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Biomedical subjects

J M Cooperman

Publications and source records attributed to J M Cooperman.

At least 19 recordsLinked to original sources
PubMed1998

Intergenerational transfer of psychosocial risk in women with childhood histories of aggression, withdrawal, or aggression and withdrawal.

Intergenerational transfer of risk between mothers and children, based on mothers' childhood aggression and social withdrawal, was examined in an inner-city sample. Each of the 3 studies reported involved a subset of the 909 female participants in the Concordia Longitudinal Risk Project, initiated when the participants were of school age. Using medical records, Study 1 (n = 853) focused on prediction of teen motherhood, delivery complications during childbirth, multiparity, and close spacing of births. Study 2 (n = 428) examined pathways to school dropout and teen parenthood. Study 3 (n = 89) involved prediction of observed parent and child behavior from mothers' childhood characteristics. Mothers' childhood aggression was consistently predictive of negative outcomes in each area of intergenerational risk, especially when combined with social withdrawal and low levels of academic achievement. Education was protective: Mothers' years of schooling predicted positive outcomes.

Achievement↗
PubMed1990

Reliability and validity of judgments of the integrity of the anterior cruciate ligament of the knee using the Lachman's test.

This study assessed the intratester and intertester reliability and the validity of judgments of the integrity of the anterior cruciate ligament (ACL) based on the use of the Lachman's test. End-feel and tibial translation judgments made during the Lachman's test were also assessed. Patients with unilateral knee problems (N = 32), 13 of whom had documented ACL damage, were examined by two physical therapists and two orthopedic surgeons. Intratester Kappa values for whether the test was positive or negative were .44 for physical therapists, .60 for orthopedic surgeons, and .51 for all examiners. Intertester Kappa values were .69 for the therapists, .61 for the surgeons, and .42 for all examiners. The predictive value of a positive test was 47% for all examiners, whereas the predictive value of a negative test was 70%. Results indicate that Lachman's test judgments have limited reliability and may be more useful for predicting that a patient does not have an ACL injury than for predicting that the ACL is injured. [Cooperman JM, Riddle, DL, Rothstein JM: Reliability and validity of judgments of the integrity of the anterior cruciate ligament of the knee using the Lachman's test.

Adolescent↗
PubMed1988

Riboflavin metabolism in the hypothyroid newborn.

In the hypothyroid rat the flavin adenine dinucleotide (FAD) content of the liver is similar to that observed in rats maintained on a riboflavin-deficient diet. Thyroxine regulates the enzyme flavin kinase. Human adults with hypothyroidism have levels of erythrocyte glutathione reductase (EGR), an FAD-containing enzyme, in the range indicative of riboflavin deficiency, which can be corrected with thyroxine therapy. In the present study six newborns with severe congenital hypothyroidism because of athyrosis, ectopic thyroidism, or congenital hypothyroidism with Down's syndrome had normal levels of EGR, and treatment with thyroxine had no effect on these levels.

Congenital Hypothyroidism↗
PubMed1987

Riboflavin metabolism in the hypothyroid human adult.

It had been shown that thyroxine regulates the conversion of riboflavin to riboflavin mononucleotide and flavin adenine dinucleotide (FAD) in laboratory animals. In the hypothyroid rat, the flavin adenine dinucleotide level of the liver decreases to levels observed in riboflavin deficiency. We have shown that in six hypothyroid human adults, the activity of erythrocyte glutathione reductase, an accessible FAD-containing enzyme, is decreased to levels observed during riboflavin deficiency. Thyroxine therapy resulted in normal levels of this enzyme while the subjects were on a controlled dietary regimen. This demonstrates that thyroid hormone regulates the enzymatic conversion of riboflavin to its active coenzyme forms in the human adult.

Aged↗
PubMed1985

Nutritional deficiencies in institutionalized mentally retarded and physically disabled individuals.

The folic acid, riboflavin, and vitamin A status of 150 individuals in a hospital for mentally retarded persons was examined. Because many of the subjects were incontinent, it was necessary to use blood samples. Folic acid deficiency was determined from plasma levels and from examination of stained peripheral blood smears for megaloblastic changes in the leucocytes. Riboflavin deficiency was determined from estimation of erythrocyte glutathione reductase and vitamin A in plasma by a colorimetric method. Twenty percent of the subjects had evidence of folic acid deficiency, 17% had evidence of riboflavin deficiency, and none had vitamin A deficiency.

Adolescent↗
PubMed1985

Effect of diet on vitamin deficiencies in retarded individuals receiving drugs.

A population of mentally retarded and physically disabled individuals on long-term therapy with anticonvulsant drugs had a high prevalence of folic acid and riboflavin deficiency, 20% and 17%, respectively, as they entered an institution devoted to their care. Their previous diet was probably nutritionally marginal, as it was cooked and prepared to baby food consistency, and milk was rarely given. They were fed in the recumbent position, resulting in frequent vomiting. In this institution, a carefully planned dietary regimen that was adequate in essential nutrients was fed by trained personnel. Drug therapy was continued. After a year no signs of folic acid or riboflavin deficiency were evident. We conclude that these weak vitamin antagonists may precipitate deficiencies on marginally adequate diets. A good dietary regimen prevented the appearance of these vitamin deficiencies.

