课题基金 / 基金详情

CELL BIOLOGY OF GLOMERULAR ULTRAFILTRATION

CELL BIOLOGY OF GLOMERULAR ULTRAFILTRATION
肾小球超滤的细胞生物学
批准号:
3152203
负责人:
PETER MICHAEL ANDREWS
金额:
$8.4万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1983
资助国家:
美国
项目状态:
已结题
起止时间:
1983-06-01 至 1987-02-28

项目摘要

项目成果

PETER MICHAEL ANDREWS的其他基金

相似基金

相关文献

中文摘要
翻译
调节肾小球滤过率的能力对于 肾脏功能正常。近几年来,很明显, 肾小球壁和/或通透性的显著改变 可用于超滤的表面积(即超滤 系数)可与多种重要的荷尔蒙反应, 肾毒性化合物,以及其他改变的生理状态。目前, 与肾小球细胞和形态变化有关的 这些超滤系数的变化是非常推测的。 或者是未知的。在拟议的研究中,体外和体内研究 旨在仔细评估细胞的形态反应 肾小球上皮足细胞、肾小球内皮细胞和 肾小球间皮细胞在改变超滤的情况下 慕尼黑-Wistar大鼠的系数。我们将特别注意 细胞质收缩因子、细胞骨架因子、 钙离子和前列腺素在影响超微结构变化中的作用 在这些牢房里。综上所述,相信上述研究将会 提供对不同组织所扮演的角色的重要见解 肾小球在调节滤液流动中的构成类型 穿过肾小球壁,构成其基础的细胞生物学参数 超滤系数与这些细胞的形态变化有关, 并将有助于确定许多重要化合物的作用机制 和条件。
英文摘要
The ability to regulate glomerular filtration rate is essential for the normal functioning of kidneys. In recent years, it has become evident that significant alterations in the permeability of the glomerular wall and/or surface area available for ultrafiltration (i.e. the ultrafiltration coefficient) can occur in response to a wide variety of important hormones, nephrotoxic compounds, and other altered physiological states. At present, the glomerular cells and morphological changes which are responsible for these alterations in the ultrafiltration coefficient are very speculative or unknown. In the proposed investigations, in vitro and in vivo studies are designed to carefully evaluate the morphological responses of glomerular epithelial podocytes, the glomerular endothelium, and the glomerular mesothelial cells in situations which alter the ultrafiltration coefficient in Munich-Wistar rats. Particular attention will be paid to the roles that cytoplasmic contractile elements, cytoskeletal elements, calcium ions, and prostaglandins play in affecting ultrastructural changes in these cells. Together, it is believed that the above studies will provide important insights into the roles played by the different cell types which make up the kidney glomerulus in regulating flow of filtrate across the glomerular wall, the cell biological parameters which underlie ultrafiltration coefficient related morphological changes in these cells, and will help define the mechanisms of action of many important compounds and conditions.
期刊论文(9)
专著(0)
科研奖励(0)
会议论文
Dietary protein prior to renal ischemia dramatically affects postischemic kidney function.
肾缺血前的膳食蛋白质显着影响缺血后的肾功能。
DOI: 10.1038/ki.1986.184
发表时间: 1986
期刊: Kidney international
影响因子: 19.6
作者: [Andrews,PM, Bates,SB]
通讯作者: Bates,SB
Dietary protein prior to renal ischemia and postischemic kidney function.
肾缺血前和缺血后肾功能的膳食蛋白质。
DOI: --
发表时间: 1987
期刊: Kidney international. Supplement
影响因子: --
作者: [Andrews,PM, Bates,SB]
通讯作者: Bates,SB
Dietary protein as a risk factor in gentamicin nephrotoxicity.
膳食蛋白质是庆大霉素肾毒性的危险因素。
DOI: 10.3109/08860228709047650
发表时间: 1987
期刊: Renal failure
影响因子: 3
作者: [Andrews,PM, Bates,SB]
通讯作者: Bates,SB
Effects of dietary protein on uranyl-nitrate-induced acute renal failure.
膳食蛋白质对硝酸铀酰诱导的急性肾衰竭的影响。
DOI: 10.1159/000184167
发表时间: 1987
期刊: Nephron
影响因子: 2.5
作者: [Andrews,PM, Bates,SB]
通讯作者: Bates,SB
共 6 条
    Non-Invasive Evaluation of Transplant Kidney using OCT
    • 批准号:
      8696002
    • 项目类别:
    • 资助金额:
      $52.08万
    • 财政年份:
      2014
    • 负责人:
      PETER MICHAEL ANDREWS
    • 依托单位:
    Non-Invasive Evaluation of Transplant Kidney using OCT
    • 批准号:
      8822287
    • 项目类别:
    • 资助金额:
      $38.89万
    • 财政年份:
      2014
    • 负责人:
      PETER MICHAEL ANDREWS
    • 依托单位:
    TSCM ASSESSMENT OF COLD STORED KIDNEYS
    • 批准号:
      2536607
    • 项目类别:
    • 资助金额:
      $10.0万
    • 财政年份:
      1998
    • 负责人:
      PETER MICHAEL ANDREWS
    • 依托单位:
    PROTECTING KIDNEYS FROM ISCHEMIC INJURY
    • 批准号:
      3152218
    • 项目类别:
    • 资助金额:
      $9.18万
    • 财政年份:
      1983
    • 负责人:
      PETER MICHAEL ANDREWS
    • 依托单位:
    海外基金