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PMC1794508_F3_9411.jpg | What stands out most in this visual? | Collagen type IV staining in healthy and arthritic synovial tissue. Collagen type IV was found in the lining layer of synovial biopsies from (a) healthy human subjects and (c) rheumatoid arthritis (RA) patients. Relative isotype controls are shown in (b,d). Double staining was performed to reveal the cellular origin of the type IV collagen. (e) Double staining was found in the lining layer. For a clearer picture, succeeding slices were stained with (f) CD55 or (g) collagen type IV. (h) Isotype control. Arrows indicate collagen IV, CD55 or double staining in the lining layer. (i) PCR results: top, collagen type IV mRNA expression in fibroblast-like synoviocytes from 10 RA patients and 11 healthy controls; bottom, β2-microglobulin (β2M) mRNA expression in the same samples. |
PMC1794508_F3_9407.jpg | What's the most prominent thing you notice in this picture? | Collagen type IV staining in healthy and arthritic synovial tissue. Collagen type IV was found in the lining layer of synovial biopsies from (a) healthy human subjects and (c) rheumatoid arthritis (RA) patients. Relative isotype controls are shown in (b,d). Double staining was performed to reveal the cellular origin of the type IV collagen. (e) Double staining was found in the lining layer. For a clearer picture, succeeding slices were stained with (f) CD55 or (g) collagen type IV. (h) Isotype control. Arrows indicate collagen IV, CD55 or double staining in the lining layer. (i) PCR results: top, collagen type IV mRNA expression in fibroblast-like synoviocytes from 10 RA patients and 11 healthy controls; bottom, β2-microglobulin (β2M) mRNA expression in the same samples. |
PMC1794515_F2_9428.jpg | What is the core subject represented in this visual? | Cell surface expression of fibroblast activation protein (FAP). Gene expression analysis is completed by immunohistochemical staining. FAP-specific staining was performed on synovial samples of five individuals of each entity (rheumatoid arthritis [RA] and osteoarthritis [OA]), demonstrating the stronger expression at the protein level in the inflamed synovia of patients with refractory RA. Magnification, ×100. |
PMC1794515_F2_9424.jpg | What is the central feature of this picture? | Cell surface expression of fibroblast activation protein (FAP). Gene expression analysis is completed by immunohistochemical staining. FAP-specific staining was performed on synovial samples of five individuals of each entity (rheumatoid arthritis [RA] and osteoarthritis [OA]), demonstrating the stronger expression at the protein level in the inflamed synovia of patients with refractory RA. Magnification, ×100. |
PMC1794515_F2_9426.jpg | What is the principal component of this image? | Cell surface expression of fibroblast activation protein (FAP). Gene expression analysis is completed by immunohistochemical staining. FAP-specific staining was performed on synovial samples of five individuals of each entity (rheumatoid arthritis [RA] and osteoarthritis [OA]), demonstrating the stronger expression at the protein level in the inflamed synovia of patients with refractory RA. Magnification, ×100. |
PMC1794515_F2_9421.jpg | What stands out most in this visual? | Cell surface expression of fibroblast activation protein (FAP). Gene expression analysis is completed by immunohistochemical staining. FAP-specific staining was performed on synovial samples of five individuals of each entity (rheumatoid arthritis [RA] and osteoarthritis [OA]), demonstrating the stronger expression at the protein level in the inflamed synovia of patients with refractory RA. Magnification, ×100. |
PMC1794515_F2_9423.jpg | What is the central feature of this picture? | Cell surface expression of fibroblast activation protein (FAP). Gene expression analysis is completed by immunohistochemical staining. FAP-specific staining was performed on synovial samples of five individuals of each entity (rheumatoid arthritis [RA] and osteoarthritis [OA]), demonstrating the stronger expression at the protein level in the inflamed synovia of patients with refractory RA. Magnification, ×100. |
PMC1794515_F2_9422.jpg | Describe the main subject of this image. | Cell surface expression of fibroblast activation protein (FAP). Gene expression analysis is completed by immunohistochemical staining. FAP-specific staining was performed on synovial samples of five individuals of each entity (rheumatoid arthritis [RA] and osteoarthritis [OA]), demonstrating the stronger expression at the protein level in the inflamed synovia of patients with refractory RA. Magnification, ×100. |
PMC1794515_F2_9425.jpg | What key item or scene is captured in this photo? | Cell surface expression of fibroblast activation protein (FAP). Gene expression analysis is completed by immunohistochemical staining. FAP-specific staining was performed on synovial samples of five individuals of each entity (rheumatoid arthritis [RA] and osteoarthritis [OA]), demonstrating the stronger expression at the protein level in the inflamed synovia of patients with refractory RA. Magnification, ×100. |
PMC1794515_F3_9415.jpg | What is the central feature of this picture? | Immunohistochemical analysis of activation markers in synovial membranes of osteoarthritis. Phenotypic markers that are instrumental in extracellular matrix alteration are detectable only at a low level (MMP-1, CD44v7/8) in areas that are slightly FAP-positive. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F3_9413.jpg | What is shown in this image? | Immunohistochemical analysis of activation markers in synovial membranes of osteoarthritis. Phenotypic markers that are instrumental in extracellular matrix alteration are detectable only at a low level (MMP-1, CD44v7/8) in areas that are slightly FAP-positive. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F3_9417.jpg | What is the dominant medical problem in this image? | Immunohistochemical analysis of activation markers in synovial membranes of osteoarthritis. Phenotypic markers that are instrumental in extracellular matrix alteration are detectable only at a low level (MMP-1, CD44v7/8) in areas that are slightly FAP-positive. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F3_9419.jpg | What is the principal component of this image? | Immunohistochemical analysis of activation markers in synovial membranes of osteoarthritis. Phenotypic markers that are instrumental in extracellular matrix alteration are detectable only at a low level (MMP-1, CD44v7/8) in areas that are slightly FAP-positive. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F3_9418.jpg | What stands out most in this visual? | Immunohistochemical analysis of activation markers in synovial membranes of osteoarthritis. Phenotypic markers that are instrumental in extracellular matrix alteration are detectable only at a low level (MMP-1, CD44v7/8) in areas that are slightly FAP-positive. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F5_9435.jpg | What's the most prominent thing you notice in this picture? | Comparison of immunohistochemical detection of activation markers. Analysis of representative areas of synovial tissue samples taken from patients with end-stage osteoarthritis (OA) or refractory rheumatoid arthritis (RA) is shown. Expression pattern and staining intensity of RA samples represent the stronger intensity of synovial inflammation when compared with OA samples. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F5_9432.jpg | What is the focal point of this photograph? | Comparison of immunohistochemical detection of activation markers. Analysis of representative areas of synovial tissue samples taken from patients with end-stage osteoarthritis (OA) or refractory rheumatoid arthritis (RA) is shown. Expression pattern and staining intensity of RA samples represent the stronger intensity of synovial inflammation when compared with OA samples. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F5_9431.jpg | What can you see in this picture? | Comparison of immunohistochemical detection of activation markers. Analysis of representative areas of synovial tissue samples taken from patients with end-stage osteoarthritis (OA) or refractory rheumatoid arthritis (RA) is shown. Expression pattern and staining intensity of RA samples represent the stronger intensity of synovial inflammation when compared with OA samples. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F5_9438.jpg | What does this image primarily show? | Comparison of immunohistochemical detection of activation markers. Analysis of representative areas of synovial tissue samples taken from patients with end-stage osteoarthritis (OA) or refractory rheumatoid arthritis (RA) is shown. Expression pattern and staining intensity of RA samples represent the stronger intensity of synovial inflammation when compared with OA samples. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F5_9437.jpg | Describe the main subject of this image. | Comparison of immunohistochemical detection of activation markers. Analysis of representative areas of synovial tissue samples taken from patients with end-stage osteoarthritis (OA) or refractory rheumatoid arthritis (RA) is shown. Expression pattern and staining intensity of RA samples represent the stronger intensity of synovial inflammation when compared with OA samples. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F5_9429.jpg | What is the principal component of this image? | Comparison of immunohistochemical detection of activation markers. Analysis of representative areas of synovial tissue samples taken from patients with end-stage osteoarthritis (OA) or refractory rheumatoid arthritis (RA) is shown. Expression pattern and staining intensity of RA samples represent the stronger intensity of synovial inflammation when compared with OA samples. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F5_9436.jpg | What is the dominant medical problem in this image? | Comparison of immunohistochemical detection of activation markers. Analysis of representative areas of synovial tissue samples taken from patients with end-stage osteoarthritis (OA) or refractory rheumatoid arthritis (RA) is shown. Expression pattern and staining intensity of RA samples represent the stronger intensity of synovial inflammation when compared with OA samples. Magnification, ×400. FAP, fibroblast activation protein; MMP, matrix metalloproteinase. |
