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Multiple pathways contribute to nonalcoholic fatty liver disease (NAFLD) in response to high fat diets (HFD). A homolog of mammalian JNK-interacting protein 3 (JIP3), also known as JSAP-1, activates different components in various signaling pathways to modulate cellular processes. The purpose of this study was to examine the role of JIP3 in obesity-related pathologies pathway. Wild-type (WT) C57BL/6 and JIP3-knockout (JIP3-/-) mice were randomized to chow or HFD. HFD-fed WT mice increased hepatic JIP3 expression. Mice lacking JIP3 exhibited reduced weight gain, hepatic steatosis, insulin resistance, lipid accumulation, oxidative stress and inflammatory response in mice fed a HFD, which were, importantly, dependent on various signaling pathways. Lipogenesis-linked pathway was inhibited in JIP3-/- mice after HFD, while PPARα/γ were increased. Additionally, JIP3-/- inhibited hepatic oxidative stress, evidenced by down-regulation of total reactive oxygen species (ROS), H2O2, O2-, malondialdehyde (MDA), xanthine oxidase (XO), inducible nitric oxide synthase (iNOS), and up-regulation of superoxide dismutase (SOD) and total antioxidant capacity (TAC) in mice after HFD feeding, which might be related to nuclear respiratory factor 2 (Nrf-2) pathway activation. Further, inflammatory response was blocked in JIP3-/- mice fed with HFD. The process might be attributed to the suppression of toll-like receptors (TLRs), p-nuclear factor kappa B (NF-κB) and p-c-Jun-N-terminal kinase (JNK). Thus, JIP3 absence is associated with decreased lipogenesis, oxidative stress and inflammation, supplying a new target for NAFLD treatment.

study question: Is there an association between exposure to phthalates and the timing of female puberty? summaryanswer: Our study suggests that the early onset of puberty is related to increased kisspeptin secretion. what is known already: Girls are maturing earlier than in past decades and the quantity of phthalates used in consumer products has concurrently risen. The hypothesis that exposure to phthalates may increase kisspeptin secretion and thereby cause early-onset puberty is unexplored. studydesign,size,duration: This case– control study ran from 2006 to 2009. We enrolled 104 girls. Girls in the central precocious puberty (CPP) (case) group were recruited from a pediatric endocrinology policlinic in Taiwan; prepubescent controls were recruited from local elementary schools and all were categorized based on a pediatrician’s diagnosis. participants/materials, setting, methods: The physical characteristics of puberty were assessed and levels of LH, FSH estradiol and kisspeptin-54 in blood samples were evaluated using radioimmunoassay. Reversed-phase high-performance liquid chromatography-tandem mass spectrometry was used to analyze seven urinary phthalate metabolites. Non-parametric analyses, trend tests and linear regressions were performed on the data. main results and the role of chance: All seven urinary phthalate metabolites in the CPP group were significantly (P , 0.05) higher than in prepubescent controls. Serum kisspeptin-54 levels were higher (P ¼ 0.022) in the CPP group than controls and were still significantly higher after adjusting for age (P ¼ 0.03). There was a significant increasing trend (Ptrend ¼ 0.005) between levels of kisspeptin and the stages of puberty. The concentration of kisspeptin-54 did not change in girls treated with leuprorelin acetate. There was a significant positive correlation between kisspeptin-54 and urinary mono-n-butyl phthalate (ng/ml: R 2 ¼ 0.251, P , 0.001; mg/g-creatinine: R 2 ¼ 0.109, P ¼ 0.024). limitations, reasons forcaution: The study duration was short and the sample size relatively small; therefore, we were unable to collect sufficient evidence to support the temporality between exposure to phthalates and the subsequent occurrence of PP. wider implications of the findings: Kisspeptin may promote the onset of puberty in girls who are exposed to a high level of phthalates, especially di-n-butyl phthalate. These data suggest that developing a kisspeptin antagonist might be an alternative strategy for treating PP.

Aqueous two-phase copolymerization of acrylamide (AM) and dimethylaminoethyl methacrylate methyl chloride (DMMC) was carried out in polyethylene glycol 20000 (PEG 20000) aqueous solution and with 2,2'-azobis(2- amidinopropane) dihydrochloride (V-50) as the initiator. The effects of the temperature, the PEG 20000 concentration, the DMMC/AM molar ratio and the V- 50 concentration on the initial monomer copolymerization rate (Rp), the total monomers conversion and the molecular weight of copolymers were systematically investigated. The initial copolymerization rate increased with an increase of temperature and V-50 content, contrary to the concentration of the PEG 20000 and DMMC. The molecular weight of the copolymers decreased with increasing the reaction parameters above mentioned. The apparent copolymerization activation energy of the system was calculated to be 65.7 kJ·mol-1 according to Arrhenius equation. The optimal PEG 20000 content of the system was 15%~25% (based on the raw materials). The relationship between the initial copolymerization rate (Rp) and the initiator concentration was discussed, and the kinetics equation was Rp~ [I]0.94.

We present an RC-model approach for understanding and analysis of holographic storage in photorefractive materials. In this model the resistor, capacitor and the current source are completely defined based on material parameters and light intensities. The model has good accuracy for the practical applications. It can also be used to understand and improve the properties of photorefractive materials for holographic recording. One interesting application of the model is the qualitative analysis of two-center recording. We also discuss this application in detail.

Purpose 2,3-Oxidosqualene cyclase (OSC), an important enzyme of cholesterol biosynthesis, catalyzes the highly selective cyclization of 2,3-monoepoxysqualene to lanosterol. Intermittent hypoxia (IH) is a hallmark feature in obstructive sleep apnea (OSA) which is increasingly recognized as an independent risk factor for liver injury. The aim of this study was to determine the effect of IH on OSC expression and evaluate the role of OSC in the IH-induced apoptosis in hepatic cell line human liver cell (HL-02). Methods HL-02 cells were exposed to normoxia or IH. Cell Counting Kit-8 (CCK-8) assay was used to value cell proliferation, and flow cytometry was used to determine cell apoptosis. The expression of OSC messenger RNA (mRNA) was evaluated by quantitative real-time PCR, and the expression of OSC protein was determined by Western blot. To further investigate the function of OSC in IH-induced apoptosis, oxidosqualene cyclase-enhanced green fluorescence protein (OSC-EGFP) plasmid was constructed to over-express OSC protein. Triglyceride content in HL-02 cells was analyzed by oil red staining or Triglyceride Quantification Kit. Results We found that IH inhibited HL-02 cell proliferation and accelerated cell apoptosis. IH decreased OSC expression, and over-expression of OSC could protect HL-02 cells against the IH-induced hepatic cell injury. Moreover, over-expression of OSC could attenuate IH-induced cellular triglyceride accumulation. Conclusions These findings suggest that OSC are involved in IH-induced hepatic cell injury. These results may contribute to the further understanding of the mechanism underlying the liver injury in OSA patients.