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PMC1797186_F3_9551.jpg | What does this image primarily show? | Specific expression of reporter by the Rev-dependent lentiviral vector in HIV-infected primary macrophages. M-CSF-treated monocyte-derived macrophages were infected or were not infected with HIVAD8, followed by Rev-dependent reporter virus vNL-GFP-RRE(SA). (A). Bright-field image of fixed cells with black bar representing 50 micrometers. Nuclei are prominent. Cells that were found to stain positive for HIV p24 are numbered in this image. B. Red fluorescence of identical field. All cells were stained for anti-p24 antibody, followed by a secondary red fluorescent antibody to detect productively infected cells. Intracellular red fluorescent foci identify productive infection; nine cells were identified in this field (B). We examined macrophage populations with four concentrations of HIV input (36, 72, 169, and 361 ng p24 HIVAD8/106 cells) followed by a constant input of reporter lentiviral vector (5 ng p24 vNL-GFP-RRE(SA)/106 cells; VSV-G envelope). Independent of the input of HIV, approximately one fifth of the p24-positive cells expressed GFP (23.0 ± 2.8%; mean ± SD; n = 4), as shown by green fluorescence in this same field (C). Magnification was identical on all three images. The reporter virus was demonstrated to function in macrophages from three donors. |
PMC1797186_F3_9553.jpg | What is shown in this image? | Specific expression of reporter by the Rev-dependent lentiviral vector in HIV-infected primary macrophages. M-CSF-treated monocyte-derived macrophages were infected or were not infected with HIVAD8, followed by Rev-dependent reporter virus vNL-GFP-RRE(SA). (A). Bright-field image of fixed cells with black bar representing 50 micrometers. Nuclei are prominent. Cells that were found to stain positive for HIV p24 are numbered in this image. B. Red fluorescence of identical field. All cells were stained for anti-p24 antibody, followed by a secondary red fluorescent antibody to detect productively infected cells. Intracellular red fluorescent foci identify productive infection; nine cells were identified in this field (B). We examined macrophage populations with four concentrations of HIV input (36, 72, 169, and 361 ng p24 HIVAD8/106 cells) followed by a constant input of reporter lentiviral vector (5 ng p24 vNL-GFP-RRE(SA)/106 cells; VSV-G envelope). Independent of the input of HIV, approximately one fifth of the p24-positive cells expressed GFP (23.0 ± 2.8%; mean ± SD; n = 4), as shown by green fluorescence in this same field (C). Magnification was identical on all three images. The reporter virus was demonstrated to function in macrophages from three donors. |
PMC1797188_F6_9555.jpg | What's the most prominent thing you notice in this picture? | Removal of the 2 mM thymidine post-treatment at 48 hours, but not at 72 hours, prevents cellular senescence. Cells were treated with 1 mM thymidine prior to electroporation and then recovered in 1 mM thymidine. At 48 hours and 72 hours, as indicated, cultures were washed 2× with PBS and fresh medium was added ("w/o": washed out). At 144 hours, cells were assayed for senescence-associated β-galactosidase activity. All images are at 20× magnification. |
PMC1797188_F6_9556.jpg | What does this image primarily show? | Removal of the 2 mM thymidine post-treatment at 48 hours, but not at 72 hours, prevents cellular senescence. Cells were treated with 1 mM thymidine prior to electroporation and then recovered in 1 mM thymidine. At 48 hours and 72 hours, as indicated, cultures were washed 2× with PBS and fresh medium was added ("w/o": washed out). At 144 hours, cells were assayed for senescence-associated β-galactosidase activity. All images are at 20× magnification. |
PMC1797188_F6_9557.jpg | What's the most prominent thing you notice in this picture? | Removal of the 2 mM thymidine post-treatment at 48 hours, but not at 72 hours, prevents cellular senescence. Cells were treated with 1 mM thymidine prior to electroporation and then recovered in 1 mM thymidine. At 48 hours and 72 hours, as indicated, cultures were washed 2× with PBS and fresh medium was added ("w/o": washed out). At 144 hours, cells were assayed for senescence-associated β-galactosidase activity. All images are at 20× magnification. |
PMC1797188_F6_9554.jpg | Can you identify the primary element in this image? | Removal of the 2 mM thymidine post-treatment at 48 hours, but not at 72 hours, prevents cellular senescence. Cells were treated with 1 mM thymidine prior to electroporation and then recovered in 1 mM thymidine. At 48 hours and 72 hours, as indicated, cultures were washed 2× with PBS and fresh medium was added ("w/o": washed out). At 144 hours, cells were assayed for senescence-associated β-galactosidase activity. All images are at 20× magnification. |
PMC1797189_F2_9560.jpg | What key item or scene is captured in this photo? | In situ expression pattern of germ cell-related markers (MAGE-A4 and TSPY) in OGCTs and sex centromere material in interphase nuclei from OGCTs. MAGE-A4 in A1: Dysgerminoma and A2: In foetal ovary of GW 28 with strong expression in oogonia (lower left), and no expression in developing follicles (top right); TSPY in B1: Gonadoblastoma (Case PT-04) and B2: Dysgerminoma (Case PT-57). Scalebar = 25μm. Fluorescence in situ hybridisation of two different dysgerminomas with sex chromosome centromeres: C. Presence of X and Y chromosome material (Case PT-04) and D. Presence only of X chromosome material (Case PT-14). E-F: Inserts are control DAPI-only. |
PMC1797189_F2_9558.jpg | What is being portrayed in this visual content? | In situ expression pattern of germ cell-related markers (MAGE-A4 and TSPY) in OGCTs and sex centromere material in interphase nuclei from OGCTs. MAGE-A4 in A1: Dysgerminoma and A2: In foetal ovary of GW 28 with strong expression in oogonia (lower left), and no expression in developing follicles (top right); TSPY in B1: Gonadoblastoma (Case PT-04) and B2: Dysgerminoma (Case PT-57). Scalebar = 25μm. Fluorescence in situ hybridisation of two different dysgerminomas with sex chromosome centromeres: C. Presence of X and Y chromosome material (Case PT-04) and D. Presence only of X chromosome material (Case PT-14). E-F: Inserts are control DAPI-only. |
PMC1797189_F2_9559.jpg | What does this image primarily show? | In situ expression pattern of germ cell-related markers (MAGE-A4 and TSPY) in OGCTs and sex centromere material in interphase nuclei from OGCTs. MAGE-A4 in A1: Dysgerminoma and A2: In foetal ovary of GW 28 with strong expression in oogonia (lower left), and no expression in developing follicles (top right); TSPY in B1: Gonadoblastoma (Case PT-04) and B2: Dysgerminoma (Case PT-57). Scalebar = 25μm. Fluorescence in situ hybridisation of two different dysgerminomas with sex chromosome centromeres: C. Presence of X and Y chromosome material (Case PT-04) and D. Presence only of X chromosome material (Case PT-14). E-F: Inserts are control DAPI-only. |
PMC1797189_F2_9563.jpg | Describe the main subject of this image. | In situ expression pattern of germ cell-related markers (MAGE-A4 and TSPY) in OGCTs and sex centromere material in interphase nuclei from OGCTs. MAGE-A4 in A1: Dysgerminoma and A2: In foetal ovary of GW 28 with strong expression in oogonia (lower left), and no expression in developing follicles (top right); TSPY in B1: Gonadoblastoma (Case PT-04) and B2: Dysgerminoma (Case PT-57). Scalebar = 25μm. Fluorescence in situ hybridisation of two different dysgerminomas with sex chromosome centromeres: C. Presence of X and Y chromosome material (Case PT-04) and D. Presence only of X chromosome material (Case PT-14). E-F: Inserts are control DAPI-only. |
PMC1797619_ppat-0030020-g004_9564.jpg | What stands out most in this visual? | Electron Micrographs of TBE Virus at pH 8.0, 10.0, and 5.4TBE virus was preincubated at pH 8.0 (A), 10.0 (B), and 5.4 (C), fixed with formalin, and negatively stained by phosphotungstic acid adjusted to pH 8.0 (samples A and B) or pH 6.0 (sample C). Arrows in (B) point to the rough surface generated by alkaline pH and in (C) to the bulky spikes generated by low pH treatment. All micrographs have been recorded at the same magnification. In (B) and (C), the virions lost their shell-like icosahedral envelope structure, at least at the particle surface, and as a consequence display irregular shapes that give the impression that the virus diameter is smaller than in (A). However, in all cases, the core diameter of the best-preserved virions has a similar value. In (C), the virions are aggregated, a characteristic of TBE virus maintained at low pH. |
PMC1797619_ppat-0030020-g004_9565.jpg | What object or scene is depicted here? | Electron Micrographs of TBE Virus at pH 8.0, 10.0, and 5.4TBE virus was preincubated at pH 8.0 (A), 10.0 (B), and 5.4 (C), fixed with formalin, and negatively stained by phosphotungstic acid adjusted to pH 8.0 (samples A and B) or pH 6.0 (sample C). Arrows in (B) point to the rough surface generated by alkaline pH and in (C) to the bulky spikes generated by low pH treatment. All micrographs have been recorded at the same magnification. In (B) and (C), the virions lost their shell-like icosahedral envelope structure, at least at the particle surface, and as a consequence display irregular shapes that give the impression that the virus diameter is smaller than in (A). However, in all cases, the core diameter of the best-preserved virions has a similar value. In (C), the virions are aggregated, a characteristic of TBE virus maintained at low pH. |
PMC1797619_ppat-0030020-g004_9566.jpg | What is the focal point of this photograph? | Electron Micrographs of TBE Virus at pH 8.0, 10.0, and 5.4TBE virus was preincubated at pH 8.0 (A), 10.0 (B), and 5.4 (C), fixed with formalin, and negatively stained by phosphotungstic acid adjusted to pH 8.0 (samples A and B) or pH 6.0 (sample C). Arrows in (B) point to the rough surface generated by alkaline pH and in (C) to the bulky spikes generated by low pH treatment. All micrographs have been recorded at the same magnification. In (B) and (C), the virions lost their shell-like icosahedral envelope structure, at least at the particle surface, and as a consequence display irregular shapes that give the impression that the virus diameter is smaller than in (A). However, in all cases, the core diameter of the best-preserved virions has a similar value. In (C), the virions are aggregated, a characteristic of TBE virus maintained at low pH. |
PMC1797619_ppat-0030020-g007_9567.jpg | Can you identify the primary element in this image? | Electron Micrographs of TBE Virus Interacting with Liposomes at pH 5.4 and 10.0(A) Electron micrographs of a virus particle in the process of low pH–induced fusion with a liposome. Solid arrow points to low pH–induced projections at the virion surface; dotted arrow points to an electrodense structure presumed to be the nucleocapsid in the process of release.(B) Virus particles attached to liposomal membranes at alkaline pH. Negative stain by phosphotungstic acid adjusted to pH 8.0. |
PMC1797619_ppat-0030020-g007_9568.jpg | What object or scene is depicted here? | Electron Micrographs of TBE Virus Interacting with Liposomes at pH 5.4 and 10.0(A) Electron micrographs of a virus particle in the process of low pH–induced fusion with a liposome. Solid arrow points to low pH–induced projections at the virion surface; dotted arrow points to an electrodense structure presumed to be the nucleocapsid in the process of release.(B) Virus particles attached to liposomal membranes at alkaline pH. Negative stain by phosphotungstic acid adjusted to pH 8.0. |
PMC1797620_ppat-0030021-g006_9569.jpg | What key item or scene is captured in this photo? | OspF Is Associated with Attenuation of the Host Innate Immune ResponseThe images shown are of hematoxylin- and eosin-stained sections of lungs of mice 24 h after infection with wild-type or ΔospF Shigella or injection with equivalent volume of phosphate buffered saline. |
PMC1797620_ppat-0030021-g006_9571.jpg | What is the core subject represented in this visual? | OspF Is Associated with Attenuation of the Host Innate Immune ResponseThe images shown are of hematoxylin- and eosin-stained sections of lungs of mice 24 h after infection with wild-type or ΔospF Shigella or injection with equivalent volume of phosphate buffered saline. |
PMC1797621_ppat-0030023-g002_9575.jpg | What is the core subject represented in this visual? | Viral Antigens in the Brain of Wild-Type and shiverer MiceMice were inoculated intracranially with 106 PFU of TMEV. The brain was dissected out 5 d p.i., snap-frozen, and 10-μm cryostat sections were cut. Sections were stained with an anti-NeuN antibody (green) and an anti-TMEV capsid serum (red). Nuclei were stained with DAPI. (A–D) Wild-type mice. (E–H) shiverer mice. The virus was predominantly found in cortex (A and E), hippocampus (B and F), hypothalamus (C and G), and thalamus (not shown). The distribution was the same in wild-type and in shiverer mice. (D and H) Examples of infected neurons in, respectively, wild-type and shiverer mice. Optical sections were obtained with the Zeiss ApoTome device. wt, wild-type; shi, shiverer.
