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PMC1855435_pone-0000420-g003_10687.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 |
PMC1855623_fig02_10688.jpg | What is the principal component of this image? | Coronal cresyl violet-stained sections through the frontal lobe in the three cases (S1, S2 and S3) that received injections of neurotoxin into the left ventrolateral frontal cortex. The most anterior section in each case is at the top of the figure and the most posterior at the bottom. Compare the left, lesioned hemisphere of each section with the right, intact hemisphere; arrows indicate the extent of the lesions. Scale bar, 5 mm (applies to all sections). |
PMC1855623_fig02_10690.jpg | What does this image primarily show? | Coronal cresyl violet-stained sections through the frontal lobe in the three cases (S1, S2 and S3) that received injections of neurotoxin into the left ventrolateral frontal cortex. The most anterior section in each case is at the top of the figure and the most posterior at the bottom. Compare the left, lesioned hemisphere of each section with the right, intact hemisphere; arrows indicate the extent of the lesions. Scale bar, 5 mm (applies to all sections). |
PMC1855623_fig02_10689.jpg | What is the central feature of this picture? | Coronal cresyl violet-stained sections through the frontal lobe in the three cases (S1, S2 and S3) that received injections of neurotoxin into the left ventrolateral frontal cortex. The most anterior section in each case is at the top of the figure and the most posterior at the bottom. Compare the left, lesioned hemisphere of each section with the right, intact hemisphere; arrows indicate the extent of the lesions. Scale bar, 5 mm (applies to all sections). |
PMC1855985_pone-0000426-g005_10693.jpg | What is the focal point of this photograph? | Structural modeling of the FGFR4 Glu681Lys amino acid substitution.A. The FGFR4 WT and E681K mutant structures are predicted using the PROTINFO software (38) provided by the (PS)2 server (National Chiao Tung University, Taiwan). These predictions are based on crystallographic structure for FGFR1 tyrosine kinase domain (PDB accession 1FGK) (33), as no FGFR4 structure is available, and visualized using VMD (39). FGFR4 Glu681 (yellow), ATP binding site (pink), activation loop (green) and catalytic loop (white). Glu681 (yellow) is nestled between the TK activation and catalytic loops. B. 3D close-up of the surfaces of Glu681 (yellow), Arg650 (green) in the activation loop, and Ala615 (white) in the catalytic loop. Since Glu681 is strongly negatively charged and Arg650 is strongly positively charged, ionic bonding between these two closely juxtaposed residues may be assumed. C. 3D close-up of the surfaces of mutated Lys681 (orange), Arg650 and Ala615. The glutamic acid to lysine substitution at position 681 could structurally and functionally alter the kinase domain by flipping the charge of residue 681 and disrupting ionic bonds with neighboring residues, particularly the closely juxtaposed Arg650. |
PMC1855985_pone-0000426-g005_10694.jpg | What is the main focus of this visual representation? | Structural modeling of the FGFR4 Glu681Lys amino acid substitution.A. The FGFR4 WT and E681K mutant structures are predicted using the PROTINFO software (38) provided by the (PS)2 server (National Chiao Tung University, Taiwan). These predictions are based on crystallographic structure for FGFR1 tyrosine kinase domain (PDB accession 1FGK) (33), as no FGFR4 structure is available, and visualized using VMD (39). FGFR4 Glu681 (yellow), ATP binding site (pink), activation loop (green) and catalytic loop (white). Glu681 (yellow) is nestled between the TK activation and catalytic loops. B. 3D close-up of the surfaces of Glu681 (yellow), Arg650 (green) in the activation loop, and Ala615 (white) in the catalytic loop. Since Glu681 is strongly negatively charged and Arg650 is strongly positively charged, ionic bonding between these two closely juxtaposed residues may be assumed. C. 3D close-up of the surfaces of mutated Lys681 (orange), Arg650 and Ala615. The glutamic acid to lysine substitution at position 681 could structurally and functionally alter the kinase domain by flipping the charge of residue 681 and disrupting ionic bonds with neighboring residues, particularly the closely juxtaposed Arg650. |
PMC1857702_F8_10695.jpg | What can you see in this picture? | Careful examination of the series of sixteen individual optical sections along the Z axis reveals that LANA-1 induces a major rearrangement in the positioning of 3MK9H3 positive chromocenter remnants from the inside of the nucleus to the periphery of the nucleus. (LANA-1 – red, 3MK9H3 – green, DNA – blue). |
PMC1857702_F8_10696.jpg | What is shown in this image? | Careful examination of the series of sixteen individual optical sections along the Z axis reveals that LANA-1 induces a major rearrangement in the positioning of 3MK9H3 positive chromocenter remnants from the inside of the nucleus to the periphery of the nucleus. (LANA-1 – red, 3MK9H3 – green, DNA – blue). |
PMC1857702_F9_10697.jpg | Can you identify the primary element in this image? | 3D reconstitution of the triple-stained nuclei shows that LANA-1 staining and the 3MK9H3 positive remnants of the heterochromatic chromocenters are non-overlapping. See the full rotational image sequences in the supplementary material [see Additional file 1]. The selected middle sections (5–9) demonstrate the extensive peripheral localization of the chromocenters. High magnification representation of a single section shows mutual avoidance of 3MK9H3 staining and LANA-1 distribution. 3D reconstitution of LANA-1 transfected nuclei also reveals well-defined nuclear areas that are devoid of LANA-1 staining. The identity and molecular content of these areas are currently unknown but they apparently include the nucleoli and the chromocentric remnants. The 3 dimensional digital cast of the LANA-1 negative areas in relation to 3mK9H3 and DNA staining is shown as image sequence in the supplementary material [see Additional file 2]. (LANA-1 – red, 3MK9H3 – green, DNA – blue). |
PMC1857702_F13_10699.jpg | What can you see in this picture? | Deletion mutant (del 275–972) lacking the central acidic repeats and the adjacent N terminal region show effective targeting to the surface of heterochromatin both in human MCF7 and in mouse L-cells without any visible effect on the chromatin organization or positioning of chromocenters. (ΔLANA-1 – green, DNA – blue). |
PMC1857702_F13_10700.jpg | What is the dominant medical problem in this image? | Deletion mutant (del 275–972) lacking the central acidic repeats and the adjacent N terminal region show effective targeting to the surface of heterochromatin both in human MCF7 and in mouse L-cells without any visible effect on the chromatin organization or positioning of chromocenters. (ΔLANA-1 – green, DNA – blue). |
PMC1857822_pone-0000437-g002_10706.jpg | What is shown in this image? | FAZ restricts basal body migration.A–C. Top panels, detergent-extracted cytoskeletons of DHC1bRNAi cells induced for 41 h stained with MAb22 (basal body marker [BB], yellow), L3B2 (FAZ marker, red) and DAPI (blue). Bottom panels: 2-fold magnification of the basal body area of the above images. Diagrams show the position of the old (with a flagellum) and new (without a flagellum) basal bodies as well as positioning of the flagellum (black lines) and the FAZ filament (red lines). DAPI has been omitted from phase contrast images to facilitate visualisation of the flagellar structures. A–B. Presence of a short new FAZ contacting the old one (orange arrows) appears to refrain new basal body migration. C. Extensive basal body migration when the new FAZ is not in contact with the old one (green arrow). D–E. Detergent-extracted cytoskeletons of non-induced (D) or 48h-induced (E) DHC1bRNAi cells stained with L3B2 (immunogold) showing interaction between new and old FAZ (orange arrows). Basal bodies (BB) are found at the proximal end of the flagella (when present) and are easily recognised by their thicker wall (due to the presence of triplet microtubules [12]). |
PMC1857822_pone-0000437-g002_10702.jpg | What is shown in this image? | FAZ restricts basal body migration.A–C. Top panels, detergent-extracted cytoskeletons of DHC1bRNAi cells induced for 41 h stained with MAb22 (basal body marker [BB], yellow), L3B2 (FAZ marker, red) and DAPI (blue). Bottom panels: 2-fold magnification of the basal body area of the above images. Diagrams show the position of the old (with a flagellum) and new (without a flagellum) basal bodies as well as positioning of the flagellum (black lines) and the FAZ filament (red lines). DAPI has been omitted from phase contrast images to facilitate visualisation of the flagellar structures. A–B. Presence of a short new FAZ contacting the old one (orange arrows) appears to refrain new basal body migration. C. Extensive basal body migration when the new FAZ is not in contact with the old one (green arrow). D–E. Detergent-extracted cytoskeletons of non-induced (D) or 48h-induced (E) DHC1bRNAi cells stained with L3B2 (immunogold) showing interaction between new and old FAZ (orange arrows). Basal bodies (BB) are found at the proximal end of the flagella (when present) and are easily recognised by their thicker wall (due to the presence of triplet microtubules [12]). |
PMC1857822_pone-0000437-g002_10703.jpg | What is the main focus of this visual representation? | FAZ restricts basal body migration.A–C. Top panels, detergent-extracted cytoskeletons of DHC1bRNAi cells induced for 41 h stained with MAb22 (basal body marker [BB], yellow), L3B2 (FAZ marker, red) and DAPI (blue). Bottom panels: 2-fold magnification of the basal body area of the above images. Diagrams show the position of the old (with a flagellum) and new (without a flagellum) basal bodies as well as positioning of the flagellum (black lines) and the FAZ filament (red lines). DAPI has been omitted from phase contrast images to facilitate visualisation of the flagellar structures. A–B. Presence of a short new FAZ contacting the old one (orange arrows) appears to refrain new basal body migration. C. Extensive basal body migration when the new FAZ is not in contact with the old one (green arrow). D–E. Detergent-extracted cytoskeletons of non-induced (D) or 48h-induced (E) DHC1bRNAi cells stained with L3B2 (immunogold) showing interaction between new and old FAZ (orange arrows). Basal bodies (BB) are found at the proximal end of the flagella (when present) and are easily recognised by their thicker wall (due to the presence of triplet microtubules [12]). |
