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      • KCI등재

        Hyperbaric Oxygen Pretreatment Improves Cognition and Reduces Hippocampal Damage Via p38 Mitogen-Activated Protein Kinase in a Rat Model

        Baisong Zhao,Xingrong Song,Yongying Pan,Zixin Wang,Haiping Xu 연세대학교의과대학 2017 Yonsei medical journal Vol.58 No.1

        Purpose: To investigate the effects of hyperbaric oxygen (HBO) pretreatment on cognitive decline and neuronal damage in an Alzheimer’sdisease (AD) rat model. Materials and Methods: Rats were divided into three groups: normal saline (NS), AD, and HBO+AD. In the AD group, amyloid β peptide (Aβ)1-40 was injected into the hippocampal CA1 region of the brain. NS rats received NS injection. In the HBO+AD group, rats received 5 days of daily HBO therapy following Aβ1-40 injection. Learning and memory capabilities were examined using the Morris water maze task. Neuronal damage and astrocyte activation were evaluated by hematoxylin-eosin staining and immunohistochemistry,respectively. Dendritic spine density was determined by Golgi-Cox staining. Tumor necrosis factor-α, interleukin-1β, and interleukin-10 production was assessed by enzyme-linked immunosorbent assay. Neuron apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling. Protein expression was examined by western blotting. Results: Learning and memory dysfunction was ameliorated in the HBO+AD group, as shown by significantly lower swimming distances and escape latency, compared to the AD group. Lower rates of neuronal damage, astrocyte activation, dendritic spine loss, and hippocampal neuron apoptosis were seen in the HBO+AD than in the AD group. A lower rate of hippocampal p38 mitogen-activated protein kinase (MAPK) phosphorylation was observed in the HBO+AD than in the AD group. Conclusion: HBO pretreatment improves cognition and reduces hippocampal damage via p38 MAPK in AD rats.

      • KCI등재

        A novel hybrid compound fault pattern identification method for gearbox based on NIC, MFDFA and WOASVM

        Xin Zhang,Jianmin Zhao,Xinghui Zhang,Xianglong Ni,Haiping Li,Fucheng Sun 대한기계학회 2019 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.33 No.3

        Gearbox compound fault pattern recognition is challenging because of its complexity and non-stationarity of the vibration signal. In this study is proposed a novel hybrid method based on narrow band interference canceller (NIC), multifractal detrended fluctuation analysis (MFDFA) and support vector machine optimized by whale optimization algorithm (WOASVM) for compound fault pattern recognition of gearbox. Specifically, the raw signal is processed by NIC to filter the deterministic signal which interferes with the fault signal, and then the multifractal features are extracted from the residual signal via MFDFA. Finally, the compound fault pattern is identified via WOASVM. Compound fault experiments of a gearbox under fixed condition and variable condition were done to evaluate the performance of the proposed method. The results show that the proposed method can effectively identify the compound faults and it outperforms other methods mentioned in this paper.

      • SCIESCOPUSKCI등재

        Effects of chromium picolinate on fat deposition, activity and genetic expression of lipid metabolism-related enzymes in 21 day old Ross broilers

        Chen, Guangxin,Gao, Zhenhua,Chu, Wenhui,Cao, Zan,Li, Chunyi,Zhao, Haiping Asian Australasian Association of Animal Productio 2018 Animal Bioscience Vol.31 No.4

        Objective: This experiment was conducted to investigate the effects of chromium picolinate (CrP) on fat deposition, genetic expression and enzymatic activity of lipid metabolism-related enzymes. Methods: Two hundred forty one-day-old Ross broilers were randomly divided into 5 groups with 4 replicates per group and 12 Ross broiler chicks per replicate. The normal control group was fed a basal diet, and the other groups fed the same basal diet supplemented with 0.1, 0.2, 0.4, and 0.8 mg/kg CrP respectively. The experiment lasted for 21 days. Results: Added CrP in the basal diet decreased the abdominal fat, had no effects on subcutaneous fat thickness and inter-muscular fat width; 0.2 mg/kg CrP significantly decreased the fatty acid synthase (FAS) enzymatic (p<0.05); acetyl-CoA carboxylase (ACC) enzymatic activity decreased in all CrP groups (p<0.05); hormone-sensitive lipase (HSL) enzymatic activity also decreased, but the change was not significant (p>0.05); 0.4 mg/kg CrP group significantly decreased the lipoprotein lipase (LPL) enzymatic activity. FAS mRNA expression increased in all experimental groups, and the LPL mRNA expression significantly increased in all experimental groups (p<0.05), but not 0.2 mg/kg CrP group. Conclusion: The results indicated that adding CrP in basal diet decreased the abdominal fat percentage, had no effects on subcutaneous fat thickness and inter-muscular fat width, decreased the enzymatic activity of FAS, ACC, LPL and HSL and increased the genetic expression levels of FAS and LPL.

      • KCI등재

        LncSNHG3 promotes hepatocellular carcinoma epithelial mesenchymal transition progression through the miR-152-3p/JAK1 pathway

        Li Hong,Wu Yu,Wang Runmei,Guo Junmei,Yu Qin,Zhang Lihe,Zhao Haiping,Yang Hao 한국유전학회 2022 Genes & Genomics Vol.44 No.1

        Background: The dysregulation of LncRNAs is related to the malignant progression of many cancers. Objective: The study aimed to investigate the expression and the biological role of LncSNHG3 in hepatocellular carcinoma (HCC). Methods: The TCGA data of the LncSNHG3 in HCC were analyzed. The expression in HCC cell lines was detected by qRT-PCR. Proliferation, migration, and invasion of HepG2 and Huh7 were examined by cell counting kit-8, colony formation, transwell assays, and wound healing assays. At the same time, the interactions among LncSNHG3, miR-152-3p, and JAK1 were confirmed by dual-luciferase reporter assay, RNA immunoprecipitation, subcellular distribution. Xenograft tumor-bearing mice models were used to measure the effect of LncSNHG3 on the growth of HCC in vivo. The apoptosis and epithelial mesenchymal transition (EMT)-associated proteins were checked by WB and IHC. Results: LncSNHG3 was overexpressed in HCC tissues and cell lines. In addition, it is correlated with the tumor stage and survival time of HCC patients. Down-regulated LncSNHG3 could significantly suppress the EMT progression of HCC in vivo and in vitro. LncSNHG3 could promote the JAK1 expression by sponging miR-152-3p. Conclusions: LncSNHG3 acted as an oncogene and promoted the EMT procession in HCC by binding miR-152-3p and promoting JAK1 expression. Predictably, LncSNHG3 was used as a potential marker and will be used as a novel therapy target for HCC in the future.

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