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PMC1797621_ppat-0030023-g002_9577.jpg | What's the most prominent thing you notice in this picture? | Viral Antigens in the Brain of Wild-Type and shiverer MiceMice were inoculated intracranially with 106 PFU of TMEV. The brain was dissected out 5 d p.i., snap-frozen, and 10-μm cryostat sections were cut. Sections were stained with an anti-NeuN antibody (green) and an anti-TMEV capsid serum (red). Nuclei were stained with DAPI. (A–D) Wild-type mice. (E–H) shiverer mice. The virus was predominantly found in cortex (A and E), hippocampus (B and F), hypothalamus (C and G), and thalamus (not shown). The distribution was the same in wild-type and in shiverer mice. (D and H) Examples of infected neurons in, respectively, wild-type and shiverer mice. Optical sections were obtained with the Zeiss ApoTome device. wt, wild-type; shi, shiverer.
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PMC1797621_ppat-0030023-g002_9572.jpg | What is the focal point of this photograph? | Viral Antigens in the Brain of Wild-Type and shiverer MiceMice were inoculated intracranially with 106 PFU of TMEV. The brain was dissected out 5 d p.i., snap-frozen, and 10-μm cryostat sections were cut. Sections were stained with an anti-NeuN antibody (green) and an anti-TMEV capsid serum (red). Nuclei were stained with DAPI. (A–D) Wild-type mice. (E–H) shiverer mice. The virus was predominantly found in cortex (A and E), hippocampus (B and F), hypothalamus (C and G), and thalamus (not shown). The distribution was the same in wild-type and in shiverer mice. (D and H) Examples of infected neurons in, respectively, wild-type and shiverer mice. Optical sections were obtained with the Zeiss ApoTome device. wt, wild-type; shi, shiverer.
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PMC1797621_ppat-0030023-g002_9578.jpg | What object or scene is depicted here? | Viral Antigens in the Brain of Wild-Type and shiverer MiceMice were inoculated intracranially with 106 PFU of TMEV. The brain was dissected out 5 d p.i., snap-frozen, and 10-μm cryostat sections were cut. Sections were stained with an anti-NeuN antibody (green) and an anti-TMEV capsid serum (red). Nuclei were stained with DAPI. (A–D) Wild-type mice. (E–H) shiverer mice. The virus was predominantly found in cortex (A and E), hippocampus (B and F), hypothalamus (C and G), and thalamus (not shown). The distribution was the same in wild-type and in shiverer mice. (D and H) Examples of infected neurons in, respectively, wild-type and shiverer mice. Optical sections were obtained with the Zeiss ApoTome device. wt, wild-type; shi, shiverer.
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PMC1797621_ppat-0030023-g002_9576.jpg | What's the most prominent thing you notice in this picture? | Viral Antigens in the Brain of Wild-Type and shiverer MiceMice were inoculated intracranially with 106 PFU of TMEV. The brain was dissected out 5 d p.i., snap-frozen, and 10-μm cryostat sections were cut. Sections were stained with an anti-NeuN antibody (green) and an anti-TMEV capsid serum (red). Nuclei were stained with DAPI. (A–D) Wild-type mice. (E–H) shiverer mice. The virus was predominantly found in cortex (A and E), hippocampus (B and F), hypothalamus (C and G), and thalamus (not shown). The distribution was the same in wild-type and in shiverer mice. (D and H) Examples of infected neurons in, respectively, wild-type and shiverer mice. Optical sections were obtained with the Zeiss ApoTome device. wt, wild-type; shi, shiverer.
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PMC1797621_ppat-0030023-g002_9579.jpg | What is the focal point of this photograph? | Viral Antigens in the Brain of Wild-Type and shiverer MiceMice were inoculated intracranially with 106 PFU of TMEV. The brain was dissected out 5 d p.i., snap-frozen, and 10-μm cryostat sections were cut. Sections were stained with an anti-NeuN antibody (green) and an anti-TMEV capsid serum (red). Nuclei were stained with DAPI. (A–D) Wild-type mice. (E–H) shiverer mice. The virus was predominantly found in cortex (A and E), hippocampus (B and F), hypothalamus (C and G), and thalamus (not shown). The distribution was the same in wild-type and in shiverer mice. (D and H) Examples of infected neurons in, respectively, wild-type and shiverer mice. Optical sections were obtained with the Zeiss ApoTome device. wt, wild-type; shi, shiverer.
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PMC1797809_F2_9582.jpg | What is shown in this image? | Kinetics of DENV-2 midgut infection after oral challenge of Aedes aegypti. Chetumal mosquito midguts dissected at different time points (n = 30 for each time point) were assayed by IFA to detect DENV-2 viral antigen (green). At each time point two representative midguts from Chetumal mosquitoes are presented. Controls are an uninfected midgut and a dengue infected midgut (in red midgut musculature). The magnification was 100×. |
PMC1797809_F2_9580.jpg | What object or scene is depicted here? | Kinetics of DENV-2 midgut infection after oral challenge of Aedes aegypti. Chetumal mosquito midguts dissected at different time points (n = 30 for each time point) were assayed by IFA to detect DENV-2 viral antigen (green). At each time point two representative midguts from Chetumal mosquitoes are presented. Controls are an uninfected midgut and a dengue infected midgut (in red midgut musculature). The magnification was 100×. |
PMC1797809_F2_9583.jpg | What is the main focus of this visual representation? | Kinetics of DENV-2 midgut infection after oral challenge of Aedes aegypti. Chetumal mosquito midguts dissected at different time points (n = 30 for each time point) were assayed by IFA to detect DENV-2 viral antigen (green). At each time point two representative midguts from Chetumal mosquitoes are presented. Controls are an uninfected midgut and a dengue infected midgut (in red midgut musculature). The magnification was 100×. |
PMC1797809_F2_9586.jpg | What is the main focus of this visual representation? | Kinetics of DENV-2 midgut infection after oral challenge of Aedes aegypti. Chetumal mosquito midguts dissected at different time points (n = 30 for each time point) were assayed by IFA to detect DENV-2 viral antigen (green). At each time point two representative midguts from Chetumal mosquitoes are presented. Controls are an uninfected midgut and a dengue infected midgut (in red midgut musculature). The magnification was 100×. |
PMC1797809_F2_9581.jpg | What does this image primarily show? | Kinetics of DENV-2 midgut infection after oral challenge of Aedes aegypti. Chetumal mosquito midguts dissected at different time points (n = 30 for each time point) were assayed by IFA to detect DENV-2 viral antigen (green). At each time point two representative midguts from Chetumal mosquitoes are presented. Controls are an uninfected midgut and a dengue infected midgut (in red midgut musculature). The magnification was 100×. |
PMC1797809_F2_9584.jpg | What is the central feature of this picture? | Kinetics of DENV-2 midgut infection after oral challenge of Aedes aegypti. Chetumal mosquito midguts dissected at different time points (n = 30 for each time point) were assayed by IFA to detect DENV-2 viral antigen (green). At each time point two representative midguts from Chetumal mosquitoes are presented. Controls are an uninfected midgut and a dengue infected midgut (in red midgut musculature). The magnification was 100×. |
PMC1797838_f4-ehp0115-000080_9589.jpg | What is shown in this image? | Representative photomicrographs of mammary glands from adult females (PND110) exposed in utero to vehicle (control; A, C, E) or 25 BPA (B, D, F, G, H). Tissue sections were either stained with H&E (A–D) or immunostained to identify mast cells (E–F), myoepithelial cells (G), or epithelial phenotype (H). Differences between normal ducts in control (A) and hyperplastic ducts (B) in BPA-treated animals are shown. The adipose tissue of the control mammary gland (C) consists of mainly fat cells, with few fibroblasts or blood vessels. Treatment with 25 BPA (D) promoted a significant increase of nuclear density in the stromal compartment. After BPA treatment, we found an increase in the volume density of mast cells (arrows) surrounding the hyperplastic duct (F) compared with few mast cells observed near the normal duct (E). The insets in (E) and (F) show mast cells at higher magnification. (G) and (H) show a higher magnification of a hyperplastic duct from a BPA-treated mammary gland; the epithelial phenotype of the cells layers within the hyperplastic ducts was confirmed by the positive CK8 immunostaining (H), whereas myoepithelial cells were labelled with p63 (G). Bars = 75 μm. |
PMC1797838_f4-ehp0115-000080_9590.jpg | Describe the main subject of this image. | Representative photomicrographs of mammary glands from adult females (PND110) exposed in utero to vehicle (control; A, C, E) or 25 BPA (B, D, F, G, H). Tissue sections were either stained with H&E (A–D) or immunostained to identify mast cells (E–F), myoepithelial cells (G), or epithelial phenotype (H). Differences between normal ducts in control (A) and hyperplastic ducts (B) in BPA-treated animals are shown. The adipose tissue of the control mammary gland (C) consists of mainly fat cells, with few fibroblasts or blood vessels. Treatment with 25 BPA (D) promoted a significant increase of nuclear density in the stromal compartment. After BPA treatment, we found an increase in the volume density of mast cells (arrows) surrounding the hyperplastic duct (F) compared with few mast cells observed near the normal duct (E). The insets in (E) and (F) show mast cells at higher magnification. (G) and (H) show a higher magnification of a hyperplastic duct from a BPA-treated mammary gland; the epithelial phenotype of the cells layers within the hyperplastic ducts was confirmed by the positive CK8 immunostaining (H), whereas myoepithelial cells were labelled with p63 (G). Bars = 75 μm. |
