Wintersgibbs1231

Soybean seeds contain many antioxidants, including flavonoids and other phytochemicals. Isoflavone is a phytoestrogen that mimics estrogenic effects on target tissues and also exerts antioxidant activity by sequestering free radicals. Despite many cultivars developed to date, varietal differences in flavonoid content and antioxidant activity in Japanese soybean accessions remain less well characterized. Here, we evaluated the seed content of isoflavones, total flavonoids, and total phenolics in 26 soybean accessions. Tanespimycin solubility dmso Next, the antioxidant activity of each accession was examined using antioxidant responsive element (ARE) linked to a luciferase reporter in human HepG2 stable cells. The relative ARE luciferase activity rate of all soybean accessions varied up to 4-fold which ranged from 1.00 to 4.02; and 22 accessions exhibited significant antioxidant activities. Correlation analysis indicated that the level of total isoflavone moderately correlated with antioxidant activity.

This study aimed to describe pulmonary high-resolution CT (HRCT) findings in Takayasu arteritis (TA) and to determine possible causes.

A total of 243 TA patients were enrolled from a prospective cohort after excluding patients with other pulmonary disorders or incomplete data. Patients were divided into two groups those with normal lung HRCT and those with abnormal lung HRCT. Clinical characteristics were compared between groups and binary logistic regression analysis was applied to identify possible causes of the lung lesions. Follow-up HRCT (obtained in 64 patients) was analysed to study changes in pulmonary lesions after treatment.

Of the 243 patients, 107 (44.0%) had normal lung HRCT while 136 (56.0%) had abnormal lung HRCT, including stripe opacity (60.3%), nodules (44.9%), patchy opacity (25.0%), pleural thickening (15.4%), pleural effusion (10.3%), ground-glass opacity (8.1%), pulmonary infarction (6.6%), mosaic attenuation (4.4%), bronchiectasis (3.7%) and pulmonary oedema (2.2%). Patients with abnormal HRCT were significantly more likely to have type II arterial involvement (25% vs 12.2%, P = 0.04), pulmonary arterial involvement (PAI; 21.3% vs 5.6%, P < 0.001), pulmonary hypertension (20.6% vs 8.4%, P = 0.01) and abnormal heart function (27.9% vs 7.6%, P < 0.001). Logistic regression analysis demonstrated that PAI, worsened heart function and age were associated with presence of pulmonary lesions. Pulmonary infarction, pleural effusion and patchy opacities improved partially after treatment.

Pulmonary lesions are not rare in patients with TA. Age, PAI and worsened heart function are potential risk factors for presence of pulmonary lesions in TA.

Pulmonary lesions are not rare in patients with TA. Age, PAI and worsened heart function are potential risk factors for presence of pulmonary lesions in TA.Prostate cancer (PCa) is one of the important factors of cancer deaths especially in the western countries. Hispidulin (4',5,7-trihydroxy-6-methoxyflavone) is a phenolic flavonoid compound proved to possess anticancer properties, but its effects on PCa are left to be released. The aims of this study were to investigate the effects and the relative mechanisms of Hispidulin on PCa development. Hispidulin administration inhibited proliferation, invasion, and migration, while accelerated apoptosis in Du145 and VCaP cells, which was accompanied by PPARγ activation and autophagy enhancement. The beneficial effects of Hispidulin could be diminished by PPARγ inhibition. Besides, Hispidulin administration suppressed PCa tumorigenicity in Xenograft models, indicating the anticancer properties in vivo. Therefore, our work revealed that the anticancer properties of Hispidulin might be conferred by its activation on PPARγ and autophagy.N6-methyladenosine (m6A) catalyzed by METTL3 regulates the maternal-to-zygotic transition in zebrafish and mice. However, the role and mechanism of METTL3-mediated m6A methylation in blastocyst development remains unclear. Here, we show that METTL3-mediated m6A methylation sustains porcine blastocyst development via negatively modulating autophagy. We found that reduced m6A levels triggered by METTL3 knockdown caused embryonic arrest during morula-blastocyst transition and developmental defects in trophectoderm cells. Intriguingly, overexpression of METTL3 in early embryos resulted in increased m6A levels and these embryos phenocopied METTL3 knockdown embryos. Mechanistically, METTL3 knockdown or overexpression resulted in a significant increase or decrease in expression of ATG5 (a key regulator of autophagy) and LC3 (an autophagy marker) in blastocysts, respectively. m6A modification of ATG5 mRNA mainly occurs at 3'UTR, and METTL3 knockdown enhanced ATG5 mRNA stability, suggesting that METTL3 negatively regulated autophagy in an m6A dependent manner. Furthermore, single-cell qPCR revealed that METTL3 knockdown only increased expression of LC3 and ATG5 in trophectoderm cells, indicating preferential inhibitory effects of METTL3 on autophagy activity in the trophectoderm lineage. Importantly, autophagy restoration by 3MA (an autophagy inhibitor) treatment partially rescued developmental defects of METTL3 knockdown blastocysts. Taken together, these results demonstrate that METTL3-mediated m6A methylation negatively modulates autophagy to support blastocyst development.Interleukin-1 receptor-associated kinase-3 (IRAK3) has a distinctive role in regulating inflammation. However, the functional role of IRAK3 and regulatory mechanism underlying the pathogenesis of osteoarthritis (OA) remain unclear. Here, we first found that IRAK3 was upregulated, while miR-33b-3p was downregulated in the cartilage of OA patients and IL-1β-induced CHON-001 cells. IRAK3 was confirmed as the direct target of miR-33b-3p and negatively regulated by miR-33b-3p. There was an inverse correlation between IRAK3 mRNA expression and miR-33b-3p expression in OA cartilage tissues. The in vitro functional experiments showed that miR-33b-3p overexpression caused a remarkable increase in viability, a significant decrease in inflammatory mediators (IL-1β and TNF-α), and apoptosis in IL-1β-induced CHON-001 cells. Importantly, IRAK3 knockdown imitated, while overexpression reversed the effects of miR-33b-3p on IL-1β-induced inflammation and apoptosis in CHON-001 cells. Collectively, miR-33b-3p significantly alleviated IL-1β-induced inflammation and apoptosis by downregulating IRAK3, which may serve as a promising target for OA.