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1
Dorfi, Hans Robert. "Acoustoelasticity: stress identification based on ultrasonic measurements /". The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487856906257899.
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Howell, Geoffrey Peter. "Identification of plastic strain using thermoelastic stress analysis". Thesis, University of Southampton, 2017. https://eprints.soton.ac.uk/412636/.
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Identification of regions containing plastic strain arising from the welding process is performed through the application of thermoelastic stress analysis (TSA) and finite element (FE) modelling. An approach is developed that removes the requirement to have a physical reference specimen for the component studied by developing a 'synthetic reference bitmap' using finite element analysis. The regions containing plastic strain can be identified with TSA by collecting data from a 'reference' plastic strain free specimen from the TSA data and creating a resultant bitmap. Here, a synthetic bitmap is developed that mimics the thermoelastic response of a physical reference specimen. The approach is validated against physical reference specimens of different geometries and materials (AL2024 and 316L stainless steel) and is shown to accurately model the thermoelastic response. The newly developed synthetic bit map approach is applied to specimens containing welds and it is shown that the regions that contain plastic strain in the heat affected zone (HAZ) of a double bead welded 316L stainless steel specimen can be revealed. The predicted changes in thermoelastic response are compared to plastic strain predictions generated by thermomechanical modelling of the welded specimen and the distribution of plastic strain found by the TSA matches that given by the model. The relationship between the change in thermoelastic response and plastic strain has been investigated and the results suggest there is a change in the thermoelastic response as a result of plastic straining. However, uncertainties in the data resulting from detector noise and other errors mean that further development of the experiments and the equipment is required to provide a conclusive and quantitative relationship. It has also been demonstrated that TSA can be used outside of the laboratory in onsite trials in two coal fired power stations. Thermoelastic data was successfully recorded from pipe welds in-situ. To achieve this a new means of loading the pipes was devised based on vibration excitation, and the difficulties of performing surface measurements on heavily corroded pipes were overcome. The results from the onsite tests show that TSA can be used as an in-situ assessment technique and that is no longer restricted to being a laboratory based technique.
3
Chierichetti, Maria. "Combined analytical and experimental approaches to dynamic component stress prediction". Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/44850.
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In modern times, the ability to investigate the aeroelastic behavior of dynamic components on rotorcraft has become essential for the prediction of their useful fatigue life. At the same time, the aeroelastic modeling of a rotorcraft is particularly complex and costly.
Inaccuracies in numerical predictions are mostly due to imprecisions in the structural modeling, to the presence of structural degradation or to the limited information on aerodynamic loads.
The integration of experimental measurements on dynamic components such as rotor blades has the potential to improve fatigue estimation, augment the knowledge of the dynamic behavior and inform numerical models.
The objective of this research is the development of a combined numerical and experimental approach, named Confluence Algorithm, that accurately predicts the response of dynamic components with a limited set of experimental data.
The integration of experimental measurements into a numerical algorithm enables the continuous and accurate tracking of the dynamic strain and stress fields.
The Confluence Algorithm systematically updates the numerical model of the external loads, and mass and stiffness distributions to improve the representation and extrapolation of the experimental data, and to extract information on the response of the system at non-measured locations.
The capabilities of this algorithm are first verified in a numerical framework and with well-controlled lab experiments.
Numerical results from a comprehensive UH-60A multibody model are then compared with available experimental data. These analyses demonstrate that the integration of the Confluence Algorithm improves the accuracy of the numerical prediction of the dynamic response of systems characterized by a periodic behavior, even in presence of non-linearities. The algorithm enables the use of simplified models that are corrected through experimental data to achieve accurate tracking of the system.
4
Stålhand, Jonas. "Arterial mechanics : noninvasive identification of constitutive parameters and residual stress /". Linköping : Dept. of Mechanical Engineering, Univ, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/tek941s.pdf.
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Emery, Trystan Ross. "Identification of damage in composite materials using thermoelastic stress analysis". Thesis, University of Southampton, 2007. https://eprints.soton.ac.uk/51292/.
