image
stringlengths 20
66
| question
stringclasses 16
values | answer
stringlengths 3
10.7k
|
|---|---|---|
PMC9431707_fig4_390204.jpg | What key item or scene is captured in this photo? | 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_390194.jpg | What does this image primarily show? | 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_390200.jpg | What key item or scene is captured in this photo? | 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_390206.jpg | What is the focal point of this photograph? | 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_390198.jpg | What is the focal point of this photograph? | 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. |
PMC9432349_F1_390229.jpg | What object or scene is depicted here? | Silk of P. conspersa. (A)
P. conspersa larvae; (B)
P. conspersa silken net in the natural environment; (C–F) Scanning electron microscopy (SEM) of the silk fibers spun by the larvae in laboratory conditions caught on the surface of an aluminum holder at various magnifications. It is clearly distinguishable that the fibers are composed of two filaments, and they are slightly flattened. The arrows indicate the mass of adhesive material that stretches between the fibers. Asterisks mark a piece of plant debris that the fibres attached to. Scale-bars: (A,B) 1 mm; (C–F) 10 μm. |
PMC9432349_F1_390225.jpg | What is shown in this image? | Silk of P. conspersa. (A)
P. conspersa larvae; (B)
P. conspersa silken net in the natural environment; (C–F) Scanning electron microscopy (SEM) of the silk fibers spun by the larvae in laboratory conditions caught on the surface of an aluminum holder at various magnifications. It is clearly distinguishable that the fibers are composed of two filaments, and they are slightly flattened. The arrows indicate the mass of adhesive material that stretches between the fibers. Asterisks mark a piece of plant debris that the fibres attached to. Scale-bars: (A,B) 1 mm; (C–F) 10 μm. |
PMC9432349_F1_390226.jpg | What is being portrayed in this visual content? | Silk of P. conspersa. (A)
P. conspersa larvae; (B)
P. conspersa silken net in the natural environment; (C–F) Scanning electron microscopy (SEM) of the silk fibers spun by the larvae in laboratory conditions caught on the surface of an aluminum holder at various magnifications. It is clearly distinguishable that the fibers are composed of two filaments, and they are slightly flattened. The arrows indicate the mass of adhesive material that stretches between the fibers. Asterisks mark a piece of plant debris that the fibres attached to. Scale-bars: (A,B) 1 mm; (C–F) 10 μm. |
PMC9432349_F2_390234.jpg | What is shown in this image? | Morphology of the silk gland (SG) from P. conspersa last instar larvae. (A) Schematic illustration of the SG anatomy in the larval body; blue arrowheads show the boundaries of the SG compartments, i.e., where anterior, middle, and posterior SG (ASG, MSG, and PSG) part. Vertical red lines marked by small letters (b–e) refer to the whole-body sections (B–E) and show the approximate position where the glands were cut in the respective transverse paraplast sections; (B–E) Transverse paraplast sections through the body of a fifth instar larva stained with Masson trichrome stain. Inserted images show higher magnification of the SG section pointed by the arrowheads; (B–D) MSG front, middle and rear portions; (E) PSG. Scale-bars: (A) 1,000 μm; (B–E), 200 μm; inset images, 50 μm. |
PMC9432349_F2_390231.jpg | What is the dominant medical problem in this image? | Morphology of the silk gland (SG) from P. conspersa last instar larvae. (A) Schematic illustration of the SG anatomy in the larval body; blue arrowheads show the boundaries of the SG compartments, i.e., where anterior, middle, and posterior SG (ASG, MSG, and PSG) part. Vertical red lines marked by small letters (b–e) refer to the whole-body sections (B–E) and show the approximate position where the glands were cut in the respective transverse paraplast sections; (B–E) Transverse paraplast sections through the body of a fifth instar larva stained with Masson trichrome stain. Inserted images show higher magnification of the SG section pointed by the arrowheads; (B–D) MSG front, middle and rear portions; (E) PSG. Scale-bars: (A) 1,000 μm; (B–E), 200 μm; inset images, 50 μm. |
PMC9432349_F2_390233.jpg | What is being portrayed in this visual content? | Morphology of the silk gland (SG) from P. conspersa last instar larvae. (A) Schematic illustration of the SG anatomy in the larval body; blue arrowheads show the boundaries of the SG compartments, i.e., where anterior, middle, and posterior SG (ASG, MSG, and PSG) part. Vertical red lines marked by small letters (b–e) refer to the whole-body sections (B–E) and show the approximate position where the glands were cut in the respective transverse paraplast sections; (B–E) Transverse paraplast sections through the body of a fifth instar larva stained with Masson trichrome stain. Inserted images show higher magnification of the SG section pointed by the arrowheads; (B–D) MSG front, middle and rear portions; (E) PSG. Scale-bars: (A) 1,000 μm; (B–E), 200 μm; inset images, 50 μm. |
PMC9432349_F2_390232.jpg | What does this image primarily show? | Morphology of the silk gland (SG) from P. conspersa last instar larvae. (A) Schematic illustration of the SG anatomy in the larval body; blue arrowheads show the boundaries of the SG compartments, i.e., where anterior, middle, and posterior SG (ASG, MSG, and PSG) part. Vertical red lines marked by small letters (b–e) refer to the whole-body sections (B–E) and show the approximate position where the glands were cut in the respective transverse paraplast sections; (B–E) Transverse paraplast sections through the body of a fifth instar larva stained with Masson trichrome stain. Inserted images show higher magnification of the SG section pointed by the arrowheads; (B–D) MSG front, middle and rear portions; (E) PSG. Scale-bars: (A) 1,000 μm; (B–E), 200 μm; inset images, 50 μm. |
PMC9432461_F1_390236.jpg | Can you identify the primary element in this image? | Brain scan of a patient with left frontotemporal glioblastoma multiforme who had relapsed from surgery, standard chemoradiotherapy regimen, and ten cycles of adjuvant temozolomide, and then had progressed after bevacizumab treatment. Comparison of imaging findings between pre-treatment (A) and post-treatment at 4 months of apatinib monotherapy (B) by contrast-enhanced MRI and MRI-Flair. The patient achieved partial response after treatment and had a progression-free survival time of 5.3 months. |
PMC9432461_F1_390237.jpg | What can you see in this picture? | Brain scan of a patient with left frontotemporal glioblastoma multiforme who had relapsed from surgery, standard chemoradiotherapy regimen, and ten cycles of adjuvant temozolomide, and then had progressed after bevacizumab treatment. Comparison of imaging findings between pre-treatment (A) and post-treatment at 4 months of apatinib monotherapy (B) by contrast-enhanced MRI and MRI-Flair. The patient achieved partial response after treatment and had a progression-free survival time of 5.3 months. |
PMC9432720_F1_390246.jpg | What is the main focus of this visual representation? | Baseline data. (A) Computed tomography (CT) images. (B) Magnetic resonance imaging (MRI). (C) Positron emission tomography-computed tomography (PET-CT) image. (D) Representative histopathological image of the tumor (H&E staining). (E) Next-generation sequencing showed a p.N771-P772insH (c.2311-2312insACC) mutation in EGFR exon 20. |
PMC9432720_F1_390247.jpg | What is the principal component of this image? | Baseline data. (A) Computed tomography (CT) images. (B) Magnetic resonance imaging (MRI). (C) Positron emission tomography-computed tomography (PET-CT) image. (D) Representative histopathological image of the tumor (H&E staining). (E) Next-generation sequencing showed a p.N771-P772insH (c.2311-2312insACC) mutation in EGFR exon 20. |
