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PMC9430814_fig2_390076.jpg | What is being portrayed in this visual content? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390065.jpg | What is the central feature of this picture? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390083.jpg | What key item or scene is captured in this photo? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390077.jpg | What is the focal point of this photograph? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390080.jpg | What is being portrayed in this visual content? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390064.jpg | Describe the main subject of this image. | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390075.jpg | Can you identify the primary element in this image? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390081.jpg | Describe the main subject of this image. | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390066.jpg | What's the most prominent thing you notice in this picture? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390068.jpg | What does this image primarily show? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390067.jpg | What stands out most in this visual? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390082.jpg | What is the principal component of this image? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390079.jpg | What is the focal point of this photograph? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430814_fig2_390071.jpg | What is the dominant medical problem in this image? | Probiotic consortia protect colon structures and inhibit macrophage infiltration in a DSS-induced colitis mouse model. (A) Representative images of H&E staining. (B) Representative images of F4/80 immunohistochemistry (IHC). |
PMC9430859_fig3_390087.jpg | Describe the main subject of this image. | Pseudohyphal-like growth of the Candida glabrata ML72254 strain was observed by direct microscopy after incubation on a Sabouraud dextrose agar-human serum (SDA-HS) plate under standard atmospheric conditions. (A to C) Cells were clumped together and showed branching patterns. (D) C. glabrata reference strain ATCC 90030 grown on SDA-HS showed solitary and budding cells. |
PMC9430859_fig3_390085.jpg | What is the main focus of this visual representation? | Pseudohyphal-like growth of the Candida glabrata ML72254 strain was observed by direct microscopy after incubation on a Sabouraud dextrose agar-human serum (SDA-HS) plate under standard atmospheric conditions. (A to C) Cells were clumped together and showed branching patterns. (D) C. glabrata reference strain ATCC 90030 grown on SDA-HS showed solitary and budding cells. |
PMC9430879_F1_390088.jpg | What is the dominant medical problem in this image? | pre-operative radiograph showing distoproximal caries (A); access opening showing threw canal orifices in mesiobuccal root (B); working length determination (C); evaluation of master cone fit (D); obturation with gutta percha (E) |
PMC9430879_F1_390092.jpg | What is the core subject represented in this visual? | pre-operative radiograph showing distoproximal caries (A); access opening showing threw canal orifices in mesiobuccal root (B); working length determination (C); evaluation of master cone fit (D); obturation with gutta percha (E) |
PMC9430879_F1_390091.jpg | What object or scene is depicted here? | pre-operative radiograph showing distoproximal caries (A); access opening showing threw canal orifices in mesiobuccal root (B); working length determination (C); evaluation of master cone fit (D); obturation with gutta percha (E) |
PMC9430879_F1_390090.jpg | What is the principal component of this image? | pre-operative radiograph showing distoproximal caries (A); access opening showing threw canal orifices in mesiobuccal root (B); working length determination (C); evaluation of master cone fit (D); obturation with gutta percha (E) |
PMC9430885_F1_390094.jpg | What object or scene is depicted here? | abdominal CT scan findings |
PMC9430885_F2_390095.jpg | Can you identify the primary element in this image? | (A,B) abdominal MRI findings |
PMC9430885_F2_390096.jpg | What is the main focus of this visual representation? | (A,B) abdominal MRI findings |
PMC9430915_fig4_390098.jpg | What is the main focus of this visual representation? | JEV caused neuronal damage in pig brains. Neuropathology in the cerebral cortex and thalamus of the JEV-infected pig. Black arrows indicate neuronal degeneration or necrosis and parenchymal infiltration by inflammatory cells. The black arrowhead indicates perivascular cuffing with lymphocytes, glial cell aggregates, neuronal degeneration, and necrosis with focal neuronophagia. The red arrow indicates multifocal glial nodules. The red arrowhead indicates the satellite phenomenon. Magnification, ×10 and ×40. Slides were analyzed by an independent pathologist in a blind manner. |
PMC9430915_fig4_390099.jpg | What does this image primarily show? | JEV caused neuronal damage in pig brains. Neuropathology in the cerebral cortex and thalamus of the JEV-infected pig. Black arrows indicate neuronal degeneration or necrosis and parenchymal infiltration by inflammatory cells. The black arrowhead indicates perivascular cuffing with lymphocytes, glial cell aggregates, neuronal degeneration, and necrosis with focal neuronophagia. The red arrow indicates multifocal glial nodules. The red arrowhead indicates the satellite phenomenon. Magnification, ×10 and ×40. Slides were analyzed by an independent pathologist in a blind manner. |
PMC9430915_fig4_390102.jpg | Can you identify the primary element in this image? | JEV caused neuronal damage in pig brains. Neuropathology in the cerebral cortex and thalamus of the JEV-infected pig. Black arrows indicate neuronal degeneration or necrosis and parenchymal infiltration by inflammatory cells. The black arrowhead indicates perivascular cuffing with lymphocytes, glial cell aggregates, neuronal degeneration, and necrosis with focal neuronophagia. The red arrow indicates multifocal glial nodules. The red arrowhead indicates the satellite phenomenon. Magnification, ×10 and ×40. Slides were analyzed by an independent pathologist in a blind manner. |
PMC9430915_fig4_390103.jpg | Describe the main subject of this image. | JEV caused neuronal damage in pig brains. Neuropathology in the cerebral cortex and thalamus of the JEV-infected pig. Black arrows indicate neuronal degeneration or necrosis and parenchymal infiltration by inflammatory cells. The black arrowhead indicates perivascular cuffing with lymphocytes, glial cell aggregates, neuronal degeneration, and necrosis with focal neuronophagia. The red arrow indicates multifocal glial nodules. The red arrowhead indicates the satellite phenomenon. Magnification, ×10 and ×40. Slides were analyzed by an independent pathologist in a blind manner. |
PMC9430915_fig4_390101.jpg | What does this image primarily show? | JEV caused neuronal damage in pig brains. Neuropathology in the cerebral cortex and thalamus of the JEV-infected pig. Black arrows indicate neuronal degeneration or necrosis and parenchymal infiltration by inflammatory cells. The black arrowhead indicates perivascular cuffing with lymphocytes, glial cell aggregates, neuronal degeneration, and necrosis with focal neuronophagia. The red arrow indicates multifocal glial nodules. The red arrowhead indicates the satellite phenomenon. Magnification, ×10 and ×40. Slides were analyzed by an independent pathologist in a blind manner. |