PMC1794515_F6_9443.jpg | What is shown in this image? | Immunohistochemical characterisation of fibroblast populations. Collected samples were snap-frozen, and sequential sections were stained for expression of Thy-1, fibroblast activation protein (FAP), or smooth muscle actin (SMA). Antigen-positive cells were identified by pink-brown colouration. Tissue samples of both entities, rheumatoid arthritis (RA) and osteoarthritis (OA), show distinct synovial fibroblast populations. Associated expression of SMA and FAP distinguishes myofibroblasts of the intimal synovial lining from Thy-1-positive fibroblasts or only SMA-expressing perivascular smooth muscle cells. Staining of anti-human FAP and anti-human SMA is more intense in RA tissue samples when compared with OA. Magnification, ×100. |
PMC1794515_F6_9447.jpg | What does this image primarily show? | Immunohistochemical characterisation of fibroblast populations. Collected samples were snap-frozen, and sequential sections were stained for expression of Thy-1, fibroblast activation protein (FAP), or smooth muscle actin (SMA). Antigen-positive cells were identified by pink-brown colouration. Tissue samples of both entities, rheumatoid arthritis (RA) and osteoarthritis (OA), show distinct synovial fibroblast populations. Associated expression of SMA and FAP distinguishes myofibroblasts of the intimal synovial lining from Thy-1-positive fibroblasts or only SMA-expressing perivascular smooth muscle cells. Staining of anti-human FAP and anti-human SMA is more intense in RA tissue samples when compared with OA. Magnification, ×100. |
PMC1794515_F6_9445.jpg | What is the core subject represented in this visual? | Immunohistochemical characterisation of fibroblast populations. Collected samples were snap-frozen, and sequential sections were stained for expression of Thy-1, fibroblast activation protein (FAP), or smooth muscle actin (SMA). Antigen-positive cells were identified by pink-brown colouration. Tissue samples of both entities, rheumatoid arthritis (RA) and osteoarthritis (OA), show distinct synovial fibroblast populations. Associated expression of SMA and FAP distinguishes myofibroblasts of the intimal synovial lining from Thy-1-positive fibroblasts or only SMA-expressing perivascular smooth muscle cells. Staining of anti-human FAP and anti-human SMA is more intense in RA tissue samples when compared with OA. Magnification, ×100. |
PMC1794515_F6_9448.jpg | Can you identify the primary element in this image? | Immunohistochemical characterisation of fibroblast populations. Collected samples were snap-frozen, and sequential sections were stained for expression of Thy-1, fibroblast activation protein (FAP), or smooth muscle actin (SMA). Antigen-positive cells were identified by pink-brown colouration. Tissue samples of both entities, rheumatoid arthritis (RA) and osteoarthritis (OA), show distinct synovial fibroblast populations. Associated expression of SMA and FAP distinguishes myofibroblasts of the intimal synovial lining from Thy-1-positive fibroblasts or only SMA-expressing perivascular smooth muscle cells. Staining of anti-human FAP and anti-human SMA is more intense in RA tissue samples when compared with OA. Magnification, ×100. |
PMC1794515_F6_9449.jpg | What is shown in this image? | Immunohistochemical characterisation of fibroblast populations. Collected samples were snap-frozen, and sequential sections were stained for expression of Thy-1, fibroblast activation protein (FAP), or smooth muscle actin (SMA). Antigen-positive cells were identified by pink-brown colouration. Tissue samples of both entities, rheumatoid arthritis (RA) and osteoarthritis (OA), show distinct synovial fibroblast populations. Associated expression of SMA and FAP distinguishes myofibroblasts of the intimal synovial lining from Thy-1-positive fibroblasts or only SMA-expressing perivascular smooth muscle cells. Staining of anti-human FAP and anti-human SMA is more intense in RA tissue samples when compared with OA. Magnification, ×100. |
PMC1794515_F7_9450.jpg | What is the core subject represented in this visual? | Double-staining of fibroblast activation protein (FAP) and smooth muscle actin (SMA). Synovial tissue samples from patients with destructive rheumatoid arthritis were stained to demonstrate the simultaneous expression of both antigens. FAP-positive fibroblasts in the intimal synovial lining were coloured brown (DAB [3,3'-diaminobenzidin]). Coexpression of SMA is visualised in red (fast red). Magnification, ×400. |
PMC1794515_F7_9451.jpg | Describe the main subject of this image. | Double-staining of fibroblast activation protein (FAP) and smooth muscle actin (SMA). Synovial tissue samples from patients with destructive rheumatoid arthritis were stained to demonstrate the simultaneous expression of both antigens. FAP-positive fibroblasts in the intimal synovial lining were coloured brown (DAB [3,3'-diaminobenzidin]). Coexpression of SMA is visualised in red (fast red). Magnification, ×400. |
PMC1794515_F7_9454.jpg | What does this image primarily show? | Double-staining of fibroblast activation protein (FAP) and smooth muscle actin (SMA). Synovial tissue samples from patients with destructive rheumatoid arthritis were stained to demonstrate the simultaneous expression of both antigens. FAP-positive fibroblasts in the intimal synovial lining were coloured brown (DAB [3,3'-diaminobenzidin]). Coexpression of SMA is visualised in red (fast red). Magnification, ×400. |
PMC1794515_F7_9452.jpg | What is being portrayed in this visual content? | Double-staining of fibroblast activation protein (FAP) and smooth muscle actin (SMA). Synovial tissue samples from patients with destructive rheumatoid arthritis were stained to demonstrate the simultaneous expression of both antigens. FAP-positive fibroblasts in the intimal synovial lining were coloured brown (DAB [3,3'-diaminobenzidin]). Coexpression of SMA is visualised in red (fast red). Magnification, ×400. |
PMC1794534_F1_9457.jpg | What can you see in this picture? | X-ray of a normal proximal femur, showing the intertrochanteric region (rectangle) used for sampling. |
PMC1794534_F1_9455.jpg | What does this image primarily show? | X-ray of a normal proximal femur, showing the intertrochanteric region (rectangle) used for sampling. |
PMC1794550_F4_9460.jpg | What is the central feature of this picture? | Representative sections of nasal mucosa fromewes 14 days post-inoculation with ovine or human B. parapertussis. (Hematoxylin and eosin stain, 400× magnification.) (a) Ewe inoculated with ovine strain. The epithelium has intact epithelial cells. The section lackssignificant infiltrates of inflammatory cells. (b) Ewe inoculated with human strain. The epithelium is covered by mucinous materialadmixed with neutrophils, eosinophils, necrotic cell debris, and seroproteinaceous fluid. Within the epithelium and lamina propria are moderate infiltrates of neutrophils (open arrowheads)and eosinophils (filled arrowheads). The lamina propria is moderately expanded by edema. |
PMC1794550_F4_9459.jpg | What object or scene is depicted here? | Representative sections of nasal mucosa fromewes 14 days post-inoculation with ovine or human B. parapertussis. (Hematoxylin and eosin stain, 400× magnification.) (a) Ewe inoculated with ovine strain. The epithelium has intact epithelial cells. The section lackssignificant infiltrates of inflammatory cells. (b) Ewe inoculated with human strain. The epithelium is covered by mucinous materialadmixed with neutrophils, eosinophils, necrotic cell debris, and seroproteinaceous fluid. Within the epithelium and lamina propria are moderate infiltrates of neutrophils (open arrowheads)and eosinophils (filled arrowheads). The lamina propria is moderately expanded by edema. |
PMC1796545_F1_9461.jpg | What is the main focus of this visual representation? | 53-year old Korean man with a remote history of facial trauma, and a four day history of diplopia and right third cranial nerve palsy. Lateral digital subtraction angiogram, right internal carotid artery. During this early phase, there is visualization of the cervical and intracranial carotid artery; in addition, early filling of the cavernous sinus (arrow) is noted. |
PMC1796545_F3_9462.jpg | What is the dominant medical problem in this image? | 53-year old Korean man with a remote history of facial trauma, and a four day history of diplopia and right third cranial nerve palsy. Anteroposterior digital subtraction angiogram, right internal carotid artery. Mid-arterial phase image demonstrates early filling of the cavernous sinus with filling of the contralateral inferior petrosal sinus (arrow). |
PMC1796545_F4_9463.jpg | What is shown in this image? | Anomalous origin on the right subclavian artery. Serial images from a helical CT scan of the superior mediastinum, cranial to caudal. Notice the large enhancing vascular structure posterior to the esophagus (*). On the more caudal images, a direct origin of this vessel from the aortic arch, distal to the origin of the left subclavian artery, is noted. |
