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Biomedical subjects

S M Wolfe

Publications and source records attributed to S M Wolfe.

At least 55 records · Page 3Linked to original sources
PubMed1987

Myopathy in sarcoidosis: clinical and pathologic study of four cases and review of the literature.

The clinical course and muscle biopsy findings of four adults with sarcoidosis who developed a myopathy are described. Three patients had evidence of an inflammatory myopathy and elevated CPK. Two patients had no detectable granulomas at muscle biopsy and may represent a separate autoimmune disorder (polymyositis) concurrent with sarcoidosis. Asymptomatic muscle disease in sarcoidosis probably occurs with a much greater frequency than symptomatic disease. Isolated sarcoid myopathy without prior or concurrent organ involvement has been described, but comprehensive autopsy studies to confirm this are lacking. The origin of symptoms associated with granulomas is obscure and may be mediated through the effects of lymphokines and monokines. Corticosteroids seem to play a useful role in therapy, but treatment over a prolonged period may be necessary. The use of cytotoxic agents is largely untested.

Adult↗
PubMed1987

Hypertrophic osteoarthropathy associated with a rejected liver transplant.

A patient with severe hepatic transplant rejection presented with evidence of hypertrophic osteoarthropathy. The classic triad of clubbing, periostitis, and arthritis was present along with typical radiographic and bone scan findings. A second liver transplant was not successful and the patient died secondary to massive bleeding. Although hypertrophic osteoarthropathy is known to occur rarely in association with chronic liver disease, it has not been reported accompanying liver transplant rejection. This syndrome is to be differentiated from other causes of arthritis and musculoskeletal pain in liver transplant patients and may contribute towards additional morbidity in these patients.

Adult↗
PubMed1982

Benoxaprofen.

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Advertising↗
PubMed1982

The marketing of a drug.

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Chemical and Drug Induced Liver Injury↗
PubMed1975

Oxygen consumption of human blood platelets. I. Effect of thrombin.

The effect of thrombin on the oxygen consumption of washed human platelets was measured polarographically with the Clark oxygen electrode. The average basal respiratory rate was 18 plus or minus 1.6 (mean plus or minus S.E.) natoms oxygen per min per 10-9 platelets. Thrombin (1.9 units/ml) caused a 4-13-fold increase in the rate of oxygen consumption (138 plus or minus 14 (mean plus or minus S.E.) natoms oxygen per min per 10-9 platelets). The thrombin-stimulated increase of oxygen consumption was transient, lasting from 1 to 1.5 min before returning to the respiratory rate observed before the thrombin addition. Release of platelet constituents appeared to precede the stimulation of oxygen consumption. These results may provide a basis for explaining the discrepancy in the literature concerning the effects of thrombin on platelet respiration.

Blood Platelets↗
PubMed1975

Oxygen consumption of human blood platelets. II. Effect of inhibitors on thrombin-induced oxygen burst.

The effect of selected inhibitors on the thrombin-stimulated burst and the basal oxygen consumption of washed human platelets were investigated and compared with inhibition of the release reaction. Cyanide (0.2 mM) caused complete inhibition of the basal respiration, but only 15% inhibition of the thrombin-stimulated burst of oxygen consumption. Similar differential inhibitory effects were observed with oligomycin, antimycin, rotenone and N-ethylmaleimide. Prostaglandin E1 (0.03 mM) and acetylsalicylic acid (0.8 mM) had little effect on basal respiration, but inhibited the thrombin-stimulated burst of oxygen consumption. N-Ethylmaleimide (0.4 mM) inhibited the release of calcium from platelets by 90%, while prostaglandin E1, acetylsalicylic acid and the above mitochondrial inhibitors caused no more than 30% inhibition of the release reaction. Our results provide evidence that basal respiration and a portion of the thrombin-stimulated burst of oxygen consumption are involved in respiratory chain phosphorylation, and that this component of the thrombin-stimulated burst may be coupled to the maintenance of the release reaction.

Antimetabolites↗