Role of illness representations and coping in patients with atopic dermatitis: a cross-sectional study.

Background: Atopic dermatitis (AD) is a skin disease accompanied by psychological burden. It has been shown for other chronic diseases that illness representations and coping strategies are associated with disease-related burden and other outcome variables like time until patients return to work or health care use.

Objective: The goal of this cross-sectional study was to investigate whether illness representations and coping strategies are correlated with the severity of AD and self-rated physical impairment of the patients.

Phorbol ester-stimulated adherence of neutrophils to endothelial cells is reduced by adenosine A2 receptor agonists.

In this study we investigated the effect of adenosine receptor agonists on the adherence of PMA-stimulated human neutrophils to cultured porcine aortic endothelial cells. Additionally, we studied the influence of adenosine analogues on the second messenger cAMP in neutrophils and cultured endothelial cells. In the presence of 10 ng/ml PMA, there was a rapid and stable increase on adherence of neutrophils to the endothelial layer.

Adenosine A1 and A2 receptor agonists alter cardiac functions and prostacyclin release in the isolated guinea-pig heart.

The actions of the adenosine A1 receptor agonist CCPA (2-chloro-N6-cyclopentyladenosine) and the adenosine A2 receptor agonist CGS 21680 (2-[p-(2-carboxyethyl(phenethylamino]-5'-N- ethylcarboxamidoadenosine) on myocardial functions and prostacyclin release were studied in Langendorff-perfused guinea-pig hearts. In spontaneously beating hearts, perfused at constant pressure, CCPA reduced heart rate and left ventricular actively developed pressure with EC50 values of 54.4 +/- 8.

Ramiprilat prevents PAF-induced myocellular and endothelial injury in a neutrophil-perfused heart preparation.

This study investigates the action of PAF-stimulated human polymorphonuclear leukocytes (PMN) on myocardial integrity and function in Langendorff-perfused guinea-pig hearts. Infusion of 10(6) PMN/ml resulted in a negative inotropic effect without larger biochemical evidence for myocardial tissue injury while infusion of PAF (1 microM) did not cause any permanent effect at all. However, the combined administration of PAF-stimulated PMN resulted in severely depressed myocardial contractile function and biochemical evidence for myocardial tissue injury.