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PMC1239918_F2_3304.jpg | Describe the main subject of this image. | P75NTR expression in the lesioned olfactory bulb: Olfactory bulb sections from sham and NMDA lesioned animals that were either estrogen or control-pellet replaced were probed for p75NTR expression and counter-stained with a nuclear dye (DAPI). A low magnification photomontage of olfactory bulb illuminated for DAPI is shown in (a). P75NTR is normally expressed in the glomerular layer of the olfactory bulb (b), photographed from the region indicated by the solid line box in (a). P75NTR is poorly expressed in other regions of the olfactory bulb, an example of which is shown in (c), taken from the region indicated by the wire frame in (a). However, in a comparable region of the NMDA-lesioned animals, diffuse p75NTR staining is seen in cells and fibers at the injury site (d). In estrogen-treated, lesioned animals p75NTR immunoreactivity is seen in cells associated with the walls of microvessels (e; g), identified by their curved nuclei (f; h) surrounding a lumen. Arrows indicate the same cells photgraphed under fluorescein (p75NTR; e,g) or UV illumination (DAPI nuclear dye; f,h). A double-labeled cell photographed under both fluoresein and UV is shown in (i). P75NTR labeling was not seen in microvessel walls in lesioned animals that received a control pellet (j) or in sections from estrogen-replaced lesioned animals that were incubated without a primary antibody (immunohistochemical control, l). Corresponding nuclear dye images are in k and m. Magnification bar: b-d = 160 μm; e-m = 25 μm. |
PMC1239923_F3_3314.jpg | What can you see in this picture? | CT-guided FNA of anterior peritoneal mass, showing a somewhat cohesive large cluster of highly pleomorphic cells (Diff-Quik, ×200). |
PMC1239923_F3_3315.jpg | What key item or scene is captured in this photo? | CT-guided FNA of anterior peritoneal mass, showing a somewhat cohesive large cluster of highly pleomorphic cells (Diff-Quik, ×200). |
PMC1242133_F2_3317.jpg | What is the central feature of this picture? | BRC-230 cells after Dox (0.1 μg/ml)→Pacl (0.1 μg/ml)→48-h washout→5-FU (1 μg/ml) treatment. Apoptotic nuclei stained with DAPI show intense fluorescence corresponding to chromatin condensation (arrow heads) and fragmentation (arrows). |
PMC1242133_F2_3316.jpg | What is the principal component of this image? | BRC-230 cells after Dox (0.1 μg/ml)→Pacl (0.1 μg/ml)→48-h washout→5-FU (1 μg/ml) treatment. Apoptotic nuclei stained with DAPI show intense fluorescence corresponding to chromatin condensation (arrow heads) and fragmentation (arrows). |
PMC1242212_F6_3320.jpg | What is the principal component of this image? | Δydr065w mutants are defective for vacuolar acidification. Wild-type (BY4743) and BY4743 Δydr065w cells were harvested in exponential phase, incubated with LysoSensor Green DND-189, and then examined by differential interference contrast (DIC) (left panel) and fluorescence (right panel) microscopy. Failure to accumulate the fluorophore indicates defective vacuolar acidification. Intact vacuoles in the mutant cells are apparent in the DIC image. |
PMC1242212_F6_3318.jpg | What is shown in this image? | Δydr065w mutants are defective for vacuolar acidification. Wild-type (BY4743) and BY4743 Δydr065w cells were harvested in exponential phase, incubated with LysoSensor Green DND-189, and then examined by differential interference contrast (DIC) (left panel) and fluorescence (right panel) microscopy. Failure to accumulate the fluorophore indicates defective vacuolar acidification. Intact vacuoles in the mutant cells are apparent in the DIC image. |
PMC1242212_F6_3319.jpg | What is the central feature of this picture? | Δydr065w mutants are defective for vacuolar acidification. Wild-type (BY4743) and BY4743 Δydr065w cells were harvested in exponential phase, incubated with LysoSensor Green DND-189, and then examined by differential interference contrast (DIC) (left panel) and fluorescence (right panel) microscopy. Failure to accumulate the fluorophore indicates defective vacuolar acidification. Intact vacuoles in the mutant cells are apparent in the DIC image. |
PMC1242212_F6_3321.jpg | What object or scene is depicted here? | Δydr065w mutants are defective for vacuolar acidification. Wild-type (BY4743) and BY4743 Δydr065w cells were harvested in exponential phase, incubated with LysoSensor Green DND-189, and then examined by differential interference contrast (DIC) (left panel) and fluorescence (right panel) microscopy. Failure to accumulate the fluorophore indicates defective vacuolar acidification. Intact vacuoles in the mutant cells are apparent in the DIC image. |
PMC1242218_F1_3323.jpg | What is the dominant medical problem in this image? | MRI scan showing the intramedullary lesion at conus medullaris. The lesion is hyperintense on T1WI and isointense on T2WI. |
PMC1242218_F1_3322.jpg | What's the most prominent thing you notice in this picture? | MRI scan showing the intramedullary lesion at conus medullaris. The lesion is hyperintense on T1WI and isointense on T2WI. |
PMC1242220_F3_3324.jpg | What can you see in this picture? | Clinical photograph of the hard palate lesion after biopsy. |
PMC1242259_F1_3326.jpg | What can you see in this picture? | Enhanced abdominal CT scan of upper abdomen showing a 6 cm sized mass in the right lower quadrant of the abdomen at the first operation. The mass contained air bubbles, tiny calcifications and hematoma. |
PMC1242259_F4_3328.jpg | What is the core subject represented in this visual? | Microscopic findings of the angiosarcoma in the small intestine. 4a) Atypical spindle or epithelioid tumor cells were arranged in sheets, and rudimentary lumen formation was rarely noted. (H&E, × 200) 4b) The tumor cells are strongly positive for anti-CD31. (PAP, × 100) |
PMC1242259_F4_3327.jpg | What is the main focus of this visual representation? | Microscopic findings of the angiosarcoma in the small intestine. 4a) Atypical spindle or epithelioid tumor cells were arranged in sheets, and rudimentary lumen formation was rarely noted. (H&E, × 200) 4b) The tumor cells are strongly positive for anti-CD31. (PAP, × 100) |
PMC1243239_F2_3332.jpg | What does this image primarily show? | Immunohistochemical detection of ZIP1 transporter protein in malignant and nonmalignant loci of a representative prostate cancer tissue section. (A) BPH, magnification is 1000×, bar = 10 μm. (B) Normal, magnification is 400×, bar = 25 μm. (C) PIN, magnification is 400×, bars = 25 μm. (D) Adenocarcinoma, magnification 400×, bar = 10 μm Note the immuno-positivity of the plasma membrane of BPH and normal glands. The malignant and PIN loci show no detectable ZIP1 so that the plasma membrane of these cells is not visible. |
