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PMC1762384_pone-0000018-g005_8203.jpg | What does this image primarily show? | Evolution of JAK2 V617F-induced polycythemia to “spent” phase with myelofibrosis.(A) Box-style plots of hematocrit (red squares, left axis) and reticulocyte counts (blue triangles, right axis) in a cohort (n = 12) of Balb/c recipients of syngeneic JAK2 V617F-transduced BM, followed for over eight months after transplantation.Similar data were observed for a B6 cohort (data not shown).(B) Increasing fibrosis (demonstrated by reticulin staining) in spleen (left panels) and BM (right panels) of representative JAK2 V617F recipients at about 3 months (middle panels) and 7 months (bottom panels) after transplantation.Note the marked increase in reticulin staining at 7 months in the JAK2 V617F recipients, but not in recipients of JAK2 WT-transduced BM (top panels).(C): Efficient transfer of the PV-like MPD by transplantation of BM from primary mice sacrificed either in the early, polycythemic phase (left, n = 3, sacrificed 72–167 days post-transplant) or the late, myelofibrotic phase (right, n = 2, sacrificed 208 days post-transplant), to lethally irradiated syngeneic secondary recipients (n = 6 for early phase and n = 4 for late phase).The graphs depict mean hematocrit (black, left axis), reticulocyte count (white, right axis) and peripheral blood leukocyte count (grey, right axis) of the donors at the time of sacrifice, and of the recipients at day 30–70 post-transplant.For transplants performed in the late phase of the disease, the hematocrit and reticulocyte counts of recipients were significantly higher than of the donors (P = 0.0407 and P = 0.0337, respectively, unpaired t-test), while there was no significant difference between donors and recipients transplanted in the early phase. |
PMC1762394_pone-0000023-g006_8213.jpg | What is being portrayed in this visual content? | Mice bearing microscopic NB-1643 tumors were injected intravenously with 2 million HB1.F3.C1 cells pre-labeled with CM-DiI Red Cell Tracker.Normal and tumor-bearing organs were harvested, sectioned, and stained with DAPI. HB1.F3.C1 cells were not detected in normal (A) brain, (B) kidney, (C) heart, (D) intestine, or (E) skin tissue.Rare, single, HB1.F3.C1 cells (white arrows) were seen in (F) lung, (G) liver and (H) spleen.Scale bars: 200 µm (A–E), 100 µm (F–H). |
PMC1762394_pone-0000023-g006_8209.jpg | What key item or scene is captured in this photo? | Mice bearing microscopic NB-1643 tumors were injected intravenously with 2 million HB1.F3.C1 cells pre-labeled with CM-DiI Red Cell Tracker.Normal and tumor-bearing organs were harvested, sectioned, and stained with DAPI. HB1.F3.C1 cells were not detected in normal (A) brain, (B) kidney, (C) heart, (D) intestine, or (E) skin tissue.Rare, single, HB1.F3.C1 cells (white arrows) were seen in (F) lung, (G) liver and (H) spleen.Scale bars: 200 µm (A–E), 100 µm (F–H). |
PMC1762394_pone-0000023-g006_8207.jpg | What's the most prominent thing you notice in this picture? | Mice bearing microscopic NB-1643 tumors were injected intravenously with 2 million HB1.F3.C1 cells pre-labeled with CM-DiI Red Cell Tracker.Normal and tumor-bearing organs were harvested, sectioned, and stained with DAPI. HB1.F3.C1 cells were not detected in normal (A) brain, (B) kidney, (C) heart, (D) intestine, or (E) skin tissue.Rare, single, HB1.F3.C1 cells (white arrows) were seen in (F) lung, (G) liver and (H) spleen.Scale bars: 200 µm (A–E), 100 µm (F–H). |
PMC1762394_pone-0000023-g006_8208.jpg | What is the dominant medical problem in this image? | Mice bearing microscopic NB-1643 tumors were injected intravenously with 2 million HB1.F3.C1 cells pre-labeled with CM-DiI Red Cell Tracker.Normal and tumor-bearing organs were harvested, sectioned, and stained with DAPI. HB1.F3.C1 cells were not detected in normal (A) brain, (B) kidney, (C) heart, (D) intestine, or (E) skin tissue.Rare, single, HB1.F3.C1 cells (white arrows) were seen in (F) lung, (G) liver and (H) spleen.Scale bars: 200 µm (A–E), 100 µm (F–H). |
PMC1762394_pone-0000023-g006_8206.jpg | What is the dominant medical problem in this image? | Mice bearing microscopic NB-1643 tumors were injected intravenously with 2 million HB1.F3.C1 cells pre-labeled with CM-DiI Red Cell Tracker.Normal and tumor-bearing organs were harvested, sectioned, and stained with DAPI. HB1.F3.C1 cells were not detected in normal (A) brain, (B) kidney, (C) heart, (D) intestine, or (E) skin tissue.Rare, single, HB1.F3.C1 cells (white arrows) were seen in (F) lung, (G) liver and (H) spleen.Scale bars: 200 µm (A–E), 100 µm (F–H). |
PMC1762423_pone-0000119-g003_8214.jpg | What is the main focus of this visual representation? | SEM images of adult mouse neural stem cells (NSC) embedded in designer peptide nanofiber scaffold RADA16-BMHP1 (1% v/w) after 14 day in vitro cultures. I) Cluster of three visible NSCs (white circle) embedded in 3-D self-assembling RADA16-BMHP1. II) A single cell at different magnification with extended processes embedded in the scaffold is shown (a–c). White arrows point to the image areas enlarged in the consecutive pictures. d) High-magnification picture focusing on the interface between the nanofiber scaffold and the round shaped cell body. The black arrow in (b) points to a cellular process. Cells and processes are thus embedded in the self-assembling peptide nanofiber scaffold in a true 3-D environment, which may likely promote cell adhesions in 3-D similar to the natural cellular environment. Adult mouse neural stem cells have been cultured and could be differentiated in vitro for several weeks. The scale bars are shown on each image. |
