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Biomedical subjects

M Brin

Publications and source records attributed to M Brin.

At least 37 records · Page 2Linked to original sources
PubMed1982

Thiamin in the elderly--relation to alcoholism and to neurological degenerative disease.

Status of thiamin in the elderly North American population is reviewed. Most Americans eat sufficient thiamin but about 5% of those over 60 yr old show impaired thiamin status. This is more marked in the poor, those confined in institutions, or those with illness. Thiamin responsive heart disease and Wernicke Korsakoff CNS syndromes occur in the elderly but there is no increased prevalence. Minor heart or neurological syndromes related to thiamin deficiency cannot be identified. The Recommended Dietary Allowance of thiamin provides at least 50% excess thiamin for those over 60 yr old--this amount is adequate. There is no known toxicity for thiamin.

Adolescent↗
PubMed1982

Biopotency of alpha-tocopherols as determined by curative myopathy bioassay in the rat.

The decrease in plasma pyruvate kinase activity after administration of various tocopherols to vitamin E-deficient rats provided the basis for a 3-point parallel-slope assay for vitamin E activity. Based on 6 replicate assays, RRR-alpha-tocopheryl acetate (RRR-alpha-TA) was 141% as active as all-rac-alpha-tocopheryl acetate (all-rac-alpha-TA). This confirms many previous reports with other bioassays and is in agreement with the unit-weight relationships assigned by The National Formulary. 2-ambo-alpha-Tocopheryl acetate was 97% as active as all-rac-alpha-TA indicating that only the configuration of the 2-position on the chromanol ring is important in determining the biological activity of alpha-tocopherol.

Animals↗
PubMed1982

[Cerebral metastases of malignant germinal tumors of the testis].

Cerebral metastases occur in 6% of cases of testicular cancer. In our study of 5 cases they occurred during the course of the disease (with a delay of 4-18 months, at the same time as pulmonary and abdominal metastases). The prognosis in these cases is poor (presence of choriocarcinomatous or vitelline elements, advanced stages). The diagnosis is easily established (clinical, encephalogram, scanner); the prognosis is hopeless (5 deaths in 3-90 days). When a metastasis is the first diagnostic clue (one case), the prognosis is slightly better (9 month survival). The incidence of cerebral metastasis is the same now as it was before the introduction of effective chemotherapy in patients who die from testicular cancer, but the death rate from this malignancy has decreased since the introduction of active chemotherapy with cisplatin. Hence, there is no indication for prophylactic treatment for cerebral metastases in patients in remission since metastases only appear in cases which are resistant to treatment.

Abdominal Neoplasms↗
PubMed1980

A decrease in irreversibly sickled erythrocytes in sicle cell anemia patients given vitamin E.

Patients with sickle cell anemia were given 450 IU of vitamin E (as alpha-tocopherol) per day for 6 to 35 weeks. Plasma tocopherol levels increased from 0.7 +/- 0.2 mg/g lipid pretreatment, to 2.3 +/- 0.3 mg/g lipid. The percentage of circulating irreversibly sickled red cells decreased from 25 +/- 3% pretreatment to 11 +/- 1% after vitamin E administration (P less than 0.001). The percentage of irreversibly sickled red cells remained below pretreatment levels as long as the vitamin was administered (up to 35 weeks). The biochemical and clinical implications of these observations are discussed.

Anemia, Sickle Cell↗
PubMed1980

Effects of aspirin and related drugs in vitamin E-deficient rats.

Evidence from the literature indicates that in vitamin E-deficient animals prostaglandin (PG) synthesis in platelets is enhanced while it is decreased in the muscle and testis. In the present study the effects of aspirin, a known inhibitor of PG biosynthesis, on vitamin E deficiency signs in the rat were investigated. Administration of aspirin to vitamin E-deficient rats had no protective effect on fetal mortality, incisor depigmentation, body weight gain or red blood cell peroxidative hemolysis. Aspirin prevented the anemia and thrombocythemia observed in vitamin E-deficient rats. Aspirin, salicylic acid and a carbazole prostaglandin inhibitor exacerbated testis degeneration in vitamin E-deficient animals. Addition of aspirin to the diet more than doubled the vitamin E requirement for reversal of necrotizing myopathy.

Animals↗
PubMed1979

Antiscorbutic activity of ascorbic acid phosphate in the rhesus monkey and the guinea pig.

Rhesus monkeys fed an ascorbic acid-free, purified liquid diet, developed scurvy in 70 to 105 days as evidenced by loss of weight, anemia, bleeding gums, inflamed palate, diarrhea, and inability to stand. Oral administration of either 10 mg/kg body weight of ascorbic acid or an equimolar amount of the magnesium salt of 1-ascorbic acid phosphate cured all symptoms of scurvy. Similarly, oral administration of 1-ascorbic acid phosphate cured all symptoms of scurvy in the guinea pig and resulted in liver ascorbate levels equal to those of animals feed ascorbic acid. It is concluded that ascorbic acid phosphate is a readily available source of ascorbic acid activity in vivo.