PMC1857822_pone-0000437-g002_10704.jpg | What is shown in this image? | FAZ restricts basal body migration.A–C. Top panels, detergent-extracted cytoskeletons of DHC1bRNAi cells induced for 41 h stained with MAb22 (basal body marker [BB], yellow), L3B2 (FAZ marker, red) and DAPI (blue). Bottom panels: 2-fold magnification of the basal body area of the above images. Diagrams show the position of the old (with a flagellum) and new (without a flagellum) basal bodies as well as positioning of the flagellum (black lines) and the FAZ filament (red lines). DAPI has been omitted from phase contrast images to facilitate visualisation of the flagellar structures. A–B. Presence of a short new FAZ contacting the old one (orange arrows) appears to refrain new basal body migration. C. Extensive basal body migration when the new FAZ is not in contact with the old one (green arrow). D–E. Detergent-extracted cytoskeletons of non-induced (D) or 48h-induced (E) DHC1bRNAi cells stained with L3B2 (immunogold) showing interaction between new and old FAZ (orange arrows). Basal bodies (BB) are found at the proximal end of the flagella (when present) and are easily recognised by their thicker wall (due to the presence of triplet microtubules [12]). |
PMC1857822_pone-0000437-g002_10701.jpg | What key item or scene is captured in this photo? | FAZ restricts basal body migration.A–C. Top panels, detergent-extracted cytoskeletons of DHC1bRNAi cells induced for 41 h stained with MAb22 (basal body marker [BB], yellow), L3B2 (FAZ marker, red) and DAPI (blue). Bottom panels: 2-fold magnification of the basal body area of the above images. Diagrams show the position of the old (with a flagellum) and new (without a flagellum) basal bodies as well as positioning of the flagellum (black lines) and the FAZ filament (red lines). DAPI has been omitted from phase contrast images to facilitate visualisation of the flagellar structures. A–B. Presence of a short new FAZ contacting the old one (orange arrows) appears to refrain new basal body migration. C. Extensive basal body migration when the new FAZ is not in contact with the old one (green arrow). D–E. Detergent-extracted cytoskeletons of non-induced (D) or 48h-induced (E) DHC1bRNAi cells stained with L3B2 (immunogold) showing interaction between new and old FAZ (orange arrows). Basal bodies (BB) are found at the proximal end of the flagella (when present) and are easily recognised by their thicker wall (due to the presence of triplet microtubules [12]). |
PMC1857823_pone-0000440-g001_10709.jpg | What is shown in this image? | Design and plasma membrane expression of VSFP2s.A: A pair of CFP (donor) and YFP (acceptor) is attached to the 4-transmembrane-voltage-sensing domain (VSD) of Ci-VSP. B, C: Confocal fluorescence (B) and transmission images (C) of PC12 cells transfected with VSFP2D. Note the targeting of the fluorescent protein to the plasma membrane. Scale bar is 30 μm. |
PMC1857823_pone-0000440-g001_10708.jpg | Describe the main subject of this image. | Design and plasma membrane expression of VSFP2s.A: A pair of CFP (donor) and YFP (acceptor) is attached to the 4-transmembrane-voltage-sensing domain (VSD) of Ci-VSP. B, C: Confocal fluorescence (B) and transmission images (C) of PC12 cells transfected with VSFP2D. Note the targeting of the fluorescent protein to the plasma membrane. Scale bar is 30 μm. |
PMC1858686_F2_10715.jpg | What object or scene is depicted here? | Double immunostainings of embryoid bodies sprouts for CD31, von Willebrand factor (vWF) and NG2 proteoglycan. CJ7 ES cells were allowed to differentiate in the presence of angiogenic growth factors (VEGF+FGF2) added at day 0. EBs angiogenic sprouts were analyzed at day 11 of differentiation. vWF immunoreactivity (red fluorescence) located in Weibel-Palade bodies can be observed in several sprouting CD31-positive cells (green fluorescence) (upper panels). Elongated NG2 proteoglycan-positive cells (red fluorescence) can be seen close to CD31-positive cells constituting endothelial sprouts (lower panels). Scale bar = 50 μm. |
PMC1858686_F2_10710.jpg | What is the principal component of this image? | Double immunostainings of embryoid bodies sprouts for CD31, von Willebrand factor (vWF) and NG2 proteoglycan. CJ7 ES cells were allowed to differentiate in the presence of angiogenic growth factors (VEGF+FGF2) added at day 0. EBs angiogenic sprouts were analyzed at day 11 of differentiation. vWF immunoreactivity (red fluorescence) located in Weibel-Palade bodies can be observed in several sprouting CD31-positive cells (green fluorescence) (upper panels). Elongated NG2 proteoglycan-positive cells (red fluorescence) can be seen close to CD31-positive cells constituting endothelial sprouts (lower panels). Scale bar = 50 μm. |
PMC1858686_F2_10713.jpg | What is the central feature of this picture? | Double immunostainings of embryoid bodies sprouts for CD31, von Willebrand factor (vWF) and NG2 proteoglycan. CJ7 ES cells were allowed to differentiate in the presence of angiogenic growth factors (VEGF+FGF2) added at day 0. EBs angiogenic sprouts were analyzed at day 11 of differentiation. vWF immunoreactivity (red fluorescence) located in Weibel-Palade bodies can be observed in several sprouting CD31-positive cells (green fluorescence) (upper panels). Elongated NG2 proteoglycan-positive cells (red fluorescence) can be seen close to CD31-positive cells constituting endothelial sprouts (lower panels). Scale bar = 50 μm. |
PMC1858686_F2_10714.jpg | What is the focal point of this photograph? | Double immunostainings of embryoid bodies sprouts for CD31, von Willebrand factor (vWF) and NG2 proteoglycan. CJ7 ES cells were allowed to differentiate in the presence of angiogenic growth factors (VEGF+FGF2) added at day 0. EBs angiogenic sprouts were analyzed at day 11 of differentiation. vWF immunoreactivity (red fluorescence) located in Weibel-Palade bodies can be observed in several sprouting CD31-positive cells (green fluorescence) (upper panels). Elongated NG2 proteoglycan-positive cells (red fluorescence) can be seen close to CD31-positive cells constituting endothelial sprouts (lower panels). Scale bar = 50 μm. |
PMC1858686_F2_10712.jpg | What does this image primarily show? | Double immunostainings of embryoid bodies sprouts for CD31, von Willebrand factor (vWF) and NG2 proteoglycan. CJ7 ES cells were allowed to differentiate in the presence of angiogenic growth factors (VEGF+FGF2) added at day 0. EBs angiogenic sprouts were analyzed at day 11 of differentiation. vWF immunoreactivity (red fluorescence) located in Weibel-Palade bodies can be observed in several sprouting CD31-positive cells (green fluorescence) (upper panels). Elongated NG2 proteoglycan-positive cells (red fluorescence) can be seen close to CD31-positive cells constituting endothelial sprouts (lower panels). Scale bar = 50 μm. |
PMC1860057_F1_10718.jpg | What is the main focus of this visual representation? | Representative microscopic images of fibroblast-like synovial cells post-lipopolysaccharide challenge. Representative microscopic images (400× magnification) of fibroblast-like synovial cells (a), (c), and (e) 2 hours post-lipopolysaccharide (LPS) challenge and (b), (d), and (f) 24 hours post-LPS challenge. Cells treated with the higher molecular weight hyaluronan (HA) product (group 4, pretreatment and sustained treatment with higher molecular weight HA) were protected from (d) and (e) the morphologic changes induced by LPS, including the loss of cell attachment to the culture flask and the pronounced cellular contraction that were seen in (a), (b) group 2 (LPS control) and (c), (d) group 3 (preteatment and sustained treatment with lower molecular weight HA). |
PMC1860057_F1_10716.jpg | What is being portrayed in this visual content? | Representative microscopic images of fibroblast-like synovial cells post-lipopolysaccharide challenge. Representative microscopic images (400× magnification) of fibroblast-like synovial cells (a), (c), and (e) 2 hours post-lipopolysaccharide (LPS) challenge and (b), (d), and (f) 24 hours post-LPS challenge. Cells treated with the higher molecular weight hyaluronan (HA) product (group 4, pretreatment and sustained treatment with higher molecular weight HA) were protected from (d) and (e) the morphologic changes induced by LPS, including the loss of cell attachment to the culture flask and the pronounced cellular contraction that were seen in (a), (b) group 2 (LPS control) and (c), (d) group 3 (preteatment and sustained treatment with lower molecular weight HA). |
PMC1860057_F1_10719.jpg | Describe the main subject of this image. | Representative microscopic images of fibroblast-like synovial cells post-lipopolysaccharide challenge. Representative microscopic images (400× magnification) of fibroblast-like synovial cells (a), (c), and (e) 2 hours post-lipopolysaccharide (LPS) challenge and (b), (d), and (f) 24 hours post-LPS challenge. Cells treated with the higher molecular weight hyaluronan (HA) product (group 4, pretreatment and sustained treatment with higher molecular weight HA) were protected from (d) and (e) the morphologic changes induced by LPS, including the loss of cell attachment to the culture flask and the pronounced cellular contraction that were seen in (a), (b) group 2 (LPS control) and (c), (d) group 3 (preteatment and sustained treatment with lower molecular weight HA). |
PMC1860057_F1_10717.jpg | What is the central feature of this picture? | Representative microscopic images of fibroblast-like synovial cells post-lipopolysaccharide challenge. Representative microscopic images (400× magnification) of fibroblast-like synovial cells (a), (c), and (e) 2 hours post-lipopolysaccharide (LPS) challenge and (b), (d), and (f) 24 hours post-LPS challenge. Cells treated with the higher molecular weight hyaluronan (HA) product (group 4, pretreatment and sustained treatment with higher molecular weight HA) were protected from (d) and (e) the morphologic changes induced by LPS, including the loss of cell attachment to the culture flask and the pronounced cellular contraction that were seen in (a), (b) group 2 (LPS control) and (c), (d) group 3 (preteatment and sustained treatment with lower molecular weight HA). |
