狼疮性肾炎发病机理的研究进展

系统性红斑狼疮 (SLE)是一种累及多脏器的自身免疫性炎症性结缔组织病 ,病因复杂 ,受遗传、免疫、神经内分泌、环境等多因素影响。狼疮性肾炎(LN)是SLE最常见而严重的临床表现 ,已成为国内外风湿病学界研究的热点 ,本文将其发病机理的研究近况作一综述。1　遗传因素小鼠狼疮性肾炎 (LN)模型的遗传分析及人类SLE家系研究表明 ,遗传因素确实促进SLE发病 ,具有复杂的多基因遗传的特点 ,LN相关的易感基因不断被揭示。 (SWR×NewZealandBlack(NZB) )F(1)(或SNF(1) )鼠有倾向发展成LN ,虽然NZB鼠狼疮的几个易感遗传位点已被证实 ,S…     

HBV转基因小鼠在肝炎发病机理研究中的应用

应用HBV转基因小鼠研究肝炎发病机理,发现CTL可触发肝细胞凋亡,介导非细胞毒性病毒的清除,在发病中具有重要作用.此外,对病毒生理、机体耐受性、肝癌的发生等也进行了探讨.     

Alzheimer病转基因小鼠模型的研究进展

Ａｌｚｈｅｉｍｅｒ病 (Ａｌｚｈｅｉｍｅｒ’ｓｄｉｓｅａｓｅ,ＡＤ)是一种进行性的精神衰退的疾病 ,又称早老性痴呆。在老年人中ＡＤ的发病率很高 ,而且 ,随着年龄的增长呈指数性增加。世界上 6 5岁以上人群中ＡＤ的发病率在 5 % - 10 % ,在 85岁以上的老年人中发病率约为 2 5 % ,其中 ,10 %的患者具有明显的ＡＤ家族史 ,在这些家族性ＡＤ患者中 ,5 % - 10 %的病例具有常染色体显性遗传的特点[1] 。ＡＤ临床表现为慢性进行性的病变过程 ,发病早期出现短期记忆力丧失 ,随后 ,发展为进行性痴呆 ,主要表现为记忆力丧失 ,定向障碍 ,判断和推理…     

炎症性肠病发病机理研究概况

炎症性肠病是一组病因不明的慢性肠道炎症性疾病 ,包含了两个独立的疾病 ,溃疡性结肠炎和克隆氏病 ,其发病与环境、感染、遗传、免疫因素有关 .本文综述了近年来该病发病机理的研究进展 ,细菌感染是一种促发因素 ,炎症性肠病有遗传性并发现了与其可能有关的易感基因 ,异常的免疫炎症反应在炎症性肠病的发生发展中起重要作用 .溃疡性结肠炎和克隆氏病的发病机理许多方面是相似的但又有不同特征 .     

炎症性肠病发病机理研究概况

炎症性肠病是一组病因不明的慢性肠道炎症性疾病,包含了两个独立的疾病,溃疡性结肠炎和克隆氏病,其发病与环境、感染、遗传、免疫因素有关.本文综述了近年来该病发病机理的研究进展,细菌感染是一种促发因素,炎症性肠病有遗传性并发现了与其可能有关的易感基因,异常的免疫炎症反应在炎症性肠病的发生发展中起重要作用.溃疡性结肠炎和克隆氏病的发病机理许多方面是相似的但又有不同特征.     

糖网病发病机理的研究进展

糖尿病视网膜病变是致盲的常见原因 ,因而最引人注意。多年来 ,国内外学者对糖网病进行了大量实验性和应用性研究 ,取得了一定的进展。本文在简要回顾糖网病病理变化的基础上 ,对其发病机制 ,诸如高血糖与糖网病、糖网病与糖代谢异常的学说以及血管生成因子的作用等作一综述。     

急性肾功能衰竭发病机理的研究进展

本文综述急性肾功能衰竭中肾小管能量耗竭、ca~(2+)蓄积、自由基、磷脂酶和细胞因子等对肾上管细胞的损伤作用,肾小管细胞脱落和再粘附的机理,以及内皮素、一氧化氮等介质和内皮细胞功能改变所致的继发性肾小球血液动力学变化等方面的研究进展,并探讨肾小管细胞修复和肾小球滤过功能恢复的可能机理。     

