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Biomedical subjects

J S Kaufmann

Publications and source records attributed to J S Kaufmann.

11 recordsLinked to original sources
PubMed1984

Effects of benoxaprofen on human neutrophil function.

In vitro assays of human neutrophil phagocytosis, adherence, enzyme release, and response to chemotactic factors were utilized to determine the effects of benoxaprofen on these cells. At concentrations of 30 and 300 micrograms/ml benoxaprofen partially inhibited phagocytosis without affecting adherence. High concentrations (300 micrograms/ml) of benoxaprofen, but not aspirin or gold, enhanced the release of the granular enzymes beta-glucuronidase and lysozyme, but not the release of the cytoplasmic enzyme lactic dehydrogenase from both resting and phagocytosing neutrophils. High concentrations (300 micrograms/ml) of benoxaprofen also inhibited the response of neutrophils to chemotactic factors as determined by both the leading front and leukotactic index methods. These unique in vitro effects of this antiinflammatory agent are compatible with recent clinical reports concerning its efficacy and toxicity.

Cell Adhesion↗
PubMed1977

Fenoprofen, aspirin, and gold induction in rheumatoid arthritis.

Fenoprofen calcium (2,400 mg/day) or aspirin (3,900 mg/day) was administered in double-blind fashion to 20 rheumatoid patients during 6 months of gold induction therapy, and to 20 rheumatoid patients not receiving gold. Among both the gold-treated and nongold-treated patients, the fenoprofen and aspirin groups improved equally in all but one parameter of disease activity. Fenoprofen and aspirin did not differ significantly in the observed prevalences of abdominal discomfort, guaiac-positive stools, or peptic ulcers. Aspirin was associated with significantly higher mean serum glutamic oxaloacetic transaminase (SGOT) levels than fenoprofen, but only among patients undergoing gold induction. Comparison of efficacy parameters between patients treated with gold and patients treated with oral drugs alone revealed significant differences favoring gold.

Adult↗
PubMed1976

Ultrasonic enhancement of nitrogen mustard cytotoxicity in mouse leukemia.

Mouse leukemia L1210 cells were exposed to continuous wave 2 MHz, 10 W/cm(2) ultrasound for 10 minutes while suspended in nitrogen mustard solution in vitro. Mice subsequently inoculated with these cells had longer survival times than control animals that received cells exposed to the drug but not ultrasound. Without the drug, ultrasound did not alter survival time. Tracer studies revealed increased cellular accumulation of drug under the influence of ultrasound.

Animals↗
PubMed1973

Effects of a false neurotransmitter, p-hydroxynorephedrine, on the function of adrenergic neurons in hypertensive patients.

Previous studies have shown that amphetamine and p-hydroxyamphetamine impair adrenergic transmission, and it has been suggested that this effect is mediated by an active metabolite, p-hydroxynorephedrine (PHN). Studies in experimental animals have shown that PHN can deplete and substitute for norepinephrine (NE) in the transmitter pool, thus meeting the criteria of a false neurotransmitter. The pharmacologic effects of PHN on adrenergic function and NE synthesis were studied in eight hypertensive patients and compared with placebo. Mean erect and supine blood pressure (BP) decreased 22/14 and 9/6 mm Hg, respectively, during PHN 600 mg daily. The post-Valsalva diastolic overshoot was abolished. The pressor sensitivity to tyramine decreased whereas the pressor response to NE was enhanced. A mild natriuresis occurred. The 24 h urinary excretion of catecholamines and catecholamine metabolites during the administration of PHN compared with placebo changed as follows: vanillylmandelic acid (VMA), 42% decrease; NE. 42% decrease; normetanephrine (NM), 400% increase: metanephrine, unchanged; dopamine, 40% decrease; while homovanillic acid was unchanged. The sum of VMA, NE, and NM decreased 23%. The posttreatment urinary excretion of PHN was biexponential with first and second phase half-lives of 13 and 55 h. respectively. The time of the second phase closely approximated the recovery of the changes in BP and excretion of VMA. No effects of PHN on the central nervous system were observed. These studies show that PHN acts peripherally to interfere with adrenergic function and NE synthesis in hypertensive patients with a resultant decrease in BP.

Adult↗