NADPH氧化酶家族在心血管疾病中作用的研究进展

烟酰胺腺嘌呤二核苷酸磷酸氧化酶是心血管系统中活性氧(reactive oxygen species,ROS)的主要来源,它包 括7种亚型并分别表达在不同的心血管细胞及其细胞器中,参与调节细胞增殖、迁移、分化、凋亡、衰老和炎症反应 等多种活动,其衍生的ROS参与高血压、动脉粥样硬化、糖尿病血管病变、心肌梗死后心室重构等多种心血管疾病 的病理过程。     

7-硝基吲唑对大鼠脑缺血再灌流保护作用的研究

目的：探讨神经元型一氧化氮合酶抑制剂（ｎＮＯＳＩ）７－硝基吲唑（７－ｎｉｔｒｏｉｎｄａｚｏｌｅ,７－ＮＩ）对脑缺血再灌流保护作用的机理。方法：选用体重１８０－２２０ｇ的雌性Ｗｉｓｔａｒ大鼠,随机分组,左颈外动脉管腔内置渔线经颈内动脉送至大脑中动脉内,使之闭塞。     

QT Dispersion Level and Its Clinical Significance.in Dilated Cardiomyopathy

［1］Richardson CP, Mckenna RM, Bristow CM, et al.Report of the 1995 Word Health Organization/International Society and Federation of Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation, 1996,93: 841 ［2］Barr CS, Naas A, Freeman M, et al. QT dispersion and sudden unexpected death in chronic heart failure. Lancet, 1994,343:327 ［3］Martin AB, Garson A, Perry JC, et al. Prolonged QT interval in hypertropic and dilated cardiomyopathy in children. Am Heart J, 1994,127(1):64 ［4］Pye M, Quinn AC, Cobble SM. QT dispersion: a non-invasive marker of susceptibility to arrhythmia in patients with sustained ventricular arrhythmias?Br Heart J, 1994,71(5):51 ［5］Berger RD, Kasper EK, Baughman KL, et al. Beat to beat QT interval variability: novel evidence for repolarization lability in ischemic and non ischemic dilated cardiomyopathy. Circulation, 1997, 96 (5):1557 ［6］Wolfram G, Ulrike S, Volker M, et al. QT dispersion and arrhythmic events in idiopathic dilated cardiomyopathy. Am J Cardiol, 1997,78: 458 ［7］Fei L, Goldman JH, Prasal K, et al. QT dispersion and RR variations on 12-lead ECGs in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy. Eur Heart J, 1996,17: 258 ［8］Pan YZ, Guo NS, Xing ZF, et al. The relation between QT dispersion and ventricular arrhythmia of dilated cardiomyopathy. Chin J Inter Medi, 1996,35(11):73 ［9］Galinier M, Vialette JC, Fourcade J, et al. QT interval dispersion as a predictor of arrhythmic events in congestive heart failure. Importance of aetiology. Eur Heart J, 1998,19(7) :1054     

新生儿缺氧缺血性脑病血浆及脑脊液一氧化氮水平的变化

目的 :了解新生儿缺氧缺血性脑病 (HIE)时血浆和脑脊液 (CSF)中 NO水平的动态变化。方法 :采用硝酸根还原酶法 ,对 35例 HIE患儿 (轻度 10例、中度 13例、重度 12例 )分别于急性期、恢复期进行了血浆和 CSF NO水平测定。结果 :HIE急性期血浆 NO水平除轻度组外 ,中、重度组明显高于对照组 ,重度组又明显高于轻、中度组 ;恢复期轻、中、重度组血浆 NO水平均降至正常 ,与对照组比较差异无显著性。CSF中 NO水平增加的幅度与血浆成正比。结论 :血浆和 CSF中 NO水平与 HIE的脑损伤程度密切相关     

Presynaptic inhibition of synaptic transmission in the rat hippocampus by activation of muscarinic receptors: involvement of presynaptic calcium influx

1. Modulation of presynaptic voltage-dependent calcium channels (VDCCs) by muscarinic receptors at the CA3–CA1 synapse of rat hippocampal slices was investigated by using the calcium indicator fura-2. Stimulation-evoked presynaptic calcium transients ([Ca_pre]_t) and field excitatory postsynaptic potentials (fe.p.s.ps) were simultaneously recorded. The relationship between presynaptic calcium influx and synaptic transmission was studied.
2. Activation of muscarinic receptors inhibited [Ca_pre]_t, thereby reducing synaptic transmission. Carbachol (CCh, 10 μM) inhibited [Ca_pre]_t by 35% and reduced fe.p.s.p. by 85%. The inhibition was completely antagonized by 1 μM atropine. An approximate 4^th power relationship was found between presynaptic calcium influx and postsynaptic responses.
3. Application of the N-type VDCC-blocking peptide toxin ω-conotoxin GVIA (ω-CTx GVIA, 1 μM) inhibited [Ca_pre]_t and fe.p.s.ps by 21% and 49%, respectively, while the P/Q-type VDCC blocker ω-agatoxin IVA (ω-Aga IVA, 1 μM) reduced [Ca_pre]_t and fe.p.s.ps by 35% and 85%, respectively.
4. Muscarinic receptor activation differentially inhibited distinct presynaptic VDCCs. ω-CTx GVIA-sensitive calcium channels were inhibited by muscarinic receptors, while ω-Aga IVA-sensitive channels were not. The percentage inhibition of ω-CTx GVIA-sensitive [Ca_pre]_t was about 63%.
5. Muscarinic receptors inhibited presynaptic VDCCs in a way similar to adenosine (Ad) receptors. The percentage inhibition of ω-CTx GVIA-sensitive [Ca_pre]_t by Ad (100 μM) was about 59%. There was no significant inhibition of ω-Aga IVA-sensitive channels by Ad. The inhibitions of [Ca_pre]_t by CCh and Ad were mutually occlusive.
6. These results indicate that inhibition of synaptic transmission by muscarinic receptors is mainly the consequence of a reduction of the [Ca_pre]_t due to inhibition of presynaptic VDCCs.

