Core-Shell Structured Carbon Nanofiber-Based Electrodes for High-Performance Supercapacitors.

The combination of multiple electrode materials and their reasonable structural design are conducive to the preparation of composite electrodes with excellent performance. In this study, based on carbon nanofibers grown with Ni(OH)2 and NiO (CHO) prepared by electrospinning, hydrothermal growth, and low-temperature carbonization, five transition metal sulfides (MnS, CoS, FeS, CuS, and NiS) were hydrothermally grown on their surfaces, exhibiting that CHO/NiS had the optimal electrochemical properties. Subsequently, the effect of hydrothermal growth time on CHO/NiS revealed that the electrochemical performance of CHO/NiS-3h was optimal, with a specific capacitance of up to 1717 F g-1 (1 A g-1), due to its multistage core-shell structure. Moreover, the diffusion-controlled process of CHO/NiS-3h dominated its charge energy storage mechanism. Finally, the asymmetric supercapacitor assembled with CHO/NiS-3h as the positive electrode demonstrated an energy density of 27.76 Wh kg-1 at a maximum power density of 4000 W kg-1, and it still maintained a power density of 800 W kg-1 at a maximum energy density of 37.97 Wh kg-1, exhibiting the potential application of multistage core-shell composite materials in high-performance supercapacitors.

Experimental studies on computed tomographic peritoneography. Peritoneal and residual renal function tolerance to iodinated contrast media injected into the peritoneal cavity.

Computed tomographic (CT) peritoneography has been widely used as reference standard to evaluate continuous ambulatory peritoneal dialysis-related complications. However, given the varying CT peritoneography approaches used across different institutions, there is no standard value for non-ionic iodinated contrast media (ICM) concentration. Few studies have currently investigated whether non-ionic iodinated contrast media (non-ionic ICM) affects peritoneal function or residual renal function (RRF). This study aimed to determine whether different non-ionic ICM concentrations affect peritoneum and RRF and attempted to evaluate CT peritoneography images to identify the optimal non-ionic ICM concentrations in animals. To this end, 25 male Sprague-Dawley rats were used to establish uraemic models, after which they were injected with a 40-mL mixture of peritoneal dialysate and iohexol at varying concentrations prior to CT peritoneography. Thereafter, two experienced radiologists blinded to the rat groupings evaluated image quality, peritoneal morphology and thickness were assessed using hematoxylin and eosin and Masson staining, and RRF was evaluated using serum creatinine levels hematoxylin and eosin staining of pathological kidney sections. Briefly, non-ionic ICM had negligible effects on the peritoneum and RRF. Our results suggest that a mixture containing 50 mL (350 mgI/mL) iohexol/2 L peritoneal dialysate can be used as reference in rats.

BMP6 regulates AMH expression via SMAD1/5/8 in goat ovarian granulosa cells.

Anti-Müllerian hormone (AMH) is produced by ovarian granulosa cells (GCs)and plays a major role in inhibiting the recruitment of primordial follicles and reducing the sensitivity of growing follicles to follicle-stimulating hormone (FSH). Bone morphogenetic protein 6 (BMP6) has similar spatiotemporal expression to AMH during follicular development, suggesting that BMP6 may regulate AMH expression. However, the specific mechanism by which BMP6 regulates AMH expression remains unclear. The objectives of this study were to examine the molecular pathway by which BMP6 regulates AMH expression. The results showed that BMP6 promoted the secretion and expression of AMH in goat ovarian GCs. Mechanistically, BMP6 upregulated the expression of sex-determining region Y-box 9 (SOX9) and GATA-binding factor 4 (GATA4), which was associated with the transcriptional initiation of AMH. AMH expression was significantly decreased by GATA4 knockdown. Moreover, BMP6 treatment promoted the phosphorylation of SMAD1/5/8, whereas inhibiting the SMAD1/5/8 signaling pathway significantly abolished BMP6-induced upregulation of AMH and GATA4 expression. Interestingly, the activation of SMAD1/5/8 alone did not affect the expression of AMH or GATA4. The results suggested that BMP6 upregulated GATA4 through the SMAD1/5/8 signaling pathway, which in turn promoted AMH expression.