Animals↗
PubMed1979

Availability of adipose tissue tocopherol in the guinea pig.

Young guinea pigs were fed a purified diet containing vitamin E for 3 weeks and then fed the diet without vitamin E for 8 weeks. Levels of vitamin E in plasma and liver decreased to low values within a week. Depletion rates for heart and muscle were much slower, whereas the rate of loss from fat was negligible. In experiments with more mature guinea pigs and a depletion period of 4 months, the depletion rate of tocopherol from fat was also barely detectable. Both yound and mature guinea pigs developed myopathy after 8 weeks of depletion. Apparently, tocopherol in adipose tissue is not sufficiently available to maintain plasma tocopherol levels or to prevent signs of vitamin E deficiency. Even during fasting, adipose tissue tocopherol was not mobilized readily. During a 4 day fast, adipose tissue mass diminished considerably, but there was no appreciable loss of tocopherol.

Adipose Tissue↗
PubMed1978

Vitamin needs of the elderly.

Vitamin deficiency is a result of gradual depletion of body stores secondary to poor dietary habits or to disease. Marginal or preclinical vitamin deficiency results in nonspecific symptoms such as malaise, irritability or somnolence, loss of appetite and weight, and impairment of psychologic and physical performance socially or at work. These signs precede clinical signs of disease. The elderly are particularly vulnerable to vitamin deficiency because of the high incidence of illness and disability in the later years of life and because of other common problems, such as low income, poor appetite, and social isolation.

Aged↗
PubMed1978

Plasma activity of pyruvate kinase and glutamic oxalacetic transaminase as indices of myopathy in the vitamin E deficient rat.

Weanling rats were fed vitamin E deficient diets for 6 to 15 weeks and then given vitamin E orally for 4 days. Plasma obtained 1 day after the last dose was assayed for glutamic oxalacetic transaminase (GOT) and pyruvate kinase activity (PK). Administration of vitamin E resulted in reduction in activity of both enzymes. Plasma levels of alkaline phosphatase, lactic dehydrogenase, and bilirubin were unaffected by vitamin E and there was no histological evidence of liver degeneration. The number of phagocytized muscle fibers was greatly reduced by vitamin E treatment, but a substantial number of necrotic fibers were still present. With more prolonged (8 days) treatment, plasma PK and GOT levels were reduced to levels found in plasma of vitamin E replete animals and few degenerated muscle fibers could be observed. It was concluded that resolution of the necrotizing myopathy in vitamin E deficient rats is a rapid process and that the decreased activity of PK and GOT in plasma is a sensitive indicator of the resolution process. The decrease in plasma enzyme levels is an easily quantitated and reproducible biological response to vitamin E administration. Thus, this approach provides a basis for a sensitive and accurate bioassay for vitamin E activity.

Animals↗
PubMed1978

The effect of medium-chain triglycerides on the bioavailability of vitamin E.

Overnight fasted, normal rats were fed a single dose of isotopically labeled vitamin E emulsified in either medium-chain or long-chain triglyceride (MCT or LCT). The animals were sacrificed at various time intervals of up to 72 hours. Levels of radioactivity in the small intestinal wall, liver, plasma, skeletal muscle and adipose tissue were higher in animals in which tocopherol was administered in MCT rather than LCT. Thus, the intestinal absorption of vitamin E was enhanced by solubilization in MCT. These findings are consistent with the theory that the gastrointestinal absorption of dietary tocopherol is dependent upon the simultaneous digestion and absorption of the fat in which the vitamin is solubilized.

Animals↗
PubMed1977

Effects of a prolonged vitamin E deficiency in the rat.

Rats fed a vitamin E-deficient diet containing 10% "stripped" corn oil had reduced growth rate and elevated platelet count by 12 weeks of age, and a normocytic anemia with elevated reticulocytes by 16 weeks of age. After 5 months, rats became emaciated and developed kyphoscoliosis. Some rats developed skin ulcers and tremors, and mortality was high. Neuromuscular lesions included a chronic necrotizing myopathy and localized axonal dystrophy. There was also a selective activation of lysosomes in the central nervous system microcirculation. Liver ascorbic acid of deficient rats was the same as in those receiving vitamin E. Urinary excretion of p-hydroxyphenylpyruvate after a tyrosine load was also the same in deficient and control rats. It was concluded that neither vitamin C synthesis or utilization was affected the E-deficient rats.

Age Factors↗
PubMed1976

Lack of antiscorbutic activity of ascorbate 2-sulfate in the rhesus monkey.

Oral administration of 10 mg per kilogram of body weight of ascorbic acid (AA) completely prevented development of scurvy in juvenile rhesus monkey (Mucaca mulata) fed an AA-free liquid diet. The same dose cured scurvy when injected intramuscularly. An equimolar dose of ascorbic acid 2-sulfate (AA-2-S) did not prevent or cure scurvy. Neither AA nor AA-2-S altered serum cholesterol. AA but not AA-2-S reduced serum triglyceride. A case of scurvy in an AA-2-S treated monkey is described in detail.

Alkaline Phosphatase↗