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PMC1808484_pbio-0050072-g002_9846.jpg | Describe the main subject of this image. | Behavioral and Electrophysiological Analyses Reveal That Synaptic Transmission Is Not Blocked in the syx3–69 Mutant Fly at Restrictive Temperatures(A and B) Temperature-sensitive paralysis and recovery of the syx3–69 mutant fly. (A) shows the still image of both wild type (+/+) and the syx3–69 mutant before, during, and after exposure to the restrictive temperature (38 °C). Although the wild-type flies are not paralyzed at 38 °C, the syx3–69 mutant flies are. However, the syx3–69 flies recover rapidly to standing position within 2–3 min once returned to the permissive temperature. The quantification of the recovery kinetics is shown in (B). Error bars in this and all other figures indicate the standard errors.(C) The paralyzed syx3–69 mutant flies remain capable of responding to stimuli via the polysynaptic giant fiber (GF) pathway. The flies are anchored on a glass slide upside down with modeling clay while a stimulating electrode is inserted into one of the compound eyes (arrows). The syx3–69 fly constantly shakes its legs, head, and abdomen while paralyzed at 38 °C. In response to electrical stimulation of the giant fiber neuron, the mutant fly extends its legs phase-locked with each stimulus. However, the Shits1 fly is completely paralyzed and does not respond to the stimuli at the same restrictive temperature. The right-most panels summarize the cumulative spontaneous and electrical stimulation–evoked movements of legs in syx3–69 flies and the lack of leg movement in Shits1 flies. These behavioral observations strongly indicate that exposing the syx3–69 fly to 38 °C does not block synaptic transmission. See also Videos S4 and S5.(D) Recordings from indirect flight muscles confirm that synaptic transmission is not blocked in syx3–69 flies at the restrictive temperature. Action potentials in DLMs driven by polysynaptic stimuli along the giant fiber pathway remain the same in the syx3–69 mutant fly as in the wild-type control fly before, during, and after exposure to the restrictive temperature. Synaptic-induced high-frequency action potentials are often observed in both the wild type and the syx3–69 mutant (unpublished data). These high-frequency action potentials also occur spontaneously in the mutant. (An example is shown in the inset box.) |
PMC1808485_pbio-0050071-g002_9856.jpg | What is the dominant medical problem in this image? | Histological Characteristics of WBR in B. leachi
Regenerating vasculature fragments that were sacrificed at sequential daily intervals exhibit cellular events during the regeneration process.(A and B) Phase I events: Haemocytes are attached to vasculature epithelium (A) (arrows). Vascular detachment from the tunic (B) (arrows) enables subsequent relocation of blood vessels.(C–E) Phase II events: 2 d after dissection, aggregated haemocytes of various sizes and shapes were observed in the regeneration niches (C) (arrows). Extensive cell proliferation formed an opaque ball of cells (D) with exclusive PCNA staining (E).(F–L) Phase III events: 1 d later, continuous cell proliferation increased the size of cell aggregates and formed blastula-like structures of different shapes (F and G) (arrowheads). At this stage, multibuds developed simultaneously in various regenerating niches (G) (arrowheads and red arrows, respectively), although separation between compartments had not been completed (G) (arrow). PCNA specifically stained newly formed bud spheres and blastula-like structures inside the regeneration niches (H). As development proceeded, axial polarity was observed with the appearance of differential cell layers (I) (arrowheads). From day 5, two invaginations from both corners of the thick vesicle wall creating two elongated double-walled folds were observed (J) (arrows). Between 10–14 days postseparation, the regeneration process reached the final stages, whereby a fully functional adult zooid was developed, including the formation of palleal buds (K). Only one zooid per regenerating fragment reached this final stage, while the others degenerated (L) (arrow).(M–P) TUNEL analysis clearly shows staining in degenerating buds. Bud that was normally developed did not stain for TUNEL and exhibits a normal blastula-like structure with clear polarization: (M) and enlargement in (O). Bud that failed to develop went through a degenerating process and was stained for TUNEL: (N) and enlargement in (P). Note that it failed to develop a normal blastula structure, and cells started to fall apart. b, bud; i, intestine; ph, pharynx. Scale bar represents 100 μm. In (O) and (P) scale bars represent 30 μm. |
PMC1808485_pbio-0050071-g002_9855.jpg | Describe the main subject of this image. | Histological Characteristics of WBR in B. leachi
Regenerating vasculature fragments that were sacrificed at sequential daily intervals exhibit cellular events during the regeneration process.(A and B) Phase I events: Haemocytes are attached to vasculature epithelium (A) (arrows). Vascular detachment from the tunic (B) (arrows) enables subsequent relocation of blood vessels.(C–E) Phase II events: 2 d after dissection, aggregated haemocytes of various sizes and shapes were observed in the regeneration niches (C) (arrows). Extensive cell proliferation formed an opaque ball of cells (D) with exclusive PCNA staining (E).(F–L) Phase III events: 1 d later, continuous cell proliferation increased the size of cell aggregates and formed blastula-like structures of different shapes (F and G) (arrowheads). At this stage, multibuds developed simultaneously in various regenerating niches (G) (arrowheads and red arrows, respectively), although separation between compartments had not been completed (G) (arrow). PCNA specifically stained newly formed bud spheres and blastula-like structures inside the regeneration niches (H). As development proceeded, axial polarity was observed with the appearance of differential cell layers (I) (arrowheads). From day 5, two invaginations from both corners of the thick vesicle wall creating two elongated double-walled folds were observed (J) (arrows). Between 10–14 days postseparation, the regeneration process reached the final stages, whereby a fully functional adult zooid was developed, including the formation of palleal buds (K). Only one zooid per regenerating fragment reached this final stage, while the others degenerated (L) (arrow).(M–P) TUNEL analysis clearly shows staining in degenerating buds. Bud that was normally developed did not stain for TUNEL and exhibits a normal blastula-like structure with clear polarization: (M) and enlargement in (O). Bud that failed to develop went through a degenerating process and was stained for TUNEL: (N) and enlargement in (P). Note that it failed to develop a normal blastula structure, and cells started to fall apart. b, bud; i, intestine; ph, pharynx. Scale bar represents 100 μm. In (O) and (P) scale bars represent 30 μm. |
PMC1808485_pbio-0050071-g002_9857.jpg | What is the focal point of this photograph? | Histological Characteristics of WBR in B. leachi
Regenerating vasculature fragments that were sacrificed at sequential daily intervals exhibit cellular events during the regeneration process.(A and B) Phase I events: Haemocytes are attached to vasculature epithelium (A) (arrows). Vascular detachment from the tunic (B) (arrows) enables subsequent relocation of blood vessels.(C–E) Phase II events: 2 d after dissection, aggregated haemocytes of various sizes and shapes were observed in the regeneration niches (C) (arrows). Extensive cell proliferation formed an opaque ball of cells (D) with exclusive PCNA staining (E).(F–L) Phase III events: 1 d later, continuous cell proliferation increased the size of cell aggregates and formed blastula-like structures of different shapes (F and G) (arrowheads). At this stage, multibuds developed simultaneously in various regenerating niches (G) (arrowheads and red arrows, respectively), although separation between compartments had not been completed (G) (arrow). PCNA specifically stained newly formed bud spheres and blastula-like structures inside the regeneration niches (H). As development proceeded, axial polarity was observed with the appearance of differential cell layers (I) (arrowheads). From day 5, two invaginations from both corners of the thick vesicle wall creating two elongated double-walled folds were observed (J) (arrows). Between 10–14 days postseparation, the regeneration process reached the final stages, whereby a fully functional adult zooid was developed, including the formation of palleal buds (K). Only one zooid per regenerating fragment reached this final stage, while the others degenerated (L) (arrow).(M–P) TUNEL analysis clearly shows staining in degenerating buds. Bud that was normally developed did not stain for TUNEL and exhibits a normal blastula-like structure with clear polarization: (M) and enlargement in (O). Bud that failed to develop went through a degenerating process and was stained for TUNEL: (N) and enlargement in (P). Note that it failed to develop a normal blastula structure, and cells started to fall apart. b, bud; i, intestine; ph, pharynx. Scale bar represents 100 μm. In (O) and (P) scale bars represent 30 μm. |
