In this work, a multilayer security solution for digital communication systems is provided by considering the joint effects of physical-layer security channel codes with application-layer cryptography. We address two problems: first, the cryptanalysis of error-prone ciphertext; second, the design of a practical physical-layer security coding scheme. To our knowledge, the cryptographic attack model of the noisy-ciphertext attack is a novel concept. The more traditional assumption that the attacker has the ciphertext is generally assumed when performing cryptanalysis. However, with the ever-increasing amount of viable research in physical-layer security, it now becomes essential to perform the analysis when ciphertext is unreliable. We do so for the simple substitution cipher using an information-theoretic framework, and for stream ciphers by characterizing the success or failure of fast-correlation attacks when the ciphertext contains errors. We then present a practical coding scheme that can be used in conjunction with cryptography to ensure positive error rates in an eavesdropper's observed ciphertext, while guaranteeing error-free communications for legitimate receivers. Our codes are called stopping set codes, and provide a blanket of security that covers nearly all possible system configurations and channel parameters. The codes require a public authenticated feedback channel. The solutions to these two problems indicate the inherent strengthening of security that can be obtained by confusing an attacker about the ciphertext, and then give a practical method for providing the confusion. The aggregate result is a multilayer security solution for transmitting secret data that showcases security enhancements over standalone cryptography.

This thesis aims to expand knowledge about the management of domestic water consumption. Among the various factors that influence water consumption, price and other economic variables have already been addressed by much research on this topic, obviously because of their implications for demand management. However, other factors such as the dominant urban model, the demographic structure and certain social values may also play a very important mediating role. This thesis aims to explore the factors (demographic, regional, socioeconomic, cultural, etc.) that influence domestic water consumption in two different but complementary scales: a local scale (municipalities in the Girona counties of Alt Empordà, Baix Empordà, Gironès, Pla de l’Estany and Selva) and a household scale (in suburban areas in the municipalities of Blanes, Caldes de Malavella, Lloret de Mar, Maçanet de la Selva, Santa Coloma de Farners, Sils, Tossa de Mar, Vidreres and Vilobí d’Onyar) / La present tesi té com a objectiu principal ampliar els coneixements la gestió de l’aigua per a usos domèstics. Entre els diferents factors que influeixen en el consum d’aigua, els preus i altres variables econòmiques han estat objecte de bona part de les investigacions sobre el tema. No obstant això, altres factors com, per exemple, el model d’ocupació urbana dominant, l’estructura demogràfica o certs valors socials, poden tenir també un rol molt rellevant. En aquesta tesi es proposa aprofundir sobre els factors (demogràfics, territorials, socioeconòmics, culturals, etc.) que incideixen en la demanda d’aigua per a usos domèstics, a dues escales diferents però complementàries: la municipal (municipis de les comarques gironines de l’Alt Empordà, Baix Empordà, Gironès, Pla de l’Estany i La Selva) i la llar (urbanitzacions dels municipis de Blanes, Caldes de Malavella, Lloret de Mar, Maçanet de la Selva, Santa Coloma de Farners, Sils, Tossa de Mar, Vidreres i Vilobí d’Onyar)

The VLSI implementation complexity of a low density parity check (LDPC) decoder is largely influenced by the interconnect and the storage requirements. This dissertation presents the decoder architectures for regular and irregular LDPC codes that provide substantial gains over existing academic and commercial implementations. Several structured properties of LDPC codes and decoding algorithms are observed and are used to construct hardware implementation with reduced processing complexity. The proposed architectures utilize an on-the-fly computation paradigm which permits scheduling of the computations in a way that the memory requirements and re-computations are reduced. Using this paradigm, the run-time configurable and multi-rate VLSI architectures for the rate compatible array LDPC codes and irregular block LDPC codes are designed. Rate compatible array codes are considered for DSL applications. Irregular block LDPC codes are proposed for IEEE 802.16e, IEEE 802.11n, and IEEE 802.20. When compared with a recent implementation of an 802.11n LDPC decoder, the proposed decoder reduces the logic complexity by 6.45x and memory complexity by 2x for a given data throughput. When compared to the latest reported multi-rate decoders, this decoder design has an area efficiency of around 5.5x and energy efficiency of 2.6x for a given data throughput. The numbers are normalized for a 180nm CMOS process. Properly designed array codes have low error floors and meet the requirements of magnetic channel and other applications which need several Gbps of data throughput. A high throughput and fixed code architecture for array LDPC codes has been designed. No modification to the code is performed as this can result in high error floors. This parallel decoder architecture has no routing congestion and is scalable for longer block lengths. When compared to the latest fixed code parallel decoders in the literature, this design has an area efficiency of around 36x and an energy efficiency of 3x for a given data throughput. Again, the numbers are normalized for a 180nm CMOS process. In summary, the design and analysis details of the proposed architectures are described in this dissertation. The results from the extensive simulation and VHDL verification on FPGA and ASIC design platforms are also presented.