PMC1796545_F5_9465.jpg | What's the most prominent thing you notice in this picture? | Anomalous origin on the right subclavian artery. Serial images from a helical CT scan of the superior mediastinum, cranial to caudal. Notice the large enhancing vascular structure posterior to the esophagus (*). On the more caudal images, a direct origin of this vessel from the aortic arch, distal to the origin of the left subclavian artery, is noted. |
PMC1796545_F8_9468.jpg | What key item or scene is captured in this photo? | 36-year old woman, s/p motor vehicle collision. On admission, an angiogram demonstrated a pseudoaneurysm of the thoracic aorta, as well as a grade 3 (pseudoaneurysm) of her left internal carotid artery. Her aorta was repaired immediately; on follow-up angiography of her carotid injury, her pseudoaneurysm had progressed and there was significant narrowing of the adjacent internal carotid artery. Digital subtraction angiogram of the left internal carotid artery, s/p stent placement. A 6 mm × 47 mm Magic Wallstent (Boston Scientific, Watertown, MA) was placed. Notice the immediate and nearly complete resolution of the pseudoaneurysms. |
PMC1796545_F8_9469.jpg | What key item or scene is captured in this photo? | 36-year old woman, s/p motor vehicle collision. On admission, an angiogram demonstrated a pseudoaneurysm of the thoracic aorta, as well as a grade 3 (pseudoaneurysm) of her left internal carotid artery. Her aorta was repaired immediately; on follow-up angiography of her carotid injury, her pseudoaneurysm had progressed and there was significant narrowing of the adjacent internal carotid artery. Digital subtraction angiogram of the left internal carotid artery, s/p stent placement. A 6 mm × 47 mm Magic Wallstent (Boston Scientific, Watertown, MA) was placed. Notice the immediate and nearly complete resolution of the pseudoaneurysms. |
PMC1796545_F11_9470.jpg | What is being portrayed in this visual content? | 25-year old woman involved in a rollover motor vehicle collision. On admission to the hospital, a screening four-vessel angiogram revealed a pseudoaneurysm of the left vertebral artery at the level of the C1–C2 disc space. Follow-up angiography performed 7 days later revealed enlargement of the pseudoaneurysm and concomitant narrowing of the vertebral artery. Due to the tortuosity of the vertebral artery, stent placement was not deemed a viable option and the vertebral artery was embolized. Unsubtracted image demonstrating coils placed distal and proximal to the pseudoaneurysm, trapping the diseased segment of vessel. |
PMC1796545_F12_9472.jpg | What is the focal point of this photograph? | 25-year old woman involved in a rollover motor vehicle collision. On admission to the hospital, a screening four-vessel angiogram revealed a pseudoaneurysm of the left vertebral artery at the level of the C1–C2 disc space. Follow-up angiography performed 7 days later revealed enlargement of the pseudoaneurysm and concomitant narrowing of the vertebral artery. Due to the tortuosity of the vertebral artery, stent placement was not deemed a viable option and the vertebral artery was embolized. Post-embolization anteroposterior digital subtraction angiogram, right vertebral artery. There is normal filling of the basilar artery, and reflux of contrast into the distal left vertebral artery which fills the left posterior inferior cerebellar artery (arrow). Images courtesy of Guido Scatorchia, MD. |
PMC1796659_fig06_9473.jpg | What key item or scene is captured in this photo? | phAE87Δ17mt3 is viable but has shorter tails that its parent phage. Electron micrographs of representative particles of phAE87 (A) and phAE87Δ17mt3 (B). The average tail length is 200 ± 10 nm for phAE87 and 180 ± 6 for phAE87Δ17mt3. The tail lengths of 30 individual phage particles for each phage were measured. |
PMC1796852_F3_9478.jpg | Can you identify the primary element in this image? | Morphology of Splenic marginal zone lymphoma. Characteristic micronodular pattern in the SMZL centred in the white pulp, with variable red pulp infiltration (H&E, original magnification ×100). |
PMC1796852_F5_9476.jpg | What is being portrayed in this visual content? | Morphology of Splenic marginal zone lymphoma. Tumor cells express CD79a (EnVision Plus, original magnification ×200). |
PMC1796854_F2_9479.jpg | Can you identify the primary element in this image? | Endoscopic identification of the left recurrent laryngeal nerve (RLN), upper (UPG) and lower (LPG) parathyroid glands. |
PMC1796893_F2_9482.jpg | What key item or scene is captured in this photo? | Examples of amounts of fat in the lumbar multifidus muscles as seen on axial T1- weighted magnetic resonance imaging scans. These were rated as grade 0 if normal condition; grade 1 for slight fat infiltration (10–50%), and grade 2 for severe fat infiltration (>50%). |
PMC1796893_F2_9481.jpg | What is shown in this image? | Examples of amounts of fat in the lumbar multifidus muscles as seen on axial T1- weighted magnetic resonance imaging scans. These were rated as grade 0 if normal condition; grade 1 for slight fat infiltration (10–50%), and grade 2 for severe fat infiltration (>50%). |
PMC1796893_F2_9480.jpg | What stands out most in this visual? | Examples of amounts of fat in the lumbar multifidus muscles as seen on axial T1- weighted magnetic resonance imaging scans. These were rated as grade 0 if normal condition; grade 1 for slight fat infiltration (10–50%), and grade 2 for severe fat infiltration (>50%). |
PMC1796906_pmed-0040039-g005_9498.jpg | What is shown in this image? | Neurotransmitter Differentiation of Grafted Human NSCsPhotomicrographs (A–J) illustrate evidence of glutamatergic (A and B, G and H), GABAergic (C–F), and cholinergic (I and J) neurotransmission in NSC grafts. As in previous figures, confocal microscopy is used primarily to confirm the colocalization of two markers in the same cellular compartment along three planes of sectioning.(A and B) These sections, stained for HNu and the prevalent AMPA receptor epitope GluR2/3, show both cytoplasmic and synaptic staining by epifluorescence (A) or confocal (B) microscopy. Insets in (A) represent magnifications of indicated neurons in main image; top- and bottom-left insets show two medium-size HNu (+) cells with cytoplasmic immunoreactivity, whereas bottom-right inset illustrates a larger HNu (+) cell containing multiple GluR2/3 (+) boutons.(C and D) These sections are stained for HNu and the GABA-synthesizing enzyme GAD and visualized with epifluorescence (C) or confocal microscopy (D). Arrows in (C) indicate multiple HNu (+) cells with cytoplasmic GAD immunoreactivity.(E and F) Confocal microscopy of a field stained with both human Syn (red in single-channel image on top left, to label graft-derived terminals) and GAD (green in single-channel image on bottom left, to label GABAergic terminals) shows colocalization of the two proteins (yellow color in merged images in F) in multiple synaptic boutons. Nearly all graft-derived boutons are inhibitory (F).(G and H) These sections (G, epifluorescence; H, confocal) are stained for human Syn to label graft-derived terminals (red) and mixed VGLUT1/ VGLUT2 antibodies to label glutamatergic terminals in the field (green). Despite significant overlap and apposition of graft-derived and VGLUT1/2 (+) terminals (G), the two groups of terminals are separate (H).(I and J) These two sections were dually stained for: HNu and choline acetyltransferase (I and insert) epifluorescence; confocal microscopy (J); and show that some of the largest NSC-derived neurons express cholinergic phenotypes. These cells elaborate multiple primary dendrites (I and insert). (J) is the confocal image of the neuron in the inset.Scale bars: (A), (C), (G), (I) 20 μm; (B), (D–F), (H), (J) 10 μm. |
PMC1796906_pmed-0040039-g005_9489.jpg | What is the dominant medical problem in this image? | Neurotransmitter Differentiation of Grafted Human NSCsPhotomicrographs (A–J) illustrate evidence of glutamatergic (A and B, G and H), GABAergic (C–F), and cholinergic (I and J) neurotransmission in NSC grafts. As in previous figures, confocal microscopy is used primarily to confirm the colocalization of two markers in the same cellular compartment along three planes of sectioning.(A and B) These sections, stained for HNu and the prevalent AMPA receptor epitope GluR2/3, show both cytoplasmic and synaptic staining by epifluorescence (A) or confocal (B) microscopy. Insets in (A) represent magnifications of indicated neurons in main image; top- and bottom-left insets show two medium-size HNu (+) cells with cytoplasmic immunoreactivity, whereas bottom-right inset illustrates a larger HNu (+) cell containing multiple GluR2/3 (+) boutons.(C and D) These sections are stained for HNu and the GABA-synthesizing enzyme GAD and visualized with epifluorescence (C) or confocal microscopy (D). Arrows in (C) indicate multiple HNu (+) cells with cytoplasmic GAD immunoreactivity.(E and F) Confocal microscopy of a field stained with both human Syn (red in single-channel image on top left, to label graft-derived terminals) and GAD (green in single-channel image on bottom left, to label GABAergic terminals) shows colocalization of the two proteins (yellow color in merged images in F) in multiple synaptic boutons. Nearly all graft-derived boutons are inhibitory (F).(G and H) These sections (G, epifluorescence; H, confocal) are stained for human Syn to label graft-derived terminals (red) and mixed VGLUT1/ VGLUT2 antibodies to label glutamatergic terminals in the field (green). Despite significant overlap and apposition of graft-derived and VGLUT1/2 (+) terminals (G), the two groups of terminals are separate (H).(I and J) These two sections were dually stained for: HNu and choline acetyltransferase (I and insert) epifluorescence; confocal microscopy (J); and show that some of the largest NSC-derived neurons express cholinergic phenotypes. These cells elaborate multiple primary dendrites (I and insert). (J) is the confocal image of the neuron in the inset.Scale bars: (A), (C), (G), (I) 20 μm; (B), (D–F), (H), (J) 10 μm. |
