小儿紫绀型先天性心脏病血浆MDA和血液流变学变化

测定３５例青紫型先天性心脏病患儿红细胞、血浆丙二醛（ＭＤＡ）含量、红细胞膜微粘度及血液流变学指标。结果患儿红细胞、血浆ＭＤＡ、膜微粘度、全血粘度、经细胞比积、红细胞聚集指数、刚性指数均显著高于正常组；ＭＤＡ含量，膜微粘度、红细胞刚性指数、聚集指数及全血粘度之间均存在正相关关系。提示患儿红细胞脂质过氧化反应增强，导致膜流动性降低、红细胞变形性差，聚集性增加，可能是血液粘度增加较为主要的原因。     

高胆固醇饲料诱导兔红细胞膜脂蛋白、脂质过氧化和膜流动性的改变

观察１４只雄性家兔在高胆固醇饲料的喂养下可能诱发的红细胞膜脂蛋白、脂质过氧化和膜流动性的改变。在喂养二个月前后的对比观察中，发现血浆总胆固醇和低密度脂蛋白胆固醇显著升高（Ｐ＜０．００１），红细胞膜低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、膜共轭双烯和膜流动性均显示明显差异（Ｐ＜０．０１～０．００１）。结果提示，高胆固醇饲料不仅可以引起高脂血症，而且可以诱导红细胞膜脂蛋白成分、脂质过氧化和膜流动性的改变。红细胞膜的这些物理和化学性质的改变，可能同微血管流变性质的改变有密切联系     

老年糖尿病患者红细胞膜脂质成分的改变

本文测定２８例老年ＮＩＤＤＭ患者红细胞膜脂质成分和脂质过氧化水平。结果显示：老年ＮＩＤＤＭ患者红细胞膜胆固醇，胆固醇／磷脂比值及过氧化脂质水平明显升高，膜磷脂降低；膜脂质成分改变与高血糖，高血脂及血浆脂蛋白异常存在一定关系。提示老年糖尿病患者红细胞膜成分存在异常，膜成分异常与代谢紊乱存在一定关系。     

NIDDM患者红细胞膜脂质过氧化作用与红细胞免疫功能之间的关系

对58例非胰岛素依赖型糖尿病(NIDDM)患者检测了红细胞免疫指标,同时测定了血浆和红细胞膜脂质过氧化水平。结果显示,NIDDM患者红细胞C3b受体活性明显降低,血浆和红细胞膜脂质过氧化水平明显升高;在NIDDM有血管并发症者上述变化更为显著,同时伴有红细胞免疫复合物花环率降低;红细胞C3b受体活性降低和血浆及红细胞膜脂质过氧化水平升高呈负相关,进一步多元逐步回归分析红细胞腆脂质过氧化水平升高和红细胞C3b受体活性降低关系更为密切。提示红细胞膜脂质过氧化损坏可能是引起红细胞免疫功能降低的一重要因素。     

大鼠高脂血症与血液粘度关系研究

目的：研究血脂与全血粘度、血浆粘度及其相关因素的关系。方法：以高脂血症大鼠模型，大鼠饲以高脂饲料，连续7周测血脂。结果：血浆TG增加2倍，TC增加13．2倍，LDL增加51．8倍，而HDL无明显改变。随血浆脂质的升高，大鼠血浆粘度也显增加，而红细胞刚性指数、红细胞变形指数及红细胞聚集指数显下降；全血高、中、低切粘度，全血还原粘度，红细胞计数、红细胞压积及红细胞电泳时间均无明显改变。与此同时，血浆纤维蛋白溶酶活性降低而血小板聚集功能增高。结论：上述结果表明，高脂血症主要导致血浆粘度增加，纤维蛋白溶酶活性和血小板聚集功能异常改变。     

肺心病患者红细胞膜脂质过氧化作用与红细胞免疫功能之间的关系

目的：探讨肺心病患者脂质过氧化对红细胞免疫功能的影响。方法：采用红细胞酵母菌混合花环法和硫代巴比土酸（ＴＢＡ）法检测了肺心病患者红细胞Ｃ３ｂ受体、血浆及红细胞膜丙二醛（ＭＤＡ）水平。结果：肺心病患者红细胞Ｃ３ｂ受体明显降低;血浆ＭＤＡ和红细胞膜ＭＤＡ明显升高;在急性期肺心病患者上述变化更为显著,同时伴有红细胞免疫复合物花环率降低;红细胞Ｃ３ｂ受体和血浆ＭＤＡ及红细胞膜ＭＤＡ呈负相关,多元逐步回归分     