PMC1860057_F1_10720.jpg | What is the central feature of this picture? | Representative microscopic images of fibroblast-like synovial cells post-lipopolysaccharide challenge. Representative microscopic images (400× magnification) of fibroblast-like synovial cells (a), (c), and (e) 2 hours post-lipopolysaccharide (LPS) challenge and (b), (d), and (f) 24 hours post-LPS challenge. Cells treated with the higher molecular weight hyaluronan (HA) product (group 4, pretreatment and sustained treatment with higher molecular weight HA) were protected from (d) and (e) the morphologic changes induced by LPS, including the loss of cell attachment to the culture flask and the pronounced cellular contraction that were seen in (a), (b) group 2 (LPS control) and (c), (d) group 3 (preteatment and sustained treatment with lower molecular weight HA). |
PMC1860057_F1_10721.jpg | What is the central feature of this picture? | Representative microscopic images of fibroblast-like synovial cells post-lipopolysaccharide challenge. Representative microscopic images (400× magnification) of fibroblast-like synovial cells (a), (c), and (e) 2 hours post-lipopolysaccharide (LPS) challenge and (b), (d), and (f) 24 hours post-LPS challenge. Cells treated with the higher molecular weight hyaluronan (HA) product (group 4, pretreatment and sustained treatment with higher molecular weight HA) were protected from (d) and (e) the morphologic changes induced by LPS, including the loss of cell attachment to the culture flask and the pronounced cellular contraction that were seen in (a), (b) group 2 (LPS control) and (c), (d) group 3 (preteatment and sustained treatment with lower molecular weight HA). |
PMC1860066_F3_10723.jpg | What is the core subject represented in this visual? | Scanning electron micrographs of articular cartilage surface of the medial tibial plateau. These micrographs were taken at 19 weeks after anterior cruciate ligament transection surgery and the magnification is ×6,000 (scale bar is 10 μm). (a) Normal group. (b) Nutritive mixture solution (NMS) group. (c) Normal saline (NS) group. |
PMC1860066_F3_10724.jpg | What does this image primarily show? | Scanning electron micrographs of articular cartilage surface of the medial tibial plateau. These micrographs were taken at 19 weeks after anterior cruciate ligament transection surgery and the magnification is ×6,000 (scale bar is 10 μm). (a) Normal group. (b) Nutritive mixture solution (NMS) group. (c) Normal saline (NS) group. |
PMC1860066_F3_10722.jpg | Describe the main subject of this image. | Scanning electron micrographs of articular cartilage surface of the medial tibial plateau. These micrographs were taken at 19 weeks after anterior cruciate ligament transection surgery and the magnification is ×6,000 (scale bar is 10 μm). (a) Normal group. (b) Nutritive mixture solution (NMS) group. (c) Normal saline (NS) group. |
PMC1860072_F3_10749.jpg | What is the main focus of this visual representation? | High magnification images of sagittal sections of articular cartilage, stained with safranin-O and fast-green, reveal detailed cartilage histology. (a) Healthy-appearing sham cartilage has intact superficial, mid, and deep zones (from top to bottom of image) that stain deeply with safranin-O (red) for glycosaminoglycans. The chondrocytes are arranged in columns. (b) Two week FM ipsilateral cartilage demonstrates delamination (del) of the superficial zone. (c) Four week FM ipsilateral cartilage shows the development of vertical fissures (vf) into the mid-zone, and loss of glycosaminoglycans (pale green stain in mid-zone is red in panel a). (d) Matrix erosion of the superficial and mid-zones is evident by 8 weeks in FM ipsilateral cartilage, as well as the formation of chondrocyte clusters (cc). (e) By 16 weeks, NM ipsilateral cartilage shows almost complete denudation (dn) of the articular cartilage, and evidence of bone repair appears beneath the subchondral plate (br). (f) Fibrocartilage-like tissue (fc) is evident in the articular cartilage of 20-week FM ipsilateral joints, which is indicative of abnormal repair processes. All images are shown at the same magnification, indicated by the scale bar. FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F3_10750.jpg | Can you identify the primary element in this image? | High magnification images of sagittal sections of articular cartilage, stained with safranin-O and fast-green, reveal detailed cartilage histology. (a) Healthy-appearing sham cartilage has intact superficial, mid, and deep zones (from top to bottom of image) that stain deeply with safranin-O (red) for glycosaminoglycans. The chondrocytes are arranged in columns. (b) Two week FM ipsilateral cartilage demonstrates delamination (del) of the superficial zone. (c) Four week FM ipsilateral cartilage shows the development of vertical fissures (vf) into the mid-zone, and loss of glycosaminoglycans (pale green stain in mid-zone is red in panel a). (d) Matrix erosion of the superficial and mid-zones is evident by 8 weeks in FM ipsilateral cartilage, as well as the formation of chondrocyte clusters (cc). (e) By 16 weeks, NM ipsilateral cartilage shows almost complete denudation (dn) of the articular cartilage, and evidence of bone repair appears beneath the subchondral plate (br). (f) Fibrocartilage-like tissue (fc) is evident in the articular cartilage of 20-week FM ipsilateral joints, which is indicative of abnormal repair processes. All images are shown at the same magnification, indicated by the scale bar. FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F3_10751.jpg | What is the central feature of this picture? | High magnification images of sagittal sections of articular cartilage, stained with safranin-O and fast-green, reveal detailed cartilage histology. (a) Healthy-appearing sham cartilage has intact superficial, mid, and deep zones (from top to bottom of image) that stain deeply with safranin-O (red) for glycosaminoglycans. The chondrocytes are arranged in columns. (b) Two week FM ipsilateral cartilage demonstrates delamination (del) of the superficial zone. (c) Four week FM ipsilateral cartilage shows the development of vertical fissures (vf) into the mid-zone, and loss of glycosaminoglycans (pale green stain in mid-zone is red in panel a). (d) Matrix erosion of the superficial and mid-zones is evident by 8 weeks in FM ipsilateral cartilage, as well as the formation of chondrocyte clusters (cc). (e) By 16 weeks, NM ipsilateral cartilage shows almost complete denudation (dn) of the articular cartilage, and evidence of bone repair appears beneath the subchondral plate (br). (f) Fibrocartilage-like tissue (fc) is evident in the articular cartilage of 20-week FM ipsilateral joints, which is indicative of abnormal repair processes. All images are shown at the same magnification, indicated by the scale bar. FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F3_10752.jpg | What is being portrayed in this visual content? | High magnification images of sagittal sections of articular cartilage, stained with safranin-O and fast-green, reveal detailed cartilage histology. (a) Healthy-appearing sham cartilage has intact superficial, mid, and deep zones (from top to bottom of image) that stain deeply with safranin-O (red) for glycosaminoglycans. The chondrocytes are arranged in columns. (b) Two week FM ipsilateral cartilage demonstrates delamination (del) of the superficial zone. (c) Four week FM ipsilateral cartilage shows the development of vertical fissures (vf) into the mid-zone, and loss of glycosaminoglycans (pale green stain in mid-zone is red in panel a). (d) Matrix erosion of the superficial and mid-zones is evident by 8 weeks in FM ipsilateral cartilage, as well as the formation of chondrocyte clusters (cc). (e) By 16 weeks, NM ipsilateral cartilage shows almost complete denudation (dn) of the articular cartilage, and evidence of bone repair appears beneath the subchondral plate (br). (f) Fibrocartilage-like tissue (fc) is evident in the articular cartilage of 20-week FM ipsilateral joints, which is indicative of abnormal repair processes. All images are shown at the same magnification, indicated by the scale bar. FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10729.jpg | What is the central feature of this picture? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10731.jpg | Can you identify the primary element in this image? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10728.jpg | Describe the main subject of this image. | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10725.jpg | What is the principal component of this image? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10743.jpg | What does this image primarily show? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10730.jpg | What can you see in this picture? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10739.jpg | What's the most prominent thing you notice in this picture? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10737.jpg | Can you identify the primary element in this image? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10740.jpg | What is the focal point of this photograph? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10734.jpg | What's the most prominent thing you notice in this picture? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10735.jpg | What can you see in this picture? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10733.jpg | What is the central feature of this picture? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10732.jpg | Describe the main subject of this image. | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10736.jpg | What is the dominant medical problem in this image? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F5_10742.jpg | What is the main focus of this visual representation? | Micro-CT analysis of subchondral changes over the time course. Knee joints from (a) NM and (b) FM groups of animals were assessed by micro-CT for morphologic changes in subchondral bone in contralateral and ipsilateral joints, compared with sham controls at 2, 12, and 20 weeks. Each sagittal slice at 12 and 20 weeks is shown at the same distance into the medial joint compartment (from the medial margin) as the corresponding histologic section in Figure 2. Subchondral trabecular architecture was maintained in both sham and contralateral joints, regardless of mobilization group. Note the more extensive subchondral spaces in FM compared with NM ipsilateral joints (white arrows). Sclerotic bone (S) appeared earlier in FM (12 weeks) than in NM ipsilateral joints (20 weeks). Collapse of the subchondral plate was evident in 20 week FM joints (arrowhead). All images are shown at the same magnification, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F7_10744.jpg | Describe the main subject of this image. | Reconstruction of micro-CT volumes reveals subchondral plate degeneration and osteophytes. Qualitative assessment of (a,b) subchondral plate integrity and (c,d) femoral osteophyte formation is shown. Reconstruction of the three-dimensional micro-CT volumes and surface rendering was used to assess the integrity of the subchondral plate in (a) NM and (b) FM ipsilateral joints at 20 weeks. Dorsal views of the reconstructed knee joints are shown. In panel a the tibial subchondral plate of NM joints exhibited minor plate breakdown (arrowhead) in the medial plateau, whereas in panel b FM plates were completely compromised by erosion and pitting (arrowheads). Coronal sections of (c) NM and (d) FM ipsilateral joints at 20 weeks reveal the presence of osteophytes (arrows). FM joints exhibit many well developed osteophytes on both medial (left) and lateral (right) joint margins, whereas NM joints show only slight medial osteophyte development (containing little mineral content). The magnification of each image is the same, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F7_10747.jpg | What is the main focus of this visual representation? | Reconstruction of micro-CT volumes reveals subchondral plate degeneration and osteophytes. Qualitative assessment of (a,b) subchondral plate integrity and (c,d) femoral osteophyte formation is shown. Reconstruction of the three-dimensional micro-CT volumes and surface rendering was used to assess the integrity of the subchondral plate in (a) NM and (b) FM ipsilateral joints at 20 weeks. Dorsal views of the reconstructed knee joints are shown. In panel a the tibial subchondral plate of NM joints exhibited minor plate breakdown (arrowhead) in the medial plateau, whereas in panel b FM plates were completely compromised by erosion and pitting (arrowheads). Coronal sections of (c) NM and (d) FM ipsilateral joints at 20 weeks reveal the presence of osteophytes (arrows). FM joints exhibit many well developed osteophytes on both medial (left) and lateral (right) joint margins, whereas NM joints show only slight medial osteophyte development (containing little mineral content). The magnification of each image is the same, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F7_10746.jpg | What key item or scene is captured in this photo? | Reconstruction of micro-CT volumes reveals subchondral plate degeneration and osteophytes. Qualitative assessment of (a,b) subchondral plate integrity and (c,d) femoral osteophyte formation is shown. Reconstruction of the three-dimensional micro-CT volumes and surface rendering was used to assess the integrity of the subchondral plate in (a) NM and (b) FM ipsilateral joints at 20 weeks. Dorsal views of the reconstructed knee joints are shown. In panel a the tibial subchondral plate of NM joints exhibited minor plate breakdown (arrowhead) in the medial plateau, whereas in panel b FM plates were completely compromised by erosion and pitting (arrowheads). Coronal sections of (c) NM and (d) FM ipsilateral joints at 20 weeks reveal the presence of osteophytes (arrows). FM joints exhibit many well developed osteophytes on both medial (left) and lateral (right) joint margins, whereas NM joints show only slight medial osteophyte development (containing little mineral content). The magnification of each image is the same, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1860072_F7_10745.jpg | What is the central feature of this picture? | Reconstruction of micro-CT volumes reveals subchondral plate degeneration and osteophytes. Qualitative assessment of (a,b) subchondral plate integrity and (c,d) femoral osteophyte formation is shown. Reconstruction of the three-dimensional micro-CT volumes and surface rendering was used to assess the integrity of the subchondral plate in (a) NM and (b) FM ipsilateral joints at 20 weeks. Dorsal views of the reconstructed knee joints are shown. In panel a the tibial subchondral plate of NM joints exhibited minor plate breakdown (arrowhead) in the medial plateau, whereas in panel b FM plates were completely compromised by erosion and pitting (arrowheads). Coronal sections of (c) NM and (d) FM ipsilateral joints at 20 weeks reveal the presence of osteophytes (arrows). FM joints exhibit many well developed osteophytes on both medial (left) and lateral (right) joint margins, whereas NM joints show only slight medial osteophyte development (containing little mineral content). The magnification of each image is the same, indicated by the scale bars. CT, computed tomography; FM, forced mobilization; NM, nonmobilized. |
PMC1863425_F3_10761.jpg | What stands out most in this visual? | Photomicrographs of DCs, Apo-Nec cells and the phagocytic process at different time points. A – Characteristic morphologies of monocyte-derived iDC (left) and mDC (LPS-treated) (right) are shown under phase contrast microscopy (original magnification: 1000×). B – Electron microscopy of an apoptotic body (Apo-Nec sample) showing chromatin condensation; original magnification: 8000×. C – Representative pictures of the phagocytic process at 0, 6, 12, 24, 48 and 72 hs. In order to observe whole cells ultrathin slices (0.5 μm) stained by Toluidine blue were analyzed as described under methods. An Apo-Nec cell and a DC are indicated (upper and lower arrows, respectively). Original magnification: 1000×. D – Detail of a phagocytic DC observed under electron microscopy (4000×) showing digested material at higher magnification (10,000×). |
PMC1863425_F3_10757.jpg | What object or scene is depicted here? | Photomicrographs of DCs, Apo-Nec cells and the phagocytic process at different time points. A – Characteristic morphologies of monocyte-derived iDC (left) and mDC (LPS-treated) (right) are shown under phase contrast microscopy (original magnification: 1000×). B – Electron microscopy of an apoptotic body (Apo-Nec sample) showing chromatin condensation; original magnification: 8000×. C – Representative pictures of the phagocytic process at 0, 6, 12, 24, 48 and 72 hs. In order to observe whole cells ultrathin slices (0.5 μm) stained by Toluidine blue were analyzed as described under methods. An Apo-Nec cell and a DC are indicated (upper and lower arrows, respectively). Original magnification: 1000×. D – Detail of a phagocytic DC observed under electron microscopy (4000×) showing digested material at higher magnification (10,000×). |
PMC1863425_F3_10754.jpg | What stands out most in this visual? | Photomicrographs of DCs, Apo-Nec cells and the phagocytic process at different time points. A – Characteristic morphologies of monocyte-derived iDC (left) and mDC (LPS-treated) (right) are shown under phase contrast microscopy (original magnification: 1000×). B – Electron microscopy of an apoptotic body (Apo-Nec sample) showing chromatin condensation; original magnification: 8000×. C – Representative pictures of the phagocytic process at 0, 6, 12, 24, 48 and 72 hs. In order to observe whole cells ultrathin slices (0.5 μm) stained by Toluidine blue were analyzed as described under methods. An Apo-Nec cell and a DC are indicated (upper and lower arrows, respectively). Original magnification: 1000×. D – Detail of a phagocytic DC observed under electron microscopy (4000×) showing digested material at higher magnification (10,000×). |
PMC1863425_F3_10755.jpg | What is the principal component of this image? | Photomicrographs of DCs, Apo-Nec cells and the phagocytic process at different time points. A – Characteristic morphologies of monocyte-derived iDC (left) and mDC (LPS-treated) (right) are shown under phase contrast microscopy (original magnification: 1000×). B – Electron microscopy of an apoptotic body (Apo-Nec sample) showing chromatin condensation; original magnification: 8000×. C – Representative pictures of the phagocytic process at 0, 6, 12, 24, 48 and 72 hs. In order to observe whole cells ultrathin slices (0.5 μm) stained by Toluidine blue were analyzed as described under methods. An Apo-Nec cell and a DC are indicated (upper and lower arrows, respectively). Original magnification: 1000×. D – Detail of a phagocytic DC observed under electron microscopy (4000×) showing digested material at higher magnification (10,000×). |
PMC1863425_F3_10756.jpg | What is the dominant medical problem in this image? | Photomicrographs of DCs, Apo-Nec cells and the phagocytic process at different time points. A – Characteristic morphologies of monocyte-derived iDC (left) and mDC (LPS-treated) (right) are shown under phase contrast microscopy (original magnification: 1000×). B – Electron microscopy of an apoptotic body (Apo-Nec sample) showing chromatin condensation; original magnification: 8000×. C – Representative pictures of the phagocytic process at 0, 6, 12, 24, 48 and 72 hs. In order to observe whole cells ultrathin slices (0.5 μm) stained by Toluidine blue were analyzed as described under methods. An Apo-Nec cell and a DC are indicated (upper and lower arrows, respectively). Original magnification: 1000×. D – Detail of a phagocytic DC observed under electron microscopy (4000×) showing digested material at higher magnification (10,000×). |
PMC1863425_F3_10764.jpg | Can you identify the primary element in this image? | Photomicrographs of DCs, Apo-Nec cells and the phagocytic process at different time points. A – Characteristic morphologies of monocyte-derived iDC (left) and mDC (LPS-treated) (right) are shown under phase contrast microscopy (original magnification: 1000×). B – Electron microscopy of an apoptotic body (Apo-Nec sample) showing chromatin condensation; original magnification: 8000×. C – Representative pictures of the phagocytic process at 0, 6, 12, 24, 48 and 72 hs. In order to observe whole cells ultrathin slices (0.5 μm) stained by Toluidine blue were analyzed as described under methods. An Apo-Nec cell and a DC are indicated (upper and lower arrows, respectively). Original magnification: 1000×. D – Detail of a phagocytic DC observed under electron microscopy (4000×) showing digested material at higher magnification (10,000×). |