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A quantitative damage assessment methodology for composite materials has been achieved using Thermoelastic Stress Analysis (TSA). The TSA technique provides fullfield data which is collected in a non-contacting and real time manner. The damage assessment methodology proposed requires a means of calibrating and temperature correcting the thermoelastic signal; these are developed and presented in this thesis. The thermoelastic theory for calibrating thermoelastic data from orthotropic bodies has traditionally been based on a stress formulation. There are difficulties in calibrating orthotropic materials in this manner and an alternative calibration routine has been devised and validated. The calibration routine provides the thermoelastic theory as a function of strain and permits a simplified calibration route as the laminate strains are the basis and can be measured in a straightforward manner. During damage propagation in laminated structures the specimen heats. The increase in temperature has a significant effect on the thermoelastic data and necessitates that the thermoelastic data be corrected to remove the effect of temperature from the data. A routine is developed that enables the correction of the thermoelastic data in a point-bypoint manner. By combining the strain calibration and temperature correction procedures a damage assessment methodology has been devised. The application of the methodology is demonstrated on glass / epoxy laminate specimens that are fatigue damaged and the damage state assessed using this method; the extent and type of damage is verified qualitatively using visual inspection methods. The work described is applicable to any orthotropic material. The effect of fatigue damage is assessed by periodically collecting thermoelastic data during the specimen life. This data is analysed using damage metrics based on the calibrated strain obtained from the TSA. The wider application of the TSA damage assessment methodology is considered by assessing the ability to locate subsurface damage. A complementary IR technique is used in conjunction with TSA known as Pulse Phase Thermography (PPT). Initial studies demonstrate the ability to resolve the spatial extents of subsurface damage. The purpose of this step is to guide TSA to areas of concern that can subsequently be assessed using the damage metrics to characterise the effect of damage on the residual life of the component. The strain calibration and temperature correction methods that enable TSA to be applied quantitatively to damaged composite materials have not been accomplished prior to this work. They provide novel methods by which TSA data can be assessed, and their application is not restricted to damage studies alone. The ability to temperature correct TSA data has been shown to be of vital importance if thermoelastic data is to be compared in a quantitative fashion. The strain calibration procedure presented will enable thermoelastic studies to be reported quantitatively and expand the application of TSA particularly in validation studies. The damage assessment methodology presented represents a step forward in the application of TSA to the damage assessment of composite materials.
6
Li, Aiqing. "Identification Of Proteins Associated With Insect Diapause And Stress Tolerance". The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1211487603.
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Nguyen, Cong Uy. "Hybrid stress visco-plasticity : formulation, discrete approximation, and stochastic identification". Thesis, Compiègne, 2022. http://www.theses.fr/2022COMP2695.
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Dans cette thèse, une nouvelle approche est développée pour les problèmes de viscoplasticité et de dynamique non linéaire. En particulier, les équations variationnelles sont élaborées selon le principe de Helligner-Reissner, de sorte que les champs de contrainte et de déplacement apparaissent comme des champs inconnus sous la forme faible. Trois nouveaux éléments finis sont développés. Le premier élément fini est formulé pour le problème axisymétrique, dans lequel le champ de contraintes est approximé par des polynômes d’ordre inférieur tels que des fonctions linéaires. Cette approche donne des solutions précises spécifiquement dans les problèmes incompressibles et rigides. De plus, un élément fini de flexion de membrane et de plaque est nouvellement conçu en discrétisant le champ de contraintes en utilisant l’espace vectoriel de Raviart-Thomas d’ordre le plus bas RT0. Cette approche garantit la continuité du champ de contraintes sur tout un domaine discret, ce qui est un avantage significatif dans la méthode numérique, notamment pour les problèmes de propagation des ondes. Les développements sont effectués pour le comportement constitutif visco-plastique des matériaux, où les équations d’évolution correspondantes sont obtenues en faisant appel au principe de dissipation maximale. Pour résoudre les équations d’équilibre dynamique, des schémas de conservation et de décroissance de l’énergie sont formulés en conséquence. Le schéma de conservation de l’énergie est inconditionnellement stable, car il peut préserver l’énergie totale d’un système donné sous une vibration libre, tandis que le schéma décroissant peut dissiper des modes de vibration à plus haute fréquence. La dernière partie de cette thèse présente les procédures d’upscaling du comportement des matériaux visco-plastiques. Plus précisément, la mise à l’échelle est effectuée par une méthode d’identification stochastique via une mise à jour baysienne en utilisant le filtre de Gauss-Markov-Kalman pour l’assimilation des propriétés importantes des matériaux dans les régimes élastique et inélastiqueIn this thesis, a novel approach is developed for visco-plasticity and nonlinear dynamics problems. In particular, variational equations are elaborated following the Helligner-Reissner principle, so that both stress and displacement fields appear as unknown fields in the weak form. Three novel finite elements are developed. The