樊均明
循证肾脏病学、糖尿病肾病、肾脏间质纤维化、腹膜透析营养和代谢研究
个性化签名
- 姓名:樊均明
- 目前身份:
- 担任导师情况:
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学术头衔:
博士生导师
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学科领域:
内科学
- 研究兴趣:循证肾脏病学、糖尿病肾病、肾脏间质纤维化、腹膜透析营养和代谢研究
樊均明,男,博士,教授,肾病学博士生导师。 1982年毕业于四川泸洲医学院,1989年获华西医科大学硕士学位。1986-1992年在云南昆明医学院肾脏内科工作,1992-1995年在中山医科大学附一院肾研所工作。1995年获中山医科大学肾脏内科学博士学位,毕业后受聘到华西医科大学附一院工作。1997-1998年赴澳大利亚蒙那什大学医学中心进行博士后研究。1998年晋升副主任医师、副教授,1999年升任硕士研究生导师,2002年破格晋升为主任医师、教授,2003年升任博士生导师。现任四川大学华西医院肾内科教授。
学术兼职:中国中西医结合学会全国青年委员;中国中西医结合肾脏病委员会全国委员;四川省中西医学会青年工作委员会主任委员;四川省中西医结合肾脏病学会副主任委员;四川省中西医结合学会副秘书长;四川省中西医结合资深专家委员会秘书;中华医学会四川肾脏病学会委员;中华医学会四川成都肾脏病学会副主任委员;《中国循证医学杂志》编委;《中国中西医结合肾病杂志》编委;《中药新药与临床药理》编委;《国外医学》(泌尿系统分册)编委;《西部医学杂志》编委;《中华实用医学杂志》编委;《中国实用内科杂志》编委;《临床肾脏病杂志》编委。
从医学23年,肾脏内科学临床、教学和研究20年,擅长糖尿病肾病、慢性肾炎、慢性肾功衰竭、尿路感染、狼疮性肾炎诊断、治疗。对循证肾脏病学、糖尿病肾病、肾脏间质纤维化、腹膜透析营养和代谢研究具有较高的造诣。作为博士后导师、博士硕士导师培养研究生45名,已毕业28名。至今申请和参与在研科研项目十五项。1996年和2001年二项申请国家自然科学基金,国家教委留学回国人员启动基金一项、省市和院校基金六项。开展中西医结合肾病研究和循证医学研究,发表中西医结合研究文章30多篇,其中MEDLIN收录文章2篇。至今发表文章160多篇,其中国外影响因子2以上杂志发表6篇,SCI、MEDLIN收录文章13篇。以我国第一作者和单位在国际肾脏病学会杂志(Kidney Int. 1999;56:1455-67)发表一文,研究细胞图片选为杂志当期封面,影响因子5.21,至今被国际外文杂志引用130次,应邀澳大利亚新西兰年会大会发言交流。参编专著八部,副主编《肾脏病诊疗手册》人民卫生出版社2000年10月第一版。至今获国家和省市科研奖8项。2004年获国际肾脏病学会2004肾脏疾病进展预防大会最佳论文奖;2003年获中华人民共和国教育部《 循证医学的引进、研究和推广》二等奖。
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樊均明, Yee-Yung Ng, Jun-Ming Fan, Wei Mu, David J. Nikolic-Paterson, Wu-Chang Yang, Tung-Po Huang, Robert C. Atkins and Hui Y. Lan
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-1年11月30日
Background. Glomerular cellular crescents consist of epithelial cells and macrophages, which can undergo an irreversible process of fibrous organization. However, the origin of the fibroblast-type cells that mediate this fibrous organization is unclear. Methods. This study examined glomerular epithelial myofibroblast transdifferentiation (GEMT) in the formation and evolution of glomerular crescents in two distinct rat models of glomerulonephritis: 5/6 nephrectomy and antiglomerular basement membrane (GBM) disease. Results. Early in the course of both disease models, and prior to crescent formation, immunohistochem-istry staining and in-situ hybridization demonstrated de novo expression of alpha-smooth-muscle actin (α-SMA), a marker of smooth muscle cells and myofib-roblasts, by glomerular parietal epithelial cells (GPEC). The expression of α-SMA by GPEC was accompanied by a loss of E-cadherin staining, a marker of epithelial cells. At this early stage of GEMT, ultra-structural studies identified the presence of character-istic actin microfilaments and dense bodies within GPEC which retained a normal epithelial morphology with apical-basal polarity and microvilli. A late stage of transdifferentiation was seen in fibrocellular cres-cents. In this case, GPEC attached to intact segments of the capsular basement membrane contained large bundles of actin microfilaments throughout the cell, and this was accompanied by a loss of polarity, micro-villi, and tight junctions. There was a significant cor-relation between the presence of α-SMA+ GPEC and glomerular crescent formation. Cellular crescents con-tained small numbers of α-SMA+ myofibroblasts. These cells become the dominant population in fibro-cellular crescents, which was associated with marked local proliferation. Relatively few α-SMA+ myofibro-blasts remained in fibrotic/organizing crescents. Most cells within cellular and fibrocellular crescents expressed transforming growth factor-β(TGF-β) and basic fibroblast growth factor (FGF-2), suggesting that these growth factors may regulate this GEMT process during the evolution of glomerular crescents. Conclusions. This study provides the first phenotypic and morphological evidence that glomerular epithelial-myofibroblast transdifferentiation participates in the formation and evolution of glomerular crescents.
