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It is a debated topic if there are any observable precursor anomalies prior to the earthquake (EQ hereafter) and if the stronger EQ can be successfully predicted. During last few decades quite a lot of observable electromagnetic (EM) precursors were published by using techniques equipped in either satellites or on ground-based stations. But there are only a few cases that the short-term precursor anomalies of EM field before earthquakes were observed by using alternate EM fields on ground. This paper will present a new EM observation network built in recent years and show a new finding of EM field with the variation of a one-year cycle observed using the network. As an example, the short-term precursor anomalies of apparent resistivity before the Yangbi EQ (Ms 5.1) occurred on March 27, 2017 in Yunnan Province will be studied. The observed anomalous phenomena indicate that the anomaly before the EQ can be captured only if reasonable effective methods including sophisticated analytical techniques are used, and it is believed that continuously observed data on the fixed observation network for a long time is an effective means for studying anomalies that appeared before earthquakes. This network can also play an important role in studying the EM environment from space.

Results show that Laser Shock Processing (LSP) improves the fatigue life of the aluminum alloy 2024T62 with 4.5-9.8 times higher than that of unshocked specimens. Data further indicate that LSP influences surface hardness, microstructure, and fracture section of the specimens as well.

Exposure to carbon blacks (CBs) has been associated with the progression of pulmonary fibrosis, whereas the mechanism is still not clear. We therefore aimed to investigate the effect of RhoA/ROCK pathway on pulmonary fibrosis caused by CBs exposure. Western blot analysis indicated that CBs could promote the activation of RhoA/ROCK pathway and phosphorylation of p65 and IκBα in mice lung. However, ROCK inhibitor Y‐27632 could attenuate phosphorylation levels of p65 and IκBα and restore histopathological changes of the lung tissue. Then, we evaluated the effect of RhoA/ROCK pathway on pulmonary fibrosis by detecting the expression levels of α‐SMA, vimentin, and Collagen type‐I (Col‐I), which could be partly inhibited by Y‐27632. It was assumed that inhibition of ROCK could be a promising therapeutic candidate for CBs‐induced pulmonary fibrosis, which possibly through the blockage of RhoA/ROCK/NF‐κB pathway. [ABSTRACT FROM AUTHOR]

Objectives: Long-term treatment of olanzapine, the most widely-prescribed second-generation antipsychotic, remarkably increases the risk of non-alcoholic fatty liver disease (NAFLD), whereas the mechanism for olanzapine-induced NAFLD remains unknown. Excessive hepatic fat accumulation is the basis for the pathogenesis of NAFLD, which results from the disturbance of TG metabolism in the liver. Apolipoprotein A5 (ApoA5) is a key regulator for TG metabolism in vivo that promotes TG accumulation in hepatocytes, thereby resulting in the development of NAFLD. However, there are no data indicating the role of apoA5 in olanzapine-induced NAFLD. Therefore, this study aims to investigate the role of apoA5 in olanzapine-induced NAFLD., Methods: This study was carried out via animal studies, cell experiment, and ApoA5 gene knockdown experiment. Six-week-old male C57BL/6J mice were randomized into a control group, a low-dose group, and a high-dose group, which were treated by 10% DMSO, 3 mg/(kg·d) olanzapine, and 6 mg/(kg·d) olanzapine, respectively for 8 weeks. The lipid levels in plasma, liver function indexes, and expression levels of ApoA5 were detected. HepG2 cells were treated with 0.1% DMSO (control group), 25 μmol/L olanzapine (low-dose group), 50 μmol/L olanzapine (medium-dose group), and 100 μmol/L olanzapine (high-dose group) for 24 h. HepG2 cells pretreated with 100 μmol/L olanzapine were transfected with siRNA and scrambled siRNA (negative control), respectively. We observed the changes in lipid droplets within liver tissues and cells using oil red O staining and fat deposition in liver tissues using HE staining. The mRNA and protein levels of ApoA5 were determined by real-time PCR and Western blotting, respectively., Results: After intervention with 3 and 6 mg/(kg·d) olanzapine for 8 weeks, there was no significant difference in body weight among the 3 groups ( P >0.05). Olanzapine dose-dependently increased the plasma TG, ALT and AST levels, and reduced plasma ApoA5 levels (all P <0.05), whereas there was no significant difference in plasma cholesterol (HDL-C, LDL-C, and TC) levels among the 3 groups (all P >0.05). Olanzapine dose-dependently up-regulated ApoA5 protein levels in liver tissues (all P <0.05), but there was no significant change in ApoA5 mRNA expression among groups ( P >0.05). In the control group, the structure of liver tissues was intact, the morphology of liver cells was regular, and only a few scattered lipid droplets were found in the cells. In the olanzapine-treated group, there was a large amount of lipid deposition in hepatocytes, and cells were balloon-like and filled with lipid droplet vacuoles. The nucleus located at the edge of cell, and the number of lipid droplets was increased significantly, especially in the high-dose group. Likewise, when HepG2 cells were treated with olanzapine for 24 h, the number and size of lipid droplets were significantly elevated in a dose-dependent manner. Moreover, olanzapine dose-dependently up-regulated ApoA5 protein levels in HepG2 cells (all P <0.05), but there was no significant difference in ApoA5 mRNA expression among groups ( P >0.05). Compared with the HepG2 cells transfected with scrambled siRNA, the number and size of lipid droplets in HepG2 cells transfected with ApoA5 siRNA were significantly reduced., Conclusions: The short-term intervention of olanzapine does not significantly increase body weight of mice, but it can directly induce hypertriglyceridemia and NAFLD in mice. Olanzapine inhibits hepatic apoA5 secretion but does not affect hepatic apoA5 synthesis, resulting in the pathogenesis of NAFLD. Inhibition of apoA5 secretion plays a key role in the development of olanzapine-related NAFLD, which may serve as an intervention target for this disease.

Objective: To investigate the effects of Sanren decoction on the immune function of rats with spleen-stomach damp-heat (DHSS) syndrome., Methods: Fifty male SD rats were randomly allocated into normal control group, DHSS model group, and 3 Sanren decoction groups (high, medium and low doses). The effects of the decoction on the body mass, rectal temperature (RT), water and food intake, histopathological changes of the gastrointestinal mucosa and serum levels of interleukin (IL)-4 and interferon (IFN)-γ were evaluated., Results: The serum levels of IFN-γ and IL-4 in the model group significantly increased compared with those in the control group (P<0.01), with a slightly increased IFN-γ/IL-4 ratio (P>0.05). Sanren decoction obviously reduced the rectal temperature and significantly decreased the production of both cytokines. High-dose Sanren decoction caused more markedly decreased IL-4 level (P<0.05) to result in a significantly increased IFN-γ/IL-4 ratio (P<0.05)., Conclusions: A shift of Th1/Th2 balance toward Th1 immune response is demonstrated in rats with DHSS syndrome, and Sanren decoction produces a protective effect on the gastrointestinal mucosa by immunoregulation.