Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.     

持续性非卧床腹膜透析腹膜炎的致病菌及其耐药性

目的：探讨持续性非卧床腹膜透析（CAPD）腹膜炎的致病菌及其耐药性。方法：回顾性分析109例CAPD腹膜炎的临床表现、致病菌、耐药性和转归情况。结果：43例培养阳性,透出液培养阳性率为39．4％,其中11例为革兰阳性球菌,19例为革兰阴性杆菌,13例为真菌。主要的革兰阴性杆菌包括肺炎克雷白氏杆菌、大肠杆菌、不动杆菌和铜绿假单胞菌。革兰阴性杆菌对氨苄西林的耐药率最高,达85．7％;对阿米卡星的耐药率最低,为17．6％;庆大霉素的耐药率为44．4％;而头孢他啶的耐药率也高达42．9％。所有革兰阳性球菌对万古霉素敏感,大部分（71．4％）对头孢唑林敏感。腹腔内用抗真菌药对真菌性腹膜炎疗效不佳。腹膜炎CAPD的退出率为20．2％（22／109）。结论：革兰阴性杆菌腹膜炎比例有所增加,致病菌对庆大霉素和头孢他啶的耐药性较高,而对阿米卡星较敏感,宜作为经验用药。     

川芎嗪抗腹膜间皮细胞损伤的实验研究

目的：观察含川芎嗪腹透液体外对腹膜间皮细胞活力,细胞增殖的影响。方法：分离,培养大鼠腹膜间皮细胞,用细胞计数法,四唑氨蓝（MTT）法,乳酸脱氢酶（LDH）法检测腹膜间皮细胞活力,细胞增殖能力。结果：培养的腹膜间皮细胞暴露于常规使用的4．25％高糖透析液30min后,间皮细胞数量显降低,MTT法示OD值显低于正常对照组,LDH释放增加,提示间皮细胞活力降低,增殖受到显抑制,加入低剂量川芎嗪后,间皮细胞数,MTTOD值较之单纯高糖透析液组均显增高,LDH显降低,但随着剂量的加大,川芎嗪的上述作用减低乃至消失,结论：适当剂量的川芎嗪能对抗常规腹透液引起的间皮细胞抑制和损伤,从而具有保护间皮细胞的作用。     

肾素血管紧张素系统阻断的发展与糖尿病肾治疗的新视点

2003年,国际肾脏病学会(ISN)和国际糖尿病联盟(IDF)基于糖尿病和糖尿病肾病(DN)在全球流行所带来的严重性,共同向世界发出了迅速采取行动的呼吁:Diabetes and kidney disease:time to act.如今,7年过去后,人类面对糖尿病和DN危害的挑战更趋严峻.全国糖尿病流行病学调查(2007-2008)结果显示,在我国20岁以上的人群中,糖尿病男女性的患病率分别达.10.6%和8.8%,总体糖尿病患病率为9.7%[1].科学家预测从2007年至2025年,全球糖尿病患者将从24 600万增加到38 000万[2],并且.无论在发达国家或发展中国家,DN已成为终末期肾病(ESRD)的主要病因.故此,由ISN和国际肾脏基金会(IFKF)联合发起的世界肾脏日把2010年的主题定为Diabetic kidney disease-act now or pay later,再次向世人发出了警钟[3].     

Fractalkine/CX3CR1介导的肾小管上皮细胞对巨噬细胞的趋化作用

巨噬细胞浸润的程度与肾功能的丧失和组织学的损害密切相关,是预测肾脏疾病转归的重要指标之一[1]。Fractalkine是趋化因子CX3C亚家族的惟一成员[2],其受体CX3CR1主要表达在单核巨噬细胞、T细胞和NK细胞上[3],介导fractalkine表达细胞对上述细胞的趋化作用。本研究意在观察     

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??Abstract??There have been studies showing the importance of genetic risk factors to the pathogenesis of IgAN.Recent years??the rise of genome-wide association study (GWAS) provided the new tactics of genetics study.Our GWAS in Chinese Han population for IgAN identified two new susceptibility loci at chromosome loci 17p13 and 8p23.In addition??we confirmed two previously reported susceptibility loci at 22q12 and MHC region??and found several genes were associated with the clinical phenotypes of IgAN.GWAS has important scientific significance and practical value for revealing the genetic pathogenesis of IgAN and further exploring new targets of IgAN intervention.     

急进性肾炎12例临床分析

回顾性总结了１２例急进性肾炎（ＲＰＧＮ）患者的临床表现，实验室及病理资料及对不同治疗方法的反应。结果显示：原发性ＲＰＧＮ９例、免疫球蛋白Ａ肾病、系统性红斑狼疮、Ｇｏｏｄ－Ｐａｓｔｕｒｅ综合征各１例。１２例患者均表现不同程度的蛋白尿、血尿、，其中４例表现为肾病综合征（ＮＳ），４例呈发作性肉眼血尿，７例血压增高；３例经糖皮质激素、环磷酰胺冲击或血浆置换治疗后肾功能基本恢复，其余７例依赖长期的存活，２例