👤 Wang Zhe

To explore the dynamic evolution of symptom clusters in patients with gynecologic malignancies during the early postoperative period and identify key transition points and influencing factors, providing evidence for precision symptom management in clinical nursing. A longitudinal study was conducted among 324 patients using the MDASI-PeriOp-GYN on postoperative days 1 (T1), 5 (T2), and 7 (T3). Exploratory factor analysis identified symptom clusters at each time point, and growth mixture modeling (GMM) was applied to examine trajectory patterns. Latent profile analysis (LPA) and network analysis were performed at T2 to identify patient subgroups, influencing factors, and core symptoms. Five symptom clusters were identified: disease behavior, gastrointestinal, endocrine, neurological, and emotional. The emotional cluster, independent at T1 and T3, merged with the disease behavior cluster at T2. GMM indicated that all clusters declined from T1 to T2, followed by divergence after T2. LPA identified high- and low-symptom subgroups. Patients with ovarian cancer and those with KPS₁ were more likely to belong to the high-symptom group. Network analysis revealed "poor appetite" as the most central symptom at T2. Postoperative day 5 (T2) represents a critical transition point in symptom evolution. Ovarian and KPS₁ are at higher risk for severe symptoms, and "poor appetite" plays a key driving role. Targeted assessment and intervention at T2 may reduce symptom burden and improve recovery outcomes in patients with gynecologic malignancies. Show less

Both glucocorticoid and insulin are known to have an anabolic effect on lipogenesis. Acetyl-CoA, an intermediate product of glycolysis, is supplied for fatty acid synthesis when carbohydrate intake is sufficient. Acetyl-CoA carboxylase (ACC), consisting of two isoenzymes ACC1 and ACC2, mediates the conversion from acetyl-CoA to malonyl-CoA, and thus plays a key role for the regulation of lipogenesis. In this study, we surveyed the effects of glucocorticoid and insulin on the transcriptional activity of the alternative promoters of ACCs (PI-PIII for ACC1, and PI and PII for ACC2) using the HepG2 human hepatocyte cell line in vitro. We also examined the roles of the insulin and/or glucose-regulated transcriptional factor(s) such as SREBP1c, LXRalpha/beta, and ChREBP on each promoter of the ACC genes. We found that both insulin and glucocorticoid had potent positive effects on all the promoters examined, and additive effects of both hormones were recognized in ACC1 PI and ACC2 PI. Furthermore, a representative insulin-responsive transcription factor SREBP1c showed significant stimulatory effects on all the promoters of ACC genes, among which those on ACC1 PIII and ACC2 PI were most prominent. On the other hand, the effect of LXRalpha was rather selective; it showed a marked stimulatory effect only on ACC1 PII. LXRbeta and ChREBP had minimal, if any, effects on some of the promoters. Altogether, our data suggest that insulin and glucocorticoid have positive effects on both ACC1 and ACC2 gene transcription. SREBP1c might be a master regulator of the expression of both genes regardless of the promoter utilized, whereas LXRalpha seems to play a promoter-specific role. Since ACC1 facilitates lipogenesis by stimulating fatty acid synthesis and ACC2 inhibits lipolysis, both insulin and glucocorticoid seem to play an important role in the pathogenesis of obesity and/or hepatic steatosis. Show less