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Primary membranous nephropathy (PMN) is associated with the highest risk for developing venous thrombosis compared with other nephrotic diseases. The aim of the study was to assess the predictive value of the pathognomonic anti-phospholipase A2 receptor (PLA2R) antibody with regard to incidence of venous thrombosis in PMN. A total of 365 in-hospital patients diagnosed with PMN were enrolled in the study. Anti-PLA2R antibody was detected by commercial enzyme-linked immunosorbent assay. Multivariate logistic regression was used to detect the independent risk factors for venous thrombosis. Thirty-seven patients (10.14%) had venous thrombosis. Patients with venous thrombosis had higher levels of cholesterol (CHOL), low-density lipoprotein (LDL), and D-dimer than those without venous thrombosis (p <.05). Patients with venous thrombosis had significantly lower levels of albumin (23.95 ± 5.53 vs. 26.18 ± 6.59 g/L, p =.049). No significant differences were found in proteinuria, serum creatinine, estimated glomerular filtration rate, platelets, and fibrinogen between patients with and without thrombosis. Anti-PLA2R antibody levels in patients with venous thrombosis were significantly higher than in patients without it (p =.002). In the univariate logistic regression, Ln anti-PLA2R antibody (OR: 1.340; p =.004), albumin (OR: 0.945; p =.050), CHOL (OR: 1.191; p =.006), and LDL (OR: 1.271, p =.006) were associated with venous thrombosis. Ln anti-PLA2R antibody (OR = 1.269; 95%CI: 1.032–1.561), and LDL (OR = 1.213; 95%CI: 1.017–1.448) were the independent risk factors for venous thrombosis (p <.05) in multivariate analysis. Anti-PLA2R antibody was the independent risk factor for venous thrombosis in PMN. Larger prospective studies were warranted to verify the results in future. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the effects of ardipusilloside I isolated from Ardisia pusilla on tumor angiogenesis and its mechanism of action. The anti-angiogenic effect in vivo was evaluated on xenograft in the athymic mice model and the chicken chorioallantoic membrane (CAM) neovascularization model, the inhibition of growth in vitro was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, and the mechanism was demonstrated through detecting microvessel density (MVD), vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2) and P-VEGFR2 protein expressions, as well as mRNA expressions of VEGF and VEGFR2. The results showed that ardipusilloside I had a good inhibitory effect on A549 xenografted tumor growth, angiogenesis of CAM, and A549 cell growth. Compared to the negative control, MVD protein and mRNA expressions of VEGF and VEGFR were significantly inhibited by ardipusilloside I in a dose-dependent manner. These findings suggested that ardipusilloside I might be a promising candidate as angiogenesis inhibitors. [ABSTRACT FROM AUTHOR]

Chronic stress is considered to predispose to various cardiovascular events such as coronary artery disease, hypertension, and even heart failure. In this study, rats were exposed to stress for 1 day, 1, 2, 3, and 4 weeks to establish a chronic stress model. A specific toll-like receptor 4 (TLR4) antagonist eritoran was used to block the activity of TLR4. On the second day after the last stress exposure, the animals were killed. The expression of TLR4 mRNA and nuclear factor-kappa B (NF-κB) DNA-binding activity in the myocardium were measured using reverse transcriptase polymerase chain reaction and electrophoretic mobility shift assay. The proinflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL-6) in myocardium were assayed by enzyme-linked immunosorbent assay. Myocardial injury was evident after chronic stress for 2 weeks. The TLR4 mRNA expression reached a peak after stress for 1 week. It was sustained at a stable level after stress exposure for 3 weeks and was restored to a nearly normal level in the fourth week. NF-κB DNA-binding activity was significantly enhanced after the stress for 1 day and markedly enhanced again after a 2-week stress exposure. It was weakened and reached a normal level after stress exposure for 4 weeks. The levels of TNF-α and IL-6 gradually increased and reached peaks after stress for 4 weeks. Meanwhile, eritoran significantly decreased the TLR4 mRNA expression and NF-κB activity in rats from the 2-week stress group. However, it did not downregulate the levels of TNF-α and IL-6. Importantly, it significantly improved the myocardial injury induced by the chronic stress. In conclusion, TLR4/NF-κB participates in myocardial injury during chronic stress. [ABSTRACT FROM AUTHOR]