Partis et recompositions politiques : quelques enseignements du « Printemps arabe »

National audienceLongtemps délaissés par les sciences sociales, les partis politiques dans le monde arabe suscitent depuis quelques années un regain d’intérêt. Vingt ans après un travail coordonné par Pierre-Robert Baduel sur le Maghreb dans la Revue des Mondes Musulmans et de la Méditerranée (1996), dix ans après un numéro dirigé par Myriam Catusse dans la même revue sur le Machrek (2006) il semble que l’appel à un renouveau de l’approche du fait partisan ait été entendu. Ce numéro de Confluences Méditerranée se propose de présenter quelques-uns de ces récents travaux, pour certains encore inédits, et, adoptant une perspective comparatiste, d’explorer avec eux les pistes qu’ils ouvrent quant aux recompositions politiques dans la région. En rassemblant ses auteurs autour d’un même objet, d’une même séquence historique, et d’une même approche, ce numéro entend ainsi souligner l’intérêt du parti à la fois comme lieu d’observation privilégié des transformations socio-politiques que connaît le monde arabe depuis 2011, et des partisans comme acteurs de ces recompositions

Dynamics of Stratospheric Sudden Warming Events: Data Analysis and Modelling

The polar vortex is a large scale cyclone located in the middle atmosphere near to the planet’s geographic poles. These vortices form during the hemispheric winter and break down in the spring of the following year. They may also break down in mid winter, causing a sudden stratospheric warming event (SSW). The vortex is thought to be preconditioned leading up to these warming events, resulting in the breakdown of the vortex. Integral diagnostics are used to investigate the stripping of air from the vortex as part of this preconditioning. Contour diagnostics of mass and circulation are calculated using ERA-40 reanalysis data for the stratosphere. The edge of the vortex is easily identifiable in these diagnostics as a high gradient of Ertel’s potential vorticity (PV), and the warming events are also clearly visible. From these the amount of air removed from the vortex is determined from the balance equation of the mass integral. These terms show that there are significant amounts of air removed from the vortex, with several stripping events identifiable in them through the winter, especially in those during which a major sudden warming event occurred. These stripping events can be seen in corresponding PV maps, where tongues of PV can be seen to be stripped from the vortex and mixed into the surrounding surf zone of turbulent air. From the integral diagnostics a Lagrangian measure of the meridional circulation in the stratosphere is also calculated. In the final part of the thesis a shallow water model is used to investigate a quantitative link between forcing and the amount of stripping of the vortex. It is found that when the forcing is large enough there is significant stripping of mass from the vortex. This does not lead to SSWs in all cases, and the total amount of stripping is not found to be proportional to the maximum amplitude of the forcing.EPSR

Does Obesity Cause Thyroid Cancer? A Mendelian Randomization Study

Background: The incidence of thyroid cancer is rising, and relatively little is known about modifiable risk factors for the condition. Observational studies have suggested a link between adiposity and thyroid cancer; however, these are subject to confounding and reverse causality. Here, we used data from the UK Biobank and Mendelian randomization approaches to investigate whether adiposity causes benign nodular thyroid disease and differentiated thyroid cancer. Methods: We analyzed data from 379 708 unrelated participants of European ancestry in the UK Biobank and identified 1812 participants with benign nodular thyroid disease and 425 with differentiated thyroid carcinoma. We tested observational associations with measures of adiposity and type 2 diabetes mellitus. One and 2-sample Mendelian randomization approaches were used to investigate causal relationships. Results: Observationally, there were positive associations between higher body mass index (odds ratio [OR], 1.15; 95% confidence interval [CI], 1.08-1.22), higher waist-hip ratio (OR, 1.16; 95% CI, 1.09-1.23), and benign nodular thyroid disease, but not thyroid cancer. Mendelian randomization did not support a causal link for obesity with benign nodular thyroid disease or thyroid cancer, although it did provide some evidence that individuals in the highest quartile for genetic liability of type 2 diabetes had higher odds of thyroid cancer than those in the lowest quartile (OR, 1.45; CI, 1.11-1.90). Conclusions: Contrary to the findings of observational studies, our results do not confirm a causal role for obesity in benign nodular thyroid disease or thyroid cancer. They do, however, suggest a link between type 2 diabetes and thyroid cancer.This article is freely available via Open Access. Click on the Publisher URL to access it via the publisher's site.WT_/Wellcome Trust/United Kingdompublished version, accepted version (12 month embargo), submitted versio

Telomere length and risk of idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease:a mendelian randomisation study

