scholarly journals 3H Leucine Incorporation Into Myofibrils of Normal and Dystrophic Mouse Skeletal Muscle

1975 ◽  
Vol 2 (1) ◽  
pp. 1-4 ◽  
Author(s):  
G. Monckton ◽  
H. Marusyk
Keyword(s):  
Skeletal Muscle ◽  
Muscular Dystrophy ◽  
Leucine Incorporation ◽  
Mouse Skeletal Muscle ◽  
Dystrophic Mouse ◽  
Before And After ◽  
Em Autoradiography ◽  
Marked Drop

SUMMARY:The study of 3H leucine incorporation into skeletal muscle of mouse muscular dystrophy (129 ReJ/dy Bar Harbour strain) shows the uptake of isotope into myofibrils. The techniques employed were light and EM autoradiography before and after glycerination (Szent-Gyorgyi 1947). The results indicate a marked drop in uptake of the 3H-Leucine into myofibrils in the dystrophic animals, supporting the contention of Nihei et al (1971) that reduced myosin synthesis occurs in mouse muscular dystrophy.

Enzyme studies of skeletal muscle in mice with hereditary muscular dystrophy

1963 ◽  
Vol 205 (5) ◽  
pp. 897-901 ◽  
Author(s):  
Marilyn W. McCaman
Keyword(s):  
Skeletal Muscle ◽  
Muscular Dystrophy ◽  
Glutathione Reductase ◽  
Enzyme Activities ◽  
Lactic Dehydrogenase ◽  
Normal Muscle ◽  
Dystrophic Muscle ◽  
Nerve Section ◽  
Mouse Muscle ◽  
Dystrophic Mouse

The activities of 20 enzymes in normal, heterozygous, and dystrophic mouse muscle were studied by means of quantitative microchemical methods. Enzyme activities in normal and heterozygous muscle were essentially the same. In dystrophic muscle glucose-6-P dehydrogenase, 6-P-gluconic dehydrogenase, glutathione reductase, peptidase, ß-glucuronidase, and glucokinase activities were significantly higher than in normal muscle, while α-glycero-P dehydrogenase and lactic dehydrogenase activities were significantly lower. The pattern of enzyme activities found in normal gastrocnemius denervated by nerve section was strikingly similar to that in dystrophic muscle.

scholarly journals Subproteomics analysis of Ca2+-binding proteins demonstrates decreased calsequestrin expression in dystrophic mouse skeletal muscle

2004 ◽  
Vol 271 (19) ◽  
pp. 3943-3952 ◽  
Author(s):  
Philip Doran ◽  
Paul Dowling ◽  
James Lohan ◽  
Karen McDonnell ◽  
Stephan Poetsch ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Binding Proteins ◽  
Mouse Skeletal Muscle ◽  
Dystrophic Mouse

Pliometric contraction-induced injury of mouse skeletal muscle: effect of initial length

1997 ◽  
Vol 82 (1) ◽  
pp. 278-283 ◽  
Author(s):  
Kam D. Hunter ◽  
John A. Faulkner
Keyword(s):  
Skeletal Muscle ◽  
Fiber Length ◽  
Isometric Force ◽  
Force Production ◽  
Initial Length ◽  
Average Force ◽  
Mouse Skeletal Muscle ◽  
Before And After ◽  
Work Input ◽  
Initial Fiber

Hunter, Kam D., and John A. Faulkner. Pliometric contraction-induced injury of mouse skeletal muscle: effect of initial length. J. Appl. Physiol. 82(1): 278–283, 1997.—For single pliometric (lengthening) contractions initiated from optimal fiber length ( L f), the most important factor determining the subsequent force deficit is the work input during the stretch. We tested the hypothesis that regardless of the initial length, the force deficit is primarily a function of the work input. Extensor digitorum longus muscles of mice were maximally activated in situ and lengthened at 2 L f /s from one of three initial fiber lengths (90, 100, or 120% of L f) to one of three final fiber lengths (150, 160, or 170% of L f). Maximal isometric force production was assessed before and after the pliometric contraction. No single mechanical factor, including the work input ( r 2= 0.34), was sufficient to explain the differences in force deficits observed among groups. Therefore, the force deficit appears to arise from a complex interaction of mechanical events. With the data grouped by initial fiber length, the correlation between the average work and the average force deficit was high ( r 2= 0.97–0.99). Consequently, differences in force deficits among groups were best explained on the basis of the initial fiber length and the work input during the stretch.

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