CONTROL OF CORNEAL HYDRATION AND TRANSPARENCY
控制角膜水合和透明度
基本信息
- 批准号:3255413
- 负责人:
- 金额:$ 18.47万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1978
- 资助国家:美国
- 起止时间:1978-09-01 至 1993-08-31
- 项目状态:已结题
- 来源:
- 关键词:NAD(H) phosphate adenosinetriphosphatase aldehyde reductase antioxidants bicarbonates chemical hydration chemoattractants chromatography cornea disorder cornea edema corneal endothelium corneal epithelium corneal stroma cytoskeleton diabetic ophthalmopathy electron microscopy electrophysiology enzyme inhibitors fluorescence microscopy free radicals glucose metabolism glutathione homeostasis human tissue hyperglycemia inflammation inositol intraocular fluid keratoplasty laboratory rabbit laboratory rat lactates light adverse effect membrane lipids membrane permeability membrane proteins membrane transport proteins oxidation reduction reaction peroxidation physiologic stressor pyridine nucleotide radioimmunoassay sodium potassium exchanging ATPase sorbitol stress ultraviolet radiation visual photosensitivity
项目摘要
The proposed research is designed to investigate two models of
stress in the corneal endothelium and to establish on a
quantitative basis the nature of the ion transport mechanisms in
this cell layer are responsible for maintaining corneal hydration
and transparency.
A study of the effects of ultraviolet light on the corneal
endothelium will seek to determine what is the primary site of
injury that results in an increase in corneal hydration and marked
changes in the appearance of the endothelium. It is postulated
that an oxidative mechanism, provoked by the formation of free
radicals following absorption of the high energy photons, causes
damage to enzymes or membrane proteins and lipids. Structural
changes that follow may result from alteration of cytoskeletal
elements or from release of chemotactic factors that cause
invasion of leukocytes that become attached to the endothelium.
The hypothesis will be tested by assessing metabolic changes after
UV exposure and the effects of changes in anti-oxidants and
detoxifying or protective enzymes on the corneal response to UV.
Defining the nature and origin of the structural changes will
entail examination by a number of microscopy techniques,
modification of the inflammatory response, and in vitro systems
for testing chemotaxis and leukocyte recruitment.
The diabetic study will seek in an animal model the basis for the
failure of diabetic patients to withstand intraocular surgery
without more severe corneal swelling than other patients. It is
postulated that the endothelium is compromised by the disease in
a manner which reduces the effectiveness or capacity of
defensive or maintenance mechanisms, such that the pump or
barrier functions are more vulnerable to subsequent insults. The
effects of hyperglycaemia on the concentrations of sorbitol and
inositol and upon inositol metabolism will be measured, as these
may regulate protein kinase and Na+-K+ ATPase activities, and
endothelial morphology and cell pattern will be followed to detect
weakening of the barrier characteristics. Additional stresses and
inhibitors of aldose reductase will be used to identify the key sites
of damage.
The study of ion transport in the endothelium will focus on the
absolute values of fluxes and the extent of coupling in order to
provide sound data for assessment of postulated mechanisms.
本研究旨在探讨两个模型
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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MICHAEL V RILEY其他文献
MICHAEL V RILEY的其他文献
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{{ truncateString('MICHAEL V RILEY', 18)}}的其他基金
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