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Cette thèse concerne la spectroscopie atomique pour le développement de microcellules photoniques à base de vapeur atomique alcaline (PMC). Le travail est motivé par reproduire les performances remarquables obtenues dans les domaines des références de fréquences et de l’optique cohérente en environnement laboratoire et à les transférer dans des dispositifs très compacts et autonomes accessibles à une communauté scientifique plus large ou à un marché commercial. Dans notre cas, ces futurs composants seront basés sur une fibre à cristal photonique à coeur creux (HC-PCF) remplie d'un matériau en phase gazeuse pour former la PMC et se distingue par une longueur d'interaction ultra longue associée à des dimensions modales transverses micrométriques. Cependant, cette échelle micrométrique du coeur creux de la fibre contenant les atomes soulève plusieurs défis techniques et scientifiques. Parmi les défis techniques, nous énumérons le développement d'un processus efficace pour le chargement d'atomes dans une telle fibre optique, la suppression ou l'atténuation de la réactivité physio-chimique des atomes (c'est-à-dire le rubidium) avec la surface interne silice entourant le coeur de la fibre, etc... En parallèle, le rapport large surface / volume du coeur de la fibre soulève des questions comme la dynamique de relaxation de la cohérence et la nature et l'effet de l'interaction atome-surface. Ainsi, les travaux de thèse reposent sur l’utilisation de revêtements spécifiques de la surface interne du coeur de la fibre avec différents matériaux pour atténuer ces réactions physico-chimiques, sur l'amincissement des larges coeurs creux des HC-PCF Kagomé à couplage inhibé et sur une technique de soudure qui garantit de faibles pertes d’insertion et l’absence de réactivité avec les atomes. Parallèlement, la thèse rapporte un ensemble d'expériences de spectroscopie pour évaluer la dynamique de relaxation des atomes à l'intérieur des HC-PCF et l’observation de nouvelles transparences sous-Doppler. / This thesis reported on atomic spectroscopy for the development of alkaline atomic vapor photonic microcell (PMC). The work is motivated by reproducing the outstanding laboratory environment based performances achieved in the fields of frequency standard and coherent optics in highly compact and stand-alone devices that can be accessible to a wider scientific community or to a commercial market. In our case these future devices will be based a Hollow-core photonic crystal fiber (HC-PCF) filled with a gas phase material to form a PMC, and outstands with an ultra-long long interaction length and micrometric modal area. However, the micrometric scale of the fiber core harboring the atoms raises several technical and scientific challenges. Among the technical challenges, we list the development of efficient process for atom loading inside long hollow fiber with small core diameter, the suppression or mitigation of physio-chemical reactivity of the atoms (i.e. Rubidium) with the fiber core inner-surface silica etc. In parallel, the large surface-to-volume ratio of the fiber-core raises questions like the coherence relaxation dynamics and the nature and effect of the atom-surface interaction. The thesis reports on fiber-core inner surface coating with different materials to mitigate the physio-chemical reactions of the confined atoms with the surface, on tapering large core inhibited coupling Kagome HC-PCF, and splicing technique that ensures low splice loss and no atomic reactivity during the splicing process. In parallel, the thesis reports on a set of spectroscopy experiments to assess the relaxation dynamics of atoms inside HC-PCF and to report on novel sub-Doppler transparencies.

