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PMC1853120_pgen-0030062-g001_10556.jpg | What is the main focus of this visual representation? | Expression of Dmrt7 mRNA and Protein(A) RT-PCR analysis of Dmrt7 mRNA from ten organs of adult mouse. cDNA from each organ was amplified with primers specific for Dmrt7 (top row) and β-actin (bottom row).(B) Dmrt7 mRNA expression during the first round of spermatogenesis. cDNAs obtained from testis at the indicated days after birth were amplified as in (A).(C) DMRT7 protein expression. Immunofluorescence of testis sections from 6-wk-old male stained with antibody to DMRT7 (green) and DAPI (blue).(D) DMRT7 subcellular localization to XY body. Testis sections from 6-wk-old male stained with antibodies to DMRT7 (red) and SUMO-1 (green). SUMO-1 is localized to the XY body. Right-most panel shows merge of other two panels. Inserts show higher magnification of pachytene spermatocytes with XY bodies. |
PMC1853120_pgen-0030062-g001_10558.jpg | What can you see in this picture? | Expression of Dmrt7 mRNA and Protein(A) RT-PCR analysis of Dmrt7 mRNA from ten organs of adult mouse. cDNA from each organ was amplified with primers specific for Dmrt7 (top row) and β-actin (bottom row).(B) Dmrt7 mRNA expression during the first round of spermatogenesis. cDNAs obtained from testis at the indicated days after birth were amplified as in (A).(C) DMRT7 protein expression. Immunofluorescence of testis sections from 6-wk-old male stained with antibody to DMRT7 (green) and DAPI (blue).(D) DMRT7 subcellular localization to XY body. Testis sections from 6-wk-old male stained with antibodies to DMRT7 (red) and SUMO-1 (green). SUMO-1 is localized to the XY body. Right-most panel shows merge of other two panels. Inserts show higher magnification of pachytene spermatocytes with XY bodies. |
PMC1853120_pgen-0030062-g001_10557.jpg | What is the main focus of this visual representation? | Expression of Dmrt7 mRNA and Protein(A) RT-PCR analysis of Dmrt7 mRNA from ten organs of adult mouse. cDNA from each organ was amplified with primers specific for Dmrt7 (top row) and β-actin (bottom row).(B) Dmrt7 mRNA expression during the first round of spermatogenesis. cDNAs obtained from testis at the indicated days after birth were amplified as in (A).(C) DMRT7 protein expression. Immunofluorescence of testis sections from 6-wk-old male stained with antibody to DMRT7 (green) and DAPI (blue).(D) DMRT7 subcellular localization to XY body. Testis sections from 6-wk-old male stained with antibodies to DMRT7 (red) and SUMO-1 (green). SUMO-1 is localized to the XY body. Right-most panel shows merge of other two panels. Inserts show higher magnification of pachytene spermatocytes with XY bodies. |
PMC1853120_pgen-0030062-g001_10559.jpg | What is being portrayed in this visual content? | Expression of Dmrt7 mRNA and Protein(A) RT-PCR analysis of Dmrt7 mRNA from ten organs of adult mouse. cDNA from each organ was amplified with primers specific for Dmrt7 (top row) and β-actin (bottom row).(B) Dmrt7 mRNA expression during the first round of spermatogenesis. cDNAs obtained from testis at the indicated days after birth were amplified as in (A).(C) DMRT7 protein expression. Immunofluorescence of testis sections from 6-wk-old male stained with antibody to DMRT7 (green) and DAPI (blue).(D) DMRT7 subcellular localization to XY body. Testis sections from 6-wk-old male stained with antibodies to DMRT7 (red) and SUMO-1 (green). SUMO-1 is localized to the XY body. Right-most panel shows merge of other two panels. Inserts show higher magnification of pachytene spermatocytes with XY bodies. |
PMC1853238_pone-0000409-g003_10566.jpg | Describe the main subject of this image. | Reversibility of Plk1 inhibition of cytokinesis and anaphase B.A) DIC images from a timelapse video of HeLa cells treated with BTO-1 for 15 minutes after anaphase onset. Inhibitor was removed at 15 minutes, second panel represents first timelapse image after inhibitor removal. Time in minutes after anaphase is shown in the lower right hand corner. B) Normalized spindle length in cells after inhibitor washout. Control data is the same data shown previously in Figure 2C for reference. BTO-1 washout (closed triangles) represents an average of 5 timelapse recordings. C) Normalized furrow width showing cytokinesis recovery after BTO-1 washout (closed triangles) (n = 5). Dashed lines represent time of washout. The half-time of furrow ingression following BTO-1 washout is 23.46±3.72 minutes post anaphase onset. T1/2 is shown±SD. |
PMC1853238_pone-0000409-g003_10563.jpg | What is the core subject represented in this visual? | Reversibility of Plk1 inhibition of cytokinesis and anaphase B.A) DIC images from a timelapse video of HeLa cells treated with BTO-1 for 15 minutes after anaphase onset. Inhibitor was removed at 15 minutes, second panel represents first timelapse image after inhibitor removal. Time in minutes after anaphase is shown in the lower right hand corner. B) Normalized spindle length in cells after inhibitor washout. Control data is the same data shown previously in Figure 2C for reference. BTO-1 washout (closed triangles) represents an average of 5 timelapse recordings. C) Normalized furrow width showing cytokinesis recovery after BTO-1 washout (closed triangles) (n = 5). Dashed lines represent time of washout. The half-time of furrow ingression following BTO-1 washout is 23.46±3.72 minutes post anaphase onset. T1/2 is shown±SD. |
PMC1853238_pone-0000409-g003_10565.jpg | Can you identify the primary element in this image? | Reversibility of Plk1 inhibition of cytokinesis and anaphase B.A) DIC images from a timelapse video of HeLa cells treated with BTO-1 for 15 minutes after anaphase onset. Inhibitor was removed at 15 minutes, second panel represents first timelapse image after inhibitor removal. Time in minutes after anaphase is shown in the lower right hand corner. B) Normalized spindle length in cells after inhibitor washout. Control data is the same data shown previously in Figure 2C for reference. BTO-1 washout (closed triangles) represents an average of 5 timelapse recordings. C) Normalized furrow width showing cytokinesis recovery after BTO-1 washout (closed triangles) (n = 5). Dashed lines represent time of washout. The half-time of furrow ingression following BTO-1 washout is 23.46±3.72 minutes post anaphase onset. T1/2 is shown±SD. |
PMC1853238_pone-0000409-g003_10564.jpg | Describe the main subject of this image. | Reversibility of Plk1 inhibition of cytokinesis and anaphase B.A) DIC images from a timelapse video of HeLa cells treated with BTO-1 for 15 minutes after anaphase onset. Inhibitor was removed at 15 minutes, second panel represents first timelapse image after inhibitor removal. Time in minutes after anaphase is shown in the lower right hand corner. B) Normalized spindle length in cells after inhibitor washout. Control data is the same data shown previously in Figure 2C for reference. BTO-1 washout (closed triangles) represents an average of 5 timelapse recordings. C) Normalized furrow width showing cytokinesis recovery after BTO-1 washout (closed triangles) (n = 5). Dashed lines represent time of washout. The half-time of furrow ingression following BTO-1 washout is 23.46±3.72 minutes post anaphase onset. T1/2 is shown±SD. |
PMC1853239_pone-0000410-g009_10567.jpg | Describe the main subject of this image. | Regions of the visual cortex that were most sensitive to stimulus position.A. The positive (red-orange) and negative (green-blue) BOLD response to the flickering Gabors for a representative subject. B. Position discrimination slopes (as in Fig. 7) were measured for every possible 5 mm3 ROI in the occipital lobe (see Materials and methods). Those overlapping ROIs that showed the steepest position discrimination slopes are shown in dark blue and outlined with a dashed white line. Notice that the region of the visual cortex that is most sensitive to stimulus position (within the white dashed line) falls between the positive and negative BOLD regions in (A). This supports the idea that the edges of the object representation, where the BOLD response changes from positive to negative, are especially important for object localization [37], [48]. |
PMC1853239_pone-0000410-g009_10568.jpg | What is the main focus of this visual representation? | Regions of the visual cortex that were most sensitive to stimulus position.A. The positive (red-orange) and negative (green-blue) BOLD response to the flickering Gabors for a representative subject. B. Position discrimination slopes (as in Fig. 7) were measured for every possible 5 mm3 ROI in the occipital lobe (see Materials and methods). Those overlapping ROIs that showed the steepest position discrimination slopes are shown in dark blue and outlined with a dashed white line. Notice that the region of the visual cortex that is most sensitive to stimulus position (within the white dashed line) falls between the positive and negative BOLD regions in (A). This supports the idea that the edges of the object representation, where the BOLD response changes from positive to negative, are especially important for object localization [37], [48]. |
PMC1854901_F2_10569.jpg | What is the main focus of this visual representation? | 3-D volume rendering of the medial portion of the foot (Yin qiao mai meridian): the points studied correspond to: 1) Tendino-muscular segment of the flexor digitorum longus, 2) Tendon of the flexor digitorum longus on the talus, and 3) abductor hallucis muscle. |
PMC1854901_F3_10570.jpg | What is the central feature of this picture? | 3-D volume rendering of the lateral portion of the foot (Yang qiao mai meridian): the points studied correspond to: 4) Tendino-muscular segment of the peroneus brevis, 5) Tendon of the peroneus longus on the lateral ankle, 6) Lateral surface of the calcaneus, 7) abductor digiti minimi muscle. |
PMC1854912_pbio-0050119-g002_10577.jpg | Describe the main subject of this image. | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10576.jpg | What object or scene is depicted here? | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10573.jpg | What key item or scene is captured in this photo? | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10583.jpg | What stands out most in this visual? | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10580.jpg | What does this image primarily show? | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10579.jpg | Describe the main subject of this image. | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10575.jpg | What can you see in this picture? | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10581.jpg | What's the most prominent thing you notice in this picture? | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10582.jpg | Can you identify the primary element in this image? | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10578.jpg | What is the focal point of this photograph? | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g002_10574.jpg | What does this image primarily show? | Small Strokes Escape Immediate Damage to Dendrites(A) Images from a YFP mouse showing the vasculature (red) and dendrites (green) (maximal intensity projection of first 100 μm of the cortex) before and 30 min after photoactivation (1 min) of RB in an animal that resulted in severe ischemia and dendritic damage (>0.40 mm2 surrounding area with clotted vessels). Vessels labeled with TR-dextran were all clotted in the imaged region.(B) A higher magnification view of the white-boxed region in (A) before and 30 min after photothrombosis.(C) Dorsal view of the microvasculature (maximal intensity projection) from 100 planar scans acquired every 1 μm before, 30 min, and 1 h after photoactivation of RB in a different animal with a small stroke (0.13 mm2 of cortical surface with clotted vessels) only affecting a subset of vessels. Flowing vessels can be assessed by the streaked images of vessels reflecting scanning of moving RBCs. The percentage of clotted vessels was 34% and 32% for 30 min and 1 h, respectively. The red arrowhead shows a capillary that was clotted at 30 min and was reperfused at 1 h, and the blue arrowheads mark a capillary that was flowing at 30 min but was clotted at 1 h.(D) Z-projection of dendrites from the yellow-boxed region in (C) showing relatively slow degeneration of dendritic structure for this relatively small stroke with partial reduction in blood flow.(E) Magnified view (yellow box in [D]) showing spine structural changes. |
PMC1854912_pbio-0050119-g004_10601.jpg | What is shown in this image? | The Relationship between Dendritic Damage Borders and Flowing Vessels(A) Image of the vasculature (maximal intensity projection of first 100 μm of the cortex) 90 min after laser-induced photoactivation of RB. Small flowing vessels are marked in red. The dashed line indicates a large flowing vessel. Green lines denote dendritic damage border as shown in (B).(B) A sub-stack Z-projection (20 μm) showing dendritic structure and dendritic damage border (green lines) 90 min after laser-induced photoactivation of RB. The blue box indicates areas in which dendritic damage borders were examined. Because it was possible that flowing vessels could be located near the edge of an image, a 50-μm buffer zone indicated by the blue line was used to avoid measurements near the border. Distances between the damage border and the nearest small (<15 μm) or large flowing vessel (>15 μm) were made at 10 μm intervals along the green borderline.(C) Representative flowing vessels labeled in (A). Flowing vessels were assessed by determining whether streaking or banding was present (see below).(D) Representative stalled vessels labeled in (A).(E) An example showing vessel streaking or banding that are indicative of objects moving parallel or perpendicular to the direction of scanning (horizontal). The images shown are the average of three consecutive frames, which compresses the width of the bands due to overlap. This single vessel was oriented both parallel and perpendicular to the scan axis and shows that streaks are converted to bands when the angle between the scan direction and the vessel changes (this was also demonstrated by turning the scan angle 90 degrees, not shown). A single linescan through the horizontal part of this flowing vessel is shown on the right showing the velocity and supply rate of RBCs for this vessel.(F) Group data from ten different animals show the cumulative probability distribution of distances between the dendritic damage border and the nearest flowing small or large vessel; to small vessel (n = 673 measurements, red line); to large vessel (n = 704 measurements, black line) after RB photothrombosis. The cumulative probability distribution of distances between individual spines and the nearest flowing capillary in normal animals (green line) are also shown for comparison; from n = 3 animals (250 measurements) from [15]. The cumulative probability distributions were significantly different between groups (Kolmogorov-Smirnov test, p < 0.0001). |
