17β-雌二醇对子宫内膜异位症患者在位子宫内膜间质细胞β-catenin mRNA和蛋白表达的影响

目的研究17β-雌二醇(17β-E2)对子宫内膜异位症(内异症)患者在位子宫内膜间质细胞β-catenin mRNA和蛋白表达的影响,探讨Wnt/β-catenin信号通路在介导雌激素促进内异症发生发展的作用。方法体外分离培养内异症患者在位子宫内膜间质细胞。用不同浓度17β-E2处理子宫内膜间质细胞48 h;此后选用10-10mol/L 17β-E2处理子宫内膜间质细胞12、24和48 h,逆转录聚合酶链反应(RT-PCR)和免疫印迹法(Western blotting)检测17β-E2处理前后子宫内膜间质细胞β-catenin mRNA和蛋白的表达水平。同法分析雌激素受体拮抗剂ICI182,780(10-6mol/L)对17β-E2促进β-catenin mRNA和蛋白表达的影响。免疫组织化学染色观察17β-E2作用后β-catenin在子宫内膜间质细胞中的定位。结果17β-E2能明显促进内异症患者在位子宫内膜间质细胞β-catenin mRNA和蛋白的表达,并呈剂量和时间依赖性,于10-10mol/L作用48 h最明显。雌激素受体拮抗剂ICI182,780能明显抑制17β-E2对子宫内膜间质细胞β-catenin mRNA和蛋白的表达。免疫组织化学染色发现17β-E2能促进β-catenin在子宫内膜间质细胞核内的表达。结论雌激素可能通过激活Wnt/β-catenin信号通路促进内异症在位子宫内膜的异位种植。     

二甲双胍在多囊卵巢综合征的作用

生殖及代谢异常是多囊卵巢综合征(PCOS)的特征性表现。已证实高胰岛素血症及胰岛素抵抗,导致血中雄激素水平过高,是PCOS的重要发病机制。二甲双胍(metformin)称为胰岛素增敏剂,用于治疗PCOS后,可减轻高雄激素血症,使月经周期规律,改善卵巢对诱导排卵的反应,提高妊娠率,降低早孕流产率,且能减低发展为II型糖尿病及心血管疾病的危险性。本文就国外近年有关metformin运用于PCOS的进展作一综述。     

氨茶碱治疗病态窦房结综合征患者的观察与护理

采用氨茶碱治疗病态窦房结综合征３０例，近期有效率为８７．０％，远期有效率（１０个月）为７４．１％。护理重点：①按时按量用药；②保证足够的用药时间；③密切监测血中氨茶碱浓度；④加强药物副反应的观察；⑤定期心电监测，严密观察病情，做好心理护理。     

Localization of mRNA for inflammatory cytokines in radicular cyst tissue by in situ hybridization, and induction of inflammatory cytokines by human gingival fibroblasts in response to radicular cyst contents

The expression of mRNA encoding the inflammatory cytokines interleukin-1α (IL-1α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor α (TNF-α) have been examined in radicular cysts by in situ hybridization. Furthermore, the biological activity of the contents of radicular cysts (RCC) has been assayed by adding extracts of RCC to cultured human gingival fibroblasts (HGFs) and analyzing the culture medium for the release of inflammatory cytokines. In the epithelial layer, keratinocytes expressed all cytokine mRNAs examined at various levels. Basal layer cells expressed mRNA for each cytokine. In the subepithelial granulation tissue of the cysts, fibroblasts and macrophages expressed mRNA for IL-6, IL-8, IL-1β and TNF-α mRNA at varying levels; especially clear expression of TNF-α and IL-1β mRNA was detected on macrophages. The infiltrating lymphoid cells, largely composed of T cells and plasma cells, expressed these cytokine mRNAs, especially those encoding IL-6 and IL-8, at various levels. In vitro analysis indicated dose-dependent release of both IL-6 and IL-8 by HGFs in response to RCC. After heating to 100°C for 10 min, RCC almost completely failed to stimulate IL-6 release from HGFs. Furthermore, anti-IL-1β antibody (neutralization test) did not prevent the stimulation of IL-6 release by RCC. Significant amounts of IL-6 and IL-8 were detected in RCC in two cases, and a trace amount of IL-1β was detected in one case. This study demonstrated the wide expression of mRNA encoding inflammatory cytokines in radicular cyst tissues, and RCC itself was capable of stimulating 1L-6 and 1L-8 production from HGFs.     

