The dystrophin-deficient (mdx) mouse remains the most commonly used model for Duchenne muscular dystrophy (DMD). Mdx mice show a predominantly covert cardiomyopathy, the hallmark of which is fibrosis. We compared mdx and normal mice at six ages (3, 6, 9, 12, 15, and 18 months) using in vivo assessment of cardiac function, selective collagen staining, and measures of TGF-β mRNA, Evans blue dye infiltration, macrophage infiltration, and aortic wall thickness.
View Article and Find Full Text PDFThe mdx mouse mutation arises from a C-to-T point mutation, which terminates the translation of dystrophin and results in the loss of a functional dystrophin protein. mdx mice are used widely in studies of the role of dystrophin and of potential treatments for Duchenne muscular dystrophy, thus accurate genotyping is essential. Current methods require labor-intensive efforts and can often lead to misconstrued results.
View Article and Find Full Text PDFSeventy-two lactic acid producing bacterial isolates (excluding streptococci) were cultured from the gastrointestinal tract of six horses. Two of the horses were orally dosed with raftilose to induce lactic acidosis and laminitis while the remaining four were maintained on a roughage diet. Near complete 16S rDNA was amplified by PCR from the genomic DNA of each isolate.
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