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PMC1617090_F2_7489.jpg | What is being portrayed in this visual content? | PET scan demonstrating a focus of intense FDG activity (arrow mark) in the left lung field. |
PMC1617090_F2_7488.jpg | What can you see in this picture? | PET scan demonstrating a focus of intense FDG activity (arrow mark) in the left lung field. |
PMC1617090_F2_7485.jpg | What is the core subject represented in this visual? | PET scan demonstrating a focus of intense FDG activity (arrow mark) in the left lung field. |
PMC1617090_F2_7477.jpg | What's the most prominent thing you notice in this picture? | PET scan demonstrating a focus of intense FDG activity (arrow mark) in the left lung field. |
PMC1617090_F2_7486.jpg | What is the focal point of this photograph? | PET scan demonstrating a focus of intense FDG activity (arrow mark) in the left lung field. |
PMC1617090_F2_7479.jpg | What stands out most in this visual? | PET scan demonstrating a focus of intense FDG activity (arrow mark) in the left lung field. |
PMC1617090_F2_7476.jpg | What is the principal component of this image? | PET scan demonstrating a focus of intense FDG activity (arrow mark) in the left lung field. |
PMC1617093_F2_7496.jpg | What is shown in this image? | FNAC (Fine Needle Aspiration Cytology) from the mass shows polygonal cells forming microacini at places. Features consistent with Hepatocellular Carcinoma. (Papanicolaou Stain × 400) |
PMC1617093_F3_7497.jpg | Describe the main subject of this image. | Histopathological examination of the excised mass. Shows that the tumour is made of thick hepatocyte cell plates with foci of acinar formation from the margins. (H&E stain, 10× HPF) |
PMC1617094_F1_7498.jpg | What does this image primarily show? | Hematoxylin and eosin staining of EpiGingival tissues (magnification, ×400). Upon arrival, the tissues were cultured for 12 hours prior to viral infection, fixed with Streck Tissue Fixative, frozen in 2-methylbutane submerged in liquid nitrogen, cross-sectioned at 9 μm using a LEICA cryostat LC1900 sectioner, stained with hematoxylin and eosin, and visualized with a Nikon TE300 microscope. |
PMC1617110_F1_7500.jpg | What is shown in this image? | The sup45-sl23ts mutation is lethal in the strain 33G-D373-rSL23-ΔS35, carrying the SUP35-C or SUP35-MC alleles. The LEU2 plasmids with SUP35-C or SUP35-MC can not replace the resident URA3 plasmid pRS316-SUP35 carrying wild type SUP35 in the strain 33G-D373-rSL23-ΔS35. Transformants were incubated on 5FOA-containing medium for 3 days. Plasmids: SUP35-C, pRS315-SUP35C; SUP35-MC, pRS315-SUP35MC; SUP35, pRS315-SUP35; empty vector, pRS315. |
PMC1617112_F3_7501.jpg | Describe the main subject of this image. | The hyaline globules in the amorphous material do not show any organisms with GMS stain (a, b). Compare this with appearance of PCP in positive control (c, d), which shows frothy casts with the characteristic crushed ping-pong ball like organisms (c) with small central to eccentric dots (arrow in d). (Bronchoalveolar lavage; Gomori-Silver Methanamine (GMS) stained SurePath Prep™). |
PMC1617112_F3_7503.jpg | What stands out most in this visual? | The hyaline globules in the amorphous material do not show any organisms with GMS stain (a, b). Compare this with appearance of PCP in positive control (c, d), which shows frothy casts with the characteristic crushed ping-pong ball like organisms (c) with small central to eccentric dots (arrow in d). (Bronchoalveolar lavage; Gomori-Silver Methanamine (GMS) stained SurePath Prep™). |
PMC1617132_pcbi-0020139-g001_7511.jpg | What is the dominant medical problem in this image? | Spatial Relationship between Endogenous CBP and DNAShown here are representative high-resolution (100×) deconvolved images of an interphase 10T1/2 cell (A) and an IM cell (B) immunofluorescently labeled with anti-CBP and counterstained with DAPI. A combined image of the single planes is presented as the “Merge,” with the CBP and DNA shown in green and red, respectively. A 3-D projection of the entire nucleus is presented (Proj). The linescan (bottom row) demonstrates that endogenous CBP preferentially localizes within euchromatin (less intense DAPI signal) or in regions immediately adjacent to intensely staining heterochromatic regions (intense DAPI signal). Scale bars represent 3 μm. |
PMC1617132_pcbi-0020139-g001_7507.jpg | What's the most prominent thing you notice in this picture? | Spatial Relationship between Endogenous CBP and DNAShown here are representative high-resolution (100×) deconvolved images of an interphase 10T1/2 cell (A) and an IM cell (B) immunofluorescently labeled with anti-CBP and counterstained with DAPI. A combined image of the single planes is presented as the “Merge,” with the CBP and DNA shown in green and red, respectively. A 3-D projection of the entire nucleus is presented (Proj). The linescan (bottom row) demonstrates that endogenous CBP preferentially localizes within euchromatin (less intense DAPI signal) or in regions immediately adjacent to intensely staining heterochromatic regions (intense DAPI signal). Scale bars represent 3 μm. |
PMC1618388_F1_7514.jpg | Describe the main subject of this image. | Abdominal magnetic resonance imaging demonstrating the dilated left hepatic duct, without the presence of any space-occupying lesion. |
PMC1618388_F1_7515.jpg | What is the central feature of this picture? | Abdominal magnetic resonance imaging demonstrating the dilated left hepatic duct, without the presence of any space-occupying lesion. |
PMC1618397_F1_7517.jpg | What is the principal component of this image? | Typical staining of tumour samples with a single-chain antibody against Eag1. Eag1 shows homogeneous cytoplasmic staining with perinuclear localization. Shown are representative examples for the different intensities of Eag1 staining leading to the scoring of 0 (A, morphologically non-malignant skeletal muscle from a rhabdomyosarcoma case), 1+ (B, malignant fibrous histiocytoma), 2+ (C, leiomyosarcoma) and 3+ (D, rhabdomyosarcoma) used for further analysis. Magnification: 20×. |
PMC1618397_F1_7519.jpg | What is the dominant medical problem in this image? | Typical staining of tumour samples with a single-chain antibody against Eag1. Eag1 shows homogeneous cytoplasmic staining with perinuclear localization. Shown are representative examples for the different intensities of Eag1 staining leading to the scoring of 0 (A, morphologically non-malignant skeletal muscle from a rhabdomyosarcoma case), 1+ (B, malignant fibrous histiocytoma), 2+ (C, leiomyosarcoma) and 3+ (D, rhabdomyosarcoma) used for further analysis. Magnification: 20×. |
PMC1618402_F4_7522.jpg | What is the focal point of this photograph? | Cytological examination of the labeled DNA distribution in MCF-7 cells. (a) Several minutes incubation of MCF-7 cells with FITC-labeled fragmented human DNA. The main part of the label is localized to the cytoplasm. (b) 14-h incubation of MCF-7 cells with FITC-labeled fragmented human DNA. The label is concentrated in the nucleus and is undetectable in the cytoplasm. |
PMC1618808_fig03_7528.jpg | What is being portrayed in this visual content? | Distribution of internalized wtFc in rFcRn-MDCK, rFcRn-GFP-MDCK and vector-only MDCK cellsFilter-grown monolayers were incubated with 1 μM wtFc (recombinant Fc derived from rat IgG2a) for 1 h at pH 6 or pH 7.4 and processed for immunofluorescence using antibodies against wtFc (red) and the tight junction marker ZO-1 (blue). The heavy chain of rFcRn (green) was detected using GFP fluorescence (rFcRn-GFP-MDCK cells) or an antibody against the rFcRn heavy chain (rFcRn-MDCK and vector-only MDCK cells). Optical sections were taken every 2 μm below the level of the tight junctions. |
PMC1618808_fig03_7532.jpg | Describe the main subject of this image. | Distribution of internalized wtFc in rFcRn-MDCK, rFcRn-GFP-MDCK and vector-only MDCK cellsFilter-grown monolayers were incubated with 1 μM wtFc (recombinant Fc derived from rat IgG2a) for 1 h at pH 6 or pH 7.4 and processed for immunofluorescence using antibodies against wtFc (red) and the tight junction marker ZO-1 (blue). The heavy chain of rFcRn (green) was detected using GFP fluorescence (rFcRn-GFP-MDCK cells) or an antibody against the rFcRn heavy chain (rFcRn-MDCK and vector-only MDCK cells). Optical sections were taken every 2 μm below the level of the tight junctions. |
PMC1618808_fig03_7530.jpg | What is the focal point of this photograph? | Distribution of internalized wtFc in rFcRn-MDCK, rFcRn-GFP-MDCK and vector-only MDCK cellsFilter-grown monolayers were incubated with 1 μM wtFc (recombinant Fc derived from rat IgG2a) for 1 h at pH 6 or pH 7.4 and processed for immunofluorescence using antibodies against wtFc (red) and the tight junction marker ZO-1 (blue). The heavy chain of rFcRn (green) was detected using GFP fluorescence (rFcRn-GFP-MDCK cells) or an antibody against the rFcRn heavy chain (rFcRn-MDCK and vector-only MDCK cells). Optical sections were taken every 2 μm below the level of the tight junctions. |
PMC1618808_fig03_7543.jpg | What is shown in this image? | Distribution of internalized wtFc in rFcRn-MDCK, rFcRn-GFP-MDCK and vector-only MDCK cellsFilter-grown monolayers were incubated with 1 μM wtFc (recombinant Fc derived from rat IgG2a) for 1 h at pH 6 or pH 7.4 and processed for immunofluorescence using antibodies against wtFc (red) and the tight junction marker ZO-1 (blue). The heavy chain of rFcRn (green) was detected using GFP fluorescence (rFcRn-GFP-MDCK cells) or an antibody against the rFcRn heavy chain (rFcRn-MDCK and vector-only MDCK cells). Optical sections were taken every 2 μm below the level of the tight junctions. |
