Effects of Selenium and Cadmium on Human Liver and Kidney Functions in Exposed Black Shale Areas.

Animal experiments suggest that selenium (Se) may alleviate cadmium (Cd) toxicity in animal liver and kidneys, but its effect on human liver and kidneys remains uncertain. In China, areas with black shale have shown elevated levels of Se and Cd. According to the USEPA (U.S. Environmental Protection Agency) evaluation method, the soil and rice in these areas pose significant risks. In black shale regions such as Enshi and Zhuxi County, residents who long-term consume local rice may surpass safe Se and Cd intake levels. Significantly high median blood Se (B-Se) and urine selenium (U-Se) levels were detected in these areas, measuring 416.977 µg/L and 352.690 µg/L and 104.527 µg/L and 51.820 µg/L, respectively. Additionally, the median blood Cd (B-Cd) and urine Cd (U-Cd) levels were markedly elevated at 4.821 µg/L and 3.848 µg/L and at 7.750 µg/L and 7.050 µg/L, respectively, indicating substantial Cd exposure. Nevertheless, sensitive liver and kidney biomarkers in these groups fall within healthy reference ranges, suggesting a potential antagonistic effect of Se on Cd in the human body. Therefore, the USEPA method may not accurately assess Cd risk in exposed black shale areas. However, within the healthy ranges, residents in the Enshi study area had significantly greater median levels of serum creatinine and cystatin C, measuring 67.3 µmol/L and 0.92 mg/L, respectively, than those in Zhuxi did (53.6 µmol/L and 0.86 mg/L). In cases of excessive Se and Cd exposure, high Se and Cd levels impact the filtration function of the human kidney to some extent.

A crosslinked network polypyrrole coated cobalt doped Fe2O3@carbon cloth flexible anode material for quasi-solid asymmetric supercapacitors.

Iron(III) oxide (Fe2O3) exhibits a substantial theoretical specific capacitance and a broad operational voltage window, making it a prospective anode material. The crystal structure of Fe2O3 was altered through cobalt doping, and its electronic conductivity was improved by supporting it with carbon cloth (Co-Fe2O3@CC). Subsequently, a crosslinked network of polypyrrole (PPy) was synthesized onto Co-Fe2O3@CC via an ice-water bath, resulting in the formation of PPy/Co-Fe2O3@CC. This PPy nano-crosslinked network not only established three-dimensional electron transport pathways on the Fe2O3 surface but also amplified the composite material's specific surface area to 45.229 m2 g-1, thereby promoting its electrochemical performance. At a current density of 2 mA cm-2, PPy/Co-Fe2O3@CC displayed an area specific capacitance of 704 mF cm-2, a value 2.2 times higher than that of Co-Fe2O3@CC. The assembled PPy/Co-Fe2O3@CC//Ni-MnO2@CC asymmetric supercapacitor demonstrated an energy density of 1.41 mW h cm-3 at a power density of 54 mW cm-3, making the synthesized electrode material a promising candidate for flexible supercapacitors.

microRNA-15b-5p shuttled by mesenchymal stem cell-derived extracellular vesicles protects podocytes from diabetic nephropathy via downregulation of VEGF/PDK4 axis.

Diabetic nephropathy (DN) is a severe complication of diabetes lethal for end-stage renal disease, with less treatment methodologies and uncertain pathogenesis. In the current study, we determined the role of mesenchymal stem cells (MSCs)-derived extracellular vesicles (EVs) containing microRNA (miR)-15b-5p in DN. After extraction and identification of MSC-derived EVs, mouse podocyte line MPC5 was selected to establish an in vitro high-glucose (HG) cell model, where expression of miR-15b-5p, pyruvate dehydrogenase kinase 4 (PDK4) and VEGFA expression in tissues and cells were determined. The loss- and gain- function assays were conducted to determine the roles of miR-15b-5p, PDK4 and VEGFA. MPC5 cells were then co-cultured with MSC-derived EVs and their biological behaviors were detected by Western blot, CCK-8 assay, and flow cytometry. The binding relationship between miR-15b-5p and PDK43 by dual luciferase reporter gene assay. The expression of miR-15b-5p was downregulated in podocytes under HG environment, but highly expressed in mouse MSCs-derived EVs. EVs-derived miR-15b-5p could protect MPC5 cell apoptosis and inflammation. miR-15b-5p inhibited the expression of PDK4 by directly bound to the 3'UTR region of PDK4 gene. miR-15b-5p inhibits VEGF expression by binding to PDK4. Inhibition of PDK4 decreased VEGFA expression and reduced apoptosis and inflammation. Collectively, miR-15b-5p shuttled by MSC-derived EV can play protective roles in HG-induced mouse podocyte injury, possibly by targeting PDK4 and decreasing the VEGFA expression.