PMC1762423_pone-0000119-g003_8218.jpg | What is the focal point of this photograph? | SEM images of adult mouse neural stem cells (NSC) embedded in designer peptide nanofiber scaffold RADA16-BMHP1 (1% v/w) after 14 day in vitro cultures. I) Cluster of three visible NSCs (white circle) embedded in 3-D self-assembling RADA16-BMHP1. II) A single cell at different magnification with extended processes embedded in the scaffold is shown (a–c). White arrows point to the image areas enlarged in the consecutive pictures. d) High-magnification picture focusing on the interface between the nanofiber scaffold and the round shaped cell body. The black arrow in (b) points to a cellular process. Cells and processes are thus embedded in the self-assembling peptide nanofiber scaffold in a true 3-D environment, which may likely promote cell adhesions in 3-D similar to the natural cellular environment. Adult mouse neural stem cells have been cultured and could be differentiated in vitro for several weeks. The scale bars are shown on each image. |
PMC1762423_pone-0000119-g003_8216.jpg | What stands out most in this visual? | SEM images of adult mouse neural stem cells (NSC) embedded in designer peptide nanofiber scaffold RADA16-BMHP1 (1% v/w) after 14 day in vitro cultures. I) Cluster of three visible NSCs (white circle) embedded in 3-D self-assembling RADA16-BMHP1. II) A single cell at different magnification with extended processes embedded in the scaffold is shown (a–c). White arrows point to the image areas enlarged in the consecutive pictures. d) High-magnification picture focusing on the interface between the nanofiber scaffold and the round shaped cell body. The black arrow in (b) points to a cellular process. Cells and processes are thus embedded in the self-assembling peptide nanofiber scaffold in a true 3-D environment, which may likely promote cell adhesions in 3-D similar to the natural cellular environment. Adult mouse neural stem cells have been cultured and could be differentiated in vitro for several weeks. The scale bars are shown on each image. |
PMC1762424_pone-0000122-g004_8220.jpg | What object or scene is depicted here? |
lb is required for proper leg muscle performance and walking behaviourA The ball test see Videos S10–S12. The abilities of flies to catch, maintain and rotate a polystyrene ball were tested. The number of individuals tested males only is indicated in upper case after the genotype. Each male performed each of the tests three times. The number of asterisks max. 5 illustrates the average performance. Notice that the RNAi-based attenuation of lb leads to a reduced ability to catch about 20% of failures and especially to maintain the ball about 60% of failures with slower and irregular rotations. Defects in catching, maintaining and rotating the ball were comparatively stronger in flies overexpressing lb. About 60% of flies were unable to catch the ball and more than 80% lost it in less than 30 s. B The ‘leg-print’ test for walking pattern. Two-day old flies were allowed to walk on a carbon-soot coated glass slide and their tracks were examined. The direction of movement is towards the top of each panel. The imprints made by the first 1 second 2 and third leg 3 of the left hemisegment are marked in each panel. Wild type flies B′ show a stereotypic pattern of prints, a consequence of a ‘tripod’ gait. In male flies where UAS-lbRNAi expression is under the control of the 1151GAL4 driver B″ the legs are held closer to the body and the leg-print is the consequence of a shuffling gait. In male flies where UAS-lbe expression is under the control of the 1151GAL4 driver the pattern of prints B′″ illustrates a bias towards one side, a consequence of the legs being abnormally positioned with respect to the body. |
PMC1762424_pone-0000122-g004_8219.jpg | What is the central feature of this picture? |
lb is required for proper leg muscle performance and walking behaviourA The ball test see Videos S10–S12. The abilities of flies to catch, maintain and rotate a polystyrene ball were tested. The number of individuals tested males only is indicated in upper case after the genotype. Each male performed each of the tests three times. The number of asterisks max. 5 illustrates the average performance. Notice that the RNAi-based attenuation of lb leads to a reduced ability to catch about 20% of failures and especially to maintain the ball about 60% of failures with slower and irregular rotations. Defects in catching, maintaining and rotating the ball were comparatively stronger in flies overexpressing lb. About 60% of flies were unable to catch the ball and more than 80% lost it in less than 30 s. B The ‘leg-print’ test for walking pattern. Two-day old flies were allowed to walk on a carbon-soot coated glass slide and their tracks were examined. The direction of movement is towards the top of each panel. The imprints made by the first 1 second 2 and third leg 3 of the left hemisegment are marked in each panel. Wild type flies B′ show a stereotypic pattern of prints, a consequence of a ‘tripod’ gait. In male flies where UAS-lbRNAi expression is under the control of the 1151GAL4 driver B″ the legs are held closer to the body and the leg-print is the consequence of a shuffling gait. In male flies where UAS-lbe expression is under the control of the 1151GAL4 driver the pattern of prints B′″ illustrates a bias towards one side, a consequence of the legs being abnormally positioned with respect to the body. |
PMC1762424_pone-0000122-g004_8221.jpg | What key item or scene is captured in this photo? |
