted here? | TEM of infected CEM cells. Control (A top panel, B, and C) or AdOx-treated HIV-1 infected CEM (A bottom panel, D E, and F) were thin sectioned and examined by TEM. A) Viewed at 100,000 × showing typical HIV-1 assembly structures. B and C) Viewed 100,000 × and 50,000 ×, respectively, show HIV-1 that are primarily ~100 nm in diameter. A large HIV particle (~150 nm) observed in control sections is indicated by an arrow in B. D) Viewed at 50,000 × shows many typical HIV-1 particles. Two larger virus particles with a diameter of ~150 to ~180 nm are depicted by the arrows. Large HIV-1 particles were present in all sections of AdOx treated cells and two more examples are shown in E and F (both at 100,000 ×). E depicts a particle which appears to contain two core structures. |
PMC1766371_pone-0000104-g003_8438.jpg | What does this image primarily show? | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1766371_pone-0000104-g003_8429.jpg | What can you see in this picture? | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1766371_pone-0000104-g003_8437.jpg | Describe the main subject of this image. | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1766371_pone-0000104-g003_8433.jpg | What is the focal point of this photograph? | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1766371_pone-0000104-g003_8430.jpg | What does this image primarily show? | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1766371_pone-0000104-g003_8424.jpg | What is the central feature of this picture? | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1766371_pone-0000104-g003_8426.jpg | What object or scene is depicted here? | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1766371_pone-0000104-g003_8428.jpg | Describe the main subject of this image. | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1766371_pone-0000104-g003_8436.jpg | What is the main focus of this visual representation? | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1766371_pone-0000104-g003_8431.jpg | Can you identify the primary element in this image? | Defects in vasculogenesis and hematopoeisis observed in Tg (fli-1:eGFP (green)) or Tg (gata-1:DsRed (red)) embryos following MO inactivation of select CTT genes.(A) Normal vascular development observed in untreated Tg (fli-1:eGFP) embryos. (B, L) Decreases in the number of vascular sprouts (arrow heads) observed following injection of MO targeting Syndecan-2[20]. (C, M) Gaps within the caudal vein plexus (small arrow heads) observed following injection of MO targeting heparin sulfatetransferase-6-O 2-sulfotransferase (HSST6O-2)[21]. (D, N) Loss of integrity in the caudal vein plexus (arrow) observed following injection of MO targeting MAGP1[22]. Premature return in caudal vein flow shown by gata-1:dsRed expression to varying severities (arrowheads) following injection of MOs targeting Ephrin B2 (E,O), SPPL2b (F,P), predicted protein LOC407708 (G, Q), and C1q (H, R). Note: the premature return defects were not shown by fli-1:eGFP expression (E, F, G, H), however, were confirmed by other vascular markers (data not shown). (K) Normal blood development observed in untreated Tg (gata-1:DsRed) embryos. Decreased number of blood cells observed in 2 dpf embryos following injection with MO against Synaptotagmin13 (S) or Novel Protein similar to SLC27A2 (T). Accompanying panels (I) and (J) display no major vasculature defects for each of these genes respectively. |
