老年糖尿病患者冠状动脉血流储备变化的初步观察

目的　应用彩色多普勒超声仪检测冠状动脉血流储备 (coronaryflowreserve ,CFR) ,初步观察老年糖尿病患者中CFR的变化。方法　 2 5例老年糖尿病患者及 2 5例健康志愿者作对照组 ,比较两组的空腹血糖 (FBG)、早餐后 2h血糖 (P2hBG)、糖化血红蛋白A1c (HbA1c)、总胆固醇 (TC)、低密度脂蛋白胆固醇 (LDL C)及甘油三酯(TG)、内皮素 1(ET 1)、静息状态时患者冠状动脉的基础血流速度 (bFV)、潘生丁注射后的最大冠脉血流速度(mFV)及CFR。结果　糖尿病组的FBG、P2hBG、TG及ET 1水平显著高于对照组 [分别为 :(9 1± 3 3)mmol/L与 (5 3± 0 7)mmol/L ;(15 8± 5 0 )mmol/L与 (8 5± 2 4 )mmol/L ;(2 96± 0 5 6 )与 (1 6 9± 0 82 )mmol/L及(15 3 80± 13 5 0 )ng/L与 (76 2 3± 10 78)ng/L ,均P <0 0 1],糖尿病组静息时的基础冠脉血流速度 (bFV)及TC、LDL C水平与对照组比较 ,差异均无显著性意义 (均P >0 0 5 ) ,而潘生丁注射后mFV及CFR (CFR =mFV/bFV)较对照组明显下降 [分别为 (5 8 1± 7 9)cm/s与 (73 5± 9 8)cm/s及 2 31± 0 4 9与 3 5 8± 0 4 6 ,P均 <0 0 1]。结论　老年糖尿病患者冠状动脉血流储备明显下降。     

氧化型低密度脂蛋白对人脐静脉内皮细胞ICAM-1及NO表达的影响

目的研究氧化型低密度脂蛋白(oxidized low density liprotein,ox-LDL)对脐静脉内皮细胞细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)及一氧化氮(nitric oxide,NO)表达的影响.方法采用细胞ELISA法测定细胞表面ICAM-l的含量,硝酸还原酶法测定细胞培养上清液中NO,免疫组化法结合图象分析测定细胞一氧化氮合酶(nitric oxide synthase,NOS)含量.结果 ox-LDL可明显增加脐静脉内皮细胞ICAM-l的表达,并减少NO及NOS的表达,且有浓度依赖性,但无明显的时间依赖性.结论 ox-LDL可损害内皮细胞的功能,减少内皮细胞NO、NOS的表达并增加内皮细胞ICAM-1的表达.这可能为ox-LDL促进动脉粥样硬化的机制之一.     

Zn~(2+)预处理对离体大鼠缺血再灌注损伤心肌的保护作用

目的 :观察Zn2 + 预处理诱导金属硫蛋白 (MT)在心肌细胞的表达及对离体大鼠缺血再灌注损伤心肌的保护作用。方法 :3 2只Sprague Dawley大鼠随机分为对照组及实验组 ,实验组按腹腔注射ZnSO4 到建立再灌注模型的时间分为E1 2h,E2 4h及E4 8h组 ,每组各 8只。检测LDH ,CK、ATP含量及心功能指标 (LVSP与±dp/dtmax) ,用1 0 9Cd/血红素饱和法测量心肌组织中金属硫蛋白的含量。结果 :E2 4h及E4 8h组MT表达量较对照组高 (P <0 .0 1) ,E1 2h组虽有表达 ,但其与对照组间差异无显著性。E2 4h及E4 8h组LDH与CK较其它二组低 ,而ATP较其它二组高 ,心功能指标较其它二组改善。E1 2h组及对照组之间相应各指标 (LDH ,CK、ATP、LVSP与±dp/dtmax)间差异无显著性 (P >0 .0 5 )。结论 :Zn2 + 预处理可诱导MT在心肌细胞的表达而对离体大鼠缺血再灌注损伤心肌具有保护作用。     