Mayer-Rokitansky-Küster-Hauser Syndrome with a Solitary Duplex Kidney and Anal Stenosis: Report of a Rare Case.

BACKGROUND: To date, only 23 cases of Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome with duplex kidney have been reported. We present the first reported case of MRKH syndrome with solitary duplex kidney and anal stenosis. CASE: A 17-year-old Chinese girl presented with primary amenorrhea and fully developed secondary sex characteristics. Ultrasonography of the abdomen and pelvis revealed the absence of the right kidney, a left duplex kidney, and a primordial uterus. Surgery for anal stenosis was performed when she was 1 year of age. The patient had a normal 46, XX karyotype.

MiR-490-3p modulates the proliferation of vascular smooth muscle cells induced by ox-LDL through targeting PAPP-A.

AIMS: Oxidized low-density lipoprotein (ox-LDL) can induce vascular smooth muscle cell (VSMC) proliferation and differentiation, which is the important mechanism of the pro-atherogenic effects of ox-LDL. Although miRNAs are crucial regulators of the ox-LDL effects on VSMC, the detailed mechanisms are not fully elucidated. So, we investigated the miRNAs changes in the proliferation of human coronary artery smooth muscle cells (hCASMCs) induced by ox-LDL and the functional significance of some miRNAs, which were regulated significantly. METHODS AND RESULTS: Using miRNA microarray, real-time PCR, and luciferase reporter assay, our study showed that miR-490-3p and insulin-like growth factor-1 (IGF1) expression were down-regulated, whereas pregnancy-associated plasma protein A (PAPP-A) and IGF2 expression were up-regulated significantly in hCASMC treated by ox-LDL and/or in human atherosclerotic plaque. Further studies indicated PAPP-A was the target gene of miR-490-3p. The miR-490-3p mimic could inhibit the up-regulation of PAPP-A induced by ox-LDL in hCASMC, which resulted in the suppression of the metalloprotease effect of PAPP-A on IGF-binding protein-4 (IGFBP-4). All these effects led to the inhibition of the proliferation of hCASMC induced by ox-LDL. CONCLUSION: Ox-LDL could inhibit the expression of miR-490-3p and IGF1, whereas increase IGF2 expression. The inhibition of miR0-490-3p up-regulated its target gene PAPP-A and then increased the proteolysis of IGFBP-4. The increased expression of IGF2 and proteolysis of IGFBP-4 might activate pathways independent or dependent on IGF axis by autocrine and paracrine mechanisms and resulted in the VSMC proliferation. Our results could help us to understand the mechanisms of the pro-atherogenic effects of ox-LDL and the effects of PAPP-A on atherosclerosis development.

The association between the Survivin A9194G exon polymorphisms and papillary thyroid carcinoma risk in the Han Chinese population.

The dysregulation of apoptosis plays a key role in carcinogenesis. This study was designed to investigate the association of apoptosis-related gene survivin A9194G single-nucleotide polymorphisms (SNPs) with papillary thyroid carcinoma (PTC) susceptibility. A case-control study of 126 patients and 198 controls was performed to investigate the association between Survivin A9194G polymorphisms and PTC susceptibility by polymerase chain reaction (PCR) following DNA sequencing methods. Moreover, the distribution of genotype frequency and the association of genotype with clinicopathologic characteristics were analyzed. We found that the survivin A9194G genotype was at a decreased risk of PTC (P=0.003; odds ratio (OR)=0.56). Furthermore, compared to the PTCs of the AA and AG phenotypes, the GG genotype thyroid cancers were significantly more common in younger patients and in cases of lower pathologic stages. In conclusion, the survivin (A9194G) polymorphism was found to play a protective role in the susceptibility to PTC. Nevertheless, further investigation with a larger sample size is needed to support our results.