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K-ras deficient mice develop thin ventricular walls and die prematurely, suggesting a potentially important role for KIAA137in heart development.
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In support of this, Igf receptor 1 KO mice develop a thin, disrupted epidermis with reduced HF abundance (Liu et al., 1993).
Heterozygotes may develop thin basement membrane disease/familial haematuria±proteinuria and sometimes renal impairment (OMIM #141200).
RESULTS: β-Secretase knockout mice develop significant retinal pathology including retinal thinning, vascular abnormalities and an increase in the age pigment, lipofuscin.
Here we show that BACE1−/− mice develop significant retinal pathology including retinal thinning, apoptosis, reduced retinal vascular density and an increase in the age pigment, lipofuscin.
These mice develop normally for a short period and then proceed to display sarcopenia, thinning of the subcutaneous fat, hair loss, hair greying, osteopenia, lordokyphosis and significantly shortened lifespan.
Transgenic female mice with gain-of-function FST, in which mouse follistatin was over-expressed, developed thin uteri and small ovaries, resulting in infertility [ 99].
Supplementary Figure 6 Pik3cdE1020K/+ mice develop IgM autoantibodies.
Aged Pten-ΔTreg mice develop non-malignant TH1 inflammation.
Four patients (28.6%) developed thin fibrin formation.
Parasite growth was monitored on Giemsa-stained thin blood films, counting parasites daily in 1,000 40,000 erythrocytes until mice developed severe disease.
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