Objective To analyze the relationship between visceral obesity and hyperuricemia (HUA), and to provide the basis for the further study of obesity and HUA. Methods A total of 1 824 participants came from Tianjin Heping District Health Education Guidance Center in 2014 were selected in this study. The investigation was performed with physical examination and laboratory test for all subjects. Body fat analyzer was used to measure the visceral fat area (VFA). The Logistic regression analysis was used to evaluate the relationship between visceral obesity and HUA. Results The prevalence of HUA in men and women increased gradually with VFA increasing (P<0.05). There was a positive correlation between VFA, waist circumference (WC), waist-to-hip ratio (WHR) and serum uric acid (SUA) level (P<0.05). According to the results of Logistic regression analysis, VFA (OR=1.805,95%CI=1.166-2.794) and WHR (OR=2.108,95%CI=1.061-4.189) were the risk factors of HUA in men. And in women, VFA (OR=1.775,95%CI=1.154-2.732), WC (OR=2.015, 95%CI=1.137- 3.570) and WHR (OR=2.489, 95% CI=1.400- 4.426) were the risk factors of HUA. Conclusion The accumulation of visceral fat will increase the risk of HUA. So it is necessary to strengthen the detection of visceral obesity to prevent the development of HUA.

Polycyclic aromatic hydrocarbons (PAHs) are a class of persistent pollutants that are widely distributed in the environment. Due to their stable structure and poor degradability, PAHs exhibit carcinogenic, teratogenic, and mutagenic toxicity to the ecological environment and organisms, thus increasing attentions have been paid to their removals and remediation. Green, safe and economical technologies are widely used in the bioremediation of PAHs-contaminated soil. This article summarizes the present status of PAHs pollution in soil of China from the aspects of origin, migration, fate, and pollution level. Meanwhile, the types of microorganisms and plants capable of degrading PAHs, as well as the underlying mechanisms, are summarized. The features of three major bioremediation technologies, i.e., microbial remediation, phytoremediation, and joint remediation, are compared. Analysis of the interaction mechanisms between plants and microorganisms, selection and cultivation of stress-resistant strains and plants, as well as safety and efficacy evaluation of practical applications, are expected to become future directions in this field.
Biodegradation, Environmental ; Polycyclic Aromatic Hydrocarbons/toxicity* ; Soil ; Soil Microbiology ; Soil Pollutants

The gut microbiota is profoundly involved in glucose and lipid metabolism, in part by regulating bile acid (BA) metabolism and affecting multiple BA-receptor signaling pathways. BAs are synthesized in the liver by multi-step reactions catalyzed via two distinct routes, the classical pathway (producing the 12α-hydroxylated primary BA, cholic acid), and the alternative pathway (producing the non-12α-hydroxylated primary BA, chenodeoxycholic acid). BA synthesis and excretion is a major pathway of cholesterol and lipid catabolism, and thus, is implicated in a variety of metabolic diseases including obesity, insulin resistance, and nonalcoholic fatty liver disease. Additionally, both oxysterols and BAs function as signaling molecules that activate multiple nuclear and membrane receptor-mediated signaling pathways in various tissues, regulating glucose, lipid homeostasis, inflammation, and energy expenditure. Modulating BA synthesis and composition to regulate BA signaling is an interesting and novel direction for developing therapies for metabolic disease. In this review, we summarize the most recent findings on the role of BA synthetic pathways, with a focus on the role of the alternative pathway, which has been under-investigated, in treating hyperglycemia and fatty liver disease. We also discuss future perspectives to develop promising pharmacological strategies targeting the alternative BA synthetic pathway for the treatment of metabolic diseases.

Plasticity in the glutamatergic synapses on striatal medium spiny neurons (MSNs) is not only essential for behavioral adaptation but also extremely vulnerable to drugs of abuse. Modulation on these synapses by even a single exposure to an addictive drug may interfere with the plasticity required by behavioral learning and thus produce impairment. In the present work, we found that the negative reinforcement learning, escaping mild foot-shocks by correct nose-poking, was impaired by a single in vivo exposure to 20 mg/kg cocaine 24 h before the learning in mice. Either a single exposure to cocaine or reinforcement learning potentiates the glutamatergic synapses on MSNs expressing the striatal dopamine 1 (D1) receptor (D1-MSNs). However, 24 h after the cocaine exposure, the potentiation required for reinforcement learning was disrupted. Specific manipulation of the activity of striatal D1-MSNs in D1-cre mice demonstrated that activation of these MSNs impaired reinforcement learning in normal D1-cre mice, but inhibition of these neurons reversed the reinforcement learning impairment induced by cocaine. The results suggest that cocaine potentiates the activity of direct pathway neurons in the dorsomedial striatum and this potentiation might disrupt the potentiation produced during and required for reinforcement learning.