The neurotrophic factors in non-neuronal tissues

Although neurotrophic factors are defined as molecules that maintain neuronal cells, they possess a range of functions outside the nervous system. For example, glial cell line-derived neurotrophic factor is essential for ureteric branching in kidney morphogenesis and for regulating the fate of stem cells during spermatogenesis. Leukemia inhibitory factor, a member of the interleukin-6 (IL-6) ciliary neurotrophic factor family, inhibits differentiation of embryonic stem cells, induces tubulogenesis in the embryonic kidney, and regulates sperm differentiation. Other IL-6 family members are important in cardiac differentiation and they have pleiotropic functions in the hematopoietic and immune systems. Although neurotrophin receptors have been found on a number of non-neuronal tissues, they represent mostly truncated receptor isoforms that are incapable of signal transduction and may have scavenger or dominant negative functions. However, several examples can be presented of essential non-neuronal functions played by neurotrophins in e.g., cardiac, hair follicle, and vascular differentiation, and the maintenance of immune cells.     

卡托普利和肾切除对肾性高血压大鼠左室心肌MHC基因转录变化的影响

用二肾一夹（２ＫＩＣ）肾性高血压大鼠模型，探讨心肌肥厚发生和逆转以及肌球蛋白重链（ｍｙｏｓｉｎｈｅａｖｙｃｈａｉｎ，ＭＨＣ）基因表达的改变。结果表明：１）２ＫＩＣ肾性高血压大鼠术后第２～１２周，动脉血压持续升高、左室重量／体重（ＬＶＷ／ＢＷ）明显升高、左心室α－ＭＨＣ基因表达明显减弱、β－ＭＨＣ基因表达明显增强；２）在术后第４周给予血管紧张素转换酶抑制剂卡托普利和术后第８周切除肾动脉狭窄侧肾脏可使２ＫＩＣ肾性高血压大鼠动脉血压下降、左心室肥厚发生逆转、抑制左心室α－ＭＨＣ基因表达减弱和β－ＮＨＣ基因表达增强。这些结果提示在２Ｋ１Ｃ肾性高血压中，动脉血压升高是左心室肥厚、左心室肌球蛋白ＭＨＣ基因表型转换的重要因素；肾素———血管紧张素系统可能参与２ＫＩＣ肾性高血压过程中的心肌肥厚和ＭＨＣ基因表型的转移。     

返流性肾病尿微量蛋白变化与肾损害的关系

目的：了解返流性肾病尿微量蛋白变化与肾损害的关系。方法：用放射免疫法对确诊为返流性肾病病儿尿β２微球蛋白（β２－Ｍ）、白蛋白（Ａｌｂ）及免疫球蛋白Ｇ（ＩｇＧ）、Ｔａｍｍ－Ｈｏｒｓｆａｌｌ蛋白（ＴＨＰ）等４项蛋白进行检测。结果：尿β２－Ｍ、Ａｌｂ、ＩｇＧ在返流性肾病的患儿均较正常组增高。重度膀胱输尿管返流的返流性肾病病儿尿ＴＨＰ明显降低，而轻度者尿ＴＨＰ未见降低。结论：返流性肾病病儿除肾小管损害外，     

Alteration of mitochondrial bioenergetics due to intravenous injection of a perfluorocarbon emulsion

Wistar albino rats were intravenously injected with 1 ml of an oxyphoretic emulsion of perfluorobutylfurane and killed 3, 7 or 30 days later. Mitochondria isolated from the liver and kidneys of treated rats showed a small decrease in the transmembrane electrical potential and a substantial depression of the rates of both ATP synthesis and ADP-stimulated respiration. These alterations in mitochondrial oxidative phosphorylation appear to be induced by perfluorocarbon and/or tensioactive molecules interacting with hydrophobic cell structures.     

全球慢性肾病防治药物研究进展

慢性肾病(chronic kidney disease,CKD)具有病因复杂、治疗难度大等特点,已成为全球性的公共卫生问题,其影响了全球约10％的人群,并可导致更高的心血管疾病和死亡的发生风险等.CKD防治的关键环节之一是阻止或延缓CKD进展.总结了CKD的流行病学、风险因素、研发投入和防治药物,以详细了解CKD的现状...     

去卵巢合并单侧输尿管结扎诱导小鼠肾脏病变的研究

为研究去卵巢合并单侧输尿管结扎引起小鼠肾脏的病理变化及可能机制,选取C57BL/6J雌性小鼠为研究对象,分别设立对照组和模型组.手术3周后,取肾脏样本.使用HE,Masson’s Trichrome两种方法进行肾石蜡切片染色,通过RT-PCR技术检测肾纤维化相关因子TGF-β,CTGF,VEGF,fibronectin,炎症因子MCP-1,RANTES,肾素-血管紧张素系统(RAS)组分肾素(renin)、肾素受体(renin receptor)、血管紧张素原(AGT)的mRNA表达.结果显示,模型组小鼠肾小球萎缩,肾小管腔隙体积增加、膨大,肾小管间质纤维化.模型组小鼠肾脏fibronectin,MCP-1,RANTES的mRNA表达都显著上调,RAS组分renin receptor的基因表达显著上调.研究表明,去卵巢合并单侧输尿管结扎通过上调肾脏肾素受体表达,诱发肾脏纤维化与炎症反应.     

用药的误区及其理论分析

使用药物是我们日常生活的一个重要部分。但是，人们对药物的使用普遍存在着误区，这些误区导致临床上产生许多药源性的疾病和不可逆的脏器损害。此文章通过对这些误区的分析，给人们正确、合理使用药物提供科学的理论依据。     

Incorporation of32P into renal phospholipids of mice during postnatal growth

Summary During the first 40 days of life the rate of incorporation of³²P into total phospholipids and into phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, sphingomyelin, diphosphatidylglycerol, phosphatidic acid and phosphatidylinositol of mouse kidney was by some 25–35% higher than in older animals. Results suggest a different involvement of cellular membranes during of normal and compensatory renal growth.     

长吻鮠肾和膀胱的组织结构

长吻鮠的肾脏由肾小体、肾小管、集合管及拟淋巴组织等构成．肾小体在肾前段最多(2．2个／mm^2)，中段次之(约1．7个／mm^2)，后段最少(约1个／mm^2)；拟淋巴组织在肾的中后段逐渐增多；肾小球直径较小，在60～78μm之间；膀胱体积远比一般真骨鱼类大，移行上皮中有大型分泌细胞，最大径达100μm．纵肌和环肌同等发达，厚280～700μm。     

中西医结合治疗原发性肾病综合症的临床研究

目的:观察中西医结合治疗原发性肾病综合症的临床疗效,并初步探讨其机理.方法:选择68例中医辨证为脾肾阳虚兼挟血瘀湿浊的PNS患者,随机分对照组33例,用标准激素治疗.治疗组35例,在标准激素治疗基础上加服中药汤剂.结果:治疗组能明显改善症状和体征,减少尿蛋白,降低血粘度及血脂水平(P均＜0.01).治疗组总有效率达91.42%,明显优于对照组78.78%(P＜0.01).