Low Density Parity Check (LDPC) codes are the parity check codes of long block length, whose parity check matrices have relatively few non-zero entries. To improve the performance at relatively short block lengths, LDPC codes are constructed by either pseudo-random or quasi-cyclic methods instead of random construction methods. In this thesis, pseudo-random code construction methods, the effects of closed loops and the graph connectivity on the performance of pseudo-random LDPC codes are investigated. Moreover, quasi-cyclic LDPC codes, which have encoding and storage advantages over pseudo-random LDPC codes, their construction methods and performances are reviewed. Finally, performance comparison between pseudo-random and quasi-cyclic LDPC codes is given for both regular and irregular cases.

Traditional solutions to information security in communication systems act in the application layer and are oblivious to the effects in the physical layer. Physical-layer security methods, of which information-theoretic security is a special case, try to extract security from the random effects in the physical layer. In information-theoretic security, there are two asymptotic notions of secrecy---weak and strong secrecy This dissertation investigates the problem of information-theoretic strong secrecy on the binary erasure wiretap channel (BEWC) with a specific focus on designing practical codes. The codes designed in this work are based on analysis and techniques from error-correcting codes. In particular, the dual codes of certain low-density parity-check (LDPC) codes are shown to achieve strong secrecy in a coset coding scheme. First, we analyze the asymptotic block-error rate of short-cycle-free LDPC codes when they are transmitted over a binary erasure channel (BEC) and decoded using the belief propagation (BP) decoder. Under certain conditions, we show that the asymptotic block-error rate falls according to an inverse square law in block length, which is shown to be a sufficient condition for the dual codes to achieve strong secrecy. Next, we construct large-girth LDPC codes using algorithms from graph theory and show that the asymptotic bit-error rate of these codes follow a sub-exponential decay as the block length increases, which is a sufficient condition for strong secrecy. The secrecy rates achieved by the duals of large-girth LDPC codes are shown to be an improvement over that of the duals of short-cycle-free LDPC codes.

No description available.

Les maladies cardiovasculaires (MCV) demeurent au tournant de ce siècle la principale cause de mortalité dans le monde. Parmi les facteurs de risque, l’hypercholestérolémie et l’obésité abdominale sont directement liées au développement précoce de l’athérosclérose. L’hypercholestérolémie familiale, communément associée à une déficience des récepteurs des lipoprotéines de basse densité (LDLR), est connue comme cause de maladie précoce d’athérosclérose et de calcification aortique chez l’humain. La subtilisine convertase proprotéine/kexine du type 9 (PCSK9), membre de la famille des proprotéines convertases, est trouvée indirectement associée aux MCV par son implication dans la dégradation du LDLR. Chez l'humain, des mutations du gène PCSK9 conduisent soit à une hypercholestérolémie familiale, soit à une hypocholestérolémie, selon que la mutation entraîne un gain ou une perte de fonction, respectivement. Il demeure incertain si les individus porteurs de mutations causant un gain de fonction de la PCSK9 développeront une calcification aortique ou si des mutations entraînant une perte de fonction provoqueront une obésité abdominale. Dans cette étude, nous avons examiné : 1) l’effet d’une surexpression de PCSK9 dans le foie de souris sur la calcification aortique ; 2) les conséquences d’une déficience en PCSK9 (Pcsk9 KO), mimant une inhibition pharmacologique, sur le tissu graisseux. Nous avons utilisé un modèle de souris transgénique (Tg) surexprimant le cDNA de PCSK9 de souris dans les hépatocytes de souris et démontrons par tomographie calculée qu’une calcification survient de façon moins étendue chez les souris PCSK9 Tg que chez les souris déficientes en LDLR. Alors que le PCSK9 Tg et la déficience en LDLR causaient tous deux une hypercholestérolémie familiale, les niveaux seuls de cholestérol circulant ne parvenaient pas à prédire le degré de calcification aortique. Dans une seconde étude, nous utilisions des souris génétiquement manipulées dépourvues de PSCK9 et démontrons que l’accumulation de graisses viscérales (adipogenèse) apparaît régulée par la PCSK9 circulante. Ainsi, en l’absence de PCSK9, l’adipogenèse viscérale augmente vraisemblablement par régulation post-traductionnelle des récepteurs à lipoprotéines de très basse densité (VLDLR) dans le tissu adipeux. Ces deux modèles mettent en évidence un équilibre dynamique de la PCSK9 dans des voies métaboliques différentes, réalisant un élément clé dans la santé cardiovasculaire. Par conséquent, les essais d’investigations et d’altérations biologiques de la PCSK9 devraient être pris en compte dans un modèle animal valide utilisant une méthode sensible et en portant une attention prudente aux effets secondaires de toute intervention. / Cardiovascular disease (CVD) is the leading cause of death in the 21st century. Among risk factors, hypercholesterolemia and abdominal obesity are directly linked to premature development of atherosclerosis. Familial hypercholesterolemia, commonly due to low-density lipoprotein receptor (LDLR) deficiency, is known to cause premature atherosclerosis and aortic calcification in humans. Proprotein convertase subtilisin/kexin 9 (PCSK9), a member of the proprotein convertase family, is indirectly associated with CVD through enhanced LDLR degradation. Mutations in the human PCSK9 gene lead to either familial hypercholesterolemia or hypocholesterolemia, depending on whether the mutation causes a gain or a loss of function, respectively. It is uncertain if individuals carrying mutations causing a gain-of-function of PCSK9 will develop aortic calcification or whether loss-of-function mutations will lead to abdominal obesity. In this thesis, we investigated: 1) the effect of PCSK9 overexpression on aortic calcification; 2) the consequences of PSCK9 deficiency, mimicking pharmacological inhibition of PCSK9 on fat tissue. We employed a transgenic (Tg) mouse model overexpressing mouse PCSK9 and illustrated by micro-computerized tomography that calcification occurs to a lesser extent in PCSK9 Tg mice than in LDLR-deficient mice. While both PCSK9 Tg and LDLR deficiency caused familial hypercholesterolemia, circulating cholesterol levels alone could not dictate the degree of aortic calcification. In another study, we used genetically modified mice lacking PCSK9 and demonstrated that visceral fat accumulation (adipogenesis) is regulated by circulating PCSK9. Thus in the absence of PCSK9, visceral adipogenesis increases likely via post-translational regulation of very-low-density lipoproteins receptors (VLDLR) in the adipose tissue. In conclusion, these two studies highlight the dynamic balance of PCSK9 in different metabolic pathways, making it a key element in cardiovascular health. Consequently, attempts to survey and/or alter PCSK9 biology should be performed in a valid animal model using sensitive methods and with careful attention to side effects of any given intervention.

