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PMC449870_pbio-0020207-g003_151.jpg | What is shown in this image? | FISH Confirmation of a Human-Specific Duplication of a Gene Cluster on Chromosome 5q13.3 Detected by Interspecies cDNA aCGH(A) Human duplication of a cluster of genes at Chromosome 5q13.3. is shown by two separate, and sometimes multiple, red BAC probe (CTD-2288G5) signals in interphase cells, with only one green BAC probe signal (RP11-1077O1) for a flanking region. Metaphase FISH shows both probes at band 5q13. The third nucleus in (A) shows four signals of the control probe (green) and eight copies of the BAC probe duplicated in the aCGH assay, consistent with the pattern expected in an S/G2 nucleus.(B–E) Bonobo (B), chimpanzee (C), gorilla (D), and orangutan (E) interphase FISH studies all show no increased signal for the human duplicated gene cluster, with signals of comparable size for the CTD-2288G5 (red) and the flanking RP11-107701 (green) probes. Metaphase FISH analyses show the gene cluster to be in the p arm of Chromosomes 4 (corresponding to the human Chromosome 5) in both the bonobo and chimpanzee, in the q arm of Chromosome 4 (corresponding to the human Chromosome 5) in the orangutan, and in the p arm of the gorilla Chromosome 19 (syntenic regions to human Chromosomes 5 and 17). |
PMC479042_pbio-0020244-g007_159.jpg | What is being portrayed in this visual content? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_154.jpg | Describe the main subject of this image. | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_165.jpg | What can you see in this picture? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_160.jpg | What is being portrayed in this visual content? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_164.jpg | What is the dominant medical problem in this image? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_156.jpg | What is shown in this image? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_158.jpg | What is the core subject represented in this visual? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_171.jpg | Can you identify the primary element in this image? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_153.jpg | What stands out most in this visual? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_155.jpg | What does this image primarily show? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_172.jpg | What is the main focus of this visual representation? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_169.jpg | What is the dominant medical problem in this image? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_170.jpg | What is the principal component of this image? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_161.jpg | What does this image primarily show? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_157.jpg | What is the principal component of this image? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_167.jpg | What is the main focus of this visual representation? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_168.jpg | What is the principal component of this image? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_162.jpg | What key item or scene is captured in this photo? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC479042_pbio-0020244-g007_163.jpg | What object or scene is depicted here? | Anterior Hyoid Crest Cells Display Aberrant Behavior in integrinα5 MutantsConfocal time-lapse recordings show hyoid cartilage development in wild-type fli1-GFP (Videos S1 and S2) and integrinα5−; fli1-GFP (Video S3) animals from 38 hpf to 86 hpf (nwt = 3; nitga5 = 4). Videos S1 and S2 are different depths of the same time-lapse recording. Representative imaging stills of Video S1 (A–F), Video S2 (G–L), and Video S3 (M–R) were taken at 38 hpf (A, G, and M), 44 hpf (B, H, and N), 50 hpf (C, I , and O), 56 hpf (D, J, and P), 62 hpf (E, K, and Q), and 86 hpf (F, L, and R). At the beginning of the recordings (A, G, and M), the mandibular (1) and hyoid (2) arches are numbered and an arrow denotes the first pouch (p1). At the end of the recordings (F, L, and R), the cartilage regions are clearly visible as large cells with thick matrix (pseudocolored blue). The outline of the HS cartilage, a composite of SY and HM regions, is shown in (F) and (L). As a reference, the opercle bone and ao/lo hyoid muscle mass are pseudocolored purple and red, respectively, and the eye and ear are labeled. In Video S1 (A–F), red arrowheads denote a cluster of cells adjacent to the first pouch that undergo cellular rearrangements and form the long, anterior SY extension in wild-type animals. (G′–R′) show magnifications of HM-forming regions taken from (G–R) and correspond to areas within white boxes given in (G) and (L) for (G–L) and in (M) and (R) for (M–R). In wild-type development, hyoid crest cells adjacent to the first pouch remain a tightly packed mass as aHM chondrifies (e.g., cells denoted by red arrowheads in G′–L′). In integrinα5 mutants, the first pouch is missing (white arrow in [M]), and anterior hyoid crest cells are disorganized at 38 hpf (e.g., arrowhead in [M′]). Over time, anterior hyoid crest cells migrate out of the region and do not contribute to cartilage (e.g., arrowheads in [N′–Q′]). In contrast, the pHM region and the opercle bone develop normally from more posterior hyoid crest in integrinα5− animals (R). Scale bar: 50 μm. |
PMC493280_F1_173.jpg | What object or scene is depicted here? | The string-of-beads sign with alternating regions of lumen narrowing and vessel dilatation on angiogram of the ICA (arrows) in a 52-year-old woman sufferning from recurrent transient ischemic attacks. |
PMC493280_F2_174.jpg | What can you see in this picture? | The string-of-beads sign in the color Doppler image in a 51-year-old patient with low-grade stenosing FMD of the ICA. The patient suffered from migraine-like headache. |
PMC497042_F1_184.jpg | What is the dominant medical problem in this image? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_180.jpg | What key item or scene is captured in this photo? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_182.jpg | What is the principal component of this image? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_192.jpg | What stands out most in this visual? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_181.jpg | What key item or scene is captured in this photo? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_194.jpg | What stands out most in this visual? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_186.jpg | What does this image primarily show? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_188.jpg | What is the focal point of this photograph? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_193.jpg | What key item or scene is captured in this photo? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_191.jpg | What object or scene is depicted here? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_185.jpg | Can you identify the primary element in this image? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F1_183.jpg | What is being portrayed in this visual content? | Localization of chlamydial inclusions and caveolin-2 in HeLa cells. HeLa 229 cells were infected with chlamydial strains for 48 h. Cells were fixed and double stained with a rabbit anti-Chlamydia and a mouse anti-caveolin-2 antibody. Inclusions of C. pneumoniae (AR39) Cpn, C. Psittaci (guinea pig inclusion conjunctivitis, GPIC strain), C. trachomatis serovars A/Har-13, Har36B, C/TW-3, K, (E/VW-KX and F not shown), are seen to co-localize with caveolin-2. Inclusions of C. trachomatis Mouse pnuemonitis agent (MoPn) and Lymphogranuloma venereum biovar (LGV 434) [not shown] do not colocalize with caveolin-2. Scale bar represents 25 μm and original magnification: 600X |
PMC497042_F2_175.jpg | What is the core subject represented in this visual? | Optical Z-axis sections of caveolin-2 associated with chlamydial inclusion membranes. FRT cells were infected with C. trachomatis serovar K for 48 h. Cells were fixed with 10% cold methanol and double stained with a guinea pig anti-Chlamydia and a mouse anti-caveolin-2 antibody. The secondary antibodies were FITC-conjugated goat anti-mouse and TRITC-conjugated goat anti-guinea pig antibody. Slides were examined using a laser confocal microscope and optical Z-axis sections were taken at 0.5 μm depth and images merged using the Confocal Assistant™ version 4.02 Image Processing Software. Original magnification: 600X; the scale bar is 25 μm in length. |
PMC497042_F2_178.jpg | What is the dominant medical problem in this image? | Optical Z-axis sections of caveolin-2 associated with chlamydial inclusion membranes. FRT cells were infected with C. trachomatis serovar K for 48 h. Cells were fixed with 10% cold methanol and double stained with a guinea pig anti-Chlamydia and a mouse anti-caveolin-2 antibody. The secondary antibodies were FITC-conjugated goat anti-mouse and TRITC-conjugated goat anti-guinea pig antibody. Slides were examined using a laser confocal microscope and optical Z-axis sections were taken at 0.5 μm depth and images merged using the Confocal Assistant™ version 4.02 Image Processing Software. Original magnification: 600X; the scale bar is 25 μm in length. |