PMC1618808_fig03_7546.jpg | What does this image primarily show? | Distribution of internalized wtFc in rFcRn-MDCK, rFcRn-GFP-MDCK and vector-only MDCK cellsFilter-grown monolayers were incubated with 1 μM wtFc (recombinant Fc derived from rat IgG2a) for 1 h at pH 6 or pH 7.4 and processed for immunofluorescence using antibodies against wtFc (red) and the tight junction marker ZO-1 (blue). The heavy chain of rFcRn (green) was detected using GFP fluorescence (rFcRn-GFP-MDCK cells) or an antibody against the rFcRn heavy chain (rFcRn-MDCK and vector-only MDCK cells). Optical sections were taken every 2 μm below the level of the tight junctions. |
PMC1618808_fig03_7535.jpg | What is the core subject represented in this visual? | Distribution of internalized wtFc in rFcRn-MDCK, rFcRn-GFP-MDCK and vector-only MDCK cellsFilter-grown monolayers were incubated with 1 μM wtFc (recombinant Fc derived from rat IgG2a) for 1 h at pH 6 or pH 7.4 and processed for immunofluorescence using antibodies against wtFc (red) and the tight junction marker ZO-1 (blue). The heavy chain of rFcRn (green) was detected using GFP fluorescence (rFcRn-GFP-MDCK cells) or an antibody against the rFcRn heavy chain (rFcRn-MDCK and vector-only MDCK cells). Optical sections were taken every 2 μm below the level of the tight junctions. |
PMC1618808_fig03_7529.jpg | What key item or scene is captured in this photo? | Distribution of internalized wtFc in rFcRn-MDCK, rFcRn-GFP-MDCK and vector-only MDCK cellsFilter-grown monolayers were incubated with 1 μM wtFc (recombinant Fc derived from rat IgG2a) for 1 h at pH 6 or pH 7.4 and processed for immunofluorescence using antibodies against wtFc (red) and the tight junction marker ZO-1 (blue). The heavy chain of rFcRn (green) was detected using GFP fluorescence (rFcRn-GFP-MDCK cells) or an antibody against the rFcRn heavy chain (rFcRn-MDCK and vector-only MDCK cells). Optical sections were taken every 2 μm below the level of the tight junctions. |
PMC1618844_F1_7548.jpg | What is the focal point of this photograph? | CT scan showing the renal mass. |
PMC1619848_fig02_7553.jpg | What is the core subject represented in this visual? | Lymphatics in the normal kidney (D2-40 immunostaining). b, Lymphatic capillaries are evident in the interstitium around the glomerulus. c, Lymphatics exhibiting a slit-like structure are distributed around the interlobular artery and vein in the cortex. c, In the interstitium around a dilated interlobular vein, many lymphatic capillaries are evident. A few lymphatic capillaries are present just beneath the venous endothelium. d, A lymphatic capillary is recognizable in the centre of the figure showing a normal medulla. |
PMC1619848_fig02_7551.jpg | What is shown in this image? | Lymphatics in the normal kidney (D2-40 immunostaining). b, Lymphatic capillaries are evident in the interstitium around the glomerulus. c, Lymphatics exhibiting a slit-like structure are distributed around the interlobular artery and vein in the cortex. c, In the interstitium around a dilated interlobular vein, many lymphatic capillaries are evident. A few lymphatic capillaries are present just beneath the venous endothelium. d, A lymphatic capillary is recognizable in the centre of the figure showing a normal medulla. |
PMC1619848_fig02_7552.jpg | What is shown in this image? | Lymphatics in the normal kidney (D2-40 immunostaining). b, Lymphatic capillaries are evident in the interstitium around the glomerulus. c, Lymphatics exhibiting a slit-like structure are distributed around the interlobular artery and vein in the cortex. c, In the interstitium around a dilated interlobular vein, many lymphatic capillaries are evident. A few lymphatic capillaries are present just beneath the venous endothelium. d, A lymphatic capillary is recognizable in the centre of the figure showing a normal medulla. |
PMC1619848_fig03_7556.jpg | What can you see in this picture? | Large blood vessel-related lymphatics in the normal kidney. a, Lymphatic vessels positive for D2-40 are abundantly distributed in the interstitium around the interlobar artery. b, Many lymphatics are shown around the interlobar veins. Longitudinal aspect of a lymphatic vessel is recognized in the interstitium adjacent to a central vein. c, Elastica van Gieson staining demonstrates a vessel (arrowheads) containing erythrocytes in the lumen and running alongside the interlobar vein. d, Figure showing the same area as (c) in a serial section. A vessel (arrowheads) containing erythrocytes found in (c) is positive for D2-40, which indicates that it is a lymphatic vessel. e, The arcuate vein in the centre of the figure shows positivity for CD31. Capillaries adjacent to the vein are also immunopositive for CD31 (arrows). f, Figure showing the same area as (d) in a serial section immunostained with D2-40. Note two capillaries (arrows) positive for D2-40, which are also positive for CD31, as shown in (e). |
PMC1619848_fig03_7555.jpg | What is the focal point of this photograph? | Large blood vessel-related lymphatics in the normal kidney. a, Lymphatic vessels positive for D2-40 are abundantly distributed in the interstitium around the interlobar artery. b, Many lymphatics are shown around the interlobar veins. Longitudinal aspect of a lymphatic vessel is recognized in the interstitium adjacent to a central vein. c, Elastica van Gieson staining demonstrates a vessel (arrowheads) containing erythrocytes in the lumen and running alongside the interlobar vein. d, Figure showing the same area as (c) in a serial section. A vessel (arrowheads) containing erythrocytes found in (c) is positive for D2-40, which indicates that it is a lymphatic vessel. e, The arcuate vein in the centre of the figure shows positivity for CD31. Capillaries adjacent to the vein are also immunopositive for CD31 (arrows). f, Figure showing the same area as (d) in a serial section immunostained with D2-40. Note two capillaries (arrows) positive for D2-40, which are also positive for CD31, as shown in (e). |
PMC1619848_fig03_7554.jpg | What key item or scene is captured in this photo? | Large blood vessel-related lymphatics in the normal kidney. a, Lymphatic vessels positive for D2-40 are abundantly distributed in the interstitium around the interlobar artery. b, Many lymphatics are shown around the interlobar veins. Longitudinal aspect of a lymphatic vessel is recognized in the interstitium adjacent to a central vein. c, Elastica van Gieson staining demonstrates a vessel (arrowheads) containing erythrocytes in the lumen and running alongside the interlobar vein. d, Figure showing the same area as (c) in a serial section. A vessel (arrowheads) containing erythrocytes found in (c) is positive for D2-40, which indicates that it is a lymphatic vessel. e, The arcuate vein in the centre of the figure shows positivity for CD31. Capillaries adjacent to the vein are also immunopositive for CD31 (arrows). f, Figure showing the same area as (d) in a serial section immunostained with D2-40. Note two capillaries (arrows) positive for D2-40, which are also positive for CD31, as shown in (e). |
PMC1619848_fig03_7558.jpg | Can you identify the primary element in this image? | Large blood vessel-related lymphatics in the normal kidney. a, Lymphatic vessels positive for D2-40 are abundantly distributed in the interstitium around the interlobar artery. b, Many lymphatics are shown around the interlobar veins. Longitudinal aspect of a lymphatic vessel is recognized in the interstitium adjacent to a central vein. c, Elastica van Gieson staining demonstrates a vessel (arrowheads) containing erythrocytes in the lumen and running alongside the interlobar vein. d, Figure showing the same area as (c) in a serial section. A vessel (arrowheads) containing erythrocytes found in (c) is positive for D2-40, which indicates that it is a lymphatic vessel. e, The arcuate vein in the centre of the figure shows positivity for CD31. Capillaries adjacent to the vein are also immunopositive for CD31 (arrows). f, Figure showing the same area as (d) in a serial section immunostained with D2-40. Note two capillaries (arrows) positive for D2-40, which are also positive for CD31, as shown in (e). |
PMC1619848_fig07_7562.jpg | What stands out most in this visual? | Immunohistochemistry of kidney with renal cell carcinoma (RCC). a, The central area of RCC has abundant blood vessels positive for CD31. b, Figure showing the same area in a serial section of (a). D2-40 immunostaining reveals a negative result. c, At the tumour margin, two lymphatics positive for D2-40 are invaded by tumour cells (arrows). d, In the fibrous interstitium around the tumour, lymphatics positive for D2-40 are abundantly distributed. Arrowheads indicate the boundary between the tumour and the tumour-free cortex. |
PMC1619848_fig07_7563.jpg | What does this image primarily show? | Immunohistochemistry of kidney with renal cell carcinoma (RCC). a, The central area of RCC has abundant blood vessels positive for CD31. b, Figure showing the same area in a serial section of (a). D2-40 immunostaining reveals a negative result. c, At the tumour margin, two lymphatics positive for D2-40 are invaded by tumour cells (arrows). d, In the fibrous interstitium around the tumour, lymphatics positive for D2-40 are abundantly distributed. Arrowheads indicate the boundary between the tumour and the tumour-free cortex. |