first finite element is formulated for the axisymmetric problem, in which the stress field is approximated by low-order polynomials such as linear functions. This approach yields accurate solutions specifically in incompressible and stiff problems. In addition, a membrane and plate bending finite element are newly designed by discretizing the stress field using the lowest order Raviart-Thomas vector space RT0. This approach guarantees the continuity of the stress field over an entire discrete domain, which is a significant advantage in the numerical method, especially for the wave propagation problems. The developments are carried out for the viscoplastic constitutive behavior of materials, where the corresponding evolution equations are obtained by appealing to the principle of maximum dissipation. To solve the dynamic equilibrium equations, energy conserving and decaying schemes are formulated correspondingly. The energy conserving scheme is unconditional stable, since it can preserve the total energy of a given system under a free vibration, while the decaying scheme can dissipate higher frequency vibration modes. The last part of this thesis presents procedures for upscaling of the visco-plastic material behavior. Specifically, the upscaling is performed by stochastic identification method via Baysian updating using the Gauss-Markov-Kalman filter for assimilation of important material properties in the elastic and inelastic regimes
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Gauthier, David. "Financial stress and the business cycle". Thesis, Paris 1, 2019. http://www.theses.fr/2019PA01E057.
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Le fil directeur de cette thèse est l’étude du stress financier et en particulier de ses implications pour les fluctuations économiques. Comment expliquer l’impact des crises financières ? Quel est le rôle du système bancaire dans la propagation des chocs financiers ? Comment reconnaître et prévoir une crise financière ? Chacun des chapitres de cette thèse a pour but d’apporter des éléments de réponse nouveaux à ces grandes questions de la macroéconomie moderne. Dans le premier chapitre, réalisé en collaboration avec Yvan Bécard, nous estimons un modèle d’équilibre général dans lequel les banques ajustent leurs conditions de crédit selon leur capacité à liquider le collatéral de leurs emprunteurs. Nous montrons que les chocs de collatéral, c’est-à-dire des chocs affectant l’efficacité des banques à liquider le collatéral, permettent de comprendre le cycle des affaires américain et en particulier les variations de la consommation, des volumes de prêts et des taux d’emprunt. Les chocs de collatéral ont aussi la particularité de ressembler aux conditions de crédits bancaires observées ces trente dernières années pour les firmes et les ménages. Dans un second chapitre, je développe un modèle d’équilibre général où le système bancaire est organisé en compétition de monopole. J’utilise le modèle pour étudier le rôle de la compétition bancaire dans la propagation des crises financières. Je trouve qu’un faible degré de compétition du système bancaire peut limiter l’impact des chocs financiers lorsque l’efficacité de la politique monétaire est limitée par la borne à taux zéro. Dans le troisième chapitre, j’étudie l’évolution des choix de financement des firmes américaines en réponse à différent types de chocs économiques. Je trouve que seuls les chocs financiers impliquent des mouvements opposés pour les prêts bancaires et les prêts obligataires. J’utilise ce résultat couplé avec une méthode dite de restriction de signe pour identifier les chocs financiers dans un modèle VAR. Je trouve que les chocs ainsi identifiés expliquent une large partie du cycle des affaires et en particulier les deux dernières récessions. Finalement, cette stratégie d’identification me permet de calculer une mesure de stress financier capable de prédire l’évolution des spreads obligatairesIn this thesis, I investigate the implications of financial stress for economic fluctuations along several dimensions. What is it that makes financial crisis so disruptive? What is the role of the banking system in their propagation? How to identify and forecast financial distress? Each chapter brings new elements to complement the literature on these broad questions. In the first chapter of this thesis, written together with Yvan Bécard, we estimate a general equilibrium model where banks can adjust their lending standards for households and firms depending on their ability to liquidate the collateral of their borrowers. We find that collateral shocks, shocks that modify the liquidity of banks’ collateral, explain most of the US business cycle fluctuations for investment, consumption, loan volumes, and the credit spreads. In addition, the collateral shocks resemble measures of bank lending standard as observed over the past 30 years for households and firms. In the second chapter, I develop a model where the banking system is characterized by monopolistic competition and used to study the role of bank competition in the propagation of financial crises. I find that low competition in the banking system can dampen the impact of financial stress in situations where monetary policy is impeded by the ZLB. In the last chapter, I study the evolution of firm debt choices in response to different types of aggregate shocks. I find that only financial shocks imply opposite movements in bond and loan volumes. I use this result with sign-restriction methods to identify financial shocks in a VAR model. I find that financial shocks identified with bond and loan series explain a large share of the business cycle and especially the two last recessions. I also use the identification strategy to recover a measure of financial stress. This measure allows predicting the evolution of corporate bond spreads
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Martínez, Cebrián Gerard 1992. "Identification of novel histone marks required for the transcriptional stress response". Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668153.