PMC1797838_f4-ehp0115-000080_9587.jpg | What stands out most in this visual? | Representative photomicrographs of mammary glands from adult females (PND110) exposed in utero to vehicle (control; A, C, E) or 25 BPA (B, D, F, G, H). Tissue sections were either stained with H&E (A–D) or immunostained to identify mast cells (E–F), myoepithelial cells (G), or epithelial phenotype (H). Differences between normal ducts in control (A) and hyperplastic ducts (B) in BPA-treated animals are shown. The adipose tissue of the control mammary gland (C) consists of mainly fat cells, with few fibroblasts or blood vessels. Treatment with 25 BPA (D) promoted a significant increase of nuclear density in the stromal compartment. After BPA treatment, we found an increase in the volume density of mast cells (arrows) surrounding the hyperplastic duct (F) compared with few mast cells observed near the normal duct (E). The insets in (E) and (F) show mast cells at higher magnification. (G) and (H) show a higher magnification of a hyperplastic duct from a BPA-treated mammary gland; the epithelial phenotype of the cells layers within the hyperplastic ducts was confirmed by the positive CK8 immunostaining (H), whereas myoepithelial cells were labelled with p63 (G). Bars = 75 μm. |
PMC1797838_f4-ehp0115-000080_9594.jpg | What object or scene is depicted here? | Representative photomicrographs of mammary glands from adult females (PND110) exposed in utero to vehicle (control; A, C, E) or 25 BPA (B, D, F, G, H). Tissue sections were either stained with H&E (A–D) or immunostained to identify mast cells (E–F), myoepithelial cells (G), or epithelial phenotype (H). Differences between normal ducts in control (A) and hyperplastic ducts (B) in BPA-treated animals are shown. The adipose tissue of the control mammary gland (C) consists of mainly fat cells, with few fibroblasts or blood vessels. Treatment with 25 BPA (D) promoted a significant increase of nuclear density in the stromal compartment. After BPA treatment, we found an increase in the volume density of mast cells (arrows) surrounding the hyperplastic duct (F) compared with few mast cells observed near the normal duct (E). The insets in (E) and (F) show mast cells at higher magnification. (G) and (H) show a higher magnification of a hyperplastic duct from a BPA-treated mammary gland; the epithelial phenotype of the cells layers within the hyperplastic ducts was confirmed by the positive CK8 immunostaining (H), whereas myoepithelial cells were labelled with p63 (G). Bars = 75 μm. |
PMC1797838_f4-ehp0115-000080_9591.jpg | What object or scene is depicted here? | Representative photomicrographs of mammary glands from adult females (PND110) exposed in utero to vehicle (control; A, C, E) or 25 BPA (B, D, F, G, H). Tissue sections were either stained with H&E (A–D) or immunostained to identify mast cells (E–F), myoepithelial cells (G), or epithelial phenotype (H). Differences between normal ducts in control (A) and hyperplastic ducts (B) in BPA-treated animals are shown. The adipose tissue of the control mammary gland (C) consists of mainly fat cells, with few fibroblasts or blood vessels. Treatment with 25 BPA (D) promoted a significant increase of nuclear density in the stromal compartment. After BPA treatment, we found an increase in the volume density of mast cells (arrows) surrounding the hyperplastic duct (F) compared with few mast cells observed near the normal duct (E). The insets in (E) and (F) show mast cells at higher magnification. (G) and (H) show a higher magnification of a hyperplastic duct from a BPA-treated mammary gland; the epithelial phenotype of the cells layers within the hyperplastic ducts was confirmed by the positive CK8 immunostaining (H), whereas myoepithelial cells were labelled with p63 (G). Bars = 75 μm. |
PMC1797838_f4-ehp0115-000080_9588.jpg | What object or scene is depicted here? | Representative photomicrographs of mammary glands from adult females (PND110) exposed in utero to vehicle (control; A, C, E) or 25 BPA (B, D, F, G, H). Tissue sections were either stained with H&E (A–D) or immunostained to identify mast cells (E–F), myoepithelial cells (G), or epithelial phenotype (H). Differences between normal ducts in control (A) and hyperplastic ducts (B) in BPA-treated animals are shown. The adipose tissue of the control mammary gland (C) consists of mainly fat cells, with few fibroblasts or blood vessels. Treatment with 25 BPA (D) promoted a significant increase of nuclear density in the stromal compartment. After BPA treatment, we found an increase in the volume density of mast cells (arrows) surrounding the hyperplastic duct (F) compared with few mast cells observed near the normal duct (E). The insets in (E) and (F) show mast cells at higher magnification. (G) and (H) show a higher magnification of a hyperplastic duct from a BPA-treated mammary gland; the epithelial phenotype of the cells layers within the hyperplastic ducts was confirmed by the positive CK8 immunostaining (H), whereas myoepithelial cells were labelled with p63 (G). Bars = 75 μm. |
PMC1797838_f4-ehp0115-000080_9593.jpg | What can you see in this picture? | Representative photomicrographs of mammary glands from adult females (PND110) exposed in utero to vehicle (control; A, C, E) or 25 BPA (B, D, F, G, H). Tissue sections were either stained with H&E (A–D) or immunostained to identify mast cells (E–F), myoepithelial cells (G), or epithelial phenotype (H). Differences between normal ducts in control (A) and hyperplastic ducts (B) in BPA-treated animals are shown. The adipose tissue of the control mammary gland (C) consists of mainly fat cells, with few fibroblasts or blood vessels. Treatment with 25 BPA (D) promoted a significant increase of nuclear density in the stromal compartment. After BPA treatment, we found an increase in the volume density of mast cells (arrows) surrounding the hyperplastic duct (F) compared with few mast cells observed near the normal duct (E). The insets in (E) and (F) show mast cells at higher magnification. (G) and (H) show a higher magnification of a hyperplastic duct from a BPA-treated mammary gland; the epithelial phenotype of the cells layers within the hyperplastic ducts was confirmed by the positive CK8 immunostaining (H), whereas myoepithelial cells were labelled with p63 (G). Bars = 75 μm. |
PMC1797842_f3-ehp0115-000107_9596.jpg | What stands out most in this visual? | Pathologic findings of toxic hepatitis cases. (A) PAS-stained liver from case 5 showing spotty necrosis of hepatocytes and clumped Kupffer cells containing PAS-positive material (arrows); these find-ings are compatible with the remission stage of acute hepatitis and with toxic hepatitis (magnification, 400×). (B) Hematoxylin and eosin (H&E)–stained liver from case 1 showing portal tracts that are slightly enlarged and infiltrated with inflammatory cells (magnification, 400×). (C) H&E-stained liver from case 5 showing central to portal bridging necrosis (magnification, 200×). (D) Masson trichrome staining of liver from case 4 showing wide periportal necrosis extending into the portal-to-portal area, with regenerative nodules present (magnification, 100×). |
PMC1797842_f3-ehp0115-000107_9597.jpg | What is being portrayed in this visual content? | Pathologic findings of toxic hepatitis cases. (A) PAS-stained liver from case 5 showing spotty necrosis of hepatocytes and clumped Kupffer cells containing PAS-positive material (arrows); these find-ings are compatible with the remission stage of acute hepatitis and with toxic hepatitis (magnification, 400×). (B) Hematoxylin and eosin (H&E)–stained liver from case 1 showing portal tracts that are slightly enlarged and infiltrated with inflammatory cells (magnification, 400×). (C) H&E-stained liver from case 5 showing central to portal bridging necrosis (magnification, 200×). (D) Masson trichrome staining of liver from case 4 showing wide periportal necrosis extending into the portal-to-portal area, with regenerative nodules present (magnification, 100×). |
PMC1800344_pone-0000259-g003_9600.jpg | What is the central feature of this picture? | Differential responses to actively and passively learned melodies.Increased BOLD effect in response to the actively learned melodies compared with the passively learned melodies was located in the left anterior insula, extending to the deep fronto-opercular cortex (p<0.005, k>100, Z-score>3.0, slices are at x = −39 and y = 9). |
PMC1800344_pone-0000259-g003_9599.jpg | What is being portrayed in this visual content? | Differential responses to actively and passively learned melodies.Increased BOLD effect in response to the actively learned melodies compared with the passively learned melodies was located in the left anterior insula, extending to the deep fronto-opercular cortex (p<0.005, k>100, Z-score>3.0, slices are at x = −39 and y = 9). |
PMC1800857_F1_9606.jpg | Can you identify the primary element in this image? | Functional brain responses collected during the four experimental phases are depicted. The brain scans show consistently stronger functional activation for stimuli conditions relative to silent control obtained from the second out three volumes. All functional contrasts are thresholded at T = 3.79, p ≤ 0.001 (uncorrected α-level, k ≥ 10) and superimposed on transverse and sagittal slices of the MNI-T1-weighted standard brain. Tables 1-4 list peak activations (T-values) of distinct activation clusters and anatomical areas. [A] Visual habituation, [B] Auditory habituation, [C] Conditioning phase, [D] Test phase (extinction). |
PMC1800857_F1_9603.jpg | What is the core subject represented in this visual? | Functional brain responses collected during the four experimental phases are depicted. The brain scans show consistently stronger functional activation for stimuli conditions relative to silent control obtained from the second out three volumes. All functional contrasts are thresholded at T = 3.79, p ≤ 0.001 (uncorrected α-level, k ≥ 10) and superimposed on transverse and sagittal slices of the MNI-T1-weighted standard brain. Tables 1-4 list peak activations (T-values) of distinct activation clusters and anatomical areas. [A] Visual habituation, [B] Auditory habituation, [C] Conditioning phase, [D] Test phase (extinction). |
PMC1800857_F1_9601.jpg | What stands out most in this visual? | Functional brain responses collected during the four experimental phases are depicted. The brain scans show consistently stronger functional activation for stimuli conditions relative to silent control obtained from the second out three volumes. All functional contrasts are thresholded at T = 3.79, p ≤ 0.001 (uncorrected α-level, k ≥ 10) and superimposed on transverse and sagittal slices of the MNI-T1-weighted standard brain. Tables 1-4 list peak activations (T-values) of distinct activation clusters and anatomical areas. [A] Visual habituation, [B] Auditory habituation, [C] Conditioning phase, [D] Test phase (extinction). |
