体外培养人增生性瘢痕成纤维细胞胶原合成及结缔组织生长因子的表达

目的　探讨结缔组织生长因子在人增生性瘢痕发病机制中的作用。方法　体外培养人正常皮肤和增生性瘢痕成纤维细胞 ,通过H3 脯氨酸掺入法检测细胞胶原合成 ,通过免疫细胞化学染色和逆转录聚合酶链反应检测细胞结缔组织生长因子蛋白质和mRNA的表达。结果　和正常皮肤成纤维细胞相比 ,增生性瘢痕成纤维细胞的胶原合成和结缔组织生长因子蛋白质及mRNA的表达均显著增高 (P <0 0 1)。结论　结缔组织生长因子可能在增生性瘢痕纤维化过程中发挥重要促进作用。     

山谷型垃圾填埋场渗滤液场内收集管网系统的设计计算方法研究

以苏州七子山垃圾填埋场为背景，采用理论分析的方法，探讨山谷型垃圾填埋场合理的渗滤液收集系统的形式和定量计算方法。     

垃圾填埋场渗沥液处理工程环境监理要点

分析并总结了垃圾填埋场渗沥液处理工程环境监理要点,即制订切实的监理方案,对工程的关键部位、 关键工序做好巡视、旁站监理工作,在实施过程中做好水土保持、生态保护、移民迁移的监理工作等     

Modeling the pharmacokinetics and pharmacodynamics of dexamethasone in depressed patients

Summary Changes in time course effected by cortisol suppression and the relationship of these changes to the plasma dexamethasone concentration of suppressor and non-suppressor patients are described in this report on a combined pharmacokinetic-pharmacodynamic model.Thirteen depressed patients (8 suppressors and 5 non-suppressors) received an intravenous dose (1.5 mg) of dexamethasone. The drug-induced effect changes are found to lag behind, in time, the plasma drug level changes. To accurately relate the temporal relationship of effect changes to plasma dexamethasone levels, a pharmacodynamic model (sigmoid-Emax) was combined with a pharmacokinetic model that incorporated an effect compartment. The magnitude of the time-lag was quantified by the half-time of equilibration between concentrations in the hypothetical effect compartment and the plasma dexamethasone levels (t_&frac;k_eo).The t_&frac;k_eo of the nonsuppressing group was about 50 of that of the suppressing group, indicating that for a given plasma level the onset and termination of effect for the nonsuppressing group is about two times more rapid than for the suppressing group. Moreover, the model can estimate the effect-site concentration that causes one-half of the maximal predicted effect (EC₅₀), a measure of an individual's sensitivity to dexamethasone. The receptor sensitivity (as determined from the EC₅₀ ratio) of the suppressing group was about twice that of the nonsuppressing group.     

解放军医学图书馆电子阅览室的技术特点

从阅览室网络拓扑结构、硬盘保护、网络控制、网址限制及视频点播等几个方面对电子阅览室采用技术的特点逐一做了简要介绍,并以此阐明通过综合管理,使阅览室各计算机能够正常、安全的运行,从而达到既可为读者提供优质服务又可保证系统安全的目的.     

Effect of Sirpα1 on the expression of nuclear factor-kappa B in hepatocellular carcinoma