PMC9430915_fig4_390104.jpg | What is the focal point of this photograph? | JEV caused neuronal damage in pig brains. Neuropathology in the cerebral cortex and thalamus of the JEV-infected pig. Black arrows indicate neuronal degeneration or necrosis and parenchymal infiltration by inflammatory cells. The black arrowhead indicates perivascular cuffing with lymphocytes, glial cell aggregates, neuronal degeneration, and necrosis with focal neuronophagia. The red arrow indicates multifocal glial nodules. The red arrowhead indicates the satellite phenomenon. Magnification, ×10 and ×40. Slides were analyzed by an independent pathologist in a blind manner. |
PMC9430915_fig4_390100.jpg | What can you see in this picture? | JEV caused neuronal damage in pig brains. Neuropathology in the cerebral cortex and thalamus of the JEV-infected pig. Black arrows indicate neuronal degeneration or necrosis and parenchymal infiltration by inflammatory cells. The black arrowhead indicates perivascular cuffing with lymphocytes, glial cell aggregates, neuronal degeneration, and necrosis with focal neuronophagia. The red arrow indicates multifocal glial nodules. The red arrowhead indicates the satellite phenomenon. Magnification, ×10 and ×40. Slides were analyzed by an independent pathologist in a blind manner. |
PMC9430915_fig4_390097.jpg | What is the main focus of this visual representation? | JEV caused neuronal damage in pig brains. Neuropathology in the cerebral cortex and thalamus of the JEV-infected pig. Black arrows indicate neuronal degeneration or necrosis and parenchymal infiltration by inflammatory cells. The black arrowhead indicates perivascular cuffing with lymphocytes, glial cell aggregates, neuronal degeneration, and necrosis with focal neuronophagia. The red arrow indicates multifocal glial nodules. The red arrowhead indicates the satellite phenomenon. Magnification, ×10 and ×40. Slides were analyzed by an independent pathologist in a blind manner. |
PMC9430915_fig9_390107.jpg | What stands out most in this visual? | JEV antigen colocated with TNF-α-, CD172a-, and iNOS-positive cells. (A to C) Tonsils were sectioned into 5-μm slides and stained with antibodies against TNF-α (green) (A), CD172a (red) (B), iNOS (green) (C), E antigen (red), or NS3 antigen (green). Nuclei were stained with DAPI (blue). Magnification, ×10. The colocalization of cell markers and JEV antigen was analyzed with ImageJ software. Representative immunofluorescence images and colocalization line graphs of three independent experiments are shown. |
PMC9431268_fig3_390114.jpg | What stands out most in this visual? | CT of a 49-year-old man (the sixth patient). (a, b) The initial CT scan (2 days after the onset) showed infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (c, d) The follow-up CT scan (15 days after the onset) showed there were still infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (e, f) The follow-up CT scan (28 days after the onset) showed the area of infiltrates and consolidations in the lower lobe of left lung had disappeared. |
PMC9431268_fig3_390117.jpg | What object or scene is depicted here? | CT of a 49-year-old man (the sixth patient). (a, b) The initial CT scan (2 days after the onset) showed infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (c, d) The follow-up CT scan (15 days after the onset) showed there were still infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (e, f) The follow-up CT scan (28 days after the onset) showed the area of infiltrates and consolidations in the lower lobe of left lung had disappeared. |
PMC9431268_fig3_390116.jpg | What object or scene is depicted here? | CT of a 49-year-old man (the sixth patient). (a, b) The initial CT scan (2 days after the onset) showed infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (c, d) The follow-up CT scan (15 days after the onset) showed there were still infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (e, f) The follow-up CT scan (28 days after the onset) showed the area of infiltrates and consolidations in the lower lobe of left lung had disappeared. |
PMC9431268_fig3_390113.jpg | What is the main focus of this visual representation? | CT of a 49-year-old man (the sixth patient). (a, b) The initial CT scan (2 days after the onset) showed infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (c, d) The follow-up CT scan (15 days after the onset) showed there were still infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (e, f) The follow-up CT scan (28 days after the onset) showed the area of infiltrates and consolidations in the lower lobe of left lung had disappeared. |
PMC9431268_fig3_390115.jpg | What is the core subject represented in this visual? | CT of a 49-year-old man (the sixth patient). (a, b) The initial CT scan (2 days after the onset) showed infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (c, d) The follow-up CT scan (15 days after the onset) showed there were still infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (e, f) The follow-up CT scan (28 days after the onset) showed the area of infiltrates and consolidations in the lower lobe of left lung had disappeared. |
PMC9431268_fig3_390112.jpg | What is the central feature of this picture? | CT of a 49-year-old man (the sixth patient). (a, b) The initial CT scan (2 days after the onset) showed infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (c, d) The follow-up CT scan (15 days after the onset) showed there were still infiltrates, reticular shadows, and consolidations with bronchograms in the lower lobe of left lung. (e, f) The follow-up CT scan (28 days after the onset) showed the area of infiltrates and consolidations in the lower lobe of left lung had disappeared. |
PMC9431367_F4_390121.jpg | What is the core subject represented in this visual? | Scaling the effect of TI-HFS at 130 Hz in the human head. (A). Placement of electrodes on the skin of the human cadaver. About 10 SEEGs were implanted in the brain for MTLE patients to record the stimulation potentials inside the brain. (B) Co-registration with the scanner and a template MRI show the amplitude of the envelope recorded during the TI-HFS session. It gives an indication on where the focus of stimulation is and the amplitude of the envelope of stimulation. Here, 1 and 3 mA were chosen to better target the anterior hippocampus in this specific cadaver and the field modulation envelope can reach an amplitude of 7 mV. (C) Electrode f is used to show the depth of the focal stimulation of TI-HFS in both square and sine waves. For TCS-like 130 Hz, it shows stronger stimulating fields in the cortex, which is primarily activated, compared to the deep structures, unlike for TI with sine waves or square waves (PWM TI). |
PMC9431367_F4_390118.jpg | Describe the main subject of this image. | Scaling the effect of TI-HFS at 130 Hz in the human head. (A). Placement of electrodes on the skin of the human cadaver. About 10 SEEGs were implanted in the brain for MTLE patients to record the stimulation potentials inside the brain. (B) Co-registration with the scanner and a template MRI show the amplitude of the envelope recorded during the TI-HFS session. It gives an indication on where the focus of stimulation is and the amplitude of the envelope of stimulation. Here, 1 and 3 mA were chosen to better target the anterior hippocampus in this specific cadaver and the field modulation envelope can reach an amplitude of 7 mV. (C) Electrode f is used to show the depth of the focal stimulation of TI-HFS in both square and sine waves. For TCS-like 130 Hz, it shows stronger stimulating fields in the cortex, which is primarily activated, compared to the deep structures, unlike for TI with sine waves or square waves (PWM TI). |