PMC1769357_F2_8446.jpg | Can you identify the primary element in this image? | Green fluorescent protein (GFP) expression in Tg(myf5(80K):GFP) transgenic embryos recapitulates endogenous myf5 expression in muscle precursors. GFP fluorescence is detected in the presomitic mesoderm of embryos by 10.5 hours postfertilization (hpf) (A), in the somites and the presomitic mesoderm in 16 hpf embryos (B). Endogenous myf5 transcripts (C,D,E) and GFP mRNA (F,G) were detectable at 7.5, 10.5, and 16 hpf. (A,D,G) Dorsal views, rostral to the left; (B,C,E,F) side views, rostral to the left, dorsal to the top. Scale bars: 100 μm in all panels. |
PMC1769357_F2_8440.jpg | What is shown in this image? | Green fluorescent protein (GFP) expression in Tg(myf5(80K):GFP) transgenic embryos recapitulates endogenous myf5 expression in muscle precursors. GFP fluorescence is detected in the presomitic mesoderm of embryos by 10.5 hours postfertilization (hpf) (A), in the somites and the presomitic mesoderm in 16 hpf embryos (B). Endogenous myf5 transcripts (C,D,E) and GFP mRNA (F,G) were detectable at 7.5, 10.5, and 16 hpf. (A,D,G) Dorsal views, rostral to the left; (B,C,E,F) side views, rostral to the left, dorsal to the top. Scale bars: 100 μm in all panels. |
PMC1769357_F2_8442.jpg | What is the core subject represented in this visual? | Green fluorescent protein (GFP) expression in Tg(myf5(80K):GFP) transgenic embryos recapitulates endogenous myf5 expression in muscle precursors. GFP fluorescence is detected in the presomitic mesoderm of embryos by 10.5 hours postfertilization (hpf) (A), in the somites and the presomitic mesoderm in 16 hpf embryos (B). Endogenous myf5 transcripts (C,D,E) and GFP mRNA (F,G) were detectable at 7.5, 10.5, and 16 hpf. (A,D,G) Dorsal views, rostral to the left; (B,C,E,F) side views, rostral to the left, dorsal to the top. Scale bars: 100 μm in all panels. |
PMC1769357_F2_8445.jpg | What can you see in this picture? | Green fluorescent protein (GFP) expression in Tg(myf5(80K):GFP) transgenic embryos recapitulates endogenous myf5 expression in muscle precursors. GFP fluorescence is detected in the presomitic mesoderm of embryos by 10.5 hours postfertilization (hpf) (A), in the somites and the presomitic mesoderm in 16 hpf embryos (B). Endogenous myf5 transcripts (C,D,E) and GFP mRNA (F,G) were detectable at 7.5, 10.5, and 16 hpf. (A,D,G) Dorsal views, rostral to the left; (B,C,E,F) side views, rostral to the left, dorsal to the top. Scale bars: 100 μm in all panels. |
PMC1769357_F2_8443.jpg | What stands out most in this visual? | Green fluorescent protein (GFP) expression in Tg(myf5(80K):GFP) transgenic embryos recapitulates endogenous myf5 expression in muscle precursors. GFP fluorescence is detected in the presomitic mesoderm of embryos by 10.5 hours postfertilization (hpf) (A), in the somites and the presomitic mesoderm in 16 hpf embryos (B). Endogenous myf5 transcripts (C,D,E) and GFP mRNA (F,G) were detectable at 7.5, 10.5, and 16 hpf. (A,D,G) Dorsal views, rostral to the left; (B,C,E,F) side views, rostral to the left, dorsal to the top. Scale bars: 100 μm in all panels. |
PMC1769357_F3_8448.jpg | What is being portrayed in this visual content? | Tg(myf5(80k):GFP) transgenic embryos express green fluorescent protein (GFP) in both slow and fast muscle fibers. (A,B) GFP expression in somites labeled with the F59 antibody. White dash lines indicate the location of head. (B) Higher magnification view of the boxed region shown in A. (C-E) Cross-section along the plane indicated by the white line in panel (B). GFP signals are observed in both fast (C, green signals) and slow muscle fibers (F, yellow signals). (A,B) Side views, rostral to the left, dorsal to the top; (C-D) dorsal to the top. 28 hpf. Scale bars: 400 μm in A; 200 μm in B; 100 μm in C-E. |
