肥胖儿童血管内皮运动功能障碍及其对左心结构和血压的影响

目的观察肥胖儿童早期血管内皮功能改变及其对左心结构和血压的影响。方法学龄期单纯性肥胖儿童及正常对照儿童各40例,分别测定血浆内皮素(ET)、6-酮前列环素(6-k-PGF     

人内皮细胞和4种细胞因子对正常人和再生障碍性贫血患者粒系造血的影响

通过人脐静脉内皮细胞为铺层的双层细胞培养,观察内皮细胞和几种细胞因子对正常人和再障患者粒系造血的影响。方法以人内皮细胞作铺层,作体外骨髓CFU-GM半固体双层培养,并在培养体系中加入细胞因子GM-CSF、IL-2、IL-6和LAK细胞上清,观察内皮细胞和细胞因子对正常人和再障患者粒系造血的影响。结果在有内皮细胞的培养体系中CFU-GM的产率均显著高于无内皮细胞的相应培养体系。在无内皮细胞时,IL-6和LAK上清显示出与GM-CSF相似的粒系造血刺激作用。对15例初诊慢性再障患者骨髓粒系祖细胞培养结果表明,无内皮细胞存在时,无论向培养体系中加入何种细胞因子,均无集落生成,而在有内皮细胞的双层培养中,部分患者骨髓可见CFU-GM集落生成。结论内皮细胞对正常和再障粒系造血均有明显影响,并提示再障造血障碍有微环境因素。     

脂蛋白对人血管内皮细胞间隙连接通讯功能的影响

用激光扫描共聚焦显微镜及荧光漂白后回复技术,观察HDL,LDL及维生素对培养的人血管内皮细胞间隙连接通讯功能的影响。结果：培养条件下的人血管内皮细胞之间可形成功能性的间隙连接。LDL组的荧光回复率分别为6．691±2．634,4．153±2．125,2.441±0.720,与对照组比较及两两比较,有显著性差异（P＜0.05）;HDL组及维生素C组的荧光回复率与对照组比较,无显著性差异;LDL＋HDL组的荧光回复率分别为3．500±0.890,4．339±1．126,5．243±1．278,与对照组比较及两两比较,有显著性差异（P＜0．05）;LDL＋维生素C组的荧光回复率分别为3．959±1．088,4．974±1．194,8．673±2．488,与对照组比较及两两比较,有显著性差异（P＜0．05）。以上结果提示：LDL对内皮细胞的间隙连接通讯功能具有明显的抑制作用,而HDL与维生素C可改善之。LDL致动脉粥样硬化的机理之一可能是抑制了内皮细胞的间隙连接通讯功能,但亦有可能这仅是内皮细胞对损伤的一种代偿反应。而HDL及维生素C对内皮细胞的保护作用可能是通过改善间隙连接的通讯功能来实现的。     

雌激素和异黄酮类药物对内皮细胞粘附分子CD54表达的影响

为探讨雌激素和异黄酮类药物对内皮细胞粘附分子CD54表达的影响,作者采用10ng/ml肿瘤坏死因子(TNFα)处理人脐静脉内皮细胞6小时,并加用不同浓度的异黄酮(WZ1,WZ2)和雌激素(WZ3,WZ4)进行干预48小时,而后用流式细胞仪定量测定细胞表面粘附分子CD54的表达,并进行统计学分析.结果:①10ng/ml的TNFα可使内皮细胞表面粘附分子CD54的表达升高4倍,与对照组相比具有统计学差异(P＜0.05);②10-10mol/L、10-8mol/L、10-6mol/L异黄酮和异卟黄酮对由TNFα诱导的内皮细胞的CD54表达有轻度促进作用;③哌嗪雌酚酮和雌二醇预处理内皮细胞48小时后再加TNFα激活,内皮细胞表面CD54平均荧光强度与单纯TNFα组相比下降明显(P＜0.05),各浓度组之间不具统计学差异(P＞0.05).以上结果提示:异黄酮和异卟黄酮对内皮细胞粘附分子CD54的表达无抑制作用;哌嗪雌酚酮和雌二醇可在一定程度上抑制CD54的表达,从而为抗粘附疗法提供了一条新思路.     

川芎嗪对凝血酶诱导血管内皮细胞释放vWF组织因子途径抑制物及表达组织因子的影响

目的 :探讨川芎嗪对凝血酶诱导的血管内皮细胞释放vWF、组织因子途径抑制物及表达组织因子的影响。方法 :传代培养的新生牛主动脉内皮细胞取上清液测vWF、组织因子途径抑制物 ;细胞冻融液测组织因子的活性。结果 :①与对照相比凝血酶能明显促进内皮细胞表达组织因子 ( 1 2 .8± 2 .43,P <0 .0 0 1 )和释放vWF( 1 8.43± 3.2 0 ,P <0 .0 0 1 ) ,川芎嗪则抑制组织因子表达 ( 0 .52± 0 .1 3,P <0 .0 0 1 )抑制vWF释放 ( 1 3.3± 5.6,P <0 .0 1 ) ;②与对照相比 ( 2 .64± 0 .93) ,凝血酶明显抑制内皮细胞释放组织因子途径抑制物 ( 0 .81± 0 .52 ,P <0 .0 0 1 ) ,但川芎嗪无明显作用 ,也不能抑制凝血酶的效应。结论 :川芎嗪可以抑制内皮细胞表达组织因子和释放vWF。     