Background: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease accounting for 1% of UK deaths. In the familial form of pulmonary fibrosis, causal genes have been identified in about 30% of cases, and a majority of these causal genes are associated with telomere maintenance. Prematurely shortened leukocyte telomere length is associated with IPF and chronic obstructive pulmonary disease (COPD), a disease with similar demographics and shared risk factors. Using mendelian randomisation, we investigated evidence supporting a causal role for short telomeres in IPF and COPD. Methods: Mendelian randomisation inference of telomere length causality was done for IPF (up to 1369 cases) and COPD (13 538 cases) against 435 866 controls of European ancestry in UK Biobank. Polygenic risk scores were calculated and two-sample mendelian randomisation analyses were done using seven genetic variants previously associated with telomere length, with replication analysis in an IPF cohort (2668 cases vs 8591 controls) and COPD cohort (15 256 cases vs 47 936 controls). Findings: In the UK Biobank, a genetically instrumented one-SD shorter telomere length was associated with higher odds of IPF (odds ratio [OR] 4·19, 95% CI 2·33–7·55; p=0·0031) but not COPD (1·07, 0·88–1·30; p=0·51). Similarly, an association was found in the IPF replication cohort (12·3, 5·05–30·1; p=0·0015) and not in the COPD replication cohort (1·04, 0·71–1·53; p=0·83). Meta-analysis of the two-sample mendelian randomisation results provided evidence inferring that shorter telomeres cause IPF (5·81 higher odds of IPF, 95% CI 3·56–9·50; p=2·19 × 10−12). There was no evidence to infer that telomere length caused COPD (OR 1·07, 95% CI 0·90–1·27; p=0·46). Interpretation: Cellular senescence is hypothesised as a major driving force in IPF and COPD; telomere shortening might be a contributory factor in IPF, suggesting divergent mechanisms in COPD. Defining a key role for telomere shortening enables greater focus in telomere-related diagnostics, treatments, and the search for a cure in IPF. Investigation of therapies that improve telomere length is warranted. Funding: Medical Research Council.</p

Telomere length and risk of idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease:a mendelian randomisation study

Background: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease accounting for 1% of UK deaths. In the familial form of pulmonary fibrosis, causal genes have been identified in about 30% of cases, and a majority of these causal genes are associated with telomere maintenance. Prematurely shortened leukocyte telomere length is associated with IPF and chronic obstructive pulmonary disease (COPD), a disease with similar demographics and shared risk factors. Using mendelian randomisation, we investigated evidence supporting a causal role for short telomeres in IPF and COPD. Methods: Mendelian randomisation inference of telomere length causality was done for IPF (up to 1369 cases) and COPD (13 538 cases) against 435 866 controls of European ancestry in UK Biobank. Polygenic risk scores were calculated and two-sample mendelian randomisation analyses were done using seven genetic variants previously associated with telomere length, with replication analysis in an IPF cohort (2668 cases vs 8591 controls) and COPD cohort (15 256 cases vs 47 936 controls). Findings: In the UK Biobank, a genetically instrumented one-SD shorter telomere length was associated with higher odds of IPF (odds ratio [OR] 4·19, 95% CI 2·33–7·55; p=0·0031) but not COPD (1·07, 0·88–1·30; p=0·51). Similarly, an association was found in the IPF replication cohort (12·3, 5·05–30·1; p=0·0015) and not in the COPD replication cohort (1·04, 0·71–1·53; p=0·83). Meta-analysis of the two-sample mendelian randomisation results provided evidence inferring that shorter telomeres cause IPF (5·81 higher odds of IPF, 95% CI 3·56–9·50; p=2·19 × 10−12). There was no evidence to infer that telomere length caused COPD (OR 1·07, 95% CI 0·90–1·27; p=0·46). Interpretation: Cellular senescence is hypothesised as a major driving force in IPF and COPD; telomere shortening might be a contributory factor in IPF, suggesting divergent mechanisms in COPD. Defining a key role for telomere shortening enables greater focus in telomere-related diagnostics, treatments, and the search for a cure in IPF. Investigation of therapies that improve telomere length is warranted. Funding: Medical Research Council.</p

The influence of transmitted and non-transmitted parental BMI-associated alleles on the risk of overweight in childhood

Overweight in children is strongly associated with parental body mass index (BMI) and overweight. We assessed parental transmitted and non-transmitted genetic contributions to overweight in children from the Danish National Birth Cohort by constructing genetic risk scores (GRSs) from 941 common genetic variants associated with adult BMI and estimating associations of transmitted maternal/paternal and non-transmitted maternal GRS with child overweight. Maternal and paternal BMI (standard deviation (SD) units) had a strong association with childhood overweight [Odds ratio (OR): 2.01 (95% confidence interval (CI) 1.74; 2.34) and 1.64 (95% CI 1.43; 1.89)]. Maternal and paternal transmitted GRSs (SD-units) increased odds for child overweight equally [OR: 1.30 (95% CI 1.16; 1.46) and 1.30 (95% CI 1.16; 1.47)]. However, both the parental phenotypic and the GRS associations may depend on maternal BMI, being weaker among mothers with overweight. Maternal non-transmitted GRS was not associated with child overweight [OR 0.98 (95% CI 0.88; 1.10)] suggesting no specific influence of maternal adiposity as such. In conclusion, parental transmitted GRSs, based on adult BMI, contribute to child overweight, but in overweight mothers other genetic and environmental factors may play a greater role.This article is freely available via Open Access. Click on the Publisher URL to access it via the publisher's site.WT104150/Wellcome Trust (Wellcome)published version, accepted version, submitted versio

