Do socioeconomic inequalities in mortality vary between different Spanish cities? a pooled cross-sectional analysis

Background: The relationship between deprivation and mortality in urban settings is well established. This relationship has been found for several causes of death in Spanish cities in independent analyses (the MEDEA project). However, no joint analysis which pools the strength of this relationship across several cities has ever been undertaken. Such an analysis would determine, if appropriate, a joint relationship by linking the associations found. Methods: A pooled cross-sectional analysis of the data from the MEDEA project has been carried out for each of the causes of death studied. Specifically, a meta-analysis has been carried out to pool the relative risks in eleven Spanish cities. Different deprivation-mortality relationships across the cities are considered in the analysis (fixed and random effects models). The size of the cities is also considered as a possible factor explaining differences between cities. Results: Twenty studies have been carried out for different combinations of sex and causes of death. For nine of them (men: prostate cancer, diabetes, mental illnesses, Alzheimer’s disease, cerebrovascular disease; women: diabetes, mental illnesses, respiratory diseases, cirrhosis) no differences were found between cities in the effect of deprivation on mortality; in four cases (men: respiratory diseases, all causes of mortality; women: breast cancer, Alzheimer’s disease) differences not associated with the size of the city have been determined; in two cases (men: cirrhosis; women: lung cancer) differences strictly linked to the size of the city have been determined, and in five cases (men: lung cancer, ischaemic heart disease; women: ischaemic heart disease, cerebrovascular diseases, all causes of mortality) both kinds of differences have been found. Except for lung cancer in women, every significant relationship between deprivation and mortality goes in the same direction: deprivation increases mortality. Variability in the relative risks across cities was found for general mortality for both sexes. Conclusions: This study provides a general overview of the relationship between deprivation and mortality for a sample of large Spanish cities combined. This joint study allows the exploration of and, if appropriate, the quantification of the variability in that relationship for the set of cities considered.

Trends in socioeconomic inequalities in amenable mortality in urban areas of Spanish cities, 1996-2007

Background: While research continues into indicators such as preventable and amenable mortality in order to evaluate quality, access, and equity in the healthcare, it is also necessary to continue identifying the areas of greatest risk owing to these causes of death in urban areas of large cities, where a large part of the population is concentrated, in order to carry out specific actions and reduce inequalities in mortality. This study describes inequalities in amenable mortality in relation to socioeconomic status in small urban areas, and analyses their evolution over the course of the periods 1996–99, 2000–2003 and 2004–2007 in three major cities in the Spanish Mediterranean coast (Alicante, Castellón, and Valencia). Methods: All deaths attributed to amenable causes were analysed among non-institutionalised residents in the three cities studied over the course of the study periods. Census tracts for the cities were grouped into 3 socioeconomic status levels, from higher to lower levels of deprivation, using 5 indicators obtained from the 2001 Spanish Population Census. For each city, the relative risks of death were estimated between socioeconomic status levels using Poisson’s Regression models, adjusted for age and study period, and distinguishing between genders. Results: Amenable mortality contributes significantly to general mortality (around 10%, higher among men), having decreased over time in the three cities studied for men and women. In the three cities studied, with a high degree of consistency, it has been seen that the risks of mortality are greater in areas of higher deprivation, and that these excesses have not significantly modified over time. Conclusions: Although amenable mortality decreases over the time period studied, the socioeconomic inequalities observed are maintained in the three cities. Areas have been identified that display excesses in amenable mortality, potentially attributable to differences in the healthcare system, associated with areas of greater deprivation. Action must be taken in these areas of greater inequality in order to reduce the health inequalities detected. The causes behind socioeconomic inequalities in amenable mortality must be studied in depth.

Variación espacial de la exposición a contaminación atmosférica en la ciudad de Valencia y su relación con un índice de privación

Objetivo: Evaluar la variación espacial de la exposición a dióxido de nitrógeno (NO2) en la ciudad de Valencia y su relación con la privación socioeconómica y la edad. Métodos: La población por sección censal (SC) procede del Instituto Nacional de Estadística. Los niveles de NO2 se midieron en 100 puntos del área de estudio, mediante captadores pasivos, en tres campañas entre 2002 y 2004. Se utilizó regresión por usos del suelo (LUR) para obtener el mapa de los niveles de NO2. Las predicciones del LUR se compararon con las proporcionadas por: a) el captador más cercano de la red de vigilancia, b) el captador pasivo más cercano, c) el conjunto de captadores en un entorno y d) kriging. Se asignaron niveles de contaminación para cada SC. Se analizó la relación entre los niveles de NO2, un índice de privación con cinco categorías y la edad (≥65 años). Resultados: El modelo LUR resultó el método más preciso. Más del 99% de la población superó los niveles de seguridad propuestos por la Organización Mundial de la Salud. Se encontró una relación inversa entre los niveles de NO2 y el índice de privación (β = –2,01 μg/m3 en el quintil de mayor privación respecto al de menor, IC95%: –3,07 a –0,95), y una relación directa con la edad (β = 0,12 μg/m3 por incremento en unidad porcentual de población ≥65 años, IC95%: 0,08 a 0,16). Conclusiones: El método permitió obtener mapas de contaminación y describir la relación entre niveles de NO2 y características sociodemográficas.