PMC1808485_pbio-0050071-g002_9861.jpg | What is the central feature of this picture? | Histological Characteristics of WBR in B. leachi
Regenerating vasculature fragments that were sacrificed at sequential daily intervals exhibit cellular events during the regeneration process.(A and B) Phase I events: Haemocytes are attached to vasculature epithelium (A) (arrows). Vascular detachment from the tunic (B) (arrows) enables subsequent relocation of blood vessels.(C–E) Phase II events: 2 d after dissection, aggregated haemocytes of various sizes and shapes were observed in the regeneration niches (C) (arrows). Extensive cell proliferation formed an opaque ball of cells (D) with exclusive PCNA staining (E).(F–L) Phase III events: 1 d later, continuous cell proliferation increased the size of cell aggregates and formed blastula-like structures of different shapes (F and G) (arrowheads). At this stage, multibuds developed simultaneously in various regenerating niches (G) (arrowheads and red arrows, respectively), although separation between compartments had not been completed (G) (arrow). PCNA specifically stained newly formed bud spheres and blastula-like structures inside the regeneration niches (H). As development proceeded, axial polarity was observed with the appearance of differential cell layers (I) (arrowheads). From day 5, two invaginations from both corners of the thick vesicle wall creating two elongated double-walled folds were observed (J) (arrows). Between 10–14 days postseparation, the regeneration process reached the final stages, whereby a fully functional adult zooid was developed, including the formation of palleal buds (K). Only one zooid per regenerating fragment reached this final stage, while the others degenerated (L) (arrow).(M–P) TUNEL analysis clearly shows staining in degenerating buds. Bud that was normally developed did not stain for TUNEL and exhibits a normal blastula-like structure with clear polarization: (M) and enlargement in (O). Bud that failed to develop went through a degenerating process and was stained for TUNEL: (N) and enlargement in (P). Note that it failed to develop a normal blastula structure, and cells started to fall apart. b, bud; i, intestine; ph, pharynx. Scale bar represents 100 μm. In (O) and (P) scale bars represent 30 μm. |
PMC1808485_pbio-0050071-g002_9858.jpg | What's the most prominent thing you notice in this picture? | Histological Characteristics of WBR in B. leachi
Regenerating vasculature fragments that were sacrificed at sequential daily intervals exhibit cellular events during the regeneration process.(A and B) Phase I events: Haemocytes are attached to vasculature epithelium (A) (arrows). Vascular detachment from the tunic (B) (arrows) enables subsequent relocation of blood vessels.(C–E) Phase II events: 2 d after dissection, aggregated haemocytes of various sizes and shapes were observed in the regeneration niches (C) (arrows). Extensive cell proliferation formed an opaque ball of cells (D) with exclusive PCNA staining (E).(F–L) Phase III events: 1 d later, continuous cell proliferation increased the size of cell aggregates and formed blastula-like structures of different shapes (F and G) (arrowheads). At this stage, multibuds developed simultaneously in various regenerating niches (G) (arrowheads and red arrows, respectively), although separation between compartments had not been completed (G) (arrow). PCNA specifically stained newly formed bud spheres and blastula-like structures inside the regeneration niches (H). As development proceeded, axial polarity was observed with the appearance of differential cell layers (I) (arrowheads). From day 5, two invaginations from both corners of the thick vesicle wall creating two elongated double-walled folds were observed (J) (arrows). Between 10–14 days postseparation, the regeneration process reached the final stages, whereby a fully functional adult zooid was developed, including the formation of palleal buds (K). Only one zooid per regenerating fragment reached this final stage, while the others degenerated (L) (arrow).(M–P) TUNEL analysis clearly shows staining in degenerating buds. Bud that was normally developed did not stain for TUNEL and exhibits a normal blastula-like structure with clear polarization: (M) and enlargement in (O). Bud that failed to develop went through a degenerating process and was stained for TUNEL: (N) and enlargement in (P). Note that it failed to develop a normal blastula structure, and cells started to fall apart. b, bud; i, intestine; ph, pharynx. Scale bar represents 100 μm. In (O) and (P) scale bars represent 30 μm. |
PMC1808485_pbio-0050071-g002_9850.jpg | What is the dominant medical problem in this image? | Histological Characteristics of WBR in B. leachi
Regenerating vasculature fragments that were sacrificed at sequential daily intervals exhibit cellular events during the regeneration process.(A and B) Phase I events: Haemocytes are attached to vasculature epithelium (A) (arrows). Vascular detachment from the tunic (B) (arrows) enables subsequent relocation of blood vessels.(C–E) Phase II events: 2 d after dissection, aggregated haemocytes of various sizes and shapes were observed in the regeneration niches (C) (arrows). Extensive cell proliferation formed an opaque ball of cells (D) with exclusive PCNA staining (E).(F–L) Phase III events: 1 d later, continuous cell proliferation increased the size of cell aggregates and formed blastula-like structures of different shapes (F and G) (arrowheads). At this stage, multibuds developed simultaneously in various regenerating niches (G) (arrowheads and red arrows, respectively), although separation between compartments had not been completed (G) (arrow). PCNA specifically stained newly formed bud spheres and blastula-like structures inside the regeneration niches (H). As development proceeded, axial polarity was observed with the appearance of differential cell layers (I) (arrowheads). From day 5, two invaginations from both corners of the thick vesicle wall creating two elongated double-walled folds were observed (J) (arrows). Between 10–14 days postseparation, the regeneration process reached the final stages, whereby a fully functional adult zooid was developed, including the formation of palleal buds (K). Only one zooid per regenerating fragment reached this final stage, while the others degenerated (L) (arrow).(M–P) TUNEL analysis clearly shows staining in degenerating buds. Bud that was normally developed did not stain for TUNEL and exhibits a normal blastula-like structure with clear polarization: (M) and enlargement in (O). Bud that failed to develop went through a degenerating process and was stained for TUNEL: (N) and enlargement in (P). Note that it failed to develop a normal blastula structure, and cells started to fall apart. b, bud; i, intestine; ph, pharynx. Scale bar represents 100 μm. In (O) and (P) scale bars represent 30 μm. |
PMC1808485_pbio-0050071-g002_9862.jpg | What is the dominant medical problem in this image? | Histological Characteristics of WBR in B. leachi
