课题基金 / 基金详情

CELL MEMBRANE MICROVISCOSITY

CELL MEMBRANE MICROVISCOSITY
细胞膜微粘度
批准号:
3942060
负责人:
R KNAZEK
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

项目摘要

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中文摘要
翻译
细胞膜微粘度的变化表明 调节其受体的功能,推测是通过 改变他们重新定位到或多或少活跃的位置的能力。 1)饱和长链脂肪酸的异常积累 在遗传性疾病中肾上腺脑白质营养不良也会导致 用于培养人肾上腺皮质细胞的硬膜 在他们的存在下,需要15倍以上的ACTH才能达到 皮质醇的合成。这可能解释了这种机制 这种疾病会出现哪种肾上腺功能不全。2)棉酚 一种饮食中导致不孕不育爆发的酚类物质 中国在几个省份。这种化合物会增加 颗粒细胞膜微粘度降低 她们对卵泡刺激素的雌激素反应。更改的功能 靶组织上的促性腺激素受体可能是通过 这种不孕不育现象就会发生。3)我们已经展示了 人类精液中独特的19OH前列腺素抑制 淋巴细胞对有丝分裂原的反应是PGE2的30倍。 初步研究表明,它们可以减少 人类淋巴细胞膜的微粘度--一种现象 这可能对解释增加的 同性恋者对各种感染性因素的易感性。其他 初步研究表明,这些同样的前列腺素 使人的微粘度显著下降 膜,这一观察可能与它们在 男性生殖生理学。免疫系统之间的直接联系 生存系统和肾上腺是在 人类单核细胞被证明阐述了一种可溶的因子 刺激人肾上腺皮质细胞合成皮质醇 体外培养。初步研究表明,单核细胞和 糖尿病患者外周血粒细胞代谢花生四烯酸 一种不寻常的时尚。这些代谢物的特性是 建立和可能在微血管疾病中的作用 人们正在对糖尿病进行研究。
英文摘要
Change in the microviscosity of cell membranes were shown to modulate the functionality of their receptors, presumably by altering their ability to reorient into more or less active positions. 1) The abnormal accumulation of saturated long chain fatty acids in the inherited disease of adrenoleukodystrophy also result in stiff membranes for when human adrenocortical cells are cultured in their presence, 15 times more ACTH is needed to achieve level of cortisol synthesis. This probably explains the mechanism by which adrenal insufficiency occurs in this disease. 2) Gossypol is a dietary phenolic that has caused outbreaks of infertility in several provinces in china. This compound causes an increase in granulosa cell membrane microviscosity and thereby decreases their estrogen response to FSH. Altered functionality of gonadotropin receptors on target tissues is a likely mechanism by which this phenomenon of infertility occurs. 3) We have shown that the unique 19OH prostaglandins in human semen suppress lymphocytes' response to mitogens 30 times more than PGE2. Preliminary studies demonstrated that they reduce the microviscosity of human lymphocyte membranes, a phenomenon that may be extremely important in explaining the increased susceptability of homosexuals to various infective agents. Other preliminary studies have shown that these same prostaglandins cause a marked decrease in the microviscosity of human membranes, an observation that may be relevant to their role in male reproductive physiology. A direct link between the immune surviellance system and the adrenal gland was established when human monocytes were shown to elaborate a soluble factor that stimulates human adrenocortical cells to synthesize cortisol in vitro. Preliminary studies have indicated that the monocytes and granulocytes of diabetic patients metabolize arachidonic acid in an abnormal fashion. The identity of these metabolites is being established and the possible role in the microvascular disease of diabetes is being studied.
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