Dissertations / Theses on the topic 'Stress suppression'
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Bridgett, Stephen John. "Detail suppression of stress analysis models." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387980.
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Chen, Chun-Chun. "Response to social stress : sensory input, stress response and the neural substrates of reproductive suppression /." May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
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N'Guessan, Prudence. "Décryptage du rôle de TP53INP1 dans la suppression de tumeur." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22070.
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Notre laboratoire a caractérisé TP53INP1 comme un gène clé de réponse au stress cellulaire. Cible de p53, TP53INP1 est ubiquitairement exprimé et fortement induit lors de différents stress in vivo et in vitro. Sa surexpression ectopique induit un arrêt du cycle cellulaire et la mort cellulaire. Nous avons montré que l’expression de TP53INP1 est perdue dans plusieurs cancers chez l’homme et que sa réexpression dans les cellules cancéreuses inhibe la croissance tumorale. De plus, les souris TP53INP1-déficientes sont très susceptibles au développement de tumeurs induites et présentent un stress oxydatif permanent caractérisé par une augmentation du taux de ROS. L’ensemble de ces résultats indique que TP53INP1 possède une fonction suppressive de tumeur probablement en lien avec son implication dans la régulation du statut redox cellulaire. Le but de mon travail de thèse est de décrypter cette fonction an niveau cellulaire et moléculaire en exploitant le modèle des souris déficientes. Mes travaux montrent que l’absence de TP53INP1 affecte tous les processus biologiques dérégulés lors de la tumorigenèse. En effet, la perte de TP53INP1 se caractérise par une augmentation de la prolifération cellulaire, de la migration cellulaire, de l’angiogenèse et de l’instabilité génétique. De façon paradoxale, les cellules déficientes pour TP53INP1 présentent une sensibilité accrue à l’apoptose induite par un stress indépendant ou non de p53. Cette sensibilité se base probablement sur un fort défaut de l’autophagie dans ces cellules. Nous observons également une diminution du taux des petites molécules antioxydantes liée au stress oxydatif constitutif observé dans ces souris. Les défauts observés en absence de TP53INP1 sont corrigés par un traitement avec un antioxydant, le N-Acetylcystéine, ce qui démontre le lien entre le rôle suppresseur de tumeur de TP53INP1 et son implication dans le contrôle du stress oxydatif. Ce travail a permis de mieux comprendre le rôle antioxydant TP53INP1 en lien avec sa fonction de suppresseur de tumeurOur laboratory has characterized TP53INP1 as a key gene in cell stress response. Target of p53, TP53INP1 is ubiquitously expressed and strongly induced during various stress-inducing treatments in vivo and in vitro. Its ectopic overexpression induces cell cycle arrest and cell death. We have shown that the expression of TP53INP1 is lost in many human cancers and that its re-expression in cancer cells inhibits tumor growth. In addition, TP53INP1-deficient mice are highly susceptible to induced tumors and show a permanent oxidative stress characterized by increased ROS levels. Taken together, these results indicate that TP53INP1 has a tumor suppressor function likely related to its involvement in the regulation of cellular redox status. The purpose of my PhD is to decipher the cellular and molecular function of TP53INP1 by exploiting the model of deficient mice. My work shows that the absence of TP53INP1 affects all biological processes deregulated in tumorigenesis. Indeed, the loss of TP53INP1 is characterized by an increase in cell proliferation, cell migration, angiogenesis and genetic instability. Paradoxically, TP53INP1-deficient cells have increased susceptibility to stress-induced apoptosis, independently or not of p53. This sensitivity is probably based on a strong impairment of autophagy in these cells. We also observed a decrease in the rate of small antioxidant molecules related to constitutive oxidative stress in these mice. The defects observed in the absence of TP53INP1 are corrected by treatment with an antioxidant, N-acetylcysteine, demonstrating the link between the role of TP53INP1 in tumor suppression and its involvement in redox control. This work has led to a better understanding of the antioxidant role of TP53INP1 linked to its function as a tumor suppressor
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Blake-Mortimer, Jane. "Lymphocytic 5'-ectonucleotidase : a marker of psychological stress-induced immune suppression /." Title page, contents and abstract only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09phb6364.pdf.
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Amstadter, Ananda Beth Laura L. Vernon Laura L. Burkhart Barry R. "Physiological effects of suppression of neutral and traumatic thoughts in posttraumatic stress disorder." Auburn, Ala, 2008. http://repo.lib.auburn.edu/EtdRoot/2008/SUMMER/Psychology/Dissertation/AMSTADTER_ANA_20.pdf.
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Kennedy, Sarah L. "Stress-induced suppression of an antibody response: A role for splenic norepinephrine." Diss., Connect to online resource, 2005. http://wwwlib.umi.com/dissertations/fullcit/3165815.
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Drysdale, Shara D. "Posttraumatic stress disorder, thought suppression and the self-regulatory executive function model." Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368151.
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Stoeser, Casey J. "Expressive suppression : relation to post-traumatic stress disorder symptoms and emotional experience /." Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1456295331&sid=7&Fmt=2&clientId=1509&RQT=309&VName=PQD.
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Davies, Mark Ian. "Vulnerability to analogue post-traumatic intrusions and experimental investigations of thought suppression." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308667.
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Arensdorf, Angela Marie. "The Mechanisms and Consequences of Gene Suppression During the Unfolded Protein Response." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/4816.
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The endoplasmic reticulum (ER) facilitates the synthesis, assembly and quality control of all secretory, transmembrane, and resident proteins of the endomembrane system. An accumulation of unfolded proteins or a disruption in the specialized folding environment within the organelle causes ER stress, thus impairing the folding capacity of the ER. In response to this stress, the ER initiates a signaling cascade called the unfolded protein response (UPR) in an attempt to restore ER homeostasis.
The vertebrate UPR is propagated by three ER-resident transmembrane proteins (i.e., PERK, IRE1α, and ATF6α), each initiating a signaling cascade that ultimately culminates in production of a transcriptional activator. The UPR was originally characterized as a pathway for the upregulation of ER chaperones, and a comprehensive body of subsequent work has shown that protein synthesis, folding, oxidation, trafficking, and degradation are all transcriptionally enhanced by the UPR. However, UPR activation is also accompanied by extensive mRNA suppression. The mechanisms responsible for this suppression and its consequences for physiological processes beyond the realm of ER protein folding and processing are only now beginning to be described.
The overall goal of my thesis work was to explore this process of UPR-mediated gene suppression by identifying the mechanisms involved and the cellular processes affected. As a result, I characterized a novel mechanism of UPR-mediated transcriptional repression involving the translational regulation of the transcription factor C/EBPβ resulting in the suppression of the gene Il4ra, encoding an essential subunit of the IL-4/IL-13 receptor. As a consequence of this suppression, a novel effect of ER stress was identified in the impairment of IL-4/IL-13 signaling, a finding of potential significance in the study of inflammatory disease. In addition to this mechanism, I validated a novel approach to the identification of UPR-regulated transcription factors using publically available bioinformatic software. Through this analysis, I identified the transcription factor HNF4α as a novel post-translational UPR-regulated transcription factor, the regulation of which, resulted in the suppression of a number of lipid metabolic genes. This analysis not only identified a novel UPR-regulated transcription factor, but also presented a new tool for the characterization of UPR-mediated gene suppression.
My work represents an independent and original investigation into the process of UPR-mediated gene suppression; and reveals that the UPR facilitates transcriptional suppression through the transcriptional, translational, and post-translational regulation of multiple transcription factors, resulting in the coordinated attenuation of physiological pathways. This function of the UPR is likely to contribute to metabolic, inflammatory, and other chronic disease states.
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Teager, Alistair James. "Examining the Effect of Detached Mindfulness, Habituation, and Suppression on Intrusive Thoughts following Exposure to Stress." Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.525239.
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Knauft, Katherine Marie. "Buffering Effects of Grit and Cognitive Reappraisal in the Context of Perceived Stress." Miami University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=miami1557500405928633.
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Côté, Marilou. "Liens entre le stress conjugal, la suppression émotionnelle et la prise alimentaire au sein de couples hétérosexuels." Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/27443.