PMC1796906_pmed-0040039-g005_9494.jpg | Can you identify the primary element in this image? | Neurotransmitter Differentiation of Grafted Human NSCsPhotomicrographs (A–J) illustrate evidence of glutamatergic (A and B, G and H), GABAergic (C–F), and cholinergic (I and J) neurotransmission in NSC grafts. As in previous figures, confocal microscopy is used primarily to confirm the colocalization of two markers in the same cellular compartment along three planes of sectioning.(A and B) These sections, stained for HNu and the prevalent AMPA receptor epitope GluR2/3, show both cytoplasmic and synaptic staining by epifluorescence (A) or confocal (B) microscopy. Insets in (A) represent magnifications of indicated neurons in main image; top- and bottom-left insets show two medium-size HNu (+) cells with cytoplasmic immunoreactivity, whereas bottom-right inset illustrates a larger HNu (+) cell containing multiple GluR2/3 (+) boutons.(C and D) These sections are stained for HNu and the GABA-synthesizing enzyme GAD and visualized with epifluorescence (C) or confocal microscopy (D). Arrows in (C) indicate multiple HNu (+) cells with cytoplasmic GAD immunoreactivity.(E and F) Confocal microscopy of a field stained with both human Syn (red in single-channel image on top left, to label graft-derived terminals) and GAD (green in single-channel image on bottom left, to label GABAergic terminals) shows colocalization of the two proteins (yellow color in merged images in F) in multiple synaptic boutons. Nearly all graft-derived boutons are inhibitory (F).(G and H) These sections (G, epifluorescence; H, confocal) are stained for human Syn to label graft-derived terminals (red) and mixed VGLUT1/ VGLUT2 antibodies to label glutamatergic terminals in the field (green). Despite significant overlap and apposition of graft-derived and VGLUT1/2 (+) terminals (G), the two groups of terminals are separate (H).(I and J) These two sections were dually stained for: HNu and choline acetyltransferase (I and insert) epifluorescence; confocal microscopy (J); and show that some of the largest NSC-derived neurons express cholinergic phenotypes. These cells elaborate multiple primary dendrites (I and insert). (J) is the confocal image of the neuron in the inset.Scale bars: (A), (C), (G), (I) 20 μm; (B), (D–F), (H), (J) 10 μm. |
PMC1796906_pmed-0040039-g005_9491.jpg | What stands out most in this visual? | Neurotransmitter Differentiation of Grafted Human NSCsPhotomicrographs (A–J) illustrate evidence of glutamatergic (A and B, G and H), GABAergic (C–F), and cholinergic (I and J) neurotransmission in NSC grafts. As in previous figures, confocal microscopy is used primarily to confirm the colocalization of two markers in the same cellular compartment along three planes of sectioning.(A and B) These sections, stained for HNu and the prevalent AMPA receptor epitope GluR2/3, show both cytoplasmic and synaptic staining by epifluorescence (A) or confocal (B) microscopy. Insets in (A) represent magnifications of indicated neurons in main image; top- and bottom-left insets show two medium-size HNu (+) cells with cytoplasmic immunoreactivity, whereas bottom-right inset illustrates a larger HNu (+) cell containing multiple GluR2/3 (+) boutons.(C and D) These sections are stained for HNu and the GABA-synthesizing enzyme GAD and visualized with epifluorescence (C) or confocal microscopy (D). Arrows in (C) indicate multiple HNu (+) cells with cytoplasmic GAD immunoreactivity.(E and F) Confocal microscopy of a field stained with both human Syn (red in single-channel image on top left, to label graft-derived terminals) and GAD (green in single-channel image on bottom left, to label GABAergic terminals) shows colocalization of the two proteins (yellow color in merged images in F) in multiple synaptic boutons. Nearly all graft-derived boutons are inhibitory (F).(G and H) These sections (G, epifluorescence; H, confocal) are stained for human Syn to label graft-derived terminals (red) and mixed VGLUT1/ VGLUT2 antibodies to label glutamatergic terminals in the field (green). Despite significant overlap and apposition of graft-derived and VGLUT1/2 (+) terminals (G), the two groups of terminals are separate (H).(I and J) These two sections were dually stained for: HNu and choline acetyltransferase (I and insert) epifluorescence; confocal microscopy (J); and show that some of the largest NSC-derived neurons express cholinergic phenotypes. These cells elaborate multiple primary dendrites (I and insert). (J) is the confocal image of the neuron in the inset.Scale bars: (A), (C), (G), (I) 20 μm; (B), (D–F), (H), (J) 10 μm. |
PMC1796906_pmed-0040039-g005_9495.jpg | What can you see in this picture? | Neurotransmitter Differentiation of Grafted Human NSCsPhotomicrographs (A–J) illustrate evidence of glutamatergic (A and B, G and H), GABAergic (C–F), and cholinergic (I and J) neurotransmission in NSC grafts. As in previous figures, confocal microscopy is used primarily to confirm the colocalization of two markers in the same cellular compartment along three planes of sectioning.(A and B) These sections, stained for HNu and the prevalent AMPA receptor epitope GluR2/3, show both cytoplasmic and synaptic staining by epifluorescence (A) or confocal (B) microscopy. Insets in (A) represent magnifications of indicated neurons in main image; top- and bottom-left insets show two medium-size HNu (+) cells with cytoplasmic immunoreactivity, whereas bottom-right inset illustrates a larger HNu (+) cell containing multiple GluR2/3 (+) boutons.(C and D) These sections are stained for HNu and the GABA-synthesizing enzyme GAD and visualized with epifluorescence (C) or confocal microscopy (D). Arrows in (C) indicate multiple HNu (+) cells with cytoplasmic GAD immunoreactivity.(E and F) Confocal microscopy of a field stained with both human Syn (red in single-channel image on top left, to label graft-derived terminals) and GAD (green in single-channel image on bottom left, to label GABAergic terminals) shows colocalization of the two proteins (yellow color in merged images in F) in multiple synaptic boutons. Nearly all graft-derived boutons are inhibitory (F).(G and H) These sections (G, epifluorescence; H, confocal) are stained for human Syn to label graft-derived terminals (red) and mixed VGLUT1/ VGLUT2 antibodies to label glutamatergic terminals in the field (green). Despite significant overlap and apposition of graft-derived and VGLUT1/2 (+) terminals (G), the two groups of terminals are separate (H).(I and J) These two sections were dually stained for: HNu and choline acetyltransferase (I and insert) epifluorescence; confocal microscopy (J); and show that some of the largest NSC-derived neurons express cholinergic phenotypes. These cells elaborate multiple primary dendrites (I and insert). (J) is the confocal image of the neuron in the inset.Scale bars: (A), (C), (G), (I) 20 μm; (B), (D–F), (H), (J) 10 μm. |
PMC1796906_pmed-0040039-g005_9490.jpg | What does this image primarily show? | Neurotransmitter Differentiation of Grafted Human NSCsPhotomicrographs (A–J) illustrate evidence of glutamatergic (A and B, G and H), GABAergic (C–F), and cholinergic (I and J) neurotransmission in NSC grafts. As in previous figures, confocal microscopy is used primarily to confirm the colocalization of two markers in the same cellular compartment along three planes of sectioning.(A and B) These sections, stained for HNu and the prevalent AMPA receptor epitope GluR2/3, show both cytoplasmic and synaptic staining by epifluorescence (A) or confocal (B) microscopy. Insets in (A) represent magnifications of indicated neurons in main image; top- and bottom-left insets show two medium-size HNu (+) cells with cytoplasmic immunoreactivity, whereas bottom-right inset illustrates a larger HNu (+) cell containing multiple GluR2/3 (+) boutons.(C and D) These sections are stained for HNu and the GABA-synthesizing enzyme GAD and visualized with epifluorescence (C) or confocal microscopy (D). Arrows in (C) indicate multiple HNu (+) cells with cytoplasmic GAD immunoreactivity.(E and F) Confocal microscopy of a field stained with both human Syn (red in single-channel image on top left, to label graft-derived terminals) and GAD (green in single-channel image on bottom left, to label GABAergic terminals) shows colocalization of the two proteins (yellow color in merged images in F) in multiple synaptic boutons. Nearly all graft-derived boutons are inhibitory (F).(G and H) These sections (G, epifluorescence; H, confocal) are stained for human Syn to label graft-derived terminals (red) and mixed VGLUT1/ VGLUT2 antibodies to label glutamatergic terminals in the field (green). Despite significant overlap and apposition of graft-derived and VGLUT1/2 (+) terminals (G), the two groups of terminals are separate (H).(I and J) These two sections were dually stained for: HNu and choline acetyltransferase (I and insert) epifluorescence; confocal microscopy (J); and show that some of the largest NSC-derived neurons express cholinergic phenotypes. These cells elaborate multiple primary dendrites (I and insert). (J) is the confocal image of the neuron in the inset.Scale bars: (A), (C), (G), (I) 20 μm; (B), (D–F), (H), (J) 10 μm. |
