c-Jun (Phospho-Ser73) ELISA Kit

Background: Nowadays, it has not been reported in detail which factors have adverse effects on renal function after PNCL surgery in solitary kidney patients with staghorn calculi. To evaluate the risk factors that deteriorate the renal function in solitary kidney patients with staghorn calculi after percutaneous nephrolithotomy (PCNL). Methods: A retrospective study was performed on solitary kidney patients with staghorn calculi between March 2014 and Jun 2019. Renal function-related indexes were collected pre-operatively, and at 1 and 6 months post-operatively. These pre- and post-operative indexes were compared to study the risk factors on renal function. Results: Totally 71 solitary kidney patients with staghorn calculi were included with a male-to-female ratio of 53:18 and mean age of 54.3 +/- 10.2 years old. The mean pre-operative estimated glomerular filtration rate (eGFR) and serum creatinine were 55.1 +/- 18.9 mL/min/1.73 m(2) and 130.9 +/- 41.0 mu mol/L, respectively. The mean diameter of largest stones was 5.0 +/- 1.7 cm, and the stone-free rate was 71.8%. Univariate analysis showed urinary tract infection (UTI) was a significant risk factor for deteriorating renal function after PCNL. At 1 to 6 months after surgery, renal function deteriorated by both UTI and combined diseases. The surgical side at the right kidney, mild hydronephrosis, and surgical time without 20 min or beyond 40 min can deteriorate renal function. Multivariate analysis demonstrated UTI was the main factor leading to deteriorated renal function with increasing serum creatinine and declining eGFR. Conclusions: Preoperative UTI can deteriorate the renal function at 1 month after PCNL, and diabetes can deteriorate the postoperative renal function at 6 months after PCNL. Controlled perioperative UTI, diabetes and factors play a crucial role in protecting renal function after PCNL for solitary kidney patients with staghorn calculi.

Molecular mechanisms underlying luteinization (terminal differentiation of granulosa and theca cells after ovulation) and luteolysis (demise of corpus luteum) are poorly understood in human ovary. Here we report that activin-A, after binding to its cognate receptors induces a functional luteolytic state and reverses luteinization phenotype by downregulating the expression of the steroidogenic enzymes, LH receptor and VEGF and reducing estradiol (E-2) progesterone (P-4) production and upregulating FSH receptor and cyclin D1 expression in human primary luteinized granulosa cells. Further, this action of activin-A involves downregulation of JNK signaling pathway and is opposite to that of human chorionic gonadotropin (hCG), which acts as a luteotropic hormone and improves luteal function through the activation of JNK pathway in the same cell type. Reversal of luteinization phenotype in luteal granulosa cells by activin-A potentially makes this hormone an attractive candidate for use under certain clinical situations, where induction of luteolysis and rapid reduction of endogenous sex steroid levels are beneficial such as ovarian hyperstimulation syndrome (OHSS), in which the ovaries hyper-respond to gonadotropin stimulation by producing too many growing follicles along with development of ascites, pleural effusion, and hemo-concentrations as a result of increased vascular permeability and leakage of intravascular volume into third spaces. Our work unveils a previously undefined role for activin-A and JNK signaling pathway in human corpus luteum biology, that might have a direct clinical impact in assisted reproductive technologies.