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The normal mice developed a fatty liver and became resistant to insulin.
The severely septic mice developed a mixed respiratory and metabolic acidosis with hyperlactataemia.
The compound also acted on the pancreas, meaning the mice developed a mild form of diabetes and lost weight.
The majority of transplanted mice developed a progressive pancytopenia with histopathological features of a myelodysplastic syndrome (MDS)–like disorder.
In the initial phase of disease, mice developed a specific Th1-driven immune response independent of inoculum concentration.
Most importantly, the surviving double knockout (FancD2−/−Aldh2−/−) mice developed a typical FA phenotype with various malformations, progressive bone marrow failure, and death due to leukemia.
Treated mice developed a profound yet transient elevation of multilineage hematopoiesis, which showed morphologic features of a chronic myeloproliferative disorder (CMPD) with progressive pancytopenia.
Lck-GM-CSF transgenic mice developed a disseminated histiocytosis and had increased circulating IL-17 producing T helper cells related cytokines.
Both lines of mice have significant increases in dermal vasculature but only the KC-Tie2-overexpressing mice developed a cutaneous psoriasiform phenotype.
Surprisingly, uko/3cv mice developed a much milder phenotype.
The histological analysis demonstrated that the transgenic mice developed a kidney disease similar to human FSGS.
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