PMC497042_F2_177.jpg | Can you identify the primary element in this image? | Optical Z-axis sections of caveolin-2 associated with chlamydial inclusion membranes. FRT cells were infected with C. trachomatis serovar K for 48 h. Cells were fixed with 10% cold methanol and double stained with a guinea pig anti-Chlamydia and a mouse anti-caveolin-2 antibody. The secondary antibodies were FITC-conjugated goat anti-mouse and TRITC-conjugated goat anti-guinea pig antibody. Slides were examined using a laser confocal microscope and optical Z-axis sections were taken at 0.5 μm depth and images merged using the Confocal Assistant™ version 4.02 Image Processing Software. Original magnification: 600X; the scale bar is 25 μm in length. |
PMC497042_F2_176.jpg | What is the core subject represented in this visual? | Optical Z-axis sections of caveolin-2 associated with chlamydial inclusion membranes. FRT cells were infected with C. trachomatis serovar K for 48 h. Cells were fixed with 10% cold methanol and double stained with a guinea pig anti-Chlamydia and a mouse anti-caveolin-2 antibody. The secondary antibodies were FITC-conjugated goat anti-mouse and TRITC-conjugated goat anti-guinea pig antibody. Slides were examined using a laser confocal microscope and optical Z-axis sections were taken at 0.5 μm depth and images merged using the Confocal Assistant™ version 4.02 Image Processing Software. Original magnification: 600X; the scale bar is 25 μm in length. |
PMC497045_F1_200.jpg | What can you see in this picture? | Representative immunostaining of paraffin sections with antibodies against Topoisomerase 2A and Aquaporin 1. (A) Upper panel shows two TOP2A positive cores from GBMs; lower panel shows two negative cores on the same tissue micro-array. (B) Upper panel from left to right: cortex and white matter; lower panel from left to right: spinal cord and hypocampus. All stained with anti-TOP2A antibodies. (C – D) Paraffin section of GBM showing nuclear staining of TOP2A; D shows a higher magnification and E is the corresponding negative control with mouse IgG1 and no primary antibodies. (F – G) Paraffin section of GBM showing cytoplasmatic staining with anti-aquaporin 1 antibodies; G shows a higher magnification and H is the negative control. |
PMC497045_F1_199.jpg | What can you see in this picture? | Representative immunostaining of paraffin sections with antibodies against Topoisomerase 2A and Aquaporin 1. (A) Upper panel shows two TOP2A positive cores from GBMs; lower panel shows two negative cores on the same tissue micro-array. (B) Upper panel from left to right: cortex and white matter; lower panel from left to right: spinal cord and hypocampus. All stained with anti-TOP2A antibodies. (C – D) Paraffin section of GBM showing nuclear staining of TOP2A; D shows a higher magnification and E is the corresponding negative control with mouse IgG1 and no primary antibodies. (F – G) Paraffin section of GBM showing cytoplasmatic staining with anti-aquaporin 1 antibodies; G shows a higher magnification and H is the negative control. |
PMC497045_F1_201.jpg | What is the main focus of this visual representation? | Representative immunostaining of paraffin sections with antibodies against Topoisomerase 2A and Aquaporin 1. (A) Upper panel shows two TOP2A positive cores from GBMs; lower panel shows two negative cores on the same tissue micro-array. (B) Upper panel from left to right: cortex and white matter; lower panel from left to right: spinal cord and hypocampus. All stained with anti-TOP2A antibodies. (C – D) Paraffin section of GBM showing nuclear staining of TOP2A; D shows a higher magnification and E is the corresponding negative control with mouse IgG1 and no primary antibodies. (F – G) Paraffin section of GBM showing cytoplasmatic staining with anti-aquaporin 1 antibodies; G shows a higher magnification and H is the negative control. |
PMC497045_F1_197.jpg | What does this image primarily show? | Representative immunostaining of paraffin sections with antibodies against Topoisomerase 2A and Aquaporin 1. (A) Upper panel shows two TOP2A positive cores from GBMs; lower panel shows two negative cores on the same tissue micro-array. (B) Upper panel from left to right: cortex and white matter; lower panel from left to right: spinal cord and hypocampus. All stained with anti-TOP2A antibodies. (C – D) Paraffin section of GBM showing nuclear staining of TOP2A; D shows a higher magnification and E is the corresponding negative control with mouse IgG1 and no primary antibodies. (F – G) Paraffin section of GBM showing cytoplasmatic staining with anti-aquaporin 1 antibodies; G shows a higher magnification and H is the negative control. |
PMC497045_F1_202.jpg | Can you identify the primary element in this image? | Representative immunostaining of paraffin sections with antibodies against Topoisomerase 2A and Aquaporin 1. (A) Upper panel shows two TOP2A positive cores from GBMs; lower panel shows two negative cores on the same tissue micro-array. (B) Upper panel from left to right: cortex and white matter; lower panel from left to right: spinal cord and hypocampus. All stained with anti-TOP2A antibodies. (C – D) Paraffin section of GBM showing nuclear staining of TOP2A; D shows a higher magnification and E is the corresponding negative control with mouse IgG1 and no primary antibodies. (F – G) Paraffin section of GBM showing cytoplasmatic staining with anti-aquaporin 1 antibodies; G shows a higher magnification and H is the negative control. |
PMC497045_F1_196.jpg | What is the core subject represented in this visual? | Representative immunostaining of paraffin sections with antibodies against Topoisomerase 2A and Aquaporin 1. (A) Upper panel shows two TOP2A positive cores from GBMs; lower panel shows two negative cores on the same tissue micro-array. (B) Upper panel from left to right: cortex and white matter; lower panel from left to right: spinal cord and hypocampus. All stained with anti-TOP2A antibodies. (C – D) Paraffin section of GBM showing nuclear staining of TOP2A; D shows a higher magnification and E is the corresponding negative control with mouse IgG1 and no primary antibodies. (F – G) Paraffin section of GBM showing cytoplasmatic staining with anti-aquaporin 1 antibodies; G shows a higher magnification and H is the negative control. |
PMC497045_F1_203.jpg | What is the dominant medical problem in this image? | Representative immunostaining of paraffin sections with antibodies against Topoisomerase 2A and Aquaporin 1. (A) Upper panel shows two TOP2A positive cores from GBMs; lower panel shows two negative cores on the same tissue micro-array. (B) Upper panel from left to right: cortex and white matter; lower panel from left to right: spinal cord and hypocampus. All stained with anti-TOP2A antibodies. (C – D) Paraffin section of GBM showing nuclear staining of TOP2A; D shows a higher magnification and E is the corresponding negative control with mouse IgG1 and no primary antibodies. (F – G) Paraffin section of GBM showing cytoplasmatic staining with anti-aquaporin 1 antibodies; G shows a higher magnification and H is the negative control. |
PMC497050_F1_204.jpg | Describe the main subject of this image. | Stored fluoroscopy following placement of the two Amplatzer septal occluders (ASOs). TEE – Transesophageal echocardiography probe. |
PMC497050_F2_206.jpg | What object or scene is depicted here? | Transesophageal echocardiography four-chamber image following deployment of the two Amplatzer septal occluders (ASO). LA – left atrium, LV – left ventricle, RA – right atrium, RV – right ventricle. |
PMC497050_F2_205.jpg | What does this image primarily show? | Transesophageal echocardiography four-chamber image following deployment of the two Amplatzer septal occluders (ASO). LA – left atrium, LV – left ventricle, RA – right atrium, RV – right ventricle. |
PMC499548_F1_210.jpg | What is the focal point of this photograph? | Anterior-posterior angiogram of right common carotid artery injection of a Papio anubis with a 6 Fr catheter in place both (A.) during vessel spasm on catheter, and (B.) 10 minutes after infusion of intraluminal verapamil (2 mg). Overlay images showing 6 Fr catheter position in CCA (gold) during spasm (C.) and after alleviation with verapamil (D.). Arrows (→) indicate tip of catheter. |
PMC499548_F1_208.jpg | What is shown in this image? | Anterior-posterior angiogram of right common carotid artery injection of a Papio anubis with a 6 Fr catheter in place both (A.) during vessel spasm on catheter, and (B.) 10 minutes after infusion of intraluminal verapamil (2 mg). Overlay images showing 6 Fr catheter position in CCA (gold) during spasm (C.) and after alleviation with verapamil (D.). Arrows (→) indicate tip of catheter. |