lb is required for proper leg muscle performance and walking behaviourA The ball test see Videos S10–S12. The abilities of flies to catch, maintain and rotate a polystyrene ball were tested. The number of individuals tested males only is indicated in upper case after the genotype. Each male performed each of the tests three times. The number of asterisks max. 5 illustrates the average performance. Notice that the RNAi-based attenuation of lb leads to a reduced ability to catch about 20% of failures and especially to maintain the ball about 60% of failures with slower and irregular rotations. Defects in catching, maintaining and rotating the ball were comparatively stronger in flies overexpressing lb. About 60% of flies were unable to catch the ball and more than 80% lost it in less than 30 s. B The ‘leg-print’ test for walking pattern. Two-day old flies were allowed to walk on a carbon-soot coated glass slide and their tracks were examined. The direction of movement is towards the top of each panel. The imprints made by the first 1 second 2 and third leg 3 of the left hemisegment are marked in each panel. Wild type flies B′ show a stereotypic pattern of prints, a consequence of a ‘tripod’ gait. In male flies where UAS-lbRNAi expression is under the control of the 1151GAL4 driver B″ the legs are held closer to the body and the leg-print is the consequence of a shuffling gait. In male flies where UAS-lbe expression is under the control of the 1151GAL4 driver the pattern of prints B′″ illustrates a bias towards one side, a consequence of the legs being abnormally positioned with respect to the body. |
PMC1762424_pone-0000122-g005_8223.jpg | What is the core subject represented in this visual? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8225.jpg | What stands out most in this visual? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8227.jpg | What is the focal point of this photograph? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8234.jpg | What is the dominant medical problem in this image? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8226.jpg | What can you see in this picture? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8232.jpg | What stands out most in this visual? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8231.jpg | Describe the main subject of this image. | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8224.jpg | What is the core subject represented in this visual? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8233.jpg | What is being portrayed in this visual content? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8230.jpg | What key item or scene is captured in this photo? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762424_pone-0000122-g005_8228.jpg | What is the focal point of this photograph? | Wg signals are required for Lbe expression and play a key role in leg myogenesisA–I Confocal images of third instar leg imaginal discs. A–C Wild type leg disc stained for Lbe and Vestigial Vg. Lbe positive myoblasts are seen in leg disc proper B and green in merge C, while the myoblasts associated with the dorsal proximal region corresponding to the ventral thorax express Vg A and red in merge C. Vg myoblasts are devoid of Lbe asterisk in B. A Yellow arrowhead shows myoblasts expressing high levels of Vg and white arrowhead those expressing Vg at lower levels. D–F Leg disc, in which a dominant-negative TCF has been expressed in the myoblasts. Myoblasts are present as shown by anti-Twist antibody staining D and blue in merge F, but Lbe expression in myoblasts is lost asterisks in E and green in F. G–I Leg disc, in which activated Armadillo Arm transgene has been expressed in the myoblasts. Lbe is ectopically expressed in dorsal proximal myoblasts arrow in H and green in merge I, normally devoid of Lbe. Myoblasts are visualised with anti-Twi antibody G and blue in I. J–J′ show adult muscle phenotypes in the femur region induced by 1151-Gal4-driven forced expression of a dominant-negative TCF. Ventral muscles tidm are partially lost asterisks in J or completely lost asterisks in J′ and dorsal muscles tilm are severely affected. Muscles are visualised using MHC-tauGFP. Anterior views from the 3D reconstructions of confocal scans. K A schematic showing position of Lbe-expressing dorsal tilm and ventral tidm precursors of femur muscles green areas with respect to epithelial Wg expression domain violet triangle. The dorsal tilm myoblasts, located comparatively far from the Wg domain, receive a lower level of Wg morphogen long thin arrow than ventrally located tidm myoblasts short thick arrow. |
PMC1762426_pone-0000107-g003_8254.jpg | What is being portrayed in this visual content? | The presequence of β-F1-ATPase precursor targets gfp to mitochondria.The expression of gfp in C9 (A,B) and BHK (C) cells was assessed by fluorescence (A), immunofluorescence (B) and immunoelectron (C) microscopy. A, Illustrates by phase contrast (upper panel) and immunofluorescence (lower panel) the same low magnification field of C9-pβGFP3′β cells. B, C9-pβGFP3′β cells analyzed by immunofluorescence microscopy using anti-β-F1-ATPase antibody at 63× magnification. Upper panel, green gfp fluorescence; middle panel, red β-F1-ATPase immunostaining; lower panel, yellow merged image. C, Specific immunogold labeling (10 nm gold) of BHK mitochondria (m). Note the lack of gold labeling of other structures in the cytoplasm or in the nucleus (n) of the cell. D, Western blots of C9 (lane 1) and BHK cells (lanes 2–4) transfected with the pβGFP3′β construct. Fractionated proteins from the cellular extracts were probed with anti-gfp and anti-tubulin, the later as loading control. The migration of the pβ-gfp chimera is also indicated. In lane 3, BHK cells have been previously treated with FCCP (4 µM) plus oligomycin (2 µM) for 1 hour. Note the accumulation of pβ-gfp. In lane 4, BHK cells treated as in lane 3 were washed for 40 minutes before fractionation. Note the processing of pβ-gfp to mature gfp. |