BACKGROUND:Signal regulatory protein alpha1(Sirpα1) is a member of Sirps families containing four immunoreceptor tyrosine-based inhibitory motifs(ITIMs) domains in the cytoplasm of and an activated substrate of receptor tyrosine kinase(RTK),that negatively regulates the RTK-dependent cell proliferating signal transduction pathway.Previously we found that Sirpα1 was closely associated with the occurrence and development of hepatocellular carcinoma(HCC)as well as liver regeneration.Since it is unclear about the regulatory mechanisms,we established the cell line transfected Sirpα1 gene and preliminarily clarified the mechanisms by which Sirpα1 negatively regulates the carcinogenesis and development of HCC. METHODS:Liver cancer Sk-Hep1 cell was respectively transfected with plasmids of pLXSN,pLXSN-Sirpα1 and pLXSN-Sirpα1Δ4Y 2 ,screened with the drug of G418(1200 μg/ml),and various transfected Sk-Hep1 cell lines were obtained.The protein expressions of P65,P50,IκBα,cyclin D1 and Fas in various Sk-Hep1 cell lines were determined by Western blotting,and P65 and P50 were localized by the immunofluorescence technique. RESULTS:Sirpα1 could significantly upregulate the protein expression of IκBα(vs.other cell lines,P<0.05) in the Sk-Hep1 cell,and downregulate the protein expressions of P65,P50 and cyclin D1(vs.other cell lines, P<0.05)in the Sk-Hep1 cell.P65 protein expression was mainly localized in the cytoplasm in the pLXSN Sk-Hep1 cell,and in the nucleus of the Sk-Hep1 cell with mutantSirpα1Δ4Y 2 ,but in nucleus of the Sk-Hep1 cell with wild Sirpα1.P50 protein expression was localized in the cytoplasm and nucleus of the pLXSN Sk-Hep1 cell,but in the nucleus of the Sk-Hep1 cell with wild Sirpα1 and mutant Sirpα1Δ4Y 2 plasmid. CONCLUSIONS:Sirpα1 might negatively regulate and control the abnormal proliferation of liver cancer cells by influencing the protein content and localization of nuclear factor-kappa B,then influence the expression of cyclins such as cyclin D1 in the signal transduction pathway.It may be one of the important mechanisms by which Sirpα1 negatively regulates the carcinogenesis and development of HCC.     

Editorial

Aim: Wall stress‐independent signalling pathways were studied for endothelin‐1 (ET‐1)‐induced c‐fos expression in rat intact mesenteric small arteries. Methods: Arteries were kept unmounted in Krebs buffer, equilibrated for 1 h and stimulated with vasoactive substances for 15–60 min. The c‐fos mRNA expression was determined by real‐time polymerase chain reaction. Results: Stimulation with fetal bovine serum (FBS), phorbol 12‐myristate 13‐acetate (PMA) and ET‐1 caused about a doubling of c‐fos mRNA. The ET‐1‐induced c‐fos expression was steady (15–60 min) and was inhibited by the inhibitor of the ET_A receptor, BQ‐123. Platelet‐derived growth factor‐B, angiotensin II and U46619 did not cause increased c‐fos mRNA levels. The broad specificity inhibitor staurosporine inhibited the response to ET‐1, but inhibitors of Rho‐A kinase and phosphatidylinositol 3‐kinase had no effect. However, inhibitors to tyrosine kinases, the MAP kinases [extracellular signal‐regulated kinase 1/2 (ERK1/2), c‐Jun amino‐terminal kinase, p38], and to conventional protein kinase C showed no inhibition. Consistent with these findings, ET‐1 did not cause activation of ERK1/2, a finding also seen in vessels held under pressure. In contrast, ET‐1‐induced c‐fos expression was inhibited by the calcium chelator BAPTA, suggesting a role for intracellular calcium. This possibility was supported by the finding that raising the extracellular K⁺ concentration caused increased expression of c‐fos in a concentration‐dependent manner. Conclusion: The results suggest that in the absence of wall stress, ET‐1 is able to induce increased expression of c‐fos independent of traditional growth pathways, such as MAP kinase. The mechanism appears to be calcium‐dependent.     

垃圾处置场填埋作业区整体布局的完善设计

目的：完善上海市老港垃圾处置场，有效地缓解“垃圾包围城市”的局面和城市垃圾出路难的问题。方法：对老港场的整体布局进行完善设计．结果：在老港场完成1期工程的基础上，2期工程的设计相应增加了填埋区的供电、供水，修筑隔堤、道路、污水处理等土建设施和运输车辆、填埋作业机械配套等，并增加了环境保护措施，如污水收集和处理系统，沼气导排，营造绿化隔离带等．