image stringlengths 20 66 | question stringclasses 16
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PMC1563467_F1_7067.jpg | What is the focal point of this photograph? | CT scan post contrast media injection reveals a huge low density compressive lesion in the posteromedial mediastinum. Notice the dislodgment of the thoracic vertebral body, the different dimensions of the spinal foramens and the different angles between the vertebral body and the traverse apophyses. |
PMC1563477_F7_7071.jpg | What is the main focus of this visual representation? | ERK1/2 phosphorylation in wild-type and mutant cultures is required for early wound response. (A–D) Immunolabeling of phospho-ERK1/2, (A) 10 minutes after wounding in Pax6+/+ cultures; (B) 30 minutes after wounding in Pax6+/+ cultures and (C) 10 minutes after wounding in Pax6+/- cultures. (D) Exposing Pax6+/- cells to EGF 90 s before wounding elicited a large phospho-ERK1/2 response after 10 minutes. In all cases, * indicates the wounded region. Scale bars = 100 μm. (E) Western blots of protein lysate of Pax6+/+ and Pax6+/- cultures. The same blot was probed sequentially with antibodies against Pax6, phospho-ERK1/2 (P-ERK1/2), and β-actin. Left hand lane: Pax6+/- cultures with 10 minute EGF exposure as described above. Middle lane: Pax6+/- cultures with no EGF exposure. Right hand lane: control Pax6+/+ cultures. Correcting for the volume of actin staining, phosphor-ERK1/2 staining in control heterozygous cultures was estimated at 80% of wild-type levels. Addition of EGF prior to wounding did not change Pax6 levels in Pax6+/- cultures, but increased phospho-ERK1/2 staining to levels comparable with or greater than Pax6+/+. All samples were taken from pools of at least six corneal epithelial cell cultures treated identically. (F) Rates of wound healing of wild-type and mutant cells with addition of 10 μM U0126 (an inhibitor of phosphor-ERK1/2 signaling), 0.1% DMSO, 15 minutes prior to wounding (U), or with addition of U0126 prior to wounding and replacement of drug in fresh medium every 2 hours (U*), or Pax6+/+ and Pax6+/- cultures with addition of 0.1% DMSO only. (*, p < 0.01 compared with wild-type control). |
PMC1563477_F7_7073.jpg | What is shown in this image? | ERK1/2 phosphorylation in wild-type and mutant cultures is required for early wound response. (A–D) Immunolabeling of phospho-ERK1/2, (A) 10 minutes after wounding in Pax6+/+ cultures; (B) 30 minutes after wounding in Pax6+/+ cultures and (C) 10 minutes after wounding in Pax6+/- cultures. (D) Exposing Pax6+/- cells to EGF 90 s before wounding elicited a large phospho-ERK1/2 response after 10 minutes. In all cases, * indicates the wounded region. Scale bars = 100 μm. (E) Western blots of protein lysate of Pax6+/+ and Pax6+/- cultures. The same blot was probed sequentially with antibodies against Pax6, phospho-ERK1/2 (P-ERK1/2), and β-actin. Left hand lane: Pax6+/- cultures with 10 minute EGF exposure as described above. Middle lane: Pax6+/- cultures with no EGF exposure. Right hand lane: control Pax6+/+ cultures. Correcting for the volume of actin staining, phosphor-ERK1/2 staining in control heterozygous cultures was estimated at 80% of wild-type levels. Addition of EGF prior to wounding did not change Pax6 levels in Pax6+/- cultures, but increased phospho-ERK1/2 staining to levels comparable with or greater than Pax6+/+. All samples were taken from pools of at least six corneal epithelial cell cultures treated identically. (F) Rates of wound healing of wild-type and mutant cells with addition of 10 μM U0126 (an inhibitor of phosphor-ERK1/2 signaling), 0.1% DMSO, 15 minutes prior to wounding (U), or with addition of U0126 prior to wounding and replacement of drug in fresh medium every 2 hours (U*), or Pax6+/+ and Pax6+/- cultures with addition of 0.1% DMSO only. (*, p < 0.01 compared with wild-type control). |
PMC1563477_F7_7070.jpg | What is the focal point of this photograph? | ERK1/2 phosphorylation in wild-type and mutant cultures is required for early wound response. (A–D) Immunolabeling of phospho-ERK1/2, (A) 10 minutes after wounding in Pax6+/+ cultures; (B) 30 minutes after wounding in Pax6+/+ cultures and (C) 10 minutes after wounding in Pax6+/- cultures. (D) Exposing Pax6+/- cells to EGF 90 s before wounding elicited a large phospho-ERK1/2 response after 10 minutes. In all cases, * indicates the wounded region. Scale bars = 100 μm. (E) Western blots of protein lysate of Pax6+/+ and Pax6+/- cultures. The same blot was probed sequentially with antibodies against Pax6, phospho-ERK1/2 (P-ERK1/2), and β-actin. Left hand lane: Pax6+/- cultures with 10 minute EGF exposure as described above. Middle lane: Pax6+/- cultures with no EGF exposure. Right hand lane: control Pax6+/+ cultures. Correcting for the volume of actin staining, phosphor-ERK1/2 staining in control heterozygous cultures was estimated at 80% of wild-type levels. Addition of EGF prior to wounding did not change Pax6 levels in Pax6+/- cultures, but increased phospho-ERK1/2 staining to levels comparable with or greater than Pax6+/+. All samples were taken from pools of at least six corneal epithelial cell cultures treated identically. (F) Rates of wound healing of wild-type and mutant cells with addition of 10 μM U0126 (an inhibitor of phosphor-ERK1/2 signaling), 0.1% DMSO, 15 minutes prior to wounding (U), or with addition of U0126 prior to wounding and replacement of drug in fresh medium every 2 hours (U*), or Pax6+/+ and Pax6+/- cultures with addition of 0.1% DMSO only. (*, p < 0.01 compared with wild-type control). |
PMC1563485_pbio-0040313-g003_7079.jpg | What can you see in this picture? | BMP Signaling Can Also Repress Expression of vnd
(A) Scheme for generating ventro-lateralized embryos with a uniform level of Dorsal adjusted to that present in the ventral neuroectoderm (e.g., vnd expressing cells). These embryos were collected from gd
7
sog
U2/gd
7
; Tl
3/+ mothers (B and C) or sog
Y506 brkm68/FM7; Tl
r4/Tl
r4 mothers (D and E).(B and C) ush (yellow) and vnd (cyan) expression in a sog−; st2-dpp ventro-lateralized embryo. Note that while ush expression is induced in response to dpp expression in this embryo (bracket), the pattern of vnd expression remains unaffected.(D and E) ush (yellow) and vnd (cyan) expression in a brk− sog−; st2-dpp ventro-lateralized embryo.(D) The level and width of ush expression (bracket) is greater than in sog− single mutants (compare with [B]).(E) Note the broad domain of reduced vnd expression (bracket), which extends anterior to the st2-dpp expression domain.(F−H) Expression of msh (red), ind (green), and vnd (blue) in a st2-brk embryo that has a normal Dorsal gradient.(F) A mid-blastoderm stage embryo showing shifts in the dorsal and ventral borders of ind expression. The inset shows higher magnification of the ind/vnd border in the region of st2-brk expression, which is consistently shifted dorsally by 1−2 cells within the stripe of brk expression. This shift is most clearly revealed by a consistent flattening of what is normally a continuous arc in the ind/vnd border at the position of st2-brk expression. The inset also shows that vnd expression extends up to the ind border and that there is no gap between these gene expression domains. We quantitated the shift in the ind/vnd border in nine st2-brk and nine wild-type embryos by counting the number of ind negative cells above a line spanning the ventral border of ind expression in the head and abdomen comprising a zone four cells wide centered within the st2 domain (or its approximate corresponding position in wild-type embryos). ind is better than vnd for performing this measurement since the ventral ind border is sharper (i.e., more all-or-none) than the dorsal vnd border. This analysis reveals that in st2-brk embryos there is an average of 5.4 ± 2.65 ind negative (vnd positive) cells above the line (which corresponds to an average shift of the ind/vnd border of 5.4/4 = 1.35 cells dorsally). In contrast, for control wild-type embryos we counted an average of 0.44 ± 0.88 cells above the line corresponding to an average of 0.11 cells. This represents a 10-fold difference between wild-type and st2-brk embryos, which is highly significant in a students' t-test (p < 0.0003).(G) Lateral view of a slightly older embryo than that shown in (F) showing a significant dorsal shift of the msh/ind border and a smaller shift of the ind/vnd border. The carets in (F and G) indicate the approximate trajectories of the ind/vnd and msh/ind borders in wild-type embryos.(H) Dorsal view of the same embryo shown in (G) revealing that msh expression expands to the dorsal midline. |
PMC1563485_pbio-0040313-g003_7074.jpg | What can you see in this picture? | BMP Signaling Can Also Repress Expression of vnd
(A) Scheme for generating ventro-lateralized embryos with a uniform level of Dorsal adjusted to that present in the ventral neuroectoderm (e.g., vnd expressing cells). These embryos were collected from gd
7
sog
U2/gd
7
; Tl
3/+ mothers (B and C) or sog
Y506 brkm68/FM7; Tl
r4/Tl
r4 mothers (D and E).(B and C) ush (yellow) and vnd (cyan) expression in a sog−; st2-dpp ventro-lateralized embryo. Note that while ush expression is induced in response to dpp expression in this embryo (bracket), the pattern of vnd expression remains unaffected.(D and E) ush (yellow) and vnd (cyan) expression in a brk− sog−; st2-dpp ventro-lateralized embryo.(D) The level and width of ush expression (bracket) is greater than in sog− single mutants (compare with [B]).(E) Note the broad domain of reduced vnd expression (bracket), which extends anterior to the st2-dpp expression domain.(F−H) Expression of msh (red), ind (green), and vnd (blue) in a st2-brk embryo that has a normal Dorsal gradient.(F) A mid-blastoderm stage embryo showing shifts in the dorsal and ventral borders of ind expression. The inset shows higher magnification of the ind/vnd border in the region of st2-brk expression, which is consistently shifted dorsally by 1−2 cells within the stripe of brk expression. This shift is most clearly revealed by a consistent flattening of what is normally a continuous arc in the ind/vnd border at the position of st2-brk expression. The inset also shows that vnd expression extends up to the ind border and that there is no gap between these gene expression domains. We quantitated the shift in the ind/vnd border in nine st2-brk and nine wild-type embryos by counting the number of ind negative cells above a line spanning the ventral border of ind expression in the head and abdomen comprising a zone four cells wide centered within the st2 domain (or its approximate corresponding position in wild-type embryos). ind is better than vnd for performing this measurement since the ventral ind border is sharper (i.e., more all-or-none) than the dorsal vnd border. This analysis reveals that in st2-brk embryos there is an average of 5.4 ± 2.65 ind negative (vnd positive) cells above the line (which corresponds to an average shift of the ind/vnd border of 5.4/4 = 1.35 cells dorsally). In contrast, for control wild-type embryos we counted an average of 0.44 ± 0.88 cells above the line corresponding to an average of 0.11 cells. This represents a 10-fold difference between wild-type and st2-brk embryos, which is highly significant in a students' t-test (p < 0.0003).(G) Lateral view of a slightly older embryo than that shown in (F) showing a significant dorsal shift of the msh/ind border and a smaller shift of the ind/vnd border. The carets in (F and G) indicate the approximate trajectories of the ind/vnd and msh/ind borders in wild-type embryos.(H) Dorsal view of the same embryo shown in (G) revealing that msh expression expands to the dorsal midline. |