PMC1796906_pmed-0040039-g005_9493.jpg | What is being portrayed in this visual content? | Neurotransmitter Differentiation of Grafted Human NSCsPhotomicrographs (A–J) illustrate evidence of glutamatergic (A and B, G and H), GABAergic (C–F), and cholinergic (I and J) neurotransmission in NSC grafts. As in previous figures, confocal microscopy is used primarily to confirm the colocalization of two markers in the same cellular compartment along three planes of sectioning.(A and B) These sections, stained for HNu and the prevalent AMPA receptor epitope GluR2/3, show both cytoplasmic and synaptic staining by epifluorescence (A) or confocal (B) microscopy. Insets in (A) represent magnifications of indicated neurons in main image; top- and bottom-left insets show two medium-size HNu (+) cells with cytoplasmic immunoreactivity, whereas bottom-right inset illustrates a larger HNu (+) cell containing multiple GluR2/3 (+) boutons.(C and D) These sections are stained for HNu and the GABA-synthesizing enzyme GAD and visualized with epifluorescence (C) or confocal microscopy (D). Arrows in (C) indicate multiple HNu (+) cells with cytoplasmic GAD immunoreactivity.(E and F) Confocal microscopy of a field stained with both human Syn (red in single-channel image on top left, to label graft-derived terminals) and GAD (green in single-channel image on bottom left, to label GABAergic terminals) shows colocalization of the two proteins (yellow color in merged images in F) in multiple synaptic boutons. Nearly all graft-derived boutons are inhibitory (F).(G and H) These sections (G, epifluorescence; H, confocal) are stained for human Syn to label graft-derived terminals (red) and mixed VGLUT1/ VGLUT2 antibodies to label glutamatergic terminals in the field (green). Despite significant overlap and apposition of graft-derived and VGLUT1/2 (+) terminals (G), the two groups of terminals are separate (H).(I and J) These two sections were dually stained for: HNu and choline acetyltransferase (I and insert) epifluorescence; confocal microscopy (J); and show that some of the largest NSC-derived neurons express cholinergic phenotypes. These cells elaborate multiple primary dendrites (I and insert). (J) is the confocal image of the neuron in the inset.Scale bars: (A), (C), (G), (I) 20 μm; (B), (D–F), (H), (J) 10 μm. |
PMC1796906_pmed-0040039-g006_9484.jpg | What is the core subject represented in this visual? | Maturation of Human NSC-Derived Neurons Based on the Elaboration of Axons, Synapses, and Innervation by Host Neurons(A) This photograph was taken through the ventral horn of a HNu/70 kDa neurofilament protein stained section 3 mo postgrafting and shows bundles of human 70 kDa neurofilament protein (+) axons (indicated with white arrows) originating in HNu (+) grafts (one indicated with an asterisk on top right) and coursing together (red arrows on bottom left) toward the ventral white matter.(B) This photograph shows an NSC graft in the ventral horn of a human Syn-stained section three months postgrafting. The sharp colocalization of Syn (+) puncta with the graft region (boundaries demarcated with arrows) is due to the selectivity of the antibody for human, but not rat, Syn protein.(C and D) These images (C, epifluorescence; D, confocal) were taken from triple-stained sections with HNu (red), TUJ1 (blue), and the presynaptic marker Bsn (green). The Bsn antibody used here recognizes rat and mouse, but not human, protein. (C) depicts a dense field of rat Bsn (+) terminals in proximity to HNu and TUJ1 (+) profiles. Examples of contacts between rat terminals and NSC-derived neurons are shown with arrowheads in the inset, which is a magnification of the profile at the center of the main image. The very large number of such terminals on NSC-derived cell bodies is best illustrated with confocal microscopy (D).(E and F) These photographs (E, epifluorescence; F, confocal) were taken from sections stained with HNu (red), TUJ1 (blue), and mixed VGLUT1/VGLUT2 antibodies (green) and show the innervation of HNu and TUJ1 (+) cells by glutamatergic terminals putatively originating in the host.Scale bars: (A) 80 μm; (B) 20 μm; (C–F) 10 μm. |
PMC1796906_pmed-0040039-g006_9487.jpg | What is the central feature of this picture? | Maturation of Human NSC-Derived Neurons Based on the Elaboration of Axons, Synapses, and Innervation by Host Neurons(A) This photograph was taken through the ventral horn of a HNu/70 kDa neurofilament protein stained section 3 mo postgrafting and shows bundles of human 70 kDa neurofilament protein (+) axons (indicated with white arrows) originating in HNu (+) grafts (one indicated with an asterisk on top right) and coursing together (red arrows on bottom left) toward the ventral white matter.(B) This photograph shows an NSC graft in the ventral horn of a human Syn-stained section three months postgrafting. The sharp colocalization of Syn (+) puncta with the graft region (boundaries demarcated with arrows) is due to the selectivity of the antibody for human, but not rat, Syn protein.(C and D) These images (C, epifluorescence; D, confocal) were taken from triple-stained sections with HNu (red), TUJ1 (blue), and the presynaptic marker Bsn (green). The Bsn antibody used here recognizes rat and mouse, but not human, protein. (C) depicts a dense field of rat Bsn (+) terminals in proximity to HNu and TUJ1 (+) profiles. Examples of contacts between rat terminals and NSC-derived neurons are shown with arrowheads in the inset, which is a magnification of the profile at the center of the main image. The very large number of such terminals on NSC-derived cell bodies is best illustrated with confocal microscopy (D).(E and F) These photographs (E, epifluorescence; F, confocal) were taken from sections stained with HNu (red), TUJ1 (blue), and mixed VGLUT1/VGLUT2 antibodies (green) and show the innervation of HNu and TUJ1 (+) cells by glutamatergic terminals putatively originating in the host.Scale bars: (A) 80 μm; (B) 20 μm; (C–F) 10 μm. |
PMC1796906_pmed-0040039-g006_9488.jpg | Can you identify the primary element in this image? | Maturation of Human NSC-Derived Neurons Based on the Elaboration of Axons, Synapses, and Innervation by Host Neurons(A) This photograph was taken through the ventral horn of a HNu/70 kDa neurofilament protein stained section 3 mo postgrafting and shows bundles of human 70 kDa neurofilament protein (+) axons (indicated with white arrows) originating in HNu (+) grafts (one indicated with an asterisk on top right) and coursing together (red arrows on bottom left) toward the ventral white matter.(B) This photograph shows an NSC graft in the ventral horn of a human Syn-stained section three months postgrafting. The sharp colocalization of Syn (+) puncta with the graft region (boundaries demarcated with arrows) is due to the selectivity of the antibody for human, but not rat, Syn protein.(C and D) These images (C, epifluorescence; D, confocal) were taken from triple-stained sections with HNu (red), TUJ1 (blue), and the presynaptic marker Bsn (green). The Bsn antibody used here recognizes rat and mouse, but not human, protein. (C) depicts a dense field of rat Bsn (+) terminals in proximity to HNu and TUJ1 (+) profiles. Examples of contacts between rat terminals and NSC-derived neurons are shown with arrowheads in the inset, which is a magnification of the profile at the center of the main image. The very large number of such terminals on NSC-derived cell bodies is best illustrated with confocal microscopy (D).(E and F) These photographs (E, epifluorescence; F, confocal) were taken from sections stained with HNu (red), TUJ1 (blue), and mixed VGLUT1/VGLUT2 antibodies (green) and show the innervation of HNu and TUJ1 (+) cells by glutamatergic terminals putatively originating in the host.Scale bars: (A) 80 μm; (B) 20 μm; (C–F) 10 μm. |
PMC1796910_pmed-0040060-g001_9501.jpg | What does this image primarily show? | Distribution of Hemangioblastomas in the Central Nervous Systems of Study Patients(A) Schematic representation of the distribution of CNS hemangioblastomas (red dots) in the 25 von Hippel-Lindau disease patients on MRI. Most (98%) of hemangioblastomas were found below the level of the tentorium in the cerebellum, brainstem, and spinal cord.(B–D) Contrast-enhanced MRI demonstrating representative locations of hemangioblastomas including the cerebellum (B), brainstem (C) and spinal cord (D). (B) Axial view through the cerebellum demonstrating a hyperintense enhancing hemangioblastoma (arrow) with surrounding edema (hypointense area surrounding the tumor) that frequently is associated with these lesions. (C) Sagittal view through the posterior fossa demonstrating a hyperintense enhancing brainstem (medullary) hemangioblastoma (arrow) with surrounding edema. (D) Sagittal view through the thoracic and lumbar spinal cord demonstrating two hyperintense enhancing hemangioblastomas (arrows). The superior tumor is associated with a large intraspinal cyst (syrinx) that is common with these neoplasms (arrowhead). |
PMC1796910_pmed-0040060-g001_9500.jpg | What is the main focus of this visual representation? | Distribution of Hemangioblastomas in the Central Nervous Systems of Study Patients(A) Schematic representation of the distribution of CNS hemangioblastomas (red dots) in the 25 von Hippel-Lindau disease patients on MRI. Most (98%) of hemangioblastomas were found below the level of the tentorium in the cerebellum, brainstem, and spinal cord.(B–D) Contrast-enhanced MRI demonstrating representative locations of hemangioblastomas including the cerebellum (B), brainstem (C) and spinal cord (D). (B) Axial view through the cerebellum demonstrating a hyperintense enhancing hemangioblastoma (arrow) with surrounding edema (hypointense area surrounding the tumor) that frequently is associated with these lesions. (C) Sagittal view through the posterior fossa demonstrating a hyperintense enhancing brainstem (medullary) hemangioblastoma (arrow) with surrounding edema. (D) Sagittal view through the thoracic and lumbar spinal cord demonstrating two hyperintense enhancing hemangioblastomas (arrows). The superior tumor is associated with a large intraspinal cyst (syrinx) that is common with these neoplasms (arrowhead). |