PMC1769357_F3_8447.jpg | What's the most prominent thing you notice in this picture? | Tg(myf5(80k):GFP) transgenic embryos express green fluorescent protein (GFP) in both slow and fast muscle fibers. (A,B) GFP expression in somites labeled with the F59 antibody. White dash lines indicate the location of head. (B) Higher magnification view of the boxed region shown in A. (C-E) Cross-section along the plane indicated by the white line in panel (B). GFP signals are observed in both fast (C, green signals) and slow muscle fibers (F, yellow signals). (A,B) Side views, rostral to the left, dorsal to the top; (C-D) dorsal to the top. 28 hpf. Scale bars: 400 μm in A; 200 μm in B; 100 μm in C-E. |
PMC1769357_F3_8449.jpg | What is the main focus of this visual representation? | Tg(myf5(80k):GFP) transgenic embryos express green fluorescent protein (GFP) in both slow and fast muscle fibers. (A,B) GFP expression in somites labeled with the F59 antibody. White dash lines indicate the location of head. (B) Higher magnification view of the boxed region shown in A. (C-E) Cross-section along the plane indicated by the white line in panel (B). GFP signals are observed in both fast (C, green signals) and slow muscle fibers (F, yellow signals). (A,B) Side views, rostral to the left, dorsal to the top; (C-D) dorsal to the top. 28 hpf. Scale bars: 400 μm in A; 200 μm in B; 100 μm in C-E. |
PMC1769357_F3_8450.jpg | What is being portrayed in this visual content? | Tg(myf5(80k):GFP) transgenic embryos express green fluorescent protein (GFP) in both slow and fast muscle fibers. (A,B) GFP expression in somites labeled with the F59 antibody. White dash lines indicate the location of head. (B) Higher magnification view of the boxed region shown in A. (C-E) Cross-section along the plane indicated by the white line in panel (B). GFP signals are observed in both fast (C, green signals) and slow muscle fibers (F, yellow signals). (A,B) Side views, rostral to the left, dorsal to the top; (C-D) dorsal to the top. 28 hpf. Scale bars: 400 μm in A; 200 μm in B; 100 μm in C-E. |
PMC1769357_F4_8459.jpg | What can you see in this picture? | Expression of green fluorescent protein (GFP) in Tg(myf5(80K):GFP) transgenics matches the dynamic pattern of endogenous myf5 expression in cranial muscles. (A-D) GFP fluorescence is apparent in pectoral fin muscle (pm), dorsal rostral muscle (drm), and hypaxial muscle (hy). (C-E) GFP fluorescence is detected in the occipital somite (os; precursors of sternohyoideus, sh) and some cranial muscles, such as the superior oblique (so) and inferior oblique (io). (F-H) Endogenous myf5 transcripts are also detected in cranial muscles, including so and io by whole-mount mRNA in situ hybridization. (A,C,F) Side views, rostral to the left, dorsal to the top; (B,D,G) dorsal views, rostral to the left; (E,H) ventral views, rostral to the left. Scale bars: 200 μm. |
PMC1769357_F4_8454.jpg | Can you identify the primary element in this image? | Expression of green fluorescent protein (GFP) in Tg(myf5(80K):GFP) transgenics matches the dynamic pattern of endogenous myf5 expression in cranial muscles. (A-D) GFP fluorescence is apparent in pectoral fin muscle (pm), dorsal rostral muscle (drm), and hypaxial muscle (hy). (C-E) GFP fluorescence is detected in the occipital somite (os; precursors of sternohyoideus, sh) and some cranial muscles, such as the superior oblique (so) and inferior oblique (io). (F-H) Endogenous myf5 transcripts are also detected in cranial muscles, including so and io by whole-mount mRNA in situ hybridization. (A,C,F) Side views, rostral to the left, dorsal to the top; (B,D,G) dorsal views, rostral to the left; (E,H) ventral views, rostral to the left. Scale bars: 200 μm. |
