Synthesis of ultra-thin graphene-like nanosheets from lignin based on evaporation induced self-assembly for supercapacitors.

Graphene-like carbon materials are widely used in power devices due to their excellent structural characteristics. In this study, ultra-thin graphene-like nanosheets (LGLNs) with rich surface wrinkles were prepared by classical evaporation induced self-assembly (EISA) using lignin biomass as carbon precursor, followed by chemical activation with KHCO3. The obtained LGLN900 material calcined at 900 °C had a thickness of ca. 3 nm, a large specific surface area of 2886 m2 g-1 with a high specific pore volume of 2.10 cm3 g-1. In addition, a large number of wrinkles on the surface of LGLN900 endows its effective compression resistance. When the LGLN900 material was used as electrode material of supercapacitor, a high specific capacitance of 388 F g-1 was obtained at 0.2 A g-1 current density in 6 M KOH aqueous solution, and 269 F g-1 specific capacitance could be at remained at 40 A g-1. The supercapacitor assembled with LGLN900 afforded a specific energy density of (11.0-13.7) Wh kg-1 at a power density of (128.8-6465) W kg-1. This work provides a facile and green strategy for the synthesis of highly wrinkled ultra-thin graphene-like nanosheets from sustainable biomass resources, which should have wide applications in adsorption, catalysis and energy storage.

Circular RNA-9119 suppresses in ovarian cancer cell viability via targeting the microRNA-21-5p-PTEN-Akt pathway.

We aimed to assess the regulatory role of circular RNA (circRNA)-9119 (circ9119) in ovarian cancer (OC) cell viability. The expression of circ9119 was clearly reduced in OC tissues and cell lines, whereas the microRNA-21-5p (miR-21) levels were elevated compared with those in normal healthy control tissues and immortalized fallopian epithelial cell line FTE187. Further, circ9119 was overexpressed, causing a notable decrease in the viability and proliferation of OC cells and an increase in apoptosis. Further study showed that circ9119 upregulation resulted in a decrease in miR-21 levels. Bioinformatics forecasting (starBase and TargetScan) and dual luciferase reporter assay demonstrated that circ9119 acts as an miR-21 sponge. Recovery of miR-21 expression in circ9119-overexpressing OC cells showed that miR-21 exhibited the opposite effect on circ9119; moreover, its recovery could suppress the effects of circ9119 overexpression, recover cell proliferation, and reduce apoptosis. Furthermore, miR-21 was found to target phosphatase and tensin homologue (PTEN) 3' untranslated region. PTEN protein and mRNA expression was reduced in OC tissues and cells, whereas it was increased on transfection with an miR-21 inhibitor. Thus, circ9119 could regulate cell proliferation and apoptosis of OC cells via by acting as an miR-21 sponge and targeting the PTEN-Akt pathway.

LncRNA MIR4435-2HG is a potential early diagnostic marker for ovarian carcinoma.

LncRNA MIR4435-2HG is characterized as an oncogene in lung cancer. However, its role in ovarian carcinoma (OC) is unclear. In this study, we aimed to investigate the role of MIR4435-2HG in OC. We found that both MIR4435-2HG and transforming growth factor beta 1 (TGF-ß1) were upregulated in OC. MIR4435-2HG is associated with tumor metastasis but not with tumor size. Upregulation of MIR4435-2HG distinguished early stage (Stage I and II) OC patients from healthy controls. Correlation analysis showed that plasma levels of MIR4435-2HG and TGF-ß1 were positively correlated only in OC patients. qPCR and western blot analysis results showed that MIR4435-2HG overexpression led to upregulation of TGF-ß1 in OC cells, while TGF-ß1 treatment did not significantly affect MIR4435-2HG expression. Transwell invasion and migration assays showed that MIR4435-2HG and TGF-ß1 promoted the invasion and migration of OC cells while TGF-ß inhibitor suppressed the invasion and migration of these cells. Further analysis of the Transwell invasion and migration assay results showed that TGF-ß inhibitor reduced the effects of MIR4435-2HG overexpression. Therefore, our results suggested that lncRNA MIR4435-2HG may promote OC by upregulating TGF-ß1. Further characterization of the functions of MIR4435-2HG in OC may provide novel targets for cancer therapies.

"Gilbert's-like" syndrome as part of a spectrum of persistent unconjugated hyperbilirubinemia in post-chronic hepatitis patients.