BMP6 Promotes the Secretion of 17 Beta-Estradiol and Progesterone in Goat Ovarian Granulosa Cells.

The purpose of this study was to investigate the effects of BMP6 on the function of goat ovarian granulosa cells (GCs). The results showed that the exogenous addition of BMP6 did not affect the EdU-positive ratio of ovarian GCs and had no significant effect on the mRNA and protein expression levels of the proliferation-related gene PCNA (p > 0.05). Meanwhile, BMP6 had no significant effect on the cycle phase distribution of GCs but increased the mRNA expression of CDK4 (p < 0.05) and CCND1 (p < 0.01) and decreased the mRNA expression of CCNE1 (p < 0.01). Moreover, BMP6 had no significant effect on the apoptosis rate of GCs and did not affect the mRNA expression levels of apoptosis-related genes BAX, BCL2, and Caspase3 (p > 0.05). Importantly, BMP6 upregulated the secretion of 17 beta-estradiol (E2) and progesterone (P4) in ovarian GCs (p < 0.01). Further studies found that BMP6 inhibited the mRNA expression of 3ß-HSD and steroid synthesis acute regulator (StAR) but significantly promoted the mRNA expression of the E2 synthesis rate-limiting enzyme CYP19A1 and the P4 synthesis rate-limiting enzyme CYP11A1 (p < 0.01). Taken together, these results showed that the exogenous addition of BMP6 did not affect the proliferation, cell cycle, and apoptosis of goat ovarian GCs but promoted the secretion of E2 and progesterone P4 in ovarian GCs by upregulating the mRNA expressions of CYP19A1 and CYP11A1.

Metabolomic profiling identifies a novel mechanism for heat stroke­related acute kidney injury.

Heat stroke can induce a systemic inflammatory response, which may lead to multi­organ dysfunction including acute kidney injury (AKI) and electrolyte disturbances. To investigate the pathogenesis of heat stroke (HS)­related AKI, a mouse model of HS was induced by increasing the animal's core temperature to 41˚C. Blood samples obtained from the tail vein were used to measure plasma glucose and creatinine levels. Micro­positron emission tomography­computed tomography (micro­PET/CT), H&E staining and transmission electron microscopy were conducted to examine metabolic and morphological changes in the mouse kidneys. Immunohistochemistry (IHC) and western blot analyses were performed to investigate the expression of apoptosis­inducing factor mitochondria­associated 2 (Aifm2), high­mobility group box 1 (HMGB1) and receptor for advanced glycosylation end products (RAGE). Liquid chromatography­mass spectrometry analysis was conducted to find differential metabolites and signaling pathways. The HS mouse model was built successfully, with significantly increased creatinine levels detected in the serum of HS mice compared with controls, whereas micro­PET/CT revealed active metabolism in the whole body of HS mice. H&E and TUNEL staining revealed that the kidneys of HS mice exhibited signs of hemorrhage and apoptosis. IHC and western blotting demonstrated significant upregulation of Aifm2, HMGB1 and RAGE in response to HS. Finally, 136 differential metabolites were screened out, and enrichment of the 'biosynthesis of unsaturated fatty acids' pathway was detected. HS­associated AKI is the renal manifestation of systemic inflammatory response syndrome, and may be triggered by the HMGB1/RAGE pathway. Metabolomics indicated increased adrenic acid, docosahexaenoic acid and eicosapentaenoic acid may serve as metabolic biomarkers for AKI in HS. The findings suggested that a correlation between the HMGB1/RAGE pathway and biosynthesis of unsaturated fatty acids may contribute to the progression of HS­related AKI.

The mechanism of Single strand binding protein-RecG binding: Implications for SSB interactome function.