PMC503391_F4_211.jpg | What is the main focus of this visual representation? | Bowing of the median nerve. Ultrasound images of the median nerve in the distal upper arm (upper) with the shoulder girdle in neutral and (lower) protracted. Note substantial bowing with the shoulder girdle in the neutral compared to protracted position. Bar = 10 mm. |
PMC503391_F4_212.jpg | Can you identify the primary element in this image? | Bowing of the median nerve. Ultrasound images of the median nerve in the distal upper arm (upper) with the shoulder girdle in neutral and (lower) protracted. Note substantial bowing with the shoulder girdle in the neutral compared to protracted position. Bar = 10 mm. |
PMC509289_pbio-0020196-g001_216.jpg | What object or scene is depicted here? | Col Expression during Lymph Gland Ontogeny(A) Col expression in lymph gland precursors is first observed in two separate clusters of cells (black arrows) in the dorsal-most mesoderm of thoracic segments T2 and T3 at stage 11 (stages according to Campos-Ortega and Hartenstein [1997]). Col expression in the head region is ectodermal (parasegment 0) and related to its function in head segmentation (Crozatier et al. 1999).(B and C) The clusters of Col-expressing cells get closer between stage 12 and early stage 13 (B) before coalescing (C).(D and E) Col expression becomes progressively restricted to the posterior-most cells of the forming lymph glands (arrowhead) during stage 14, as shown by the partial overlap between Odd-skipped (Odd) and Col expression.(F and G) Enlarged view of lymph glands after completion of embryogenesis, stage 16. Col expression marks the prospective PSC (Lebestky et al. 2003) in a dorsal-posterior position (arrowheads).(H) Schematic representation of Col expression in the lymph glands and pericardial cells in stage 16 embryos.(I) A srp6G mutant embryo arrested at stage 13. Col is expressed in the presumptive lymph gland primordium (black arrow), although it is not possible to distinguish between high and low levels of expression. All embryos are oriented anterior to the left. (A–C), (G), and (I) are lateral views; (D–F) are dorsal views. (B), (C), and (E–G) are higher magnifications of the dorsal thoracic region. White arrows in (A) and (I) indicate Col expression in a developing dorsal muscle (Crozatier and Vincent 1999). |
PMC509289_pbio-0020196-g001_214.jpg | Can you identify the primary element in this image? | Col Expression during Lymph Gland Ontogeny(A) Col expression in lymph gland precursors is first observed in two separate clusters of cells (black arrows) in the dorsal-most mesoderm of thoracic segments T2 and T3 at stage 11 (stages according to Campos-Ortega and Hartenstein [1997]). Col expression in the head region is ectodermal (parasegment 0) and related to its function in head segmentation (Crozatier et al. 1999).(B and C) The clusters of Col-expressing cells get closer between stage 12 and early stage 13 (B) before coalescing (C).(D and E) Col expression becomes progressively restricted to the posterior-most cells of the forming lymph glands (arrowhead) during stage 14, as shown by the partial overlap between Odd-skipped (Odd) and Col expression.(F and G) Enlarged view of lymph glands after completion of embryogenesis, stage 16. Col expression marks the prospective PSC (Lebestky et al. 2003) in a dorsal-posterior position (arrowheads).(H) Schematic representation of Col expression in the lymph glands and pericardial cells in stage 16 embryos.(I) A srp6G mutant embryo arrested at stage 13. Col is expressed in the presumptive lymph gland primordium (black arrow), although it is not possible to distinguish between high and low levels of expression. All embryos are oriented anterior to the left. (A–C), (G), and (I) are lateral views; (D–F) are dorsal views. (B), (C), and (E–G) are higher magnifications of the dorsal thoracic region. White arrows in (A) and (I) indicate Col expression in a developing dorsal muscle (Crozatier and Vincent 1999). |
PMC509289_pbio-0020196-g001_222.jpg | Describe the main subject of this image. | Col Expression during Lymph Gland Ontogeny(A) Col expression in lymph gland precursors is first observed in two separate clusters of cells (black arrows) in the dorsal-most mesoderm of thoracic segments T2 and T3 at stage 11 (stages according to Campos-Ortega and Hartenstein [1997]). Col expression in the head region is ectodermal (parasegment 0) and related to its function in head segmentation (Crozatier et al. 1999).(B and C) The clusters of Col-expressing cells get closer between stage 12 and early stage 13 (B) before coalescing (C).(D and E) Col expression becomes progressively restricted to the posterior-most cells of the forming lymph glands (arrowhead) during stage 14, as shown by the partial overlap between Odd-skipped (Odd) and Col expression.(F and G) Enlarged view of lymph glands after completion of embryogenesis, stage 16. Col expression marks the prospective PSC (Lebestky et al. 2003) in a dorsal-posterior position (arrowheads).(H) Schematic representation of Col expression in the lymph glands and pericardial cells in stage 16 embryos.(I) A srp6G mutant embryo arrested at stage 13. Col is expressed in the presumptive lymph gland primordium (black arrow), although it is not possible to distinguish between high and low levels of expression. All embryos are oriented anterior to the left. (A–C), (G), and (I) are lateral views; (D–F) are dorsal views. (B), (C), and (E–G) are higher magnifications of the dorsal thoracic region. White arrows in (A) and (I) indicate Col expression in a developing dorsal muscle (Crozatier and Vincent 1999). |
PMC509289_pbio-0020196-g001_220.jpg | What is shown in this image? | Col Expression during Lymph Gland Ontogeny(A) Col expression in lymph gland precursors is first observed in two separate clusters of cells (black arrows) in the dorsal-most mesoderm of thoracic segments T2 and T3 at stage 11 (stages according to Campos-Ortega and Hartenstein [1997]). Col expression in the head region is ectodermal (parasegment 0) and related to its function in head segmentation (Crozatier et al. 1999).(B and C) The clusters of Col-expressing cells get closer between stage 12 and early stage 13 (B) before coalescing (C).(D and E) Col expression becomes progressively restricted to the posterior-most cells of the forming lymph glands (arrowhead) during stage 14, as shown by the partial overlap between Odd-skipped (Odd) and Col expression.(F and G) Enlarged view of lymph glands after completion of embryogenesis, stage 16. Col expression marks the prospective PSC (Lebestky et al. 2003) in a dorsal-posterior position (arrowheads).(H) Schematic representation of Col expression in the lymph glands and pericardial cells in stage 16 embryos.(I) A srp6G mutant embryo arrested at stage 13. Col is expressed in the presumptive lymph gland primordium (black arrow), although it is not possible to distinguish between high and low levels of expression. All embryos are oriented anterior to the left. (A–C), (G), and (I) are lateral views; (D–F) are dorsal views. (B), (C), and (E–G) are higher magnifications of the dorsal thoracic region. White arrows in (A) and (I) indicate Col expression in a developing dorsal muscle (Crozatier and Vincent 1999). |
PMC509289_pbio-0020196-g001_219.jpg | Can you identify the primary element in this image? | Col Expression during Lymph Gland Ontogeny(A) Col expression in lymph gland precursors is first observed in two separate clusters of cells (black arrows) in the dorsal-most mesoderm of thoracic segments T2 and T3 at stage 11 (stages according to Campos-Ortega and Hartenstein [1997]). Col expression in the head region is ectodermal (parasegment 0) and related to its function in head segmentation (Crozatier et al. 1999).(B and C) The clusters of Col-expressing cells get closer between stage 12 and early stage 13 (B) before coalescing (C).(D and E) Col expression becomes progressively restricted to the posterior-most cells of the forming lymph glands (arrowhead) during stage 14, as shown by the partial overlap between Odd-skipped (Odd) and Col expression.(F and G) Enlarged view of lymph glands after completion of embryogenesis, stage 16. Col expression marks the prospective PSC (Lebestky et al. 2003) in a dorsal-posterior position (arrowheads).(H) Schematic representation of Col expression in the lymph glands and pericardial cells in stage 16 embryos.(I) A srp6G mutant embryo arrested at stage 13. Col is expressed in the presumptive lymph gland primordium (black arrow), although it is not possible to distinguish between high and low levels of expression. All embryos are oriented anterior to the left. (A–C), (G), and (I) are lateral views; (D–F) are dorsal views. (B), (C), and (E–G) are higher magnifications of the dorsal thoracic region. White arrows in (A) and (I) indicate Col expression in a developing dorsal muscle (Crozatier and Vincent 1999). |
