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Biomedical subjects

B Jensen

Publications and source records attributed to B Jensen.

At least 145 records · Page 8Linked to original sources

Rat testicular lipids and dietary isomeric fatty acids in essential fatty acid deficiency.

Weanling rats were fed essential fatty acid-deficient diets, either completely fat-free, or with partially hydrogenated fish oil (PHFO, 28 wt %), or with fractions derived from PHFO containing primarily positional isomers of trans-eicosenoate (20:1, 3 wt %) or trans-docosenoate (22:1, 3 wt %). Control animals were fed a peanut oil-containing diet (28 wt %). After 5 or 15 weeks on the diet, the content of neutral and phosphorus-containing lipids in the testes was determined. The fatty acid distribution in major lipid classes was analyzed for animals fed the diets for 15 weeks. The testicular stage of maturation or degeneration was assessed by histology. The group fed PHFO exhibited signs of complete testicular degeneration, or lack of maturation, already after 5 weeks, whereas the animals on the diets with the very long chain monoenoic acids suffered severe degenerations only after 15 weeks. In the PHFO-fed rats, a sharp decline in the concentration of testicular triacylglycerols was observed. In all of the essential fatty acid-deficient groups, an increase in testicular sphingomyelin was observed. Cholesterol levels were fairly similar among all dietary groups. The total testicular fatty acids of the PHFO-fed animals contained somewhat more eicosadienoic acid than found in the other groups, and somewhat less (n-9)-acids. In all EFA-deficient groups, (n-6)-acids were lowered, in particular in triacylglycerols and phosphatidyl cholines. The PHFO group did not show a lower (n-6)-concentration than the other deficient groups, in spite of the more severe symptoms of deficiency. There was no evidence of a major accumulation of long chain isomeric fatty acids in the degenerated testes of the PHFO-, 20:1-, and 22:1-fed groups.

Animals↗

Amylo-1,60glucosidase deficiency (glycogenosis type III) in the Faroe Islands.

Seven cases of glycogenosis type III (amylo-1,6-glucosidase deficiency) in two probably related families from the Faroe Islands are presented. The group of patients comprised two pairs of sibs. In a total of 78 members of the two families case histories were obtained and clinical examinations, analyses of amylo-1,6-glycosidase activity in erythrocytes and leucocytes, determinations of red cell, serum and enzyme groups as well as HL-A types were performed. In addition, all patients were subjected to studies of liver function. The distribution patients in these families supports the assumption of autosomal recessive inheritance. Heterozygotes could not be diagnosed with certainty by the methods of enzyme activity analysis employed. The incidence of glycogenosis type III with amylo-1,6-glucosidase deficiency was found to be high in the Faroe Islands.

Adolescent↗

The crystal structure of acetylcholine beta-resorcylate.

Acetylcholine beta-resorcylate, C14H21NO6, crystallizes in space group P21/c with a unit cell having dimensions a=14.562(6), b=14.109(4), c=15.096(6) A, and beta=106.90(3) degrees. Z=8. The structure was determined by direct methods from diffractometer collected three-dimensional X-ray data and refined by full-matrix least-squares techniques to an R index of 0.078. Layers of beta-resorcylate ions alternate with layers of acetylcholine ions. The beta-resorcylate ions are linked together in infinite chains by strong hydrogen bonds while no hydrogen bonds involve the acetylcholine ions.

Acetylcholine↗