血管内皮祖细胞与老年缺血性心血管病的血管新生

<正> 1997年国内外报道血管内皮祖细胞(endothelial progenitorcelhs,EPCs)分离培养成功,从而使:EPCs成为当前干细胞研究热潮中的一个分支。EPCs是一群具有游走性特征、能进一步增殖分化的幼稚内皮细胞,由干细胞经成血管细胞分化发育而来,由于缺乏成熟内皮细胞的特征性表型,因此,有人提出对于EPCs的鉴别分离主要靠其特异性的分子标志(CD34+、flk-1、AC133+);此外也可通过EPCs培养分化形     

血管内皮功能障碍及其治疗进展

内皮细胞不仅仅是血管腔内的一层防护细胞,而且还能分泌一系列血管活怀物质,调节血管张力及血管生长,具有防止血栓形成等我种生理功能。因此内皮细胞功能障碍与动脉粥样硬化、高血压及心力衰竭等疾病的发生、发展有密切关系。对内皮功能障碍进行逆转性治疗,已成为心血管疾病治疗领域的一个新的发展趋势。目前主要治疗措施包括：改善血管内环境;促进ＮＯＲ 形成;应用血管紧张素转化产（ＡＣＥ）抑制剂,钙拮抗剂、雌激素等。     

血脂异常冠心病血管内皮损伤机制的研究

目的:研究血脂异常冠心病大鼠血管内皮损伤机制.方法:根据培养方法,20只大鼠被均分为健康对照组和血脂异常冠心病组.观察比较两组培养后血脂水平、血清TNF-α、IL-1β、IL-6、SOD、GSH、MDA水平、VEGF、Bcl-2及半胱氨酸蛋白酶(Caspase-9)相对表达量.结果:与健康对照组比较,血脂异常冠心病组血...     

血管内皮功能研究现状

自从生理学家Ｈｉｓ于 186 5年首先提出内皮这一概念后 ,人类对它的研究始终方兴未艾。新近越来越多的研究发现血管内皮功能失调参与多种心血管疾病的发病 ,并认为内皮功能失调是发生动脉粥样硬化的最初事件即“启动子”[1 ] 。如今 ,遴选出一种既经济又简便的方法来评估血管内皮功能以及采取某种合适的方式来保护或挽救血管内皮功能将是心血管疾病防治史上的一个新的里程碑。我们着重对血管内皮的功能及其评估方法、内皮功能失调的治疗作一综述。1　正常血管内皮的功能1.1　屏障作用　血管内皮衬于血管内壁 ,起屏障作用 ,将血管内外分开 ,…     

内皮依赖性超极化因子的研究概况

内皮依赖性超极化因子是一个不同于一氧化氮和前列环素的内皮舒张因子，它在调节血管平滑肌张力及心血管的病理、生理方面发挥重要作用。     

血管内皮功能与血管重塑

血管内皮具有强大的生理功能,内皮功能障碍参与心血管疾病的发生、发展.近年的研究表明,血管重塑对心血管疾病的意义愈见明显,而内皮细胞在血管重塑过程中发挥重要作用,内皮功能障碍可影响血管重塑的程度和性质.本文就正常血管内皮功能及其在血管重塑过程中的作用以及内皮功能障碍与血管重塑的关系作一综述.     

辛伐他汀和粒细胞集落刺激因子对血管内皮损伤的修复效应

目的探讨在大鼠颈动脉球囊损伤模型中,通过刺激骨髓,加强内皮祖细胞向周围血动员对损伤血管内皮修复和抑制新生内膜的效果。方法制备大鼠颈动脉球囊损伤模型。对照组(n=14)给予生理盐水灌胃,辛伐他汀组(n=12)及合并使用辛伐他汀与粒细胞集落刺激因子(G-CSF)组(n=12)给予辛伐他汀10mg/(kg.d)灌胃,辛伐他汀与G-CSF组加用G-CSF100μg/(kg.d)腹腔注射,给药均从术前1周至术后2周。测定损伤血管内皮修复率、新生内膜/中膜面积比(IA/MA)、增殖性细胞核抗原(PCNA)阳性细胞指数、外周血一氧化氮(NO)含量,流式细胞仪检测CD34 血管内皮生长因子受体2(VEGFR-2) 双荧光阳性细胞比例。结果成功建立大鼠颈动脉损伤模型。与对照组比较,辛伐他汀组内皮修复率增加12.3%,IA/MA减少18.4%、外周血NO含量增加33.9%(P均<0.05);PCNA阳性表达指数降低5.7%(P>0.05);辛伐他汀与G-CSF组上述指标分别为38.2%,50.3%,33.9%和37.2%(P均<0.05)。与对照组比较辛伐他汀可增加外周血CD34 VEGFR-2 双荧光阳性细胞比例87.6%,合用辛伐他汀与G-CSF则可增加达343.4%(P均<0.05)。结论在颈动脉球囊损伤模型,辛伐他汀可以促进损伤血管内皮修复达到抑制新生内膜增殖的效果,其机制可能涉及加强骨髓中内皮祖细胞向外周血的动员。在辛伐他汀基础上合用G-CSF刺激骨髓,可以使上述效应进一步加强。     

