RESUMO
Almost 16 million Germans are treated annually in an emergency room (ER). Most patients are seen in a specialty ER and only 10-20% of all hospitals have a centralized ER facility. Clinical emergency medicine is currently not adequately reimbursed, but represents a major patient entry point for most hospitals. It remains unclear whether the implementation of specialized ER physicians is more cost-effective than centralized specialization. However, it appears reasonable to centralize all ER resources, to optimize the workflow using electronic patient charts and order entry sets and to incorporate the general practitioner into the treatment of simple medical problems.
Assuntos
Comportamento Cooperativo , Serviço Hospitalar de Emergência/organização & administração , Administração Hospitalar , Comunicação Interdisciplinar , Serviços Centralizados no Hospital/economia , Serviços Centralizados no Hospital/organização & administração , Análise Custo-Benefício , Grupos Diagnósticos Relacionados/economia , Grupos Diagnósticos Relacionados/organização & administração , Serviço Hospitalar de Emergência/economia , Medicina Geral/economia , Alemanha , Administração Hospitalar/economia , Humanos , Sistemas de Registro de Ordens Médicas/economia , Sistemas de Registro de Ordens Médicas/organização & administração , Sistemas Computadorizados de Registros Médicos/economia , Sistemas Computadorizados de Registros Médicos/organização & administração , Programas Nacionais de Saúde/economia , Programas Nacionais de Saúde/organização & administração , Mecanismo de Reembolso/economia , Mecanismo de Reembolso/organização & administração , Fluxo de TrabalhoRESUMO
The cystic fibrosis transmembrane conductance regulator (CFTR) has been shown previously to be regulated by inhibitory G proteins. In the present study, we demonstrate inhibition of CFTR by alphaG(i2) and alphaG(i1), but not alphaG(0), in Xenopus oocytes. We further examined whether regulators of G protein signaling (RGS) proteins interfere with alphaG(i)-dependent inhibition of CFTR. Activation of CFTR by IBMX and forskolin was attenuated in the presence of alphaG(i2), indicating inhibition of CFTR by alphaG(i2) in Xenopus oocytes. Coexpression of the proteins RGS3 and RGS7 together with CFTR and alphaG(i2) partially recovered activation by IBMX/forskolin. 14-3-3, a protein that is known to interfere with RGS proteins, counteracted the effects of RGS3. These data demonstrate the regulation of CFTR by alphaG(i) in Xenopus oocytes. Because RGS proteins interfere with the G protein-dependent regulation of CFTR, this may offer new potential pathways for pharmacological intervention in cystic fibrosis.