Background: 3 billion people worldwide rely on polluting fuels and technologies for domestic cooking and heating. We estimate the global, regional, and national health burden associated with exposure to household air pollution. Methods: For the systematic review and meta-analysis, we systematically searched four databases for studies published from database inception to April 2, 2020, that evaluated the risk of adverse cardiorespiratory, paediatric, and maternal outcomes from exposure to household air pollution, compared with no exposure.
Cardiovascular causes have been estimated to be responsible for more than two thirds of the considerable mortality attributed to air pollution. There is now a substantial body of research demonstrating that exposure to air pollution has many detrimental effects throughout the cardiovascular system. Multiple biological mechanisms are responsible, however, oxidative stress is a prominent observation at many levels of the cardiovascular impairment induced by pollutant exposure.
We examined whether cognitive reserve (CR) impacts level of, or rate of change in, biomarkers of Alzheimer's disease (AD) and small-vessel cerebrovascular disease in >250 individuals who were cognitively normal and middle-aged and older at the baseline. The four primary biomarker categories commonly examined in studies of AD were measured longitudinally: cerebrospinal fluid measures of amyloid (A) and tau (T); cerebrospinal fluid and neuroimaging measures of neuronal injury (N); and neuroimaging measures of white matter hyperintensities (WMHs) to assess cerebrovascular pathology (V).
Traumatic brain injury (TBI) is one the most common human afflictions, contributing to long-term disability in survivors. Emerging data indicate that functional improvement or deterioration can occur years after TBI. In this regard, TBI is recognized as risk factor for late-life neurodegenerative disorders. TBI encompasses a heterogeneous disease process in which diverse injury subtypes and multiple molecular mechanisms overlap.
Alzheimer's disease (AD) is considered a polygenic disorder. This view is clouded, however, by lingering uncertainty over how to treat the quasi “monogenic” role of apolipoprotein E (APOE). The APOE4 allele is not only the strongest genetic risk factor for AD, it also affects risk for cardiovascular disease, stroke, and other neurodegenerative disorders. This review, based mostly on data from human studies, ranges across a variety of APOE-related pathologies, touching on evolutionary genetics and risk mitigation by ethnicity and sex.
Background Established in 2000, Millennium Development Goal 4 (MDG4) catalysed extraordinary political, financial, and social commitments to reduce under-5 mortality by two-thirds between 1990 and 2015. At the country level, the pace of progress in improving child survival has varied markedly, highlighting a crucial need to further examine potential drivers of accelerated or slowed decreases in child mortality.
Background China has experienced a remarkable epidemiological and demographic transition during the past three decades. Far less is known about this transition at the subnational level. Timely and accurate assessment of the provincial burden of disease is needed for evidence-based priority setting at the local level in China. Methods Following the methods of the Global Burden of Disease Study 2013 (GBD 2013), we have systematically analysed all available demographic and epidemiological data sources for China at the provincial level.