PMC1563485_pbio-0040313-g003_7078.jpg | What is the main focus of this visual representation? | BMP Signaling Can Also Repress Expression of vnd
(A) Scheme for generating ventro-lateralized embryos with a uniform level of Dorsal adjusted to that present in the ventral neuroectoderm (e.g., vnd expressing cells). These embryos were collected from gd
7
sog
U2/gd
7
; Tl
3/+ mothers (B and C) or sog
Y506 brkm68/FM7; Tl
r4/Tl
r4 mothers (D and E).(B and C) ush (yellow) and vnd (cyan) expression in a sog−; st2-dpp ventro-lateralized embryo. Note that while ush expression is induced in response to dpp expression in this embryo (bracket), the pattern of vnd expression remains unaffected.(D and E) ush (yellow) and vnd (cyan) expression in a brk− sog−; st2-dpp ventro-lateralized embryo.(D) The level and width of ush expression (bracket) is greater than in sog− single mutants (compare with [B]).(E) Note the broad domain of reduced vnd expression (bracket), which extends anterior to the st2-dpp expression domain.(F−H) Expression of msh (red), ind (green), and vnd (blue) in a st2-brk embryo that has a normal Dorsal gradient.(F) A mid-blastoderm stage embryo showing shifts in the dorsal and ventral borders of ind expression. The inset shows higher magnification of the ind/vnd border in the region of st2-brk expression, which is consistently shifted dorsally by 1−2 cells within the stripe of brk expression. This shift is most clearly revealed by a consistent flattening of what is normally a continuous arc in the ind/vnd border at the position of st2-brk expression. The inset also shows that vnd expression extends up to the ind border and that there is no gap between these gene expression domains. We quantitated the shift in the ind/vnd border in nine st2-brk and nine wild-type embryos by counting the number of ind negative cells above a line spanning the ventral border of ind expression in the head and abdomen comprising a zone four cells wide centered within the st2 domain (or its approximate corresponding position in wild-type embryos). ind is better than vnd for performing this measurement since the ventral ind border is sharper (i.e., more all-or-none) than the dorsal vnd border. This analysis reveals that in st2-brk embryos there is an average of 5.4 ± 2.65 ind negative (vnd positive) cells above the line (which corresponds to an average shift of the ind/vnd border of 5.4/4 = 1.35 cells dorsally). In contrast, for control wild-type embryos we counted an average of 0.44 ± 0.88 cells above the line corresponding to an average of 0.11 cells. This represents a 10-fold difference between wild-type and st2-brk embryos, which is highly significant in a students' t-test (p < 0.0003).(G) Lateral view of a slightly older embryo than that shown in (F) showing a significant dorsal shift of the msh/ind border and a smaller shift of the ind/vnd border. The carets in (F and G) indicate the approximate trajectories of the ind/vnd and msh/ind borders in wild-type embryos.(H) Dorsal view of the same embryo shown in (G) revealing that msh expression expands to the dorsal midline. |
PMC1563485_pbio-0040313-g003_7076.jpg | What is the dominant medical problem in this image? | BMP Signaling Can Also Repress Expression of vnd
(A) Scheme for generating ventro-lateralized embryos with a uniform level of Dorsal adjusted to that present in the ventral neuroectoderm (e.g., vnd expressing cells). These embryos were collected from gd
7
sog
U2/gd
7
; Tl
3/+ mothers (B and C) or sog
Y506 brkm68/FM7; Tl
r4/Tl
r4 mothers (D and E).(B and C) ush (yellow) and vnd (cyan) expression in a sog−; st2-dpp ventro-lateralized embryo. Note that while ush expression is induced in response to dpp expression in this embryo (bracket), the pattern of vnd expression remains unaffected.(D and E) ush (yellow) and vnd (cyan) expression in a brk− sog−; st2-dpp ventro-lateralized embryo.(D) The level and width of ush expression (bracket) is greater than in sog− single mutants (compare with [B]).(E) Note the broad domain of reduced vnd expression (bracket), which extends anterior to the st2-dpp expression domain.(F−H) Expression of msh (red), ind (green), and vnd (blue) in a st2-brk embryo that has a normal Dorsal gradient.(F) A mid-blastoderm stage embryo showing shifts in the dorsal and ventral borders of ind expression. The inset shows higher magnification of the ind/vnd border in the region of st2-brk expression, which is consistently shifted dorsally by 1−2 cells within the stripe of brk expression. This shift is most clearly revealed by a consistent flattening of what is normally a continuous arc in the ind/vnd border at the position of st2-brk expression. The inset also shows that vnd expression extends up to the ind border and that there is no gap between these gene expression domains. We quantitated the shift in the ind/vnd border in nine st2-brk and nine wild-type embryos by counting the number of ind negative cells above a line spanning the ventral border of ind expression in the head and abdomen comprising a zone four cells wide centered within the st2 domain (or its approximate corresponding position in wild-type embryos). ind is better than vnd for performing this measurement since the ventral ind border is sharper (i.e., more all-or-none) than the dorsal vnd border. This analysis reveals that in st2-brk embryos there is an average of 5.4 ± 2.65 ind negative (vnd positive) cells above the line (which corresponds to an average shift of the ind/vnd border of 5.4/4 = 1.35 cells dorsally). In contrast, for control wild-type embryos we counted an average of 0.44 ± 0.88 cells above the line corresponding to an average of 0.11 cells. This represents a 10-fold difference between wild-type and st2-brk embryos, which is highly significant in a students' t-test (p < 0.0003).(G) Lateral view of a slightly older embryo than that shown in (F) showing a significant dorsal shift of the msh/ind border and a smaller shift of the ind/vnd border. The carets in (F and G) indicate the approximate trajectories of the ind/vnd and msh/ind borders in wild-type embryos.(H) Dorsal view of the same embryo shown in (G) revealing that msh expression expands to the dorsal midline. |
PMC1563485_pbio-0040313-g003_7081.jpg | What stands out most in this visual? | BMP Signaling Can Also Repress Expression of vnd
(A) Scheme for generating ventro-lateralized embryos with a uniform level of Dorsal adjusted to that present in the ventral neuroectoderm (e.g., vnd expressing cells). These embryos were collected from gd
7
sog
U2/gd
7
; Tl
3/+ mothers (B and C) or sog
Y506 brkm68/FM7; Tl
r4/Tl
r4 mothers (D and E).(B and C) ush (yellow) and vnd (cyan) expression in a sog−; st2-dpp ventro-lateralized embryo. Note that while ush expression is induced in response to dpp expression in this embryo (bracket), the pattern of vnd expression remains unaffected.(D and E) ush (yellow) and vnd (cyan) expression in a brk− sog−; st2-dpp ventro-lateralized embryo.(D) The level and width of ush expression (bracket) is greater than in sog− single mutants (compare with [B]).(E) Note the broad domain of reduced vnd expression (bracket), which extends anterior to the st2-dpp expression domain.(F−H) Expression of msh (red), ind (green), and vnd (blue) in a st2-brk embryo that has a normal Dorsal gradient.(F) A mid-blastoderm stage embryo showing shifts in the dorsal and ventral borders of ind expression. The inset shows higher magnification of the ind/vnd border in the region of st2-brk expression, which is consistently shifted dorsally by 1−2 cells within the stripe of brk expression. This shift is most clearly revealed by a consistent flattening of what is normally a continuous arc in the ind/vnd border at the position of st2-brk expression. The inset also shows that vnd expression extends up to the ind border and that there is no gap between these gene expression domains. We quantitated the shift in the ind/vnd border in nine st2-brk and nine wild-type embryos by counting the number of ind negative cells above a line spanning the ventral border of ind expression in the head and abdomen comprising a zone four cells wide centered within the st2 domain (or its approximate corresponding position in wild-type embryos). ind is better than vnd for performing this measurement since the ventral ind border is sharper (i.e., more all-or-none) than the dorsal vnd border. This analysis reveals that in st2-brk embryos there is an average of 5.4 ± 2.65 ind negative (vnd positive) cells above the line (which corresponds to an average shift of the ind/vnd border of 5.4/4 = 1.35 cells dorsally). In contrast, for control wild-type embryos we counted an average of 0.44 ± 0.88 cells above the line corresponding to an average of 0.11 cells. This represents a 10-fold difference between wild-type and st2-brk embryos, which is highly significant in a students' t-test (p < 0.0003).(G) Lateral view of a slightly older embryo than that shown in (F) showing a significant dorsal shift of the msh/ind border and a smaller shift of the ind/vnd border. The carets in (F and G) indicate the approximate trajectories of the ind/vnd and msh/ind borders in wild-type embryos.(H) Dorsal view of the same embryo shown in (G) revealing that msh expression expands to the dorsal midline. |
PMC1563485_pbio-0040313-g003_7077.jpg | What is the central feature of this picture? | BMP Signaling Can Also Repress Expression of vnd
(A) Scheme for generating ventro-lateralized embryos with a uniform level of Dorsal adjusted to that present in the ventral neuroectoderm (e.g., vnd expressing cells). These embryos were collected from gd
7
sog
U2/gd
7
; Tl
3/+ mothers (B and C) or sog
Y506 brkm68/FM7; Tl
r4/Tl