肾综合征出血热地鼠肾细胞Ⅱ型灭活疫苗的安全性、免疫性及其流行病学效果考核

目的：考核HFRS地鼠肾细胞Ⅱ型灭活疫苗的安全性、免疫法及其流行病学效果。方法：采用间接免疫荧光抗体试验（IFA）、微量细胞变性中和试验（MCPENT），检测接种者血中荧光抗体及中和抗体水平；调查接种组与对照组发病情况。结果：以怀宁、广德两县18个村为疫苗观察现场，接种组7499人，对照组7261人，中强反应率为224％（5／223）。3针全程免疫后中和抗体阳转率为63．33％（19／30），荧光抗体阳转率为38.58％（27／70）；接种后1年内接种组无发病，对照组发病3例。结论：该疫苗的安全性较好；有一定水平的免疫应答，但防病效果应进一步观察确证。     

Congenital cardiac malformations in Adams-Oliver syndrome

Whole genomic hprt clones were used in Southern analysis to screen the integrity of the hprt gene in a family that includes a patient with HPRT enzyme deficiency causal to Lesch-Nyhan syndrome. A 5 kb DNA sequence deletion was found to have its endpoints in the first and third introns. The probes identified the carrier status of female family members, aided by an RFLP carried by the mother's normal X-chromosome.     

蝮蛇抗栓酶与肝素抗凝治疗小儿肾病的疗效比较

本文对60例小儿肾病患儿随机分为3组,蝮蛇抗栓酶治疗组,肝素治疗组,常规治疗组(对照组),结果总有效率分别为95％,90％,60％。蝮蛇抗栓酶组与对照组比较,差异有极显著性(P<0.01),肝素组与对照组比较,差异有显著性(P<0.05)。结果提示抗凝治疗对小儿肾病高凝状态有明显改善作用,能增加临床疗效。蝮蛇抗栓酶抗凝效果优于肝素。     

不同剂量辛伐他汀对肾病综合征高脂血症的近期疗效

目的 :观察辛伐地他汀 -舒降之对肾病综合征高脂血症的近期疗效及安全性 ,比较不同剂量辛伐他汀的降脂作用。方法 :72例均系肾综合并高脂血症的患者 ,随机分治疗组 (5 6例 )和对照组 (16例 ) ,在积极治疗原发病的同时 ,治疗组给予服辛伐他汀每晚 5～ 2 0mg ,14例混合性高脂血症患者同时服用非诺贝特 ;对照组未用降脂药。观察治疗前及治疗后 1周、2周血脂全套 (TC ,TG ,LDL和HDL)、肝功能 (AST ,ALT ,TP和ALB)、肾功能 (BUN ,Scr)、及尿蛋白定量的变化。结果 :辛伐他汀每晚 2 0mg服用 1周可使 6 3%的患者总胆固醇 (TC)下降 33% ,服用 2周可使 84%的患者血TC降至正常 ;单用辛伐他汀在降低TC的同时 ,可使甘油三酯 (TC)下降 43.16 % ,若与非诺贝特合用可使TG下降达 6 4.2 2 % ,未见不良反应发生 ;辛伐他汀的降脂作用与剂量及用药时间密切相关 ,2 0mg >10mg >5mg ,每晚服用 5mg共 2周仅能使 6 0 %的患者TC下降 12 .5 %。结论 :辛伐他汀 (每晚 2 0mg)能安全、快速有效降低肾病综合征患者的高脂血症 ,而对减少尿蛋白、改善肾功能近期无作用     

The Lewis blood group--a new genetic marker of ischaemic heart disease.

In a cohort of 3383 men aged 53 to 74 in the Copenhagen Male Study we investigated the association between ischaemic heart disease (IHD) and the Lewis blood group, assigned to chromosome 19. Among men with the Le(a-b-) phenotype, 8% had a history of non-fatal myocardial infarction, among others the frequency was 4%. The corresponding odds ratio was (95% confidence interval: CI) 1.9 (1.2-3.0) P < 0.01, men with Le(a-b-) had a risk-factor profile and pattern of disease resembling that of Reaven's syndrome X. In a subsequent prospective study 343 men with arteriosclerotic stigmas were excluded. The men had their morbidity and mortality recorded over the next 4 years. One-hundred-and-one men suffered IHD; 26 dying from IHD. In total 162 men died. Men with Le(a-b-) had an increased risk of death from IHD compared with others. Adjusted for age, relative risk (RR) (95% CI) was: 4.4 (1.9-10.3), P < 0.001, and for all causes of mortality: RR = 1.6 (1.0-2.6), P < 0.05. Men with the Le(a-b-) phenotype had an increased risk of an IHD event compared to men with other phenotypes (RR = 1.6 (0.9-2.8), P = 0.10) and a significantly higher IHD case fatality rate (RR = 2.8 (1.5-5.2), P = 0.01). The finding that the Le(a-b-) phenotype is a genetic marker of IHD risk may have implications in terms of prevention. The Le(a-b-) phenotype may also contribute to providing an explanation for the substantial ethnic differences found in the incidence of IHD. The similar risk-factor profile and pattern of disease found between Le(a-b-) men and individuals with Reaven's syndrome X is hypothesized to be due to a close genetic relationship on chromosome 19.