PMC1619848_fig07_7561.jpg | What can you see in this picture? | Immunohistochemistry of kidney with renal cell carcinoma (RCC). a, The central area of RCC has abundant blood vessels positive for CD31. b, Figure showing the same area in a serial section of (a). D2-40 immunostaining reveals a negative result. c, At the tumour margin, two lymphatics positive for D2-40 are invaded by tumour cells (arrows). d, In the fibrous interstitium around the tumour, lymphatics positive for D2-40 are abundantly distributed. Arrowheads indicate the boundary between the tumour and the tumour-free cortex. |
PMC1619848_fig07_7560.jpg | What is the dominant medical problem in this image? | Immunohistochemistry of kidney with renal cell carcinoma (RCC). a, The central area of RCC has abundant blood vessels positive for CD31. b, Figure showing the same area in a serial section of (a). D2-40 immunostaining reveals a negative result. c, At the tumour margin, two lymphatics positive for D2-40 are invaded by tumour cells (arrows). d, In the fibrous interstitium around the tumour, lymphatics positive for D2-40 are abundantly distributed. Arrowheads indicate the boundary between the tumour and the tumour-free cortex. |
PMC1621068_F4_7565.jpg | What is the core subject represented in this visual? | Localisation of CFSE-stained Bb-HP incubated with human neutrophils. Confocal microscopy was used to demonstrate intracellular localisation of CFSE-stained Bb-HP. Neutrophils and CFSE-stained Bb-Hp were incubated for 5 min (A) or 30 min (B) before the reaction was stopped by adding ice-cold PBS and samples were fixed. The white arrow on panel (A) indicates a borrelia bacterium attached to neutrophil surface. In panel (C), neutrophils were pre-treated for 10 min with 5 μg/ml Cytochalasin B before addition of CFSE-stained Bb-HP for 30 min. Images shown are "stack images" taken at a defined cross section of the neutrophil, as close to the centre of the cell as possible. The white bar represents 10 μm. Images are representative of two to three samples carried out with neutrophils from two to three different donors. |
PMC1621068_F4_7564.jpg | What is the principal component of this image? | Localisation of CFSE-stained Bb-HP incubated with human neutrophils. Confocal microscopy was used to demonstrate intracellular localisation of CFSE-stained Bb-HP. Neutrophils and CFSE-stained Bb-Hp were incubated for 5 min (A) or 30 min (B) before the reaction was stopped by adding ice-cold PBS and samples were fixed. The white arrow on panel (A) indicates a borrelia bacterium attached to neutrophil surface. In panel (C), neutrophils were pre-treated for 10 min with 5 μg/ml Cytochalasin B before addition of CFSE-stained Bb-HP for 30 min. Images shown are "stack images" taken at a defined cross section of the neutrophil, as close to the centre of the cell as possible. The white bar represents 10 μm. Images are representative of two to three samples carried out with neutrophils from two to three different donors. |
PMC1621068_F4_7566.jpg | What is shown in this image? | Localisation of CFSE-stained Bb-HP incubated with human neutrophils. Confocal microscopy was used to demonstrate intracellular localisation of CFSE-stained Bb-HP. Neutrophils and CFSE-stained Bb-Hp were incubated for 5 min (A) or 30 min (B) before the reaction was stopped by adding ice-cold PBS and samples were fixed. The white arrow on panel (A) indicates a borrelia bacterium attached to neutrophil surface. In panel (C), neutrophils were pre-treated for 10 min with 5 μg/ml Cytochalasin B before addition of CFSE-stained Bb-HP for 30 min. Images shown are "stack images" taken at a defined cross section of the neutrophil, as close to the centre of the cell as possible. The white bar represents 10 μm. Images are representative of two to three samples carried out with neutrophils from two to three different donors. |
PMC1621078_F7_7568.jpg | Describe the main subject of this image. | Whole chromosome-6-paint FISH analysis of monochromatic ES cell clones that had lost heterozygosity at both the ROSA26 locus and D6Mit159. Metaphase chromosomes were hybridized to a chromosome 6 probe labeled with FITC. Chromosomes were counter stained red with propidium iodide (PI). Images shown were produced by merging FITC and PI epifluorescence images. Copies of chromosome 6 are yellow. Other chromosomes are red. Panels A and B show metaphase chromosomes from cells that expressed CFP only or YFP only, respectively. 400× magnification. |
PMC1621081_F1_7569.jpg | What stands out most in this visual? | Non-contrast computed tomography of head showing the hypoechoeic mass without any intracranial extension. |
PMC1624827_F4_7572.jpg | What is shown in this image? | Membrane phospholipid perturbation patterns in Jurkat T lymphoblasts after unipolar and bipolar pulse exposure. (a) FM1-43 fluorescence increase appears only at the anode (bottom) pole of the cell after 4, 30 ns, 2.5 MV/m pulses. (b) Bipolar pulses (50, 15 ns, 2.8 MV/m) produce phospholipid rearrangement and PS externalization at both electrode-facing poles of the cell. (c) Cellular fluorescence intensity profile 10 s after bipolar pulse exposure. The frequency of pulse delivery was 10 Hz. Each bipolar pulse was delivered as a pair of pulses, first negative, then positive, each 15 ns wide. Total energy delivered for the unipolar and bipolar pulses was approximately the same, and no poration is observed by conventional methods at these pulse exposure levels. |
PMC1624827_F4_7573.jpg | What is the principal component of this image? | Membrane phospholipid perturbation patterns in Jurkat T lymphoblasts after unipolar and bipolar pulse exposure. (a) FM1-43 fluorescence increase appears only at the anode (bottom) pole of the cell after 4, 30 ns, 2.5 MV/m pulses. (b) Bipolar pulses (50, 15 ns, 2.8 MV/m) produce phospholipid rearrangement and PS externalization at both electrode-facing poles of the cell. (c) Cellular fluorescence intensity profile 10 s after bipolar pulse exposure. The frequency of pulse delivery was 10 Hz. Each bipolar pulse was delivered as a pair of pulses, first negative, then positive, each 15 ns wide. Total energy delivered for the unipolar and bipolar pulses was approximately the same, and no poration is observed by conventional methods at these pulse exposure levels. |
PMC1624850_F3_7575.jpg | What does this image primarily show? | Hand x-ray showed synostosis between capitate-hamate-and lunate-triquetrum. |
PMC1624850_F4_7576.jpg | What can you see in this picture? | Foot x ray showed multiple fusions, talo-calcanear, talo-navicular, naviculo-calcanear, cunieform2-cuneiform 3. |
PMC1626408_f1-ehp0114-a00580_7577.jpg | What's the most prominent thing you notice in this picture? | Harming while healing?Concerns about potential reproductive effects of exposure to the plasticizer DEHP, including those to infants from uses in medical tubing and other equipment, prompted a new examination of the available health data by the NTP. |
PMC1626476_F2_7579.jpg | What is the core subject represented in this visual? | Superficial nodal recurrence (ipsilateral dorsolateral node) in a patient with a pT2 pN2b supraglottic larynx carcinoma. Preoperative diagnostic images did not show any suspicious superficial nodes, nor were any enlarged nodes visible in the postoperative planning computed tomography a: IMRT treatment plan, PTV1 (black line): 'build up' effect in the skin/subcutaneous region of interest (ROI, white dotted line) which was not intended to be included into the PTV1. b: posttreatment follow up computed tomography scan revealed a superficial lymph node metastasis (ROI), located in the former 'build up' area |
PMC1626485_F1_7580.jpg | What can you see in this picture? | Computed tomography (CT) of the thorax showed a well defined lesion in the anterior segment of the left upper lobe. |
PMC1626485_F3_7582.jpg | What stands out most in this visual? | Microscopic examination showed a variety of cell lines – squamous epithelium and sebaceous glands (Fig. 3A), cartilage (Fig. 3B), pancreatic tissue (Fig. 3C), gastric glands (Fig. 3D). |
PMC1626486_F3_7583.jpg | What stands out most in this visual? | Figure shows the effect of AVD on mitral regurgitation severity. Mitral inflow pulsed Doppler (A) and color Doppler showing mitral regurgitation in the apical 4 chamber view (B) at a paced AV delay of 150 ms and mitral inflow pulsed Doppler (C) and color Doppler showing mitral regurgitation severity in the apical 4 chamber view (D) at paced AV delay of 50 ms. Diastolic mitral regurgitation is seen at an AV delay of 150 ms (black arrowheads, A). Note significant mitral regurgitation in panel B which decreased in panel D at short AV delay. |
PMC1626486_F3_7584.jpg | What key item or scene is captured in this photo? | Figure shows the effect of AVD on mitral regurgitation severity. Mitral inflow pulsed Doppler (A) and color Doppler showing mitral regurgitation in the apical 4 chamber view (B) at a paced AV delay of 150 ms and mitral inflow pulsed Doppler (C) and color Doppler showing mitral regurgitation severity in the apical 4 chamber view (D) at paced AV delay of 50 ms. Diastolic mitral regurgitation is seen at an AV delay of 150 ms (black arrowheads, A). Note significant mitral regurgitation in panel B which decreased in panel D at short AV delay. |