PMC1854912_pbio-0050119-g004_10596.jpg | Describe the main subject of this image. | The Relationship between Dendritic Damage Borders and Flowing Vessels(A) Image of the vasculature (maximal intensity projection of first 100 μm of the cortex) 90 min after laser-induced photoactivation of RB. Small flowing vessels are marked in red. The dashed line indicates a large flowing vessel. Green lines denote dendritic damage border as shown in (B).(B) A sub-stack Z-projection (20 μm) showing dendritic structure and dendritic damage border (green lines) 90 min after laser-induced photoactivation of RB. The blue box indicates areas in which dendritic damage borders were examined. Because it was possible that flowing vessels could be located near the edge of an image, a 50-μm buffer zone indicated by the blue line was used to avoid measurements near the border. Distances between the damage border and the nearest small (<15 μm) or large flowing vessel (>15 μm) were made at 10 μm intervals along the green borderline.(C) Representative flowing vessels labeled in (A). Flowing vessels were assessed by determining whether streaking or banding was present (see below).(D) Representative stalled vessels labeled in (A).(E) An example showing vessel streaking or banding that are indicative of objects moving parallel or perpendicular to the direction of scanning (horizontal). The images shown are the average of three consecutive frames, which compresses the width of the bands due to overlap. This single vessel was oriented both parallel and perpendicular to the scan axis and shows that streaks are converted to bands when the angle between the scan direction and the vessel changes (this was also demonstrated by turning the scan angle 90 degrees, not shown). A single linescan through the horizontal part of this flowing vessel is shown on the right showing the velocity and supply rate of RBCs for this vessel.(F) Group data from ten different animals show the cumulative probability distribution of distances between the dendritic damage border and the nearest flowing small or large vessel; to small vessel (n = 673 measurements, red line); to large vessel (n = 704 measurements, black line) after RB photothrombosis. The cumulative probability distribution of distances between individual spines and the nearest flowing capillary in normal animals (green line) are also shown for comparison; from n = 3 animals (250 measurements) from [15]. The cumulative probability distributions were significantly different between groups (Kolmogorov-Smirnov test, p < 0.0001). |
PMC1854912_pbio-0050119-g004_10600.jpg | What object or scene is depicted here? | The Relationship between Dendritic Damage Borders and Flowing Vessels(A) Image of the vasculature (maximal intensity projection of first 100 μm of the cortex) 90 min after laser-induced photoactivation of RB. Small flowing vessels are marked in red. The dashed line indicates a large flowing vessel. Green lines denote dendritic damage border as shown in (B).(B) A sub-stack Z-projection (20 μm) showing dendritic structure and dendritic damage border (green lines) 90 min after laser-induced photoactivation of RB. The blue box indicates areas in which dendritic damage borders were examined. Because it was possible that flowing vessels could be located near the edge of an image, a 50-μm buffer zone indicated by the blue line was used to avoid measurements near the border. Distances between the damage border and the nearest small (<15 μm) or large flowing vessel (>15 μm) were made at 10 μm intervals along the green borderline.(C) Representative flowing vessels labeled in (A). Flowing vessels were assessed by determining whether streaking or banding was present (see below).(D) Representative stalled vessels labeled in (A).(E) An example showing vessel streaking or banding that are indicative of objects moving parallel or perpendicular to the direction of scanning (horizontal). The images shown are the average of three consecutive frames, which compresses the width of the bands due to overlap. This single vessel was oriented both parallel and perpendicular to the scan axis and shows that streaks are converted to bands when the angle between the scan direction and the vessel changes (this was also demonstrated by turning the scan angle 90 degrees, not shown). A single linescan through the horizontal part of this flowing vessel is shown on the right showing the velocity and supply rate of RBCs for this vessel.(F) Group data from ten different animals show the cumulative probability distribution of distances between the dendritic damage border and the nearest flowing small or large vessel; to small vessel (n = 673 measurements, red line); to large vessel (n = 704 measurements, black line) after RB photothrombosis. The cumulative probability distribution of distances between individual spines and the nearest flowing capillary in normal animals (green line) are also shown for comparison; from n = 3 animals (250 measurements) from [15]. The cumulative probability distributions were significantly different between groups (Kolmogorov-Smirnov test, p < 0.0001). |
PMC1854912_pbio-0050119-g004_10595.jpg | Describe the main subject of this image. | The Relationship between Dendritic Damage Borders and Flowing Vessels(A) Image of the vasculature (maximal intensity projection of first 100 μm of the cortex) 90 min after laser-induced photoactivation of RB. Small flowing vessels are marked in red. The dashed line indicates a large flowing vessel. Green lines denote dendritic damage border as shown in (B).(B) A sub-stack Z-projection (20 μm) showing dendritic structure and dendritic damage border (green lines) 90 min after laser-induced photoactivation of RB. The blue box indicates areas in which dendritic damage borders were examined. Because it was possible that flowing vessels could be located near the edge of an image, a 50-μm buffer zone indicated by the blue line was used to avoid measurements near the border. Distances between the damage border and the nearest small (<15 μm) or large flowing vessel (>15 μm) were made at 10 μm intervals along the green borderline.(C) Representative flowing vessels labeled in (A). Flowing vessels were assessed by determining whether streaking or banding was present (see below).(D) Representative stalled vessels labeled in (A).(E) An example showing vessel streaking or banding that are indicative of objects moving parallel or perpendicular to the direction of scanning (horizontal). The images shown are the average of three consecutive frames, which compresses the width of the bands due to overlap. This single vessel was oriented both parallel and perpendicular to the scan axis and shows that streaks are converted to bands when the angle between the scan direction and the vessel changes (this was also demonstrated by turning the scan angle 90 degrees, not shown). A single linescan through the horizontal part of this flowing vessel is shown on the right showing the velocity and supply rate of RBCs for this vessel.(F) Group data from ten different animals show the cumulative probability distribution of distances between the dendritic damage border and the nearest flowing small or large vessel; to small vessel (n = 673 measurements, red line); to large vessel (n = 704 measurements, black line) after RB photothrombosis. The cumulative probability distribution of distances between individual spines and the nearest flowing capillary in normal animals (green line) are also shown for comparison; from n = 3 animals (250 measurements) from [15]. The cumulative probability distributions were significantly different between groups (Kolmogorov-Smirnov test, p < 0.0001). |
PMC1854912_pbio-0050119-g005_10588.jpg | What is the core subject represented in this visual? | No Relationship between Accelerated Extravasation and Loss of Spines after RB Photothrombosis(A) Low-magnification image of the vasculature (maximal intensity projection, 50 μm) before and after photoactivation of RB. A total of 24% percent of vessels were clotted over an ischemic area of 0.05 mm2.(B) Shown are two channel images (a subregion Z-projection) from the boxed region in (A) showing the vasculature (red) and YFP-labeled dendrites (green) before and 1, 4, and 5 h after photoactivation of RB. Vessels were labeled with TR-dextran. The red fluorescence in the tissue indicates extravasation or leakage of plasma containing TR-dextran.(C) A higher-magnification view of a dendritic segment (box in [B]) showing no significant damage or loss of spines despite time-dependent acceleration in extravasation.(D) Quantification of extravasation and spine number over time for this animal. Extravasation was quantified by determining the percentage of vessel TR-dextran fluorescence intensity present in the tissue. Spine number expressed as percentage of the number present before RB photoactivation (n = 174 spines). These data indicated that small strokes are not associated with any significant change in spine number over a 5 h period despite a significant increase in extravasation.(E) Group data from nine different animals show relative changes in extravascation and spine number (data aligned by the timepoint when the maximal rate of extravasaton was observed; set as the 0 timepoint) after RB stroke. A one-way analysis of variance indicated a significant effect of time on both spine loss and extravasation. Individual timepoints were compared to the 0 timepoint using Dunnett's post hoc test. We did not observe a significant change in spine number when the rate of extravasation was maximal.(F) There was no significant correlation between the rate of spine loss, change in spine number between consecutive 1-h timepoints, and extravasation at different times (r
2 = 0.02; p = 0.75; nonparametric Spearman correlation coefficient; same data as [E] analyzed differently). |
PMC1854912_pbio-0050119-g005_10586.jpg | Can you identify the primary element in this image? | No Relationship between Accelerated Extravasation and Loss of Spines after RB Photothrombosis(A) Low-magnification image of the vasculature (maximal intensity projection, 50 μm) before and after photoactivation of RB. A total of 24% percent of vessels were clotted over an ischemic area of 0.05 mm2.(B) Shown are two channel images (a subregion Z-projection) from the boxed region in (A) showing the vasculature (red) and YFP-labeled dendrites (green) before and 1, 4, and 5 h after photoactivation of RB. Vessels were labeled with TR-dextran. The red fluorescence in the tissue indicates extravasation or leakage of plasma containing TR-dextran.(C) A higher-magnification view of a dendritic segment (box in [B]) showing no significant damage or loss of spines despite time-dependent acceleration in extravasation.(D) Quantification of extravasation and spine number over time for this animal. Extravasation was quantified by determining the percentage of vessel TR-dextran fluorescence intensity present in the tissue. Spine number expressed as percentage of the number present before RB photoactivation (n = 174 spines). These data indicated that small strokes are not associated with any significant change in spine number over a 5 h period despite a significant increase in extravasation.(E) Group data from nine different animals show relative changes in extravascation and spine number (data aligned by the timepoint when the maximal rate of extravasaton was observed; set as the 0 timepoint) after RB stroke. A one-way analysis of variance indicated a significant effect of time on both spine loss and extravasation. Individual timepoints were compared to the 0 timepoint using Dunnett's post hoc test. We did not observe a significant change in spine number when the rate of extravasation was maximal.(F) There was no significant correlation between the rate of spine loss, change in spine number between consecutive 1-h timepoints, and extravasation at different times (r
2 = 0.02; p = 0.75; nonparametric Spearman correlation coefficient; same data as [E] analyzed differently). |
PMC1854912_pbio-0050119-g005_10587.jpg | What is the central feature of this picture? | No Relationship between Accelerated Extravasation and Loss of Spines after RB Photothrombosis(A) Low-magnification image of the vasculature (maximal intensity projection, 50 μm) before and after photoactivation of RB. A total of 24% percent of vessels were clotted over an ischemic area of 0.05 mm2.(B) Shown are two channel images (a subregion Z-projection) from the boxed region in (A) showing the vasculature (red) and YFP-labeled dendrites (green) before and 1, 4, and 5 h after photoactivation of RB. Vessels were labeled with TR-dextran. The red fluorescence in the tissue indicates extravasation or leakage of plasma containing TR-dextran.(C) A higher-magnification view of a dendritic segment (box in [B]) showing no significant damage or loss of spines despite time-dependent acceleration in extravasation.(D) Quantification of extravasation and spine number over time for this animal. Extravasation was quantified by determining the percentage of vessel TR-dextran fluorescence intensity present in the tissue. Spine number expressed as percentage of the number present before RB photoactivation (n = 174 spines). These data indicated that small strokes are not associated with any significant change in spine number over a 5 h period despite a significant increase in extravasation.(E) Group data from nine different animals show relative changes in extravascation and spine number (data aligned by the timepoint when the maximal rate of extravasaton was observed; set as the 0 timepoint) after RB stroke. A one-way analysis of variance indicated a significant effect of time on both spine loss and extravasation. Individual timepoints were compared to the 0 timepoint using Dunnett's post hoc test. We did not observe a significant change in spine number when the rate of extravasation was maximal.(F) There was no significant correlation between the rate of spine loss, change in spine number between consecutive 1-h timepoints, and extravasation at different times (r
2 = 0.02; p = 0.75; nonparametric Spearman correlation coefficient; same data as [E] analyzed differently). |