Anticonvulsants↗
PubMed1982

The folate in human milk.

In previous studies of the folate content of human milk, samples were prepared for assay by a method that resulted in a turbid solution that was then assayed by a turbidimetric microbiological method. We have used an improved microbiological assay in which the milks were treated with rennin to precipitate casein and heated in a buffered ascorbate to coagulate lactalbumin and lactoglobulin. Milks were obtained serially from nursing mothers for periods ranging from 1 day to 6 months postpartum. The results showed that the folate in human milk has few glutamate residues since treatment with a purified folate conjugase preparation release no additional folate activity for Lactobacillus casei. Colostrum is relatively low in folate, but milk folate increases as lactation proceeds. During each stage of lactation there was great variation in milk folate content among the women. In the case of a folate-deficient woman, supplementation with folic acid resulted in a prompt increase in milk folate level.

Adult↗
PubMed1980

Nutrition in the pathogenesis of alcoholic pancreatitis.

The pathogenesis of chronic alcoholic pancreatitis is unclear. Some European studies have shown that alcoholics who develop pancreatitis consume a diet richer in protein and fat than normal controls. The infrequency of alcoholic cirrhosis in patients with alcoholic pancreatitis in these studies was explained by this enhanced nutritional intake protecting the liver but not the pancreas. In this study we evaluated by an oral recall method the nutritional intake of patients with alcoholic pancreatitis or alcoholic cirrhosis prior to the onset of symptomatology and compared the data with established norms. Our data did not confirm the European observation that pancreatitis patients consume amounts of protein and fat, more than the general population and more than alcoholics with cirrhosis. Furthermore, the combined incidence of cirrhosis and pancreatitis was not infrequent. Our observations do not disprove that a high fat and/or protein diet predispose to pancreatitis but suggest that such a diet is not a prerequisite for alcoholics to develop pancreatitis.

Adult↗
PubMed1980

Riboflavin deficiency in an adolescent population in New York City.

An adolescent population ranging in age from 13 to 19 years and of a low socioeconomic status in New York City was surveyed for riboflavin deficiency. Deficiency was determined from estimation of erythrocyte glutathione reductase activity, an accurate reflector of riboflavin nutritional status. The overall prevalence of deficiency among those not on vitamin supplements was 26.6%. The prevalence did not depend on sex or age. There was a correlation between milk consumption and riboflavin nutritional status. The prevalence was highest among those consuming less than 1 cup/week and least among those taking 3 or more cups a day. The latter group was comparable in this respect to those receiving daily vitamin supplements. Adolescents are at a high risk for nutritional deficiencies because of their notoriously poor dietary habits, and the estimation of riboflavin deficiency may be an indicator of overall nutritional status.

Adolescent↗
PubMed1978

Riboflavin deficiency in women taking oral contraceptive agents.

The effect of oral contraceptive agents (OCA) on riboflavin nutritional status of women of child-bearing age in a low socioeconomic population was studied. For a control group, 100 women in the same age and socioeconomic group using alternate forms of contraception were selected. Riboflavin deficiency was determined by measuring erythrocyte glutathione reductase activity, a reliable index of the deficiency. None of the women was on vitamin supplements or had clinical conditions effecting dietary intake or utilization. Eleven of 100 women in the control group had biochemical evidence of deficiency. This compared to 24 of 56 OCA users who were deficient. The frequency of deficiency increased among those on OCA for longer periods of time. Thirteen of 17 OCA users for 3 years or more, compared to 11 of 39 users under 3 years were deficient. There were no discernable dietary differences between the groups. These studies demonstrate that riboflavin deficiency is a problem of women in the lower socioeconomic level in the child-bearing age. The use of OCA aggravates the prevalence of deficiency.

Adolescent↗
PubMed1977

Light (phototherapy)--induced riboflavin deficiency in the neonate.

Phototherapy with blue light decomposes riboflavin, which has a maximum absorption at 450 nm. A study was designed to determine whether riboflavin deficiency developed in neonates who received phototherapy for moderate hyperbilirubinemia. Twenty-one infants with normal erythrocyte glucose-6-phosphate dehydrogenase activity were investigated. Five infants with moderate hyperbilirubinemia who did not require phototherapy served as the controls. Riboflavin deficiency was determined from the degree of saturation of erythrocyte glutathione reductase, a method shown to reflect riboflavin nutritional status in the neonate. Sixteen of 21 infants who were exposed to phototherapy developed riboflavin deficiency; all who had phototherapy for 49 hours or more developed the deficiency. That the concentration of serum bilirubin or the duration of hyperbilirubinemia was not a factor is supported by the fact that none of the controls became deficient. This observation may have important metabolic and clinical consequences for the neonate.

Female↗