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Biomedical subjects

R Khardori

Publications and source records attributed to R Khardori.

49 records · Page 3Linked to original sources
PubMed1979

Adrenocortical function in experimental protein malnutrition.

Adrenocorticoid activity was investigated in experimentally induced protein malnutrition in Rhesus monkeys. Control studies were carried out in the same animals before inducing protein malnutrition. Plasma cortisol levels were elevated in the protein malnourished state. There was a total abolition of the diurnal rhythm of cortisol secretion. Fasting hypoglycemia was also observed in the protein malnourished state. It is concluded that increased adrenocorticoid activity and sustained steroidogenesis result from protein deficiency. Hypoglycemia may be an important stimulus, in addition to the metabolic stress imposed by the protein deprivation. The recognition of increased adrenocorticoid activity is important in a protein-deficient host, since the defense against infections might be impaired in such a situation.

Adrenal Cortex↗
PubMedDate not supplied

Insulin secretion and carbohydrate metabolism in experimental protein malnutrition.

In order to study the evolution of endocrine and metabolic changes in protein malnutrition, we created a replica of this human syndrome in a primate model. This model was free from stress factors like infestations, and infections and provided an opportunity to study the details more closely. Our results showed that definite endocrine and metabolic changes are established by six weeks of protein deprivation. The study demonstrated that protein deprivation results in decreased fasting blood glucose levels associated with diminution in fasting, and total insulin output when presented with a glucose load. There is also deterioration of carbohydrate tolerance. It is suggested that decreased fasting blood glucose is a consequence of impaired breakdown and/or depletion of glycogen stores, and hepatic dysfunction secondary to fatty infiltration. The exact cause of decrease in insulin output remains to be clearly elucidated. The carbohydrate intolerance is attributed to insulin lack, hepatic dysfunction and decreased glucose disposal consequent to protein deprivation.

Animals↗
PubMedDate not supplied

Clinical and molecular studies in a unique family with autosomal dominant limb-girdle muscular dystrophy and Paget disease of bone.

PURPOSE: To characterize the clinical features and perform linkage analysis of candidate loci in a large Illinois family with autosomal dominant limb-girdle muscular dystrophy (LGMD) and Paget disease of bone (PDB). METHODS: The family includes 11 affected individuals (8 M, 3 F). Clinical, biochemical and radiologic evaluations were performed to delineate clinical features of the disorder. Linkage analysis with polymorphic markers was performed for previously identified LGMD, PDB and cardiomyopathy loci. RESULTS: Onset of PDB is early, at a mean age of 35 y, with classic distribution involving the spine, pelvis, and skull. Muscle weakness and atrophy is progressive with mildly elevated to normal creatine phosphokinase levels. Muscle biopsy in the oldest male revealed vacuolated fibers, however, in others revealed nonspecific myopathy. Affected individuals die from progressive muscle weakness, and respiratory and cardiac failure in their 40s-60s. Linkage analysis excluded autosomal dominant and recessive LGMD, PDB, and cardiomyopathy loci. CONCLUSION: Autosomal dominant LGMD associated with PDB is an unusual disorder. Linkage analysis indicates a unique locus in this family.

Adult↗
PubMedDate not supplied

Diabetes mellitus and optic atrophy in two siblings: a report on a new association and a review of the literature.

Two siblings with diabetes mellitus and optic atrophy (Wolfram syndrome) are described. As often noted, they also had atonic urinary bladders. Only one of the siblings had some impairment of hearing. Other findings not previously reported that appeared in each subject were esophageal dysphagia and vertigo. An autopsy in one revealed brain stem hypoplasia and thinning and flattening of the optic nerves with atrophy of the lateral geniculate bodies.

Adult↗
PubMedDate not supplied

Hyperparathyroid crisis manifesting as respiratory and heart failure.

OBJECTIVE: To describe a case of hyperparathyroid crisis manifesting as respiratory failure and congestive heart failure and to emphasize the implications of hypercalcemia and hypophosphatemia in this setting. METHODS: A case report and a review of the pertinent literature are presented. RESULTS: A 71-year-old man was transferred to our care because of respiratory failure and congestive heart failure. He had no change in cardiorespiratory status until the significance of hypercalcemia and hypophosphatemia was recognized and therapy was directed at correction of these abnormalities. Primary hyperparathyroidism was the cause of these electrolyte abnormalities. CONCLUSION: To our knowledge, hyperparathyroid crisis manifesting as respiratory insufficiency and congestive heart failure has not been described previously. Phosphate depletion may account for the neuromuscular features seen in hyperparathyroidism.

Journal Article↗