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Tableau d'honneur de la Faculté des études supérieures et postdoctorales, 2016-2017L’étude de l’alimentation induite par le stress et les émotions négatives a été largement menée jusqu’à maintenant en vue d’identifier différentes caractéristiques individuelles pouvant être désignées comme facteur de risque à la suralimentation. À cet effet, le fait de souffrir de surpoids ou d’obésité, de même que la présentation d’un profil alimentaire restrictif ont été identifiés. Bien que certaines études se soient intéressées à la variation des types de stress auxquels sont soumis les individus, aucune n’a élargie sa perspective aux relations de couple. Pourtant, les émotions vécues au sein du couple et la régulation qui en est faite peuvent sans contredit contribuer à l’installation et l’exacerbation de comportements alimentaires problématiques pouvant mener à une prise de poids. En ce sens, à l’aide d’une expérimentation en laboratoire impliquant l’induction d’un stress de nature conjugale, la thèse vise à approfondir les connaissances actuelles quant aux liens qui unissent les émotions vécues dans le contexte d’une discussion conjugale stressante et la prise alimentaire qui s’en suit chez des individus en couple hétérosexuel. Pour ce faire, 80 couples ont été recrutés et ont discuté, en laboratoire, d’aspects qu’ils aimeraient voir changer chez l’autre. La quantité de nourriture consommée suite à la discussion a été mesurée, à leur insu, à l’aide d’un test de goût. Les couples ont été invités à évaluer leur humeur ainsi que la suppression émotionnelle qu’ils ont exercée pendant la discussion, de même qu’à remplir des questionnaires auto-rapportés. L’indice de masse corporelle (IMC) des partenaires a été calculé à partir de mesures objectives. Le premier objectif spécifique de la thèse vise plus particulièrement à étudier l’impact d’un changement d’humeur suite à la discussion conjugale stressante sur la prise alimentaire subséquente des hommes et des femmes, et de tester l’effet modérateur de l’IMC et de la restriction alimentaire sur cette relation. Les résultats indiquent d’abord des associations différentes chez les hommes et les femmes en réponse à la situation expérimentale. Chez les hommes, seules les perceptions d’appétit prédisent la prise alimentaire, tandis que chez les femmes, un patron plus complexe se dessine. Un sous-groupe de femmes à risque de se suralimenter en réponse au stress conjugal est identifié, soit les femmes présentant un IMC élevé et un profil alimentaire restrictif. Ces résultats ajoutent à la littérature actuelle en ce sens où l’impact d’un stresseur de nature conjugale sur la prise alimentaire n’avait jamais été testé auparavant. De plus, ils soulignent l’importance de tenir compte en concomitance de l’IMC et de la restriction dans la compréhension du phénomène de l’alimentation induite par le stress chez les femmes. Le deuxième objectif spécifique de la thèse a pour but d’examiner, à l’aide d’un modèle dyadique, l’effet médiateur de la suppression émotionnelle sur le lien entre le changement d’humeur suite à la discussion conjugale stressante et la prise alimentaire subséquente, en fonction de l’IMC des deux membres du couple. Les résultats de cette étude révèlent que la suppression émotionnelle est un médiateur valide de la relation entre le changement d’humeur et la prise alimentaire, et met également en évidence l’effet modérateur de l’IMC sur cette médiation. Plus particulièrement, la dégradation de l’humeur des individus présentant un IMC élevé est associée à une plus grande prise alimentaire via l’adoption de suppression émotionnelle pendant la discussion avec le partenaire, tandis que chez les individus présentant un IMC faible, la dégradation de l’humeur est plutôt associée à une plus faible prise alimentaire via la suppression. D’un point de vue dyadique, la suppression émotionnelle d’un membre du couple agit comme médiateur de la relation entre le changement émotionnel et la prise alimentaire de son partenaire, sans égard à l’IMC des conjoints. En d’autres mots, la dégradation de l’humeur de l’un mène à une plus grande consommation via la suppression émotionnelle de l’autre. Ces résultats font ressortir le rôle clé de la suppression émotionnelle dans l’alimentation induite par le stress conjugal non seulement au plan individuel, mais également au plan dyadique. Ils soulignent la pertinence de s’intéresser aux interrelations entre les membres d’un couple pour prédire leurs comportements alimentaires. Dans leur ensemble, les travaux de la thèse suggèrent que le couple puisse générer du stress et des affects négatifs qui peuvent mener à la suralimentation. Une attention grandissante devrait être portée à ce type de stresseur dans l’avenir, de même qu’à l’étude de la réponse alimentaire d’un sous-groupe de personnes précis face au stress conjugal, soit les femmes qui présentent des difficultés de régulation du poids et de l’alimentation.
Stress-induced eating has been widely studied up until now in order to identify individual characteristics which may be designated as risk factors to overeating. Being overweight or obese, as well as being a restrained eater, have been identified. Although some studies have investigated the impact of different types of stressors on eating, none has broadened its investigation on romantic relationships. However, emotions experienced through couple interactions as well as the way partners deal with (or regulate) those emotions may certainly contribute to the development and exacerbation of problematic eating behaviors that can lead to weight gain. Thus, using a laboratory experiment involving a dyadic stress, the present thesis aims to deepen the current understanding of the relationship between emotions following a stressful couple discussion and food intake among heterosexual couples. Eighty couples were recruited and discussed an aspect that they wanted their partner to change. Food intake was measured following the discussion with a bogus taste test. Both partners assessed their mood state, as well as emotion suppression, and completed self-reported questionnaires. Body mass index (BMI) was calculated with objective measures. The first specific objective of the thesis was to examine the impact of mood change induced by a stressful couple discussion on food intake in both spouses, while simultaneously taking into account the moderating effect of BMI and restraint on this association. First, results showed different responses in men and women following the discussion. Among men, only appetite perceptions significantly predicted food intake, while a more complex pattern emerged among women. A subgroup of women at risk to overeat in response to dyadic stress was identified, those with a high BMI and a restrictive eating profile. These results add to the current literature since the impact of a dyadic stressor on food intake had never been tested before. Moreover, these results highlight the importance of considering the concomitant effect of BMI and restraint in the understanding of stress-induced eating among women. The second specific objective of the thesis was to examine, using dyadic analysis, whether emotion suppression was a valid mediator in the relationship between mood change following a stressful couple discussion and subsequent food intake among couples, while taking into account spouses’ BMI. Results showed that emotion suppression was a valid mediator in the relationship between mood change and food intake, and that BMI significantly moderated this mediation. That is, mood worsening was related to high food intake through emotion suppression among high BMI spouses, while for low BMI spouses, mood worsening rather predicted low food intake through emotion suppression. Dyadic analysis revealed that emotion suppression in one partner acted as a mediator in the association between mood change and food intake in the other partner, regardless of BMI. In other words, mood worsening of one partner led to a greater consumption of food via emotion suppression in the other partner. These results emphasise the key role of emotion suppression in the relationship between mood change and food intake in the context of a stressful couple discussion. They also underscore the relevance to focus on the interrelationships between spouses to predict their eating behaviors. Taken together, the thesis results suggest that romantic relationships can generate stress and negative emotions that can lead to overeating. More attention should be paid to this type of stressor in the future, as well as to the study of the eating response to dyadic stress of a specific subgroup of people, i.e. women presenting eating and weight regulation issues.
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Millet, Yves. "Suppression of Arabidopsis thaliana root innate immunity by Pseudomonas syringae phytotoxin coronatine and functional studies of the cytochrome P450 CYP76C2." Strasbourg, 2009. https://publication-theses.unistra.fr/public/theses_doctorat/2009/MILLET_Yves_2009.pdf.