PMC1769357_F4_8457.jpg | What is the focal point of this photograph? | Expression of green fluorescent protein (GFP) in Tg(myf5(80K):GFP) transgenics matches the dynamic pattern of endogenous myf5 expression in cranial muscles. (A-D) GFP fluorescence is apparent in pectoral fin muscle (pm), dorsal rostral muscle (drm), and hypaxial muscle (hy). (C-E) GFP fluorescence is detected in the occipital somite (os; precursors of sternohyoideus, sh) and some cranial muscles, such as the superior oblique (so) and inferior oblique (io). (F-H) Endogenous myf5 transcripts are also detected in cranial muscles, including so and io by whole-mount mRNA in situ hybridization. (A,C,F) Side views, rostral to the left, dorsal to the top; (B,D,G) dorsal views, rostral to the left; (E,H) ventral views, rostral to the left. Scale bars: 200 μm. |
PMC1769357_F8_8461.jpg | What is the dominant medical problem in this image? | The myf5 upstream region contains modules that regulate expression in spinal cord, bones, eyes and olfactory-pits. (A,B) Green fluorescent protein (GFP) fluorescence at 48 hours postfertilization (hpf) (A) and 72 hpf (B); the star in A indicates the location of hindbrain. (C,D) Cross-sections along the plane indicated by lines C and D in B, GFP signals are apparent in spinal cord (sc) and surface ectoderm. (E-J) GFP expression is observed in bones at 21 dpf (E and F), in bones at 60 dpf (G and H) in eyes (H and I), and olfactory pits (J). (K) The same embryo as (J) with brightfield illumination. am, adductor mandibulae; bh, basihyal; mc, Meckel's cartilage; n, notochord; op, olfactory pits; pq, palatoquadrate; sc, spinal cord. (A,B,E,H) Lateral views, rostral to the left, dorsal to the top; (F,G) ventral views, rostral to the left; (I-K) frontal views, dorsal to the top. Scare bars: 500 μm in A, E-H; 250 μm in I; 200 μm in B; 100 μm in C, D, J, K. |
PMC1769357_F8_8467.jpg | What stands out most in this visual? | The myf5 upstream region contains modules that regulate expression in spinal cord, bones, eyes and olfactory-pits. (A,B) Green fluorescent protein (GFP) fluorescence at 48 hours postfertilization (hpf) (A) and 72 hpf (B); the star in A indicates the location of hindbrain. (C,D) Cross-sections along the plane indicated by lines C and D in B, GFP signals are apparent in spinal cord (sc) and surface ectoderm. (E-J) GFP expression is observed in bones at 21 dpf (E and F), in bones at 60 dpf (G and H) in eyes (H and I), and olfactory pits (J). (K) The same embryo as (J) with brightfield illumination. am, adductor mandibulae; bh, basihyal; mc, Meckel's cartilage; n, notochord; op, olfactory pits; pq, palatoquadrate; sc, spinal cord. (A,B,E,H) Lateral views, rostral to the left, dorsal to the top; (F,G) ventral views, rostral to the left; (I-K) frontal views, dorsal to the top. Scare bars: 500 μm in A, E-H; 250 μm in I; 200 μm in B; 100 μm in C, D, J, K. |
PMC1769357_F8_8469.jpg | What is the principal component of this image? | The myf5 upstream region contains modules that regulate expression in spinal cord, bones, eyes and olfactory-pits. (A,B) Green fluorescent protein (GFP) fluorescence at 48 hours postfertilization (hpf) (A) and 72 hpf (B); the star in A indicates the location of hindbrain. (C,D) Cross-sections along the plane indicated by lines C and D in B, GFP signals are apparent in spinal cord (sc) and surface ectoderm. (E-J) GFP expression is observed in bones at 21 dpf (E and F), in bones at 60 dpf (G and H) in eyes (H and I), and olfactory pits (J). (K) The same embryo as (J) with brightfield illumination. am, adductor mandibulae; bh, basihyal; mc, Meckel's cartilage; n, notochord; op, olfactory pits; pq, palatoquadrate; sc, spinal cord. (A,B,E,H) Lateral views, rostral to the left, dorsal to the top; (F,G) ventral views, rostral to the left; (I-K) frontal views, dorsal to the top. Scare bars: 500 μm in A, E-H; 250 μm in I; 200 μm in B; 100 μm in C, D, J, K. |
