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      • KCI등재

        Asymmetric Reduction of Ethyl Acetoacetate Catalyzed by Immobilized Acetobacter sp. CCTCC M209061 Cells in Hydrophilic Ionic Liquid Hybrid System

        Ping Wei,Pei Xu,Xiao-Ting Wang,Wen-Yong Lou,Min-Hua Zong 한국생물공학회 2015 Biotechnology and Bioprocess Engineering Vol.20 No.2

        The asymmetric reduction of ethyl acetoacetate (EAA) to ethyl (R)-3-hydroxybutyrate [(R)-EHB] using immobilized Acetobacter sp. CCTCC M209061 cells was successfully conducted in a hydrophilic ionic liquid (IL)- containing system. The best one of all the tested watermiscible ILs was 1-(hydroxyethyl)-3-methylimidazolium hydrochloride (C2OHMIM·Cl). In C2OHMIM·Cl-aqueous buffer hybrid system, it was found that the optimal IL concentration, substrate and co-substrate concentration, reaction temperature, buffer pH and shaking rate were 0.5mol/L, 45 mmol/L, 80 mmol/L, 35oC, pH 5.5 and 200 rpm, respectively. Under the optimized reaction conditions, the initial reaction rate, the yield and the product e.e. reached 4.90 μmol/min, 95.3 and > 99.0%, respectively, which were much higher than the corresponding values reported previously. The efficient biocatalytic process mediated by the immobilized cells was feasible on 500 mL preparative scale, and the biocatalysts showed good operational stability and could be recycled for at least 10 batches.

      • SCIESCOPUS

        The establishment of IB-SEM numerical method and verification of fluid-solid interaction

        Wang, Jing,Li, Shu-cai,Mao, Xuerui,Li, Li-ping,Shi, Shao-shuai,Zhou, Zong-qing Techno-Press 2018 Geomechanics & engineering Vol.15 No.6

        The interaction between particles and fluid was investigated by IB-SEM numerical method which is a combination of combing the spectral/hp element method and the rigid immersed boundary method. The accuracy of this numerical method was verified based on the computed results with the traditional body-fitted mesh in numerical simulation of the flow through the cylinder. Then the governing equations of particles motion and contact in fluid are constructed. The movement of the particles and the interaction between the fluid and the particles are investigated. This method avoided the problem of low computational efficiency and error caused by the re-division of the grid when the solids moved. Finally, the movement simulation of multi particles in the fluid was carried out, which can provide a completely new numerical simulation method.

      • KCI등재

        N-acetylcysteine protects against cadmium-induced oxidative stress in rat hepatocytes

        Jicang Wang,Huali Zhu,Xue-Zhong Liu,Zong-Ping Liu 대한수의학회 2014 Journal of Veterinary Science Vol.15 No.4

        Cadmium (Cd) is a well-known hepatotoxic environmentalpollutant. We used rat hepatocytes as a model to studyoxidative damage induced by Cd, effects on the antioxidantsystems, and the role of N-acetylcysteine (NAC) in protectingcells against Cd toxicity. Hepatocytes were incubated for 12and 24 h with Cd (2.5, 5, 10 μM). Results showed that Cd caninduce cytotoxicity: 10 μM resulted in 36.2% mortality after12 h and 47.8% after 24 h. Lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase activitiesincreased. Additionally, reactive oxygen species (ROS)generation increased in Cd-treated hepatocytes along withmalondialdehyde levels. Glutathione concentrationssignificantly decreased after treatment with Cd for 12 h butincreased after 24 h of Cd exposure. In contrast, glutathioneperoxidase activity significantly increased after treatmentwith Cd for 12 h but decreased after 24 h. superoxidedismutase and catalase activities increased at 12 h and 24 h. glutathione S-transferase and glutathione reductase activitiesdecreased, but not significantly. Rat hepatocytes incubatedwith NAC and Cd simultaneously had significantly increasedviability and decreased Cd-induced ROS generation. Ourresults suggested that Cd induces ROS generation that leads to oxidative stress. Moreover, NAC protects rat hepatocytes from cytotoxicity associated with Cd.

      • KCI등재

        Is Folate Status a Risk Factor for Asthma or Other Allergic Diseases?

        Ting Wang,Zong-An Liang,Yu-Lin Ji,Hong-Ping Zhang,Xin Zhang,Gang Wang 대한천식알레르기학회 2015 Allergy, Asthma & Immunology Research Vol.7 No.6

        Purpose: It is controversial whether folate status is a risk factor for the development of asthma or other allergic diseases. This study was conducted to investigate whether indirect or direct exposure to folate and impaired folate metabolism, reflected as methylene-tetrahydrofolate reductase (MTHFR) C677T polymorphism, would contribute to the development of asthma and other allergic diseases. Methods: Electronic databases were searched to identify all studies assessing the association between folate status and asthma or other allergic diseases. Two reviewers independently assessed the eligibility of studies and extracted data. The relative risk (RR) or odds ratio (OR) with 95% confidence intervals (CI) was calculated and pooled. Results: Twenty-six studies (16 cohort, 7 case-control, and 3 cross-sectional studies) were identified. Maternal folic acid supplementation was not associated with the development of asthma, atopic dermatitis (AD), eczema, and sensitization in the offspring, whereas exposure during early pregnancy was related to wheeze occurrence in the offspring (RR=1.06, 95% CI=[1.02-1.09]). The TT genotype of MTHFR C677T polymorphism was at high risk of asthma (OR=1.41, 95% CI=[1.07-1.86]). Conclusions: It is indicated that maternal folic acid supplementation during early pregnancy may increase the risk of wheeze in early childhood and that the TT genotype of MTHFR C677T polymorphism impairing folic acid metabolism would be at high risk of asthma development. These results might provide additional information for recommendations regarding forced folate consumption or folic acid supplements during pregnancy based on its well-established benefits for the prevention of congenital malformations. However, currently available evidence is of low quality which is needed to further elucidate.