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Upon environmental stresses such as temperature fluctuations or increases in osmolarity, yeast
Saccharomyces cerevisiae induces a transcriptional reprograming in order to survive and adapt to
the stress. Histone post-translational modifications are key regulatory elements known to modulate
transcription. By using a complete collection of histone mutants, we performed a high throughput
transcriptional screening to assess the histone residues required for a proper induction of stressresponsive fluorescent reporters upon heat and osmotic stress. From our screening, we could
extract general conclusions regarding the histone residues required for the stress-induced
transcription. We observed poor overlap between the residues necessary for heat and osmotic
stress. Results from the screening also suggested accessible and modifiable residues were more
prone to affect stress-induced transcription when mutated. Following such indications, we selected
the accessible and modifiable residues H4-S47 and H4-T30 as their mutation rendered
transcriptional defects upon osmotic and heat stress respectively. We validated and characterized
the extent of their transcriptional defects by northern blot and RNA sequencing. We also identified
and characterized Cla4 and Ste20 for H4-S47 and Ste11 for the H4-T30 as the putative kinases
phosphorylating these residues upon stress. In addition, the study of other residues identified in
the screening opens new possibilities to identify novel histone modifications relevant for the
transcriptional stress response.Durant estressos ambientals, com ara fluctuacions de temperatura o augment de l'osmolaritat, el llevat Saccharomyces cerevisiae indueix una reprogramació transcripcional per sobreviure i adaptar-se a l'estrès. Les modificacions post-traduccionals d'histones són elements reguladors clau coneguts per modular la transcripció. Utilitzant una col·lecció complet de mutants d'histona, vam realitzar un cribratge transcripcional a gran escala per a avaluar els residus d'histona necessaris per a una inducció adequada de senyalitzadors fluorescents que responen a estrès osmòtic i tèrmic. Del nostre cribratge, vam poder extreure conclusions generals sobre els residus d'histona necessaris per a la transcripció induïda per estrès. Vam observar poc solapament entre els residus necessaris per l’estrès tèrmic i osmòtic. Els resultats del cribratge també suggereixen que els residus accessibles i modificables, quan se’ls mutava, eren més propensos a afectar la transcripció induïda per l'estrès. Seguint aquestes indicacions, vam seleccionar els residus accessibles i modificables H4-S47 i H4-T30 ja que la seva mutació proporcionava defectes transcripcionals en estrès osmòtic i tèrmic respectivament. Vam validar i caracteritzar l’extensió dels seus defectes transcripcionals mitjançant norther blot i seqüenciació d’ARN. També vam identificar i caracteritzar Cla4 i Ste20 per a H4-S47 i Ste11 per a H4-T30 com a possibles quinases que fosforilen els dos residus en estrès. A més, l'estudi d'altres residus identificats en el cribratge obre noves possibilitats per identificar noves modificacions d'histona rellevants per a la resposta transcripcional en estrès.
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Herrmann, Leonie. "Identification and characterization of novel candidate molecules for posttraumatic stress disorder". Diss., Ludwig-Maximilians-Universität München, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-157327.
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Tripp, Charlotte E. "The identification and characterisation of novel suppressors of DNA replication stress". Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/20385/.
