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Exact(5)

These data suggest that the process we propose, namely the negative regulation of the endothelial relaxation by the smooth muscle, could also be of great interest in vascular pathophysiological conditions.

These data suggest that p43 overexpression in skeletal muscle could also induce a similar event, hence inducing an oxidative stress which might contribute to muscle wasting via proteolysis activation.

Hyperpolarization and relaxation of mesenteric artery smooth muscle could also be evoked by a combination of the concentration selective SKCa and IKCa agonists cyclohexyl-[2- 3,5-dimethyl-pyrazol-1-yl -6-methyl-pyrimidin-4-yl]-amine (cyclohexyl-[2- 3,5-dimethyl-pyrazol-1-yl -6-methyl-pyrimidin-4-yl]-amine300 µM [16], [30]) in arteries from cyclohexyl-[2- 3,5-dimethyl-pyrazol-1-yl -6-methyl-pyrimidin-4-yl]-amine

The accumulation of mtDNA deletions in skeletal muscle could also be secondary to a failure to clear mitochondria with damaged DNA (Chen et al, 2010).

Timing and complexity of the mussel immune response as well as the immunostimulation protocol (following shell notching, small mantle wounds may have attracted the hemocytes and induced their degranulation far from the adductor muscle) could also explain the progressive AMP down-regulation observed in the hemocytes of the Vibrio-challenged mussels.

Similar(55)

Thus the smaller force decline in our aged muscles could also reflect an age-related increase in the densities of the Na+/K+ ATPase in the t-tubule membrane.

The decreased expression of the skeletal and cardiac α-actin that occurred in mutant muscle and to a lesser extent in aging muscles could also contribute to the atrophy and to the alterations in sarcomere organization that are observed in mutants.

Together these results from elderly muscle indicate increased muscle inflammation susceptibility [ 69] and an altered acute muscle adaptive response to exercise in elderly muscle, which could also contribute to the muscle deficits in RA patients.

A pectoralis major muscle flap or a sternocleidomastoid muscle flap could also have been an option as the injury was near the neck.

The muscle mass-independent decrease in muscle function could also be partly restored by supplementation with the specific nutritional combination (TB-SNC).

Therapy of congenital and degenerative muscle diseases could also benefit from findings in muscle tissue engineering research [ 27, 28].

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