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Au cours de l’évolution, les plantes ont développé des mécanismes de défense sophistiqués contre les pathogènes. L’une des premières lignes de défense se base sur la reconnaissance par la plante de motifs moléculaires très conservés associés aux pathogènes (PAMP/MAMP). Cette reconnaissance active divers mécanismes de défense, en particulier le dépôt de callose au niveau de la zone infectée. Malgré l’abondance des interactions racine-microbes, la réponse aux MAMPs dans cette partie de la plante reste largement inexplorée. Nous avons développé un système de culture hydroponique qui nous a permis d’étudier cette réponse chez Arabidopsis thaliana en se basant sur l’étude de lignées promoteur:GUS ainsi que sur le dépôt de callose Nous avons trouvé que les racines répondent fortement aux MAMPs dans des régions bien spécifiques, en particulier dans la zone d’élongation. Cette réponse dépend de la voie de signalisation de l’éthylène, du facteur de transcription MYB51, du cytochrome P450 CYP81F2 ainsi que de la myrosinase PEN2. En outres, nous montrons que Pseudomonas syringae et Pseudomonas fluorescens sont capables de bloquer ce mécanisme de défense. En particulier, dans le cas de P. Syringae, cette suppression s’effectue grâce à la production de coronatine (COR). L’action de la COR est dépendante de l’E3 ligase COI1 et du facteur de transcription JIN1/MYC2. Un screen génétique m’a permis d’isoler de nouveaux mutants incapables de bloquer la réponse aux MAMPs, dans le but d’identifier de nouveaux gènes impliqués dans la réponse à la COR. Enfin, ma thèse a porté sur l’étude du cytochrome P450 CYP76C2, fortement induit par les pathogènes. CYP76C2 est activé localement lors d’une infection par P. Syringae ou Botrytis cinerea ainsi que lors des mécanismes de mort cellulaire. Je démontre que l'activation de CYP76C2 est partiellement dépendante de la voie de signalisation de l’acide salicylique et que ce gène est potentiellement impliqué dans le contrôle du stress oxydatifOver the course of evolution, plants developed sophisticated defense mechanisms against bacterial and fungal pathogens. One of the first layers of plant defense is called PAMP triggered immunity (PTI) and is based on the recognition of conserved epitopes of pathogen-derived molecules called PAMPs/MAMPs (Pathogen/Microbe Associated Molecular Patterns). This recognition activates defense responses including the deposition of callose at the site of pathogen attack. Despite the fact that roots are the organs most subject to microbial interactions, MAMP signaling in roots remains largely unexplored. I developed an Arabidopsis thaliana seedling assay to study PTI in roots based on the detection of callose and the activation of promoter:GUS reporters of MAMP-responsive genes. I found that MAMPs trigger a strong response in roots dependent on ethylene signaling, the MYB51 transcription factor, the cytochrome P450 CYP81F2, and the PEN2 myrosinase, but independent of salicylic acid signaling. In addition, I show that the bacteria Pseudomonas syringae and Pseudomonas fluorescens suppress this response and that P. Syringae is doing so by producing the phytotoxi coronatine. I found that coronatine acts via the E3 ligase COI1 and the transcription factor JIN1/MYC2. I performed a forward genetic screen to isolate mutants impaired in COR-mediated suppression in an attempt to identify new players involved in COR signaling. In this thesis, I also present data concerning CYP76C2, a gene encoding a cytochrome P450 that is highly induced by MAMPs and pathogens in Arabidopsis leaves. I confirmed that CYP76C2 is activated during pathogen infection and various cell death elicited scenarios. Furthermore, I demonstrate that CYP76C2 is partially dependent on SA signaling and may be involved in controlling oxidative damage during infection
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Tseng, Raymond J. "Stress-induced suppression of natural killer cell activity during influenza viral infection the role of glucocorticoids and opioids /." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1148586277.
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Gupta, Prachi. "SYNTHESIS AND CHARACTERIZATION OF ANTIOXIDANT CONJUGATED POLY(ΒETA-AMINO ESTER) MICRO/NANOGELS FOR THE SUPPRESSION OF OXIDATIVE STRESS." UKnowledge, 2016. http://uknowledge.uky.edu/cme_etds/58.
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Oxidative stress is a pathophysiological condition defined by an increased production of reactive oxygen species (ROS), which can result in the growth arrest of cells followed by cell disintegration or necrosis. A number of small molecule antioxidants (e.g. curcumin, quercetin and resveratrol) are capable of directly scavenging ROS, thereby short-circuiting the self-propagating oxidative stress state. However, poor solubility and rapid 1st pass metabolism results in overall low bioavailability and acts as a barrier for its use as a drug to suppress oxidative stress efficiently.
To overcome this limitation, these small molecule antioxidants were covalently conjugated into poly(β-amino ester) (PβAE) cross-linked networks to formulate prodrug gel microparticles and nanoparticles (nanogels). Being hydrolytically degradable in nature, these PβAE crosslinked systems released antioxidants in their original structural form in a sustained controlled fashion.
Both quercetin and curcumin-PβAE nanogels showed prolonged suppression of cellular oxidative stress induced by H2O2. Curcumin PβAE nanogels also demonstrated protection against mitochondrial oxidative stress induced by H2O2 and polychlorinated biphenyls.
Curcumin-PβAE gel microparticles were also developed as a platform to treat oral mucositis through a local antioxidant delivery route. The same synthesis chemistry was transferred to formulate resveratrol PβAE gel microparticles for topical applications, to treat UV radiation induced oxidative stress. Both formulations showed suppression of induced oxidative stress. An in vivo trial with curcumin-PβAE microparticles further showed relatively reduced the severity of induced oral mucositis (OM) in hamster check pouch as compared to placebo.
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Vincent, Annabelle Carole. "Effets de la suppression du stress de la naissance et de l'adoption sur le développement et le comportement de jeunes rats." Rouen, 2003. http://www.theses.fr/2003ROUEL458.
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Chez les Mammifères au moins, la naissance représente un stress physique important pour le nouveau né. Notre étude a pour objet de déterminer les effets de la suppression de ce "stress de la naissance" chez des rats nés à terme, suivis jusqu'à l'âge adulte. Notre recherche s'intéresse également aux conséquences à court et long terme de l'adoption à la naissance. Nous avons conduit plusieurs expériences dans lesquelles nous avons fait varier, d'une part, le mode de naissance (par césarienne ou par voie vaginale) la césarienne permettant aux fœtus d'éviter de subir le stress dû à leur compression dans les voies génitales lors des contractions utérines et la situation d'hypoxie, d'autre part, l'environnement de développement post-natal (adoption ou élévage par la mère biologique). Les mères adoptives mettent bas naturellement soit deux jours avant, soit à la même période que les autres mères et leur comportement est aussi étudié. Les résultats et les comparaisons statistiques ont montré que : -la corticostéronémie, à la naissance, est plus faible chez les ratons nés par césarienne que chez ceux nés par voie vaginale, suggérant que la naissance naturelle est bien un évenement stressant. -l'adoption intra-lignée modifie seulement certaines composantes, orientées directement vers les jeunes, du comportement des mères, mais le mode de naissance des ratons n'engendre pas d'effets majeurs sur leurs conduites. -l'adoption provoque une mortalitée immédiatement suivant la procédure, qui se poursuit au moins jusqu'à l'âge d'un mois chez les rats adoptés par des mères ayant mis bas deux jours avant associée à une lente évolution pondérale néonatale, un accroissement de l'anxiété de trait, des modifications du comportement social, ainsi qu'une atteinte des fonctions mnésiques seulement à court terme. - la naissance par césarienne a des effets dramatiques sur la survie ainsi que sur la croissance pondérale au moins pendant toute la période néonatale, entraîne une hyper-activité durable uniquement chez les rats adoptés par des mères ayant mis bas deux jours avant l'adoption, des perturbations du comportement émotionnel, des changements comportementaux au cours d'interactions sociales, ainsi qu'une modification des capacités menésiques à court ou long terme. Ansi une légère modification des conditions de naissance ou un changement précoce de l'environnement maternel suffit à influencer le développement des jeunes et le comportement émotionnel et cognitif des animaux adultesAt least in mammals, birth represents an important physical stress for the newborn. The present study was aimed to dtermine the effects of elimination of this "birth stress" on development and behavior of young term rats, observed until the adult stage. The second aim of this study was to determine the short-and-long-term consequences of fostering at birth. Several experiments were organized to test the influence of the mode of delivery (cesarean section or spontaneous vaginal delivery), the cesarean delivery allowing the avoidance by fetuses of suffering stress due to their compression of the genital tract during strong uterine contractions and acute birth hypoxia, and the postnatal development environment (fostering or rearing by the natural mother). The foster dams were spontaneously dillivered two days peviously or at the same time than other biological dams, and their behavior was also studied. The results show that : - corticoid secretion, at birth, was lower in rat pups delivered by cesarean section than in those naturally born, indicating that natural birth is indeed a stressful event. - in-fostering modified dam's activities directly towards the pups, but the mode of pups'birth seemed to have no major effect on maternal behavior - in-fostering per se resulted in mortality of neonates soon following adoption but; which continued at least throughout the first month of life, with a neonatal growth retardation of surviving pups fostered by dams which were delivered two days previously, an enhanced trait anxiety, modifications of social behavior, and impairments of working memory. - cesarean section birth had catastrophic effects on death and weight gain of survivors at least throughout the neonatalperiod, and elicited a long-lasting hyperactivity only in rats fostered by dams which delivered two days previously, disturbances of emotional behavior, behavioral modifications during social interactions and dysfunction in short-or long-term memory. Thus, mild modification of birth conditions or early change of maternal environment is sufficient to influence the development of young and the emotional and cognitive functions of adult
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Malueg, Amanda Leah. "Stress in the Red-cockaded Woodpecker: Hormonal Mechanisms of Reproductive Suppression in Helper Males and Impacts of Military Training Activities." Thesis, Virginia Tech, 2007. http://hdl.handle.net/10919/35091.
