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141.
应用细胞原位杂交技术,观察经重组小鼠白细胞介素-19(IL-1β)处理后的体外培养的新生1d大鼠中脑黑质神经元c-jun基因的表达.结果显示,培养的黑质细胞多为酪氨酸羟化酶阳性神经元,IL-1β可诱导体外培养的黑质神经元c-junmRNA表达,高水平的表达出现在IL-1β处理后2~4h。说明IL-1β有兴奋黑质神经元的作用,并提示黑质神经元上可能存在IL-1β受体. 相似文献
142.
乳腺癌ER,PR状态与细胞超微结构变化的形态定量分析 总被引:1,自引:0,他引:1
用免疫组化PAP法检测30例乳腺癌雌激素受体(ER)和孕激素受体(PR),从中选取ER、PR阳性者(E^+P^+)6例,阴性者(E^-P^-)5例作透射电镜观察,对部分细胞器连接的变化进行形态定量分析。结果E^-P^-组癌细胞内线粒体、粗面内质网及溶酶体的含量明显高于E^+P^+组,且差异有显著性(P<0.05,0.01,0.01);E^-P^-组细胞间的桥粒及镶嵌连接有减少趋势,但差异无显著性 相似文献
143.
食管癌三维适形放射治疗疗效的Meta分析 总被引:6,自引:0,他引:6
目的分析三维适形放射治疗技术(3-DCRT)治疗食管癌的疗效和放射毒性反应。方法检索国内有关数据库查找符合条件的临床随机对照试验,采用Meta分析方法,对国内公开发表的有关3-DCRT治疗食管癌的临床随机对照试验研究文献进行综合分析,在RevMan4.2.7软件中统计分析相应的研究指标。结果有8项独立的临床随机对照试验研究进入了本次meta分析。3-DCRT组的近期疗效,1、2、3年局控率及1、2、3年生存率均优于对照组(p〈0.01)。两组毒副反应的差异无统计学显著性意义。结论3-DCRT治疗食管癌的近期疗效优于常规放射治疗方法,远期疗效和毒副反应有待进一步观察随访和研究。 相似文献
144.
Objective: To investigate the ultra structure of amelanotic melanocytes (AMMC). Methods: The hair follicles obtained from normal human scalp by 0.50% collagenase type V treatment were washed with 0.1mol/L phosphate buffer salt (PBS). Hair-follicle cell suspensions were prepared by trypsin treatment and cultured in melanocyte medium. Remaining keratinocytes were removed by differential trypsinization. 100μg/ml geneticin was used to eliminate the contaminating fibroblasts. At third passage, the cells were trypsinized, and then washed in phosphate-buffered saline and processed for transmission electron microscopy. Results: Under transmission electron microscope, the cultured cells showed round or oval shape, with single large nuclear and the karyotheca were double deck. There were obvious euchromosome within the nucleus, and sparse heterochromosome. There were various organelles in the cytoplasm, including plentiful melanosomes with nearly similar size, mitochondria, rough endoplasmic reticule (RER) and ribosome. The electron density granules in most of the melanosomes disposed along concentric circularities. Golgi apparatus in the cells was inconspicuous. Conclusion: The ultra structure of AMMC from human hair follicles is different from that of epidermal melanocytes, and these characteristics determine the functional immature of AMMC. 相似文献
145.
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147.
人Nanog基因的克隆及其在COS-7L细胞中的表达 总被引:2,自引:0,他引:2
目的 :克隆人Nanog基因 ,构建其真核表达载体 ,并观察其在哺乳动物细胞COS 7L中的表达。方法 :利用HE2 93细胞的人基因组DNA为模板 ,以LA PCR技术 ,扩增Nango的基因 ,定向克隆到带Flag标签的pCMV载体中 ,测序后 ,挑选序列正确的真核表达质粒pFlag Nanog转染COS 7L细胞。用抗Flag标签的抗体 ,进行Westernblot和间接免疫荧光染色法检测Nango蛋白的表达。结果 :从人基因组DNA中克隆到序列正确的Nanog全长编码序列。所构建的Nanog质粒在COS 7L细胞中获得高效表达。结论 :人Nanog基因的克隆、真核表达载体的构建及在COS 7L中的表达均获得成功 ,为进一步研究其功能 ,尤其是探讨其在神经干细胞中的作用奠定了基础。 相似文献
148.
149.
Yu G Boone T Delaney J Hawkins N Kelley M Ramakrishnan M McCabe S Qiu WR Kornuc M Xia XZ Guo J Stolina M Boyle WJ Sarosi I Hsu H Senaldi G Theill LE 《Nature immunology》2000,1(3):252-256
We report that the tumor neurosis factor homolog APRIL (a proliferation-inducing ligand) stimulates in vitro proliferation of primary B and T cells and increases spleen weight due to accumulation of B cells in vivo. APRIL functions via binding to BCMA (B cell maturation antigen) and TACI (transmembrane activator and CAML-interactor) and competes with TALL-I (also called BLyS or BAFF) for receptor binding. Soluble BCMA and TACI specifically prevent binding of APRIL and block APRIL-stimulated proliferation of primary B cells. BCMA-Fc also inhibits production of antibodies against keyhole limpet hemocyanin and Pneumovax in mice, indicating that APRIL and/or TALL-I signaling via BCMA and/or TACI are required for generation of humoral immunity. Thus, APRIL-TALL-I and BCMA-TACI form a two ligands-two receptors pathway involved in stimulation of B and T cell function. 相似文献
150.
Anti-RMA: a murine monoclonal antibody that activates rat macrophages. I. Distribution and characterization of the RMA antigen. 总被引:2,自引:0,他引:2
M Yamin D Lazarus E E Schneeberger K McCarthy W J Xia R Kradin 《American journal of respiratory cell and molecular biology》1990,2(2):207-215
Activated macrophages participate in inflammation by eliminating foreign cells, promoting wound healing, and modulating the immune response. A murine monoclonal antibody, designated anti-rat macrophage activator (RMA), was raised against alveolar macrophages (AM) activated with interferon-gamma (IFN-gamma) and phorbol myristate acetate (PMA). The RMA antigen is expressed by resident macrophages but not by other cells. Binding to AM by anti-RMA is not competitively inhibited by the murine monoclonal antibodies MRC OX-41, OX-42, and OX-43. Surface membrane expression of RMA antigens is upregulated by lipopolysaccharide, PMA, and tumor necrosis factor-alpha but not by IFN-gamma. Stimulation of AM with anti-RMA yields distinct ultrastructural alterations, as well as de novo protein and DNA synthesis. Immunoprecipitation of [35S]methionine metabolically labeled AM yields a 120 kD protein by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) that is not altered by chemical reduction. We conclude that the RMA antigen is macrophage specific and that binding of anti-RMA to AM promotes functional activities in a subset of these cells. 相似文献