7 research outputs found

    Survival of islet allografts from the donors of WT mice and PD L1-deficient mice.

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    <p>Blood glucose levels and islet graft survival in the recipients bearing islets from WT mice and PDL1- deficient mice are shown (N = 8). Diabetes was induced in BALB/c mice with STZ, followed by transplantation of four hundred islets isolated from WT or PDL1- deficient mice. The blood glucose levels are shown in Fig 2A in comparison with the glucose levels of the recipients transplanted with the islets from WT mice. Euglycemia was maintained for a shorter duration in the recipients bearing islets from PD-L1-deficient mice (Fig 2B). Graft survival was calculated by the Kaplan-Meier method and compared using a log-rank test (P = 0.0008). The results show that the survival time of the recipients transplanted with islets from PD-L1-deficient mice was clearly shorter compared with that of the recipients bearing islets from WT mice.</p

    Differential expression of <i>PD-1</i> and <i>CTLA-4</i> and related immunotherapy in patients in the two risk groups.

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    (A-B) represents the differential expression of PD-1 and CTLA-4 in the two risk groups. (C–F) represents the difference analysis of patients in the two risk groups when receiving immunotherapy for anti-PD-1 and CTLA-4.</p

    The mRNA levels of the four hub genes.

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    (A–D) Expression of the four genes in 12 pairs of ccRCC and para-cancer tissues by qRT-PCR. (E–H) expression of the four hub genes in cancer cells and normal kidney cells by qRT-PCR (**PP<0.05).</p

    HFD treatment reduces the level of MG53 in blood circulation.

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    <p>(A) Western blotting MG53 levels in serum of ND (n = 5) and HFD (n = 7)-treated mice. (B) Quantification of western blot densities reveals reduced MG53 serum levels in mice on HFD. The results are presented as mean ± SEM. ** p<0.01.</p

    HFD treatment induces MG53 localization to the plasma membrane and mitochondria in skeletal muscle.

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    <p>(A) IHC staining of longitudinal sections of skeletal muscle reveals striated patterns of MG53 in ND-treated mice (left). HFD treatment results in the aggregation of MG53 near the plasma membrane (middle). mg53-/- muscle cells show no staining (right). Scale bar: 20 μm. (B) Cross-sections of TA muscle tissue reveal punctated distribution of MG53 inside the muscle fibers of HFD-treated mice (lower panels), which was not witnessed in those subjected to normal conditions (upper panels). COX IV staining (green) suggests the possibility of MG53 (red) localization around mitochondria, since COX IV positive signals were detected in the center of MG53 punctates (please see the right panels with high magnification). Scale bar: 10 μm.</p

    HFD-treated mice exhibit metabolic syndrome.

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    <p>(<b>A</b>) HFD-treated mice are glucose intolerant and (<b>B</b>) insulin resistant. n = 5 normal diet (ND), n = 8 high fat diet (HFD). (<b>C</b>) HFD induces mice obesity. (<b>D</b>) Lipid profiling shows elevated total cholesterol and low-density lipoprotein (LDL) levels in HFD-induced mice. The results are presented as mean ± SEM. * p<0.05; ** p<0.01.</p
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