9 research outputs found

    Relationship between visual field loss and maximal combined electroretinographic responses in retinitis pigmentosa : comparison among genetically different types

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    1984年から1996年までに千葉大学眼科を受診した定型網膜色素変性症228例について常優26例, 常劣64例, 孤発例138例に分け動的量的視野および網膜電図を検討した。Goldmann視野におけるV-4イソプターでは5から10cm^2までと150から250cm^2までの2群に別れ, 1-4イソプターでは5cm^2以下の群のみ認められた。加齢及び遺伝形式による差異は認められなかった。網膜電図ではa, b波ともに正常対照群より減少してはいるものの, 遺伝形式による差異は認められなかった。また, 網膜電図で振幅を認められる割合はV-4イソプターおよびI-4イソプターの面積と相関していることが示唆されたが, 遺伝形式による差異は認められなかった。網膜電図の振幅の比であるb/a比は正常対象群に対して疾患群は減少していたが, 常備は特に他に比べ有意に減少していた。定型網膜色素変性症の網膜電図や視野の検討は数多くなされてきたが, b/a比について統計的考察がなされてきたことはない。a波およびb波は組織学的に発生起源が異なっており, b波はa波のインパルスによって二次的に引き起こされることは以前より知られてきている。網膜電図において常備のb/a比が有意な低下を示すことは, 網膜障害の機序が他と異なる可能性が示唆された。Analyses were performed on 228 Japanese patients with retinitis pigmentosa (RP) who were classified with autosomal dominant (ADRP, n=26), autosomal recessive (ARRP, n=64), and simplex (simplex RP, rc=138) inheritance. Visual fields were tested with Goldmann perimetry. Maximal combined responses of electroretinogram (ERG) with 20-Joule white flash stimulation were recorded after dark adaptation for 20 minutes. The visual field with the V-4 isopter demonstrated two unique groups, represented by dense areas between 5 and 10cm^2 and between 150 and 250cm^2, while only one unique group was observed within the 5cm^2 area with the 1-4 isopter. No age or inheritance type of effect was seen. A-and b-wave amplitudes were equally low in the 3 groups, as compared with normal subjects. The b/a ratio was significantly smaller in the ADRP group, compared with the others. The rate of detectable ERG responses decreased as the visual field became smaller. There was no inheritance effect. A lower b/a ratio in ADRP patients suggested that retinal functional abnormalities differed from ARRP and simplex RP patients

    Knockdown constructs shows Sdc1 is necessary for NPC maintenance and proliferation in vivo.

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    <p>In utero electroporation was performed at E13 and results assessed at E15. (A) Sdc1 UTR and ORF shRNAs reduced NPC proliferation and promoted neuronal differentiation, indicated by Ki67 and Tuj1, respectively (scale bar = 50 um), as quantified in (B) (scrambled, N = 4; Sdc1 UTR, N = 3; Sdc1 ORF, N = 5). (C) Sdc1 UTR and ORF shRNAs decreased both RGC and IPC populations, indicated by reduced Pax6 and Tbr2, respectively (scale bar = 50 um) and quantified in (D) (scrambled, N = 4; Sdc1 UTR, N = 3; Sdc1 ORF, N = 5). (E) The distribution of eGFP<sup>+</sup> cells in the cortical layers (scrambled, N = 5; Sdc1 ORF, N = 4). CP, cortical plate; IZ, intermediate zone; SVZ, subventricular zone; VZ, ventricular zone. Error bars represent S.E.M, *P<0.05, **P<0.01, ***p<0.001.</p

    Sdc1 modulates NPC to response to Wnt ligand.

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    <p>(A) Knocking down Sdc1 reduced the total β-catenin protein level compared to scrambled control group, quantified in (B) after normalized to GAPDH. (C) Schematic depicting the GSK 3β inhibitor (Chir 99021) treatment experiment (D) Chir 99021 treatment partially rescued proliferation of Sdc1 UTR or Sdc1 ORF treated NPCs (scale bar = 50 um), assessed by Ki67 and quantified in (E). (F) Schematic diagram depicting the Wnt3a conditioned medium treatment experiment. (G) Wnt3a increased proliferation in scrambled control treated NPCs, but had no significant effect in Sdc1 UTR or Sdc1 ORF treated NPCs (scale bar = 50 um), assessed by Ki67 and quantified in (H). Error bars represent S.E.M, *P<0.05, **P<0.01, ***p<0.001, NS = not significant.</p

    Sdc1 knockdown reduces NPC maintenance and proliferation in vitro.

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    <p>(A) The FUWG H1 lentiviral vector expresses a shRNA under the H1 promoter and eGFP under the ubiquitin promoter. Two different shRNAs (Sdc1 UTR and Sdc1 ORF) specifically targeting Sdc1 inhibit Sdc1 expression at mRNA (B) and protein (C) levels. (D) E11 cortical NPCs were treated with scrambled control, Sdc1 UTR and Sdc1 ORF lentiviruses and assessed at 4 DIV. Knocking down Sdc1 reduces the NPC population and their proliferation, indicated by Nestin and Ki67, respectively; knocking down Sdc1 also promotes neuronal differentiation, indicated by Tuj1 staining (scale bar = 50 um). Data are quantified in (E). (F) Knocking down Sdc1 does not increase cell apoptosis, assessed by active Caspase-3. (G) Knocking down Sdc1 reduces neurosphere generation, assessed at 7 DIV and quantified in (H) (N = 3) (scale bar = 200 um). Error bars represent S.E.M, *P<0.05, **P<0.01, ***p<0.001.</p

    Sdc1 is highly expressed in the germinal zones of the developing mouse cerebral cortex.