PMC1243239_F2_3329.jpg | What can you see in this picture? | Immunohistochemical detection of ZIP1 transporter protein in malignant and nonmalignant loci of a representative prostate cancer tissue section. (A) BPH, magnification is 1000×, bar = 10 μm. (B) Normal, magnification is 400×, bar = 25 μm. (C) PIN, magnification is 400×, bars = 25 μm. (D) Adenocarcinoma, magnification 400×, bar = 10 μm Note the immuno-positivity of the plasma membrane of BPH and normal glands. The malignant and PIN loci show no detectable ZIP1 so that the plasma membrane of these cells is not visible. |
PMC1243239_F2_3331.jpg | Describe the main subject of this image. | Immunohistochemical detection of ZIP1 transporter protein in malignant and nonmalignant loci of a representative prostate cancer tissue section. (A) BPH, magnification is 1000×, bar = 10 μm. (B) Normal, magnification is 400×, bar = 25 μm. (C) PIN, magnification is 400×, bars = 25 μm. (D) Adenocarcinoma, magnification 400×, bar = 10 μm Note the immuno-positivity of the plasma membrane of BPH and normal glands. The malignant and PIN loci show no detectable ZIP1 so that the plasma membrane of these cells is not visible. |
PMC1243239_F2_3330.jpg | What object or scene is depicted here? | Immunohistochemical detection of ZIP1 transporter protein in malignant and nonmalignant loci of a representative prostate cancer tissue section. (A) BPH, magnification is 1000×, bar = 10 μm. (B) Normal, magnification is 400×, bar = 25 μm. (C) PIN, magnification is 400×, bars = 25 μm. (D) Adenocarcinoma, magnification 400×, bar = 10 μm Note the immuno-positivity of the plasma membrane of BPH and normal glands. The malignant and PIN loci show no detectable ZIP1 so that the plasma membrane of these cells is not visible. |
PMC1243240_F2_3337.jpg | Describe the main subject of this image. | Immunoreactivity of TLR2, TLR3 and TLR4 in nasal mucosa. Immunohistochemical localization of TLR2, TLR3 and TLR4 in biopsies of nasal mucosa. Representative pictures of control (A) and TLR-stained (B-F) sections. No immunoreactivity was observed in control sections when the primary antibody was omitted (A). In an adjacent section, immunoreactivity for TLR3 is seen in the apical part of the epithelial lining and in a few scattered intraepithelial leukocytes (B). Pictures C and D illustrate representative staining patterns of TLR2 and TLR4, respectively. Areas with a thin repairing epithelium display a particularly intense staining, TLR3 (E) and TLR4 (F). Scale bars: A, B and D = 85 μm, C = 30 μm, E and F= 50 μm. |
PMC1243240_F2_3333.jpg | What is the central feature of this picture? | Immunoreactivity of TLR2, TLR3 and TLR4 in nasal mucosa. Immunohistochemical localization of TLR2, TLR3 and TLR4 in biopsies of nasal mucosa. Representative pictures of control (A) and TLR-stained (B-F) sections. No immunoreactivity was observed in control sections when the primary antibody was omitted (A). In an adjacent section, immunoreactivity for TLR3 is seen in the apical part of the epithelial lining and in a few scattered intraepithelial leukocytes (B). Pictures C and D illustrate representative staining patterns of TLR2 and TLR4, respectively. Areas with a thin repairing epithelium display a particularly intense staining, TLR3 (E) and TLR4 (F). Scale bars: A, B and D = 85 μm, C = 30 μm, E and F= 50 μm. |
PMC1243240_F2_3338.jpg | What is the focal point of this photograph? | Immunoreactivity of TLR2, TLR3 and TLR4 in nasal mucosa. Immunohistochemical localization of TLR2, TLR3 and TLR4 in biopsies of nasal mucosa. Representative pictures of control (A) and TLR-stained (B-F) sections. No immunoreactivity was observed in control sections when the primary antibody was omitted (A). In an adjacent section, immunoreactivity for TLR3 is seen in the apical part of the epithelial lining and in a few scattered intraepithelial leukocytes (B). Pictures C and D illustrate representative staining patterns of TLR2 and TLR4, respectively. Areas with a thin repairing epithelium display a particularly intense staining, TLR3 (E) and TLR4 (F). Scale bars: A, B and D = 85 μm, C = 30 μm, E and F= 50 μm. |
PMC1243240_F2_3336.jpg | What can you see in this picture? | Immunoreactivity of TLR2, TLR3 and TLR4 in nasal mucosa. Immunohistochemical localization of TLR2, TLR3 and TLR4 in biopsies of nasal mucosa. Representative pictures of control (A) and TLR-stained (B-F) sections. No immunoreactivity was observed in control sections when the primary antibody was omitted (A). In an adjacent section, immunoreactivity for TLR3 is seen in the apical part of the epithelial lining and in a few scattered intraepithelial leukocytes (B). Pictures C and D illustrate representative staining patterns of TLR2 and TLR4, respectively. Areas with a thin repairing epithelium display a particularly intense staining, TLR3 (E) and TLR4 (F). Scale bars: A, B and D = 85 μm, C = 30 μm, E and F= 50 μm. |
PMC1243240_F2_3334.jpg | What does this image primarily show? | Immunoreactivity of TLR2, TLR3 and TLR4 in nasal mucosa. Immunohistochemical localization of TLR2, TLR3 and TLR4 in biopsies of nasal mucosa. Representative pictures of control (A) and TLR-stained (B-F) sections. No immunoreactivity was observed in control sections when the primary antibody was omitted (A). In an adjacent section, immunoreactivity for TLR3 is seen in the apical part of the epithelial lining and in a few scattered intraepithelial leukocytes (B). Pictures C and D illustrate representative staining patterns of TLR2 and TLR4, respectively. Areas with a thin repairing epithelium display a particularly intense staining, TLR3 (E) and TLR4 (F). Scale bars: A, B and D = 85 μm, C = 30 μm, E and F= 50 μm. |
PMC1243240_F2_3335.jpg | What can you see in this picture? | Immunoreactivity of TLR2, TLR3 and TLR4 in nasal mucosa. Immunohistochemical localization of TLR2, TLR3 and TLR4 in biopsies of nasal mucosa. Representative pictures of control (A) and TLR-stained (B-F) sections. No immunoreactivity was observed in control sections when the primary antibody was omitted (A). In an adjacent section, immunoreactivity for TLR3 is seen in the apical part of the epithelial lining and in a few scattered intraepithelial leukocytes (B). Pictures C and D illustrate representative staining patterns of TLR2 and TLR4, respectively. Areas with a thin repairing epithelium display a particularly intense staining, TLR3 (E) and TLR4 (F). Scale bars: A, B and D = 85 μm, C = 30 μm, E and F= 50 μm. |