冠脉循环中血小板活化状态对冠心病致病作用的研究

目的：探讨冠脉循环中血小板活化状态在冠心病（ＣＨＤ）发病学中的意义。方法：用放免等方法对受试冠状静脉窦（ＣＳ）及升主动脉（ＡＯ）血行血小板膜表面α－颗粒膜蛋白（α－ＧＭＰ－１４０）和循环内皮细胞（ＣＥＣ）等测定。结果：ＣＨＤ患冠脉循环中α－ＧＭＰ－１４０含量和ＣＥＣ浓度均明显升高（Ｐ〈０．０１）,以急心肌梗塞（ＡＭＩ）组为明显,冠脉狭窄愈严重,二升高愈明显,病灶多发比单发升高明显。结论：ＣＨＤ患冠脉循环中血小板高度激活,在ＣＨＤ的发生发展中有一定的意义。     

Study of platelet-rich fibrin promoting endothelial cell differentiation and angiogenesis induced by transplantation of adipose-derived stem cells

Diabetic patients are characterized by long wound healing time, and adipose stem cells (ADSCs) can secrete growth factors to promote angiogenesis and improve diabetic wound healing. In this research, we attempted to interrogate the impact of platelet-rich fibrin (PRF) on ADSCs in diabetic wound healing. ADSCs were harvested from human adipose tissues and identified through flow cytometry. After pretreatment with cultured medium supplemented with different concentrations of PRF (2.5%, 5%, and 7.5%), proliferation and differentiation capacity of ADSCs were assessed by CCK-8 assay, qRT-PCR and immunofluorescence (IF), respectively. Tube formation assay measured angiogenesis. Western blot analysis analyzed expression of endothelial markers and the extracellular signal-regulated kinase (ERK) and serine/threonine kinase (Akt) pathways in PRF-induced ADSCs. The CCK-8 experiment indicated that PRF enhanced proliferation of ADSCs in dose-dependent manner, relative to normal control group. The expression of endothelial markers and the capacity of tube formation were significantly promoted by 7.5% PRF. The release of growth factors containing vascular endothelial grow factor (VEGF) and insulin-like growth factor-1 (IGF-1) from PRF was increased with the extension of detection time. When the receptors of VEGF or/and IGF-1 were neutralized, ADSCs differentiation into endothelial cells were obviously inhibited. Additionally, PRF stimulated ERK and Akt pathways, and the inhibitors of ERK and Akt attenuated PRF-induced differentiation of ADSCs into endothelial cells. In conclusion, PRF promoted endothelial cell differentiation and angiogenesis induced by ADSCs in diabetic wound healing, which appears to give guidance for treating patients.     

Inhibition of neovascularization in vivo by gold compounds

As mononuclear cell infiltration and growth of pannus critically depend on synovial neovascularization in rheumatoid arthritis (RA), inhibition of the synovial blood vessels would have the potential to reduce rheumatoid inflammation. In this investigation, we studied the effect of gold sodium thiomalate (GST) and auranofin (AUR) on neovascularization in vivo by using a micropocket technique. Both GST and AUR suppressed rabbit corneal neovascularization in a dose-dependent fashion. Significant inhibition was observed by 3 mg/kg GST and 1 mg/kg AUR injected intravenously every other day. These injections maintained serum gold concentrations at the level of 2–5 g/ml and less than 2 g/ml in GST-and AUR-injected rabbits, respectively. These are concentrations attained in the serum or synovium of rheumatoid patients treated by gold compounds. Similar inhibition was observed by both intramuscular administration of GST and oral administration of AUR. In contrast, no inhibition was observed when non-steroidal anti-inflammatory drugs (NSAIDs; 20 mg/kg acetylsalicylic acid, 10 mg/kg ibuprofen and 10 mg/kg indomethacin) were injected intravenously on a daily basis. These results suggested that gold compounds have an antiangiogenic effect in vivo. The inhibition of neovascularization by gold compounds suggested that they may suppress rheumatoid synovitis by reducing the number of small blood vessels required for mononuclear cell infiltration and synovial tissue proliferation.     

Periventricular- intraventricular hemorrhage in the premature infant- A historical perspective

The objective of this chapter is to trace the evolution of intraventricular hemorrhage in the premature infant highlighting the importance of the germinal matrix, a critical role for cerebral blood flow changes in the genesis of hemorrhage, clinical factors that increase the bleeding risk, and potential preventative strategies. In 1976, neuropathological studies demonstrated capillary rupture within the germinal matrix as the precursor of hemorrhage. In 1980, introduction of cranial ultrasound facilitated diagnosis of intraventricular hemorrhage. In 1979, loss of cerebral autoregulation in sick newborn infants was demonstrated. In the 1980’s, studies demonstrated the importance of intravascular factors in provoking hemorrhage. In 1983, the association of cerebral blood flow velocity fluctuations and subsequent hemorrhage was demonstrated. In 1994, antenatal steroids use to accelerate lung development was recommended. This was associated with an unanticipated reduction in hemorrhage. In the mid 1990’s early indomethacin administration was associated with a reduction of severe hemorrhage.