Corruption and Media Concentration: A Panel Data Analysis

My master thesis studies the relationship between media concentration and corruption based on a panel data analysis, with a panel dataset which provides information about 29 countries over a span of 19 years. Based on a cross-section analysis Djankov, McLiesh, Nenova and Shleifer (2003, JLE) which focused on the relationship between corruption and media state-ownership, I enhance their results thanks to panel data fixed effects, to control for more unobservable effects, and several robustness checks. As Djankov et al did, we focus on two specific media markets: television (TV) and daily newspapers. Thanks to new data from the book “Who Owns the World‟s Media?” (Noam, 2016), I broaden the spectrum of their article to focus on the correlations between corruption and all types of media concentration (public, private and the industry). I confine their previous results: a positive correlation is found only for public TV with large shares of the market. In fact, I find a negative correlation between public TV shares and corruption for lower levels of state-ownership, especially in the case of developed countries. Contrary to daily newspapers, this result remains after many robustness checks. I provide evidence that low-levels of state-ownership limit concentration of private media, reducing the risk of media capture. Indeed, competition within the private sector is found to be negatively correlated with corruption. Finally, I find weak evidence for a positive correlation between corruption and media industry concentration in only two cases: when considering all types of media and when considering TV alone

Corruption and Media Concentration: A Panel Data Analysis

My master thesis studies the relationship between media concentration and corruption based on a panel data analysis, with a panel dataset which provides information about 29 countries over a span of 19 years. Based on a cross-section analysis Djankov, McLiesh, Nenova and Shleifer (2003, JLE) which focused on the relationship between corruption and media state-ownership, I enhance their results thanks to panel data fixed effects, to control for more unobservable effects, and several robustness checks. As Djankov et al did, we focus on two specific media markets: television (TV) and daily newspapers. Thanks to new data from the book “Who Owns the World‟s Media?” (Noam, 2016), I broaden the spectrum of their article to focus on the correlations between corruption and all types of media concentration (public, private and the industry). I confine their previous results: a positive correlation is found only for public TV with large shares of the market. In fact, I find a negative correlation between public TV shares and corruption for lower levels of state-ownership, especially in the case of developed countries. Contrary to daily newspapers, this result remains after many robustness checks. I provide evidence that low-levels of state-ownership limit concentration of private media, reducing the risk of media capture. Indeed, competition within the private sector is found to be negatively correlated with corruption. Finally, I find weak evidence for a positive correlation between corruption and media industry concentration in only two cases: when considering all types of media and when considering TV alone

Time and resource constrained offloading with multi-task in a mobile edge computing node

In recent years, the importance of the mobile edge computing (MEC) paradigm along with the 5G, the Internet of Things (IoT) and virtualization of network functions is well noticed. Besides, the implementation of computation-intensive applications at the mobile device level is limited by battery capacity, processing capabalities and execution time. To increase the batteries life and improve the quality of experience for computationally intensive and latency-sensitive applications, offloading some parts of these applications to the MEC is proposed. This paper presents a solution for a hard decision problem that jointly optimizes the processing time and computing resources in a mobile edge-computing node. Hence, we consider a mobile device with an offloadable list of heavy tasks and we jointly optimize the offloading decisions and the allocation of IT resources to reduce the latency of tasks’ processing. Thus, we developped a heuristic solution based on the simulated annealing algorithm, which can improve the offloading rate and reduce the total task latency while meeting short decision time. We performed a series of experiments to show its efficiency. Finally, the obtained results in terms of full-time treatrement are very encouraging. In addition, our solution makes offloading decisions within acceptable and achievable deadlines

Energy and Processing Time Efficiency for an Optimal Offloading in a Mobile Edge Computing Node

This article describes a processing time, energy and computing resources optimization in a Mobile Edge Computing (MEC). We consider a mobile user MEC system, where a smart mobile device (SMD) demand computation offloading to a MEC server. For that, we consider a SMD contains a set of heavy tasks that can be offloadable. The formulated optimization problem takes into account both the dedicated energy capacity and the processing times. We proposed a heuristic solution schema. To evaluate our solution, we realized a range of simulation experiments. The results obtained in terms of treatment time and energy consumption are very

