RESUMO
The road traffic crash injury burden significantly impacts the lives of South African children. This study aimed to assess the fatal and non-fatal pattern of road traffic crash injury of children under 13 years old from Metro West, City of Cape Town, from 1 January until 31 December 2014. The data were stratified by age, sex and mechanism of road traffic crash. The overall mortality rate was 8.7 per 100 000 population and pedestrians contributed the most to this burden (72.5%). There were more male children involved in a road traffic crash (p = 0.0001). The greatest proportion of fatal and non-fatal road traffic crash injuries was observed in children aged 5-9 years. Fractures contributed to the greatest rate of years lived with disability (3.0 years of life lived with disability per 100 000). Our study found that the burden of road traffic crashes primarily affects male pedestrians aged 5-9 years old.
Assuntos
Acidentes de Trânsito/mortalidade , Pedestres/estatística & dados numéricos , Ferimentos e Lesões/epidemiologia , Escala Resumida de Ferimentos , Adolescente , Distribuição por Idade , Criança , Pré-Escolar , Cidades/epidemiologia , Feminino , Humanos , Lactente , Masculino , Fatores de Risco , Distribuição por Sexo , África do Sul/epidemiologiaRESUMO
Melatonin protects the heart against myocardial ischemia/reperfusion injury via the activation of the survivor activating factor enhancement (SAFE) pathway which involves tumor necrosis factor alpha (TNFα) and the signal transducer and activator of transcription 3 (STAT3). Toll-like receptor 4 (TLR4) plays a crucial role in myocardial ischemia/reperfusion injury and activates TNFα. In this study, we investigated whether melatonin may target TLR4 to activate the SAFE pathway. Isolated hearts from rats or mice were subjected to ischemia/reperfusion injury. Melatonin (75 ng/L) and/or TAK242 (a specific inhibitor of TLR4 signaling, 500 nm) were administered to the rat hearts before the induction of ischemia. Pre-ischemic myocardial STAT3 was evaluated by Western blotting. Lipopolysaccharide (LPS, a stimulator of TLR4) was administered to wild type, TNFα receptor 2 knockout or cardiomyocyte-specific STAT3-deficient mice (2.8 mg/kg, i.p) 45 min before the heart isolation. Myocardial infarct size was measured as an endpoint. Compared to the control, administration of melatonin reduced myocardial infarct size (34.7 ± 2.8% versus 62.6 ± 2.7%, P < 0.01). This protective effect was abolished in the presence of TAK242 (49.2 ± 6.5%). Melatonin administered alone increased the pre-ischemic activation of mitochondrial STAT3, and this effect was attenuated with TAK242. Furthermore, stimulation of TLR4 with LPS pretreatment to mice reduced myocardial infarct size of the hearts isolated from wild-type animals but failed to protect the hearts isolated from TNFα receptor 2-knockout mice or cardiomyocyte-specific STAT3-deficient mice (P < 0.001). Taken together, these data suggest that cardioprotection induced by melatonin is mediated by TLR4 to activate the SAFE pathway.
Assuntos
Cardiotônicos/farmacologia , Melatonina/farmacologia , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/metabolismo , Animais , Masculino , Camundongos , Camundongos Knockout , Traumatismo por Reperfusão Miocárdica/genética , Traumatismo por Reperfusão Miocárdica/metabolismo , Traumatismo por Reperfusão Miocárdica/patologia , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/patologia , Ratos , Ratos Wistar , Receptores Tipo II do Fator de Necrose Tumoral/genética , Receptores Tipo II do Fator de Necrose Tumoral/metabolismo , Fator de Transcrição STAT3/genética , Fator de Transcrição STAT3/metabolismo , Transdução de Sinais/genética , Sulfonamidas/farmacologia , Receptor 4 Toll-Like/genética , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismoRESUMO
BACKGROUND: Many epidemiological, clinical and laboratory studies suggest that chronic and moderate consumption of red wine benefits cardiovascular health, because of the alcoholic content or the polyphenols/flavonoids. AIMS: The antioxidant and cardioprotective properties of a French red wine (cabernet sauvignon, 12% alcohol by volume) were compared with those of the same wine subjected to reverse osmosis for partial removal of alcohol (6% alcohol by volume). METHODS: Antioxidant capacity was assessed in vitro using the oxygen radical absorbance capacity (ORAC) assay. To test the cardioprotective effect of 12% v. 6% wine, the drinking water of rats used for controls was supplemented with red wine (12% or 6%). After 10 days, hearts were isolated on a Langendorff system and subjected to 30 minutes of global ischaemia plus 30 minutes of reperfusion (I/R). RESULTS: No differences in antioxidant capacity were observed between wine of 12% and 6% alcohol content (n=8 per group). Control hearts subjected to I/R presented a rate pressure product (heart rate x left ventricular developed pressure, expressed as a percentage of baseline value) of 16±4% (mean±standard error). Pretreatment with wine 12% or 6% improved the rate pressure product to 40±6% and 43±6%, respectively (p<0.05 v. control). CONCLUSION: Our findings suggest that the reduction of alcohol content from 12% to 6% in wine did not alter its antioxidant and cardioprotective properties. Moderate and regular consumption of lower alcohol content wines may confer beneficial effects without the risks associated with traditional wines of higher alcohol content.