Regenerating vasculature fragments that were sacrificed at sequential daily intervals exhibit cellular events during the regeneration process.(A and B) Phase I events: Haemocytes are attached to vasculature epithelium (A) (arrows). Vascular detachment from the tunic (B) (arrows) enables subsequent relocation of blood vessels.(C–E) Phase II events: 2 d after dissection, aggregated haemocytes of various sizes and shapes were observed in the regeneration niches (C) (arrows). Extensive cell proliferation formed an opaque ball of cells (D) with exclusive PCNA staining (E).(F–L) Phase III events: 1 d later, continuous cell proliferation increased the size of cell aggregates and formed blastula-like structures of different shapes (F and G) (arrowheads). At this stage, multibuds developed simultaneously in various regenerating niches (G) (arrowheads and red arrows, respectively), although separation between compartments had not been completed (G) (arrow). PCNA specifically stained newly formed bud spheres and blastula-like structures inside the regeneration niches (H). As development proceeded, axial polarity was observed with the appearance of differential cell layers (I) (arrowheads). From day 5, two invaginations from both corners of the thick vesicle wall creating two elongated double-walled folds were observed (J) (arrows). Between 10–14 days postseparation, the regeneration process reached the final stages, whereby a fully functional adult zooid was developed, including the formation of palleal buds (K). Only one zooid per regenerating fragment reached this final stage, while the others degenerated (L) (arrow).(M–P) TUNEL analysis clearly shows staining in degenerating buds. Bud that was normally developed did not stain for TUNEL and exhibits a normal blastula-like structure with clear polarization: (M) and enlargement in (O). Bud that failed to develop went through a degenerating process and was stained for TUNEL: (N) and enlargement in (P). Note that it failed to develop a normal blastula structure, and cells started to fall apart. b, bud; i, intestine; ph, pharynx. Scale bar represents 100 μm. In (O) and (P) scale bars represent 30 μm. |
PMC1808485_pbio-0050071-g002_9852.jpg | What is the focal point of this photograph? | Histological Characteristics of WBR in B. leachi
Regenerating vasculature fragments that were sacrificed at sequential daily intervals exhibit cellular events during the regeneration process.(A and B) Phase I events: Haemocytes are attached to vasculature epithelium (A) (arrows). Vascular detachment from the tunic (B) (arrows) enables subsequent relocation of blood vessels.(C–E) Phase II events: 2 d after dissection, aggregated haemocytes of various sizes and shapes were observed in the regeneration niches (C) (arrows). Extensive cell proliferation formed an opaque ball of cells (D) with exclusive PCNA staining (E).(F–L) Phase III events: 1 d later, continuous cell proliferation increased the size of cell aggregates and formed blastula-like structures of different shapes (F and G) (arrowheads). At this stage, multibuds developed simultaneously in various regenerating niches (G) (arrowheads and red arrows, respectively), although separation between compartments had not been completed (G) (arrow). PCNA specifically stained newly formed bud spheres and blastula-like structures inside the regeneration niches (H). As development proceeded, axial polarity was observed with the appearance of differential cell layers (I) (arrowheads). From day 5, two invaginations from both corners of the thick vesicle wall creating two elongated double-walled folds were observed (J) (arrows). Between 10–14 days postseparation, the regeneration process reached the final stages, whereby a fully functional adult zooid was developed, including the formation of palleal buds (K). Only one zooid per regenerating fragment reached this final stage, while the others degenerated (L) (arrow).(M–P) TUNEL analysis clearly shows staining in degenerating buds. Bud that was normally developed did not stain for TUNEL and exhibits a normal blastula-like structure with clear polarization: (M) and enlargement in (O). Bud that failed to develop went through a degenerating process and was stained for TUNEL: (N) and enlargement in (P). Note that it failed to develop a normal blastula structure, and cells started to fall apart. b, bud; i, intestine; ph, pharynx. Scale bar represents 100 μm. In (O) and (P) scale bars represent 30 μm. |
PMC1808486_pbio-0050069-g005_9868.jpg | What does this image primarily show? | Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar. |
PMC1808486_pbio-0050069-g005_9867.jpg | What is the dominant medical problem in this image? | Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar. |
PMC1808486_pbio-0050069-g005_9873.jpg | What is shown in this image? | Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar. |
PMC1808486_pbio-0050069-g005_9865.jpg | Describe the main subject of this image. | Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar. |
PMC1808486_pbio-0050069-g005_9871.jpg | Describe the main subject of this image. | Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar. |
PMC1808486_pbio-0050069-g005_9869.jpg | Can you identify the primary element in this image? | Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar. |
PMC1808486_pbio-0050069-g005_9870.jpg | Can you identify the primary element in this image? | Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar. |
PMC1808486_pbio-0050069-g005_9872.jpg | What is the central feature of this picture? | Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar. |
PMC1808486_pbio-0050069-g005_9866.jpg | What is the core subject represented in this visual? | Cell Movement in the Neural Plate(A and B) Schematic overview of the results obtained by the fate-mapping experiments. Colours at prim5 stage correspond to the territories labelled at bud stage.(C–E) Time-lapse analysis of nuclei (red) movement in the neural plate in her5pac:egfp (green): 3D rendering of a 200-μm z-series done at (C) bud stage and (D) 5-somite stage. (E) Schematic overview of the trajectories of individual nuclei over the recorded time (time-lapse movie can be seen in Video S1), with labelled nuclei in white. Wavy lines and dark to light colours of the lines represent the timeline of nuclei movement. Some lines are shorter because nuclei moved out of or into the observed area over the recorded time. We observed three types of movement: the basal cells move anteriorly (green arrow), posterior alar cells move towards the midline and then anteriorly (yellow arrow), and anterior alar cells move diagonally towards the midline (red arrow).(F–L) Transplantation of basal cells: (F) animal pole view in which labelled cells (green) are transplanted on top of the shield; (G) schematic lateral view of shield stage embryo in which transplanted cells are going to move towards the animal pole during gastrulation; (H) schematic lateral view of bud stage embryo in which transplanted cells are spread along the midline of the embryo; and (I) shhGFP is shown in green, transplanted cells in red, at 22 hpf in a live embryo. (J–L) shh is shown in red, transplanted cells in green; at 30 hpf, basally derived cells form a large proportion of the brain, showing that just the tip of the ZLI is formed by alar plate cells (white arrow), the basal ZLI is composed of basal cells (white double arrow), and the ventral part of the developing thalamus is built by basal cells (yellow arrow). The yellow line in (K) indicates the border between alar and basal plate; the arrowhead in (K) points to a single basal cell moving alar. |
PMC1808500_pbio-0050039-g004_9879.jpg | What is the core subject represented in this visual? | Loss of Postsynaptic Target Cells but Not Local Striatal Interneurons in DAT-Retlx/lx MiceImmunohistochemical stainings of dorsal striatum of 2-y-old control (A, D, and G) and DAT-Retlx/lx mutants (B, E, and H) for NeuN (A and B), DARPP-32 (D and E), or parvalbumin (G and H). Histograms showing the number of NeuN-positive (C), DARPP-32–positive (F), and parvalbumin-positive cells (I) in DAT-Retlx/lx mutants and age-matched controls (n = 3–5 each genotype). Note also the reduced staining intensities for NeuN and DARPP-32 in DAT-Retlx/lx compared to control mice. *, p < 0.05; **, p < 0.01 (Student t-test). Scale bars indicate 50 μm. |
PMC1808500_pbio-0050039-g004_9875.jpg | What can you see in this picture? | Loss of Postsynaptic Target Cells but Not Local Striatal Interneurons in DAT-Retlx/lx MiceImmunohistochemical stainings of dorsal striatum of 2-y-old control (A, D, and G) and DAT-Retlx/lx mutants (B, E, and H) for NeuN (A and B), DARPP-32 (D and E), or parvalbumin (G and H). Histograms showing the number of NeuN-positive (C), DARPP-32–positive (F), and parvalbumin-positive cells (I) in DAT-Retlx/lx mutants and age-matched controls (n = 3–5 each genotype). Note also the reduced staining intensities for NeuN and DARPP-32 in DAT-Retlx/lx compared to control mice. *, p < 0.05; **, p < 0.01 (Student t-test). Scale bars indicate 50 μm. |
PMC1808500_pbio-0050039-g004_9878.jpg | Describe the main subject of this image. | Loss of Postsynaptic Target Cells but Not Local Striatal Interneurons in DAT-Retlx/lx MiceImmunohistochemical stainings of dorsal striatum of 2-y-old control (A, D, and G) and DAT-Retlx/lx mutants (B, E, and H) for NeuN (A and B), DARPP-32 (D and E), or parvalbumin (G and H). Histograms showing the number of NeuN-positive (C), DARPP-32–positive (F), and parvalbumin-positive cells (I) in DAT-Retlx/lx mutants and age-matched controls (n = 3–5 each genotype). Note also the reduced staining intensities for NeuN and DARPP-32 in DAT-Retlx/lx compared to control mice. *, p < 0.05; **, p < 0.01 (Student t-test). Scale bars indicate 50 μm. |
