ABSTRACT
Abstract Background Health expectancy indicators aim at capturing the quality dimension of total life expectancy.; however, the underlying approach, definition of health, and information source differ considerably among the indicators available. Objective (1) Review the main concepts and approaches used to estimate health expectancy focusing on two widely used European health indicators: Health-Adjusted Life Expectancy (HALE) and Healthy Life Years (HLY); (2) identify underlying differences between the results yielded by these two indicators. Method Statistical differences between the HALE and HLY indicators by sex at ages 50, 60, and 70 were tested using pairwise and global Student´s t-tests and z-scores based on standard deviation. Data for 29 European countries were collected from the European Health Expectancy Monitoring Unit (EHEMU) information system and the World Health Organization (WHO) Global Burden of Disease Study 2016 (GBD 2016). Results The HALE indicator estimates were smoother across European countries compared with those of the HLY indicator, present a narrower sex gap in morbidity, higher z-scores compared with the average distribution across Europe, and results less sensitive to cross-national variations. Conclusion The HALE estimates indicate that morbidity is more compressed for both sexes, whereas the HLY estimates suggest that morbidity is more compressed for males but more expanded for females. These contrasting results demonstrate that health expectancy indicators should be interpreted with caution.
Resumo Introdução Os indicadores de expectativa de vida saudável visam capturar uma dimensão de qualidade na expectativa de vida total. No entanto, os pressupostos, a definição de saúde e a fonte de informação diferem consideravelmente entre os indicadores. Objetivo (1) Revisar os principais conceitos e abordagens para estimar as expectativas de saúde com foco em dois indicadores de saúde usados no caso europeu (HALE e HLY); e (2) Identificar diferenças subjacentes nos resultados gerados por esses dois indicadores. Método As diferenças estatísticas entre HALE e HLY por sexo nas idades de 50, 60 e 70 são testadas através dos testes t de Student emparelhados e globais e escores z com base no desvio padrão. Os dados são de 29 países europeus do Sistema Europeu de Informação da Unidade de Monitoramento de Expectativas de Saúde (EHEMU) e do estudo OMS-GBD para o ano de 2016. Resultados As estimativas da HALE possuem menor variabilidade entre os países europeus do que a HLY, apresentam uma diferença de morbidade menor por sexo, apresentam escores-z mais altos em comparação com a distribuição média europeia e têm resultados menos sensíveis às variações entre países. Conclusão As estimativas da HALE indicam que a morbidade é mais comprimida para ambos os sexos, enquanto a HLY sugere que a morbidade para os homens é mais comprimida e para mulheres mais expandida. Esses resultados contrastantes implicam que se deve ter cuidado com os indicadores de expectativa de vida saudável e sua interpretação.
ABSTRACT
Neuronal apoptosis is one of the essential mechanisms of early brain injury after subarachnoid hemorrhage (SAH). Recently, HLY78 has been shown to inhibit apoptosis in tumor cells and embryonic cells caused by carbon ion radiation through activation of the Wnt/β-catenin pathway. This study was designed to explore the anti-apoptotic role of HLY78 in experimental SAH. The results demonstrated that HLY78 attenuated neuronal apoptosis and the neurological deficits after SAH through the activation of low-density lipoprotein receptor-related protein 6 (LRP6), which subsequently increased the level of phosphorylated glycogen synthesis kinase 3 beta (p-GSK3β) (Ser9), β-catenin, and Bcl-2, accompanied by a decrease of p-β-catenin, Bax, and cleaved caspase 3. An LRP6 small-interfering ribonucleic acid reversed the effects of HLY78. In conclusion, HLY78 attenuates neuronal apoptosis and improves neurological deficits through the LRP6/GSK3β/β-catenin signaling pathway after SAH in rats. HLY78 is a promising therapeutic agent to attenuate early brain injury after SAH.
ABSTRACT
Neuronal apoptosis is one of the essential mechanisms of early brain injury after subarachnoid hemorrhage (SAH). Recently, HLY78 has been shown to inhibit apoptosis in tumor cells and embryonic cells caused by carbon ion radiation through activation of the Wnt/β-catenin pathway. This study was designed to explore the anti-apoptotic role of HLY78 in experimental SAH. The results demonstrated that HLY78 attenuated neuronal apoptosis and the neurological deficits after SAH through the activation of low-density lipoprotein receptor-related protein 6 (LRP6), which subsequently increased the level of phosphorylated glycogen synthesis kinase 3 beta (p-GSK3β) (Ser9), β-catenin, and Bcl-2, accompanied by a decrease of p-β-catenin, Bax, and cleaved caspase 3. An LRP6 small-interfering ribonucleic acid reversed the effects of HLY78. In conclusion, HLY78 attenuates neuronal apoptosis and improves neurological deficits through the LRP6/GSK3β/β-catenin signaling pathway after SAH in rats. HLY78 is a promising therapeutic agent to attenuate early brain injury after SAH.