     

小儿肾小球疾病血清微量元素测定与分析

采用原子吸收分光光度法,测定了７８ 例肾小球疾病患儿血清铜、锌、铁、镁４ 种元素。结果显示,单纯性肾病组、肾炎性肾病组、紫癜性肾病组及肾炎组血清锌均显著低于正常组（ Ｐ＜ ００５）,血清铁、镁与正常组比较无显著差异。单纯性肾病组,肾炎性肾病组血清铜显著低于正常组（ Ｐ＜ ００５）。提示血清铜、锌、铁、镁含量的变化与疾病发生和疾病状态有关。     

端头修饰PEO有序膜的制备及其微摩擦性能的初步研究

以对氨基苯磺酸修饰聚乙二醇端头,制备兼具刚性与极性端头的聚合物,考察其制备ＬＢ膜与自组装膜的条件,用原子力／摩擦力显微镜表征自组装膜的表面形貌,对其微摩擦性能进行初步的探讨。     

α1-抗糜蛋白酶基因、早老素1基因 与阿尔茨海默病的相关分析

目的探讨中国汉族人中α１抗糜蛋白酶（ＡＡＣＴ）基因、早老素１（ＰＳ１）基因多态性与阿尔茨海默病（Ａｌｚｈｅｉｍｅｒｓｄｉｓｅａｓｅ,ＡＤ）的相关情况。方法应用ＰＣＲＲＦＬＰ方法,在１２３例患者和１４０例正常人中观察ＡＡＣＴ信号肽和ＰＳ１基因多态性的分布,进行关联分析。结果１ＡＤ患者与ＰＳ１基因等位基因１正关联,与等位基因２和基因型２／２负关联,但与１／１基因型无关;２ＡＡＣＴ信号肽基因多态性与ＡＤ无关联;３在三种ＰＳ１基因型中,ＡＡＣＴ信号肽基因多态性与ＡＤ均无关;４在ＡＡＣＴ基因ＡＡ、ＴＴ基因型中,ＰＳ１基因多态性与ＡＤ负关联,而ＴＡ型中ＰＳ１基因与ＡＤ无显著相关。结论中国人群中,ＡＤ与ＰＳ１基因２／２型负关联,而与ＡＡＣＴ信号肽基因多态性无关;ＡＡＣＴ信号肽和ＰＳ１基因多态性之间也无明显的相互影响。     

Human allogeneic vascular rejection after arterial transplantation and peripheral lymphoid reconstitution in severe combined immunodeficient mice

BACKGROUND: Interspecies differences create important shortcomings in existing animal models used to describe in vivo events responsible for allograft rejection. Alloimmune destruction of human dermal microvessels, histologically consistent with rejection, has been demonstrated in human skin-grafted severe combined immunodeficient (SCID) mice receiving allogeneic human peripheral blood mononuclear cells (PBMC). We have now documented human alloimmune injury in a vascularized, SCID-human arterial transplantation model. METHODS: Fresh human artery was used to replace the CB.17 SCID/beige mouse infrarenal aorta. Seven days later, 3x10(8) human PBMC were administered intraperitoneally, and lymphocyte engraftment was considered successful when circulating human CD3+ cells were later identified in peripheral blood. RESULTS: Forty-six of 49 (94%) mice undergoing transplantation survived, including 14 controls with arterial grafts receiving no PBMC. Twenty-eight of 32 mice demonstrated circulating human CD3+ cells, 14 days after PBMC administration. Animals were killed at 14, 21, or 28 days after receiving allogeneic PBMC, and arteries were recovered for histology and immunohistology. All 14 control mice had patent transplanted grafts with normal vascular histology and no lymphoid infiltration. Damage to transplanted arteries among lymphocyte-engrafted mice was apparent by 14 and 21 days in some animals, whereas 16 of 22 exhibited moderate to severe intimal, medial, and/or adventitial lymphocytic infiltration with intimal expansion by day 28. The infiltrate consisted of HLA-A, -B, -C+, and -DR+, human CD3+ cells, approximately equally distributed as CD4+ and CD8+ subsets. Some infiltrating lymphocytes were cytolytic cells as demonstrated by perforin staining. The endothelium of transplanted human arteries exhibited endothelialitis, and the endothelial cells stained intensely with anti-HLA-A, -B, -C and anti-HLA-DR antibodies. The expanded intima was predominantly smooth muscle cells, staining positively for smooth muscle alpha-actin, HLA-A, -B, -C and HLA-DR. Medial necrosis was not observed. CONCLUSION: The results provide evidence of alloimmune-mediated vascular rejection in this human arterial transplantation model.