髂总动脉分支及其临床意义

在78具成年尸体上详细观察了髂总动脉的分支。髂总动脉外侧支的出现率为30.76%,多起于髂总动脉远侧1/3段(43.33%),始端外径为2.38±0.06(0.90～4.20)mm.起自髂总动脉的髂腰动脉的出现率为10.26%,也多起于髂总动脉远侧1/3段,其始端外径为3.03±0.14(2.50～3.80)mm。记录了此两支动脉的走行和分布,并讨论了它们的临床意义。     

胎牛血清外泌体对成骨细胞增殖的作用

背景:研究表明外泌体具有促进骨再生的能力,但从胎牛血清中提取的外泌体是否可以促进骨形成仍存在争议。目的:观察胎牛血清外泌体对成骨细胞增殖能力的影响,从而为临床治疗骨破坏提供新思路。方法:通过超速离心法从胎牛血清中提取外泌体,采用透射电子显微镜和Western blot法验证外泌体是否提取成功;然后用10 mg/L胎牛血清外泌体干预成骨前体细胞MC3T3-E1,通过CCK-8实验检测外泌体对成骨细胞增殖能力的影响,Western blot检测外泌体对成骨细胞骨形态发生蛋白2和骨桥蛋白表达的影响。以不含外泌体的胎牛血清培养的MC3T3-E1细胞为对照组。结果与结论:①胎牛血清外泌体具有典型的脂质双层膜结构,大小在30-150 nm之间,外泌体表面标记因子CD81表达呈阳性,而微囊表面标记物CD40表达呈阴性;②外泌体组的增殖能力明显高于对照组,差异有显著性意义(P<0.05);外泌体组成骨标志性因子骨形态发生蛋白2和骨桥蛋白的表达水平明显高于对照组,差异有显著性意义(P<0.05);③结果表明,胎牛血清外泌体对成骨细胞的增殖起促进作用,可为临床治疗骨破坏提供新思路。     

Predictive validity of a national examination for medical graduates in the People's Republic of China

National examinations for medical graduates were introduced on an experimental basis in the People's Republic of China in 1982. To estimate the predictive validity of the National Medical Examination (NME), an investigation of the postgraduate competence of a sample of the participating examinees was conducted in 1984. The sample consisted of 1,717 of the 4,995 graduates from 13 medical colleges who had taken the initial NME. Their scores on the NME and the ratings given them by directors of postgraduate programs in nine aspects of clinical competence were compared by frequency distribution and product-moment correlation coefficients. Scores on the NME were consistent with measures of postgraduate clinical competence and, as a whole, correlated significantly with the ratings of clinical competence, supporting the use of the score on the NME as a predictor of postgraduate clinical competence. However, the extent of the relationship between the NME score and postgraduate clinical competence varied according to the specialty program of postgraduate medical training.     

缺血预处理对缺血/再灌注脑的保护及其与微循环调节功能的关系研究

目的:探讨缺血预处理(IPC)是否对缺血/再灌注(I/R)脑细胞具有保护效应及其与微循环调节功能间的关系。方法:I/R与IPC组大鼠均复制脑I/R损伤模型,IPC组增加于I/R之前24h进行的短暂脑缺血预处理。动物均开颅窗观察缺血前、缺血后、再灌后脑软膜微循环指标;并取脑组织作红四氮唑(TTC)染色观察缺血损伤情况。结果:I/R组TTC染色后大多数出现不规则的缺血损伤的淡染区,而IPC组明显少见。IPC组缺血及再灌之后毛细血管累计总长度、微循环血流量、微血管内血流速度之相对增加值均大于I/R组。I/R组于再灌注之后有无复流现象;而IPC组此时呈灌注增加的过程。结论:IPC通过提高微循环的调节功能,促进毛细血管的相对性开放和血流的相对性加快,减轻缺血期组织血流低灌注和再灌注期无复流现象,从而对I/R脑产生一定保护作用。     