血管内皮功能及检测方法

长期以来血管内皮被认为不过是血液和组织之同的一个物理屏障。直到20世纪70年代后期，Furchgott等阐明了内皮依赖的血管反应，相继发现的内皮源性一氧化氮（NO），说明内皮细胞是有生理功能的，彻底改变了血管内皮仅仅是一层简单的分隔血液和组织的血管内层组织及半透膜性屏障的认识。血管内皮是一个具有高度活性的代谢和分泌器官。它既是感应细胞又是效应细胞，能感知血液中的炎性信号、激素水平、切应力、压力等信息。同时通过释放活性物质对这些信息作出反应。内皮源性舒张因子和收缩因子之间存在平衡，任何偏离这种平衡状态的现象都被认为内皮功能障碍。近年来血管内皮功能不全被认为是动脉粥样硬化形成的早期特征，很多与动脉粥样硬化有关的危险因素也损害内皮功能，而一些干预措施可以改善内皮功能，从而减少心血管事件的发生。     

HIV感染及高效抗逆转录病毒治疗对心血管疾病的影响

近几年来,我国HIV感染人群不断扩大,全国感染人数已接近100万,严重威胁我国人民的生命健康;随着我国艾滋病患者免费抗病毒治疗的实施,许多严重并发症随之出现,最常见的并发症之一是心血管疾病.     

老年大鼠损伤血管过度增殖与内皮Jagged1表达的关系

目的 探讨增龄促进大鼠损伤血管过度增殖与内皮Jaggedl表达的关系. 方法 健康雄性SD大鼠(幼年3月龄.老年22月龄)40只随机分为对照组和胸主动脉球囊损伤组各20只,胸主动脉球囊损伤组分别于术后,术后7、14、28 d(每个时间点老年与幼年组分别为5只)取靶血管行免疫组化染色观察内皮Jaggedl和新生内膜增殖细胞核抗原(PCNA)的动态变化,计算28 d时新生内膜与中膜比值.培养大鼠主动脉内皮和平滑肌细胞,用流式细胞法分析年龄对内皮Jaggedl表达率的影响.并将内皮接种于下室、平滑肌和上室建立共培养体系,用3H-TdR掺人和平滑肌迁移计数检测不同月龄大鼠内皮对血小板源生长因子(PDGF)刺激的平滑肌增生迁移的影响. 结果 老年大鼠新生内膜与中膜比值明显高于幼年大鼠(分别为0.35±0.02与0.28±0.01.,P＜0.01);与幼年大鼠比较,老年大鼠再生内皮Jagged1呈上调延迟并迅速下降的变化模式,而PCNA升高幅度大、维持时间长;流式细胞分析结果 表明,老年大鼠内皮Jaggedl表达率(46.6±6.3)%·低于幼年大鼠的(85.4±4.0)%,P＜0.05;PDGF(10 ng/ml)能显著促进幼年和老年内皮组平滑肌细胞增生迁移,但与老年大鼠内皮共培养的平滑肌增生迁移更明显[3H-TdR掺入:(26 438±1857)cpm/孔与(16 698±2076)cpm/孔,P＜0.05;迁移:(32±4)个/高倍视野与(18±5)个/高倍视野,P＜0.05]结论 老年大鼠血管损伤后内皮Jaggedl上调障碍,与老龄促进平滑肌增生迁移密切相关,提示Jagged1可能参与了老龄加重损伤血管过度增殖的调控.     