La transplantation d'hépatocytes représente une alternative à la transplantation hépatique pour le traitement de certaines maladies métaboliques dont l'hypercholestérolémie familiale. Les cellules souches embryonnaires (ES) et les cellules souches pluripotentes induites (iPS) humaines représentent de nouvelles sources de cellules hépatiques. Nous avons mis au point une approche de différenciation des cellules souches humaines en cellules hépatiques et généré ainsi des cellules dérivées de cellules iPS de patients atteints d'hypercholestérolémie familiale.

Les estrogènes confèrent aux femmes une protection cardiovasculaire jusqu’à la ménopause. En effet, la perte des fonctions ovariennes engendre plusieurs désordres du profil lipidique qui s’accompagnent d’une accumulation de triglycérides au foie appelée stéatose hépatique. Le retrait des estrogènes perturbe de nombreuses voies de contrôle de la cholestérolémie, provoquant simultanément une hypercholestérolémie et une stéatose hépatiques. Toutefois, à ce jour, les mécanismes d’action du retrait des estrogènes sur le métabolisme du cholestérol favorisant le stockage de triglycérides au foie demeurent imprécis. À cet égard, les travaux de cette thèse visaient à clarifier l’ensemble des effets du retrait des estrogènes sur le métabolisme du cholestérol pouvant mener à la pathogenèse de la stéatose hépatique. Lors de la première étude, l’ovariectomie (Ovx) chez la rate, un modèle bien établi de la stéatose, avait permis d’identifier la voie d’assemblage des lipoprotéines à très faible densité (VLDL) comme élément contributif à la stéatose. La voie des VLDL reliant étant également une voie de transport du cholestérol, l’étude suivante a été réalisée afin de comprendre le rôle du cholestérol alimentaire sur les lipides hépatiques. Dans cette deuxième étude, le modèle de la diète riche en lipides et en cholestérol (HFHC), aussi reconnu pour induire une stéatose hépatique, a permis d’établir des liens étroits entre le métabolisme du cholestérol et celui des lipides hépatiques. Étonnamment, de manière similaire à l’Ovx, la diète HFHC perturbait la voie d’assemblage des VLDL. En outre, les données recueillies au cours de ces travaux indiquaient qu’une dysrégulation du métabolisme des acides biliaires avait contribué à la sévérité de la stéatose hépatique induite par cette diète HFHC. Dans la continuité de ces deux premiers projets, nous nous sommes intéressés aux effets concomitants du retrait des estrogènes et d’une diète HFHC sur la stéatose hépatique. De manière intéressante, lorsque combinés, l’Ovx et la diète HFHC potentialisaient non seulement l’accumulation de lipides hépatiques, mais également les perturbations moléculaires des voies sous-jacentes à la stéatose, dont l’assemblage des VLDL et de la sécrétion d’acides biliaires. Dans l’ensemble, les données présentées dans la revue de littérature et dans les trois études reliées à cette thèse indiquent qu’une dysrégulation du métabolisme du cholestérol en réponse au retrait des estrogènes entraîne des complications favorisant l’accumulation de lipides dans le foie. / Estrogens confer to women a cardiovascular protection until menopause. Indeed, the loss of ovarian functions leads to several lipid disorders along with hepatic triglycerides accumulation called hepatic steatosis. Estrogen withdrawal disrupts several cholesterol metabolism pathways that results in both hypercholesterolemia and hepatic steatosis. However, to date, the precise mechanisms by which estrogen withdrawal affect cholesterol metabolism pathways that favour lipid storage in the liver are unclear. In this regard, works in the present thesis aimed at elucidate the effects of estrogen withdrawal on cholesterol metabolism involved in hepatic steatosis pathogenesis. In the first study, estrogen withdrawal by ovariectomy (Ovx), a well established model for hepatic steatosis and hypercholesterolemia, had enabled the identification of very low density lipoprotein (VLDL) pathway as a contributory element for hepatic steatosis. Since the VLDL pathway relates lipids and cholesterol metabolism, we conducted the second study to explore the role of dietary cholesterol on hepatic lipids. In the second study, the high fat/high cholesterol (HFHC) diet, also recognized as a model for hepatic steatosis development, was used to explore links between cholesterol metabolism and hepatic fat accumulation. Surprisingly, HFHC diet also disrupted the VLDL pathway. Additionally, data provided in this study indicated that a dysregulation of bile acids metabolism might have contributed to the severity of hepatic steatosis induced by the HFHC diet. As a continuation of these projects, we were interested in the concomitant effects of estrogen withdrawal and HFHC diet on hepatic lipid accretion. Interestingly, when combined, Ovx and HFHC diet not only potentiated hepatic lipid accumulation but also molecular disruptions involved in underlying pathways for hepatic steatosis including the VLDL pathway and bile acid secretion. Overall, data presented in the review of litterature and provided by the three studies related to the present thesis indicate that cholesterol metabolism dysregulation following estrogen withdrawal result in complications that favour hepatic lipid accumulation.