PMC509289_pbio-0020196-g001_218.jpg | What does this image primarily show? | Col Expression during Lymph Gland Ontogeny(A) Col expression in lymph gland precursors is first observed in two separate clusters of cells (black arrows) in the dorsal-most mesoderm of thoracic segments T2 and T3 at stage 11 (stages according to Campos-Ortega and Hartenstein [1997]). Col expression in the head region is ectodermal (parasegment 0) and related to its function in head segmentation (Crozatier et al. 1999).(B and C) The clusters of Col-expressing cells get closer between stage 12 and early stage 13 (B) before coalescing (C).(D and E) Col expression becomes progressively restricted to the posterior-most cells of the forming lymph glands (arrowhead) during stage 14, as shown by the partial overlap between Odd-skipped (Odd) and Col expression.(F and G) Enlarged view of lymph glands after completion of embryogenesis, stage 16. Col expression marks the prospective PSC (Lebestky et al. 2003) in a dorsal-posterior position (arrowheads).(H) Schematic representation of Col expression in the lymph glands and pericardial cells in stage 16 embryos.(I) A srp6G mutant embryo arrested at stage 13. Col is expressed in the presumptive lymph gland primordium (black arrow), although it is not possible to distinguish between high and low levels of expression. All embryos are oriented anterior to the left. (A–C), (G), and (I) are lateral views; (D–F) are dorsal views. (B), (C), and (E–G) are higher magnifications of the dorsal thoracic region. White arrows in (A) and (I) indicate Col expression in a developing dorsal muscle (Crozatier and Vincent 1999). |
PMC509289_pbio-0020196-g005_228.jpg | What object or scene is depicted here? | Col-Expressing Cells Play an Instructive Role in Lamellocyte ProductionExpression of the crystal cell marker doxA3 (Waltzer et al. 2003) (A, B, and G); of the lamellocyte markers α-ps4 (M. Meister, unpublished data) (C–F and H) and L1 (Asha et al. 2003) (J); and of Col (I and J); in wt (A, C, and E), col loss-of-function mutant (B, D, and F), and srp-Gal4/UAS-col (G–J) larvae. In (E) and (F), larvae were taken 48 h after infestation. An increased number of doxA3-positive cells (B) parallels the absence of lamellocyte differentiation (F) in col1 mutant lymph glands. Conversely, lamellocyte differentiation and a reduced number of doxA3-positive cells are observed upon enforced Col expression (G and H). Double staining for Col and L1 shows that Col-expressing cells and differentiating lamellocytes do not overlap in the lymph gland. (I) shows ectopic Col expression compared to expression in the PSC (arrowhead; not visible in [J]). Antibody and in situ probes are indicated on each panel. In all panels, larvae are oriented with the head to the left: a single primary lobe is shown, with sometimes a few secondary lobes. Bar: 50 μm. |
PMC509289_pbio-0020196-g005_230.jpg | Can you identify the primary element in this image? | Col-Expressing Cells Play an Instructive Role in Lamellocyte ProductionExpression of the crystal cell marker doxA3 (Waltzer et al. 2003) (A, B, and G); of the lamellocyte markers α-ps4 (M. Meister, unpublished data) (C–F and H) and L1 (Asha et al. 2003) (J); and of Col (I and J); in wt (A, C, and E), col loss-of-function mutant (B, D, and F), and srp-Gal4/UAS-col (G–J) larvae. In (E) and (F), larvae were taken 48 h after infestation. An increased number of doxA3-positive cells (B) parallels the absence of lamellocyte differentiation (F) in col1 mutant lymph glands. Conversely, lamellocyte differentiation and a reduced number of doxA3-positive cells are observed upon enforced Col expression (G and H). Double staining for Col and L1 shows that Col-expressing cells and differentiating lamellocytes do not overlap in the lymph gland. (I) shows ectopic Col expression compared to expression in the PSC (arrowhead; not visible in [J]). Antibody and in situ probes are indicated on each panel. In all panels, larvae are oriented with the head to the left: a single primary lobe is shown, with sometimes a few secondary lobes. Bar: 50 μm. |
PMC509289_pbio-0020196-g005_223.jpg | What is the central feature of this picture? | Col-Expressing Cells Play an Instructive Role in Lamellocyte ProductionExpression of the crystal cell marker doxA3 (Waltzer et al. 2003) (A, B, and G); of the lamellocyte markers α-ps4 (M. Meister, unpublished data) (C–F and H) and L1 (Asha et al. 2003) (J); and of Col (I and J); in wt (A, C, and E), col loss-of-function mutant (B, D, and F), and srp-Gal4/UAS-col (G–J) larvae. In (E) and (F), larvae were taken 48 h after infestation. An increased number of doxA3-positive cells (B) parallels the absence of lamellocyte differentiation (F) in col1 mutant lymph glands. Conversely, lamellocyte differentiation and a reduced number of doxA3-positive cells are observed upon enforced Col expression (G and H). Double staining for Col and L1 shows that Col-expressing cells and differentiating lamellocytes do not overlap in the lymph gland. (I) shows ectopic Col expression compared to expression in the PSC (arrowhead; not visible in [J]). Antibody and in situ probes are indicated on each panel. In all panels, larvae are oriented with the head to the left: a single primary lobe is shown, with sometimes a few secondary lobes. Bar: 50 μm. |
PMC509289_pbio-0020196-g005_226.jpg | What is shown in this image? | Col-Expressing Cells Play an Instructive Role in Lamellocyte ProductionExpression of the crystal cell marker doxA3 (Waltzer et al. 2003) (A, B, and G); of the lamellocyte markers α-ps4 (M. Meister, unpublished data) (C–F and H) and L1 (Asha et al. 2003) (J); and of Col (I and J); in wt (A, C, and E), col loss-of-function mutant (B, D, and F), and srp-Gal4/UAS-col (G–J) larvae. In (E) and (F), larvae were taken 48 h after infestation. An increased number of doxA3-positive cells (B) parallels the absence of lamellocyte differentiation (F) in col1 mutant lymph glands. Conversely, lamellocyte differentiation and a reduced number of doxA3-positive cells are observed upon enforced Col expression (G and H). Double staining for Col and L1 shows that Col-expressing cells and differentiating lamellocytes do not overlap in the lymph gland. (I) shows ectopic Col expression compared to expression in the PSC (arrowhead; not visible in [J]). Antibody and in situ probes are indicated on each panel. In all panels, larvae are oriented with the head to the left: a single primary lobe is shown, with sometimes a few secondary lobes. Bar: 50 μm. |
PMC509289_pbio-0020196-g005_227.jpg | What is the focal point of this photograph? | Col-Expressing Cells Play an Instructive Role in Lamellocyte ProductionExpression of the crystal cell marker doxA3 (Waltzer et al. 2003) (A, B, and G); of the lamellocyte markers α-ps4 (M. Meister, unpublished data) (C–F and H) and L1 (Asha et al. 2003) (J); and of Col (I and J); in wt (A, C, and E), col loss-of-function mutant (B, D, and F), and srp-Gal4/UAS-col (G–J) larvae. In (E) and (F), larvae were taken 48 h after infestation. An increased number of doxA3-positive cells (B) parallels the absence of lamellocyte differentiation (F) in col1 mutant lymph glands. Conversely, lamellocyte differentiation and a reduced number of doxA3-positive cells are observed upon enforced Col expression (G and H). Double staining for Col and L1 shows that Col-expressing cells and differentiating lamellocytes do not overlap in the lymph gland. (I) shows ectopic Col expression compared to expression in the PSC (arrowhead; not visible in [J]). Antibody and in situ probes are indicated on each panel. In all panels, larvae are oriented with the head to the left: a single primary lobe is shown, with sometimes a few secondary lobes. Bar: 50 μm. |
PMC509289_pbio-0020196-g005_225.jpg | What object or scene is depicted here? | Col-Expressing Cells Play an Instructive Role in Lamellocyte ProductionExpression of the crystal cell marker doxA3 (Waltzer et al. 2003) (A, B, and G); of the lamellocyte markers α-ps4 (M. Meister, unpublished data) (C–F and H) and L1 (Asha et al. 2003) (J); and of Col (I and J); in wt (A, C, and E), col loss-of-function mutant (B, D, and F), and srp-Gal4/UAS-col (G–J) larvae. In (E) and (F), larvae were taken 48 h after infestation. An increased number of doxA3-positive cells (B) parallels the absence of lamellocyte differentiation (F) in col1 mutant lymph glands. Conversely, lamellocyte differentiation and a reduced number of doxA3-positive cells are observed upon enforced Col expression (G and H). Double staining for Col and L1 shows that Col-expressing cells and differentiating lamellocytes do not overlap in the lymph gland. (I) shows ectopic Col expression compared to expression in the PSC (arrowhead; not visible in [J]). Antibody and in situ probes are indicated on each panel. In all panels, larvae are oriented with the head to the left: a single primary lobe is shown, with sometimes a few secondary lobes. Bar: 50 μm. |