PMC1808500_pbio-0050039-g004_9881.jpg | What stands out most in this visual? | Loss of Postsynaptic Target Cells but Not Local Striatal Interneurons in DAT-Retlx/lx MiceImmunohistochemical stainings of dorsal striatum of 2-y-old control (A, D, and G) and DAT-Retlx/lx mutants (B, E, and H) for NeuN (A and B), DARPP-32 (D and E), or parvalbumin (G and H). Histograms showing the number of NeuN-positive (C), DARPP-32–positive (F), and parvalbumin-positive cells (I) in DAT-Retlx/lx mutants and age-matched controls (n = 3–5 each genotype). Note also the reduced staining intensities for NeuN and DARPP-32 in DAT-Retlx/lx compared to control mice. *, p < 0.05; **, p < 0.01 (Student t-test). Scale bars indicate 50 μm. |
PMC1810238_F1_9884.jpg | What stands out most in this visual? | The photo shows the 3D hologram of the ventricular septal defect repaired with a patch. |
PMC1810239_F5_9889.jpg | Describe the main subject of this image. | Visual scoring compared to CMYK analysis. (A) Representative images of 256 NSCLC biopsies show plasma membrane specific EGFR-NovaRed labeling with visual scores ranging from 0–3. (B) A box and whiskers graph (median, 25% to 75% box range, min and max whiskers) representation of mean Yellow intensity of specimens shows a direct relationship with the categorical visual scores. |
PMC1810239_F5_9886.jpg | What object or scene is depicted here? | Visual scoring compared to CMYK analysis. (A) Representative images of 256 NSCLC biopsies show plasma membrane specific EGFR-NovaRed labeling with visual scores ranging from 0–3. (B) A box and whiskers graph (median, 25% to 75% box range, min and max whiskers) representation of mean Yellow intensity of specimens shows a direct relationship with the categorical visual scores. |
PMC1810239_F5_9887.jpg | What is the dominant medical problem in this image? | Visual scoring compared to CMYK analysis. (A) Representative images of 256 NSCLC biopsies show plasma membrane specific EGFR-NovaRed labeling with visual scores ranging from 0–3. (B) A box and whiskers graph (median, 25% to 75% box range, min and max whiskers) representation of mean Yellow intensity of specimens shows a direct relationship with the categorical visual scores. |
PMC1810239_F5_9888.jpg | What key item or scene is captured in this photo? | Visual scoring compared to CMYK analysis. (A) Representative images of 256 NSCLC biopsies show plasma membrane specific EGFR-NovaRed labeling with visual scores ranging from 0–3. (B) A box and whiskers graph (median, 25% to 75% box range, min and max whiskers) representation of mean Yellow intensity of specimens shows a direct relationship with the categorical visual scores. |
PMC1810241_F4_9891.jpg | What key item or scene is captured in this photo? | Morphological changes of cell cultures infected with WR and Wyeth strains at 3 days post-infection. (A) Plaque formation in Vero E6 and EA.hy926 cells. (B) Morphological changes of CV-1, primary mouse lung cells (Lung), MLEC and primary mouse kidney cells (Kidney) at 200 × magnification. Cells were infected with WR or Wyeth strains at m.o.i. 1 and observed after 2 days post-infection. |
PMC1810241_F4_9895.jpg | What is the focal point of this photograph? | Morphological changes of cell cultures infected with WR and Wyeth strains at 3 days post-infection. (A) Plaque formation in Vero E6 and EA.hy926 cells. (B) Morphological changes of CV-1, primary mouse lung cells (Lung), MLEC and primary mouse kidney cells (Kidney) at 200 × magnification. Cells were infected with WR or Wyeth strains at m.o.i. 1 and observed after 2 days post-infection. |
PMC1810241_F4_9894.jpg | Describe the main subject of this image. | Morphological changes of cell cultures infected with WR and Wyeth strains at 3 days post-infection. (A) Plaque formation in Vero E6 and EA.hy926 cells. (B) Morphological changes of CV-1, primary mouse lung cells (Lung), MLEC and primary mouse kidney cells (Kidney) at 200 × magnification. Cells were infected with WR or Wyeth strains at m.o.i. 1 and observed after 2 days post-infection. |
PMC1810241_F4_9892.jpg | What is shown in this image? | Morphological changes of cell cultures infected with WR and Wyeth strains at 3 days post-infection. (A) Plaque formation in Vero E6 and EA.hy926 cells. (B) Morphological changes of CV-1, primary mouse lung cells (Lung), MLEC and primary mouse kidney cells (Kidney) at 200 × magnification. Cells were infected with WR or Wyeth strains at m.o.i. 1 and observed after 2 days post-infection. |
PMC1810241_F4_9890.jpg | What's the most prominent thing you notice in this picture? | Morphological changes of cell cultures infected with WR and Wyeth strains at 3 days post-infection. (A) Plaque formation in Vero E6 and EA.hy926 cells. (B) Morphological changes of CV-1, primary mouse lung cells (Lung), MLEC and primary mouse kidney cells (Kidney) at 200 × magnification. Cells were infected with WR or Wyeth strains at m.o.i. 1 and observed after 2 days post-infection. |
PMC1810241_F4_9893.jpg | Describe the main subject of this image. | Morphological changes of cell cultures infected with WR and Wyeth strains at 3 days post-infection. (A) Plaque formation in Vero E6 and EA.hy926 cells. (B) Morphological changes of CV-1, primary mouse lung cells (Lung), MLEC and primary mouse kidney cells (Kidney) at 200 × magnification. Cells were infected with WR or Wyeth strains at m.o.i. 1 and observed after 2 days post-infection. |
PMC1810251_F2_9900.jpg | What is being portrayed in this visual content? | TLR9 immunoreactivity in the nasal mucosa. Immunohistochemical localization of TLR9 in biopsies of nasal mucosa is depicted in (B-F) whereas (A) illustrates a representative picture of a control slide. A) No immunoreactivity was observed in control sections where an isotype-matched control antibody was used. B) In an adjacent section, immunoreactivity for TLR9 is seen in the apical part of the epithelial lining, in scattered intra- and subepithelial leukocytes and in elongated fibroblast-like cells in the subepithelial tissue (arrow). The epithelial TLR9 immunoreactivity varied from being foremost present within the apical region of the epithelium (B) to a more even distribution (C). D) A distinct TLR9 immunoreactivity was also present in endothelial cells (arrowhead). E) Bright field micrographs demonstrating TLR9-positive large non-granulated mononuclear cells (arrowhead) and mast cells (inset). F) TLR9-positive intraepithelial lymphocytes (arrows E-F). Scale bars: A-C = 50 μm, D-E = 20 μm, and F = 350 μm. |
PMC1810251_F2_9901.jpg | What is the focal point of this photograph? | TLR9 immunoreactivity in the nasal mucosa. Immunohistochemical localization of TLR9 in biopsies of nasal mucosa is depicted in (B-F) whereas (A) illustrates a representative picture of a control slide. A) No immunoreactivity was observed in control sections where an isotype-matched control antibody was used. B) In an adjacent section, immunoreactivity for TLR9 is seen in the apical part of the epithelial lining, in scattered intra- and subepithelial leukocytes and in elongated fibroblast-like cells in the subepithelial tissue (arrow). The epithelial TLR9 immunoreactivity varied from being foremost present within the apical region of the epithelium (B) to a more even distribution (C). D) A distinct TLR9 immunoreactivity was also present in endothelial cells (arrowhead). E) Bright field micrographs demonstrating TLR9-positive large non-granulated mononuclear cells (arrowhead) and mast cells (inset). F) TLR9-positive intraepithelial lymphocytes (arrows E-F). Scale bars: A-C = 50 μm, D-E = 20 μm, and F = 350 μm. |
PMC1810251_F2_9898.jpg | What is the dominant medical problem in this image? | TLR9 immunoreactivity in the nasal mucosa. Immunohistochemical localization of TLR9 in biopsies of nasal mucosa is depicted in (B-F) whereas (A) illustrates a representative picture of a control slide. A) No immunoreactivity was observed in control sections where an isotype-matched control antibody was used. B) In an adjacent section, immunoreactivity for TLR9 is seen in the apical part of the epithelial lining, in scattered intra- and subepithelial leukocytes and in elongated fibroblast-like cells in the subepithelial tissue (arrow). The epithelial TLR9 immunoreactivity varied from being foremost present within the apical region of the epithelium (B) to a more even distribution (C). D) A distinct TLR9 immunoreactivity was also present in endothelial cells (arrowhead). E) Bright field micrographs demonstrating TLR9-positive large non-granulated mononuclear cells (arrowhead) and mast cells (inset). F) TLR9-positive intraepithelial lymphocytes (arrows E-F). Scale bars: A-C = 50 μm, D-E = 20 μm, and F = 350 μm. |