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The measurement of stress hormone levels in wild free-living animals is becoming an increasingly effective method for examining proximate mechanisms of animal behavior and the physiological impacts of human activities on wildlife. In these studies I measured plasma levels of the stress hormone corticosterone in the endangered red-cockaded woodpecker (Picoides borealis) to determine their role in the reproductive behavior of individuals in this species, and whether they are affected by human disturbance. In chapter one, I provide an introduction to the vertebrate stress response and I describe the natural history of the red-cockaded woodpecker. In chapter two, I compare corticosterone and reproductive hormone levels between breeding males and helper males to examine hormonal mechanisms of reproductive suppression in helper males. No hormonal differences existed between breeding and helper males. However, baseline corticosterone levels were lower in all males living in groups with two or more helper males, suggesting that male helpers reduce the workload of all other group members. In chapter three, I compare corticosterone levels between birds living in clusters subject to two different training restriction regimes on a military installation. Males living in clusters without training restrictions had lower baseline corticosterone than those living in clusters with training restrictions, suggesting that males habituate to chronic disturbance by downregulating baseline corticosterone levels.Master of Science
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Taniguchi, Masayuki. "Dopamine D1 receptor subtype mediates acute stress-induced dendritic growth in excitatory neurons of the medial prefrontal cortex and contributes to suppression of stress susceptibility in mice." Kyoto University, 2018. http://hdl.handle.net/2433/232116.
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Cates, Philippa Susan. "Elucidating the neural mechanisms underlying stress-induced suppression of the gonadotrophin releasing hormone pulse generator in the female rat." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392328.
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Yoshizumi, Takahiro, and Satomi Murase. "The effect of avoidant tendencies on the intensity of intrusive memories in a community sample of college students." Elsevier, 2007. http://hdl.handle.net/2237/9098.
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Mizon, Guy Andrew. "Is expressive flexibility related to recovery from a stressful task?" Thesis, University of Exeter, 2012. http://hdl.handle.net/10036/3874.
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Habitual suppression of emotions has been linked to adverse consequences such as avoidant attachment, lower social support, and reduced relationship closeness (e.g. John & Gross, 2004). However, accumulating evidence that expression and suppression can be both adaptive and maladaptive in different contexts suggests the importance of flexibility in emotional regulation. The present study examined the mechanisms underlying the only laboratory measure of emotional flexibility: the Expressive Flexibility (EF) task (Bonanno, Papa, Lalande, Westphal, & Coifman, 2004). This measure has been linked to adjustment over a one-year period, especially in the context of social threat, and among people who have experienced higher levels of life stress (Westphal, Seivert & Bonanno, 2010). We sought to test whether EF is related to physiological recovery from stress in the immediate term. Participants completed questionnaire measures, the EF Task and a stressful public speaking task. In the EF task, participants were filmed suppressing, exaggerating, and not altering facial reactions to negative and positive pictures. A “balanced EF” score was calculated reflecting their ability to suppress and exaggerate with equal success. Regression analyses used EF scores as predictors for psychophysiological indices of stress (SCR and HR) during and after the public-speaking task. The interaction of EF and social safeness (SSPS) was predictive of the magnitude of SCR recovery, such that for people with lower EF, higher SSPS is predictive of greater SCR recovery. These results converge with previous findings on the suggestion that EF is related to resilience, especially in the context of adversity.
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Yarar, Orhan Ferhat. "Effects Of Inhibitory Mechanisms And Thought Suppression Tendency On The Frequency And Intensity Of Traumatic Intrusions." Master's thesis, METU, 2011. http://etd.lib.metu.edu.tr/upload/12612926/index.pdf.
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The present study investigates the effects of cognitive inhibitory mechanisms and tendency to suppress thoughts on the frequency and intensity of traumatic intrusions within the trauma film paradigm. Non clinical participants&rsquoresponse inhibition and proactive inhibition levels and tendency to suppress thoughts were measured prior to exposure to a trauma film. One week after seeing the trauma film, participants reported the frequency and intensity of trauma film related intrusions with an intrusion diary and Impact of Events Scale. No significant effect of response inhibition, proactive inhibition and thought suppression tendency was found on the frequency and intensity of trauma film related intrusions. Findings of the study are discussed.
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Finzel, Pérez Ana [Verfasser]. "Upstream control and downstream responses of p53 are involved in its tumor suppression functions upon genotoxic stress / Ana Finzel Pérez." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/1122111193/34.
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Benayoun, Bérénice. "Foxl2 : un facteur de transcription essentiel de l'ovaire, à l'interface entre la réponse au stress cellulaire et la suppression tumorale." Paris 7, 2011. http://www.theses.fr/2011PA077006.
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FOXL2 est un facteur de transcription, muté dans le Syndrome du Blépharophimosis (BPES), qui se caractérise par des malformations craniofaciales isolées ou associées à des problèmes ovariens. Dans ce travail, nous avons montré que la protéine FOXL2 est très modifiée au niveau post-traductionnel, et découvert un nouveau mécanisme de maturation. Nous avons aussi identifié un élément de réponse de haute affinité de FoxL2. Cette identification a permis de mettre au point un outil diagnostique pour prévoir l'occurrence de problèmes ovariens en association avec le BPES. Nous avons aussi montré que FOXL2 joue un rôle la réponse au stress cellulaire. En effet, un stress oxydant dans des cellules de la granulosa fait augmenter l'expression de FOXL2, son acétylation et sa capacité de transactivation. Nous avons montré que SIRT1 inhibe FOXL2, alors que FOXL2 peut activer SIRT1, ce qui correspond à un rétrocontrôle négatif. Des études cliniques ont montré que la perturbation de FOXL2 est motrice pour la tumorigenèse des cellules de la granulosa, ce qui suggère un rôle de anti-tumoral pour FOXL2. L'étude des cibles de FOXL2 a révélé qu'il régulerait la progression du cycle cellulaire. En effet, une surexpression de FOXL2 amène les cellules à s'accumuler en phase Gl du cycle. L'inhibition de SIRT1 par le nicotinamide induit une augmentation de l’expression/activité de FOXL2, ce qui corrèle avec des perturbations de la progression du cycle cellulaire. En résumé, ce travail a permis d'impliquer FOXL2 comme un régulateur de la réponse au stress et de la prolifération, et a fourni de nouvelles pistes pour comprendre les conséquences pathogéniques de sa dérégulationFOXL2 is a transcription factor, mutated in the Blepharophimosis Syndrome (BPES), characterized by craniofacial defects, either isolated (type II) or associated with ovarian dysfunction (type I). We found that FOXL2 is a highly post-translationally modified protein, and uncovered a novel mechanism of maturation. We also identified a high-affinity FoxL2 Response Element, which was instrumental to set up a diagnostic tool predicting the occurrence of ovarian dysfunction in BPES patients. We also showed that FOXL2 was involved in the cell stress response. Indeed, we found that oxidative stress up-regulated FOXL2 in granulosa cells, increased its acetylation and its transactivation. Consistently, FOXL2 upregulation protects cells against oxidative stress. We identifiée SIRT1 as a FOXL2 negative regulator and a direct target gene, proving the existence of a negative-feedback loop. Clinical studies found that FOXL2 misregulation may drive malignant transformation of granulosa cells, pointing to a tumor suppressor role. Study of FOXL2 target genes revealed cell-cycle progression as a significant FOXL2-regulated pathway. Indeed, FOXL2 over-expression led to accumulation of cells in the Gl-phase and increased repair of DNA oxidation damage. We tested the effect of SIRT1 inhibition with nicotinamide, which increases FOXL2 levels, on granulosa tumor cells. Indeed, this treatment interfered with cell cycle progression. In short, this PhD work implicates FOXL2 as a novel regulator of stress response and proliferation in granulosa cells, which gives new insights into the pathogenic consequences of its deregulation
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Bowe, James Edward. "The role of CGRP in stress-induced suppression of the GnRH pulse generator and thermo regulatory responses in the female rat." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429402.