人白内障球结膜微血管的电镜观察

目的 :观察人球结膜微血管的超微结构 ,认识白内障时球结膜微血管的电镜改变 ,为微循环和眼科研究工作提供参考。方法 :观察对象为 5例老年性白内障、1例糖尿病性白内障 ,术前一般状态良好。在白内障手术时取球结膜标本。电镜常规固定、包埋、定位、超薄切片、用电镜观察。结果 :球结膜毛细血管多由 2～ 3个内皮细胞围绕而成。核多为长椭圆形 ,核周缘有轻度凸凹。近腔侧胞浆细胞器较多 ,微丝和微管十分发达。基底膜、周细胞与一般毛细血管相似。 6例白内障球结膜毛细血管的内皮细胞、基底膜、周细胞、管腔都有不同程度的变化。其电镜改变可以分为三类 :( 1)代偿反应性增强改变 :微丝、微管十分发达、核周深凹、胞体突入管腔内、内皮细胞突起穿越基底膜、白细胞穿壁 ;( 2 )可恢复性退变 :线粒体退变、核质周集、胞浆出现空泡、基底膜分层、弥散、小量出血 ;( 3)严重不可恢复性改变 :核质固缩、腔内红细胞融合、血红蛋白溢出弥散、管壁断裂、腔内充满退变、裂解结构 ( 2例 ) ,并通过断裂处出至基底膜外。结论 :白内障病人球结膜微血管的超微结构有程度不等的改变     

主要常见病甲襞微循环改变重复性的研究

在目前不能直接观测病人内部器官微循环改变的条件下，应用模糊聚类的理论和方法，对主要常见病有意义的的甲襞微循环改变进行聚类，同时参考国内外相关文献的结果，提出了主要常见病有意义的甲襞微循环改变群。在改变群中任意提出3、4、5、6、7、8项改变指标，形成改变组合，一种组合重复出现二次以上的重复率，随组合改变指标数的增多而减少（70．36％～4．36％）。将改变群分成重要指标和参考指标二类，从每类中提出三项形成组合，重复率仅为0．34％。说明组合方式的影响十分巨大。经过反复探索、大量实践，有可能找出对疾病的符合率较高、漏诊率较低、误诊率较小的最佳组合方式。     

Life expectancy in British Marfan syndrome populations

A total of 206 patients with Marfan syndrome were ascertained throughout genetic clinics in Wales and Scotland during the period 1970–1990. There were 45 deaths representing 22% of the cohort. Mean age at death was 45.3 ± 16.5 years. 50% median cumulative survival in the total cohort (n = 206) was 53 years for males and 72 years for females. Multivariate analysis confirmed severity as the best independent indicator of survival. These findings and survival curves will assist in the counselling of British families and individuals with Marfan syndrome.     

Frataxin is reduced in Friedreich ataxia patients and is associated with mitochondrial membranes

Friedreich ataxia is a progressive neurodegenerative disorder caused by loss of function mutations in the frataxin gene. In order to unravel frataxin function we developed monoclonal antibodies raised against different regions of the protein. These antibodies detect a processed 18 kDa protein in various human and mouse tissues and cell lines that is severely reduced in Friedreich ataxia patients. By immunocytofluorescence and immunocytoelectron microscopy we show that frataxin is located in mitochondria, associated with the mitochondrial membranes and crests. Analysis of cellular localization of various truncated forms of frataxin expressed in cultured cells and evidence of removal of an N-terminal epitope during protein maturation demonstrated that the mitochondrial targetting sequence is encoded by the first 20 amino acids. Given the shared clinical features between Friedreich ataxia, vitamin E deficiency and some mitochondriopathies, our data suggest that a reduction in frataxin results in oxidative damage.      

Reduced expression of tissue inhibitor of metalloproteinase (TIMP)-2 in gestational trophoblastic diseases

To elucidate the involvement of type IV collagenases [matrix metalloproteinase (MMP)-2 and MMP-9] and their tissue inhibitors (TIMP-1 and TIMP-2) in the development of gestational trophoblastic disease (GTD), we quantified their levels in hydatidiform mole and choriocarcinoma tissues using specific enzyme-linked immunosorbent assays, and the results were compared with those from normal first trimester placenta. Levels of pro-MMP-2 were increased in hydatidiform mole, and they were further elevated in choriocarcinoma. Levels of pro-MMP-9 in choriocarcinoma and those of TIMP-1 in both hydatidiform mole and choriocarcinoma were also increased. In contrast, TIMP-2 levels were markedly decreased in both hydatidiform mole and choriocarcinoma. Similar results were obtained by the tissue culture of first trimester placenta and hydatidiform mole. Gelatin zymography indicated that the levels of both pro- and activated forms of MMP-2 and MMP-9 were higher in hydatidiform mole and choriocarcinoma. The decreased expression of TIMP-2 in hydatidiform mole and choriocarcinoma was confirmed by Western blot, Northern blot and immunohistochemistry, with the decrease being more pronounced in choriocarcinoma. Taken together, the present study shows that both TIMP-2 mRNA and protein levels are markedly decreased in GTD and the imbalance of MMP-TIMP production, shifted toward greater MMP activity, may be involved in the pathogenesis of GTD.