Comparative analysis of CreER transgenic mice for the study of brain macrophages: A case study

Conditional mutagenesis and fate mapping have contributed considerably to our understanding of physiology and pathology. Specifically, Cre recombinase-based approaches allow the definition of cell type-specific contributions to disease development and of inter-cellular communication circuits in respective animal models. Here we compared Cx₃cr1^CreER and Sall1^CreER transgenic mice and their use to decipher the brain macrophage compartment as a showcase to discuss recent technological advances. Specifically, we highlight the need to define the accuracy of Cre recombinase expression, as well as strengths and pitfalls of these particular systems that should be taken into consideration when applying these models.     

个体化护理在结肠造口术护理中的作用

目的探讨个体化护理在结肠造口术中的作用。方法对我院2005～2008年36例结肠造口术患者手术前和手术后护理经验进行总结。结果36例患者恢复良好,无严重并发症和心理疾患的发生。结论以人为本的个体化护理是结肠造口手术成功的重要影响因素。     

A Binary Cre Transgenic Approach Dissects Microglia and CNS Border-Associated Macrophages

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大鼠海马83 ku蛋白诱导神经干细胞向乙酰胆碱酯酶阳性神经元的定向分化

背景:神经干细胞的临床应用还尚待时日,现阶段需要解决如何诱导神经干细胞分化为特定表型的神经元以替代丢失、变性的神经元细胞.目的:探讨大鼠海马组织83 ku蛋白对神经干细胞向乙酰胆碱酯酶阳性神经元分化的作用.设计、时间及地点:细胞学体外对照观察,于2003-10/2008-04在南通大学医学院完材料:清洁级SD大鼠12只,17 d龄SD胎鼠多只,均由南通大学实验动物中心提供.方法:取6只正常大鼠及6只切割海马伞后14 d大鼠的海马组织制成匀浆,进行非变性聚丙烯酰胺凝胶电泳,根据染色结果切取含有83 ku差异蛋白条带进行电洗脱,定量后调整蛋白浓度为300 mg/L.取胎鼠前脑组织,体外分离培养神经干细胞,设立3组:空白对照组加入单纯DMEM/F12无血清培养基;83 ku蚩白正常组、83 ku蛋白切割组分别加入含10 mg/L来自正常/割海马伞大鼠海码组织83 ku蛋白的DMEM/F12无血清培养基,诱导12 d.主要观察指标:用乙酰胆碱酯酶组织化学染色榆测神经干细胞分化为乙酰胆碱酯酶阳性神经元的情况.结果:诱导12d后,83 ku蛋白切割组乙酰胆碱酯酶阳性神经元较多,胞体大且分化较好,突起粗且长;83 ku蛋白正常组乙酰胆碱酯酶阳性神经元较少,胞体小,突起短;空白对照组仅见少量乙酰胆碱酯酶阳性神经元.组间乙酰胆碱酯酶阳件神经元数比较差异有显著性意义(P＜0.05),83 ku蛋白切割组＞83 ku蛋白正常组＞空白射照组.结论:大鼠海马组织中83 ku蛋白可成功诱导神经干细胞定向分化为乙酰胆碱酯酶阳性神经元.     

复方柠烯乳剂灌注治疗肝胆管术后残留结石

本文报告复方柠烯乳剂治疗３１例肝胆管结石术后残留结石的结果。３１例中肝内外胆管兼有结石的２０例，肝内胆管结石８例，肝外胆管结石３例，总治愈率６７．７％，总有效率１００％。作者认为柠烯乳剂是目前溶石中高效、无毒、价廉的较理想药物，尤适用于残石位置较高、体积较大、数量较多而又难以用器械或手术清除的胆管残留结石。     

NKG2D ligands mediate immunosurveillance of senescent cells

Cellular senescence is a stress response mechanism that limits tumorigenesis and tissue damage. Induction of cellular senescence commonly coincides with an immunogenic phenotype that promotes self-elimination by components of the immune system, thereby facilitating tumor suppression and limiting excess fibrosis during wound repair. The mechanisms by which senescent cells regulate their immune surveillance are not completely understood. Here we show that ligands of an activating Natural Killer (NK) cell receptor (NKG2D), MICA and ULBP2 are consistently up-regulated following induction of replicative senescence, oncogene-induced senescence and DNA damage - induced senescence. MICA and ULBP2 proteins are necessary for efficient NK-mediated cytotoxicity towards senescent fibroblasts. The mechanisms regulating the initial expression of NKG2D ligands in senescent cells are dependent on a DNA damage response, whilst continuous expression of these ligands is regulated by the ERK signaling pathway. In liver fibrosis, the accumulation of senescent activated stellate cells is increased in mice lacking NKG2D receptor leading to increased fibrosis. Overall, our results provide new insights into the mechanisms regulating the expression of immune ligands in senescent cells and reveal the importance of NKG2D receptor-ligand interaction in protecting against liver fibrosis.