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Cooper, Richard James. "Effects of chemical seedhead suppression on the carbohydrate status, quality, rooting, and heat stress tolerance of annual bluegrass (Poa annua L.) /." The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487260135357518.
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Friedrich, Anja [Verfasser], Sophia [Akademischer Betreuer] Sonnewald, and Sophia [Gutachter] Sonnewald. "Role of the Coxiella burnetii type IV effector protein CaeB in cell death suppression and ER stress signaling / Anja Friedrich ; Gutachter: Sophia Sonnewald ; Betreuer: Sophia Sonnewald." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2021. http://d-nb.info/1235757722/34.
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Labbé, Adam. "Profil d'expression des fibroblastes de souris embryonnaires avec une suppression dans le domaine hélicase de l'homologue du gène Werner traité avec du peroxyde d'hydrogène." Thesis, Université Laval, 2012. http://www.theses.ulaval.ca/2012/28800/28800.pdf.
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Schäfer, Claudia [Verfasser], Krämer Oliver Akademischer Betreuer] H, Frank [Akademischer Betreuer] [Große, and Martin [Akademischer Betreuer] Göttlicher. "Modulation of the replication stress response by histone deacetylases is connected to suppression of the PP2A regulatory subunit PR130 / Claudia Schäfer. Gutachter: Krämer Oliver H. ; Frank Große ; Martin Göttlicher." Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2015. http://d-nb.info/1066238278/34.
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Cunniffe, Brian. "Effect of acute and chronic exercise on immunoendocrine responses in professional rugby union." Thesis, University of South Wales, 2009. https://pure.southwales.ac.uk/en/studentthesis/effect-of-acute-and-chronic-exercise-on-immunoendocrine-responses-in-professional-rugby-union(bc7a6dfd-67e1-4e63-965e-a61333245818).html.
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Prolonged and intense exercise is known to modulate and suppress certain aspects of the immunoendocrine system. Such effects are thought to be largely mediated by the release of stress hormones and regulatory cytokines which originate from a variety of stress related paradigms in sport. These include acute physical exertion, chronic and repetitive exercise as well as other psychological and psychosocial aspects of training and competing in an elite environment. It may be of particular interest to study the effects of regular competition and training on immunoendocrine markers in rugby union players. At the professional level, rugby is an intense and physically demanding game where a significant amount of tissue trauma occurs as a result of the many game collisions. The aims of the studies outlined in this thesis were to determine the effects of acute, repeated and chronic exercise exposure on immunoendocrine markers and illness incidence in professional rugby union. Additional case studies were also undertaken to supplement main study findings. The first part of the thesis documented the effects of acute and repeated exercise on immunoendocrine markers in a cohort of international rugby union players. Data in study 1 showed that large disturbances in immunoendocine and hormone levels occur in players (n = 10) following game play. The magnitude of this response appeared dependent on game physicality (number of rucks/mauls, tackles) and the number of collisions players received during match play. Findings also showed suppression in host immunity, and in particular, innate immune function (neutrophil degranulation) which was not resolved 38 h (-29%) into the recovery period. In study 2, bloods were taken from players (n = 8) across a 21-day international rugby series. Data revealed that players entered the international camp with residual muscle damage (creatine kinase; CK) and inflammation (hs-CRP) following previous club involvement in European cup rugby. Further increases in stress related markers (cortisol, IL-6, CK, CRP) were not evident throughout the players time at the international training base. Conversely, a progressive increase in anabolic-catabolic balance (T/C ratio) was observed across time. In comparison to values on camp-entry (day 1), increases in T/C ratio were evident on day-5 (9.8%), day-7 (13%), day-19 (35%) and day-21 (45%) (P < 0.05). This data is suggestive of improved physiological recovery and was commensurate with team fitness goals (reduced volume + maintenance of training intensity) for that time. Findings suggest that monitoring of player club activities and training load preceding international duty is pertinent if they are required to represent their country inside 7 days. The second part of the thesis evaluated the stress induced effects of chronic rugby exposure in professional club players. Questionnaire data analysed from study 3 showed that players (n = 65) perceived current season length as being ‘too long’ (55%), ‘poorly structured’ (56%) and that game demands are increasing with time (52%). Furthermore, the majority of players (80%) felt that time ‘away’ from rugby was not sufficiently long enough and were in favour of a mid-season break (2 wks in duration). Investigation into the effects of chronic exercise on illness incidence, immunological and psychological state was carried out in a squad of club players (n = 30) over a competitive season (n = 48 wks) in studies 4-6. Findings revealed that specific periods in a rugby season resulted in disturbances to hormonal and immune status. These periods occurred following breaks in club game fixtures [November international and Six-nations period: February/early March], times of increased training intensity and increased ratio of conditioning/rugby activity. Peaks in number of upper respiratory illnesses (URIs) and disturbances in psychometric variables also occurred during these time periods. In 23% of all URIs, players reported that the presence of the illness either reduced activity (14.4%) or felt the need to go to bed (8.6%). Positional differences in variables were also observed. A higher incidence of URIs (3.4 vs 4.3) and lower concentrations of resting immune markers [salivary lysozyme: s-Lys (-31%); immunoglobulin A: s-IgA (-27%)] was observed in ‘backs’ (vs forwards) over the season. Higher mid-season cortisol levels was also observed in backs (P < 0.05) while conversely, greater concentrations of plasma CK and CRP were found in forwards throughout the season. These findings indicate positional specific differences in response to exercise load and point to the role of group specific recovery at certain times during the season. Data from study 6 showed that the number of training related complaints decreased across the season, findings which closely resembled corresponding decreases in plasma CRP values. This data is suggestive of a ‘repeated-bout’ effect or ‘contact adaptation’ in rugby union. Finally, comparison of methods used in the recording of illness data revealed that players were more honest when disclosing the existence of banal infections to a web-based training diary and under-reported infections to medical staff.
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Matos, Rodrigues Gabriel Eduardo de. "Suppression of Homologous Recombination by RAD51 Functional Inactivation In Vivo in Mice Replication Stress, DNA Damage, Inflammatory Cytokines and Innate Immune Response In Vivo Suppression of Homologous Recombination Leads to a Systemic Inflammation That Exacerbates Mouse Death Functional Inactivation of RAD51 in Adult Mice Leads to Premature Aging Without Tumor Development Inactivation of Trp53 Accelerates Mouse Death After RAD51 Functional Inactivation in Adult Mice Without Increasing Tumor Formation RAD51 Functional Inactivation Inhibits Mammary Tumor Initiation and Progression in Mice." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL073.