PMC1247535_f6-ehp0112-a00740_3339.jpg | What's the most prominent thing you notice in this picture? | Probing insights. Nanoprobes studded with molecules that bind ions such as zinc, calcium, and potassium are injected into cells to reveal the patterns of ion exchange that make cells function. Computer models are used to interpret the fluorescent signatures probes emit when they capture a target ion. |
PMC1247622_f4-ehp0112-001564_3341.jpg | What can you see in this picture? | Intracellular phagocytized particles in a Giemsa-stained cytospin preparation from the IS sample of an FDNY-FF exposed to WTC dust. (A) Image showing a single macrophage with intracellular particles and two adjacent lymphocytes. (B) Image showing a mixed cell population with macrophages and intracellular particles. Light microscopy; magnification, ×100. |
PMC1247622_f4-ehp0112-001564_3340.jpg | What is the focal point of this photograph? | Intracellular phagocytized particles in a Giemsa-stained cytospin preparation from the IS sample of an FDNY-FF exposed to WTC dust. (A) Image showing a single macrophage with intracellular particles and two adjacent lymphocytes. (B) Image showing a mixed cell population with macrophages and intracellular particles. Light microscopy; magnification, ×100. |
PMC1249560_F3_3349.jpg | What is the principal component of this image? | Immunoelectron micrographs demonstrating co-localization of GFP-HPS3 and clathrin. Double-labeling of anti-GFP (10-nm gold) and anti-clathrin (20-nm gold) [A, B], or the reverse labeled anti-clathrin (10-nm gold) and anti-GFP (15-nm gold) [C, D, E] in normal melanocytes electroporated with GFP-HPS3. Co-localization of the two labels was shown on small (50–100 nm) clathrin-containing vesicles (arrowheads) in the Golgi region [A and C]. Co-localization was observed on small clathrin-labeled vesicles (arrowheads) but not on neighboring large endosomal structures [B and D]. High magnification of a small clathrin containing vesicle labeled with GFP-HPS3 [E]. CM = Cell Membrane, G = Golgi area, E = Endosomal structure. Bar = 100 nm |
PMC1249560_F3_3346.jpg | Can you identify the primary element in this image? | Immunoelectron micrographs demonstrating co-localization of GFP-HPS3 and clathrin. Double-labeling of anti-GFP (10-nm gold) and anti-clathrin (20-nm gold) [A, B], or the reverse labeled anti-clathrin (10-nm gold) and anti-GFP (15-nm gold) [C, D, E] in normal melanocytes electroporated with GFP-HPS3. Co-localization of the two labels was shown on small (50–100 nm) clathrin-containing vesicles (arrowheads) in the Golgi region [A and C]. Co-localization was observed on small clathrin-labeled vesicles (arrowheads) but not on neighboring large endosomal structures [B and D]. High magnification of a small clathrin containing vesicle labeled with GFP-HPS3 [E]. CM = Cell Membrane, G = Golgi area, E = Endosomal structure. Bar = 100 nm |
PMC1249560_F3_3347.jpg | Can you identify the primary element in this image? | Immunoelectron micrographs demonstrating co-localization of GFP-HPS3 and clathrin. Double-labeling of anti-GFP (10-nm gold) and anti-clathrin (20-nm gold) [A, B], or the reverse labeled anti-clathrin (10-nm gold) and anti-GFP (15-nm gold) [C, D, E] in normal melanocytes electroporated with GFP-HPS3. Co-localization of the two labels was shown on small (50–100 nm) clathrin-containing vesicles (arrowheads) in the Golgi region [A and C]. Co-localization was observed on small clathrin-labeled vesicles (arrowheads) but not on neighboring large endosomal structures [B and D]. High magnification of a small clathrin containing vesicle labeled with GFP-HPS3 [E]. CM = Cell Membrane, G = Golgi area, E = Endosomal structure. Bar = 100 nm |
PMC1249560_F3_3348.jpg | What's the most prominent thing you notice in this picture? | Immunoelectron micrographs demonstrating co-localization of GFP-HPS3 and clathrin. Double-labeling of anti-GFP (10-nm gold) and anti-clathrin (20-nm gold) [A, B], or the reverse labeled anti-clathrin (10-nm gold) and anti-GFP (15-nm gold) [C, D, E] in normal melanocytes electroporated with GFP-HPS3. Co-localization of the two labels was shown on small (50–100 nm) clathrin-containing vesicles (arrowheads) in the Golgi region [A and C]. Co-localization was observed on small clathrin-labeled vesicles (arrowheads) but not on neighboring large endosomal structures [B and D]. High magnification of a small clathrin containing vesicle labeled with GFP-HPS3 [E]. CM = Cell Membrane, G = Golgi area, E = Endosomal structure. Bar = 100 nm |
PMC1249560_F3_3350.jpg | What is the central feature of this picture? | Immunoelectron micrographs demonstrating co-localization of GFP-HPS3 and clathrin. Double-labeling of anti-GFP (10-nm gold) and anti-clathrin (20-nm gold) [A, B], or the reverse labeled anti-clathrin (10-nm gold) and anti-GFP (15-nm gold) [C, D, E] in normal melanocytes electroporated with GFP-HPS3. Co-localization of the two labels was shown on small (50–100 nm) clathrin-containing vesicles (arrowheads) in the Golgi region [A and C]. Co-localization was observed on small clathrin-labeled vesicles (arrowheads) but not on neighboring large endosomal structures [B and D]. High magnification of a small clathrin containing vesicle labeled with GFP-HPS3 [E]. CM = Cell Membrane, G = Golgi area, E = Endosomal structure. Bar = 100 nm |
PMC1249560_F4_3343.jpg | What can you see in this picture? | Immunoelectron micrographs demonstrating no co-localization of GFP-HPS3-delCBD and clathrin.
Double-labeling of anti-clathrin (10-nm gold) and anti-GFP (15-nm gold) in normal melanocytes electroporated with GFP-HPS3-delCBD [A-D]. GFP-HPS3-delCBD (arrowheads) was largely cytoplasmic and distributed throughout the entire cell, from the perinuclear/Golgi region [A,B,D] to the tips [C]. No co-localization of the two labels (GFP-HPS3-delCBD and clathrin) was observed. N=Nucleus, G=Golgi, E=Endosomal structure, M=Melanosome. Bar = 500 nm |
PMC1249560_F4_3342.jpg | What stands out most in this visual? | Immunoelectron micrographs demonstrating no co-localization of GFP-HPS3-delCBD and clathrin.
Double-labeling of anti-clathrin (10-nm gold) and anti-GFP (15-nm gold) in normal melanocytes electroporated with GFP-HPS3-delCBD [A-D]. GFP-HPS3-delCBD (arrowheads) was largely cytoplasmic and distributed throughout the entire cell, from the perinuclear/Golgi region [A,B,D] to the tips [C]. No co-localization of the two labels (GFP-HPS3-delCBD and clathrin) was observed. N=Nucleus, G=Golgi, E=Endosomal structure, M=Melanosome. Bar = 500 nm |
PMC1249560_F4_3345.jpg | What is the principal component of this image? | Immunoelectron micrographs demonstrating no co-localization of GFP-HPS3-delCBD and clathrin.