PMC1626486_F3_7585.jpg | What does this image primarily show? | Figure shows the effect of AVD on mitral regurgitation severity. Mitral inflow pulsed Doppler (A) and color Doppler showing mitral regurgitation in the apical 4 chamber view (B) at a paced AV delay of 150 ms and mitral inflow pulsed Doppler (C) and color Doppler showing mitral regurgitation severity in the apical 4 chamber view (D) at paced AV delay of 50 ms. Diastolic mitral regurgitation is seen at an AV delay of 150 ms (black arrowheads, A). Note significant mitral regurgitation in panel B which decreased in panel D at short AV delay. |
PMC1629024_F1_7589.jpg | Describe the main subject of this image. | kal-1 overexpression in the cells responsible for the formation of the cephalopharyngeal skeleton causes alterations of the sclerotized components of the head. (A) Stage 16 wild type embryonic head. The kal-1 transcript is detected in the region of the gnathal lobes that will give rise to the anterior part of the cephalopharyngeal skeleton. (B) Schematic representation of the cephalopharyngeal skeleton of a L1 Drosophila larva. MH mouth hook, MT median tooth, HP H-piece, LG lateralgräten, DBr dorsal bridge, DP dorsal process, VP ventral process. (C) Fluorescence (left), bright-field (center), and merged (right) images of the expression in the cephalopharyngeal skeleton of a stage 17 embryo of the UAS-GFP reporter, driven by the 179y-Gal4 line. (D) Wild type stage 17 embryonic head cuticle. In the inset, a magnification of the mouth hooks. (E) Head cuticle of a stage 17 179y-Gal4/+; UAS-kal-1/+; UAS-kal-1/+ embryo. The head skeleton structure appears less sclerotized; principally the median tooth, the H-piece, and the lateralgräten, but also the dorsal bridge, the dorsal process, and the ventral process appear thinner than in the wild type. The mouth hooks lack the posterior part (inset). |
PMC1629024_F1_7595.jpg | What is the principal component of this image? | kal-1 overexpression in the cells responsible for the formation of the cephalopharyngeal skeleton causes alterations of the sclerotized components of the head. (A) Stage 16 wild type embryonic head. The kal-1 transcript is detected in the region of the gnathal lobes that will give rise to the anterior part of the cephalopharyngeal skeleton. (B) Schematic representation of the cephalopharyngeal skeleton of a L1 Drosophila larva. MH mouth hook, MT median tooth, HP H-piece, LG lateralgräten, DBr dorsal bridge, DP dorsal process, VP ventral process. (C) Fluorescence (left), bright-field (center), and merged (right) images of the expression in the cephalopharyngeal skeleton of a stage 17 embryo of the UAS-GFP reporter, driven by the 179y-Gal4 line. (D) Wild type stage 17 embryonic head cuticle. In the inset, a magnification of the mouth hooks. (E) Head cuticle of a stage 17 179y-Gal4/+; UAS-kal-1/+; UAS-kal-1/+ embryo. The head skeleton structure appears less sclerotized; principally the median tooth, the H-piece, and the lateralgräten, but also the dorsal bridge, the dorsal process, and the ventral process appear thinner than in the wild type. The mouth hooks lack the posterior part (inset). |
PMC1629024_F1_7594.jpg | What does this image primarily show? | kal-1 overexpression in the cells responsible for the formation of the cephalopharyngeal skeleton causes alterations of the sclerotized components of the head. (A) Stage 16 wild type embryonic head. The kal-1 transcript is detected in the region of the gnathal lobes that will give rise to the anterior part of the cephalopharyngeal skeleton. (B) Schematic representation of the cephalopharyngeal skeleton of a L1 Drosophila larva. MH mouth hook, MT median tooth, HP H-piece, LG lateralgräten, DBr dorsal bridge, DP dorsal process, VP ventral process. (C) Fluorescence (left), bright-field (center), and merged (right) images of the expression in the cephalopharyngeal skeleton of a stage 17 embryo of the UAS-GFP reporter, driven by the 179y-Gal4 line. (D) Wild type stage 17 embryonic head cuticle. In the inset, a magnification of the mouth hooks. (E) Head cuticle of a stage 17 179y-Gal4/+; UAS-kal-1/+; UAS-kal-1/+ embryo. The head skeleton structure appears less sclerotized; principally the median tooth, the H-piece, and the lateralgräten, but also the dorsal bridge, the dorsal process, and the ventral process appear thinner than in the wild type. The mouth hooks lack the posterior part (inset). |
PMC1629024_F1_7588.jpg | What is the core subject represented in this visual? | kal-1 overexpression in the cells responsible for the formation of the cephalopharyngeal skeleton causes alterations of the sclerotized components of the head. (A) Stage 16 wild type embryonic head. The kal-1 transcript is detected in the region of the gnathal lobes that will give rise to the anterior part of the cephalopharyngeal skeleton. (B) Schematic representation of the cephalopharyngeal skeleton of a L1 Drosophila larva. MH mouth hook, MT median tooth, HP H-piece, LG lateralgräten, DBr dorsal bridge, DP dorsal process, VP ventral process. (C) Fluorescence (left), bright-field (center), and merged (right) images of the expression in the cephalopharyngeal skeleton of a stage 17 embryo of the UAS-GFP reporter, driven by the 179y-Gal4 line. (D) Wild type stage 17 embryonic head cuticle. In the inset, a magnification of the mouth hooks. (E) Head cuticle of a stage 17 179y-Gal4/+; UAS-kal-1/+; UAS-kal-1/+ embryo. The head skeleton structure appears less sclerotized; principally the median tooth, the H-piece, and the lateralgräten, but also the dorsal bridge, the dorsal process, and the ventral process appear thinner than in the wild type. The mouth hooks lack the posterior part (inset). |
PMC1629024_F1_7587.jpg | What is the main focus of this visual representation? | kal-1 overexpression in the cells responsible for the formation of the cephalopharyngeal skeleton causes alterations of the sclerotized components of the head. (A) Stage 16 wild type embryonic head. The kal-1 transcript is detected in the region of the gnathal lobes that will give rise to the anterior part of the cephalopharyngeal skeleton. (B) Schematic representation of the cephalopharyngeal skeleton of a L1 Drosophila larva. MH mouth hook, MT median tooth, HP H-piece, LG lateralgräten, DBr dorsal bridge, DP dorsal process, VP ventral process. (C) Fluorescence (left), bright-field (center), and merged (right) images of the expression in the cephalopharyngeal skeleton of a stage 17 embryo of the UAS-GFP reporter, driven by the 179y-Gal4 line. (D) Wild type stage 17 embryonic head cuticle. In the inset, a magnification of the mouth hooks. (E) Head cuticle of a stage 17 179y-Gal4/+; UAS-kal-1/+; UAS-kal-1/+ embryo. The head skeleton structure appears less sclerotized; principally the median tooth, the H-piece, and the lateralgräten, but also the dorsal bridge, the dorsal process, and the ventral process appear thinner than in the wild type. The mouth hooks lack the posterior part (inset). |
PMC1629024_F1_7591.jpg | What key item or scene is captured in this photo? | kal-1 overexpression in the cells responsible for the formation of the cephalopharyngeal skeleton causes alterations of the sclerotized components of the head. (A) Stage 16 wild type embryonic head. The kal-1 transcript is detected in the region of the gnathal lobes that will give rise to the anterior part of the cephalopharyngeal skeleton. (B) Schematic representation of the cephalopharyngeal skeleton of a L1 Drosophila larva. MH mouth hook, MT median tooth, HP H-piece, LG lateralgräten, DBr dorsal bridge, DP dorsal process, VP ventral process. (C) Fluorescence (left), bright-field (center), and merged (right) images of the expression in the cephalopharyngeal skeleton of a stage 17 embryo of the UAS-GFP reporter, driven by the 179y-Gal4 line. (D) Wild type stage 17 embryonic head cuticle. In the inset, a magnification of the mouth hooks. (E) Head cuticle of a stage 17 179y-Gal4/+; UAS-kal-1/+; UAS-kal-1/+ embryo. The head skeleton structure appears less sclerotized; principally the median tooth, the H-piece, and the lateralgräten, but also the dorsal bridge, the dorsal process, and the ventral process appear thinner than in the wild type. The mouth hooks lack the posterior part (inset). |
PMC1629024_F1_7586.jpg | What is the principal component of this image? | kal-1 overexpression in the cells responsible for the formation of the cephalopharyngeal skeleton causes alterations of the sclerotized components of the head. (A) Stage 16 wild type embryonic head. The kal-1 transcript is detected in the region of the gnathal lobes that will give rise to the anterior part of the cephalopharyngeal skeleton. (B) Schematic representation of the cephalopharyngeal skeleton of a L1 Drosophila larva. MH mouth hook, MT median tooth, HP H-piece, LG lateralgräten, DBr dorsal bridge, DP dorsal process, VP ventral process. (C) Fluorescence (left), bright-field (center), and merged (right) images of the expression in the cephalopharyngeal skeleton of a stage 17 embryo of the UAS-GFP reporter, driven by the 179y-Gal4 line. (D) Wild type stage 17 embryonic head cuticle. In the inset, a magnification of the mouth hooks. (E) Head cuticle of a stage 17 179y-Gal4/+; UAS-kal-1/+; UAS-kal-1/+ embryo. The head skeleton structure appears less sclerotized; principally the median tooth, the H-piece, and the lateralgräten, but also the dorsal bridge, the dorsal process, and the ventral process appear thinner than in the wild type. The mouth hooks lack the posterior part (inset). |
