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Objective To investigate the role of extracellular signal regulated kinase 1/2 （ERK1/2） in colitis through the regulation of NADPH oxidase and mitochondrial fission. Methods Mice models of acute colitis were induced by 3% dextran sulfate sodium （DSS）. Thirty C57BL/6J mice were randomly divided into six groups by random number table method： control group， 3%DSS group，1% dimethyl sulfoxide （DMSO） group， ERK1/2 inhibitor（PD98059） group， 3%DSS+1%DMSO group and 3%DSS+PD98059 group， with five mice in each group. The changes of body weight， colonic length， disease activity index and colonic histopathological changes of mice in the control and 3%DSS groups were evaluated， and the expression levels of ERK1/2， p-ERK1/2， Nicotinamide adenine dinucleotide phosphate oxidase 1 （Nox1） and Nox2 in colonic mucosa of mice were detected. Mice in 1%DMSO and 3%DSS+1%DMSO groups were intraperitoneally injected with 1%DMSO. Mice in the PD98059 and 3%DSS+PD98059 groups were intraperitoneally injected with PD98059. The colonic histopathological changes were evaluated among four groups， and the expression levels of Nox1， Nox2， Dynamin related protein 1 （DRP1）， p-DRP1-S616 and p-DRP1-S637 mitochondrial fission related proteins were detected. Mitochondrial fission of colonic epithelial cells in the control and 3%DSS groups was observed by transmission electron microscopy. The co-localization of Nox2 and mitochondrial outer membrane translocator enzyme TOM complex （TOMM20） in colonic mucosa of mice in two groups was analyzed by double-immunofluorescence staining. The correlation between relative expression levels of DRP1 and Nox2 mRNA in mouse colonic mucosa was analyzed in two groups. Results Compared with the control group， mice in the 3%DSS group exhibited body weight loss， shortened colonic length， increased disease activity index and increased colonic histopathological score. The expression levels of p-ERK1/2， Nox1， Nox2 in colonic mucosa of mice were significantly up-regulated in the 3%DSS group （all P < 0.05）. In mice with colitis， mitochondrial fission in colonic epithelial cells was increased， and the colonic mucosa co-localization of DRP1 and Nox2 was elevated， and the relative mRNA expression levels of both target genes were positively correlated （r = 0.678， P < 0.05）. ERK1/2 inhibitor PD98059 improved colonic histopathological changes in mice with colitis， and down-regulated the expression levels of Nox1， Nox2， DRP1， p-DRP1-S616 in colonic mucosa. Conclusion Inhibition of ERK1/2 may ameliorate colitis by down-regulating NADPH oxidase expression and alleviating mitochondrial fission.

Objective To investigate the role ofβ-arrestin1 （ARRB1） in liver fibrosis and elucidate the mechanism of hepatic stellate cell activation induced by ARRB1/p38 signaling pathway to promote liver fibrosis. Methods Twelve male C57BJ/6L mice were randomly divided into the control （n = 6） and model groups（n = 6）. The liver fibrosis mouse model was established by 20% carbon tetrachloride. In addition， liver tissue samples from patients with liver cirrhosis and healthy controls were collected. Liver fibrosis was assessed by HE and Sirius red staining. The expression levels of ARRB1， p38， pp38， α-SMA and collagen Ⅰ were detected by immunohistochemistry， western blot and quantitative real-time PCR. The human hepatic stellate cell line LX2 was activated by TGF-β cytokine and the expression level of ARRB1 was analyzed. Furthermore， siRNA or plasmid was used to silence or overexpress ARRB1， and p38 specific inhibitor （SB203580） was adopted to reveal the regulatory relationship between ARRB1 and p38. Results ARRB1 expression was up-regulated and the activation of p38 signal was strengthened in liver fibrosis tissues（all P < 0.05）. TGF-β treatment activated hepatic stellate cells and ARRB1 and p38 signaling in hepatic stellate cell LX2. The up-regulation or down-regulation of ARRB1 expression level could correspondingly affect p38 signaling and regulate the activity of hepatic stellate cells， while the change of p38 activity exerted no effect uponthe expression of ARRB1. Conclusion The expression level of ARRB1 is up-regulated in liver fibrosis， which can activate hepatic stellate cells by activating the p38 signaling， thereby promoting the incidence and development of liver fibrosis.

Gears are often in a harsh working environment, and their vibration signals have the characteristics of non-linearity and non-stationarity. Therefore, it is of great significance to develop a fault diagnosis method suitable for gears. To solve this problem, an intelligent fault diagnosis method based on adaptive projection intrinsically transformation sine-assisted multivariate empirical mode decomposition (APIT-SA-MEMD) and Floyd local linear embedding (FLLE) algorithm is proposed. Multivariate empirical mode decomposition of adaptive projection intrinsically transformation has modal aliasing phenomenon, so APIT-SA-MEMD is proposed to reduce the modal aliasing phenomenon existing in traditional empirical mode decomposition. First, the APIT-SA-MEMD method is used to decompose the gear vibration signal, and the IMF component that can characterize the gear vibration signal is obtained. On this basis, the time domain and frequency domain features of the selected IMF components are extracted to obtain a high-dimensional feature matrix. Finally, FLLE is used to perform dimensionality reduction and clustering analysis on the high-dimensional feature matrix to realize the identification of gear fault modes. Experimental results show that the proposed method can accurately identify different types of gear faults.

Objective To explore whether β-arrestin2 plays a role by regulating autophagy in colitis. Methods 20 β-arrestin2 wild-type （WT） and 20 β-arrestin2 knockout （KO） mice were randomly and evenly divided into four groups, including β-arrestin2 WT control group and experimental group, β-arrestin2 KO control group and experimental group. In the experimental groups, the mice were given free access to 3% dextran sulfate sodium （DSS） for 7 d to induce acute colitis. In the control groups, the mice were given sterile ddH2O. The disease activity index of mice was observed and recorded in each group. The colon tissues of mice were collected, and the expression levels of autophagy-related proteins including LC3B and Beclin1 were observed and detected by immunohistochemistry and western blot. The expression of β-arrestin2 was knockdown by siRNA in HCoEpiC cells, and then the cells were treated by Earle's Balanced Salt Solution （EBSS） to induce autophagy. Then, the expression level of LC3B protein was detected. Results The expression of autophagy-related proteins was significantly up-regulated in the colon mucosal tissues of WT experimental mice. Compared with WT mice, the colonic inflammation was significantly ameliorated in β-arrestin2 KO mice after DSS treatment. And the expression levels of autophagy-related proteins LC3B-Ⅱ/Ⅰ were significantly down-regulated in β-arrestin2 KO mice in the experimental groups（P < 0.05）.There is no significant difference in the expression levels of Beclin1（P > 0.05）. After knocking down the expression of β-arrestin2 in HCoEpiC cells and EBSS treatment, the expression levels of LC3B-Ⅱ/Ⅰ were significantly down-regulated （P < 0.05）. Conclusion β-arrestin2 can regulate the autophagy in colitis, and the deficiency of β-arrestin2 can inhibit autophagy to ameliorate the colonic inflammation.