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    <p>(A) Schematic to indicate area of analysis. (B) Sdc1 expression in a coronal section of the E15 mouse cortex (area indicated by the box in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042883#pone-0042883-g001" target="_blank">Fig. 1A</a>). Sdc1 is highly expressed in both the VZ and SVZ (scale bar = 200 um). (C) Higher magnification of the boxed area indicated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0042883#pone-0042883-g001" target="_blank">Fig. 1B</a> (scale bar = 100 um). (D) Sdc1 expression in the neural germinal zone where Sox2+ RGCs are located (scale bar = 100 um). LV, Lateral ventricle; CP, cortical plate; IZ, intermediate zone; SVZ, subventricular zone; VZ, ventricular zone.</p

    Additional file 2: of Syndecan-1 induction in lung microenvironment supports the establishment of breast tumor metastases

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    Figure S2. Characterization of 4T1 primary fat pad tumors. The 4T1 tumor cells (1 × 107 cells in 10 μL) were injected into the exposed 4th mammary gland and mice were killed after 30 days. (A) Hematoxylin and eosin (H&E) stained sections of tumors in fat pad. Carcinoma cells infiltrate adipose tissue (Ad), which contains benign mammary duct (Duct). Scatter plot graph indicates wet weights of tumors excised from Sdc1+/+ and Sdc1−/− mice. (B) Immunohistochemical (IHC) labeling for proliferation marker Ki67. Graph compares Ki67 labeling index between animal genotypes. (C) IHC labeling for endothelial cell marker CD31. Graph compares CD31-positive area between animal genotypes. (D) IHC labeling for alpha smooth muscle actin (αSMA). Graph compares number of αSMA-positive cell clusters between animal genotypes. (E) IHC labeling for macrophage marker F4/80. Graph compares density of F4/80-positive macrophages between animal genotypes. (F) Tumor border imaged by second harmonic generation (SHG) microscopy. White structures indicate fibrillar collagen. Graph compares mean collagen fiber angles relative to tumor boundary between animal genotypes. (TIF 7079 kb

    Additional file 4: of Syndecan-1 induction in lung microenvironment supports the establishment of breast tumor metastases

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    Figure S4. Effect of housing temperature and host Sdc1 on T cells within lung metastases. A subset of animals was moved to a housing environment with a thermo-neutral temperature of approximately 31 °C, 2 weeks prior to inoculation and maintained at that temperature throughout the duration of the experiment. The 4T1 mouse mammary carcinoma cells were inoculated into the mammary fat pad as described. Mice were killed after 30 days and sections of lung tissue were labeled with antibodies to CD4 and CD8. CD4+ and CD8+ intratumoral and normal lung lymphocytes were counted as described in “Methods”. (A, B) Photomicrographs of adjacent sections of small lung metastasis (M) next to vessel (V) labeled with antibodies to CD4 (A) and CD8 (B) (original magnification × 400). (C, D) Density of intratumoral lymphocytes in mice segregated by housing temperature expressed as number of cells per megapixel (MP) of metastasis tissue. (E, F) Density of intratumoral lymphocytes in mice segregated by housing temperature and Sdc1 genotype (same dataset as in C, D). (G, H) Density of lymphocytes in normal lung tissue at distance from any metastases. (TIF 2897 kb

    Additional file 1: of Syndecan-1 induction in lung microenvironment supports the establishment of breast tumor metastases

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    Figure S1. Effect of host Sdc1 on metastatic efficiency of E0771 mouse mammary carcinoma cells. E0771 tumor cells (1 × 107 cells in 10 μL) were injected into the exposed 4th mammary gland as described in “Methods” and mice were killed after 30 days. (A) Metastatic lesion in lung (original magnification × 400; scale bar indicates 100 μm; M, metastasis; L, lung). (B) Number of metastatic lesions per mouse. Metastases were counted on single histologic sections of both lungs. (C) Metastatic tumor burden expressed as percent lung tissue occupied by metastatic lesions. (D) Average area of metastatic lesions expressed in pixels as measured on histologic sections. (TIF 1153 kb

    Additional file 3: of Syndecan-1 induction in lung microenvironment supports the establishment of breast tumor metastases

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    Figure S3. Effect of host Sdc1 on later stages of E0771 carcinoma cell metastasis. E0771 tumor cells (1 × 105 tumor cells in 100 μL) were injected into the tail veins of C57BL/6 mice, which were killed 15 days later. (A) Metastasis growing around pulmonary vessel (magnification ×400; scale bar indicates 100 μm; V, vessel). (B) Number of metastatic lesions per mouse. Metastases were counted on single histologic sections of both lungs. (C) Metastatic tumor burden expressed as percent lung tissue involved by metastatic lesions. (D) Average area of metastatic lesions expressed in pixels as measured on histologic sections. (TIF 880 kb
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