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The results were validated in vivo using a mouse diabetic wound healing model with impaired neovascularization.
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In the present study, using a mouse model STZ-induced diabetic cardiomyopathy, we demonstrated that left ventricular atrophy and left ventricular systolic dysfunction were attenuated in genetically engineered mice with cardiac specific overexpression of DGKζ.
Using a diabetic mouse model, islets were transplanted into the omentum pouch alone, with local administration of VEGF-A and basic fibroblast growth factor (FGF) or together with heparin-coated poly L-lactic acid/lactide) (poly L-lactic with or without VEGF-acid/lactide
In brief, we made transgenic mice using a Nonobese diabetic-mouse derived bacterial artificial chromosome in which the coding sequence for Sst was replaced while retaining approximately 118-kbp 5′ and approximately 98-kbp 3′ of the Sst-start and Sst-stop codons, respectively.
One study evaluated renal fibrosis in Mmp2−/− mice using a diabetic nephropathy model initiated by streptozotocin (STZ), a pancreatic β-cell toxin (Takamiya et al., 2013).
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They tested whether local miR-503 inhibition would improve post-ischemic reparative neovascularization and blood flow recovery in diabetic mice using a decoy strategy to lower miR-503 availability in the muscle during ischemia.
Current studies in our laboratory using nonobese diabetic mice, indicate that this procedure was able to reverse autoimmune diabetes for 5 months with no evidence of autoimmune destruction of insulin-secreting hepatocytes (B. Ren, unpublished observations), giving hope that this procedure will be useful for reversal of autoimmune diabetes.
These results are in agreement with a recent study using two other diabetic mouse models, ob/ob and kky, where hypoxia was detected in pancreatic islets.
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