PMC1863425_F3_10759.jpg | Can you identify the primary element in this image? | Photomicrographs of DCs, Apo-Nec cells and the phagocytic process at different time points. A – Characteristic morphologies of monocyte-derived iDC (left) and mDC (LPS-treated) (right) are shown under phase contrast microscopy (original magnification: 1000×). B – Electron microscopy of an apoptotic body (Apo-Nec sample) showing chromatin condensation; original magnification: 8000×. C – Representative pictures of the phagocytic process at 0, 6, 12, 24, 48 and 72 hs. In order to observe whole cells ultrathin slices (0.5 μm) stained by Toluidine blue were analyzed as described under methods. An Apo-Nec cell and a DC are indicated (upper and lower arrows, respectively). Original magnification: 1000×. D – Detail of a phagocytic DC observed under electron microscopy (4000×) showing digested material at higher magnification (10,000×). |
PMC1863425_F3_10762.jpg | What stands out most in this visual? | Photomicrographs of DCs, Apo-Nec cells and the phagocytic process at different time points. A – Characteristic morphologies of monocyte-derived iDC (left) and mDC (LPS-treated) (right) are shown under phase contrast microscopy (original magnification: 1000×). B – Electron microscopy of an apoptotic body (Apo-Nec sample) showing chromatin condensation; original magnification: 8000×. C – Representative pictures of the phagocytic process at 0, 6, 12, 24, 48 and 72 hs. In order to observe whole cells ultrathin slices (0.5 μm) stained by Toluidine blue were analyzed as described under methods. An Apo-Nec cell and a DC are indicated (upper and lower arrows, respectively). Original magnification: 1000×. D – Detail of a phagocytic DC observed under electron microscopy (4000×) showing digested material at higher magnification (10,000×). |
PMC1863429_F1_10765.jpg | What is the focal point of this photograph? | Computer tomography (CT) scan of advanced ovarian cancer before treatment showing conglomeration of the bowel. |
PMC1863432_F1_10768.jpg | Can you identify the primary element in this image? | NT2/D1 cells in expansion medium. Phase contrast images of three typical morphologies of NT2/D1 cells in expansion medium, (RPMI, FBS and antibiotics) analyzed in a CK2 Olympus microscope: A. Embryoid body-like structures, magnification 40×; B. epithelioid-like phenotype, magnification 100×; C. neuronal-like phenotype, magnification 200×. |
PMC1863432_F1_10767.jpg | What is the focal point of this photograph? | NT2/D1 cells in expansion medium. Phase contrast images of three typical morphologies of NT2/D1 cells in expansion medium, (RPMI, FBS and antibiotics) analyzed in a CK2 Olympus microscope: A. Embryoid body-like structures, magnification 40×; B. epithelioid-like phenotype, magnification 100×; C. neuronal-like phenotype, magnification 200×. |
PMC1863432_F1_10769.jpg | What does this image primarily show? | NT2/D1 cells in expansion medium. Phase contrast images of three typical morphologies of NT2/D1 cells in expansion medium, (RPMI, FBS and antibiotics) analyzed in a CK2 Olympus microscope: A. Embryoid body-like structures, magnification 40×; B. epithelioid-like phenotype, magnification 100×; C. neuronal-like phenotype, magnification 200×. |
PMC1864992_ppat-0030063-g001_10770.jpg | What is shown in this image? | Analysis of Purified SIV Virions by Cryo-Electron Tomography(A) Low-dose projection image of a plunge-frozen specimen.(B) A series of images recorded over a tilt range of −63° to +63° was used to reconstruct a 3-D volume of vitrified viruses similar to those shown in (A). Four 1-nm-thick tomographic slices at different depths from a tomogram of plunge-frozen SIV virions are shown.Scale bars are 50 nm long. The dark black spots are from 5-nm-wide gold fiducial markers used for aligning individual images in a tilt series. |
PMC1864992_ppat-0030063-g001_10771.jpg | What is the principal component of this image? | Analysis of Purified SIV Virions by Cryo-Electron Tomography(A) Low-dose projection image of a plunge-frozen specimen.(B) A series of images recorded over a tilt range of −63° to +63° was used to reconstruct a 3-D volume of vitrified viruses similar to those shown in (A). Four 1-nm-thick tomographic slices at different depths from a tomogram of plunge-frozen SIV virions are shown.Scale bars are 50 nm long. The dark black spots are from 5-nm-wide gold fiducial markers used for aligning individual images in a tilt series. |
PMC1864992_ppat-0030063-g004_10791.jpg | What is the core subject represented in this visual? | Projection Images from SIV-Infected Cells and from T Cells Exposed to SIV for Short Periods(A–C) Electron microscopic images of budding (A), immature (B), and mature (C) SIV particles in chronically infected cell suspensions. Scale bars are 50 nm long.(D and E) Distinct virus–cell contacts in chronically infected cells that are defined by a characteristic density at the interface between the virus and the cell membrane, and distinct from virus morphologies seen in (A–C). Note that in some instances (E), the curvature of the cell membrane follows the curvature of the virus where the contact is made. Scale bars are 100 nm long.(F) Projection image (higher magnifications shown in inset) of the contact region between SIV virions and T lymphocytes fixed after incubation at 37 °C for 15 min. At lower magnifications the overall context of the cell in the vicinity of the contact region is shown, while at the higher magnifications, entry claw contacts can be recognized in the projection view. Scale bar is 1 μm long. G, part of the Golgi ribbon; m, mitochondria; n, nucleus. |
PMC1864992_ppat-0030063-g004_10788.jpg | What is the central feature of this picture? | Projection Images from SIV-Infected Cells and from T Cells Exposed to SIV for Short Periods(A–C) Electron microscopic images of budding (A), immature (B), and mature (C) SIV particles in chronically infected cell suspensions. Scale bars are 50 nm long.(D and E) Distinct virus–cell contacts in chronically infected cells that are defined by a characteristic density at the interface between the virus and the cell membrane, and distinct from virus morphologies seen in (A–C). Note that in some instances (E), the curvature of the cell membrane follows the curvature of the virus where the contact is made. Scale bars are 100 nm long.(F) Projection image (higher magnifications shown in inset) of the contact region between SIV virions and T lymphocytes fixed after incubation at 37 °C for 15 min. At lower magnifications the overall context of the cell in the vicinity of the contact region is shown, while at the higher magnifications, entry claw contacts can be recognized in the projection view. Scale bar is 1 μm long. G, part of the Golgi ribbon; m, mitochondria; n, nucleus. |
PMC1864992_ppat-0030063-g004_10789.jpg | What key item or scene is captured in this photo? | Projection Images from SIV-Infected Cells and from T Cells Exposed to SIV for Short Periods(A–C) Electron microscopic images of budding (A), immature (B), and mature (C) SIV particles in chronically infected cell suspensions. Scale bars are 50 nm long.(D and E) Distinct virus–cell contacts in chronically infected cells that are defined by a characteristic density at the interface between the virus and the cell membrane, and distinct from virus morphologies seen in (A–C). Note that in some instances (E), the curvature of the cell membrane follows the curvature of the virus where the contact is made. Scale bars are 100 nm long.(F) Projection image (higher magnifications shown in inset) of the contact region between SIV virions and T lymphocytes fixed after incubation at 37 °C for 15 min. At lower magnifications the overall context of the cell in the vicinity of the contact region is shown, while at the higher magnifications, entry claw contacts can be recognized in the projection view. Scale bar is 1 μm long. G, part of the Golgi ribbon; m, mitochondria; n, nucleus. |
PMC1864992_ppat-0030063-g004_10786.jpg | What is the focal point of this photograph? | Projection Images from SIV-Infected Cells and from T Cells Exposed to SIV for Short Periods(A–C) Electron microscopic images of budding (A), immature (B), and mature (C) SIV particles in chronically infected cell suspensions. Scale bars are 50 nm long.(D and E) Distinct virus–cell contacts in chronically infected cells that are defined by a characteristic density at the interface between the virus and the cell membrane, and distinct from virus morphologies seen in (A–C). Note that in some instances (E), the curvature of the cell membrane follows the curvature of the virus where the contact is made. Scale bars are 100 nm long.(F) Projection image (higher magnifications shown in inset) of the contact region between SIV virions and T lymphocytes fixed after incubation at 37 °C for 15 min. At lower magnifications the overall context of the cell in the vicinity of the contact region is shown, while at the higher magnifications, entry claw contacts can be recognized in the projection view. Scale bar is 1 μm long. G, part of the Golgi ribbon; m, mitochondria; n, nucleus. |
PMC1864992_ppat-0030063-g004_10787.jpg | What is shown in this image? | Projection Images from SIV-Infected Cells and from T Cells Exposed to SIV for Short Periods(A–C) Electron microscopic images of budding (A), immature (B), and mature (C) SIV particles in chronically infected cell suspensions. Scale bars are 50 nm long.(D and E) Distinct virus–cell contacts in chronically infected cells that are defined by a characteristic density at the interface between the virus and the cell membrane, and distinct from virus morphologies seen in (A–C). Note that in some instances (E), the curvature of the cell membrane follows the curvature of the virus where the contact is made. Scale bars are 100 nm long.(F) Projection image (higher magnifications shown in inset) of the contact region between SIV virions and T lymphocytes fixed after incubation at 37 °C for 15 min. At lower magnifications the overall context of the cell in the vicinity of the contact region is shown, while at the higher magnifications, entry claw contacts can be recognized in the projection view. Scale bar is 1 μm long. G, part of the Golgi ribbon; m, mitochondria; n, nucleus. |