Using genetics to understand the causal influence of higher BMI on depression

Background: Depression is more common in obese than non-obese individuals, especially in women, but the causal relationship between obesity and depression is complex and uncertain. Previous studies have used genetic variants associated with BMI to provide evidence that higher body mass index (BMI) causes depression, but have not tested whether this relationship is driven by the metabolic consequences of BMI nor for differences between men and women. Methods: We performed a Mendelian randomization study using 48 791 individuals with depression and 291 995 controls in the UK Biobank, to test for causal effects of higher BMI on depression (defined using self-report and Hospital Episode data). We used two genetic instruments, both representing higher BMI, but one with and one without its adverse metabolic consequences, in an attempt to 'uncouple' the psychological component of obesity from the metabolic consequences. We further tested causal relationships in men and women separately, and using subsets of BMI variants from known physiological pathways. Results: Higher BMI was strongly associated with higher odds of depression, especially in women. Mendelian randomization provided evidence that higher BMI partly causes depression. Using a 73-variant BMI genetic risk score, a genetically determined one standard deviation (1 SD) higher BMI (4.9 kg/m2) was associated with higher odds of depression in all individuals [odds ratio (OR): 1.18, 95% confidence interval (CI): 1.09, 1.28, P = 0.00007) and women only (OR: 1.24, 95% CI: 1.11, 1.39, P = 0.0001). Meta-analysis with 45 591 depression cases and 97 647 controls from the Psychiatric Genomics Consortium (PGC) strengthened the statistical confidence of the findings in all individuals. Similar effect size estimates were obtained using different Mendelian randomization methods, although not all reached P < 0.05. Using a metabolically favourable adiposity genetic risk score, and meta-analysing data from the UK biobank and PGC, a genetically determined 1 SD higher BMI (4.9 kg/m2) was associated with higher odds of depression in all individuals (OR: 1.26, 95% CI: 1.06, 1.50], P = 0.010), but with weaker statistical confidence. Conclusions: Higher BMI, with and without its adverse metabolic consequences, is likely to have a causal role in determining the likelihood of an individual developing depression.This article is freely available via Open Access. Click on the Publisher URL to access it via the publisher's site.DH_/Department of Health/United Kingdom MC_PC_17228/MRC_/Medical Research Council/United Kingdom MC_QA137853/MRC_/Medical Research Council/United Kingdom 104150/Z/14/Z/WT_/Wellcome Trust/United Kingdom MR/M005070/1/MRC_/Medical Research Council/United Kingdom WT097835MF/WT_/Wellcome Trust/United Kingdompublished version, accepted version (12 month embargo), submitted versio

How can entrepreneurial interventions in a university context impact the entrepreneurial intention of their students?

This paper explores the link between the entrepreneurial intention of students in higher education and the entrepreneurial interventions an institution can provide to support them. The study uses data collected from 679 undergraduate students from Chinese and UK Universities. The instrument for data collection was a paper-based questionnaire. This study uses the integrated model of entrepreneurial intentions as the theoretical underpinning for this approach. The initial findings highlight the perceived need for a range of entrepreneurship interventions, with business training programmes being the highest priority, followed by mentoring, specialist business advice, low-cost finance, business networking events and enterprise clubs. It also shows that those with different Intention Horizons do request a different portfolio of interventions. The paper provides an evidence-based approach to entrepreneurship education design and the development of interventions to support a range of students with and without entrepreneurial intention. This work suggests a previously under-articulated relationship between the nascent entrepreneur’s Intention Horizon, university interventions, and entrepreneurial action. There are numerous calls for further contextualisation of entrepreneurship education which this paper fulfils (Baron and Shane in Psychol Entrepreneurship 19-39, 2007; Byrne et al. in Edward Elgar Publishing, 2014). It further develops the narrative around both contextualisation, the previous experience of the students and the range and importance of these interventions to support the creation of a new venture

How can entrepreneurial interventions in a university context impact the entrepreneurial intention of their students?

This paper explores the link between the entrepreneurial intention of students in higher education and the entrepreneurial interventions an institution can provide to support them. The study uses data collected from 679 undergraduate students from Chinese and UK Universities. The instrument for data collection was a paper-based questionnaire. This study uses the integrated model of entrepreneurial intentions as the theoretical underpinning for this approach. The initial findings highlight the perceived need for a range of entrepreneurship interventions, with business training programmes being the highest priority, followed by mentoring, specialist business advice, low-cost finance, business networking events and enterprise clubs. It also shows that those with different Intention Horizons do request a different portfolio of interventions. The paper provides an evidence-based approach to entrepreneurship education design and the development of interventions to support a range of students with and without entrepreneurial intention. This work suggests a previously under-articulated relationship between the nascent entrepreneur’s Intention Horizon, university interventions, and entrepreneurial action. There are numerous calls for further contextualisation of entrepreneurship education which this paper fulfils (Baron and Shane in Psychol Entrepreneurship 19-39, 2007; Byrne et al. in Edward Elgar Publishing, 2014). It further develops the narrative around both contextualisation, the previous experience of the students and the range and importance of these interventions to support the creation of a new venture