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1.
Am J Emerg Med ; 30(1): 174-80, 2012 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-21030189

RESUMEN

OBJECTIVES: To examine whether posturally induced changes in cardiac output differentiate patients presenting with dyspnea to the emergency department (ED) with acute heart failure (AHF) from other causes. METHODS: This was an observational study of patients presenting to the ED with dyspnea. Exclusion criteria included ischemic chest pain, electrocardiographic changes diagnostic of acute myocardial infarction, pericardial effusion or chest wall deformities causing dyspnea, or heart transplant. Hemodynamic variables of cardiac index (CI), total peripheral resistance index, and thoracic fluid content (TFC) were determined in upright seated and supine positions 3 minutes apart using bioreactance technology (Cheetah Medical Inc, Portland, Ore). Acute heart failure was defined as either B-type natriuretic peptide 100 to 500 pg/mL and discharge diagnosis of AHF or a B-type natriuretic peptide greater than 500 pg/mL. RESULTS: Of 92 patients, 25 had AHF, 23 had asthma/chronic obstructive pulmonary disease (COPD), and 44 had dyspnea related to other conditions; 41 (44.1%) were male, 56 (60.2%) were African American, and the mean age was 58 ± 15.0 years. Mean baseline TFC was higher in AHF vs asthma/COPD (59.3 ± 26.0 vs 39.7 ± 14.8 1/kW, P = .003) and trended higher compared to other patients with dyspnea (49.2 ± 22.0, P = .10). Postural changes in mean CI were lower in AHF (-0.20 ± 0.84 L min(-1) m(-2)) vs asthma/COPD (1.20 ± 1.23 L min(-1) m(-2); P = .002) and other dyspnea patients (0.82 ± 0.91 L min(-1) m(-2); P = .007). CONCLUSION: Patients with AHF have greater TFC but lower CI responses to postural changes compared to patients with asthma and COPD. Knowledge of these changes may help rapidly differentiate AHF from asthma and COPD in the ED.


Asunto(s)
Insuficiencia Cardíaca/diagnóstico , Hemodinámica , Enfermedad Aguda , Adulto , Anciano , Anciano de 80 o más Años , Biomarcadores/sangre , Gasto Cardíaco/fisiología , Femenino , Insuficiencia Cardíaca/sangre , Insuficiencia Cardíaca/fisiopatología , Humanos , Masculino , Persona de Mediana Edad , Péptido Natriurético Encefálico/sangre , Proyectos Piloto , Postura/fisiología , Resistencia Vascular/fisiología , Adulto Joven
2.
J Biol Chem ; 282(34): 25088-99, 2007 Aug 24.
Artículo en Inglés | MEDLINE | ID: mdl-17597071

RESUMEN

Caspase-3 is an essential executioner of apoptosis responsible for regulating many important cellular processes, among them the number of circulating monocytes, central players in the innate immune response. The activation of caspase-3 requires its processing from an inactive precursor. Here we show that the small heat shock protein 27 (Hsp27) associates with caspase-3 and protein-protein interaction experiments in vivo and with purified proteins demonstrate a direct interaction between Hsp27 and the amino-terminal prodomain of caspase-3. Using an in vitro caspase-3 activation assay, our results further establish that the interaction of Hsp27 with the caspase-3 prodomain inhibits the second proteolytic cleavage necessary for caspase-3 activation, revealing a novel mechanism for the regulation of this effector caspase. Hsp27 expression in monocytes is constitutive. Consistent with a central role of Hsp27 in blocking caspase-3 activation, Hsp27 down-regulation by double-stranded RNA interference induces apoptosis of macrophages, whereas Hsp27 overexpression increases the life span of monocytes by inhibiting apoptosis. Highlighting the importance of cell partitioning in the regulation of apoptosis, immunofluorescence, and subcellular fractionation studies revealed that whereas both caspase-3 and Hsp27 are cytoplasmic in fresh monocytes (i.e. not undergoing apoptosis), Hsp27 moves to the nucleus during apoptosis, a relocalization that can be blocked by promoting the differentiation of monocytes to macrophages or by inhibiting cell death. These results reveal a novel mechanism of caspase-3 regulation and underscore a novel and fundamental role of Hsp27 in the regulation of monocyte life span.


Asunto(s)
Caspasa 3/metabolismo , Inhibidores Enzimáticos/farmacología , Proteínas de Choque Térmico/metabolismo , Monocitos/patología , Apoptosis , Diferenciación Celular , Activación Enzimática , Humanos , Receptores de Lipopolisacáridos/biosíntesis , Modelos Biológicos , Monocitos/metabolismo , Unión Proteica , Estructura Terciaria de Proteína , Interferencia de ARN , Fracciones Subcelulares/metabolismo
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