glomerular crescents, glomerular epithelial cells, glomerulonephritis, myofibroblasts, trans-differentiation
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樊均明, JUN-MING FAN, YEE-YUNG NG, PRUDENCE A. HILL, DAVID J. NIKOLIC-PATERSON, WEI MU, ROBERT C. ATKINS, and HUI Y. LAN
Kidney International, Vol. 56 (1999), pp. 1455-1467,-0001,():
-1年11月30日
Transforming growth factor-β regulates tubular epithelial-myofibroblast transdifferentiation in vitro. Background. We recently found evidence of tubular epithe-lial-myofibroblast transdifferentiation (TEMT) during the de-velopment of tubulointerstitial fibrosis in the rat remnant kid-ney. This study investigated the mechanisms that induce TEMT in vitro. Methods. The normal rat kidney tubular epithelial cell line (NRK52E) was cultured for six days on plastic or collagen type I-coated plates in the presence or absence of recombinant trans-forming growth factor-j31 (TGF-β1). Transdifferentiation of tubular cells into myofibroblasts was assessed by electron mi-croscopy and by expression of α-smooth muscle actin (α-SMA) and E-cadherin. Results. NRK52E cells cultured on plastic or collagen-coated plates showed a classic cobblestone morphology. Culture in 1 ng/ml TGF-β caused only very minor changes in morphology, but culture in 10 or 50ng/ml TGF-β1 caused profound changes. This involved hypertrophy, a loss of apical-basal polarity and microvilli, with cells becoming elongated and invasive, the for-mation of a new front-end back-end polarity, and the appear-ance of actin microfilaments and dense bodies. These morpho-logjcal changes were accompanied by phenotypic changes. Double immunohistochemistry staining showed that the addi-tion of TGF-β1 to confluent cell cultures caused a loss of the epithelial marker E-cadherin and de novo expression of α-SMA. An intermediate stage in transdifferentiation could be seen with hypertrophic cells expressing both E-cadherin and α-SMA. De novo α-SMA expression was confirmed by Northern blotting, Western blotting, and flow cytometry. In particular, cells with a transformed morphology showed strong α-SMA immunostaining of characteristic microfilament struc-tures along the cell axis. There was a dose-dependent increase in the percentage of cells expressing α-SMA with increasing concentrations of TGF-β1, which was completely inhibited by the addition of a neutrafizing ant-TGF-β1 antibody. Corn
TGF-β, transdifferentiation, collagen type 1, β-smooth muscle actin, fibrosis, tubulointersfifial fibrosis.,
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樊均明, Xue Q. Yu, † Jun-Ming Fan, * David J. Nikolic-Paterson, * Nianshen Yang, † Wei Mu, * Raimund Pichler, ‡ Richard J. Johnson, ‡ Robert C. Atkins, * and Hui Y. Lan*
American Journal of Pathology, Vol. 154, No.3, March 1999,-0001,():
-1年11月30日
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