PMC1629024_F1_7592.jpg | What object or scene is depicted here? | kal-1 overexpression in the cells responsible for the formation of the cephalopharyngeal skeleton causes alterations of the sclerotized components of the head. (A) Stage 16 wild type embryonic head. The kal-1 transcript is detected in the region of the gnathal lobes that will give rise to the anterior part of the cephalopharyngeal skeleton. (B) Schematic representation of the cephalopharyngeal skeleton of a L1 Drosophila larva. MH mouth hook, MT median tooth, HP H-piece, LG lateralgräten, DBr dorsal bridge, DP dorsal process, VP ventral process. (C) Fluorescence (left), bright-field (center), and merged (right) images of the expression in the cephalopharyngeal skeleton of a stage 17 embryo of the UAS-GFP reporter, driven by the 179y-Gal4 line. (D) Wild type stage 17 embryonic head cuticle. In the inset, a magnification of the mouth hooks. (E) Head cuticle of a stage 17 179y-Gal4/+; UAS-kal-1/+; UAS-kal-1/+ embryo. The head skeleton structure appears less sclerotized; principally the median tooth, the H-piece, and the lateralgräten, but also the dorsal bridge, the dorsal process, and the ventral process appear thinner than in the wild type. The mouth hooks lack the posterior part (inset). |
PMC1629024_F1_7593.jpg | Can you identify the primary element in this image? | kal-1 overexpression in the cells responsible for the formation of the cephalopharyngeal skeleton causes alterations of the sclerotized components of the head. (A) Stage 16 wild type embryonic head. The kal-1 transcript is detected in the region of the gnathal lobes that will give rise to the anterior part of the cephalopharyngeal skeleton. (B) Schematic representation of the cephalopharyngeal skeleton of a L1 Drosophila larva. MH mouth hook, MT median tooth, HP H-piece, LG lateralgräten, DBr dorsal bridge, DP dorsal process, VP ventral process. (C) Fluorescence (left), bright-field (center), and merged (right) images of the expression in the cephalopharyngeal skeleton of a stage 17 embryo of the UAS-GFP reporter, driven by the 179y-Gal4 line. (D) Wild type stage 17 embryonic head cuticle. In the inset, a magnification of the mouth hooks. (E) Head cuticle of a stage 17 179y-Gal4/+; UAS-kal-1/+; UAS-kal-1/+ embryo. The head skeleton structure appears less sclerotized; principally the median tooth, the H-piece, and the lateralgräten, but also the dorsal bridge, the dorsal process, and the ventral process appear thinner than in the wild type. The mouth hooks lack the posterior part (inset). |
PMC1629024_F3_7601.jpg | What is the principal component of this image? | Cephalopharyngeal skeleton phenotypes induced by overexpression of the different DmKal-1 mutant proteins. (A, B, C, D, E) Head cuticle of stage 17 embryos. (A) Stage 17 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The head skeleton structure appears less sclerotized and the median tooth is altered. Moreover, the mouth hooks (arrows) lack the posterior part and appear distant from the mid-line (dotted line). (B) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S] embryo. (C) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S+N236K] embryo. (D) Stage 17 179y-Gal4/+; UAS-kal-1 [C85S] embryo. The mouth hooks base shows a reduction of the dorsal process. (E) Stage 17 179y-Gal4/+; UAS-kal-1 [R159T+R161L] embryo. In the insets, a magnification of the hooks. (F, G)) Stage 13 embryos immunostained with anti-Hind antibody. (F) 179y-Gal4/+; UAS-kal-1; UAS-kal-1 embryo. GBR occurs normally. (G) 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The embryo shows an incomplete GBR process. |
PMC1629024_F3_7598.jpg | Can you identify the primary element in this image? | Cephalopharyngeal skeleton phenotypes induced by overexpression of the different DmKal-1 mutant proteins. (A, B, C, D, E) Head cuticle of stage 17 embryos. (A) Stage 17 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The head skeleton structure appears less sclerotized and the median tooth is altered. Moreover, the mouth hooks (arrows) lack the posterior part and appear distant from the mid-line (dotted line). (B) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S] embryo. (C) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S+N236K] embryo. (D) Stage 17 179y-Gal4/+; UAS-kal-1 [C85S] embryo. The mouth hooks base shows a reduction of the dorsal process. (E) Stage 17 179y-Gal4/+; UAS-kal-1 [R159T+R161L] embryo. In the insets, a magnification of the hooks. (F, G)) Stage 13 embryos immunostained with anti-Hind antibody. (F) 179y-Gal4/+; UAS-kal-1; UAS-kal-1 embryo. GBR occurs normally. (G) 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The embryo shows an incomplete GBR process. |
PMC1629024_F3_7597.jpg | What's the most prominent thing you notice in this picture? | Cephalopharyngeal skeleton phenotypes induced by overexpression of the different DmKal-1 mutant proteins. (A, B, C, D, E) Head cuticle of stage 17 embryos. (A) Stage 17 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The head skeleton structure appears less sclerotized and the median tooth is altered. Moreover, the mouth hooks (arrows) lack the posterior part and appear distant from the mid-line (dotted line). (B) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S] embryo. (C) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S+N236K] embryo. (D) Stage 17 179y-Gal4/+; UAS-kal-1 [C85S] embryo. The mouth hooks base shows a reduction of the dorsal process. (E) Stage 17 179y-Gal4/+; UAS-kal-1 [R159T+R161L] embryo. In the insets, a magnification of the hooks. (F, G)) Stage 13 embryos immunostained with anti-Hind antibody. (F) 179y-Gal4/+; UAS-kal-1; UAS-kal-1 embryo. GBR occurs normally. (G) 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The embryo shows an incomplete GBR process. |
PMC1629024_F3_7599.jpg | What is the principal component of this image? | Cephalopharyngeal skeleton phenotypes induced by overexpression of the different DmKal-1 mutant proteins. (A, B, C, D, E) Head cuticle of stage 17 embryos. (A) Stage 17 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The head skeleton structure appears less sclerotized and the median tooth is altered. Moreover, the mouth hooks (arrows) lack the posterior part and appear distant from the mid-line (dotted line). (B) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S] embryo. (C) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S+N236K] embryo. (D) Stage 17 179y-Gal4/+; UAS-kal-1 [C85S] embryo. The mouth hooks base shows a reduction of the dorsal process. (E) Stage 17 179y-Gal4/+; UAS-kal-1 [R159T+R161L] embryo. In the insets, a magnification of the hooks. (F, G)) Stage 13 embryos immunostained with anti-Hind antibody. (F) 179y-Gal4/+; UAS-kal-1; UAS-kal-1 embryo. GBR occurs normally. (G) 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The embryo shows an incomplete GBR process. |
PMC1629024_F3_7596.jpg | What is the principal component of this image? | Cephalopharyngeal skeleton phenotypes induced by overexpression of the different DmKal-1 mutant proteins. (A, B, C, D, E) Head cuticle of stage 17 embryos. (A) Stage 17 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The head skeleton structure appears less sclerotized and the median tooth is altered. Moreover, the mouth hooks (arrows) lack the posterior part and appear distant from the mid-line (dotted line). (B) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S] embryo. (C) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S+N236K] embryo. (D) Stage 17 179y-Gal4/+; UAS-kal-1 [C85S] embryo. The mouth hooks base shows a reduction of the dorsal process. (E) Stage 17 179y-Gal4/+; UAS-kal-1 [R159T+R161L] embryo. In the insets, a magnification of the hooks. (F, G)) Stage 13 embryos immunostained with anti-Hind antibody. (F) 179y-Gal4/+; UAS-kal-1; UAS-kal-1 embryo. GBR occurs normally. (G) 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The embryo shows an incomplete GBR process. |
PMC1629024_F3_7600.jpg | What is shown in this image? | Cephalopharyngeal skeleton phenotypes induced by overexpression of the different DmKal-1 mutant proteins. (A, B, C, D, E) Head cuticle of stage 17 embryos. (A) Stage 17 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The head skeleton structure appears less sclerotized and the median tooth is altered. Moreover, the mouth hooks (arrows) lack the posterior part and appear distant from the mid-line (dotted line). (B) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S] embryo. (C) Stage 17 179y-Gal4/+; UAS-kal-1 [C127/128S+N236K] embryo. (D) Stage 17 179y-Gal4/+; UAS-kal-1 [C85S] embryo. The mouth hooks base shows a reduction of the dorsal process. (E) Stage 17 179y-Gal4/+; UAS-kal-1 [R159T+R161L] embryo. In the insets, a magnification of the hooks. (F, G)) Stage 13 embryos immunostained with anti-Hind antibody. (F) 179y-Gal4/+; UAS-kal-1; UAS-kal-1 embryo. GBR occurs normally. (G) 179y-Gal4/+; UAS-kal-1 [N236K] embryo. The embryo shows an incomplete GBR process. |
PMC1630693_F2_7603.jpg | What is the central feature of this picture? | CT scan was performed which showed a large cervical mass arising form thyroid and extending to left cervical soft tissue with displacement of trachea. |
PMC1630711_pgen-0020181-g001_7616.jpg | What key item or scene is captured in this photo? | Loss of p150CAF-1 Function Leads to Early Developmental Arrest and Alteration of Heterochromatin Organization(A) Generation of Chaf1a
