Joint Liver Center run by UCLA and First Affiliated Hospital,Zhejiang University School of Medicine was established at Hangzhou,China

A cooperation agreement was signed by University of California at Los Angeles and the First Affiliated Hospital,Zhejiang University School of Medicine on June 2,2011,indicating the establishment of a joint     

Endoxin antagonist lessens myocardial ischemia reperfusion injury

Endoxin antagonist lessens myocardial ischemia reperfusion injury@柯永胜$Department of Cardiology, Yijishan Hospital, Wannan Medical College, Wuhu, 241001 China @王德国$Department of Cardiology, Yijishan Hospital, Wannan Medical College, Wuhu, 241001 C     

醋柳愈酯的体内代谢及药代动力

本文用薄层扫描定量法研究了醋柳愈酯在大鼠体内的代射,并测定代谢物水杨酸(SLA)的血药浓度,所得药一时数据依一定程序进行曲线拟合,计算药代动力学参数。并直接观察在大鼠体内的组织分布和在尿、粪、胆汁中的排泄。以肌肉、肺最高,脾、血浆次之,肾、睾丸、心、肝、脑、脂肪均有分布。小部分SLA径肾排泄,粪及胆汁排出量极低。     

睡眠剥夺对力竭运动大鼠胸腺谷胱甘肽、丙二醛、超氧化物歧化酶的影响

目的:观察不同睡眠剥夺时间后力竭运动对大鼠胸腺谷胱甘肽、丙二醛含量和超氧化物歧化酶活性的变化,探讨睡眠剥夺对大鼠抗氧化能力的影响。方法:实验于2006-04/05在湖南师范大学体育学院运动生物化学实验室完成。实验分组:选择10周龄健康雄性SD大鼠30只,按随机数字表法分为5组,每组6只:睡眠非运动组,睡眠 力竭运动组和睡眠剥夺24,48,72h 力竭运动组。实验方法:①采用轻柔刺激法制备大鼠睡眠剥夺模型。②睡眠非运动组和睡眠 力竭运动组不进行睡眠剥夺。③睡眠 力竭运动组和睡眠剥夺各组大鼠运动方案:跑台坡度为10°,速度为19.3m/min(相当于76%VO2max),所有大鼠运动至力竭(运动末期,大鼠先后滞留跑道后1/3处达3次以上,各种刺激驱赶均无效,停跑后体征表现为呼吸急促,神情倦怠,腹卧位,对刺激反应迟钝,捕捉时,逃避反应较运动前减弱)。实验评估:①大鼠一般状态。②力竭时间。③大鼠力竭后麻醉处死,测定胸腺谷胱甘肽、丙二醛含量和超氧化物歧化酶活性。结果:纳入大鼠30只,均进入结果分析。①大鼠一般状态:睡眠 力竭运动组大鼠表现为形态正常,活泼好动,皮毛光亮,眼睛有神;睡眠剥夺48,h 力竭运动组大鼠均出现神态倦怠,眼神黯淡,四肢亦有不同程度的红肿;睡眠剥夺24h 力竭运动组大72鼠介于以上两者之间。②睡眠 力竭运动组和睡眠剥夺24,7248,h组大鼠的力竭时间分别为(232.36±37.67),(269.19±38.61),(162.42±35.70),(141.07±28.56)。③谷胱甘肽含量、超氧化物歧化酶活性:睡眠 力竭运动组谷胱甘肽含量和超氧min化物歧化酶活性均低于睡眠非运动组[分别为(25.54±0.79),(27.09±1.31)mg/g;(±0.21),(±0.10)mkat/g],差异有显4.594.88著性意义(P<0.05);睡眠剥夺24h 力竭运动组谷胱甘肽含量和超氧化物歧化酶活性均高于睡眠非运动组[分别为(28.60±0.96),(27.09±1.31)mg/g;(±0.10),(±0.10)5.234.88mkat/g],差异有显著性意义(P<0.05),睡眠剥夺48,h 力竭运动组P72均低于睡眠非运动组[分别为(23.74±1.19),(22.43±0.52),(27.09±1.31)mg/g;(±0.14),(±0.18),(±0.10)mkat/g],4.523.354.88差异均有非常显著性意义(P<0.01);睡眠剥夺各组与睡眠 力竭运动组间谷胱甘肽含量和超氧化物歧化酶活性差异均有非常P显著性意义(P<0.01);睡眠剥夺各组间比较差异有显著性意义(P<0.05)。④丙二醛浓度:睡眠 力竭运动组丙二醛浓度高于P睡眠非运动组[分别为(±0.27),(±0.24)μmol/L],差异有非常显著性意义(P<0.01);睡眠剥夺各组与睡眠非运动组之间6.565.35P差异均有非常显著性意义(P<0.01);睡眠剥夺24,48,72h 力竭运动组丙二醛含量均高于睡眠 力竭运动组[分别为(±0.12),(±P7.398.850.72),(10.89±0.82),(±0.27)μmol/L],差异有显著性意义(P<0.05;P<0.01);睡眠剥夺各组间比较,睡眠剥夺48h与睡眠剥夺24h差6.56异无显著性意义(P>0.05),睡眠剥夺72h与睡眠剥夺24h、睡眠剥夺72h与睡眠剥夺48h间比较差异有非常显著性意义(P<0.01)。结论:①睡眠剥夺24h可引起大鼠胸腺氧化应激,使氧自由基能力有所增强。②睡眠剥夺48,72h力竭运动后氧自由基能力降低。     