多替拉韦联合拉米夫定简化方案治疗初治HIV感染者真实世界研究

[摘要]　目的　初步观察多替拉韦联合拉米夫定简化方案治疗初治HIV感染者的临床疗效。方法　采用前瞻性观察研究方法,筛选我院门诊确诊的HIV/AIDS患者,接受多替拉韦联合拉米夫定简化方案治疗,观察治疗期间CD4+ T细胞计数、CD4/CD48比值、HIV载量及炎症因子的变化情况。结果　27例患者在治疗12周时病毒抑制率为62.96%,24周和48周时分别为92.31%和100%;CD4+ T细胞计数在治疗12周时上升为（340.53±235.39）个/μl,24周时上升为（430.26±291.71）个/μl（P均＜0.05）;治疗前44.44%的患者合并机会性感染,其治疗前升高的炎症因子在治疗后均逐渐下降。结论　多替拉韦联合拉米夫定简化治疗初治的HIV/AIDS患者可以获得较高的病毒抑制率,尤其可以作为晚期患者的优化方案。     

初治HIV感染者代谢水平的调查研究

目的 了解初治HIV感染者的代谢水平,初步探索与HIV疾病进展的关系.方法 收集我院2018年7月—12月期间确诊的163例初治HIV感染者的临床资料以及代谢相关指标,分析其代谢水平以及与HIV疾病进展的关系.结果 163例初治HIV感染者全部为男性,年龄中位数为28(25,32)岁,其中高血压的发生率为14.11％,...     

Foxp3+ regulatory T cells in antiretroviral-naive HIV patients

We characterized regulatory T cells from antiretroviral-naive HIV patients by flow cytometry. The proportion of CD4 cells positive for CD25 and Foxp3 was increased, mainly in those with CD4 cell counts less than 200 cells/microl. The total number of Foxp3-positive cells correlated with the CD4 cell count. Further studies are needed on whether Foxp3-positive cell numbers or function explain the susceptibility to autoimmune and inflammatory diseases seen in some patients with advanced HIV.     

HIV／AIDS患者血浆病毒载量及外周血T淋巴细胞亚群的变化

目的：观察国内HIV／AIDS患者血浆病毒载量和外周血CD4^ 、CD8^ T淋巴细胞的变化，探讨这些变化的临床意义。方法：选择未经抗病毒治疗的HIV／AIDS患者124例，用bDNA法检测血浆病毒载量，并用流式细胞仪检测外周血CD4^ 、CD8^ T淋巴细胞。结果：AIDS患者的血浆病毒载量明显高于HIV感染者，血浆病毒载量与CD4^ 细胞计数呈显著负相关，但其最高峰位于CD4^ 细胞计数100／μl处，然后随着CD4^ 细胞计数的下降而减少。CD4^ T细胞计数为AIDS组＜HIV组＜正常对照组：HIV感染者的CD8^ T细胞计数显著高于正常组和AIDS组，而AIDS患者CD8^ T细胞数则随着CD4^ T细胞减少而下降。结论：血浆病毒载量随着疾病进展而显著升高，但在疾病晚期则有所降低。外周血CD4^ T细胞计数随着疾病的进展而进行性减少；CD8^ T细胞计数在感染早期显著升高，进入晚期则减少。在评价HIV感染者和AIDS患者病情时，应结合病毒载量、CD4^ 、CD8^ T细胞计数综合分析。     

成人HIV／AIDS CD^4＋细胞数与病毒载量之间关系分析

目的分析成人HIV/AIDS患者CD4~+细胞数与病毒载量(VL)之间的关系。方法对1990年—2001年在本院就诊的200例HIV/AIDS患者进行跟踪分析。结果 CD4~+≥200/μl时,血浆VL(log10)为4.17±0.79;CD4~+<200/μl时,血浆VL(log10)为5.01±0.72,VL水平明显高于CD~+≥200/μl组(P<0.01)。其中CD4~+>350/μl时,血浆VL(log10)为3.95±0.82;CD4~+200～350/μl时.血浆VL(log10)为4.43±0.63;CD4~+100～200/μl时,血浆VL(log10)为4.85±0.68;CD4~+<100/μl时,血浆VL(log10)为5.16±0.68。结论 HIV/AIDS患者CD4~+细胞数与病毒复制有非常密切的关系,外周血CD4~+细胞数与血浆VL的变化呈负相关关系。当血浆VL(log10)>5.01±0.72时,应考虑患者已进入艾滋病期。     

Extended antiretroviral treatment interruption in HIV-infected patients with long-term suppression of plasma HIV RNA