Efficient Multi-task offloading with energy and computational resources optimization in a mobile edge computing node

With the fifth-generation (5G) networks, Mobile edge computing (MEC) is a promising paradigm to provide near computing and storage capabilities to smart mobile devices. In addition, mobile devices are most of the time battery dependent and energy constrained while they are characterized by their limited processing and storage capacities. Accordingly, these devices must offload a part of their heavy tasks that require a lot of computation and are energy consuming. This choice remains the only option in some circumstances, especially when the battery drains off. Besides, the local CPU frequency allocated to processing has a huge impact on devices energy consumption. Additionally, when mobile devices handle many tasks, the decision of the part to offload becomes critical. Actually, we must consider the wireless network state, the available processing resources at both sides, and particularly the local available battery power. In this paper, we consider a single mobile device that is energy constrained and that retains a list of heavy offloadable tasks that are delay constrained. Therefore, we formulated the corresponding optimization problem, and proposed a Simulated Annealing based heuristic solution scheme. In order to evaluate our solution, we carried out a set of simulation experiments. Finally, the obtained results in terms of energy are very encouraging. Moreover, our solution performs the offloading decisions within an acceptable and feasible timeframes

Offloading Decisions in a Mobile Edge Computing Node with Time and Energy Constraints

This article describes a simulated annealing based offloading decision with processing time, energy consumption and resource constraints in a Mobile Edge Computing Node. Edge computing mostly deals with mobile devices subject to constraints. Especially because of their limited processing capacity and the availability of their battery, these devices have to offload some of their heavy tasks, which require a lot of calculations. We consider a single mobile device with a list of heavy tasks that can be offloadable. The formulated optimization problem takes into account both the dedicated energy capacity and the total execution time. We proposed a heuristic solution schema. To evaluate our solution, we performed a set of simulation experiments. The results obtained in terms of processing time and energy consumption are very encouraging

Hibernation impact on the catalytic activities of the mitochondrial D-3-hydroxybutyrate dehydrogenase in liver and brain tissues of jerboa (Jaculus orientalis)

BACKGROUND: Jerboa (Jaculus orientalis) is a deep hibernating rodent native to subdesert highlands. During hibernation, a high level of ketone bodies i.e. acetoacetate (AcAc) and D-3-hydroxybutyrate (BOH) are produced in liver, which are used in brain as energetic fuel. These compounds are bioconverted by mitochondrial D-3-hydroxybutyrate dehydrogenase (BDH) E.C. 1.1.1.30. Here we report, the function and the expression of BDH in terms of catalytic activities, kinetic parameters, levels of protein and mRNA in both tissues i.e brain and liver, in relation to the hibernating process. RESULTS: We found that: 1/ In euthemic jerboa the specific activity in liver is 2.4- and 6.4- fold higher than in brain, respectively for AcAc reduction and for BOH oxidation. The same differences were found in the hibernation state. 2/ In euthermic jerboa, the Michaelis constants, K(M )BOH and K(M )NAD(+ )are different in liver and in brain while K(M )AcAc, K(M )NADH and the dissociation constants, K(D )NAD(+)and K(D )NADH are similar. 3/ During prehibernating state, as compared to euthermic state, the liver BDH activity is reduced by half, while kinetic constants are strongly increased except K(D )NAD(+). 4/ During hibernating state, BDH activity is significantly enhanced, moreover, kinetic constants (K(M )and K(D)) are strongly modified as compared to the euthermic state; i.e. K(D )NAD(+ )in liver and K(M )AcAc in brain decrease 5 and 3 times respectively, while K(D )NADH in brain strongly increases up to 5.6 fold. 5/ Both protein content and mRNA level of BDH remain unchanged during the cold adaptation process. CONCLUSIONS: These results cumulatively explained and are consistent with the existence of two BDH enzymatic forms in the liver and the brain. The apoenzyme would be subjected to differential conformational folding depending on the hibernation state. This regulation could be a result of either post-translational modifications and/or a modification of the mitochondrial membrane state, taking into account that BDH activity is phospholipid-dependent