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Replication stress is present in cancers cells at higher than normal levels due to the increased proliferation caused by oncogene activation. This results in elevated levels of phosphorylated RPA2 (pRPA2) and DNA damage, which can ultimately result in genetic instability. By inhibiting suppressors of replication stress, it may be possible to target this cancer-specific phenotype to selectively kill tumour cells. Attempts were therefore made to develop a high throughput whole genome RNAi screen to detect increased endogenous levels of pRPA2 foci formation following gene knockdown, however, this proved unsuccessful. As a contingency measure a selected panel of kinases, identified as putative replication stress suppressors and potential druggable targets, were assessed for their ability to induce pRPA2 foci following gene knockdown. This approach identified several hits, which were then evaluated for their ability to preferentially kill cells lacking p53 signalling or overexpressing several clinically relevant oncogenes (Cyclin E, H-RAS and MYC-N). They were also assessed for their ability to potentiate the effects of the replication stress inducing drugs Gemcitabine and 5-Flurouracil as well as the PARP inhibitor Olaparib. In addition, the putative DNA damage repair factor CCDC15, which has been hypothesised to act in the resolution of replication impeding lesions, was also investigated as a potential replication stress suppressor. However, it does not appear to modulate DNA replication stress as its loss does not induce pRPA2 and the formation of DNA damage following its knockdown is independent of entry into S phase. Interestingly, depletion of CCDC15 sensitised certain cell lines to the effects of DNA crosslinking agents. Furthermore, knockdown of CCDC15 also slightly increased the formation of endogenous FANCD2 foci, but not in cells treated with DNA crosslinking agents. However, CCDC15-depleted cells exhibited delayed formation and resolution of RAD51 foci following DNA damage, which were not due to perturbations in cell cycle progression. Although CCDC15 appears to have little effect on the cell cycle distribution of cycling cells, its loss potentially delays re-entry into the cycle of cells paused in G1 phase.
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Müller-Rudorf, Alina [Verfasser], Anna Lena [Akademischer Betreuer] Illert i Robert [Akademischer Betreuer] Zeiser. "Crosstalk between the stress axes: Identification of the NIPA - p53 interaction". Freiburg : Universität, 2019. http://d-nb.info/1231232285/34.
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Adams, Leslie Allen. "Identification of early stress in a zebrafish model of familial ALS". The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1375373734.
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Simoni, L. "Gene-trap based identification of stress-activated genes in Arabidopsis thaliana". Doctoral thesis, Università degli Studi di Milano, 2007. http://hdl.handle.net/2434/56604.
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We employed a large scale gene trap approach to identify genes involved in osmotic stress responses. This strategy allows the analysis of stress-induced Gus expression, so we realized a selective screening of the EXOTIC (EXOn Trapping Insert Consortium) collection, by using Mannitol as selective agent. Moreover this strategy allows the analysis of cell-specific Gus expression, so we searched the EXOTIC lines for guard cell-specific activation of the reporter gene. We identified 3 lines that showed GUS expression only after exposure to Mannitol. In one line we mapped the transposon insertion in the At3g03350 gene, coding for a putative dehydrogenase/reductase protein. At3g03350 is specifically activated by Mannitol in roots, but it is constitutively expressed in the endosperm. We observed an arrest of embryo development at the globular stage in homozygous mutant seeds and verified that it is due to knockout of the At3g03350 gene. Both mutant embryo and endosperm did not show morphological defects. This phenotype suggests that the enzyme is involved in early seed development, particularly in energy metabolism.Subsequently we employed the gene trap approach to identify genes expressed in guard cells. We identified five lines in which the reporter gene was exclusively or preferentially expressed in guard cells. In 3 lines we mapped the DsG insertion in intergenic regions while in 2 lines we mapped the DsG insertion in two annotated genes. CYP86A2, coding for a cytochrome P450 protein, is involved in cutin monomers biosynthesis in stomata and we hypothesize that it is involved in stomatal responses to pathogen attacks. AtPDR3 (pleiotropic drug resistance 3) is an ABC transporter and we provide evidence that it is involved in the modulation of guard cell responses to ABA.
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Partridge, Charles Randal. "Identification and molecular characterization of novel genomic targets in oxidant-induced vascular injury". Diss., Texas A&M University, 2005. http://hdl.handle.net/1969.1/5024.