PMC1810251_F2_9897.jpg | What stands out most in this visual? | TLR9 immunoreactivity in the nasal mucosa. Immunohistochemical localization of TLR9 in biopsies of nasal mucosa is depicted in (B-F) whereas (A) illustrates a representative picture of a control slide. A) No immunoreactivity was observed in control sections where an isotype-matched control antibody was used. B) In an adjacent section, immunoreactivity for TLR9 is seen in the apical part of the epithelial lining, in scattered intra- and subepithelial leukocytes and in elongated fibroblast-like cells in the subepithelial tissue (arrow). The epithelial TLR9 immunoreactivity varied from being foremost present within the apical region of the epithelium (B) to a more even distribution (C). D) A distinct TLR9 immunoreactivity was also present in endothelial cells (arrowhead). E) Bright field micrographs demonstrating TLR9-positive large non-granulated mononuclear cells (arrowhead) and mast cells (inset). F) TLR9-positive intraepithelial lymphocytes (arrows E-F). Scale bars: A-C = 50 μm, D-E = 20 μm, and F = 350 μm. |
PMC1810251_F2_9902.jpg | What is the principal component of this image? | TLR9 immunoreactivity in the nasal mucosa. Immunohistochemical localization of TLR9 in biopsies of nasal mucosa is depicted in (B-F) whereas (A) illustrates a representative picture of a control slide. A) No immunoreactivity was observed in control sections where an isotype-matched control antibody was used. B) In an adjacent section, immunoreactivity for TLR9 is seen in the apical part of the epithelial lining, in scattered intra- and subepithelial leukocytes and in elongated fibroblast-like cells in the subepithelial tissue (arrow). The epithelial TLR9 immunoreactivity varied from being foremost present within the apical region of the epithelium (B) to a more even distribution (C). D) A distinct TLR9 immunoreactivity was also present in endothelial cells (arrowhead). E) Bright field micrographs demonstrating TLR9-positive large non-granulated mononuclear cells (arrowhead) and mast cells (inset). F) TLR9-positive intraepithelial lymphocytes (arrows E-F). Scale bars: A-C = 50 μm, D-E = 20 μm, and F = 350 μm. |
PMC1810426_pone-0000302-g004_9919.jpg | What is the focal point of this photograph? | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g004_9909.jpg | What is shown in this image? | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g004_9917.jpg | What is the principal component of this image? | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g004_9916.jpg | Describe the main subject of this image. | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g004_9911.jpg | What is the core subject represented in this visual? | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g004_9914.jpg | Describe the main subject of this image. | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g004_9915.jpg | What is the principal component of this image? | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g004_9918.jpg | What is shown in this image? | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g004_9912.jpg | What is being portrayed in this visual content? | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g004_9913.jpg | What is the dominant medical problem in this image? | Lateral Speciation on Singling-out Epidermal Ionocyte Progenitors is Mediated by deltaC Ligand and notch1a/notch3 Receptors.(A) Fluorescence double in situ hybridization shows the overlapping expression between deltaC (green, left) and foxi3a (red, middle) on the epidermal ionocyte domain of the ventral ectoderm at the tail bud (tb) stage. The angles of the deltaC and foxi3a expression domain are presented as the mean±S.D. (B) The area demarcated by the dotted line in (A) is viewed at high magnification. Basically, foxi3a+ epidermal ionocyte progenitors (red) also co-express deltaC (green, asterisks). However, some deltaC+ cells outside the epidermal ionocyte domain are negative for foxi3a, suggesting that they are not epidermal ionocytes. (C–D) Fluorescent double in situ hybridization with deltaC (green) and foxi3a (red) probes to show that deltaC is transiently expressed in the epidermal ionocyte lineage. As development proceeds, deltaC is sharply downregulated in the epidermal ionocyte lineage. (E–L) Evaluation of foxi3a expression by genetic mutants or morphants with reduced or enhanced Notch activity at the tb stage. foxi3a expression in the epidermal ionocyte domain was more homogeneous in deltaC mutants of beatit446 (E) and beatw212b (F), in a notch1a mutant of desth35b (G), and in a notch3 MO-injected desth35b mutant (I). The foxi3a expression in the epidermal ionocyte domain was severely reduced in notch1a intracellular domain (ICD) RNA- (J) or notch3 ICD RNA-injected embryos (K). (H) notch1a/des th35b mutants injected with the notch1b MO showed no significant difference with uninjected mutants. N1a, notch1a; N1b, notch1b; N3, notch3; ICD, intra-cellular domain; MO, morpholino. |
PMC1810426_pone-0000302-g005_9905.jpg | What is the principal component of this image? |
deltaC is Positively Regulated by ascl1a and Receives Negative Feedback by notch.
(A) Misexpression of VP16:ascl1a mRNA was sufficient to generate ectopic deltaC expression outside the epidermal ionocyte domain. foxi3a expression, on the contrary, was not affected by VP16:ascl1a mRNA misexpression. (B–F) Evaluation of deltaC expression by genetic mutants or mRNA-injected embryos with enhanced or reduced Notch activity. Compared to the wild-type (B), deltaC expression in the epidermal ionocyte domain was more homogeneous in mibta52b (C), beatit446 (D), and X-Su(H)DBM mRNA-injected embryos (E). On the contrary, deltaC expression in the epidermal ionocyte domain was completely abolished in X-Su(H)/Ank mRNA-injected embryos (F). Embryos in the upper panel of all photos are oriented in ventral view, with the anterior to the top, while in the lower panel, all are oriented in lateral view, with the anterior to the left. Epidermal ionocyte domains are highlighted by dotted lines. hpf, hour post-fertilization; tb, tail bud. |
PMC1810426_pone-0000302-g005_9904.jpg | What object or scene is depicted here? |
deltaC is Positively Regulated by ascl1a and Receives Negative Feedback by notch.
(A) Misexpression of VP16:ascl1a mRNA was sufficient to generate ectopic deltaC expression outside the epidermal ionocyte domain. foxi3a expression, on the contrary, was not affected by VP16:ascl1a mRNA misexpression. (B–F) Evaluation of deltaC expression by genetic mutants or mRNA-injected embryos with enhanced or reduced Notch activity. Compared to the wild-type (B), deltaC expression in the epidermal ionocyte domain was more homogeneous in mibta52b (C), beatit446 (D), and X-Su(H)DBM mRNA-injected embryos (E). On the contrary, deltaC expression in the epidermal ionocyte domain was completely abolished in X-Su(H)/Ank mRNA-injected embryos (F). Embryos in the upper panel of all photos are oriented in ventral view, with the anterior to the top, while in the lower panel, all are oriented in lateral view, with the anterior to the left. Epidermal ionocyte domains are highlighted by dotted lines. hpf, hour post-fertilization; tb, tail bud. |
PMC1810426_pone-0000302-g005_9907.jpg | What is the main focus of this visual representation? |
deltaC is Positively Regulated by ascl1a and Receives Negative Feedback by notch.
(A) Misexpression of VP16:ascl1a mRNA was sufficient to generate ectopic deltaC expression outside the epidermal ionocyte domain. foxi3a expression, on the contrary, was not affected by VP16:ascl1a mRNA misexpression. (B–F) Evaluation of deltaC expression by genetic mutants or mRNA-injected embryos with enhanced or reduced Notch activity. Compared to the wild-type (B), deltaC expression in the epidermal ionocyte domain was more homogeneous in mibta52b (C), beatit446 (D), and X-Su(H)DBM mRNA-injected embryos (E). On the contrary, deltaC expression in the epidermal ionocyte domain was completely abolished in X-Su(H)/Ank mRNA-injected embryos (F). Embryos in the upper panel of all photos are oriented in ventral view, with the anterior to the top, while in the lower panel, all are oriented in lateral view, with the anterior to the left. Epidermal ionocyte domains are highlighted by dotted lines. hpf, hour post-fertilization; tb, tail bud. |
PMC1810426_pone-0000302-g005_9908.jpg | What is the dominant medical problem in this image? |
deltaC is Positively Regulated by ascl1a and Receives Negative Feedback by notch.