r4 mothers (D and E).(B and C) ush (yellow) and vnd (cyan) expression in a sog−; st2-dpp ventro-lateralized embryo. Note that while ush expression is induced in response to dpp expression in this embryo (bracket), the pattern of vnd expression remains unaffected.(D and E) ush (yellow) and vnd (cyan) expression in a brk− sog−; st2-dpp ventro-lateralized embryo.(D) The level and width of ush expression (bracket) is greater than in sog− single mutants (compare with [B]).(E) Note the broad domain of reduced vnd expression (bracket), which extends anterior to the st2-dpp expression domain.(F−H) Expression of msh (red), ind (green), and vnd (blue) in a st2-brk embryo that has a normal Dorsal gradient.(F) A mid-blastoderm stage embryo showing shifts in the dorsal and ventral borders of ind expression. The inset shows higher magnification of the ind/vnd border in the region of st2-brk expression, which is consistently shifted dorsally by 1−2 cells within the stripe of brk expression. This shift is most clearly revealed by a consistent flattening of what is normally a continuous arc in the ind/vnd border at the position of st2-brk expression. The inset also shows that vnd expression extends up to the ind border and that there is no gap between these gene expression domains. We quantitated the shift in the ind/vnd border in nine st2-brk and nine wild-type embryos by counting the number of ind negative cells above a line spanning the ventral border of ind expression in the head and abdomen comprising a zone four cells wide centered within the st2 domain (or its approximate corresponding position in wild-type embryos). ind is better than vnd for performing this measurement since the ventral ind border is sharper (i.e., more all-or-none) than the dorsal vnd border. This analysis reveals that in st2-brk embryos there is an average of 5.4 ± 2.65 ind negative (vnd positive) cells above the line (which corresponds to an average shift of the ind/vnd border of 5.4/4 = 1.35 cells dorsally). In contrast, for control wild-type embryos we counted an average of 0.44 ± 0.88 cells above the line corresponding to an average of 0.11 cells. This represents a 10-fold difference between wild-type and st2-brk embryos, which is highly significant in a students' t-test (p < 0.0003).(G) Lateral view of a slightly older embryo than that shown in (F) showing a significant dorsal shift of the msh/ind border and a smaller shift of the ind/vnd border. The carets in (F and G) indicate the approximate trajectories of the ind/vnd and msh/ind borders in wild-type embryos.(H) Dorsal view of the same embryo shown in (G) revealing that msh expression expands to the dorsal midline. |
PMC1563485_pbio-0040313-g003_7075.jpg | What key item or scene is captured in this photo? | BMP Signaling Can Also Repress Expression of vnd
(A) Scheme for generating ventro-lateralized embryos with a uniform level of Dorsal adjusted to that present in the ventral neuroectoderm (e.g., vnd expressing cells). These embryos were collected from gd
7
sog
U2/gd
7
; Tl
3/+ mothers (B and C) or sog
Y506 brkm68/FM7; Tl
r4/Tl
r4 mothers (D and E).(B and C) ush (yellow) and vnd (cyan) expression in a sog−; st2-dpp ventro-lateralized embryo. Note that while ush expression is induced in response to dpp expression in this embryo (bracket), the pattern of vnd expression remains unaffected.(D and E) ush (yellow) and vnd (cyan) expression in a brk− sog−; st2-dpp ventro-lateralized embryo.(D) The level and width of ush expression (bracket) is greater than in sog− single mutants (compare with [B]).(E) Note the broad domain of reduced vnd expression (bracket), which extends anterior to the st2-dpp expression domain.(F−H) Expression of msh (red), ind (green), and vnd (blue) in a st2-brk embryo that has a normal Dorsal gradient.(F) A mid-blastoderm stage embryo showing shifts in the dorsal and ventral borders of ind expression. The inset shows higher magnification of the ind/vnd border in the region of st2-brk expression, which is consistently shifted dorsally by 1−2 cells within the stripe of brk expression. This shift is most clearly revealed by a consistent flattening of what is normally a continuous arc in the ind/vnd border at the position of st2-brk expression. The inset also shows that vnd expression extends up to the ind border and that there is no gap between these gene expression domains. We quantitated the shift in the ind/vnd border in nine st2-brk and nine wild-type embryos by counting the number of ind negative cells above a line spanning the ventral border of ind expression in the head and abdomen comprising a zone four cells wide centered within the st2 domain (or its approximate corresponding position in wild-type embryos). ind is better than vnd for performing this measurement since the ventral ind border is sharper (i.e., more all-or-none) than the dorsal vnd border. This analysis reveals that in st2-brk embryos there is an average of 5.4 ± 2.65 ind negative (vnd positive) cells above the line (which corresponds to an average shift of the ind/vnd border of 5.4/4 = 1.35 cells dorsally). In contrast, for control wild-type embryos we counted an average of 0.44 ± 0.88 cells above the line corresponding to an average of 0.11 cells. This represents a 10-fold difference between wild-type and st2-brk embryos, which is highly significant in a students' t-test (p < 0.0003).(G) Lateral view of a slightly older embryo than that shown in (F) showing a significant dorsal shift of the msh/ind border and a smaller shift of the ind/vnd border. The carets in (F and G) indicate the approximate trajectories of the ind/vnd and msh/ind borders in wild-type embryos.(H) Dorsal view of the same embryo shown in (G) revealing that msh expression expands to the dorsal midline. |
PMC1564002_F3_7091.jpg | Can you identify the primary element in this image? | Injury-induced proliferating retinal progenitors express rx1, vsx2, and pax6a. A) – D) Histology of the heat-lesioned retina at 1 and 3 dpl; the boxed area in A) is magnified in B). Cell loss is mainly confined to the retinal pigmented epithelium (RPE) and photoreceptors in the outer nuclear layer, ONL. The CMZ (arrow in A) is at the junction between the neural retina and the ciliary epithelium (CE), which is continuous anteriorly with the iris epithelium (IE). Scale bar (A) = 150 μm. C) At 3 dpl double cones immunoreactive with zpr1 (red) are missing from the lesioned area and elongated nuclei appear in the inner nuclear layer (white arrows). Counterstained with DAPI (blue). D) By 3 dpl, radial fibers of Müller glia in the inner nuclear layer, INL, are visible in the region of the lesion (black arrows), indicative of reactive gliosis. Scale bar = 50 μm. D) Proliferating cells in the inner and outer nuclear layers of the retina in the lesioned area (asterisks) at 5 dpl incorporated BrdU (green) injected at 4 dpl. E) Injury-induced proliferating cells are also immunoreactive for proliferating cell nuclear antigen, PCNA (green) and are associated with radial fibers of Müller glia (magenta, anti-human GFAP). Note: the commercial polyclonal GFAP antibody used here is not selective for GFAP in zebrafish but labels other intermediate filaments (data not shown). In contrast, the monoclonal zrf1, which was generated against zebrafish proteins, selectively labels zebrafish GFAP [97]. Scale bar = 50 μm. F) – L) A 4 h or 24 h pulse of BrdU at 4 or 5 dpl labels clusters of nuclei (magenta) that extend between the INL and ONL and express rx1 (F) and vsx2 (J) as visualized by in situ hybridization (red). DAPI (blue); zrf1 (green, anti-zebrafish GFAP). Scale bar = 25 μm. Higher magnification views of rx1 (G,H, I) and vsx2 (K, L) in BrdU+ progenitors enclosed in a basket of zrf1+ Müller glial fibers. |
PMC1564002_F3_7090.jpg | What key item or scene is captured in this photo? | Injury-induced proliferating retinal progenitors express rx1, vsx2, and pax6a. A) – D) Histology of the heat-lesioned retina at 1 and 3 dpl; the boxed area in A) is magnified in B). Cell loss is mainly confined to the retinal pigmented epithelium (RPE) and photoreceptors in the outer nuclear layer, ONL. The CMZ (arrow in A) is at the junction between the neural retina and the ciliary epithelium (CE), which is continuous anteriorly with the iris epithelium (IE). Scale bar (A) = 150 μm. C) At 3 dpl double cones immunoreactive with zpr1 (red) are missing from the lesioned area and elongated nuclei appear in the inner nuclear layer (white arrows). Counterstained with DAPI (blue). D) By 3 dpl, radial fibers of Müller glia in the inner nuclear layer, INL, are visible in the region of the lesion (black arrows), indicative of reactive gliosis. Scale bar = 50 μm. D) Proliferating cells in the inner and outer nuclear layers of the retina in the lesioned area (asterisks) at 5 dpl incorporated BrdU (green) injected at 4 dpl. E) Injury-induced proliferating cells are also immunoreactive for proliferating cell nuclear antigen, PCNA (green) and are associated with radial fibers of Müller glia (magenta, anti-human GFAP). Note: the commercial polyclonal GFAP antibody used here is not selective for GFAP in zebrafish but labels other intermediate filaments (data not shown). In contrast, the monoclonal zrf1, which was generated against zebrafish proteins, selectively labels zebrafish GFAP [97]. Scale bar = 50 μm. F) – L) A 4 h or 24 h pulse of BrdU at 4 or 5 dpl labels clusters of nuclei (magenta) that extend between the INL and ONL and express rx1 (F) and vsx2 (J) as visualized by in situ hybridization (red). DAPI (blue); zrf1 (green, anti-zebrafish GFAP). Scale bar = 25 μm. Higher magnification views of rx1 (G,H, I) and vsx2 (K, L) in BrdU+ progenitors enclosed in a basket of zrf1+ Müller glial fibers. |
PMC1564002_F3_7098.jpg | What is the main focus of this visual representation? | Injury-induced proliferating retinal progenitors express rx1, vsx2, and pax6a. A) – D) Histology of the heat-lesioned retina at 1 and 3 dpl; the boxed area in A) is magnified in B). Cell loss is mainly confined to the retinal pigmented epithelium (RPE) and photoreceptors in the outer nuclear layer, ONL. The CMZ (arrow in A) is at the junction between the neural retina and the ciliary epithelium (CE), which is continuous anteriorly with the iris epithelium (IE). Scale bar (A) = 150 μm. C) At 3 dpl double cones immunoreactive with zpr1 (red) are missing from the lesioned area and elongated nuclei appear in the inner nuclear layer (white arrows). Counterstained with DAPI (blue). D) By 3 dpl, radial fibers of Müller glia in the inner nuclear layer, INL, are visible in the region of the lesion (black arrows), indicative of reactive gliosis. Scale bar = 50 μm. D) Proliferating cells in the inner and outer nuclear layers of the retina in the lesioned area (asterisks) at 5 dpl incorporated BrdU (green) injected at 4 dpl. E) Injury-induced proliferating cells are also immunoreactive for proliferating cell nuclear antigen, PCNA (green) and are associated with radial fibers of Müller glia (magenta, anti-human GFAP). Note: the commercial polyclonal GFAP antibody used here is not selective for GFAP in zebrafish but labels other intermediate filaments (data not shown). In contrast, the monoclonal zrf1, which was generated against zebrafish proteins, selectively labels zebrafish GFAP [97]. Scale bar = 50 μm. F) – L) A 4 h or 24 h pulse of BrdU at 4 or 5 dpl labels clusters of nuclei (magenta) that extend between the INL and ONL and express rx1 (F) and vsx2 (J) as visualized by in situ hybridization (red). DAPI (blue); zrf1 (green, anti-zebrafish GFAP). Scale bar = 25 μm. Higher magnification views of rx1 (G,H, I) and vsx2 (K, L) in BrdU+ progenitors enclosed in a basket of zrf1+ Müller glial fibers. |