缺血性中风红细胞变形能力与膜微粘度及膜生化改变的相关性研究

本文通过对脑梗塞患者及健康对照者进行红细胞变形能力与红细胞膜微粘度及膜生化成份的测定,发现两组有显著差异,且患者组红细胞变形能力与膜微粘度、胆固醇/磷脂比值、膜脂质过氧化物含量呈显著负相关,与膜唾液酸含量呈显著正相关,按影响程度大小排列依次为膜微粘度、脂质过氧化物含量、唾液酸、胆固醇/磷脂比值。     

48例Binswanger病血液流变学分析

本文调查了48例Binswanger病血液流变学10项指标，并与44例正常老年人及47例脑梗塞患者作对照。结果表明；（1）Binswanger病组全血粘度、血浆高切粘度、血沉、红细胞聚集指数、红细胞刚性指数、血沉方程K值、全血还原粘度显著高于正常对照组（P＜0．001）；全血粘度、血浆高切粘度、红细胞聚集指数、红细胞刚性指数、全血还原粘度与脑梗塞组相似。（2）Binswanger病组红细胞变形指数明显低于正常对照组（P＜0．001），但显著高于脑梗塞组（P＜0．01）。结论：Binswanger病患者血液流变学处于一种高粘状态。     

缺血性中风红细胞变形能力与膜微粘度及膜生化改变的相关…

本文通过对脑梗塞患者及健康对照者进行红细胞变形能力与红细胞膜微粘度及膜生化成份的测定，发现两组有显著差异，且患者组红细胞变形能力与膜微粘度、胆固醇／磷脂比值、膜脂质过氧化物含量呈显著负相关，与膜唾液酸含量呈显著正相关，按影响程度大小排列依次为膜微粘度、脂质过氧化物含量、唾液酸、胆固醇／磷脂比值。     

体外循环转流期间红细胞膜流动性的变化

对25例心脏手术行体外循环患者转流期间红细胞膜流动性（fluidity,FLU)、血浆脂质过氧化物（LPO）和红细胞超氧化物岐化酶（SOD）动态变化进行观察,结果转流后期FLU显著降低,LPO显著升高,而SOD活性转流初期升高明显,至转流后24小时恢复到转流前水平,并且红细胞膜FLU降低血浆LPO改变呈负相关。提示：转流期间脂质过氧化增强,可能是红细胞膜流动性降低的原因之一。     

Muscarine-sensitive voltage-dependent potassium current in cultured murine spinal cord neurons

Muscarine produced membrane depolarization and decreased membrane conductance of mouse spinal cord neurons in dissociated cell culture. When the neurons were voltage clamped, muscarine evoked inward currents which increased with membrane depolarization and decreased with membrane hyperpolarization. However, the muscarine-induced inward currents did not invert at large negative potentials, suggesting that muscarine decreased a voltage-dependent potassium current (m-current) [2]. Using the voltage-jump current-relaxation technique, m-current was demonstrated in spinal cord neurons and shown to be a muscarine-sensitive potassium current.     

血管内皮细胞生长过程中与衰老相关的细胞生物学特征的变化

目的 探讨内皮细胞衰老过程中细胞生物学特征变化。方法 体外培养人脐静脉内皮细胞。通过传代形成细胞的衰老模型。光镜下观察细胞各代的形态结构；流式细胞术检测细胞周期和细胞内自发荧光产物的变化；线粒体膜电位特异染料法检测线粒体膜电位的演变。结果 随着细胞传代次数的增加，内皮细胞结构逐步退化，细胞分裂减缓，细胞周期趋向停滞于G0／G1期。细胞自发荧光有显著性增加，线粒体膜电位则有显著性降低。结论 内皮细胞在复制性衰老过程中，伴随着细胞形态退化、细胞周期异常，细胞内自发荧光产物增加，线粒体膜电位降低。反映内皮细胞衰老时，细胞内线粒体功能降低，脂质过氧化反应增强。     