(A) Misexpression of VP16:ascl1a mRNA was sufficient to generate ectopic deltaC expression outside the epidermal ionocyte domain. foxi3a expression, on the contrary, was not affected by VP16:ascl1a mRNA misexpression. (B–F) Evaluation of deltaC expression by genetic mutants or mRNA-injected embryos with enhanced or reduced Notch activity. Compared to the wild-type (B), deltaC expression in the epidermal ionocyte domain was more homogeneous in mibta52b (C), beatit446 (D), and X-Su(H)DBM mRNA-injected embryos (E). On the contrary, deltaC expression in the epidermal ionocyte domain was completely abolished in X-Su(H)/Ank mRNA-injected embryos (F). Embryos in the upper panel of all photos are oriented in ventral view, with the anterior to the top, while in the lower panel, all are oriented in lateral view, with the anterior to the left. Epidermal ionocyte domains are highlighted by dotted lines. hpf, hour post-fertilization; tb, tail bud. |
PMC1810521_F2_9922.jpg | What's the most prominent thing you notice in this picture? | A and B. Light microscopy of total nerve fibers in a normal (A) and haemangiomatous (B) artery of the face stained using Bodian's method. The adventitia was separated from other layers of the artery wall and stretched on a slice. As can be seen, there are fewer nerve fibers in the haemangiomatous artery (B) than in the normal artery (A) (magnification 400×; bar 100 μm). |
PMC1810521_F2_9923.jpg | What is being portrayed in this visual content? | A and B. Light microscopy of total nerve fibers in a normal (A) and haemangiomatous (B) artery of the face stained using Bodian's method. The adventitia was separated from other layers of the artery wall and stretched on a slice. As can be seen, there are fewer nerve fibers in the haemangiomatous artery (B) than in the normal artery (A) (magnification 400×; bar 100 μm). |
PMC1810521_F3_9924.jpg | What can you see in this picture? | A and B. Fluorescent light microscopy of a transversal section of a normal (A) artery of the face stained using Falck's method for the staining of adrenergic nerve fibers compared with a haemangiomatous artery (B). A = adventitia; M = medium layer; E = endothelial layer; L = lumen (magnification 400×; bar 100 μm). |
PMC1810521_F3_9925.jpg | What stands out most in this visual? | A and B. Fluorescent light microscopy of a transversal section of a normal (A) artery of the face stained using Falck's method for the staining of adrenergic nerve fibers compared with a haemangiomatous artery (B). A = adventitia; M = medium layer; E = endothelial layer; L = lumen (magnification 400×; bar 100 μm). |
PMC1810538_F1_9927.jpg | What is being portrayed in this visual content? | Cross sectional cut of CT scan of abdomen at the time of clinical presentation. Multiple hypoechoic densities are present in the spleen (arrows). |
PMC1810538_F2_9926.jpg | What key item or scene is captured in this photo? | Hematoxylin and eosin stain of lymph node biopsy showing a stellate granuloma and microabscesses. |
PMC1810561_F4_9928.jpg | What can you see in this picture? | Effects of Hg2+ on ethidium-labeling in the renal cortex. Animals were treated with Hg2+ (3.5 mg/kg, ip) for 24 h and the left kidneys were infused with ethidium homodimer. Cryosections of the kidneys were then fixed, permeabilized and labeled with DAPI as described in the Methods section. Panels A, D, G are high-powered (HP) images from control animals and panels B, E, H are from 3.5 mg/kg Hg2+-treated animals. Panels C, F, I represent low-powered (LP) images from 3.5 mg/kg Hg2+-treated animals. Panels A-C show phase-contrast images of the same fields in D-F and G-I, respectively. Panels D-F show total nuclei labeled in each field by DAPI, G-I show labeled nuclei by ethidium homodimer. The white arrow in panel I indicates the boundary between inner medulla and the renal cortex. The scale bar in the top left image represents 100 μm and the scale bar in the top right image represents 500 μm. |
PMC1810561_F4_9929.jpg | Can you identify the primary element in this image? | Effects of Hg2+ on ethidium-labeling in the renal cortex. Animals were treated with Hg2+ (3.5 mg/kg, ip) for 24 h and the left kidneys were infused with ethidium homodimer. Cryosections of the kidneys were then fixed, permeabilized and labeled with DAPI as described in the Methods section. Panels A, D, G are high-powered (HP) images from control animals and panels B, E, H are from 3.5 mg/kg Hg2+-treated animals. Panels C, F, I represent low-powered (LP) images from 3.5 mg/kg Hg2+-treated animals. Panels A-C show phase-contrast images of the same fields in D-F and G-I, respectively. Panels D-F show total nuclei labeled in each field by DAPI, G-I show labeled nuclei by ethidium homodimer. The white arrow in panel I indicates the boundary between inner medulla and the renal cortex. The scale bar in the top left image represents 100 μm and the scale bar in the top right image represents 500 μm. |
PMC1810561_F4_9933.jpg | Describe the main subject of this image. | Effects of Hg2+ on ethidium-labeling in the renal cortex. Animals were treated with Hg2+ (3.5 mg/kg, ip) for 24 h and the left kidneys were infused with ethidium homodimer. Cryosections of the kidneys were then fixed, permeabilized and labeled with DAPI as described in the Methods section. Panels A, D, G are high-powered (HP) images from control animals and panels B, E, H are from 3.5 mg/kg Hg2+-treated animals. Panels C, F, I represent low-powered (LP) images from 3.5 mg/kg Hg2+-treated animals. Panels A-C show phase-contrast images of the same fields in D-F and G-I, respectively. Panels D-F show total nuclei labeled in each field by DAPI, G-I show labeled nuclei by ethidium homodimer. The white arrow in panel I indicates the boundary between inner medulla and the renal cortex. The scale bar in the top left image represents 100 μm and the scale bar in the top right image represents 500 μm. |
PMC1810561_F4_9932.jpg | Describe the main subject of this image. | Effects of Hg2+ on ethidium-labeling in the renal cortex. Animals were treated with Hg2+ (3.5 mg/kg, ip) for 24 h and the left kidneys were infused with ethidium homodimer. Cryosections of the kidneys were then fixed, permeabilized and labeled with DAPI as described in the Methods section. Panels A, D, G are high-powered (HP) images from control animals and panels B, E, H are from 3.5 mg/kg Hg2+-treated animals. Panels C, F, I represent low-powered (LP) images from 3.5 mg/kg Hg2+-treated animals. Panels A-C show phase-contrast images of the same fields in D-F and G-I, respectively. Panels D-F show total nuclei labeled in each field by DAPI, G-I show labeled nuclei by ethidium homodimer. The white arrow in panel I indicates the boundary between inner medulla and the renal cortex. The scale bar in the top left image represents 100 μm and the scale bar in the top right image represents 500 μm. |
PMC1810561_F4_9935.jpg | What object or scene is depicted here? | Effects of Hg2+ on ethidium-labeling in the renal cortex. Animals were treated with Hg2+ (3.5 mg/kg, ip) for 24 h and the left kidneys were infused with ethidium homodimer. Cryosections of the kidneys were then fixed, permeabilized and labeled with DAPI as described in the Methods section. Panels A, D, G are high-powered (HP) images from control animals and panels B, E, H are from 3.5 mg/kg Hg2+-treated animals. Panels C, F, I represent low-powered (LP) images from 3.5 mg/kg Hg2+-treated animals. Panels A-C show phase-contrast images of the same fields in D-F and G-I, respectively. Panels D-F show total nuclei labeled in each field by DAPI, G-I show labeled nuclei by ethidium homodimer. The white arrow in panel I indicates the boundary between inner medulla and the renal cortex. The scale bar in the top left image represents 100 μm and the scale bar in the top right image represents 500 μm. |
PMC1810561_F4_9930.jpg | What can you see in this picture? | Effects of Hg2+ on ethidium-labeling in the renal cortex. Animals were treated with Hg2+ (3.5 mg/kg, ip) for 24 h and the left kidneys were infused with ethidium homodimer. Cryosections of the kidneys were then fixed, permeabilized and labeled with DAPI as described in the Methods section. Panels A, D, G are high-powered (HP) images from control animals and panels B, E, H are from 3.5 mg/kg Hg2+-treated animals. Panels C, F, I represent low-powered (LP) images from 3.5 mg/kg Hg2+-treated animals. Panels A-C show phase-contrast images of the same fields in D-F and G-I, respectively. Panels D-F show total nuclei labeled in each field by DAPI, G-I show labeled nuclei by ethidium homodimer. The white arrow in panel I indicates the boundary between inner medulla and the renal cortex. The scale bar in the top left image represents 100 μm and the scale bar in the top right image represents 500 μm. |
