INSULIN RESISTANCE AND POLYCYSTIC OVARY SYNDROME IN A CHINESE POPULATION.

OBJECTIVE: Our study aimed to investigate glucose and lipid level as well as insulin resistance (IR) in patients with polycystic ovary syndrome (PCOS). METHODS: In a case-control study, 426 patients with PCOS were diagnosed according to Rotterdam criteria, and they were conducted in the morning after a 10-h fast. Participants received standard 75-g oral glucose tolerance test (OGTT). Plasma glucose and insulin levels were obtained at 0, 30, 60, 120, and 180 min. They also received the lipid evaluation; 95 healthy women with normal menstrual cycles served as controls. Thus, by modifying the homeostasis model assessment of insulin resistance (HOMA-IR) with the use of individual time-course values of glucose and insulin plasma levels, we developed a new assessment method, HOMA-Mx. RESULTS: In our study, 23.71% of patients had abnormal glucose metabolism. With further impairment in glucose metabolism, the glucose and lipid level gradually increased (P<0.05), while the impaired glucose regulation (IGR) group showed greater insulin response than a type 2 diabetes mellitus (T2DM) group. Compared with healthy controls, both lean and obese PCOS patients with normal glucose tolerance (NGT) had a higher body mass index (BMI), and higher serum glucose, insulin, and lipid values. Additionally, the insulin value peaked at 30 min and 60 min in the lean and obese groups, respectively. HOMA-M30 proved to be the best predictive parameter (cutoff: 20.36, area under the curve [AUC]: 0.753) for assessment of IR in normal-weight patients and HOMA-IR (cutoff: 32.17, AUC: 0.868) was optimal in obese PCOS patients. CONCLUSIONS: A new assessment method was developed for these groups: HOMA-M30 for lean PCOS patients and HOMA-M60 for obese patients, in order to focus on peak insulin values for early detection of IR.

Promoter aberrant methylation status of ADRA1A is associated with hepatocellular carcinoma.

The aim of our study was to explore the relationship between the methylation status of the alpha-1A adrenergic receptor (ADRA1A) gene and hepatocellular carcinoma (HCC). We combined our in-house data-set with the Cancer Genome Atlas (TCGA) data-set to screen and identify the methylation status and expression of adrenergic receptor (AR) genes in HCC. Immunohistochemistry and western blot were performed to assess the expression of ADRA1A in HCC cell lines and tissues. We further evaluated the methylation levels of the ADRA1A promoter region in 160 HCC patients using the Sequenom MassARRAY® platform and investigated the association between methylation of ADRA1A and clinical characteristics. The expression levels of ADRA1A mRNA and protein were significantly decreased in HCC tissues. Compared with that in paired normal tissues, the mean methylation level of the ADRA1A promoter region was significantly increased in tumour tissues from 160 HCC patients (25.2% vs. 17.0%, P < 0.0001). We found that a DNA methyltransferase inhibitor (decitabine) could increase the expression of ADRA1A mRNA in HCC cell lines. Moreover, hypermethylation of the ADRA1A gene in HCC samples was associated with clinical characteristics, including alcohol intake (P = 0.0097) and alpha-fetoprotein (P = 0.0411). Receiver operator characteristic (ROC) curve analysis demonstrated that the mean methylation levels of ADRA1A could discriminate between HCC tissues and adjacent non-cancerous tissues (AUC = 0.700, P < 0.0001). mRNA sequencing indicated that the main enriched pathways were pathways in cancer, cytokine-cytokine receptor interaction and metabolic pathways (P < 0.01). ADRA1A gene hypermethylation might contribute to HCC initiation and is a promising biomarker for the diagnosis of HCC.

Production of L-lactic acid from corncob.

The optimum temperature, initial pH, amount of added enzyme and substrate (corncob) for the hydrolysis of corncob by Acremonium cellulase were 35 degrees C, 4.5, 10 u/g-corncob and 100 g/l, respectively. Under the optimum conditions, more than 55 g/l of reducing sugars were hydrolyzed from 100 g/l of corncob to 34 g/l of glucose and 12 g/l of xylose based on dried corncob. More than 25 g/l of L-lactic acid was produced from this enzymatic hydrolyzate and less than 5 g/l of xylose remained in the 3-l airlift bioreactor. The production of L-lactic acid by simultaneous saccharification and fermentation (SSF) was also carried out in the 3-l airlift bioreactor using Acremonium thermophilus (cellulose-producer) and Rhizopus sp. MK-96-1196 (lactic acid-producer). More than 24 g/l of L-lactic acid was produced from 100 g/l of untreated raw corncob.

22q11.2 deletion mosaicism in patients with conotruncal heart defects.

BACKGROUND: Some patients with conotruncal heart defects (CTDs) have a chromosome 22q11.2 deletion, but we do not know whether patients with CTDs who are missing the peripheral blood-cell chromosome 22q11.2 deletion are also missing the 22q11.2 deletion in myocardial cells, and whether patients with the 22q11.2 deletion can show a different 22q11.2 deletion in peripheral blood cells and myocardial cells due to a postzygotic mutation during the embryonic period. METHODS: A total of 32 Chinese pediatric nonsyndromic CTD patients (21 with tetralogy of fallot [TOF], 9 with double outlet right ventricle [DORV], 1 with pulmonary artery atresia with ventricular septal defect [PAA/VSD], and 1 with congenitally corrected transposition of the great arteries [CCTGA]), 12 females and 20 males ranging in age from 5 months to 7 years, were included in our study. We used fluorescence in situ hybridization (FISH) to find the chromosome 22q11.2 deletion in peripheral blood cells and compared genotypes of 15 short tandem repeat (STR) markers within 22q11.2 between peripheral blood cells and myocardial cells to search for genetic mosaicism of the chromosome 22q11.2 deletion. RESULTS: Three patients, 2 with TOF and 1 with DORV, were determined to have the peripheral blood cell chromosome 22q11.2 deletion. There was no STR genotypic difference observed between peripheral blood cells and myocardial cells in patients with or without the chromosome 22q11.2 deletion. CONCLUSIONS: Genetic mosaicism may not play a major role in the etiology of isolated CTDs.