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Biomedical subjects

D C Williams

Publications and source records attributed to D C Williams.

At least 181 records · Page 10Linked to original sources
PubMed1980

The effect of chloroform inhalation on hepatic glucuronidation and de-glucuronidation mechanisms.

The effect of 2, 4, 6 or 8 exposures to chloroform vapour on hepatic glucuronidating (UDPGA transferase) and de-glucuronidating (beta-glucuronidase) levels has been studied in rats. Successive treatments progressively decreased hepatic UDPGA transferase to a minimum of 53% of the control level. beta-Glucuronidase activity was increased two-fold after only two exposures and remained elevated for subsequent exposures. Cytochrome P450 levels decreased with each exposure. The level of this coenzyme in the treated animals remained lower than that of the control animals for at least 48 hours after treatment. UDPGA transferase was diminished to its lowest levels 9 hours after the final exposure to chloroform and did not achieve the control value for a further 48 hours. The beta-glucuronidase activity remained elevated for 12 hours after final exposure. The present experiment demonstrates that inhalation of toxic solvents such as chloroform decreases the glucuronidating capacity of the liver.

Animals↗
PubMed1980

The effect of isolation stress on some hepatic drug and carcinogen metabolising enzymes in rats.

Rats were subjected to stress by isolation for periods of up to eight days, which produced an elevation in plasma cortisol. In vivo drug metabolism as estimated by the plasma elimination rate of orally-administered antipyrine was not significantly affected by this treatment although there was an apparent decrease in the absorption rate of the drug. In vitro experiments on hepatic microsomal preparations derived from stressed animals indicate that this stress increased in the activity of some enzyme systems concerned with benzo(a)pyrene activation and this correlated with an increased binding of the carcinogen to DNA. The activity of conjugating enzyme which could catalyze the excretion of such carcinogens was not significantly altered. The results indicated that stress could have an important bearing on carcinogenesis by enhancing to a greater extent enzyme systems responsible for activation than those involved in the excretion of polycyclic aromatic hydrocarbons.

Animals↗
PubMed1980

Controlling physician oversupply through certificate of need.

By 1990 the aggregate supply of physicians in the United States is likely to exceed the population's requirements by 10 percent or more. State and regional aggregate and specialty-specific surpluses may be more extreme. Since the demand for physician services appears to be determined to a significant degree by the supply of physicians, the number of physicians who can maintain financially viable practices in a region is not likely to be limited effectively by the normal market interaction of supply and demand. Excessive physician supplies may, however, have a number of deleterious effects, including rapid escalation of health care costs, fragmentation of patient care, and a decrease in the quality of patient care. In this Article, the authors review the potential effectiveness of a number of policy interventions that might be employed to optimize physician supplies in areas of excess. They evaluate the following alternatives: (1) a limit on the number of medical school graduates; (2) control of physician residencies by number and by specialty; (3) creation or implementation of incentive policies; (4) control by hospitals--indirectly by limiting the number of beds, or directly by denying staff privileges; (5) widespread development of HMOs; (6) direct employment by the federal government of the majority of practicing physicians; and (7) creation of certificate of need for physician licensure is the alternative that shows the greatest promise of enabling the number and specialties of physicians providing patient care in areas facing a physician surplus to be managed in such a way that the populations of such areas can obtain adequate medical care at a reasonable cost.

Certificate of Need↗
PubMed1979

Plasminogen activation transforms the morphology of quiescent 3T3 cell monolayers and initiates growth.

Plasminogen activator of cell origin converts the plasma protein plasminogen to the proteolytic enzyme plasmin. Recently, high levels of activator have been observed to be particularly associated with tumours and transformed cells, and a functional relationship between plasminogen activation and malignancy has been proposed. In this paper we have attempted to induce transformation-like morphology and growth in a population of confluent quiescent cells in tissue culture, by inducing plasminogen activation. Untransformed 3T3 cells grown to confluence in plasminogen-free medium were subjected to plasminogen activation by the addition of urokinase and plasminogen or plasminogen-containing acid-treated serum, or plasmin. Under these conditions, the previously well ordered monolayers became disrupted, with multilayering, and discontinuities in the cell sheet, and the cells simultaneously grew to significantly higher densities. Removal of the plasmin-containing medium supplements effected some restoration of normal morphology. Thus, lhen plasmin was present 3T3 cells did not become transformed, but expresses transformation-like features. Well ordered monolayer morphology and quiescence in 3T3 cells at confluence are therefore dependent upon the absence of plasminogen activation.

Animals↗
PubMed1979

Reported physiological and psychological symptoms of tobacco smoke pollution in nonsmoking and smoking college students.