PMC1564002_F3_7093.jpg | What key item or scene is captured in this photo? | Injury-induced proliferating retinal progenitors express rx1, vsx2, and pax6a. A) – D) Histology of the heat-lesioned retina at 1 and 3 dpl; the boxed area in A) is magnified in B). Cell loss is mainly confined to the retinal pigmented epithelium (RPE) and photoreceptors in the outer nuclear layer, ONL. The CMZ (arrow in A) is at the junction between the neural retina and the ciliary epithelium (CE), which is continuous anteriorly with the iris epithelium (IE). Scale bar (A) = 150 μm. C) At 3 dpl double cones immunoreactive with zpr1 (red) are missing from the lesioned area and elongated nuclei appear in the inner nuclear layer (white arrows). Counterstained with DAPI (blue). D) By 3 dpl, radial fibers of Müller glia in the inner nuclear layer, INL, are visible in the region of the lesion (black arrows), indicative of reactive gliosis. Scale bar = 50 μm. D) Proliferating cells in the inner and outer nuclear layers of the retina in the lesioned area (asterisks) at 5 dpl incorporated BrdU (green) injected at 4 dpl. E) Injury-induced proliferating cells are also immunoreactive for proliferating cell nuclear antigen, PCNA (green) and are associated with radial fibers of Müller glia (magenta, anti-human GFAP). Note: the commercial polyclonal GFAP antibody used here is not selective for GFAP in zebrafish but labels other intermediate filaments (data not shown). In contrast, the monoclonal zrf1, which was generated against zebrafish proteins, selectively labels zebrafish GFAP [97]. Scale bar = 50 μm. F) – L) A 4 h or 24 h pulse of BrdU at 4 or 5 dpl labels clusters of nuclei (magenta) that extend between the INL and ONL and express rx1 (F) and vsx2 (J) as visualized by in situ hybridization (red). DAPI (blue); zrf1 (green, anti-zebrafish GFAP). Scale bar = 25 μm. Higher magnification views of rx1 (G,H, I) and vsx2 (K, L) in BrdU+ progenitors enclosed in a basket of zrf1+ Müller glial fibers. |
PMC1564002_F3_7097.jpg | What object or scene is depicted here? | Injury-induced proliferating retinal progenitors express rx1, vsx2, and pax6a. A) – D) Histology of the heat-lesioned retina at 1 and 3 dpl; the boxed area in A) is magnified in B). Cell loss is mainly confined to the retinal pigmented epithelium (RPE) and photoreceptors in the outer nuclear layer, ONL. The CMZ (arrow in A) is at the junction between the neural retina and the ciliary epithelium (CE), which is continuous anteriorly with the iris epithelium (IE). Scale bar (A) = 150 μm. C) At 3 dpl double cones immunoreactive with zpr1 (red) are missing from the lesioned area and elongated nuclei appear in the inner nuclear layer (white arrows). Counterstained with DAPI (blue). D) By 3 dpl, radial fibers of Müller glia in the inner nuclear layer, INL, are visible in the region of the lesion (black arrows), indicative of reactive gliosis. Scale bar = 50 μm. D) Proliferating cells in the inner and outer nuclear layers of the retina in the lesioned area (asterisks) at 5 dpl incorporated BrdU (green) injected at 4 dpl. E) Injury-induced proliferating cells are also immunoreactive for proliferating cell nuclear antigen, PCNA (green) and are associated with radial fibers of Müller glia (magenta, anti-human GFAP). Note: the commercial polyclonal GFAP antibody used here is not selective for GFAP in zebrafish but labels other intermediate filaments (data not shown). In contrast, the monoclonal zrf1, which was generated against zebrafish proteins, selectively labels zebrafish GFAP [97]. Scale bar = 50 μm. F) – L) A 4 h or 24 h pulse of BrdU at 4 or 5 dpl labels clusters of nuclei (magenta) that extend between the INL and ONL and express rx1 (F) and vsx2 (J) as visualized by in situ hybridization (red). DAPI (blue); zrf1 (green, anti-zebrafish GFAP). Scale bar = 25 μm. Higher magnification views of rx1 (G,H, I) and vsx2 (K, L) in BrdU+ progenitors enclosed in a basket of zrf1+ Müller glial fibers. |
PMC1564002_F3_7095.jpg | What is the core subject represented in this visual? | Injury-induced proliferating retinal progenitors express rx1, vsx2, and pax6a. A) – D) Histology of the heat-lesioned retina at 1 and 3 dpl; the boxed area in A) is magnified in B). Cell loss is mainly confined to the retinal pigmented epithelium (RPE) and photoreceptors in the outer nuclear layer, ONL. The CMZ (arrow in A) is at the junction between the neural retina and the ciliary epithelium (CE), which is continuous anteriorly with the iris epithelium (IE). Scale bar (A) = 150 μm. C) At 3 dpl double cones immunoreactive with zpr1 (red) are missing from the lesioned area and elongated nuclei appear in the inner nuclear layer (white arrows). Counterstained with DAPI (blue). D) By 3 dpl, radial fibers of Müller glia in the inner nuclear layer, INL, are visible in the region of the lesion (black arrows), indicative of reactive gliosis. Scale bar = 50 μm. D) Proliferating cells in the inner and outer nuclear layers of the retina in the lesioned area (asterisks) at 5 dpl incorporated BrdU (green) injected at 4 dpl. E) Injury-induced proliferating cells are also immunoreactive for proliferating cell nuclear antigen, PCNA (green) and are associated with radial fibers of Müller glia (magenta, anti-human GFAP). Note: the commercial polyclonal GFAP antibody used here is not selective for GFAP in zebrafish but labels other intermediate filaments (data not shown). In contrast, the monoclonal zrf1, which was generated against zebrafish proteins, selectively labels zebrafish GFAP [97]. Scale bar = 50 μm. F) – L) A 4 h or 24 h pulse of BrdU at 4 or 5 dpl labels clusters of nuclei (magenta) that extend between the INL and ONL and express rx1 (F) and vsx2 (J) as visualized by in situ hybridization (red). DAPI (blue); zrf1 (green, anti-zebrafish GFAP). Scale bar = 25 μm. Higher magnification views of rx1 (G,H, I) and vsx2 (K, L) in BrdU+ progenitors enclosed in a basket of zrf1+ Müller glial fibers. |
PMC1564002_F3_7096.jpg | What is the main focus of this visual representation? | Injury-induced proliferating retinal progenitors express rx1, vsx2, and pax6a. A) – D) Histology of the heat-lesioned retina at 1 and 3 dpl; the boxed area in A) is magnified in B). Cell loss is mainly confined to the retinal pigmented epithelium (RPE) and photoreceptors in the outer nuclear layer, ONL. The CMZ (arrow in A) is at the junction between the neural retina and the ciliary epithelium (CE), which is continuous anteriorly with the iris epithelium (IE). Scale bar (A) = 150 μm. C) At 3 dpl double cones immunoreactive with zpr1 (red) are missing from the lesioned area and elongated nuclei appear in the inner nuclear layer (white arrows). Counterstained with DAPI (blue). D) By 3 dpl, radial fibers of Müller glia in the inner nuclear layer, INL, are visible in the region of the lesion (black arrows), indicative of reactive gliosis. Scale bar = 50 μm. D) Proliferating cells in the inner and outer nuclear layers of the retina in the lesioned area (asterisks) at 5 dpl incorporated BrdU (green) injected at 4 dpl. E) Injury-induced proliferating cells are also immunoreactive for proliferating cell nuclear antigen, PCNA (green) and are associated with radial fibers of Müller glia (magenta, anti-human GFAP). Note: the commercial polyclonal GFAP antibody used here is not selective for GFAP in zebrafish but labels other intermediate filaments (data not shown). In contrast, the monoclonal zrf1, which was generated against zebrafish proteins, selectively labels zebrafish GFAP [97]. Scale bar = 50 μm. F) – L) A 4 h or 24 h pulse of BrdU at 4 or 5 dpl labels clusters of nuclei (magenta) that extend between the INL and ONL and express rx1 (F) and vsx2 (J) as visualized by in situ hybridization (red). DAPI (blue); zrf1 (green, anti-zebrafish GFAP). Scale bar = 25 μm. Higher magnification views of rx1 (G,H, I) and vsx2 (K, L) in BrdU+ progenitors enclosed in a basket of zrf1+ Müller glial fibers. |
PMC1564002_F3_7089.jpg | Describe the main subject of this image. | Injury-induced proliferating retinal progenitors express rx1, vsx2, and pax6a. A) – D) Histology of the heat-lesioned retina at 1 and 3 dpl; the boxed area in A) is magnified in B). Cell loss is mainly confined to the retinal pigmented epithelium (RPE) and photoreceptors in the outer nuclear layer, ONL. The CMZ (arrow in A) is at the junction between the neural retina and the ciliary epithelium (CE), which is continuous anteriorly with the iris epithelium (IE). Scale bar (A) = 150 μm. C) At 3 dpl double cones immunoreactive with zpr1 (red) are missing from the lesioned area and elongated nuclei appear in the inner nuclear layer (white arrows). Counterstained with DAPI (blue). D) By 3 dpl, radial fibers of Müller glia in the inner nuclear layer, INL, are visible in the region of the lesion (black arrows), indicative of reactive gliosis. Scale bar = 50 μm. D) Proliferating cells in the inner and outer nuclear layers of the retina in the lesioned area (asterisks) at 5 dpl incorporated BrdU (green) injected at 4 dpl. E) Injury-induced proliferating cells are also immunoreactive for proliferating cell nuclear antigen, PCNA (green) and are associated with radial fibers of Müller glia (magenta, anti-human GFAP). Note: the commercial polyclonal GFAP antibody used here is not selective for GFAP in zebrafish but labels other intermediate filaments (data not shown). In contrast, the monoclonal zrf1, which was generated against zebrafish proteins, selectively labels zebrafish GFAP [97]. Scale bar = 50 μm. F) – L) A 4 h or 24 h pulse of BrdU at 4 or 5 dpl labels clusters of nuclei (magenta) that extend between the INL and ONL and express rx1 (F) and vsx2 (J) as visualized by in situ hybridization (red). DAPI (blue); zrf1 (green, anti-zebrafish GFAP). Scale bar = 25 μm. Higher magnification views of rx1 (G,H, I) and vsx2 (K, L) in BrdU+ progenitors enclosed in a basket of zrf1+ Müller glial fibers. |
PMC1564002_F5_7085.jpg | What is the principal component of this image? | Injury-induced retinal progenitors regenerate cone photoreceptors within a week. A) At 4 dpl, proliferating cells (BrdU; magenta) fill the lesioned area (asterisks) in which double cones immunoreactive for zpr1 (green) are missing. Scale bar = 250 μm. B) By 7 dpl, some retinal progenitors that were labeled with BrdU (magenta) at 4 dpl have begun to differentiate into cones and are double-labeled with zpr1 (green). Boxed areas are shown at higher magnification in the insets; double-labeled cells are white. C) By 31 dpl fully differentiated, regenerated cone photoreceptors (zpr1; green) are labeled with BrdU (magenta) injected at 3 dpl (double-labeled white nuclei are indicated by black arrows). Unidentified BrdU+ nuclei are seen in the inner retina. D) Cocktail of riboprobes to cone opsins (green) identifies BrdU+ (magenta), regenerated cones at 31 dpl (double-labeled white nuclei are indicated by black arrows). BrdU+ rod nuclei (magenta) are in the inner part of the outer nuclear layer, ONL. E) Müller glia in a transgenic zebrafish Tg(gfap:GFP)mi2001 are labeled with anti-GFP (green) and co-express apoE (magenta, in situ hybridization) in their cell bodies. F) At 4 dpl, most BrdU+ proliferating nuclei are in the outer nuclear layer, ONL, but a few apoE+ Müller glial cells are also BrdU+ (inset). Radial fibers of Müller glia are labeled with zpr1/anti-GFAP (blue). |