Altérations mitochondriales et processus inflammatoire dans la déficience en acyl- Coenzyme A oxydase 1 peroxysomale

L acyl-CoA oxydase 1 (ACOX1) est l enzyme qui catalyse la première étape de la voie classique de la b-oxydation peroxysomale. Cette voie catabolise exclusivement les acides gras à très longue chaîne (AGTLC). Chez l homme, la déficience en ACOX1 est à l origine de la pseudo adrénoleucodystrophie néonatale (P-NALD), une maladie neurodégénérative rare caractérisée par une accumulation des AGTLC dans le plasma et les tissus, une hépatomégalie, un retard du développement moteur et une démyélinisation de la matière blanche cérébrale. Chez la souris, l extinction du gène Acox1 provoque une accumulation des AGTLC dans le plasma, un retard de croissance, une stéatose hépatique et le développement d une hépatocarcinogenèse avec l âge. Cependant, ces souris ne développent pas de symptômes cérébraux contrairement aux patients P NALD. Au cours de ce travail, on a pu montrer sur des fibroblastes issus de patients atteints de P NALD qu en absence d activité ACOX1, les peroxysomes sont diminués en nombre et augmentés en taille avec un niveau de b-oxydation peroxysomale fortement réduit. L accumulation des AGTLC suite à la déficience en ACOX1 dans ces cellules provoque, au niveau transcriptionnel, la perturbation de la voie de synthèse du cholestérol et déclenche une réaction inflammatoire caractérisée par l activation de la voie de l IL-1 et la sécrétion d IL-6 et d IL-8. Le rôle métabolique important que joue l ACOX1 dans l homéostasie énergétique cellulaire a pu être souligné chez l homme et chez la souris. En effet, la déficience en ACOX1 dans les fibroblastes de patients P-NALD perturbe la morphologie de la mitochondrie qui apparaît anormale ainsi que le métabolisme énergétique mitochondrial caractérisé par une inhibition de PGC-1a par acétylation, une surexpression de l activité du complexe V et une diminution du taux d ATP mitochondrial. L absence dans le foie de l activité ACOX1, chez la souris Acox1-/-, se traduit par des perturbations, au niveau mitochondrial, dela biogenèse et du métabolisme énergétique. Ces perturbations mitochondriales se caractérisent par une diminution de l activité du complexe IV de la chaîne respiratoire accompagnée d une diminution de la respiration. Cependant, ces perturbations n affectent pas le taux d ATP total. Les altérations mitochondriales observées chez les souris Acox1-/- sont en grande partie corrigées par l expression de l ACOX1 humaine. Ceci montre le rôle indispensable de l ACOX1 dans l homéostasie de la fonction mitochondriale.L ensemble des résultats obtenus au cours de ce travail confirme l importance de l activité acyl-CoA oxydase 1 pour la dégradation des AGTLC au niveau du système de b-oxydation peroxysomale et pour la biogenèse du peroxysome. L accumulation des substrats non métabolisés en absence d ACOX1 pourrait être à l origine de la perturbation de la fonction mitochondriale montrant à quel point l activité de l ACOX1 est indispensable au métabolisme cellulaireAcyl-CoA oxidase 1 (ACOX1) is the rate-limiting enzyme of the peroxisomal fatty acid b-oxidation pathway of very-long-chain fatty acid (VLCFAs). In humans, ACOX1 deficiency, also called pseudo-neonatal adrenoleukodystrophy, is an autosomal recessive and a severe form of the peroxisomal b-oxidation deficiency. Patients suffer from severe delayed motor development followed by a progressive neurological regression including progressive hypodensity of cerebral white matter, hepatomegaly and deafness and die during late-infantile period. Elevated plasma and tissues VLCFAs levels are detected in these patients. Mice lacking ACOX1 develop severe microvesicular steatohepatitis with increased intrahepatic H2O2 levels and hepatocellular regeneration. Liver cell proliferation in Acox1-/- mice leads to complete replacement of steatotic hepatocytes with hepatocytes that exhibit massive spontaneous peroxisome proliferation. Older mice develop hepatocellular carcinomas due to the sustained activation of peroxisome proliferator-activated receptor-alpha (PPARa). Contrary to humans, mice lacking ACOX1 have no apparent neurological disorder. Based on fibroblasts cell model from P-NALD patients, we show that ACOX1 deficiency lead to abolition of peroxysomal b-oxidation of cerotic acid (C26:0) and modification of peroxysomal morphology which appear reduced in number and enlarged in size. Moreover, accumulation of VLCFAs in ACOX1 deficiency in human fibroblasts interferes at the transcription level with cholesterol synthesis pathway. Furthermore, these cells show activation of interleukin-1b pathway with elevated production of interleukin-6 and interleukin-8 as an inflammatory response to metabolic disturbance due to VLCFAs accumulation. Furthermore, we show in this study that the ACOX1 deficiency in human fibroblasts and in mice liver leads to alteration of the mitochondrial ultra structure, changes in the expression and activity of mitochondrial chain complexes. These alterations of mitochondrial functions are accompanied by reduction in mitochondrial ATP levels in human fibroblasts and decreased mitochondrial respiration in ACOX1 deficient mice. Interestingly, the mitochondrial changes observed in Acox1-/- mice are restored by expression of human ACOX1 in liver suggesting an essential role of human and murine Acyl-CoA oxidase 1 activity in preventing mitochondrial and lipid disturbance.Together, the results presented in this work underscore the important role of ACOX1 in humans and mice to ensure peroxisomal b-oxidation, VLCFAs catabolism and to preserve peroxisomal morphology. Given mitochondrial perturbation in ACOX1 deficiency, it is clear that this enzyme plays a pivotal role in preventing VLCFAs accumulation and their cellular toxicity and guarantees mitochondrial normal morphology and function in response to energy demandDIJON-BU Doc.électronique (212319901) / SudocSudocFranceF