OBJECTIVES: Evaluation of extended treatment interruption (TI) in chronic HIV infection among patients successfully treated with antiretroviral therapy. METHODS: An observational analysis of 25 patients in a prospectively followed cohort with chronic HIV infection, viral loads <500 HIV-1 RNA copies/mL for at least 6 months, and an interruption in therapy of >/=28 days duration was carried out. Follow up was divided into 3-month time periods for analysis. The effects of time period, stratification group and stratification group by time period interactions on CD4 counts were tested using a mixed model. Univariate comparisons among patient characteristics and responses were performed using Fisher's exact test or the Wilcoxon rank sum test. RESULTS: At initiation of TI, the median CD4 count was 799 cells/microL. TI duration was a median of 7.1 months. HIV RNA rebounded to a median maximum level of 75 000 copies/mL. Maximum viral rebound was significantly greater in patients who were male, had lipodystrophy and had zenith HIV RNA prior to TI of >/=50 000 copies/mL. Lower CD4 cell counts were observed during TI in patients with lipodystrophy, zenith HIV RNA >/=50 000 copies/mL, history of AIDS, HIV infection >/=5 years and presuppression CD4 count 相似文献   

Effects of HIV disease on lipid, glucose and insulin levels: results from a large antiretroviral-naive cohort

OBJECTIVES: With the use of potent antiretroviral therapy in patients with HIV disease, changes in lipid parameters and glucose homeostasis have been noted. However, these effects have been difficult to interpret because of the varied demographic and treatment characteristics of the cohorts and the complexity of differentiating the effect of HIV disease from that of the drugs used in its treatment. This study was designed to explore these issues. METHODS: Demographic information and fasting blood samples were collected from 419 antiretroviral-naive HIV-1-infected patients. RESULTS: The average age of the participants was 38.2 years, with 21% being female, 60% being African American, and 14% having a history of injection drug use. The mean CD4 lymphocyte count was 216 cells/microL, the mean baseline log10 HIV viral load was 4.98 HIV-1 RNA copies/mL, and 26% of patients had a history of AIDS-defining events. Women and African Americans had significantly higher levels of high-density lipoprotein (HDL) cholesterol, and older age was associated with higher total cholesterol levels. Lower CD4 lymphocyte counts and higher HIV RNA levels were independently associated with lower HDL cholesterol levels. Additionally, higher HIV RNA level was associated with lower levels of low-density lipoprotein (LDL) cholesterol and higher levels of very-low-density lipoprotein (VLDL) cholesterol and triglycerides. A history of AIDS-defining events was associated with higher total cholesterol, VLDL cholesterol and triglyceride concentrations. With respect to glucose homeostasis, a higher CD4 lymphocyte count was associated with less evidence of insulin resistance. However, a higher body mass index was associated with higher lipid levels and with more evidence of insulin resistance. CONCLUSIONS: Both HIV disease and demographic characteristics were found to influence lipid values and glucose homeostasis in the absence of antiretroviral treatment. More advanced HIV disease was associated with less favourable lipid and glucose homeostatic profiles. The independent association between HIV RNA levels and various lipid parameters suggests that viral replication had a direct effect on lipid levels. Interpretation of the effects of various HIV treatment regimen and drugs on metabolic parameters must take into account the stage of HIV disease and the demographic characteristics of the population studied.     

Genetic polymorphisms and resistance mutations of HIV type 2 in antiretroviral-naive patients in Burkina Faso

Natural polymorphisms in the pol gene of HIV-2 may influence the susceptibility to antiretroviral drugs and the choice of treatment. We collected samples in centers for anonymous HIV testing in Ouagadougou, Burkina Faso, in patients supposedly naive for any antiretroviral treatment. Eighty-four samples were first tested as HIV-2 positive in Burkina Faso and then shipped to Brussels, Belgium, for confirmation of the serological status and plasma viral load. Fifty-two samples were confirmed as HIV-2 positive in Belgium. Twelve others were HIV-1 positive and 20 were dually reactive. Twenty-one of HIV-2 confirmed samples had an HIV-2 plasma viral load higher than 1000 copies/ml. These viruses were sequenced in the protease and reverse trancriptase genes and 17 sequences of the pol gene were obtained. Highly polymorphic positions were identified in protease and RT genes. Two samples harbored known resistance mutations: M184V RT mutation in one and Q151M with M184V in the other. Phylogenetic analysis showed that viruses in Burkina Faso did not cluster separately from published sequences from neighboring countries. The two resistant strains were unrelated. Our findings imply either that resistant viruses are circulating in Burkina Faso or that some individuals take unsupervised treatment. Both hypotheses present problems.