Le Corbusier tente de ramener l’architecture à l’utilité et de créer une esthétique de pureté en parfaite harmonie avec celle-ci. Or s’il est conduit à s’opposer à tout excès et à économiser l’espace, ses choix esthétiques semblent mal répondre à cet impératif. Un seul superflu demeure un tabou chez lui: l’ornement. Le refus de cet ajout constitue ainsi un angle pour la compréhension du caractère de ses œuvres. Une enquête sur les causes de ce rejet mène à la conclusion que l’architecture nouvelle doit avoir comme principes l’esprit puriste, l’esprit scientifique déterministe et l’esprit individualiste. Pourtant, en même temps qu’elle les incarne, elle les enfreint systématiquement jusqu’à un certain point en vue de l’obtention des effets artistiques. De cette transgression de l’interdit résultent la réintroduction du superflu, une esthétique mi-authentique mi-inauthentique, et la qualification de l’espace de création corbuséen par la « parergonalité sans parergon ». Comme l’utilité ramenée en soi implique l’économie du temps, l’examen porte aussi sur les expériences temporelles que permet l’architecture nouvelle. Il montre qu’avec la « parergonalité sans parergon », celle-ci fait éprouver la décroissance du temps, sa suspension, son enchevêtrement avec l’objet, l’éternel présent présentiste, la logique de l’accroissement sous la logique de la réduction, des vécus semblables aux troubles de l’insomnie, etc. En même temps, cette architecture se remet en question, ouvrant ainsi d’autres historicités à l’art de bâtir et à l’homme, dont l’économie de l’espace ne valorise que le comportement corporel / Le Corbusier intends to bring architecture back to the utility and to create an aesthetics of purity in perfect harmony with this latter one. Yet if he is led to oppose all excess and to economize the space, his aesthetic choises do not seem to well respond to this imperative. One single surplus remains a taboo to him: the ornament. The opposition to this addition becomes then an angle for understanding the characteristic of his works. A conclusion of the inquiry into causes of this rejection is that the new architecture must hold the purist spirit, the scientific determinist spirit and the individualist spirit as principles. However, while embodying them actually, at the same time it infringes them systematically to a certain degree in order to create artistic effects. The outcomes of this transgression of the inhibited are the reintroduction of the surplus, a half authentic, half inauthentic aesthetics, and the characterization of Le Corbusier’s space of creation by “parergonality without parergon”. Since the utility brought back to itself implying the economy of time, we proceed as well to examine the temporal experiences made possible by the new architecture, and demonstrate that by means of the “parergonality without parergon”, it brings forth experiences like diminution of the time, its suspension, its entanglement with the object, the presentist eternal present, the logic of the increase under the logic of the reduction, effects similar to insomnia disorders, etc. Meanwhile, this architecture calls itself in question, opening then different historicities to architecture and to human being of which the economy of space values only the corporal movement

Understanding of the fate of oil in the environment is of utmost importance; however, accurate, predictive models are still in very early stages. To aid in the development of these models, photodegradation of selected polycyclic aromatic hydrocarbons (PAHs) in an n-alkane hydrocarbon matrix was followed for individual PAHs and mixtures of PAHs similar to that found in the Deepwater Horizon spill. Tetracene in tetradecane photodegraded quickest of all observed PAHs, with a loss of 99% after only one hour of irradiation. Binary mixtures of PAHs showed different degradation amounts, including changes in PAH kinetics. These results suggest that the formation of dimers or aggregates as well as photosensitization reaction is important in the degradation of PAHs in oil. Kinetics of PAH photodegradation and PAH sensitized photodegradation will be presented. This information will provide a better understanding of the fate of oil in environmental systems.

An adult female sample of childhood sexual abuse survivors (N=467) were surveyed to determine whether internalized shame moderated the effects of sexual inhibited difficulties. Other variables such as severity, duration, and frequency of sexual abuse, as well as whether physical abuse was also part of their experience, were examined to determine their role in later sexual inhibition. It was predicted that there would be a significant positive relationship between 1) Scores on variables of physical abuse, severity of abuse, frequency of abuse, duration of abuse, identity of the perpetrator and scores on the variable of inhibited sexual difficulties; 2) Scores of internalized shame and scores of inhibited sexual difficulties and 3) Scores on variable of physical abuse, severity of abuse, frequency of abuse, duration of abuse, identity of the perpetrator and scores on the variables of internalized shame. Through Structural Equation Modeling using AMOS, the results indicated a statistically significant positive relationship between severity, frequency and inhibited sexual disturbances but found no direct relationship between physical abuse, the identity of the perpetrator, the duration of the abuse and inhibited sexual disturbances. Results also indicated that shame had a direct positive relationship to inhibited sexual disturbances. The third finding was that physical abuse and severity of abuse had a significant positive relationship with shame which implies that shame is a moderating variable for inhibited sexual disturbances in adult women survivors of childhood sexual abuse. Internalized shame may be an important factor for therapists to consider in helping survivors overcome sexual inhibition as a result of childhood sexual abuse. If a woman develops a shame-prone identity she may be at risk for experiencing inhibition in her sexuality.