PMC9432720_F1_390241.jpg | What's the most prominent thing you notice in this picture? | Baseline data. (A) Computed tomography (CT) images. (B) Magnetic resonance imaging (MRI). (C) Positron emission tomography-computed tomography (PET-CT) image. (D) Representative histopathological image of the tumor (H&E staining). (E) Next-generation sequencing showed a p.N771-P772insH (c.2311-2312insACC) mutation in EGFR exon 20. |
PMC9432720_F2_390248.jpg | What key item or scene is captured in this photo? | Tumor progression of the patient before and after treatment. (A) Representative computed tomography images at various points. CT images revealed lesions in the lower right lung. (B) Magnetic resonance images at various points. PFS, progression-free survival. The timeline of therapies, therapeutic regimens and tumor progression are indicated (top). The tumor is indicated by red arrows. SD, stable disease; PD, progressive disease; PR, partial response. |
PMC9432720_F2_390250.jpg | What is being portrayed in this visual content? | Tumor progression of the patient before and after treatment. (A) Representative computed tomography images at various points. CT images revealed lesions in the lower right lung. (B) Magnetic resonance images at various points. PFS, progression-free survival. The timeline of therapies, therapeutic regimens and tumor progression are indicated (top). The tumor is indicated by red arrows. SD, stable disease; PD, progressive disease; PR, partial response. |
PMC9432720_F2_390249.jpg | What does this image primarily show? | Tumor progression of the patient before and after treatment. (A) Representative computed tomography images at various points. CT images revealed lesions in the lower right lung. (B) Magnetic resonance images at various points. PFS, progression-free survival. The timeline of therapies, therapeutic regimens and tumor progression are indicated (top). The tumor is indicated by red arrows. SD, stable disease; PD, progressive disease; PR, partial response. |
PMC9432740_pone.0273674.g001_390259.jpg | What's the most prominent thing you notice in this picture? | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary (A-C) and secondary (D-F) ERM. (A) Epiretinal membrane specimen from a 69-year-old female patient with primary ERM, showing negative staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with partial retinoschisis but no EZ defect. (D) Epiretinal membrane specimen from a 61-year-old male patient with secondary ERM from rhegmatogenous retinal detachment (RRD), showing positive staining for S1P (arrows). (E) Ultrawide field retinal photograph that shows a retinal tear with laser scars (arrows). (F) Image of SD-OCT that shows ERM with EZ defect (arrowheads). |
PMC9432740_pone.0273674.g001_390260.jpg | What is the dominant medical problem in this image? | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary (A-C) and secondary (D-F) ERM. (A) Epiretinal membrane specimen from a 69-year-old female patient with primary ERM, showing negative staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with partial retinoschisis but no EZ defect. (D) Epiretinal membrane specimen from a 61-year-old male patient with secondary ERM from rhegmatogenous retinal detachment (RRD), showing positive staining for S1P (arrows). (E) Ultrawide field retinal photograph that shows a retinal tear with laser scars (arrows). (F) Image of SD-OCT that shows ERM with EZ defect (arrowheads). |
PMC9432740_pone.0273674.g001_390262.jpg | Describe the main subject of this image. | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary (A-C) and secondary (D-F) ERM. (A) Epiretinal membrane specimen from a 69-year-old female patient with primary ERM, showing negative staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with partial retinoschisis but no EZ defect. (D) Epiretinal membrane specimen from a 61-year-old male patient with secondary ERM from rhegmatogenous retinal detachment (RRD), showing positive staining for S1P (arrows). (E) Ultrawide field retinal photograph that shows a retinal tear with laser scars (arrows). (F) Image of SD-OCT that shows ERM with EZ defect (arrowheads). |
PMC9432740_pone.0273674.g001_390261.jpg | What object or scene is depicted here? | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary (A-C) and secondary (D-F) ERM. (A) Epiretinal membrane specimen from a 69-year-old female patient with primary ERM, showing negative staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with partial retinoschisis but no EZ defect. (D) Epiretinal membrane specimen from a 61-year-old male patient with secondary ERM from rhegmatogenous retinal detachment (RRD), showing positive staining for S1P (arrows). (E) Ultrawide field retinal photograph that shows a retinal tear with laser scars (arrows). (F) Image of SD-OCT that shows ERM with EZ defect (arrowheads). |
PMC9432740_pone.0273674.g001_390258.jpg | Describe the main subject of this image. | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary (A-C) and secondary (D-F) ERM. (A) Epiretinal membrane specimen from a 69-year-old female patient with primary ERM, showing negative staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with partial retinoschisis but no EZ defect. (D) Epiretinal membrane specimen from a 61-year-old male patient with secondary ERM from rhegmatogenous retinal detachment (RRD), showing positive staining for S1P (arrows). (E) Ultrawide field retinal photograph that shows a retinal tear with laser scars (arrows). (F) Image of SD-OCT that shows ERM with EZ defect (arrowheads). |
PMC9432740_pone.0273674.g002_390254.jpg | What object or scene is depicted here? | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary ERM with (A-C) or without (D-F) ellipsoid zone (EZ) defects. (A) Epiretinal membrane specimen from a 64-year-old female patient with primary ERM with EZ defect, showing higher positive staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with EZ defect (arrowheads). (D) Epiretinal membrane specimen from a 73-year-old female patient with primary ERM without EZ defect, showing lower positive staining for S1P. Only a couple of cells were stained with S1P (arrows). (E) Ultrawide field retinal photography that shows no specific underlying retinal disease. (F) Image of SD-OCT that shows ERM without EZ defect. |
PMC9432740_pone.0273674.g002_390253.jpg | What key item or scene is captured in this photo? | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary ERM with (A-C) or without (D-F) ellipsoid zone (EZ) defects. (A) Epiretinal membrane specimen from a 64-year-old female patient with primary ERM with EZ defect, showing higher positive staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with EZ defect (arrowheads). (D) Epiretinal membrane specimen from a 73-year-old female patient with primary ERM without EZ defect, showing lower positive staining for S1P. Only a couple of cells were stained with S1P (arrows). (E) Ultrawide field retinal photography that shows no specific underlying retinal disease. (F) Image of SD-OCT that shows ERM without EZ defect. |
PMC9432740_pone.0273674.g002_390252.jpg | What object or scene is depicted here? | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary ERM with (A-C) or without (D-F) ellipsoid zone (EZ) defects. (A) Epiretinal membrane specimen from a 64-year-old female patient with primary ERM with EZ defect, showing higher positive staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with EZ defect (arrowheads). (D) Epiretinal membrane specimen from a 73-year-old female patient with primary ERM without EZ defect, showing lower positive staining for S1P. Only a couple of cells were stained with S1P (arrows). (E) Ultrawide field retinal photography that shows no specific underlying retinal disease. (F) Image of SD-OCT that shows ERM without EZ defect. |