PMC1564002_F5_7083.jpg | What is being portrayed in this visual content? | Injury-induced retinal progenitors regenerate cone photoreceptors within a week. A) At 4 dpl, proliferating cells (BrdU; magenta) fill the lesioned area (asterisks) in which double cones immunoreactive for zpr1 (green) are missing. Scale bar = 250 μm. B) By 7 dpl, some retinal progenitors that were labeled with BrdU (magenta) at 4 dpl have begun to differentiate into cones and are double-labeled with zpr1 (green). Boxed areas are shown at higher magnification in the insets; double-labeled cells are white. C) By 31 dpl fully differentiated, regenerated cone photoreceptors (zpr1; green) are labeled with BrdU (magenta) injected at 3 dpl (double-labeled white nuclei are indicated by black arrows). Unidentified BrdU+ nuclei are seen in the inner retina. D) Cocktail of riboprobes to cone opsins (green) identifies BrdU+ (magenta), regenerated cones at 31 dpl (double-labeled white nuclei are indicated by black arrows). BrdU+ rod nuclei (magenta) are in the inner part of the outer nuclear layer, ONL. E) Müller glia in a transgenic zebrafish Tg(gfap:GFP)mi2001 are labeled with anti-GFP (green) and co-express apoE (magenta, in situ hybridization) in their cell bodies. F) At 4 dpl, most BrdU+ proliferating nuclei are in the outer nuclear layer, ONL, but a few apoE+ Müller glial cells are also BrdU+ (inset). Radial fibers of Müller glia are labeled with zpr1/anti-GFAP (blue). |
PMC1564002_F5_7084.jpg | What is the dominant medical problem in this image? | Injury-induced retinal progenitors regenerate cone photoreceptors within a week. A) At 4 dpl, proliferating cells (BrdU; magenta) fill the lesioned area (asterisks) in which double cones immunoreactive for zpr1 (green) are missing. Scale bar = 250 μm. B) By 7 dpl, some retinal progenitors that were labeled with BrdU (magenta) at 4 dpl have begun to differentiate into cones and are double-labeled with zpr1 (green). Boxed areas are shown at higher magnification in the insets; double-labeled cells are white. C) By 31 dpl fully differentiated, regenerated cone photoreceptors (zpr1; green) are labeled with BrdU (magenta) injected at 3 dpl (double-labeled white nuclei are indicated by black arrows). Unidentified BrdU+ nuclei are seen in the inner retina. D) Cocktail of riboprobes to cone opsins (green) identifies BrdU+ (magenta), regenerated cones at 31 dpl (double-labeled white nuclei are indicated by black arrows). BrdU+ rod nuclei (magenta) are in the inner part of the outer nuclear layer, ONL. E) Müller glia in a transgenic zebrafish Tg(gfap:GFP)mi2001 are labeled with anti-GFP (green) and co-express apoE (magenta, in situ hybridization) in their cell bodies. F) At 4 dpl, most BrdU+ proliferating nuclei are in the outer nuclear layer, ONL, but a few apoE+ Müller glial cells are also BrdU+ (inset). Radial fibers of Müller glia are labeled with zpr1/anti-GFAP (blue). |
PMC1564002_F5_7086.jpg | What can you see in this picture? | Injury-induced retinal progenitors regenerate cone photoreceptors within a week. A) At 4 dpl, proliferating cells (BrdU; magenta) fill the lesioned area (asterisks) in which double cones immunoreactive for zpr1 (green) are missing. Scale bar = 250 μm. B) By 7 dpl, some retinal progenitors that were labeled with BrdU (magenta) at 4 dpl have begun to differentiate into cones and are double-labeled with zpr1 (green). Boxed areas are shown at higher magnification in the insets; double-labeled cells are white. C) By 31 dpl fully differentiated, regenerated cone photoreceptors (zpr1; green) are labeled with BrdU (magenta) injected at 3 dpl (double-labeled white nuclei are indicated by black arrows). Unidentified BrdU+ nuclei are seen in the inner retina. D) Cocktail of riboprobes to cone opsins (green) identifies BrdU+ (magenta), regenerated cones at 31 dpl (double-labeled white nuclei are indicated by black arrows). BrdU+ rod nuclei (magenta) are in the inner part of the outer nuclear layer, ONL. E) Müller glia in a transgenic zebrafish Tg(gfap:GFP)mi2001 are labeled with anti-GFP (green) and co-express apoE (magenta, in situ hybridization) in their cell bodies. F) At 4 dpl, most BrdU+ proliferating nuclei are in the outer nuclear layer, ONL, but a few apoE+ Müller glial cells are also BrdU+ (inset). Radial fibers of Müller glia are labeled with zpr1/anti-GFAP (blue). |
PMC1564002_F5_7087.jpg | What can you see in this picture? | Injury-induced retinal progenitors regenerate cone photoreceptors within a week. A) At 4 dpl, proliferating cells (BrdU; magenta) fill the lesioned area (asterisks) in which double cones immunoreactive for zpr1 (green) are missing. Scale bar = 250 μm. B) By 7 dpl, some retinal progenitors that were labeled with BrdU (magenta) at 4 dpl have begun to differentiate into cones and are double-labeled with zpr1 (green). Boxed areas are shown at higher magnification in the insets; double-labeled cells are white. C) By 31 dpl fully differentiated, regenerated cone photoreceptors (zpr1; green) are labeled with BrdU (magenta) injected at 3 dpl (double-labeled white nuclei are indicated by black arrows). Unidentified BrdU+ nuclei are seen in the inner retina. D) Cocktail of riboprobes to cone opsins (green) identifies BrdU+ (magenta), regenerated cones at 31 dpl (double-labeled white nuclei are indicated by black arrows). BrdU+ rod nuclei (magenta) are in the inner part of the outer nuclear layer, ONL. E) Müller glia in a transgenic zebrafish Tg(gfap:GFP)mi2001 are labeled with anti-GFP (green) and co-express apoE (magenta, in situ hybridization) in their cell bodies. F) At 4 dpl, most BrdU+ proliferating nuclei are in the outer nuclear layer, ONL, but a few apoE+ Müller glial cells are also BrdU+ (inset). Radial fibers of Müller glia are labeled with zpr1/anti-GFAP (blue). |
PMC1564010_F3_7100.jpg | What does this image primarily show? | Comparison between subtraction images. Subtraction images before [left] and after [right] registration. In the right note the portal and hepatic veins, their course and the better identification of several anatomic details. Recognition of the enhancing lesion in 8th segment is improved (open arrow in the right image). It is clear on the subtracted image after registration that the round zone of enhancement in 4th segment is not a focal lesion but a branching portal ramus (white arrow in the right image). Finally, the high signal intensity artifact on the lateral and anterior margins of the liver disappears after registration (arrows in the left image). |
PMC1564010_F3_7099.jpg | What is being portrayed in this visual content? | Comparison between subtraction images. Subtraction images before [left] and after [right] registration. In the right note the portal and hepatic veins, their course and the better identification of several anatomic details. Recognition of the enhancing lesion in 8th segment is improved (open arrow in the right image). It is clear on the subtracted image after registration that the round zone of enhancement in 4th segment is not a focal lesion but a branching portal ramus (white arrow in the right image). Finally, the high signal intensity artifact on the lateral and anterior margins of the liver disappears after registration (arrows in the left image). |
PMC1564010_F6_7102.jpg | What is the central feature of this picture? | Metastatic liver lesions from breast cancer. Tl-weighted 3D post-contrast image [left] and corresponding 3D subtraction image, [right]. The arrows show metastatic lesions from breast cancer, better reveled in the subtraction image. See text for further details. |
PMC1564010_F6_7101.jpg | What is the focal point of this photograph? | Metastatic liver lesions from breast cancer. Tl-weighted 3D post-contrast image [left] and corresponding 3D subtraction image, [right]. The arrows show metastatic lesions from breast cancer, better reveled in the subtraction image. See text for further details. |
PMC1564019_F2_7104.jpg | What is the principal component of this image? | All tumour cells on immunohistochemical study showed finely granular immunoreactivity of the cytoplasm with antimitochondrial antibody (a: ×200), cytoplasmatic and membranous positivity for antikeratin antibody (b: ×200) and cytoplasmatic positivity for alpha-1-antichymotripsina (c and d: × 200; in c yet note neoplastic perineural infiltration). |
PMC1564019_F2_7105.jpg | What stands out most in this visual? | All tumour cells on immunohistochemical study showed finely granular immunoreactivity of the cytoplasm with antimitochondrial antibody (a: ×200), cytoplasmatic and membranous positivity for antikeratin antibody (b: ×200) and cytoplasmatic positivity for alpha-1-antichymotripsina (c and d: × 200; in c yet note neoplastic perineural infiltration). |
PMC1564019_F2_7103.jpg | What is being portrayed in this visual content? | All tumour cells on immunohistochemical study showed finely granular immunoreactivity of the cytoplasm with antimitochondrial antibody (a: ×200), cytoplasmatic and membranous positivity for antikeratin antibody (b: ×200) and cytoplasmatic positivity for alpha-1-antichymotripsina (c and d: × 200; in c yet note neoplastic perineural infiltration). |
PMC1564030_F1_7108.jpg | What can you see in this picture? | Tumor cells were mainly epithelioid with abundant eosinophilic and granular cytoplasm. Occasional nuclear inclusions were present (hematoxylin-eosin, original magnification ×400). |
PMC1564030_F2_7107.jpg | What is the core subject represented in this visual? | Tumor cells demonstrated strong and diffuse cytoplasmic positivity for HMB45 and Melan-A (Melan-A immunoperoxidase, original magnification ×400). |
PMC1564030_F3_7109.jpg | What is the focal point of this photograph? | Tumor cells showed strong and diffuse membranous positivity for smooth muscle actin (smooth muscle actin immunoperoxidase, original magnification ×400). |
PMC1564038_F3_7117.jpg | Can you identify the primary element in this image? | Time course of serial stimulation. Micrographs before stimulation (a), after first stimulation (b), after first phagocytosis started (c, d), after second stimulation started (e, f), after first phagocytosis was complete (g), second phagocytosis started (h, i), and after second phagocytosis was complete (j). Schematic explanation of time-course of series stimulation (k). White arrows in micrographs indicate the position of zymosan. |
