HIV-Ⅰ CN54株gagprotease基因嵌合脊髓灰质炎病毒cDNA质粒的构建和表达研究

目的 构建HIV-1 CN54株gagprotease基因嵌合脊髓灰质炎病毒cDNA的表达质粒，并鉴定、检测基因及其表达。方法 用PCR技术获得人免疫缺陷病毒CN54株的gagprotease基因，并使其两端带上合适的酶切住点，将其定向插入到包含脊髓灰质炎病毒cDNA的表达质粒pSVA14中，替代其部分结构基因，构建HIV基因嵌合缺陷性脊髓灰质炎病毒基因组的表达质粒。经筛选、鉴定后用脂质体转染技术将新构建的质粒转入Hela细胞内，用Western Blot方法检测目的基因在Hela细胞内的表达。结果 PCR技术扩增所得的人免疫缺陷病毒CN54株gagprotease基因经琼脂糖凝胶电泳、DNA测序证实成功获得，未引入突变碱基，筛选、鉴定证明gagprotease基因被正确定向插入到脊髓灰质炎病毒的cDNA序列之中，Western Blot检测到gagpro-tcase基因正确表达了相关蛋白。结论 成功构建了表达人免疫缺陷病毒CN54株gagprotease基因的缺陷性脊髓灰质炎病毒基因组嵌合质粒，为利用脊髓灰质炎病毒作人免疫缺陷病毒基因的表达载体奠定了基础，此研究对开发以脊髓灰质炎病毒为艾滋病的疫苗载体有重要意义。     

自我效能感与晕船症状的相关研究

目的 探讨自我效能感与晕船症状的相关，以期寻找影响晕船的心理因素。方法 对某院校参加海上实习的123名医疗本科学员用一般自我效能感量表、晕船自我效能感量表于出海作业前进行施测，用晕船症状评分量表于出海作业返回后进行评估。结果 晕船自我效能感与晕船症状显著负相关（r=-0．470，P〈0．01），而一般自我效能感量表与晕船症状的相关无统计学意义（r=-0．102，P〉0．05）。结论 晕船自我效能感可能为个体发生晕船的心理影响因素之一。     

羟基磷灰石/聚合物复合材料的研究进展

该文对羟基磷灰石与天然生物材料、人工合成的医用可生物降解高分子材料以及医用非降解高分子材料的研究应用与进展进行了总结.并对羟基磷灰石/聚合物复合材料的发展趋势进行了探讨.     

维持性血液透析患者血清胱抑素C浓度与左心室肥厚的相关分析

比较64例维持性血液透析(MHD)患者和20例健康对照者一般临床资料和临床常用血生化指标;采用乳胶颗粒增强免疫透射比浊法检测血清胱抑素C浓度,超声心动图测定心脏腔径及心功能参数.结果 示MHD患者随透析时间延长,血清胱抑素C浓度逐渐增加,且左心室肥厚发生率显著增高.左心室肥厚者收缩压、左心室重量指数和血胱抑素C浓度明显高于无左心室肥厚者.胱抑素C与左心室重量指数、收缩压相关(r=0.633,0.397,均P<0.01).提示MHD患者血清胱抑素C变化可能与左心室肥厚密切相关,并可能是透析患者远期心血管并发症的影响因素.     

宁波市镇海区社区居民高血压干预前后KAP调查

目的进行高血压综合干预效果评价,了解社区居民的KAP的改变情况,探讨社区健康促进对高血压病人的血压控制作用.方法采用二阶段随机抽样的方法分别在干预前后进行问卷调查.结果高血压患者干预后血压控制率达71.9%,较干预前的56.8%有显著性提高(P＜0.05).居民高血压知识平均得分为85.5分,及格率达96.6%.有更多的居民开始控制每日的食盐摄入量,每日食用蔬菜和水果的情况都有改变.高血压患者定期测量血压率由31.3%上升到56.7%.居民对开展社区高血压健康促进持正性态度的明显增多.结论社区高血压综合干预有助于高血压病人的血压控制.     

Detection of mononucleotide repeat sequence alterations in a large background of normal DNA for screening high-frequency microsatellite instability cancers.

PURPOSE: Mutations in mononucleotide repeat sequence (MRS) are good indicators of high-frequency microsatellite instability (MSI-H) cancers, but it has been a challenge to detect such mutations in a large background of wild-type DNA; as in this setting, PCR errors often generate false positive mutant alleles. In this study, we developed a general strategy, referred to as probe clamping primer extension-PCR (PCPE-PCR), to detect MRS alterations in a large background of wild-type DNA. EXPERIMENTAL DESIGN: In PCPE-PCR, genomic DNA is first subjected to PCPE, in which mutant single-strand DNA molecules are preferentially produced. Next, genomic DNA is removed to enrich for the mutant DNA fraction. Thereafter, PCR is carried out using the remaining single-strand DNA molecules as templates. Finally, the PCR products are analyzed to reveal the MSI-H status. In this study, the sensitivity of this new method was first examined by spiking mutant DNA into wild-type DNA at specific ratios followed by studying whether this method is applicable to fecal DNA testing. RESULTS: We showed that PCPE-PCR could detect both mutated BAT26 and transforming growth factor-beta-RII (A)10 markers in the presence of 500-fold excess of normal DNA and that as few as three copies of mutated DNA could be detected. In addition, we showed that this technology could detect MSI-H colorectal cancer by fecal DNA analysis. CONCLUSION: PCPE-PCR is sensitive. In addition, PCPE-PCR is simple and amendable to a cost-effective and high-throughput screening operation. This technology may be applicable to noninvasive screening of MSI-H cancer.     