PMC509289_pbio-0020196-g005_224.jpg | What is being portrayed in this visual content? | Col-Expressing Cells Play an Instructive Role in Lamellocyte ProductionExpression of the crystal cell marker doxA3 (Waltzer et al. 2003) (A, B, and G); of the lamellocyte markers α-ps4 (M. Meister, unpublished data) (C–F and H) and L1 (Asha et al. 2003) (J); and of Col (I and J); in wt (A, C, and E), col loss-of-function mutant (B, D, and F), and srp-Gal4/UAS-col (G–J) larvae. In (E) and (F), larvae were taken 48 h after infestation. An increased number of doxA3-positive cells (B) parallels the absence of lamellocyte differentiation (F) in col1 mutant lymph glands. Conversely, lamellocyte differentiation and a reduced number of doxA3-positive cells are observed upon enforced Col expression (G and H). Double staining for Col and L1 shows that Col-expressing cells and differentiating lamellocytes do not overlap in the lymph gland. (I) shows ectopic Col expression compared to expression in the PSC (arrowhead; not visible in [J]). Antibody and in situ probes are indicated on each panel. In all panels, larvae are oriented with the head to the left: a single primary lobe is shown, with sometimes a few secondary lobes. Bar: 50 μm. |
PMC509293_pbio-0020218-g003_248.jpg | What is the main focus of this visual representation? | Plasticity of Isolated Myofibers(A) Phase-contrast micrograph of a live cell at 3 d after plating, showing a lobulated structure in the middle of the fiber.(B) Micrograph of a live fiber at 2 d after plating, showing budding of nuclei at one end. The cell has been counterstained with Syto 13.(C) Fluorescence micrograph of a myofiber at 24 h after microinjection with TR–dextran. The cell has been counterstained with Syto 13 dye to show the nuclei.(D) Fluorescence micrograph of a colony formed from a single myofiber injected 24 h earlier with TR–dextran. The cell has flattened on the substrate and the nuclei are stained with Syto 13 dye.(E) Fluorescence micrograph of a colony formed from the progeny of several myofibers in proximity that were injected 5 d earlier with TR–dextran.(F) Analysis of the DNA content of cells derived from myofibers injected 5 d earlier with TR–dextran. The DNA content was determined by image analysis of the nuclei of mononucleate TR-positive cells that had been stained with Hoechst (see Materials and Methods). The green arrow is the value for G0 nuclei in quiescent myofibers, while the blue arrow is the G2/M value determined for mononucleate cells with anti-phosphohistone H3. The red arrow is the G1 value determined for mononucleate cells.(G) Photomicrograph of a live myofiber, 48 h after plating, showing a binucleate bud formed at the end. The cell was stained as for (B).(H) Fluorescence micrograph of a bud containing three nuclei stained with Syto13 (yellow) derived from a myofiber that contained at least five nuclei and that was injected with TR–dextran (red).Scale bars: (B), (C), and (G), 100 μm; (A), (E), and (H), 50 μm; and (D), 10 μm. |
PMC509293_pbio-0020218-g003_246.jpg | What is the focal point of this photograph? | Plasticity of Isolated Myofibers(A) Phase-contrast micrograph of a live cell at 3 d after plating, showing a lobulated structure in the middle of the fiber.(B) Micrograph of a live fiber at 2 d after plating, showing budding of nuclei at one end. The cell has been counterstained with Syto 13.(C) Fluorescence micrograph of a myofiber at 24 h after microinjection with TR–dextran. The cell has been counterstained with Syto 13 dye to show the nuclei.(D) Fluorescence micrograph of a colony formed from a single myofiber injected 24 h earlier with TR–dextran. The cell has flattened on the substrate and the nuclei are stained with Syto 13 dye.(E) Fluorescence micrograph of a colony formed from the progeny of several myofibers in proximity that were injected 5 d earlier with TR–dextran.(F) Analysis of the DNA content of cells derived from myofibers injected 5 d earlier with TR–dextran. The DNA content was determined by image analysis of the nuclei of mononucleate TR-positive cells that had been stained with Hoechst (see Materials and Methods). The green arrow is the value for G0 nuclei in quiescent myofibers, while the blue arrow is the G2/M value determined for mononucleate cells with anti-phosphohistone H3. The red arrow is the G1 value determined for mononucleate cells.(G) Photomicrograph of a live myofiber, 48 h after plating, showing a binucleate bud formed at the end. The cell was stained as for (B).(H) Fluorescence micrograph of a bud containing three nuclei stained with Syto13 (yellow) derived from a myofiber that contained at least five nuclei and that was injected with TR–dextran (red).Scale bars: (B), (C), and (G), 100 μm; (A), (E), and (H), 50 μm; and (D), 10 μm. |
PMC509293_pbio-0020218-g003_247.jpg | What is the core subject represented in this visual? | Plasticity of Isolated Myofibers(A) Phase-contrast micrograph of a live cell at 3 d after plating, showing a lobulated structure in the middle of the fiber.(B) Micrograph of a live fiber at 2 d after plating, showing budding of nuclei at one end. The cell has been counterstained with Syto 13.(C) Fluorescence micrograph of a myofiber at 24 h after microinjection with TR–dextran. The cell has been counterstained with Syto 13 dye to show the nuclei.(D) Fluorescence micrograph of a colony formed from a single myofiber injected 24 h earlier with TR–dextran. The cell has flattened on the substrate and the nuclei are stained with Syto 13 dye.(E) Fluorescence micrograph of a colony formed from the progeny of several myofibers in proximity that were injected 5 d earlier with TR–dextran.(F) Analysis of the DNA content of cells derived from myofibers injected 5 d earlier with TR–dextran. The DNA content was determined by image analysis of the nuclei of mononucleate TR-positive cells that had been stained with Hoechst (see Materials and Methods). The green arrow is the value for G0 nuclei in quiescent myofibers, while the blue arrow is the G2/M value determined for mononucleate cells with anti-phosphohistone H3. The red arrow is the G1 value determined for mononucleate cells.(G) Photomicrograph of a live myofiber, 48 h after plating, showing a binucleate bud formed at the end. The cell was stained as for (B).(H) Fluorescence micrograph of a bud containing three nuclei stained with Syto13 (yellow) derived from a myofiber that contained at least five nuclei and that was injected with TR–dextran (red).Scale bars: (B), (C), and (G), 100 μm; (A), (E), and (H), 50 μm; and (D), 10 μm. |
PMC509293_pbio-0020218-g003_243.jpg | What is shown in this image? | Plasticity of Isolated Myofibers(A) Phase-contrast micrograph of a live cell at 3 d after plating, showing a lobulated structure in the middle of the fiber.(B) Micrograph of a live fiber at 2 d after plating, showing budding of nuclei at one end. The cell has been counterstained with Syto 13.(C) Fluorescence micrograph of a myofiber at 24 h after microinjection with TR–dextran. The cell has been counterstained with Syto 13 dye to show the nuclei.(D) Fluorescence micrograph of a colony formed from a single myofiber injected 24 h earlier with TR–dextran. The cell has flattened on the substrate and the nuclei are stained with Syto 13 dye.(E) Fluorescence micrograph of a colony formed from the progeny of several myofibers in proximity that were injected 5 d earlier with TR–dextran.(F) Analysis of the DNA content of cells derived from myofibers injected 5 d earlier with TR–dextran. The DNA content was determined by image analysis of the nuclei of mononucleate TR-positive cells that had been stained with Hoechst (see Materials and Methods). The green arrow is the value for G0 nuclei in quiescent myofibers, while the blue arrow is the G2/M value determined for mononucleate cells with anti-phosphohistone H3. The red arrow is the G1 value determined for mononucleate cells.(G) Photomicrograph of a live myofiber, 48 h after plating, showing a binucleate bud formed at the end. The cell was stained as for (B).(H) Fluorescence micrograph of a bud containing three nuclei stained with Syto13 (yellow) derived from a myofiber that contained at least five nuclei and that was injected with TR–dextran (red).Scale bars: (B), (C), and (G), 100 μm; (A), (E), and (H), 50 μm; and (D), 10 μm. |
