Creatine kinase and myofibrillar proteins in hereditary muscular dystrophy and vitamin E deficiency

1974 ◽  
Vol 27 (10) ◽  
pp. 1117-1129 ◽  
Author(s):  
Robert Eugene Olson
1961 ◽  
Vol 2 (1) ◽  
pp. 67-72 ◽  
Author(s):  
N. Lannek ◽  
P. Lindberg ◽  
G. Nilsson ◽  
G. Nordström ◽  
K. Orstadius

1958 ◽  
Vol 193 (3) ◽  
pp. 530-533 ◽  
Author(s):  
Nome Baker ◽  
William H. Blahd ◽  
P. Hart

Exchangeable body potassium (Ke), muscle potassium and muscle sodium concentrations have been measured in hereditarily dystrophic mice and in their normal littermates. Both Ke and K39/gm muscle were depressed in the dystrophics approximately 20% below the mean normal value; however, the concentration of Na23/gm muscle was higher by 50%, on the average, in the dystrophic tissue. The data suggest a partial replacement of intracellular by extracellular space in the dystrophic mice. Thus, this form of hereditary muscular dystrophy is qualitatively similar, with regard to K and Na concentrations, to human muscular dystrophy, vitamin E deficiency in rabbits, nutritional dystrophy in calves, and denervation in puppies.


1939 ◽  
Vol 39 (6) ◽  
pp. 643-652 ◽  
Author(s):  
Archer John Porter Martin ◽  
Thomas Moore

IN an early preliminary communication we (Martin & Moore, 1936) reported that in rats maintained for prolonged periods on diets deficient in vitamin E a brown discoloration of the uterus occurred. Degeneration of the convoluted tubules of the kidneys was also found. In a more recent paper we (Martin & Moore, 1938) described a less intense discoloration in the skeletal muscles, which was localized in distribution. The muscles of the hindlegs, which displayed the paresis described by Ringsted (1935), were always noticeably discoloured. In both the uterine and leg muscles discoloration was found to be associated with muscular degeneration. The similarity of the condition in the leg muscles to the nutritional muscular dystrophy first reported by Goettsch & Pappenheimer (1931) in guinea-pigs was noted. The purpose of this communication is to give a detailed account of this work, including its most recent developments (Moore, 1939).


1966 ◽  
Vol 3 (3) ◽  
pp. 208-225 ◽  
Author(s):  
Norman F. Cheville

Syndromes of encephalomalacia, exudative diathesis and muscular dystrophy were produced in day-old chicks placed on a torula yeast base diet deficient in vitamin E. Changes in the percentage of dietary lipid were responsible for variation in the disease processes. Chicks receiving 3-9% lipid had vascular alterations which determined, in most cases, the severity of the resulting tissue changes. Encephalomalacia occurred only in chicks on 9% dietary lipid. Muscular lesions were seen in all chicks and were thought to be due to damage to the mitochondria. Acid phosphatase activity was not directly associated with degeneration of muscle.


1957 ◽  
Vol 105 (5) ◽  
pp. 395-402 ◽  
Author(s):  
James S. Dinning ◽  
Paul L. Day

Eight young rhesus monkeys were fed a purified diet devoid of vitamin E. After from 6 to 13 months of feeding, all the animals developed signs of vitamin E deficiency. The signs of vitamin E deficiency in the monkey include muscular dystrophy, elevated excretion of creatine, allantoin, and free amino acids and decreased excretion of creatinine. The vitamin E-deficient monkeys all developed anemia and granulocytosis. Anemia was the first sign of vitamin E deficiency which was observed. All of these signs of vitamin E deficiency were reversed by treatment with α-tocopherol.


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