不同静脉给药方法对尼莫地平注射液稳定性影响

目的考察尼莫地平注射液在不同静脉给药方法下的稳定性。方法采用高效液相色谱法测定尼莫地平含量。结果尼莫地平注射液在输液泵给药途径下,8 h后浓度下降约1%;在常规输液途径下,尼莫地平注射液于玻璃瓶装0.9%氯化钠注射液中比较稳定,8 h后浓度下降约10%,但经过PVC输液器之后,浓度迅速下降,8 h后仅为初始浓度的45%左右。结论输液泵静脉给药方式是尼莫地平的临床最佳给药途径。     

The pathogenesis of autosomal dominant polycystic kidney disease: an update

The identification of PKD1 and PKD2, the two major genes responsible for autosomal dominant polycystic kidney disease, are the seminal discoveries upon which much of the current investigation into the pathogenesis of this common heritable disease is based. A major mechanistic insight was achieved with the discovery that autosomal dominant polycystic kidney disease occurs by a two-hit mechanism requiring somatic inactivation of the normal allele in individual polarized epithelial cells. Most recent advances are focused on the function of the respective protein products, polycystin-1 and polycystin-2. Indirect evidence supports an interaction between polycystin-1 and -2, albeit it is unlikely that they work in concert in all tissues and at all times. They associate in yeast two hybrid and cotransfection assays and there is a striking similarity in the renal and pancreatic cystic phenotypes of Pkd2-/- and Pkd1del34/del34 mice. Also, the respective homologues of both proteins are expressed in the same sensory neuronal cells in the nematode and the human disease phenotypes remain completely overlapping with the major difference being in relative severity. Mounting evidence supports the hypothesis that polycystin-1 is a cell surface receptor. A close homologue in the sea urchin sperm mediates the acrosome reaction in response to contact with egg-jelly, the nematode homologue functions in mechano- or chemosensation, and the solution structure of the repeated extracellular polycystic kidney disease domains reveals a beta-sandwich fold commonly found in surface receptor molecules. Indirect evidence also supports the initial hypothesis that polycystin-2 is a calcium channel subunit. Several closely related homologues retain the calcium channel signature motif but differ in their predicted interaction domains, and one of these homologues has been shown to be a calcium regulated cation channel. Several important distinctions in polcystin-1 and -2 function have also been discovered. Polycystin-2 has a role in cardiac development that polcystin-1 does not. High level polycystin-2 expression in renal epithelial cells coincides with maturation and elongation of tubules and, unlike polycystin-1, persists into adulthood. In cells in tissue culture, polycystin-2 is expressed exclusively in the endoplasmic reticulum whilst the cellular expression of polycystin-1 remains unknown. Overall, the difficult task of understanding the autosomal dominant polycystic disease process is proceeding apace.     

Use of infliximab in the treatment of Crohn's disease in children and adolescents

BACKGROUND: Crohn's disease is often poorly responsive to conventional therapy with corticosteroids and immunomodulators. A novel chimeric antibody to tumor necrosis factor-alpha, infliximab, has shown utility in the treatment of refractory Crohn's disease in adults. PURPOSE: To evaluate the efficacy of open-label administration of infliximab in children and adolescents with active intestinal Crohn's disease. METHODS: Chart review of the experience with 19 subjects (mean age 14.4 years, range 9 to 19 years) receiving 1 to 3 infusions of infliximab (5 mg/kg/dose) over a 12-week period for corticosteroid-resistant disease (n = 7) or corticosteroid dependence (n = 12). Disease activity was monitored by physician global assessment and the Pediatric Crohn's Disease Activity Index. RESULTS: Significant initial improvement (first 4 weeks after infusion) was noted in all subjects, with Pediatric Crohn's Disease Activity Index values decreasing significantly (mean +/- SD, 42.1 +/- 13.7 to 10.0 +/- 5.6, P <.0001). Over the subsequent 8-week period, 8 of 19 treated subjects had worsening of symptoms, although none deteriorated to severe activity. The mean Pediatric Crohn's Disease Activity Index at 12 weeks was 26.8 +/- 16. 4. The mean daily prednisone dosages at baseline, 4 weeks, and 12 weeks were 28 +/- 14 mg, 20 +/- 12 mg, and 8 +/- 12 mg, respectively (P <.01). Adverse effects were noted in 3 patients during infusion (dyspnea, rash) and were self-limited. CONCLUSIONS: Infliximab is associated with short-term clinical improvement in children and adolescents with severe Crohn's disease. The rapid return of disease activity in some patients suggests that additional dosing strategies may be required. Long-term safety necessitates close monitoring.