PMC1854912_pbio-0050119-g005_10591.jpg | Can you identify the primary element in this image? | No Relationship between Accelerated Extravasation and Loss of Spines after RB Photothrombosis(A) Low-magnification image of the vasculature (maximal intensity projection, 50 μm) before and after photoactivation of RB. A total of 24% percent of vessels were clotted over an ischemic area of 0.05 mm2.(B) Shown are two channel images (a subregion Z-projection) from the boxed region in (A) showing the vasculature (red) and YFP-labeled dendrites (green) before and 1, 4, and 5 h after photoactivation of RB. Vessels were labeled with TR-dextran. The red fluorescence in the tissue indicates extravasation or leakage of plasma containing TR-dextran.(C) A higher-magnification view of a dendritic segment (box in [B]) showing no significant damage or loss of spines despite time-dependent acceleration in extravasation.(D) Quantification of extravasation and spine number over time for this animal. Extravasation was quantified by determining the percentage of vessel TR-dextran fluorescence intensity present in the tissue. Spine number expressed as percentage of the number present before RB photoactivation (n = 174 spines). These data indicated that small strokes are not associated with any significant change in spine number over a 5 h period despite a significant increase in extravasation.(E) Group data from nine different animals show relative changes in extravascation and spine number (data aligned by the timepoint when the maximal rate of extravasaton was observed; set as the 0 timepoint) after RB stroke. A one-way analysis of variance indicated a significant effect of time on both spine loss and extravasation. Individual timepoints were compared to the 0 timepoint using Dunnett's post hoc test. We did not observe a significant change in spine number when the rate of extravasation was maximal.(F) There was no significant correlation between the rate of spine loss, change in spine number between consecutive 1-h timepoints, and extravasation at different times (r
2 = 0.02; p = 0.75; nonparametric Spearman correlation coefficient; same data as [E] analyzed differently). |
PMC1854912_pbio-0050119-g005_10590.jpg | What key item or scene is captured in this photo? | No Relationship between Accelerated Extravasation and Loss of Spines after RB Photothrombosis(A) Low-magnification image of the vasculature (maximal intensity projection, 50 μm) before and after photoactivation of RB. A total of 24% percent of vessels were clotted over an ischemic area of 0.05 mm2.(B) Shown are two channel images (a subregion Z-projection) from the boxed region in (A) showing the vasculature (red) and YFP-labeled dendrites (green) before and 1, 4, and 5 h after photoactivation of RB. Vessels were labeled with TR-dextran. The red fluorescence in the tissue indicates extravasation or leakage of plasma containing TR-dextran.(C) A higher-magnification view of a dendritic segment (box in [B]) showing no significant damage or loss of spines despite time-dependent acceleration in extravasation.(D) Quantification of extravasation and spine number over time for this animal. Extravasation was quantified by determining the percentage of vessel TR-dextran fluorescence intensity present in the tissue. Spine number expressed as percentage of the number present before RB photoactivation (n = 174 spines). These data indicated that small strokes are not associated with any significant change in spine number over a 5 h period despite a significant increase in extravasation.(E) Group data from nine different animals show relative changes in extravascation and spine number (data aligned by the timepoint when the maximal rate of extravasaton was observed; set as the 0 timepoint) after RB stroke. A one-way analysis of variance indicated a significant effect of time on both spine loss and extravasation. Individual timepoints were compared to the 0 timepoint using Dunnett's post hoc test. We did not observe a significant change in spine number when the rate of extravasation was maximal.(F) There was no significant correlation between the rate of spine loss, change in spine number between consecutive 1-h timepoints, and extravasation at different times (r
2 = 0.02; p = 0.75; nonparametric Spearman correlation coefficient; same data as [E] analyzed differently). |
PMC1854912_pbio-0050119-g005_10593.jpg | Describe the main subject of this image. | No Relationship between Accelerated Extravasation and Loss of Spines after RB Photothrombosis(A) Low-magnification image of the vasculature (maximal intensity projection, 50 μm) before and after photoactivation of RB. A total of 24% percent of vessels were clotted over an ischemic area of 0.05 mm2.(B) Shown are two channel images (a subregion Z-projection) from the boxed region in (A) showing the vasculature (red) and YFP-labeled dendrites (green) before and 1, 4, and 5 h after photoactivation of RB. Vessels were labeled with TR-dextran. The red fluorescence in the tissue indicates extravasation or leakage of plasma containing TR-dextran.(C) A higher-magnification view of a dendritic segment (box in [B]) showing no significant damage or loss of spines despite time-dependent acceleration in extravasation.(D) Quantification of extravasation and spine number over time for this animal. Extravasation was quantified by determining the percentage of vessel TR-dextran fluorescence intensity present in the tissue. Spine number expressed as percentage of the number present before RB photoactivation (n = 174 spines). These data indicated that small strokes are not associated with any significant change in spine number over a 5 h period despite a significant increase in extravasation.(E) Group data from nine different animals show relative changes in extravascation and spine number (data aligned by the timepoint when the maximal rate of extravasaton was observed; set as the 0 timepoint) after RB stroke. A one-way analysis of variance indicated a significant effect of time on both spine loss and extravasation. Individual timepoints were compared to the 0 timepoint using Dunnett's post hoc test. We did not observe a significant change in spine number when the rate of extravasation was maximal.(F) There was no significant correlation between the rate of spine loss, change in spine number between consecutive 1-h timepoints, and extravasation at different times (r
2 = 0.02; p = 0.75; nonparametric Spearman correlation coefficient; same data as [E] analyzed differently). |
PMC1854912_pbio-0050119-g005_10594.jpg | What object or scene is depicted here? | No Relationship between Accelerated Extravasation and Loss of Spines after RB Photothrombosis(A) Low-magnification image of the vasculature (maximal intensity projection, 50 μm) before and after photoactivation of RB. A total of 24% percent of vessels were clotted over an ischemic area of 0.05 mm2.(B) Shown are two channel images (a subregion Z-projection) from the boxed region in (A) showing the vasculature (red) and YFP-labeled dendrites (green) before and 1, 4, and 5 h after photoactivation of RB. Vessels were labeled with TR-dextran. The red fluorescence in the tissue indicates extravasation or leakage of plasma containing TR-dextran.(C) A higher-magnification view of a dendritic segment (box in [B]) showing no significant damage or loss of spines despite time-dependent acceleration in extravasation.(D) Quantification of extravasation and spine number over time for this animal. Extravasation was quantified by determining the percentage of vessel TR-dextran fluorescence intensity present in the tissue. Spine number expressed as percentage of the number present before RB photoactivation (n = 174 spines). These data indicated that small strokes are not associated with any significant change in spine number over a 5 h period despite a significant increase in extravasation.(E) Group data from nine different animals show relative changes in extravascation and spine number (data aligned by the timepoint when the maximal rate of extravasaton was observed; set as the 0 timepoint) after RB stroke. A one-way analysis of variance indicated a significant effect of time on both spine loss and extravasation. Individual timepoints were compared to the 0 timepoint using Dunnett's post hoc test. We did not observe a significant change in spine number when the rate of extravasation was maximal.(F) There was no significant correlation between the rate of spine loss, change in spine number between consecutive 1-h timepoints, and extravasation at different times (r
2 = 0.02; p = 0.75; nonparametric Spearman correlation coefficient; same data as [E] analyzed differently). |
PMC1854912_pbio-0050119-g006_10617.jpg | What stands out most in this visual? | The Relationship between Loss of Dendritic Structure and Activity Dependent Hemodynamic Responses in Animals with Photothrombotic Stroke Targeted to Individual Arteries(A) Shown are laser-speckle surface blood flow images, darker tones indicate lower speckle contrast and higher velocities of blood flow. Left: control speckle contrast image of the right somatosensory cortex (oriented rostral up and medial left). A middle cerebral artery branch and sites where laser induced photothrombosis was performed are indicated by two red lines. Middle: 20 min after targeted photothrombosis blood flow has stopped in photoactivated segment. Blue arrowheads indicate changes in venous blood flow at distant sites. A small black box indicates the location of two-photon imaging shown in (B). Right: 4.5 h after stroke blood flow is still lost within the targeted MCA segment.(B) Image of RB photoactivation location on the MCA branch is indicated by the red line (left-most line). Upstream, to the right of the photoactivation spot a clot can be seen developing. Middle panel: dendritic damage border image taken 90 min after photothrombosis (approximate border indicated by a dashed green line, dendritic damage was reduced below the dashed line). Right: 4 h after photothrombosis dendritic damage worsened, although the approximate border for dendritic damage was in a similar location as that observed at the 90-min timepoint (note the structural transition and some intact dendrites in the lower part of the image).(C) Left: IOS map of contralateral forelimb (FL) and hindlimb (HL) responsive areas (average of 40 trials). Middle: 1 h after stroke the forelimb map has retreated while the hindlimb map is largely preserved (average of 40 trials collected 30–60 min poststroke). Right: raw image of change in reflectance for the 1 h poststroke contralateral forelimb map (images scaled from −0.05% to 0.05% change). The white diagonal and horizontal lines indicate the size and location used for determining response profiles in (D). The locations of MCA branches activated by forelimb stimulation are indicated; the arteries are clearly visible as lighter structures.(D) Quantification of forelimb and hindlimb IOS response from smoothed line profiles indicated in (C) (right). The profiles show a large change in the border of the forelimb territory (left). For the 1-h maps the edge of blebbed dendritic structure was 511 μm from the edge of the forelimb response. The hindlimb functional border was largely unaffected (middle panel). The approximate border locations for IOS responses were maintained for both 1- and 4.5–6-h timepoints. Right: average group data from nine different animals showing distance between the IOS map border and the center of the map for control conditions (column 1) and after stroke (column 2). The distance between the border of morphological dendritic damage and the center of the IOS map is in the third column. The last bar is the difference between bars 2 and 3 for each animal; a measure of the distance between the morphological edge of stroke damage and edge of the IOS response after stroke. Paired t-tests compared column 1 to 2 or 3 (asterisks indicate p < 0.02, alpha reduced since two comparisons were performed). |
PMC1854912_pbio-0050119-g006_10614.jpg | What is the core subject represented in this visual? | The Relationship between Loss of Dendritic Structure and Activity Dependent Hemodynamic Responses in Animals with Photothrombotic Stroke Targeted to Individual Arteries(A) Shown are laser-speckle surface blood flow images, darker tones indicate lower speckle contrast and higher velocities of blood flow. Left: control speckle contrast image of the right somatosensory cortex (oriented rostral up and medial left). A middle cerebral artery branch and sites where laser induced photothrombosis was performed are indicated by two red lines. Middle: 20 min after targeted photothrombosis blood flow has stopped in photoactivated segment. Blue arrowheads indicate changes in venous blood flow at distant sites. A small black box indicates the location of two-photon imaging shown in (B). Right: 4.5 h after stroke blood flow is still lost within the targeted MCA segment.(B) Image of RB photoactivation location on the MCA branch is indicated by the red line (left-most line). Upstream, to the right of the photoactivation spot a clot can be seen developing. Middle panel: dendritic damage border image taken 90 min after photothrombosis (approximate border indicated by a dashed green line, dendritic damage was reduced below the dashed line). Right: 4 h after photothrombosis dendritic damage worsened, although the approximate border for dendritic damage was in a similar location as that observed at the 90-min timepoint (note the structural transition and some intact dendrites in the lower part of the image).(C) Left: IOS map of contralateral forelimb (FL) and hindlimb (HL) responsive areas (average of 40 trials). Middle: 1 h after stroke the forelimb map has retreated while the hindlimb map is largely preserved (average of 40 trials collected 30–60 min poststroke). Right: raw image of change in reflectance for the 1 h poststroke contralateral forelimb map (images scaled from −0.05% to 0.05% change). The white diagonal and horizontal lines indicate the size and location used for determining response profiles in (D). The locations of MCA branches activated by forelimb stimulation are indicated; the arteries are clearly visible as lighter structures.(D) Quantification of forelimb and hindlimb IOS response from smoothed line profiles indicated in (C) (right). The profiles show a large change in the border of the forelimb territory (left). For the 1-h maps the edge of blebbed dendritic structure was 511 μm from the edge of the forelimb response. The hindlimb functional border was largely unaffected (middle panel). The approximate border locations for IOS responses were maintained for both 1- and 4.5–6-h timepoints. Right: average group data from nine different animals showing distance between the IOS map border and the center of the map for control conditions (column 1) and after stroke (column 2). The distance between the border of morphological dendritic damage and the center of the IOS map is in the third column. The last bar is the difference between bars 2 and 3 for each animal; a measure of the distance between the morphological edge of stroke damage and edge of the IOS response after stroke. Paired t-tests compared column 1 to 2 or 3 (asterisks indicate p < 0.02, alpha reduced since two comparisons were performed). |
