改良性治疗法联合西地那非治疗勃起功能障碍维吾尔族患者2505例回顾性分析

目的:性治疗法目前尚未普及,本研究旨在评价性治疗法联合西地那非治疗勃起功能障碍(ED)的疗效。方法:根据治疗方法的不同将在本院治疗随访过的3130例维吾尔族ED患者分成2组。对照组625例,单纯口服西地那非3个月;试验组2505例,采用性治疗法联合西地那非治疗3个月。采用国际勃起功能问卷表(IIEF-5)在各组治疗前、后进行疗效评估,并随访12个月。结果:对照组治疗前、后及在6个月、12个月随访的IIEF-5评分分别为12.80±3.76、18.10±2.61、17.35±2.73和16.64±2.63;试验组治疗前、后及在6个月、12个月随访的IIEF-5评分分别为12.73±3.52、19.06±4.07、19.86±2.42和20.47±2.38。两组治疗前后IIEF-5评分自身对比差异均有显著性(P<0.05)。组间比较,试验组较对照组6个月和12个月随访IIEF-5评分均有显著性差异(P<0.05)。结论:性治疗法联合西地那非治疗ED的效果优于单纯西地那非治疗,并在12个月的随访中稳定性良好。     

Role of the B domain for factor VIII and factor V expression and function

Factor V and factor VIII are homologous cofactors in the blood coagulation cascade that have the domain structure A1-A2-B-A3-C1-C2, of which the B domain has extensively diverged. In transfected COS-1 monkey cells, expression of factor VIII is approximately 10-fold less efficient than that of factor V, primarily because of inefficient protein secretion and, to a lesser extent, reduced mRNA expression. To study the functional significance and effect of the B domain on expression and activity, chimeric cDNAs were constructed in which the B domains of factor V and factor VIII were exchanged. Expression of a factor VIII chimera harboring the B-domain of factor V yielded a fully functional factor VIII molecule that was expressed twofold more efficiently than wild-type factor VIII because of increased mRNA expression. Thus, sequences within the factor VIII B domain were not responsible for the inefficient secretion of factor VIII compared with factor V. Expression of a factor V chimera harboring the B domain of factor VIII was slightly reduced compared with wild-type factor V, although the secreted molecule had significantly reduced procoagulant activity correlating with dissociated heavy and light chains and resistance to thrombin activation. Interestingly, the factor V chimera containing the factor VIII B domain was efficiently activated by Russell's viper venum (RVV). A factor V B domain deletion (residues 710- 1545) molecule also exhibited significantly reduced procoagulant activity caused by resistance to thrombin cleavage and activation, although this molecule was activatable by RVV. These results show that, in contrast to factor VIII, thrombin activation of factor V requires sequences within the B domain. In addition, thrombin activation of factor V occurs through a different mechanism than activation by RVV.     

Identification of the molecular defect in the erythrocyte membrane skeleton of some kindreds with hereditary spherocytosis

We have localized the molecular alteration in the membrane skeleton of two of four kindreds with hereditary spherocytosis (HS) to an alteration in the spectrin-protein-4.1 interaction due to a defective spectrin molecule. The defective spectrin-protein-4.1 interaction in these kindreds (referred to as type I HS) leads to a weakened spectrin- protein-4.1-actin ternary complex, which in turn may lead to the friable membrane skeleton and suggested membrane instability related to this disorder. Type I HS spectrin binds approximately 63% as much protein-4.1 as normal spectrin (with equal affinity). This defect does not correlate with splenic function or erythrocyte age in the circulation. However, the approximately 37% reduction in binding of protein-4.1 to HS spectrin approaches the theoretical value of 50% expected in this autosomal dominant disorder. All other type I membrane skeletal interactions (spectrin-syndein, spectrin heterodimer- heterodimer, syndein-band-3) were found to be normal. It would appear therefore that the defective HS spectrin-protein-4.1 interaction in type I hereditary spherocytosis may be the primary molecular defect rather than a secondary phenomena.     

再发骨质疏松性椎体压缩骨折保守治疗患者出院后生存质量

目的：对比初次和再发骨质疏松性椎体压缩骨折(osteoporotic vertebral compression fractures,OVCFs)患者保 守治疗的生存质量,了解再次骨折对此类患者生存质量各方面的影响。方法：回顾性观察治疗OVCFs后出现再骨折 的患者30名(再骨折组)和同时期行保守治疗OVCFs后未发生再骨折的基本条件相似的患者30例(对照组),比较两组出 院后3个月时SF-36简明健康健康状况调查表的调查结果。结果：再骨折组治疗后的8个维度均不同程度较对照组变差 (均P<0.01)。结论：再骨折组患者的生存质量明显低于对照组,并且会进一步影响患者的心理预期、情绪和社会活动 的各个方面。