PMC1796945_pone-0000246-g004_9504.jpg | What is the main focus of this visual representation? | Angio (A) and noninvasive coronary angiography using MSCT (B) and MRI (C) all demonstrate absence of significant stenoses in the right coronary artery (arrow) in a 45-year-old female patient with atypical angina pectoris. Note that MSCT due to higher spatial resolution allows better delineation of the distal segments of the right coronary artery than MRI (asterisks). |
PMC1796945_pone-0000246-g004_9505.jpg | What is the dominant medical problem in this image? | Angio (A) and noninvasive coronary angiography using MSCT (B) and MRI (C) all demonstrate absence of significant stenoses in the right coronary artery (arrow) in a 45-year-old female patient with atypical angina pectoris. Note that MSCT due to higher spatial resolution allows better delineation of the distal segments of the right coronary artery than MRI (asterisks). |
PMC1796945_pone-0000246-g004_9503.jpg | What object or scene is depicted here? | Angio (A) and noninvasive coronary angiography using MSCT (B) and MRI (C) all demonstrate absence of significant stenoses in the right coronary artery (arrow) in a 45-year-old female patient with atypical angina pectoris. Note that MSCT due to higher spatial resolution allows better delineation of the distal segments of the right coronary artery than MRI (asterisks). |
PMC1797045_F2_9509.jpg | What is the dominant medical problem in this image? | MRI of bilateral elastofibroma with the tumour being located between the thoracic wall, the anterior serratus, and the latissimus dorsi muscle (coronal (2a) and axial (2c) T1-weighted images): The small arrows indicate the medial margins of the lesions containing fatty (bright) and fibrous (dark) tissue. The tumours are located between the thoracic wall, the anterior serratus, and the latissimus dorsi muscle. The large arrows points to the margo inferior of the scapula. Figures [2b] and [2d] show the corresponding STIR -sequences with a slightly inhomogenous signal intensity within the elastofibromas. |
PMC1797045_F2_9506.jpg | What key item or scene is captured in this photo? | MRI of bilateral elastofibroma with the tumour being located between the thoracic wall, the anterior serratus, and the latissimus dorsi muscle (coronal (2a) and axial (2c) T1-weighted images): The small arrows indicate the medial margins of the lesions containing fatty (bright) and fibrous (dark) tissue. The tumours are located between the thoracic wall, the anterior serratus, and the latissimus dorsi muscle. The large arrows points to the margo inferior of the scapula. Figures [2b] and [2d] show the corresponding STIR -sequences with a slightly inhomogenous signal intensity within the elastofibromas. |
PMC1797045_F2_9507.jpg | What object or scene is depicted here? | MRI of bilateral elastofibroma with the tumour being located between the thoracic wall, the anterior serratus, and the latissimus dorsi muscle (coronal (2a) and axial (2c) T1-weighted images): The small arrows indicate the medial margins of the lesions containing fatty (bright) and fibrous (dark) tissue. The tumours are located between the thoracic wall, the anterior serratus, and the latissimus dorsi muscle. The large arrows points to the margo inferior of the scapula. Figures [2b] and [2d] show the corresponding STIR -sequences with a slightly inhomogenous signal intensity within the elastofibromas. |
PMC1797045_F4_9510.jpg | What is shown in this image? | Microscopic findings in elastofibroma dorsi: 4a): Fibrous, collagenous strands intermingled with fat cells (hematoxylin-eosine-staining). 4b): Collagenous material and roundly shaped elastic fibres, mesenchymal cells with bland nuclei (hematoxylin-eosine-staining). 4c): Elastic fibres and structures forming discs and globules stained dark brown to black using an elastic stain (Elastica-van-Gieson). |
PMC1797045_F4_9512.jpg | What is the main focus of this visual representation? | Microscopic findings in elastofibroma dorsi: 4a): Fibrous, collagenous strands intermingled with fat cells (hematoxylin-eosine-staining). 4b): Collagenous material and roundly shaped elastic fibres, mesenchymal cells with bland nuclei (hematoxylin-eosine-staining). 4c): Elastic fibres and structures forming discs and globules stained dark brown to black using an elastic stain (Elastica-van-Gieson). |
PMC1797045_F4_9511.jpg | What is the dominant medical problem in this image? | Microscopic findings in elastofibroma dorsi: 4a): Fibrous, collagenous strands intermingled with fat cells (hematoxylin-eosine-staining). 4b): Collagenous material and roundly shaped elastic fibres, mesenchymal cells with bland nuclei (hematoxylin-eosine-staining). 4c): Elastic fibres and structures forming discs and globules stained dark brown to black using an elastic stain (Elastica-van-Gieson). |
PMC1797156_F1_9514.jpg | What is the main focus of this visual representation? | A) Mild staining of epidermal keratinocytes and lack of staining in dermal cells in non lesional skin biopsy. B) Strong cytoplasmic staining of epidermal keratinocytes, dermal endothelial and inflammatory cells. IL-8 IHC, DAB, Hx counterstaining × 40 |
PMC1797156_F1_9513.jpg | What stands out most in this visual? | A) Mild staining of epidermal keratinocytes and lack of staining in dermal cells in non lesional skin biopsy. B) Strong cytoplasmic staining of epidermal keratinocytes, dermal endothelial and inflammatory cells. IL-8 IHC, DAB, Hx counterstaining × 40 |
PMC1797159_F4_9520.jpg | What key item or scene is captured in this photo? | Islets from Idd9 congenic mice are intrinsically resistant to cytokine and CD8 T cell-mediated autoimmune destruction. Islets isolated from 5 week old Idd9 congenic and NOD donors were transplanted under the kidney capsule of NODScid recipients. After allowing 7 days for the grafts to revascularize, splenocytes from 8.3NODScid mice (30 million cells) were adoptively transferred into graft recipients. Control mice did not receive splenocytes. Five days later, graft destruction was analyzed by H&E staining of graft sections, as shown in (A) (i-iv). Scoring of graft destruction (B) was determined by anti-glucagon staining (A) (v-vi) as described in the methods. NOD grafts (n = 4), NOD control grafts (n = 2), Idd9 congenic grafts (n = 3) and Idd9 control grafts (n = 2) were assessed, and a total of 24, 11, 26 and 32 islets scored, respectively, for each group. Graph shows average % healthy islets in each graft +/- SEM. Results representative of 3 independent experiments. (C) Confocal live/dead viability staining of islets from 5 week old Idd9 congenic and NOD mice treated with, or without, TNF (2,000 U/ml) and IFNγ (1,000 U/ml) for 6 days. Live cells stain green, and the nuclei of dead cells stain red. For each assay, 7–9 islets (250–500 cells) were analyzed and the average % dead cells per field +/- SEM is shown in (D). Results representative of 3 independent experiments. |
PMC1797159_F4_9521.jpg | What key item or scene is captured in this photo? | Islets from Idd9 congenic mice are intrinsically resistant to cytokine and CD8 T cell-mediated autoimmune destruction. Islets isolated from 5 week old Idd9 congenic and NOD donors were transplanted under the kidney capsule of NODScid recipients. After allowing 7 days for the grafts to revascularize, splenocytes from 8.3NODScid mice (30 million cells) were adoptively transferred into graft recipients. Control mice did not receive splenocytes. Five days later, graft destruction was analyzed by H&E staining of graft sections, as shown in (A) (i-iv). Scoring of graft destruction (B) was determined by anti-glucagon staining (A) (v-vi) as described in the methods. NOD grafts (n = 4), NOD control grafts (n = 2), Idd9 congenic grafts (n = 3) and Idd9 control grafts (n = 2) were assessed, and a total of 24, 11, 26 and 32 islets scored, respectively, for each group. Graph shows average % healthy islets in each graft +/- SEM. Results representative of 3 independent experiments. (C) Confocal live/dead viability staining of islets from 5 week old Idd9 congenic and NOD mice treated with, or without, TNF (2,000 U/ml) and IFNγ (1,000 U/ml) for 6 days. Live cells stain green, and the nuclei of dead cells stain red. For each assay, 7–9 islets (250–500 cells) were analyzed and the average % dead cells per field +/- SEM is shown in (D). Results representative of 3 independent experiments. |
PMC1797159_F4_9519.jpg | What can you see in this picture? | Islets from Idd9 congenic mice are intrinsically resistant to cytokine and CD8 T cell-mediated autoimmune destruction. Islets isolated from 5 week old Idd9 congenic and NOD donors were transplanted under the kidney capsule of NODScid recipients. After allowing 7 days for the grafts to revascularize, splenocytes from 8.3NODScid mice (30 million cells) were adoptively transferred into graft recipients. Control mice did not receive splenocytes. Five days later, graft destruction was analyzed by H&E staining of graft sections, as shown in (A) (i-iv). Scoring of graft destruction (B) was determined by anti-glucagon staining (A) (v-vi) as described in the methods. NOD grafts (n = 4), NOD control grafts (n = 2), Idd9 congenic grafts (n = 3) and Idd9 control grafts (n = 2) were assessed, and a total of 24, 11, 26 and 32 islets scored, respectively, for each group. Graph shows average % healthy islets in each graft +/- SEM. Results representative of 3 independent experiments. (C) Confocal live/dead viability staining of islets from 5 week old Idd9 congenic and NOD mice treated with, or without, TNF (2,000 U/ml) and IFNγ (1,000 U/ml) for 6 days. Live cells stain green, and the nuclei of dead cells stain red. For each assay, 7–9 islets (250–500 cells) were analyzed and the average % dead cells per field +/- SEM is shown in (D). Results representative of 3 independent experiments. |
