Results point to two potentially orthogonal predisease mechanisms that warrant special attention: cardiovascular activation and sleep dysfunction. Health behavior and cortisol regulation, however, may require more sensitive measures and large sample sizes to discern their roles in loneliness and health.

Enhanced external counterpulsation reduces angina and extends time to exercise-induced ischemia in patients with symptomatic CAD. Treatment was relatively well tolerated and free of limiting side effects in most patients.

No abstract

Significant health-related quality of life improvements were measurable up to 12 months after the completion of treatment with EECP. Improvements in this controlled study are consistent with HQOL changes reported in case series and patient registries. Larger studies are warranted.

The mechanism leading to changes in the superstructure of endothelial cells exposed to ischemia and reperfusion remains uncharacterized. We show that in posthypoxic endothelial cells, the simple re-addition of oxygen induces a profound reorganization of the actin cytoskeleton. The total filamentous actin pool increases by 41% and translocation of actin filaments to the submembranous network is observed. Concurrent with the actin polymerization, increased tyrosine phosphorylation of endothelial cell substrates is detected on Western blots. Overexpression of superoxide dismutase using replication incompetent adenovirus inhibits the actin and tyrosine phosphorylation responses to reoxygenation. Inhibition of tyrosine kinases with the isoflavone genistein also suppressed the actin polymerization response to reoxygenation, but unlike superoxide dismutase, genistein also induced the collapse of the superstructure of endothelial cells upon reoxygenation. These experiments support the concept that reoxygenation following a period of hypoxia can induce the remodeling of the actin cytoskeleton in endothelial cells. Such a response requires the intact coupling of superoxide producing pathway(s) with tyrosine kinase pathway(s).Angiogenesis can either rescue ischemic tissues by re-establishing an appropriate blood supply, or neovascularize proliferating tissues such as developing organs and neoplastic lesions (1, 2). Substantial progress has been made in the characterization of growth factors that promote or antagonize the angiogenic response (1-3). Vascular endothelial growth factor has been shown to be produced by the cells of ischemic tissues (glioblastoma and lung) (4, 5), and the receptors for vascular endothelial growth factor (flt and KDR) are up-regulated on the surface of endothelial cells in these tissues (4 -7). However, little is known about the molecular control of the cellular machinery (the actin cytoskeleton) that mediates the translocation of endothelial cells to ischemic areas, a process that is necessary, although not sufficient, for angiogenesis to take place.The vascular endothelial growth factor receptor, like most growth factor receptors, is a receptor tyrosine kinase (8 -10), whose signaling cascade is mediated by the clustering of effector molecules through the binding of SH2 domains to tyrosinephosphorylated residues. We found out recently that, in addition to tyrosine phosphorylation, the activity of growth factor receptors is also coupled to the production of reactive oxygen species (ROS) 1 such as superoxide or hydrogen peroxide (H 2 O 2 ) (11). Thus, activation of rat vascular smooth muscle cells with platelet-derived growth factor (PDGF) leads to H 2 O 2 production. Catalase or ROS chelators block the tyrosine kinase and mitogenic response to platelet-derived growth factor (11). Moreover, while ROS have been recognized in the past as mediators of intercellular interactions, we and others have recently identified ROS as major intracellular signal transduction messengers used by several small GTP...

Summary:Studies over the past several decades support the hypothesis that enhanced external counterpulsation (EECP) can provide long-term benefits in patients with angina secondary to chronic coronary disease. Numerous non-sham controlled trials have recently been substantiated by a multicenter, randomized trial. Although the mechanism by which this mechanical treatment effects an alteration in cellular processes within the myocardium remains unclear, recent scientific investigations suggest that shear stress induced by chronic exposure to EECP might result in the release of a variety of growth factors and the subsequent stimulation of angiogenesis in the coronary beds. Ongoing clinical trials in patients with significant left ventricular dysfunction, an international registry, and additional clinical trials may help to elucidate further the role of this novel and unique therapy in our clinical armamentarium.

No abstract

An analysis of the data from the Ontario longitudinal study of aging was carried out to investigate the associations between self-reported income and perceived health status, using cross-tabulations and logistic regression models. Reported income, educational level, and smoking status were associated with perceived health status. Reported income was associated with perceived health status independently of the effects of education and smoking. The data also indicate that changes in income are related significantly to changes in perceived health status. A reduced income was associated with a worsening of health and a weak relationship was apparent between increased income and better health. The analyses further suggest that income changes precede health changes. The possible mechanisms through which an income change may lead to health changes are discussed.