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La recombinaison homologue (RH) est un processus conservé dans l'évolution qui joue un rôle de premier plan dans la plasticité du génome, contrôlant l'équilibre de stabilité/diversité génétique. L'étape charnière des RH, c'est-à-dire la recherche d'homologie d'ADN et l'échange de brins, est régi par le filament RAD51-ssDNA (ADN simple brin) qui doit être bien ordonné, donc représentant les espèces actives centrales de la RH. La déficience de la HR est liée au développement de syndromes et cancer chez l’humain. Cependant, puisque Rad51 est un gène essentiel chez la souris, les conséquences de la perturbation fonctionnelle de RAD51 reste à être étudié in vivo. Ici, nous avons développé un forme inductible du dominante négative de RAD51 (SMRAD51) pour poissonnier la RH in vivo. En utilisant des approches biochimiques, nous démontrons que SMRAD51 perturbe les échanges de brins d’ADN dépendant de RAD51 et la formation du filament RAD51-ssDNA. L'expression SMRAD51 conduit à le stresse réplicatif in vitro et in vivo, déclenchant épuisement des progéniteurs. Nous montrons que l’inactivation fonctionnelle de RAD51 chez la souris en croissance (commence 12 à 14 jours après la naissance) déclenche une réponse inflammatoire entraînant la mort de la souris dans quelques jours. Chez la souris adulte, l’inactivation fonctionnelle de RAD51 induit des phénotypes de vieillissement prématuré et diminue la durée de vie avant un possible tumorigenèse. De plus, nous montrons que l'inactivation fonctionnelle de RAD51 inhibe initiation et progression tumorale dans un modèle murin de cancer du sein. Dans l'ensemble, je découvre ici de nouveaux mécanismes pro-vieillissement et anti-tumoraux générés par l'inactivation fonctionnelle de RAD51Homologous recombination (HR) is an evolutionary conserved process that plays a prominent role in genome plasticity, controlling the balance of genetic stability/diversity. The pivotal step of HR,i.e. DNA homology search and strand exchange, is governed by the RAD51-ssDNA (single-stranded DNA) filament that must be well ordered, thus representing the actual active species of HR. HR impairment is linked to human developmental syndromes and cancer. However, since RAD51 is an essential gene in mice, the consequences of functional disruption of RAD51 remain to be studied in vivo. Here we developed an inducible dominant negative form of RAD51 (SMRAD51) to poison HR in vivo. Using biochemical approaches, we demonstrate that SMRAD51 disrupts RAD51-dependent strand-exchange and RAD51-ssDNA filament formation. SMRAD51 expression leads to replicative stress in vitro and in vivo, triggering progenitor exhaustion. We show that functional inactivation of RAD51 in growing mice (starting from 12 to 14 days after birth) triggers a systemic inflammatory response causing mouse death within a few days. Meanwhile, RAD51 functional disruption in adult mice induces premature aging phenotypes and reduced lifespan prior to putative tumorigenesis. In addition, we show that RAD51 functional inactivation inhibits tumor initiation and progression in a mouse model of breast cancer. Overall, here I uncover new pro-aging and anti-tumor mechanisms generated by the functional inactivation of RAD51
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Huang, Shirley Chien-Chieh 1978. "Control of tumor suppressor p53 by protein phosphorylation and ER stress." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78384.
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Tumor suppressor p53 is a mediator of stress-induced cell cycle arrest and apoptosis. The kinase inhibitor 2-aminopurine (2-AP) is an adenine analog shown to cause cells to bypass DNA damage-induced cellular arrest through unknown mechanisms, and may potentially target p53. Although p53 plays vital roles in adaptation to many stresses, its role in cellular response to endoplasmic reticulum (ER) stress is unclear. Here, stress-induced p53 stabilization and checkpoint control in the presence of 2-AP are examined, as well as p53 regulation upon ER stress induction. I show that 2-aminopurine suppresses p53 stabilization in response to different forms of DNA damage. Biologically, 2-AP exposure enables cells to bypass adriamycin-induced G2/M arrest in a p53-dependent manner, but rescues the clonogenic survival of cells exposed to adriamycin in a p53-independent manner. Next, I show that pharmacological and physiological inducers of ER stress can inhibit stress-induced p53 function by promoting p53 cytoplasmic retention.
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Curato, John. "Inheritance of resistance to wheat streak mosaic virus in wheat line KS06HW79." Thesis, Kansas State University, 2016. http://hdl.handle.net/2097/32918.
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Master of ScienceDepartment of Agronomy
Guorong Zhang
Guihua Bai
Wheat streak mosaic virus (WSMV) is a disease that causes significant yield losses in wheat (Triticum aestivum L.). Host resistance is the primary approach for control. KS06HW79 is a wheat line with WSMV resistance up to 21°C. To study the inheritance of resistance in KS06HW79, it was crossed with two WSMV-susceptible wheat genotypes, KS020638-M-5 and Brawl CL Plus. Parental lines, F₁, F₂, and check varieties were mechanically inoculated and evaluated for WSMV resistance at 21°C in growth chambers. The segregation pattern in two F₂ populations fit a one-recessive-gene model (1 resistant : 3 susceptible) and a dominant-suppression-epistasis model (3 resistant : 13 susceptible). To determine which model was a better fit, WSMV resistance was evaluated for F₂:₃ families generated from resistant F₂ plants in both crosses. Approximately two thirds of the F₂:₃ families in each cross showed segregation for WSMV resistance, suggesting that the dominant-suppression epistasis model better explained the WSMV resistance in KS06HW79. This model was also supported by two KS06HW79-derived doubled haploid populations, which had a segregation ratio of 1 resistant : 3 susceptible. Therefore, the WSMV resistance in KS06HW79 is likely controlled by two dominant genes, one of which is a suppressor.
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Latonen, Leena. "Tumor suppressor p53 and transcriptional changes in cellular stress responses to UV radiation." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/haart/vk/latonen/.
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Hata, Masayuki. "KUS121, a VCP modulator, attenuates ischemic retinal cell death via suppressing endoplasmic reticulum stress." Kyoto University, 2018. http://hdl.handle.net/2433/232075.
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Tang, Kei-shuen, and 鄧紀旋. "Role of BRCA1 in stress-induced autophagy in breast and ovarian cancercells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45847204.
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Aflalo, Bernardo Santos. "CFD and CAA analysis of single stream isothermal jets with noise suppression devices." Instituto Tecnológico de Aeronáutica, 2009. http://www.bd.bibl.ita.br/tde_busca/arquivo.php?codArquivo=1210.
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Since the 50's, with the appearance of the turbojet engines, the jet noise is being exhaustively studied, because it is one of the most important source of aircraft noise. Many attempts have been made to reduce the jet noise, including higher by-pass turbofan engines. Chevron nozzles also have been used by the industry to try to reduce the jet noise with a low performance and weight penalty. This work shows a computation procedure to assess how this noise suppression devices impact on both fluid dynamics and acoustics of single isothermal jets. Towards this goal, different chevron nozzles, with 6, 8 and 12 lobes have been analyzed. The calculation procedure is based on a Reynolds Average Navier-Stokes calculation, followed by a stochastic noise generation and radiation method, resulting in a relatively fast noise calculation procedure. The simulations have been carried out using the commercial software CFD++. The calculation procedure has predicted the expected fluid dynamic and acoustic behavior for chevron nozzles, e.g., shortening the potential core length, high frequency noise increase and low frequency noise attenuation. The parametric study of the number of lobes has shown that this parameter impacts the mixing region. Moreover, varying this parameter is a way to attain different low frequency reductions, without great impacts on the highest frequencies. Although the procedure did not capture correctly the absolute values of the acoustic response, the results show that this relatively simple and quick analysis reproduced important parameters in designing new nozzles and can be used as a way to better understand the influence of chevrons.
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Husaini, Roslina. "Towards the Investigation of the Effects of Nitration on the Activity of the Human p53 Tumour Suppressor Protein. Nitration of the p53 Tumour Suppressor Protein." Thesis, University of Bradford, 2014. http://hdl.handle.net/10454/14788.
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Upon responding to cellular stress, p53 protein becomes stabilised and acts as a transcription factor mainly resulting from phosphorylation and acetylation of the protein. Nitration of p53 protein is poorly characterised by comparison with phosphorylation and acetylation. The main aim of this work was to study the effects of nitration on p53 functional activities and on p53-MDM2 protein-protein interactions. Preliminary work was to characterise the nitration of p53 protein over-expressed in E. coli BL21(DE3) which was then purified by a series of column chromatography. GST-MDM2 protein along with control GST protein were also overexpressed in BL21 which were subsequently purified by a single step batch purification before subjected to nitration. Peroxynitrite, a nitrating agent used in this study, was generated in vitro. Preliminary nitration work was carried out using BSA as a model protein as it is easily nitrated owing to its high number of tyrosine residues (19 residues). The present results showed that p53 and GST-MDM2 proteins were hardly nitrated as no strong nitro-tyrosine signals were obtained. This might be due to these proteins, being overexpressed in E. coli, were not properly folded resulting in hidden/cryptic tyrosine residues of which making nitration difficult to achieve. Peroxynitrite was shown to have a degrading property, reducing protein levels of peroxynitrite-treated p53, GST-MDM2 and GST proteins. Immunoprecipitation studies of cancer cell lysates with different p53 status treated with peroxynitrite showed very weak signals of nitro-p53 protein in mutant p53 cells whereby no nitro-p53 protein signal in wild-type p53 MCF7 cells. In addition, NO donor GSNO-treated MCF7 cells showed weak nitro-p53 protein signals.Ministry of Science, Technology and Innovation (MOSTI) of Malaysia
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Kwan, Wai-yin. "Glucose-regulated protein 78 as a novel target of BRCA1 for inhibiting stress-induced apoptosis." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4163391X.