The Escherichia coli single-strand DNA binding protein (SSB) is essential to viability where it functions to regulate SSB interactome function. Here it binds to single-stranded DNA and to target proteins that comprise the interactome. The region of SSB that links these two essential protein functions is the intrinsically disordered linker. Key to linker function is the presence of three, conserved PXXP motifs that mediate binding to oligosaccharide-oligonucleotide binding folds (OB-fold) present in SSB and its interactome partners. Not surprisingly, partner OB-fold deletions eliminate SSB binding. Furthermore, single point mutations in either the PXXP motifs or, in the RecG OB-fold, obliterate SSB binding. The data also demonstrate that, and in contrast to the view currently held in the field, the C-terminal acidic tip of SSB is not required for interactome partner binding. Instead, we propose the tip has two roles. First, and consistent with the proposal of Dixon, to regulate the structure of the C-terminal domain in a biologically active conformation that prevents linkers from binding to SSB OB-folds until this interaction is required. Second, as a secondary binding domain. Finally, as OB-folds are present in SSB and many of its partners, we present the SSB interactome as the first family of OB-fold genome guardians identified in prokaryotes.

Schisandrin B Improves the Renal Function of IgA Nephropathy Rats Through Inhibition of the NF-κB Signalling Pathway.

Schisandrin B (SchB) is an active compound extracted from the Chinese herb Schisandra chinensis and shows excellent anti-inflammatory activity. This study was performed to examine the effects of SchB in a rat model of IgA nephropathy (IgAN). IgAN was established in Sprague-Dawley rats by immunization with lipopolysaccharide (LPS), bovine serum albumin, and carbon tetrachloride. Renal function was evaluated by determining the levels of urinary red blood cells, proteinuria, blood urea nitrogen (BUN), and creatinine (Cr). Renal tissue and protein samples were collected for further analysis. Pre-treatment and treatment with SchB significantly ameliorated renal function of IgAN rats, which was evidenced by decreased levels of proteinuria, hematuria, BUN, and Cr. IgAN rats exhibited increased serum IgA, renal IgA deposition, mesangial cell proliferation, and inflammatory cell infiltration, which were significantly attenuated by intervention with SchB. Moreover, SchB inhibited infiltration of CD3+ and CD11b+ cells, decreased levels of tumour necrosis factor-alpha, interleukin-1ß, and monocyte chemoattractant protein-1 in the kidney, and decreased the numbers of CD3+CD69+ cells in the spleen. Of note, SchB therapy significantly increased cytoplasmic p65 and IκB expression and decreased nuclear p65 levels both in the damaged renal tissue and LPS-stimulated HK-2 cells, indicating a direct inhibitory effect on the NF-κB pathway in IgAN rats. Taken together, our data provide insight into a new application of SchB for the treatment of IgAN and represent a novel mechanism behind these effects.

[Aliskiren inhibits angiotensin II/angiotensin 1-7(Ang II/Ang1-7) signal pathway in rats with diabetic nephropathy].

Objective To investigate the role of aliskiren (AL) in the angiotensinII/ angiotensin 1-7 (AngII/Ang1-7) signal pathway in renal tissue of diabetic nephropathy (DN) rats. Methods 40 male SD rats were randomly divided into 4 groups including normal group, diabetes group, AL group and valsartan (Val) group. Animal models of diabetes were induced by high fat diet combined with small dose of streptozotocin injection. Rats in AL group were administered 50 mg/(kg.d) AL by gavage, and rats in Val group were administered 30 mg/(kg.d)Val by gavage. 24-hour urine protein (24 h-UP) were observed by Coomassie blue colorimetry at 2, 4 and 6 weeks after modeling, serum creatinine was detected by automatic biochemical analyser, kidney index [kidneys mass(g)/body mass (kg)] was measured. HE and PAS staining were used to observe renal pathological changes. Immunohistochemistry was used to detect the expression of ACE2, MAS receptor, AT1R and AT2R in the kidney. Results After 6 weeks of modeling, there was no significant difference in creatinine level among groups. The levels of glucose, 24 h-UP and kidney index in diabetes group, AL group and Val group significantly increased. Compared with diabetes group, the levels of 24 h-UP and kidney index were lower in AL group and Val group. Immunohistochemistry showed that the expression of AT2R and ACE2 was lower and the expression of MAS receptor was higher in AL group than diabetes group and Val group. Compared to normal group and Val group, AT1R expression was significantly up-regulated in AL group, without significant difference between diabetes group and AL group. Conclusion AL down-regulates the expression of AT2R and ACE2, thus inhibits the AngII/ Ang1-7 signal axis and improves/alleviates the symptoms in diabetic rats.