Glutathione peroxidase (GPX1) - Selenocysteine metabolism preserves the follicular fluid's (FF) redox homeostasis via IGF-1- NMD cascade in follicular ovarian cysts (FOCs).

Follicular ovarian cysts (FOCs) are characterized by follicles in the ovaries that are >20 mm in diameter and persist for >10 days without the corpus luteum, leading to anovulation, dysregulation of folliculogenesis and subfertility in humans and livestock species. Despite their clinical significance, the precise impact of FOCs on oocyte reserve, maturation, and quality still needs to be explored. While FOCs are observed in both human and livestock populations, they are notably prevalent in livestock species. Consequently, livestock species serve as valuable models for investigating the molecular intricacies of FOCs. Thus, in this study, using goat FOCs, we performed integrated proteomic, metabolomic and functional analyses to demonstrate that oocyte maturation is hampered due to increased reactive oxygen species (ROS) in FOCs follicular fluid (FF) via downregulation of glutathione peroxidase (GPX1), a critical antioxidant seleno enzyme required to negate oxidative stress. Notably, GPX1 reduction was positively correlated with the FF's decline of free selenium and selenocysteine metabolic enzymes, O-phosphoryl-tRNA (Sec) selenium transferase (SEPSECS) and selenocysteine lyase (SCLY) levels. Adding GPX1, selenocysteine, or selenium to the culture media rescued the oocyte maturation abnormalities caused by FOCs FF by down-regulating the ROS. Additionally, we demonstrate that substituting GPX1 regulator, Insulin-like growth factor-I (IGF-1) in the in vitro maturation media improved the oocyte maturation in the cystic FF by down-regulating the ROS activity via suppressing Non-sense-mediated decay (NMD) of GPX1. In contrast, inhibition of IGF-1R and the target of rapamycin complex 1 (mTORC1) hampered the oocyte maturation via NMD up-regulation. These findings imply that the GPX1 regulation via selenocysteine metabolism and the IGF-1-mediated NMD may be critical for the redox homeostasis of FF. We propose that GPX1 enhancers hold promise as therapeutics for enhancing the competence of FOCs oocytes. However, further in vivo studies are necessary to validate these findings observed in vitro.

Blue emissive amidinate-based tetra-coordinated boron compounds.

A series of novel amidinate ligated four-coordinated boron compounds, [(Ar)-C(tBuN)2BF2] (1BF2-6BF2), were synthesised and structurally characterised (Ar = 1-phenyl, 2-naphthyl, 2-anthryl, 9-anthryl, 9-phenanthryl and 1-pyrene). The increased π-conjugation of Ar-substitution on the amidinate ligand results in dark blue-emission in compounds 3BF2-6BF2. All these compounds are emissive in the solution state. The 2-anthryl substituted compound 3BF2 was found to exhibit a maximum quantum yield of 48% in dichloromethane. Theoretical studies were carried out which validate the hypothesis about the increased π-conjugation.

Endotoxemia predicts outcome in acute pancreatitis.

The incidence of complications of acute pancreatitis is high in patients with endotoxemia, and so we determined the endotoxin levels in the blood and peritoneal fluid of patients with acute severe pancreatitis to correlate the levels with any sequelae. Fourteen patients with acute severe pancreatitis were examined with regard to clinical features, biochemical tests, and laparotomy (n = 9). In all coagulation profiles, blood gas analysis, chest and abdominal x-rays, ultrasound, and abdominal computed tomography scan (n = 10) were performed. Qualitative estimation of endotoxin levels was done in peripheral blood and peritoneal and peripancreatic fluid. Ten (71.42%) of 14 patients had endotoxin in the blood, and 9 (64.28%) had it in the peritoneal fluid. Twelve (85.7%) had pulmonary involvement, with hypoxia being the most common (85.7%); among them endotoxin was found in the blood of 10 (83.32%) and in the peritoneal fluid of 8 (66.66%) patients. Renal dysfunction was found in 4 (28.57%) patients; endotoxin was present in the blood of all 4 patients and in the peritoneal fluid of 3 (75%) patients. Cardiovascular abnormality was detected in 8 (57.14%) patients, and endotoxin was present in the blood and peritoneal fluid of all patients. Metabolic abnormality was present in 8 (57.14%) patients; endotoxin was present in the blood of all 8 patients and in the peritoneal fluid of 7 (87.6%) patients. Eight (88.88%) of the 9 patients who required surgery had endotoxemia. Three (30%) patients with endotoxemia survived, whereas all 4 patients without endotoxemia survived. Mean hospital stay was 61.2 days and 46.7 days for endotoxin-positive and endotoxin-negative patients, respectively. We conclude that the presence of endotoxin in blood and peritoneal fluid correlates with the severity, systemic complications, and mortality rates of acute pancreatitis. Endotoxin estimation can identify patients at risk in the early stages of acute pancreatitis.