PMC1854912_pbio-0050119-g006_10613.jpg | What is the core subject represented in this visual? | The Relationship between Loss of Dendritic Structure and Activity Dependent Hemodynamic Responses in Animals with Photothrombotic Stroke Targeted to Individual Arteries(A) Shown are laser-speckle surface blood flow images, darker tones indicate lower speckle contrast and higher velocities of blood flow. Left: control speckle contrast image of the right somatosensory cortex (oriented rostral up and medial left). A middle cerebral artery branch and sites where laser induced photothrombosis was performed are indicated by two red lines. Middle: 20 min after targeted photothrombosis blood flow has stopped in photoactivated segment. Blue arrowheads indicate changes in venous blood flow at distant sites. A small black box indicates the location of two-photon imaging shown in (B). Right: 4.5 h after stroke blood flow is still lost within the targeted MCA segment.(B) Image of RB photoactivation location on the MCA branch is indicated by the red line (left-most line). Upstream, to the right of the photoactivation spot a clot can be seen developing. Middle panel: dendritic damage border image taken 90 min after photothrombosis (approximate border indicated by a dashed green line, dendritic damage was reduced below the dashed line). Right: 4 h after photothrombosis dendritic damage worsened, although the approximate border for dendritic damage was in a similar location as that observed at the 90-min timepoint (note the structural transition and some intact dendrites in the lower part of the image).(C) Left: IOS map of contralateral forelimb (FL) and hindlimb (HL) responsive areas (average of 40 trials). Middle: 1 h after stroke the forelimb map has retreated while the hindlimb map is largely preserved (average of 40 trials collected 30–60 min poststroke). Right: raw image of change in reflectance for the 1 h poststroke contralateral forelimb map (images scaled from −0.05% to 0.05% change). The white diagonal and horizontal lines indicate the size and location used for determining response profiles in (D). The locations of MCA branches activated by forelimb stimulation are indicated; the arteries are clearly visible as lighter structures.(D) Quantification of forelimb and hindlimb IOS response from smoothed line profiles indicated in (C) (right). The profiles show a large change in the border of the forelimb territory (left). For the 1-h maps the edge of blebbed dendritic structure was 511 μm from the edge of the forelimb response. The hindlimb functional border was largely unaffected (middle panel). The approximate border locations for IOS responses were maintained for both 1- and 4.5–6-h timepoints. Right: average group data from nine different animals showing distance between the IOS map border and the center of the map for control conditions (column 1) and after stroke (column 2). The distance between the border of morphological dendritic damage and the center of the IOS map is in the third column. The last bar is the difference between bars 2 and 3 for each animal; a measure of the distance between the morphological edge of stroke damage and edge of the IOS response after stroke. Paired t-tests compared column 1 to 2 or 3 (asterisks indicate p < 0.02, alpha reduced since two comparisons were performed). |
PMC1854912_pbio-0050119-g006_10618.jpg | What is the core subject represented in this visual? | The Relationship between Loss of Dendritic Structure and Activity Dependent Hemodynamic Responses in Animals with Photothrombotic Stroke Targeted to Individual Arteries(A) Shown are laser-speckle surface blood flow images, darker tones indicate lower speckle contrast and higher velocities of blood flow. Left: control speckle contrast image of the right somatosensory cortex (oriented rostral up and medial left). A middle cerebral artery branch and sites where laser induced photothrombosis was performed are indicated by two red lines. Middle: 20 min after targeted photothrombosis blood flow has stopped in photoactivated segment. Blue arrowheads indicate changes in venous blood flow at distant sites. A small black box indicates the location of two-photon imaging shown in (B). Right: 4.5 h after stroke blood flow is still lost within the targeted MCA segment.(B) Image of RB photoactivation location on the MCA branch is indicated by the red line (left-most line). Upstream, to the right of the photoactivation spot a clot can be seen developing. Middle panel: dendritic damage border image taken 90 min after photothrombosis (approximate border indicated by a dashed green line, dendritic damage was reduced below the dashed line). Right: 4 h after photothrombosis dendritic damage worsened, although the approximate border for dendritic damage was in a similar location as that observed at the 90-min timepoint (note the structural transition and some intact dendrites in the lower part of the image).(C) Left: IOS map of contralateral forelimb (FL) and hindlimb (HL) responsive areas (average of 40 trials). Middle: 1 h after stroke the forelimb map has retreated while the hindlimb map is largely preserved (average of 40 trials collected 30–60 min poststroke). Right: raw image of change in reflectance for the 1 h poststroke contralateral forelimb map (images scaled from −0.05% to 0.05% change). The white diagonal and horizontal lines indicate the size and location used for determining response profiles in (D). The locations of MCA branches activated by forelimb stimulation are indicated; the arteries are clearly visible as lighter structures.(D) Quantification of forelimb and hindlimb IOS response from smoothed line profiles indicated in (C) (right). The profiles show a large change in the border of the forelimb territory (left). For the 1-h maps the edge of blebbed dendritic structure was 511 μm from the edge of the forelimb response. The hindlimb functional border was largely unaffected (middle panel). The approximate border locations for IOS responses were maintained for both 1- and 4.5–6-h timepoints. Right: average group data from nine different animals showing distance between the IOS map border and the center of the map for control conditions (column 1) and after stroke (column 2). The distance between the border of morphological dendritic damage and the center of the IOS map is in the third column. The last bar is the difference between bars 2 and 3 for each animal; a measure of the distance between the morphological edge of stroke damage and edge of the IOS response after stroke. Paired t-tests compared column 1 to 2 or 3 (asterisks indicate p < 0.02, alpha reduced since two comparisons were performed). |
PMC1854912_pbio-0050119-g006_10609.jpg | What does this image primarily show? | The Relationship between Loss of Dendritic Structure and Activity Dependent Hemodynamic Responses in Animals with Photothrombotic Stroke Targeted to Individual Arteries(A) Shown are laser-speckle surface blood flow images, darker tones indicate lower speckle contrast and higher velocities of blood flow. Left: control speckle contrast image of the right somatosensory cortex (oriented rostral up and medial left). A middle cerebral artery branch and sites where laser induced photothrombosis was performed are indicated by two red lines. Middle: 20 min after targeted photothrombosis blood flow has stopped in photoactivated segment. Blue arrowheads indicate changes in venous blood flow at distant sites. A small black box indicates the location of two-photon imaging shown in (B). Right: 4.5 h after stroke blood flow is still lost within the targeted MCA segment.(B) Image of RB photoactivation location on the MCA branch is indicated by the red line (left-most line). Upstream, to the right of the photoactivation spot a clot can be seen developing. Middle panel: dendritic damage border image taken 90 min after photothrombosis (approximate border indicated by a dashed green line, dendritic damage was reduced below the dashed line). Right: 4 h after photothrombosis dendritic damage worsened, although the approximate border for dendritic damage was in a similar location as that observed at the 90-min timepoint (note the structural transition and some intact dendrites in the lower part of the image).(C) Left: IOS map of contralateral forelimb (FL) and hindlimb (HL) responsive areas (average of 40 trials). Middle: 1 h after stroke the forelimb map has retreated while the hindlimb map is largely preserved (average of 40 trials collected 30–60 min poststroke). Right: raw image of change in reflectance for the 1 h poststroke contralateral forelimb map (images scaled from −0.05% to 0.05% change). The white diagonal and horizontal lines indicate the size and location used for determining response profiles in (D). The locations of MCA branches activated by forelimb stimulation are indicated; the arteries are clearly visible as lighter structures.(D) Quantification of forelimb and hindlimb IOS response from smoothed line profiles indicated in (C) (right). The profiles show a large change in the border of the forelimb territory (left). For the 1-h maps the edge of blebbed dendritic structure was 511 μm from the edge of the forelimb response. The hindlimb functional border was largely unaffected (middle panel). The approximate border locations for IOS responses were maintained for both 1- and 4.5–6-h timepoints. Right: average group data from nine different animals showing distance between the IOS map border and the center of the map for control conditions (column 1) and after stroke (column 2). The distance between the border of morphological dendritic damage and the center of the IOS map is in the third column. The last bar is the difference between bars 2 and 3 for each animal; a measure of the distance between the morphological edge of stroke damage and edge of the IOS response after stroke. Paired t-tests compared column 1 to 2 or 3 (asterisks indicate p < 0.02, alpha reduced since two comparisons were performed). |
PMC1854912_pbio-0050119-g006_10616.jpg | What is shown in this image? | The Relationship between Loss of Dendritic Structure and Activity Dependent Hemodynamic Responses in Animals with Photothrombotic Stroke Targeted to Individual Arteries(A) Shown are laser-speckle surface blood flow images, darker tones indicate lower speckle contrast and higher velocities of blood flow. Left: control speckle contrast image of the right somatosensory cortex (oriented rostral up and medial left). A middle cerebral artery branch and sites where laser induced photothrombosis was performed are indicated by two red lines. Middle: 20 min after targeted photothrombosis blood flow has stopped in photoactivated segment. Blue arrowheads indicate changes in venous blood flow at distant sites. A small black box indicates the location of two-photon imaging shown in (B). Right: 4.5 h after stroke blood flow is still lost within the targeted MCA segment.(B) Image of RB photoactivation location on the MCA branch is indicated by the red line (left-most line). Upstream, to the right of the photoactivation spot a clot can be seen developing. Middle panel: dendritic damage border image taken 90 min after photothrombosis (approximate border indicated by a dashed green line, dendritic damage was reduced below the dashed line). Right: 4 h after photothrombosis dendritic damage worsened, although the approximate border for dendritic damage was in a similar location as that observed at the 90-min timepoint (note the structural transition and some intact dendrites in the lower part of the image).(C) Left: IOS map of contralateral forelimb (FL) and hindlimb (HL) responsive areas (average of 40 trials). Middle: 1 h after stroke the forelimb map has retreated while the hindlimb map is largely preserved (average of 40 trials collected 30–60 min poststroke). Right: raw image of change in reflectance for the 1 h poststroke contralateral forelimb map (images scaled from −0.05% to 0.05% change). The white diagonal and horizontal lines indicate the size and location used for determining response profiles in (D). The locations of MCA branches activated by forelimb stimulation are indicated; the arteries are clearly visible as lighter structures.(D) Quantification of forelimb and hindlimb IOS response from smoothed line profiles indicated in (C) (right). The profiles show a large change in the border of the forelimb territory (left). For the 1-h maps the edge of blebbed dendritic structure was 511 μm from the edge of the forelimb response. The hindlimb functional border was largely unaffected (middle panel). The approximate border locations for IOS responses were maintained for both 1- and 4.5–6-h timepoints. Right: average group data from nine different animals showing distance between the IOS map border and the center of the map for control conditions (column 1) and after stroke (column 2). The distance between the border of morphological dendritic damage and the center of the IOS map is in the third column. The last bar is the difference between bars 2 and 3 for each animal; a measure of the distance between the morphological edge of stroke damage and edge of the IOS response after stroke. Paired t-tests compared column 1 to 2 or 3 (asterisks indicate p < 0.02, alpha reduced since two comparisons were performed). |