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Pluquet, Olivier. "Activation de la protéine onco-suppressive P53 par le cytoprotecteur amifostine : définition d'une voie signalétique d'activation indépendante du stress-génotoxique." Paris 5, 2002. http://www.theses.fr/2002PA05P616.
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La protéine oncosupressive p53 est un facteur de transcription inductible après stress génotoxiques (radiations, médicaments anti-cancéreux) et non-génotoxiques. Le WR1065 est un aminothiol utilisé en thérapie pour protéger les cellules saines des thérapies anti-cancéreuses. Ses effets protecteurs sont en partie dus à sa capacité à piéger les espèces réactives de l'oxygène, mais les bases moléculaires de sa spécificité pour les cellules normales ne sont pas connues. La protéine oncosuppressive p53, qui possède une sensibilité redox intrinsèque, est très souvent inactivée dans les cancers, elle pourrait représenter une cible importante du WR1065. Nos résultats montrent que dans notre modèle cellulaire, l'aminothiol WR1065 active p53 dans des cellules en culture, induit l'expression de ses gènes cibles, provoque un arrêt du cycle cellulaire en G1 dépendant de p53 et induit une cytoprotection au moins en partie dépendante de p53. Cette induction de p53 de caractérise par une voie signalétique qui diffère de celle utilisée par les agents endommageant l'ADN. La signalisation implique une voie de stress non génotoxique par l'intermédiaire de la protéine kinase JNK. JNK contrôle la stabilité et l'activité de p53 par un mécanisme complémentaire de celui utilisé par la plupart des agents cytotoxiques. .The p53 protein is a trancription factor activated in response to genotoxic stresses (radiation, chemotherapeutic drugs) and non-genotoxic stresses. WR1065 is an aminothiol used in therapy to protect healthy cells from the side effects of anti-cancer therapies. Its protective effects are thought to be mediated by its ability to scavenge reactive oxygen species, however, the molecular basis of its specificity for normal tissues is unknown. The p53 protein, which is sensitive to redox conditions, is often inactivated in cancers. P53 could be an important target of WR1065. Our results show that in our cellular model, WR1065 activates p53, which transactivates its target genes and induces a p53-dependent G1 arrest. Moreover, WR1065 induces at least in part, a p53-dependent cytoprotection. Induction of p53 is characterized by a signaling pathway which differs from the one used by DNA damaging agents. .
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Chaudhuri, Leena. "Manganese superoxide dismutase (MnSOD) 3'-untranslated region: a novel molecular sensor for environmental stress." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/2682.
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Eukaryotic gene expression is a complex process and can be controlled at the level of transcription, post-transcription or translation and post-translation. In recent years, there is a growing interest in understanding the role of 3'-untranslated region (UTR) in regulating mRNA turnover and translation. The 3'-UTR harbors the poly(A) signal and post-transcriptional regulatory sequences like miRNA and AU-rich elements (AREs). The presence of multiple poly(A) sites often results in multiple transcripts; shorter transcripts correlating with more protein abundance. Manganese superoxide dismutase (MnSOD) is a nuclear encoded and mitochondrial matrix localized antioxidant enzyme that converts mitochondrial generated superoxide to hydrogen peroxide. Human MnSOD has two poly(A) sites resulting in two transcripts: 1.5 and 4.2 kb. We hypothesize that the 3'-UTR of MnSOD regulates its mRNA and protein levels as well as activity in response to growth states and environmental stress. Results from a Q-RT-PCR assay showed a preferential accumulation of the shorter MnSOD transcript during quiescence, which correlated with an increase in MnSOD activity. The accumulation of the longer MnSOD transcript during proliferation was associated with a decrease in MnSOD activity. Log transformed expression ratio of the longer to shorter transcript was also higher in proliferating epithelial non-cancerous (mammary: MCF-10A) and cancer cells (mammary: MB-231, SUM 159; oral squamous: SQ20B, FaDu, Cal27; and lung: A549, H292), suggesting that the abundance of the longer transcript is independent of cellular transformation status, instead it is dependent on cellular growth state. Interestingly, the abundance of the longer transcript directly correlated with percent S-phase (R2=0.86). The shorter transcript was enriched in irradiated MB-231 cells. MCF-10A cells exposed to 2-(4-chlorophenyl)benzo-1,4-quinone (4-Cl-BQ), a metabolite of the environmental pollutant polychlorinated biphenyl 3, showed a significant decrease in the abundance of the 4.2 kb transcript due to a faster mRNA turnover, 14 h compared to 20 h in untreated control cells. The decrease in the 4.2 kb transcript levels was associated with a corresponding decrease in MnSOD protein levels and activity, which resulted in a significant inhibition of quiescent cells entry into the proliferative cycle. Deletion and reporter assays showed: (a) a significant decrease in reporter activity in constructs carrying multiple AREs that are present in the 3'-UTR of the longer MnSOD transcript; (b) irradiation increased the reporter activity of the constructs carrying the 3'-UTR sequence of the shorter MnSOD transcript and (c) N-acetyl-cysteine increased the reporter activity of constructs carrying multiple AREs. Because the longer transcript carries AREs, our results identified redox sensitive AREs as novel regulators of MnSOD transcript levels. We conclude that MnSOD 3'-UTR is a novel molecular sensor regulating MnSOD mRNA levels in response to different growth states and environmental stress. A better understanding of the 3'-UTR regulating gene expression could lead to the development of new molecular biology-based redox therapy designed to treat proliferative disorders.
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Schmerr, Martin J. "THE FUNCTIONAL SIGNIFICANCE OF AN ALTERNATELY SPLICED PRODUCT OF THE HDM2GENE." Ohio : Ohio University, 2007. http://www.ohiolink.edu/etd/view.cgi?ohiou1173370332.
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Wang, Di. "Extending Complex Event Processing for Advanced Applications." Digital WPI, 2013. https://digitalcommons.wpi.edu/etd-dissertations/235.
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Recently numerous emerging applications, ranging from on-line financial transactions, RFID based supply chain management, traffic monitoring to real-time object monitoring, generate high-volume event streams. To meet the needs of processing event data streams in real-time, Complex Event Processing technology (CEP) has been developed with the focus on detecting occurrences of particular composite patterns of events. By analyzing and constructing several real-world CEP applications, we found that CEP needs to be extended with advanced services beyond detecting pattern queries. We summarize these emerging needs in three orthogonal directions. First, for applications which require access to both streaming and stored data, we need to provide a clear semantics and efficient schedulers in the face of concurrent access and failures. Second, when a CEP system is deployed in a sensitive environment such as health care, we wish to mitigate possible privacy leaks. Third, when input events do not carry the identification of the object being monitored, we need to infer the probabilistic identification of events before feed them to a CEP engine. Therefore this dissertation discusses the construction of a framework for extending CEP to support these critical services. First, existing CEP technology is limited in its capability of reacting to opportunities and risks detected by pattern queries. We propose to tackle this unsolved problem by embedding active rule support within the CEP engine. The main challenge is to handle interactions between queries and reactions to queries in the high-volume stream execution. We hence introduce a novel stream-oriented transactional model along with a family of stream transaction scheduling algorithms that ensure the correctness of concurrent stream execution. And then we demonstrate the proposed technology by applying it to a real-world healthcare system and evaluate the stream transaction scheduling algorithms extensively using real-world workload. Second, we are the first to study the privacy implications of CEP systems. Specifically we consider how to suppress events on a stream to reduce the disclosure of sensitive patterns, while ensuring that nonsensitive patterns continue to be reported by the CEP engine. We formally define the problem of utility-maximizing event suppression for privacy preservation. We then design a suite of real-time solutions that eliminate private pattern matches while maximizing the overall utility. Our first solution optimally solves the problem at the event-type level. The second solution, at event-instance level, further optimizes the event-type level solution by exploiting runtime event distributions using advanced pattern match cardinality estimation techniques. Our experimental evaluation over both real-world and synthetic event streams shows that our algorithms are effective in maximizing utility yet still efficient enough to offer near real time system responsiveness. Third, we observe that in many real-world object monitoring applications where the CEP technology is adopted, not all sensed events carry the identification of the object whose action they report on, so called €œnon-ID-ed€� events. Such non-ID-ed events prevent us from performing object-based analytics, such as tracking, alerting and pattern matching. We propose a probabilistic inference framework to tackle this problem by inferring the missing object identification associated with an event. Specifically, as a foundation we design a time-varying graphic model to capture correspondences between sensed events and objects. Upon this model, we elaborate how to adapt the state-of-the-art Forward-backward inference algorithm to continuously infer probabilistic identifications for non-ID-ed events. More important, we propose a suite of strategies for optimizing the performance of inference. Our experimental results, using large-volume streams of a real-world health care application, demonstrate the accuracy, efficiency, and scalability of the proposed technology.
