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For example, both inbred and genetically heterogeneous mouse strains develop glucose intolerance with oral administration of encapsulated rapamycin [ 11, 37, 38].
Although a number of mouse strains develop obesity and obesity-associated insulin resistance under certain conditions [ 25, 26] most of these models are resistant to atherosclerosis [ 27].
Regarding tubular functions, a limit of the adriamycin model is that sensitive mouse strains develop not only focal segmental glomerulosclerosis but also tubulo-interstitial fibrosis and tubular lesions that rapidly progress towards renal insufficiency [ 40].
All infected mouse strains develop acute myocarditis from day 8 to 12 post infection (pi), but only certain strains such as A/J and BALB/c develop DCM by day 35 pi [ 11].
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All arthritis susceptible mouse strains developed a strong antibody response to human G6PI (hG6PI; Fig. 3a).
Interestingly, the different mouse strains developed either peripheral or central neuropathy.
Objective The STR/ort mouse strain develops osteoarthritis (OA) of the medial tibial cartilage whilst CBA mice do not develop this disease.
Upon challenge with H1N1 swine flu virus, this mouse strain develops signs of disease, nevertheless the mice recover after two weeks [22].
This mouse strain develops and reproduces exactly like control BALB/c mice, and the thymic epithelial function and thymocyte maturation is indistinguishable from wild type controls [24].
Interestingly, each knockout mouse strain develops tumors in a specific subset of tissues, but none of these mice develop mammary tumors [11], [12], [13], [14], [15], [16], [17], [18].
The NZM2410 mouse strain develops spontaneous lupus nephritis that shares a number of characteristics with human SLE [ 21].
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