Trends in socioeconomic inequalities in preventable mortality in urban areas of 33 Spanish cities, 1996–2007 (MEDEA project)

Background: Preventable mortality is a good indicator of possible problems to be investigated in the primary prevention chain, making it also a useful tool with which to evaluate health policies particularly public health policies. This study describes inequalities in preventable avoidable mortality in relation to socioeconomic status in small urban areas of thirty three Spanish cities, and analyses their evolution over the course of the periods 1996–2001 and 2002–2007. Methods: We analysed census tracts and all deaths occurring in the population residing in these cities from 1996 to 2007 were taken into account. The causes included in the study were lung cancer, cirrhosis, AIDS/HIV, motor vehicle traffic accidents injuries, suicide and homicide. The census tracts were classified into three groups, according their socioeconomic level. To analyse inequalities in mortality risks between the highest and lowest socioeconomic levels and over different periods, for each city and separating by sex, Poisson regression were used. Results: Preventable avoidable mortality made a significant contribution to general mortality (around 7.5%, higher among men), having decreased over time in men (12.7 in 1996–2001 and 10.9 in 2002–2007), though not so clearly among women (3.3% in 1996–2001 and 2.9% in 2002–2007). It has been observed in men that the risks of death are higher in areas of greater deprivation, and that these excesses have not modified over time. The result in women is different and differences in mortality risks by socioeconomic level could not be established in many cities. Conclusions: Preventable mortality decreased between the 1996–2001 and 2002–2007 periods, more markedly in men than in women. There were socioeconomic inequalities in mortality in most cities analysed, associating a higher risk of death with higher levels of deprivation. Inequalities have remained over the two periods analysed. This study makes it possible to identify those areas where excess preventable mortality was associated with more deprived zones. It is in these deprived zones where actions to reduce and monitor health inequalities should be put into place. Primary healthcare may play an important role in this process.

Survey on Rules on Loss of Nationality in International Treaties and Case Law. CEPS Paper in Liberty and Security in Europe No. 57, 30 August 2013

This paper offers a picture of the obligations existing under international and European law in respect of the loss of nationality. It describes international instruments including obligations in this field with direct relevancy for the loss of nationality of Member States of the European Union, but also obligations regarding loss of nationality in regional non-European treaties. Attention is given to two important judicial decisions of the European Court of Justice (Janko Rottmann) and the European Court of Human Rights (Genovese v Malta) regarding nationality. Special attention is devoted to Article 15 of the Universal Declaration of Human Rights, which forbids the arbitrary deprivation of nationality. A survey is provided of possible sub-principles that can be derived from this rule. Finally, some observations are made on the burden of proof in cases of loss of nationality.

Contribution différentielle de Neuroligine‐1 et d’EphA4 à la régulation du sommeil

Le sommeil est un besoin vital et le bon fonctionnement de l’organisme dépend de la quantité et de la qualité du sommeil. Le sommeil est régulé par deux processus : un processus circadien qui dépend de l’activité des noyaux suprachiasmatiques de l’hypothalamus et qui régule le moment durant lequel nous allons dormir, et un processus homéostatique qui dépend de l’activité neuronale et se reflète dans l’intensité du sommeil. En effet, le sommeil dépend de l’éveil qui le précède et plus l’éveil dure longtemps, plus le sommeil est profond tel que mesuré par des marqueurs électroencéphalographiques (EEG). Des études ont montré que le bon fonctionnement de ces deux processus régulateurs du sommeil dépend de la plasticité synaptique. Ainsi, les éléments synaptiques régulant la communication et la force synaptique sont d’importants candidats pour agir sur la physiologie de la régulation du sommeil. Les molécules d’adhésion cellulaire sont des acteurs clés dans les mécanismes de plasticité synaptique. Elles régulent l’activité et la maturation des synapses. Des études ont montré que leur absence engendre des conséquences similaires au manque de sommeil. Le but de ce projet de thèse est d’explorer l’effet de l’absence de deux familles de molécule d’adhésion cellulaire, les neuroligines et la famille des récepteur Eph et leur ligand les éphrines dans les processus régulateurs du sommeil. Notre hypothèse est que l’absence d’un des membres de ces deux familles de molécule affecte les mécanismes impliqués dans le processus homéostatique de régulation du sommeil. Afin de répondre à notre hypothèse, nous avons étudié d’une part l’activité EEG chez des souris mutantes n’exprimant pas Neuroligine‐1 (Nlgn1) ou le récepteur EphA4 en condition normale et après une privation de sommeil. D’autre part, nous avons mesuré les changements moléculaires ayant lieu dans ces deux modèles après privation de sommeil. Au niveau de l’activité EEG, nos résultats montrent que l’absence de Nlgn1 augmente la densité des ondes lentes en condition normale et augment l’amplitude et la pente des ondes lentes après privation de sommeil. Nlgn1 est nécessaire au fonctionnement normal de la synchronie corticale, notamment après une privation de sommeil, lui attribuant ainsi un rôle clé dans l’homéostasie du sommeil. Concernant le récepteur EphA4, son absence affecte la durée du sommeil paradoxal ainsi que l’activité sigma qui dépendent du processus circadien. Nos résultats suggèrent donc que ce récepteur est un élément important dans la régulation circadienne du sommeil. Les changements transcriptionnels en réponse à la privation de sommeil des souris n’exprimant pas Nlgn1 et EphA4 ne sont pas différents des souris sauvages. Toutefois, nous avons montré que la privation de sommeil affectait la distribution des marques épigénétiques sur le génome, tels que la méthylation et l’hydroxyméthylation, et que l’expression des molécules régulant ces changements est modifiée chez les souris mutantes pour le récepteur EphA4. Nos observations mettent en évidence que les molécules d’adhésion cellulaire, Nlgn1 et le récepteur EphA4, possèdent un rôle important dans les processus homéostatique et circadien du sommeil et contribuent de manière différente à la régulation du sommeil.