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Gene expression was examined in vascular smooth muscle cells to study the complex interaction between oxidative injury and the pathogenesis of vascular disease. Extensive vascular remodeling coupled to increased production of 8-epi-PGF2ñ nuclear localization of NFúB, and alterations in glutathione homeostasis were identified as major responses of the vascular wall to oxidative stress. Transcriptional profiling studies, supported by immunohistochemistry and in situ hybridization measurements, identified genes involved in adhesion and extracellular matrix deposition (ñ1 integrin, collagen), cytoskeletal rearrangements (ñ-smooth muscle actin, ñ-tropomyosin), and signal transduction (NFúB, osteopontin, and LINE) as targets of oxidant injury. In the case of osteopontin (OPN), elevation of OPN levels in vSMCs was shown to be mediated by redox-regulated transcriptional mechanisms. A 200bp region located in the 5' UTR of the osteopontin promoter was found to be responsive to oxidative stress. This regulatory region contained two distinct cis acting elements involved in promoter inducibility. These elements were tentatively identified as NFKB and TIEG-1 binding sites and shown to be highly responsive to hydrogen peroxide and chemical antioxidants. Collectively these studies answer central questions regarding the mechanisms underlying the vascular response to oxidative stress and the involvement of OPN in diseases of the vascular wall.
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Misiewicz, Michael. "Identification of a novel endoplasmic reticulum stress response element regulated by XBP1". Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116963.
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The Prion protein (PrP), which is the causative agent of scrapie diseases, has a still unclear physiological function, despite 30 years of research on its nature. However, a preponderance of evidence is beginning to support the idea that cellular prion protein (PrPC) has a pro-survival function. Here, we study the regulation of the prion protein gene (PRNP) in this context, as the regulation of the PRNP gene is not well understood. By homology, we identified in the PRNP a novel promoter element which bears similarity to the Endoplasmic Reticulum Stress Response Element (ERSE). This novel ERSE ("ERSE-26") is able to regulate PRNP endogenously in response to endoplasmic reticulum (ER) stress. In order to determine whether or not the ERSE-26 exists elsewhere in the genome and what is co-regulated with PRNP, we conducted a bioinformatic search and identified 38 other genes with an ERSE-26. Their expression was confirmed by treating cultured primary human neurons and MCF-7 cells with the ER stressors Brefeldin A, Tunicamycin and Thapsigargin and conducting Reverse Transcriptase PCR or Quantitative PCR. We found that the genes SESN2, GADD45B and PRNP were significantly upregulated, and others showed an upward trend. Finally, a luciferase reporter construct containing the ERSE-26 only was used to identify that the ER stress transcription factor XBP1 is a transcription factor that induces ERSE-26 activity. Finally, we conducted a literature search to determine what functions of the cell are co-regulated with PRNP with the ERSE-26. Oxidative stress response and pro-survival genes were found in the ERSE-26 genes and found to be the most upregulated by the ERSE-26, strengthening the case for PrPC as a pro-survival gene.La protéine Prion (PrP), qui est l'agent infectieux causant les encéphalopathies transmissibles, n'a pas toujours un rôle bien identifié dans la cellule, malgré 30 ans de recherche sur sa fonction physiologique. Cependant, de plus en plus de preuves commencent à impliquer PrP dans des fonctions de protection dans la cellule. Dans cette étude, nous avons étudié la régulation peu connue du promoteur du gène qui encode PrP (PRNP). Par homologie de séquence, nous avons identifié un nouvel élément dans le promoteur de PRNP qui ressemble à l'Endoplasmic Reticulum Stress Response Element (ERSE). Ce nouvel ERSE (appelé ERSE-26) est capable de réguler l'expression du PRNP de manière endogène en réponse au stress dans le réticulum endoplasmique (RE). Pour savoir si l'ERSE-26 existe ailleurs dans le génome et afin de trouver d'autres gènes régulé avec PRNP, nous avons fait une recherche bioinformatique dans le génome entier. Nous avons identifié 38 gènes contenant aussi un ERSE-26 dans leur promoteur. Afin de confirmer l'expression de ces gènes en réponse au stress ER, nous avons traité des cultures de neurones primaires humains et des cellules MCF-7 avec les activateurs du stress RE Brefeldin A, Tunicamycin et Thapsigargin, puis vérifié l'expression par Transcriptase Inverse PCR (RT-PCR) ou RT-PCR quantitative. Nous avons montré l'induction des gènes GADD45B, SESN2 et PRNP, et d'autres ont montré une tendance positive. Ensuite, un plasmide rapporteur luciferase contenant l'ERSE-26 seulement a été utilisé pour montrer que le facteur de transcription du stress ER XBP1 est un facteur de transcription responsable pour l'activité de l'ERSE-26. Finalement, nous avons fait une recherche dans la littérature afin de déterminer la fonction des gènes contenant ERSE-26. Les gènes répondant au stress oxydant et les gènes pro-survie étaient parmi les gènes ERSE-26, et aussi ont été le plus induits, soutenant le rôle protecteur du PrP dans la cellule.