Double-labeling of anti-clathrin (10-nm gold) and anti-GFP (15-nm gold) in normal melanocytes electroporated with GFP-HPS3-delCBD [A-D]. GFP-HPS3-delCBD (arrowheads) was largely cytoplasmic and distributed throughout the entire cell, from the perinuclear/Golgi region [A,B,D] to the tips [C]. No co-localization of the two labels (GFP-HPS3-delCBD and clathrin) was observed. N=Nucleus, G=Golgi, E=Endosomal structure, M=Melanosome. Bar = 500 nm |
PMC1249575_F6_3352.jpg | What is the principal component of this image? | Antigen trapping and long-term retention. FDC-like cells (a, c) or macrophages (b, d), were pulsed for 30 min with HRPO/human IgG complexes. a, b, Cells were fixed after 4 days and double stained by a standard HRPO substrate reaction (brown) and for CD35 (red). a, In FDC-like cells antigen was present in its enzymatic active form, and CD35 was expressed. b, In macrophages only traces of antigen was detectable and CD35 is weakly positive. c, d, Cells were cultured for 16 days. In FDC-like cells (c) enzyme activity is still detectable, whereas in macrophages enzyme activity is absent. |
PMC1249575_F6_3351.jpg | What is the main focus of this visual representation? | Antigen trapping and long-term retention. FDC-like cells (a, c) or macrophages (b, d), were pulsed for 30 min with HRPO/human IgG complexes. a, b, Cells were fixed after 4 days and double stained by a standard HRPO substrate reaction (brown) and for CD35 (red). a, In FDC-like cells antigen was present in its enzymatic active form, and CD35 was expressed. b, In macrophages only traces of antigen was detectable and CD35 is weakly positive. c, d, Cells were cultured for 16 days. In FDC-like cells (c) enzyme activity is still detectable, whereas in macrophages enzyme activity is absent. |
PMC1249575_F6_3353.jpg | What key item or scene is captured in this photo? | Antigen trapping and long-term retention. FDC-like cells (a, c) or macrophages (b, d), were pulsed for 30 min with HRPO/human IgG complexes. a, b, Cells were fixed after 4 days and double stained by a standard HRPO substrate reaction (brown) and for CD35 (red). a, In FDC-like cells antigen was present in its enzymatic active form, and CD35 was expressed. b, In macrophages only traces of antigen was detectable and CD35 is weakly positive. c, d, Cells were cultured for 16 days. In FDC-like cells (c) enzyme activity is still detectable, whereas in macrophages enzyme activity is absent. |
PMC1249577_F1_3356.jpg | What is being portrayed in this visual content? | Routine MRI showing the extent of the lesion in the left hemisphere on an axial view, at (A) 3 months of age with T2-weighted image, (B) 12 months of age with an inversion recovery T1-weighted image, and (C) 20 months of age with a T1-weighted gradient-echo image. |
PMC1249577_F1_3354.jpg | What does this image primarily show? | Routine MRI showing the extent of the lesion in the left hemisphere on an axial view, at (A) 3 months of age with T2-weighted image, (B) 12 months of age with an inversion recovery T1-weighted image, and (C) 20 months of age with a T1-weighted gradient-echo image. |
PMC1249577_F3_3357.jpg | What's the most prominent thing you notice in this picture? | (A) fMRI statistically significant areas of activation (at p < 0.001, uncorrected) were projected on axial slices of the anatomical volume of the infant. Positive activation is shown in red colors and negative activation is shown with blue colors. The strongest activation is negative, in the occipital lobe. Note the activation in the left (injured) visual hemisphere. (B) The shape of the event-related hemodynamic response of the left visual cortex activation. (C) Correspondence between the DTI tracts and the fMRI activation in the left hemisphere is illustrated on three views. The functional activation is indicated with a white cluster superimposed on the anatomical volume of the infant. The optic radiation is shown with green color and the inter-hemispheric connections with pink color. |
PMC1249577_F3_3363.jpg | Can you identify the primary element in this image? | (A) fMRI statistically significant areas of activation (at p < 0.001, uncorrected) were projected on axial slices of the anatomical volume of the infant. Positive activation is shown in red colors and negative activation is shown with blue colors. The strongest activation is negative, in the occipital lobe. Note the activation in the left (injured) visual hemisphere. (B) The shape of the event-related hemodynamic response of the left visual cortex activation. (C) Correspondence between the DTI tracts and the fMRI activation in the left hemisphere is illustrated on three views. The functional activation is indicated with a white cluster superimposed on the anatomical volume of the infant. The optic radiation is shown with green color and the inter-hemispheric connections with pink color. |
PMC1249577_F3_3362.jpg | What is the focal point of this photograph? | (A) fMRI statistically significant areas of activation (at p < 0.001, uncorrected) were projected on axial slices of the anatomical volume of the infant. Positive activation is shown in red colors and negative activation is shown with blue colors. The strongest activation is negative, in the occipital lobe. Note the activation in the left (injured) visual hemisphere. (B) The shape of the event-related hemodynamic response of the left visual cortex activation. (C) Correspondence between the DTI tracts and the fMRI activation in the left hemisphere is illustrated on three views. The functional activation is indicated with a white cluster superimposed on the anatomical volume of the infant. The optic radiation is shown with green color and the inter-hemispheric connections with pink color. |
PMC1249577_F3_3359.jpg | What can you see in this picture? | (A) fMRI statistically significant areas of activation (at p < 0.001, uncorrected) were projected on axial slices of the anatomical volume of the infant. Positive activation is shown in red colors and negative activation is shown with blue colors. The strongest activation is negative, in the occipital lobe. Note the activation in the left (injured) visual hemisphere. (B) The shape of the event-related hemodynamic response of the left visual cortex activation. (C) Correspondence between the DTI tracts and the fMRI activation in the left hemisphere is illustrated on three views. The functional activation is indicated with a white cluster superimposed on the anatomical volume of the infant. The optic radiation is shown with green color and the inter-hemispheric connections with pink color. |
PMC1253509_F1_3368.jpg | What object or scene is depicted here? | Preoperative CT scan. Preoperative axial CT scan which shows a large hyperdense tumor arising from the petrous portion of the right temporal bone with intracranial extension and impending uncal herniation. |
PMC1253509_F1_3370.jpg | Describe the main subject of this image. | Preoperative CT scan. Preoperative axial CT scan which shows a large hyperdense tumor arising from the petrous portion of the right temporal bone with intracranial extension and impending uncal herniation. |
PMC1253509_F2_3365.jpg | What is being portrayed in this visual content? | Preoperative CT scan. The figure shows the sagittal and coronal reconstruction of the tumor. |
PMC1253509_F2_3366.jpg | What key item or scene is captured in this photo? | Preoperative CT scan. The figure shows the sagittal and coronal reconstruction of the tumor. |
PMC1253515_F1_3375.jpg | What is the central feature of this picture? | Computerized Tomography showing areas of focal decreased enhancement of the anterior lower poles (white arrow) of the right kidney suggesting renal infarction versus pyelonephritis. |
PMC1253525_F1_3376.jpg | What does this image primarily show? | a y b: Papamicolaou; c: biopsy; d: CD45; e: neuron specific enolase; f: vimentin. |
