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3.
Am J Psychiatry ; 150(1): 7-18, 1993 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-8417583

RESUMEN

Concerns about cost, access, and quality of health care in the United States have led to a variety of legislative proposals that would reform our health care system and its financing. Health insurance benefits for mental illness, including substance abuse, are treated differently from medical/surgical benefits, with stricter limits on outpatient visits and hospital days. Medicare, Medicaid, and most private health insurance plans contain this historic disparity of coverage for mental illness compared to general medical illness. Psychiatric services are also distinguishable because of the large public sector reimbursement for mental illness treatment and support. Principles for a more equitable design of mental health benefits include a non-discriminatory approach; payment on the basis of service rather than diagnosis; application of cost containment for care of mental illness on the same basis as care of general medical illness; retention of the public sector as a backup system for high-cost, long-term care; encouragement of lower-cost alternatives to the hospital through the development of a continuum of care; and a recognition of the distinction between psychotherapy and medical management. All current approaches to universal health care fall short of these principles. A research agenda is needed now more than ever in order to articulate the case for complete coverage of mental illness and substance abuse.


Asunto(s)
Atención a la Salud/legislación & jurisprudencia , Seguro Psiquiátrico/normas , National Health Insurance, United States/legislación & jurisprudencia , Atención Ambulatoria , Control de Costos , Atención a la Salud/economía , Atención a la Salud/normas , Predicción , Política de Salud/economía , Política de Salud/tendencias , Humanos , Seguro de Hospitalización , Seguro Psiquiátrico/economía , Seguro Psiquiátrico/legislación & jurisprudencia , Trastornos Mentales/terapia , National Health Insurance, United States/economía , National Health Insurance, United States/normas , Pautas de la Práctica en Medicina , Estados Unidos
5.
Acad Psychiatry ; 15(1): 33-9, 1991 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-24430403

RESUMEN

This paper reviews the various resources available to psychiatrists for keeping abreast of the current literature and research in the field and reports the results of a survey that assesses psychiatrists' current practices in tracking the literature. The respondents' knowledge of available resources, their usual searching practices, and their satisfaction with the resource network are presented. The authors draw conclusions about the most efficient means of tracking the literature for various purposes and offer suggestions about improving resources.

6.
Metabolism ; 34(1): 30-5, 1985 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-3965860

RESUMEN

Very low-density lipoproteins (VLDL) contain sialylated apolipoproteins (apo) (eg, apo CIII1-3) that inhibit apo CII activation of lipoprotein lipase (LPL) and also uptake of triglyceride (TG)-rich lipoproteins by the liver. Hypertriglyceridemic patients can have an excess of sialylated apo CIII (apo CIII1 or apo CIII2) in VLDL. These observations have prompted the notion that sialic acid in VLDL may impede LPL or receptor-mediated clearance of VLDL and thus result in hypertriglyceridemia. The aim of this study was to determine whether desialylation of VLDL altered their property as a substrate for LPL. VLDL isolated from five hypertriglyceridemic patients was desialylated with neuraminidase, labeled with a fluorescent probe, dansyl phosphatidylethanolamine and 600 micrograms of labeled VLDL TG were incubated with a constant amount of purified bovine LPL. The change in fluorescence against time was monitored on a recorder to yield curves representing continuous lipolysis of VLDL by LPL. Mean initial velocity of reaction (Vi) and extent of lipolysis measured as total increase in fluorescence over baseline at 30 minutes (F30/FO) were similar (Vi = 10.2 +/- 0.37 control v 10.2 +/- 0.42 u/min desialylated VLDL; F30/FO = 4.1 +/- 0.15, control v 4.1 +/- 0.07 desialylated VLDL; n = 5). Thus, sialic acid does not influence VLDL catabolism by LPL. Our study does not exclude a possible role of the sialic acid in receptor mediated uptake of remnants produced by initial catabolism of VLDL by LPL.


Asunto(s)
Lipoproteína Lipasa/metabolismo , Lipoproteínas VLDL/metabolismo , Hígado/metabolismo , Ácidos Siálicos/metabolismo , Adulto , Fenómenos Químicos , Química , Femenino , Humanos , Técnicas In Vitro , Focalización Isoeléctrica , Lipólisis , Masculino , Persona de Mediana Edad , Ácido N-Acetilneuramínico , Neuraminidasa/metabolismo , Espectrometría de Fluorescencia
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