http://stroke.ahajournals.org/content/45/9/e177.extract?etoc
- Ulrich Dirnagl, MD
+ Author Affiliations
- Correspondence to Ulrich Dirnagl, MD, Center for Stroke Research Berlin, Charité Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany. E-mail ulrich.dirnagl@charite.de
Introduction
Sixty-five million years have passed
since mouse and man shared a common ancestor. The principles of
evolution, as well as
the scientific literature, suggest that there
are many similarities between both mammal species but also significant
differences.
Humans are definitely no 75 kg mice,1 but is it true that “the mouse model has been totally misleading for at least three major killers—sepsis, burns, and trauma,”
as the New York Times concluded after the publication of a study by Seok et al?2
By looking at transcriptional responses of blood cells, this study
found “that, although acute inflammatory stresses from
different etiologies result in highly similar
genomic responses in humans, the responses in corresponding mouse
models correlate
poorly with the human conditions and also,
one another.”
The results of the Seok et al2 study are by no means surprising or new,3
but they nevertheless carry an important message for experimental
stroke research. The authors used male mice of the C57
BL/6J strain, which is exquisitely resistant
to sepsis: more than one million-fold doses of endotoxin are required to
cause
shock in this mouse strain. The mice are
inbred and raised under specific pathogen-free conditions, so at the
time of the
study, the 8-week-old mice had a naive and
immature immune system.
In contrast, rodents are as
sensitive to focal cerebral ischemia as humans. The evolution of the
infarct and surrounding penumbra
has similar temporal and histopathologic
dynamics, and the time windows for thrombolysis after embolic stroke are
practically
…
No comments:
Post a Comment