涂植光
个性化签名
- 姓名:涂植光
- 目前身份:
- 担任导师情况:
- 学位:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
药物化学
- 研究兴趣:
涂植光,男,1946.8.月出生。教授,博士生导师。1970年毕业于重庆医学院儿科系本科, 1981年药理学专业研究生毕业并获硕士学位。曾赴英国研修。
重庆市首批该学科学术带头人,享受国务院政府特殊津贴,曾被评为“在工作中做出突出贡献的中国硕士学位获得者”。现任教育部医学技术教学指导委员会副主任、全国高等医学教育学会医学检验分会理事长、全国临床检验学会常委、卫生部临床检验中心专家委员会委员、重庆市第二届学位委员会委员等。
先后主持国家自然科学基金、教委优秀年轻教师基金、教育部重点科学技术项目等多项科研课题。发表科研论文100余篇,其中被SCI收录英文论文13篇。多本全国性专业学术杂志编委、常务编委或副主编。分别担任教育部及卫生部本科、7年制和8年制规划教材7部主编、副主编或编委,主编的“临床检验生物化学”评为“普通高等教育‘十一五’国家级规划教材”。曾获国家教学成果二等奖1项,省(市)教学、科技成果一、二、三等奖4项。招收培养硕士生38名,博士生21名。
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主页访问
1992
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关注数
0
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成果阅读
102
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成果数
2
涂植光, TU Zhi-Guang, ZHAO Liang-Li
中国药理学报,1996,17(6):541~544,-0001,():
-1年11月30日
To compare the inhibitory effectS of quinidine and quinine on liver microsome bufuralol 1Aydroxylase (BH). aryr hydrocarbon hydroxyl- ase (AHH). and 7-ethoxycoumarin O-deethylase (ED) activities in man and rat. METHODS: A normal phase HPLC and the fluorescence spectrometry were used to assay the enzyme activities. RESULTS: Both quinidine and quinine produced a concentration-dependent inhibition to liver microsome BH, AHH, and ED in man and rat. Thelr median inhibitory concentrations (ICsO) oii liver microscme BH, AHH. and ED low and high atfinjfy phases were 0.2. 378. 2952P and >5000 moI.L-1 for quinine in man. 290, 613 1465. 1595. UmoI.L-1 for quinidine in rat; 29, 207, 808, and >5000 umoI.L-l for quinine in man. and 31, 54, 597, and 2508 UmoI.L-1 for quinine in rat, respectively. CONCLUSlON: Quinidine is a species- and stereo-selective potent inhibitor to human liver microscme BH.
quinidine, quinine, liver micro-somes, pharmacogenetics, bufuralol, 7-alkoxy-coumarin O-dealkylase, aryl hydrocarbon hydroxylases
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【期刊论文】M etoprolol α-hydroxylation capacity in 96 Chinese Han volunteers
涂植光, TU Zhi-Guang, ZHAO Liang-Li
中国药理学报,1995,16(4):325-329,-0001,():
-1年11月30日
AIM: To study the ability of oxidizing meto-proloi (Met) to form α-hydroxymetoprolol (HM) in Chinese in vivo and in vitro. METHODS: An ion pair reverse phase high performance liquid chromatography was used. RESULTS: In v/vo study, the 8-h urinary recoveries of Met and HM after po Met tartrate 100 mg were tested in 96 unrelated healthy Chinese Hart volunteers, and the capaeity of Met α-hydroxylation expressed by lg Met/HM (metabolic ratio. MR). The frequency histogram of lg MR showed the characteristic hi modal distribution of monogenie control variation, and the phenotypieal antinaode of lg MR was 1.09. Only 1 man with lg MR=2,30 was identified as poor metabolizer of Met α-hydroxylation, The urinary recoveries of Met and HM and the MR in 95 extensive metabohzer were 6.8±3.3%. 3.0±1.5% of dose mole and 3.1±2. 5; respectively, The sex difierence, smoking and tea consuming had no effects on the urinary excretions of Met, and HM. and the MR, In vitro, the adding of NADH did not affect the activities of human liver microsome Met α-hydroxylase. The enzyme kinetics parameters were Km=89.60 umol L-1 and Vmax=39.5 ng HM mg-1 min-1. No functional absence of liver mierosome Met α-hydroxylase was found in the tested liver samples from 8 people, and the activities of liver mierosome Met α-hydroxylase were 31 ±22ng mg-1 min-1, CONCLUSION: The incidence of poor metabolizer phenotype for Met α-hydroxylation in Chinese Hart nationality is low, and the NADH is riot involved in human liver microsome Met α-hydroxylation.
metoprolol, a-hydroxymetoprolol, liver microsomes, pharmacogeneties, polymorphism
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