PMC1854912_pbio-0050119-g006_10615.jpg | What is the core subject represented in this visual? | The Relationship between Loss of Dendritic Structure and Activity Dependent Hemodynamic Responses in Animals with Photothrombotic Stroke Targeted to Individual Arteries(A) Shown are laser-speckle surface blood flow images, darker tones indicate lower speckle contrast and higher velocities of blood flow. Left: control speckle contrast image of the right somatosensory cortex (oriented rostral up and medial left). A middle cerebral artery branch and sites where laser induced photothrombosis was performed are indicated by two red lines. Middle: 20 min after targeted photothrombosis blood flow has stopped in photoactivated segment. Blue arrowheads indicate changes in venous blood flow at distant sites. A small black box indicates the location of two-photon imaging shown in (B). Right: 4.5 h after stroke blood flow is still lost within the targeted MCA segment.(B) Image of RB photoactivation location on the MCA branch is indicated by the red line (left-most line). Upstream, to the right of the photoactivation spot a clot can be seen developing. Middle panel: dendritic damage border image taken 90 min after photothrombosis (approximate border indicated by a dashed green line, dendritic damage was reduced below the dashed line). Right: 4 h after photothrombosis dendritic damage worsened, although the approximate border for dendritic damage was in a similar location as that observed at the 90-min timepoint (note the structural transition and some intact dendrites in the lower part of the image).(C) Left: IOS map of contralateral forelimb (FL) and hindlimb (HL) responsive areas (average of 40 trials). Middle: 1 h after stroke the forelimb map has retreated while the hindlimb map is largely preserved (average of 40 trials collected 30–60 min poststroke). Right: raw image of change in reflectance for the 1 h poststroke contralateral forelimb map (images scaled from −0.05% to 0.05% change). The white diagonal and horizontal lines indicate the size and location used for determining response profiles in (D). The locations of MCA branches activated by forelimb stimulation are indicated; the arteries are clearly visible as lighter structures.(D) Quantification of forelimb and hindlimb IOS response from smoothed line profiles indicated in (C) (right). The profiles show a large change in the border of the forelimb territory (left). For the 1-h maps the edge of blebbed dendritic structure was 511 μm from the edge of the forelimb response. The hindlimb functional border was largely unaffected (middle panel). The approximate border locations for IOS responses were maintained for both 1- and 4.5–6-h timepoints. Right: average group data from nine different animals showing distance between the IOS map border and the center of the map for control conditions (column 1) and after stroke (column 2). The distance between the border of morphological dendritic damage and the center of the IOS map is in the third column. The last bar is the difference between bars 2 and 3 for each animal; a measure of the distance between the morphological edge of stroke damage and edge of the IOS response after stroke. Paired t-tests compared column 1 to 2 or 3 (asterisks indicate p < 0.02, alpha reduced since two comparisons were performed). |
PMC1854912_pbio-0050119-g007_10608.jpg | What is being portrayed in this visual content? | Dendritic Structural Borders after Complete Removal of the Hindlimb Functional Map(A) Laser-speckle surface blood flow image showing the approximate location of the hindlimb territory (green circle) and two sites where photoactivation of RB was performed using a fluorescence arc lamp (red lines). Right: laser-speckle image 20 min after stroke induction shows a loss of surface blood flow to at least half of the hindlimb territory.(B) Raw change in IOS after contralateral forelimb stimulation 40–70 min after stroke indicates a significant forelimb response (darkening in area under FL, images scaled from −0.1% to 0.1% change). In this image branches of the MCA (indicated) that supply both the forelimb and hindlimb area are seen in bright white. This image shows that part of the hindlimb territory is still undergoing changes in blood flow in response to activity.(C) IOS maps for hindlimb and forelimb regions in the animal before stroke induction. The mixed forelimb and hindlimb response presumably reflects some degree of noise (yellow pixels).(D) The hindlimb response was completely lost (no significant response was observed so a color map could not be created) 40–70 min after photothrombotic stroke, while a response in the forelimb area was still present. The white box and enlarged image to the right indicates the area where two-photon imaging established the border of dendritic damage.(E) Quantification of the forelimb and hindlimb IOS responses from smoothed line profiles over the region indicated in (B) by the dotted black lines. Upper panel: contralateral forelimb stimulation results in approximately 0.15% reduction in light reflectance. After stroke reflectance decreases to approximately 0.07%. Lower graph: the contralateral hindlimb stimulus response profile was completely lost following stroke as the red line was not different from 0. The contralateral hindlimb response was visible under control conditions and is observed (in the response profile graph) about −750 μm from the center of the forelimb area. |
PMC1854912_pbio-0050119-g007_10602.jpg | What is the core subject represented in this visual? | Dendritic Structural Borders after Complete Removal of the Hindlimb Functional Map(A) Laser-speckle surface blood flow image showing the approximate location of the hindlimb territory (green circle) and two sites where photoactivation of RB was performed using a fluorescence arc lamp (red lines). Right: laser-speckle image 20 min after stroke induction shows a loss of surface blood flow to at least half of the hindlimb territory.(B) Raw change in IOS after contralateral forelimb stimulation 40–70 min after stroke indicates a significant forelimb response (darkening in area under FL, images scaled from −0.1% to 0.1% change). In this image branches of the MCA (indicated) that supply both the forelimb and hindlimb area are seen in bright white. This image shows that part of the hindlimb territory is still undergoing changes in blood flow in response to activity.(C) IOS maps for hindlimb and forelimb regions in the animal before stroke induction. The mixed forelimb and hindlimb response presumably reflects some degree of noise (yellow pixels).(D) The hindlimb response was completely lost (no significant response was observed so a color map could not be created) 40–70 min after photothrombotic stroke, while a response in the forelimb area was still present. The white box and enlarged image to the right indicates the area where two-photon imaging established the border of dendritic damage.(E) Quantification of the forelimb and hindlimb IOS responses from smoothed line profiles over the region indicated in (B) by the dotted black lines. Upper panel: contralateral forelimb stimulation results in approximately 0.15% reduction in light reflectance. After stroke reflectance decreases to approximately 0.07%. Lower graph: the contralateral hindlimb stimulus response profile was completely lost following stroke as the red line was not different from 0. The contralateral hindlimb response was visible under control conditions and is observed (in the response profile graph) about −750 μm from the center of the forelimb area. |
PMC1854912_pbio-0050119-g007_10605.jpg | What is the main focus of this visual representation? | Dendritic Structural Borders after Complete Removal of the Hindlimb Functional Map(A) Laser-speckle surface blood flow image showing the approximate location of the hindlimb territory (green circle) and two sites where photoactivation of RB was performed using a fluorescence arc lamp (red lines). Right: laser-speckle image 20 min after stroke induction shows a loss of surface blood flow to at least half of the hindlimb territory.(B) Raw change in IOS after contralateral forelimb stimulation 40–70 min after stroke indicates a significant forelimb response (darkening in area under FL, images scaled from −0.1% to 0.1% change). In this image branches of the MCA (indicated) that supply both the forelimb and hindlimb area are seen in bright white. This image shows that part of the hindlimb territory is still undergoing changes in blood flow in response to activity.(C) IOS maps for hindlimb and forelimb regions in the animal before stroke induction. The mixed forelimb and hindlimb response presumably reflects some degree of noise (yellow pixels).(D) The hindlimb response was completely lost (no significant response was observed so a color map could not be created) 40–70 min after photothrombotic stroke, while a response in the forelimb area was still present. The white box and enlarged image to the right indicates the area where two-photon imaging established the border of dendritic damage.(E) Quantification of the forelimb and hindlimb IOS responses from smoothed line profiles over the region indicated in (B) by the dotted black lines. Upper panel: contralateral forelimb stimulation results in approximately 0.15% reduction in light reflectance. After stroke reflectance decreases to approximately 0.07%. Lower graph: the contralateral hindlimb stimulus response profile was completely lost following stroke as the red line was not different from 0. The contralateral hindlimb response was visible under control conditions and is observed (in the response profile graph) about −750 μm from the center of the forelimb area. |
PMC1854912_pbio-0050119-g007_10606.jpg | What is the principal component of this image? | Dendritic Structural Borders after Complete Removal of the Hindlimb Functional Map(A) Laser-speckle surface blood flow image showing the approximate location of the hindlimb territory (green circle) and two sites where photoactivation of RB was performed using a fluorescence arc lamp (red lines). Right: laser-speckle image 20 min after stroke induction shows a loss of surface blood flow to at least half of the hindlimb territory.(B) Raw change in IOS after contralateral forelimb stimulation 40–70 min after stroke indicates a significant forelimb response (darkening in area under FL, images scaled from −0.1% to 0.1% change). In this image branches of the MCA (indicated) that supply both the forelimb and hindlimb area are seen in bright white. This image shows that part of the hindlimb territory is still undergoing changes in blood flow in response to activity.(C) IOS maps for hindlimb and forelimb regions in the animal before stroke induction. The mixed forelimb and hindlimb response presumably reflects some degree of noise (yellow pixels).(D) The hindlimb response was completely lost (no significant response was observed so a color map could not be created) 40–70 min after photothrombotic stroke, while a response in the forelimb area was still present. The white box and enlarged image to the right indicates the area where two-photon imaging established the border of dendritic damage.(E) Quantification of the forelimb and hindlimb IOS responses from smoothed line profiles over the region indicated in (B) by the dotted black lines. Upper panel: contralateral forelimb stimulation results in approximately 0.15% reduction in light reflectance. After stroke reflectance decreases to approximately 0.07%. Lower graph: the contralateral hindlimb stimulus response profile was completely lost following stroke as the red line was not different from 0. The contralateral hindlimb response was visible under control conditions and is observed (in the response profile graph) about −750 μm from the center of the forelimb area. |
PMC1854912_pbio-0050119-g007_10603.jpg | What is the dominant medical problem in this image? | Dendritic Structural Borders after Complete Removal of the Hindlimb Functional Map(A) Laser-speckle surface blood flow image showing the approximate location of the hindlimb territory (green circle) and two sites where photoactivation of RB was performed using a fluorescence arc lamp (red lines). Right: laser-speckle image 20 min after stroke induction shows a loss of surface blood flow to at least half of the hindlimb territory.(B) Raw change in IOS after contralateral forelimb stimulation 40–70 min after stroke indicates a significant forelimb response (darkening in area under FL, images scaled from −0.1% to 0.1% change). In this image branches of the MCA (indicated) that supply both the forelimb and hindlimb area are seen in bright white. This image shows that part of the hindlimb territory is still undergoing changes in blood flow in response to activity.(C) IOS maps for hindlimb and forelimb regions in the animal before stroke induction. The mixed forelimb and hindlimb response presumably reflects some degree of noise (yellow pixels).(D) The hindlimb response was completely lost (no significant response was observed so a color map could not be created) 40–70 min after photothrombotic stroke, while a response in the forelimb area was still present. The white box and enlarged image to the right indicates the area where two-photon imaging established the border of dendritic damage.(E) Quantification of the forelimb and hindlimb IOS responses from smoothed line profiles over the region indicated in (B) by the dotted black lines. Upper panel: contralateral forelimb stimulation results in approximately 0.15% reduction in light reflectance. After stroke reflectance decreases to approximately 0.07%. Lower graph: the contralateral hindlimb stimulus response profile was completely lost following stroke as the red line was not different from 0. The contralateral hindlimb response was visible under control conditions and is observed (in the response profile graph) about −750 μm from the center of the forelimb area. |
PMC1854912_pbio-0050119-g007_10604.jpg | What object or scene is depicted here? | Dendritic Structural Borders after Complete Removal of the Hindlimb Functional Map(A) Laser-speckle surface blood flow image showing the approximate location of the hindlimb territory (green circle) and two sites where photoactivation of RB was performed using a fluorescence arc lamp (red lines). Right: laser-speckle image 20 min after stroke induction shows a loss of surface blood flow to at least half of the hindlimb territory.(B) Raw change in IOS after contralateral forelimb stimulation 40–70 min after stroke indicates a significant forelimb response (darkening in area under FL, images scaled from −0.1% to 0.1% change). In this image branches of the MCA (indicated) that supply both the forelimb and hindlimb area are seen in bright white. This image shows that part of the hindlimb territory is still undergoing changes in blood flow in response to activity.(C) IOS maps for hindlimb and forelimb regions in the animal before stroke induction. The mixed forelimb and hindlimb response presumably reflects some degree of noise (yellow pixels).(D) The hindlimb response was completely lost (no significant response was observed so a color map could not be created) 40–70 min after photothrombotic stroke, while a response in the forelimb area was still present. The white box and enlarged image to the right indicates the area where two-photon imaging established the border of dendritic damage.(E) Quantification of the forelimb and hindlimb IOS responses from smoothed line profiles over the region indicated in (B) by the dotted black lines. Upper panel: contralateral forelimb stimulation results in approximately 0.15% reduction in light reflectance. After stroke reflectance decreases to approximately 0.07%. Lower graph: the contralateral hindlimb stimulus response profile was completely lost following stroke as the red line was not different from 0. The contralateral hindlimb response was visible under control conditions and is observed (in the response profile graph) about −750 μm from the center of the forelimb area. |