PMC9431367_F4_390124.jpg | What's the most prominent thing you notice in this picture? | Scaling the effect of TI-HFS at 130 Hz in the human head. (A). Placement of electrodes on the skin of the human cadaver. About 10 SEEGs were implanted in the brain for MTLE patients to record the stimulation potentials inside the brain. (B) Co-registration with the scanner and a template MRI show the amplitude of the envelope recorded during the TI-HFS session. It gives an indication on where the focus of stimulation is and the amplitude of the envelope of stimulation. Here, 1 and 3 mA were chosen to better target the anterior hippocampus in this specific cadaver and the field modulation envelope can reach an amplitude of 7 mV. (C) Electrode f is used to show the depth of the focal stimulation of TI-HFS in both square and sine waves. For TCS-like 130 Hz, it shows stronger stimulating fields in the cortex, which is primarily activated, compared to the deep structures, unlike for TI with sine waves or square waves (PWM TI). |
PMC9431367_F4_390122.jpg | What object or scene is depicted here? | Scaling the effect of TI-HFS at 130 Hz in the human head. (A). Placement of electrodes on the skin of the human cadaver. About 10 SEEGs were implanted in the brain for MTLE patients to record the stimulation potentials inside the brain. (B) Co-registration with the scanner and a template MRI show the amplitude of the envelope recorded during the TI-HFS session. It gives an indication on where the focus of stimulation is and the amplitude of the envelope of stimulation. Here, 1 and 3 mA were chosen to better target the anterior hippocampus in this specific cadaver and the field modulation envelope can reach an amplitude of 7 mV. (C) Electrode f is used to show the depth of the focal stimulation of TI-HFS in both square and sine waves. For TCS-like 130 Hz, it shows stronger stimulating fields in the cortex, which is primarily activated, compared to the deep structures, unlike for TI with sine waves or square waves (PWM TI). |
PMC9431367_F4_390120.jpg | What can you see in this picture? | Scaling the effect of TI-HFS at 130 Hz in the human head. (A). Placement of electrodes on the skin of the human cadaver. About 10 SEEGs were implanted in the brain for MTLE patients to record the stimulation potentials inside the brain. (B) Co-registration with the scanner and a template MRI show the amplitude of the envelope recorded during the TI-HFS session. It gives an indication on where the focus of stimulation is and the amplitude of the envelope of stimulation. Here, 1 and 3 mA were chosen to better target the anterior hippocampus in this specific cadaver and the field modulation envelope can reach an amplitude of 7 mV. (C) Electrode f is used to show the depth of the focal stimulation of TI-HFS in both square and sine waves. For TCS-like 130 Hz, it shows stronger stimulating fields in the cortex, which is primarily activated, compared to the deep structures, unlike for TI with sine waves or square waves (PWM TI). |
PMC9431431_fig1_390136.jpg | What is the core subject represented in this visual? | Microscopic evaluation of the susceptibility of LLC-MK2 cells and human respiratory epithelial cells (HRECs) to HCoV-NL63 infection. Confluent monolayer (submerged) cultures of LLC-MK2 cells and HRECs were inoculated with HCoV-NL63 at 1 × 105 TCID50/mL or mock inoculated (infection medium) and incubated for 96 h (n = 3). (A to F) Brightfield images of LLC-MK2 and HREC cultures at 96 h postinoculation (hpi). Mock-inoculated with LLC-MK2 cells (A), HRECs (B), and ALI-HRECs (C). (D) Cytopathic effects (CPE) in HCoV-NL63-infected LLC-MK2 cells, including clumping of cells and cytoplasmic stranding with cell detachment (see arrows). (E to F) Absence of CPE in HREC and ALI-HREC cultures. (G to L) Immunofluorescence staining for HCoV-NL63 N protein (green) and DAPI nuclear counterstain (blue). The indirect immunofluorescence assay (IFA) was performed using an IgG1 mouse monoclonal anti-HCoV-NL63 N protein (2D4; Ingenasa-Eurofins) at a final concentration of 0.25 μg/mL, followed by incubation with 20 μg/mL of FITC-conjugated goat anti-mouse IgG antibody (KPL; SeraCare Life Sciences Inc.), while cell nuclei were stained using NucBlue Fixed cell ReadyProbes reagent (DAPI; Invitrogen, Thermo Fisher Scientific). (G to I) Absence of unspecific fluorescence in mock-inoculated IFA controls for LLC-MK2 cells (G), HRECs (H), and ALI-HRECs (I). (J to L) HCoV-NL63 N protein (green) was detected in LLC-MK2 cells (J) but not in HRECs (K) nor in ALI-HRECs (L). Scale bar = 100 μm. |
PMC9431431_fig1_390127.jpg | What's the most prominent thing you notice in this picture? | Microscopic evaluation of the susceptibility of LLC-MK2 cells and human respiratory epithelial cells (HRECs) to HCoV-NL63 infection. Confluent monolayer (submerged) cultures of LLC-MK2 cells and HRECs were inoculated with HCoV-NL63 at 1 × 105 TCID50/mL or mock inoculated (infection medium) and incubated for 96 h (n = 3). (A to F) Brightfield images of LLC-MK2 and HREC cultures at 96 h postinoculation (hpi). Mock-inoculated with LLC-MK2 cells (A), HRECs (B), and ALI-HRECs (C). (D) Cytopathic effects (CPE) in HCoV-NL63-infected LLC-MK2 cells, including clumping of cells and cytoplasmic stranding with cell detachment (see arrows). (E to F) Absence of CPE in HREC and ALI-HREC cultures. (G to L) Immunofluorescence staining for HCoV-NL63 N protein (green) and DAPI nuclear counterstain (blue). The indirect immunofluorescence assay (IFA) was performed using an IgG1 mouse monoclonal anti-HCoV-NL63 N protein (2D4; Ingenasa-Eurofins) at a final concentration of 0.25 μg/mL, followed by incubation with 20 μg/mL of FITC-conjugated goat anti-mouse IgG antibody (KPL; SeraCare Life Sciences Inc.), while cell nuclei were stained using NucBlue Fixed cell ReadyProbes reagent (DAPI; Invitrogen, Thermo Fisher Scientific). (G to I) Absence of unspecific fluorescence in mock-inoculated IFA controls for LLC-MK2 cells (G), HRECs (H), and ALI-HRECs (I). (J to L) HCoV-NL63 N protein (green) was detected in LLC-MK2 cells (J) but not in HRECs (K) nor in ALI-HRECs (L). Scale bar = 100 μm. |
PMC9431431_fig1_390126.jpg | What can you see in this picture? | Microscopic evaluation of the susceptibility of LLC-MK2 cells and human respiratory epithelial cells (HRECs) to HCoV-NL63 infection. Confluent monolayer (submerged) cultures of LLC-MK2 cells and HRECs were inoculated with HCoV-NL63 at 1 × 105 TCID50/mL or mock inoculated (infection medium) and incubated for 96 h (n = 3). (A to F) Brightfield images of LLC-MK2 and HREC cultures at 96 h postinoculation (hpi). Mock-inoculated with LLC-MK2 cells (A), HRECs (B), and ALI-HRECs (C). (D) Cytopathic effects (CPE) in HCoV-NL63-infected LLC-MK2 cells, including clumping of cells and cytoplasmic stranding with cell detachment (see arrows). (E to F) Absence of CPE in HREC and ALI-HREC cultures. (G to L) Immunofluorescence staining for HCoV-NL63 N protein (green) and DAPI nuclear counterstain (blue). The indirect immunofluorescence assay (IFA) was performed using an IgG1 mouse monoclonal anti-HCoV-NL63 N protein (2D4; Ingenasa-Eurofins) at a final concentration of 0.25 μg/mL, followed by incubation with 20 μg/mL of FITC-conjugated goat anti-mouse IgG antibody (KPL; SeraCare Life Sciences Inc.), while cell nuclei were stained using NucBlue Fixed cell ReadyProbes reagent (DAPI; Invitrogen, Thermo Fisher Scientific). (G to I) Absence of unspecific fluorescence in mock-inoculated IFA controls for LLC-MK2 cells (G), HRECs (H), and ALI-HRECs (I). (J to L) HCoV-NL63 N protein (green) was detected in LLC-MK2 cells (J) but not in HRECs (K) nor in ALI-HRECs (L). Scale bar = 100 μm. |