PMC1762426_pone-0000107-g003_8257.jpg | What's the most prominent thing you notice in this picture? | The presequence of β-F1-ATPase precursor targets gfp to mitochondria.The expression of gfp in C9 (A,B) and BHK (C) cells was assessed by fluorescence (A), immunofluorescence (B) and immunoelectron (C) microscopy. A, Illustrates by phase contrast (upper panel) and immunofluorescence (lower panel) the same low magnification field of C9-pβGFP3′β cells. B, C9-pβGFP3′β cells analyzed by immunofluorescence microscopy using anti-β-F1-ATPase antibody at 63× magnification. Upper panel, green gfp fluorescence; middle panel, red β-F1-ATPase immunostaining; lower panel, yellow merged image. C, Specific immunogold labeling (10 nm gold) of BHK mitochondria (m). Note the lack of gold labeling of other structures in the cytoplasm or in the nucleus (n) of the cell. D, Western blots of C9 (lane 1) and BHK cells (lanes 2–4) transfected with the pβGFP3′β construct. Fractionated proteins from the cellular extracts were probed with anti-gfp and anti-tubulin, the later as loading control. The migration of the pβ-gfp chimera is also indicated. In lane 3, BHK cells have been previously treated with FCCP (4 µM) plus oligomycin (2 µM) for 1 hour. Note the accumulation of pβ-gfp. In lane 4, BHK cells treated as in lane 3 were washed for 40 minutes before fractionation. Note the processing of pβ-gfp to mature gfp. |
PMC1762426_pone-0000107-g005_8251.jpg | Describe the main subject of this image. | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8235.jpg | What does this image primarily show? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8246.jpg | Can you identify the primary element in this image? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8244.jpg | What's the most prominent thing you notice in this picture? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8237.jpg | What is the central feature of this picture? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8245.jpg | Describe the main subject of this image. | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8241.jpg | What is being portrayed in this visual content? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8242.jpg | Describe the main subject of this image. | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8248.jpg | What is being portrayed in this visual content? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8236.jpg | What does this image primarily show? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8240.jpg | What is the central feature of this picture? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8243.jpg | What's the most prominent thing you notice in this picture? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8252.jpg | What object or scene is depicted here? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762426_pone-0000107-g005_8239.jpg | What can you see in this picture? | Morphological changes in the cellular mitochondrial network during mitosis.Synchronized mitochondria-tagged C9-pβGFP3′β cells were analyzed by immunofluorescence microscopy at four hours after release from the metabolic block. Typical morphologies of cells in interphase (a,f), prophase (b), metaphase (c,g), anaphase (d) and telophase (e,h) are shown at 60× magnification. The red fluorescence identifies the cytoskeletal proteins α-tubulin (a–e) and β-actin (f–h). The green fluorescence identifies mitochondria. The blue fluorescence reveals the stained nuclear DNA with the To-Pro probe. |
PMC1762430_pone-0000126-g001_8261.jpg | What is being portrayed in this visual content? | Evoked catecholeamine release is absent in syntaxin deleted chromaffin cells. (A) Fluorescent image of cultured chromaffin cells incubated with SFV-egfp or SFV BoNT/C-ires-egfp, and immunostained for syntaxin, showing a reduced syntaxin staining at the plasma membrane after BoNT/C expression. The syntaxin staining after BoNT/C was slightly overexposed to emphasize the persistence of cytosolic staining (as opposed to plasma membrane staining). Scale bars represent 2 µm. (B) Examples of amperometric recordings in control and BoNT/C infected chromaffin cells during stimulation with a 30 mM K+ solution. |
PMC1762430_pone-0000126-g001_8258.jpg | What does this image primarily show? | Evoked catecholeamine release is absent in syntaxin deleted chromaffin cells. (A) Fluorescent image of cultured chromaffin cells incubated with SFV-egfp or SFV BoNT/C-ires-egfp, and immunostained for syntaxin, showing a reduced syntaxin staining at the plasma membrane after BoNT/C expression. The syntaxin staining after BoNT/C was slightly overexposed to emphasize the persistence of cytosolic staining (as opposed to plasma membrane staining). Scale bars represent 2 µm. (B) Examples of amperometric recordings in control and BoNT/C infected chromaffin cells during stimulation with a 30 mM K+ solution. |
PMC1762430_pone-0000126-g001_8260.jpg | What can you see in this picture? | Evoked catecholeamine release is absent in syntaxin deleted chromaffin cells. (A) Fluorescent image of cultured chromaffin cells incubated with SFV-egfp or SFV BoNT/C-ires-egfp, and immunostained for syntaxin, showing a reduced syntaxin staining at the plasma membrane after BoNT/C expression. The syntaxin staining after BoNT/C was slightly overexposed to emphasize the persistence of cytosolic staining (as opposed to plasma membrane staining). Scale bars represent 2 µm. (B) Examples of amperometric recordings in control and BoNT/C infected chromaffin cells during stimulation with a 30 mM K+ solution. |
