| 1 | Virological course of hepatitis A virus as determined by real time RT-PCR: Correlation with biochemical, immunological and genotypic profiles显示文摘瞄准:承担肝炎 A 的分析,并且相关病毒的负担,丙氨酸 aminotransferase (中高音) ,和有病毒血的持续时间的病毒的遗传型有控制调停房间的免疫的 CD4 (+)/ CD8 (+) 淋巴细胞人口的这些参数。方法:房间计数用用荧光在乙二胺四乙酸小瓶收集的新鲜全血被执行激活的房间 sorter。肝炎 A 病毒(HAV ) RNA 从血浆液被提取,抄录进 cDNA 并且由实时聚合酶链反应确定了并且是 genotyped 的颠倒。结果:在 11 个病人之中, 10 能完全被分析。这些, 3 有严重尖锐肝炎(s -- 啊) 并且剩余物有自我限制尖锐肝炎 A (啊哈) ,在第 4 d 上与有暴发性的疾病(脑病等级 IV ) 的一个病人一起死。中高音水平在啊哈两个都是显著地更高的(1070.9 +/- 894.3;P = 0.0014 ) 并且 s -- 啊(1713.9 +/- 886.3;P = 0.001 ) 与正常控制相比(23.6 +/- 7.2 ) 。在 s 的前凝血酶时间 -- 啊病人(21.0 +/- 2.0;P = 0.02 ) 比在啊哈显著地高(14.3 +/- 1.1;P = 0.44 ) 。在啊哈病人的 CD4 (+)/CD8 (+) 比率(1.17 +/- 0.11;P = 0.22 ) 并且 s -- 啊(0.83 +/- 0.12;P = 0.0002 ) 比在正常健康控制(1.52 ) 看低。有的自我限制盒子达到顶点在分析的开始的病毒的负担当时在 s -- 啊病人这发生在第 15 或第 30 d。在敏锐、严格的组,一耐心的各个属于遗传型 IA,与仍然是 8 个盒子属于遗传型 IIIA。唯一的暴发性的肝的失败大小写属于遗传型 IA。在自我限制感染的全部功课期间收集的 HAV 病毒的负担和中高音价值直接为 s 被相关,但是这不是事实 -- 啊病人。结论:基于小规模的研究, s 的固执地更高的病毒的负担 -- 啊可能由于减少的细胞免疫和溶血。病毒血的持续时间依赖于主人,当病毒的遗传型没在 AVH 和 s 的临床的结果有明显的角色 -- 啊盒子。 | Zahid Hussain Bhudev C Das Syed A Husain Sunil K Polipalli Tanzeel Ahmed Nargis Begum Subhash Medhi Alice Verghese Mohammad Raish Apiradee Theamboonlers Yong Poovorawan Premashis Kar | 2006 | World Journal of Gastroenterology2006，12，29： | 10 |
| 5 | Hepatitis B virus genotypes in chronic liver disease patients from New Delhi,India显示文摘AIM: To study the Hepatitis B virus (HBV) genotypes and their effect on the progression and outcome in patients with chronic liver diseases from New Delhi, India. METHODS: Sera from 100 HBV-related chronic liver disease (CLDB) cases were tested for HBV genotype using Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) and Type-specific primers-based PCR (TSP-PCR) targeting to the surface (S) gene encoding hepatitis B surface antigen. RESULTS: Only genotypes A and D were present and genotype D was dominant. Genotype D was present in all CLDB patient categories. The genotype distribution for the 100 patients with CLDB was as follows: genotype A, 16/100 (16%) (7/40- 17% chronic hepatitis B (CHB); 8/47, 17%, HBV-related cirrhosis (CRB); 1/13, 7.6%, HBV-related hepatocellular carcinoma (HCCB); genotype D- 84/100 (84%) (32/40- 80% CHB; 38/47- 81%, CRB; 11/13, 85%, HCCB); genotype A + D, 3/100 (3%) (1/40- 3% CHB; 1/47- 2%, CRB; 1/13, 7.6%, HCCB); C, 0; B, 0; E, 0; F, 0; G 0, H 0; (P < 0.01, genotype D vs A). CONCLUSION: Only HBV genotypes A and D were present in patients with CLDB from New Delhi, India. Compared with genotype D, genotype A patients had no significant clinical or biochemical differences (P > 0.05). Mixed infection with genotype A and D were seen in 3% of the cases. Genotype D was the dominant genotype prevalent in all patient categories. | Saket Chattopadhyay Bhudev Chandra Das Premashis Kar | 2006 | World Journal of Gastroenterology2006，12，41： | 1 |
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