PMC509293_pbio-0020218-g003_245.jpg | What stands out most in this visual? | Plasticity of Isolated Myofibers(A) Phase-contrast micrograph of a live cell at 3 d after plating, showing a lobulated structure in the middle of the fiber.(B) Micrograph of a live fiber at 2 d after plating, showing budding of nuclei at one end. The cell has been counterstained with Syto 13.(C) Fluorescence micrograph of a myofiber at 24 h after microinjection with TR–dextran. The cell has been counterstained with Syto 13 dye to show the nuclei.(D) Fluorescence micrograph of a colony formed from a single myofiber injected 24 h earlier with TR–dextran. The cell has flattened on the substrate and the nuclei are stained with Syto 13 dye.(E) Fluorescence micrograph of a colony formed from the progeny of several myofibers in proximity that were injected 5 d earlier with TR–dextran.(F) Analysis of the DNA content of cells derived from myofibers injected 5 d earlier with TR–dextran. The DNA content was determined by image analysis of the nuclei of mononucleate TR-positive cells that had been stained with Hoechst (see Materials and Methods). The green arrow is the value for G0 nuclei in quiescent myofibers, while the blue arrow is the G2/M value determined for mononucleate cells with anti-phosphohistone H3. The red arrow is the G1 value determined for mononucleate cells.(G) Photomicrograph of a live myofiber, 48 h after plating, showing a binucleate bud formed at the end. The cell was stained as for (B).(H) Fluorescence micrograph of a bud containing three nuclei stained with Syto13 (yellow) derived from a myofiber that contained at least five nuclei and that was injected with TR–dextran (red).Scale bars: (B), (C), and (G), 100 μm; (A), (E), and (H), 50 μm; and (D), 10 μm. |
PMC509293_pbio-0020218-g004_236.jpg | What is the principal component of this image? | Analysis of Nuclear Migration and Fragmentation by Time-Lapse Microscopy(A) Single frames illustrating the migration of three nuclei (yellow arrows) along a myofiber, of which two are incorporated into a terminal aggregate by 11.4 h. One nucleus (green arrow) remained stationary during this period.(B) Single frames illustrating the production of viable multinucleate fragments from a myofiber. Note the presence of a trinucleate aggregate (arrowed green) that separates after lateral breakage of the fiber (0 min, arrowed yellow). This fragment subsequently extends cytoplasmic processes (14.3 and 15.4 h) and migrates over the culture substratum.Series (A) and (B) begin at 6 h after plating. Scale bars: (A) 50 μm; (B) 200 μm. |
PMC509293_pbio-0020218-g004_238.jpg | What's the most prominent thing you notice in this picture? | Analysis of Nuclear Migration and Fragmentation by Time-Lapse Microscopy(A) Single frames illustrating the migration of three nuclei (yellow arrows) along a myofiber, of which two are incorporated into a terminal aggregate by 11.4 h. One nucleus (green arrow) remained stationary during this period.(B) Single frames illustrating the production of viable multinucleate fragments from a myofiber. Note the presence of a trinucleate aggregate (arrowed green) that separates after lateral breakage of the fiber (0 min, arrowed yellow). This fragment subsequently extends cytoplasmic processes (14.3 and 15.4 h) and migrates over the culture substratum.Series (A) and (B) begin at 6 h after plating. Scale bars: (A) 50 μm; (B) 200 μm. |
PMC509293_pbio-0020218-g004_232.jpg | What is the focal point of this photograph? | Analysis of Nuclear Migration and Fragmentation by Time-Lapse Microscopy(A) Single frames illustrating the migration of three nuclei (yellow arrows) along a myofiber, of which two are incorporated into a terminal aggregate by 11.4 h. One nucleus (green arrow) remained stationary during this period.(B) Single frames illustrating the production of viable multinucleate fragments from a myofiber. Note the presence of a trinucleate aggregate (arrowed green) that separates after lateral breakage of the fiber (0 min, arrowed yellow). This fragment subsequently extends cytoplasmic processes (14.3 and 15.4 h) and migrates over the culture substratum.Series (A) and (B) begin at 6 h after plating. Scale bars: (A) 50 μm; (B) 200 μm. |
PMC509293_pbio-0020218-g004_242.jpg | What's the most prominent thing you notice in this picture? | Analysis of Nuclear Migration and Fragmentation by Time-Lapse Microscopy(A) Single frames illustrating the migration of three nuclei (yellow arrows) along a myofiber, of which two are incorporated into a terminal aggregate by 11.4 h. One nucleus (green arrow) remained stationary during this period.(B) Single frames illustrating the production of viable multinucleate fragments from a myofiber. Note the presence of a trinucleate aggregate (arrowed green) that separates after lateral breakage of the fiber (0 min, arrowed yellow). This fragment subsequently extends cytoplasmic processes (14.3 and 15.4 h) and migrates over the culture substratum.Series (A) and (B) begin at 6 h after plating. Scale bars: (A) 50 μm; (B) 200 μm. |
PMC509293_pbio-0020218-g004_233.jpg | What is the core subject represented in this visual? | Analysis of Nuclear Migration and Fragmentation by Time-Lapse Microscopy(A) Single frames illustrating the migration of three nuclei (yellow arrows) along a myofiber, of which two are incorporated into a terminal aggregate by 11.4 h. One nucleus (green arrow) remained stationary during this period.(B) Single frames illustrating the production of viable multinucleate fragments from a myofiber. Note the presence of a trinucleate aggregate (arrowed green) that separates after lateral breakage of the fiber (0 min, arrowed yellow). This fragment subsequently extends cytoplasmic processes (14.3 and 15.4 h) and migrates over the culture substratum.Series (A) and (B) begin at 6 h after plating. Scale bars: (A) 50 μm; (B) 200 μm. |
PMC509293_pbio-0020218-g004_241.jpg | What is the central feature of this picture? | Analysis of Nuclear Migration and Fragmentation by Time-Lapse Microscopy(A) Single frames illustrating the migration of three nuclei (yellow arrows) along a myofiber, of which two are incorporated into a terminal aggregate by 11.4 h. One nucleus (green arrow) remained stationary during this period.(B) Single frames illustrating the production of viable multinucleate fragments from a myofiber. Note the presence of a trinucleate aggregate (arrowed green) that separates after lateral breakage of the fiber (0 min, arrowed yellow). This fragment subsequently extends cytoplasmic processes (14.3 and 15.4 h) and migrates over the culture substratum.Series (A) and (B) begin at 6 h after plating. Scale bars: (A) 50 μm; (B) 200 μm. |
PMC509293_pbio-0020218-g004_237.jpg | What does this image primarily show? | Analysis of Nuclear Migration and Fragmentation by Time-Lapse Microscopy(A) Single frames illustrating the migration of three nuclei (yellow arrows) along a myofiber, of which two are incorporated into a terminal aggregate by 11.4 h. One nucleus (green arrow) remained stationary during this period.(B) Single frames illustrating the production of viable multinucleate fragments from a myofiber. Note the presence of a trinucleate aggregate (arrowed green) that separates after lateral breakage of the fiber (0 min, arrowed yellow). This fragment subsequently extends cytoplasmic processes (14.3 and 15.4 h) and migrates over the culture substratum.Series (A) and (B) begin at 6 h after plating. Scale bars: (A) 50 μm; (B) 200 μm. |
PMC509293_pbio-0020218-g004_234.jpg | Can you identify the primary element in this image? | Analysis of Nuclear Migration and Fragmentation by Time-Lapse Microscopy(A) Single frames illustrating the migration of three nuclei (yellow arrows) along a myofiber, of which two are incorporated into a terminal aggregate by 11.4 h. One nucleus (green arrow) remained stationary during this period.(B) Single frames illustrating the production of viable multinucleate fragments from a myofiber. Note the presence of a trinucleate aggregate (arrowed green) that separates after lateral breakage of the fiber (0 min, arrowed yellow). This fragment subsequently extends cytoplasmic processes (14.3 and 15.4 h) and migrates over the culture substratum.Series (A) and (B) begin at 6 h after plating. Scale bars: (A) 50 μm; (B) 200 μm. |
PMC509293_pbio-0020218-g004_240.jpg | What is shown in this image? | Analysis of Nuclear Migration and Fragmentation by Time-Lapse Microscopy(A) Single frames illustrating the migration of three nuclei (yellow arrows) along a myofiber, of which two are incorporated into a terminal aggregate by 11.4 h. One nucleus (green arrow) remained stationary during this period.(B) Single frames illustrating the production of viable multinucleate fragments from a myofiber. Note the presence of a trinucleate aggregate (arrowed green) that separates after lateral breakage of the fiber (0 min, arrowed yellow). This fragment subsequently extends cytoplasmic processes (14.3 and 15.4 h) and migrates over the culture substratum.Series (A) and (B) begin at 6 h after plating. Scale bars: (A) 50 μm; (B) 200 μm. |