PMC1800857_F1_9605.jpg | What is the central feature of this picture? | Functional brain responses collected during the four experimental phases are depicted. The brain scans show consistently stronger functional activation for stimuli conditions relative to silent control obtained from the second out three volumes. All functional contrasts are thresholded at T = 3.79, p ≤ 0.001 (uncorrected α-level, k ≥ 10) and superimposed on transverse and sagittal slices of the MNI-T1-weighted standard brain. Tables 1-4 list peak activations (T-values) of distinct activation clusters and anatomical areas. [A] Visual habituation, [B] Auditory habituation, [C] Conditioning phase, [D] Test phase (extinction). |
PMC1800857_F1_9604.jpg | What is the central feature of this picture? | Functional brain responses collected during the four experimental phases are depicted. The brain scans show consistently stronger functional activation for stimuli conditions relative to silent control obtained from the second out three volumes. All functional contrasts are thresholded at T = 3.79, p ≤ 0.001 (uncorrected α-level, k ≥ 10) and superimposed on transverse and sagittal slices of the MNI-T1-weighted standard brain. Tables 1-4 list peak activations (T-values) of distinct activation clusters and anatomical areas. [A] Visual habituation, [B] Auditory habituation, [C] Conditioning phase, [D] Test phase (extinction). |
PMC1800859_F2_9611.jpg | What key item or scene is captured in this photo? | Coeliac angiogram. Figure 2A is an angiogram of the coeliac trunk. This demonstrates a highly vascular mass around the duodenum and pancreas and its blood supply from the pancreaticoduodenal arteries. Numerous other small vascular blushes are seen which represent further pancreatic metastases. Figure 2B is taken post- embolisation and demonstrates successful occlusion of the tumour's blood supply. |
PMC1800906_F6_9615.jpg | What key item or scene is captured in this photo? | Photomicrographs illustrating c-Fos-immunopositive nuclei and TrpOH-immunopositive neurons in the mid-rostrocaudal DRVL (−8.18 mm Bregma) of rats exposed to A) CO, B) HA, C) LL, and D) HL conditions. Black boxes indicate regions shown at higher magnification in insets in the lower right hand corner of each panel. Arrowheads indicate examples of c-Fos-immunopositive cells (blue/black nuclear staining); arrows indicate TrpOH-immunopositive (serotonergic) neurons (brown/orange cytoplasmic staining). c-Fos-immunopositive/TrpOH-immunopositive neurons were rarely observed. Abbreviation: bv, blood vessels characteristic of the DRVL region at this rostrocaudal level. Scale bar, 50 μm, inset 25 μm. |
PMC1800906_F6_9612.jpg | What is the dominant medical problem in this image? | Photomicrographs illustrating c-Fos-immunopositive nuclei and TrpOH-immunopositive neurons in the mid-rostrocaudal DRVL (−8.18 mm Bregma) of rats exposed to A) CO, B) HA, C) LL, and D) HL conditions. Black boxes indicate regions shown at higher magnification in insets in the lower right hand corner of each panel. Arrowheads indicate examples of c-Fos-immunopositive cells (blue/black nuclear staining); arrows indicate TrpOH-immunopositive (serotonergic) neurons (brown/orange cytoplasmic staining). c-Fos-immunopositive/TrpOH-immunopositive neurons were rarely observed. Abbreviation: bv, blood vessels characteristic of the DRVL region at this rostrocaudal level. Scale bar, 50 μm, inset 25 μm. |
PMC1800906_F6_9614.jpg | What is the principal component of this image? | Photomicrographs illustrating c-Fos-immunopositive nuclei and TrpOH-immunopositive neurons in the mid-rostrocaudal DRVL (−8.18 mm Bregma) of rats exposed to A) CO, B) HA, C) LL, and D) HL conditions. Black boxes indicate regions shown at higher magnification in insets in the lower right hand corner of each panel. Arrowheads indicate examples of c-Fos-immunopositive cells (blue/black nuclear staining); arrows indicate TrpOH-immunopositive (serotonergic) neurons (brown/orange cytoplasmic staining). c-Fos-immunopositive/TrpOH-immunopositive neurons were rarely observed. Abbreviation: bv, blood vessels characteristic of the DRVL region at this rostrocaudal level. Scale bar, 50 μm, inset 25 μm. |
PMC1802066_F2_9619.jpg | What is being portrayed in this visual content? | Low concentrations of exogenous TGF-β1 induce morphogenesis of branching tubules. (A) J3B1A cells grown in a collagen gel in defined medium for a total of 10 days. (B) Parallel culture in which J3B1A cells were grown in a collagen gel for 6 days to allow cyst formation and were subsequently treated with 50 pg/ml TGF-β1 for an additional 4 days. TGF-β1 has induced the outgrowth of tube-like structures from the wall of existing cysts. (C) Treatment with 2 ng/ml TGF-β1 has resulted in the formation of numerous thin cell cords extending out into the surrounding collagen matrix. Notably, at this relatively high concentration, TGF-β1 also disrupts the organization of preformed cysts, resulting in lumen obliteration. (D) Higher magnification view of a multicellular structure formed in a culture treated with 20 pg/ml TGF-β1 for 4 days. The outgrowths enclose a patent lumen, which at least in some tubes is continuous with the cavity of the cyst. (E) Semi-thin section of a collagen gel culture of J3B1A cells treated with 50 pg/ml TGF-β1 for 4 days. Bars (A-E), 200 μm. (F) Quantitative analysis of TGF-β1-induced tubulogenesis. J3B1A cells were grown in a collagen gel for 6 days to allow cyst formation and were subsequently treated with different concentrations of TGF-β1. Tube formation was evaluated as described in Materials and Methods after 4 days of treatment. Data were expressed as mean number of outgrowths per colony ± s.e.m. from three separate experiments. p < 0.0005 for values of 20 pg/ml TGF-β1 at 2 days compared with control at 2 days, as well as for values of 100 pg/ml TGF-β1 at 2 days compared with 50 pg/ml TGF-β1 at 2 days; p < 0.0025 for values of 50 pg/ml TGF-β1 at 4 days compared with 2 days; p < 0.01 for values of 50 pg/ml TGF-β1 at 4 days compared with 20 pg/ml TGF-β1 at 4 days; p < 0.025 for values of 50 pg/ml TGF-β1 at 2 days compared with 20 pg/ml TGF-β1 at 2 days, as well as for values of 20 pg/ml TGF-β1 at 4 days compared with 2 days. |
PMC1802066_F2_9618.jpg | What is shown in this image? | Low concentrations of exogenous TGF-β1 induce morphogenesis of branching tubules. (A) J3B1A cells grown in a collagen gel in defined medium for a total of 10 days. (B) Parallel culture in which J3B1A cells were grown in a collagen gel for 6 days to allow cyst formation and were subsequently treated with 50 pg/ml TGF-β1 for an additional 4 days. TGF-β1 has induced the outgrowth of tube-like structures from the wall of existing cysts. (C) Treatment with 2 ng/ml TGF-β1 has resulted in the formation of numerous thin cell cords extending out into the surrounding collagen matrix. Notably, at this relatively high concentration, TGF-β1 also disrupts the organization of preformed cysts, resulting in lumen obliteration. (D) Higher magnification view of a multicellular structure formed in a culture treated with 20 pg/ml TGF-β1 for 4 days. The outgrowths enclose a patent lumen, which at least in some tubes is continuous with the cavity of the cyst. (E) Semi-thin section of a collagen gel culture of J3B1A cells treated with 50 pg/ml TGF-β1 for 4 days. Bars (A-E), 200 μm. (F) Quantitative analysis of TGF-β1-induced tubulogenesis. J3B1A cells were grown in a collagen gel for 6 days to allow cyst formation and were subsequently treated with different concentrations of TGF-β1. Tube formation was evaluated as described in Materials and Methods after 4 days of treatment. Data were expressed as mean number of outgrowths per colony ± s.e.m. from three separate experiments. p < 0.0005 for values of 20 pg/ml TGF-β1 at 2 days compared with control at 2 days, as well as for values of 100 pg/ml TGF-β1 at 2 days compared with 50 pg/ml TGF-β1 at 2 days; p < 0.0025 for values of 50 pg/ml TGF-β1 at 4 days compared with 2 days; p < 0.01 for values of 50 pg/ml TGF-β1 at 4 days compared with 20 pg/ml TGF-β1 at 4 days; p < 0.025 for values of 50 pg/ml TGF-β1 at 2 days compared with 20 pg/ml TGF-β1 at 2 days, as well as for values of 20 pg/ml TGF-β1 at 4 days compared with 2 days. |
PMC1802066_F2_9621.jpg | What's the most prominent thing you notice in this picture? | Low concentrations of exogenous TGF-β1 induce morphogenesis of branching tubules. (A) J3B1A cells grown in a collagen gel in defined medium for a total of 10 days. (B) Parallel culture in which J3B1A cells were grown in a collagen gel for 6 days to allow cyst formation and were subsequently treated with 50 pg/ml TGF-β1 for an additional 4 days. TGF-β1 has induced the outgrowth of tube-like structures from the wall of existing cysts. (C) Treatment with 2 ng/ml TGF-β1 has resulted in the formation of numerous thin cell cords extending out into the surrounding collagen matrix. Notably, at this relatively high concentration, TGF-β1 also disrupts the organization of preformed cysts, resulting in lumen obliteration. (D) Higher magnification view of a multicellular structure formed in a culture treated with 20 pg/ml TGF-β1 for 4 days. The outgrowths enclose a patent lumen, which at least in some tubes is continuous with the cavity of the cyst. (E) Semi-thin section of a collagen gel culture of J3B1A cells treated with 50 pg/ml TGF-β1 for 4 days. Bars (A-E), 200 μm. (F) Quantitative analysis of TGF-β1-induced tubulogenesis. J3B1A cells were grown in a collagen gel for 6 days to allow cyst formation and were subsequently treated with different concentrations of TGF-β1. Tube formation was evaluated as described in Materials and Methods after 4 days of treatment. Data were expressed as mean number of outgrowths per colony ± s.e.m. from three separate experiments. p < 0.0005 for values of 20 pg/ml TGF-β1 at 2 days compared with control at 2 days, as well as for values of 100 pg/ml TGF-β1 at 2 days compared with 50 pg/ml TGF-β1 at 2 days; p < 0.0025 for values of 50 pg/ml TGF-β1 at 4 days compared with 2 days; p < 0.01 for values of 50 pg/ml TGF-β1 at 4 days compared with 20 pg/ml TGF-β1 at 4 days; p < 0.025 for values of 50 pg/ml TGF-β1 at 2 days compared with 20 pg/ml TGF-β1 at 2 days, as well as for values of 20 pg/ml TGF-β1 at 4 days compared with 2 days. |
