Genetics of multiple sclerosis [published erratum appears in Hum Mol Genet 1997 Nov;6(12):2189]

Multiple Sclerosis (MS) is a common chronic central nervous system disease in young adults. Relative familial risk appears to be determined largely by genes while population risk is strongly influenced by environmental factors. This is supported by genetic epidemiological studies which also suggest an oligogenic inheritance of susceptibility. The HLA DRB1*1501, DQA1*0102, DQB1 0602 haplotype is associated with the disease but HLA contributes only modestly to overall susceptibility. The results of three genomic searches are concordant with the genetic epidemiology and imply a number of genes with interacting effects will be found. Importantly, no single region has been identified with a major influence on familial risk.      

丙氧鸟苷对转TK基因的人外周血单个核细胞的毒性作用

目的 探讨减少异体干细胞移植中移植抗宿主病（GVHD）,同时最大限度提高移植抗白血病（GVL）效应的有效方法。方法 采用逆转录病毒介导的基因转移方法将I型单纯疱疹病毒胸苷激酶（HSV－TK）基因、绿色荧光蛋白（GFP）基因及抗新霉素（NeoR）基因插入人外周血单个核细胞（PBMC）,MTT法测定丙氧鸟苷（GCV）对转化细胞抑制率。结果 转化细胞表达GFP,且主要为T淋巴细胞,占11．4％,而且被转化的T淋巴细胞中,CD4阳性细胞转化率较高,占7．6％,CD8,CD19,CD33阳性细胞转化率分别为2．9％,2．1％和4．7％,PCR鉴定表明,转染的人外周血单个核细胞DNA中整合中有NeoR基因,MTT法测定丙氧鸟苷（GCV）对转化细胞与未转化细胞抑制率,显示转化细胞生长明显受抑。结论 异体干细胞移植后,如产生严重GVHD应用GCV选择性清除HSV－TK基因转导的T淋巴细胞,使控制GVHD已成可能。     

Effect of Transforming Growth Factor-β_2 on Phagocytosis in Cultured Bovine Trabecular Meshwork Cells

A gradual loss of cells occurs within the humantrabecular meshwork (TM) during normal aging andappears to be increased in patients with primary openangle glaucoma (POAG) [1] .The exactmechanism bywhich cells are lost in either condition is not known,however phagocytosis has been suggested[2 ] .It hasbeen found that,when compared with the non- POAGpatients,the level of transforming growth factor- β2(TGF- β2 ) which may be involved in the pathogenesisof POAG increased in the aqueous humo…     

Irritable bowel syndrome: A technical review for practice guideline development

This article has no abstract. To view the article, select the "View Print Version (PDF)" link above.     

Epidemiology, values, and the meaning of paradigm

Use of the term paradigm has recently reached the epidemiological milieu. This article provides a critical analysis of a classification of "epidemiological paradigms" as proposed by Almeida-Filho. It was initially ascertained that values were not considered fundamental elements for the construction of paradigms, and that they therefore distanced themselves from the Kuhnian matrix. Systematization sought to unite antithetical tendencies and thus seemed closer to the Foucaltian epistéme. Finally, hegemony was considered a more appropriate term than paradigm for systematizing epidemiological periods, since the values of the different watersheds are committed to particularity (principally social class).     

左旋卡尼汀治疗不稳定型心绞痛疗效观察

目的:探讨左旋卡尼汀治疗不稳定性心绞痛的临床疗效.方法:86例不稳定性心绞痛患者随机分为两组,每组43例.在常规治疗基础上,治疗组应用左旋卡尼汀,对照组应用极化液.结果:心绞痛缓解有效率治疗组为93.02%,对照组心绞痛缓解有效率为65.12%(P＜0.01);静息心电图缺血性ST段恢复有效率治疗组为76.74%,对照组为48.84%(P＜0.01).结论:左旋卡尼汀辅助治疗不稳定性心绞痛的是一种安全有效的方法,它能改善缺血心肌的能量代谢.     

Monocyte-dependent regulation of T lymphocyte activation through CD98

CD98 is a 125 kDa heterodimer, which is strongly expressed on the surface of activated and proliferating cells. Its expression is strikingly regulated during T cell differentiation and activation, but the role of CD98 during T lymphocyte responses is not yet understood. We report here that proliferation of resting peripheral blood mononuclear cells (PBMC) induced by lectin, superantigen (SAg) or conventional antigens was blocked by anti-CD98 heavy chain (CD98hc) mAb. In contrast, anti-CD98hc did not block responses of T cell clones or lines. Anti-CD98hc inhibited IL-2 receptor expression and progression of T cells from G1 to S phase, but did not reduce expression of the IL-2 gene. Anti-CD98hc mAb did not regulate the initial activation events involving the TCR and co-receptor structures, but instead inhibited T lymphocyte responses even when added 18 h or more after the activation stimulus. Further experiments demonstrated that anti-CD98 was not directly affecting T cells in this system, but was instead acting on accessory cells. This was supported using a novel xenogeneic system that takes advantage of the lack of xenoreactivity of purified human T cells against mouse splenocytes. Despite absence of a direct xenoresponse to murine spleen cells, human T cells were activated by SAg presented by murine splenic antigen-presenting cells (APC). Murine anti-human CD98hc did not block T cell proliferation in this system. Furthermore, responses using monocyte-depleted PBMC as APC were not blocked by anti-CD98hc. Taken together, the present data suggests that triggering of human monocyte CD98 can suppress T cell proliferation by a process that halts progression through the cell cycle of recently activated T lymphocytes. This may represent a novel pathway for monocyte regulation of T cell activation.