The availability of gene-disrupted (knockout) mice has allowed an intensive investigation of specific immunological parameters that are associated with disease in the murine models.
In addition, these mice display poor survival and a markedly reduced capacity for experimental clot lysis.
Furthermore, no disease could be transmitted from these mice to either transgenic or non-transgenic mice.
However, it is now clear from classical experiments in mice and from examples of human genetic disease that this is not the case.
More than half of them, however, used mice.
Modelling coxsackie-virus infection in pregnant mice in long-term experiment.
Mtmr2-null mice also have defects in spermatogenesis, which become apparent from 3 to 4 weeks of age.
Homozygous -thalassaemia is embryonic lethal in mice, since the globin switch occurs in utero.