PMC1253525_F1_3377.jpg | What object or scene is depicted here? | a y b: Papamicolaou; c: biopsy; d: CD45; e: neuron specific enolase; f: vimentin. |
PMC1253525_F1_3381.jpg | What stands out most in this visual? | a y b: Papamicolaou; c: biopsy; d: CD45; e: neuron specific enolase; f: vimentin. |
PMC1253525_F1_3379.jpg | What is the main focus of this visual representation? | a y b: Papamicolaou; c: biopsy; d: CD45; e: neuron specific enolase; f: vimentin. |
PMC1253525_F1_3380.jpg | What can you see in this picture? | a y b: Papamicolaou; c: biopsy; d: CD45; e: neuron specific enolase; f: vimentin. |
PMC1253525_F2_3382.jpg | What is being portrayed in this visual content? | a, b, c: Papanicolaou; d: HMB-45; e: skin biopsy; f, g, h: breast tumor. |
PMC1253525_F2_3383.jpg | What's the most prominent thing you notice in this picture? | a, b, c: Papanicolaou; d: HMB-45; e: skin biopsy; f, g, h: breast tumor. |
PMC1253525_F2_3389.jpg | What is the core subject represented in this visual? | a, b, c: Papanicolaou; d: HMB-45; e: skin biopsy; f, g, h: breast tumor. |
PMC1253525_F2_3388.jpg | What stands out most in this visual? | a, b, c: Papanicolaou; d: HMB-45; e: skin biopsy; f, g, h: breast tumor. |
PMC1253525_F2_3385.jpg | What object or scene is depicted here? | a, b, c: Papanicolaou; d: HMB-45; e: skin biopsy; f, g, h: breast tumor. |
PMC1253525_F2_3386.jpg | What key item or scene is captured in this photo? | a, b, c: Papanicolaou; d: HMB-45; e: skin biopsy; f, g, h: breast tumor. |
PMC1253525_F2_3384.jpg | What key item or scene is captured in this photo? | a, b, c: Papanicolaou; d: HMB-45; e: skin biopsy; f, g, h: breast tumor. |
PMC1253535_F9_3390.jpg | What stands out most in this visual? | Transduction of neural stem cells by a HIV-2 based GFP lentiviral vector packaged by SIV-2 Gag-Pol. (A) Phase contrast image through growing neurosphere (upper left). (B) Fluorescent image of neurosphere in A expressing GFP 72 hours post transduction (upper right). (C) Confocal image through neurosphere expressing GFP (lower left) (D) Neurons derived from human neurosphere 7 days post differentiation (lower right). Red represents β tubulin III, green – GFP, Hoechst stain (blue) nuclei. Arrow denotes double labelled cell. Magnification in A and B = 10×, in C = 100×, D = 40× |
PMC1253535_F9_3392.jpg | What is the central feature of this picture? | Transduction of neural stem cells by a HIV-2 based GFP lentiviral vector packaged by SIV-2 Gag-Pol. (A) Phase contrast image through growing neurosphere (upper left). (B) Fluorescent image of neurosphere in A expressing GFP 72 hours post transduction (upper right). (C) Confocal image through neurosphere expressing GFP (lower left) (D) Neurons derived from human neurosphere 7 days post differentiation (lower right). Red represents β tubulin III, green – GFP, Hoechst stain (blue) nuclei. Arrow denotes double labelled cell. Magnification in A and B = 10×, in C = 100×, D = 40× |
PMC1253535_F9_3391.jpg | Can you identify the primary element in this image? | Transduction of neural stem cells by a HIV-2 based GFP lentiviral vector packaged by SIV-2 Gag-Pol. (A) Phase contrast image through growing neurosphere (upper left). (B) Fluorescent image of neurosphere in A expressing GFP 72 hours post transduction (upper right). (C) Confocal image through neurosphere expressing GFP (lower left) (D) Neurons derived from human neurosphere 7 days post differentiation (lower right). Red represents β tubulin III, green – GFP, Hoechst stain (blue) nuclei. Arrow denotes double labelled cell. Magnification in A and B = 10×, in C = 100×, D = 40× |
PMC1253535_F9_3393.jpg | What is the main focus of this visual representation? | Transduction of neural stem cells by a HIV-2 based GFP lentiviral vector packaged by SIV-2 Gag-Pol. (A) Phase contrast image through growing neurosphere (upper left). (B) Fluorescent image of neurosphere in A expressing GFP 72 hours post transduction (upper right). (C) Confocal image through neurosphere expressing GFP (lower left) (D) Neurons derived from human neurosphere 7 days post differentiation (lower right). Red represents β tubulin III, green – GFP, Hoechst stain (blue) nuclei. Arrow denotes double labelled cell. Magnification in A and B = 10×, in C = 100×, D = 40× |
PMC1253663_f3-ehp0112-001704_3397.jpg | What is shown in this image? | Histologic examination of tumors formed in nude mice. Tumors showing a hyperplastic stratified epithelium with prominent parakeratosis formed by injection of A1 cells (A) or A2 cells (B). Tumors with more malignant characteristics formed by injection of cell lines T1 (C) or T4 (D). Bars = 50 μm. |
PMC1253663_f3-ehp0112-001704_3394.jpg | What's the most prominent thing you notice in this picture? | Histologic examination of tumors formed in nude mice. Tumors showing a hyperplastic stratified epithelium with prominent parakeratosis formed by injection of A1 cells (A) or A2 cells (B). Tumors with more malignant characteristics formed by injection of cell lines T1 (C) or T4 (D). Bars = 50 μm. |
PMC1253663_f3-ehp0112-001704_3396.jpg | What is the central feature of this picture? | Histologic examination of tumors formed in nude mice. Tumors showing a hyperplastic stratified epithelium with prominent parakeratosis formed by injection of A1 cells (A) or A2 cells (B). Tumors with more malignant characteristics formed by injection of cell lines T1 (C) or T4 (D). Bars = 50 μm. |
PMC1253679_f9-ehp0112-a00994_3398.jpg | What is being portrayed in this visual content? | Crop casualties. Many Colombian farmers believe their crops, like these bananas, are being ruined by drift from herbicide spraying of illegal poppy and coca crops. Many of the ruined crops were planted at the urging of the government as alternatives to the illegal plants. |
PMC1253714_f4-ehp0113-000083_3401.jpg | What stands out most in this visual? | Immunoreactivity of VCAM-1 antiserum against sections of mouse aortic arches. (A) Olive oil. (B) Olive oil plus PCB. (C) Corn oil. (D) Corn oil plus PCB. See “Materials and Methods” for details. Red staining reflects positive chromogen development for VCAM-1 immunostaining on the endothelial surface (B–D) and in subendothelial tissue (D). Magnification, 400×. |
PMC1253714_f4-ehp0113-000083_3402.jpg | What key item or scene is captured in this photo? | Immunoreactivity of VCAM-1 antiserum against sections of mouse aortic arches. (A) Olive oil. (B) Olive oil plus PCB. (C) Corn oil. (D) Corn oil plus PCB. See “Materials and Methods” for details. Red staining reflects positive chromogen development for VCAM-1 immunostaining on the endothelial surface (B–D) and in subendothelial tissue (D). Magnification, 400×. |
PMC1253714_f4-ehp0113-000083_3400.jpg | What does this image primarily show? | Immunoreactivity of VCAM-1 antiserum against sections of mouse aortic arches. (A) Olive oil. (B) Olive oil plus PCB. (C) Corn oil. (D) Corn oil plus PCB. See “Materials and Methods” for details. Red staining reflects positive chromogen development for VCAM-1 immunostaining on the endothelial surface (B–D) and in subendothelial tissue (D). Magnification, 400×. |
PMC1253714_f4-ehp0113-000083_3399.jpg | What does this image primarily show? | Immunoreactivity of VCAM-1 antiserum against sections of mouse aortic arches. (A) Olive oil. (B) Olive oil plus PCB. (C) Corn oil. (D) Corn oil plus PCB. See “Materials and Methods” for details. Red staining reflects positive chromogen development for VCAM-1 immunostaining on the endothelial surface (B–D) and in subendothelial tissue (D). Magnification, 400×. |
PMC1253716_f1-ehp0113-000096_3403.jpg | What does this image primarily show? | Hematoxylin and eosin stain, right knee skin biopsy. Magnification, 40×. |