PMC1762430_pone-0000126-g002_8275.jpg | What is being portrayed in this visual content? | Syntaxin deletion decreases the number of morphologically docked secretory vesicles. (A) Electron micrographs of control and BoNT/C expressing chromaffin cell. For each cell a magnification of a sub-membrane region is shown indicating severely impaired vesicle docking after acute BoNT/C expression compared to the control cell that contains many morphologically docked vesicles at the plasma membrane. Scale bars represent 200 nm. (B) Normalized cumulative distribution of secretory vesicles as a function of distance from the plasma membrane in control cells expressing EFGP or BoNT/C. Inset shows cumulative vesicle distribution in the sub-membrane region within 0–100 nm. Grey line represents the vesicle distribution in the absence of Munc18-1 as shown before [24]. (C–E) Number of docked vesicles (C), vesicles>0–30 and within 30–100 nm (D), and the total number of vesicles (E). Data are mean±SEM from the following number of cells (n) and animals (N): control+EGFP, n = 20, N = 4; control+BoNT/C, n = 20, N = 4 (**p<0.05 and ***p<0.001, ANOVA and student's t-test). |
PMC1762430_pone-0000126-g002_8271.jpg | What can you see in this picture? | Syntaxin deletion decreases the number of morphologically docked secretory vesicles. (A) Electron micrographs of control and BoNT/C expressing chromaffin cell. For each cell a magnification of a sub-membrane region is shown indicating severely impaired vesicle docking after acute BoNT/C expression compared to the control cell that contains many morphologically docked vesicles at the plasma membrane. Scale bars represent 200 nm. (B) Normalized cumulative distribution of secretory vesicles as a function of distance from the plasma membrane in control cells expressing EFGP or BoNT/C. Inset shows cumulative vesicle distribution in the sub-membrane region within 0–100 nm. Grey line represents the vesicle distribution in the absence of Munc18-1 as shown before [24]. (C–E) Number of docked vesicles (C), vesicles>0–30 and within 30–100 nm (D), and the total number of vesicles (E). Data are mean±SEM from the following number of cells (n) and animals (N): control+EGFP, n = 20, N = 4; control+BoNT/C, n = 20, N = 4 (**p<0.05 and ***p<0.001, ANOVA and student's t-test). |
PMC1762430_pone-0000126-g005_8266.jpg | What object or scene is depicted here? | Distribution of Munc18-1 is altered in syntaxin deleted chromaffin cells. (A) Immunolocalization of syntaxin (blue) and Munc18-1 (red) in SFV-egfp or BoNT/C-ires-egfp infected chromaffin cells. Scale bars represent 2 µm. (B) Average pixel intensity of Munc18-1 expression obtained from line scans through a confocal section of a BoNT/C and EGFP expressing cell. Inset shows how line scans were made from a to b (C) Quantification of the Munc18-1 expression at the plasma membrane. Numbers indicate mean±SEM. from n = 22 cells and N = 3 animals (***p<0.01, ANOVA and student's t-test, comparison to control). |
PMC1762430_pone-0000126-g005_8263.jpg | What is the focal point of this photograph? | Distribution of Munc18-1 is altered in syntaxin deleted chromaffin cells. (A) Immunolocalization of syntaxin (blue) and Munc18-1 (red) in SFV-egfp or BoNT/C-ires-egfp infected chromaffin cells. Scale bars represent 2 µm. (B) Average pixel intensity of Munc18-1 expression obtained from line scans through a confocal section of a BoNT/C and EGFP expressing cell. Inset shows how line scans were made from a to b (C) Quantification of the Munc18-1 expression at the plasma membrane. Numbers indicate mean±SEM. from n = 22 cells and N = 3 animals (***p<0.01, ANOVA and student's t-test, comparison to control). |
PMC1762430_pone-0000126-g005_8265.jpg | What is shown in this image? | Distribution of Munc18-1 is altered in syntaxin deleted chromaffin cells. (A) Immunolocalization of syntaxin (blue) and Munc18-1 (red) in SFV-egfp or BoNT/C-ires-egfp infected chromaffin cells. Scale bars represent 2 µm. (B) Average pixel intensity of Munc18-1 expression obtained from line scans through a confocal section of a BoNT/C and EGFP expressing cell. Inset shows how line scans were made from a to b (C) Quantification of the Munc18-1 expression at the plasma membrane. Numbers indicate mean±SEM. from n = 22 cells and N = 3 animals (***p<0.01, ANOVA and student's t-test, comparison to control). |
PMC1762430_pone-0000126-g005_8267.jpg | What object or scene is depicted here? | Distribution of Munc18-1 is altered in syntaxin deleted chromaffin cells. (A) Immunolocalization of syntaxin (blue) and Munc18-1 (red) in SFV-egfp or BoNT/C-ires-egfp infected chromaffin cells. Scale bars represent 2 µm. (B) Average pixel intensity of Munc18-1 expression obtained from line scans through a confocal section of a BoNT/C and EGFP expressing cell. Inset shows how line scans were made from a to b (C) Quantification of the Munc18-1 expression at the plasma membrane. Numbers indicate mean±SEM. from n = 22 cells and N = 3 animals (***p<0.01, ANOVA and student's t-test, comparison to control). |
PMC1762430_pone-0000126-g005_8264.jpg | What is the core subject represented in this visual? | Distribution of Munc18-1 is altered in syntaxin deleted chromaffin cells. (A) Immunolocalization of syntaxin (blue) and Munc18-1 (red) in SFV-egfp or BoNT/C-ires-egfp infected chromaffin cells. Scale bars represent 2 µm. (B) Average pixel intensity of Munc18-1 expression obtained from line scans through a confocal section of a BoNT/C and EGFP expressing cell. Inset shows how line scans were made from a to b (C) Quantification of the Munc18-1 expression at the plasma membrane. Numbers indicate mean±SEM. from n = 22 cells and N = 3 animals (***p<0.01, ANOVA and student's t-test, comparison to control). |
PMC1764004_F1_8280.jpg | What key item or scene is captured in this photo? | Abdominal computed tomographic scan showing an iliac vein thrombosis (a) and ascending thrombosis of the right ovarian vein (b). |
PMC1764004_F2_8281.jpg | What is the core subject represented in this visual? | Abdominal computed tomographic scan showing a common iliac vein thrombosis. |
PMC1764006_F2_8282.jpg | What is the core subject represented in this visual? | Macrodontia of upper central incisors is a constant feature of KBG syndrome (a). Fusion of upper and lateral right incisors is evident in this other patient on physical (b) and panorex film (c) examination. |