PMC1854917_pbio-0050117-g002_10622.jpg | What's the most prominent thing you notice in this picture? | Ablation of the X, 2-Entire, 3-Entire Chromosomes and Identification of Mutant Embryos(A, C, E, and H) Live embryos were imaged using an up-right microscope. Arrowhead indicates the phenotypes associated with each chromosomal ablation. (A) shows a WT embryo. In (C), an X− embryo shows the irregular cellularization front (nullo phenotype) due to the failure to form furrow canals around some nuclei. (E) The 2− embryo developed the characteristic halo phenotype: a dark cytoplasmic halo below the nuclei. (H) The 3− embryo developed the bottleneck phenotype. Nuclei failed to be incorporated in the cellularization front because of the early and uncontrolled contractility of the actin-myosin network.(B, D, F, G, I, and J) Immunostaining using anti-Armadillo (B and D) and anti Myosin-2 antibodies (F, G, I, and J). (B) and (D) show the apical surface, top view, of WT and X− embryos respectively. Arrowhead indicates the irregular conformation of the apical membrane in the X− embryo. (F and G) Optical cross section of WT (F) and 2− (G) embryos stained with anti-myosin-2 antibodies. Note the lack of cell membranes in 2− embryos and failure to localize myosin-2 to the basal side of the cellularization front. (I and J) Top view of WT (I) and 3− (J) embryos stained with anti-myosyn-2 antibodies showing the typical bottleneck phenotype, arrowhead in (J).(K) Table summarizing the results of each chromosomal manipulation. The chromosomal location of down-regulated genes (3-fold, p < 0.001) is plotted next to the corresponding embryo. Data were obtained using four biological replicates (ablation of chromosome X and 2) and two biological replicates (ablation of Chromosome 3 entire). |
PMC1854917_pbio-0050117-g002_10627.jpg | What key item or scene is captured in this photo? | Ablation of the X, 2-Entire, 3-Entire Chromosomes and Identification of Mutant Embryos(A, C, E, and H) Live embryos were imaged using an up-right microscope. Arrowhead indicates the phenotypes associated with each chromosomal ablation. (A) shows a WT embryo. In (C), an X− embryo shows the irregular cellularization front (nullo phenotype) due to the failure to form furrow canals around some nuclei. (E) The 2− embryo developed the characteristic halo phenotype: a dark cytoplasmic halo below the nuclei. (H) The 3− embryo developed the bottleneck phenotype. Nuclei failed to be incorporated in the cellularization front because of the early and uncontrolled contractility of the actin-myosin network.(B, D, F, G, I, and J) Immunostaining using anti-Armadillo (B and D) and anti Myosin-2 antibodies (F, G, I, and J). (B) and (D) show the apical surface, top view, of WT and X− embryos respectively. Arrowhead indicates the irregular conformation of the apical membrane in the X− embryo. (F and G) Optical cross section of WT (F) and 2− (G) embryos stained with anti-myosin-2 antibodies. Note the lack of cell membranes in 2− embryos and failure to localize myosin-2 to the basal side of the cellularization front. (I and J) Top view of WT (I) and 3− (J) embryos stained with anti-myosyn-2 antibodies showing the typical bottleneck phenotype, arrowhead in (J).(K) Table summarizing the results of each chromosomal manipulation. The chromosomal location of down-regulated genes (3-fold, p < 0.001) is plotted next to the corresponding embryo. Data were obtained using four biological replicates (ablation of chromosome X and 2) and two biological replicates (ablation of Chromosome 3 entire). |
PMC1854917_pbio-0050117-g002_10623.jpg | What is the central feature of this picture? | Ablation of the X, 2-Entire, 3-Entire Chromosomes and Identification of Mutant Embryos(A, C, E, and H) Live embryos were imaged using an up-right microscope. Arrowhead indicates the phenotypes associated with each chromosomal ablation. (A) shows a WT embryo. In (C), an X− embryo shows the irregular cellularization front (nullo phenotype) due to the failure to form furrow canals around some nuclei. (E) The 2− embryo developed the characteristic halo phenotype: a dark cytoplasmic halo below the nuclei. (H) The 3− embryo developed the bottleneck phenotype. Nuclei failed to be incorporated in the cellularization front because of the early and uncontrolled contractility of the actin-myosin network.(B, D, F, G, I, and J) Immunostaining using anti-Armadillo (B and D) and anti Myosin-2 antibodies (F, G, I, and J). (B) and (D) show the apical surface, top view, of WT and X− embryos respectively. Arrowhead indicates the irregular conformation of the apical membrane in the X− embryo. (F and G) Optical cross section of WT (F) and 2− (G) embryos stained with anti-myosin-2 antibodies. Note the lack of cell membranes in 2− embryos and failure to localize myosin-2 to the basal side of the cellularization front. (I and J) Top view of WT (I) and 3− (J) embryos stained with anti-myosyn-2 antibodies showing the typical bottleneck phenotype, arrowhead in (J).(K) Table summarizing the results of each chromosomal manipulation. The chromosomal location of down-regulated genes (3-fold, p < 0.001) is plotted next to the corresponding embryo. Data were obtained using four biological replicates (ablation of chromosome X and 2) and two biological replicates (ablation of Chromosome 3 entire). |
PMC1854917_pbio-0050117-g002_10621.jpg | What is the core subject represented in this visual? | Ablation of the X, 2-Entire, 3-Entire Chromosomes and Identification of Mutant Embryos(A, C, E, and H) Live embryos were imaged using an up-right microscope. Arrowhead indicates the phenotypes associated with each chromosomal ablation. (A) shows a WT embryo. In (C), an X− embryo shows the irregular cellularization front (nullo phenotype) due to the failure to form furrow canals around some nuclei. (E) The 2− embryo developed the characteristic halo phenotype: a dark cytoplasmic halo below the nuclei. (H) The 3− embryo developed the bottleneck phenotype. Nuclei failed to be incorporated in the cellularization front because of the early and uncontrolled contractility of the actin-myosin network.(B, D, F, G, I, and J) Immunostaining using anti-Armadillo (B and D) and anti Myosin-2 antibodies (F, G, I, and J). (B) and (D) show the apical surface, top view, of WT and X− embryos respectively. Arrowhead indicates the irregular conformation of the apical membrane in the X− embryo. (F and G) Optical cross section of WT (F) and 2− (G) embryos stained with anti-myosin-2 antibodies. Note the lack of cell membranes in 2− embryos and failure to localize myosin-2 to the basal side of the cellularization front. (I and J) Top view of WT (I) and 3− (J) embryos stained with anti-myosyn-2 antibodies showing the typical bottleneck phenotype, arrowhead in (J).(K) Table summarizing the results of each chromosomal manipulation. The chromosomal location of down-regulated genes (3-fold, p < 0.001) is plotted next to the corresponding embryo. Data were obtained using four biological replicates (ablation of chromosome X and 2) and two biological replicates (ablation of Chromosome 3 entire). |
PMC1854917_pbio-0050117-g002_10630.jpg | What is shown in this image? | Ablation of the X, 2-Entire, 3-Entire Chromosomes and Identification of Mutant Embryos(A, C, E, and H) Live embryos were imaged using an up-right microscope. Arrowhead indicates the phenotypes associated with each chromosomal ablation. (A) shows a WT embryo. In (C), an X− embryo shows the irregular cellularization front (nullo phenotype) due to the failure to form furrow canals around some nuclei. (E) The 2− embryo developed the characteristic halo phenotype: a dark cytoplasmic halo below the nuclei. (H) The 3− embryo developed the bottleneck phenotype. Nuclei failed to be incorporated in the cellularization front because of the early and uncontrolled contractility of the actin-myosin network.(B, D, F, G, I, and J) Immunostaining using anti-Armadillo (B and D) and anti Myosin-2 antibodies (F, G, I, and J). (B) and (D) show the apical surface, top view, of WT and X− embryos respectively. Arrowhead indicates the irregular conformation of the apical membrane in the X− embryo. (F and G) Optical cross section of WT (F) and 2− (G) embryos stained with anti-myosin-2 antibodies. Note the lack of cell membranes in 2− embryos and failure to localize myosin-2 to the basal side of the cellularization front. (I and J) Top view of WT (I) and 3− (J) embryos stained with anti-myosyn-2 antibodies showing the typical bottleneck phenotype, arrowhead in (J).(K) Table summarizing the results of each chromosomal manipulation. The chromosomal location of down-regulated genes (3-fold, p < 0.001) is plotted next to the corresponding embryo. Data were obtained using four biological replicates (ablation of chromosome X and 2) and two biological replicates (ablation of Chromosome 3 entire). |
PMC1854917_pbio-0050117-g002_10631.jpg | What is the central feature of this picture? | Ablation of the X, 2-Entire, 3-Entire Chromosomes and Identification of Mutant Embryos(A, C, E, and H) Live embryos were imaged using an up-right microscope. Arrowhead indicates the phenotypes associated with each chromosomal ablation. (A) shows a WT embryo. In (C), an X− embryo shows the irregular cellularization front (nullo phenotype) due to the failure to form furrow canals around some nuclei. (E) The 2− embryo developed the characteristic halo phenotype: a dark cytoplasmic halo below the nuclei. (H) The 3− embryo developed the bottleneck phenotype. Nuclei failed to be incorporated in the cellularization front because of the early and uncontrolled contractility of the actin-myosin network.(B, D, F, G, I, and J) Immunostaining using anti-Armadillo (B and D) and anti Myosin-2 antibodies (F, G, I, and J). (B) and (D) show the apical surface, top view, of WT and X− embryos respectively. Arrowhead indicates the irregular conformation of the apical membrane in the X− embryo. (F and G) Optical cross section of WT (F) and 2− (G) embryos stained with anti-myosin-2 antibodies. Note the lack of cell membranes in 2− embryos and failure to localize myosin-2 to the basal side of the cellularization front. (I and J) Top view of WT (I) and 3− (J) embryos stained with anti-myosyn-2 antibodies showing the typical bottleneck phenotype, arrowhead in (J).(K) Table summarizing the results of each chromosomal manipulation. The chromosomal location of down-regulated genes (3-fold, p < 0.001) is plotted next to the corresponding embryo. Data were obtained using four biological replicates (ablation of chromosome X and 2) and two biological replicates (ablation of Chromosome 3 entire). |
PMC1855055_F2_10633.jpg | Can you identify the primary element in this image? | Phenotypic changes in primary cultured alveolar epithelial cells stimulated with PAR4 agonists or TGF-β. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) various agonists (thrombin, AYPGKF-NH2 or TGF-β) for 72 h, and stained for E-cadherin or α-SMA using specific antibodies as described in Method section. |
PMC1855055_F2_10632.jpg | Describe the main subject of this image. | Phenotypic changes in primary cultured alveolar epithelial cells stimulated with PAR4 agonists or TGF-β. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) various agonists (thrombin, AYPGKF-NH2 or TGF-β) for 72 h, and stained for E-cadherin or α-SMA using specific antibodies as described in Method section. |
PMC1855055_F2_10635.jpg | Describe the main subject of this image. | Phenotypic changes in primary cultured alveolar epithelial cells stimulated with PAR4 agonists or TGF-β. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) various agonists (thrombin, AYPGKF-NH2 or TGF-β) for 72 h, and stained for E-cadherin or α-SMA using specific antibodies as described in Method section. |
PMC1855055_F2_10634.jpg | What object or scene is depicted here? | Phenotypic changes in primary cultured alveolar epithelial cells stimulated with PAR4 agonists or TGF-β. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) various agonists (thrombin, AYPGKF-NH2 or TGF-β) for 72 h, and stained for E-cadherin or α-SMA using specific antibodies as described in Method section. |
PMC1855055_F8_10639.jpg | What does this image primarily show? | Effects of AG1478 and PP2 on PAR4 agonist induced phenotypic changes in primary cultured alveolar epithelial cells. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) AYPGKF-NH2 (100 μM) for 72 h in the presence or absence of each inhibitor (30 nM AG1478 or 300 nM PP2), and stained using each specific antibody as described in Method section. |
PMC1855055_F8_10641.jpg | What's the most prominent thing you notice in this picture? | Effects of AG1478 and PP2 on PAR4 agonist induced phenotypic changes in primary cultured alveolar epithelial cells. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) AYPGKF-NH2 (100 μM) for 72 h in the presence or absence of each inhibitor (30 nM AG1478 or 300 nM PP2), and stained using each specific antibody as described in Method section. |
PMC1855055_F8_10636.jpg | What stands out most in this visual? | Effects of AG1478 and PP2 on PAR4 agonist induced phenotypic changes in primary cultured alveolar epithelial cells. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) AYPGKF-NH2 (100 μM) for 72 h in the presence or absence of each inhibitor (30 nM AG1478 or 300 nM PP2), and stained using each specific antibody as described in Method section. |
PMC1855055_F8_10642.jpg | What object or scene is depicted here? | Effects of AG1478 and PP2 on PAR4 agonist induced phenotypic changes in primary cultured alveolar epithelial cells. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) AYPGKF-NH2 (100 μM) for 72 h in the presence or absence of each inhibitor (30 nM AG1478 or 300 nM PP2), and stained using each specific antibody as described in Method section. |
PMC1855055_F8_10640.jpg | Describe the main subject of this image. | Effects of AG1478 and PP2 on PAR4 agonist induced phenotypic changes in primary cultured alveolar epithelial cells. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) AYPGKF-NH2 (100 μM) for 72 h in the presence or absence of each inhibitor (30 nM AG1478 or 300 nM PP2), and stained using each specific antibody as described in Method section. |
PMC1855055_F8_10637.jpg | What is the central feature of this picture? | Effects of AG1478 and PP2 on PAR4 agonist induced phenotypic changes in primary cultured alveolar epithelial cells. Immunofluorescence images for a specific marker for epithelial cell (E-cadherin; rhodamine red, upper panel) or myofibroblast (α-SMA; FITC green, lower panel) captured with confocal lasar microscopy. Cells were treated with or without (control) AYPGKF-NH2 (100 μM) for 72 h in the presence or absence of each inhibitor (30 nM AG1478 or 300 nM PP2), and stained using each specific antibody as described in Method section. |
