华南、华北人群HLA-DQB1等位基因多态性

目的从基因水平调查了中国华南、华北地区人群HLA-DQB1等位基因频率，并研究比较两地区人群HLA-DQB1多态性分布。方法采用深圳益生堂生物企业有限公司研制开发的“HLA-DQB1低分辨率分型基因芯片检测试剂盒”，应用聚合酶链反应．序列特异性引物＋序列特异性寡核苷酸探针芯片检测技术，对700名南方地区的中国人和320名北方地区的中国人进行基因分型。结果鉴定了10个HLA-DQB1等位基因，获得了一组准确、科学的统计数据。结论得到了中国华南、华北地区人群HLA-DQB1等位基因频率差异的数据，证明中国人群HLA-DQB1＊02，05，0601，0602，0603的分布南北差异有统计学意义（P〈0．05），为疾病相关性研究、人文科学研究提供了可靠的遗传学数据。     

Nitric Oxide Synthase Expression in Macrophages of Histoplasma capsulatum-Infected Mice Is Associated with Splenocyte Apoptosis and Unresponsiveness

Splenic macrophages from Histoplasma capsulatum-infected mice express inducible nitric oxide synthase (iNOS), and the iNOS expression correlates with severity of the infection. We examined whether production of NO is responsible for apoptosis and the anti-lymphoproliferative response of splenocytes from mice infected with H. capsulatum. In situ terminal deoxynucleotidyl transferase nick end labeling revealed apoptotic nuclei in cryosections of spleen from infected but not normal mice. Splenocytes of infected mice were unresponsive to stimulation by either concanavalin A or heat-killed H. capsulatum yeast cells. Splenocyte responsiveness was restored by addition to the medium of N^G-monomethyl-l-arginine, a known inhibitor of NO production. The proliferative response of splenocytes from infected mice was also restored by depletion of macrophages or by replacement with macrophages from normal mice. In addition, expression of iNOS returned to its basal level when the animals had recovered from infection. These results suggest that suppressor cell activity of macrophages is associated with production of NO, which also appears to be an effector molecule for apoptosis of cultured splenocytes from infected mice.

Nitric oxide (NO) has been reported to induce apoptosis in many cells including smooth muscle cells (20), oligodendrocytes (27), pancreatic β cells (11), melanoma cells (35), thymocytes (7), B lymphocytes (4), and macrophages (2). Fehsel et al. recently demonstrated apoptosis in freshly isolated thymocytes after exposure to NO (7). In the same report, they also showed apoptotic foci in close proximity to blood vessels after lipopolysaccharide treatment. Capillary endothelial and dendritic cells adjacent to apoptotic foci stained strongly for inducible nitric oxide synthase (iNOS), suggesting that NO may be the mediator for thymic apoptosis (7). Data from another laboratory also showed that cloned thymic stromal cell monolayers eliminate thymocytes in vitro through production of NO (26). Furthermore, apoptosis has been suggested as a mechanism by which the immune system replenishes itself and maintains homeostasis (30).The dimorphic fungus Histoplasma capsulatum is a facultative intracellular pathogen of the macrophage (32). Although it is not an obligate intracellular pathogen, the organism is found almost exclusively inside host cells during histoplasmosis (5). In our in vitro studies, H. capsulatum exhibits uninhibited growth in normal unstimulated murine macrophages (32). In activated macrophages, either peritoneal macrophages and cells from the Raw 264.7 line stimulated by gamma interferon (IFN-γ) or splenic macrophages stimulated by IFN-γ and lipopolysaccharide, growth of the fungus is inhibited (13, 18, 32). Furthermore, the anti-histoplasma activity of macrophages is dependent on the expression of iNOS and the production of NO (14, 18). However, the significance of NO production in immunoregulation of histoplasmosis is not clearly defined.In this study, we examined whether NO can act as a regulator of apoptosis in lymphoproliferative responses of splenocytes from H. capsulatum-infected mice. We showed that iNOS was induced in splenic macrophages during active infection and the expression of iNOS coincided with active infection. We also observed by in situ terminal deoxynucleotidyl transferase (TdT) nick end labeling (TUNEL) of spleen sections that apoptosis occurred in immune cells in the spleens of infected mice but was minimal in control mice. The link between apoptosis and NO production was established by inclusion of N^G-monomethyl-l-arginine (NMMA) in the culture medium. Inhibition of NO production reduced the amount of apoptosis in splenocyte culture. Thereby, we also confirmed the findings of Zhou et al. (36) that production of NO by splenocytes of H. capsulatum-infected mice suppressed the splenic lymphocyte proliferative response. In addition, we showed that macrophages were mediators of splenocyte unresponsiveness through the NO that they produced and that NO production was associated with apoptotic changes in cultured splenocytes from infected mice.     