协同受体与艾滋病发病机理的研究进展

我们着重就协同受体与艾滋病发病机理的研究进展作一介绍。1　协同受体介导病毒感染细胞ＨＩＶ 1感染人体后引起进行性的艾滋病病变 ,通常经历三个典型的时期 ,第一为急性感染期 ,表现为病毒血症 ;接着是无症状期 ,此时在淋巴器官中大多可检测出病毒的复制 ;最后是免疫系统破坏 ,伴随病毒血症的再次出现。并产生继发性感染等而导致病人死亡。引起人体艾滋病的ＨＩＶ 1病毒株有以下几种 :①嗜巨噬细胞ＨＩＶ 1株 ;②嗜Ｔ细胞ＨＩＶ 1病毒株 ;③部分原代ＨＩＶ 1分离株是双嗜性的 ,既感染嗜巨噬细胞 ,又感染Ｔ细胞[1 3] 。决定ＨＩＶ 1嗜细胞…     

蛋白粒子及蛋白粒子病发病机理的分子基础

一、１９９７年诺贝尔生理学或医学奖与蛋白粒子：１９９７年诺贝尔生理学或医学奖颁给美国学者ＳｔａｎｌｅｙＢ．Ｐｒｕｓｉｎｅｒ以表彰他在发现蛋白粒子（Ｐｒｉｏｎ）和阐明其致病机理的研究中所作的贡献。蛋白粒子是一种能在动物和人类中引起多种中枢神经系统变性疾...     

肌性斜颈的病因及发病机理

肌性斜颈是由于一侧胸锁乳突肌挛缩所致头部向患侧偏斜 ,并随患者年龄增长而逐渐引起面部及头颅畸形的一种常见病。该病以儿童为主 ,在婴幼儿发病率为 0 .4%～1.3% 〔1 ,2〕。若早期得不到合理治疗 ,随年龄增长畸形将逐渐加重 ,将对患者心理、工作、婚姻带来很大的影响。对该病虽已有几百年的认识 ,但目前对其病因及发病机理尚无定论 ,各家说法不一。Mc Daniel〔3〕报道引起斜颈的病因达 40余种 ,Kiwak〔4〕报道有 80余种 ,故对该病的病因及发病机理仍需进一步探讨 ,为临床诊断治疗该病提供确切的理论依据。1　血肿学说早在 1838年 Strom …     

家族性腺瘤性息肉病与高脂血症的关系

家族性腺瘤性息肉病（familial adenomatous polyposis,FAP）是由APC（adenomatous polyposis coli）基因突变引起的常染色体显性遗传病。高脂血症作为FAP的肠外伴随症状逐渐被关注,同时在FAP的经典模型Apc基因突变的Min小鼠上也出现了高血脂症状。本文从高脂血症、FAP以及APC基因突变的角度,阐述三者的相互联系,期望对病人的预防与治疗提供有价值的参考。     

A Model of Combined Gastroduodenitis and Hyperlipidemia in Rats

We elaborated a model of gastroduodenitis combined with hyperlipidemia in rats. This model is based on alimentary lipid disturbances and morphological changes in the gastroduodenal mucosa caused by exogenous damaging factors. Morphological assay revealed gastroduodenitis; biochemical studies of the blood and liver demonstrated hyperlipidemia. This model holds much promise for evaluating pathogenetic mechanisms of combined gastroduodenal and heart diseases.     

Support for linkage of familial combined hyperlipidemia to chromosome 1q21-q23 in Chinese and German families