PMC9432740_pone.0273674.g002_390251.jpg | What is the core subject represented in this visual? | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary ERM with (A-C) or without (D-F) ellipsoid zone (EZ) defects. (A) Epiretinal membrane specimen from a 64-year-old female patient with primary ERM with EZ defect, showing higher positive staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with EZ defect (arrowheads). (D) Epiretinal membrane specimen from a 73-year-old female patient with primary ERM without EZ defect, showing lower positive staining for S1P. Only a couple of cells were stained with S1P (arrows). (E) Ultrawide field retinal photography that shows no specific underlying retinal disease. (F) Image of SD-OCT that shows ERM without EZ defect. |
PMC9432740_pone.0273674.g002_390255.jpg | What is the main focus of this visual representation? | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary ERM with (A-C) or without (D-F) ellipsoid zone (EZ) defects. (A) Epiretinal membrane specimen from a 64-year-old female patient with primary ERM with EZ defect, showing higher positive staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with EZ defect (arrowheads). (D) Epiretinal membrane specimen from a 73-year-old female patient with primary ERM without EZ defect, showing lower positive staining for S1P. Only a couple of cells were stained with S1P (arrows). (E) Ultrawide field retinal photography that shows no specific underlying retinal disease. (F) Image of SD-OCT that shows ERM without EZ defect. |
PMC9432740_pone.0273674.g002_390256.jpg | What is the core subject represented in this visual? | Representative images of stained epiretinal membrane (ERM) specimens and retinal images from patients with primary ERM with (A-C) or without (D-F) ellipsoid zone (EZ) defects. (A) Epiretinal membrane specimen from a 64-year-old female patient with primary ERM with EZ defect, showing higher positive staining for sphingosine-1-phosphate (S1P). (B) Ultrawide field retinal photograph that shows no specific underlying retinal disease. (C) Image of spectral-domain optical coherence tomography (SD-OCT) that shows ERM with EZ defect (arrowheads). (D) Epiretinal membrane specimen from a 73-year-old female patient with primary ERM without EZ defect, showing lower positive staining for S1P. Only a couple of cells were stained with S1P (arrows). (E) Ultrawide field retinal photography that shows no specific underlying retinal disease. (F) Image of SD-OCT that shows ERM without EZ defect. |
PMC9432748_pone.0273921.g006_390265.jpg | What's the most prominent thing you notice in this picture? | Electronmicrographs of kidney tissue in all experimental solution groups.Kidney tissue damage was ultrastructurally characterized by effacement of pedicels in podocytes, thickening of glomerular basal laminae in UW (A) group. Degenerated podocytes and disturbed glomerular basal membranes were observed in UW-g solution group (B). Mildly degenerated podocytes were reflecting low degree of glomerular injury in UW-m group (C). Minimal proximal tubular degenerations were also noticed in this group. Mild degree of podocytes degeneration and moderately thickened glomerular basal laminae in mUW (D) and mUW-g (E) groups. Mild podocytes degeneration and thickening of glomerular basal laminae in mUW-m (F) group. (original magnifications; UW group; x20.000, UW-g group; x20,000, UW-m group; x5000, mUW; x7,500, mUW-g; x7,500, mUW-m; x12,000). |
PMC9432748_pone.0273921.g006_390266.jpg | What is shown in this image? | Electronmicrographs of kidney tissue in all experimental solution groups.Kidney tissue damage was ultrastructurally characterized by effacement of pedicels in podocytes, thickening of glomerular basal laminae in UW (A) group. Degenerated podocytes and disturbed glomerular basal membranes were observed in UW-g solution group (B). Mildly degenerated podocytes were reflecting low degree of glomerular injury in UW-m group (C). Minimal proximal tubular degenerations were also noticed in this group. Mild degree of podocytes degeneration and moderately thickened glomerular basal laminae in mUW (D) and mUW-g (E) groups. Mild podocytes degeneration and thickening of glomerular basal laminae in mUW-m (F) group. (original magnifications; UW group; x20.000, UW-g group; x20,000, UW-m group; x5000, mUW; x7,500, mUW-g; x7,500, mUW-m; x12,000). |
PMC9432748_pone.0273921.g006_390264.jpg | What is the core subject represented in this visual? | Electronmicrographs of kidney tissue in all experimental solution groups.Kidney tissue damage was ultrastructurally characterized by effacement of pedicels in podocytes, thickening of glomerular basal laminae in UW (A) group. Degenerated podocytes and disturbed glomerular basal membranes were observed in UW-g solution group (B). Mildly degenerated podocytes were reflecting low degree of glomerular injury in UW-m group (C). Minimal proximal tubular degenerations were also noticed in this group. Mild degree of podocytes degeneration and moderately thickened glomerular basal laminae in mUW (D) and mUW-g (E) groups. Mild podocytes degeneration and thickening of glomerular basal laminae in mUW-m (F) group. (original magnifications; UW group; x20.000, UW-g group; x20,000, UW-m group; x5000, mUW; x7,500, mUW-g; x7,500, mUW-m; x12,000). |
PMC9432748_pone.0273921.g006_390267.jpg | What is the dominant medical problem in this image? | Electronmicrographs of kidney tissue in all experimental solution groups.Kidney tissue damage was ultrastructurally characterized by effacement of pedicels in podocytes, thickening of glomerular basal laminae in UW (A) group. Degenerated podocytes and disturbed glomerular basal membranes were observed in UW-g solution group (B). Mildly degenerated podocytes were reflecting low degree of glomerular injury in UW-m group (C). Minimal proximal tubular degenerations were also noticed in this group. Mild degree of podocytes degeneration and moderately thickened glomerular basal laminae in mUW (D) and mUW-g (E) groups. Mild podocytes degeneration and thickening of glomerular basal laminae in mUW-m (F) group. (original magnifications; UW group; x20.000, UW-g group; x20,000, UW-m group; x5000, mUW; x7,500, mUW-g; x7,500, mUW-m; x12,000). |
PMC9432748_pone.0273921.g006_390268.jpg | What stands out most in this visual? | Electronmicrographs of kidney tissue in all experimental solution groups.Kidney tissue damage was ultrastructurally characterized by effacement of pedicels in podocytes, thickening of glomerular basal laminae in UW (A) group. Degenerated podocytes and disturbed glomerular basal membranes were observed in UW-g solution group (B). Mildly degenerated podocytes were reflecting low degree of glomerular injury in UW-m group (C). Minimal proximal tubular degenerations were also noticed in this group. Mild degree of podocytes degeneration and moderately thickened glomerular basal laminae in mUW (D) and mUW-g (E) groups. Mild podocytes degeneration and thickening of glomerular basal laminae in mUW-m (F) group. (original magnifications; UW group; x20.000, UW-g group; x20,000, UW-m group; x5000, mUW; x7,500, mUW-g; x7,500, mUW-m; x12,000). |
PMC9432748_pone.0273921.g006_390263.jpg | What is the dominant medical problem in this image? | Electronmicrographs of kidney tissue in all experimental solution groups.Kidney tissue damage was ultrastructurally characterized by effacement of pedicels in podocytes, thickening of glomerular basal laminae in UW (A) group. Degenerated podocytes and disturbed glomerular basal membranes were observed in UW-g solution group (B). Mildly degenerated podocytes were reflecting low degree of glomerular injury in UW-m group (C). Minimal proximal tubular degenerations were also noticed in this group. Mild degree of podocytes degeneration and moderately thickened glomerular basal laminae in mUW (D) and mUW-g (E) groups. Mild podocytes degeneration and thickening of glomerular basal laminae in mUW-m (F) group. (original magnifications; UW group; x20.000, UW-g group; x20,000, UW-m group; x5000, mUW; x7,500, mUW-g; x7,500, mUW-m; x12,000). |
