15 research outputs found

    Additional file 2: of Loss of XBP1 accelerates age-related decline in retinal function and neurodegeneration

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    Figure S2. No differences in ERG responses between WT and XBP1 cKO mice at 10 weeks of age or in implicit times at any age. (A) Graph of the a-wave and b-wave responses for a transient, light-adapted ERG for XBP1 fl/fl (WT, black, n = 5) and XBP1 fl/fl; Chx10-Cre (cKO, grey, n = 5) at 10 weeks of age shows no differences in the amplitude of the a-wave or b-wave. (B) In addition, the implicit times for b-wave onset are not different for WT and XBP1 cKO in transient, light adapted ERG responses at any age measured. (C and D) Similarly, implicit times for the a-wave and b-wave are not different for the 10-step dark adapted ERG responses between (C) 6–8 month old WT and XBP1 cKO mice nor between (D) 12–14 month old WT and XBP1 cKO mice. (TIFF 449 kb

    Additional file 1: of Loss of XBP1 accelerates age-related decline in retinal function and neurodegeneration

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    Figure S1. Multiple retinal markers reveal no differences between WT and XBP1 cKO at P15 or 12 months of age. Cryosections of retina from P15 or 12 month old wild type (WT) and XBP1 fl/fl; Chx10-cre (cKO) mice immunolabeled with antibodies against the listed proteins. (A) At P15 there is no difference in the appearance of labeling for calbindin, a horizontal cell marker, between XBP1 cKO and WT. (B and C) There are no differences in labeling for Pax6 at (B) P15 or (C) 12 months between XBP1 cKO and WT retinas. (D) Double labeling for the bipolar cell marker, PKC-α, and the Ribeye antibody appears identical between XBP1 cKO and WT at P15. (E and F) We see no differences between XBP1 cKO and WT in staining for the MG marker, glutamine synthetase (GS) at P15 or 12 months of age. GCL, ganglion cell layer; INL, inner nuclear layer; ONL, outer nuclear layer. Scale bar = 40 μm. (TIFF 1571 kb

    Additional file 1: of Impact of hyperuricemia on clinical outcomes after percutaneous coronary intervention for in-stent restenosis

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    Table S1. Changes in serum uric acid level, Table S2. In-stent restenosis patterns at the index procedure, Table S3. Cumulative incidence of clinical events between patients with lower uric acid level (≤6.8 mg/dL) and those with higher uric acid level (> 6.8 mg/dL), Table S4. Cumulative incidence of clinical events between patients with lower uric acid level (≤5.3 mg/dL) and those with higher uric acid level (> 5.3 mg/dL), Table S5. Subgroup analyses of the cumulative incidence of clinical events between the low uric acid group and the high uric acid group, Table S6. Cox-proportional hazard models for non-target vessel revascularization, Figure S1. Kaplan–Meier curve for major adverse event between patients with lower uric acid level (≤5.3 mg/dL) and those with higher uric acid level (> 5.3 mg/dL). UA, uric acid. (DOCX 134 kb

    Additional file 1: of Predictors of adverse pathologic features after radical prostatectomy in low-risk prostate cancer

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    Figure S1. Receiver operator characteristics (ROC) curve of PSA levels, number of positive cores and multivariable logistic regression model incorporating PSA levels and number of positive cores for predicting presence of adverse pathologic features. If we considered both parameters to predict APFs, it would have shown slightly better outcomes for predictions (AUC = 0.662). (JPG 31 kb

    Additional file 8: Figure S8. of α-Synuclein accumulation and GBA deficiency due to L444P GBA mutation contributes to MPTP-induced parkinsonism

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    GBA overexpression inhibits MPTP-reduced mitochondrial protein level in GBA +/L444P mice. a Immunoblots of SDHA, PDH, VDAC, TH, GBA, and α-synuclein from AAV5-Con injected WT, AAV5-hGBA injected WT, AAV5-Con injected heterozygous, and AAV5-hGBA injected heterozygous mice treated with saline or MPTP. VMB lysates were immunoblotted with anti-SDHA, anti-PDH, anti-VDAC, anti-TH, and anti-GBA antibodies. b SDHA, c PDH, d VDAC, e TH, f GBA, and g α-synuclein expression levels were normalized against β-actin. Error bars represent the mean ± S.E.M. (n = three mice per group). Two-way ANOVA was used for statistical analysis followed by post-hoc Bonferroni test for multiple group comparison. *P < 0.05, **P < 0.01, ***P < 0.001 vs. saline-treated WT with AAV-Con or saline-treated GBA +/L444P with AAV5-Con or MPTP-treated WT with AAV5-Con or MPTP-treated GBA +/L444P with AAV5-Con group. (PDF 683 kb

    Additional file 5: Figure S5. of α-Synuclein accumulation and GBA deficiency due to L444P GBA mutation contributes to MPTP-induced parkinsonism

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    Lysosomal calcium concentration. SH-SY5Y cells were transfected with indicated constructs for 48 h. The cells were then labeled with CellLight® Lysosome-RFP (LAMP1; red) and loaded with 0.1 mg/ml of lysosomal calcium indicator Oregon Green BAPTA-1 dextran (BAPTA-1; green) for 12 h. The Oregon Green BAPTA-1 signals that co-localized to lysosome (LAMP-1; red) were used for measuring lysosomal calcium concentration. [Ca2+]lys was measured using ratiometric methods via confocal microscopy. Two-way ANOVA was used to test for statistical analysis followed by post-hoc Bonferroni test for multiple group comparison. ***P < 0.001. (PDF 1122 kb
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