PMC1769357_F8_8468.jpg | Describe the main subject of this image. | The myf5 upstream region contains modules that regulate expression in spinal cord, bones, eyes and olfactory-pits. (A,B) Green fluorescent protein (GFP) fluorescence at 48 hours postfertilization (hpf) (A) and 72 hpf (B); the star in A indicates the location of hindbrain. (C,D) Cross-sections along the plane indicated by lines C and D in B, GFP signals are apparent in spinal cord (sc) and surface ectoderm. (E-J) GFP expression is observed in bones at 21 dpf (E and F), in bones at 60 dpf (G and H) in eyes (H and I), and olfactory pits (J). (K) The same embryo as (J) with brightfield illumination. am, adductor mandibulae; bh, basihyal; mc, Meckel's cartilage; n, notochord; op, olfactory pits; pq, palatoquadrate; sc, spinal cord. (A,B,E,H) Lateral views, rostral to the left, dorsal to the top; (F,G) ventral views, rostral to the left; (I-K) frontal views, dorsal to the top. Scare bars: 500 μm in A, E-H; 250 μm in I; 200 μm in B; 100 μm in C, D, J, K. |
PMC1769357_F8_8460.jpg | What is the main focus of this visual representation? | The myf5 upstream region contains modules that regulate expression in spinal cord, bones, eyes and olfactory-pits. (A,B) Green fluorescent protein (GFP) fluorescence at 48 hours postfertilization (hpf) (A) and 72 hpf (B); the star in A indicates the location of hindbrain. (C,D) Cross-sections along the plane indicated by lines C and D in B, GFP signals are apparent in spinal cord (sc) and surface ectoderm. (E-J) GFP expression is observed in bones at 21 dpf (E and F), in bones at 60 dpf (G and H) in eyes (H and I), and olfactory pits (J). (K) The same embryo as (J) with brightfield illumination. am, adductor mandibulae; bh, basihyal; mc, Meckel's cartilage; n, notochord; op, olfactory pits; pq, palatoquadrate; sc, spinal cord. (A,B,E,H) Lateral views, rostral to the left, dorsal to the top; (F,G) ventral views, rostral to the left; (I-K) frontal views, dorsal to the top. Scare bars: 500 μm in A, E-H; 250 μm in I; 200 μm in B; 100 μm in C, D, J, K. |
PMC1769361_F2_8477.jpg | What is being portrayed in this visual content? | Cyclin D1 and phospho-cyclin D1 staining patterns. (A) MRC5 cells were pulsed with BrdU and stained as described in Figure 1. Fluorescence photographs of BrdU, cyclin D1 and DNA stains for a single group of cells are presented. Separate cells stain for cyclin D1 and BrdU. (B) NIH3T3 cells were fixed and stained with antibodies against total cyclin D1, or cyclin D1 phosphorylated on Thr-286. This procedure was performed on untreated cells, or following a three hr treatment with MG132 to block proteasomal degradation. Fluorescence images of the same area of cells are presented, along with DAPI stained DNA. No accumulation of cytoplasmic cyclin D1 or phospho-cyclin D1 is apparent in any of these cells. |
PMC1769361_F2_8474.jpg | What's the most prominent thing you notice in this picture? | Cyclin D1 and phospho-cyclin D1 staining patterns. (A) MRC5 cells were pulsed with BrdU and stained as described in Figure 1. Fluorescence photographs of BrdU, cyclin D1 and DNA stains for a single group of cells are presented. Separate cells stain for cyclin D1 and BrdU. (B) NIH3T3 cells were fixed and stained with antibodies against total cyclin D1, or cyclin D1 phosphorylated on Thr-286. This procedure was performed on untreated cells, or following a three hr treatment with MG132 to block proteasomal degradation. Fluorescence images of the same area of cells are presented, along with DAPI stained DNA. No accumulation of cytoplasmic cyclin D1 or phospho-cyclin D1 is apparent in any of these cells. |