PMC1864992_ppat-0030063-g004_10793.jpg | Describe the main subject of this image. | Projection Images from SIV-Infected Cells and from T Cells Exposed to SIV for Short Periods(A–C) Electron microscopic images of budding (A), immature (B), and mature (C) SIV particles in chronically infected cell suspensions. Scale bars are 50 nm long.(D and E) Distinct virus–cell contacts in chronically infected cells that are defined by a characteristic density at the interface between the virus and the cell membrane, and distinct from virus morphologies seen in (A–C). Note that in some instances (E), the curvature of the cell membrane follows the curvature of the virus where the contact is made. Scale bars are 100 nm long.(F) Projection image (higher magnifications shown in inset) of the contact region between SIV virions and T lymphocytes fixed after incubation at 37 °C for 15 min. At lower magnifications the overall context of the cell in the vicinity of the contact region is shown, while at the higher magnifications, entry claw contacts can be recognized in the projection view. Scale bar is 1 μm long. G, part of the Golgi ribbon; m, mitochondria; n, nucleus. |
PMC1864992_ppat-0030063-g004_10792.jpg | What does this image primarily show? | Projection Images from SIV-Infected Cells and from T Cells Exposed to SIV for Short Periods(A–C) Electron microscopic images of budding (A), immature (B), and mature (C) SIV particles in chronically infected cell suspensions. Scale bars are 50 nm long.(D and E) Distinct virus–cell contacts in chronically infected cells that are defined by a characteristic density at the interface between the virus and the cell membrane, and distinct from virus morphologies seen in (A–C). Note that in some instances (E), the curvature of the cell membrane follows the curvature of the virus where the contact is made. Scale bars are 100 nm long.(F) Projection image (higher magnifications shown in inset) of the contact region between SIV virions and T lymphocytes fixed after incubation at 37 °C for 15 min. At lower magnifications the overall context of the cell in the vicinity of the contact region is shown, while at the higher magnifications, entry claw contacts can be recognized in the projection view. Scale bar is 1 μm long. G, part of the Golgi ribbon; m, mitochondria; n, nucleus. |
PMC1864992_ppat-0030063-g004_10785.jpg | What is the core subject represented in this visual? | Projection Images from SIV-Infected Cells and from T Cells Exposed to SIV for Short Periods(A–C) Electron microscopic images of budding (A), immature (B), and mature (C) SIV particles in chronically infected cell suspensions. Scale bars are 50 nm long.(D and E) Distinct virus–cell contacts in chronically infected cells that are defined by a characteristic density at the interface between the virus and the cell membrane, and distinct from virus morphologies seen in (A–C). Note that in some instances (E), the curvature of the cell membrane follows the curvature of the virus where the contact is made. Scale bars are 100 nm long.(F) Projection image (higher magnifications shown in inset) of the contact region between SIV virions and T lymphocytes fixed after incubation at 37 °C for 15 min. At lower magnifications the overall context of the cell in the vicinity of the contact region is shown, while at the higher magnifications, entry claw contacts can be recognized in the projection view. Scale bar is 1 μm long. G, part of the Golgi ribbon; m, mitochondria; n, nucleus. |
PMC1864992_ppat-0030063-g004_10790.jpg | Describe the main subject of this image. | Projection Images from SIV-Infected Cells and from T Cells Exposed to SIV for Short Periods(A–C) Electron microscopic images of budding (A), immature (B), and mature (C) SIV particles in chronically infected cell suspensions. Scale bars are 50 nm long.(D and E) Distinct virus–cell contacts in chronically infected cells that are defined by a characteristic density at the interface between the virus and the cell membrane, and distinct from virus morphologies seen in (A–C). Note that in some instances (E), the curvature of the cell membrane follows the curvature of the virus where the contact is made. Scale bars are 100 nm long.(F) Projection image (higher magnifications shown in inset) of the contact region between SIV virions and T lymphocytes fixed after incubation at 37 °C for 15 min. At lower magnifications the overall context of the cell in the vicinity of the contact region is shown, while at the higher magnifications, entry claw contacts can be recognized in the projection view. Scale bar is 1 μm long. G, part of the Golgi ribbon; m, mitochondria; n, nucleus. |
PMC1864992_ppat-0030063-g005_10781.jpg | What stands out most in this visual? | Electron Tomography of Virus–Cell Contact in Chronically and Acutely Infected Cells(A–C) Single 1-nm slices extracted from a dual axis tomogram reconstructed by weighted back-projection where part of an entry claw is captured in a chronically infected cell. One combination of three rods can be seen in one plane (A), while a different combination of three rods can be seen in the other (B). Four of the rods can be seen clearly in orthogonal view sectioned close to the plane of contact between virus and cell (C), with the densities arranged in a zig-zag manner. The black arrows point to the four densities in both transverse and top views.(D) A 1-nm tomographic slice from SIV–T cell contact region in cells fixed 15 min after warming to 37 °C following incubation with high viral concentrations.Scale bars are 100 nm long in (A–D).(E) 3-D rendering of the same contact region presented in panel (D), showing the viral envelope (magenta), contact rods (red), core (yellow), and cell membrane (blue). Note that there are almost no spikes on the virion surface away from the region of viral–cell contact. |
PMC1864992_ppat-0030063-g005_10784.jpg | Can you identify the primary element in this image? | Electron Tomography of Virus–Cell Contact in Chronically and Acutely Infected Cells(A–C) Single 1-nm slices extracted from a dual axis tomogram reconstructed by weighted back-projection where part of an entry claw is captured in a chronically infected cell. One combination of three rods can be seen in one plane (A), while a different combination of three rods can be seen in the other (B). Four of the rods can be seen clearly in orthogonal view sectioned close to the plane of contact between virus and cell (C), with the densities arranged in a zig-zag manner. The black arrows point to the four densities in both transverse and top views.(D) A 1-nm tomographic slice from SIV–T cell contact region in cells fixed 15 min after warming to 37 °C following incubation with high viral concentrations.Scale bars are 100 nm long in (A–D).(E) 3-D rendering of the same contact region presented in panel (D), showing the viral envelope (magenta), contact rods (red), core (yellow), and cell membrane (blue). Note that there are almost no spikes on the virion surface away from the region of viral–cell contact. |
PMC1864992_ppat-0030063-g005_10780.jpg | Can you identify the primary element in this image? | Electron Tomography of Virus–Cell Contact in Chronically and Acutely Infected Cells(A–C) Single 1-nm slices extracted from a dual axis tomogram reconstructed by weighted back-projection where part of an entry claw is captured in a chronically infected cell. One combination of three rods can be seen in one plane (A), while a different combination of three rods can be seen in the other (B). Four of the rods can be seen clearly in orthogonal view sectioned close to the plane of contact between virus and cell (C), with the densities arranged in a zig-zag manner. The black arrows point to the four densities in both transverse and top views.(D) A 1-nm tomographic slice from SIV–T cell contact region in cells fixed 15 min after warming to 37 °C following incubation with high viral concentrations.Scale bars are 100 nm long in (A–D).(E) 3-D rendering of the same contact region presented in panel (D), showing the viral envelope (magenta), contact rods (red), core (yellow), and cell membrane (blue). Note that there are almost no spikes on the virion surface away from the region of viral–cell contact. |
PMC1864992_ppat-0030063-g005_10782.jpg | What is shown in this image? | Electron Tomography of Virus–Cell Contact in Chronically and Acutely Infected Cells(A–C) Single 1-nm slices extracted from a dual axis tomogram reconstructed by weighted back-projection where part of an entry claw is captured in a chronically infected cell. One combination of three rods can be seen in one plane (A), while a different combination of three rods can be seen in the other (B). Four of the rods can be seen clearly in orthogonal view sectioned close to the plane of contact between virus and cell (C), with the densities arranged in a zig-zag manner. The black arrows point to the four densities in both transverse and top views.(D) A 1-nm tomographic slice from SIV–T cell contact region in cells fixed 15 min after warming to 37 °C following incubation with high viral concentrations.Scale bars are 100 nm long in (A–D).(E) 3-D rendering of the same contact region presented in panel (D), showing the viral envelope (magenta), contact rods (red), core (yellow), and cell membrane (blue). Note that there are almost no spikes on the virion surface away from the region of viral–cell contact. |