PMC1797159_F4_9518.jpg | What key item or scene is captured in this photo? | Islets from Idd9 congenic mice are intrinsically resistant to cytokine and CD8 T cell-mediated autoimmune destruction. Islets isolated from 5 week old Idd9 congenic and NOD donors were transplanted under the kidney capsule of NODScid recipients. After allowing 7 days for the grafts to revascularize, splenocytes from 8.3NODScid mice (30 million cells) were adoptively transferred into graft recipients. Control mice did not receive splenocytes. Five days later, graft destruction was analyzed by H&E staining of graft sections, as shown in (A) (i-iv). Scoring of graft destruction (B) was determined by anti-glucagon staining (A) (v-vi) as described in the methods. NOD grafts (n = 4), NOD control grafts (n = 2), Idd9 congenic grafts (n = 3) and Idd9 control grafts (n = 2) were assessed, and a total of 24, 11, 26 and 32 islets scored, respectively, for each group. Graph shows average % healthy islets in each graft +/- SEM. Results representative of 3 independent experiments. (C) Confocal live/dead viability staining of islets from 5 week old Idd9 congenic and NOD mice treated with, or without, TNF (2,000 U/ml) and IFNγ (1,000 U/ml) for 6 days. Live cells stain green, and the nuclei of dead cells stain red. For each assay, 7–9 islets (250–500 cells) were analyzed and the average % dead cells per field +/- SEM is shown in (D). Results representative of 3 independent experiments. |
PMC1797159_F4_9522.jpg | What is being portrayed in this visual content? | Islets from Idd9 congenic mice are intrinsically resistant to cytokine and CD8 T cell-mediated autoimmune destruction. Islets isolated from 5 week old Idd9 congenic and NOD donors were transplanted under the kidney capsule of NODScid recipients. After allowing 7 days for the grafts to revascularize, splenocytes from 8.3NODScid mice (30 million cells) were adoptively transferred into graft recipients. Control mice did not receive splenocytes. Five days later, graft destruction was analyzed by H&E staining of graft sections, as shown in (A) (i-iv). Scoring of graft destruction (B) was determined by anti-glucagon staining (A) (v-vi) as described in the methods. NOD grafts (n = 4), NOD control grafts (n = 2), Idd9 congenic grafts (n = 3) and Idd9 control grafts (n = 2) were assessed, and a total of 24, 11, 26 and 32 islets scored, respectively, for each group. Graph shows average % healthy islets in each graft +/- SEM. Results representative of 3 independent experiments. (C) Confocal live/dead viability staining of islets from 5 week old Idd9 congenic and NOD mice treated with, or without, TNF (2,000 U/ml) and IFNγ (1,000 U/ml) for 6 days. Live cells stain green, and the nuclei of dead cells stain red. For each assay, 7–9 islets (250–500 cells) were analyzed and the average % dead cells per field +/- SEM is shown in (D). Results representative of 3 independent experiments. |
PMC1797159_F4_9517.jpg | What can you see in this picture? | Islets from Idd9 congenic mice are intrinsically resistant to cytokine and CD8 T cell-mediated autoimmune destruction. Islets isolated from 5 week old Idd9 congenic and NOD donors were transplanted under the kidney capsule of NODScid recipients. After allowing 7 days for the grafts to revascularize, splenocytes from 8.3NODScid mice (30 million cells) were adoptively transferred into graft recipients. Control mice did not receive splenocytes. Five days later, graft destruction was analyzed by H&E staining of graft sections, as shown in (A) (i-iv). Scoring of graft destruction (B) was determined by anti-glucagon staining (A) (v-vi) as described in the methods. NOD grafts (n = 4), NOD control grafts (n = 2), Idd9 congenic grafts (n = 3) and Idd9 control grafts (n = 2) were assessed, and a total of 24, 11, 26 and 32 islets scored, respectively, for each group. Graph shows average % healthy islets in each graft +/- SEM. Results representative of 3 independent experiments. (C) Confocal live/dead viability staining of islets from 5 week old Idd9 congenic and NOD mice treated with, or without, TNF (2,000 U/ml) and IFNγ (1,000 U/ml) for 6 days. Live cells stain green, and the nuclei of dead cells stain red. For each assay, 7–9 islets (250–500 cells) were analyzed and the average % dead cells per field +/- SEM is shown in (D). Results representative of 3 independent experiments. |
PMC1797165_F6_9524.jpg | What is the focal point of this photograph? | Panoramic radiograph taken at the beginning of distraction showing the osteomies. |
PMC1797165_F7_9523.jpg | What is the dominant medical problem in this image? | Radiograph taken after consolidation phase showing the formation of new bone at the distraction site. |
PMC1797166_F1_9526.jpg | What does this image primarily show? | Contrast enhanced CT scan shows a soft tissue mass, 16 × 17 mm in size in the lateral part of the right external auditory canal posterior wall. Diagnosis was reported to be schwannoma by histologic examination. |
PMC1797166_F1_9525.jpg | What key item or scene is captured in this photo? | Contrast enhanced CT scan shows a soft tissue mass, 16 × 17 mm in size in the lateral part of the right external auditory canal posterior wall. Diagnosis was reported to be schwannoma by histologic examination. |
PMC1797168_F4_9535.jpg | What stands out most in this visual? | Sheep skull benchmark object. a): Photo. b) Matching the photo, this shows the 3D model obtained using ATOS-II 3D scanner. c) Matching the photo, this shows the 3D model obtained using QTSculptor scanner. Details of the scratch contained on the surface were reproduced photographically (d), on the ATOS-II scanner (e) and QTSculptor (f). See text for feature description. Bar is 5 mm. |
PMC1797168_F4_9534.jpg | What is shown in this image? | Sheep skull benchmark object. a): Photo. b) Matching the photo, this shows the 3D model obtained using ATOS-II 3D scanner. c) Matching the photo, this shows the 3D model obtained using QTSculptor scanner. Details of the scratch contained on the surface were reproduced photographically (d), on the ATOS-II scanner (e) and QTSculptor (f). See text for feature description. Bar is 5 mm. |
PMC1797168_F5_9530.jpg | What is the focal point of this photograph? | Rock benchmark object. a): Photo. b) Matching the photo, this shows the 3D model obtained using ATOS-II 3D scanner. c) Matching the photo, this shows the 3D model obtained using QTSculptor scanner. A detailed region of this surface was reproduced photographically (d), on the ATOS-II scanner (e) and QTSculptor (f). See text for feature description. Bar is 5 mm. |
PMC1797168_F5_9528.jpg | What stands out most in this visual? | Rock benchmark object. a): Photo. b) Matching the photo, this shows the 3D model obtained using ATOS-II 3D scanner. c) Matching the photo, this shows the 3D model obtained using QTSculptor scanner. A detailed region of this surface was reproduced photographically (d), on the ATOS-II scanner (e) and QTSculptor (f). See text for feature description. Bar is 5 mm. |
PMC1797168_F5_9531.jpg | Describe the main subject of this image. | Rock benchmark object. a): Photo. b) Matching the photo, this shows the 3D model obtained using ATOS-II 3D scanner. c) Matching the photo, this shows the 3D model obtained using QTSculptor scanner. A detailed region of this surface was reproduced photographically (d), on the ATOS-II scanner (e) and QTSculptor (f). See text for feature description. Bar is 5 mm. |
PMC1797168_F5_9527.jpg | What key item or scene is captured in this photo? | Rock benchmark object. a): Photo. b) Matching the photo, this shows the 3D model obtained using ATOS-II 3D scanner. c) Matching the photo, this shows the 3D model obtained using QTSculptor scanner. A detailed region of this surface was reproduced photographically (d), on the ATOS-II scanner (e) and QTSculptor (f). See text for feature description. Bar is 5 mm. |
PMC1797170_F3_9540.jpg | What is the principal component of this image? | Eye phenotypes induced by intercellular injection of anti-Pax6 monoclonal antibody. (a-d) Intercellular distribution of FITC-labeled anti-mouse antibody injected at the blastula stage. Embryos were analyzed in toto (a,c) or using confocal microscopy (b,d) either 1 hour after injection (a,b) or at the shield stage (c,d). Note that the staining is concentrated in the intercellular space and is virtually absent from the cell interior. (e-m) Prototypical eye phenotypes (quantifications in Figure 4): Embryo 1 (e-g) has a severely reduced right eye (lateral view (e)) compared with left eye (lateral view (f)) and no right retina or lens (section in (g)). Embryo 2 (h-j) has a strongly reduced left eye (frontal view in (h), lateral view in (i)). The horizontal section (j) confirms the phenotypes and indicates that the left lens is also reduced (arrow). Embryo 3 has two reduced eyes with disorganized morphologies (lateral views in (k,l)) and a reduced and misplaced left lens (red arrow in (l,m)). In all horizontal sections, rostral is to the left. |
