Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects reproductive dysfunction and metabolism in women of childbearing age. An increasing number of studies have suggested that the bone morphogenetic protein 15 (BMP15) signalling pathway serves an important role in the pathogenesis of PCOS; however, the full mechanism remains unknown. The present study revealed that intrinsic follicular dysplasia may be associated with regulation disorders of ovarian granulosa cell apoptosis. Compared with the control group, body mass index, luteinising hormone and testosterone levels were significantly increased (P<0.05). The percentage of S phase cells was significantly higher, cells in G2/M phase cells was significantly lower, and cells undergoing apoptosis was significantly higher in the PCOS group compared with the control group (P<0.05). The expression levels of B‑cell lymphoma 2 was significantly decreased in granulosa cells of PCOS group, whereas the expression of caspase‑3 was higher than the control group (P<0.05). The rate of apoptosis of granulosa cells was measured by a terminal deoxynucleotide transferase dUTP nick‑end labelling assay. The relative mRNA expression levels of BMP receptor 2 and SMAD1 were significantly decreased in granulosa cells in the PCOS group compared with the control (P<0.05). In addition, the expression of BMP15 in follicular fluid and Smad1 in granulosa cells was significantly decreased in the PCOS group compared with the control (P<0.05). The data suggested that the BMP15/Smad1 signalling pathway may be involved in granulosa cell apoptosis, and may be a target for clinical treatment for PCOS.

No abstract

Polycystic ovary syndrome (PcoS) is one of the most common endocrine metabolic disorders characterized by hyperandrogenism, polycystic ovaries and ovulatory dysfunction. Several studies have suggested that the aberrant expression of micrornas (mirnas/mirs) plays an important role in the pathogenesis of PcoS; however, the role and underlying mechanisms of mir-132 in the development of PcoS remain unclear. in the present study, the expression of mir-132 in granulosa cells (Gcs) derived from 26 patients with PcoS and 30 healthy controls was detected by reverse transcription-quantitative Pcr (rT-qPcr). The apoptosis of Gcs was examined using a Tunel assay. The human ovarian granulosa-like tumor cell line, KGn, was cultured for cell counting Kit-8 assays following the overexpression or knockdown of mir-132. TargetScan was applied to identify the potential targets of mir-132, which was further verified by a luciferase assay, RT-qPCR and western blotting. The expression of mir-132 was decreased in Gcs from patients with PcoS. Moreover, the Gcs of patients with PCOS exhibited significantly increased apoptotic nuclei. Furthermore, the overexpression of mir-132 inhibited the viability of KGN cells. In addition, the results verified that mir-132 directly targeted forkhead box protein a1 (Foxa1), the knockdown of which suppressed KGn cell viability. on the whole, the findings of the present study demonstrated that mir-132 inhibited cell viability and induced apoptosis by directly interacting with Foxa1. Thus, mir-132 may be a potential target for the treatment of patients with PcoS.

Objective. To summarize the advantages of peritoneal dialysis (PD) catheters without capsular puncture (only one pneumoperitoneum needle) puncture technique conducted by our center. Methods. The study examines the clinical data of PD patients (including the general situation of patients, intraoperative and postoperative characteristics, and complications) undergoing pneumoperitoneum needle catheterization from January 2019 to May 2021 in the Department of Nephrology at the First Affiliated Hospital of Hebei North University (the largest peritoneal dialysis center in Zhangjiakou). Results. A total of 153 surgical cases were collected. There were 91 males and 62 females. The mean (± standard deviation) age was 56.1 ± 18.6 years, and the mean (± standard deviation) follow-up time was 16.7 ± 8.2 months. The average operation time was 30.33 minutes with a standard deviation of 14.80 minutes. The length of abdominal incision is 2.38 ± 0.42   cm , and the blood loss was about 26.3 ± 9.2   ml , including 2 cases of laparoscopic reposition of drift tube, 0 case of pipe blockage, 3 cases of fluid leakage, 1 case of peritoneal dialysis catheter tunnel infection, 4 cases of outlet infection, 12 occurrences of peritonitis, 121.3 patient months in peritonitis, and 0 times in omentum wrapping without bladder injury, incisional hernia, or intestinal injury. Conclusion. Relative to open operation, the peritoneal dialysis (PD) catheters with pneumoperitoneum needle puncture technique has the following advantages: simpler operation, shorter operation time, less bleeding, less injury, less complications, and higher safety. Moreover, there are no additional costs compared with open operation. Thus, the technique is recommended for clinical applications.

SH3 and cysteine-rich protein 3 (STAC3), a small adapter protein originally identified as a core component of excitation–contraction coupling machinery, regulates the voltage-induced Ca2+ release in skeletal muscle. However, the possibility of additional, as yet unknown, non-muscle effects of STAC3 cannot be ruled out. Herein, we provide the evidence for the expression and functional involvement of STAC3 in spermatogenesis. STAC3 expression was localized in the testicular interstitium of rodent and human testes. By using the cytotoxic drug ethylene dimethane sulfonate (EDS), STAC3 expression was observed to be decreased sharply in rat testis after selective withdrawal of Leydig cells (LCs), and reappeared immediately after LCs repopulation, indicating that testicular expression of STAC3 mainly stems from LCs. From a functional standpoint, in vivo lentiviral vector–mediated suppression of STAC3 resulted in a significant decrease in testosterone production, and thereafter caused impairment of male fertility by inducing oligozoospermia and asthenospermia. The indispensible involvement of STAC3 in testicular steroidogenesis was validated using the in vivo knockdown model with isolated primary LCs as well as in vitro experiments with primary LCs. By generating the TM3Stac3−/− cells, we further revealed that STAC3 depletion attenuated mitochondrial membrane potential and StAR processing in db-cAMP-stimulated LCs. Thus, the inhibitory effect of STAC3 deficiency on testicular steroidogenesis may be ascribed to a disturbed mitochondrial homeostasis. Collectively, the present results strongly suggest that STAC3 may function as a novel regulator linking mitochondrial homeostasis and testicular steroidogenesis in LCs. Our data underscore an unexpected reproductive facet of this muscle-derived factor.