脂联素（adiponectin,ADPN）是脂肪细胞分泌的一种特异性蛋白质,具有改善胰岛素抵抗、抗炎、抗动脉粥样硬化、降血糖、保护血管内皮等作用[1],生理浓度范围内的脂联素通过抑制NF-κB信号传导通路能够剂量依赖性地抑制肿瘤坏死因子（TNF-α）诱导的血管内皮细胞黏附分子的表达。本研究通过将人脂联素基因重组腺病毒感染人脐静脉内皮细胞（human umbilical veins endothelial cells,HUVECs）,研究其对人脐静脉内皮细胞分泌单核细胞超化因子1（MCP-1）和细胞间粘附分子（intercellular adhesion molecule,ICAM-1）和mRNA表达的影响。

<正>由动脉粥样硬化(AS)导致的心血管疾病发病率及患病率逐年升高,已成为全球范围内人类主要死因。流行病学提示,黄酮类化合物在促进健康和防治心血管疾病方面具有良好的疗效。花色苷(Anthocyanins)属于黄酮类物质,现已在植物性

目的研究替米沙坦对心肌梗死后心室重构的影响。方法应用冠状动脉结扎法建立大鼠心肌梗死(MI)模型,24 h后存活大鼠随机分为安慰剂对照组和替米沙坦治疗组,另设假手术组。8 w后,测量心室重量/体重(HW/BW),非梗死区胶原含量,多普勒超声评价心脏功能。结果对照组与假手术组比较HW/BW、左心室舒张末期内径(LVDd)、E/A比值、非梗死区胶原含量、射血分数(EF)、短轴缩短率(FS)、后壁(PW)增厚率均降低(均P<0.01)。治疗组与对照组比较,上述指标显著改善(均P<0.01)。结论替米沙坦可抑制并减轻MI后左室重构。

Objective To investigate the relationship of serum adiponectin (APN) with left ventricular hypertrophy (LVH) and carotid athcrosclerosis (AS),and to observe the change of serum adiponectin levels in patients with hypertension and obesity.Methods Patients with essential hypertension (50 cases) were divided into simple hypertension group (23 cases) and hypertension with obesity group(27 cases),and 45 normotensives were divided into control group (24 cases) and simple obesity group (21 cases).The levels of serum adiponectin were determined by enzyme immunoassay.Common carotid artery intima-media thickness (CCA-IMT),carotid artery diameter (CADIA) and left ventricular relevant index were measured by color doppler ultrasonography,and left ventricular mass index (LVMI) was calculated.Results In control group,simple obesity group,simple hypertension group and hypertension with obesity group,serum APN levels were decreased by turn,CADIA reduced gradually,LVMI values were increased by turn,CCA-IMT values were increased gradually (F=28.34,10.26,36.52,14.73,all P＜0.01).Correlation analysis showed that serum APN levels were significantly negatively correlated with LVMI and CCA-IMT(r=-0.870,-0.710,both P＜0.01),and were positively related with CADIA (r=0.742,P＜0.00).APN,SBP and BMI were the main influencing factors on left ventricular hypertrophy (β =-0.909,0.126,-0.053).Conclusions The presence of both hypertension and obesity may play a synergistic role in accelerating the process of left ventricular hypertrophy and atherosclerosis.Lower APN levels and/or rising BMI may accelerate occurrence and development of LVH and AS in aged patients with hypertension and obesity.

目的研究内皮型一氧化氮合酶(eNOS)基因导入对高血压大鼠心脏、肾脏细胞凋亡的影响。方法将实验大鼠分为自发性高血压大鼠(SHR)组、AAV-LacZ组和AAV-eNOS组,每组8只,另设8只正常血压(WKY)大鼠为WKY组。AAV-eNOS组经尾静脉注射AAV-eNOS 200μl(含eNOS基因拷贝1×1012),AAV-LacZ组注射AAV-LacZ 200μl,WKY及SHR组大鼠分别经尾静脉给予等量0.1 mol/L PBS。应用原位末端标记(TUNEL)法检测各组大鼠心、肾组织中的细胞凋亡,免疫组织化学方法检测eNOS的表达。结果①SHR组大鼠心肌组织及肾脏组织染色阳性信号明显增多,与WKY组比较具有显著性差异(P<0.05),AAV-eNOS组凋亡阳性信号明显低于SHR组,差异显著(P<0.05)。②SHR组及AAV-LacZ组大鼠心肌组织eNOS表达低于WKY组,差异具有显著性(P<0.05);与SHR组大鼠比较,AAV-eNOS组eNOS表达明显增加,差异具有显著性(P<0.05)。各组大鼠肾脏eNOS蛋白表达未见明显差异。结论 eNOS基因导入可明显抑制心肌及肾脏组织细胞的凋亡,保护靶器官。

目的研究替米沙坦对自发性高血压大鼠(SHR)左心室重构的影响。方法 16只12周龄雄性SHR,随机分为替米沙坦组和SHR空白对照组,每组8只;另设同龄Wistar大鼠(WKY)8只为正常对照组。治疗组给予替米沙坦10 mg.kg-1.d-1灌胃给药,饲养8 w后处死动物,测量左心室重量及心肌厚度,计算左心室重量与体重比(LVW/BW);通过Van Gieson染色法观察左心室心肌胶原纤维变化,对左心室心肌胶原容积分数(CVF)和血管周围胶原面积(PVCA)进行分析;电镜和HE染色观察左室心肌超微结构。结果与正常对照组WKY大鼠相比,SHR空白对照组的尾动脉收缩压(SBP)、LVW/BW、左室壁厚度、CVF、PVCA均显著增高(P<0.01);与SHR空白对照组相比,替米沙坦组能有效降低SHR的SBP,改善左心室肥厚(P<0.01),减少心肌间质及心肌小动脉周围的胶原(P<0.01),组织病理及电镜显示,替米沙坦治疗能显著改善SHR左心室重构。结论替米沙坦能有效降低SHR血压,改善左心室重构。

近年来,血源性传播疾病已经越来越引起医护人员的关注.手术室护士由于自身工作的特殊性,工作中直接接触患者的开放性伤口、血液、体液等,存在着被感染的高度危险,是护理人员中最易受到血源性感染的人群[1].