PMC509297_pbio-0020225-g003_254.jpg | What is shown in this image? | Lesion AnalysisRepresentative photomicrographs of cresyl-violet-stained coronal brain sections taken from subjects belonging to each of the three lesion groups—partial hippocampal lesion (A), sham lesion (B), and complete hippocampal lesion (C). In each case, sections corresponding to anterior, middle, and posterior levels of the hippocampus are displayed. The mean area of spared hippocampal tissue in each group (see Materials and Methods for calculation) is plotted below in (D). Note that the volumes of spared tissue in the septal and temporal halves of the hippocampus are plotted separately, but these values are still expressed as percentages of the entire hippocampal volume—hence the value of 50% per half in shams. The cartoon hippocampi accompanying the graph indicate lesioned tissue in dark grey, and spared tissue in light cream. As intended, partially lesioned rats exhibited substantial sparing only in the septal (dorsal) half of the hippocampus, and rats with complete hippocampal lesions exhibited minimal sparing (less than 5% at either pole). |
PMC509297_pbio-0020225-g003_255.jpg | What is being portrayed in this visual content? | Lesion AnalysisRepresentative photomicrographs of cresyl-violet-stained coronal brain sections taken from subjects belonging to each of the three lesion groups—partial hippocampal lesion (A), sham lesion (B), and complete hippocampal lesion (C). In each case, sections corresponding to anterior, middle, and posterior levels of the hippocampus are displayed. The mean area of spared hippocampal tissue in each group (see Materials and Methods for calculation) is plotted below in (D). Note that the volumes of spared tissue in the septal and temporal halves of the hippocampus are plotted separately, but these values are still expressed as percentages of the entire hippocampal volume—hence the value of 50% per half in shams. The cartoon hippocampi accompanying the graph indicate lesioned tissue in dark grey, and spared tissue in light cream. As intended, partially lesioned rats exhibited substantial sparing only in the septal (dorsal) half of the hippocampus, and rats with complete hippocampal lesions exhibited minimal sparing (less than 5% at either pole). |
PMC509297_pbio-0020225-g003_253.jpg | What is the main focus of this visual representation? | Lesion AnalysisRepresentative photomicrographs of cresyl-violet-stained coronal brain sections taken from subjects belonging to each of the three lesion groups—partial hippocampal lesion (A), sham lesion (B), and complete hippocampal lesion (C). In each case, sections corresponding to anterior, middle, and posterior levels of the hippocampus are displayed. The mean area of spared hippocampal tissue in each group (see Materials and Methods for calculation) is plotted below in (D). Note that the volumes of spared tissue in the septal and temporal halves of the hippocampus are plotted separately, but these values are still expressed as percentages of the entire hippocampal volume—hence the value of 50% per half in shams. The cartoon hippocampi accompanying the graph indicate lesioned tissue in dark grey, and spared tissue in light cream. As intended, partially lesioned rats exhibited substantial sparing only in the septal (dorsal) half of the hippocampus, and rats with complete hippocampal lesions exhibited minimal sparing (less than 5% at either pole). |
PMC509297_pbio-0020225-g003_252.jpg | What can you see in this picture? | Lesion AnalysisRepresentative photomicrographs of cresyl-violet-stained coronal brain sections taken from subjects belonging to each of the three lesion groups—partial hippocampal lesion (A), sham lesion (B), and complete hippocampal lesion (C). In each case, sections corresponding to anterior, middle, and posterior levels of the hippocampus are displayed. The mean area of spared hippocampal tissue in each group (see Materials and Methods for calculation) is plotted below in (D). Note that the volumes of spared tissue in the septal and temporal halves of the hippocampus are plotted separately, but these values are still expressed as percentages of the entire hippocampal volume—hence the value of 50% per half in shams. The cartoon hippocampi accompanying the graph indicate lesioned tissue in dark grey, and spared tissue in light cream. As intended, partially lesioned rats exhibited substantial sparing only in the septal (dorsal) half of the hippocampus, and rats with complete hippocampal lesions exhibited minimal sparing (less than 5% at either pole). |
PMC509297_pbio-0020225-g003_258.jpg | What can you see in this picture? | Lesion AnalysisRepresentative photomicrographs of cresyl-violet-stained coronal brain sections taken from subjects belonging to each of the three lesion groups—partial hippocampal lesion (A), sham lesion (B), and complete hippocampal lesion (C). In each case, sections corresponding to anterior, middle, and posterior levels of the hippocampus are displayed. The mean area of spared hippocampal tissue in each group (see Materials and Methods for calculation) is plotted below in (D). Note that the volumes of spared tissue in the septal and temporal halves of the hippocampus are plotted separately, but these values are still expressed as percentages of the entire hippocampal volume—hence the value of 50% per half in shams. The cartoon hippocampi accompanying the graph indicate lesioned tissue in dark grey, and spared tissue in light cream. As intended, partially lesioned rats exhibited substantial sparing only in the septal (dorsal) half of the hippocampus, and rats with complete hippocampal lesions exhibited minimal sparing (less than 5% at either pole). |
PMC509297_pbio-0020225-g003_250.jpg | What is being portrayed in this visual content? | Lesion AnalysisRepresentative photomicrographs of cresyl-violet-stained coronal brain sections taken from subjects belonging to each of the three lesion groups—partial hippocampal lesion (A), sham lesion (B), and complete hippocampal lesion (C). In each case, sections corresponding to anterior, middle, and posterior levels of the hippocampus are displayed. The mean area of spared hippocampal tissue in each group (see Materials and Methods for calculation) is plotted below in (D). Note that the volumes of spared tissue in the septal and temporal halves of the hippocampus are plotted separately, but these values are still expressed as percentages of the entire hippocampal volume—hence the value of 50% per half in shams. The cartoon hippocampi accompanying the graph indicate lesioned tissue in dark grey, and spared tissue in light cream. As intended, partially lesioned rats exhibited substantial sparing only in the septal (dorsal) half of the hippocampus, and rats with complete hippocampal lesions exhibited minimal sparing (less than 5% at either pole). |
PMC509297_pbio-0020225-g003_251.jpg | What is the central feature of this picture? | Lesion AnalysisRepresentative photomicrographs of cresyl-violet-stained coronal brain sections taken from subjects belonging to each of the three lesion groups—partial hippocampal lesion (A), sham lesion (B), and complete hippocampal lesion (C). In each case, sections corresponding to anterior, middle, and posterior levels of the hippocampus are displayed. The mean area of spared hippocampal tissue in each group (see Materials and Methods for calculation) is plotted below in (D). Note that the volumes of spared tissue in the septal and temporal halves of the hippocampus are plotted separately, but these values are still expressed as percentages of the entire hippocampal volume—hence the value of 50% per half in shams. The cartoon hippocampi accompanying the graph indicate lesioned tissue in dark grey, and spared tissue in light cream. As intended, partially lesioned rats exhibited substantial sparing only in the septal (dorsal) half of the hippocampus, and rats with complete hippocampal lesions exhibited minimal sparing (less than 5% at either pole). |
PMC509304_pbio-0020242-g002_260.jpg | Describe the main subject of this image. | Metastasis of Primary SCC to Lymph Nodes and Lungs in p19 Arf-Deficient Mice(A) Underside of skin from tumor-bearing mouse shows newly formed blood vessels surrounding tumor site (arrow) and leading to inguinal lymph node (arrowhead).(B) Enlarged inquinal lymph node (left) containing metastatic SCC and blood vessel formation (arrow) compared to normal lymph node (right).(C) H&E stain of carcinoma section with prominent blood vessel (bv). Carcinoma cells (ca) have penetrated blood vessel wall (arrow).(D) H&E stain of lymph node bearing infiltrating SCC cells (arrow) among normal lymphocytes (arrowhead).(E) H&E stain of lymph node bearing metastatic differentiated SCC.(F) Immunostain with pan-keratin antibody of papilloma.(G) Immunostain with pan-keratin antibody of lymph node with metastatic SCC.(H and I) H&E stain of normal lung (arrowhead) with large metastatic SCC deposit (arrow).(J) H&E stain of lung metastasis with secondary site of infiltration (arrow).(D–G, J): 20× magnification. Inserts in (E–G): 40× magnification. |
