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1.
Health Care Manag Sci ; 6(3): 175-88, 2003 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-12943153

RESUMO

Profit-seeking nursing facilities have been found to be overwhelmingly more cost efficient than nonprofit facilities. However, the question remains as to whether these organizational-efficiency differences are the result of operating structural differences (i.e., agency relationship costs) or differences in the quality of care rendered. Using traditional cost- and profit-function regression analyses which include a new index measure for quality, we conclude that quality influences costs and profits marginally, efficiency differences reflect agency costs and differences in organizational goals, and the belief that increases in quality require increases in cost does not hold when facility capacity is significantly underutilized.


Assuntos
Eficiência Organizacional/economia , Qualidade da Assistência à Saúde/organização & administração , Instituições de Cuidados Especializados de Enfermagem/organização & administração , Comportamento do Consumidor , Instituições Privadas de Saúde/economia , Instituições Privadas de Saúde/organização & administração , Auditoria Administrativa , Modelos Econômicos , Organizações sem Fins Lucrativos/economia , Organizações sem Fins Lucrativos/organização & administração , Qualidade da Assistência à Saúde/economia , Qualidade de Vida , Análise de Regressão , Instituições de Cuidados Especializados de Enfermagem/economia , Texas
2.
Cancer Res ; 54(22): 5848-55, 1994 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-7954413

RESUMO

Ninety potential chemopreventive agents were screened using 6 chemoprevention-associated biochemical end points. These compounds were tested using rodent (tracheal epithelial or liver) cells and human cells [neonatal foreskin fibroblasts, bronchial epithelial cells, or human leukemic cells (HL-60)]. The effects measured were: (a) inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tyrosine kinase activity in HL-60 cells; (b) inhibition of TPA-induced ornithine decarboxylase (ODC) activity in rat tracheal epithelial cells; (c) inhibition of poly(ADP-ribose)polymerase in propane sultone-treated primary human fibroblasts; (d) inhibition of benzo[a]pyrene(B[a]P)-DNA binding in human bronchial epithelial cells; (e) induction of reduced glutathione in Buffalo rat liver cells; and (f) inhibition of TPA-induced free radical formation in primary human fibroblasts or HL-60 cells. Fifty compounds were highly effective in inhibiting TPA-induced tyrosine kinase activity. This assay identified compounds from a wide variety of chemical classes as effective inhibitors, including all the vitamins, retinoic acid analogues, protein kinase C inhibitors, and chemicals belonging to the amino acid category. Fifty-two chemicals were classified as highly positive compounds when examined for their ability to inhibit TPA-induced ODC activity. These agents showed a dose-dependent inhibition or inhibition at all doses. Retinoids, in general, exhibited strong inhibition of ODC activity. A category of compounds showing dose-dependent inhibition were the sulfur compounds, especially the thiols and thiones. Among the natural products, terpenes were strong inhibitors of ODC. Forty-seven compounds were classified as strong inhibitors of poly(ADP-ribose)polymerase. In the carcinogen-DNA binding inhibition assay, 21 compounds were identified as strong inhibitors, which include phenolic compounds as well as sulfur compounds. Vitamins and their analogues were also good inhibitors. Testing for induced glutathione yielded 19 compounds that were good inducers. Sulfur-containing compounds and most of the phenolic compounds were also inducers of glutathione. Twenty compounds were highly positive for inhibition of TPA-induced free radical formation. A significant number of phenolic and sulfur compounds were again strong oxygen radical scavengers. Some antiinflammatory agents were also identified as free radical inhibitors. In general, retinoids were quite active in all the assays. Eight compounds were positive in all of the six assays; these were vitamin C (ascorbic acid), bismuththiol, esculetin, etoperidone, folic acid, hydrocortisone, indole-3-carbinol, and tocopherol succinate. Agents that were positive in these assays may inhibit the carcinogenesis process by similar mechanisms in humans and are identified as candidates for development as chemopreventive agents.(ABSTRACT TRUNCATED AT 400 WORDS)