PMC1855058_F4_10647.jpg | Can you identify the primary element in this image? | Representative examples of anti-BrdU immunohistochemistry in the ovaries of IO and BR mice. A. BrdU immuno-positive cells in the OSE (arrows) adjacent to a follicle (foll) and a corpus luteum in a 9-month IO ovary on the afternoon of estrous. Note the labeled cells in the theca and stroma just beneath the OSE. B. Negative control (no primary antibody added) of an adjacent section to A. C. Numerous BrdU immuno-positive nuclei (arrows) in the OSE at the base of a recently ovulated follicle (rof) in a 6-month BR ovary. D. A single BrdU immuno-positive cell (arrow) is present in this group of three rete ovarii tubules from a 9-month BR ovary. E. BrdU incorporation in cells present in a hilar cyst (c) in a 12-month BR ovary. F. BrdU incorporation in cells, including hobnail cells with clear cytoplasm, lining a cortical cyst in a 12-month IO ovary. Bars = 75 μm; original magnification 200 ×. |
PMC1855058_F4_10645.jpg | What is being portrayed in this visual content? | Representative examples of anti-BrdU immunohistochemistry in the ovaries of IO and BR mice. A. BrdU immuno-positive cells in the OSE (arrows) adjacent to a follicle (foll) and a corpus luteum in a 9-month IO ovary on the afternoon of estrous. Note the labeled cells in the theca and stroma just beneath the OSE. B. Negative control (no primary antibody added) of an adjacent section to A. C. Numerous BrdU immuno-positive nuclei (arrows) in the OSE at the base of a recently ovulated follicle (rof) in a 6-month BR ovary. D. A single BrdU immuno-positive cell (arrow) is present in this group of three rete ovarii tubules from a 9-month BR ovary. E. BrdU incorporation in cells present in a hilar cyst (c) in a 12-month BR ovary. F. BrdU incorporation in cells, including hobnail cells with clear cytoplasm, lining a cortical cyst in a 12-month IO ovary. Bars = 75 μm; original magnification 200 ×. |
PMC1855058_F4_10643.jpg | What key item or scene is captured in this photo? | Representative examples of anti-BrdU immunohistochemistry in the ovaries of IO and BR mice. A. BrdU immuno-positive cells in the OSE (arrows) adjacent to a follicle (foll) and a corpus luteum in a 9-month IO ovary on the afternoon of estrous. Note the labeled cells in the theca and stroma just beneath the OSE. B. Negative control (no primary antibody added) of an adjacent section to A. C. Numerous BrdU immuno-positive nuclei (arrows) in the OSE at the base of a recently ovulated follicle (rof) in a 6-month BR ovary. D. A single BrdU immuno-positive cell (arrow) is present in this group of three rete ovarii tubules from a 9-month BR ovary. E. BrdU incorporation in cells present in a hilar cyst (c) in a 12-month BR ovary. F. BrdU incorporation in cells, including hobnail cells with clear cytoplasm, lining a cortical cyst in a 12-month IO ovary. Bars = 75 μm; original magnification 200 ×. |
PMC1855058_F4_10644.jpg | What is shown in this image? | Representative examples of anti-BrdU immunohistochemistry in the ovaries of IO and BR mice. A. BrdU immuno-positive cells in the OSE (arrows) adjacent to a follicle (foll) and a corpus luteum in a 9-month IO ovary on the afternoon of estrous. Note the labeled cells in the theca and stroma just beneath the OSE. B. Negative control (no primary antibody added) of an adjacent section to A. C. Numerous BrdU immuno-positive nuclei (arrows) in the OSE at the base of a recently ovulated follicle (rof) in a 6-month BR ovary. D. A single BrdU immuno-positive cell (arrow) is present in this group of three rete ovarii tubules from a 9-month BR ovary. E. BrdU incorporation in cells present in a hilar cyst (c) in a 12-month BR ovary. F. BrdU incorporation in cells, including hobnail cells with clear cytoplasm, lining a cortical cyst in a 12-month IO ovary. Bars = 75 μm; original magnification 200 ×. |
PMC1855058_F4_10648.jpg | What is the principal component of this image? | Representative examples of anti-BrdU immunohistochemistry in the ovaries of IO and BR mice. A. BrdU immuno-positive cells in the OSE (arrows) adjacent to a follicle (foll) and a corpus luteum in a 9-month IO ovary on the afternoon of estrous. Note the labeled cells in the theca and stroma just beneath the OSE. B. Negative control (no primary antibody added) of an adjacent section to A. C. Numerous BrdU immuno-positive nuclei (arrows) in the OSE at the base of a recently ovulated follicle (rof) in a 6-month BR ovary. D. A single BrdU immuno-positive cell (arrow) is present in this group of three rete ovarii tubules from a 9-month BR ovary. E. BrdU incorporation in cells present in a hilar cyst (c) in a 12-month BR ovary. F. BrdU incorporation in cells, including hobnail cells with clear cytoplasm, lining a cortical cyst in a 12-month IO ovary. Bars = 75 μm; original magnification 200 ×. |
PMC1855079_pone-0000418-g001_10650.jpg | What is the core subject represented in this visual? | Avian vaginal morphology.(A) Typical tubular avian vagina from domestic Pheasant (Phasianus colchicus) (connective tissue removed). Note the lack of any elaborations. (B) Vagina (V) of Pekin duck (domestic Anas plathyrhynchos) (connective tissue removed). Note the complexity of the structure. (C) Longitudinal dissection of Pekin Duck vagina showing structural complexity. Pockets (*) are closer to the cloaca (Cl) and their lumen in shown between the traces lines. Spirals (white arrows) are closer to the uterus (or shell gland) (U). S.S. = Area of sperm storage tubules. (Scale bar in all pictures = 2 cm). |
PMC1855079_pone-0000418-g001_10651.jpg | What is the main focus of this visual representation? | Avian vaginal morphology.(A) Typical tubular avian vagina from domestic Pheasant (Phasianus colchicus) (connective tissue removed). Note the lack of any elaborations. (B) Vagina (V) of Pekin duck (domestic Anas plathyrhynchos) (connective tissue removed). Note the complexity of the structure. (C) Longitudinal dissection of Pekin Duck vagina showing structural complexity. Pockets (*) are closer to the cloaca (Cl) and their lumen in shown between the traces lines. Spirals (white arrows) are closer to the uterus (or shell gland) (U). S.S. = Area of sperm storage tubules. (Scale bar in all pictures = 2 cm). |
PMC1855313_F1_10652.jpg | What is the main focus of this visual representation? | CT Scan showing area of sqaumous cell carcinoma. |
PMC1855328_F6_10654.jpg | What is the principal component of this image? | Phenotypic effects of altering SRF expression. 6a) An open wild-type flower. 6b-f) Flowers of same age as in 6a. Note the absence of mature pollen. 6 g) Leaves of plants with altered SRF4 activity. The 35S::SRF4 (line 1–5), Col, and srf4-3 plants are indicated. Leaves are enlarged and reduced, respectively. Note the regular leaf shapes. Scale bars: 0.5 mm |
PMC1855328_F6_10655.jpg | What is the core subject represented in this visual? | Phenotypic effects of altering SRF expression. 6a) An open wild-type flower. 6b-f) Flowers of same age as in 6a. Note the absence of mature pollen. 6 g) Leaves of plants with altered SRF4 activity. The 35S::SRF4 (line 1–5), Col, and srf4-3 plants are indicated. Leaves are enlarged and reduced, respectively. Note the regular leaf shapes. Scale bars: 0.5 mm |
PMC1855328_F6_10653.jpg | What is the core subject represented in this visual? | Phenotypic effects of altering SRF expression. 6a) An open wild-type flower. 6b-f) Flowers of same age as in 6a. Note the absence of mature pollen. 6 g) Leaves of plants with altered SRF4 activity. The 35S::SRF4 (line 1–5), Col, and srf4-3 plants are indicated. Leaves are enlarged and reduced, respectively. Note the regular leaf shapes. Scale bars: 0.5 mm |
PMC1855328_F6_10657.jpg | What is the main focus of this visual representation? | Phenotypic effects of altering SRF expression. 6a) An open wild-type flower. 6b-f) Flowers of same age as in 6a. Note the absence of mature pollen. 6 g) Leaves of plants with altered SRF4 activity. The 35S::SRF4 (line 1–5), Col, and srf4-3 plants are indicated. Leaves are enlarged and reduced, respectively. Note the regular leaf shapes. Scale bars: 0.5 mm |
PMC1855328_F6_10656.jpg | What is being portrayed in this visual content? | Phenotypic effects of altering SRF expression. 6a) An open wild-type flower. 6b-f) Flowers of same age as in 6a. Note the absence of mature pollen. 6 g) Leaves of plants with altered SRF4 activity. The 35S::SRF4 (line 1–5), Col, and srf4-3 plants are indicated. Leaves are enlarged and reduced, respectively. Note the regular leaf shapes. Scale bars: 0.5 mm |
PMC1855328_F6_10658.jpg | What is the core subject represented in this visual? | Phenotypic effects of altering SRF expression. 6a) An open wild-type flower. 6b-f) Flowers of same age as in 6a. Note the absence of mature pollen. 6 g) Leaves of plants with altered SRF4 activity. The 35S::SRF4 (line 1–5), Col, and srf4-3 plants are indicated. Leaves are enlarged and reduced, respectively. Note the regular leaf shapes. Scale bars: 0.5 mm |
PMC1855328_F6_10659.jpg | What is the central feature of this picture? | Phenotypic effects of altering SRF expression. 6a) An open wild-type flower. 6b-f) Flowers of same age as in 6a. Note the absence of mature pollen. 6 g) Leaves of plants with altered SRF4 activity. The 35S::SRF4 (line 1–5), Col, and srf4-3 plants are indicated. Leaves are enlarged and reduced, respectively. Note the regular leaf shapes. Scale bars: 0.5 mm |
PMC1855344_F7_10663.jpg | What's the most prominent thing you notice in this picture? | Gαi2 immunostaining imaged by confocal microscopy. Upper row, reference antibody against Gαi2 (Dr. Tomiko Asano); lower row, commercial antibody against Gαi2 (red) and Calbindin D-28 (green). Both antibodies show intense staining of ependymal cilia in ODN control (nonsense oligodeoxynucleotide) and saline control groups and attenuation of Gαi2 signal in AS-ODN (antisense-oligodeoxynucleotide against Gαi2) treated animals. Background staining with Calbindin D-28k (CaBP) was used to better visualize intracellular staining in endoplasmic reticulum with Chemicon antibody. Scale bar: 10 μm. |
PMC1855344_F7_10665.jpg | What can you see in this picture? | Gαi2 immunostaining imaged by confocal microscopy. Upper row, reference antibody against Gαi2 (Dr. Tomiko Asano); lower row, commercial antibody against Gαi2 (red) and Calbindin D-28 (green). Both antibodies show intense staining of ependymal cilia in ODN control (nonsense oligodeoxynucleotide) and saline control groups and attenuation of Gαi2 signal in AS-ODN (antisense-oligodeoxynucleotide against Gαi2) treated animals. Background staining with Calbindin D-28k (CaBP) was used to better visualize intracellular staining in endoplasmic reticulum with Chemicon antibody. Scale bar: 10 μm. |
PMC1855344_F7_10662.jpg | What's the most prominent thing you notice in this picture? | Gαi2 immunostaining imaged by confocal microscopy. Upper row, reference antibody against Gαi2 (Dr. Tomiko Asano); lower row, commercial antibody against Gαi2 (red) and Calbindin D-28 (green). Both antibodies show intense staining of ependymal cilia in ODN control (nonsense oligodeoxynucleotide) and saline control groups and attenuation of Gαi2 signal in AS-ODN (antisense-oligodeoxynucleotide against Gαi2) treated animals. Background staining with Calbindin D-28k (CaBP) was used to better visualize intracellular staining in endoplasmic reticulum with Chemicon antibody. Scale bar: 10 μm. |
PMC1855344_F7_10664.jpg | What is the focal point of this photograph? | Gαi2 immunostaining imaged by confocal microscopy. Upper row, reference antibody against Gαi2 (Dr. Tomiko Asano); lower row, commercial antibody against Gαi2 (red) and Calbindin D-28 (green). Both antibodies show intense staining of ependymal cilia in ODN control (nonsense oligodeoxynucleotide) and saline control groups and attenuation of Gαi2 signal in AS-ODN (antisense-oligodeoxynucleotide against Gαi2) treated animals. Background staining with Calbindin D-28k (CaBP) was used to better visualize intracellular staining in endoplasmic reticulum with Chemicon antibody. Scale bar: 10 μm. |
PMC1855344_F7_10661.jpg | What is the central feature of this picture? | Gαi2 immunostaining imaged by confocal microscopy. Upper row, reference antibody against Gαi2 (Dr. Tomiko Asano); lower row, commercial antibody against Gαi2 (red) and Calbindin D-28 (green). Both antibodies show intense staining of ependymal cilia in ODN control (nonsense oligodeoxynucleotide) and saline control groups and attenuation of Gαi2 signal in AS-ODN (antisense-oligodeoxynucleotide against Gαi2) treated animals. Background staining with Calbindin D-28k (CaBP) was used to better visualize intracellular staining in endoplasmic reticulum with Chemicon antibody. Scale bar: 10 μm. |
PMC1855433_pone-0000424-g005_10670.jpg | What stands out most in this visual? | Individual activation maps and percent BOLD signal change (% BSC) in the left lateral occipitotemporal (LO) cortex for Experiment 1.
a) The exact position of the left LO localized by comparing size discrimination versus pattern discrimination is shown in the clearest sagittal slice for each of the nine subjects. In each subject, LO was below the posterior end of the inferior temporal sulcus (ITS, dotted line). Note that in 2 of the 9 subjects, LO was activated by the reverse contrast of pattern versus size discrimination (reported in blue). b) Bar graphs display the magnitude of peak activation in %BSC in each experimental condition at the level of single subject and group average (the rightmost bars). c) Line graphs indicate the event‐related averaged time courses in % BSC with time zero indicating visual stimuli onset. Both magnitude of peak activation and event‐related averaged time courses showed that size discrimination was higher than pattern discrimination and moreover that grasping did not differ from reaching. |
PMC1855433_pone-0000424-g005_10675.jpg | What's the most prominent thing you notice in this picture? | Individual activation maps and percent BOLD signal change (% BSC) in the left lateral occipitotemporal (LO) cortex for Experiment 1.
a) The exact position of the left LO localized by comparing size discrimination versus pattern discrimination is shown in the clearest sagittal slice for each of the nine subjects. In each subject, LO was below the posterior end of the inferior temporal sulcus (ITS, dotted line). Note that in 2 of the 9 subjects, LO was activated by the reverse contrast of pattern versus size discrimination (reported in blue). b) Bar graphs display the magnitude of peak activation in %BSC in each experimental condition at the level of single subject and group average (the rightmost bars). c) Line graphs indicate the event‐related averaged time courses in % BSC with time zero indicating visual stimuli onset. Both magnitude of peak activation and event‐related averaged time courses showed that size discrimination was higher than pattern discrimination and moreover that grasping did not differ from reaching. |
PMC1855433_pone-0000424-g005_10666.jpg | What does this image primarily show? | Individual activation maps and percent BOLD signal change (% BSC) in the left lateral occipitotemporal (LO) cortex for Experiment 1.
