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Customized training concentrating on self-management improved upon the data and self-management actions associated with older people along with atrial fibrillation: Any randomized controlled demo.
Objective To explore the development of cholestatic fibrosis induced by α-naphthylisothiocyanate (ANIT) and the inflammation pathways. Methods Fifteen 129/Sv mice weighing (23±2) g were randomly divided into 2 groups control group (n=5) and experiment group (n=10). The control group was fed commercial chow diet and the experiment group was fed the same diet supplemented with 0. 05% ANIT. Five mice in the experiment group were sacrificed on day 14 and 28 respectively. The gallbladder, serum and liver samples were collected. Biochemical indicators of cholestasis were detected following the procedures in the kit. Liver injury was evaluated by histopathological. Hepatic fibrosis and inflammatory response were analyzed by Q-PCR and WB. Results Compared with the control group, total bile acid (TBA), the main cholestasis biomarker, was increased from (3. 2±0. 9) μmol/L to (31. 6±4. 3) μmol/L in A-D14 group. AST and ALT, the biomarkers of liver injury, were also increased significantly (P＜0. 05). The expression levels of fibrotic factor tissue inhibitors of metalloproteinases 1 (TIMP-1), monocyte chemoattractant protein 1 (MCP-1) and collagen protein I (Collagen I) were higher than those of control group (P＜0. 05). The expressions of fibrosis protein Collagen I and α-SMA were also up-regulated. The collagen fibers of the liver were largely deposited and the liver fibrosis occurred (P＜0. 05). The expression of inflammatory factors was higher than the control group, JNK, c-Jun and STAT3 were activated (P＜0. 05). In A-D28 group, except AST, matrix metalloproteinases 2 (MMP-2) and Collagen I indicators were slightly decreased, other indicators of cholestasis, liver injury, liver fibrosis and inflammation continued to be up-regulated or stable (P＜0. 05). Conclusion After 14-day treatment with 0. 05% ANIT diet, significant cholestatic liver fibrosis occurred in mice. After 28 days of treatment, cholestasis liver fibrosis kept stable. The JNK inflammatory pathway played a crucial role in the development of liver fibrosis.Objective To investigate the improvement effects of Xiaotan Huayu Liqiao Formula on cognitive impairment in mice exposed to chronic intermittent hypoxia (CIH), and to explore the related mechanisms. SF2312 chemical structure Methods Forty-eight male C57 BL/6 mice were randomly divided into four groups as Normoxia, CIH, Formula+CIH and Formula group. Mice were exposed to normoxia in the normoxia and formula group, or intermittent hypoxia in CIH or Formula+CIH group (in the chambers, mice were filled with 100% N2 to produce FiO2 of 9% for 1. 5 min. The FiO2 gradually returned to 21% over the remainder of each cycle. The exposure cycle was repeated every 3 min, 8 h/day for 35 days). Mice were treated with Xiaotan Huayu Liqiao Formula at the dose of 26. 8 g/kg by intragastric administration before CIH exposure. Meanwhile, mice in CIH and normoxia group were given the same volume of normal saline. When the experiment lasts for 26-35 d, Morris water maze was used to detect cognitive dysfunction in mice. At the end of 35 days, Y-maze was per＜0. 01). Conclusion Xiaotan Huayu Liqiao Formula could alleviate the structural and functional impairment of the postsynaptic dense area, and improved CIH-induced cognitive dysfunction.Objective To investigate the effects of butylphthalide (NBP) on learning and memory related ability, hydrogen sulfide (H2S) content in hippocampus and amygdala, cystathionine-β-synthase (CBS) expression and mitochondrial ATPase activity in rats with chronic alcoholism. Methods Ninety SD male rats were randomly divided into three groups normal control group (NC), model group (M) and butylphthalide remedy group (BR). Except for the control group, the water solution containing 6% (v/v) alcohol was used as the sole source of drinking water in the other two groups. After 14 days of feeding, the butylphthalide remedy group was injected with NBP intraperitoneally at the dose of 5 mg/kg once a day for 14 consecutive days, and the remaining two groups were injected with the same dose of normal saline. The control group subsequently used the Morris water maze method to observe and record the animals after entering the water. The time required for the underwater platform, their strategies and their swimming trajectoriesf hippocampus and the increase of ATPase activity.Objective To observe the effects of repeated horizontal -Gx acceleration exposure on cardiac structure in New Zealand rabbits. Methods Twenty New Zealand rabbits were divided into 2 groups (n=10) control group and -Gx acceleration exposure group. The rabbits in -Gx acceleration exposure group were exposed to -3. 6 Gx with 2 s, at intervals of 5 min, repeated 20 times daily, with a total of 30 d; the control group didn't undergo the acceleration stress. After the last -Gx acceleration exposure, the animals were killed by intravenous injection of air, and two small pieces of myocardium were immediately dissected from the left ventricles for structure examination using optical microscope and transmission electron microscope. Results There was no significant difference in the myocardial cell morphology and arrangement observed under the optical microscope between the -Gx acceleration exposure group and the control group; the myocardial fibers arranged in disorder, myocardial cell edema, nuclear membrane expansion, vascular endothelial basement membrane separation were observed in the -Gx acceleration exposure group under transmission electron microscope, compared with the control group. Conclusion -Gx acceleration exposure can lead to ultrastructural damage in rabbit cardiac myocytes. It suggested that the more attention should be paid to the effect and protection of long-term horizontal -Gx acceleration exposure on the cardiac function of carrier fighter pilots.Objective To study the effects of mice macrophages on myogenic differentiation and insulin sensitivity of skeletal muscle cells under high glucose condition. Methods C2C12 myoblasts and RAW264. 7 macrophages were co-cultured in transwell and treated with 60 mmol/L glucose. They were randomly divided into single culture control group (SC group, n=12), co-culture control group (CC group, n=12), single culture high glucose group (SH group, n=12) and co-culture high glucose group (CH group, n=12). Cell morphology was observed by phase contrast microscope. C2C12 were collected after 1 and 3 days of co-culture. Cell viability was measured by CCK-8. Embryonic myosin heavy chain (E-MHC) and glucose transporters 4 (GLUT4) protein expressions were detected by immunofluorescence. The expressions of myogenic factor 5 (Myf5), myogenic determination gene (MyoD) and myogenin gene were detected by real-time PCR. 2-(N-(7-nitrobenz-2-oxa-13-diazol-4-yl) amino)-2-deoxyglucose (2-NBDG) assay was used to detect the cellular basis and insulin-stimulated glucose uptake.
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