PMC1802742_F6_9623.jpg | What is being portrayed in this visual content? | H&E and LFB staining of brain sections reveal the absence of pathologic autoimmunity. Perfusion-fixed brains were obtained from GL261-bearing mice treated with GAA-vaccine and poly-ICLC on day 90 after the tumor-inoculation. Frozen sections were stained with LFB (B and D). Cryostat sections were also stained with H&E to evaluate the overall infiltration of mononuclear immune cells (A and C). Images were taken from the basal ganglia. The thick bundle strongly stained with LFB indicates internal capsule. All images were obtained from the corresponding visual fields. The original magnifications are × 10 (for A and B), and × 20 (for C and D). There was no evidence of demyelination, hemorrhage, or pathological immune cell infiltration throughout the brain. |
PMC1802742_F6_9622.jpg | What is the core subject represented in this visual? | H&E and LFB staining of brain sections reveal the absence of pathologic autoimmunity. Perfusion-fixed brains were obtained from GL261-bearing mice treated with GAA-vaccine and poly-ICLC on day 90 after the tumor-inoculation. Frozen sections were stained with LFB (B and D). Cryostat sections were also stained with H&E to evaluate the overall infiltration of mononuclear immune cells (A and C). Images were taken from the basal ganglia. The thick bundle strongly stained with LFB indicates internal capsule. All images were obtained from the corresponding visual fields. The original magnifications are × 10 (for A and B), and × 20 (for C and D). There was no evidence of demyelination, hemorrhage, or pathological immune cell infiltration throughout the brain. |
PMC1802742_F6_9624.jpg | What does this image primarily show? | H&E and LFB staining of brain sections reveal the absence of pathologic autoimmunity. Perfusion-fixed brains were obtained from GL261-bearing mice treated with GAA-vaccine and poly-ICLC on day 90 after the tumor-inoculation. Frozen sections were stained with LFB (B and D). Cryostat sections were also stained with H&E to evaluate the overall infiltration of mononuclear immune cells (A and C). Images were taken from the basal ganglia. The thick bundle strongly stained with LFB indicates internal capsule. All images were obtained from the corresponding visual fields. The original magnifications are × 10 (for A and B), and × 20 (for C and D). There was no evidence of demyelination, hemorrhage, or pathological immune cell infiltration throughout the brain. |
PMC1802742_F6_9625.jpg | What is the principal component of this image? | H&E and LFB staining of brain sections reveal the absence of pathologic autoimmunity. Perfusion-fixed brains were obtained from GL261-bearing mice treated with GAA-vaccine and poly-ICLC on day 90 after the tumor-inoculation. Frozen sections were stained with LFB (B and D). Cryostat sections were also stained with H&E to evaluate the overall infiltration of mononuclear immune cells (A and C). Images were taken from the basal ganglia. The thick bundle strongly stained with LFB indicates internal capsule. All images were obtained from the corresponding visual fields. The original magnifications are × 10 (for A and B), and × 20 (for C and D). There was no evidence of demyelination, hemorrhage, or pathological immune cell infiltration throughout the brain. |
PMC1802756_pbio-0050053-g002_9628.jpg | What stands out most in this visual? | Regionally Confined Cell Shape Changes Accompany Chamber Emergence(A and B) Phalloidin staining (red) of wild-type hearts expressing Tg(cmlc2:egfp). Insets show representative cell shapes filled in white.(C and D) Bar graphs depict surface area and circularity measurements of LHT, IC, and OC cells. Bar height indicates the mean value of a dataset, and error bars indicate standard error. An asterisk indicates statistically significant differences compared to LHT data (p < 0.0001). See Materials and Methods for details of morphometric analyses. (C) Surface area measurements in fixed samples demonstrate that IC and OC cells are significantly larger than LHT cells. (D) Cell shape assessments in fixed samples demonstrate that OC cells are significantly elongated relative to the more circular LHT and IC cells.(E–L) Confocal projections of live Tg(cmlc2:egfp)-expressing hearts that exhibit mosaic expression of Tg(cmlc2:dsredt4). Arrows point to representative cells expressing both dsredt4 and egfp. Three-dimensional assessment of cell morphologies in live embryos confirms that LHT (E and I) and IC (H and L) cells are relatively cuboidal, whereas OC cells are flattened and elongated (F, G, J, and K). OC cells are typically oriented with their long axes perpendicular to the arterial–venous axis (F and J), although some examples do not exhibit obvious orientation (G and K). |
PMC1802756_pbio-0050053-g002_9629.jpg | What's the most prominent thing you notice in this picture? | Regionally Confined Cell Shape Changes Accompany Chamber Emergence(A and B) Phalloidin staining (red) of wild-type hearts expressing Tg(cmlc2:egfp). Insets show representative cell shapes filled in white.(C and D) Bar graphs depict surface area and circularity measurements of LHT, IC, and OC cells. Bar height indicates the mean value of a dataset, and error bars indicate standard error. An asterisk indicates statistically significant differences compared to LHT data (p < 0.0001). See Materials and Methods for details of morphometric analyses. (C) Surface area measurements in fixed samples demonstrate that IC and OC cells are significantly larger than LHT cells. (D) Cell shape assessments in fixed samples demonstrate that OC cells are significantly elongated relative to the more circular LHT and IC cells.(E–L) Confocal projections of live Tg(cmlc2:egfp)-expressing hearts that exhibit mosaic expression of Tg(cmlc2:dsredt4). Arrows point to representative cells expressing both dsredt4 and egfp. Three-dimensional assessment of cell morphologies in live embryos confirms that LHT (E and I) and IC (H and L) cells are relatively cuboidal, whereas OC cells are flattened and elongated (F, G, J, and K). OC cells are typically oriented with their long axes perpendicular to the arterial–venous axis (F and J), although some examples do not exhibit obvious orientation (G and K). |
PMC1802756_pbio-0050053-g002_9627.jpg | What is the core subject represented in this visual? | Regionally Confined Cell Shape Changes Accompany Chamber Emergence(A and B) Phalloidin staining (red) of wild-type hearts expressing Tg(cmlc2:egfp). Insets show representative cell shapes filled in white.(C and D) Bar graphs depict surface area and circularity measurements of LHT, IC, and OC cells. Bar height indicates the mean value of a dataset, and error bars indicate standard error. An asterisk indicates statistically significant differences compared to LHT data (p < 0.0001). See Materials and Methods for details of morphometric analyses. (C) Surface area measurements in fixed samples demonstrate that IC and OC cells are significantly larger than LHT cells. (D) Cell shape assessments in fixed samples demonstrate that OC cells are significantly elongated relative to the more circular LHT and IC cells.(E–L) Confocal projections of live Tg(cmlc2:egfp)-expressing hearts that exhibit mosaic expression of Tg(cmlc2:dsredt4). Arrows point to representative cells expressing both dsredt4 and egfp. Three-dimensional assessment of cell morphologies in live embryos confirms that LHT (E and I) and IC (H and L) cells are relatively cuboidal, whereas OC cells are flattened and elongated (F, G, J, and K). OC cells are typically oriented with their long axes perpendicular to the arterial–venous axis (F and J), although some examples do not exhibit obvious orientation (G and K). |
PMC1802756_pbio-0050053-g002_9632.jpg | What's the most prominent thing you notice in this picture? | Regionally Confined Cell Shape Changes Accompany Chamber Emergence(A and B) Phalloidin staining (red) of wild-type hearts expressing Tg(cmlc2:egfp). Insets show representative cell shapes filled in white.(C and D) Bar graphs depict surface area and circularity measurements of LHT, IC, and OC cells. Bar height indicates the mean value of a dataset, and error bars indicate standard error. An asterisk indicates statistically significant differences compared to LHT data (p < 0.0001). See Materials and Methods for details of morphometric analyses. (C) Surface area measurements in fixed samples demonstrate that IC and OC cells are significantly larger than LHT cells. (D) Cell shape assessments in fixed samples demonstrate that OC cells are significantly elongated relative to the more circular LHT and IC cells.(E–L) Confocal projections of live Tg(cmlc2:egfp)-expressing hearts that exhibit mosaic expression of Tg(cmlc2:dsredt4). Arrows point to representative cells expressing both dsredt4 and egfp. Three-dimensional assessment of cell morphologies in live embryos confirms that LHT (E and I) and IC (H and L) cells are relatively cuboidal, whereas OC cells are flattened and elongated (F, G, J, and K). OC cells are typically oriented with their long axes perpendicular to the arterial–venous axis (F and J), although some examples do not exhibit obvious orientation (G and K). |
PMC1802827_pgen-0030028-g003_9646.jpg | What is the main focus of this visual representation? | SA1 Location in the Grasshopper E. plorans First Meiotic Prophase Spermatocytes(A and B) Leptotene and pachytene spermatocytes. Note that, despite the fact that this image corresponds to the proyection of several focal planes, there is no SA1 signaling in the leptotene spermatocyte. Le, leptotene; Nu, nucleolus.(C and D) Zygotene and pachytene spermatocytes. Note the presence of short SA1 threads in the zygotene nucleus. Zy, zygotene.(E) Magnification of the periphery of a pachytene nucleus. Note the accumulation of SA1 at the ends of the linear structures formed by SA1 at their contact with the nuclear envelope.(F and G) Enlargements of this association in frontal (F) and lateral (G) views, respectively.(H and I) Projection of all focal planes throughout the univalent sex chromosome from a pachytene spermatocyte. The chromatin of this chromosome is easily distinguished. Note the absence of SA1 signal inside the sex chromosome.(J) Merged image of the SA1 staining and the chromatin counterstaining. The presence of SA1 signaling in the autosomes is quite evident.(K and L) Early diplotene cell in which a barbed wire–like staining of SA1 is seen.(M and N) Late diplotene spermatocyte showing SA1 staining at the interchromatid domain. Note the SA1 accumulations present at the homologous centromere regions of the bivalents (arrowheads). (B, D, I, L, and N) correspond to the DAPI-stained chromatin of the spermatocytes. The position of the single sex chromosome is marked with an X. (A, B, C, D, H, I, and J) are images from confocal microscopy. (E, F, G, K, L, M, and N) are images from fluorescence microscopy. |
