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In contrast, older AnkbR1788W/R1788W and AnkbL1622I/L1622I mice developed increased adiposity, a phenotype that was reproduced in cultured adipocytes, and insulin resistance.
P. copri easily took up residence, and the researchers found that the mice developed increased inflammation, especially in the gut.
All imaged mice developed increased T2 values in the infected left thigh muscle, which were visualized by T2 maps (Fig. 1A/C, Fig. 2A/C).
In the present study, female mice developed increased RVP following Dfen-administration; however, RVH remained unaffected.
In addition, streptozotocin (STZ) diabetic mice developed increased oxidative stress and kidney damage when subjected to a selenium deficient diet [ 14].
Despite having similar increases in blood pressure and heart hypertrophy, the PPARγ P465L mice developed increased fibrosis in response to AngII compared with WT littermates.
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Others have shown that Il10−/− mice develop increased gut permeability prior to development of colitis [32].
Muscle-specific PPARgamma-deficient mice develop increased adiposity and insulin resistance but respond to thiazolidinediones.
Herein, we report that following coxsackievirus infection, IL-6KO mice develop increased chronic autoimmune myocarditis.
Two other pathological results of interest are that AD-LBV mice develop increased levels of insoluble Aβ42 tau at younger ages than 3xTg-AD mice.
In support of an anti-fibrotic role for COX-2 in lung fibrosis, COX-2-deficient mice develop increased fibrosis following bleomycin-induced injury (Keerthisingam et al., 2001).
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