PMC1564038_F3_7118.jpg | What is the core subject represented in this visual? | Time course of serial stimulation. Micrographs before stimulation (a), after first stimulation (b), after first phagocytosis started (c, d), after second stimulation started (e, f), after first phagocytosis was complete (g), second phagocytosis started (h, i), and after second phagocytosis was complete (j). Schematic explanation of time-course of series stimulation (k). White arrows in micrographs indicate the position of zymosan. |
PMC1564038_F3_7125.jpg | What key item or scene is captured in this photo? | Time course of serial stimulation. Micrographs before stimulation (a), after first stimulation (b), after first phagocytosis started (c, d), after second stimulation started (e, f), after first phagocytosis was complete (g), second phagocytosis started (h, i), and after second phagocytosis was complete (j). Schematic explanation of time-course of series stimulation (k). White arrows in micrographs indicate the position of zymosan. |
PMC1564038_F3_7126.jpg | What can you see in this picture? | Time course of serial stimulation. Micrographs before stimulation (a), after first stimulation (b), after first phagocytosis started (c, d), after second stimulation started (e, f), after first phagocytosis was complete (g), second phagocytosis started (h, i), and after second phagocytosis was complete (j). Schematic explanation of time-course of series stimulation (k). White arrows in micrographs indicate the position of zymosan. |
PMC1564038_F3_7119.jpg | What is the principal component of this image? | Time course of serial stimulation. Micrographs before stimulation (a), after first stimulation (b), after first phagocytosis started (c, d), after second stimulation started (e, f), after first phagocytosis was complete (g), second phagocytosis started (h, i), and after second phagocytosis was complete (j). Schematic explanation of time-course of series stimulation (k). White arrows in micrographs indicate the position of zymosan. |
PMC1564038_F3_7122.jpg | What is the dominant medical problem in this image? | Time course of serial stimulation. Micrographs before stimulation (a), after first stimulation (b), after first phagocytosis started (c, d), after second stimulation started (e, f), after first phagocytosis was complete (g), second phagocytosis started (h, i), and after second phagocytosis was complete (j). Schematic explanation of time-course of series stimulation (k). White arrows in micrographs indicate the position of zymosan. |
PMC1564038_F3_7124.jpg | What can you see in this picture? | Time course of serial stimulation. Micrographs before stimulation (a), after first stimulation (b), after first phagocytosis started (c, d), after second stimulation started (e, f), after first phagocytosis was complete (g), second phagocytosis started (h, i), and after second phagocytosis was complete (j). Schematic explanation of time-course of series stimulation (k). White arrows in micrographs indicate the position of zymosan. |
PMC1564038_F3_7127.jpg | What is the main focus of this visual representation? | Time course of serial stimulation. Micrographs before stimulation (a), after first stimulation (b), after first phagocytosis started (c, d), after second stimulation started (e, f), after first phagocytosis was complete (g), second phagocytosis started (h, i), and after second phagocytosis was complete (j). Schematic explanation of time-course of series stimulation (k). White arrows in micrographs indicate the position of zymosan. |
PMC1564038_F3_7123.jpg | What is being portrayed in this visual content? | Time course of serial stimulation. Micrographs before stimulation (a), after first stimulation (b), after first phagocytosis started (c, d), after second stimulation started (e, f), after first phagocytosis was complete (g), second phagocytosis started (h, i), and after second phagocytosis was complete (j). Schematic explanation of time-course of series stimulation (k). White arrows in micrographs indicate the position of zymosan. |
PMC1564038_F4_7113.jpg | What is the principal component of this image? | Time course of single stimulation. Micrographs before stimulation (a), after first stimulation (b, c), after phagocytosis started (d, e), after phagocytosis was complete (f). The time in the figure is averaged result of 6 samples. |
PMC1564038_F4_7110.jpg | What is the focal point of this photograph? | Time course of single stimulation. Micrographs before stimulation (a), after first stimulation (b, c), after phagocytosis started (d, e), after phagocytosis was complete (f). The time in the figure is averaged result of 6 samples. |
PMC1564038_F4_7112.jpg | What is the principal component of this image? | Time course of single stimulation. Micrographs before stimulation (a), after first stimulation (b, c), after phagocytosis started (d, e), after phagocytosis was complete (f). The time in the figure is averaged result of 6 samples. |
PMC1564038_F4_7114.jpg | What is being portrayed in this visual content? | Time course of single stimulation. Micrographs before stimulation (a), after first stimulation (b, c), after phagocytosis started (d, e), after phagocytosis was complete (f). The time in the figure is averaged result of 6 samples. |
PMC1564042_F1_7128.jpg | What object or scene is depicted here? | Scanning magnification view of a pure adenoid basal lesion (adenoid basal epithelioma), showing an infiltrative proliferation of basaloid nests. (hematoxylin and eosin, original magnification 10×) |
PMC1564043_F1_7130.jpg | What does this image primarily show? | Clinical photography. Conjunctival hyperemia, mild corneal edema, posterior synechiae and cataract. |
PMC1564043_F2_7131.jpg | What is the core subject represented in this visual? | Computed Tomography. Total exsudative retinal detachment in the right eye. |
PMC1564130_F9_7134.jpg | What can you see in this picture? | Oregon Green labeled fibrinogen (0.5 mg/ml; Molecular Probes, Eugene, OR) was treated with thrombin (1.25 U) in the presence of 4 mM GPRP-NH2 to produce fluorescently labeled sFn. A375 cells were incubated with labeled sFn for 20 min in a Bioptechs FCS2 enclosed stage incubator. The residual sFn was washed away by perfusion and the cells were imaged on an Olympus BX61 fluorescence microscope equipped with a long pass 535 nm dichroic filter. Considerable binding of sFn was observed. A is a representative image showing tumor cell sFn binding. In contrast, little or no binding was observed when cells were pre-incubated with peptides P1 + P2 (B), or sFn with P3 + P4 (C). Similarly, sFn bound readily to monocytes (D), but was inhibited when cells were pre-incubated with P1 + P2 (E), or sFn was pre-treated with P3 + P4 (F). |
PMC1564130_F9_7133.jpg | What is the dominant medical problem in this image? | Oregon Green labeled fibrinogen (0.5 mg/ml; Molecular Probes, Eugene, OR) was treated with thrombin (1.25 U) in the presence of 4 mM GPRP-NH2 to produce fluorescently labeled sFn. A375 cells were incubated with labeled sFn for 20 min in a Bioptechs FCS2 enclosed stage incubator. The residual sFn was washed away by perfusion and the cells were imaged on an Olympus BX61 fluorescence microscope equipped with a long pass 535 nm dichroic filter. Considerable binding of sFn was observed. A is a representative image showing tumor cell sFn binding. In contrast, little or no binding was observed when cells were pre-incubated with peptides P1 + P2 (B), or sFn with P3 + P4 (C). Similarly, sFn bound readily to monocytes (D), but was inhibited when cells were pre-incubated with P1 + P2 (E), or sFn was pre-treated with P3 + P4 (F). |
PMC1564130_F9_7132.jpg | What is the main focus of this visual representation? | Oregon Green labeled fibrinogen (0.5 mg/ml; Molecular Probes, Eugene, OR) was treated with thrombin (1.25 U) in the presence of 4 mM GPRP-NH2 to produce fluorescently labeled sFn. A375 cells were incubated with labeled sFn for 20 min in a Bioptechs FCS2 enclosed stage incubator. The residual sFn was washed away by perfusion and the cells were imaged on an Olympus BX61 fluorescence microscope equipped with a long pass 535 nm dichroic filter. Considerable binding of sFn was observed. A is a representative image showing tumor cell sFn binding. In contrast, little or no binding was observed when cells were pre-incubated with peptides P1 + P2 (B), or sFn with P3 + P4 (C). Similarly, sFn bound readily to monocytes (D), but was inhibited when cells were pre-incubated with P1 + P2 (E), or sFn was pre-treated with P3 + P4 (F). |
PMC1564130_F9_7137.jpg | What is the central feature of this picture? | Oregon Green labeled fibrinogen (0.5 mg/ml; Molecular Probes, Eugene, OR) was treated with thrombin (1.25 U) in the presence of 4 mM GPRP-NH2 to produce fluorescently labeled sFn. A375 cells were incubated with labeled sFn for 20 min in a Bioptechs FCS2 enclosed stage incubator. The residual sFn was washed away by perfusion and the cells were imaged on an Olympus BX61 fluorescence microscope equipped with a long pass 535 nm dichroic filter. Considerable binding of sFn was observed. A is a representative image showing tumor cell sFn binding. In contrast, little or no binding was observed when cells were pre-incubated with peptides P1 + P2 (B), or sFn with P3 + P4 (C). Similarly, sFn bound readily to monocytes (D), but was inhibited when cells were pre-incubated with P1 + P2 (E), or sFn was pre-treated with P3 + P4 (F). |
PMC1564130_F9_7136.jpg | What is the core subject represented in this visual? | Oregon Green labeled fibrinogen (0.5 mg/ml; Molecular Probes, Eugene, OR) was treated with thrombin (1.25 U) in the presence of 4 mM GPRP-NH2 to produce fluorescently labeled sFn. A375 cells were incubated with labeled sFn for 20 min in a Bioptechs FCS2 enclosed stage incubator. The residual sFn was washed away by perfusion and the cells were imaged on an Olympus BX61 fluorescence microscope equipped with a long pass 535 nm dichroic filter. Considerable binding of sFn was observed. A is a representative image showing tumor cell sFn binding. In contrast, little or no binding was observed when cells were pre-incubated with peptides P1 + P2 (B), or sFn with P3 + P4 (C). Similarly, sFn bound readily to monocytes (D), but was inhibited when cells were pre-incubated with P1 + P2 (E), or sFn was pre-treated with P3 + P4 (F). |
