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1.
BMC Public Health ; 18(1): 71, 2017 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-28764686

RESUMO

BACKGROUND: It is now universally acknowledged that climate change constitutes a major threat to human health. At the same time, some of the measures to reduce greenhouse gas emissions, so-called climate change mitigation measures, have significant health co-benefits (e.g., walking or cycling more; eating less meat). The goal of limiting global warming to 1,5° Celsius set by the Conference of the Parties to the United Nations Framework Convention on Climate Change in Paris in 2015 can only be reached if all stakeholders, including households, take actions to mitigate climate change. Results on whether framing mitigation measures in terms of their health co-benefits increases the likelihood of their implementation are inconsistent. The present study protocol describes the transdisciplinary project HOPE (HOuseholds' Preferences for reducing greenhouse gas emissions in four European high-income countries) that investigates the role of health co-benefits in households' decision making on climate change mitigation measures in urban households in France, Germany, Norway and Sweden. METHODS: HOPE employs a mixed-methods approach combining status-quo carbon footprint assessments, simulations of the reduction of households' carbon footprints, and qualitative in-depth interviews with a subgroup of households. Furthermore, a policy analysis of current household oriented climate policies is conducted. In the simulation of the reduction of households' carbon footprints, half of the households are provided with information on health co-benefits of climate change mitigation measures, the other half is not. Households' willingness to implement the measures is assessed and compared in between-group analyses of variance. DISCUSSION: This is one of the first comprehensive mixed-methods approaches to investigate which mitigation measures households are most willing to implement in order to reach the 1,5° target set by the Paris Agreement, and whether health co-benefits can serve as a motivator for households to implement these measures. The comparison of the empirical data with current climate policies will provide knowledge for tailoring effective climate change mitigation and health policies.


Assuntos
Mudança Climática , Conservação dos Recursos Naturais , Comportamentos Relacionados com a Saúde , Política de Saúde , Promoção da Saúde/métodos , Países Desenvolvidos , França , Alemanha , Humanos , Noruega , Paris , Suécia
4.
Mol Cell Biol ; 31(1): 63-80, 2011 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-20974805

RESUMO

An early lesion in many kidney diseases is damage to podocytes, which are critical components of the glomerular filtration barrier. A number of proteins are essential for podocyte filtration function, but the signaling events contributing to development of nephrotic syndrome are not well defined. Here we show that class II phosphoinositide 3-kinase C2α (PI3KC2α) is expressed in podocytes and plays a critical role in maintaining normal renal homeostasis. PI3KC2α-deficient mice developed chronic renal failure and exhibited a range of kidney lesions, including glomerular crescent formation and renal tubule defects in early disease, which progressed to diffuse mesangial sclerosis, with reduced podocytes, widespread effacement of foot processes, and modest proteinuria. These findings were associated with altered expression of nephrin, synaptopodin, WT-1, and desmin, indicating that PI3KC2α deficiency specifically impacts podocyte morphology and function. Deposition of glomerular IgA was observed in knockout mice; importantly, however, the development of severe glomerulonephropathy preceded IgA production, indicating that nephropathy was not directly IgA mediated. PI3KC2α deficiency did not affect immune responses, and bone marrow transplantation studies also indicated that the glomerulonephropathy was not the direct consequence of an immune-mediated disease. Thus, PI3KC2α is critical for maintenance of normal glomerular structure and function by supporting normal podocyte function.


Assuntos
Glomérulos Renais/anatomia & histologia , Glomérulos Renais/fisiologia , Fosfatidilinositol 3-Quinases/fisiologia , Animais , Antígenos de Superfície/metabolismo , Transplante de Medula Óssea , Glomerulonefrite/etiologia , Glomerulonefrite/patologia , Glomerulonefrite/fisiopatologia , Glomerulonefrite por IGA/etiologia , Glomerulonefrite por IGA/patologia , Glomerulonefrite por IGA/fisiopatologia , Humanos , Imunoglobulina A/metabolismo , Imunoglobulina G/metabolismo , Glomérulos Renais/enzimologia , Glomérulos Renais/patologia , Proteínas de Membrana/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Proteínas dos Microfilamentos/metabolismo , Fosfatidilinositol 3-Quinases/deficiência , Fosfatidilinositol 3-Quinases/genética , Podócitos/enzimologia , Podócitos/patologia , Podócitos/fisiologia , Insuficiência Renal/etiologia , Insuficiência Renal/patologia , Insuficiência Renal/fisiopatologia , Quimeras de Transplante
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