小儿喘咳液对哮喘豚鼠肺超微结构变化的电镜观察

利用透射式电子显微镜观察小儿喘咳液对过敏性哮喘豚鼠肺超微结构变化情况。结果显示:连续雾化吸入卵清蛋白后第1d肺毛细血管壁充血并挤压毛细血管壁,第8d肺毛细血管壁增厚,胶原纤维增生。而用小儿喘咳液连续治疗7d后肺毛细血管壁增厚程度减轻,无胶原纤维增生。证明小儿喘咳液对哮喘有良好的治疗效果。     

高效液相色谱法测定七叶莲胶囊中延胡索酸的含量

目的:建立七叶莲胶囊中延胡索酸的HPLC含量测定方法.方法:采用C18色谱柱,流动相:乙腈-0.4%磷酸二氢钾溶液(20∶80),检测波长 210 nm.结果:在 0.010 5～0.084 μg 范围内,延胡索酸对照品浓度与峰面积呈良好的线性关系,r＝0.999 4,样品的平均回收率为99.87%,RSD＝1.21%.结论:采用HPLC法测定七叶莲胶囊中延胡索酸的含量,方法简便易行,结果可靠.     

海参猴桃液辅以少量rIL-2对免疫杀伤细胞活性的正向调节研究

目的 :探讨用中药海参猴桃液 (SSAP)辅以基因重组人白细胞介素 2 (rIL -2 )体外培养扩增、激活免疫杀伤细胞LAK的机理 ,观察SSAP辅以少量rIL -2能否提高及在多大程度上提高LAK细胞的杀瘤活性。方法 :通过提取健康供血者的外周血单个核细胞作为待培养细胞 ,设空白对照组 (加等量生理盐水 )、阳性对照组 (1 0 0 0U/mlrIL -2 1ml)、实验 1组 (1 0 0 0U/mlrIL -2 0 .5ml +30 0 0 μg/mlSSAP 1ml)、实验 2组 (1 0 0 0U/mlrIL -20 .1ml+30 0 0 μg/mlSSAP 1ml) ,4组在不同条件下培养LAK细胞 ,分别用H -TdR释放法检定其体外对人肝癌BEF -740 4杀伤活性。结果 :30 0 0 μg/ml的SSAP +1 0 0 0U/mlrIL -20 .1ml在培养第 3天便能测出杀伤活性 ,第 9天达峰值 [杀瘤率 (75 .5± 1 3.6 ) % ],杀瘤活性与 1 0倍量rIL -2单独诱导激活的LAK细胞杀瘤活性相近 [杀瘤率 (92 .9± 2 1 .3) % ],两组比较无显著性差异 (P >0 .0 5 ) ,而且杀瘤活性持续 1 8天。结论 :SSAP辅以少量的rIL -2能大量扩增激活LAK细胞 ,增强其对肿瘤细胞的杀伤力 ,更重要的意义在于获得的LAK细胞杀伤力强大而持久 ,同时可减少rIL -2的用量     

Epidermal Neural Crest Stem Cells (EPI-NCSC) and Pluripotency

This article serves three purposes. We summarize current knowledge of the origin and characteristics of EPI-NCSC, review their application in a mouse model of spinal cord injury, and we present new data that highlight aspects of pluripotency of EPI-NCSC. EPI-NCSC are multipotent stem cells, which are derived from the embryonic neural crest and are located in the bulge of hair follicles. EPI-NCSC can undergo self-renewal and they are able to generate all major neural crest derivatives, including neurons, nerve supporting cells, smooth muscle cells, bone/cartilage cells and melanocytes. Despite their ectodermal origin, neural crest cells can also generate cell types that typically are derived from mesoderm. We were therefore interested in exploring aspects of EPI-NCSC pluripotency. We here show that EPI-NCSC can fuse with adult skeletal muscle fibers and that incorporated EPI-NCSC nuclei are functional. Furthermore, we show that adult skeletal muscle represents an environment conducive to long-term survival of neurogenic EPI-NCSC. Genes used to create induced pluripotent stem (iPS) cells are present in our EPI-NCSC longSAGE gene expression library. Here we have corroborated this notion by real-time PCR. Our results show similarities in the expression of Myc, Klf4, Sox2 and Lin28 genes between EPI-NCSC and embryonic stem cells (ESC). In contrast there were major differences in Nanog and Pou5f1 (Oct-4) expression levels between EPI-NCSC and ESC, possibly explaining why EPI-NCSC are not tumorigenic. Overall, as embryonic remnants in an adult location EPI-NCSC show several attractive characteristics for future cell replacement therapy and/or biomedical engineering: Due to their ability to migrate, EPI-NCSC can be isolated as a highly pure population of multipotent stem cells by minimally-invasive procedures. The cells can be expanded in vitro into millions of stem cells/progenitors and they share some characteristics with pluripotent stem cells without being tumorigenic. Since the patients’ own EPI-NCSC could be used for autologous transplantation, this would avoid graft rejection.     

Direct inhibition of rat leydig cell function by tamoxifen

The effects of tamoxifen on rat testicular steroidogenesis were studied using dispersed interstitial cells. Tamoxifen significantly inhibited LH-, and 8-bromo-adenosine 3′,5′-monophosphate (8-bromo-cyclic AMP)-stimulated testosterone synthesis in a dose-dependent manner. Tamoxifen (10^?5M) also reduced LH-stimulated cyclic AMP formation. The addition of equimolar concentrations of 17β-estradiol or tamoxifen separately to interstitial cells resulted in similar inhibition of LH-stimulated testosterone synthesis. When equimolar concentrations of 17β-estradiol and tamoxifen were added concomitantly to interstitial cells, the inhibition was additive. Present studies demonstrate that tamoxifen has direct inhibitory effects on testicular steroidogenesis: both at the plasma membrane resulting in decreased cyclic AMP formation and also at steps subsequent to cyclic AMP.