Sentence examples for model of limb from inspiring English sources

In a syngeneic murine model of limb ischemia, ESCs or ESC-ECs were delivered by intramuscular (IM), intrafemoral artery (IA), or intrafemoral vein injections (n=5 in each group).

Using a mouse model of limb girdle muscular dystrophy engineered with a null allele of γ-sarcoglycan, we bred the identical γ-sarcoglycan mutation into four different genetic backgrounds.

An assessment of limb asymmetry was also performed revealing a non-dominant arm matching advantage but only for children and only in the task requiring interhemispheric transfer of a memory-based model of limb position.

It has been possible to develop a reproducible model of limb lengthening in this species.

The feasibility and accuracy of nuclear perfusion imaging has already been demonstrated by Stacy et al. in a pig model of limb ischemia [27].

The results of these experiments document the feasibility of imaging and quantifying RAGE expression in the hind limbs of a relevant mouse model of limb ischemia and show the effect of diabetes to increase the expression and thereby reduce angiogenesis.

Wu, B. et al. Glucocorticoid steroid and alendronate treatment alleviates dystrophic phenotype with enhanced functional glycosylation of alpha-dystroglycan in mouse model of limb-girdle muscular dystrophy with FKRPP448L mutation.

Tranilast has been administered to sarcoglycan-deficient Bio14.6 hamsters, a rodent model of limb-girdle muscular dystrophy (LGMD).

Muscle atrophy caused in mutant caveolin-3 transgenic mice, a model of limb-girdle muscular dystrophy (LGMD) 1C, was reduced dramatically by crossing these mice with myostatin propeptide transgenic mice [ 63].

In addition, tranilast administration was found to be efficacious in reducing muscle fibrosis in the Bio14.6 hamster model of limb-girdle muscular dystrophy and reducing serum creatine kinase levels in mdx dystrophic mice, effects they suggest may be a result of tranilast-mediated inhibition of the Ca2+-permeable growth factor-regulated channel (TRPV2 or GRC) [ 18, 25].

The mechanism of slowed reuptake appears to be due to decreased SERCA activity, which has been observed in microsomes from boys with DMD, Sgcd −/− mice (mouse model of limb-girdle MD due to loss of δ-sarcoglycan gene, which similarly disrupts the dystrophin-glycoprotein complex similar to that observed in mdx mice with the loss of dystrophin) and dy 2j /dy 2j mice that have a mutation in Lama2.