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Biomedical subjects

N W Levin

Publications and source records attributed to N W Levin.

At least 163 records · Page 9Linked to original sources
PubMed1977

Focal glomerulonephritis and interstitial nephritis in methicillin-treated, heroin-related infective endocarditis.

A drug addict with staphylococcal endocarditis treated with methicillin, who developed massive proteinuria and acute nephritic syndrome is described. Discontinuation of methicillin therapy and appropriate antibiotic treatment of endocarditis led to clinical improvement, emphasizing the need to promptly discontinue potential nephrotoxic agents when abnormalities in renal function appear. The clinical course and results of renal biopsy studies suggest multiple causes of the renal lesions in this patient.

Adult↗
PubMed1977

18F scintigraphy in the early diagnosis of osteonecrosis of the femoral head in chronic hemodialysis and transplantation.

Osteonecrosis of the femoral head results in an increased uptake of 18F due to a reparative reaction in the necrotic area and its surroundings. Twenty hemodialysis and twenty-seven post-transplant patients were studied serially. In the hemodialysis group, nine patients had positive scintigraphs and eleven had negative studies. All were asymptomatic. In the transplant group, twelve were positive and fifteen were negative. Four patients with positive scans later developed unequivocal clinical and radiographic evidence of osteonecrosis. Patients with negative scans have been asymptomatic and without radiological abnormalities. Age, sex, duration of dialysis, bone mineral densitometry, total steroid dose, duration of hospitalization after transplantation, and serum chemistries were not different in positive and negative patients. All patients on alternate-day steroids have negative scans. A positive 18F scintigraph antedates the occurrence of clinical and radiological findings of osteonecrosis.

Adult↗
PubMed1976

Ribonucleic acid synthesis in the renal cortex at the initiation of compensatory growth.

The mechanisms responsible for the increase in RNA per cell during the first 48h of renal compensatory growth were studied in the renal cortex. Unilaterally nephrectomized, sham-operated or non-operated rats were used. Incorporation into RNA of labelled precursors was studied in vivo and in vitro. Sham-operation produced significant changes in precursor incorporation, absolute amounts of UTP and RNA, and the rate of RNA synthesis. At 6h after surgery, the amount of RNA decreased in sham-operated controls, whereas that in growing cortex remained unchanged. Incorporation into RNA in vivo was greater in the growing cortex, although the rate of RNA synthesis was not increased. At 24h, precursor incorporation into RNA and UTP and RNA synthesis were all increased in the growing cortex. In contrast with results obtained in vivo, slices of growing cortex incorporated less labelled precursor into RNA than did cortex slices from sham-operated controls, from 3 to 48h. Maximal differences were found from 6 to 24h. An attempt was made to equalize endogenous precursor pool sizes by increasing the concentration of unlabelled uridine in the media; incorporation differences were narrowed significantly. Serum from nephrectomized animals did not increase precursor incorporation into RNA in vitro. An increase in RNA synthesis is an important factor in RNA accretion in the renal cortex beyond 12h of compensatory growth. This is accompanied by increased UTP content and preceded by expansion of other pools. The amount of labelled precursor incorporated into RNA is greatly influenced by its delivery rate to the growing kidney in vivo and by intracellular dilution of expanded precursor pools in vitro.

Animals↗
PubMed1975

Relation of renal growth to diabetic glomerulosclerosis.

In diabetes mellitus abnormal quantiites of glycoprotein may be formed in the basement membrane of the glomerulus and both renal function and size may increase. It is suggested that these changes, of quite different potential significance, have a common origin an increased rate of uridine-triphosphate synthesis resulting from hyperglycemia.

Animals↗
PubMed1973

Inhibition of primary ADP-induced platelet aggregation in normal subjects after administration of nitrofurantoin (furadantin).

The evidence indicating that platelets may play a role in the occurrence of certain thromboembolic phenomena has stimulated a search for inhibitors of platelet function. This report presents data to indicate that nitrofurantoin is a potent inhibitor of primary ADP-induced platelet aggregation. The addition of 10 muM nitrofurantoin to citrated platelet-rich plasma obtained from 12 normal subjects produced a 29+/-6% (2 SD) inhibition of the velocity of platelet aggregation induced by 2 muM ADP. The inhibitory effect of nitrofurantoin demonstrated competitive kinetics in respect to ADP. The intravenous (180 mg) or oral (200 mg) administration of nitrofurantoin produced a serum nitrofurantoin concentration ranging from 2.7 to 23 muM in 28 normal subjects. Platelet-rich plasma obtained from these subjects demonstrated inhibition of the velocity of ADP-induced platelet aggregation that correlated with the log of the serum nitrofurantoin concentration (P < 0.001). Collagen-induced platelet aggregation was also inhibited in a dose-related manner, and the bleeding time was significantly prolonged in the two subjects with the highest serum nitrofurantoin concentration. These studies indicate that nitrofurantoin in vivo inhibits platelet function to a degree that is proportional to the serum nitrofurantoin concentration.

Adenosine Diphosphate↗