Biomedical subjects

D A Patterson

Publications and source records attributed to D A Patterson.

14 recordsLinked to original sources

PubMed1996

An optimization model for constrained discriminant analysis and numerical experiments with iris, thyroid, and heart disease datasets.

A nonlinear 0/1 mixed integer programming model is presented for a constrained discriminant analysis problem. The model enables controlling misclassification probabilities by placing restrictions on the numbers of misclassifications allowed among the training entities and incorporating a "reserved-judgment" region to which entities whose classifications are difficult to determine may be allocated. A linearization of the model is given, and preliminary numerical results for two medical and one non medical domain are presented.

Databases, Factual↗

PubMed1995

Field trial of the Global Assessment of Functioning Scale--Modified.

OBJECTIVE: A field trial of the Global Assessment of Functioning Scale--Modified was conducted to test its construct validity. A slightly altered form of the scale, the Social and Occupational Functioning Assessment Scale, was used in DSM-IV. METHOD: Social, occupational, and clinical data on 196 subjects receiving outpatient mental health services were analyzed. RESULTS: Six significant predictors were found that accounted for 51.75% of the variation in scores on the Global Assessment of Functioning Scale--Modified. Scores were independent of axis I, axis II, and psychoactive substance dependence diagnoses from DSM-III-R. CONCLUSIONS: The construct validity of the Global Assessment of Functioning Scale--Modified and the Social and Occupational Functioning Assessment Scale is supported by these findings.

Ambulatory Care↗

PubMed1995

Definition of the bleeding tendency in factor XI-deficient kindreds--a clinical and laboratory study.

Individuals with severe factor XI deficiency are prone to excessive bleeding after injury or surgery, but the existence of a haemorrhagic tendency in partial factor XI deficiency is controversial. In this study, 172 members of 30 kindreds (20 non-Jewish) transmitting factor XI deficiency in North West England were interviewed and a bleeding history questionnaire completed. Blood was taken for coagulation assays. The questionnaires were categorised independently by two assessors to determine presence or absence of a bleeding tendency, in the absence of information about the factor XI level or family history. Analysis shows that 48% of heterozygotes have a bleeding tendency. Eighteen (60%) families came to attention because of bleeding problems in heterozygotes. Comparison of histories between partially deficient and non-deficient individuals demonstrated a higher incidence of menstrual problems, an increase in significant bruising, and an increased likelihood of excessive bleeding after tonsillectomy and dental extractions. The incidence of von Willebrand's disease was not increased, but individuals with heterozygous factor XI deficiency who were bleeders tended to have lower levels of factor VIIIc and von Willebrand factor, and were more commonly of blood group 0. These features may contribute to the bleeding tendency. There was no evidence of alteration in factor VII activity (as defined by the ratio of activity to antigen) between the bleeders and non-bleeders. This is convincing evidence for abnormal bleeding in factor XI deficiency which is not confined to severely deficient patients.

Adolescent↗

PubMed1988

Hydrogen peroxide-mediated inhibition of T-cell response to mitogens is a result of direct action on T cells.

Hydrogen peroxide, a reactive oxygen intermediate produced by activated neutrophils, has been shown to inhibit the response of human T lymphocytes to mitogens and alloantigens. Since hydrogen peroxide is known to react with iron and to induce lipid peroxidation, we compared the effects of hydrogen peroxide and a lipid peroxidation product, malondialdehyde, on the response of human peripheral blood mononuclear cells to T-cell mitogens. Peripheral blood mononuclear cells pretreated with 1 mmol/L of malondialdehyde, washed, and resuspended in fresh medium exhibited no inhibition of phytohemagglutinin responsiveness. Peripheral blood mononuclear cells treated in the same manner but with 200 mumol/L of hydrogen peroxide were inhibited by more than 95%. The addition of ferric edetate did not alter the inhibitory effects of 50 to 100 mumol/L of hydrogen peroxide, nor did the addition of deferoxamine, an iron chelator. These studies suggest that exogenous lipid peroxidation does not affect lymphocyte activation but that hydrogen peroxide has a direct inhibitory effect. Although monocytes are necessary for T-cell mitogenic responses, the effect of hydrogen peroxide was found to be directed at T lymphocytes. Exposure of T cells to a single dose of 200 mumol/L of hydrogen peroxide resulted in more than 71% suppression of the proliferative response measured 48 hours later, but the effect was spontaneously reversed by 72 to 96 hours. Repeated exposure of the cells to hydrogen peroxide resulted in continued inhibition of the proliferative response. These findings suggest that hydrogen peroxide produced by inflammatory phagocytic cells might be capable of suppressing the immune response of nearby T lymphocytes.

Deferoxamine↗

PubMed1988