Rsad2 mediates Bisphenol A-induced actin cytoskeletal disruption in mouse spermatocytes.

Bisphenol A (BPA) is widely exposed in populations worldwide and has negative effects on spermatogenesis both in animals and humans. The homeostasis of the actin cytoskeleton in the spermatogenic epithelium is crucial for spermatogenesis. Actin cytoskeleton destruction in the seminiferous epithelium is one of the important reasons for BPA-induced spermatogenesis disorder. However, the underlying molecular mechanisms remain largely unexplored. Herein, we explored the role and mechanism of Rsad2, an interferon-stimulated gene in BPA-induced actin cytoskeleton disorder in mouse GC-2 spermatocyte cell lines. After BPA exposure, the actin cytoskeleton was dramatically disrupted and the cell morphology was markedly altered accompanied by a significant increase in Rsad2 expression both in mRNA and protein levels in GC-2 cells. Furthermore, the phalloidin intensities and cell morphology were restored obviously when interfering with the expression of Rsad2 in BPA-treated GC-2 cells. In addition, we observed a significant decrease in intracellular ATP levels after BPA treatment, while the ATP level was obviously upregulated when knocking down the expression of Rsad2 in BPA-treated cells compared to cells treated with BPA alone. Moreover, Rsad2 relocated to mitochondria after BPA exposure in GC-2 cells. BPA promoted Rsad2 expression by activating type I IFN-signaling in GC-2 cells. In summary, Rsad2 mediated BPA-induced actin cytoskeletal disruption in GC-2 cells, which provided data to reveal the mechanism of BPA-induced male reproductive toxicity.

Polystyrene nanoplastics exposure triggers spermatogenic cell senescence via the Sirt1/ROS axis.

Polystyrene nanoplastics (PS-NPs) have been reported to accumulate in the testes and constitute a new threat to reproductive health. However, the exact effects of PS-NPs exposure on testicular cells and the underlying mechanisms remain largely unknown. The C57BL/6 male mice were orally administered with PS-NPs (80 nm) at different dosages (0, 10, and 40 mg/kg/day) for 60 days, and GC-1 cells were treated with PS-NPs in this study. Enlarged seminiferous tubule lumens and a loose and vacuolated layer of spermatogenic cells were observed in PS-NPs-exposed mice. Spermatogenic cells which may be one of the target cells for this reproductive damage, were decreased in the mice from PS-NPs group. PS-NPs caused spermatogenic cells to undergo senescence, manifested as elevated SA-ß-galactosidase activity and activated senescence-related signaling p53-p21/Rb-p16 pathways, and induced cell cycle arrest. Mechanistically, Gene Ontology (GO) enrichment suggested the key role of reactive oxygen species (ROS) in PS-NPs-induced spermatogenic cell senescence, and this result was confirmed by measuring ROS levels. Moreover, ROS inhibition partially attenuated the senescence phenotype of spermatogenic cells and DNA damage. Using the male health atlas (MHA) database, Sirt1 was filtrated as the critical molecule in the regulation of testicular senescence. PS-NPs induced overexpression of the main ROS generator Nox2, downregulated Sirt1, increased p53 and acetylated p53 in vivo and in vitro, whereas these disturbances were partially restored by pterostilbene. In addition, pterostilbene intervention significantly alleviated the PS-NPs-induced spermatogenic cell senescence and attenuated ROS burst. Collectively, our study reveals that PS-NPs exposure can trigger spermatogenic cell senescence mediated by p53-p21/Rb-p16 signaling by regulating the Sirt1/ROS axis. Importantly, pterostilbene intervention may be a promising strategy to alleviate this damage.

Clinical nutrition service capacity of 445 secondary or above hospitals in Sichuan, China: the 2021 annual survey.

BACKGROUND AND OBJECTIVES: To investigate the capacity of clinical nutrition services in secondary and tertiary hospitals in the Sichuan Province, China. METHODS AND STUDY DESIGN: Convenience sampling was used. E-questionnaires were distributed to all eligible medical institutions in Sichuan through the official network of provincial and municipal clinical nutrition quality control centers. The data obtained were sorted in Microsoft Excel and analyzed by SPSS. RESULTS: A total of 519 questionnaires were returned, of which 455 were valid. Only 228 hospitals were accessible to clinical nutrition services, of which 127 hospitals had independently set up clinical nutrition departments (CNDs). The ratio of clinical nutritionists to beds was 1:214. During the last decade, the rate of constructing new CNDs was maintained at approximately 5 units/year. A total of 72.4% of hospitals managed their clinical nutrition units as part of their medical technology departments. The specialist number ratio of senior, associate, intermediate and junior is approximately 1:4:8:10. There were 5 common charges for clinical nutrition. CONCLUSIONS: The sample representation was limited, and the capacity of clinical nutrition services may have been overestimated. Secondary and tertiary hospitals in Sichuan are currently in the second high tide of department establishment, with a positive trend of departmental affiliation standardization and a basic formation of a talent echelon.

Efficacy of immune nutrients in severe acute pancreatitis: A network meta-analysis.

BACKGROUND: The use of immune nutrients in the treatment of severe pancreatitis remains controversial. No study has yet compared the effects of different immune nutrients on patients with severe acute pancreatitis. This study aimed to compare the effects of different immune nutrients in treating severe acute pancreatitis through a network meta-analysis. METHODS: PubMed, Embase, Cochrane Library, Web of Science, and Scopus were used to search randomized controlled trials from the inception to July 2023. Information was collected from patients with severe acute pancreatitis and their intervention methods, which included the administration of glutamine, omega-3 polyunsaturated fatty acids, arginine, and nucleotides. The evaluated outcomes included mortality, infection, the length of the hospital stay (LOH), the length of intensive care unit stay (LOI), and C-reactive protein (CRP). Risk ratio (95% confidence interval [CI]) and mean difference (MD) (95% CI) were calculated using a network meta-analysis random-effects model. The ranking between interventions was calculated using the surface under the cumulative ranking curve. The Cochrane Risk of Bias tool 2 was used to assess the risk of bias. The sources of heterogeneity were assessed using sensitivity analysis and network meta-regression. The credibility of the evidence was assessed using grading of recommendations assessment, development, and evaluation. RESULTS: Nineteen studies with 1035 patients were included in this network meta-analysis. Parenteral glutamine was more effective in reducing mortality, infection, LOH, and LOI, as well as in the downregulation of CRP compared to the control. Risk ratio (95%CI) or MD (95%CI) were 0.38 (0.16, 0.90), 0.35 (0.14, 0.90), -3.32 (-4.90, -1.75), -2.53 (-4.46, -0.61), and -17.78 (-28.77, -6.78), respectively. Parenteral omega-3 polyunsaturated fatty acids was more effective in reducing LOH and LOI, as well as in the downregulation of CRP. MD (95%CI) were -6.77 (-11.40, -2.14), -5.19 (-7.80, -2.57), and -26.20 (-39.71, -12.68), respectively. Immune nutrients in the other groups did not exert any effect compared to the control regarding all the outcomes. Parenteral glutamine ranked best in reducing infections. Parenteral omega-3 polyunsaturated fatty acids ranked best in reducing mortality, LOH, and LOI, as well as in the downregulation of CRP. CONCLUSION: Some immune nutrients were beneficial for patients with severe acute pancreatitis. Parenteral administration could be better than enteral administration.