Gilbert's syndrome (GS) patients present with remittent unconjugated hyperbilirubinemia. In this study, we investigated the correlation between polymorphisms in the gene encoding UDP-glucuronosyltransferase, UGT1A1, and the development of unconjugated hyperbilirubinemia in clinical GS and post-hepatitis hyperbilirubinemia. Blood samples were collected from 285 patients, including 85 patients who were clinically diagnosed with GS, 70 patients who had indirect hyperbilirubinemia during the recovery period of chronic liver diseases, 109 patients with normal hepatic function and 21 chronic active hepatitis patients. All samples were tested for the presence of the *28/*6 UGT1A1 genotype by pyrosequencing. Compared with the GS-control group, a significant difference in variations of the UGT1A1*28/*6 allele gene was found in GS patients. The post-hepatitis group showed a significant difference in the UGT1A1*28/*6 allele gene frequency distribution relative to that in the hepatitis control group. There were no significant differences between the GS group and post-hepatitis group in the distribution of the UGT1A1*28/*6 allele gene frequency and UGT1A1 diplotypes. UGT1A1*28/*6 gene polymorphisms in patients who had indirect hyperbilirubinemia while recovering from chronic liver diseases presented similar patterns as those seen for GS patients. These findings suggest that a "Gilbert's-like" syndrome might be part of the spectrum of persistent unconjugated hyperbilirubinemia in post-chronic hepatitis patients.

Dehydroepiandrosterone-Regulated Testosterone Biosynthesis via Activation of the ERK1/2 Signaling Pathway in Primary Rat Leydig Cells.

BACKGROUND: Dehydroepiandrosterone decreases with age and this reduction has been shown to be associated with physical health in human. Some studies have suggested that the effects of DHEA are exerted after it is biotransformed into more biologically-active hormones in peripheral target cells. This study investigated the effects of DHEA on the testosterone biosynthesis and possible signaling pathway mechanism underlying these DHEA effects were also explored in primary rat Leydig cells. METHODS: Primary Leydig cells were treated with DHEA and then detected testosterone content by RIA and steroidogenic enzymes, ERK1/2 signal pathway factors protein expression level by Western blot. RESULTS: Incubation of primary Leydig cells with DHEA significantly increased testosterone content and 3ß-HSD and 17ß-HSD protein expression levels, while aromatase protein expression levels were decreased. Compared with the control group, p-ERK1/2 and p-CREB protein levels were significantly increased in DHEA-treated groups. Testosterone content was significantly decreased in the DHEA-treated group pre-incubated with U0126 (p-ERK1/2 inhibitor). Additionally, the rise in p-ERK1/2, 3ß-HSD and 17ß-HSD protein levels induced by DHEA was reversed when cells were pre-incubated with U0126. Interestingly, no significant difference was found in aromatase protein expression level in cells pretreated with U0126. CONCLUSION: These findings demonstrate that (a) exogenous DHEA might preferentially convert to testosterone rather than estradiol due to the up-regulation of 3ß-HSD and 17ß-HSD protein levels and the down-regulation of aromatase protein level in primary Leydig cells, and (b) the action of DHEA is at least partly associated with the elevation of p-ERK1/2 and p-CREB protein levels.

Ample Evidence: Dehydroepiandrosterone (DHEA) Conversion into Activated Steroid Hormones Occurs in Adrenal and Ovary in Female Rat.

Dehydroepiandrosterone (DHEA) is important for human health, especially for women. All estrogens and practically half of androgens are synthesized from DHEA in peripheral tissues. However, the mechanism and exact target tissues of DHEA biotransformation in the female are not fully clear. The present study showed that maximal content of androstenedione (AD) and testosterone (T) were observed at 3h after DHEA administration in female rats, which was 264% and 8000% above the control, respectively. Estradiol (E2) content significantly increased at 6h after DHEA administration, which was 113% higher than that in control group. Gavage with DHEA could significantly reduce 3ß-hydroxysteroid dehydrogenase (3ß-HSD) mRNA level at 3-12h and 17ß-hydroxysteroid dehydrogenase (17ß-HSD) mRNA level at 12h in ovary, while increasing aromatase mRNA levels at 6, 24, and 48 h. It is interesting that administration of DHEA caused a significant increase of 17ß-HSD, 3ß-HSD and aromatase mRNA levels in adrenal. The AD and T contents also markedly increased by 537% and 2737% after DHEA administration in ovariectomised rats, in company with a significant increase in 17ß-HSD and 3ß-HSD mRNA levels and decreased aromatase mRNA level in adrenal. However, DHEA administration did not restore the decreased E2, estrone (E1), and progesterone (P) caused by the removal of the ovaries in females. These results clearly illustrated that exogenous DHEA is preferentially converted into androgens in adrenal, while its conversion to estrogens mainly happens in the ovary through steroidogenic enzyme in female rats.