自发性脑出血发病危险因素的Logistic回归分析

目的:分析抚顺地区自发性脑出血发病的危险因素。方法:①选择2002-09/2005-08抚顺市第二医院神经内外科和重症监护病房收治的自发性脑出血患者250例,男202例,女48例,年龄37～79岁。脑力劳动105例,有高血压史153例,情绪行为障碍87例,高胆固醇血症5例,冠心病31例,心电图异常者62例,吸烟47例,嗜酒55例,有糖尿病史23例,超重79例。均符合中华神经科学会、中华神经外科学会《各类脑血管疾病诊断要点》中自发性脑出血诊断标准,且经CT或MRI检查证实;均对检查项目知情同意;居住地为抚顺市望花区。②于患者入院后1周内进行一般资料和住院资料及自发性脑出血危险因素调查。高血压史:在发病前至少2次或以上收缩压>140mmHg(1mmHg=0.133kPa)或舒张压>90mmHg。情绪行为障碍表现为符合美国精神疾病诊断分类与统计手册(第四版)抑郁症诊断标准。高胆固醇血症:总胆固醇≥6.5mmol/L;糖尿病诊断以1999年世界卫生组织、国际糖尿病联合会公布为标准;超重定义为体质量指数≥25kg/m2。③采用多因素非条件Logistic回归分析对自发性脑出血发病的可能相关因素进行分析。以OR>1为自发性脑出血发生的危险因素;OR<1为自发性脑出血发生的保护因素。结果:自发性脑出血患者250例均进入结果分析。自发性脑出血患者脑力劳动OR=2.568,P=0.000;高血压OR=6.513,P=0.000;情绪行为障碍OR=4.053,P=0.000;心电图异常OR=13.397,P=0.000;糖尿病OR=4.013,P=0.006;超重OR=4.179,P=0.000;以上因素为自发性脑出血发生的危险因素。高胆固醇血症OR=0.150,P=0.005,为自发性脑出血发生的保护因素。结论:脑力劳动、高血压史、糖尿病史、情绪行为障碍、心电图异常、超重是抚顺市望花地区人群自发性脑出血发病的危险因素。     

血管内皮生长因子在口腔颌面骨组织工程中的应用

目的:了解血管内皮生长因子促进骨再生和修复作用的机制及应用方式,探讨其在口腔颌面骨组织工程中的应用前景。资料来源:应用计算机检索PubMed数据库1994-01/2006-02有关血管内皮生长因子促进成骨的文章,检索词“Vascular endothelial growth factor,Bone formation,Maxillofacial bone,Bone defect”,限定文章语言种类为English。同时计算机检索中国期刊全文数据库1994-01/2006-02期间的相关文章,检索词“血管内皮生长因子、成骨、颌骨”,限定文章语言种类为中文。资料选择:对资料进行初审,选取符合要求的有关文章找全文。纳入标准:①血管内皮生长因子及其受体分子结构方面的文章。②血管内皮生长因子促进成骨作用的基础研究和临床研究。③血管内皮生长因子在颌骨组织工程中应用的基础研究和临床研究。排除标准:重复或类似的同一研究、Meta分析、个案报道。资料提炼:共收集到186篇有关血管内皮生长因子促进成骨作用的文章,排除重复或类似的同一研究,30篇符合要求(其中2篇为血管内皮生长因子及其受体分子结构方面的文献,18篇为血管内皮生长因子促进成骨作用的基础研究和临床研究方面的文献,10篇涉及血管内皮生长因子在颌骨组织工程中应用的研究)。资料综合:①国内外有关血管内皮生长因子促进成骨作用的机制为:通过促进内皮细胞增殖、血管生成,调节骨组织血供并参与骨的发育形成;作为旁分泌因子参与骨形成代谢;通过调节成骨细胞和破骨细胞的活性促进骨组织的再生、修复和重建。②血管内皮生长因子在骨组织工程中的应用方式主要有外源性应用和内源性应用,外源性应用就是将外源性血管内皮细胞生长因子加入到支架和细胞的复合体中,使它通过促进血管化、调节参与成骨的多种因子及成骨细胞和破骨细胞的活性,提高成骨效能。内源性应用就是利用基因技术,将人血管内皮细胞生长因子基因转入种子细胞,使种子细胞持续的产生血管内皮细胞生长因子,为骨形成提供足够的血管化和调节骨细胞的活性。③动物实验已证实血管内皮生长因子对颌骨牵张成骨和颌骨缺损修复起着促进作用。结论:应用外源性和内源性血管内皮生长因子构建的组织工程骨可促进骨形成和骨缺损修复,用它来加快颌面骨组织工程的骨形成和缩短疗程在理论上是可行的。     