Altered membrane anisotropy gradients of plasma membranes of living peripheral blood leukocytes in aging and Alzheimer's disease

Several reports have suggested that membrane rigidity, a term that refers to the relative motion of membrane constituents, is decreased in Alzheimer's Disease. Accordingly, a series of fluorescent membrane probes was used to evaluate the rigidity from the surface to the center of the outer hemi-leaflet of the plasma membrane of living neutrophils, monocytes and lymphocytes. Anisotropy, a parameter which increases with increasing membrane rigidity, was calculated from flow cytometric measurements of vertically and horizontally polarized components of the fluorescence emission of the probes. These preliminary experiments suggest that whereas membrane rigidity in certain regions of the plasma membrane of peripheral blood leukocytes is increased as expected in elderly controls, it is decreased in Alzheimer's disease.     

Decreased microsomal membrane fluidity in the development of cholesterol-induced atherosclerosis in the rabbit

The hypothesis was examined that arterial microsomal membrane fluidity is decreased in atherosclerosis. To investigate this hypothesis, the fluorescence anisotropy (r) of 1,6-diphenylhexa-1,3,5-triene was measured in aortic microsomes isolated from normal and atherosclerotic rabbits. A decrease in membrane fluidity, as indicated by a significant increase in r, was observed in microsomes from atherosclerotic rabbits. Notably, the increase in r occurred prior to macroscopic lesion development. The data support the hypothesis that membrane fluidity is decreased in atherosclerosis and indicate that this decrease occurs early in the atherogenic process. The hypothesis that decreased microsomal membrane fluidity contributes to the increased activity of acyl-CoA:cholesterol acyltransferase (ACAT) in atherosclerosis was also investigated. The hypothesis was rejected on the basis that enrichment of microsomes from normal rabbits with exogenous cholesterol to achieve r values equal to that of microsomes from atherosclerotic rabbits did not result in comparable ACAT activity.     

衰老血管内皮细胞线粒体膜电位与活性氧的变化

背景：血管内皮细胞衰老、凋亡与再生的平衡对正常血管的功能维持具有极其重要的作用。而线粒体是机体细胞内的重要细胞器,除了合成ATP为细胞提供能量外,还控制细胞程序性死亡、以及衰老等多种病理生理的代谢过程。 目的：通过检测脐静脉内皮细胞传代过程中线粒体膜电位与活性氧的改变及其相互关系,从而探讨细胞衰老过程中所产生的功能障碍。 方法：体外培养人脐静脉内皮细胞,选取传代过程中的第2,4,6,8代细胞,采用流式细胞术检测细胞线粒体膜电位及活性氧变化。选取第2,8代细胞行透射电镜检查,观察正常及衰老细胞超微结构的改变。 结果与结论：传代衰老过程中,血管内皮细胞线粒体膜电位逐代降低,而胞内活性氧则出现由增加转而降低的过程。传代后期血管内皮细胞同早期内皮细胞相比,线粒体及内质网明显减少。说明内皮细胞在传代导致的复制性衰老过程中,线粒体膜电位降低,线粒体受损。而在早期传代过程中线粒体轻度受损,而活性氧产生增加,但在线粒体严重受损、功能严重退化过程中,活性氧产生降低。     

银杏内酯B对体外培养的视网膜神经细胞内钙离子浓度和线粒体功能的影响

目的： 观察银杏内酯B对体外培养的大鼠视网膜神经细胞内钙离子浓度和线粒体功能的影响。方法: 采用体外原代培养的大鼠视网膜神经细胞,建立谷氨酸损伤的视网膜神经细胞凋亡模型,与银杏内酯B共同培养,用激光扫描共聚焦显微镜检测对视网膜神经细胞内钙离子浓度和线粒体膜电位的影响。结果: 谷氨酸（8 mmol/L）作用后,视网膜神经细胞存活率降低,细胞凋亡增加,细胞内钙离子浓度增加,线粒体膜电位下降。GB干预后,钙离子浓度降低,线粒体膜电位显著升高,细胞凋亡明显减少。结论: GB能对抗谷氨酸兴奋性毒性, 保护视网膜神经细胞,这一作用可能是通过降低细胞内钙离子浓度和升高线粒体膜电位来实现的。     

