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Biomedical subjects

H Bergman

Publications and source records attributed to H Bergman.

At least 145 records · Page 8Linked to original sources
PubMed1983

Alcohol consumption, neuropsychological status and computer-tomographic findings in a random sample of men and women from the general population.

There was no correlation between reported amount of alcohol consumed on each drinking occasion per se and neuropsychological and neuroradiological signs of cerebral disorder in age-stratified random sample of 200 men and 200 women taken from the general population. Furthermore, moderate to heavy social drinking as assessed by an index based on amount of alcohol consumed on each drinking occasion and the responses to some other alcohol-habit questions was not associated with signs of cerebral disorder. Alcohol dependence, however, was associated with signs often diagnosed in alcoholic patients but milder in degree. There were indications of important differences between men and women with regard to the relationship between advanced alcohol-habits and cerebral disorder.

Adult↗
PubMed1983

Fibrosarcoma of the penis: case report and review of the literature.

We report a case of fibrosarcoma of the penis and review the literature. We believe that amputation is the most effective therapy and the role of lymphadenectomy is equivocal. All cases should be reported to better define the roles of various oncologic modalities of therapy.

Aged↗
PubMed1983

Variation in cell surface morphology of two 90Sr-induced osteosarcomas serially transplanted in CBA mice.

The induction of skeletal tumours, which can be classified as osteosarcomas of many different types, is considered to be the primary carcinogenic effect of radiostrontium. In the present report the cell surface morphology in vivo of 90Sr-induced osteosarcoma cells was investigated, since a variety of tumour cells--and especially those investigated in vitro--have been shown to possess morphologic changes compared with their normal counterparts. Using scanning electron microscopy, variations in cell surface morphology were observed in 2 tumour series, which were serially transplanted in mice for 45 and 60 transfer generations, respectively. The slow-growing osteosarcoma cells of the early transfer generations, of osteoblastic as well as fibroblastic type, seemed to have more cytopodia than the fast-growing osteosarcoma cells from later generations. This may be due to the fact that slowly growing cell populations have a large proportion of cells in G1, in which stage there is a higher frequency of cellular cytopodia.

Animals↗
PubMed1982

Induction of porphyria in the rat by chronic versus acute exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Chronic oral administration of 1 microgram . kg-1 . week-1 of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to female rats for 16 weeks resulted in hepatic porphyria. In contrast, administration of single oral doses as high as 30 micrograms/kg did not produce porphyria, either acutely or 16 weeks later. Activities of hepatic drug-metabolizing enzymes [aryl hydrocarbon hydroxylase (AHH) and glucuronyl transferase] were increased by chronic oral doses of TCDD as low as 0.01 microgram . kg-1 . week-1. When animals were dosed with TCDD chronically and then allowed to recover for 6 months, AHH and glucuronyl transferase activities returned toward normal (98 and 86% recovery). However, animals showed only partial recovery from TCDD-induced porphyria. Hepatic porphyrin levels did decrease during this period, but urinary porphyrins and the rate-limiting enzyme in porphyrin synthesis, delta-aminolevulinic acid synthetase, remained maximally elevated during the 6-month recovery period. It is concluded that single doses of TCDD do not produce porphyria in the rat, but that TCDD is porphyrogenic when given chronically. Moreover, when TCDD administration is stopped, recovery from the porphyrogenic effects of TCDD is very slow and does not correlate with the biological half-life of TCDD in the rat.

5-Aminolevulinate Synthetase↗
PubMed1982

Inhibition of benzo(a)pyrene monooxygenase by alpha-naphthoflavone may be partially mediated by the metabolite 9-hydroxy-alpha-naphthoflavone.

alpha-Naphthoflavone (ANF) inhibits beta-naphthoflavone-induced rat liver microsomal benzo(a)pyrene metabolism and is transformed by these microsomes into alpha-naphthoflavone metabolites. We determined the inhibitory effect on benzo(a)pyrene (B(a)P) metabolism of several of these metabolites and of 6-methoxy-ANF, using beta-naphthoflavone-induced rat liver microsomes. 9-Hydroxy-ANF was the most active inhibitor (I50 = 1.47 microM) and was metabolized from ANF by these hepatic microsomes in concentrations which are inhibitory. Therefore, 9-hydroxy-ANF a microsomal metabolite of ANF, may play a role in the inhibition of B(a)P oxidation by ANF.