PMC1764006_F2_8284.jpg | What is the focal point of this photograph? | Macrodontia of upper central incisors is a constant feature of KBG syndrome (a). Fusion of upper and lateral right incisors is evident in this other patient on physical (b) and panorex film (c) examination. |
PMC1764006_F2_8283.jpg | What is the core subject represented in this visual? | Macrodontia of upper central incisors is a constant feature of KBG syndrome (a). Fusion of upper and lateral right incisors is evident in this other patient on physical (b) and panorex film (c) examination. |
PMC1764006_F3_8286.jpg | What is the central feature of this picture? | Common skeletal defects observed in KBG syndrome include supernumerary cervical rib (a, arrow), schisis of the posterior arch of cervical (b, arrow) and/or sacral (c, arrow) vertebrae. Left hand X-ray of a 10-year-old male KBG patient (d) showing shortened tubular bones especially of the III-IV-V metacarpus, the I distal and the V middle phalanges with clinodactylous V finger. Bone age is delayed in particular with respect to carpal bones. |
PMC1764006_F3_8287.jpg | What is the dominant medical problem in this image? | Common skeletal defects observed in KBG syndrome include supernumerary cervical rib (a, arrow), schisis of the posterior arch of cervical (b, arrow) and/or sacral (c, arrow) vertebrae. Left hand X-ray of a 10-year-old male KBG patient (d) showing shortened tubular bones especially of the III-IV-V metacarpus, the I distal and the V middle phalanges with clinodactylous V finger. Bone age is delayed in particular with respect to carpal bones. |
PMC1764006_F3_8288.jpg | Describe the main subject of this image. | Common skeletal defects observed in KBG syndrome include supernumerary cervical rib (a, arrow), schisis of the posterior arch of cervical (b, arrow) and/or sacral (c, arrow) vertebrae. Left hand X-ray of a 10-year-old male KBG patient (d) showing shortened tubular bones especially of the III-IV-V metacarpus, the I distal and the V middle phalanges with clinodactylous V finger. Bone age is delayed in particular with respect to carpal bones. |
PMC1764006_F3_8285.jpg | What is the central feature of this picture? | Common skeletal defects observed in KBG syndrome include supernumerary cervical rib (a, arrow), schisis of the posterior arch of cervical (b, arrow) and/or sacral (c, arrow) vertebrae. Left hand X-ray of a 10-year-old male KBG patient (d) showing shortened tubular bones especially of the III-IV-V metacarpus, the I distal and the V middle phalanges with clinodactylous V finger. Bone age is delayed in particular with respect to carpal bones. |
PMC1764169_f3-ehp0114-a00700_8290.jpg | What is shown in this image? | Biomarkers of biologically effective dose assess the interaction of toxicants with molecular targets such as protein receptors. |
PMC1764169_f3-ehp0114-a00700_8289.jpg | What is the central feature of this picture? | Biomarkers of biologically effective dose assess the interaction of toxicants with molecular targets such as protein receptors. |
PMC1764417_F2_8292.jpg | What is shown in this image? | (A) A 77 year old woman presented ten years after craniotomy for acoustic neuroma resection with deafness. An axial MRI of the brain after gadolinium administration demonstrated radiographic progression of disease within the left internal acoustic meatus. (B) Planning CT scan with IV contrast. The patient was treated with 2500 cGy to the 84% isodose line in five stages. |
PMC1764417_F2_8291.jpg | What's the most prominent thing you notice in this picture? | (A) A 77 year old woman presented ten years after craniotomy for acoustic neuroma resection with deafness. An axial MRI of the brain after gadolinium administration demonstrated radiographic progression of disease within the left internal acoustic meatus. (B) Planning CT scan with IV contrast. The patient was treated with 2500 cGy to the 84% isodose line in five stages. |
PMC1764419_F3_8294.jpg | What is the focal point of this photograph? | Cellular uptake of methanol C60. (A). Phase contrast image of a MDA MB231 cell which has internalized a C60 cluster. Intracellular C60 retains its PL signature. Scale bar is 20 μm. (B). Confocal microscopy of internalized C60 aggregates (red) identified with arrows. Methanol C60-treated MCF10A cells were plated on collagen coated chamber slides, fixed, counterstained with FITC-phalloidin. A compiled 3-dimensional projection of optically sectioned z-stack is shown. Scale bar is 5 μm. |
PMC1764419_F3_8293.jpg | What can you see in this picture? | Cellular uptake of methanol C60. (A). Phase contrast image of a MDA MB231 cell which has internalized a C60 cluster. Intracellular C60 retains its PL signature. Scale bar is 20 μm. (B). Confocal microscopy of internalized C60 aggregates (red) identified with arrows. Methanol C60-treated MCF10A cells were plated on collagen coated chamber slides, fixed, counterstained with FITC-phalloidin. A compiled 3-dimensional projection of optically sectioned z-stack is shown. Scale bar is 5 μm. |
PMC1764420_F2_8295.jpg | What is the central feature of this picture? | Scanning electron microscopy (SEM) and energy-dispersive X-ray analysis (EDAX) of the coal sample containing the most sulphur (NIST # 2685b). The top image A shows grains of carbonaceous material with a cluster of 'bright' crystals. Image B is shows the 'bright' crystals magnified and an EDAX spectrum focused on the crystals reveals the presence of iron and sulfur (C). An equivalent spectrum was recorded on a pyrite sample (not shown). An energy of 15 kV and a working distance of 8 mm were used for both A and B, 1500 × and 15000 × magnifications were used for A and B, respectively. |
