Notes

Psychometric Attributes from the Icelandic Form of the actual Revised Edmonton Indicator Review Size.
hibitor group was significantly lower than that in DM group. According to qRT-PCR results, compared with those in Control group, mRNA expressions of Notch mRNA and miR-135a in the rat kidney tissues were substantially raised in DM group (p less then 0.05), and they were notably lowered in miR-13a inhibitor group compared with those in DM group (p less then 0.05). Finally, Western blotting results manifested that the protein levels of Notch, NIC, and Hes1 in the renal tissues of rats in DM group were considerably higher than those in Control group (p less then 0.05), and that their protein expression levels in miR-135a inhibitor group were markedly lower than those in DM group (p less then 0.05). CONCLUSIONS Inhibition of miR-135a can reduce the renal fibrosis in DKD rats through the Notch pathway.OBJECTIVE The aim of this study was to research the potential mechanism of INHBC and CSF1R in diabetic nephropathy. MATERIALS AND METHODS 30 SD rats were selected and randomly divided into Con group, Sham group, and DN group. In the DN group, intraperitoneal injection of the streptozotocin-citrate solution was conducted to construct the DN model. In the Sham group, intraperitoneal injection of equal citrate solution was conducted. The Con group did not do anything. After successful modeling, blood glucose, insulin, biochemical indexes, and levels of inflammatory cytokines in blood samples were detected. The expression levels of INHBC, CSF1R, apoptosis-related proteins and IGF-1 were detected by Western blot. MRNA expression levels of INHBC, CSF1R, IGF-1 and inflammatory cytokines were detected by qPCR. RESULTS Compared with the Con group, the expression levels of blood glucose, insulin, biochemical indexes, INHBC, CSF1R, IGF-1, IL-6, TNF-α and Bcl2 increased in the DN group, while the expression levels of IL-10, Caspase 3, Caspase 9, and Bax decreased. INHBC mRNA was positively correlated with IGF-1 mRNA. CSF1R was negatively correlated with Caspase 3, Caspase 9, Bax, and IL-10, and positively correlated with IL-6, TNF-α, and Bcl2. CONCLUSIONS NHBC and CSF1R induced the secretion of IL-6 and TNF-α, inhibited the production of IL-10, inhibited apoptosis of cells, and promoted the proliferation of renal cells during DN disease. Therefore, INHBC and CSF1R can be used as target objects of DN treatment strategies.OBJECTIVE Atherosclerosis (AS), with high risk of stroke or cerebrovascular disease, is one of the most common causes of death worldwide. Increasing evidence shows that long non-coding RNA (lncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) is related to atherothrombotic stroke susceptibility and contributes to AS progression. However, the underlying mechanism was not explained yet. PATIENTS AND METHODS Human aorta vascular smooth muscle cells (HA-VSMCs) and human umbilical vein endothelial cells (HUVECs) were treated with oxidized Low Density Lipoprotein (ox-LDL) and considered as AS cell models. Quantitative reverse transcriptase PCR (qRT-PCR) and Western blotting were employed to investigate the mRNA and protein expression level, respectively. Microscopic examination through fluorescent in situ hybridization (FISH) was used to determine the location of ANRIL. Cell proliferation and migration assays were demonstrated to evaluate the functional role of ANRIL in AS. Potential target of ANRIL was determined using Luciferase reporter assay and RNA immunoprecipitation (RIP). RESULTS ANRIL was upregulated and miR-399-5p was down-regulated in both human atherosclerotic plaques and ox-LDL-induced cells. ANRIL was located in cytoplasm and promoted cell proliferation and migration by sponging miR-399-5p. Further analysis identified fibroblast growth factor receptor substrate 2 (FRS2) as a direct target of miR-399-5p. 4-Hydroxynonenal Finally, RAS/RAF/ERK signal pathway was proved to be involved in the regulation of ANRIL on the progression of AS. CONCLUSIONS These results revealed the underlying mechanism that ANRIL promoted AS progression by sponging miR-399-5p and regulating RAS/RAF/ERK signal pathway, suggesting that ANRIL might be a potential target for the therapeutic strategy of AS.OBJECTIVE Increasing evidence has shown that HSF1 is involved in glycemia regulation, and SIRPα plays a pivotal role in islet β-cell viability. However, it is still unknown whether SIRPα is associated with HSF1 in regulating the cell viability and cell death of islet β-cells. MATERIALS AND METHODS Western blot and qPCR were applied to determine protein and mRNA levels of HSF1 and SIRPα. Cell viability and death were investigated by cell counting kit-8 and trypan blue exclusion assay. Meanwhile, cell apoptosis was analyzed by detecting caspase3 activity. Moreover, luciferase reporter assay was applied to explore the mechanism by which HSF1 transcriptionally upregulated SIRPα expression. RESULTS Our study reveals that HSF1 expression was lower in islets from T1DM compared to normal mice. We found that overexpression of HSF1 decreased the apoptosis of islet β-cell lines. Moreover, we demonstrated that overexpression of HSF1 decreased the apoptosis of islet β-cells through increasing the expression of SIRPα. In terms of mechanism, luciferase reporter assays showed that HSF1 upregulated SIRPα expression by activating its gene promoter region. The binding site (-1809 to -1795) was required for HSF1-induced increase of SIRPα gene promoter activity. CONCLUSIONS These results indicate that the low expression of HSF1/SIRPα may be one of the mechanisms of islet β-cell death and targeting HSF1/SIRPα may be a novel strategy for the treatment of T1DM.OBJECTIVE The importance of the circular ribonucleic acid (RNA) in malignant tumors causes more attention of researchers. Melanoma is one of the most ordinary malignant tumors. This study aims to identify how circ_0017247 functions in the progression of melanoma. PATIENTS AND METHODS Circ_0017247 expression of both melanoma patients' tissue samples and cell lines were detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the function of circ_0017247 was identified by performing the Wound healing assay, the transwell assay, and the Matrigel assay in vitro. Besides, the mechanism assays were performed to uncover the interaction between circ_0017247 and miR-145. In addition, the tumor metastasis assays were also conducted in vivo. RESULTS In this study, circ_0017247 expression was significantly higher in melanoma tissues compared with that in the skin tissues with a melanocytic nevus. The migrated length of the melanoma cells was reduced after circ_0017247 was silenced. Moreover, the number of migrated and invaded melanoma cells was reduced after circ_0017247 was silenced.
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