PMC9431431_fig1_390134.jpg | Can you identify the primary element in this image? | Microscopic evaluation of the susceptibility of LLC-MK2 cells and human respiratory epithelial cells (HRECs) to HCoV-NL63 infection. Confluent monolayer (submerged) cultures of LLC-MK2 cells and HRECs were inoculated with HCoV-NL63 at 1 × 105 TCID50/mL or mock inoculated (infection medium) and incubated for 96 h (n = 3). (A to F) Brightfield images of LLC-MK2 and HREC cultures at 96 h postinoculation (hpi). Mock-inoculated with LLC-MK2 cells (A), HRECs (B), and ALI-HRECs (C). (D) Cytopathic effects (CPE) in HCoV-NL63-infected LLC-MK2 cells, including clumping of cells and cytoplasmic stranding with cell detachment (see arrows). (E to F) Absence of CPE in HREC and ALI-HREC cultures. (G to L) Immunofluorescence staining for HCoV-NL63 N protein (green) and DAPI nuclear counterstain (blue). The indirect immunofluorescence assay (IFA) was performed using an IgG1 mouse monoclonal anti-HCoV-NL63 N protein (2D4; Ingenasa-Eurofins) at a final concentration of 0.25 μg/mL, followed by incubation with 20 μg/mL of FITC-conjugated goat anti-mouse IgG antibody (KPL; SeraCare Life Sciences Inc.), while cell nuclei were stained using NucBlue Fixed cell ReadyProbes reagent (DAPI; Invitrogen, Thermo Fisher Scientific). (G to I) Absence of unspecific fluorescence in mock-inoculated IFA controls for LLC-MK2 cells (G), HRECs (H), and ALI-HRECs (I). (J to L) HCoV-NL63 N protein (green) was detected in LLC-MK2 cells (J) but not in HRECs (K) nor in ALI-HRECs (L). Scale bar = 100 μm. |
PMC9431431_fig1_390130.jpg | What's the most prominent thing you notice in this picture? | Microscopic evaluation of the susceptibility of LLC-MK2 cells and human respiratory epithelial cells (HRECs) to HCoV-NL63 infection. Confluent monolayer (submerged) cultures of LLC-MK2 cells and HRECs were inoculated with HCoV-NL63 at 1 × 105 TCID50/mL or mock inoculated (infection medium) and incubated for 96 h (n = 3). (A to F) Brightfield images of LLC-MK2 and HREC cultures at 96 h postinoculation (hpi). Mock-inoculated with LLC-MK2 cells (A), HRECs (B), and ALI-HRECs (C). (D) Cytopathic effects (CPE) in HCoV-NL63-infected LLC-MK2 cells, including clumping of cells and cytoplasmic stranding with cell detachment (see arrows). (E to F) Absence of CPE in HREC and ALI-HREC cultures. (G to L) Immunofluorescence staining for HCoV-NL63 N protein (green) and DAPI nuclear counterstain (blue). The indirect immunofluorescence assay (IFA) was performed using an IgG1 mouse monoclonal anti-HCoV-NL63 N protein (2D4; Ingenasa-Eurofins) at a final concentration of 0.25 μg/mL, followed by incubation with 20 μg/mL of FITC-conjugated goat anti-mouse IgG antibody (KPL; SeraCare Life Sciences Inc.), while cell nuclei were stained using NucBlue Fixed cell ReadyProbes reagent (DAPI; Invitrogen, Thermo Fisher Scientific). (G to I) Absence of unspecific fluorescence in mock-inoculated IFA controls for LLC-MK2 cells (G), HRECs (H), and ALI-HRECs (I). (J to L) HCoV-NL63 N protein (green) was detected in LLC-MK2 cells (J) but not in HRECs (K) nor in ALI-HRECs (L). Scale bar = 100 μm. |
PMC9431431_fig1_390133.jpg | What stands out most in this visual? | Microscopic evaluation of the susceptibility of LLC-MK2 cells and human respiratory epithelial cells (HRECs) to HCoV-NL63 infection. Confluent monolayer (submerged) cultures of LLC-MK2 cells and HRECs were inoculated with HCoV-NL63 at 1 × 105 TCID50/mL or mock inoculated (infection medium) and incubated for 96 h (n = 3). (A to F) Brightfield images of LLC-MK2 and HREC cultures at 96 h postinoculation (hpi). Mock-inoculated with LLC-MK2 cells (A), HRECs (B), and ALI-HRECs (C). (D) Cytopathic effects (CPE) in HCoV-NL63-infected LLC-MK2 cells, including clumping of cells and cytoplasmic stranding with cell detachment (see arrows). (E to F) Absence of CPE in HREC and ALI-HREC cultures. (G to L) Immunofluorescence staining for HCoV-NL63 N protein (green) and DAPI nuclear counterstain (blue). The indirect immunofluorescence assay (IFA) was performed using an IgG1 mouse monoclonal anti-HCoV-NL63 N protein (2D4; Ingenasa-Eurofins) at a final concentration of 0.25 μg/mL, followed by incubation with 20 μg/mL of FITC-conjugated goat anti-mouse IgG antibody (KPL; SeraCare Life Sciences Inc.), while cell nuclei were stained using NucBlue Fixed cell ReadyProbes reagent (DAPI; Invitrogen, Thermo Fisher Scientific). (G to I) Absence of unspecific fluorescence in mock-inoculated IFA controls for LLC-MK2 cells (G), HRECs (H), and ALI-HRECs (I). (J to L) HCoV-NL63 N protein (green) was detected in LLC-MK2 cells (J) but not in HRECs (K) nor in ALI-HRECs (L). Scale bar = 100 μm. |
PMC9431444_fig1_390138.jpg | What can you see in this picture? | Clinical signs of diseased yellow catfish. (A) Diseased yellow catfish hanging head up in water and exhibiting disoriented behavior; (B) diseased yellow catfish showing hemorrhages on head, mouth, lower jaw, and fin base; (C) spleen of diseased fish, showing a dark color; (D) kidney showing severe hemorrhagic and necrosis; (E) diseased fish spleen showing various-sized vacuolation (red arrow) by H&E staining; (F) diseased fish kidney showing edema and a moderate to heavy infiltration of lymphocytes (blue arrows) and condensed and marginated nuclei of glomerulus cells (black arrow) by H&E staining. |
PMC9431444_fig1_390140.jpg | What is being portrayed in this visual content? | Clinical signs of diseased yellow catfish. (A) Diseased yellow catfish hanging head up in water and exhibiting disoriented behavior; (B) diseased yellow catfish showing hemorrhages on head, mouth, lower jaw, and fin base; (C) spleen of diseased fish, showing a dark color; (D) kidney showing severe hemorrhagic and necrosis; (E) diseased fish spleen showing various-sized vacuolation (red arrow) by H&E staining; (F) diseased fish kidney showing edema and a moderate to heavy infiltration of lymphocytes (blue arrows) and condensed and marginated nuclei of glomerulus cells (black arrow) by H&E staining. |
PMC9431444_fig1_390141.jpg | Describe the main subject of this image. | Clinical signs of diseased yellow catfish. (A) Diseased yellow catfish hanging head up in water and exhibiting disoriented behavior; (B) diseased yellow catfish showing hemorrhages on head, mouth, lower jaw, and fin base; (C) spleen of diseased fish, showing a dark color; (D) kidney showing severe hemorrhagic and necrosis; (E) diseased fish spleen showing various-sized vacuolation (red arrow) by H&E staining; (F) diseased fish kidney showing edema and a moderate to heavy infiltration of lymphocytes (blue arrows) and condensed and marginated nuclei of glomerulus cells (black arrow) by H&E staining. |