+/− mice by homologous recombination in ES cells. (Top) Scheme of the p150CAF1 protein indicating the interacting domains (ID) for HP1 and p60CAF-1, and the acidic domain (AD). (Middle) Structure of the murine Chaf1a gene. Blocks and lines represent exons and introns, respectively. A star indicates the translation initiation site. Below is shown the Chaf1a targeting vector, which includes genomic DNA homology regions (5 HR and 3 HR), the diphtheria toxin (DT), and neomycin selection genes. Recombined (Rec) ES cells and mice were identified by Southern blot using ScaI (S) and the indicated probe.(B) Breeding strategy used for the production of E4 Chaf1a
−/− embryos. Genotyping was performed by PCR using the three oligonucleotide primers indicated in (A) (1, 2, and 3). An example of the result of a genotyping experiment is shown.(C) Immunodetection of p150CAF-1 (green) and HP1α (red) in E4 embryos derived from Chaf1a
+/− intercrosses. Because Chaf1a
+/+ and Chaf1a
+/− embryos both stain positively for the presence of p150CAF-1, they are both designated as wild-type. p150CAF-1 expression, which indicates ongoing S phase, can be detected in most cells within the wild-type blastocyst (upper panel). The lower panel shows a 12-cell embryo labeling negatively for p150CAF-1. Only nonspecific background labeling can be observed. In each panel, the right-hand image shows the merge between the HP1α fluorescence and DAPI-stained DNA in blue. Pink color indicates the association of HP1 with DAPI-dense material. The bottom of each panel shows the magnification of a nucleus selected from the above embryo (white square). The arrowhead indicates the typical heterochromatin foci revealed by DAPI and HP1α staining in wild-type embryos. These foci are not visible in Chaf1a
−/− embryos. DAPI and HP1α staining are diffuse within the nucleus of p150CAF-1-depleted embryos, with enrichment at the nuclear periphery, revealing abnormal heterochromatin organization. Scale bars represent 10 μm.(E) Wild-type embryos isolated at embryonic day 2 (E2, two cells), E2.5 (four cells), E3 (eight cells), E3.5 (16 cells), and E4 (32 cells) are shown. Heterochromatin was monitored by DAPI staining (upper panel) and HP1 immunolabeling (in red, lower panel).(F) Magnification of a nucleus (DAPI-stained) representative of each stage. The right-hand panel shows the nucleus of an ES cell. Scale bar represents 10 μm. |
PMC1630711_pgen-0020181-g001_7617.jpg | What is the dominant medical problem in this image? | Loss of p150CAF-1 Function Leads to Early Developmental Arrest and Alteration of Heterochromatin Organization(A) Generation of Chaf1a
+/− mice by homologous recombination in ES cells. (Top) Scheme of the p150CAF1 protein indicating the interacting domains (ID) for HP1 and p60CAF-1, and the acidic domain (AD). (Middle) Structure of the murine Chaf1a gene. Blocks and lines represent exons and introns, respectively. A star indicates the translation initiation site. Below is shown the Chaf1a targeting vector, which includes genomic DNA homology regions (5 HR and 3 HR), the diphtheria toxin (DT), and neomycin selection genes. Recombined (Rec) ES cells and mice were identified by Southern blot using ScaI (S) and the indicated probe.(B) Breeding strategy used for the production of E4 Chaf1a
−/− embryos. Genotyping was performed by PCR using the three oligonucleotide primers indicated in (A) (1, 2, and 3). An example of the result of a genotyping experiment is shown.(C) Immunodetection of p150CAF-1 (green) and HP1α (red) in E4 embryos derived from Chaf1a
+/− intercrosses. Because Chaf1a
+/+ and Chaf1a
+/− embryos both stain positively for the presence of p150CAF-1, they are both designated as wild-type. p150CAF-1 expression, which indicates ongoing S phase, can be detected in most cells within the wild-type blastocyst (upper panel). The lower panel shows a 12-cell embryo labeling negatively for p150CAF-1. Only nonspecific background labeling can be observed. In each panel, the right-hand image shows the merge between the HP1α fluorescence and DAPI-stained DNA in blue. Pink color indicates the association of HP1 with DAPI-dense material. The bottom of each panel shows the magnification of a nucleus selected from the above embryo (white square). The arrowhead indicates the typical heterochromatin foci revealed by DAPI and HP1α staining in wild-type embryos. These foci are not visible in Chaf1a
−/− embryos. DAPI and HP1α staining are diffuse within the nucleus of p150CAF-1-depleted embryos, with enrichment at the nuclear periphery, revealing abnormal heterochromatin organization. Scale bars represent 10 μm.(E) Wild-type embryos isolated at embryonic day 2 (E2, two cells), E2.5 (four cells), E3 (eight cells), E3.5 (16 cells), and E4 (32 cells) are shown. Heterochromatin was monitored by DAPI staining (upper panel) and HP1 immunolabeling (in red, lower panel).(F) Magnification of a nucleus (DAPI-stained) representative of each stage. The right-hand panel shows the nucleus of an ES cell. Scale bar represents 10 μm. |
PMC1630711_pgen-0020181-g001_7615.jpg | What can you see in this picture? | Loss of p150CAF-1 Function Leads to Early Developmental Arrest and Alteration of Heterochromatin Organization(A) Generation of Chaf1a
+/− mice by homologous recombination in ES cells. (Top) Scheme of the p150CAF1 protein indicating the interacting domains (ID) for HP1 and p60CAF-1, and the acidic domain (AD). (Middle) Structure of the murine Chaf1a gene. Blocks and lines represent exons and introns, respectively. A star indicates the translation initiation site. Below is shown the Chaf1a targeting vector, which includes genomic DNA homology regions (5 HR and 3 HR), the diphtheria toxin (DT), and neomycin selection genes. Recombined (Rec) ES cells and mice were identified by Southern blot using ScaI (S) and the indicated probe.(B) Breeding strategy used for the production of E4 Chaf1a
−/− embryos. Genotyping was performed by PCR using the three oligonucleotide primers indicated in (A) (1, 2, and 3). An example of the result of a genotyping experiment is shown.(C) Immunodetection of p150CAF-1 (green) and HP1α (red) in E4 embryos derived from Chaf1a
+/− intercrosses. Because Chaf1a
+/+ and Chaf1a
+/− embryos both stain positively for the presence of p150CAF-1, they are both designated as wild-type. p150CAF-1 expression, which indicates ongoing S phase, can be detected in most cells within the wild-type blastocyst (upper panel). The lower panel shows a 12-cell embryo labeling negatively for p150CAF-1. Only nonspecific background labeling can be observed. In each panel, the right-hand image shows the merge between the HP1α fluorescence and DAPI-stained DNA in blue. Pink color indicates the association of HP1 with DAPI-dense material. The bottom of each panel shows the magnification of a nucleus selected from the above embryo (white square). The arrowhead indicates the typical heterochromatin foci revealed by DAPI and HP1α staining in wild-type embryos. These foci are not visible in Chaf1a
−/− embryos. DAPI and HP1α staining are diffuse within the nucleus of p150CAF-1-depleted embryos, with enrichment at the nuclear periphery, revealing abnormal heterochromatin organization. Scale bars represent 10 μm.(E) Wild-type embryos isolated at embryonic day 2 (E2, two cells), E2.5 (four cells), E3 (eight cells), E3.5 (16 cells), and E4 (32 cells) are shown. Heterochromatin was monitored by DAPI staining (upper panel) and HP1 immunolabeling (in red, lower panel).(F) Magnification of a nucleus (DAPI-stained) representative of each stage. The right-hand panel shows the nucleus of an ES cell. Scale bar represents 10 μm. |
PMC1630711_pgen-0020181-g004_7611.jpg | What is shown in this image? | Depletion of p150CAF-1 Leads to Loss of Clustering, Altered Localization, and Decondensation of Pericentric Heterochromatin DomainsDistribution of pericentric (red) and centric (green) domains was analyzed in the interphase nuclei of mouse ES cells by DNA FISH, using major satellite (pSAT) [47] and minor satellite (pMR150) [48] DNA probes, respectively. (A) In ES cells expressing control (cont) siRNA, pericentric regions from several chromosomes associate in clusters (red). These chromocenters form foci as revealed by DAPI staining (left-hand image), while centric regions (green) remain independent entities at the periphery of these domains. The right-hand image shows the merge between the pericentric and centric FISH signals.(B) The organization of pericentric domains was altered in cells expressing p150CAF-1 siRNA. Instead of forming well-defined chromocenters, pericentric domains were found either isolated or associated in heterogeneous aggregates of various sizes, often at the nuclear periphery. Scale bar = 10 μm.(C) Control ES cells. Fluorescence was quantified along a line randomly drawn across the nucleus in the merged image and data were plotted. One can distinguish clear peaks corresponding to chromocenters (red) and the condensed minor satellites (green).(D) ES cells expressing p150CAF-1 siRNA. p150CAF-1 depletion led to a lower fluorescence intensity and a broader distribution of signals corresponding to DAPI (blue) and major satellite hybridization (red, plot) while the organization of the minor satellites remained unaffected. Insets in the right-hand images show a typical chromocenter in control cells (C) and a disrupted chromocenter in p150CAF-1-depleted cells (D). |