Notch1表达下调抑制病理性瘢痕成纤维细胞增殖并诱导其凋亡

目的探讨慢病毒介导的Notch1表达下调对病理瘢痕成纤维细胞(PSF)中caspase-9活化水平及线粒体膜电位的影响。方法分离培养增生性PSFs,感染Notch1 siRNA慢病毒和阴性对照慢病毒。分别采用RT-qPCR和Western blot检测细胞中Notch1mRNA和蛋白表达;MTT法检测细胞增殖;PI单染法检测细胞周期;Annexin V-FITC/PI法检测细胞凋亡;Western blot检测细胞周期蛋白D1(cyclin D1)、细胞周期依赖性蛋白激酶4(CDK4)、活化的caspase-3(c-caspase-3)和caspase-9(c-caspase-9)蛋白及胞质和线粒体中细胞色素C(cytochrome C)蛋白;JC-1法检测细胞线粒体膜电位。结果Notch1 siRNA慢病毒感染后的PSFs中Notch1表达水平明显低于阴性对照慢病毒和未感染的PSFs的表达水平(P<0.05)。下调Notch1后的PSFs增殖能力降低(P<0.05);细胞G0/G1期比例升高(P<0.05);细胞凋亡率升高(P<0.05);c-caspase-3和c-caspase-9蛋白表达升高(P<0.05);细胞线粒体膜电位明显下降(P<0.05);细胞中cyclin D1和CDK4蛋白水平降低(P<0.05);胞质内的cytochrome C蛋白含量升高(P<0.05)及线粒体中cytochrome C蛋白水平降低(P<0.05)。结论Notch1表达下调抑制PSFs增殖并诱导凋亡。     

基牙数目对游离端附着体义齿支持组织应力分布的影响

目的探讨不同基牙数目下,下颌双侧游离缺损冠外附着体义齿支持组织的应力分布情况。方法建立下颌KennedyⅠ类牙列缺损冠外附着体义齿修复的三维有限元模型,分析在垂直载荷作用下采用不同基牙数目时,基牙牙周组织及缺牙区牙槽嵴的von Mises应力分布。结果末端基牙牙周膜应力集中区位于远中的牙颈部,牙槽嵴的高应力区主要位于牙槽嵴顶的近远中两侧。随着基牙数目的增加,基牙牙周组织及缺牙区牙嵴的最大应力值都呈下降趋势,应力分布趋于均匀。当基牙数目从1颗增加到2颗时到再增加到3颗时,牙周膜的最大应力约呈等梯度下降,而基牙牙槽骨和牙槽嵴的下降量则明显减少。结论在下颌游离缺损修复中,冠外附着体义齿支持组织应力的减少与基牙数目的增加不完全成比例,在临床上应根据具体的情况确定联合基牙的数目。     

Changes in electrical resistivity of swine liver after occlusion and postmortem

The resistivity of swine liver tissue was measured in vivo, during induced ischaemia and post-mortem, so that associated changes in resistivity could be quantified. Plunge electrodes, the four-terminal method and a computer-automated measurement system were used to acquire resistivities between 10 Hz and 1 MHz. Liver resistivity was measured in vivo in three animals at 11 locations. At 10 Hz, resistivity was 758±170 Ω·cm. At 1 MHz, the resistivity was 250±40Ω·cm. The resistivity time course was measured during the first 10 min after the liver blood supply in one animal had been occluded. Resistivity increased steadily during occlusion. The change in resistivity of an excised tissue sample was measured during the first 12h after excision in one animal. Resistivity increased during the first 2h by 53% at 10 Hz and by 32% at 1MHz. After 2h, resistivity decreased, probably owing to membrane breakdown. The resistivity data were fitted to a Cole-Cole circle, from which extracellular resistance R_e, intracellular resistance R_i and cell membrane capacitance C_m were estimated. R_e increased during the first 2h by 95% and then decreased, suggesting an increase in extracellular volume. C_m increased during the first 4h by 40%, possibly owing to closure of membrane channels, and then decreased, suggesting membrane breakdown. R_i stayed constant during the initial 6h and then increased.