PMC1764420_F2_8296.jpg | What's the most prominent thing you notice in this picture? | Scanning electron microscopy (SEM) and energy-dispersive X-ray analysis (EDAX) of the coal sample containing the most sulphur (NIST # 2685b). The top image A shows grains of carbonaceous material with a cluster of 'bright' crystals. Image B is shows the 'bright' crystals magnified and an EDAX spectrum focused on the crystals reveals the presence of iron and sulfur (C). An equivalent spectrum was recorded on a pyrite sample (not shown). An energy of 15 kV and a working distance of 8 mm were used for both A and B, 1500 × and 15000 × magnifications were used for A and B, respectively. |
PMC1764428_F7_8298.jpg | What is the main focus of this visual representation? | Ribbon representations. Ribbon diagram corresponding to the prediction of the tertiary structure of K. lactis β-galactosidase (A), A. niger β-galactosidase (B) and hybrid β-galactosidase (C) using the Swiss-Model program. The residues mentioned in Figure 1 have been drawn as spheres of colours (E482 blue, M522 green, Y523 yellow, E551 red). D1–D5 identify the five domains of K. lactis β-galactosidase (A) predicted by alignment in comparison with the sequence of the E. coli β-galactosidase (Figure 1). The fifth domain of the A. niger β-galactosidase is coloured in green (B and C). The white arrow (C) shows the slight opening of the third domain in the hybridβ-galactosidase. |
PMC1764428_F7_8299.jpg | What is being portrayed in this visual content? | Ribbon representations. Ribbon diagram corresponding to the prediction of the tertiary structure of K. lactis β-galactosidase (A), A. niger β-galactosidase (B) and hybrid β-galactosidase (C) using the Swiss-Model program. The residues mentioned in Figure 1 have been drawn as spheres of colours (E482 blue, M522 green, Y523 yellow, E551 red). D1–D5 identify the five domains of K. lactis β-galactosidase (A) predicted by alignment in comparison with the sequence of the E. coli β-galactosidase (Figure 1). The fifth domain of the A. niger β-galactosidase is coloured in green (B and C). The white arrow (C) shows the slight opening of the third domain in the hybridβ-galactosidase. |
PMC1764429_F2_8309.jpg | What is the principal component of this image? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8314.jpg | What's the most prominent thing you notice in this picture? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8313.jpg | What can you see in this picture? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8306.jpg | Describe the main subject of this image. | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8311.jpg | What is the main focus of this visual representation? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8316.jpg | What is the main focus of this visual representation? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8310.jpg | What's the most prominent thing you notice in this picture? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8308.jpg | What key item or scene is captured in this photo? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8315.jpg | What is the main focus of this visual representation? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8305.jpg | Can you identify the primary element in this image? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764429_F2_8312.jpg | What object or scene is depicted here? | Top row, left: Admission CT showing hypoattenuation of the right lentiform nucleus and insular cortex as well as slight swelling of cortical sulci in the right frontoparietal region. Top row, the third and the fourth pictures: The perfusion CT on admission, with flow and mean transit time CT showing a broad perfusion deficit in the right MCA region. Top row, the second picture: The volume chart shows only a small deficit in the right MCA region, consistent with the presence of a large ischemic penumbra in the cortical cerebral tissue. Middle row: The follow-up brain MRI showing the presence of a limited subcortical infarct on the distal region of the right lentiform nucleus and corona radiata. Signs of only a subtle cortical infarction are seen. From left to right: FLAIR MRI, T2-diffusion-weighted MRI, apparent diffusion coefficient. Middle row, right: The persistence of the right MCA occlusion on the follow up MRA. Bottom row: Day 2 CT showed that the extent of the subcortical infarct was substantially smaller than that of the perfusion deficit found in the CT perfusion brain scan obtained on admission. |
PMC1764431_F1_8302.jpg | What object or scene is depicted here? | Immunohistochemical labeling of CD8+ and CD3+/FOXP3+ T cells of representative colon cancer specimens with one case demonstrating a high number of CD8+ T cells (A) and CD3+ T cells (red, membranous) with a high proportion of regulatory T cells co-expressing FOXP3 (brown, nuclear) in the stroma (C) and the malignant epithelium of the tumor (inset) and another case with a low number of CD8+ T cells (B) and only a few CD3+ T cells and FOXP3+ Treg (D). |
PMC1764431_F1_8301.jpg | What is the dominant medical problem in this image? | Immunohistochemical labeling of CD8+ and CD3+/FOXP3+ T cells of representative colon cancer specimens with one case demonstrating a high number of CD8+ T cells (A) and CD3+ T cells (red, membranous) with a high proportion of regulatory T cells co-expressing FOXP3 (brown, nuclear) in the stroma (C) and the malignant epithelium of the tumor (inset) and another case with a low number of CD8+ T cells (B) and only a few CD3+ T cells and FOXP3+ Treg (D). |
PMC1764431_F1_8303.jpg | Describe the main subject of this image. | Immunohistochemical labeling of CD8+ and CD3+/FOXP3+ T cells of representative colon cancer specimens with one case demonstrating a high number of CD8+ T cells (A) and CD3+ T cells (red, membranous) with a high proportion of regulatory T cells co-expressing FOXP3 (brown, nuclear) in the stroma (C) and the malignant epithelium of the tumor (inset) and another case with a low number of CD8+ T cells (B) and only a few CD3+ T cells and FOXP3+ Treg (D). |