The pathogenesis of oral submucous fibrosis (OSMF) is due to a complex interplay between the production and degradation of extracellular matrix (ECM) protein components. In tissue fibrosis, there is a net accumulation of collagen as a result of an imbalance between enhanced production, deposition and impaired degradation of ECM components. OSMF is a chronic inflammatory condition of the oral cavity and regulation of a number of pro-inflammatory and fibrogenic cytokines such as interleukine-1, -6 and -8 isoforms, TGF-β, PDGF, bFGF, IFN-γ and TNF-α has been reported in OSMF tissues. The expression of these growth factors has a bearing on the epithelial changes as well as proliferation and differentiation of oral fibroblasts into ECM protein producing myofibroblast cells. One key modulator of fibrosis in several organs has been TGF-β. Overproduction of TGF-β mRNA and protein has been reported in several fibrotic disorders including that of skin, lungs, liver, kidney and heart. This is mainly due to stimulation of ECM genes by TGF-β. Although there have been few reports suggesting the over production of TGF-β in OSMF tissues, the specific isoforms involved or the mechanisms are poorly understood. Areca nut components, especially arecoline have been implicated in the pathophysiology of OSMF. Few reports indicate the involvement of arecoline in the regulation of collagen production and activity of collagenases and their inhibitors in oral fibroblast cells. Moreover, the alkaloid is involved in initiating epithelial inflammation by inducing COX-2, prostaglandin E2, IL-1α, IL-6 and IL-8 in KB oral carcinoma cells and oral fibroblast cells. These and other reports strongly suggest that changes in gene expression mediated by Arecoline may be central to the progression of OSMF. Not much is known about arecoline-mediated cellular signaling events except for few recent reports that suggest the activation of MAPK pathways. In neuronal and colonic smooth muscle cells of mouse, rat and rabbit, the actions of Arecoline have been reported to be through the activation of muscarinic acetylcholine receptors. Direct binding of arecoline to human M1, 2 and 3 muscarinic receptor isoforms have been shown in brain tissues. Stimulation of these receptors alters the intracellular levels of Ca+2 and cAMP, which are important second messengers. The cholinergic potential of arecoline may be important for their roles in arecoline-mediated signaling events. The expression of muscarinic acetylcholine receptors has been reported in several cell types besides neuronal and excitatory cells. Although several gene expression changes have been reported following Arecoline treatment of a variety of cells, the mechanism of such regulations is not established. Hence in order to understand the role of arecoline in OSMF disease process, we undertook studies that provide insights into arecoline action in epithelial and fibroblast cells and possible molecular mechanisms. The objectives are to study: 1. The role of arecoline in cellular proliferation, cell-cycle regulation and apoptosis in human normal keratinocytes. 2. Mechanism of regulation of gene expression by arecoline in normal keratinocytes. 3. Mechanism of regulation of gene expression by arecoline in human normal oral fibroblasts. In order to achieve the above objectives, a human keratinocyte cell line, HaCaT and an oral periodontal fibroblast cell line (PDC) were utilized. The cells were treated with arecoline and a variety of assays including RT-PCR analysis of mRNA of several genes, phosphorylation status of MAPK pathway intermediates, cell cycle analysis and other cellular and molecular methods have been employed. Following arecoline treatment, there is induction of oxidative stress, growth arrest and epithelial cell death. Since actions of TGF-β are central to most fibrotic disorders and arecoline has been implicated in OSMF, it is hypothesized that arecoline may influence fibrosis via TGF-β pathway. Towards this, several TGF-β target genes that may have a possible role in fibrosis have been studied in arecoline treated epithelial and fibroblast cells. Since arecoline mediated oxidative stress has been reported, the regulation of genes that are involved in stress response pathway have been studied for induction