Honorary treasurer: it's not all about money.
Explore the source record for details and available documents.
Economics↗
Biomedical subjects
Richard Dixon
Publications and source records attributed to Richard Dixon.
Do health plans influence quality of care?
OBJECTIVE: To investigate the relative impact of physician groups and health plans on quality of care measures. DESIGN: Secondary data analysis of receipt of preventive care services included in the Health Plan Employer Data and Information Set (HEDIS) among 10 758 patients representing 21 health maintenance organizations and 22 large provider groups in the San Francisco and Los Angeles, California, areas in 1997. Each patient was eligible for (at least) one of six HEDIS-measured services. Data identify whether or not the service was provided, the patient's health plan, and the provider group responsible for the care. We used logistic regression to examine variations across plans in HEDIS rates, and whether variations persist after controls for provider groups are included. SETTING: Patients from 21 health maintenance organizations serving San Francisco and Los Angeles, California, in 1997. MAIN OUTCOME MEASURES: Breast cancer screening, childhood immunizations, cervical cancer screening, diabetic retinal exam, prenatal care in the first trimester, and check-ups after delivery among patients for whom these services are appropriate. RESULTS: There are statistically significant differences across health plans in utilization rates for the six services examined. These differences are not substantially affected when we control for the provider group that cared for the patient. That is, controlling for provider group does not explain variations across plans, consistent with the view that health plans have an impact on HEDIS quality measures independent of the providers that they contract with. CONCLUSIONS: There are activities that plans can undertake which influence their HEDIS scores. On the face of it, these results suggest that plans can independently improve quality, in contrast to hypotheses that plans would be "too far" from patients to have an influence. Continued attention to collecting plan-level data is warranted. Further work should address other possible sources of variations in HEDIS scores, such as variability in the quality of plan administrative databases.
California↗
STRIDE 1: effects of the selective ET(A) receptor antagonist, sitaxsentan sodium, in a patient population with pulmonary arterial hypertension that meets traditional inclusion criteria of previous pulmonary arterial hypertension trials.
Sitaxsentan (SITAX; Thelin, Encysive Corporation, Bellaire, TX, U.S.A.) is a highly selective oral endothelin-A receptor antagonist. STRIDE-1, a 12-week randomized, doubleblind, placebo-controlled trial of sitaxsentan for pulmonary arterial hypertension showed significant benefit in 6-minute walk distance, functional class and hemodynamics. Pulmonary arterial hypertension clinical trials traditionally limit enrolment to class III/IV patients with idiopathic pulmonary arterial hypertension or pulmonary arterial hypertension related to connective tissue disease, who have a baseline 6-minute walk distance of < 450 m. In contrast, STRIDE-1 included milder cases: class II patients, no baseline 6- minute walk cut-off, and congenital heart disease patients. We now present the STRIDE-1 subset who would have qualified under traditional inclusion criteria. The results were: change for placebo (mean +/- SE) vs change for sitaxsentan (mean +/- SE) vs treatment effect (mean), all statistically significant: 6-minute walk (m): -26 +/- 13, 39 +/- 10, 65; mean right atrial pressure (mmHg): 2.1 +/- 0.8, -1.2 +/- 0.5, -3.3; mean pulmonary arterial pressure (mmHg): 0.4 +/- 1.5, -4.7 +/- 1.5, -5.1; cardiac index (L/min per m): -0.09 +/- 0.09, 0.38 +/- 0.06, 0.47; pulmonary vascular resistance (dyne.s.cm): 85 +/- 60, -274 +/- 47, -359. A 45% improvement in functional class was seen in sitaxsentan-treated patients (P = 0.0005). Thus, in the STRIDE-1 subpopulation that met enrolment criteria of previous pulmonary arterial hypertension trials, improvement in efficacy parameters with sitaxsentan therapy was even greater than seen in the entire STRIDE-1 population.
Administration, Oral↗
Blockade of cell adhesion by a small molecule selectin antagonist attenuates myocardial ischemia/reperfusion injury.
Reperfusion injury is related closely to inflammatory reactions such as the activation and accumulation of neutrophils. We investigated the efficacy of a novel small molecule selectin antagonist (bimosiamose) in a rat model of transient left coronary artery occlusion (30 min) and reperfusion (24 h). Treatment with bimosiamose (25 mg/kg, intravenously at reperfusion) showed a significant reduction in infarction area/area at risk of approximately 41% compared to vehicle control (P=0.01) and preserved the left ventricular function. The accumulation of polymorphonuclear neutrophils at the site of area at risk was decreased significantly, accompanied by 78% reduction of the myeloperoxidase activity. Parallel-plate flow chamber analysis revealed that bimosiamose showed a significant inhibition in rolling (62%, P<0.001) and adhesion (38%, P<0.05) of HL-60 cells to activated human umbilical vein endothelial cells compared with vehicle control. This study demonstrates for the first time that bimosiamose, a novel small molecule selectin antagonist, attenuates significantly ischemia/reperfusion injury.
Animals↗
IL-18 receptor beta-induced changes in the presentation of IL-18 binding sites affect ligand binding and signal transduction.
IL-18 is a pleiotropic proinflammatory cytokine that is involved in induction of inflammatory mediators, regulation of the cytotoxic activity of NK cells and T cells, and differentiation and activation of both Th1 and Th2 cells. IL-18 signals through its specific cell surface receptor IL-18R, which comprises two subunits: IL-18R alpha and IL-18R beta. IL-18R alpha alone has a weak affinity for IL-18 binding, while the IL-18R alpha/beta complex has a high affinity. By using several anti-IL-18 mAbs and IL-18 binding protein, we have examined whether these site-specific inhibitors could block the binding of IL-18 to IL-18R alpha and to the IL-18R alpha/beta complex. Here we show that IL-18 binding to IL-18R alpha was inhibited by a neutralizing mAb, 125-2H, while binding of IL-18 to the alpha/beta receptor complex was not. This suggests that IL-18R beta-induced conformational changes may occur in IL-18R alpha upon dimerization, leading to changes in the presentation of IL-18 binding sites. Epitope mapping of 125-2H using human-mouse IL-18 chimeras identified a region in IL-18 that was required for 125-2H recognition. This region, as examined by IL-18R binding and functional analysis, appeared to be critical for triggering signal transduction through the heterodimeric receptor.
Animals↗