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( Zi Zhong Tang ),( Hui Chen ),( Li Jiao Chen ),( San Liu ),( Xue Yi Han ),( Qi Wu ) 한국미생물 · 생명공학회 2014 Journal of microbiology and biotechnology Vol.24 No.4
The carbohydrate-binding module (CBM) is an important domain of most cellulases that plays a key role in the hydrolysis of cellulose. The neutral endoglucanase (EG1) gene was reconstructed. A redesigned endoglucanase, named EG2, was constructed with a CBM containing a linker from Corticium rolfsii (GenBank Accession No. D49448). The redesigned EG genes were expressed in Escherichia coli, and their characteristics are discussed. Results showed that the degradation of cellulose by EG2 was about double that by EG1. The specific activities of EG1 and EG2 were tested under optimal conditions, and EG2 had higher activity (169.1 ± 2.74 U/mg) toward CMC-Na than did EG1 (84.0 ± 1.98) in the process of cellulose degradation. The optimal pH and temperature, pH stability, and heat stability of EG1 and EG2 were similar. Results indicated that the CBM plays an essential role in the hydrolysis of cellulose. We can improve EG`s catalytic power by adding the CBM from Corticium rolfsii.
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Yu Qing,Wu Li-bin,Zhang Fan,Wei Xiao-tong,Chen Pian-pian,Wang Shuai-ya,Cai Mei-yi,Shu Qi,Li Liao-yuan,Wu Zi-jian,Cai Rong-lin,Hu Ling 사단법인약침학회 2021 Journal of Acupuncture & Meridian Studies Vol.14 No.6
Background: Myocardial ischemia reperfusion injury (MIRI) is an important mechanism of post-myocardial infarction injury and a main cause of death in patients with ischemic heart disease. Electroacupuncture (EA) pretreatment is effective for the prevention and treatment of MIRI, but mechanisms mediating the effects of cardiovascular disease EA treatments remain unclear. Objectives: To determine whether the lateral hypothalamus (LHA) and the cerebellar fastigial nucleus (FN) are involved in the protective effects of EA stimulation on MIRI. Methods: EA pretreatment was performed for 7 days before the establishment of the MIRI model. ST-segment changes on electrocardiograms were recorded and the Curtis–Walker arrhythmia score was used to evaluate changes in reperfusion injury. Hematoxylin–eosin staining was applied to evaluate the pathological and morphological changes in myocardial tissue. c-fos expression in the LHA and FN was determined by immunofluorescence staining. Glutamic (Glu) and γ-Aminobutyric acid (GABA) levels were measured using a high-performance liquid chromatography-electrochemical method. Results: EA pretreatment reduced ST-segment elevation, arrhythmia scores, and morphological changes in MIRI myocardial cells in rats, and decreased the c-fos protein expression in LHA/FN nuclei. MIRI was associated with an imbalance between GABA and Glu levels, whereas EA pretreatment increased GABA levels and decreased Glu levels in the LHA/FN. Conclusion: FN and LHA are involved in the EA-mediated attenuation of MIRI. Pretreatment with EA plays a protective role in the myocardium by regulating Glu and GABA release in the LHA and FN.
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( Xing Yu Li ),( Zi Chao Mao ),( Yue Hu Wang ),( Yi Xing Wu ),( Yue Qiu He ),( Chun Lin Long ) 한국미생물 · 생명공학회 2013 Journal of microbiology and biotechnology Vol.23 No.3
Bacillus subtilis XF-1, a strain with demonstrated ability to control clubroot disease caused by Plasmodiophora brassicae, was studied to elucidate its mechanism of antifungal activity against P. brassicae. Fengycin-type cyclopeptides (FTCPs), a well-known class of compounds with strong fungitoxic activity, were purified by acid precipitation, methanol extraction, and chromatographic separation. Eight homologs of fengycin, seven homologs of dehydroxyfengycin, and six unknown FTCPs were characterized with LC/ESI-MS, LC/ESI-MS/MS, and NMR. FTCPs (250μg/ml) were used to treat the resting spores of P. brassicae (107/ml) by detecting leakage of the cytoplasm components and cell destruction. After 12 h treatment, the absorbencies at 260 nm (A260) and at 280 nm (A280) increased gradually to approaching the maximum of absorbance, accompanying the collapse of P. brassicae resting spores, and nearly no complete cells were observed at 24 h treatment. The results suggested that the cells could be cleaved by the FTCPs of B. subtilis XF-1, and the diversity of FTCPs was mainly attributed to a mechanism of clubroot disease biocontrol.
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Si-Qi Dong,Tong-Min Wang,Jiang-Bo Zhang,Yong-Qiao He,Wen-Qiong Xue,Zi-Yi Wu,Da-Wei Yang,Lian-Jing Cao,Jing-Wen Huang,Xi-Zhao Li,Pei-Fen Zhang,Xiao-Hui Zheng,Wei-Hua Jia 대한암학회 2021 Cancer Research and Treatment Vol.53 No.3
Purpose Capecitabine is an extensively used oral prodrug of 5-fluorouracil in treatment of colon cancer and is known to cause hand-foot syndrome (HFS). As the target enzyme for capecitabine, thymidylate synthase (TYMS) plays a key role for 5-fluorouracil metabolism and has been associated with some side effects caused by capecitabine. The aim of our study is to identify the possible genetic predictors of capecitabine-induced HFS (CAP-HFS) in Chinese colorectal cancer patients.Materials and Methods Whole exons of TYMS were sequenced for 288 extreme phenotype HFS patients, including 144 severe or early-onset (first 2 cycles) moderate HFS extreme cases and 144 extreme controls with no reported HFS. The associations between polymorphisms and CAP-HFS were analyzed using logistic regression under an additive model.Results We identified a novel risk mutation (c.1A>G, chr18:657743), was associated with severe HFS in an extreme case who was affected during the first cycle of treatment. Moreover, we identified three new variants, rs3786362, rs699517, rs2790, and two previously reported variants, 5’VNTR 2R/3R and 3′-untranslated region 6-bp ins-del, which were significantly associated with CAP-HFS (p < 0.05). In silico analysis revealed that the effect of these polymorphisms in the TYMS region on the development of HFS might not be restricted solely to the regulation of TYMS expression, but also the TYMS catalytic activity through the indirect effect on ENOSF1 expression.Conclusion This study identified new polymorphisms in TYMS gene significantly associated with CAP-HFS, which may serve as useful genetic predictors for CAP-HFS and help to elucidate the underlying mechanism of HFS.
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