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These transgenic mice have delayed hair growth, underdeveloped ears, and shorter tails.

Since the increase in FAA was slower to develop in orexin KO mice but reaches a similar magnitude (20 25% of total high activity occurs in ZT 7 9), this suggests that orexin KO mice have delayed acquisition of but no impairment in FAA.

Vimentin knockout mice have delayed wound healing [ 38].

During development Thra1 PV /+ mice have delayed closure of the skull sutures, severe growth retardation, delayed bone age, and impaired bone mineral accrual (22).

Surviving mice have delayed growth and development (both m−/+ and +/p−), but only the m−/+ adult mice exhibit PTH resistance, with elevation of PTH and decreased serum calcium levels.

Sdc4-null mice have delayed wound healing, impaired angiogenesis and defects in muscle satellite cells, but no apparent early developmental defects have been described (Cornelison et al., 2004; Echtermeyer et al., 2001; Ishiguro et al., 2000).

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Since S.mansoni chronically-infected galectin-3−/− mice had delayed monocyte-macrophage differentiation [22], we propose that the disorganization on B lymphocyte and plasma cell niches is narrowly associated with this eminent macrophage dysfunction.

In another study, we showed that Axl knock-out mice had delayed recovery and prolonged axonal damage following cuprizone toxicity, supporting the observation that the Axl receptor was important for recovery [25].

In contrast, 129S1/SvImJ mice had delayed transition to decompensated heart failure, with relatively mild alterations in histology and markers of hypertrophy at five weeks post-TAC and preserved systolic function until eight weeks post-TAC, suggesting that 129S1/SvImJ genetic modifiers might protect against the earlier and more severe pathological changes seen in C57BL/6J mice [39].

In summary, there were rough correlations between the presence of viral antigens and viral titers in the given organs, and rZH501-M847-G-infected mice had delayed development of lesions or showed less severe lesions than did other infected mouse groups.

The researchers found that crossing G60S mutant mice with HER2-overexpressing mice in which tumorigenesis is induced by carcinogen (DMBA) exposure revealed unexpected findings where G60S mice had delayed tumor onset but increased metastasis [ 28].

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