We examined familial combined hyperlipidemia (FCHL) families from nonisolated regions in Germany and China to see if we could corroborate support for a chromosome 1q FCHL locus in more general populations. We recruited 24 German families with 137 members, 92 of whom met the criteria of affected in terms of the low density lipoprotein (LDL) and triglyceride levels in excess of the 90th percentile for age and gender. In China, we recruited 12 families with a total of 81 members. All affected persons had total cholesterol concentrations >240 mg/dl and triglyceride concentrations >250 mg/dl. We examined the markers APOA2, D1S1677, D1S104, D1S194, D1S426, and D1S196. Two-point linkage analysis allowing for heterogeneity gave a maximum linkage of disorder score (HLOD) of 2.60 right over D1S194, estimating the proportion of linked families at 36%. This marker is adjacent to D1S104. The evidence for linkage was roughly the same both in the German (HLOD 1.40) and Chinese families (HLOD 1.52). Marker D1S194 is close to the retinoid X receptor (RXR) gene locus, which was found to be linked to triglyceride levels in an earlier twin study from our laboratory. We interpret our observations as encouraging support for the recent findings indicating the presence of a gene for FCHL on chromosome 1q. Furthermore, since DIS194 is adjacent to the gene for the RXR, we suggest that RXR is an attractive candidate for involvement in FCHL.     

Recent Advances in Kawasaki Disease

Kawasaki disease (KD) is characterized with acute systemic vasculitis, occurs predominantly in children between 6 months to 5 years of age. Patients with this disease recover well and the disease is self-limited in most cases. Since it can lead to devastating cardiovascular complications, KD needs special attention. Recent reports show steady increases in the prevalence of KD in both Japan and Korea. However, specific pathogens have yet to be found. Recent advances in research on KD include searches for genetic susceptibility related to KD and research on immunopathogenesis based on innate and acquired immunity. Also, search for etiopathogenesis and treatment of KD has been actively sought after using animal models. In this paper, the recent progress of research on KD was discussed.     

Genetic abnormalities and pathogenesis of familial amyloidotic polyneuropathy

Familial amyloidotic polyneuropathy (FAP) is an autosomal inherited disease, characterized by extracellular amyloid deposits and by peripheral neuropathy. Amyloid fibrils derived from most types of FAP consist of variant transthyretin (TTR) with single amino acid substitutions, and methionine 30 TTR is the most common variant TTR. TTR is mainly produced in the liver and the choroid plexus. Biochemical and molecular biological techniques have been revealing the amyloidogenicity of variant TTR in vitro and in vivo using the transgenic mouse as a model. It will be important for the development of effective therapy to find out the factors, other than variant TTR, which affect amyloid deposition and define the tissue specificity of amyloid.     

Genetic backgrounds and diagnosis of familial hypercholesterolemia

Lipid disorders play a critical role in the intricate development of atherosclerosis and its clinical consequences, such as coronary heart disease and stroke. These disorders are responsible for a significant number of deaths in many adult populations worldwide. Familial hypercholesterolemia (FH) is a genetic disorder that causes extremely high levels of LDL cholesterol. The most common mutations occur in genes responsible for low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), or proprotein convertase subtilisin/kexin type 9 (PCSK9). While genetic testing is a dependable method for diagnosing the disease, it may not detect primary mutations in 20%–40% of FH cases.     

抑郁症动物模型的评价及认知行为变化

目的研究抑郁症动物模型的评价方法及认知行为变化。方法造模前后分别测量摄食量和体重,使用Y型电迷宫评价抑郁症动物模型的认知,强迫游泳试验评价抗抑郁药物作用后动物行为的变化。结果造模前后动物的体重增加量,造模后的动物摄食量,药物干预后动物强迫游泳实验中的静止时间在两组之间有显著差异。结论体重增加量,摄食量,电迷宫实验可以作为抑郁症动物模型的评价方法。强迫游泳试验可以评价抗抑郁药物干预后动物行为的变化。慢性应激抑郁动物模型存在认知行为的变化。     

SIV Infection of Macaques as a Model for AIDS Pathogenesis

Simian immunodeficiency virus (SIV) infection of macaques is the best available animal model for studying the pathogenesis of AIDS. Experimental inoculation of macaques with SIV results in a persistent infection that leads to immunodeficiency, opportunistic infections, and death. Most aspects of the illness, including immunologic and virologic parameters, are easily quantified. Furthermore, pathologic processes can be evaluated throughout the course of experimental infection. Recently, molecular clones of SIV proviral DNA have been used to study genetic variation and specific viral determinants of pathogenesis. Considered together, these observations support the continued detailed study of SIV infection of macaques as a model for human AIDS.