PMC1630711_pgen-0020181-g004_7614.jpg | What's the most prominent thing you notice in this picture? | Depletion of p150CAF-1 Leads to Loss of Clustering, Altered Localization, and Decondensation of Pericentric Heterochromatin DomainsDistribution of pericentric (red) and centric (green) domains was analyzed in the interphase nuclei of mouse ES cells by DNA FISH, using major satellite (pSAT) [47] and minor satellite (pMR150) [48] DNA probes, respectively. (A) In ES cells expressing control (cont) siRNA, pericentric regions from several chromosomes associate in clusters (red). These chromocenters form foci as revealed by DAPI staining (left-hand image), while centric regions (green) remain independent entities at the periphery of these domains. The right-hand image shows the merge between the pericentric and centric FISH signals.(B) The organization of pericentric domains was altered in cells expressing p150CAF-1 siRNA. Instead of forming well-defined chromocenters, pericentric domains were found either isolated or associated in heterogeneous aggregates of various sizes, often at the nuclear periphery. Scale bar = 10 μm.(C) Control ES cells. Fluorescence was quantified along a line randomly drawn across the nucleus in the merged image and data were plotted. One can distinguish clear peaks corresponding to chromocenters (red) and the condensed minor satellites (green).(D) ES cells expressing p150CAF-1 siRNA. p150CAF-1 depletion led to a lower fluorescence intensity and a broader distribution of signals corresponding to DAPI (blue) and major satellite hybridization (red, plot) while the organization of the minor satellites remained unaffected. Insets in the right-hand images show a typical chromocenter in control cells (C) and a disrupted chromocenter in p150CAF-1-depleted cells (D). |
PMC1630711_pgen-0020181-g007_7606.jpg | What is being portrayed in this visual content? | Alteration of Epigenetic Marking at Pericentric Heterochromatin in p150CAF-1-Depleted Cells(A) p150CAF-1 depletion leads to reduced H4K20me3 and H3K9me3 at pericentric heterochromatin. Enrichment of histone marks at major satellite repeats was determined by ChIP from control (cont) and p150CAF-1 (p150) siRNA-expressing ES cells. DNA prepared from the input and the antibody-bound fraction were run onto an agarose gel and analyzed by Southern blot with the pSAT major satellite repeat probe [47].(B) Hybridization signals were quantified using an Instant Imager. After autoradiography, the membrane was stripped and rehybridized with a minor satellite probe [49]. After quantification, the membrane was stripped and rehybridized with an IAP LTR probe [50]. Results are presented as the amount of DNA immunoprecipitated from p150CAF-1-depleted ES cells divided by the DNA obtained from control cells. The figure shows the mean value and standard deviation of three independent ChIP experiments.(C and D) H3K9me3 and H4K20me3 fluorescence patterns are severely altered in p150CAF-1-depleted ES cells. Immunodetection of H3K9me3 (C, green), H4K20me3 (D, green), and HP1α (red) in control and p150CAF-1 siRNA-expressing ES cells. Merging of HP1α with H3K9me3 (C) and H4K20me3 (D) is shown in yellow. Scale bars represent 10 μm. |
PMC1630711_pgen-0020181-g007_7609.jpg | Can you identify the primary element in this image? | Alteration of Epigenetic Marking at Pericentric Heterochromatin in p150CAF-1-Depleted Cells(A) p150CAF-1 depletion leads to reduced H4K20me3 and H3K9me3 at pericentric heterochromatin. Enrichment of histone marks at major satellite repeats was determined by ChIP from control (cont) and p150CAF-1 (p150) siRNA-expressing ES cells. DNA prepared from the input and the antibody-bound fraction were run onto an agarose gel and analyzed by Southern blot with the pSAT major satellite repeat probe [47].(B) Hybridization signals were quantified using an Instant Imager. After autoradiography, the membrane was stripped and rehybridized with a minor satellite probe [49]. After quantification, the membrane was stripped and rehybridized with an IAP LTR probe [50]. Results are presented as the amount of DNA immunoprecipitated from p150CAF-1-depleted ES cells divided by the DNA obtained from control cells. The figure shows the mean value and standard deviation of three independent ChIP experiments.(C and D) H3K9me3 and H4K20me3 fluorescence patterns are severely altered in p150CAF-1-depleted ES cells. Immunodetection of H3K9me3 (C, green), H4K20me3 (D, green), and HP1α (red) in control and p150CAF-1 siRNA-expressing ES cells. Merging of HP1α with H3K9me3 (C) and H4K20me3 (D) is shown in yellow. Scale bars represent 10 μm. |
PMC1630711_pgen-0020181-g007_7605.jpg | What is the core subject represented in this visual? | Alteration of Epigenetic Marking at Pericentric Heterochromatin in p150CAF-1-Depleted Cells(A) p150CAF-1 depletion leads to reduced H4K20me3 and H3K9me3 at pericentric heterochromatin. Enrichment of histone marks at major satellite repeats was determined by ChIP from control (cont) and p150CAF-1 (p150) siRNA-expressing ES cells. DNA prepared from the input and the antibody-bound fraction were run onto an agarose gel and analyzed by Southern blot with the pSAT major satellite repeat probe [47].(B) Hybridization signals were quantified using an Instant Imager. After autoradiography, the membrane was stripped and rehybridized with a minor satellite probe [49]. After quantification, the membrane was stripped and rehybridized with an IAP LTR probe [50]. Results are presented as the amount of DNA immunoprecipitated from p150CAF-1-depleted ES cells divided by the DNA obtained from control cells. The figure shows the mean value and standard deviation of three independent ChIP experiments.(C and D) H3K9me3 and H4K20me3 fluorescence patterns are severely altered in p150CAF-1-depleted ES cells. Immunodetection of H3K9me3 (C, green), H4K20me3 (D, green), and HP1α (red) in control and p150CAF-1 siRNA-expressing ES cells. Merging of HP1α with H3K9me3 (C) and H4K20me3 (D) is shown in yellow. Scale bars represent 10 μm. |
PMC1634748_F2_7622.jpg | Describe the main subject of this image. | Dilated lymphatics with multifocal areas resembling early KS (H&E stain, magnification ×100). |
PMC1634748_F3_7621.jpg | What is being portrayed in this visual content? | KS in-situ area at higher magnification comprised of small vessels and adjacent spindled cells arising from dilated lymphatics (H&E stain, magnification ×400). |
PMC1634748_F4_7623.jpg | What is the dominant medical problem in this image? | HHV8 positive cells lining dilated lymphatics and focal spindle-shaped cells (LNA-1 immunohistochemical stain; magnification ×400). |
PMC1634861_F1_7626.jpg | What is the main focus of this visual representation? | The CT scan showed the irregular hypodense lesion with fat stranding nearby the cecum without obvious enlarged lymph nodes. |
PMC1634861_F2_7625.jpg | What stands out most in this visual? | A heterogenous hypodense lesion with adjacent fat stranding in the right inguinal canal was noted on the CT scan. |
PMC1634861_F3_7624.jpg | What stands out most in this visual? | No oral contrast media leaking from the cecum into the peritoneal cavity was noted on the CT scan. |
PMC1635062_F1_7628.jpg | What stands out most in this visual? | The method of thoracic ratios. Chest radiograph to show the method of measurement of calculation of thoracic ratios (TRs). H represents the distance from the upper end-plate of the T1 vertebral body and the lower end plate of T12 vertebral body. DR (DL) represents the distance from the midpoint of the distal end-plate of each vertebra body (T1–12) to the outline of the lateral border of the right (left) thoracic cage. These distances are standardised by dividing by the measured T1 – T12 distance (H). They are termed segmental right and left thoracic ratios TRs. Ratios are also calculated segmentally for the total width of the chest (right plus left measured lengths), [12]. |
PMC1635062_F1_7630.jpg | What's the most prominent thing you notice in this picture? | The method of thoracic ratios. Chest radiograph to show the method of measurement of calculation of thoracic ratios (TRs). H represents the distance from the upper end-plate of the T1 vertebral body and the lower end plate of T12 vertebral body. DR (DL) represents the distance from the midpoint of the distal end-plate of each vertebra body (T1–12) to the outline of the lateral border of the right (left) thoracic cage. These distances are standardised by dividing by the measured T1 – T12 distance (H). They are termed segmental right and left thoracic ratios TRs. Ratios are also calculated segmentally for the total width of the chest (right plus left measured lengths), [12]. |
PMC1635062_F1_7629.jpg | What key item or scene is captured in this photo? | The method of thoracic ratios. Chest radiograph to show the method of measurement of calculation of thoracic ratios (TRs). H represents the distance from the upper end-plate of the T1 vertebral body and the lower end plate of T12 vertebral body. DR (DL) represents the distance from the midpoint of the distal end-plate of each vertebra body (T1–12) to the outline of the lateral border of the right (left) thoracic cage. These distances are standardised by dividing by the measured T1 – T12 distance (H). They are termed segmental right and left thoracic ratios TRs. Ratios are also calculated segmentally for the total width of the chest (right plus left measured lengths), [12]. |