PMC9432763_pone.0272561.g004_390272.jpg | What does this image primarily show? | Field photographs.(a) general view of structure E, showing the walls built using different techniques and the internal stratification; (b) general view of structure A, characterized by two parallel rows of vertical posts, a central hearth, and a well-preserved sandy-clay floor; (c) detail of structure F walls, built using horizontally lying timber and branches woven around vertical posts (‘wattle and post’); (d) detail of a corner of structure F, showing walls built using the wattle and post technique. |
PMC9432763_pone.0272561.g004_390269.jpg | What can you see in this picture? | Field photographs.(a) general view of structure E, showing the walls built using different techniques and the internal stratification; (b) general view of structure A, characterized by two parallel rows of vertical posts, a central hearth, and a well-preserved sandy-clay floor; (c) detail of structure F walls, built using horizontally lying timber and branches woven around vertical posts (‘wattle and post’); (d) detail of a corner of structure F, showing walls built using the wattle and post technique. |
PMC9432763_pone.0272561.g004_390271.jpg | Describe the main subject of this image. | Field photographs.(a) general view of structure E, showing the walls built using different techniques and the internal stratification; (b) general view of structure A, characterized by two parallel rows of vertical posts, a central hearth, and a well-preserved sandy-clay floor; (c) detail of structure F walls, built using horizontally lying timber and branches woven around vertical posts (‘wattle and post’); (d) detail of a corner of structure F, showing walls built using the wattle and post technique. |
PMC9432763_pone.0272561.g008_390273.jpg | What stands out most in this visual? | Interpretation of thin section OPP 76 (structure F) and related μXRF map.(a) Interpretation of thin section OPP 76, with a SMT assigned to each identified sub-unit. Note the alternating sequence of SMT 2 (dung mixed with ashes) and SMT 1 (ash mixed with charcoal)/SMT 1a (ash mixed with herbivore dung and charcoal). Non-interpreted version of thin section OPP 76 is available in S1 Appendix; (b-e) μXRF maps showing the abundance of specific elements superimposed on the PPL scan of thin section OPP 76. In (b), note the correspondence between high S signal and SMT 2 sub-units and–in minor amount–SMT 1a sub-units that still contain fragments of herbivore dung. In (c) and (e), note that the highest concentrations of P and Ca are visible in SMT 1 sub-units (n° 5, 9, 13), while SMT 2 sub-units show very low P values. In SMT 2, the coarse elements with high P signal are bone fragments. |
PMC9432763_pone.0272561.g008_390274.jpg | What is the focal point of this photograph? | Interpretation of thin section OPP 76 (structure F) and related μXRF map.(a) Interpretation of thin section OPP 76, with a SMT assigned to each identified sub-unit. Note the alternating sequence of SMT 2 (dung mixed with ashes) and SMT 1 (ash mixed with charcoal)/SMT 1a (ash mixed with herbivore dung and charcoal). Non-interpreted version of thin section OPP 76 is available in S1 Appendix; (b-e) μXRF maps showing the abundance of specific elements superimposed on the PPL scan of thin section OPP 76. In (b), note the correspondence between high S signal and SMT 2 sub-units and–in minor amount–SMT 1a sub-units that still contain fragments of herbivore dung. In (c) and (e), note that the highest concentrations of P and Ca are visible in SMT 1 sub-units (n° 5, 9, 13), while SMT 2 sub-units show very low P values. In SMT 2, the coarse elements with high P signal are bone fragments. |
PMC9432763_pone.0272561.g008_390275.jpg | What is being portrayed in this visual content? | Interpretation of thin section OPP 76 (structure F) and related μXRF map.(a) Interpretation of thin section OPP 76, with a SMT assigned to each identified sub-unit. Note the alternating sequence of SMT 2 (dung mixed with ashes) and SMT 1 (ash mixed with charcoal)/SMT 1a (ash mixed with herbivore dung and charcoal). Non-interpreted version of thin section OPP 76 is available in S1 Appendix; (b-e) μXRF maps showing the abundance of specific elements superimposed on the PPL scan of thin section OPP 76. In (b), note the correspondence between high S signal and SMT 2 sub-units and–in minor amount–SMT 1a sub-units that still contain fragments of herbivore dung. In (c) and (e), note that the highest concentrations of P and Ca are visible in SMT 1 sub-units (n° 5, 9, 13), while SMT 2 sub-units show very low P values. In SMT 2, the coarse elements with high P signal are bone fragments. |
PMC9432863_f1_390284.jpg | What key item or scene is captured in this photo? | The histologic features of well-differentiated liposarcoma (WDL) and corresponding fluorescence in situ hybridization (FISH) images. Lipoma-like WDL showing variation in adipocyte size, with the presence of bizarre, hyperchromatic stromal cells (A hematoxylin and eosin staining [H&E]; magnification: 200×). Inflammatory WDL with predominant inflammatory cell arrogation and atypical, hyperchromatic cells can be identified in the stroma (B H&E; magnification: 200×). WDL with extensive myxoid change showing abundant myxoid stroma and containing small branching vessels (C H&E; magnification: 200×). FISH analysis identified MDM2 amplification in the WDL (case 17) (D). |
PMC9432863_f1_390282.jpg | What is the core subject represented in this visual? | The histologic features of well-differentiated liposarcoma (WDL) and corresponding fluorescence in situ hybridization (FISH) images. Lipoma-like WDL showing variation in adipocyte size, with the presence of bizarre, hyperchromatic stromal cells (A hematoxylin and eosin staining [H&E]; magnification: 200×). Inflammatory WDL with predominant inflammatory cell arrogation and atypical, hyperchromatic cells can be identified in the stroma (B H&E; magnification: 200×). WDL with extensive myxoid change showing abundant myxoid stroma and containing small branching vessels (C H&E; magnification: 200×). FISH analysis identified MDM2 amplification in the WDL (case 17) (D). |
PMC9432863_f1_390283.jpg | What is shown in this image? | The histologic features of well-differentiated liposarcoma (WDL) and corresponding fluorescence in situ hybridization (FISH) images. Lipoma-like WDL showing variation in adipocyte size, with the presence of bizarre, hyperchromatic stromal cells (A hematoxylin and eosin staining [H&E]; magnification: 200×). Inflammatory WDL with predominant inflammatory cell arrogation and atypical, hyperchromatic cells can be identified in the stroma (B H&E; magnification: 200×). WDL with extensive myxoid change showing abundant myxoid stroma and containing small branching vessels (C H&E; magnification: 200×). FISH analysis identified MDM2 amplification in the WDL (case 17) (D). |
PMC9432863_f1_390285.jpg | Describe the main subject of this image. | The histologic features of well-differentiated liposarcoma (WDL) and corresponding fluorescence in situ hybridization (FISH) images. Lipoma-like WDL showing variation in adipocyte size, with the presence of bizarre, hyperchromatic stromal cells (A hematoxylin and eosin staining [H&E]; magnification: 200×). Inflammatory WDL with predominant inflammatory cell arrogation and atypical, hyperchromatic cells can be identified in the stroma (B H&E; magnification: 200×). WDL with extensive myxoid change showing abundant myxoid stroma and containing small branching vessels (C H&E; magnification: 200×). FISH analysis identified MDM2 amplification in the WDL (case 17) (D). |