PMC1802827_pgen-0030028-g003_9641.jpg | What is the focal point of this photograph? | SA1 Location in the Grasshopper E. plorans First Meiotic Prophase Spermatocytes(A and B) Leptotene and pachytene spermatocytes. Note that, despite the fact that this image corresponds to the proyection of several focal planes, there is no SA1 signaling in the leptotene spermatocyte. Le, leptotene; Nu, nucleolus.(C and D) Zygotene and pachytene spermatocytes. Note the presence of short SA1 threads in the zygotene nucleus. Zy, zygotene.(E) Magnification of the periphery of a pachytene nucleus. Note the accumulation of SA1 at the ends of the linear structures formed by SA1 at their contact with the nuclear envelope.(F and G) Enlargements of this association in frontal (F) and lateral (G) views, respectively.(H and I) Projection of all focal planes throughout the univalent sex chromosome from a pachytene spermatocyte. The chromatin of this chromosome is easily distinguished. Note the absence of SA1 signal inside the sex chromosome.(J) Merged image of the SA1 staining and the chromatin counterstaining. The presence of SA1 signaling in the autosomes is quite evident.(K and L) Early diplotene cell in which a barbed wire–like staining of SA1 is seen.(M and N) Late diplotene spermatocyte showing SA1 staining at the interchromatid domain. Note the SA1 accumulations present at the homologous centromere regions of the bivalents (arrowheads). (B, D, I, L, and N) correspond to the DAPI-stained chromatin of the spermatocytes. The position of the single sex chromosome is marked with an X. (A, B, C, D, H, I, and J) are images from confocal microscopy. (E, F, G, K, L, M, and N) are images from fluorescence microscopy. |
PMC1802827_pgen-0030028-g003_9640.jpg | What object or scene is depicted here? | SA1 Location in the Grasshopper E. plorans First Meiotic Prophase Spermatocytes(A and B) Leptotene and pachytene spermatocytes. Note that, despite the fact that this image corresponds to the proyection of several focal planes, there is no SA1 signaling in the leptotene spermatocyte. Le, leptotene; Nu, nucleolus.(C and D) Zygotene and pachytene spermatocytes. Note the presence of short SA1 threads in the zygotene nucleus. Zy, zygotene.(E) Magnification of the periphery of a pachytene nucleus. Note the accumulation of SA1 at the ends of the linear structures formed by SA1 at their contact with the nuclear envelope.(F and G) Enlargements of this association in frontal (F) and lateral (G) views, respectively.(H and I) Projection of all focal planes throughout the univalent sex chromosome from a pachytene spermatocyte. The chromatin of this chromosome is easily distinguished. Note the absence of SA1 signal inside the sex chromosome.(J) Merged image of the SA1 staining and the chromatin counterstaining. The presence of SA1 signaling in the autosomes is quite evident.(K and L) Early diplotene cell in which a barbed wire–like staining of SA1 is seen.(M and N) Late diplotene spermatocyte showing SA1 staining at the interchromatid domain. Note the SA1 accumulations present at the homologous centromere regions of the bivalents (arrowheads). (B, D, I, L, and N) correspond to the DAPI-stained chromatin of the spermatocytes. The position of the single sex chromosome is marked with an X. (A, B, C, D, H, I, and J) are images from confocal microscopy. (E, F, G, K, L, M, and N) are images from fluorescence microscopy. |
PMC1802827_pgen-0030028-g003_9647.jpg | What is the central feature of this picture? | SA1 Location in the Grasshopper E. plorans First Meiotic Prophase Spermatocytes(A and B) Leptotene and pachytene spermatocytes. Note that, despite the fact that this image corresponds to the proyection of several focal planes, there is no SA1 signaling in the leptotene spermatocyte. Le, leptotene; Nu, nucleolus.(C and D) Zygotene and pachytene spermatocytes. Note the presence of short SA1 threads in the zygotene nucleus. Zy, zygotene.(E) Magnification of the periphery of a pachytene nucleus. Note the accumulation of SA1 at the ends of the linear structures formed by SA1 at their contact with the nuclear envelope.(F and G) Enlargements of this association in frontal (F) and lateral (G) views, respectively.(H and I) Projection of all focal planes throughout the univalent sex chromosome from a pachytene spermatocyte. The chromatin of this chromosome is easily distinguished. Note the absence of SA1 signal inside the sex chromosome.(J) Merged image of the SA1 staining and the chromatin counterstaining. The presence of SA1 signaling in the autosomes is quite evident.(K and L) Early diplotene cell in which a barbed wire–like staining of SA1 is seen.(M and N) Late diplotene spermatocyte showing SA1 staining at the interchromatid domain. Note the SA1 accumulations present at the homologous centromere regions of the bivalents (arrowheads). (B, D, I, L, and N) correspond to the DAPI-stained chromatin of the spermatocytes. The position of the single sex chromosome is marked with an X. (A, B, C, D, H, I, and J) are images from confocal microscopy. (E, F, G, K, L, M, and N) are images from fluorescence microscopy. |
PMC1802827_pgen-0030028-g003_9642.jpg | What is the focal point of this photograph? | SA1 Location in the Grasshopper E. plorans First Meiotic Prophase Spermatocytes(A and B) Leptotene and pachytene spermatocytes. Note that, despite the fact that this image corresponds to the proyection of several focal planes, there is no SA1 signaling in the leptotene spermatocyte. Le, leptotene; Nu, nucleolus.(C and D) Zygotene and pachytene spermatocytes. Note the presence of short SA1 threads in the zygotene nucleus. Zy, zygotene.(E) Magnification of the periphery of a pachytene nucleus. Note the accumulation of SA1 at the ends of the linear structures formed by SA1 at their contact with the nuclear envelope.(F and G) Enlargements of this association in frontal (F) and lateral (G) views, respectively.(H and I) Projection of all focal planes throughout the univalent sex chromosome from a pachytene spermatocyte. The chromatin of this chromosome is easily distinguished. Note the absence of SA1 signal inside the sex chromosome.(J) Merged image of the SA1 staining and the chromatin counterstaining. The presence of SA1 signaling in the autosomes is quite evident.(K and L) Early diplotene cell in which a barbed wire–like staining of SA1 is seen.(M and N) Late diplotene spermatocyte showing SA1 staining at the interchromatid domain. Note the SA1 accumulations present at the homologous centromere regions of the bivalents (arrowheads). (B, D, I, L, and N) correspond to the DAPI-stained chromatin of the spermatocytes. The position of the single sex chromosome is marked with an X. (A, B, C, D, H, I, and J) are images from confocal microscopy. (E, F, G, K, L, M, and N) are images from fluorescence microscopy. |
PMC1802827_pgen-0030028-g003_9648.jpg | What is the central feature of this picture? | SA1 Location in the Grasshopper E. plorans First Meiotic Prophase Spermatocytes(A and B) Leptotene and pachytene spermatocytes. Note that, despite the fact that this image corresponds to the proyection of several focal planes, there is no SA1 signaling in the leptotene spermatocyte. Le, leptotene; Nu, nucleolus.(C and D) Zygotene and pachytene spermatocytes. Note the presence of short SA1 threads in the zygotene nucleus. Zy, zygotene.(E) Magnification of the periphery of a pachytene nucleus. Note the accumulation of SA1 at the ends of the linear structures formed by SA1 at their contact with the nuclear envelope.(F and G) Enlargements of this association in frontal (F) and lateral (G) views, respectively.(H and I) Projection of all focal planes throughout the univalent sex chromosome from a pachytene spermatocyte. The chromatin of this chromosome is easily distinguished. Note the absence of SA1 signal inside the sex chromosome.(J) Merged image of the SA1 staining and the chromatin counterstaining. The presence of SA1 signaling in the autosomes is quite evident.(K and L) Early diplotene cell in which a barbed wire–like staining of SA1 is seen.(M and N) Late diplotene spermatocyte showing SA1 staining at the interchromatid domain. Note the SA1 accumulations present at the homologous centromere regions of the bivalents (arrowheads). (B, D, I, L, and N) correspond to the DAPI-stained chromatin of the spermatocytes. The position of the single sex chromosome is marked with an X. (A, B, C, D, H, I, and J) are images from confocal microscopy. (E, F, G, K, L, M, and N) are images from fluorescence microscopy. |
PMC1802827_pgen-0030028-g003_9644.jpg | What is the focal point of this photograph? | SA1 Location in the Grasshopper E. plorans First Meiotic Prophase Spermatocytes(A and B) Leptotene and pachytene spermatocytes. Note that, despite the fact that this image corresponds to the proyection of several focal planes, there is no SA1 signaling in the leptotene spermatocyte. Le, leptotene; Nu, nucleolus.(C and D) Zygotene and pachytene spermatocytes. Note the presence of short SA1 threads in the zygotene nucleus. Zy, zygotene.(E) Magnification of the periphery of a pachytene nucleus. Note the accumulation of SA1 at the ends of the linear structures formed by SA1 at their contact with the nuclear envelope.(F and G) Enlargements of this association in frontal (F) and lateral (G) views, respectively.(H and I) Projection of all focal planes throughout the univalent sex chromosome from a pachytene spermatocyte. The chromatin of this chromosome is easily distinguished. Note the absence of SA1 signal inside the sex chromosome.(J) Merged image of the SA1 staining and the chromatin counterstaining. The presence of SA1 signaling in the autosomes is quite evident.(K and L) Early diplotene cell in which a barbed wire–like staining of SA1 is seen.(M and N) Late diplotene spermatocyte showing SA1 staining at the interchromatid domain. Note the SA1 accumulations present at the homologous centromere regions of the bivalents (arrowheads). (B, D, I, L, and N) correspond to the DAPI-stained chromatin of the spermatocytes. The position of the single sex chromosome is marked with an X. (A, B, C, D, H, I, and J) are images from confocal microscopy. (E, F, G, K, L, M, and N) are images from fluorescence microscopy. |