by arecoline in epithelial cells. The results presented in this thesis suggest the up regulation of oxidative stress-responsive genes in HaCaT cells including HOX-1, FTL, G6PD, GCLC and GRD in HaCaT cells. Oxidative stress is a major inducer of inflammatory response in the epithelial tissues. The expression of IL-1α, an important inflammatory cytokine is induced by arecoline in HaCaT cells in response to oxidative stress via the activation of p38 MAPK pathway. Interestingly, activation of MAPK pathways by arecoline is involved in the regulation of common target genes of arecoline and TGF-β and also in the induction of TGF-β−responsive promoter reporter construct, p3TP-lux activity in HaCaT cells. Due to the involvement of TGF-β in fibrosis, regulation of TGF-β pathway genes by arecoline has been studied both in HaCaT and PDC cells. In HaCaT cells, arecoline induces the expression of TGF-β2 mRNA while TβRII expression is down regulated. The expression of the rest of TGF-β/SMAD pathway genes including TGF-β1, β3, TβRI, SMAD1, 2, 3, 4 and 7 are not affected by arecoline in HaCaT cells. Over expression of TGF-β2 is also observed in most of the OSMF tissues compared to normal oral tissues. However, in normal oral fibroblast cells, we observed that the TGF-β/SMAD pathway genes are not regulated by arecoline. These results suggest the possible involvement of arecoline-mediated induction of TGF-β2 in epithelial cells in OSMF disease development. We investigated the signaling pathways involved in the regulation of TGF-β2 and found that stimulation of M3 muscarinic receptor by arecoline leads to the induction of TGF-β2 expression in HaCaT cells via PKC pathway. TGM-2 is an important TGF-β target gene involved in the cross linking of ECM proteins. Arecoline-mediated induction of TGM2 mRNA and transglutaminase activity are observed in oral fibroblast cells, PDC. The induction of TGM-2 was found to be independent of oxidative stress and TGF-β, but dependent on muscarinic acid receptor activation by arecoline and involves cytosolic cAMP. When tested in OSMF tissues, there was an increased expression of TGF-β2, TSP1 and TGM2 as compared to normal tissues suggesting a possible role of these genes in arecoline-mediated progression of OSMF. Interleukin-8 (IL-8), which is involved in inflammation has been reported to be regulated by TGF-β in a cell type specific manner. In several cell types including human endometrial stromal cells, LnCaP (prostate cancer cells), human retinal pigment epithelial cells and rat lung alveolar epithelial (LM5) cells etc., TGF-β up regulates the expression of IL-8 mRNA. Arecoline was found to down regulate IL-8 expression in PDC cells as measured by RT-PCR. Interestingly, the presence of serum along with arecoline induces the expression of IL-8 in PDC cells suggesting the modulation of arecoline-mediated gene regulation by a serum activated signaling pathway. Intriguingly, arecoline treatment led to down regulation of collagens in PDC cells. However, collagen genes are induced in PDC cells in the presence of HaCaT spent medium by arecoline suggesting a role for factor(s) secreted by epithelial cells in the regulation of collagen genes by arecoline. This factor could be an isoform of TGF-β as shown by blocking the induction of collagens by the TGF-β inhibitor, βLAP. Taken together, all these results indicate the ability of arecoline to cause fibrosis in a tissue environment where both epithelial and fibroblasts respond to arecoline and mutually contribute to the disease manifestation. Major conclusions from this study includes, 1] cell death in epithelial cells due to oxidative stress following arecoline treatment, 2] regulation of gene expression by arecoline involves MAPK, PKC pathways, 3] muscarinic acid receptor and oxidative stress are also important for regulation gene expression by arecoline. The most important inference from this study is the possible paracrine influence of TGF-β isoforms secreted by epithelial cells on the oral fibroblasts in determining the progression of OSMF. In summary, in this thesis, an attempt has been made to study the molecular mechanisms and role of arecoline, an alkaloid in conferring gene expression changes that may lead to the initiation and progression of oral sub mucous fibrosis.