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排序方式: 共有886条查询结果,搜索用时 15 毫秒
881.
882.
HLA-C was shown to be a highly polymorphic gene that can be accurately typed by sequencing methodologies. We report two novel HLA-C alleles identified during sequence-based typing of East African populations; the novel alleles were confirmed by sequencing two separate polymerase chain reaction products and by molecular cloning and sequencing multiple clones. The first new allele is identical to Cw*0701 except for a single-nucleotide synonymous substitution at codon 182 (GCA-->GCG). The new allele has been named by the WHO nomenclature committee as Cw*070105. The second new allele is identical to Cw*1403 except for a nonsynonomous change at codon 21 (CAC-->CGC), changed from histidine to arginine. The new allele has been named by the WHO nomenclature committee as Cw*1408. 相似文献
883.
Longitudinal analysis of genotype distribution of influenza A virus from 2003 to 2005 总被引:1,自引:0,他引:1
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Mak A Rahmanian R Lei V Lawrence D Krajden M Brunham RC Skowronski D Li Y Booth T Goh SH Petric M 《Journal of clinical microbiology》2006,44(10):3583-3588
Influenza A viruses cause yearly epidemics, in part, due to their ability to overcome immunity from previous infections through acquisition of mutations. Amino acid sequences encoded by genes 4 (HA), 6 (NA), 7 (M), and 8 (NS) from 77 H3N2 influenza A isolates, collected between November 2003 and March 2005, were analyzed to determine the extent to which the viruses mutated within epidemic periods and between the epidemics. Nucleotide and amino acid sequences were stable throughout the epidemics but experienced substantial changes between epidemics. Major changes occurred in the HA gene in 5 to 7 amino acids and the NA gene in 11 to 13 amino acids and changes of 5 amino acids occurred in the M and NS genes. In the HA gene, changes occurred in sites known to be epitopes that determine the hemagglutination inhibition reactivity, and these were shown to be associated with a change of strain from A/Fujian/411/2002-like to A/California/7/2004-like viruses. Our findings indicate that genotype determination promises to be a rapid approach for detecting new strains of influenza A viruses in a population. 相似文献
884.
CR de Andrade PF Leite AC Montezano DA Casolari A Yogi RC Tostes R Haddad MN Eberlin FRM Laurindo HP de Souza FMA Corr��a AM de Oliveira 《British journal of pharmacology》2009,157(4):568-580
Background and purpose:
There are interactions between endothelin-1 (ET-1) and endothelial vascular injury in hyperhomocysteinemia (HHcy), but the underlying mechanisms are poorly understood. Here we evaluated the effects of HHcy on the endothelin system in rat carotid arteries.Experimental approach:
Vascular reactivity to ET-1 and ETA and ETB receptor antagonists was assessed in rings of carotid arteries from normal rats and those with HHcy. ETA and ETB receptor expression was assessed by mRNA (RT-PCR), immunohistochemistry and binding of [125I]-ET-1.Key results:
HHcy enhanced ET-1-induced contractions of carotid rings with intact endothelium. Selective antagonism of ETA or ETB receptors produced concentration-dependent rightward displacements of ET-1 concentration response curves. Antagonism of ETA but not of ETB receptors abolished enhancement in HHcy tissues. ETA and ETB receptor gene expressions were not up-regulated. ETA receptor expression in the arterial media was higher in HHcy arteries. Contractions to big ET-1 served as indicators of endothelin-converting enzyme activity, which was decreased by HHcy, without reduction of ET-1 levels. ET-1-induced Rho-kinase activity, calcium release and influx were increased by HHcy. Pre-treatment with indomethacin reversed enhanced responses to ET-1 in HHcy tissues, which were reduced also by a thromboxane A2 receptor antagonist. Induced relaxation was reduced by BQ788, absent in endothelium-denuded arteries and was decreased in HHcy due to reduced bioavailability of NO.Conclusions and implications:
Increased ETA receptor density plays a fundamental role in endothelial injury induced by HHcy. ET-1 activation of ETA receptors in HHcy changed the balance between endothelium-derived relaxing and contracting factors, favouring enhanced contractility.British Journal of Pharmacology (2009) 157, 568–580; doi:10.1111/j.1476-5381.2009.00165.x; published online 9 April 2009This article is part of a themed section on Endothelium in Pharmacology. For a list of all articles in this section see the end of this paper, or visit: http://www3.interscience.wiley.com/journal/121548564/issueyear?year=2009 相似文献885.
886.
目的:近年来,树突状细胞参与调节作用的研究较多。实验拟验证重组腺相关病毒(rAAV)介导癌胚抗原基因转染树突状细胞后其的免疫调节作用的变化。方法:实验于2006-06/2006-11在美国阿肯色大学医学院基因治疗中心完成。①实验方法:取健康人外周血(自愿捐献),采用改良Ficoll密度梯度离心的方法分离外周血单个核细胞,取贴壁细胞,分为rAAV/CEA转染组和空白对照组,均采用重组人粒细胞巨噬细胞集落刺激因子、白细胞介素4、肿瘤坏死因子-α诱导树突状细胞前体细胞成熟,将成熟树突状细胞与末梢血淋巴细胞按比例混合培养,可得到激活的细胞毒性T淋巴细胞。②实验评估:采用流式细胞仪检测树突状细胞表面标志表达,细胞毒性T淋巴细胞的免疫表型变化,细胞毒性T淋巴细胞γ-干扰素表达。采用酶联免疫吸附法(ELISA法)检测树突状细胞的白细胞介素12和白细胞介素10表达。结果:①rAAV/CEA转染树突状细胞的CD14较空白对照组降低,共刺激分子CD40、CD80、CD83、CD86表达均较空白对照组高。②成熟树突状细胞细胞因子表达中,rAAV/CEA转染组的白细胞介素12较空白对照组升高,白细胞介素10降低。③与空白对照组比较,rAAV/CEA转染组能高表达CD8 T细胞和其表型CD69,CD8/CD56的T细胞比例上调,CD25 CD4 的T细胞减少。④rAAV/CEA转染的细胞毒性T淋巴细胞表达相对较高水平的γ-干扰素,与杀伤实验结果相吻合。结论:rAAV/CEA转染树突状细胞能够激活细胞毒性T淋巴细胞的特异性杀伤作用,与树突状细胞和细胞毒性T淋巴细胞等免疫细胞表面标志变化和细胞内细胞因子水平变化相关。 相似文献