Animals↗
PubMed1981

Noradrenaline augments tetanic potentiation of transmitter release by a calcium dependent process.

Noradrenaline (25 microM-50 microM) causes an increase in tetanic potentiation and in the augmentation phase of posttetanic potentiation of miniature and plate potential frequency. These effects were observed at both the frog and the rat neuromuscular junctions. The action of noradrenaline on quantal transmitter release depends on the presence of calcium ions in the extracellular medium.

Animals↗
PubMed1981

Psychomotor performance and real driving performance of outpatients receiving diazepam.

The primary aim of this study was to compare task performance in a laboratory test and real driving performance of outpatients receiving diazepam medication with those of control subjects. Plasma and saliva samples were taken to investigate a level-response relationship. Real driving performance was measured by trained observers. The design of the laboratory test was based on a vigilance task (high attention) directly followed by a simple eye-hand coordination tasks (low attention). Twenty-two males participated in the study. Diazepam was given orally by prescription, mostly as a maintenance dose of 5 mg three times a day. Patients receiving diazepam showed impaired performance in the driving test and the low-attention task. Furthermore, the results indicate no relationship between plasma or saliva levels of diazepam and/or its metabolite N-desmethyldiazepam and real driving performance and/or laboratory task performance.

Adult↗
PubMed1981

Metabolism of alpha-naphthoflavone by rat liver microsomes.

alpha-Naphthoflavone (ANF) or 7,8-benzoflavone, a synthetic flavonoid, has been widely used in biochemical and biological studies concerning the mechanisms of action of chemical carcinogens. It has been shown previously that ANF inhibits benzo(a)pyrene metabolism by beta-naphthoflavone (BNF)-induced rat liver microsomes but has no inhibitory effects on benzo(a)pyrene metabolism in phenobarbital (PB)-induced rat liver microsomes. This study shows that ANF gives type 1 binding spectra with and is metabolized by both BNF- and PB-induced rat liver microsomes. Specific metabolites identified by ultraviolet and mass spectra and in some cases by cochromatography with authentic standards were: 6-hydroxy-alpha-naphthoflavone, 9-hydroxy-alpha-naphthoflavone, alpha-naphthoflavone-5,6-oxide, and 5,6-dihydro-5,6-dihydroxy-alpha-naphthoflavone. Metabolism at the 5,6 bond of ANF accounted for 73 and 86% of the total organic soluble metabolites produced by PB- and BNF-induced microsomes, respectively. This result is in concert with previous observations on the role of 6 substitution and the loss of inhibitory activity of ANF in BNF-induced rat liver microsomes. Metabolism of ANF is mediated by the cytochrome P-450 mixed-function oxidases, because it is dependent on NADPH and inhibited by carbon monoxide and other cytochrome P-450 inhibitors. BNF-induced microsomes metabolize ANF to 5,6-dihydro-5,6-dihydroxy-alpha-naphthoflavone to a much greater extent than do PB-induced microsomes.

Animals↗
PubMed1980

Computed-tomography of the brain and neuropsychological assessement of alcoholic patients.

The purpose of the project is to assess the state of the brain of alcoholic patients by means of computerized tomography and by neuropsychological performance and to correlate the findings with the clinical course of alcohol dependence. The investigated group is a consecutive series of 106 patients admitted for treatment of alcoholism and participating in a prospective program of mapping medical, social and psychological characteristics. Cortical changes were diagnosed in 59.6 % of the investigated patients, enlarged lateral ventricles in 33.3 % and an enlarged 3rd ventricle in 48.3 %. With regard to neuropsychological functioning 54.2 % of the sample scored in the mildly to severely impaired region of the Halstead Impairment Index and 63.5 % were considered to show signs of an intellectual impairment in the psychologist's overall assessment of test results. Cortical changes and ventricular enlargement seemed to follow different courses in the investigated group since they were uncorrelated in the sub-group of older patients with long duration of heavy drinking. The correlations between neuropsychological functioning and morphological changes were generally low. However, the results suggest that learning and memory deficits indicate subcortical changes in the brains of alcoholic patients while a high score on the Halstead Impairment Index indicated cortical changes.

Adult↗