PMC9432863_f2_390279.jpg | What is shown in this image? | The histologic features of well-differentiated liposarcoma (WDL) with unusual genetic results and corresponding fluorescence in situ hybridization (FISH) images. The WDL (case 4) showing hyperchromatic bizarre stromal cells (A H&E; magnification: 200×). FISH analysis revealed that the tumor was negative for MDM2
(B) and CDK4
(C) gene amplification but with FRS2 gene amplification (D). |
PMC9432863_f2_390278.jpg | What is being portrayed in this visual content? | The histologic features of well-differentiated liposarcoma (WDL) with unusual genetic results and corresponding fluorescence in situ hybridization (FISH) images. The WDL (case 4) showing hyperchromatic bizarre stromal cells (A H&E; magnification: 200×). FISH analysis revealed that the tumor was negative for MDM2
(B) and CDK4
(C) gene amplification but with FRS2 gene amplification (D). |
PMC9432863_f3_390289.jpg | What is the core subject represented in this visual? | The histologic features of dedifferentiated liposarcoma (DDL) and corresponding fluorescence in situ hybridization (FISH) images. DDL with undifferentiated pleomorphic sarcoma-like differentiation; tumor cells exhibited moderate cytologic atypia with obvious nuclear pleomorphism (A H&E; magnification: 400×). DDL showed a fibrosarcoma-like pattern, exhibiting marked hypercellularity and cytologic atypia. (B H&E; magnification: 400×). DDL showing areas of osteosarcoma and chondrosarcoma-like differentiation (C H&E; magnification: 100×). DDL with IMT-like features with varying degrees of chronic inflammatory cell infiltration (D H&E; magnification: 200×). DDL with low-grade fibrosarcoma-like differentiation, exhibiting mild cytologic atypia (E H&E; magnification: 200×). FISH analysis identified MDM2 amplification in the DDL (case 32) (F). |
PMC9432863_f3_390287.jpg | What is the focal point of this photograph? | The histologic features of dedifferentiated liposarcoma (DDL) and corresponding fluorescence in situ hybridization (FISH) images. DDL with undifferentiated pleomorphic sarcoma-like differentiation; tumor cells exhibited moderate cytologic atypia with obvious nuclear pleomorphism (A H&E; magnification: 400×). DDL showed a fibrosarcoma-like pattern, exhibiting marked hypercellularity and cytologic atypia. (B H&E; magnification: 400×). DDL showing areas of osteosarcoma and chondrosarcoma-like differentiation (C H&E; magnification: 100×). DDL with IMT-like features with varying degrees of chronic inflammatory cell infiltration (D H&E; magnification: 200×). DDL with low-grade fibrosarcoma-like differentiation, exhibiting mild cytologic atypia (E H&E; magnification: 200×). FISH analysis identified MDM2 amplification in the DDL (case 32) (F). |
PMC9432863_f3_390291.jpg | Can you identify the primary element in this image? | The histologic features of dedifferentiated liposarcoma (DDL) and corresponding fluorescence in situ hybridization (FISH) images. DDL with undifferentiated pleomorphic sarcoma-like differentiation; tumor cells exhibited moderate cytologic atypia with obvious nuclear pleomorphism (A H&E; magnification: 400×). DDL showed a fibrosarcoma-like pattern, exhibiting marked hypercellularity and cytologic atypia. (B H&E; magnification: 400×). DDL showing areas of osteosarcoma and chondrosarcoma-like differentiation (C H&E; magnification: 100×). DDL with IMT-like features with varying degrees of chronic inflammatory cell infiltration (D H&E; magnification: 200×). DDL with low-grade fibrosarcoma-like differentiation, exhibiting mild cytologic atypia (E H&E; magnification: 200×). FISH analysis identified MDM2 amplification in the DDL (case 32) (F). |
PMC9432863_f3_390290.jpg | Describe the main subject of this image. | The histologic features of dedifferentiated liposarcoma (DDL) and corresponding fluorescence in situ hybridization (FISH) images. DDL with undifferentiated pleomorphic sarcoma-like differentiation; tumor cells exhibited moderate cytologic atypia with obvious nuclear pleomorphism (A H&E; magnification: 400×). DDL showed a fibrosarcoma-like pattern, exhibiting marked hypercellularity and cytologic atypia. (B H&E; magnification: 400×). DDL showing areas of osteosarcoma and chondrosarcoma-like differentiation (C H&E; magnification: 100×). DDL with IMT-like features with varying degrees of chronic inflammatory cell infiltration (D H&E; magnification: 200×). DDL with low-grade fibrosarcoma-like differentiation, exhibiting mild cytologic atypia (E H&E; magnification: 200×). FISH analysis identified MDM2 amplification in the DDL (case 32) (F). |
PMC9432863_f4_390297.jpg | What is the main focus of this visual representation? | The histologic features of DDL with leiomyosarcomatous differentiation (case 33) and its corresponding immunohistochemical and fluorescence in situ hybridization (FISH) image. Sclerotic well-differentiated area outside the lung (A H&E; magnification: 200×). At low magnification, the growth of the spindle tumor cells showed cleft-like architecture, mimicking the pattern of pulmonary adenofibroma (B H&E; magnification: 200×). Spindle tumor cells display a fascicular arrangement, with hyperchromatic, cigar-shaped nuclei and mild to moderate atypia (C H&E; magnification: 200×). The tumor cells exhibited increased nuclear atypia with obvious pleomorphism (D H&E; magnification: 200×). The tumor cells showed SMA (E magnification: 200×), desmin (F magnification: 200×) and h-caldesmon (G magnification: 200×) positivity in well-differentiated areas and negativity in focal sarcoma-like areas. MDM2 amplification was identified in this case (H). |
PMC9432863_f4_390298.jpg | What is the focal point of this photograph? | The histologic features of DDL with leiomyosarcomatous differentiation (case 33) and its corresponding immunohistochemical and fluorescence in situ hybridization (FISH) image. Sclerotic well-differentiated area outside the lung (A H&E; magnification: 200×). At low magnification, the growth of the spindle tumor cells showed cleft-like architecture, mimicking the pattern of pulmonary adenofibroma (B H&E; magnification: 200×). Spindle tumor cells display a fascicular arrangement, with hyperchromatic, cigar-shaped nuclei and mild to moderate atypia (C H&E; magnification: 200×). The tumor cells exhibited increased nuclear atypia with obvious pleomorphism (D H&E; magnification: 200×). The tumor cells showed SMA (E magnification: 200×), desmin (F magnification: 200×) and h-caldesmon (G magnification: 200×) positivity in well-differentiated areas and negativity in focal sarcoma-like areas. MDM2 amplification was identified in this case (H). |
PMC9432863_f5_390307.jpg | What object or scene is depicted here? | The histologic features of myxoid pleomorphic liposarcoma and corresponding immunohistochemical and genetic results. The tumor exhibited features of pleomorphic liposarcoma with myxoid matrix, and multivacuolated lipoblasts were found (A H&E; magnification: 400×) (case 42). Myxoid liposarcoma-like areas were also identified within the tumor, displaying a well-developed plexiform vasculature pattern (B H&E; magnification: 400×). The tumor cells (case 42) showed positivity for p53 immunostaining (C magnification: 400×). FISH analysis revealed negativity for MDM2 amplification (D) or DDIT3 rearrangement (E). Sanger sequencing results showed TP53 mutations in both tumors (F). |
