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Biomedical subjects

L Berman

Publications and source records attributed to L Berman.

At least 91 records · Page 5Linked to original sources
PubMed1976

Structural abnormalities of muscle tissue in ankylosing spondylitis.

Muscle tissue of patients with ankylosing spondylitis has been studied by means of histology, histochemistry and electron microscopy and has been shown to be grossly abnormal. The underlying basis of the muscle changes is probably neuropathic and we believe that these changes form part of the over-all pathology of this disease.

Adult↗
PubMed1976

Streptozotocin and renal amyloidosis in the Syrian hamster.

In the Syrian hamster, administration of the drug streptozotocin was associated with an increased incidence and severity of renal amyloidosis. Some of the more severely affected animals showed a frankly nephrotic picture. Although some of the diseased animals showed decreased levels of serum albumin, no other definite changes in serum proteins were noted, nor was there any evidence of glomerular immunoglobulin or immune complex deposition. None of the lesions previously found after administration of streptozotocin in the Chinese hamster were encountered.

Amyloidosis↗
PubMed1975

Xanthine, hypoxanthine and muscle pain. Histochemical and biochemical observations.

A suspected case of xanthine oxidase deficiency has been further investigated. The patient complained of arthralgia and myalgia. Further studies included histochemical and ultramicroscopic analysis of muscle sarcoplasmic reticulum, and biochemical studies. High levels of xanthine and hypoxanthine were found, while uric acid was absent in the muscle extracts.

Adenosine Triphosphatases↗
PubMed1968

Hereditary sideroblastic anemia and glucose-6-phosphate dehydrogenase deficiency in a Negro family.

Detailed clinical and genetic studies have been performed in a Negro family, which segregated for sex-linked sideroblastic anemia and glucose-6-phosphate dehydrogenase (G-6-DP) deficiency. This is the first such pedigree reported. Males affected with sideroblastic anemia had growth retardation, hypochromic microcytic anemia, elevated serum iron, decreased unsaturated iron-binding capacity, increased (59)Fe clearance, low (59)Fe incorporation into erythrocytes, normal erythrocyte survival ((51)Cr), normal hemoglobin electrophoretic pattern, erythroblastic hyperplasia of marrow with increased iron, and marked increase in marrow sideroblasts, particularly ringed sideroblasts. Perinuclear deposition of ferric aggregates was demonstrated to be intramitochondrial by electron microscopy. Female carriers of the sideroblastic gene were normal but exhibited a dimorphic population of erythrocytes including normocytic and microcytic cells. The bone marrow studies in the female (mother) showed ringed marrow sideroblasts. Studies of G-6-PD involved the methemoglobin elution test for G-6-PD activity of individual erythrocytes, quantitative G-6-PD assay, and electrophoresis. In the pedigree, linkage information was obtained from a doubly heterozygous woman, four of her sons, and five of her daughters. Three sons were doubly affected, and one was normal. One daughter appeared to be a recombinant. The genes appeared to be linked in the coupling phase in the mother. The maximum likelihood estimate of the recombination value was 0.14. By means of Price-Jones curves, the microcytic red cells in peripheral blood were quantitated in female carriers. The sideroblast count in the bone marrow in the mother corresponded closely to the percentage of microcytic cells in peripheral blood. This is the second example in which the cellular expression of a sex-linked trait has been documented in the human red cells, the first one being G-6-PD deficiency. The coexistence of the two genes in doubly heterozygous females has made it possible to study correlations in cell counts; our studies showed a strong positive correlation except in the probable recombinant in which a reciprocal relation held which indicated that X-inactivation was at least regional, rather than locus by locus.

Anemia, Hypochromic↗