PMC1802827_pgen-0030028-g003_9649.jpg | What is being portrayed in this visual content? | SA1 Location in the Grasshopper E. plorans First Meiotic Prophase Spermatocytes(A and B) Leptotene and pachytene spermatocytes. Note that, despite the fact that this image corresponds to the proyection of several focal planes, there is no SA1 signaling in the leptotene spermatocyte. Le, leptotene; Nu, nucleolus.(C and D) Zygotene and pachytene spermatocytes. Note the presence of short SA1 threads in the zygotene nucleus. Zy, zygotene.(E) Magnification of the periphery of a pachytene nucleus. Note the accumulation of SA1 at the ends of the linear structures formed by SA1 at their contact with the nuclear envelope.(F and G) Enlargements of this association in frontal (F) and lateral (G) views, respectively.(H and I) Projection of all focal planes throughout the univalent sex chromosome from a pachytene spermatocyte. The chromatin of this chromosome is easily distinguished. Note the absence of SA1 signal inside the sex chromosome.(J) Merged image of the SA1 staining and the chromatin counterstaining. The presence of SA1 signaling in the autosomes is quite evident.(K and L) Early diplotene cell in which a barbed wire–like staining of SA1 is seen.(M and N) Late diplotene spermatocyte showing SA1 staining at the interchromatid domain. Note the SA1 accumulations present at the homologous centromere regions of the bivalents (arrowheads). (B, D, I, L, and N) correspond to the DAPI-stained chromatin of the spermatocytes. The position of the single sex chromosome is marked with an X. (A, B, C, D, H, I, and J) are images from confocal microscopy. (E, F, G, K, L, M, and N) are images from fluorescence microscopy. |
PMC1802827_pgen-0030028-g003_9645.jpg | What is the dominant medical problem in this image? | SA1 Location in the Grasshopper E. plorans First Meiotic Prophase Spermatocytes(A and B) Leptotene and pachytene spermatocytes. Note that, despite the fact that this image corresponds to the proyection of several focal planes, there is no SA1 signaling in the leptotene spermatocyte. Le, leptotene; Nu, nucleolus.(C and D) Zygotene and pachytene spermatocytes. Note the presence of short SA1 threads in the zygotene nucleus. Zy, zygotene.(E) Magnification of the periphery of a pachytene nucleus. Note the accumulation of SA1 at the ends of the linear structures formed by SA1 at their contact with the nuclear envelope.(F and G) Enlargements of this association in frontal (F) and lateral (G) views, respectively.(H and I) Projection of all focal planes throughout the univalent sex chromosome from a pachytene spermatocyte. The chromatin of this chromosome is easily distinguished. Note the absence of SA1 signal inside the sex chromosome.(J) Merged image of the SA1 staining and the chromatin counterstaining. The presence of SA1 signaling in the autosomes is quite evident.(K and L) Early diplotene cell in which a barbed wire–like staining of SA1 is seen.(M and N) Late diplotene spermatocyte showing SA1 staining at the interchromatid domain. Note the SA1 accumulations present at the homologous centromere regions of the bivalents (arrowheads). (B, D, I, L, and N) correspond to the DAPI-stained chromatin of the spermatocytes. The position of the single sex chromosome is marked with an X. (A, B, C, D, H, I, and J) are images from confocal microscopy. (E, F, G, K, L, M, and N) are images from fluorescence microscopy. |
PMC1802835_F3_9651.jpg | What is the principal component of this image? | A, Immunoblots of the DNP-derivatives of lung proteins of guinea pigs exposed to air or CS after day 1 and day 3. Twenty five μg protein isolated from air-exposed or CS-exposed guinea pigs were converted, without any further treatment, to the DNP-derivative followed by immunoblotting as mentioned in Materials and Methods. 1 and 3 mean exposed to air (sham control) or CS for 1 day and 3 days, respectively. B, C, Histopathology profiles of guinea pig lung tissue sections after exposure to cigarette smoke for 3 days. B shows infiltration of inflammatory cells in the septal regions. C shows accumulation of leukocytes within the alveolar cells that are in all probability macrophages (indicated by → ; magnification × 20) |
PMC1802835_F3_9650.jpg | What is the principal component of this image? | A, Immunoblots of the DNP-derivatives of lung proteins of guinea pigs exposed to air or CS after day 1 and day 3. Twenty five μg protein isolated from air-exposed or CS-exposed guinea pigs were converted, without any further treatment, to the DNP-derivative followed by immunoblotting as mentioned in Materials and Methods. 1 and 3 mean exposed to air (sham control) or CS for 1 day and 3 days, respectively. B, C, Histopathology profiles of guinea pig lung tissue sections after exposure to cigarette smoke for 3 days. B shows infiltration of inflammatory cells in the septal regions. C shows accumulation of leukocytes within the alveolar cells that are in all probability macrophages (indicated by → ; magnification × 20) |
PMC1802837_F6_9670.jpg | What is being portrayed in this visual content? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9660.jpg | What is the core subject represented in this visual? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9659.jpg | What can you see in this picture? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9662.jpg | What stands out most in this visual? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9655.jpg | What is the focal point of this photograph? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9657.jpg | What stands out most in this visual? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9667.jpg | What key item or scene is captured in this photo? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9664.jpg | What does this image primarily show? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9656.jpg | What is shown in this image? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9671.jpg | What is the core subject represented in this visual? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9663.jpg | Can you identify the primary element in this image? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9665.jpg | What is the main focus of this visual representation? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1802837_F6_9669.jpg | What is the central feature of this picture? | Short myosin XI tail length fusion constructs are insufficient to be targeted to organelles. Tobacco leaf cells after Agrobacterium infiltration with different myosin tail length fusion constructs. A-D) Complete tail constructs. E-G) 1/2 coil constructs. H-J) Nocoil constructs. K-N) 1/2 tail constructs. O-R) Dilute constructs. The yellow signal is from the YFP fusion constructs, red is chlorophyll autofluorescence. The shorter the tail, the more unspecific cytoplasmic labeling is observed. Rather few punctuate structures were observed in cells with 1/2 tail or dilute constructs. n/d = not determined. Bar = 10 μm. |
PMC1803007_ppat-0030017-g003_9677.jpg | What stands out most in this visual? | Location of GAAPs(A) U2OS-neo (top row), U2OS-v-GAAP (middle row), or U2OS-h-GAAP (lower row) cells were stained using an anti-HA mAb together with an α-GM130 Ab. All primary Abs were detected with secondary Abs conjugated to fluorescein isothiocyanate or tetramethylrhodamine isothiocyanate. Scale bars, 20 μm. The right panel shows an immunoblot analysis of U2OS stable cell lines using an α-HA mAb.(B) Top left panel: Cryo-immunoelectron microscopy was used to label the v-GAAP HA-tagged protein in U2OS v-GAAP cells with anti-HA mAb (Covance, diluted 1/10), followed by rabbit anti-mouse (Cappel) and 6-nm protein-A Au (scale bars 100 nm, top left panel). Golgi stack morphology was compared in the different cell lines by conventional thin sections of Epon-embedded samples and was examined by electron microscopy in U2OS-neo (top right panel), US-OS-v-GAAP (lower left panel), and U2OS h-GAAP (lower right panel). Scale bars, 200 nm.(C) HeLa cells were transfected with pCI-h-GAAPHA or pCI-v-GAAPHA and fixed 4 h post transfection. GAAPs were detected using an α-HA mAb, and cells were co-stained with the Golgi marker α-GM130. Scale bars, 20 μm. |
PMC1803007_ppat-0030017-g003_9679.jpg | What key item or scene is captured in this photo? | Location of GAAPs(A) U2OS-neo (top row), U2OS-v-GAAP (middle row), or U2OS-h-GAAP (lower row) cells were stained using an anti-HA mAb together with an α-GM130 Ab. All primary Abs were detected with secondary Abs conjugated to fluorescein isothiocyanate or tetramethylrhodamine isothiocyanate. Scale bars, 20 μm. The right panel shows an immunoblot analysis of U2OS stable cell lines using an α-HA mAb.(B) Top left panel: Cryo-immunoelectron microscopy was used to label the v-GAAP HA-tagged protein in U2OS v-GAAP cells with anti-HA mAb (Covance, diluted 1/10), followed by rabbit anti-mouse (Cappel) and 6-nm protein-A Au (scale bars 100 nm, top left panel). Golgi stack morphology was compared in the different cell lines by conventional thin sections of Epon-embedded samples and was examined by electron microscopy in U2OS-neo (top right panel), US-OS-v-GAAP (lower left panel), and U2OS h-GAAP (lower right panel). Scale bars, 200 nm.(C) HeLa cells were transfected with pCI-h-GAAPHA or pCI-v-GAAPHA and fixed 4 h post transfection. GAAPs were detected using an α-HA mAb, and cells were co-stained with the Golgi marker α-GM130. Scale bars, 20 μm. |
PMC1803007_ppat-0030017-g003_9681.jpg | What key item or scene is captured in this photo? | Location of GAAPs(A) U2OS-neo (top row), U2OS-v-GAAP (middle row), or U2OS-h-GAAP (lower row) cells were stained using an anti-HA mAb together with an α-GM130 Ab. All primary Abs were detected with secondary Abs conjugated to fluorescein isothiocyanate or tetramethylrhodamine isothiocyanate. Scale bars, 20 μm. The right panel shows an immunoblot analysis of U2OS stable cell lines using an α-HA mAb.(B) Top left panel: Cryo-immunoelectron microscopy was used to label the v-GAAP HA-tagged protein in U2OS v-GAAP cells with anti-HA mAb (Covance, diluted 1/10), followed by rabbit anti-mouse (Cappel) and 6-nm protein-A Au (scale bars 100 nm, top left panel). Golgi stack morphology was compared in the different cell lines by conventional thin sections of Epon-embedded samples and was examined by electron microscopy in U2OS-neo (top right panel), US-OS-v-GAAP (lower left panel), and U2OS h-GAAP (lower right panel). Scale bars, 200 nm.(C) HeLa cells were transfected with pCI-h-GAAPHA or pCI-v-GAAPHA and fixed 4 h post transfection. GAAPs were detected using an α-HA mAb, and cells were co-stained with the Golgi marker α-GM130. Scale bars, 20 μm. |