PMC1764431_F1_8304.jpg | What is shown in this image? | Immunohistochemical labeling of CD8+ and CD3+/FOXP3+ T cells of representative colon cancer specimens with one case demonstrating a high number of CD8+ T cells (A) and CD3+ T cells (red, membranous) with a high proportion of regulatory T cells co-expressing FOXP3 (brown, nuclear) in the stroma (C) and the malignant epithelium of the tumor (inset) and another case with a low number of CD8+ T cells (B) and only a few CD3+ T cells and FOXP3+ Treg (D). |
PMC1764646_pone-0000148-g003_8320.jpg | What does this image primarily show? | In situ hybridization showing bright (A, C, E, G) and corresponding dark (B, D, F, H) field views of a serial sections through an artery from the intact antler tip (A–D), and an artery from the denervated antler tip (E–H) of the same deer. A and B, E and F binding of the antisense NGF riboprobe, while C and D, and G and H show the sense NGF riboprobe. Bar = 100 um. The magnification of figure 3D applies to the figures 3E to 3H. |
PMC1764646_pone-0000148-g003_8318.jpg | What can you see in this picture? | In situ hybridization showing bright (A, C, E, G) and corresponding dark (B, D, F, H) field views of a serial sections through an artery from the intact antler tip (A–D), and an artery from the denervated antler tip (E–H) of the same deer. A and B, E and F binding of the antisense NGF riboprobe, while C and D, and G and H show the sense NGF riboprobe. Bar = 100 um. The magnification of figure 3D applies to the figures 3E to 3H. |
PMC1764646_pone-0000148-g003_8325.jpg | What stands out most in this visual? | In situ hybridization showing bright (A, C, E, G) and corresponding dark (B, D, F, H) field views of a serial sections through an artery from the intact antler tip (A–D), and an artery from the denervated antler tip (E–H) of the same deer. A and B, E and F binding of the antisense NGF riboprobe, while C and D, and G and H show the sense NGF riboprobe. Bar = 100 um. The magnification of figure 3D applies to the figures 3E to 3H. |
PMC1764646_pone-0000148-g003_8322.jpg | What is the focal point of this photograph? | In situ hybridization showing bright (A, C, E, G) and corresponding dark (B, D, F, H) field views of a serial sections through an artery from the intact antler tip (A–D), and an artery from the denervated antler tip (E–H) of the same deer. A and B, E and F binding of the antisense NGF riboprobe, while C and D, and G and H show the sense NGF riboprobe. Bar = 100 um. The magnification of figure 3D applies to the figures 3E to 3H. |
PMC1764646_pone-0000148-g003_8323.jpg | Describe the main subject of this image. | In situ hybridization showing bright (A, C, E, G) and corresponding dark (B, D, F, H) field views of a serial sections through an artery from the intact antler tip (A–D), and an artery from the denervated antler tip (E–H) of the same deer. A and B, E and F binding of the antisense NGF riboprobe, while C and D, and G and H show the sense NGF riboprobe. Bar = 100 um. The magnification of figure 3D applies to the figures 3E to 3H. |
PMC1764646_pone-0000148-g003_8319.jpg | What is the core subject represented in this visual? | In situ hybridization showing bright (A, C, E, G) and corresponding dark (B, D, F, H) field views of a serial sections through an artery from the intact antler tip (A–D), and an artery from the denervated antler tip (E–H) of the same deer. A and B, E and F binding of the antisense NGF riboprobe, while C and D, and G and H show the sense NGF riboprobe. Bar = 100 um. The magnification of figure 3D applies to the figures 3E to 3H. |
PMC1764646_pone-0000148-g003_8324.jpg | What is the core subject represented in this visual? | In situ hybridization showing bright (A, C, E, G) and corresponding dark (B, D, F, H) field views of a serial sections through an artery from the intact antler tip (A–D), and an artery from the denervated antler tip (E–H) of the same deer. A and B, E and F binding of the antisense NGF riboprobe, while C and D, and G and H show the sense NGF riboprobe. Bar = 100 um. The magnification of figure 3D applies to the figures 3E to 3H. |
PMC1764646_pone-0000148-g003_8321.jpg | What is being portrayed in this visual content? | In situ hybridization showing bright (A, C, E, G) and corresponding dark (B, D, F, H) field views of a serial sections through an artery from the intact antler tip (A–D), and an artery from the denervated antler tip (E–H) of the same deer. A and B, E and F binding of the antisense NGF riboprobe, while C and D, and G and H show the sense NGF riboprobe. Bar = 100 um. The magnification of figure 3D applies to the figures 3E to 3H. |
PMC1764646_pone-0000148-g004_8317.jpg | What stands out most in this visual? | Layer identification of unstained proliferative zone in a growing antler tip. D, RM, PC, TZ, C, are the same as shown in Figure 1. Rectangular box indicates position where tissue was sampled for in situ hybridization. |
PMC1764718_pone-0000156-g006_8337.jpg | What is the dominant medical problem in this image? | 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_8328.jpg | What is the principal component of this image? | 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_8335.jpg | What is the dominant medical problem in this image? | 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_8329.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_8334.jpg | What object or scene is depicted here? | 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_8331.jpg | Can you identify the primary element in this image? | 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_8339.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_8340.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. |
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