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1.
Pediatr Infect Dis J ; 24(4): 331-4, 2005 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15818293

RESUMO

BACKGROUND: Enterovirus 71 (EV71) can sometimes cause fatal or disabling diseases in children; therefore EV71-infected children with cardiopulmonary failure were investigated at Chang Gung Children's Hospital to discover the prognostic predictors. METHODS: We investigated 27 EV71-infected children with cardiopulmonary failure from May 2000 to September 2001 and analyzed their clinical data to find predictors associated with unfavorable outcomes of deaths or ventilator dependence. RESULTS: Of the 27 patients, 8 (30%) died and 10 (37%) were ventilator-dependent. Troponin I levels correlated most strongly with fatality, with 5 of the 6 children with troponin I levels >40 ng/ml dying (P = 0.001). Other factors correlated with fatality were cerebrospinal fluid white blood cell count > or =100/microL (P = 0.002) and initial systolic pressure < or =100 mm Hg (P = 0.05). Of the 19 survivors, 10 (53%) were left with central hypoventilation, dysphagia and/or limb weakness plus atrophy. The factors associated with ventilator dependence included higher inotrope equivalent (P < 0.001), duration of hypotension > or =40 hours, initial blood systolic pressure < or =100 mm Hg, positive EV71 isolation and age > or =12 months. CONCLUSIONS: Poor prognostic factors were related to cardiovascular and neurologic damage; therefore physicians may consider advanced cardiovascular support for EV71-infected children with cardiopulmonary failure.


Assuntos
Infecções por Enterovirus/complicações , Enterovirus/isolamento & purificação , Parada Cardíaca/etiologia , Criança , Enterovirus/classificação , Infecções por Enterovirus/microbiologia , Infecções por Enterovirus/mortalidade , Infecções por Enterovirus/fisiopatologia , Feminino , Parada Cardíaca/microbiologia , Parada Cardíaca/mortalidade , Parada Cardíaca/fisiopatologia , Humanos , Lactente , Masculino , Prognóstico , Índice de Gravidade de Doença , Ventiladores Mecânicos
2.
J Agric Food Chem ; 61(25): 6069-76, 2013 Jun 26.
Artigo em Inglês | MEDLINE | ID: mdl-23731091

RESUMO

Mulberry (Morus alba L.) has been considered to possess different benefits such as protecting liver; improving fever, urine excretion disorder, hypertension, and diabetic syndrome; and preventing cardiovascular diseases. Recently, mounting evidence has shown that mulberry anthocyanin extract (MAE) is beneficial to hyperlipidemia; however, the mechanisms remain unclear. The present study was aimed to investigate the protective effects of MAE on hepatocyte cultured with high fatty acid and the underlying mechanisms. By using human hepatoma cell HepG2 as cell model, the results showed that MAE suppressed fatty acid synthesis and enhanced fatty acid oxidation, contributing to amelioration of lipid accumulation induced by oleic acid (OA). Moreover, MAE also inhibited acetyl coenzyme A carboxylase (ACC) activities by stimulating adenosine monophosphate-activated protein kinase (AMPK). MAE attenuated the expression of sterol regulatory element-binding protein-1 (SREBP-1) and its target molecules, such as fatty acid synthase (FAS). Similar results were also found in the expressions of enzymes involved in triglyceride and cholesterol biosyntheses including glycerol-3-phosphate acyltransferase (GPAT), 3-hydroxy-3-methyl-glutaryl CoA reductase (HMGCoR), adipocyte-specific fatty acid binding protein (A-FABP), and SREBP-2. In contrast, the lipolytic enzyme expressions of peroxisome proliferator activated receptor α (PPARα) and carnitinepalmitol- transferase-1 (CPT1) were increased. This study suggests the hypolipidemic effects of MAE occur via phosphorylation of AMPK and inhibition of lipid biosynthesis and stimulation of lipolysis. Therefore, the mulberry anthocyanins may actively prevent nonalcoholic fatty liver disease.


Assuntos
Antocianinas/farmacologia , Metabolismo dos Lipídeos/efeitos dos fármacos , Lipogênese/efeitos dos fármacos , Fígado/efeitos dos fármacos , Morus/química , Ácido Oleico/metabolismo , Extratos Vegetais/farmacologia , Proteínas Quinases Ativadas por AMP/genética , Proteínas Quinases Ativadas por AMP/metabolismo , Regulação para Baixo/efeitos dos fármacos , Células Hep G2 , Hepatócitos/efeitos dos fármacos , Hepatócitos/enzimologia , Hepatócitos/metabolismo , Humanos , Fígado/enzimologia , Fígado/metabolismo , PPAR alfa/genética , PPAR alfa/metabolismo , Proteína de Ligação a Elemento Regulador de Esterol 1/genética , Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
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