Intestinal Flora is a Key Factor in Insulin Resistance and Contributes to the Development of Polycystic Ovary Syndrome.

CONTEXT: The key gut microbial biomarkers for polycystic ovarian syndrome (PCOS) and how dysbiosis causes insulin resistance and PCOS remain unclear. OBJECTIVE: To assess the characteristics of intestinal flora in PCOS and explore whether abnormal intestinal flora can affect insulin resistance and promote PCOS and whether chenodeoxycholic acid (CDCA) can activate intestinal farnesoid X receptor (FXR), improving glucose metabolism in PCOS. SETTING AND DESIGN: The intestinal flora of treatment-naïve PCOS patients and hormonally healthy controls was analyzed. Phenotype analysis, intestinal flora analysis, and global metabolomic profiling of caecal contents were performed on a letrozole-induced PCOS mouse model; similar analyses were conducted after 35 days of antibiotic treatment on the PCOS mouse model, and glucose tolerance testing was performed on the PCOS mouse model after a 35-day CDCA treatment. Mice receiving fecal microbiota transplants from PCOS patients or healthy controls were evaluated after 10 weeks. RESULTS: Bacteroides was significantly enriched in treatment-naïve PCOS patients. The enrichment in Bacteroides was reproduced in the PCOS mouse model. Gut microbiota removal ameliorated the PCOS phenotype and insulin resistance and increased relative FXR mRNA levels in the ileum and serum fibroblast growth factor 15 levels. PCOS stool-transplanted mice exhibited insulin resistance at 10 weeks but not PCOS. Treating the PCOS mouse model with CDCA improved glucose metabolism. CONCLUSIONS: Bacteroides is a key microbial biomarker in PCOS and shows diagnostic value. Gut dysbiosis can cause insulin resistance. FXR activation might play a beneficial rather than detrimental role in glucose metabolism in PCOS.

[Distribution Characteristics and Ecological Risk Assessment of Phthalate Esters in Surface Sediments of the Songhua River].

This study assesses the spatial distribution characteristics and ecological risk of phthalate esters (PAEs) in the surface sediments of the mainstream and tributaries of the Songhua River, China, using concentrations and composition of six PAEs, which were analyzed using gas chromatography-mass spectrometery (GC-MS). We assess the ∑6PAEs ecological risk using the hazard quotient (HQ) method and environmental risk levels (ERL). The results were as follows. ① It was found that the total concentrations of ∑6PAEs ranged from 6832.5 to 36298.9 ng·g-1 dry weight (average 18388.6 ng·g-1), with the main contributions coming from di-(2-ethylhexyl) phthalate (DEHP) and di-n-butyl phthalate (DBP). The difference between the main stream ∑6PAEs (6832.5-36298.9 ng·g-1, average 18616.9 ng·g-1) and the tributary ∑6PAEs (10367.6-26593.3 ng·g-1, average 18264.1 ng·g-1) was not significant (P >0.05). The mean concentrations of individual PAEs in the tributary stream differed little from that of the main stream. The ∑6PAEs concentration of the Songhua River decreased initially but then increased from the upstream to the downstream. The average ∑6PAEs concentration in natural agricultural areas (18677.5 ng·g-1) was similar to that found in urban industrial areas (18063.7 ng·g-1), and DBP and DEHP contributed 98% of ∑6PAEs. ② The main sources of ∑6PAEs were domestic, agricultural production, and industrial production using plasticizers. ③ The ecological risk assessment indicated that DMP and BBP in the surface sediments of the Songhua River did not pose an ecological risk for aquatic organisms, and that DEP was associated with a low ecological risk, whereas DEHP and DBP posed a high ecological risk for aquatic organisms.

[Treatment and etiological analysis of biliary fistula associated with liver hydatidosis: report of 13 cases].

OBJECTIVE: To explore the cause and the treatment of liver hydatidosis complicated by biliary fistula, to reduce or prevent the incidence of the complication. METHODS: From 1982 to 2002, 1 666 patients with liver hydatidosis were treated surgically in our hospital, and a retrospective analysis was conducted in 13 from the cohort, who developed biliary fisltula after the surgeries. RESULTS: The incidence of liver hydatidosis-associated biliary fistula was 0.78% (13/1666), and 8 (61.5%) out of such cases were due to the primary liver hydatidosis, 3 (15.38%) were caused by damage to the small accessory hepatic duct or parahepatic byliary duct, and 2 (7.69%) by the puncture of the needle. CONCLUSION: Biliary fistula often arises from liver hydatidosis itself, and can be partly attributed to erroneous operation on the part of the operators, and prevention of this complication, therefore, is possible through careful operation.