综合科老年住院患者抑郁症的研究

为了解综合征医疗机构中综合科老年住院患者抑郁症的患病情况,对综合性医院综合科病房218例老年住院患者进行调查,计算Zung抑郁自评量表分值（SDS）。结果表明：轻、中、重度抑郁症的患者率分别为5%、7.3%和6.8%,内科医师对重度老年期抑郁症的识别率仅为20%,老年期抑郁症症状不典型,以焦虑、少动、失眼、易激惹和食欲下降为多见。结果提示：在综合性医疗机构住院患者中,老年期抑郁症的患病率较镐,应适应医学模式的转变,提高综合科医师对此症的识别和处理能力。     

长QT综合征KCNQ1基因G983A突变体的构建、体外转录与表达

目的构建先天性长QT综合征KCNQ1基因G983A突变体,并研究其在非洲爪蟾卵母细胞上的表达。方法首先进行定点诱变,构建含KCNQ1G983A突变点的原核表达载体pSP64-KCNQ1（G983A）,并对pSP64-KCNQ1（G983A）进行纯化和线性化,然后应用SP6RNA体外转录试剂盒进行转录,并回收和鉴定转录的cRNAs。制备非洲爪蟾卵母细胞,经显微注射仪将KCNQ1（G983A）cRNAs注射至卵母细胞中,2d后采用双电极电压钳记录卵母细胞膜的电流。结果成功地构建pSP64-KCNQ1（G983A）突变体,经转录获得KCNQ1（G983A）cRNAs,并在爪蟾卵母细胞上表达。结论KCNQ1基因（G983A）突变体的成功构建及表达,为进一步探讨长QT综合征的发病机制奠定了基础。     

The Origin of Neointimal Smooth Muscle Cells in Transplant Arteriosclerosis from Recipient Bone-marrow Cells in Rat Aortic Allograft

In order to investigate the origin of neointimal smooth muscle cells in transplant arterio- sclerosis in rat aortic allograft, sex-mismatched bone marrow transplantation was performed from male Wistar rats to female Wistar rats. Four weeks after transplantation, the aortic transplant model was established by means of micro-surgery in rats. The recipients were divided into 4 groups: female Wistar-female Wistar aortic isografts, female SD-female Wistar aortic allografts, male SD-male Wis- tar aortic allografts, female SD-chimera Wistar aortic allografts. Eight weeks after transplantation, aortic grafts were removed at autopsy and processed for histological evaluation and immunohisto- chemistry. The results indicated that excessive accumulation of α-SMA-positive smooth muscle cells resulted in significant neointima formation and vascular lumen stricture in rat aortic allografts. Neointima assay revealed that the neointimal area and NIA/MA ratio of transplanted artery were sig- nificantly increased in all of aortic allograft groups as compared with those in aortic isograft group (P<0.01). Neointimal smooth muscle cells were harvested from cryostat sections of aortic allograft by microdissection method. The Sry gene-specific PCR was performed, and the result showed that a dis- tinct DNA band of 225 bp emerged in the male-male aortic allograft group and chimera aortic al- lograft group respectively, but not in the female-female aortic allograft group. It was suggested that recipient bone-marrow cells, as the origin of neointimal smooth muscle cells, contributed to the pathological neointimal hyperplasia of aortic allograft and transplant arteriosclerosis.     