PMC1810561_F4_9931.jpg | What is the main focus of this visual representation? | Effects of Hg2+ on ethidium-labeling in the renal cortex. Animals were treated with Hg2+ (3.5 mg/kg, ip) for 24 h and the left kidneys were infused with ethidium homodimer. Cryosections of the kidneys were then fixed, permeabilized and labeled with DAPI as described in the Methods section. Panels A, D, G are high-powered (HP) images from control animals and panels B, E, H are from 3.5 mg/kg Hg2+-treated animals. Panels C, F, I represent low-powered (LP) images from 3.5 mg/kg Hg2+-treated animals. Panels A-C show phase-contrast images of the same fields in D-F and G-I, respectively. Panels D-F show total nuclei labeled in each field by DAPI, G-I show labeled nuclei by ethidium homodimer. The white arrow in panel I indicates the boundary between inner medulla and the renal cortex. The scale bar in the top left image represents 100 μm and the scale bar in the top right image represents 500 μm. |
PMC1810561_F4_9934.jpg | What can you see in this picture? | Effects of Hg2+ on ethidium-labeling in the renal cortex. Animals were treated with Hg2+ (3.5 mg/kg, ip) for 24 h and the left kidneys were infused with ethidium homodimer. Cryosections of the kidneys were then fixed, permeabilized and labeled with DAPI as described in the Methods section. Panels A, D, G are high-powered (HP) images from control animals and panels B, E, H are from 3.5 mg/kg Hg2+-treated animals. Panels C, F, I represent low-powered (LP) images from 3.5 mg/kg Hg2+-treated animals. Panels A-C show phase-contrast images of the same fields in D-F and G-I, respectively. Panels D-F show total nuclei labeled in each field by DAPI, G-I show labeled nuclei by ethidium homodimer. The white arrow in panel I indicates the boundary between inner medulla and the renal cortex. The scale bar in the top left image represents 100 μm and the scale bar in the top right image represents 500 μm. |
PMC1817643_F1_9939.jpg | What's the most prominent thing you notice in this picture? | Screening and electron microscopy of bacteriophage 0305φ8-36. Bacteriophage 0305φ8-36 was initially propagated and isolated [17] from soil frequented by cattle at the King Ranch (Kingsville, Texas). The host was a locally isolated Bacillus that was typed as B. thuringiensis by sequencing of the gene for 16s ribosomal DNA, as previously described [17]. During isolation, single-plaque cloning was performed [17] in gels of 0.40%, 0.20% and 0.15% agarose. The inocula for all three Petri plates were bacteriophages from a single plaque of the previous propagation, transferred by sterile needle and then non-uniformly spread [17]. The three Petri plates were at the same temperature (±0.2 C) during incubation. Photographic images are shown of Petri plates used for propagation in agarose gels of the following percentages: (a) 0.4, (b) 0.20, (c) 0.15. (d) In a more comprehensive experiment, plots of plaque diameter as a function of agarose gel percentage were made for bacteriophages G, T4 and 0305φ8-36 (0305φ8-36 is abbreviated by 36 in the figure). The molten agarose solution was the same among the different bacteriophages in (d). The host for bacteriophage G was Bacillus megaterium; the host for T4 was Escherichia coli BB/1. All Petri plates for (d) were in contact with the same surface and the temperature did not vary among them by more than 0.2°C. (e) Electron microscopy was performed of bacteriophage 0305φ8-36 negatively stained with sodium phosphotungstate after purification from a plate stock by use of a cesium chloride step gradient [17]. The length of the bar is 0.1 μm; magnification calibration was checked with a diffraction grating. The tails of all bacteriophage particles have partially contracted. By this criterion, 0305φ8-36 is a myovirus. |
PMC1817643_F1_9937.jpg | Can you identify the primary element in this image? | Screening and electron microscopy of bacteriophage 0305φ8-36. Bacteriophage 0305φ8-36 was initially propagated and isolated [17] from soil frequented by cattle at the King Ranch (Kingsville, Texas). The host was a locally isolated Bacillus that was typed as B. thuringiensis by sequencing of the gene for 16s ribosomal DNA, as previously described [17]. During isolation, single-plaque cloning was performed [17] in gels of 0.40%, 0.20% and 0.15% agarose. The inocula for all three Petri plates were bacteriophages from a single plaque of the previous propagation, transferred by sterile needle and then non-uniformly spread [17]. The three Petri plates were at the same temperature (±0.2 C) during incubation. Photographic images are shown of Petri plates used for propagation in agarose gels of the following percentages: (a) 0.4, (b) 0.20, (c) 0.15. (d) In a more comprehensive experiment, plots of plaque diameter as a function of agarose gel percentage were made for bacteriophages G, T4 and 0305φ8-36 (0305φ8-36 is abbreviated by 36 in the figure). The molten agarose solution was the same among the different bacteriophages in (d). The host for bacteriophage G was Bacillus megaterium; the host for T4 was Escherichia coli BB/1. All Petri plates for (d) were in contact with the same surface and the temperature did not vary among them by more than 0.2°C. (e) Electron microscopy was performed of bacteriophage 0305φ8-36 negatively stained with sodium phosphotungstate after purification from a plate stock by use of a cesium chloride step gradient [17]. The length of the bar is 0.1 μm; magnification calibration was checked with a diffraction grating. The tails of all bacteriophage particles have partially contracted. By this criterion, 0305φ8-36 is a myovirus. |
PMC1817656_ppat-0030031-g002_9942.jpg | What is shown in this image? | Brain MRI of Tgbov XV Mice Infected with BSE and BASET2-weighted images of anterior-to-posterior coronal planes of (A–C) BASE-infected mouse; (D–F) BSE-infected mouse; (G–I) uninfected Tgbov XV mouse. Both BSE- and BASE-infected mice show high signal intensity in the septal region: arrowheads in (A) and (D); and cerebellum: arrowheads in (C) and (F) compared to control (G) and (I). In addition, mice challenged with BASE exhibit scattered hyperintense areas in frontal regions: arrows in (A); and midbrain: arrows in (B) that are absent in BSE-infected and uninfected mice. |
PMC1817656_ppat-0030031-g002_9950.jpg | What is shown in this image? | Brain MRI of Tgbov XV Mice Infected with BSE and BASET2-weighted images of anterior-to-posterior coronal planes of (A–C) BASE-infected mouse; (D–F) BSE-infected mouse; (G–I) uninfected Tgbov XV mouse. Both BSE- and BASE-infected mice show high signal intensity in the septal region: arrowheads in (A) and (D); and cerebellum: arrowheads in (C) and (F) compared to control (G) and (I). In addition, mice challenged with BASE exhibit scattered hyperintense areas in frontal regions: arrows in (A); and midbrain: arrows in (B) that are absent in BSE-infected and uninfected mice. |
PMC1817656_ppat-0030031-g002_9949.jpg | Describe the main subject of this image. | Brain MRI of Tgbov XV Mice Infected with BSE and BASET2-weighted images of anterior-to-posterior coronal planes of (A–C) BASE-infected mouse; (D–F) BSE-infected mouse; (G–I) uninfected Tgbov XV mouse. Both BSE- and BASE-infected mice show high signal intensity in the septal region: arrowheads in (A) and (D); and cerebellum: arrowheads in (C) and (F) compared to control (G) and (I). In addition, mice challenged with BASE exhibit scattered hyperintense areas in frontal regions: arrows in (A); and midbrain: arrows in (B) that are absent in BSE-infected and uninfected mice. |
PMC1817656_ppat-0030031-g002_9944.jpg | What can you see in this picture? | Brain MRI of Tgbov XV Mice Infected with BSE and BASET2-weighted images of anterior-to-posterior coronal planes of (A–C) BASE-infected mouse; (D–F) BSE-infected mouse; (G–I) uninfected Tgbov XV mouse. Both BSE- and BASE-infected mice show high signal intensity in the septal region: arrowheads in (A) and (D); and cerebellum: arrowheads in (C) and (F) compared to control (G) and (I). In addition, mice challenged with BASE exhibit scattered hyperintense areas in frontal regions: arrows in (A); and midbrain: arrows in (B) that are absent in BSE-infected and uninfected mice. |
PMC1817656_ppat-0030031-g002_9947.jpg | What stands out most in this visual? | Brain MRI of Tgbov XV Mice Infected with BSE and BASET2-weighted images of anterior-to-posterior coronal planes of (A–C) BASE-infected mouse; (D–F) BSE-infected mouse; (G–I) uninfected Tgbov XV mouse. Both BSE- and BASE-infected mice show high signal intensity in the septal region: arrowheads in (A) and (D); and cerebellum: arrowheads in (C) and (F) compared to control (G) and (I). In addition, mice challenged with BASE exhibit scattered hyperintense areas in frontal regions: arrows in (A); and midbrain: arrows in (B) that are absent in BSE-infected and uninfected mice. |
PMC1819365_F2_9951.jpg | What can you see in this picture? | Detection of LMP-1 expression by immunohistochemistry (red) in UNPC tumor cells. Alkaline phosphatase anti-alkaline phosphatase, original magnification ×250. |
