Search

Research question What is the effect of C-type natriuretic peptide (CNP) on human sperm capacitation in vitro and what is the mechanism of this effect? Design CNP/NPR-B expression in the female rat genital tract was examined by immunohistochemistry and western blot assay, and then the role of CNP in human sperm capacitation was determined. The signal transduction pathway of CNP in the process was determined to elucidate the regulation mechanism of CNP by enzyme-linked immunosorbent assay and flow cytometry. Results Both CNP and NPR-B were expressed in the genital tract of female rats, especially in the mucosa epithelium cell of the oviduct; the CNP level in the rat oviduct was higher than that in the cervix. Both CNP and NPR-B level in the rat oviduct varied during the oestrus cycle, maximal expression being observed at proestrus. Furthermore, intracellular cGMP level in spermatozoa was significantly enhanced by CNP (P Conclusions CNP secreted by the female genital tract might bind to NPR-B on the spermatozoa. It successively stimulated intracellular cGMP/PKG signalling, increased Ca2+ and tyrosine-phosphorylated proteins, promoted hyperactivation and induced the acrosome reaction, which ultimately facilitated sperm capacitation.

Background Measurement of the biomarker copeptin may help identify disease severity and risk of mortality for a various diseases. This study sought to determine the relationship between copeptin and all-cause mortality of patients with cardio-cerebrovascular disease. Methods Database of Medline and Web of Science were searched for studies with data involving the baseline copeptin levels and subsequent all-cause mortality outcomes. The pooled HRs of all-cause mortality were calculated and presented with 95% CI s. Subgroup analysis and sensitivity analysis were conducted to explore the possible sources of heterogeneity. Results Data from 14,395 participants were derived from 28 prospective studies. Higher copeptin significantly increased the risk of all-cause mortality (per unit copeptin: HR = 1.020, 95% CI = 1.004–1.036; log unit copeptin: HR = 2.884, 95% CI = 1.844–4.512; categorical copeptin: HR = 3.371, 95% CI = 2.077–5.472). Subgroup analysis indicated that the risk of all-cause death was higher in cerebrovascular patients (per unit copeptin: HR = 2.537, 95% CI = 0.956–6.731; log unit copeptin: HR = 3.419, 95% CI = 2.391–4.888) than cardiovascular patients (per unit copeptin: HR = 1.011, 95% CI = 1.002–1.020; log unit copeptin: HR = 2.009, 95% CI = 1.119–3.608). Conclusion Copeptin is associated with all-cause mortality of patients with cardiovascular and cerebrovascular disease. Our study suggests that copeptin seems to be a promising novel biomarker for prediction of mortality in cardio-cerebrovascular patients, especially for cerebrovascular patients.

Objective To study the functions of urokinase receptor (uPAR) during spermatogenesis by adding targeted siRNA cocktails to the co-culture of Sertoli cell with spermatogenic cells. Methods The seminiferous tubule samples from SD rats aged 20-23 d were digested with collagenase for 15-20 min, then were cut into small fragments. Tubular fragments were digested with collagenase again for 5-10 min, then gently resuspended in F12/DMEM supplemented with vitamins and hormones. Cell samples were seeded in plate and cultured at 32°C for 2 weeks. After 48 h, siRNA cocktails at a concentration of 15 nmol/L or 30 nmol/L were introduced into this cocultured Sertoli/spermatogenic cells. After then for 48 h, expression of uPAR mRNA was analyzed by real-time RT-PCR. Results Some spermatogenic cells took place morphologic changes and generated an obvious flagellum. The expression levels of uPAR mRNA silencing with siRNA cocktails at a concentration of 15 nmol/L or 30 nmol/L were significantly lower than those in nontransfected group (P Conclusion The meiosis and spermiogenesis could take place in this culture system, and the siRNA cocktails can effectively inhibit the gene expression of uPAR in co-cultured Sertoli/spermatogenic cells.