128 research outputs found

    Do We Want to Measure the Quality of Care for Vulnerable Older People? The ACOVE Approach. Syracuse Seminar on Aging.

    Get PDF
    There's limited information available about measuring the quality of medical care that is targeted to the needs of older patients. And there's very limited pressure on the system to provide high quality geriatric care. Why is that? Because the quality measures haven't been adequately developed and implemented, and it's more difficult to measure care for an older sample. Measuring care for ill older adults is complex, because they tend to have multiple medical conditions, and they demonstrate substantial variation in goals for care (Wenger and colleagues 2007). The Assessing Care of Vulnerable Elders (ACOVE) project began in 1998 as a collaboration between RAND Health and Pzizer Inc to develop and apply quality indicators (QIs) for assessment and treatment targeted at vulnerable older persons. The project involved defining and identifying the target population, identifying health conditions that cover much of the medical care provided to this population, developing quality-of-care indicators to measure how well those conditions are being addressed, and applying thoseindicators to determine the actual quality of care received by older adults.health care, medical care, elderly, assessment, geriatrics, gerontology

    Do We Want to Measure the Quality of Care for Vulnerable Older People? The ACOVE Approach.

    Get PDF
    There\u27s limited information available about measuring the quality of medical care that is targeted to the needs of older patients. And there\u27s very limited pressure on the system to provide high quality geriatric care. Why is that? Because the quality measures haven\u27t been adequately developed and implemented, and it\u27s more difficult to measure care for an older sample. Measuring care for ill older adults is complex, because they tend to have multiple medical conditions, and they demonstrate substantial variation in goals for care (Wenger and colleagues 2007). The Assessing Care of Vulnerable Elders (ACOVE) project began in 1998 as a collaboration between RAND Health and Pfizer Inc to develop and apply quality indicators (QIs) for assessment and treatment targeted at vulnerable older persons. The project involved defining and identifying the target population, identifying health conditions that cover much of the medical care provided to this population, developing quality-of-care indicators to measure how well those conditions are being addressed, and applying those indicators to determine the actual quality of care received by older adults

    CCN2 Is Required for the TGF-β Induced Activation of Smad1 - Erk1/2 Signaling Network

    Get PDF
    Connective tissue growth factor (CCN2) is a multifunctional matricellular protein, which is frequently overexpressed during organ fibrosis. CCN2 is a mediator of the pro-fibrotic effects of TGF-β in cultured cells, but the specific function of CCN2 in the fibrotic process has not been elucidated. In this study we characterized the CCN2-dependent signaling pathways that are required for the TGF-β induced fibrogenic response. By depleting endogenous CCN2 we show that CCN2 is indispensable for the TGF-β-induced phosphorylation of Smad1 and Erk1/2, but it is unnecessary for the activation of Smad3. TGF-β stimulation triggered formation of the CCN2/β3 integrin protein complexes and activation of Src signaling. Furthermore, we demonstrated that signaling through the αvβ3 integrin receptor and Src was required for the TGF-β induced Smad1 phosphorylation. Recombinant CCN2 activated Src and Erk1/2 signaling, and induced phosphorylation of Fli1, but was unable to stimulate Smad1 or Smad3 phosphorylation. Additional experiments were performed to investigate the role of CCN2 in collagen production. Consistent with the previous studies, blockade of CCN2 abrogated TGF-β-induced collagen mRNA and protein levels. Recombinant CCN2 potently stimulated collagen mRNA levels and upregulated activity of the COL1A2 promoter, however CCN2 was a weak inducer of collagen protein levels. CCN2 stimulation of collagen was dose-dependent with the lower doses (<50 ng/ml) having a stimulatory effect and higher doses having an inhibitory effect on collagen gene expression. In conclusion, our study defines a novel CCN2/αvβ3 integrin/Src/Smad1 axis that contributes to the pro-fibrotic TGF-β signaling and suggests that blockade of this pathway may be beneficial for the treatment of fibrosis

    Exercise and Cardiovascular Events - Placing the Risks Into Perspective: A Scientific Statement From the American heart Association Council on Nutrition, Physical Activity, and Metabolism and the Council on Clinical Cardiology

    Get PDF
    Habitual physical activity reduces coronary heart disease events, but vigorous activity can also acutely and transiently increase the risk of sudden cardiac death and acute myocardial infarction in susceptible persons. This scientific statement discusses the potential cardiovascular complications of exercise, their pathological substrate, and their incidence and suggests strategies to reduce these complications. Exercise-associated acute cardiac events generally occur in individuals with structural cardiac disease. Hereditary or congenital cardiovascular abnormalities are predominantly responsible for cardiac events among young individuals, whereas atherosclerotic disease is primarily responsible for these events in adults. The absolute rate of exercise-related sudden cardiac death varies with the prevalence of disease in the study population. The incidence of both acute myocardial infarction and sudden death is greatest in the habitually least physically active individuals. No strategies have been adequately studied to evaluate their ability to reduce exercise-related acute cardiovascular events. Maintaining physical fitness through regular physical activity may help to reduce events because a disproportionate number of events occur in least physically active subjects performing unaccustomed physical activity. Other strategies, such as screening patients before participation in exercise, excluding high-risk patients from certain activities, promptly evaluating possible prodromal symptoms, training fitness personnel for emergencies, and encouraging patients to avoid high-risk activities, appear prudent but have not been systematically evaluated

    3D Multi-Cell Simulation of Tumor Growth and Angiogenesis

    Get PDF
    We present a 3D multi-cell simulation of a generic simplification of vascular tumor growth which can be easily extended and adapted to describe more specific vascular tumor types and host tissues. Initially, tumor cells proliferate as they take up the oxygen which the pre-existing vasculature supplies. The tumor grows exponentially. When the oxygen level drops below a threshold, the tumor cells become hypoxic and start secreting pro-angiogenic factors. At this stage, the tumor reaches a maximum diameter characteristic of an avascular tumor spheroid. The endothelial cells in the pre-existing vasculature respond to the pro-angiogenic factors both by chemotaxing towards higher concentrations of pro-angiogenic factors and by forming new blood vessels via angiogenesis. The tumor-induced vasculature increases the growth rate of the resulting vascularized solid tumor compared to an avascular tumor, allowing the tumor to grow beyond the spheroid in these linear-growth phases. First, in the linear-spherical phase of growth, the tumor remains spherical while its volume increases. Second, in the linear-cylindrical phase of growth the tumor elongates into a cylinder. Finally, in the linear-sheet phase of growth, tumor growth accelerates as the tumor changes from cylindrical to paddle-shaped. Substantial periods during which the tumor grows slowly or not at all separate the exponential from the linear-spherical and the linear-spherical from the linear-cylindrical growth phases. In contrast to other simulations in which avascular tumors remain spherical, our simulated avascular tumors form cylinders following the blood vessels, leading to a different distribution of hypoxic cells within the tumor. Our simulations cover time periods which are long enough to produce a range of biologically reasonable complex morphologies, allowing us to study how tumor-induced angiogenesis affects the growth rate, size and morphology of simulated tumors
    corecore