PMC1819375_F10_9953.jpg | What is the core subject represented in this visual? | Histopathological image of a biopsy guided by the assessment in "Figure 9" showing keratosis with scattered nuclei (20–40 cell layers deep) and Civatte bodies at the basement membrane conducive with a diagnosis of Lichen Planus. This is at right angles (i.e. transverse section) to the plane of assessment in "Figure 9". |
PMC1819379_F1_9954.jpg | What is being portrayed in this visual content? | preoperative aortography. |
PMC1819384_F5_9957.jpg | What does this image primarily show? | Electron microscopy analysis of structure changes in E. coli challenged baboon lung. a: normal architecture of the alveolar septae in healthy baboons; b. accumulation of neutrophils (PMN) and the presence of intra-alveolar bleeding erythrocytes (arrow) can be observed at 2 hrs; c: the increased accumulation of macrophages, fibroblasts and collagen deposition at 24 hrs. av, alveola; coll, collagen; Fb, fibroblasts; Mac, macrophages; RBC, red blood cells. Magnification: ×7000. |
PMC1819384_F5_9955.jpg | Can you identify the primary element in this image? | Electron microscopy analysis of structure changes in E. coli challenged baboon lung. a: normal architecture of the alveolar septae in healthy baboons; b. accumulation of neutrophils (PMN) and the presence of intra-alveolar bleeding erythrocytes (arrow) can be observed at 2 hrs; c: the increased accumulation of macrophages, fibroblasts and collagen deposition at 24 hrs. av, alveola; coll, collagen; Fb, fibroblasts; Mac, macrophages; RBC, red blood cells. Magnification: ×7000. |
PMC1819556_pone-0000314-g003_9958.jpg | What object or scene is depicted here? |
A) Western blot confirmation of XIAP over-expression in injected eyes in P23H animals in comparison to the contralateral control uninjected eye in the same animal. Blot was probed with an anti-HA antibody. Given that the protein extracts were made from the whole retina, and only a fraction of the retina was covered by the subretinal injection, XIAP protein levels seen on the Western blot are an under-estimation of the level of over-expression at the site of injection. Some variability in XIAP expression is present between animals. Ponceau red staining of membrane confirms equal loading. (B) Anti-HA immunofluorescence (green) confirms XIAP over-expression at site of neuroprotection in a P23H animal. (C) Contralateral untreated control has no fluorescence and shows diminished ONL thickness. (D) GFP-injected retina of a S334ter animal is shown at boundary between photoreceptors covered by the virus and photoreceptors outside the range of the virus. ONL thickness is similar on either side of the virus boundary. Sections are counterstained with DAPI (nuclear stain). |
PMC1819558_pone-0000307-g001_9962.jpg | What object or scene is depicted here? | EPI data quality.A representative example of raw EPI (echoplanar imaging) data normalized to MNI space is shown in a coronar (MNI y = −7 mm) and axial (MNI z = −20 mm) section. The axial section corresponds approx. to the sections shown in [51]. The example represents the average across all EPI volumes acquired during the experimental session of one subject. The outline of the amygdala is shown (red line), enclosing the area with at least 50% probability of belonging to the amygdala (according to the probabilistic maps from [26]). The extent of the laterobasal (LB) group of the amygdala (LB, > = 80% probability) is shown in blue, the superficial group (SF) in green, and the centromedial group (CM) in magenta. In addition, the outline of the segmentation mask enclosing the area with sufficient signal for application of point spread function (PSF) based EPI distortion correction (see reference [39] for further details) is shown in yellow. In all subjects, the whole analyzed extent of the amygdala was within the segmentation mask and therefore distortion correction was possible in this region. Good EPI signal quality in the amygdala region was achieved in all subjects investigated. |
PMC1820591_F1_9964.jpg | What is the principal component of this image? | A silicone breast implant in this patient caused marked limitation of echocardiographic acoustic window and image acquisition in the parasternal long axis view obscuring left ventricular cavity and septum. |
PMC1820591_F2_9965.jpg | What stands out most in this visual? | A large shadow is seen across the right and left ventricle caused by the silicone breast implant that limited the echocardiographic window in the 4 chamber view. |
PMC1820591_F3_9966.jpg | What is the central feature of this picture? | Similar to figure 2, a large shadow is seen across the right and left ventricle secondary to the silicone breast implant in this patient limiting echocardiographic window in the 4 chamber view. |
PMC1820591_F5_9969.jpg | Describe the main subject of this image. | In order to improve the acoustic window, the parasternal long axis view was modified by the echocardiographer causing tilting of the image. |
PMC1820595_F1_9968.jpg | What is shown in this image? | Ultrasonography showing hypoechoic mass in the right breast. |
PMC1820595_F2_9967.jpg | What is the focal point of this photograph? | Computed tomography showing well-defined, round mass in the right breast (arrow). |
PMC1820595_F3_9970.jpg | What's the most prominent thing you notice in this picture? | Computed tomography showing tumour mass in the renal bed (arrow points to surgical clips). |
PMC1820597_F4_9978.jpg | What is being portrayed in this visual content? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F4_9976.jpg | What is the focal point of this photograph? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F4_9983.jpg | What is being portrayed in this visual content? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F4_9981.jpg | What object or scene is depicted here? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F4_9985.jpg | What is the principal component of this image? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F4_9980.jpg | What stands out most in this visual? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F4_9979.jpg | What is shown in this image? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F4_9977.jpg | What is the principal component of this image? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F4_9986.jpg | What key item or scene is captured in this photo? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F4_9982.jpg | What is the principal component of this image? | Effect of digitonin extraction on distribution of CLIC1 in Panc1 cells. Panc1 cells were fixed with PLP without (A, C) or with (B, D) prior extraction with digitonin. Cells were then stained with AP1089 (A, B) or with both AP1089 and 9F5 (C, D) and imaged using confocal microscopy. In A and B, images are shown from the very base of the cell (left panel) plus images at focal planes 2 (center) and 4 (right) μm higher. Collection of images in B required higher sensitivity than A. Parallel cultures stained with control antisera and imaged under identical conditions were blank (not shown). In panels C and D, cells were double stained with AP1089 with Alexafluor565-conjugated goat anti-rabbit IgG (red, left panel) and 9F5 with Alexafluor488-conjugated goat anti-mouse IgG (green, center panel) without (C) or following (D) digitonin extraction. A merged image for each pair is shown on the right. Scale bar in A and B represent 25 μm, scale bars in C and D represent 20 μm. |
PMC1820597_F8_9974.jpg | What is the core subject represented in this visual? | CLIC1 in T84 cells. Cells were grown to confluence on permeable supports, fixed, stained for CLIC1, and a stack of Z images at 0.2 μm intervals collected by confocal microscopy. A: image from the apex of the cells. 4μ: image taken 4 μm below image A. 8μ: image take 8 μm below image A. Z: vertical section generated from a 2 μm thick slice through the center of the stack of images. The scale bars represent 5 μm. |
PMC1820597_F8_9971.jpg | What can you see in this picture? | CLIC1 in T84 cells. Cells were grown to confluence on permeable supports, fixed, stained for CLIC1, and a stack of Z images at 0.2 μm intervals collected by confocal microscopy. A: image from the apex of the cells. 4μ: image taken 4 μm below image A. 8μ: image take 8 μm below image A. Z: vertical section generated from a 2 μm thick slice through the center of the stack of images. The scale bars represent 5 μm. |
PMC1820774_F1_9988.jpg | What is the dominant medical problem in this image? | Photograph of intraoperative measurement set up. Rostral is to the left, caudal to the right. Three electrodes can be seen inserted through the convex annulus of three adjacent discs. The pressure transducer is seen inserted into the middle disc. |
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