PMC1635062_F1_7627.jpg | What is shown in this image? | The method of thoracic ratios. Chest radiograph to show the method of measurement of calculation of thoracic ratios (TRs). H represents the distance from the upper end-plate of the T1 vertebral body and the lower end plate of T12 vertebral body. DR (DL) represents the distance from the midpoint of the distal end-plate of each vertebra body (T1–12) to the outline of the lateral border of the right (left) thoracic cage. These distances are standardised by dividing by the measured T1 – T12 distance (H). They are termed segmental right and left thoracic ratios TRs. Ratios are also calculated segmentally for the total width of the chest (right plus left measured lengths), [12]. |
PMC1635062_F3_7631.jpg | Can you identify the primary element in this image? | Chest radiograph of a normal girl aged 18 months, showing the difference of the shape of the thorax compared with scoliotic one (see figure 2). |
PMC1635417_F1_7632.jpg | What is the central feature of this picture? | The initial CT scan demonstrates a mass in the right iliac fossa (arrow) and a suspected metasasis in segment IV of the liver. |
PMC1635417_F1_7633.jpg | What is the core subject represented in this visual? | The initial CT scan demonstrates a mass in the right iliac fossa (arrow) and a suspected metasasis in segment IV of the liver. |
PMC1635535_pgen-0020169-g003_7636.jpg | Can you identify the primary element in this image? |
Tol2-Mediated, Long-term Expression and Gene Correction of Murine Model of Tyrosinemia Type 1(A) Schematic diagram of Tol2 transposons used for injections of FAH-deficient mice. The full-length (pTol2/FAHIL) and minimal (pminiTol2/FAHIL) versions of the transposon provide expression of both FAH and luciferase as products of a single message; pCMV-GFP served as a co-delivered control plasmid while pCMV-Tol2 provided a source of transposase protein. PmCAGGS [51], minimal chimeric CMV enhancer/chicken beta-actin fusion promoter; pAβG, rabbit beta-globin poly(A); ff-LUC, firefly luciferase; FAH, mouse fumarylacetoactate hydrolase cDNA; IRES, encephalomyocarditis virus internal ribosome entry site. Then 10 mg of pTol2/FAHIL or pminiTol2/FAHIL transposon DNA plus pCMV-GFP or -Tol2 (10 mg each) was administered by rapid, high-volume tail vein injection into sedated FAH-deficient mice (n = 3 to 5 per group).(B) The mean percentage body weight for animals in each treatment group, to determine the progression of liver disease. An asterisk (*) indicates the time when NTBC was readministered in drinking water to prevent mortality of mice that did not receive Tol2 transposase.(C) In vivo luciferase activity levels, assayed at indicated time points by whole body imaging and recorded as photons emitted per second as described in Materials and MethodsMaterials and Methods. The time courses of changes in body weight or in vivo luciferase enzyme activity are shown for groups of animals co-infused with pTol2/FAHIL and GFP (squares) or Tol2 transposase (circles), or with pminiTol2/FAHIL plus GFP (triangles) or Tol2 transposase (plus sign). The mean percentage luciferase activity at any given time point is relative to that observed at 24 h for pminiTol2/FAHIL, which demonstrated the highest transient level of luciferase activity. The 8-wk measurement of no-transposase control animals is shaded because they required administration of NTBC for survival at 7 wk.(D) Images of mice infused with pminiTol2/FAHIL plus pCMV-Tol2 at indicated times (in days; upper left box), showing tissue regeneration as seen by increasing intensity of luciferase enzyme activity detected at a location corresponding to the liver. In vivo luciferase activity levels are reported at the bottom of each image (lower left box) as photons emitted per second (×106). |
PMC1635535_pgen-0020169-g003_7635.jpg | What is shown in this image? |
Tol2-Mediated, Long-term Expression and Gene Correction of Murine Model of Tyrosinemia Type 1(A) Schematic diagram of Tol2 transposons used for injections of FAH-deficient mice. The full-length (pTol2/FAHIL) and minimal (pminiTol2/FAHIL) versions of the transposon provide expression of both FAH and luciferase as products of a single message; pCMV-GFP served as a co-delivered control plasmid while pCMV-Tol2 provided a source of transposase protein. PmCAGGS [51], minimal chimeric CMV enhancer/chicken beta-actin fusion promoter; pAβG, rabbit beta-globin poly(A); ff-LUC, firefly luciferase; FAH, mouse fumarylacetoactate hydrolase cDNA; IRES, encephalomyocarditis virus internal ribosome entry site. Then 10 mg of pTol2/FAHIL or pminiTol2/FAHIL transposon DNA plus pCMV-GFP or -Tol2 (10 mg each) was administered by rapid, high-volume tail vein injection into sedated FAH-deficient mice (n = 3 to 5 per group).(B) The mean percentage body weight for animals in each treatment group, to determine the progression of liver disease. An asterisk (*) indicates the time when NTBC was readministered in drinking water to prevent mortality of mice that did not receive Tol2 transposase.(C) In vivo luciferase activity levels, assayed at indicated time points by whole body imaging and recorded as photons emitted per second as described in Materials and MethodsMaterials and Methods. The time courses of changes in body weight or in vivo luciferase enzyme activity are shown for groups of animals co-infused with pTol2/FAHIL and GFP (squares) or Tol2 transposase (circles), or with pminiTol2/FAHIL plus GFP (triangles) or Tol2 transposase (plus sign). The mean percentage luciferase activity at any given time point is relative to that observed at 24 h for pminiTol2/FAHIL, which demonstrated the highest transient level of luciferase activity. The 8-wk measurement of no-transposase control animals is shaded because they required administration of NTBC for survival at 7 wk.(D) Images of mice infused with pminiTol2/FAHIL plus pCMV-Tol2 at indicated times (in days; upper left box), showing tissue regeneration as seen by increasing intensity of luciferase enzyme activity detected at a location corresponding to the liver. In vivo luciferase activity levels are reported at the bottom of each image (lower left box) as photons emitted per second (×106). |
PMC1635557_F6_7641.jpg | What does this image primarily show? | Nuclear envelope targeting of NETs up-regulated in C2C12 differentiation. V5 epitope tagged NETs, LAP2β and calnexin (Cnx) were transiently transfected into C2C12 cells. Cell were left untreated (- T) or extracted with 1% Triton X-100 (+ T) before fixation and immunofluorescence staining. Shown are representative images from (A) undifferentiated C2C12 cells, (B) differentiated C2C12 cells. All epitope-tagged calnexin was removed by Triton X-100 pre-extraction (not shown). Scale bar: 20 μm. |
PMC1635557_F6_7640.jpg | Can you identify the primary element in this image? | Nuclear envelope targeting of NETs up-regulated in C2C12 differentiation. V5 epitope tagged NETs, LAP2β and calnexin (Cnx) were transiently transfected into C2C12 cells. Cell were left untreated (- T) or extracted with 1% Triton X-100 (+ T) before fixation and immunofluorescence staining. Shown are representative images from (A) undifferentiated C2C12 cells, (B) differentiated C2C12 cells. All epitope-tagged calnexin was removed by Triton X-100 pre-extraction (not shown). Scale bar: 20 μm. |
PMC1635557_F6_7642.jpg | What is the focal point of this photograph? | Nuclear envelope targeting of NETs up-regulated in C2C12 differentiation. V5 epitope tagged NETs, LAP2β and calnexin (Cnx) were transiently transfected into C2C12 cells. Cell were left untreated (- T) or extracted with 1% Triton X-100 (+ T) before fixation and immunofluorescence staining. Shown are representative images from (A) undifferentiated C2C12 cells, (B) differentiated C2C12 cells. All epitope-tagged calnexin was removed by Triton X-100 pre-extraction (not shown). Scale bar: 20 μm. |
PMC1635557_F6_7639.jpg | What is the dominant medical problem in this image? | Nuclear envelope targeting of NETs up-regulated in C2C12 differentiation. V5 epitope tagged NETs, LAP2β and calnexin (Cnx) were transiently transfected into C2C12 cells. Cell were left untreated (- T) or extracted with 1% Triton X-100 (+ T) before fixation and immunofluorescence staining. Shown are representative images from (A) undifferentiated C2C12 cells, (B) differentiated C2C12 cells. All epitope-tagged calnexin was removed by Triton X-100 pre-extraction (not shown). Scale bar: 20 μm. |
PMC1635561_F5_7644.jpg | What is the main focus of this visual representation? | Two-color fluorescence detection of actin (red) and PRRSV antigen (green) in MARC-145 cells. A. Uninfected control, 20 μm; B.18 h p.i. with PRRSV, 20 μm; C. Control at 42 h p.i. with PRRSV, 50 μm; D. Drug vehicle control at 42 h p.i. with PRRSV, 50 μm. E. Colchicine-treated, 5 μM, 42 h p.i. (arrow indicates PRRSV-positive doublet; see Figure 6, A, C and D for higher magnification), 50 μm; F. AK-2 treated, 250 μm; (Length of scale bar is indicated for each panel) |
PMC1635561_F5_7646.jpg | What is shown in this image? | Two-color fluorescence detection of actin (red) and PRRSV antigen (green) in MARC-145 cells. A. Uninfected control, 20 μm; B.18 h p.i. with PRRSV, 20 μm; C. Control at 42 h p.i. with PRRSV, 50 μm; D. Drug vehicle control at 42 h p.i. with PRRSV, 50 μm. E. Colchicine-treated, 5 μM, 42 h p.i. (arrow indicates PRRSV-positive doublet; see Figure 6, A, C and D for higher magnification), 50 μm; F. AK-2 treated, 250 μm; (Length of scale bar is indicated for each panel) |
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