[A birth cohort study of the association between prenatal serum bisphenol A concentration and infant neurobehavior development].

Objective: To explore the association between maternal bisphenol A (BPA) exposure during pregnancy and neurobehavioral development in infant. Methods: Participants were from the Ma'anshan Birth Cohort, which was established from October 2008 to October 2010 based on four municipal medical and health institutions in Ma'anshan. High-performance liquid chromatography-tandem mass spectrometry was applied for the determination of serum BPA concentration in 1 783 pregnant women sampled at their first filing, and during 2.97 to 28.1 months age of the infants. Neurobehavioral development were assessed by 0-6-year-old pediatric examination table of neuropsychological development. Generalized linear model was used to analyze the association between serum BPA levels during pregnancy and infants' neurobehavioral development. Results: A total of 931 mother-child pairs had complete data on serum BPA detection during pregnancy and assessment of infants' neurobehavioral development status. The age of pregnant women at their first filing was (26.67±3.45) years old, and the M (P25,P75) of serum BPA concentration (ng/ml) was 0.23 (0.11, 0.52), with a detection rate of 84.1% (783/931). The age of infants was (13.18±5.46) months, and 53.5% (498) were boys. The developmental quotient scores of large motor, fine motor, adaptive ability, language ability and social behaviors of infants were (97.88±16.32), (97.16±15.35), (99.64±15.47), (95.3±16.04) and (98.95±14.76) points, respectively. Generalized linear model showed that after adjusting for factors such as delivery mode, feeding mode, family per capita monthly income, preterm delivery, gender, maternal age, residence, pre-pregnancy body mass index and residence time, serum BPA level in pregnancy was negatively associated with infant's development of social behavior [ß (95%CI):-2.42 (-4.71, -0.12)]. The post-stratification analysis by infant age revealed that the serum BPA level in pregnancy was only negatively associated with the development of language and social behavior developmental quotient scores in infants between the ages of 12 and 18 months, with ß (95%CI) about -6.66 (-13.06, -0.25) and -7.401 (-12.97, -1.83), respectively. Conclusion: BPA exposure during pregnancy affects language and social behavior development in infants, and the detection window is between 12 and 18 months old of the infant.

Serum uric acid and non-alcoholic fatty liver disease in non-hypertensive Chinese adults: the Cardiometabolic Risk in Chinese (CRC) study.

OBJECTIVE: The causal relationship between serum uric acid (SUA) level and non-alcoholic fatty liver disease (NAFLD) has not yet been clarified. The objective of the study was to determine the association between SUA and NAFLD, as well as assess the interactions between SUA and other metabolic risk factors regarding NAFLD. PATIENTS AND METHODS: The study samples related to a community-based health examination survey conducted in Central China. Initially, a total of 24,878 patients with medical examination were included. After excluding the individuals with confounding factors, the remaining 21,798 subjects with biomarkers available were included in the present study. RESULTS: The data show that the risk of NAFLD significantly increased with the elevated SUA levels. Further adjustments for sex, age, and other confounding metabolic factors did not change the increasing trend of NAFLD risk. The odds ratios [ORs, 95% confidence interval (CI)] of NAFLD across the increasing quintiles of SUA were 1.00, 1,530 (1.174-1.995), 2.24 (1.714-2.886), 2.636 (2.019-3.441), and 3.714 (2.828-4.877) (p for trend < 0.0001). Also, significant interaction was found between SUA and prehypertension in relation to the NAFLD risk (p for interaction < 0.05). CONCLUSIONS: SUA was significantly associated with NAFLD risk, independent of other metabolic risk factors, and SUA also had significant interaction with prehypertension regarding the risk of NAFLD.

Link between obesity and cancer: role of triglyceride/free fatty acid cycling.

Obesity has long been suspected to be a risk factor for cancer. The relationship between body fat deposition and the pathogenesis of cancer has been the subject of many studies, however, no clear consensus has emerged linking these two biological processes. Recent epidemiological studies showed a strong association between cancer-related deaths and increased body-mass index. In fact, obesity has been identified as a cause for oesophageal, colon, uterine, kidney and post-menopausal breast cancers and also as a significant risk factor for the cancers of prostate, pancreas and non-Hodgkin lymphoma. Approximately 16-20% of cancer deaths in women and 14% of cancer deaths in men were found to be due to obesity. It is also recognized that there is a positive relationship between type-2 diabetes associated hyperinsulinemia and cancer incidence. Though the recent annual report in US finds that the incidence and mortality rates for many cancers have dropped in 2003 since 1975, this decline is mostly due to a substantial decrease in tobacco use among men. However, during the same period the rise in the prevalence of obesity might have contributed to the increased risk and incidence of prostate, liver, kidney, oesophageal and breast cancers. Whether the elevated cancer risk in obesity arises from similar modulation of parallel signaling/metabolic pathways during adipogenesis and oncogenesis has not been hitherto addressed. In this Review we would like to bring out the similarities between adipogenesis and oncogenesis and how this relationship at molecular level may be relevant for the development of effective therapeutics for obesity, diabetes and cancer. While adipogenesis is the process of formation of mature adipocytes or fat cells under normal physiological conditions, oncogenesis is a pathological process, which results in the uncontrolled growth of cells leading to cancer. Though, both these processes at surface seem to be totally different, we believe that there are important common denominators for these processes that need to be recognized. We will discuss the role of two such underlying factors - (1) malonyl-CoA, an important regulator of fatty acid metabolism and (2) triglyceride/free fatty acid (TG/FFA) cycling which is central to the generation of multiple signals for controlling various metabolic, physiological and signaling pathways in the cell.

[Effect of nitric oxide in preventing myocardial dysfunction following relative ischemia/ reperfusion in the rat isolated heart].

AIM: The protective effect of L-arginine on relative ischemia/reperfusion-induced myocardial injury was investigated in the rat isolated langendorff perfused heart. METHODS: Four groups of hearts subjected to 20 min electric stimulus and 40 min reperfusion received vehicle, L-arginine, N(omega)-nitro-L-arginine methyl ester and only stimulus respectively. RESULTS: The recovery of left ventricular developed pressure and pressure-rate product at the end of reperfusion was significantly higher in the L-arginine group (89.04% +/- 2.46% and 72.16% +/- 4.40%, respectively) than in the vehicle group (64.74% +/- 7.67% and 44.57% +/- 6.89%, respectively, P < 0.05). It is suggested that N(omega)-nitro-L-arginine methyl ester inhibits the recovery of the heart function after ischemia and accelerates the myocardial injury. CONCLUSION: We propose that it is important to protect the integrity of the heart angioendothelium during ischemia/reperfusion, and promote the synthesis of NO to relieve the myocardial injury and consequently accelerate the recovery of the heart function.