Biomedical subjects
Publications and source records attributed to S Moses.
A case of noninfectious arthritis was associated with meningococcal meningitis. Elevated levels of immune complexes were demonstrated in both serum and synovial fluid by the C1q binding assay and Raji cell assay. We believe this complication of meningococcal infection is another disorder in which immune complexes may play a pathogenic role.
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The effects of several oxidant agents on metabolic and membrane parameters of glucose-6-phosphate dehydrogenase deficient erythrocytes (Mediterranean type) were examined in order to explore a possible common mechanism for their action on the deficient cells. The increase in methemoglobin and the decrease in GSH levels elicited by e oxidants were more pronounced in the deficient cells, provided glucose was present during the incubation of the cells with the drugs. However, glucose did not differentially modify other parameters: ATP level, filterability and osmotic fragility. There was no correlation between the effects produced by the oxidants on various parameters in either normal or deficient cells. It is concluded that in terms of the parameters studied more than one mechanism for the effects of the oxidants on cells should be assumed.
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The correlation between blood glucose levels, the concentration of glycogen, the activities of glycogen synthase and phosphorylase and their respective kinases and phosphatases was examined in liver of rat fetuses between day 18 of gestation and one day after birth. Between day 18 and 21 there is a rapid increase in the concentration of glycogen and in the activity of synthase a and a much slower increase in the activity of phosphorylase a. The activity of the respective kinases increased rapidly during this period and reached maximum on day 21. The activity of synthase phosphatase and phosphorylase phosphatase increased after day 18, to reach a maximum on day 19 and 20, respectively, but decreased again towards day 21. The possibility that the changes in glycogen concentration and enzyme activities were related to an effect of glucose or AMP on the respective phosphatases was considered. It was found that the Km of phosphorylase phosphatase for glucose in the prenatal period was 5--7 mM, as in the adult. Since the level of blood glucose during this period was constant (2.8 mM), an effect of glucose on phosphatase activity seems unlikely. AMP concentration increased between day 18 and 21 from 6--15 nmol/g. In view of the low level of phosphorylase a activity during this period, the increase in AMP concentration is not considered to be important in the regulation of glycogen breakdown at this time. Immediately after birth blood glucose levels dropped to 5 mg/dl. This was accompanied by a rapid decrease in glycogen concentration and in the activity of glycogen synthase and a rise in phosphorylase activity. Blood glucose levels returned to the initial level within 1 h after birth, whereas the changes in glycogen concentration and enzyme activities continued for at least 3 h after birth. On day 22 all parameters examined had reached the level found in adult rat liver. It is suggested that the rapid changes observed immediately after birth are due to an effect of gypoglycemia mediated by hormones and cannot be ascribed to direct effects of metabolites on the enzyme systems involved.
Patients with systemic lupus erythematosus (SLE) and other connective tissue diseases were surveyed for the presence of antibodies to normal DNA, antibodies to a ribonuclease-insensitive acidic nuclear protein, and immune deposits in normal skin. While 80% of patients with SLE had abnormal values for at least two of these three tests, none of the patients with other connective tissue diseases had more than one abnormal value. The presence of RBC autoantibodies was found along with one of the other abnormal laboratory tests in 76% of patients with SLE, including 14% of patients not found to have two abnormal tests. None of the other patients tested had RBC autoantibodies. These findings suggest that a set of laboratory tests can be constructed as criteria for a diagnosis of SLE that would be as specific as the presently employed American Rheumatism Association criteria.
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In a Jewish Moroccan inbred family, 8 of 12 siblings were found to have multiple deficiencies of pituitary hormones, including GH, TSH and gonadotrophins. The parents showed no deficiency and are in good health, as are the other 4 siblings. The investigations carried out indicate that in this family the etiology is hereditary in nature, probably being autosomal recessive, with the defect located in the pituitary gland.
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Two families with Dyggve-Melchior-Clausen syndrome are reported. In the first family, Jews from Morocco, six of 10 siblings are affected. In the second family, a consanguineous marriage of Arabs from Gaza, two of three children are affected. A description of the skeletal changes in patients ranging in age from 4 to 25 years is presented. The radiologic signs of generalized platyspondyly with double humped end plates and the lace-like appearance of thickened iliac crests are pathognomonic and distinctive of the syndrome. The diagnostic features of the disease are compared to those of Morguio's disease, spondyloepiphyseal dysplasia tarda, and spondylometaphyseal dysplasia.
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Sickle cell thalassemia in an Israeli family of Indian extraction is described. The family demonstrates the segregation of the betaS- and beta-thal genes and the interaction phenomenon known to exist in this condition is demonstrated clearly in the propositus.
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A four and a half year old girl with delayed appearance of traumatic hemopericardium, detected radiologically despite misleading clinical manifestations, is presented. The presence of cardiomegaly and a needle in the right upper mediastinum on the chest roentgenogram and its partial motion together with diminished cardiac pulsations at fluoroscopy led to angiocardiography. The radiological demonstration of hemopericardium due to the needle penetrating the aortic root, enabled successful surgical intervention.
Erythrocytes affected by hereditary spherocytosis (HS), obtained from several splenectomized patients, showed a varying degree of elevated osmotic fragility. In order to evaluate a possible role of the erythrocyte membrane lipids in HS, microviscosity of the membrane lipid core was measured by a fluorescence-polarization technique. Intact HS-affected red cells, as well as their ghost membranes and liposomes prepared from their lipid extract, all showed a distinctly higher micro-viscosity than the respective normal control. The increased microviscosity correlated with the severity of HS. The data support the proposition that the defect in HS-affected red cells is associated, at least in part, with alterations in the membrane lipids.
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