PMC1803030_pone-0000276-g002_9682.jpg | What is the focal point of this photograph? | Changes in local SWA homeostasis during sleep after 5-Hz rTMS conditioning. A. Topographic distribution of SWA after 5-Hz conditioning (top) and the sham control (bottom) condition. Average EEG power density at 1–4.5 Hz (n = 10 subjects) for the first 30 minutes of NREM sleep. Values were normalized by total power for the recording, color coded, plotted at the corresponding position on the planar projection of the scalp surface, and interpolated (biharmonic spline) between electrodes (dots). Values to the left of the topographic plots represent maximal and minimal power (in percentage of the overall mean) with standard errors in parenthesis. B. Topographic distribution of the t-value for the comparison between the 5-Hz conditioning and sham control condition (two-tailed paired t-test). White dots indicate electrodes showing significant differences after statistical non-parametric mapping (see methods). C. Anatomical localization of the three electrodes showing a significant difference in SWA during the first 30 min of NREM. All 60 electrodes (red pins) were digitized and co-registered with the subject's magnetic resonance images. When the topographic distribution of the percentage change of SWA after the TMS conditioning compared to the control condition was projected onto the brain, the three significant electrodes projected onto left premotor cortex (white dots). |
PMC1803030_pone-0000276-g002_9683.jpg | What is the main focus of this visual representation? | Changes in local SWA homeostasis during sleep after 5-Hz rTMS conditioning. A. Topographic distribution of SWA after 5-Hz conditioning (top) and the sham control (bottom) condition. Average EEG power density at 1–4.5 Hz (n = 10 subjects) for the first 30 minutes of NREM sleep. Values were normalized by total power for the recording, color coded, plotted at the corresponding position on the planar projection of the scalp surface, and interpolated (biharmonic spline) between electrodes (dots). Values to the left of the topographic plots represent maximal and minimal power (in percentage of the overall mean) with standard errors in parenthesis. B. Topographic distribution of the t-value for the comparison between the 5-Hz conditioning and sham control condition (two-tailed paired t-test). White dots indicate electrodes showing significant differences after statistical non-parametric mapping (see methods). C. Anatomical localization of the three electrodes showing a significant difference in SWA during the first 30 min of NREM. All 60 electrodes (red pins) were digitized and co-registered with the subject's magnetic resonance images. When the topographic distribution of the percentage change of SWA after the TMS conditioning compared to the control condition was projected onto the brain, the three significant electrodes projected onto left premotor cortex (white dots). |
PMC1803773_F1_9685.jpg | What is the main focus of this visual representation? | Non-contrast magnetic resonance imaging showing hyper-intense lesion involving the left temporal and parieto-occipital regions. The tumor is crossing the midline to the right parietal region. |
PMC1803784_F1_9687.jpg | What does this image primarily show? | Contrast enhanced CT scan showing aortoesophageal fistula. |
PMC1803784_F3_9688.jpg | What is the main focus of this visual representation? | Contrast enhanced CT scan showing psedo-aneurysm formation. |
PMC1803784_F5_9690.jpg | What key item or scene is captured in this photo? | Post-operative esophagography. |
PMC1803784_F6_9689.jpg | What is the dominant medical problem in this image? | Post-operative contrast CT showing complete healing of the lesion. |
PMC1804119_fig04_9692.jpg | What is the principal component of this image? | BP reduction in tumor volume in a syngenic rat GBM tumor in situ model. RG2 cells (5 × 104) were implanted i.c. (striatum) in F344 rats. (a) Tumor volume shown by MRI imaging of serial sections (1.5 μm thick): C1–C6 were from the vehicle control rat; BP1–BP6 from a BP-treated rat (tumor mass shown by white arrow). (b) Tumor volume was calculated using echo-planar imaging capability. Each column represents mean ± SEM (*p < 0.05, **p < 0.001). (c) Immunohistochemical staining and TUNEL assay were performed in rat brain tumor tissues (on day 16 after BP treatment). Representative photographs of sections of the control group (i, iii and v) and BP-treated group (ii, iv and vi) GBM tumors immunohistochemically stained for cell proliferation marker with Ki-67 (i and ii), cell apoptosis marker with caspase 3 (active form; iii and iv) and DNA fragmentation of apoptosis cell with TUNEL staining (v and vi). The Ki-67- and caspase 3-positive cells were stained brown and the TUNEL-positive cells were stained green (×400). |
PMC1804119_fig04_9691.jpg | What stands out most in this visual? | BP reduction in tumor volume in a syngenic rat GBM tumor in situ model. RG2 cells (5 × 104) were implanted i.c. (striatum) in F344 rats. (a) Tumor volume shown by MRI imaging of serial sections (1.5 μm thick): C1–C6 were from the vehicle control rat; BP1–BP6 from a BP-treated rat (tumor mass shown by white arrow). (b) Tumor volume was calculated using echo-planar imaging capability. Each column represents mean ± SEM (*p < 0.05, **p < 0.001). (c) Immunohistochemical staining and TUNEL assay were performed in rat brain tumor tissues (on day 16 after BP treatment). Representative photographs of sections of the control group (i, iii and v) and BP-treated group (ii, iv and vi) GBM tumors immunohistochemically stained for cell proliferation marker with Ki-67 (i and ii), cell apoptosis marker with caspase 3 (active form; iii and iv) and DNA fragmentation of apoptosis cell with TUNEL staining (v and vi). The Ki-67- and caspase 3-positive cells were stained brown and the TUNEL-positive cells were stained green (×400). |
PMC1804119_fig04_9698.jpg | Describe the main subject of this image. | BP reduction in tumor volume in a syngenic rat GBM tumor in situ model. RG2 cells (5 × 104) were implanted i.c. (striatum) in F344 rats. (a) Tumor volume shown by MRI imaging of serial sections (1.5 μm thick): C1–C6 were from the vehicle control rat; BP1–BP6 from a BP-treated rat (tumor mass shown by white arrow). (b) Tumor volume was calculated using echo-planar imaging capability. Each column represents mean ± SEM (*p < 0.05, **p < 0.001). (c) Immunohistochemical staining and TUNEL assay were performed in rat brain tumor tissues (on day 16 after BP treatment). Representative photographs of sections of the control group (i, iii and v) and BP-treated group (ii, iv and vi) GBM tumors immunohistochemically stained for cell proliferation marker with Ki-67 (i and ii), cell apoptosis marker with caspase 3 (active form; iii and iv) and DNA fragmentation of apoptosis cell with TUNEL staining (v and vi). The Ki-67- and caspase 3-positive cells were stained brown and the TUNEL-positive cells were stained green (×400). |
PMC1804119_fig04_9701.jpg | What is the central feature of this picture? | BP reduction in tumor volume in a syngenic rat GBM tumor in situ model. RG2 cells (5 × 104) were implanted i.c. (striatum) in F344 rats. (a) Tumor volume shown by MRI imaging of serial sections (1.5 μm thick): C1–C6 were from the vehicle control rat; BP1–BP6 from a BP-treated rat (tumor mass shown by white arrow). (b) Tumor volume was calculated using echo-planar imaging capability. Each column represents mean ± SEM (*p < 0.05, **p < 0.001). (c) Immunohistochemical staining and TUNEL assay were performed in rat brain tumor tissues (on day 16 after BP treatment). Representative photographs of sections of the control group (i, iii and v) and BP-treated group (ii, iv and vi) GBM tumors immunohistochemically stained for cell proliferation marker with Ki-67 (i and ii), cell apoptosis marker with caspase 3 (active form; iii and iv) and DNA fragmentation of apoptosis cell with TUNEL staining (v and vi). The Ki-67- and caspase 3-positive cells were stained brown and the TUNEL-positive cells were stained green (×400). |
PMC1804119_fig04_9697.jpg | What is being portrayed in this visual content? | BP reduction in tumor volume in a syngenic rat GBM tumor in situ model. RG2 cells (5 × 104) were implanted i.c. (striatum) in F344 rats. (a) Tumor volume shown by MRI imaging of serial sections (1.5 μm thick): C1–C6 were from the vehicle control rat; BP1–BP6 from a BP-treated rat (tumor mass shown by white arrow). (b) Tumor volume was calculated using echo-planar imaging capability. Each column represents mean ± SEM (*p < 0.05, **p < 0.001). (c) Immunohistochemical staining and TUNEL assay were performed in rat brain tumor tissues (on day 16 after BP treatment). Representative photographs of sections of the control group (i, iii and v) and BP-treated group (ii, iv and vi) GBM tumors immunohistochemically stained for cell proliferation marker with Ki-67 (i and ii), cell apoptosis marker with caspase 3 (active form; iii and iv) and DNA fragmentation of apoptosis cell with TUNEL staining (v and vi). The Ki-67- and caspase 3-positive cells were stained brown and the TUNEL-positive cells were stained green (×400). |
PMC1804119_fig04_9695.jpg | Describe the main subject of this image. | BP reduction in tumor volume in a syngenic rat GBM tumor in situ model. RG2 cells (5 × 104) were implanted i.c. (striatum) in F344 rats. (a) Tumor volume shown by MRI imaging of serial sections (1.5 μm thick): C1–C6 were from the vehicle control rat; BP1–BP6 from a BP-treated rat (tumor mass shown by white arrow). (b) Tumor volume was calculated using echo-planar imaging capability. Each column represents mean ± SEM (*p < 0.05, **p < 0.001). (c) Immunohistochemical staining and TUNEL assay were performed in rat brain tumor tissues (on day 16 after BP treatment). Representative photographs of sections of the control group (i, iii and v) and BP-treated group (ii, iv and vi) GBM tumors immunohistochemically stained for cell proliferation marker with Ki-67 (i and ii), cell apoptosis marker with caspase 3 (active form; iii and iv) and DNA fragmentation of apoptosis cell with TUNEL staining (v and vi). The Ki-67- and caspase 3-positive cells were stained brown and the TUNEL-positive cells were stained green (×400). |
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