Atherosclerosis is a progressive inflammatory disease that is characterized by the accumulation of lipids, infiltrated cells and fibrous elements in large arteries. This thesis focuses on the molecular mechanisms behind foam cell formation and inflammation, two central processes in the development of atherosclerosis. More specific, we studied the effects of proinflammatory cytokines on CXCL16 expression and its role as scavenger receptor on macrophages and smooth muscle cells in atherogenesis. CXCL16 is defined as a chemokine and a scavenger receptor, regulating adhesion and chemoattraction of CXCR6 expressing cells and uptake of oxLDL. We show that the expression of CXCL16 and its receptor CXCR6 are more pronounced in human atherosclerotic lesions compared with non-atherosclerotic vessels. Increased expression of CXCL16 was also seen in atherosclerotic aortas of apoE-/- mice compared with aortas of non-atherosclerotic, age-matched C57BL/6 mice. In vitro, IFN gamma induced CXCL16 expression in primary human monocytes and smooth muscle cells which resulted in an increased uptake of oxLDL. Treatment of mice with IFN gamma also induced CXCL16 expression in atherosclerotic lesions. Thus, we have demonstrated a role for IFN gamma in foam cell formation through upregulation of CXCL16. The expression of CXCR6 was defined to the same regions as for CXCL16 in the lesion, indicating the presence of cells able to respond to CXCL16. Consequently, CXCL16 could serve as a molecular link between lipid metabolism and immune activity in atherosclerotic lesion. CD137 belongs to the TNF family and mediates several important processes in inflammation. CD137 is involved in the activation of T cells, NK cells, B cells and monocytes and regulate cytokine production, proliferation and apoptosis in these cells. A limited number of studies have demonstrated CD137 expression on smooth muscle cells and endothelial cells. Our results show that CD137 mRNA is higher expressed in human atherosclerotic lesions compared with unaffected vessels. We found that endothelial cells express CD137 in atherosclerotic lesions and that cultured endothelial cells and smooth muscle cells express CD137 and CD137 ligand in vitro. CD137 was regulated differentially by proinflammatory cytokines (i.e. IFN gamma, TNF alpha, IL-1 beta) and bacterial lipopolysaccharide depending on cell type. Furthermore, we investigated the effects of CD137 signalling, demonstrating that binding of the CD137 ligand to its receptor increases proliferation and migration of smooth muscle cells. In summary, this thesis has focused on the expression, regulation and role of CXCL16 and CD137, two genes that have not been described earlier in the concept of atherosclerosis. The findings demonstrate some of the molecular mechanisms involved in vascular inflammation and may increase our knowledge about the development of atherosclerosis.