PMC9432863_f5_390305.jpg | Can you identify the primary element in this image? | The histologic features of myxoid pleomorphic liposarcoma and corresponding immunohistochemical and genetic results. The tumor exhibited features of pleomorphic liposarcoma with myxoid matrix, and multivacuolated lipoblasts were found (A H&E; magnification: 400×) (case 42). Myxoid liposarcoma-like areas were also identified within the tumor, displaying a well-developed plexiform vasculature pattern (B H&E; magnification: 400×). The tumor cells (case 42) showed positivity for p53 immunostaining (C magnification: 400×). FISH analysis revealed negativity for MDM2 amplification (D) or DDIT3 rearrangement (E). Sanger sequencing results showed TP53 mutations in both tumors (F). |
PMC9432863_f5_390304.jpg | What can you see in this picture? | The histologic features of myxoid pleomorphic liposarcoma and corresponding immunohistochemical and genetic results. The tumor exhibited features of pleomorphic liposarcoma with myxoid matrix, and multivacuolated lipoblasts were found (A H&E; magnification: 400×) (case 42). Myxoid liposarcoma-like areas were also identified within the tumor, displaying a well-developed plexiform vasculature pattern (B H&E; magnification: 400×). The tumor cells (case 42) showed positivity for p53 immunostaining (C magnification: 400×). FISH analysis revealed negativity for MDM2 amplification (D) or DDIT3 rearrangement (E). Sanger sequencing results showed TP53 mutations in both tumors (F). |
PMC9432863_f5_390308.jpg | What's the most prominent thing you notice in this picture? | The histologic features of myxoid pleomorphic liposarcoma and corresponding immunohistochemical and genetic results. The tumor exhibited features of pleomorphic liposarcoma with myxoid matrix, and multivacuolated lipoblasts were found (A H&E; magnification: 400×) (case 42). Myxoid liposarcoma-like areas were also identified within the tumor, displaying a well-developed plexiform vasculature pattern (B H&E; magnification: 400×). The tumor cells (case 42) showed positivity for p53 immunostaining (C magnification: 400×). FISH analysis revealed negativity for MDM2 amplification (D) or DDIT3 rearrangement (E). Sanger sequencing results showed TP53 mutations in both tumors (F). |
PMC9432863_f5_390306.jpg | What does this image primarily show? | The histologic features of myxoid pleomorphic liposarcoma and corresponding immunohistochemical and genetic results. The tumor exhibited features of pleomorphic liposarcoma with myxoid matrix, and multivacuolated lipoblasts were found (A H&E; magnification: 400×) (case 42). Myxoid liposarcoma-like areas were also identified within the tumor, displaying a well-developed plexiform vasculature pattern (B H&E; magnification: 400×). The tumor cells (case 42) showed positivity for p53 immunostaining (C magnification: 400×). FISH analysis revealed negativity for MDM2 amplification (D) or DDIT3 rearrangement (E). Sanger sequencing results showed TP53 mutations in both tumors (F). |
PMC9432863_f6_390292.jpg | What is shown in this image? | The histologic features of pleomorphic liposarcoma and corresponding immunohistochemical results. The spindled, epithelial tumor cells exhibited marked nuclear atypia (A H&E; magnification: 400×) (case 43). The bizarre lipoblasts can be identified within the lesion (B H&E; magnification: 400×). Myxoid change in focal area, resembling the morphology of myxofibrosarcoma (C H&E; magnification: 200×). The tumor cells were diffusely positive for P53 (D magnification: 400×). |
PMC9432863_f6_390295.jpg | What is being portrayed in this visual content? | The histologic features of pleomorphic liposarcoma and corresponding immunohistochemical results. The spindled, epithelial tumor cells exhibited marked nuclear atypia (A H&E; magnification: 400×) (case 43). The bizarre lipoblasts can be identified within the lesion (B H&E; magnification: 400×). Myxoid change in focal area, resembling the morphology of myxofibrosarcoma (C H&E; magnification: 200×). The tumor cells were diffusely positive for P53 (D magnification: 400×). |
PMC9432863_f6_390293.jpg | What is the central feature of this picture? | The histologic features of pleomorphic liposarcoma and corresponding immunohistochemical results. The spindled, epithelial tumor cells exhibited marked nuclear atypia (A H&E; magnification: 400×) (case 43). The bizarre lipoblasts can be identified within the lesion (B H&E; magnification: 400×). Myxoid change in focal area, resembling the morphology of myxofibrosarcoma (C H&E; magnification: 200×). The tumor cells were diffusely positive for P53 (D magnification: 400×). |
PMC9432863_f6_390294.jpg | What's the most prominent thing you notice in this picture? | The histologic features of pleomorphic liposarcoma and corresponding immunohistochemical results. The spindled, epithelial tumor cells exhibited marked nuclear atypia (A H&E; magnification: 400×) (case 43). The bizarre lipoblasts can be identified within the lesion (B H&E; magnification: 400×). Myxoid change in focal area, resembling the morphology of myxofibrosarcoma (C H&E; magnification: 200×). The tumor cells were diffusely positive for P53 (D magnification: 400×). |
PMC9433062_F4_390310.jpg | What is being portrayed in this visual content? | After incision in the fibrous scar around the pylorus (arrows), the endoscope was able to pass through the stricture. |
PMC9433062_F5_390311.jpg | What is shown in this image? | One-year follow-up upper endoscopy. The pyloric channel is open and dilated. |
PMC9433093_fig5s1_390312.jpg | What does this image primarily show? | Deletion of CAP-G2 partially rescues mutations in the basic amino acid clusters of CAP-H2.(A) Recombinant mammalian condensin II holocomplex (holo) and ΔG2 subcomplex harboring either wild-type (WT) or mutations in the H2 basic amino acid cluster (H2-BC1D, H2-BC2D, and H2-BC1/2D) were purified and subjected to SDS-PAGE. The gel was stained with Coomassie Brilliant Blue. (B) Mouse sperm nuclei were incubated in Δcond I/II extracts that had been supplemented with condensin II holocomplex (WT, H2-BC1D, H2-BC2D, or H2-BC1/2D) at 200 nM or ΔG2 subcomplexes (WT, H2-BC1D, H2-BC2D, and H2-BC1/2D) at either 25 or 200 nM. After incubation for 150 min, reactions were fixed and labeled with anti-hCAP-H2 antibody. DNA was counterstained with DAPI. Shown here is a representative image from over 15 chromosome clusters examined per condition. Scale bar, 10 µm. In samples with 200 nM addition, ΔG2 subcomplexes were overloaded on chromosomal axes but only ΔG2(WT) made longer, continuous axes while ΔG2 with H2 basic cluster mutations.
Figure 5—figure supplement 1—source data 1.Raw data uncropped gel corresponding to Figure 5—figure supplement 1.
|
PMC9433093_fig5s1_390313.jpg | What is shown in this image? | Deletion of CAP-G2 partially rescues mutations in the basic amino acid clusters of CAP-H2.(A) Recombinant mammalian condensin II holocomplex (holo) and ΔG2 subcomplex harboring either wild-type (WT) or mutations in the H2 basic amino acid cluster (H2-BC1D, H2-BC2D, and H2-BC1/2D) were purified and subjected to SDS-PAGE. The gel was stained with Coomassie Brilliant Blue. (B) Mouse sperm nuclei were incubated in Δcond I/II extracts that had been supplemented with condensin II holocomplex (WT, H2-BC1D, H2-BC2D, or H2-BC1/2D) at 200 nM or ΔG2 subcomplexes (WT, H2-BC1D, H2-BC2D, and H2-BC1/2D) at either 25 or 200 nM. After incubation for 150 min, reactions were fixed and labeled with anti-hCAP-H2 antibody. DNA was counterstained with DAPI. Shown here is a representative image from over 15 chromosome clusters examined per condition. Scale bar, 10 µm. In samples with 200 nM addition, ΔG2 subcomplexes were overloaded on chromosomal axes but only ΔG2(WT) made longer, continuous axes while ΔG2 with H2 basic cluster mutations.
Figure 5—figure supplement 1—source data 1.Raw data uncropped gel corresponding to Figure 5—figure supplement 1.