PMC1564131_F2_7140.jpg | What stands out most in this visual? | Transaxial magnetic resonance images at the levels of mid-calf (top slice images) and mid-thigh (bottom slice images) of the subjects in the study. Bright/white signals in these images are highlighting adipose tissue within these anatomical sections. Dark signals represent either muscle tissue within sections or the background of the images. Subject GL2784 is a healthy 24 year old woman whose MRI showed no infiltrated fat into calf muscle, and only small amount of infiltration in the thigh. Subject GL2990 is a normal 50 year old woman who had somewhat increased subcutaneous (sc) fat in the calves and mid-thigh with slightly more infiltration of fat into the muscle compared to the images of subject GL2784. Subject GL0658 is a 49 year old FPLD3 patient (heterozygous for mutation PPARG F388L) whose scans show moderate loss of sc fat in both the calves and mid thigh and moderate levels of fat infiltration. Subject GL0096 is a 63 year old FPLD2 patient (heterozygous for mutation LMNA R482Q) whose scan shows total sc fat loss in the calves, major sc fat loss in the mid-thigh and marbled appearance of muscle tissue due to severe amounts of fat being stored within the muscle. |
PMC1564131_F2_7139.jpg | What is being portrayed in this visual content? | Transaxial magnetic resonance images at the levels of mid-calf (top slice images) and mid-thigh (bottom slice images) of the subjects in the study. Bright/white signals in these images are highlighting adipose tissue within these anatomical sections. Dark signals represent either muscle tissue within sections or the background of the images. Subject GL2784 is a healthy 24 year old woman whose MRI showed no infiltrated fat into calf muscle, and only small amount of infiltration in the thigh. Subject GL2990 is a normal 50 year old woman who had somewhat increased subcutaneous (sc) fat in the calves and mid-thigh with slightly more infiltration of fat into the muscle compared to the images of subject GL2784. Subject GL0658 is a 49 year old FPLD3 patient (heterozygous for mutation PPARG F388L) whose scans show moderate loss of sc fat in both the calves and mid thigh and moderate levels of fat infiltration. Subject GL0096 is a 63 year old FPLD2 patient (heterozygous for mutation LMNA R482Q) whose scan shows total sc fat loss in the calves, major sc fat loss in the mid-thigh and marbled appearance of muscle tissue due to severe amounts of fat being stored within the muscle. |
PMC1564131_F2_7138.jpg | What is being portrayed in this visual content? | Transaxial magnetic resonance images at the levels of mid-calf (top slice images) and mid-thigh (bottom slice images) of the subjects in the study. Bright/white signals in these images are highlighting adipose tissue within these anatomical sections. Dark signals represent either muscle tissue within sections or the background of the images. Subject GL2784 is a healthy 24 year old woman whose MRI showed no infiltrated fat into calf muscle, and only small amount of infiltration in the thigh. Subject GL2990 is a normal 50 year old woman who had somewhat increased subcutaneous (sc) fat in the calves and mid-thigh with slightly more infiltration of fat into the muscle compared to the images of subject GL2784. Subject GL0658 is a 49 year old FPLD3 patient (heterozygous for mutation PPARG F388L) whose scans show moderate loss of sc fat in both the calves and mid thigh and moderate levels of fat infiltration. Subject GL0096 is a 63 year old FPLD2 patient (heterozygous for mutation LMNA R482Q) whose scan shows total sc fat loss in the calves, major sc fat loss in the mid-thigh and marbled appearance of muscle tissue due to severe amounts of fat being stored within the muscle. |
PMC1564147_F6_7142.jpg | What does this image primarily show? | Photomicrograph of bone biopsy showing sheet of plasma cells with a prominent 'Russell body' (Hematoxylin & Eosin × 400). |
PMC1564184_F2_7144.jpg | What stands out most in this visual? | Radiological follow up of peritoneal carcinomatosis. MS- CT axial (contrast-enhanced, portal-venous phase): Peritoneal carcinomatosis (omental cake) (A), regressive under chemotherapy (B). |
PMC1564184_F2_7143.jpg | What does this image primarily show? | Radiological follow up of peritoneal carcinomatosis. MS- CT axial (contrast-enhanced, portal-venous phase): Peritoneal carcinomatosis (omental cake) (A), regressive under chemotherapy (B). |
PMC1564284_pmed-0030293-g001_7147.jpg | What is the main focus of this visual representation? | Plain Radiograph of the Sacroiliac Joints on Presentation to the Hospital San Juan de MatucanaThe radiologist reported this radiograph as normal. |
PMC1564418_F4_7152.jpg | What is being portrayed in this visual content? | unc-18 expression in the male gonad and ventral nerve cord. Nomarski (A, D), fluorescence (B, E) and merged (C, F) images of unc-18::YFP expression in the male gonad region and part of the ventral nerve cord. (A–C) Lateral view; (D–F) dorsal view. The dashed arrow indicates the sperm in the seminal vesicle, and the solid arrow indicates the valve area where the sperm exit into the vas deferens. Arrowheads in (A–C) indicate the ventral nerve cord. |
PMC1564418_F4_7154.jpg | What is being portrayed in this visual content? | unc-18 expression in the male gonad and ventral nerve cord. Nomarski (A, D), fluorescence (B, E) and merged (C, F) images of unc-18::YFP expression in the male gonad region and part of the ventral nerve cord. (A–C) Lateral view; (D–F) dorsal view. The dashed arrow indicates the sperm in the seminal vesicle, and the solid arrow indicates the valve area where the sperm exit into the vas deferens. Arrowheads in (A–C) indicate the ventral nerve cord. |
PMC1564418_F4_7151.jpg | What can you see in this picture? | unc-18 expression in the male gonad and ventral nerve cord. Nomarski (A, D), fluorescence (B, E) and merged (C, F) images of unc-18::YFP expression in the male gonad region and part of the ventral nerve cord. (A–C) Lateral view; (D–F) dorsal view. The dashed arrow indicates the sperm in the seminal vesicle, and the solid arrow indicates the valve area where the sperm exit into the vas deferens. Arrowheads in (A–C) indicate the ventral nerve cord. |
PMC1564418_F4_7150.jpg | What is shown in this image? | unc-18 expression in the male gonad and ventral nerve cord. Nomarski (A, D), fluorescence (B, E) and merged (C, F) images of unc-18::YFP expression in the male gonad region and part of the ventral nerve cord. (A–C) Lateral view; (D–F) dorsal view. The dashed arrow indicates the sperm in the seminal vesicle, and the solid arrow indicates the valve area where the sperm exit into the vas deferens. Arrowheads in (A–C) indicate the ventral nerve cord. |
PMC1564418_F4_7153.jpg | What key item or scene is captured in this photo? | unc-18 expression in the male gonad and ventral nerve cord. Nomarski (A, D), fluorescence (B, E) and merged (C, F) images of unc-18::YFP expression in the male gonad region and part of the ventral nerve cord. (A–C) Lateral view; (D–F) dorsal view. The dashed arrow indicates the sperm in the seminal vesicle, and the solid arrow indicates the valve area where the sperm exit into the vas deferens. Arrowheads in (A–C) indicate the ventral nerve cord. |
PMC1564418_F9_7158.jpg | What is the focal point of this photograph? | Expression of reporter constructs in the male. Lateral views and all images are oriented such that posterior is left and dorsal is up. Images in (A–C) were inverted to obtain this orientation. (A–C) aex-3::UNC-18::YFP expression in the male. Nomarski (A), fluorescence (B), and merged (C) images. Slightly higher magnification than images in (D–I). Although aex-3 unc-18::YFP is expressed in the ventral cord, in (A–C) we focused on the plane that best showed the gonad expression. (D–F) acr-2::YFP expression in the male. Nomarski (D), fluorescence (E) and merged (F) images. (G–I) acr-5::YFP expression in the male. Nomarski (G), fluorescence (H), and merged (I) images. Animals shown are pha-1(e2123ts) young adult males transformed with the extrachromosomal array pha-1+ reporter::YFP. |
PMC1564418_F9_7160.jpg | What's the most prominent thing you notice in this picture? | Expression of reporter constructs in the male. Lateral views and all images are oriented such that posterior is left and dorsal is up. Images in (A–C) were inverted to obtain this orientation. (A–C) aex-3::UNC-18::YFP expression in the male. Nomarski (A), fluorescence (B), and merged (C) images. Slightly higher magnification than images in (D–I). Although aex-3 unc-18::YFP is expressed in the ventral cord, in (A–C) we focused on the plane that best showed the gonad expression. (D–F) acr-2::YFP expression in the male. Nomarski (D), fluorescence (E) and merged (F) images. (G–I) acr-5::YFP expression in the male. Nomarski (G), fluorescence (H), and merged (I) images. Animals shown are pha-1(e2123ts) young adult males transformed with the extrachromosomal array pha-1+ reporter::YFP. |
PMC1564418_F9_7157.jpg | What is being portrayed in this visual content? | Expression of reporter constructs in the male. Lateral views and all images are oriented such that posterior is left and dorsal is up. Images in (A–C) were inverted to obtain this orientation. (A–C) aex-3::UNC-18::YFP expression in the male. Nomarski (A), fluorescence (B), and merged (C) images. Slightly higher magnification than images in (D–I). Although aex-3 unc-18::YFP is expressed in the ventral cord, in (A–C) we focused on the plane that best showed the gonad expression. (D–F) acr-2::YFP expression in the male. Nomarski (D), fluorescence (E) and merged (F) images. (G–I) acr-5::YFP expression in the male. Nomarski (G), fluorescence (H), and merged (I) images. Animals shown are pha-1(e2123ts) young adult males transformed with the extrachromosomal array pha-1+ reporter::YFP. |
PMC1564418_F9_7156.jpg | What does this image primarily show? | Expression of reporter constructs in the male. Lateral views and all images are oriented such that posterior is left and dorsal is up. Images in (A–C) were inverted to obtain this orientation. (A–C) aex-3::UNC-18::YFP expression in the male. Nomarski (A), fluorescence (B), and merged (C) images. Slightly higher magnification than images in (D–I). Although aex-3 unc-18::YFP is expressed in the ventral cord, in (A–C) we focused on the plane that best showed the gonad expression. (D–F) acr-2::YFP expression in the male. Nomarski (D), fluorescence (E) and merged (F) images. (G–I) acr-5::YFP expression in the male. Nomarski (G), fluorescence (H), and merged (I) images. Animals shown are pha-1(e2123ts) young adult males transformed with the extrachromosomal array pha-1+ reporter::YFP. |
PMC1564418_F9_7162.jpg | What is shown in this image? | Expression of reporter constructs in the male. Lateral views and all images are oriented such that posterior is left and dorsal is up. Images in (A–C) were inverted to obtain this orientation. (A–C) aex-3::UNC-18::YFP expression in the male. Nomarski (A), fluorescence (B), and merged (C) images. Slightly higher magnification than images in (D–I). Although aex-3 unc-18::YFP is expressed in the ventral cord, in (A–C) we focused on the plane that best showed the gonad expression. (D–F) acr-2::YFP expression in the male. Nomarski (D), fluorescence (E) and merged (F) images. (G–I) acr-5::YFP expression in the male. Nomarski (G), fluorescence (H), and merged (I) images. Animals shown are pha-1(e2123ts) young adult males transformed with the extrachromosomal array pha-1+ reporter::YFP. |