Base moléculaire des effets de l'huile d'argan sur le métabolisme mitochondrial et peroxysomal des acides gras et sur l'inflammation

L objectif des travaux de cette thèse a été d explorer les bases moléculaires de l effet de l huile d Argan (HA) sur le métabolisme lipidique au niveau mitochondriale et peroxysomale ainsi qu élucider son potentiel anti-inflammatoire. Nous avons donc montré, dans un premier temps, que les méthodes artisanales préservaient les propriétés antioxydantes d HA empêchant l oxydation de l acide férulique contrairement à l HA d origines commerciale. Ensuite, le traitement par l HA ou par les lipopolysaccharides (LPS) de fibroblastes humains, un modèle cellulaire de la pseudo-adrénoleucodystrophie néonatale (P-NALD), révèle pour l HA une prolifération des peroxysomes indépendante de l activation du récepteur nucléaire PPARa et de son coactivateur PGC-1a. Par contre, l induction de la prolifération de peroxysomes par les LPS est accompagnée d une activation de PPAR et de PGC-1 Parallèlement, une étude a été réalisée au niveau hépatique chez des souris traitées par l HA ou par les LPS. Nous avons montré pour la première fois l activité antioxydante de l huile d Argan in vivo au niveau hépatique par l induction de l activité enzymatique de la catalase peroxysomale et une activité hypolipémiante par la stimulation des activités déshydrogénases (ACADs) de la -oxydations mitochondriale des acides gars. De plus, l HA induit la transcription des gènes PPECK et G6PH de la voie de la néoglucogenèse. Nous avons montré également pour la première fois un effet préventif de l HA contre la répression des activités déshydrogénases des voies de -oxydations mitochondriale et peroxysomale, ainsi que celle la voie de la néoglucogenèse. Nos travaux démontrent que l HA possède un potentiel anti-inflammatoire, induit par le LPS, élucidé par la répression de cytokines pro-inflammatoires IL-6 et TNFa et par l induction de cytokines anti-inflammatoires IL10 et IL-4. L ensemble de nos résultats indiquerait que l huile d Argan, du fait de sa composition riche en acide gras mono et polyinsaturés et en antioxydants, a des effets hypolipémiants et anti-inflammatoires au niveau hépatique qui se traduisent par une régulation de l expression à la fois de récepteurs nucléaires et de leur gènes cibles ainsi que de certaines cytokinesThe objective of this thesis work was to explore the molecular basis of Argan Oil (AO) effects on the mitochondrial and peroxisomal lipid metabolism and to elucidate its anti-inflammatory potential. We thus showed, initially, that the artisanal method preparation preserved the antioxidant properties of AO preventing the oxidation of the ferulic acid, by contrast to AO of commercial origin. Then, the treatment by the AO or lipopolysaccharides (LPS) of human fibroblasts, the cellular model of pseudo-neonatal adrenoleukodystrophy (P-NALD), revealed for the AO that peroxisomes proliferation is independent from the activation of the nuclear receptor PPARa and the co-activator PGC-1a. On the other side, the induction of the proliferation of peroxisomes by LPS is accompanied by