PMC9431444_fig5_390145.jpg | What is the focal point of this photograph? | FISH detection of YcCV in naturally infected yellow catfish. (A and C) FISH hybridization in YcCV-infected kidney and spleen cells, respectively; (Aa, Ca) detection of positive signals in kidney and spleen cells, respectively; (Ba, Da) absence of signal in healthy kidney and spleen cells. Arrows show positive signals. |
PMC9431444_fig5_390143.jpg | What is the central feature of this picture? | FISH detection of YcCV in naturally infected yellow catfish. (A and C) FISH hybridization in YcCV-infected kidney and spleen cells, respectively; (Aa, Ca) detection of positive signals in kidney and spleen cells, respectively; (Ba, Da) absence of signal in healthy kidney and spleen cells. Arrows show positive signals. |
PMC9431444_fig5_390146.jpg | What stands out most in this visual? | FISH detection of YcCV in naturally infected yellow catfish. (A and C) FISH hybridization in YcCV-infected kidney and spleen cells, respectively; (Aa, Ca) detection of positive signals in kidney and spleen cells, respectively; (Ba, Da) absence of signal in healthy kidney and spleen cells. Arrows show positive signals. |
PMC9431444_fig5_390144.jpg | What is the principal component of this image? | FISH detection of YcCV in naturally infected yellow catfish. (A and C) FISH hybridization in YcCV-infected kidney and spleen cells, respectively; (Aa, Ca) detection of positive signals in kidney and spleen cells, respectively; (Ba, Da) absence of signal in healthy kidney and spleen cells. Arrows show positive signals. |
PMC9431444_fig5_390147.jpg | What is the core subject represented in this visual? | FISH detection of YcCV in naturally infected yellow catfish. (A and C) FISH hybridization in YcCV-infected kidney and spleen cells, respectively; (Aa, Ca) detection of positive signals in kidney and spleen cells, respectively; (Ba, Da) absence of signal in healthy kidney and spleen cells. Arrows show positive signals. |
PMC9431493_fig1_390153.jpg | What is the principal component of this image? | Subcellular localization of Crt1-GFP under cellulase induction condition. (A) Fluorescence microscopy analysis of Crt1-GFP after inducing with 1% (wt/vol) Avicel in MA medium for 12 h. Inset a: arrows indicated the plasma membrane; Inset b: arrows indicated the nuclear envelope. Scale bar: 10 μm. (B) Colocalization of Crt1-GFP and mCherry-Xyr1 after inducing with 1% (wt/vol) Avicel for 12 h. Scale bar: 10 μm. (C) Colocalization analysis of Crt1-GFP and the NE-localized Sec61α-mCherry. The strain was cultured in MA medium with 1% (wt/vol) Avicel for 12 h and mycelia were collected for fluorescence analysis. Scale bar: 10 μm. The fluorescence was examined with a Nikon Eclipse 80i fluorescence microscope. The images shown are taken from one of at least two independent experiments. |
PMC9431493_fig1_390155.jpg | What does this image primarily show? | Subcellular localization of Crt1-GFP under cellulase induction condition. (A) Fluorescence microscopy analysis of Crt1-GFP after inducing with 1% (wt/vol) Avicel in MA medium for 12 h. Inset a: arrows indicated the plasma membrane; Inset b: arrows indicated the nuclear envelope. Scale bar: 10 μm. (B) Colocalization of Crt1-GFP and mCherry-Xyr1 after inducing with 1% (wt/vol) Avicel for 12 h. Scale bar: 10 μm. (C) Colocalization analysis of Crt1-GFP and the NE-localized Sec61α-mCherry. The strain was cultured in MA medium with 1% (wt/vol) Avicel for 12 h and mycelia were collected for fluorescence analysis. Scale bar: 10 μm. The fluorescence was examined with a Nikon Eclipse 80i fluorescence microscope. The images shown are taken from one of at least two independent experiments. |
PMC9431493_fig1_390158.jpg | What is the central feature of this picture? | Subcellular localization of Crt1-GFP under cellulase induction condition. (A) Fluorescence microscopy analysis of Crt1-GFP after inducing with 1% (wt/vol) Avicel in MA medium for 12 h. Inset a: arrows indicated the plasma membrane; Inset b: arrows indicated the nuclear envelope. Scale bar: 10 μm. (B) Colocalization of Crt1-GFP and mCherry-Xyr1 after inducing with 1% (wt/vol) Avicel for 12 h. Scale bar: 10 μm. (C) Colocalization analysis of Crt1-GFP and the NE-localized Sec61α-mCherry. The strain was cultured in MA medium with 1% (wt/vol) Avicel for 12 h and mycelia were collected for fluorescence analysis. Scale bar: 10 μm. The fluorescence was examined with a Nikon Eclipse 80i fluorescence microscope. The images shown are taken from one of at least two independent experiments. |
PMC9431493_fig1_390156.jpg | What is being portrayed in this visual content? | Subcellular localization of Crt1-GFP under cellulase induction condition. (A) Fluorescence microscopy analysis of Crt1-GFP after inducing with 1% (wt/vol) Avicel in MA medium for 12 h. Inset a: arrows indicated the plasma membrane; Inset b: arrows indicated the nuclear envelope. Scale bar: 10 μm. (B) Colocalization of Crt1-GFP and mCherry-Xyr1 after inducing with 1% (wt/vol) Avicel for 12 h. Scale bar: 10 μm. (C) Colocalization analysis of Crt1-GFP and the NE-localized Sec61α-mCherry. The strain was cultured in MA medium with 1% (wt/vol) Avicel for 12 h and mycelia were collected for fluorescence analysis. Scale bar: 10 μm. The fluorescence was examined with a Nikon Eclipse 80i fluorescence microscope. The images shown are taken from one of at least two independent experiments. |
PMC9431493_fig1_390151.jpg | What is the principal component of this image? | Subcellular localization of Crt1-GFP under cellulase induction condition. (A) Fluorescence microscopy analysis of Crt1-GFP after inducing with 1% (wt/vol) Avicel in MA medium for 12 h. Inset a: arrows indicated the plasma membrane; Inset b: arrows indicated the nuclear envelope. Scale bar: 10 μm. (B) Colocalization of Crt1-GFP and mCherry-Xyr1 after inducing with 1% (wt/vol) Avicel for 12 h. Scale bar: 10 μm. (C) Colocalization analysis of Crt1-GFP and the NE-localized Sec61α-mCherry. The strain was cultured in MA medium with 1% (wt/vol) Avicel for 12 h and mycelia were collected for fluorescence analysis. Scale bar: 10 μm. The fluorescence was examined with a Nikon Eclipse 80i fluorescence microscope. The images shown are taken from one of at least two independent experiments. |
PMC9431493_fig1_390152.jpg | Describe the main subject of this image. | Subcellular localization of Crt1-GFP under cellulase induction condition. (A) Fluorescence microscopy analysis of Crt1-GFP after inducing with 1% (wt/vol) Avicel in MA medium for 12 h. Inset a: arrows indicated the plasma membrane; Inset b: arrows indicated the nuclear envelope. Scale bar: 10 μm. (B) Colocalization of Crt1-GFP and mCherry-Xyr1 after inducing with 1% (wt/vol) Avicel for 12 h. Scale bar: 10 μm. (C) Colocalization analysis of Crt1-GFP and the NE-localized Sec61α-mCherry. The strain was cultured in MA medium with 1% (wt/vol) Avicel for 12 h and mycelia were collected for fluorescence analysis. Scale bar: 10 μm. The fluorescence was examined with a Nikon Eclipse 80i fluorescence microscope. The images shown are taken from one of at least two independent experiments. |