PMC1253759_f2-ehp0113-000323_3407.jpg | What is the focal point of this photograph? | Representative kidney sections taken from (NZB × NZW)F1 mice after 16 weeks of treatment. (A) Sham-operated mouse. (B) Ovariectomized mouse treated with chlordecone (1.8 mg/pellet). (C and D) Two ovariectomized mice, each treated with a control pellet. (A) and (B) show enlarged, cellular, and sclerotic glomeruli (arrows) with tubular atrophy and dilation (asterisks). (C) and (D) show segmental mesangial thickening, but otherwise spared, glomeruli (arrows) with normal tubules (asterisk). Sections were stained with PAS (magnification, 400×). |
PMC1253759_f2-ehp0113-000323_3408.jpg | What object or scene is depicted here? | Representative kidney sections taken from (NZB × NZW)F1 mice after 16 weeks of treatment. (A) Sham-operated mouse. (B) Ovariectomized mouse treated with chlordecone (1.8 mg/pellet). (C and D) Two ovariectomized mice, each treated with a control pellet. (A) and (B) show enlarged, cellular, and sclerotic glomeruli (arrows) with tubular atrophy and dilation (asterisks). (C) and (D) show segmental mesangial thickening, but otherwise spared, glomeruli (arrows) with normal tubules (asterisk). Sections were stained with PAS (magnification, 400×). |
PMC1253759_f2-ehp0113-000323_3405.jpg | What is the principal component of this image? | Representative kidney sections taken from (NZB × NZW)F1 mice after 16 weeks of treatment. (A) Sham-operated mouse. (B) Ovariectomized mouse treated with chlordecone (1.8 mg/pellet). (C and D) Two ovariectomized mice, each treated with a control pellet. (A) and (B) show enlarged, cellular, and sclerotic glomeruli (arrows) with tubular atrophy and dilation (asterisks). (C) and (D) show segmental mesangial thickening, but otherwise spared, glomeruli (arrows) with normal tubules (asterisk). Sections were stained with PAS (magnification, 400×). |
PMC1253759_f2-ehp0113-000323_3406.jpg | What is the central feature of this picture? | Representative kidney sections taken from (NZB × NZW)F1 mice after 16 weeks of treatment. (A) Sham-operated mouse. (B) Ovariectomized mouse treated with chlordecone (1.8 mg/pellet). (C and D) Two ovariectomized mice, each treated with a control pellet. (A) and (B) show enlarged, cellular, and sclerotic glomeruli (arrows) with tubular atrophy and dilation (asterisks). (C) and (D) show segmental mesangial thickening, but otherwise spared, glomeruli (arrows) with normal tubules (asterisk). Sections were stained with PAS (magnification, 400×). |
PMC1253843_ppat-0010016-g003_3421.jpg | What key item or scene is captured in this photo? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1253843_ppat-0010016-g003_3417.jpg | What is the focal point of this photograph? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1253843_ppat-0010016-g003_3418.jpg | What key item or scene is captured in this photo? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1253843_ppat-0010016-g003_3410.jpg | What's the most prominent thing you notice in this picture? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1253843_ppat-0010016-g003_3415.jpg | What is the main focus of this visual representation? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1253843_ppat-0010016-g003_3413.jpg | What is shown in this image? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1253843_ppat-0010016-g003_3423.jpg | Can you identify the primary element in this image? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1253843_ppat-0010016-g003_3416.jpg | What is the dominant medical problem in this image? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1253843_ppat-0010016-g003_3420.jpg | What does this image primarily show? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1253843_ppat-0010016-g003_3411.jpg | What stands out most in this visual? | YopE Selectively Inactivates Membrane-Associated Rac1.COS1 cells cotransfected with plasmids expressing mYFP-PBD and noted plasmids were challenged at 37 °C for 30 min with Y. pseudotuberculosis YP17(yopH −, yopT −, yopE −) (noted as “Control” in [A] and [B]) or YP17/pYopE (noted as “+YopE” in [A–C]). Bacteria were grown at 37 °C for 1 h to induce expression of the type III secretion system prior to infection (Materials and Methods). The C189S mutation blocks plasma membrane localization of Rac1, whereas R66A prevents extraction of Rac1 by RhoGDI from plasma membrane into cytosol.(A and B) Displayed are images of typical cells showing phase contrast, mCFP fluorescence and color-scaled sensitized FRET or normalized (Rac1 activation) for YP17 (A) or Yp17/pYopE (A and B) infected cells (Materials and Methods). White bar represents 10 μm.(C) Cytoplasmic Rac1 is not a YopE target. Normalized FRET was determined (Materials and Methods) by imaging cytoplasm of eight infected cells (Materials and Methods). Data for mCFP-Rac1 activation was normalized against mCFP-Rac1 intensity (normalized Rac1 activation) and displayed as mean ± SEM. *****, p < 5 × 10−6 between control cells and YopE-treated cells or between Rac1(WT) and Rac1C189S-transfected cells. NS, no significant difference between Rac1(WT)-transfected cells and Rac1R66A-transfected cells. |
PMC1255742_pbio-0030362-g004_3430.jpg | What is the core subject represented in this visual? | Effects of rTMS on BOLD Signals(A) rTMS effect on BOLD signals of a single participant detected pre-rTMS, post-rTMS, and 3 h after rTMS in the left SI ipsilateral to the rTMS site in the postcentral gyrus, and in the contralateral SII in the parietal operculum above the Sylvian fissure. Activations are projected on a rendered T1-weighted MRI dataset. Comparing pre- with post-rTMS fMRI sessions revealed enlarged activation and increased BOLD signal intensity in left SI ipsilateral to the rTMS site. These changes of BOLD signal characteristics recovered 3 h after termination of rTMS.(B) Psychometric functions illustrating the rTMS-induced improvement of discrimination threshold for the individual shown in (A). Correct responses in percent (red squares) are plotted as a function of separation distance together with the results of a logistic regression line (blue with blue diamonds). 50% levels of correct responses are shown as well as thresholds. Top graph, pre-rTMS; middle graph, post-rTMS condition, immediately after rTMS; bottom graph, recovery after 3 h. After rTMS there is a distinct shift in the psychometric functions towards lower separation distances by 0.20 mm, which recovers to pre-rTMS conditions 3 h later (pre-rTMS, 1.75 mm; recovered, 1.72 mm).(C) Random-effect analysis (paired t-test pre-post, right D2 stimulation) revealed significant changes of activated patterns localized in SI ipsilateral to the rTMS stimulated D2 representation (n = 12, pre- versus post-rTMS; threshold, p = 0.001, uncorrected for multiple comparisons; S1-parameters, 32 voxels; T-score = 4.15; x,y,z (mm), −54, −14, 50; Talairach position, postcentral gyrus, Brodmann area 3).(D) No changes of BOLD activity were found in the right hemisphere contralateral to the rTMS site (paired t-test pre- versus post-rTMS, left index finger stimulation; threshold, p = 0.001, uncorrected for multiple comparisons) and in SII.(E) Changes in activation pattern as obtained from random effects analysis (paired t-test pre- versus post-rTMS, right index finger stimulation; compare with [C]), superimposed on a glass brain for visualization. Views are from top (left grid), back (middle grid), and right (right grid). |
