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The inducible character of our HGF mouse model demonstrates that prenatal development is the specific stage influenced by activation of Met signalling.
The established transgenic mouse model demonstrates that adipose tissue produced hSAA enters the circulation, resulting in elevated plasma levels of hSAA.
In vivo mouse model demonstrates suppressed E. coli and S. pneumoniae clearance following acid aspiration.
In contrast, the recently described MC2R knockout mouse model demonstrates classical adrenal failure with both glucocorticoid and mineralocorticoid deficiency (8).
The mouse model demonstrates unequivocally that ASPP2 is a tumour suppressor that functions as an activator of the tumour suppressor function of p53.
The EAF2−/−VHL+/− mouse model demonstrates that these two tumor suppressors cooperate in the regulation of angiogenesis and that loss of these genes contributes to the development of neoplasia in the liver and prostate.
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Results of anti-diabetic assay using C57BL/KsJ-db/db mouse model demonstrated that compound 9 was effective at lowering blood glucose, total cholesterol and HbA1c (P < 0.01).
Additionally, studies in the DMD mdx mouse model demonstrate that cellular uptake of a PMO is enhanced by co-administration of a glucose-fructose formulation, resulting in the restoration of higher dystrophin protein levels in the skeletal muscle [97].
The BFS-1 mouse model demonstrated a tendency (p<0.09) for tumor weight reduction after treatment with the peptide (Fig. 7 (f)).
Histopathologically, the mouse model demonstrated accumulation of abnormal lysosomal inclusions in multiple tissues and neuronal cell loss with concomitant astrocyte activation [18], [19].
Experiments in mercury-induced AKI mouse model demonstrated that apoptosis, oxidative stress and toxic renal failure were significantly attenuated by pretreatment with capsids prior to the mercury insult.
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