PMC1864992_ppat-0030063-g005_10783.jpg | What is the dominant medical problem in this image? | Electron Tomography of Virus–Cell Contact in Chronically and Acutely Infected Cells(A–C) Single 1-nm slices extracted from a dual axis tomogram reconstructed by weighted back-projection where part of an entry claw is captured in a chronically infected cell. One combination of three rods can be seen in one plane (A), while a different combination of three rods can be seen in the other (B). Four of the rods can be seen clearly in orthogonal view sectioned close to the plane of contact between virus and cell (C), with the densities arranged in a zig-zag manner. The black arrows point to the four densities in both transverse and top views.(D) A 1-nm tomographic slice from SIV–T cell contact region in cells fixed 15 min after warming to 37 °C following incubation with high viral concentrations.Scale bars are 100 nm long in (A–D).(E) 3-D rendering of the same contact region presented in panel (D), showing the viral envelope (magenta), contact rods (red), core (yellow), and cell membrane (blue). Note that there are almost no spikes on the virion surface away from the region of viral–cell contact. |
PMC1864992_ppat-0030063-g007_10777.jpg | What is the principal component of this image? | Imaging of HIV-1 in Contact with T Cells(A–D) Four slices at different depths in a tomogram of the contact between HIV-1 and T cells, with cells fixed following incubation for 1 h at 37 °C. Scale bar is 100 nm long.(E) 3-D surface rendering of the tomographically derived architecture of the contact region between HIV-1 and the T cell membrane shown in panels (A–D), with color scheme as in panel (E) of Figure 5. |
PMC1864992_ppat-0030063-g007_10778.jpg | What is being portrayed in this visual content? | Imaging of HIV-1 in Contact with T Cells(A–D) Four slices at different depths in a tomogram of the contact between HIV-1 and T cells, with cells fixed following incubation for 1 h at 37 °C. Scale bar is 100 nm long.(E) 3-D surface rendering of the tomographically derived architecture of the contact region between HIV-1 and the T cell membrane shown in panels (A–D), with color scheme as in panel (E) of Figure 5. |
PMC1864992_ppat-0030063-g007_10776.jpg | What does this image primarily show? | Imaging of HIV-1 in Contact with T Cells(A–D) Four slices at different depths in a tomogram of the contact between HIV-1 and T cells, with cells fixed following incubation for 1 h at 37 °C. Scale bar is 100 nm long.(E) 3-D surface rendering of the tomographically derived architecture of the contact region between HIV-1 and the T cell membrane shown in panels (A–D), with color scheme as in panel (E) of Figure 5. |
PMC1864992_ppat-0030063-g007_10775.jpg | What is being portrayed in this visual content? | Imaging of HIV-1 in Contact with T Cells(A–D) Four slices at different depths in a tomogram of the contact between HIV-1 and T cells, with cells fixed following incubation for 1 h at 37 °C. Scale bar is 100 nm long.(E) 3-D surface rendering of the tomographically derived architecture of the contact region between HIV-1 and the T cell membrane shown in panels (A–D), with color scheme as in panel (E) of Figure 5. |
PMC1865376_F5_10795.jpg | What's the most prominent thing you notice in this picture? | NOGO-A expression during cell migration. A) H&E staining of optic tectum at HH30(E7) showing the generative zone (GZ), the migrating zone (MZ) and the first neuronal lamina (L1). B) Section in situ hybridization (sISH) of NOGO-A in an adjacent section demonstrating a corresponding radial pattern of expression in the region of migration. High magnification of the MZ (from boxed region in "A") shows the elongated processes of radial glia and associated migrating neurons. C) H&E for morphologic comparison; D) vimentin (Vim) immunohistochemistry (IHC) decorating the intermediate filaments of the radial glia; E) IHC of Neurofilament (NF) targeting migrating neurons; and F) sISH showing NOGO-A expression (red) more closely resembling NF staining. Scale bar 200 μm in A, B; 50 μm in C, D, E, F. |
PMC1865376_F5_10794.jpg | Can you identify the primary element in this image? | NOGO-A expression during cell migration. A) H&E staining of optic tectum at HH30(E7) showing the generative zone (GZ), the migrating zone (MZ) and the first neuronal lamina (L1). B) Section in situ hybridization (sISH) of NOGO-A in an adjacent section demonstrating a corresponding radial pattern of expression in the region of migration. High magnification of the MZ (from boxed region in "A") shows the elongated processes of radial glia and associated migrating neurons. C) H&E for morphologic comparison; D) vimentin (Vim) immunohistochemistry (IHC) decorating the intermediate filaments of the radial glia; E) IHC of Neurofilament (NF) targeting migrating neurons; and F) sISH showing NOGO-A expression (red) more closely resembling NF staining. Scale bar 200 μm in A, B; 50 μm in C, D, E, F. |
PMC1865376_F5_10797.jpg | What is the principal component of this image? | NOGO-A expression during cell migration. A) H&E staining of optic tectum at HH30(E7) showing the generative zone (GZ), the migrating zone (MZ) and the first neuronal lamina (L1). B) Section in situ hybridization (sISH) of NOGO-A in an adjacent section demonstrating a corresponding radial pattern of expression in the region of migration. High magnification of the MZ (from boxed region in "A") shows the elongated processes of radial glia and associated migrating neurons. C) H&E for morphologic comparison; D) vimentin (Vim) immunohistochemistry (IHC) decorating the intermediate filaments of the radial glia; E) IHC of Neurofilament (NF) targeting migrating neurons; and F) sISH showing NOGO-A expression (red) more closely resembling NF staining. Scale bar 200 μm in A, B; 50 μm in C, D, E, F. |
PMC1865376_F5_10798.jpg | What stands out most in this visual? | NOGO-A expression during cell migration. A) H&E staining of optic tectum at HH30(E7) showing the generative zone (GZ), the migrating zone (MZ) and the first neuronal lamina (L1). B) Section in situ hybridization (sISH) of NOGO-A in an adjacent section demonstrating a corresponding radial pattern of expression in the region of migration. High magnification of the MZ (from boxed region in "A") shows the elongated processes of radial glia and associated migrating neurons. C) H&E for morphologic comparison; D) vimentin (Vim) immunohistochemistry (IHC) decorating the intermediate filaments of the radial glia; E) IHC of Neurofilament (NF) targeting migrating neurons; and F) sISH showing NOGO-A expression (red) more closely resembling NF staining. Scale bar 200 μm in A, B; 50 μm in C, D, E, F. |
PMC1865376_F6_10803.jpg | Can you identify the primary element in this image? | NOGO-A Expression During Network Establishment. A) H&E and B) NOGO-A in situ hybridization (ISH) of HH36 (E10) optic tectum, prior to synaptogenesis. Transcript expression is intensified in cells of the tectal associated nuclei (TN) and cortical neuronal lamina. Note the lack of expression in the fibers of the optic tract (OT). C&D) Magnified view of tectal lamination (horizontal boxes) from A&B reveal the presumptive projection layer of the tectum, the compartment stratum griseum central (SGC), as the cortical neuronal lamina strongly expressing NOGO-A. Ventricular Zone-VZ, developing lamina-DL. E) H&E and F) NOGO-A in situ hybridization at E20 (after significant synaptogenesis) shows punctate expression localized to the large neuronal cell bodies of the tectal associated nuclei, the SGC, and to deep cellular layers of the main retinal afferent layer, the stratum griseum et fibrosum superficiale (SGFS). G&H) Magnified view of tectal lamination (horizontal boxes) from C&D. I-M) Serial sections localizing NOGO-A expression to projection neurons within a tectal associated nucleus (vertical box in C). I) H&E showing the large cell bodies of the projection neurons (inset showing large cytoplasm-rich neuron with nuclear clearing and prominent nucleolus), J) punctate NOGO-A expression, K) immunohistochemistry (IHC) of neurofilament (NF), highlighting neuronal cell bodies, L) IHC of glial fiber associated protein (GFAP) demonstrating glial supporting cells, and M) IHC for vimentin (Vim) demarcating a few immature glial cells. |
PMC1865376_F6_10801.jpg | What is shown in this image? | NOGO-A Expression During Network Establishment. A) H&E and B) NOGO-A in situ hybridization (ISH) of HH36 (E10) optic tectum, prior to synaptogenesis. Transcript expression is intensified in cells of the tectal associated nuclei (TN) and cortical neuronal lamina. Note the lack of expression in the fibers of the optic tract (OT). C&D) Magnified view of tectal lamination (horizontal boxes) from A&B reveal the presumptive projection layer of the tectum, the compartment stratum griseum central (SGC), as the cortical neuronal lamina strongly expressing NOGO-A. Ventricular Zone-VZ, developing lamina-DL. E) H&E and F) NOGO-A in situ hybridization at E20 (after significant synaptogenesis) shows punctate expression localized to the large neuronal cell bodies of the tectal associated nuclei, the SGC, and to deep cellular layers of the main retinal afferent layer, the stratum griseum et fibrosum superficiale (SGFS). G&H) Magnified view of tectal lamination (horizontal boxes) from C&D. I-M) Serial sections localizing NOGO-A expression to projection neurons within a tectal associated nucleus (vertical box in C). I) H&E showing the large cell bodies of the projection neurons (inset showing large cytoplasm-rich neuron with nuclear clearing and prominent nucleolus), J) punctate NOGO-A expression, K) immunohistochemistry (IHC) of neurofilament (NF), highlighting neuronal cell bodies, L) IHC of glial fiber associated protein (GFAP) demonstrating glial supporting cells, and M) IHC for vimentin (Vim) demarcating a few immature glial cells. |
PMC1865376_F6_10806.jpg | Describe the main subject of this image. | NOGO-A Expression During Network Establishment. A) H&E and B) NOGO-A in situ hybridization (ISH) of HH36 (E10) optic tectum, prior to synaptogenesis. Transcript expression is intensified in cells of the tectal associated nuclei (TN) and cortical neuronal lamina. Note the lack of expression in the fibers of the optic tract (OT). C&D) Magnified view of tectal lamination (horizontal boxes) from A&B reveal the presumptive projection layer of the tectum, the compartment stratum griseum central (SGC), as the cortical neuronal lamina strongly expressing NOGO-A. Ventricular Zone-VZ, developing lamina-DL. E) H&E and F) NOGO-A in situ hybridization at E20 (after significant synaptogenesis) shows punctate expression localized to the large neuronal cell bodies of the tectal associated nuclei, the SGC, and to deep cellular layers of the main retinal afferent layer, the stratum griseum et fibrosum superficiale (SGFS). G&H) Magnified view of tectal lamination (horizontal boxes) from C&D. I-M) Serial sections localizing NOGO-A expression to projection neurons within a tectal associated nucleus (vertical box in C). I) H&E showing the large cell bodies of the projection neurons (inset showing large cytoplasm-rich neuron with nuclear clearing and prominent nucleolus), J) punctate NOGO-A expression, K) immunohistochemistry (IHC) of neurofilament (NF), highlighting neuronal cell bodies, L) IHC of glial fiber associated protein (GFAP) demonstrating glial supporting cells, and M) IHC for vimentin (Vim) demarcating a few immature glial cells. |
