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@BOOK{Carter:811337,
      key          = {811337},
      editor       = {Carter, Adrian J. and Kettenmann, Helmut},
      title        = {{C}ell {C}ulture {M}odels as {A}lternatives to {A}nimal
                      {E}xperimentation for the {T}esting of {N}europrotective
                      {C}ompounds in {S}troke {R}esearch},
      volume       = {3},
      address      = {Jülich},
      publisher    = {Forschungszentrum Jülich GmbH Zentralbibliothek, Verlag},
      reportid     = {FZJ-2016-03825},
      isbn         = {3-89336-250-9},
      series       = {Schriften des Forschungszentrums Jülich. Reihe
                      Lebenswissenschaften / Life Science},
      pages        = {145 S.},
      year         = {1999},
      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. [...]},
      cin          = {PTJ-BIO},
      cid          = {I:(DE-Juel1)PTJ-BIO-20090406},
      pnm          = {899 - ohne Topic (POF3-899)},
      pid          = {G:(DE-HGF)POF3-899},
      typ          = {PUB:(DE-HGF)3},
      url          = {https://juser.fz-juelich.de/record/811337},
}