PMC509304_pbio-0020242-g002_269.jpg | What does this image primarily show? | Metastasis of Primary SCC to Lymph Nodes and Lungs in p19 Arf-Deficient Mice(A) Underside of skin from tumor-bearing mouse shows newly formed blood vessels surrounding tumor site (arrow) and leading to inguinal lymph node (arrowhead).(B) Enlarged inquinal lymph node (left) containing metastatic SCC and blood vessel formation (arrow) compared to normal lymph node (right).(C) H&E stain of carcinoma section with prominent blood vessel (bv). Carcinoma cells (ca) have penetrated blood vessel wall (arrow).(D) H&E stain of lymph node bearing infiltrating SCC cells (arrow) among normal lymphocytes (arrowhead).(E) H&E stain of lymph node bearing metastatic differentiated SCC.(F) Immunostain with pan-keratin antibody of papilloma.(G) Immunostain with pan-keratin antibody of lymph node with metastatic SCC.(H and I) H&E stain of normal lung (arrowhead) with large metastatic SCC deposit (arrow).(J) H&E stain of lung metastasis with secondary site of infiltration (arrow).(D–G, J): 20× magnification. Inserts in (E–G): 40× magnification. |
PMC509304_pbio-0020242-g002_266.jpg | What is the principal component of this image? | Metastasis of Primary SCC to Lymph Nodes and Lungs in p19 Arf-Deficient Mice(A) Underside of skin from tumor-bearing mouse shows newly formed blood vessels surrounding tumor site (arrow) and leading to inguinal lymph node (arrowhead).(B) Enlarged inquinal lymph node (left) containing metastatic SCC and blood vessel formation (arrow) compared to normal lymph node (right).(C) H&E stain of carcinoma section with prominent blood vessel (bv). Carcinoma cells (ca) have penetrated blood vessel wall (arrow).(D) H&E stain of lymph node bearing infiltrating SCC cells (arrow) among normal lymphocytes (arrowhead).(E) H&E stain of lymph node bearing metastatic differentiated SCC.(F) Immunostain with pan-keratin antibody of papilloma.(G) Immunostain with pan-keratin antibody of lymph node with metastatic SCC.(H and I) H&E stain of normal lung (arrowhead) with large metastatic SCC deposit (arrow).(J) H&E stain of lung metastasis with secondary site of infiltration (arrow).(D–G, J): 20× magnification. Inserts in (E–G): 40× magnification. |
PMC509304_pbio-0020242-g002_261.jpg | What is being portrayed in this visual content? | Metastasis of Primary SCC to Lymph Nodes and Lungs in p19 Arf-Deficient Mice(A) Underside of skin from tumor-bearing mouse shows newly formed blood vessels surrounding tumor site (arrow) and leading to inguinal lymph node (arrowhead).(B) Enlarged inquinal lymph node (left) containing metastatic SCC and blood vessel formation (arrow) compared to normal lymph node (right).(C) H&E stain of carcinoma section with prominent blood vessel (bv). Carcinoma cells (ca) have penetrated blood vessel wall (arrow).(D) H&E stain of lymph node bearing infiltrating SCC cells (arrow) among normal lymphocytes (arrowhead).(E) H&E stain of lymph node bearing metastatic differentiated SCC.(F) Immunostain with pan-keratin antibody of papilloma.(G) Immunostain with pan-keratin antibody of lymph node with metastatic SCC.(H and I) H&E stain of normal lung (arrowhead) with large metastatic SCC deposit (arrow).(J) H&E stain of lung metastasis with secondary site of infiltration (arrow).(D–G, J): 20× magnification. Inserts in (E–G): 40× magnification. |
PMC509304_pbio-0020242-g002_264.jpg | What key item or scene is captured in this photo? | Metastasis of Primary SCC to Lymph Nodes and Lungs in p19 Arf-Deficient Mice(A) Underside of skin from tumor-bearing mouse shows newly formed blood vessels surrounding tumor site (arrow) and leading to inguinal lymph node (arrowhead).(B) Enlarged inquinal lymph node (left) containing metastatic SCC and blood vessel formation (arrow) compared to normal lymph node (right).(C) H&E stain of carcinoma section with prominent blood vessel (bv). Carcinoma cells (ca) have penetrated blood vessel wall (arrow).(D) H&E stain of lymph node bearing infiltrating SCC cells (arrow) among normal lymphocytes (arrowhead).(E) H&E stain of lymph node bearing metastatic differentiated SCC.(F) Immunostain with pan-keratin antibody of papilloma.(G) Immunostain with pan-keratin antibody of lymph node with metastatic SCC.(H and I) H&E stain of normal lung (arrowhead) with large metastatic SCC deposit (arrow).(J) H&E stain of lung metastasis with secondary site of infiltration (arrow).(D–G, J): 20× magnification. Inserts in (E–G): 40× magnification. |
PMC509304_pbio-0020242-g002_263.jpg | What is the core subject represented in this visual? | Metastasis of Primary SCC to Lymph Nodes and Lungs in p19 Arf-Deficient Mice(A) Underside of skin from tumor-bearing mouse shows newly formed blood vessels surrounding tumor site (arrow) and leading to inguinal lymph node (arrowhead).(B) Enlarged inquinal lymph node (left) containing metastatic SCC and blood vessel formation (arrow) compared to normal lymph node (right).(C) H&E stain of carcinoma section with prominent blood vessel (bv). Carcinoma cells (ca) have penetrated blood vessel wall (arrow).(D) H&E stain of lymph node bearing infiltrating SCC cells (arrow) among normal lymphocytes (arrowhead).(E) H&E stain of lymph node bearing metastatic differentiated SCC.(F) Immunostain with pan-keratin antibody of papilloma.(G) Immunostain with pan-keratin antibody of lymph node with metastatic SCC.(H and I) H&E stain of normal lung (arrowhead) with large metastatic SCC deposit (arrow).(J) H&E stain of lung metastasis with secondary site of infiltration (arrow).(D–G, J): 20× magnification. Inserts in (E–G): 40× magnification. |
PMC509411_pbio-0020299-g001_271.jpg | Can you identify the primary element in this image? | Emerging leaf tips (yellow arrow) and hypocotyl (orange arrows) of an Arabidopsis mutant |
PMC509425_F5_272.jpg | What is the core subject represented in this visual? | The figure shows static acquisition images with gamma camera 2, 24, and 48 h, and 2, 24, 48 and 72 h after inoculation with 111In-Oxine-labelled iDC and mDC, respectively, for patient no. 3. Greater migration activity of mDC is clearly visible. (IS, inoculation site: LN, lymph node). |
PMC512287_F1_274.jpg | What object or scene is depicted here? | Magnetic resonance imaging of brain on hospital day six. T2 weighted image showing obstructive hydrocephalus and ventriculitis. |
PMC512287_F2_275.jpg | What is the principal component of this image? | Magnetic resonance imaging of brain on hospital day six. T1 weighted, post-gadolinium image showing obstructive hydrocephalus and ventriculitis. |
PMC512287_F3_277.jpg | What is the main focus of this visual representation? | Magnetic resonance imaging of brain on hospital day six. Diffusion image showing acute infarcts in the cerebellum. |
PMC512287_F4_276.jpg | What is being portrayed in this visual content? | Magnetic resonance imaging of brain on hospital day six. T2 weighted image showing fluid within the right mastoid air cells. |
PMC514490_pbio-0020261-g009_281.jpg | What can you see in this picture? | Immunolocalisation of Rabankyrin-5 in the Mouse KidneyMouse kidney cortex was processed for frozen section immunoelectron microscopy. Sections were (A and B) single labelled for Rabankyrin-5 (arrowheads, 10 nm) or (C and D) double labelled (arrows, 5 nm) for Rabankyrin-5 and LAMP-1.(A) Low-magnification view of the apical region of two proximal tubule cells demonstrates low labelling for Rabankyrin-5 on apical microvilli (M) but stronger labelling (arrowheads) of large subapical electron-lucent vesicular structures (asterisks). One of these structures is shown at higher magnification in (B). L, lateral membrane.(C) Rabankyrin-5 labels LAMP-1–negative subapical structures as well as compartments showing low LAMP-1 labelling (arrows and asterisk).(D) Rabankyrin-5 (arrowheads) associates with compartments, which show no or weak labelling for LAMP-1 (asterisks). In addition, low Rabankyrin-5 labelling is associated with more strongly labelled LAMP-1–positive compartments. Note that there is some nonspecific labelling of mitochondria (m). Scale bars represent 500 nm. |
PMC514490_pbio-0020261-g009_279.jpg | Can you identify the primary element in this image? | Immunolocalisation of Rabankyrin-5 in the Mouse KidneyMouse kidney cortex was processed for frozen section immunoelectron microscopy. Sections were (A and B) single labelled for Rabankyrin-5 (arrowheads, 10 nm) or (C and D) double labelled (arrows, 5 nm) for Rabankyrin-5 and LAMP-1.(A) Low-magnification view of the apical region of two proximal tubule cells demonstrates low labelling for Rabankyrin-5 on apical microvilli (M) but stronger labelling (arrowheads) of large subapical electron-lucent vesicular structures (asterisks). One of these structures is shown at higher magnification in (B). L, lateral membrane.(C) Rabankyrin-5 labels LAMP-1–negative subapical structures as well as compartments showing low LAMP-1 labelling (arrows and asterisk).(D) Rabankyrin-5 (arrowheads) associates with compartments, which show no or weak labelling for LAMP-1 (asterisks). In addition, low Rabankyrin-5 labelling is associated with more strongly labelled LAMP-1–positive compartments. Note that there is some nonspecific labelling of mitochondria (m). Scale bars represent 500 nm. |
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