PMC1255742_pbio-0030362-g004_3431.jpg | What's the most prominent thing you notice in this picture? | Effects of rTMS on BOLD Signals(A) rTMS effect on BOLD signals of a single participant detected pre-rTMS, post-rTMS, and 3 h after rTMS in the left SI ipsilateral to the rTMS site in the postcentral gyrus, and in the contralateral SII in the parietal operculum above the Sylvian fissure. Activations are projected on a rendered T1-weighted MRI dataset. Comparing pre- with post-rTMS fMRI sessions revealed enlarged activation and increased BOLD signal intensity in left SI ipsilateral to the rTMS site. These changes of BOLD signal characteristics recovered 3 h after termination of rTMS.(B) Psychometric functions illustrating the rTMS-induced improvement of discrimination threshold for the individual shown in (A). Correct responses in percent (red squares) are plotted as a function of separation distance together with the results of a logistic regression line (blue with blue diamonds). 50% levels of correct responses are shown as well as thresholds. Top graph, pre-rTMS; middle graph, post-rTMS condition, immediately after rTMS; bottom graph, recovery after 3 h. After rTMS there is a distinct shift in the psychometric functions towards lower separation distances by 0.20 mm, which recovers to pre-rTMS conditions 3 h later (pre-rTMS, 1.75 mm; recovered, 1.72 mm).(C) Random-effect analysis (paired t-test pre-post, right D2 stimulation) revealed significant changes of activated patterns localized in SI ipsilateral to the rTMS stimulated D2 representation (n = 12, pre- versus post-rTMS; threshold, p = 0.001, uncorrected for multiple comparisons; S1-parameters, 32 voxels; T-score = 4.15; x,y,z (mm), −54, −14, 50; Talairach position, postcentral gyrus, Brodmann area 3).(D) No changes of BOLD activity were found in the right hemisphere contralateral to the rTMS site (paired t-test pre- versus post-rTMS, left index finger stimulation; threshold, p = 0.001, uncorrected for multiple comparisons) and in SII.(E) Changes in activation pattern as obtained from random effects analysis (paired t-test pre- versus post-rTMS, right index finger stimulation; compare with [C]), superimposed on a glass brain for visualization. Views are from top (left grid), back (middle grid), and right (right grid). |
PMC1255742_pbio-0030362-g004_3427.jpg | What is the principal component of this image? | Effects of rTMS on BOLD Signals(A) rTMS effect on BOLD signals of a single participant detected pre-rTMS, post-rTMS, and 3 h after rTMS in the left SI ipsilateral to the rTMS site in the postcentral gyrus, and in the contralateral SII in the parietal operculum above the Sylvian fissure. Activations are projected on a rendered T1-weighted MRI dataset. Comparing pre- with post-rTMS fMRI sessions revealed enlarged activation and increased BOLD signal intensity in left SI ipsilateral to the rTMS site. These changes of BOLD signal characteristics recovered 3 h after termination of rTMS.(B) Psychometric functions illustrating the rTMS-induced improvement of discrimination threshold for the individual shown in (A). Correct responses in percent (red squares) are plotted as a function of separation distance together with the results of a logistic regression line (blue with blue diamonds). 50% levels of correct responses are shown as well as thresholds. Top graph, pre-rTMS; middle graph, post-rTMS condition, immediately after rTMS; bottom graph, recovery after 3 h. After rTMS there is a distinct shift in the psychometric functions towards lower separation distances by 0.20 mm, which recovers to pre-rTMS conditions 3 h later (pre-rTMS, 1.75 mm; recovered, 1.72 mm).(C) Random-effect analysis (paired t-test pre-post, right D2 stimulation) revealed significant changes of activated patterns localized in SI ipsilateral to the rTMS stimulated D2 representation (n = 12, pre- versus post-rTMS; threshold, p = 0.001, uncorrected for multiple comparisons; S1-parameters, 32 voxels; T-score = 4.15; x,y,z (mm), −54, −14, 50; Talairach position, postcentral gyrus, Brodmann area 3).(D) No changes of BOLD activity were found in the right hemisphere contralateral to the rTMS site (paired t-test pre- versus post-rTMS, left index finger stimulation; threshold, p = 0.001, uncorrected for multiple comparisons) and in SII.(E) Changes in activation pattern as obtained from random effects analysis (paired t-test pre- versus post-rTMS, right index finger stimulation; compare with [C]), superimposed on a glass brain for visualization. Views are from top (left grid), back (middle grid), and right (right grid). |
PMC1255742_pbio-0030362-g004_3428.jpg | What is the main focus of this visual representation? | Effects of rTMS on BOLD Signals(A) rTMS effect on BOLD signals of a single participant detected pre-rTMS, post-rTMS, and 3 h after rTMS in the left SI ipsilateral to the rTMS site in the postcentral gyrus, and in the contralateral SII in the parietal operculum above the Sylvian fissure. Activations are projected on a rendered T1-weighted MRI dataset. Comparing pre- with post-rTMS fMRI sessions revealed enlarged activation and increased BOLD signal intensity in left SI ipsilateral to the rTMS site. These changes of BOLD signal characteristics recovered 3 h after termination of rTMS.(B) Psychometric functions illustrating the rTMS-induced improvement of discrimination threshold for the individual shown in (A). Correct responses in percent (red squares) are plotted as a function of separation distance together with the results of a logistic regression line (blue with blue diamonds). 50% levels of correct responses are shown as well as thresholds. Top graph, pre-rTMS; middle graph, post-rTMS condition, immediately after rTMS; bottom graph, recovery after 3 h. After rTMS there is a distinct shift in the psychometric functions towards lower separation distances by 0.20 mm, which recovers to pre-rTMS conditions 3 h later (pre-rTMS, 1.75 mm; recovered, 1.72 mm).(C) Random-effect analysis (paired t-test pre-post, right D2 stimulation) revealed significant changes of activated patterns localized in SI ipsilateral to the rTMS stimulated D2 representation (n = 12, pre- versus post-rTMS; threshold, p = 0.001, uncorrected for multiple comparisons; S1-parameters, 32 voxels; T-score = 4.15; x,y,z (mm), −54, −14, 50; Talairach position, postcentral gyrus, Brodmann area 3).(D) No changes of BOLD activity were found in the right hemisphere contralateral to the rTMS site (paired t-test pre- versus post-rTMS, left index finger stimulation; threshold, p = 0.001, uncorrected for multiple comparisons) and in SII.(E) Changes in activation pattern as obtained from random effects analysis (paired t-test pre- versus post-rTMS, right index finger stimulation; compare with [C]), superimposed on a glass brain for visualization. Views are from top (left grid), back (middle grid), and right (right grid). |
PMC1255742_pbio-0030362-g004_3432.jpg | What can you see in this picture? | Effects of rTMS on BOLD Signals(A) rTMS effect on BOLD signals of a single participant detected pre-rTMS, post-rTMS, and 3 h after rTMS in the left SI ipsilateral to the rTMS site in the postcentral gyrus, and in the contralateral SII in the parietal operculum above the Sylvian fissure. Activations are projected on a rendered T1-weighted MRI dataset. Comparing pre- with post-rTMS fMRI sessions revealed enlarged activation and increased BOLD signal intensity in left SI ipsilateral to the rTMS site. These changes of BOLD signal characteristics recovered 3 h after termination of rTMS.(B) Psychometric functions illustrating the rTMS-induced improvement of discrimination threshold for the individual shown in (A). Correct responses in percent (red squares) are plotted as a function of separation distance together with the results of a logistic regression line (blue with blue diamonds). 50% levels of correct responses are shown as well as thresholds. Top graph, pre-rTMS; middle graph, post-rTMS condition, immediately after rTMS; bottom graph, recovery after 3 h. After rTMS there is a distinct shift in the psychometric functions towards lower separation distances by 0.20 mm, which recovers to pre-rTMS conditions 3 h later (pre-rTMS, 1.75 mm; recovered, 1.72 mm).(C) Random-effect analysis (paired t-test pre-post, right D2 stimulation) revealed significant changes of activated patterns localized in SI ipsilateral to the rTMS stimulated D2 representation (n = 12, pre- versus post-rTMS; threshold, p = 0.001, uncorrected for multiple comparisons; S1-parameters, 32 voxels; T-score = 4.15; x,y,z (mm), −54, −14, 50; Talairach position, postcentral gyrus, Brodmann area 3).(D) No changes of BOLD activity were found in the right hemisphere contralateral to the rTMS site (paired t-test pre- versus post-rTMS, left index finger stimulation; threshold, p = 0.001, uncorrected for multiple comparisons) and in SII.(E) Changes in activation pattern as obtained from random effects analysis (paired t-test pre- versus post-rTMS, right index finger stimulation; compare with [C]), superimposed on a glass brain for visualization. Views are from top (left grid), back (middle grid), and right (right grid). |
