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| Hauptseite > Publikationsdatenbank > Cell Culture Models as Alternatives to Animal Experimentation for the Testing of Neuroprotective Compounds in Stroke Research |
| Hauptseite > Publikationsdatenbank > Cell Culture Models as Alternatives to Animal Experimentation for the Testing of Neuroprotective Compounds in Stroke Research |
| Book | FZJ-2016-03825 |
;
1999
Forschungszentrum Jülich GmbH Zentralbibliothek, Verlag
Jülich
ISBN: 3-89336-250-9
Please use a persistent id in citations: http://hdl.handle.net/2128/11849
Abstract: This handbook is the result of a projeet partly financed by the German Ministry for Education, Research, Science and Technlogy (BMBF) which ran for three years from 1995 to 1998 and involved several research groups in Germany. The statement of Lord Adrian, famous for his discovery that the frequency of firing in a nerve cell is a measure of the intensity of the stimulus, quoted above is a way of ethically justifying the use of animals in research. It also contains a very important caveat. It requires us to ask ourselves carefully whether there is really $\textit{no other way}$ of conducting the research in questions. And this is the aim that we have set ourselves for our joint project. During the course of our work wo have developed and relined different cell assay techniques which can be used for investigating the effects of neuroprotective compounds in strake research. We thought it would be worthwhile to share some of the experimental details from our filldings with a wider audience. And we have therefore decided in association with the BMBF to print a handbook which summarizes these methods. But first, why have we chosen human strake as our research target? Thromboembolic stroke causes the death of nerve cells by depriving the brain of an adequate supply of oxygenated blood. The process is called cerebral ischaemia and is primarily a vascular event which leads to damage of brain tissue and impaired function. Strake is the third leading cause of death after coronary heart disease and cancer, and is an importatnt source of adult disability in industrialized nations (Bonita, 1992). Surprisingly, funding of stroke research per death by the National Institutes of Health in the United States falls well behind that of many other of these diseases (NIH, 1998). The brain depends on arterial blood for a continuous supply of oxygen and glucose. Even if blood flow is interrupted for only a few minutes, certain highly vulnerable neurons will degenerate. If the interruption is sustained, then all types of brain cells will eventually die. Fundamental to aur understanding of the pracess of cerebral ischaemia has been the presumption that brain cells do not simply die beeause of energy failure. The link betwecn ischaemia and neuronal death is considerably more complicated. Strake triggers a chain reaction of eleelrieal atld chemieal aetivity which is relatcd 10 ischaemic depolarization, the release of exeitatory amino acids and ehanges in calcium homeostasis (Matlson and Mark, 1996; Tymianski and Tator, 1996). These events act in concert to orchestrate cell death. [...]
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