<組織>技術室組織図

Demographical data (age; gender; hypertension, diabetes mellitus) type of occlusion, affected eye, SER, BCVA, AL, ONH parameters and SSI of affected and unaffected fellow eyes of our BRVO study subjects. (XLS 59 kb

The localization of TGF-β1 and -β2 mRNA in relation to markers of the penumbra and glial scar.

<p><b>A</b>: Double labeling of TGF-β1 mRNA (black <i>in situ</i> hybridization signal) and immunoreactivity of heat shock protein 70 (Hsp70), a marker of the penumbra (brown precipitate) 24 h following MCAO. The lesion is indicated by star symbols (*), and the lesion border is demarcated by black dots. Black squares demarcate the outer border of the penumbra. The framed area in Aa is shown in Ab to better appreciate the similar distribution of TGF-β1 mRNA and Hsp70 in the penumbra. Ac is a high magnification image of the framed area in Ab and demonstrates that TGF-β1 mRNA and Hsp70 immunoreactivity are not co-localized in the same cells. <b>B</b>: Double labeling of TGF-β2 mRNA (black <i>in situ</i> hybridization signal) and Hsp70 immunoreactivity (brown precipitate) 24 h following MCAO. Black squares demarcate the outer border of the penumbra. Within the penumbra, the majority of the TGF-β2 mRNA-expressing cells contain Hsp70 immunoreactivity. However, TGF-β2 mRNA expressing cells but not Hsp70-immunoreactive cells are present in the intact brain tissue. <b>C</b>: A glial scar can be identified based on the high density of intensely labeled GFAP-positive astrocytes. TGF-β1-expressing cells are present within the glial scar and also within the lesion but not in the intact tissue outside the glial scar. Abbreviations: LV - lateral ventricle. Scale bars = 1 mm for Aa, 400 µm for Ab, 100 µm for Ac, and 200 µm for both B and C.</p

TGF-β1 is induced in glial cells but not in neurons 72 h after lesion.

<p><b>A</b>: Double labeling of TGF-β1 mRNA and Iba1 immunoreactivity. The border of the lesion is demarcated by black dots. The position of the high magnification image in B is shown by the large black arrowhead. <b>B</b>: A high magnification image shows that the black <i>in situ</i> hybridization signal of TGF-β1 is located above Iba1-immunoreactive cell bodies visualized by brown precipitate. <b>C</b>: Single labeled TGF-β1 mRNA expressing cells are indicated by white arrowheads, and GFAP-immunoreactive astrocytes by black arrowheads, while double labeled cells are indicated by black arrows. <b>D</b>: TGF-β1 mRNA expressing neurons are indicated by white arrowheads, and NeuN-immunoreactive neurons by black arrowheads. No double labeled neurons are present. Abbreviations: cc – corpus callosum, LV – lateral ventricle. Scale bars = 1 mm for A, 30 µm for B, and 100 µm for C and D.</p

The induction of TGF-β1, - β2, and -β3 mRNA 72 h and 1 mo after MCAO.

<p> <i>In situ</i> hybridization sections show the expression of TGF-β mRNA. The infarct areas are indicated by the star symbol (*) and the borders of the infarcts are demarcated with white dots. A: TGF-β1 expression is induced at the perimeter of the lesion as well as within the infarct area 72 h after MCAO. High magnification bright field photomicrographs demonstrate that TGF-β1 mRNA accumulates above cell bodies within the infarct area (Aa), as well as in the corpus callosum (Ab). The locations of these pictures are indicated by the arrowheads in the left panel. B: TGF-β2 is present in layers II, III, and V of the cerebral cortex. Only a few cells demonstrate increased expression level of TGF-β2 in the vicinity of the border of the lesion at 72 h after MCAO. C: TGF-β3 is present in some neurons in layer IV of the cerebral cortex, but the level of expression is not higher than that in normal animals D: The induction of TGF-β1 mRNA is demonstrated 1 month after MCAO. TGF-β1 mRNA is abundant within the infarct area except for in a relatively small core region. The field indicated by the large black arrowhead in A is enlarged and shown in bright-field in the inlet to demonstrate that even the densest TGF-β1 signal represents labeling of individual cells as autoradiography grains accumulated above cell bodies. E: TGF-β2 mRNA is present in a few cells at the perimeter of the infarct area. Outside the lesion, TGF-β2 mRNA is distributed in the cerebral cortex as in intact animals but is not induced above normal levels. Abbreviations: ac – anterior commissure, cc – corpus callosum, CP - caudate putamen, LV - lateral ventricle. Scale bar = 2 mm for A and E, 1 mm for C, and 50 µm for B.</p

The induction of TGF-β1, -β2, and –β3 mRNA at 3 h and 24 h after middle cerebral artery occlusion (MCAO).