PMC1769361_F2_8476.jpg | What is the dominant medical problem in this image? | Cyclin D1 and phospho-cyclin D1 staining patterns. (A) MRC5 cells were pulsed with BrdU and stained as described in Figure 1. Fluorescence photographs of BrdU, cyclin D1 and DNA stains for a single group of cells are presented. Separate cells stain for cyclin D1 and BrdU. (B) NIH3T3 cells were fixed and stained with antibodies against total cyclin D1, or cyclin D1 phosphorylated on Thr-286. This procedure was performed on untreated cells, or following a three hr treatment with MG132 to block proteasomal degradation. Fluorescence images of the same area of cells are presented, along with DAPI stained DNA. No accumulation of cytoplasmic cyclin D1 or phospho-cyclin D1 is apparent in any of these cells. |
PMC1769361_F2_8473.jpg | What is the dominant medical problem in this image? | Cyclin D1 and phospho-cyclin D1 staining patterns. (A) MRC5 cells were pulsed with BrdU and stained as described in Figure 1. Fluorescence photographs of BrdU, cyclin D1 and DNA stains for a single group of cells are presented. Separate cells stain for cyclin D1 and BrdU. (B) NIH3T3 cells were fixed and stained with antibodies against total cyclin D1, or cyclin D1 phosphorylated on Thr-286. This procedure was performed on untreated cells, or following a three hr treatment with MG132 to block proteasomal degradation. Fluorescence images of the same area of cells are presented, along with DAPI stained DNA. No accumulation of cytoplasmic cyclin D1 or phospho-cyclin D1 is apparent in any of these cells. |
PMC1769361_F2_8472.jpg | What can you see in this picture? | Cyclin D1 and phospho-cyclin D1 staining patterns. (A) MRC5 cells were pulsed with BrdU and stained as described in Figure 1. Fluorescence photographs of BrdU, cyclin D1 and DNA stains for a single group of cells are presented. Separate cells stain for cyclin D1 and BrdU. (B) NIH3T3 cells were fixed and stained with antibodies against total cyclin D1, or cyclin D1 phosphorylated on Thr-286. This procedure was performed on untreated cells, or following a three hr treatment with MG132 to block proteasomal degradation. Fluorescence images of the same area of cells are presented, along with DAPI stained DNA. No accumulation of cytoplasmic cyclin D1 or phospho-cyclin D1 is apparent in any of these cells. |
PMC1769361_F2_8475.jpg | What is the dominant medical problem in this image? | Cyclin D1 and phospho-cyclin D1 staining patterns. (A) MRC5 cells were pulsed with BrdU and stained as described in Figure 1. Fluorescence photographs of BrdU, cyclin D1 and DNA stains for a single group of cells are presented. Separate cells stain for cyclin D1 and BrdU. (B) NIH3T3 cells were fixed and stained with antibodies against total cyclin D1, or cyclin D1 phosphorylated on Thr-286. This procedure was performed on untreated cells, or following a three hr treatment with MG132 to block proteasomal degradation. Fluorescence images of the same area of cells are presented, along with DAPI stained DNA. No accumulation of cytoplasmic cyclin D1 or phospho-cyclin D1 is apparent in any of these cells. |
PMC1769361_F2_8471.jpg | What object or scene is depicted here? | Cyclin D1 and phospho-cyclin D1 staining patterns. (A) MRC5 cells were pulsed with BrdU and stained as described in Figure 1. Fluorescence photographs of BrdU, cyclin D1 and DNA stains for a single group of cells are presented. Separate cells stain for cyclin D1 and BrdU. (B) NIH3T3 cells were fixed and stained with antibodies against total cyclin D1, or cyclin D1 phosphorylated on Thr-286. This procedure was performed on untreated cells, or following a three hr treatment with MG132 to block proteasomal degradation. Fluorescence images of the same area of cells are presented, along with DAPI stained DNA. No accumulation of cytoplasmic cyclin D1 or phospho-cyclin D1 is apparent in any of these cells. |
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