PMC1797170_F3_9539.jpg | What is the principal component of this image? | Eye phenotypes induced by intercellular injection of anti-Pax6 monoclonal antibody. (a-d) Intercellular distribution of FITC-labeled anti-mouse antibody injected at the blastula stage. Embryos were analyzed in toto (a,c) or using confocal microscopy (b,d) either 1 hour after injection (a,b) or at the shield stage (c,d). Note that the staining is concentrated in the intercellular space and is virtually absent from the cell interior. (e-m) Prototypical eye phenotypes (quantifications in Figure 4): Embryo 1 (e-g) has a severely reduced right eye (lateral view (e)) compared with left eye (lateral view (f)) and no right retina or lens (section in (g)). Embryo 2 (h-j) has a strongly reduced left eye (frontal view in (h), lateral view in (i)). The horizontal section (j) confirms the phenotypes and indicates that the left lens is also reduced (arrow). Embryo 3 has two reduced eyes with disorganized morphologies (lateral views in (k,l)) and a reduced and misplaced left lens (red arrow in (l,m)). In all horizontal sections, rostral is to the left. |
PMC1797170_F3_9543.jpg | What is being portrayed in this visual content? | Eye phenotypes induced by intercellular injection of anti-Pax6 monoclonal antibody. (a-d) Intercellular distribution of FITC-labeled anti-mouse antibody injected at the blastula stage. Embryos were analyzed in toto (a,c) or using confocal microscopy (b,d) either 1 hour after injection (a,b) or at the shield stage (c,d). Note that the staining is concentrated in the intercellular space and is virtually absent from the cell interior. (e-m) Prototypical eye phenotypes (quantifications in Figure 4): Embryo 1 (e-g) has a severely reduced right eye (lateral view (e)) compared with left eye (lateral view (f)) and no right retina or lens (section in (g)). Embryo 2 (h-j) has a strongly reduced left eye (frontal view in (h), lateral view in (i)). The horizontal section (j) confirms the phenotypes and indicates that the left lens is also reduced (arrow). Embryo 3 has two reduced eyes with disorganized morphologies (lateral views in (k,l)) and a reduced and misplaced left lens (red arrow in (l,m)). In all horizontal sections, rostral is to the left. |
PMC1797170_F3_9537.jpg | What is the principal component of this image? | Eye phenotypes induced by intercellular injection of anti-Pax6 monoclonal antibody. (a-d) Intercellular distribution of FITC-labeled anti-mouse antibody injected at the blastula stage. Embryos were analyzed in toto (a,c) or using confocal microscopy (b,d) either 1 hour after injection (a,b) or at the shield stage (c,d). Note that the staining is concentrated in the intercellular space and is virtually absent from the cell interior. (e-m) Prototypical eye phenotypes (quantifications in Figure 4): Embryo 1 (e-g) has a severely reduced right eye (lateral view (e)) compared with left eye (lateral view (f)) and no right retina or lens (section in (g)). Embryo 2 (h-j) has a strongly reduced left eye (frontal view in (h), lateral view in (i)). The horizontal section (j) confirms the phenotypes and indicates that the left lens is also reduced (arrow). Embryo 3 has two reduced eyes with disorganized morphologies (lateral views in (k,l)) and a reduced and misplaced left lens (red arrow in (l,m)). In all horizontal sections, rostral is to the left. |
PMC1797170_F3_9538.jpg | What is the core subject represented in this visual? | Eye phenotypes induced by intercellular injection of anti-Pax6 monoclonal antibody. (a-d) Intercellular distribution of FITC-labeled anti-mouse antibody injected at the blastula stage. Embryos were analyzed in toto (a,c) or using confocal microscopy (b,d) either 1 hour after injection (a,b) or at the shield stage (c,d). Note that the staining is concentrated in the intercellular space and is virtually absent from the cell interior. (e-m) Prototypical eye phenotypes (quantifications in Figure 4): Embryo 1 (e-g) has a severely reduced right eye (lateral view (e)) compared with left eye (lateral view (f)) and no right retina or lens (section in (g)). Embryo 2 (h-j) has a strongly reduced left eye (frontal view in (h), lateral view in (i)). The horizontal section (j) confirms the phenotypes and indicates that the left lens is also reduced (arrow). Embryo 3 has two reduced eyes with disorganized morphologies (lateral views in (k,l)) and a reduced and misplaced left lens (red arrow in (l,m)). In all horizontal sections, rostral is to the left. |
PMC1797170_F3_9545.jpg | What is the core subject represented in this visual? | Eye phenotypes induced by intercellular injection of anti-Pax6 monoclonal antibody. (a-d) Intercellular distribution of FITC-labeled anti-mouse antibody injected at the blastula stage. Embryos were analyzed in toto (a,c) or using confocal microscopy (b,d) either 1 hour after injection (a,b) or at the shield stage (c,d). Note that the staining is concentrated in the intercellular space and is virtually absent from the cell interior. (e-m) Prototypical eye phenotypes (quantifications in Figure 4): Embryo 1 (e-g) has a severely reduced right eye (lateral view (e)) compared with left eye (lateral view (f)) and no right retina or lens (section in (g)). Embryo 2 (h-j) has a strongly reduced left eye (frontal view in (h), lateral view in (i)). The horizontal section (j) confirms the phenotypes and indicates that the left lens is also reduced (arrow). Embryo 3 has two reduced eyes with disorganized morphologies (lateral views in (k,l)) and a reduced and misplaced left lens (red arrow in (l,m)). In all horizontal sections, rostral is to the left. |
PMC1797170_F3_9544.jpg | Describe the main subject of this image. | Eye phenotypes induced by intercellular injection of anti-Pax6 monoclonal antibody. (a-d) Intercellular distribution of FITC-labeled anti-mouse antibody injected at the blastula stage. Embryos were analyzed in toto (a,c) or using confocal microscopy (b,d) either 1 hour after injection (a,b) or at the shield stage (c,d). Note that the staining is concentrated in the intercellular space and is virtually absent from the cell interior. (e-m) Prototypical eye phenotypes (quantifications in Figure 4): Embryo 1 (e-g) has a severely reduced right eye (lateral view (e)) compared with left eye (lateral view (f)) and no right retina or lens (section in (g)). Embryo 2 (h-j) has a strongly reduced left eye (frontal view in (h), lateral view in (i)). The horizontal section (j) confirms the phenotypes and indicates that the left lens is also reduced (arrow). Embryo 3 has two reduced eyes with disorganized morphologies (lateral views in (k,l)) and a reduced and misplaced left lens (red arrow in (l,m)). In all horizontal sections, rostral is to the left. |
PMC1797170_F3_9541.jpg | What is the dominant medical problem in this image? | Eye phenotypes induced by intercellular injection of anti-Pax6 monoclonal antibody. (a-d) Intercellular distribution of FITC-labeled anti-mouse antibody injected at the blastula stage. Embryos were analyzed in toto (a,c) or using confocal microscopy (b,d) either 1 hour after injection (a,b) or at the shield stage (c,d). Note that the staining is concentrated in the intercellular space and is virtually absent from the cell interior. (e-m) Prototypical eye phenotypes (quantifications in Figure 4): Embryo 1 (e-g) has a severely reduced right eye (lateral view (e)) compared with left eye (lateral view (f)) and no right retina or lens (section in (g)). Embryo 2 (h-j) has a strongly reduced left eye (frontal view in (h), lateral view in (i)). The horizontal section (j) confirms the phenotypes and indicates that the left lens is also reduced (arrow). Embryo 3 has two reduced eyes with disorganized morphologies (lateral views in (k,l)) and a reduced and misplaced left lens (red arrow in (l,m)). In all horizontal sections, rostral is to the left. |
PMC1797170_F3_9536.jpg | What object or scene is depicted here? | Eye phenotypes induced by intercellular injection of anti-Pax6 monoclonal antibody. (a-d) Intercellular distribution of FITC-labeled anti-mouse antibody injected at the blastula stage. Embryos were analyzed in toto (a,c) or using confocal microscopy (b,d) either 1 hour after injection (a,b) or at the shield stage (c,d). Note that the staining is concentrated in the intercellular space and is virtually absent from the cell interior. (e-m) Prototypical eye phenotypes (quantifications in Figure 4): Embryo 1 (e-g) has a severely reduced right eye (lateral view (e)) compared with left eye (lateral view (f)) and no right retina or lens (section in (g)). Embryo 2 (h-j) has a strongly reduced left eye (frontal view in (h), lateral view in (i)). The horizontal section (j) confirms the phenotypes and indicates that the left lens is also reduced (arrow). Embryo 3 has two reduced eyes with disorganized morphologies (lateral views in (k,l)) and a reduced and misplaced left lens (red arrow in (l,m)). In all horizontal sections, rostral is to the left. |
PMC1797183_F2_9547.jpg | What stands out most in this visual? | Examples of eosin-hematoxylin stained tumor-tissue of the central (A) and peripheral (B) part of the mammary tumor in control (left) and during hyperoxic treatment (right, 1 bar, pO2 = 1.0). The images under A are scaled to the same magnification (× 4) and the images under B to the same magnification (× 10). Scale bar indicate 500 μm (A) and 100 μm (B). |
PMC1797183_F2_9548.jpg | Can you identify the primary element in this image? | Examples of eosin-hematoxylin stained tumor-tissue of the central (A) and peripheral (B) part of the mammary tumor in control (left) and during hyperoxic treatment (right, 1 bar, pO2 = 1.0). The images under A are scaled to the same magnification (× 4) and the images under B to the same magnification (× 10). Scale bar indicate 500 μm (A) and 100 μm (B). |
PMC1797183_F2_9549.jpg | What stands out most in this visual? | Examples of eosin-hematoxylin stained tumor-tissue of the central (A) and peripheral (B) part of the mammary tumor in control (left) and during hyperoxic treatment (right, 1 bar, pO2 = 1.0). The images under A are scaled to the same magnification (× 4) and the images under B to the same magnification (× 10). Scale bar indicate 500 μm (A) and 100 μm (B). |
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