PMC1257431_F3_3434.jpg | What key item or scene is captured in this photo? | Laser scanning confocal microscope (× 400) image of the double immunofluorescent assay. The expression of CD68+ (green) and CD147+ (red) cells, and the co-expression of CD68+CD147+ cells (yellow) in the lining and sublining layers of rheumatoid arthritis synovium is apparent. |
PMC1257431_F3_3433.jpg | What stands out most in this visual? | Laser scanning confocal microscope (× 400) image of the double immunofluorescent assay. The expression of CD68+ (green) and CD147+ (red) cells, and the co-expression of CD68+CD147+ cells (yellow) in the lining and sublining layers of rheumatoid arthritis synovium is apparent. |
PMC1257439_F5_3442.jpg | What is the core subject represented in this visual? | Double immunofluorescence labelling of normal and dcSSc skin biopsies. Cryosections from (a,c) normal and (b,d) dcSSc were double stained for endothelial cells using (a,b) PAL-E antibody and Thy-1 and (c,d) α-SMA and Thy-1. Thy-1 is labelled with FITC while PAL-E and α-SMA are labelled with Texas Red. In both (a) normal and (b) dcSSc, immunofluorescence for Thy-1 ((a,b) arrow, green colour) and PAL-E ((a,b) arrowhead, red colour) was consistently exclusive and showed no colocalization. In both (c) normal and (d) dcSSc, strong colocalization between Thy-1 and α-SMA was evident ((c,d) arrows, yellow colour). In normal skin, Thy-1 immunofluorescence that did not colocalize with α-SMA was observed immediately adjacent to microvessels ((c) arrowheads, green colour). Cryosections from dcSSc were double stained for (e,f,g) ED-A FN and α-SMA and (h) ED-A FN and Thy-1. ED-A FN is labelled with Texas Red while α-SMA and Thy-1 are labelled with FITC. Cell nuclei are counterstained blue with DAPI. Colocalization between α-SMA and ED-A FN was detected in dermal fibroblastic cells ((e) arrows, yellow colour) as well as in the microvascular wall ((f,g) arrows, yellow colour). Colocalization was also observed between ED-A FN and Thy-1 in both the microvascular wall ((h) arrow, yellow colour) and in dermal fibroblastic cells ((h) arrowheads, yellow colour). Original magnification (a-d,h) × 10, (e,f) × 20, (g) × 40. α-SMA, alpha smooth muscle actin; DAPI, 4,6-diamidino-2-phenylindole; dcSSc, diffuse cutaneous systemic sclerosis; ED-A FN, ED-A splice variant of fibronectin; FITC, fluorescein isothiocyanate. |
PMC1257439_F5_3441.jpg | What is shown in this image? | Double immunofluorescence labelling of normal and dcSSc skin biopsies. Cryosections from (a,c) normal and (b,d) dcSSc were double stained for endothelial cells using (a,b) PAL-E antibody and Thy-1 and (c,d) α-SMA and Thy-1. Thy-1 is labelled with FITC while PAL-E and α-SMA are labelled with Texas Red. In both (a) normal and (b) dcSSc, immunofluorescence for Thy-1 ((a,b) arrow, green colour) and PAL-E ((a,b) arrowhead, red colour) was consistently exclusive and showed no colocalization. In both (c) normal and (d) dcSSc, strong colocalization between Thy-1 and α-SMA was evident ((c,d) arrows, yellow colour). In normal skin, Thy-1 immunofluorescence that did not colocalize with α-SMA was observed immediately adjacent to microvessels ((c) arrowheads, green colour). Cryosections from dcSSc were double stained for (e,f,g) ED-A FN and α-SMA and (h) ED-A FN and Thy-1. ED-A FN is labelled with Texas Red while α-SMA and Thy-1 are labelled with FITC. Cell nuclei are counterstained blue with DAPI. Colocalization between α-SMA and ED-A FN was detected in dermal fibroblastic cells ((e) arrows, yellow colour) as well as in the microvascular wall ((f,g) arrows, yellow colour). Colocalization was also observed between ED-A FN and Thy-1 in both the microvascular wall ((h) arrow, yellow colour) and in dermal fibroblastic cells ((h) arrowheads, yellow colour). Original magnification (a-d,h) × 10, (e,f) × 20, (g) × 40. α-SMA, alpha smooth muscle actin; DAPI, 4,6-diamidino-2-phenylindole; dcSSc, diffuse cutaneous systemic sclerosis; ED-A FN, ED-A splice variant of fibronectin; FITC, fluorescein isothiocyanate. |
PMC1257439_F5_3438.jpg | What stands out most in this visual? | Double immunofluorescence labelling of normal and dcSSc skin biopsies. Cryosections from (a,c) normal and (b,d) dcSSc were double stained for endothelial cells using (a,b) PAL-E antibody and Thy-1 and (c,d) α-SMA and Thy-1. Thy-1 is labelled with FITC while PAL-E and α-SMA are labelled with Texas Red. In both (a) normal and (b) dcSSc, immunofluorescence for Thy-1 ((a,b) arrow, green colour) and PAL-E ((a,b) arrowhead, red colour) was consistently exclusive and showed no colocalization. In both (c) normal and (d) dcSSc, strong colocalization between Thy-1 and α-SMA was evident ((c,d) arrows, yellow colour). In normal skin, Thy-1 immunofluorescence that did not colocalize with α-SMA was observed immediately adjacent to microvessels ((c) arrowheads, green colour). Cryosections from dcSSc were double stained for (e,f,g) ED-A FN and α-SMA and (h) ED-A FN and Thy-1. ED-A FN is labelled with Texas Red while α-SMA and Thy-1 are labelled with FITC. Cell nuclei are counterstained blue with DAPI. Colocalization between α-SMA and ED-A FN was detected in dermal fibroblastic cells ((e) arrows, yellow colour) as well as in the microvascular wall ((f,g) arrows, yellow colour). Colocalization was also observed between ED-A FN and Thy-1 in both the microvascular wall ((h) arrow, yellow colour) and in dermal fibroblastic cells ((h) arrowheads, yellow colour). Original magnification (a-d,h) × 10, (e,f) × 20, (g) × 40. α-SMA, alpha smooth muscle actin; DAPI, 4,6-diamidino-2-phenylindole; dcSSc, diffuse cutaneous systemic sclerosis; ED-A FN, ED-A splice variant of fibronectin; FITC, fluorescein isothiocyanate. |
PMC1257439_F5_3440.jpg | What does this image primarily show? | Double immunofluorescence labelling of normal and dcSSc skin biopsies. Cryosections from (a,c) normal and (b,d) dcSSc were double stained for endothelial cells using (a,b) PAL-E antibody and Thy-1 and (c,d) α-SMA and Thy-1. Thy-1 is labelled with FITC while PAL-E and α-SMA are labelled with Texas Red. In both (a) normal and (b) dcSSc, immunofluorescence for Thy-1 ((a,b) arrow, green colour) and PAL-E ((a,b) arrowhead, red colour) was consistently exclusive and showed no colocalization. In both (c) normal and (d) dcSSc, strong colocalization between Thy-1 and α-SMA was evident ((c,d) arrows, yellow colour). In normal skin, Thy-1 immunofluorescence that did not colocalize with α-SMA was observed immediately adjacent to microvessels ((c) arrowheads, green colour). Cryosections from dcSSc were double stained for (e,f,g) ED-A FN and α-SMA and (h) ED-A FN and Thy-1. ED-A FN is labelled with Texas Red while α-SMA and Thy-1 are labelled with FITC. Cell nuclei are counterstained blue with DAPI. Colocalization between α-SMA and ED-A FN was detected in dermal fibroblastic cells ((e) arrows, yellow colour) as well as in the microvascular wall ((f,g) arrows, yellow colour). Colocalization was also observed between ED-A FN and Thy-1 in both the microvascular wall ((h) arrow, yellow colour) and in dermal fibroblastic cells ((h) arrowheads, yellow colour). Original magnification (a-d,h) × 10, (e,f) × 20, (g) × 40. α-SMA, alpha smooth muscle actin; DAPI, 4,6-diamidino-2-phenylindole; dcSSc, diffuse cutaneous systemic sclerosis; ED-A FN, ED-A splice variant of fibronectin; FITC, fluorescein isothiocyanate. |
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