Biomedical subjects
Publications and source records attributed to D Samuel.
Anterior sacral meningocele is a rare congenital meningeal cyst herniating through a bony defect in the sacrum. Since its description by Bryant in 1837, only 154 cases have been reported in the world literature. The application of ultrasound and C.T. scan following myelography is discussed.
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Fulminant hepatitis was observed in a 44-year-old patient with cirrhosis, 38 days after the beginning of a treatment by disulfiram. Hepatitis was associated with fever and hypereosinophilia. Liver transplantation was performed with success. We reviewed 15 previously published cases of disulfiram-induced hepatitis. They occurred from 10 to 180 days after the beginning of the treatment by disulfiram, aminotransferases were increased whereas alkaline phosphatases were not markedly changed; there was either focal or widespread necrosis. Fulminant hepatitis was observed mainly in patients with alcoholic chronic liver disease or in patients who continued to ingest disulfiram while jaundice was already present. An immunoallergic mechanism is thought to be responsible for disulfiram-induced hepatitis.
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Monoclonal antibodies to FITC were produced and shown to be specific for the fluorochrome. Molecular weight marker proteins labelled with FITC could be detected after SDS-PAGE and transfer onto nitrocellulose using anti-FITC followed by an anti-mouse IgG-alkaline phosphatase conjugate. The molecular weight of an antigen common to Legionella pneumophila and recognised by a monoclonal antibody could be determined accurately on a Western blot when FITC labelled markers were used as internal standards. The FITC-anti-FITC system was shown to be extremely sensitive, detecting 23.7 amol of BSA-FITC conjugate (equivalent to 1.42 x 10(7) molecules of FITC) in a dot blot assay.
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Glutamic acid decarboxylase (GAD), gamma-[3H]-aminobutyric acid [( 3H]GABA) high-affinity uptake into synaptosomes, and endogenous GABA content were measured in the rat striatum 2-3 weeks following 6-hydroxydopamine injection in the ipsilateral substantia nigra to destroy the nigrostriatal dopaminergic pathway and after kainic acid injection into the centromedial-parafascicular complex of the ipsilateral thalamus to lesion the thalamostriatal input. Both lesions resulted in apparent GAD increase concomitant with a decreased [3H]GABA uptake into striatal synaptosomes. GABA content was increased selectively following the dopaminergic lesion. Kinetic analysis of the uptake process for [3H]GABA showed selectively a decreased Vmax following the dopaminergic lesion; in animals with thalamic lesion, however, the change only concerned the Km, which showed a decreased affinity of the transport sites for [3H]GABA. Determination of Km and Vmax for GAD action on its substrate glutamic acid showed an increased affinity of GAD for glutamic acid in the case of the dopaminergic lesion without any change in Vmax, whereas the thalamic lesion resulted in GAD increase concomitant with a selective increase in Vmax. These data suggest that striatal GABA neurons are under the influence of nigrostriatal dopaminergic neurons which may reduce the GABA turnover, whereas the exact nature of the powerful control also revealed on these neurons following thalamic lesion remains to be determined. Both lesions induced adaptive neurochemical responses of striatal GABA neurons, possibly reflecting in the case of the dopaminergic deprivation an increased GABA turnover.
Voluntary exercise inhibits the reproductive regression associated with a short photoperiod in male or female hamsters. The question addressed by the present study was whether exercise would also attenuate the reproductive regression associated with injection of exogenous melatonin. In male hamsters exercise inhibited the testicular regression, decline in gonadotropin secretion, and reduction in testosterone release associated with two daily injections (15 micrograms) of melatonin in pinealectomized hamsters on long days. After the reproductive system of the sedentary melatonin group had regressed, one-half of these hamsters were placed in cages with exercise wheels. Access to the exercise wheels stimulated testicular recrudescence and restored gonadotropin secretion to levels found in vehicle-injected hamsters. Sedentary female hamsters injected with melatonin tended to go into a state of constant diestrus associated with daily afternoon increases in serum luteinizing hormone, whereas most exercising hamsters injected with melatonin generally continued having regular estrous cycles with proestrus luteinizing-hormone surges. The ability of exercise to inhibit the effect of exogenous melatonin in pinealectomized hamsters suggests that exercise acts, at least in part, by mechanisms other than altering melatonin secretion.
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Immune complexes from rheumatoid arthritis (RA IC) and Hodgkin's disease (HD IC) sera were separated on an anti-C3g affinity column and their ability to stimulate the production of IgM and IgM RF by normal and RA B lymphocytes tested in a culture system in vitro. RA IC stimulated IgM production of which up to 91.3% had IgM RF activity. HD IC were incapable of stimulating the production of IgM and IgM RF. The stimulation of IgM and IgM RF production by RA IC required de novo protein synthesis. Both RA IC and HD IC were capable of significantly inhibiting (from 47.6 to 72.0%) pokeweed mitogen (PWM)-induced and goat F(ab)2 antihuman mu-induced B lymphocyte proliferation. Thus it is proposed that IC present in human pathological sera may regulate immunoglobulin production by an effect on B lymphocyte proliferation while some may, in addition, be capable of inducing IgM RF production from such cells.
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Protoporphyria is an inherited disorder of heme biosynthesis characterized by an overproduction of protoporphyrin in the erythropoietic and hepatic tissues, the relative contribution of which in the metabolic disorder has not been directly quantitated. Excess protoporphyrin is eliminated solely by the liver into the bile and feces. We describe the case of a patient with protoporphyria complicated by severe cirrhosis in whom liver transplantation was performed and resulted in almost complete disappearance of skin photosensitivity manifestations and reduction in the level of protoporphyrin in erythrocytes. However, the level of protoporphyrin in feces was not markedly different before and after liver transplantation, which suggests that overproduction of protoporphyrin was unchanged. These findings are consistent with the view that the diseased liver and ensuing low hepatic clearance of protoporphyrin contributed to accumulation of protoporphyrin in the body and that, at least in this patient, the role of the hepatic tissue in the overproduction of protoporphyrin was small in comparison with that of the erythropoietic tissue.