PMC1865376_F6_10805.jpg | What is the dominant medical problem in this image? | NOGO-A Expression During Network Establishment. A) H&E and B) NOGO-A in situ hybridization (ISH) of HH36 (E10) optic tectum, prior to synaptogenesis. Transcript expression is intensified in cells of the tectal associated nuclei (TN) and cortical neuronal lamina. Note the lack of expression in the fibers of the optic tract (OT). C&D) Magnified view of tectal lamination (horizontal boxes) from A&B reveal the presumptive projection layer of the tectum, the compartment stratum griseum central (SGC), as the cortical neuronal lamina strongly expressing NOGO-A. Ventricular Zone-VZ, developing lamina-DL. E) H&E and F) NOGO-A in situ hybridization at E20 (after significant synaptogenesis) shows punctate expression localized to the large neuronal cell bodies of the tectal associated nuclei, the SGC, and to deep cellular layers of the main retinal afferent layer, the stratum griseum et fibrosum superficiale (SGFS). G&H) Magnified view of tectal lamination (horizontal boxes) from C&D. I-M) Serial sections localizing NOGO-A expression to projection neurons within a tectal associated nucleus (vertical box in C). I) H&E showing the large cell bodies of the projection neurons (inset showing large cytoplasm-rich neuron with nuclear clearing and prominent nucleolus), J) punctate NOGO-A expression, K) immunohistochemistry (IHC) of neurofilament (NF), highlighting neuronal cell bodies, L) IHC of glial fiber associated protein (GFAP) demonstrating glial supporting cells, and M) IHC for vimentin (Vim) demarcating a few immature glial cells. |
PMC1865376_F6_10809.jpg | What key item or scene is captured in this photo? | NOGO-A Expression During Network Establishment. A) H&E and B) NOGO-A in situ hybridization (ISH) of HH36 (E10) optic tectum, prior to synaptogenesis. Transcript expression is intensified in cells of the tectal associated nuclei (TN) and cortical neuronal lamina. Note the lack of expression in the fibers of the optic tract (OT). C&D) Magnified view of tectal lamination (horizontal boxes) from A&B reveal the presumptive projection layer of the tectum, the compartment stratum griseum central (SGC), as the cortical neuronal lamina strongly expressing NOGO-A. Ventricular Zone-VZ, developing lamina-DL. E) H&E and F) NOGO-A in situ hybridization at E20 (after significant synaptogenesis) shows punctate expression localized to the large neuronal cell bodies of the tectal associated nuclei, the SGC, and to deep cellular layers of the main retinal afferent layer, the stratum griseum et fibrosum superficiale (SGFS). G&H) Magnified view of tectal lamination (horizontal boxes) from C&D. I-M) Serial sections localizing NOGO-A expression to projection neurons within a tectal associated nucleus (vertical box in C). I) H&E showing the large cell bodies of the projection neurons (inset showing large cytoplasm-rich neuron with nuclear clearing and prominent nucleolus), J) punctate NOGO-A expression, K) immunohistochemistry (IHC) of neurofilament (NF), highlighting neuronal cell bodies, L) IHC of glial fiber associated protein (GFAP) demonstrating glial supporting cells, and M) IHC for vimentin (Vim) demarcating a few immature glial cells. |
PMC1865376_F6_10807.jpg | What is the principal component of this image? | NOGO-A Expression During Network Establishment. A) H&E and B) NOGO-A in situ hybridization (ISH) of HH36 (E10) optic tectum, prior to synaptogenesis. Transcript expression is intensified in cells of the tectal associated nuclei (TN) and cortical neuronal lamina. Note the lack of expression in the fibers of the optic tract (OT). C&D) Magnified view of tectal lamination (horizontal boxes) from A&B reveal the presumptive projection layer of the tectum, the compartment stratum griseum central (SGC), as the cortical neuronal lamina strongly expressing NOGO-A. Ventricular Zone-VZ, developing lamina-DL. E) H&E and F) NOGO-A in situ hybridization at E20 (after significant synaptogenesis) shows punctate expression localized to the large neuronal cell bodies of the tectal associated nuclei, the SGC, and to deep cellular layers of the main retinal afferent layer, the stratum griseum et fibrosum superficiale (SGFS). G&H) Magnified view of tectal lamination (horizontal boxes) from C&D. I-M) Serial sections localizing NOGO-A expression to projection neurons within a tectal associated nucleus (vertical box in C). I) H&E showing the large cell bodies of the projection neurons (inset showing large cytoplasm-rich neuron with nuclear clearing and prominent nucleolus), J) punctate NOGO-A expression, K) immunohistochemistry (IHC) of neurofilament (NF), highlighting neuronal cell bodies, L) IHC of glial fiber associated protein (GFAP) demonstrating glial supporting cells, and M) IHC for vimentin (Vim) demarcating a few immature glial cells. |
PMC1865376_F6_10800.jpg | What's the most prominent thing you notice in this picture? | NOGO-A Expression During Network Establishment. A) H&E and B) NOGO-A in situ hybridization (ISH) of HH36 (E10) optic tectum, prior to synaptogenesis. Transcript expression is intensified in cells of the tectal associated nuclei (TN) and cortical neuronal lamina. Note the lack of expression in the fibers of the optic tract (OT). C&D) Magnified view of tectal lamination (horizontal boxes) from A&B reveal the presumptive projection layer of the tectum, the compartment stratum griseum central (SGC), as the cortical neuronal lamina strongly expressing NOGO-A. Ventricular Zone-VZ, developing lamina-DL. E) H&E and F) NOGO-A in situ hybridization at E20 (after significant synaptogenesis) shows punctate expression localized to the large neuronal cell bodies of the tectal associated nuclei, the SGC, and to deep cellular layers of the main retinal afferent layer, the stratum griseum et fibrosum superficiale (SGFS). G&H) Magnified view of tectal lamination (horizontal boxes) from C&D. I-M) Serial sections localizing NOGO-A expression to projection neurons within a tectal associated nucleus (vertical box in C). I) H&E showing the large cell bodies of the projection neurons (inset showing large cytoplasm-rich neuron with nuclear clearing and prominent nucleolus), J) punctate NOGO-A expression, K) immunohistochemistry (IHC) of neurofilament (NF), highlighting neuronal cell bodies, L) IHC of glial fiber associated protein (GFAP) demonstrating glial supporting cells, and M) IHC for vimentin (Vim) demarcating a few immature glial cells. |
PMC1865376_F6_10810.jpg | What object or scene is depicted here? | NOGO-A Expression During Network Establishment. A) H&E and B) NOGO-A in situ hybridization (ISH) of HH36 (E10) optic tectum, prior to synaptogenesis. Transcript expression is intensified in cells of the tectal associated nuclei (TN) and cortical neuronal lamina. Note the lack of expression in the fibers of the optic tract (OT). C&D) Magnified view of tectal lamination (horizontal boxes) from A&B reveal the presumptive projection layer of the tectum, the compartment stratum griseum central (SGC), as the cortical neuronal lamina strongly expressing NOGO-A. Ventricular Zone-VZ, developing lamina-DL. E) H&E and F) NOGO-A in situ hybridization at E20 (after significant synaptogenesis) shows punctate expression localized to the large neuronal cell bodies of the tectal associated nuclei, the SGC, and to deep cellular layers of the main retinal afferent layer, the stratum griseum et fibrosum superficiale (SGFS). G&H) Magnified view of tectal lamination (horizontal boxes) from C&D. I-M) Serial sections localizing NOGO-A expression to projection neurons within a tectal associated nucleus (vertical box in C). I) H&E showing the large cell bodies of the projection neurons (inset showing large cytoplasm-rich neuron with nuclear clearing and prominent nucleolus), J) punctate NOGO-A expression, K) immunohistochemistry (IHC) of neurofilament (NF), highlighting neuronal cell bodies, L) IHC of glial fiber associated protein (GFAP) demonstrating glial supporting cells, and M) IHC for vimentin (Vim) demarcating a few immature glial cells. |
PMC1865376_F6_10808.jpg | What does this image primarily show? | NOGO-A Expression During Network Establishment. A) H&E and B) NOGO-A in situ hybridization (ISH) of HH36 (E10) optic tectum, prior to synaptogenesis. Transcript expression is intensified in cells of the tectal associated nuclei (TN) and cortical neuronal lamina. Note the lack of expression in the fibers of the optic tract (OT). C&D) Magnified view of tectal lamination (horizontal boxes) from A&B reveal the presumptive projection layer of the tectum, the compartment stratum griseum central (SGC), as the cortical neuronal lamina strongly expressing NOGO-A. Ventricular Zone-VZ, developing lamina-DL. E) H&E and F) NOGO-A in situ hybridization at E20 (after significant synaptogenesis) shows punctate expression localized to the large neuronal cell bodies of the tectal associated nuclei, the SGC, and to deep cellular layers of the main retinal afferent layer, the stratum griseum et fibrosum superficiale (SGFS). G&H) Magnified view of tectal lamination (horizontal boxes) from C&D. I-M) Serial sections localizing NOGO-A expression to projection neurons within a tectal associated nucleus (vertical box in C). I) H&E showing the large cell bodies of the projection neurons (inset showing large cytoplasm-rich neuron with nuclear clearing and prominent nucleolus), J) punctate NOGO-A expression, K) immunohistochemistry (IHC) of neurofilament (NF), highlighting neuronal cell bodies, L) IHC of glial fiber associated protein (GFAP) demonstrating glial supporting cells, and M) IHC for vimentin (Vim) demarcating a few immature glial cells. |
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