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11.
BMC Health Serv Res ; 12: 370, 2012 Oct 29.
Artículo en Inglés | MEDLINE | ID: mdl-23106856

RESUMEN

BACKGROUND: Mapping patient and work flow and cost analysis studies can help determine the most efficient and cost effective way of providing health services while still maintaining the best standards of care. This study used both time and motion methodology and hospital data to assess the contribution of staff time and facility usage to the overall cost of cancer care during patient visits to a comprehensive cancer centre in Quebec, using metastatic colorectal cancer as a model. METHODS: A workflow diagram was created mapping direct and indirect steps involved during a patient's physician or treatment (FOLFOX/bevacizumab or XELOX/bevacizumab) visit. Staff were timed as they performed each task and this data together with compensation amounts were used to calculate personnel costs. Mean work times and 95% confidence intervals (CI) were calculated. Operation and maintenance (O&M) costs for the Centre were calculated using information from hospital databases. All costs were presented in constant Canadian dollars for the 2010-2011 fiscal year period. RESULTS: For physician visits, direct and indirect personnel costs were $9.25 (95%CI:$7.00-$11.51) and O&M costs were $60.21, for a total of $69.46 (95%CI:$67.21-$71.72). For treatment visits, personnel and O&M costs were $71.91 (95%CI:$45.53-$98.29) and $62.00 respectively for a total of $133.91 (95%CI:$107.53-$160.29). When calculated for treatment alone, the total cost was $136.06 (95%CI:$109.16-$162.95) for FOLFOX/bevacizumab and $119.94 (95%CI:$96.89-$142.99) for XELOX/bevacizumab. The highest cumulative personnel costs were for the pharmacists and nurses ($38.87 and $34.82 respectively). Regarding patient flow, total time in between steps was 77.6 and 49.5 minutes for a physician or treatment visit respectively. CONCLUSIONS: This study from a health care provider's perspective, demonstrated that in the context of increasingly expensive therapies, costs associated with staff time and facility usage do not contribute greatly to the overall cost of treating cancer at this cancer centre. It also illustrated the need for improvements in patient and work flow to reduce wait times in the clinic.


Asunto(s)
Instituciones Oncológicas/estadística & datos numéricos , Neoplasias Colorrectales/terapia , Admisión y Programación de Personal , Flujo de Trabajo , Neoplasias Colorrectales/secundario , Atención Integral de Salud , Femenino , Humanos , Masculino , Modelos Organizacionales , Quebec , Estudios de Tiempo y Movimiento
16.
J Neurosci ; 23(13): 5789-98, 2003 Jul 02.
Artículo en Inglés | MEDLINE | ID: mdl-12843283

RESUMEN

Heat shock protein 70 (Hsp70) protects cultured motor neurons from the toxic effects of mutations in Cu/Zn-superoxide dismutase (SOD-1), which is responsible for a familial form of the disease, amyotrophic lateral sclerosis (ALS). Here, the endogenous heat shock response of motor neurons was investigated to determine whether a high threshold for activating this protective mechanism contributes to their vulnerability to stresses associated with ALS. When heat shocked, cultured motor neurons failed to express Hsp70 or transactivate a green fluorescent protein reporter gene driven by the Hsp70 promoter, although Hsp70 was induced in glial cells. No increase in Hsp70 occurred in motor neurons after exposure to excitotoxic glutamate or expression of mutant SOD-1 with a glycine--> alanine substitution at residue 93 (G93A), nor was Hsp70 increased in spinal cords of G93A SOD-1 transgenic mice or sporadic or familial ALS patients. In contrast, strong Hsp70 induction occurred in motor neurons with expression of a constitutively active form of heat shock transcription factor (HSF)-1 or when proteasome activity was sufficiently inhibited to induce accumulation of an alternative transcription factor HSF2. These results indicate that the high threshold for induction of the stress response in motor neurons stems from an impaired ability to activate the main heat shock-stress sensor, HSF1.


Asunto(s)
Esclerosis Amiotrófica Lateral/metabolismo , Proteínas de Unión al ADN/metabolismo , Regulación de la Expresión Génica , Respuesta al Choque Térmico , Neuronas Motoras/metabolismo , Esclerosis Amiotrófica Lateral/genética , Esclerosis Amiotrófica Lateral/patología , Animales , Células Cultivadas , Cisteína Endopeptidasas/metabolismo , Modelos Animales de Enfermedad , Inhibidores Enzimáticos/farmacología , Genes Reporteros , Ácido Glutámico/toxicidad , Proteínas HSP70 de Choque Térmico/genética , Proteínas HSP70 de Choque Térmico/metabolismo , Factores de Transcripción del Choque Térmico , Proteínas de Choque Térmico/metabolismo , Respuesta al Choque Térmico/fisiología , Calor , Humanos , Técnicas In Vitro , Ratones , Ratones Transgénicos , Neuronas Motoras/efectos de los fármacos , Neuronas Motoras/patología , Complejos Multienzimáticos/antagonistas & inhibidores , Complejos Multienzimáticos/metabolismo , Regiones Promotoras Genéticas , Complejo de la Endopetidasa Proteasomal , Médula Espinal/citología , Médula Espinal/metabolismo , Médula Espinal/patología , Superóxido Dismutasa/biosíntesis , Superóxido Dismutasa/genética , Factores de Transcripción/metabolismo
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