Enhanced monocyte adhesion to endothelial cells is an early event in atherogenesis. It has been shown that C-reactive protein (CRP) plays a key role in atherogenesis. Here, we investigated the effects of CRP on monocyte-endothelial cell adhesion and tested the hypothesis that NADPH oxidase (NOX)-mediated oxidative stress might play a key role in CRP-induced monocyte-endothelial cell adhesion. Firstly, 36 patients with carotid intima-media thickness (IMT) incrassation and 34 controls were enrolled in this study. The levels of glucose, lipids, CRP, monocyte chemotractant protein (MCP-1), malondialdehyde (MDA), and protein carbonylation were analyzed. The results showed that carotid IMT was associated with abnormal lipid metabolism, including elevated CRP, triglycerides (TG) (P<0.01) and decreased high density lipoprotein (HDL) level (P<0.05). The levels of CRP and MCP-1 in patients with carotid IMT incrassation were increased compared with the controls (P<0.01). Moreover, patients with carotid IMT incrassation displayed enhanced MDA and protein carbonylation levels (P<0.01), accompanied by activation and up-regulation of NOX in monocytes (P<0.05) compared with the controls. The monocytes isolated from five healthy donors were used for in vitro experiments. Reactive oxygen species (ROS) production and NOX expression in monocytes were examined. The results also indicated that CRP could promote the adhesion of monocyte-endothelial cell by up-regulation of MCP-1 expression (P<0.05). Importantly, NF? B and p38 MAPK signaling pathways, which were activated by NOX-derived ROS, were involved in CRP-induced monocyte-endothelial cell adhesion and up-regulation of MCP-1 expression. These data suggested that CRP could promote the adhesion of monocytes to endothelial cells via NOX-mediated oxidative stress. J. Cell. Biochem. 113: 857867, 2012. (C) 2011 Wiley Periodicals, Inc.

心血管系统合成和分泌多种小分子的生物活性物质,如血管活性多肽、生物活性氨基酸、细胞因子生长因子和一氧化碳、硫化氢等气体信号分子。这些生物活性分子具有分子量小、种类繁多、分布广

目的 探讨20(S)-原人参二醇(Ppd)对胃癌细胞SGC-7901细胞周期的影响.方法 采用MTT 法检测Ppd对SGC-7901细胞存活率的影响,流式细胞分析法检测凋亡小体的含量.结果 Ppd对SGC-7901细胞生长有明显的抑制作用,且呈量-效关系;IC50为2.0 μg/ml;且肿瘤细胞产生明显的G1期阻滞现象,Ppd 2.0 μg/ml时G1细胞百分率达76.08%,而在Ppd 10.0 μg/ml时为81.17%,较对照组(39.02%)明显增多(P<0.05),而S、G2～M期细胞数明显减少.流式细胞术结果也证明,不同浓度的Ppd作用SGC-7901细胞后,在G1期的前面出现一个小的亚二倍体峰,即为凋亡峰,且随着Ppd剂量增加,处于凋亡峰的细胞比例呈增加趋势.在Ppd 2.0 μg/ml时,其凋亡峰为27.58;Ppd 10.0 μg/ml时,出现最大凋亡峰为28.31.结论 Ppd促进了胃癌SGC-7901细胞凋亡,抑制了胃癌SGC-7901细胞的增殖.

<正>蓝莓(Blueberry),又名越桔、蓝浆果、红豆果等,为杜鹃花科(Ericaceae)越桔属(Vaccinium spp.)多年生落叶或常绿果树,呈灌木。在栽培学上,蓝莓属小浆果类果树。蓝莓共有450多种不同的品种,主要的优良品种有兔眼蓝莓、高丛蓝莓、半高

目的利用基因芯片检测20（S）-原人参二醇（Ppd）作用于SGC-7901细胞后的基因表达情况,从基因水平上探讨Ppd抑制SGC-7901细胞增殖的作用机制。方法 SGC-7901细胞经不同浓度Ppd处理48 h,倒置光显微镜和荧光显微镜观察细胞形态学变化,MTT法检测SGC-7901细胞的存活率,流式细胞仪检测细胞周期变化,然后提取总RNA,逆转录生成cDNA,cDNA与基因芯片杂交,扫描仪检测杂交结果。结果扫描信号分析数据显示10条基因表达有差异,p21、chk1表达上调,cyclinB1、cyclinE1、E2F1、DNA 2PK、hTERT、bcl22、jnk、VEGF表达下调。结论 Ppd可以抑制SGC-9017细胞增殖,作用机制与改变细胞周期某些调控物质的基因表达、诱导细胞凋亡有关。

老年人在心脏解剖,生理临床等方面与年轻人都有很大不同,所以在临床诊断治疗中应格外注意老年人的发病特点.