Expression of a Common LQT1 Mutation in Five Apparently Unrelated Families in a Regional Inherited Arrhythmia Clinic

Expression of a Common LQT1 Mutation. Background: The Inherited Arrhythmia Clinic at the University of Western Ontario services a catchment area of 1.5 million people and follows families with inherited arrhythmia syndromes. Methods: Patients referred for evaluation of long‐QT Syndrome (LQTS) are evaluated with resting and standing ECGs, and treadmill exercise testing. Patients with findings consistent with LQTS are offered comprehensive genetic testing with screening of all first‐degree relatives of genotype‐positive patients. Results: Among 31 probands with disease‐causing LQTS mutations, 5 probands from apparently unrelated families of Irish descent were found to have an identical disease causing transmembrane mutation in KCNQ1 (Leu266Pro). Systematic screening of 33 first‐degree relatives of genotype‐positive individuals detected 15 unaffected and 18 asymptomatic affected family members. Symptoms in 6 patients occurred later in life than reported LQT1 populations (61 ± 18 years, range 44–89). In this cohort, several family members presented with cardiac arrest during acute myocardial ischemia (n = 2), sudden death, unexplained drowning, and torsade de pointes during exercise testing. There was no identifiable common relative for this cohort after pedigree construction of the previous 4–7 generations. Affected patients had mild QT prolongation at rest with dramatic QT prolongation with exercise. Conclusions: Genetic testing in this LQTS population suggests a common KCNQ1 Leu266Pro founder effect, with the descendants clustering in our geographical region even though no common relative has been identified. The observations highlight the utility of genotypic and phenotypic correlation and a specialized clinic. (J Cardiovasc Electrophysiol, Vol. 21, pp. 296–300, March 2010)     

ANGIOTENSIN II ACTIVATES PRESSOR AND DEPRESSOR SITES OF THE PONTOMEDULLA THAT REACT TO GLUTAMATE

1. In cats anaesthetized with a mixture of α-chloralose (40 mg/kg) and urethane (400 mg/kg) and in rats anaesthetized with a mixture of α-chloralose (60 mg/kg) and urethane (800 mg/kg), changes in systemic arterial pressure (SAP), heart rate (HR) and sympathetic activities of vertebral (VNA) and renal (RNA) nerves were determined following the micro-injection of angiotensin II (AngII; 0.16 mmol/L; 50 nL) into the pressor and depressor sites of the pontomedulla previously reacted to a microinjection of monosodium l -glutamate (Glu; O.1 mol/L; 50 nL). Pressor sites included gigantocellular tegmental field (FTG) and dorsal medulla (DM) and rostral ventrolateral medulla (VLM). The depressor site was the caudal VLM (CVLM). The effects of losartan (1 mmol/L; 50 nL), a specific AT₁ receptor non-peptide antagonist for AngII, on responses induced by AngII in the VLM, DM and CVLM were also determined. 2. In 30% of pressor sites in the FTG, 55% in the VLM and 67% in the DM and in 76% of depressor sites in the CVLM previously exposed to Glu, microinjection of AngII to the same site produced pressor or depressor responses similar to that of Glu, but smaller in magnitude, particularly in the pressor VLM. Changes in both VNA and RNA induced by AngII were also smaller than those induced by Glu, particularly RNA from DM activation. 3. In the dorsal motor nucleus of the vagus, AngII, as Glu, produced marked bradycardia, but again this was smaller in magnitude than the bradycardia produced by Glu. 4. In rats, in the DM near or around the nucleus of the solitary tract where Glu increased SAP, microinjection of AngII (0.8 mmol/L; 60 nL) produced a depressor response, while the microinjection of 1.6 mmol/L (60 nL) AngII produced a pressor response. 5. Losartan blocked the increases in SAP induced by AngII in the VLM and DM. Decreases in SAP induced by AngII in the CVLM, however, were only slightly decreased by losartan. 6. Our data suggest that a significant portion of pressor and depressor sites of the pontomedulla contain neurons responsive to both AngII and Glu. In neurons in the VLM and DM, AngII produced pressor responses that were primarily mediated through AT₁ receptors, while the depressor actions of AngII in the CVLM were not mediated by AT₁ receptors.