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Christian, Kyle. "The role of hnRNP A1 and hnRNP C1/C2 in the regulation of the stress responsive genes Cyp2a5/2A6 and p53." Doctoral thesis, Uppsala University, Department of Pharmaceutical Biosciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8722.
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The family of proteins known as heterogeneous nuclear ribonucleoproteins (hnRNPs) is large and diverse. Often, one and the same hnRNP will perform multiple cellular functions, leading to their description as “multifunctional proteins”. The two hnRNPs known as hnRNP A1 and hnRNP C1/C2 are multifunctional proteins found to affect the transcription, splicing, stability, and translation of specific genes’ mRNA. They are implicated in carcinogenesis, apoptosis, and DNA damage response mechanisms.
The aims of this thesis were to study the hnRNP A1 and hnRNP C1/C2 dependent regulation of two highly stress responsive genes, the tumor suppressor p53 and the cytochrome P450 enzyme Cyp2a5/CYP2A6. We identified hnRNP C1/C2 as a DNA damage induced binding protein towards the coding region of p53 mRNA, and found that while a specific cis binding site appears to have a positive function in p53 expression, interaction of hnRNP C1/C2 with this site represses the expression. The data suggest that two distinct molecular mechanisms exist for the down-regulation of p53 by hnRNP C1/C2. One mechanism, active during transcriptional stress, is dependent upon the aforementioned site, and the other, independent. We discuss how hnRNP C1/C2 dependent repression of p53 may play a role in apoptosis.
The data presented here further suggest that the transcriptional and post-transcriptional processes controlling the expression of the murine Cyp2a5 gene are linked via hnRNP A1, by performing functions in the nucleus as a transcription factor, or in the cytoplasmic compartment as a trans factor bound to the 3’UTR of the mRNA as needed. Our studies of the human ortholog of this gene, CYP2A6, suggest that this gene is regulated post-transcriptionally in a manner similar to that of its murine counterpart, via changes in mRNA stability and interaction of hnRNP A1 with its 3’ UTR.
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Recchia, Gustavo Henrique. "Identificação de genes diferencialmente expressos em feijoeiro envolvidos na resistência ao estresse hídrico." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/64/64133/tde-11102011-085802/.
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O Brasil é o segundo maior produtor de feijão, sendo a espécie mais cultivada o Phaseolus vulgaris L. Entre as três possíveis safras exploradas no Brasil, aquela que gera a maior produção é a da seca. Por outro lado, como a maioria das lavouras emprega pouca tecnologia, um dos problemas desta cultura é o estresse hídrico, que leva a uma redução na produtividade. Dessa forma, a identificação de genes que controlam os mecanismos de defesa e adaptação do feijoeiro à falta de água seria de grande utilidade. Nos últimos anos, muitas informações ômicas do feijoeiro foram geradas, criando uma visão integrada deste organismo e oferecendo uma complexa rede de interações entre genes e seus produtos. Este trabalho teve como objetivo central à identificação de genes diferencialmente expressos no sistema radicular de um genótipo de feijoeiro resistente ao estresse hídrico (BAT 477), quando submetido a uma interrupção de irrigação durante seu desenvolvimento. Foi construída uma biblioteca subtrativa de cDNA (SSH), que representou os genes diferencialmente expressos no genótipo resistente, utilizando-se como driver o genótipo Carioca 80SH (suscetível a seca). Foram obtidos 1572 reads válidos, sendo 931 destes singletons e 189 contigs com uma média de seis reads por cluster. A anotação das sequências foi conduzida via BLASTX, sendo consideradas para anotação somente os melhores resultados dos produtos gênicos similares com E- Value \'
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Drechsler, Frank Verfasser], Jan [Akademischer Betreuer] Schirawski, and Joost T. van [Akademischer Betreuer] [Dongen. "Suppressor of apical dominance1 of the maize pathogen Sporisorium reilianum induces outgrowth of subapical ears by induction of abiotic stress response / Frank Drechsler ; Jan Schirawski, Joost Thomas van Dongen." Aachen : Universitätsbibliothek der RWTH Aachen, 2016. http://d-nb.info/1162499222/34.
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Drechsler, Frank [Verfasser], Jan Akademischer Betreuer] Schirawski, and Joost T. van [Akademischer Betreuer] [Dongen. "Suppressor of apical dominance1 of the maize pathogen Sporisorium reilianum induces outgrowth of subapical ears by induction of abiotic stress response / Frank Drechsler ; Jan Schirawski, Joost Thomas van Dongen." Aachen : Universitätsbibliothek der RWTH Aachen, 2016. http://d-nb.info/1162499222/34.
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Novas, Anabela M. P. C. "Tennis training, upper respiratory tract infections and salivary immunoglobulin A." Thesis, Queensland University of Technology, 2003. https://eprints.qut.edu.au/36789/1/36789_Digitised%20Thesis.pdf.
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Upper respiratory tract infections (URTI) are one of the most common illnesses affecting the general population and particularly athletes, often reducing the individual capacity of physical performance. Epidemiological data suggest that intensive exercise, training and competition may increase susceptibility to respiratory infections. On the other hand, some studies defend that less active subjects may reduce their risk of URTI by engaging in moderate exercise training. Nevertheless, reports are not unanimous and frequently contained various limitations. The higher incidence of infections in elite athletes has been widely attributed to immune suppression induced by exhaustive exercise, however this has not been clearly demonstrated. The present series of studies aimed to investigate the relationship between physical activity and the incidence of URTI in young healthy females with a range of physical activity levels, from sedentary to elite athletes (tennis players). Additionally, it was intended to explore the temporal association between specific characteristics of tennis training and competition, the incidence of URTI, and salivary lgA levels (μg.mr1 ; μg.min-1 ) and changes, in elite female tennis players over a 12-week period. To accomplish the objectives described, a practical method for quantifying tennis play was validated and applied. Major findings of this research include the greater incidence of URTI symptomatology in girls with low or extremely high levels of physical activity as compared to those with moderate levels. Moreover, the incidence of URTI in elite tennis players was directly correlated with the training load and competition level, on a weekly basis. In the subsequent study, one hour of intense tennis play produced a significant drop in salivary lgA secretion rate (S-lgA), and the magnitude of the immune suppression was directly associated with the amount of training undertaken during the previous day and week (P<0.05). Nevertheless, tennis training did not seem to suppress chronically salivary lgA as positive correlations were found between resting salivary lgA levels of concentration and secretion rate, and the amount of training undertaken previously. Finally, it was noted a sharper post-exercise drop in S-lgA in occasions preceding an URTI episode compared to occasions when the infection did not develop subsequently (within 7 days). However, this parameter was not a specific predictor of URTI, in this cohort of athletes.
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Gilkes, Daniele M. "Multiple modes of MDMX regulation affect p53 activation." [Tampa, Fla.] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002312.
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