Effect Of Pulsatile Electromagnetic Fields On Blood Viscosity And Coagulation

Ithasbeenprovedthatanumberofdiseasesarerelatedwithabnormalityofbloodviscosityandcoagulationinclinicalresearch.Bloodhyperviscosityandhypercoagulationcauseandaccelearatethedevelopmentofcertaindiseases,deathrateofsomeofwhicharerisingwithyears.Lookingforawaytoreducebloodviscosityandrestrainfasterandstrongercoagulationbecomesasubjectdrawingmoreattention.Theproperseofthisresearchwastofindsuchaway.Intheblood,therearechargrdRBC,WBC,PLT,inorganicions,sothattheremustbesensitiveandcomplicatedresponse…     

pp~(60c-src(+))在神经生长端的表达及其意义

目的　探索 pp60c-src( + ) 在神经生长端的表达特征及其生理意义。方法　用免疫细胞化学方法检测 pp60c-src( + ) 在初代培养鸡胚脊神经节细胞内的分布特征。结果　pp60c -src( + ) 的免疫活性分布在神经细胞的细胞膜下、核周体、神经突起 ;在生长端体部和丝状伪足 ,pp60c -src( + ) 的免疫活性较强 ,少数免疫活性较弱。在伸长的突起上有时可见 pp60c-src( + ) 免疫活性分布在串珠样膨体上。结论　pp60c-src( + ) 参与生长端的运动和生长 ;在生长端分化、神经生长过程中 ,pp60c-src( + ) 的调控作用具有时空特异性     

C1q受体研究进展

补体分子C1q具有调节各种细胞反应的能力.近年,随着C1q功能研究的深入,发现许多细胞内或者细胞表面存在结合C1q的蛋白或者受体,如C1qRp、gC1qbp、C1qRo2-、钙网素/CRT/cC1qR胶凝素受体、CR1.其中某些蛋白除结合C1q外还结合其它配体.     

Paternal mosaicism and hereditary angioedema in a Taiwanese family.

BACKGROUND: Hereditary angioedema (HAE) is a rare disorder characterized by recurrent attacks of localized subcutaneous or submucosal edema. It is inherited in an autosomal dominant fashion and caused by a deficiency of C1 inhibitor (C1 INH). Most patients with HAE have an absolute deficiency of C1 INH (type I HAE), whereas the rest (approximately 15%) synthesize a dysfunctional C1 INH protein (type II HAE). Mosaicism is rare in HAE. OBJECTIVE: To describe the clinical manifestations, laboratory findings, and molecular genetic studies in a Taiwanese family with type I HAE with paternal mosaicism. METHODS: A family that included a 34-year-old man (index patient) and his 25-year-old brother who both had recurrent peripheral angioedema was evaluated. A younger sister had died of an unexplained cause at 18 years of age. We analyzed blood levels of C3, C4, and C1 INH and sequenced the SERPING] (C1NH) gene that codes for C1 INH in 5 family members, including the parents and 3 brothers. RESULTS: The 4 men in the family had a novel mutation c.3_73del, p.N1fsX34 in exon 3 of the C1INH gene, resulting in C1 INH deficiency. Although the father carried this mutant gene, he had normal serum levels of C1 INH. Based on quantitative analysis of allele dosage by DNA fragment analysis (GeneScan), the father was determined to have genetic mosaicism. CONCLUSION: Parental mosaicism is a possible explanation for normal C1 INH plasma concentrations in both parents despite clinically apparent HAE in the children.     

16例染色体异常核型分析

目的与方法本文对189例自然流产、闭经、发育不全患者进行细胞遗传学检查,结果发现异常核型16例,异常核型涉及1、3、4、5、6、7、8、9、10、 15、X、Y染色体.其中平衡易位10例,性染色体异常3例,大Y染色体3例.结论染色体异常是导致流产、闭经、性发育异常的重要遗传因素,应引起临床医师的高度重视.     

采用MDA-MB-231细胞膜进行表皮生长因子受体活性的检测

目的　探讨能否直接利用肿瘤细胞膜进行表皮生长因子受体 (Epidermalgrowthfactorreceptor,EGFR)催化活性检测。方法　首先筛选出EGFR基因表达水平相对较高的细胞株MDA MB 2 31,通过差速离心制备细胞膜 ,采用Westernblotting检测EGFR催化磷酸化的程度。结果　底物被磷酸化 ,加入特异性拮抗剂AG14 78后 ,磷酸化被抑制。结论　利用肿瘤细胞膜检测EGFR活性的设想是成立的 ,并且其方法简便、经济。