A 147-item questionnaire concerning the relevance of the nonsmokers' right movement to college and university campuses was administered to 307 University of New Hampshire undergraduates. The fourth section of the questionnaire consisted of 28 questions on symptoms caused by smoke pollution. Responses to these questions were given on a five-category frequency of occurrence scale. Frequencies, descriptive statistics, and t tests contrasting current smokers from nonsmokers were presented. Generally sizable percentages of nonsmokers reported adverse physiological and psychological symptoms from tobacco smoke pollution. Smokers reported a similar pattern of responding but at lower frequencies of occurrence.

Adolescent↗
PubMed1979

Correlation between tumour size, metastatic spread and galactosyl transferase activity in cyclophosphamide-treated mice bearing the Lewis lung carcinoma.

Galactosyl transferase activity was measured in tumour and normal tissues of mice receiving cyclophosphamide treatment for Lewis lung carcinoma. Animals which responded to cyclophosphamide therapy had significantly smaller tumours with fewer metastases than the untreated mice. The level of galactosyl transferase was significantly reduced in the tumours which were inhibited by the cyclophosphamide treatment.

Animals↗
PubMed1979

Immunocytochemical localization of plasminogen activator on porcine kidney cell strain: LLC-PK1 (LP100).

An antibody to plasminogen activator (PA) produced by the cultured cells of the pig kidney cell strain LLC-PK1 (LP100) was used to localize PA on the cell's free (unattached) surface. Localization was accomplished by the unlabeled antibody enzyme method (PAP) at the light microscopic level and at the electron microsopic level. Localization was commonly more intense at cell to cell junctions and was associated with blebs and vesiculation in this area. We are proposing that membrane shedding by blebs and vesiculation may be the mechanism of PA release in the LLC-PK1 (LP100) cell strain.

Animals↗
PubMed1979

The effect of ascorbic acid on RNA and protein synthesis on two cultured cell lines in vitro.

Previous work in this laboratory has thrown some light on the possible mechanism involved in the anti-tumour activity of ascorbic acid (AA). In order to elucidate this mechanism further, the present studies, involving the effect of AA on protein and RNA synthesis, were carried out. The results obtained in this investigation may support the hypothesis previously put forward for the action of AA on cell proliferation.

Ascorbic Acid↗
PubMed1979

Hepatic function assessed (in rats) during chemotherapy with some anti-cancer drugs.

Using rats, we studied how best to assess hepatic damage after administering therapeutic doses of each of five anti-cancer drugs or of the hepatotoxin, carbon tetrachloride. As indexes, we compared measurement of the concentration of administered antipyrine in plasma with measurement in serum of alpha-fetoprotein or of the activities of five enzymes that reportedly best reflect hepatic damage. The biological half-life of antipyrine in the plasma was increased more than threefold on pretreating the rats with any of the five cytotoxic drugs or with carbon tetrachloride. In contrast, the concentrations of alpha-fetoprotein, alkaline phosphatase, gamma-glutamyltransferase, or glutamate dehydrogenase were not consistently increased. Of the enzymes tested in serum, aspartate aminotransferase and ornithine carbamoyltransferase best indicated hepatic impairment resulting from the treatment with anti-cancer drugs. Our results imply that determination of the pharmacokinetics of marker drugs such as antipyrine better indicates hepatic dysfunction induced by cytotoxic agents than does measurement of the enzymes liberated into serum as a result of damage to liver mitochondria.

Alkaline Phosphatase↗
PubMed1978

Chronotropic effect of tyramine on rat heart cells cultured with sympathetic neurons.

Dissociated newborn rat superior cervical ganglion neurons in culture without exogenous nerve growth factor survive and extend processes on a monolayer of rat heart ventricular cells. An increase in the contraction rate of the heart cells was observed in 83% of the co-cultures treated with 5 X 10(-6) M tyramine. No increase was seen in heart cell cultures without neurons. These results are consistent with the assumed mode of action of tyramine--the release of catecholamines from nerve terminals--and suggest that functional interaction can occur in culture between sympathetic neurons and heart ventricular cells.

Animals↗
PubMed1978

Thrombin-induced platelet aggregation is mediated by a platelet plasma membrane-bound lectin.

Throbin-activated human platelets cause agglutination of trypsinized, formalinized bovine erythrocytes. This lectin activity of stimulated platelets was blocked by galactosamine, glucosamine, mannosamine, lysine, and arginine, but not by N-acetylated sugars, other neutral sugars, or other amino acids. Inhibitors of the thrombin-induced lectin activity also blocked thrombin-induced platelet aggregation. It appears that a membrane surface component that has lectin activity mediates platelet aggregation.

Agglutinins↗