a) The exact position of the left LO localized by comparing size discrimination versus pattern discrimination is shown in the clearest sagittal slice for each of the nine subjects. In each subject, LO was below the posterior end of the inferior temporal sulcus (ITS, dotted line). Note that in 2 of the 9 subjects, LO was activated by the reverse contrast of pattern versus size discrimination (reported in blue). b) Bar graphs display the magnitude of peak activation in %BSC in each experimental condition at the level of single subject and group average (the rightmost bars). c) Line graphs indicate the event‐related averaged time courses in % BSC with time zero indicating visual stimuli onset. Both magnitude of peak activation and event‐related averaged time courses showed that size discrimination was higher than pattern discrimination and moreover that grasping did not differ from reaching. |
PMC1855433_pone-0000424-g005_10668.jpg | What's the most prominent thing you notice in this picture? | Individual activation maps and percent BOLD signal change (% BSC) in the left lateral occipitotemporal (LO) cortex for Experiment 1.
a) The exact position of the left LO localized by comparing size discrimination versus pattern discrimination is shown in the clearest sagittal slice for each of the nine subjects. In each subject, LO was below the posterior end of the inferior temporal sulcus (ITS, dotted line). Note that in 2 of the 9 subjects, LO was activated by the reverse contrast of pattern versus size discrimination (reported in blue). b) Bar graphs display the magnitude of peak activation in %BSC in each experimental condition at the level of single subject and group average (the rightmost bars). c) Line graphs indicate the event‐related averaged time courses in % BSC with time zero indicating visual stimuli onset. Both magnitude of peak activation and event‐related averaged time courses showed that size discrimination was higher than pattern discrimination and moreover that grasping did not differ from reaching. |
PMC1855433_pone-0000424-g005_10672.jpg | Can you identify the primary element in this image? | Individual activation maps and percent BOLD signal change (% BSC) in the left lateral occipitotemporal (LO) cortex for Experiment 1.
a) The exact position of the left LO localized by comparing size discrimination versus pattern discrimination is shown in the clearest sagittal slice for each of the nine subjects. In each subject, LO was below the posterior end of the inferior temporal sulcus (ITS, dotted line). Note that in 2 of the 9 subjects, LO was activated by the reverse contrast of pattern versus size discrimination (reported in blue). b) Bar graphs display the magnitude of peak activation in %BSC in each experimental condition at the level of single subject and group average (the rightmost bars). c) Line graphs indicate the event‐related averaged time courses in % BSC with time zero indicating visual stimuli onset. Both magnitude of peak activation and event‐related averaged time courses showed that size discrimination was higher than pattern discrimination and moreover that grasping did not differ from reaching. |
PMC1855433_pone-0000424-g005_10669.jpg | What key item or scene is captured in this photo? | Individual activation maps and percent BOLD signal change (% BSC) in the left lateral occipitotemporal (LO) cortex for Experiment 1.
a) The exact position of the left LO localized by comparing size discrimination versus pattern discrimination is shown in the clearest sagittal slice for each of the nine subjects. In each subject, LO was below the posterior end of the inferior temporal sulcus (ITS, dotted line). Note that in 2 of the 9 subjects, LO was activated by the reverse contrast of pattern versus size discrimination (reported in blue). b) Bar graphs display the magnitude of peak activation in %BSC in each experimental condition at the level of single subject and group average (the rightmost bars). c) Line graphs indicate the event‐related averaged time courses in % BSC with time zero indicating visual stimuli onset. Both magnitude of peak activation and event‐related averaged time courses showed that size discrimination was higher than pattern discrimination and moreover that grasping did not differ from reaching. |
PMC1855433_pone-0000424-g005_10673.jpg | What is shown in this image? | Individual activation maps and percent BOLD signal change (% BSC) in the left lateral occipitotemporal (LO) cortex for Experiment 1.
a) The exact position of the left LO localized by comparing size discrimination versus pattern discrimination is shown in the clearest sagittal slice for each of the nine subjects. In each subject, LO was below the posterior end of the inferior temporal sulcus (ITS, dotted line). Note that in 2 of the 9 subjects, LO was activated by the reverse contrast of pattern versus size discrimination (reported in blue). b) Bar graphs display the magnitude of peak activation in %BSC in each experimental condition at the level of single subject and group average (the rightmost bars). c) Line graphs indicate the event‐related averaged time courses in % BSC with time zero indicating visual stimuli onset. Both magnitude of peak activation and event‐related averaged time courses showed that size discrimination was higher than pattern discrimination and moreover that grasping did not differ from reaching. |
PMC1855433_pone-0000424-g005_10674.jpg | What is the principal component of this image? | Individual activation maps and percent BOLD signal change (% BSC) in the left lateral occipitotemporal (LO) cortex for Experiment 1.
a) The exact position of the left LO localized by comparing size discrimination versus pattern discrimination is shown in the clearest sagittal slice for each of the nine subjects. In each subject, LO was below the posterior end of the inferior temporal sulcus (ITS, dotted line). Note that in 2 of the 9 subjects, LO was activated by the reverse contrast of pattern versus size discrimination (reported in blue). b) Bar graphs display the magnitude of peak activation in %BSC in each experimental condition at the level of single subject and group average (the rightmost bars). c) Line graphs indicate the event‐related averaged time courses in % BSC with time zero indicating visual stimuli onset. Both magnitude of peak activation and event‐related averaged time courses showed that size discrimination was higher than pattern discrimination and moreover that grasping did not differ from reaching. |
PMC1855433_pone-0000424-g005_10671.jpg | What stands out most in this visual? | Individual activation maps and percent BOLD signal change (% BSC) in the left lateral occipitotemporal (LO) cortex for Experiment 1.
a) The exact position of the left LO localized by comparing size discrimination versus pattern discrimination is shown in the clearest sagittal slice for each of the nine subjects. In each subject, LO was below the posterior end of the inferior temporal sulcus (ITS, dotted line). Note that in 2 of the 9 subjects, LO was activated by the reverse contrast of pattern versus size discrimination (reported in blue). b) Bar graphs display the magnitude of peak activation in %BSC in each experimental condition at the level of single subject and group average (the rightmost bars). c) Line graphs indicate the event‐related averaged time courses in % BSC with time zero indicating visual stimuli onset. Both magnitude of peak activation and event‐related averaged time courses showed that size discrimination was higher than pattern discrimination and moreover that grasping did not differ from reaching. |
PMC1855433_pone-0000424-g006_10677.jpg | What is the principal component of this image? | Group activation maps and percent BOLD signal change (% BSC) for grasping minus reaching in Experiment 1 and Experiment 2.
a) Brain areas activated by comparing grasping vs. reaching in Experiment 1: left primary motor cortex (M1, within the central sulcus), left primary somatosensory cortex (S1, within the postcentral sulcus), the left superior postcentral sulcus (sPCS), the left and right anterior intraparietal sulcus (lAIP and rAIP), the left horizontal segment of the intraparietal sulcus (hIPS), the parieto‐occipital cortex (PO) and early visual cortices (V). The group activation map is based on the Talairach averaged group results shown on group‐averaged. b) Event‐related averaged time courses measured in each area for Experiment 1. c) Event‐related averaged time courses for Experiment 2 in each of the brain regions localized by Experiment 1. Brain activation is measured in % BSC and time zero indicates visual stimuli onset. For both experiments, Talairach coordinates for the activated areas and p values for the relevant statistical comparisons are shown in Table 1. L=left, R=right, P=posterior. |
PMC1855435_pone-0000420-g002_10681.jpg | What is the main focus of this visual representation? | Overview of PtK2 cells grown on EM grids.Light microscopy images of Ptk2 cells grown on EM-grids. A, shows several EM grid bars, whereas B is a higher magnification. Bars: 20 µm. C, low magnification electron microscopy images of Ptk2 cells cultivated on an EM-grid. Bar: 2 µm. D, intermediate magnification (typically used for recording tomographic tilt series) EM images of the Ptk2 cells, infected with VV for 5 min. arrows–actin, arrowheads-extracellular virions. Bar: 200 nm |
PMC1855435_pone-0000420-g002_10679.jpg | What can you see in this picture? | Overview of PtK2 cells grown on EM grids.Light microscopy images of Ptk2 cells grown on EM-grids. A, shows several EM grid bars, whereas B is a higher magnification. Bars: 20 µm. C, low magnification electron microscopy images of Ptk2 cells cultivated on an EM-grid. Bar: 2 µm. D, intermediate magnification (typically used for recording tomographic tilt series) EM images of the Ptk2 cells, infected with VV for 5 min. arrows–actin, arrowheads-extracellular virions. Bar: 200 nm |
PMC1855435_pone-0000420-g002_10680.jpg | What object or scene is depicted here? | Overview of PtK2 cells grown on EM grids.Light microscopy images of Ptk2 cells grown on EM-grids. A, shows several EM grid bars, whereas B is a higher magnification. Bars: 20 µm. C, low magnification electron microscopy images of Ptk2 cells cultivated on an EM-grid. Bar: 2 µm. D, intermediate magnification (typically used for recording tomographic tilt series) EM images of the Ptk2 cells, infected with VV for 5 min. arrows–actin, arrowheads-extracellular virions. Bar: 200 nm |
PMC1855435_pone-0000420-g002_10682.jpg | What is the focal point of this photograph? | Overview of PtK2 cells grown on EM grids.Light microscopy images of Ptk2 cells grown on EM-grids. A, shows several EM grid bars, whereas B is a higher magnification. Bars: 20 µm. C, low magnification electron microscopy images of Ptk2 cells cultivated on an EM-grid. Bar: 2 µm. D, intermediate magnification (typically used for recording tomographic tilt series) EM images of the Ptk2 cells, infected with VV for 5 min. arrows–actin, arrowheads-extracellular virions. Bar: 200 nm |
PMC1855435_pone-0000420-g003_10683.jpg | What does this image primarily show? | Structural changes of VV at the cell surface prior to entry.PtK2 cells were grown on gold grids, coated on one side with 1% formvar and on both sides with carbon. Cells were infected at a multiplicity of infection of 500 for 30 min at 37°C, before vitrification in liquid ethane. A, a section (12 nm thick) through a tomogram (see Movie S1) with an extra-cellular virion (V) attached to the plasma membrane (PM); in the tomograms the DNA is randomly distributed (arrow–contact sites of the outer viral membranes with the PM–magnified in C). B, surface rendered representation of the particle in A (green-actin). C, surface rendered representation of the area marked by an arrow in A, showing close contact sites (yellow) between the outer viral membrane and the plasma membrane (magnification 3× as in A and B). D, the virion reveals tubular membrane structures inside the core. E, one of the pore-like structures (arrow) in the core of the particle seen in A (cross-section and surface rendered). Bars-100 nm |
PMC1855435_pone-0000420-g003_10684.jpg | What is the main focus of this visual representation? | Structural changes of VV at the cell surface prior to entry.PtK2 cells were grown on gold grids, coated on one side with 1% formvar and on both sides with carbon. Cells were infected at a multiplicity of infection of 500 for 30 min at 37°C, before vitrification in liquid ethane. A, a section (12 nm thick) through a tomogram (see Movie S1) with an extra-cellular virion (V) attached to the plasma membrane (PM); in the tomograms the DNA is randomly distributed (arrow–contact sites of the outer viral membranes with the PM–magnified in C). B, surface rendered representation of the particle in A (green-actin). C, surface rendered representation of the area marked by an arrow in A, showing close contact sites (yellow) between the outer viral membrane and the plasma membrane (magnification 3× as in A and B). D, the virion reveals tubular membrane structures inside the core. E, one of the pore-like structures (arrow) in the core of the particle seen in A (cross-section and surface rendered). Bars-100 nm |
PMC1855435_pone-0000420-g003_10686.jpg | What object or scene is depicted here? | Structural changes of VV at the cell surface prior to entry.PtK2 cells were grown on gold grids, coated on one side with 1% formvar and on both sides with carbon. Cells were infected at a multiplicity of infection of 500 for 30 min at 37°C, before vitrification in liquid ethane. A, a section (12 nm thick) through a tomogram (see Movie S1) with an extra-cellular virion (V) attached to the plasma membrane (PM); in the tomograms the DNA is randomly distributed (arrow–contact sites of the outer viral membranes with the PM–magnified in C). B, surface rendered representation of the particle in A (green-actin). C, surface rendered representation of the area marked by an arrow in A, showing close contact sites (yellow) between the outer viral membrane and the plasma membrane (magnification 3× as in A and B). D, the virion reveals tubular membrane structures inside the core. E, one of the pore-like structures (arrow) in the core of the particle seen in A (cross-section and surface rendered). Bars-100 nm |
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