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Biomedical subjects

M Black

Publications and source records attributed to M Black.

At least 199 records · Page 11Linked to original sources
PubMed1976

Safety of the bolus administration of gentamicin.

A study was done to assess the safety of gentamicin administration by a bolus method. A total of 63 patients were randomly treated with intravenous gentamicin by bolus administration (3 to 5 min) and by slow infusion (2 h). Serum gentamicin levels were measured. Renal and audiovestibular function were monitored. Pure-tone audiometry was performed at the beginning, on day 3, and at the end of therapy. The study revealed that the bolus administration was safe and nontoxic.

Adult↗
PubMed1976

Dimensions of adolescent psychopathology and their prognostic significance for treatment outcome.

The mothers of 87 male and female adolescents accepted at a counseling agency described their offspring by completing the Institute of Juvenile Research Behavior Checklist. A factor analysis of the initial data yielded nine symptom factors. These were used in combination with selected demographic variables, to compare the 54 continuers in treatment with the 22 early defectors and the 18 cases improved after a year of a full course of treatment with the 16 unimproved cases. Both discriminant function analyses indicated that the groups could be successfully differentiated; however, variables most predictive of continuance in treatment were not most predictive of a successful outcome.

Adolescent↗
PubMed1975

Increased incidence of isoniazid hepatitis in rapid acetylators: possible relation to hydranize metabolites.

Approximately 10% to 20% of isoniazid recipients manifest biochemical evidence of liver injury. A smaller number of patients develop clinically overt hepatitis. Isoniazid is metabolized in man at extremely variable rates, and the rate is under genetic control. Two separate clinical studies have noted a possible relation between susceptibility of patients to isoniazid liver injury and rapid metabolism (acetylation) of the drug. For this reason, 21 patients who had recovered from probable isoniazid hepatitis and 5 patients who previously had manifested biochemical evidence of mild isoniazid liver injury were genetically phenotyped as rapid or slow isoniazid acetylators by the sulfamethazine method. The rapid phenotype was found in 86% of patients with probable hepatitis and in 60% of the possible ones, whereas the expected frequency was 45%. Eximination of isoniazid metabolites revealed that rapid acetylators hydrolze much more isoniazid to isonic otinic hydrazine moiety than do slow acetylators. The hydrazine moiety liberated from isoniazed is primarily acetylhydrazine, and studies in animals show this metabolite to be converted to a potent acylating agent that produces liver necrosis. We suggest that release of the hepatotoxic hydrazino moiety of isoniazid in man is responsible for isoniazid liver injury.

Acetylation↗
PubMed1975

Systematic observation of play behavior in autistic children.

The play behavior, defined as interaction with peers and objects, of five autistic children was systematically observed in four environments, i.e., a stark environment, a theraplay unit, a playroom, and an outside play deck. The preliminary results suggested that (1) with some children environment has little or no effect on their play behavior; (2) with multiple objects, autistic children frequently related to the objects rather than to their peers; (3) object play was most frequently at the manipulative stage and often included repetitive and negative behavior; (4) within a confined space with no objects present, autistic children frequently engaged in solitary repetitive behavior; and (5) within a confined space designed to facilitate a movement flow (theraplay), autistic children modeled and imitated and were involved in gross motor play together.

Aggression↗
PubMed1975

Isoniazid-associated hepatitis in 114 patients.

Analysis of the overt hepatic disease that developed in 114 patients while taking isoniazid for chemoprophylaxis of tuberculosis showed it to be mainly hepatocellular. The severity of the hepatic injury was manifested by the 13 fatalities (12.3%) and by the histological demonstration of submassive necrosis in 9 and massive necrosis in 4 patients. The 20 other patients from whom hepatic tissue was available for study included 16 with moderately severe acute hepatocellular injury (4 had a mixed hepatocellular-cholestatic pattern), and 4 with chronic hepatic diseases (1 had cirrhosis). Clinical manifestations of hepatic disease prior to the onset of jaundice included vague digestive complaints in 55% of the group and "viral' disease-like complaints in 35%, some with and some without gastrointestinal symptoms. Jaundice was the presenting complaint in 10% of patients. Fever and rash were reported in very few patients (less than 4%) and eosinophilia of modest degree was noted in approximately 10%. Hepatic injury was recognized during the 1st month of isoniazid administration in 15% and during the 2nd month in an additional 31%. In the remaining 54% of patients, the drug had been administered for periods of 2 to 11 months before hepatic injury was noted. Analyses of variables suggested that hepatic injury which presented after 2 months, especially with bilirubin levels that exceeded 20 mg per 100 ml, was more likely to have a fatal outcome than disease that presented during the first 2 months even with higher bilirubin levels. The case fatality rate was significantly higher in black females than in black males or in whites of either sex. The observations of the present study offer no support for the view that isoniazid-induced hepatic disease results from hypersensitivity to the drug. Other data that support the view that hepatotoxic metabolites of isoniazid may be responsible for the injury are considered.

Age Factors↗