Assuntos
Antineoplásicos/farmacologia , Ensaios de Seleção de Medicamentos Antitumorais/métodos , Glutationa/antagonistas & inibidores , Inibidores da Ornitina Descarboxilase , Inibidores de Poli(ADP-Ribose) Polimerases , Proteínas Tirosina Quinases/antagonistas & inibidores , Animais , Benzo(a)pireno/farmacologia , Bioensaio , Adutos de DNA/efeitos dos fármacos , Relação Dose-Resposta a Droga , Epitélio/enzimologia , Epitélio/patologia , Fibroblastos/metabolismo , Radicais Livres/metabolismo , Humanos , Leucemia Promielocítica Aguda/enzimologia , Leucemia Promielocítica Aguda/patologia , Fígado/enzimologia , Ratos , Ratos Endogâmicos BUF , Acetato de Tetradecanoilforbol/antagonistas & inibidores , Acetato de Tetradecanoilforbol/farmacologia , Tiofenos/farmacologia , Traqueia/enzimologia , Traqueia/patologia , Células Tumorais Cultivadas
3.
Life Sci ; 50(24): 1859-68, 1992.
Artigo em Inglês | MEDLINE | ID: mdl-1598072

RESUMO

Para-aminoclonidine coupled to hemocyanin was used to produce mouse monoclonal antibodies directed against clonidine. The properties of one of these, called mFE7, secreted by a clone of hybrid myeloma, are described. This antibody displayed total crossreactivity with imidazolidines and no crossreactivity at all with catecholamines or other known naturally occurring substances tested. A liquid phase radioimmunoassay permitted the detection of immunoreactivity in human brain extracts. The mFE7 antibody could be useful for immunopurifying the endogenous ligand of Imidazolines Preferring Receptors (IPR) which are catecholamines insensitive.


Assuntos
Anticorpos Monoclonais/biossíntese , Antígenos/imunologia , Clonidina/análogos & derivados , Imidazóis/imunologia , Animais , Anticorpos Monoclonais/imunologia , Anticorpos Monoclonais/metabolismo , Especificidade de Anticorpos , Reações Antígeno-Anticorpo/fisiologia , Antígenos/metabolismo , Ligação Competitiva , Encéfalo/imunologia , Clonidina/imunologia , Clonidina/metabolismo , Feminino , Glutaral/imunologia , Hemocianinas/imunologia , Humanos , Imidazóis/metabolismo , Cinética , Camundongos , Camundongos Endogâmicos BALB C , Prazosina/farmacologia , Extratos de Tecidos/imunologia , Vacinas Sintéticas/imunologia , Vacinas Sintéticas/metabolismo , Ioimbina/farmacologia
4.
Immunopharmacol Immunotoxicol ; 11(4): 715-35, 1989.
Artigo em Inglês | MEDLINE | ID: mdl-2628483

RESUMO

Ozone is an oxidant gas and an ubiquitous oxidant air pollutant with the potential to adversely affect pulmonary immune function with a consequent increase in disease susceptibility. Pulmonary natural killer (NK) activity was measured in order to assess the pulmonary immunotoxicity of continuous ozone exposure. Continuous ozone exposures at 1.0 ppm were performed for 23.5 hours per day for either 1, 5, 7, or 10 consecutive days. Pulmonary immune function was assessed by measuring natural killer (NK) activity from whole-lung homogenates of male Fischer-344 rats. Results of this study indicated that continuous ozone exposure for 1, 5, or 7 days resulted in a significant decrease in pulmonary NK activity. This suppressed pulmonary NK activity returned to control levels after continuous exposure to ozone for 10 days. The suppressed pulmonary NK response was thus attenuated and returned to normal values in the continued presence of ozone gas. This attenuation process is dynamic, complex, and doubtless involves several cell types and/or products of these cells. Pulmonary NK activity was also suppressed at 0.5 ppm ozone, but not at 0.1 ppm ozone, following 23.5 hours of exposure. NK activity is important for defense against viral, bacterial, and neoplastic disease. The depressed NK activity resulting from continuous ozone exposure could therefore result in a compromised ability to defend against pulmonary diseases.


Assuntos
Células Matadoras Naturais/efeitos dos fármacos , Pulmão/efeitos dos fármacos , Ozônio/toxicidade , Poluentes Atmosféricos/toxicidade , Animais , Citotoxicidade Imunológica/efeitos dos fármacos , Imunocompetência/efeitos dos fármacos , Imunossupressores , Células Matadoras Naturais/imunologia , Pulmão/imunologia , Masculino , Ratos , Ratos Endogâmicos F344
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