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1.
J Hosp Infect ; 92(2): 194-8, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26778130

RESUMO

An outbreak of carbapenem-resistant Acinetobacter baumannii (CRAb) occurred in an interdisciplinary intensive care unit, affecting 10 patients. Within hours of recognition of the spread of CRAb an intervention team was instituted for collection of available data, decision-making, communication and monitoring of all interventions performed, including cohorting, temporary stop of admissions, staff education, and enforcement of infection control measures. An area was defined for cohortation of patients colonized with CRAb, with a separate nursing team and a second set of mobile equipment. New transmissions were no longer observed after only four days into the institution of enhanced infection control measures.


Assuntos
Infecções por Acinetobacter/epidemiologia , Acinetobacter baumannii/isolamento & purificação , Antibacterianos/farmacologia , Carbapenêmicos/farmacologia , Surtos de Doenças , Unidades de Terapia Intensiva , Infecções por Acinetobacter/microbiologia , Acinetobacter baumannii/efeitos dos fármacos , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Controle de Infecções/métodos , Masculino , Pessoa de Meia-Idade , Resistência beta-Lactâmica
2.
Am J Physiol Lung Cell Mol Physiol ; 280(1): L165-72, 2001 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-11133506

RESUMO

Mucus hypersecretion from hyperplastic airway goblet cells is a hallmark of chronic obstructive pulmonary disease (COPD). Although cigarette smoking is thought to be involved in mucus hypersecretion in COPD, the mechanism by which cigarette smoke induces mucus overproduction is unknown. Here we show that activation of epidermal growth factor receptors (EGFR) is responsible for mucin production after inhalation of cigarette smoke in airways in vitro and in vivo. In the airway epithelial cell line NCI-H292, exposure to cigarette smoke upregulated the EGFR mRNA expression and induced activation of EGFR-specific tyrosine phosphorylation, resulting in upregulation of MUC5AC mRNA and protein production, effects that were inhibited completely by selective EGFR tyrosine kinase inhibitors (BIBX1522, AG-1478) and that were decreased by antioxidants. In vivo, cigarette smoke inhalation increased MUC5AC mRNA and goblet cell production in rat airways, effects that were prevented by pretreatment with BIBX1522. These effects may explain the goblet cell hyperplasia that occurs in COPD and may provide a novel strategy for therapy in airway hypersecretory diseases.


Assuntos
Receptores ErbB/metabolismo , Células Caliciformes/metabolismo , Mucinas/biossíntese , Mucosa Respiratória/metabolismo , Fumar/metabolismo , Animais , Diferenciação Celular/efeitos dos fármacos , Inibidores Enzimáticos/farmacologia , Células Epiteliais/citologia , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Receptores ErbB/genética , Expressão Gênica/efeitos dos fármacos , Células Caliciformes/efeitos dos fármacos , Humanos , Técnicas In Vitro , Pneumopatias Obstrutivas/etiologia , Pneumopatias Obstrutivas/metabolismo , Mucina-5AC , Mucinas/genética , Fosforilação , Proteínas Tirosina Quinases/antagonistas & inibidores , RNA Mensageiro/análise , Ratos , Mucosa Respiratória/citologia , Mucosa Respiratória/efeitos dos fármacos , Fumar/efeitos adversos , Organismos Livres de Patógenos Específicos , Tirosina/metabolismo
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