PMC9431493_fig1_390157.jpg | What is shown in this image? | Subcellular localization of Crt1-GFP under cellulase induction condition. (A) Fluorescence microscopy analysis of Crt1-GFP after inducing with 1% (wt/vol) Avicel in MA medium for 12 h. Inset a: arrows indicated the plasma membrane; Inset b: arrows indicated the nuclear envelope. Scale bar: 10 μm. (B) Colocalization of Crt1-GFP and mCherry-Xyr1 after inducing with 1% (wt/vol) Avicel for 12 h. Scale bar: 10 μm. (C) Colocalization analysis of Crt1-GFP and the NE-localized Sec61α-mCherry. The strain was cultured in MA medium with 1% (wt/vol) Avicel for 12 h and mycelia were collected for fluorescence analysis. Scale bar: 10 μm. The fluorescence was examined with a Nikon Eclipse 80i fluorescence microscope. The images shown are taken from one of at least two independent experiments. |
PMC9431498_fig7_390160.jpg | Describe the main subject of this image. | Scanning electron microscopy (SEM) showing the effect of vagococcin T on E. faecium cells (magnification, ×30,000). Cells incubated without vagococcin T showed no visible cell damage (A), while the vagococcin T-treated cells had a shriveled appearance following a 2-h incubation with 10× MIC of vagococcin T (B). Signs of cell damage and lysis are indicated by red arrows. |
PMC9431598_fig4_390172.jpg | Describe the main subject of this image. | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390167.jpg | Describe the main subject of this image. | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390164.jpg | What is being portrayed in this visual content? | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390173.jpg | What's the most prominent thing you notice in this picture? | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390170.jpg | What's the most prominent thing you notice in this picture? | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390163.jpg | Describe the main subject of this image. | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390174.jpg | What can you see in this picture? | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390168.jpg | Can you identify the primary element in this image? | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390166.jpg | What is the dominant medical problem in this image? | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390165.jpg | What is the central feature of this picture? | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390162.jpg | Describe the main subject of this image. | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431598_fig4_390169.jpg | What stands out most in this visual? | Histological analysis of antibiotic induced virulence in kidneys. Histological examination revealed the formation of abscess in ceftazidime, ampicillin and tetracycline treated groups. Photos with ×2 magnification shows the gross area of the examined tissue and abscesses are indicated by arrows. The 20× magnified photos represent the selected abscess and the staining of cells at the abscess site can be clearly seen. The production of protein A and alpha-toxin was measured by immunohistochemistry and this is visible in the same abscess region. |
PMC9431617_fig5_390175.jpg | What is the focal point of this photograph? | Light-induced toxic compound production derived from IAA. PDA containing 200 μM IAA was incubated under dark or light condition for 1 day, before sporidia (OD600 ≈ 1.0) or mating culture (1:1 mixed sporidia of opposite mating-type) were inoculated. The IAA-containing PDA without preincubation (0 days) was used as control. The inoculated PDA plates were kept under constant dark for 3 days before photographing. Three biological repeats were performed, and representative images are shown here. |
PMC9431617_fig5_390176.jpg | What key item or scene is captured in this photo? | Light-induced toxic compound production derived from IAA. PDA containing 200 μM IAA was incubated under dark or light condition for 1 day, before sporidia (OD600 ≈ 1.0) or mating culture (1:1 mixed sporidia of opposite mating-type) were inoculated. The IAA-containing PDA without preincubation (0 days) was used as control. The inoculated PDA plates were kept under constant dark for 3 days before photographing. Three biological repeats were performed, and representative images are shown here. |
PMC9431662_fig2_390178.jpg | What is the dominant medical problem in this image? | Cross-reactive dengue virus D11C antibodies augment Zika virus replication in KU812 cells across time. KU812 cells were incubated with ZIKV-PRVABC59 (MOI, 1) for 1 h with either 6 μg/mL D11C or a nonspecific isotype control antibody, washed, and resuspended with fresh growth media. Cell-free supernatants were collected 4, 48, 72, and 96 hpi. Infectious virus was quantified by plaque assay. A two-way ANOVA and a Tukey’s multiple-comparison test were used to determine whether the presence of D11C enhanced ZIKV replication compared to that of the nonspecific isotype control. Data are expressed as PFU/mL ± SEM for n = 3 independent experiments, each replicated in duplicate. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, nonsignificant. |
PMC9431662_fig2_390179.jpg | Can you identify the primary element in this image? | Cross-reactive dengue virus D11C antibodies augment Zika virus replication in KU812 cells across time. KU812 cells were incubated with ZIKV-PRVABC59 (MOI, 1) for 1 h with either 6 μg/mL D11C or a nonspecific isotype control antibody, washed, and resuspended with fresh growth media. Cell-free supernatants were collected 4, 48, 72, and 96 hpi. Infectious virus was quantified by plaque assay. A two-way ANOVA and a Tukey’s multiple-comparison test were used to determine whether the presence of D11C enhanced ZIKV replication compared to that of the nonspecific isotype control. Data are expressed as PFU/mL ± SEM for n = 3 independent experiments, each replicated in duplicate. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, nonsignificant. |
PMC9431707_fig2_390213.jpg | What is shown in this image? | Knockout of RIPK3 suppresses Enterococcus faecalis-induced necroptosis in an experimental refractory apical periodontitis (RAP) mouse model. (A) Representative hematoxylin-eosin staining of the apical region in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection (n = 6/group; 100× and 200× magnification). The yellow double arrows mark width of the periodontal membrane; yellow dotted lines mark the periapical area; dr, distal root of the mandibular first molar; ab, alveolar bone; pl, periodontal ligament; f, furcation area. (B) Representative immunohistochemical staining of p-MLKL in the apical region of mandibular first molars (n = 6/group; 200× and 400× magnification). Scale bar: 50 μm. (C) Immunoblot analysis of RIKP3, p-MLKL, and MLKL expression levels and (D) densitometric analysis. Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by the least significant difference (LSD) post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig2_390222.jpg | What does this image primarily show? | Knockout of RIPK3 suppresses Enterococcus faecalis-induced necroptosis in an experimental refractory apical periodontitis (RAP) mouse model. (A) Representative hematoxylin-eosin staining of the apical region in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection (n = 6/group; 100× and 200× magnification). The yellow double arrows mark width of the periodontal membrane; yellow dotted lines mark the periapical area; dr, distal root of the mandibular first molar; ab, alveolar bone; pl, periodontal ligament; f, furcation area. (B) Representative immunohistochemical staining of p-MLKL in the apical region of mandibular first molars (n = 6/group; 200× and 400× magnification). Scale bar: 50 μm. (C) Immunoblot analysis of RIKP3, p-MLKL, and MLKL expression levels and (D) densitometric analysis. Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by the least significant difference (LSD) post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig2_390211.jpg | What is the focal point of this photograph? | Knockout of RIPK3 suppresses Enterococcus faecalis-induced necroptosis in an experimental refractory apical periodontitis (RAP) mouse model. (A) Representative hematoxylin-eosin staining of the apical region in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection (n = 6/group; 100× and 200× magnification). The yellow double arrows mark width of the periodontal membrane; yellow dotted lines mark the periapical area; dr, distal root of the mandibular first molar; ab, alveolar bone; pl, periodontal ligament; f, furcation area. (B) Representative immunohistochemical staining of p-MLKL in the apical region of mandibular first molars (n = 6/group; 200× and 400× magnification). Scale bar: 50 μm. (C) Immunoblot analysis of RIKP3, p-MLKL, and MLKL expression levels and (D) densitometric analysis. Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by the least significant difference (LSD) post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig2_390214.jpg | Describe the main subject of this image. | Knockout of RIPK3 suppresses Enterococcus faecalis-induced necroptosis in an experimental refractory apical periodontitis (RAP) mouse model. (A) Representative hematoxylin-eosin staining of the apical region in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection (n = 6/group; 100× and 200× magnification). The yellow double arrows mark width of the periodontal membrane; yellow dotted lines mark the periapical area; dr, distal root of the mandibular first molar; ab, alveolar bone; pl, periodontal ligament; f, furcation area. (B) Representative immunohistochemical staining of p-MLKL in the apical region of mandibular first molars (n = 6/group; 200× and 400× magnification). Scale bar: 50 μm. (C) Immunoblot analysis of RIKP3, p-MLKL, and MLKL expression levels and (D) densitometric analysis. Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by the least significant difference (LSD) post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig2_390215.jpg | What object or scene is depicted here? | Knockout of RIPK3 suppresses Enterococcus faecalis-induced necroptosis in an experimental refractory apical periodontitis (RAP) mouse model. (A) Representative hematoxylin-eosin staining of the apical region in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection (n = 6/group; 100× and 200× magnification). The yellow double arrows mark width of the periodontal membrane; yellow dotted lines mark the periapical area; dr, distal root of the mandibular first molar; ab, alveolar bone; pl, periodontal ligament; f, furcation area. (B) Representative immunohistochemical staining of p-MLKL in the apical region of mandibular first molars (n = 6/group; 200× and 400× magnification). Scale bar: 50 μm. (C) Immunoblot analysis of RIKP3, p-MLKL, and MLKL expression levels and (D) densitometric analysis. Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by the least significant difference (LSD) post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig2_390217.jpg | What is the core subject represented in this visual? | Knockout of RIPK3 suppresses Enterococcus faecalis-induced necroptosis in an experimental refractory apical periodontitis (RAP) mouse model. (A) Representative hematoxylin-eosin staining of the apical region in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection (n = 6/group; 100× and 200× magnification). The yellow double arrows mark width of the periodontal membrane; yellow dotted lines mark the periapical area; dr, distal root of the mandibular first molar; ab, alveolar bone; pl, periodontal ligament; f, furcation area. (B) Representative immunohistochemical staining of p-MLKL in the apical region of mandibular first molars (n = 6/group; 200× and 400× magnification). Scale bar: 50 μm. (C) Immunoblot analysis of RIKP3, p-MLKL, and MLKL expression levels and (D) densitometric analysis. Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by the least significant difference (LSD) post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig2_390218.jpg | What does this image primarily show? | Knockout of RIPK3 suppresses Enterococcus faecalis-induced necroptosis in an experimental refractory apical periodontitis (RAP) mouse model. (A) Representative hematoxylin-eosin staining of the apical region in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection (n = 6/group; 100× and 200× magnification). The yellow double arrows mark width of the periodontal membrane; yellow dotted lines mark the periapical area; dr, distal root of the mandibular first molar; ab, alveolar bone; pl, periodontal ligament; f, furcation area. (B) Representative immunohistochemical staining of p-MLKL in the apical region of mandibular first molars (n = 6/group; 200× and 400× magnification). Scale bar: 50 μm. (C) Immunoblot analysis of RIKP3, p-MLKL, and MLKL expression levels and (D) densitometric analysis. Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way analysis of variance (ANOVA) followed by the least significant difference (LSD) post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig3_390193.jpg | What is shown in this image? | Knockout of RIPK3 alleviates bone destruction in an Enterococcus faecalis-infected refractory apical periodontitis (RAP) mouse model. (A) Micro-CT evaluation of bone destruction in the apical region of mandibular first molars in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection. Representative X-ray images and 2D images as well as 3D reconstruction. The red areas mark bone destruction. (B) Evaluation of the bone volume fraction of the residual alveolar bone. (C and D) Microstructural parameter analysis of the trabecular bone, including (C) trabecular thickness (Tb. Th) and (D) trabecular bone clearance (Tb. sp) (n = 6/group). Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA with the LSD post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig3_390187.jpg | What is shown in this image? | Knockout of RIPK3 alleviates bone destruction in an Enterococcus faecalis-infected refractory apical periodontitis (RAP) mouse model. (A) Micro-CT evaluation of bone destruction in the apical region of mandibular first molars in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection. Representative X-ray images and 2D images as well as 3D reconstruction. The red areas mark bone destruction. (B) Evaluation of the bone volume fraction of the residual alveolar bone. (C and D) Microstructural parameter analysis of the trabecular bone, including (C) trabecular thickness (Tb. Th) and (D) trabecular bone clearance (Tb. sp) (n = 6/group). Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA with the LSD post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig3_390188.jpg | What key item or scene is captured in this photo? | Knockout of RIPK3 alleviates bone destruction in an Enterococcus faecalis-infected refractory apical periodontitis (RAP) mouse model. (A) Micro-CT evaluation of bone destruction in the apical region of mandibular first molars in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection. Representative X-ray images and 2D images as well as 3D reconstruction. The red areas mark bone destruction. (B) Evaluation of the bone volume fraction of the residual alveolar bone. (C and D) Microstructural parameter analysis of the trabecular bone, including (C) trabecular thickness (Tb. Th) and (D) trabecular bone clearance (Tb. sp) (n = 6/group). Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA with the LSD post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig3_390186.jpg | What can you see in this picture? | Knockout of RIPK3 alleviates bone destruction in an Enterococcus faecalis-infected refractory apical periodontitis (RAP) mouse model. (A) Micro-CT evaluation of bone destruction in the apical region of mandibular first molars in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection. Representative X-ray images and 2D images as well as 3D reconstruction. The red areas mark bone destruction. (B) Evaluation of the bone volume fraction of the residual alveolar bone. (C and D) Microstructural parameter analysis of the trabecular bone, including (C) trabecular thickness (Tb. Th) and (D) trabecular bone clearance (Tb. sp) (n = 6/group). Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA with the LSD post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig3_390191.jpg | What object or scene is depicted here? | Knockout of RIPK3 alleviates bone destruction in an Enterococcus faecalis-infected refractory apical periodontitis (RAP) mouse model. (A) Micro-CT evaluation of bone destruction in the apical region of mandibular first molars in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection. Representative X-ray images and 2D images as well as 3D reconstruction. The red areas mark bone destruction. (B) Evaluation of the bone volume fraction of the residual alveolar bone. (C and D) Microstructural parameter analysis of the trabecular bone, including (C) trabecular thickness (Tb. Th) and (D) trabecular bone clearance (Tb. sp) (n = 6/group). Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA with the LSD post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig3_390192.jpg | What is being portrayed in this visual content? | Knockout of RIPK3 alleviates bone destruction in an Enterococcus faecalis-infected refractory apical periodontitis (RAP) mouse model. (A) Micro-CT evaluation of bone destruction in the apical region of mandibular first molars in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection. Representative X-ray images and 2D images as well as 3D reconstruction. The red areas mark bone destruction. (B) Evaluation of the bone volume fraction of the residual alveolar bone. (C and D) Microstructural parameter analysis of the trabecular bone, including (C) trabecular thickness (Tb. Th) and (D) trabecular bone clearance (Tb. sp) (n = 6/group). Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA with the LSD post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig3_390190.jpg | What key item or scene is captured in this photo? | Knockout of RIPK3 alleviates bone destruction in an Enterococcus faecalis-infected refractory apical periodontitis (RAP) mouse model. (A) Micro-CT evaluation of bone destruction in the apical region of mandibular first molars in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection. Representative X-ray images and 2D images as well as 3D reconstruction. The red areas mark bone destruction. (B) Evaluation of the bone volume fraction of the residual alveolar bone. (C and D) Microstructural parameter analysis of the trabecular bone, including (C) trabecular thickness (Tb. Th) and (D) trabecular bone clearance (Tb. sp) (n = 6/group). Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA with the LSD post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig3_390185.jpg | What is shown in this image? | Knockout of RIPK3 alleviates bone destruction in an Enterococcus faecalis-infected refractory apical periodontitis (RAP) mouse model. (A) Micro-CT evaluation of bone destruction in the apical region of mandibular first molars in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection. Representative X-ray images and 2D images as well as 3D reconstruction. The red areas mark bone destruction. (B) Evaluation of the bone volume fraction of the residual alveolar bone. (C and D) Microstructural parameter analysis of the trabecular bone, including (C) trabecular thickness (Tb. Th) and (D) trabecular bone clearance (Tb. sp) (n = 6/group). Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA with the LSD post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig3_390189.jpg | What does this image primarily show? | Knockout of RIPK3 alleviates bone destruction in an Enterococcus faecalis-infected refractory apical periodontitis (RAP) mouse model. (A) Micro-CT evaluation of bone destruction in the apical region of mandibular first molars in wild-type (WT) and RIPK3−/− mice with or without E. faecalis infection. Representative X-ray images and 2D images as well as 3D reconstruction. The red areas mark bone destruction. (B) Evaluation of the bone volume fraction of the residual alveolar bone. (C and D) Microstructural parameter analysis of the trabecular bone, including (C) trabecular thickness (Tb. Th) and (D) trabecular bone clearance (Tb. sp) (n = 6/group). Results are shown as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA with the LSD post hoc test. *, P < 0.05; **, P < 0.01; ***, P < 0.001. |
PMC9431707_fig4_390196.jpg | What is the principal component of this image? | The executioner of necroptosis colocalizes with a macrophage marker in refractory apical periodontitis (RAP) lesions. (A) Double-immunofluorescence staining of p-MLKL (red), executioner of necroptosis, and the macrophage marker CD68 (green) in healthy and RAP specimens from patients (n = 6/group). (B) Immunofluorescence colocalization of p-MLKL (red) and macrophage marker F4/80 (green) in uninfected and Enterococcus faecalis-infected RAP mouse models (n = 6/group). DAPI staining shows cell nuclei (blue; 400× magnification). Scale bar: 50 μm. The representative images were obtained from three independent experiments. |
PMC9431707_fig4_390199.jpg | What object or scene is depicted here? | The executioner of necroptosis colocalizes with a macrophage marker in refractory apical periodontitis (RAP) lesions. (A) Double-immunofluorescence staining of p-MLKL (red), executioner of necroptosis, and the macrophage marker CD68 (green) in healthy and RAP specimens from patients (n = 6/group). (B) Immunofluorescence colocalization of p-MLKL (red) and macrophage marker F4/80 (green) in uninfected and Enterococcus faecalis-infected RAP mouse models (n = 6/group). DAPI staining shows cell nuclei (blue; 400× magnification). Scale bar: 50 μm. The representative images were obtained from three independent experiments. |
PMC9431707_fig4_390202.jpg | What stands out most in this visual? | The executioner of necroptosis colocalizes with a macrophage marker in refractory apical periodontitis (RAP) lesions. (A) Double-immunofluorescence staining of p-MLKL (red), executioner of necroptosis, and the macrophage marker CD68 (green) in healthy and RAP specimens from patients (n = 6/group). (B) Immunofluorescence colocalization of p-MLKL (red) and macrophage marker F4/80 (green) in uninfected and Enterococcus faecalis-infected RAP mouse models (n = 6/group). DAPI staining shows cell nuclei (blue; 400× magnification). Scale bar: 50 μm. The representative images were obtained from three independent experiments. |
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