培哚普利对老年高血压患者颈动脉内-中膜厚度及血管内皮依赖性舒张功能的影响

目的探讨培哚普利对老年高血压患者内皮功能的影响及其机制。方法选择老年高血压患者100例,随机分为培哚普利治疗组(P组,n=50)和安慰剂组(C组,n=50);另选50例健康体检者为血压正常对照组(N组,n=50),应用无创超声检查技术,观察治疗前、后的颈动脉内中膜厚度及肱动脉内皮依赖性舒张功能的变化。结果培哚普利治疗组治疗后颈动脉内中膜厚度明显减少,肱动脉内皮依赖性舒张功能明显改善。结论培哚普利可明显改善老年高血压患者内皮功能,具有抗动脉粥样硬化的作用。     

奥美沙坦酯与缬沙坦治疗中青年原发性高血压的对照研究

目的 比较奥美沙坦酯和缬沙坦治疗中青年原发性高血压的疗效和安全性.方法 90例中青年原发性高血压患者随机接受奥美沙坦酯20 mg或缬沙坦80 mg口服治疗,每日1次,总疗程8周.对其降压效果进行观察比较.结果 治疗过程中奥美沙坦酯组2例因头痛和咳嗽退出试验,缬沙坦组1例因头痛退出.治疗前与治疗2、4、6、8周组间SBP和DBP差异均无统计学意义(P均>0.05),治疗2、4、6、8周与组内治疗前比较,差异均有统计学意义(P均<0.05).奥美沙坦酯组和缬沙坦组降压总有效率分别为86.0%(37/43)和84.1%(37/44),组间差异无统计学意义(χ2=0.065,P>0.05).结论 治疗中青年轻中度原发性高血压,奥美沙坦酯和缬沙坦疗效和不良反应均类似.     

福辛普利对X综合征患者冠脉血流储备的影响

目的:应用彩色多普勒超声仪检测冠状动脉血流储备(coronary flow reserve,CFR),观察福辛普利对X综合征患者CFR的影响。方法:选取26例X综合征患者,比较福辛普利(5mg或10mg)治疗前后患者血压、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、甘油三酯(TG)、内皮素(ET-1)、静急状态时患者冠状动脉的基础血流速度(bFV)、潘生丁注射后的最大血流速度(mFV)及冠状动脉血流储备(CFR)的变化。结果:福辛普利治疗6个月后,X综合征患者的 SBP、DBP、TC、LDL-C、TG水平轻度下降(P>0.05),ET-1水平显著下降,从(103.5±9.7)pg/ml到(77.5±12.0)pg/ml(P<0.05);患者的bFV改变不明显(P>0.05),而mFV从治疗前的(57.2±8.4)cm/s上升到(72.1±7.6)cm/s(P<0.05),CFR从治疗前的2.52±0.56上升到3.32±0.44(P<0.01)。结论:应用福辛普利治疗X综合征患者可有效改善患者的内皮功能和CFR。     

Implication of Receptor Activator of NF-κB Ligand in Wnt/β-Catenin Pathway Promoting Osteoblast-like Cell Differentiation

Recent studies showed that activation of Wnt/β-catenin pathway promoted the differentiation of osteoblast-like cells in the arterial calcification, but its mechanism remains unknown. In this study, the hypothesis that Wnt/β-catenin pathway promotes the differentiation of osteoblast-like cells by upregulating the expression of receptor activator of NF-κB ligand (RANKL) was examined. LiCl was used to activate the Wnt/β-catenin pathway. The differentiation of osteoblast-like cells was observed by Von Kossa staining, calcium content assay, alkaline phosphatase (ALP) activity assay, and detection of osteocalcin expression. Real-time PCR was performed to detect the expression of RANKL and osteoprotegerin (OPG, the decoy receptor of RANKL) during the osteoblast-like cell differentiation. Different concentrations of OPG were added to the culture media respectively to inhibit the function of RANKL, and the change in the differentiation of osteoblast-like cells was evaluated. The results showed that when the Wnt/β-catenin pathway was activated by LiCl, the expression of RANKL was significantly in-creased, which coincided with the differentiation of osteoblast-like cells (P<0.05), and the OPG treatment could partly attenuate the promoting effect of Wnt/β-catenin pathway on the differentiation of osteoblast-like cells (P<0.05), but it failed to completely abolish such effect. It was concluded that activation of Wnt/β-catenin pathway promotes the differentiation of osteoblast-like cells by both RANKL-dependent and RANKL-independent mechanisms.