PMC1564418_F9_7163.jpg | What does this image primarily show? | Expression of reporter constructs in the male. Lateral views and all images are oriented such that posterior is left and dorsal is up. Images in (A–C) were inverted to obtain this orientation. (A–C) aex-3::UNC-18::YFP expression in the male. Nomarski (A), fluorescence (B), and merged (C) images. Slightly higher magnification than images in (D–I). Although aex-3 unc-18::YFP is expressed in the ventral cord, in (A–C) we focused on the plane that best showed the gonad expression. (D–F) acr-2::YFP expression in the male. Nomarski (D), fluorescence (E) and merged (F) images. (G–I) acr-5::YFP expression in the male. Nomarski (G), fluorescence (H), and merged (I) images. Animals shown are pha-1(e2123ts) young adult males transformed with the extrachromosomal array pha-1+ reporter::YFP. |
PMC1564426_pgen-0020146-g004_7174.jpg | What is being portrayed in this visual content? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7176.jpg | What's the most prominent thing you notice in this picture? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7166.jpg | What object or scene is depicted here? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7173.jpg | What is the principal component of this image? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7177.jpg | What object or scene is depicted here? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7168.jpg | What's the most prominent thing you notice in this picture? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7164.jpg | What stands out most in this visual? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7170.jpg | Can you identify the primary element in this image? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7172.jpg | What's the most prominent thing you notice in this picture? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7178.jpg | What is the principal component of this image? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7179.jpg | What's the most prominent thing you notice in this picture? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7171.jpg | What is the focal point of this photograph? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7169.jpg | What is the focal point of this photograph? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7165.jpg | Describe the main subject of this image. | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564426_pgen-0020146-g004_7167.jpg | What stands out most in this visual? | Histological and Immunochemical Examination of P12 Skin and Teeth(A–E) P12 normal skin. (F–J) P12 mutant skin. (K–N) P12 normal oral cavity. (O–R) P12 mutant oral cavity. Stained with H&E for histology (A, F, K–L, O–P), Ki67 (B, G), β-catenin (C, H, M, Q), K14 (D, I, N, R), and K6 (E, J). Aberrant follicular morphogenesis, characterized by formation of irregularly spaced, nonpolarized hair follicles, in mutant skin is evident. Despite the abnormal histology, proliferation seems to be confined to hair bulb-like structures (arrows in [G], inset [G′] at higher magnification), but in mutant skin (arrows in [H], inset [H′] at higher magnification) and oral cavity (arrows in insets [Q′] at higher magnification) elevated cytosolic localization of β-catenin is detected in some cells. Scale bars: 50 μm for (A–F), (H–J); 250 μm for (K) and (O); 100 μm for (G), (L–N), (P–R); 20 μm for (Q′). |
PMC1564427_ppat-0020092-g009_7181.jpg | What does this image primarily show? | Grading of the Supratesticular Lymphatic Vessel Dilation of Filarial-Infected Patients Displayed by USGDilation of the supratesticular lymphatic vessels was determined by measuring the largest diameter detectable in the two-dimensional b-mode of a portable ultrasound machine. A grading system was developed to determine the degree of lymphatic dilation as follows: (A) category 1: patients with minimal lymphatic dilation of up to 0.2 cm; (B) category 2: patients with mild dilation from 0.21–0.50 cm; (C) category 3: patients with moderate dilation from 0.51–1.0 cm; and (D) category 4: patients with severe dilation of above 1.0 cm. |
PMC1564427_ppat-0020092-g009_7180.jpg | What can you see in this picture? | Grading of the Supratesticular Lymphatic Vessel Dilation of Filarial-Infected Patients Displayed by USGDilation of the supratesticular lymphatic vessels was determined by measuring the largest diameter detectable in the two-dimensional b-mode of a portable ultrasound machine. A grading system was developed to determine the degree of lymphatic dilation as follows: (A) category 1: patients with minimal lymphatic dilation of up to 0.2 cm; (B) category 2: patients with mild dilation from 0.21–0.50 cm; (C) category 3: patients with moderate dilation from 0.51–1.0 cm; and (D) category 4: patients with severe dilation of above 1.0 cm. |
PMC1564427_ppat-0020092-g009_7183.jpg | What does this image primarily show? | Grading of the Supratesticular Lymphatic Vessel Dilation of Filarial-Infected Patients Displayed by USGDilation of the supratesticular lymphatic vessels was determined by measuring the largest diameter detectable in the two-dimensional b-mode of a portable ultrasound machine. A grading system was developed to determine the degree of lymphatic dilation as follows: (A) category 1: patients with minimal lymphatic dilation of up to 0.2 cm; (B) category 2: patients with mild dilation from 0.21–0.50 cm; (C) category 3: patients with moderate dilation from 0.51–1.0 cm; and (D) category 4: patients with severe dilation of above 1.0 cm. |
PMC1569370_F6_7184.jpg | What is the main focus of this visual representation? | HCV NS3/4A colocalizes with Cardif at mitochondrial membrane. The localization of HCV proteins and Cardif was studied in Huh7 cells. The cells were transfected with HCV protein expression constructs (NS3/4A, core or NS5A) and 48 h later cells were fixed and stained. The colocalization was visualised by confocal microscopy. Cells were stained for Cardif (endogenous) (A, D, G, J), mitochondria with Mitotracker Red 580 (B), NS3/4A (E), core (H) and NS5A (K) and the signals were merged (C, F, I, L). |
PMC1569370_F6_7189.jpg | What is the principal component of this image? | HCV NS3/4A colocalizes with Cardif at mitochondrial membrane. The localization of HCV proteins and Cardif was studied in Huh7 cells. The cells were transfected with HCV protein expression constructs (NS3/4A, core or NS5A) and 48 h later cells were fixed and stained. The colocalization was visualised by confocal microscopy. Cells were stained for Cardif (endogenous) (A, D, G, J), mitochondria with Mitotracker Red 580 (B), NS3/4A (E), core (H) and NS5A (K) and the signals were merged (C, F, I, L). |
PMC1569370_F6_7187.jpg | What is the main focus of this visual representation? | HCV NS3/4A colocalizes with Cardif at mitochondrial membrane. The localization of HCV proteins and Cardif was studied in Huh7 cells. The cells were transfected with HCV protein expression constructs (NS3/4A, core or NS5A) and 48 h later cells were fixed and stained. The colocalization was visualised by confocal microscopy. Cells were stained for Cardif (endogenous) (A, D, G, J), mitochondria with Mitotracker Red 580 (B), NS3/4A (E), core (H) and NS5A (K) and the signals were merged (C, F, I, L). |
PMC1569370_F6_7193.jpg | Describe the main subject of this image. | HCV NS3/4A colocalizes with Cardif at mitochondrial membrane. The localization of HCV proteins and Cardif was studied in Huh7 cells. The cells were transfected with HCV protein expression constructs (NS3/4A, core or NS5A) and 48 h later cells were fixed and stained. The colocalization was visualised by confocal microscopy. Cells were stained for Cardif (endogenous) (A, D, G, J), mitochondria with Mitotracker Red 580 (B), NS3/4A (E), core (H) and NS5A (K) and the signals were merged (C, F, I, L). |
PMC1569370_F6_7188.jpg | What is the dominant medical problem in this image? | HCV NS3/4A colocalizes with Cardif at mitochondrial membrane. The localization of HCV proteins and Cardif was studied in Huh7 cells. The cells were transfected with HCV protein expression constructs (NS3/4A, core or NS5A) and 48 h later cells were fixed and stained. The colocalization was visualised by confocal microscopy. Cells were stained for Cardif (endogenous) (A, D, G, J), mitochondria with Mitotracker Red 580 (B), NS3/4A (E), core (H) and NS5A (K) and the signals were merged (C, F, I, L). |
PMC1569370_F6_7191.jpg | What is the dominant medical problem in this image? | HCV NS3/4A colocalizes with Cardif at mitochondrial membrane. The localization of HCV proteins and Cardif was studied in Huh7 cells. The cells were transfected with HCV protein expression constructs (NS3/4A, core or NS5A) and 48 h later cells were fixed and stained. The colocalization was visualised by confocal microscopy. Cells were stained for Cardif (endogenous) (A, D, G, J), mitochondria with Mitotracker Red 580 (B), NS3/4A (E), core (H) and NS5A (K) and the signals were merged (C, F, I, L). |
PMC1569370_F6_7185.jpg | What is shown in this image? | HCV NS3/4A colocalizes with Cardif at mitochondrial membrane. The localization of HCV proteins and Cardif was studied in Huh7 cells. The cells were transfected with HCV protein expression constructs (NS3/4A, core or NS5A) and 48 h later cells were fixed and stained. The colocalization was visualised by confocal microscopy. Cells were stained for Cardif (endogenous) (A, D, G, J), mitochondria with Mitotracker Red 580 (B), NS3/4A (E), core (H) and NS5A (K) and the signals were merged (C, F, I, L). |
PMC1569370_F6_7192.jpg | What is the central feature of this picture? | HCV NS3/4A colocalizes with Cardif at mitochondrial membrane. The localization of HCV proteins and Cardif was studied in Huh7 cells. The cells were transfected with HCV protein expression constructs (NS3/4A, core or NS5A) and 48 h later cells were fixed and stained. The colocalization was visualised by confocal microscopy. Cells were stained for Cardif (endogenous) (A, D, G, J), mitochondria with Mitotracker Red 580 (B), NS3/4A (E), core (H) and NS5A (K) and the signals were merged (C, F, I, L). |
PMC1569370_F6_7186.jpg | What is the principal component of this image? | HCV NS3/4A colocalizes with Cardif at mitochondrial membrane. The localization of HCV proteins and Cardif was studied in Huh7 cells. The cells were transfected with HCV protein expression constructs (NS3/4A, core or NS5A) and 48 h later cells were fixed and stained. The colocalization was visualised by confocal microscopy. Cells were stained for Cardif (endogenous) (A, D, G, J), mitochondria with Mitotracker Red 580 (B), NS3/4A (E), core (H) and NS5A (K) and the signals were merged (C, F, I, L). |
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