|
PMC9433123_f2_390317.jpg | What is the focal point of this photograph? | Slit-lamp visualization of a wavy retained Descemet membrane with supernumerary anterior chamber formation in the right eye on the day following penetrating keratoplasty. |
PMC9433200_fig1_390319.jpg | What is the central feature of this picture? | MRI image of brain tumor. |
PMC9433226_fig1_390322.jpg | What is the core subject represented in this visual? | (a, b) Contrast-enhanced three-dimensional computed tomography images obtained at 8 days of age. (c, d) Patient-specific three-dimensional solid cardiovascular model based on computed tomography data at 8 days of age. Computed tomography scans were not electrocardiography-gated. (a) The frontal view. The left aortic arch was interrupted after the branching of the left common carotid artery (red arrow). (b) The rear view. This image shows the left distal arch connected to the ductus arteriosus (yellow arrow) and right distal arch (small yellow arrowheads). The right dorsal aorta was long and tortuous, with hemodynamic aortic coarctation. (c) The frontal view and (d) the rear view. Arteries are colored in red. Pulmonary arteries and veins are colored in blue. The patent ductus arteriosus is colored purple. The heart and vessel model was helpful to plan and simulate surgery. |
PMC9433226_fig1_390321.jpg | What is the central feature of this picture? | (a, b) Contrast-enhanced three-dimensional computed tomography images obtained at 8 days of age. (c, d) Patient-specific three-dimensional solid cardiovascular model based on computed tomography data at 8 days of age. Computed tomography scans were not electrocardiography-gated. (a) The frontal view. The left aortic arch was interrupted after the branching of the left common carotid artery (red arrow). (b) The rear view. This image shows the left distal arch connected to the ductus arteriosus (yellow arrow) and right distal arch (small yellow arrowheads). The right dorsal aorta was long and tortuous, with hemodynamic aortic coarctation. (c) The frontal view and (d) the rear view. Arteries are colored in red. Pulmonary arteries and veins are colored in blue. The patent ductus arteriosus is colored purple. The heart and vessel model was helpful to plan and simulate surgery. |
PMC9433226_fig1_390323.jpg | What's the most prominent thing you notice in this picture? | (a, b) Contrast-enhanced three-dimensional computed tomography images obtained at 8 days of age. (c, d) Patient-specific three-dimensional solid cardiovascular model based on computed tomography data at 8 days of age. Computed tomography scans were not electrocardiography-gated. (a) The frontal view. The left aortic arch was interrupted after the branching of the left common carotid artery (red arrow). (b) The rear view. This image shows the left distal arch connected to the ductus arteriosus (yellow arrow) and right distal arch (small yellow arrowheads). The right dorsal aorta was long and tortuous, with hemodynamic aortic coarctation. (c) The frontal view and (d) the rear view. Arteries are colored in red. Pulmonary arteries and veins are colored in blue. The patent ductus arteriosus is colored purple. The heart and vessel model was helpful to plan and simulate surgery. |
PMC9433298_fig7_390325.jpg | What key item or scene is captured in this photo? | Effect of STIG and STIG+DEX on smooth muscle hypertrophy and basement membrane thickening. Lung tissues were assessed for bronchial basement membrane thickening (BM) and airway smooth muscle hyperplasia (SM) (magnification = ×40). Morphometric analysis quantified the extent of smooth muscle hypertrophy (g). Data is expressed as mean index ± SEM (n = 5). ####p < 0.0001 compared to the vehicle control group; ∗∗∗∗p < 0.0001 and ns (not significant) as compared to the disease control group using ANOVA followed by Dunnett's post hoc test. |
PMC9433298_fig7_390329.jpg | What can you see in this picture? | Effect of STIG and STIG+DEX on smooth muscle hypertrophy and basement membrane thickening. Lung tissues were assessed for bronchial basement membrane thickening (BM) and airway smooth muscle hyperplasia (SM) (magnification = ×40). Morphometric analysis quantified the extent of smooth muscle hypertrophy (g). Data is expressed as mean index ± SEM (n = 5). ####p < 0.0001 compared to the vehicle control group; ∗∗∗∗p < 0.0001 and ns (not significant) as compared to the disease control group using ANOVA followed by Dunnett's post hoc test. |
PMC9433314_F4_390332.jpg | What is the focal point of this photograph? | Stimulation target in subject 7. |
PMC9433314_F4_390334.jpg | What is being portrayed in this visual content? | Stimulation target in subject 7. |
PMC9433314_F4_390333.jpg | Can you identify the primary element in this image? | Stimulation target in subject 7. |
PMC9433314_F4_390331.jpg | What is shown in this image? | Stimulation target in subject 7. |
PMC9433320_Fig1_390352.jpg | What is the dominant medical problem in this image? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390356.jpg | Describe the main subject of this image. | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390361.jpg | What object or scene is depicted here? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390363.jpg | What is the principal component of this image? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390368.jpg | What is the main focus of this visual representation? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390359.jpg | What can you see in this picture? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390362.jpg | What is the focal point of this photograph? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390358.jpg | What is the central feature of this picture? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390354.jpg | What does this image primarily show? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390353.jpg | What is shown in this image? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390367.jpg | What is the central feature of this picture? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig1_390357.jpg | What is the central feature of this picture? | Acetylation-regulated chromatin compaction prevents microtubule perforation in mitosis.a, The contribution of condensin and histone deacetylases to mitotic chromosome compaction and congression to the spindle centre. HeLa cells with homozygously mAID-tagged SMC4 were treated with 5-PhIAA to deplete condensin (ΔCondensin) or with TSA to suppress mitotic histone deacetylation as indicated. Live-cell images with microtubules stained by SiR–tubulin; DNA was stained with Hoechst 33342. Projection of 5 z-sections. b, Quantification of chromosome congression by the fraction of chromatin localizing to the central spindle region. n = 51 (control), n = 65 (ΔCondensin), n = 34 (ΔCondensin + TSA), n = 61 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). c, Quantification of chromatin density in cells treated as described in a. n = 31 (control), n = 89 (ΔCondensin), n = 99 (ΔCondensin + TSA) and n = 74 (TSA) cells. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P < 10−15 (ΔCondensin + TSA); P < 10−15 (TSA); precision limit of floating-point arithmetic). AU, arbitrary units. d, Electron tomography analysis of wild-type prometaphase HeLa cells in the absence or presence of TSA. Magenta, chromatin surfaces; green, microtubules in cytoplasm; cyan, microtubules in chromatin. The red circles show the perforation sites. e,f, Quantification of microtubule density in chromatin (e) and cytoplasmic (f) regions as shown in d. n = 10 tomograms from 7 cells for each condition. The bars indicate the mean. Significance was tested using two-tailed Mann–Whitney U-tests (P = 1.083 × 10−5 (e); P = 0.247 (f)). Biological replicates: n = 2 (a–f). Scale bars, 5 µm (a), 2 µm (d, 250 nm section); 200 nm (tomogram slices and 3D model).Source Data |
PMC9433320_Fig4_390346.jpg | What is the focal point of this photograph? | Microtubules push liquified chromatin away from the spindle pole.a, Time-lapse microscopy analysis of liquified chromatin during monopolar spindle assembly. AluI was injected into live mitotic HeLa cells expressing H2B–mCherry and meGFP–CENP-A, stained with SiR–tubulin, in the presence of nocodazole (noco) and STLC. Nocodazole was then removed at t = 0 min during time-lapse imaging to induce monopolar spindle assembly. Projection of 5 z-sections. Time is shown as min:s. b, Quantification of bulk chromatin (H2B–mCherry) and centromeric chromatin (meGFP–CENP-A) localizing at the cell periphery relative to the region around the spindle monopole at t = 36 min. n = 15 cells. The bars indicate the mean. Significance was tested by a two-tailed Mann–Whitney U-test (P = 1.289 × 10−8). c, Model of chromatin compaction and condensin-mediated DNA looping in mitotic chromosome and spindle assembly. The illustration shows a top-down view of a chromosome cross-section. Biological replicates: n = 3 (a,b). Scale bars, 5 µm.Source Data |