      • KCI등재

        Cadmium induces apoptosis in primary rat osteoblasts through caspase and mitogen-activated protein kinase pathways

        Hong-Yan Zhao,Wei Liu,Yi Wang,Nannan Dai,Jian-Hong Gu,Yan Yuan,Xue-Zhong Liu,Jian-Chun Bian,Zong-Ping Liu 대한수의학회 2015 Journal of Veterinary Science Vol.16 No.3

        Exposure to cadmium (Cd) induces apoptosis in osteoblasts (OBs); however, little information is available regarding the specific mechanismsof Cd-induced primary rat OB apoptosis. In this study, Cd reduced cell viability, damaged cell membranes and induced apoptosis in OBs. We observed decreased mitochondrial transmembrane potentials, ultrastructure collapse, enhanced caspase-3 activity, and increasedconcentrations of cleaved PARP, cleaved caspase-9 and cleaved caspase-3 following Cd treatment. Cd also increased the phosphorylationof p38-mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK)1/2 and c-jun N-terminal kinase (JNK) in OBs. Pretreatment with the caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, ERK1/2 inhibitor (U0126), p38 inhibitor(SB203580) and JNK inhibitor (SP600125) abrogated Cd-induced cell apoptosis. Furthermore, Cd-treated OBs exhibited signs of oxidativestress protection, including increased antioxidant enzymes superoxide dismutase and glutathione reductase levels and decreased formationof reactive oxygen species. Taken together, the results of our study clarified that Cd has direct cytotoxic effects on OBs, which are mediatedby caspase- and MAPK pathways in Cd-induced apoptosis of OBs.

      • KCI등재

        Involvement of the Ca2+ signaling pathway in osteoprotegerin inhibition of osteoclast differentiation and maturation

        Ying-Xiao Fu,Jian-Hong Gu,Yi Wang,Yan Yuan,Xue-Zhong Liu,Jian-Chun Bian,Zong-Ping Liu 대한수의학회 2015 Journal of Veterinary Science Vol.16 No.2

        The purpose of this study was to determine whether the Ca2+ signaling pathway is involved in the ability of osteoprotegerin (OPG) to inhibit osteoclast differentiation and maturation. RAW264.7 cells were incubated with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-κB ligand (RANKL) to stimulate osteoclastogenesis and then treated with different concentrations of OPG, an inhibitor of osteoclast differentiation. The intracellular Ca2+ concentration [Ca2+]i and phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the different treatment groups were measured by flow cytometry and Western blotting, respectively. The results confirmed that M-CSF + RANKL significantly increased [Ca2+]i and CaMKII phosphorylation in osteoclasts (p < 0.01), and that these effects were subsequently decreased by OPG treatment. Exposure to specific inhibitors of the Ca2+ signaling pathway revealed that these changes varied between the different OPG treatment groups. Findings from the present study indicated that the Ca2+ signaling pathway is involved in both the regulation of osteoclastogenesis as well as inhibition of osteoclast differentiation and activation by OPG.

      • SCIESCOPUSKCI등재

        Characterization of the Methylation Status of Pax7 and Myogenic Regulator Factors in Cell Myogenic Differentiation

        Chao, Zhe,Zheng, Xin-Li,Sun, Rui-Ping,Liu, Hai-Long,Huang, Li-Li,Cao, Zong-Xi,Deng, Chang-Yan,Wang, Feng Asian Australasian Association of Animal Productio 2016 Animal Bioscience Vol.29 No.7

        Epigenetic processes in the development of skeletal muscle have been appreciated for over a decade. DNA methylation is a major epigenetic modification important for regulating gene expression and suppressing spurious transcription. Up to now, the importance of epigenetic marks in the regulation of Pax7 and myogenic regulatory factors (MRFs) expression is far less explored. In the present study, semi-quantitative the real-time polymerase chain reaction (RT-PCR) analyses showed MyoD and Myf5 were expressed in activated and quiescent C2C12 cells. MyoG was expressed in a later stage of myogenesis. Pax7 was weakly expressed in differentiated C2C12 cells. To further understand the regulation of expression of these genes, the DNA methylation status of Pax7, MyoD, and Myf5 was determined by bisulfite sequencing PCR. During the C2C12 myoblasts fusion process, the changes of promoter and exon 1 methylation of Pax7, MyoD, and Myf5 genes were observed. In addition, an inverse relationship of low methylation and high expression was found. These results suggest that DNA methylation may be an important mechanism regulating Pax7 and MRFs transcription in cell myogenic differentiation.

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