Molecular studies of the fourth component of complement (C4) in glomerulonephritis.
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Biomedical subjects
Publications and source records attributed to C C Porter.
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A population-based study of hemolytic-uremic syndrome (HUS) revealed that 20 child residents of Washington, DC and Baltimore, Maryland were hospitalized with HUS from January 1979 through September 1983. The number of cases peaked during the summer and fall; none occurred during the winter. Incidence of hospitalized cases was higher in Whites and girls than in Blacks or boys, and the average annual incidence was 1.08 cases/100,000 children less than 5 year old. This study demonstrates that HUS is not unique to the West Coast, as previously suggested.
Nephropathic cystinosis causes renal death by approximately age 10 years. With increased life span due to kidney transplantation, ten to 25 years of cystine accumulation has resulted in pancreatic complications in individuals with cystinosis. We noted severe hyperglycemia in five posttransplant patients, three of whom remained insulin-dependent diabetics several years after transplant. The clinical findings were not consistent with steroid-dependent or insulin-resistant diabetes. Pancreatic cystine deposition was detected histologically and biochemically on post-mortem examination of two other patients. We conclude that hyperglycemia may be anticipated in the immediate posttransplant period in cystinotic patients and that some patients will require insulin therapy years later. The use of cystine-depleting agents should be considered in posttransplant cystinosis as an attempt to prevent potential damage to the pancreas and other organs from cystine deposition.
Autoimmune thrombocytopenia unresponsive to corticosteroid therapy developed in a 16-year-old female with long-standing Sjögren's syndrome. Serial plasma exchange caused a linear decrease in platelet antibody titer associated with a concomitant rise in platelet count. Statistical analysis of sequential platelet counts revealed an increase with plasmapheresis and immunosuppression that was significantly greater than that achieved with immunosuppression alone (p less than 0.005).
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6-Chloro-2(1-piperazinyl) quinoxaline (CPQ) was examined pharmacologically and biochemically as an inhibitor of the neuronal reuptake of serotonin, dopamine and norepinephrine. The compound was 25-50 times more potent than chlorimipramine in potentiating the head-twitch response to 5-hydroxytryptophan (5-HTP) and in antagonizing p-chloromethamphetamine (PCMA)-induced depletion of brain serotonin in rats. CPQ also potentiated the forepaw clonus produced by 5HTP in rats and antagonized PCMA-induced head twitches. At dose levels 30 times those necessary to significantly affect serotoninergic systems, CPQ was ineffective in antagonizing either tetrabenazine-induced sedation in mice or the depletion of rat brain and heart norepinephrine or brain dopamine produced by 4, alpha-dimethylmeta-tyramine (H77/77). The data indicate that CPQ exhibits a high degree of potency and selectivity in inhibiting the neuronal reuptake of serotonin.
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Equipment is described for measuring the pull exerted by mice to escape tail restraint and enter a black box. Alcohol, at doses exceeding about 2.5 g/kg, intraperitoneally, significantly decreased "muscle pull", measured 5-60 min after administration. Fifty per cent depression of muscle pull was obtained with doses of about 3.04, 3.18 and 3.55 g/kg of alcohol, 15, 30 and 60 min after alcohol administration, respectively. Depression of muscle pull correlated with alcohol concentrations in the blood plasma. The data show that muscle pull was decreased in only a few animals with plasma alcohol concentrations of less than about 250 mg%, but was significantly depressed in animals with plasma alcohol concentrations of 350 mg% or more. Although differing from it in some respects, the method described is similar to the tilting-plane method which has been used in studies dealing with the effect of alcohol in rats and mice.
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