PMC9433320_Fig4_390343.jpg | What key item or scene is captured in this photo? | Microtubules push liquified chromatin away from the spindle pole.a, Time-lapse microscopy analysis of liquified chromatin during monopolar spindle assembly. AluI was injected into live mitotic HeLa cells expressing H2B–mCherry and meGFP–CENP-A, stained with SiR–tubulin, in the presence of nocodazole (noco) and STLC. Nocodazole was then removed at t = 0 min during time-lapse imaging to induce monopolar spindle assembly. Projection of 5 z-sections. Time is shown as min:s. b, Quantification of bulk chromatin (H2B–mCherry) and centromeric chromatin (meGFP–CENP-A) localizing at the cell periphery relative to the region around the spindle monopole at t = 36 min. n = 15 cells. The bars indicate the mean. Significance was tested by a two-tailed Mann–Whitney U-test (P = 1.289 × 10−8). c, Model of chromatin compaction and condensin-mediated DNA looping in mitotic chromosome and spindle assembly. The illustration shows a top-down view of a chromosome cross-section. Biological replicates: n = 3 (a,b). Scale bars, 5 µm.Source Data |
PMC9433320_Fig4_390348.jpg | What is the main focus of this visual representation? | Microtubules push liquified chromatin away from the spindle pole.a, Time-lapse microscopy analysis of liquified chromatin during monopolar spindle assembly. AluI was injected into live mitotic HeLa cells expressing H2B–mCherry and meGFP–CENP-A, stained with SiR–tubulin, in the presence of nocodazole (noco) and STLC. Nocodazole was then removed at t = 0 min during time-lapse imaging to induce monopolar spindle assembly. Projection of 5 z-sections. Time is shown as min:s. b, Quantification of bulk chromatin (H2B–mCherry) and centromeric chromatin (meGFP–CENP-A) localizing at the cell periphery relative to the region around the spindle monopole at t = 36 min. n = 15 cells. The bars indicate the mean. Significance was tested by a two-tailed Mann–Whitney U-test (P = 1.289 × 10−8). c, Model of chromatin compaction and condensin-mediated DNA looping in mitotic chromosome and spindle assembly. The illustration shows a top-down view of a chromosome cross-section. Biological replicates: n = 3 (a,b). Scale bars, 5 µm.Source Data |
PMC9433320_Fig4_390337.jpg | What can you see in this picture? | Microtubules push liquified chromatin away from the spindle pole.a, Time-lapse microscopy analysis of liquified chromatin during monopolar spindle assembly. AluI was injected into live mitotic HeLa cells expressing H2B–mCherry and meGFP–CENP-A, stained with SiR–tubulin, in the presence of nocodazole (noco) and STLC. Nocodazole was then removed at t = 0 min during time-lapse imaging to induce monopolar spindle assembly. Projection of 5 z-sections. Time is shown as min:s. b, Quantification of bulk chromatin (H2B–mCherry) and centromeric chromatin (meGFP–CENP-A) localizing at the cell periphery relative to the region around the spindle monopole at t = 36 min. n = 15 cells. The bars indicate the mean. Significance was tested by a two-tailed Mann–Whitney U-test (P = 1.289 × 10−8). c, Model of chromatin compaction and condensin-mediated DNA looping in mitotic chromosome and spindle assembly. The illustration shows a top-down view of a chromosome cross-section. Biological replicates: n = 3 (a,b). Scale bars, 5 µm.Source Data |
PMC9433320_Fig4_390338.jpg | What is being portrayed in this visual content? | Microtubules push liquified chromatin away from the spindle pole.a, Time-lapse microscopy analysis of liquified chromatin during monopolar spindle assembly. AluI was injected into live mitotic HeLa cells expressing H2B–mCherry and meGFP–CENP-A, stained with SiR–tubulin, in the presence of nocodazole (noco) and STLC. Nocodazole was then removed at t = 0 min during time-lapse imaging to induce monopolar spindle assembly. Projection of 5 z-sections. Time is shown as min:s. b, Quantification of bulk chromatin (H2B–mCherry) and centromeric chromatin (meGFP–CENP-A) localizing at the cell periphery relative to the region around the spindle monopole at t = 36 min. n = 15 cells. The bars indicate the mean. Significance was tested by a two-tailed Mann–Whitney U-test (P = 1.289 × 10−8). c, Model of chromatin compaction and condensin-mediated DNA looping in mitotic chromosome and spindle assembly. The illustration shows a top-down view of a chromosome cross-section. Biological replicates: n = 3 (a,b). Scale bars, 5 µm.Source Data |
PMC9433320_Fig4_390341.jpg | What object or scene is depicted here? | Microtubules push liquified chromatin away from the spindle pole.a, Time-lapse microscopy analysis of liquified chromatin during monopolar spindle assembly. AluI was injected into live mitotic HeLa cells expressing H2B–mCherry and meGFP–CENP-A, stained with SiR–tubulin, in the presence of nocodazole (noco) and STLC. Nocodazole was then removed at t = 0 min during time-lapse imaging to induce monopolar spindle assembly. Projection of 5 z-sections. Time is shown as min:s. b, Quantification of bulk chromatin (H2B–mCherry) and centromeric chromatin (meGFP–CENP-A) localizing at the cell periphery relative to the region around the spindle monopole at t = 36 min. n = 15 cells. The bars indicate the mean. Significance was tested by a two-tailed Mann–Whitney U-test (P = 1.289 × 10−8). c, Model of chromatin compaction and condensin-mediated DNA looping in mitotic chromosome and spindle assembly. The illustration shows a top-down view of a chromosome cross-section. Biological replicates: n = 3 (a,b). Scale bars, 5 µm.Source Data |
PMC9433320_Fig4_390345.jpg | What is the principal component of this image? | Microtubules push liquified chromatin away from the spindle pole.a, Time-lapse microscopy analysis of liquified chromatin during monopolar spindle assembly. AluI was injected into live mitotic HeLa cells expressing H2B–mCherry and meGFP–CENP-A, stained with SiR–tubulin, in the presence of nocodazole (noco) and STLC. Nocodazole was then removed at t = 0 min during time-lapse imaging to induce monopolar spindle assembly. Projection of 5 z-sections. Time is shown as min:s. b, Quantification of bulk chromatin (H2B–mCherry) and centromeric chromatin (meGFP–CENP-A) localizing at the cell periphery relative to the region around the spindle monopole at t = 36 min. n = 15 cells. The bars indicate the mean. Significance was tested by a two-tailed Mann–Whitney U-test (P = 1.289 × 10−8). c, Model of chromatin compaction and condensin-mediated DNA looping in mitotic chromosome and spindle assembly. The illustration shows a top-down view of a chromosome cross-section. Biological replicates: n = 3 (a,b). Scale bars, 5 µm.Source Data |
PMC9433320_Fig4_390351.jpg | What stands out most in this visual? | Microtubules push liquified chromatin away from the spindle pole.a, Time-lapse microscopy analysis of liquified chromatin during monopolar spindle assembly. AluI was injected into live mitotic HeLa cells expressing H2B–mCherry and meGFP–CENP-A, stained with SiR–tubulin, in the presence of nocodazole (noco) and STLC. Nocodazole was then removed at t = 0 min during time-lapse imaging to induce monopolar spindle assembly. Projection of 5 z-sections. Time is shown as min:s. b, Quantification of bulk chromatin (H2B–mCherry) and centromeric chromatin (meGFP–CENP-A) localizing at the cell periphery relative to the region around the spindle monopole at t = 36 min. n = 15 cells. The bars indicate the mean. Significance was tested by a two-tailed Mann–Whitney U-test (P = 1.289 × 10−8). c, Model of chromatin compaction and condensin-mediated DNA looping in mitotic chromosome and spindle assembly. The illustration shows a top-down view of a chromosome cross-section. Biological replicates: n = 3 (a,b). Scale bars, 5 µm.Source Data |
PMC9433320_Fig4_390349.jpg | What's the most prominent thing you notice in this picture? | Microtubules push liquified chromatin away from the spindle pole.a, Time-lapse microscopy analysis of liquified chromatin during monopolar spindle assembly. AluI was injected into live mitotic HeLa cells expressing H2B–mCherry and meGFP–CENP-A, stained with SiR–tubulin, in the presence of nocodazole (noco) and STLC. Nocodazole was then removed at t = 0 min during time-lapse imaging to induce monopolar spindle assembly. Projection of 5 z-sections. Time is shown as min:s. b, Quantification of bulk chromatin (H2B–mCherry) and centromeric chromatin (meGFP–CENP-A) localizing at the cell periphery relative to the region around the spindle monopole at t = 36 min. n = 15 cells. The bars indicate the mean. Significance was tested by a two-tailed Mann–Whitney U-test (P = 1.289 × 10−8). c, Model of chromatin compaction and condensin-mediated DNA looping in mitotic chromosome and spindle assembly. The illustration shows a top-down view of a chromosome cross-section. Biological replicates: n = 3 (a,b). Scale bars, 5 µm.Source Data |
Subsets and Splits