<p>Dark-field photomicrographs of <i>in situ</i> hybridization sections show the expression of TGF-β mRNAs. The lesion sites are indicated by the star symbols (*) and the borders of the lesions are demarcated by black and white dots. A: Giemsa counterstaining demonstrates the position of the lesion in the caudate putamen 3 h after MCAO. B: The same field of the same section is shown in a dark field image. TGF-β1 mRNA is induced around the lesion. C: TGF-β2 mRNA is present ipsilateral to the lesion. The normal distribution of TGF-β2 can be observed in layers II and V of the cerebral cortex without any apparent increase in the expression level. D: TGF-β1 expression is induced around the lesion in the cerebral cortex 24 h following MCAO. E: TGF-β1 expression is also induced in the peri-infarct area of the caudate putamen. F: TGF-β2 is induced in layers II, III, and V of the ipsilateral cerebral cortex. G: TGF-β3 has a somewhat elevated expression level in some cells of layer II of the cerebral cortex. TGF-β3 is normally present in layer IV of the cerebral cortex and is not induced in this location. Abbreviations: ac – anterior commissure, cc – corpus callosum, CP - caudate putamen, LV - lateral ventricle. Scale bars = 1 mm.</p

The expression of TGF-β proteins in different brain regions around an ischemic lesion at 24 h following a 1 h transient MCAO.

<p>The number of cells was counted in 200×400 µm areas (0.08 mm²) of coronal brain sections in cortical layers I-VI and in the caudate putamen (CP). The number of autoradiography grains was counted above TGF-β-positive cell nuclei indicated by the accumulation of autoradiography grains. Measurements were performed around the ischemic lesion (dark gray) and in the corresponding brain area on the contralateral side of the brain (light gray). Sections from 5 animals were involved in the analysis. A–C: The number of cells expressing TGF-β1, -β2, and -β3 in 0.08 mm². D-F: The number of autoradiography grains proportional to the mRNA level of TGF- β1, -β2, and -β3 in single cells. The values around the ischemic lesion and in the corresponding brain area on the contralateral side of the brain were compared using paired Students t-tests, where data obtained from the same section formed the pairs to eliminate variation from the labeling intensity of an individual staining. The star symbol (*) indicates brain regions, in which the number of TGF-β-expressing cells or the mRNA level of the particular subtype of TGF-β in single cells was significantly (p<0.05) elevated.</p

TGF-β2 is induced in neurons but not in glial cells 24 h after MCAO.

<p><b>A</b>: Double labeling of TGF-β2 mRNA (black <i>in situ</i> hybridization signal) and immunoreactivity of the microglia marker Iba1 (brown precipitate). The lesion is indicated by star symbols (*) and the lesion border is demarcated by black dots. The positions of the high-magnification images in layer III and V of the cerebral cortex are indicated by black arrowheads as Aa, and Ab, respectively. Iba1-immunoreactive microglia do not contain TGF-β2 mRNA in either layer of the cerebral cortex. <b>B</b>: Double labeling of TGF-β2 mRNA (black <i>in situ</i> hybridization signal) and NeuN-immunoreactive neurons (brown precipitate). Almost all TGF-β2 mRNA-expressing cells contained NeuN immunoreactivity in layer III (Ba), and in layer V (Bb). Examples of double-labeled cells are indicated by black arrows. <b>C</b>: TGF-β2 is not expressed in astrocytes. TGF-β2 mRNA expressing neurons are indicated by white arrowheads and GFAP-immunoreactive neurons are indicated by black arrowheads. There are no double-labeled cells present. Abbreviations: cc – corpus callosum. Scale bars = 1 mm for A, 50 µm for Ab, 200 µm for Ba, 100 µm for Bb, and 100 µm for C.</p

The induction of TGF-β mRNA by 24 h permanent occlusion of the middle cerebral artery.

<p>The infarct area is indicated by star symbol (*) and its border is demarcated with black or white dots. <b>A</b>: TTC staining demonstrates the effect of ischemia on brain tissue. <b>B</b>: TGF-β1 expression is induced in the peri-infarct area of the lesion. <b>C</b>: TGF-β2 is induced in layers II, III, and V of the ipsilateral cerebral cortex. The induction is particularly salient in layers II and III where the labeling is much more intense ipsilateral to the lesion compared with the contralateral side. <b>D</b>: TGF-β3 is induced in layer II of the ipsilateral cerebral cortex. Abbreviations: cc – corpus callosum, CP - caudate putamen, LV - lateral ventricle. Scale bars = 1 mm for B and D.</p

Additional file 1: Table 5. of Impact of 3T multiparametric MRI and FDG-PET-CT in the evaluation of occult primary cancer with cervical node metastasis

Data collection. (XLSX 22 kb