an activation of both PPARa and PGC-1a. At the same time, mice treatments by AO or by the LPS showed, for the first time, the hepatic antioxidant activity of AO through the induction of the activity of the peroxisomal catalase. In addition, we showed a hypolipidemic activity of AO, by the stimulation of dehydrogenase activities (ACADs) of the mitochondrial fatty acid b-oxidation. Moreover, the AO induces the transcription of genes involved in gluconeogenesis pathway (i.e. PEPCK and G6PH). We also revealed, for the first time, the preventive effect of AO against LPS repressions of mitochondrial and peroxisomal fatty acid degradation as well as on the gluconeogenic pathway. Furthermore, the AO anti-inflammatory potential has been shown, in mice treated by LPS, through the repression of the pro-inflammatory cytokines IL-6 and TNFa and by the induction of the anti-inflammatory cytokines IL10 and IL-4. All together, our results may indicate that the Argan oil, because of its composition rich in mono and polyunsaturated fatty acids and in antioxidants as well, has a hypolipidemic and an anti-inflammatory effects, which are revealed by the regulation of the expressions of nuclear receptors and their target genes including several cytokinesDIJON-BU Doc.électronique (212319901) / SudocSudocFranceF

NFY interacts with the promoter region of two genes involved in the rat peroxisomal fatty acid β-oxidation: the multifunctional protein type 1 and the 3-ketoacyl-CoA B thiolase

BACKGROUND: β-oxidation of long and very long chain fatty acyl-CoA derivatives occurs in peroxisomes, which are ubiquitous subcellular organelles of eukaryotic cells. This pathway releases acetyl-CoA as precursor for several key molecules such as cholesterol. Numerous enzymes participating to cholesterol and fatty acids biosynthesis pathways are co-localized in peroxisomes and some of their encoding genes are known as targets of the NFY transcriptional regulator. However, until now no interaction between NFY transcription factor and genes encoding peroxisomal β-oxidation has been reported. RESULTS: This work studied the interactions between NFY factor with the rat gene promoters of two enzymes of the fatty acid β-oxidation, MFP-1 (multifunctional protein type 1) and ThB (thiolase B) and their involvement in the cholesterol dependent-gene regulation. Binding of this nuclear factor to the ATTGG motif of the MFP-1 and of the ThB promoters was demonstrated by EMSA (Electrophoretic Mobility Shift Assay) and super shift assay. In contrast, in spite of the presence of putative Sp1 binding sites in these promoters, competitive EMSA did not reveal any binding. The promoter-dependent luciferase gene expression was downregulated by cholesterol in MFP-1 and ThB promoters harbouring constructs. CONCLUSIONS: This work describes for the first time a NFY interaction with promoter sequences of the peroxisomal β-oxidation encoding genes. It suggests that cholesterol would negatively regulate the expression of genes involved in β-oxidation, which generates the initial precursor for its own biosynthesis, via at least the NFY transcription factor