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Barth, Alexander [Verfasser]. "Identification of genetic factors involved in the regulation of stress / Alexander Barth". Bonn : Universitäts- und Landesbibliothek Bonn, 2012. http://d-nb.info/1044082038/34.
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Edmond, Avril. "The identification, rationalization and correlation of physiological and behavioural responses to stress". Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414140.
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Raymondi, Luis Guillermo Antezana, Fabricio Eduardo Aguirre Guzman, Jimmy Armas-Aguirre i Paola Agonzalez. "Technological solution for the identification and reduction of stress level using wearables". IEEE Computer Society, 2020. http://hdl.handle.net/10757/656578.
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El texto completo de este trabajo no está disponible en el Repositorio Académico UPC por restricciones de la casa editorial donde ha sido publicado.In this article, a technological solution is proposed to identify and reduce the level of mental stress of a person through a wearable device. The proposal identifies a physiological variable: Heart rate, through the integration between a wearable and a mobile application through text recognition using the back camera of a smartphone. As part of the process, the technological solution shows a list of guidelines depending on the level of stress obtained in a given time. Once completed, it can be measured again in order to confirm the evolution of your stress level. This proposal allows the patient to keep his stress level under control in an effective and accessible way in real time. The proposal consists of four phases: 1. Collection of parameters through the wearable; 2. Data reception by the mobile application; 3. Data storage in a cloud environment and 4. Data collection and processing; this last phase is divided into 4 sub-phases: 4.1. Stress level analysis, 4.2. Recommendations to decrease the level obtained, 4.3. Comparison between measurements and 4.4. Measurement history per day. The proposal was validated in a workplace with people from 20 to 35 years old located in Lima, Peru. Preliminary results showed that 80% of patients managed to reduce their stress level with the proposed solution.
Revisión por pares
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Danquah, Agyemang. "Identification and validation of key factors of stress tolerance in Arabidopsis thaliana". Thesis, Paris 11, 2013. http://www.theses.fr/2013PA112052.
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Les stress abiotiques sont la cause principale des pertes de rendement agricole dans le monde. Aujourd'hui, le développement d'espèces capables de résister à ces stress est d'une importance majeure, en particulier dans le contexte de la croissance démographique actuelle et du changement climatique mondial. La phytohormone acide abscissique (ABA) contrôle divers processus cellulaires et induit un signal de protection des plantes contre les stress abiotiques. Parmi les différents évènements moléculaires impliqués dans la voie de signalisation de l'ABA, les cascades de signalisation des mitogen activated protein kinase (MAPK) jouent un rôle important dans la transmission du signal. Cependant, seulement un nombre réduit de MAPK ont été identifiées et caractérisées jusqu'à maintenant.J'ai isolé 2 proches homologues MEKK-like MAPKKKs d'Arabidopsis, MAPKKK17 et MAPKKK18, dont le niveau d'expression étaient fortement induit en réponse à l'ABA et aux stress abiotiques. Chez les mutants insensibles à l'ABA, pyr1/pyl1/pyl2/pyl4 et hab1G246D, l'expression ABA- et sel-dépendant de ces deux gènes était fortement réduite, indiquant que ces 2 kinases agissent en aval du complexe de signalisation de l'ABA. L'utilisation de plantes transgéniques exprimant, sous le contrôle de son propre promoteur, le gène MAPKKK18 fusionné à une étiquette PC2 ou YFP a permis de montrer par western blot que la protéine s'accumulait suite à un traitement à l'ABA et non pas en réponse au stress abiotiques. Ces données montrent que l'ABA est le régulateur majeur de la fonction de MAPKKK18.Suite à une approche de yeast-2-hybrid, j'ai pu identifier MKK3 comme la seule MAPKK interagissant avec MAPKKK17 and MAPKKK18. Ces résultats ont pu être confirmés via la technique de BiFC. Dans des protoplastes de mésophylle, il apparait que MAPKKK17 et MAPKKK18 activent MKK3, indiquant que ces deux gènes codent pour des kinases fonctionnelles. Afin d'apporter des preuves génétiques, j'ai isolé les T-DNA knockout mutants de ces 3 gènes. Des analyses de germination révèlent que mkk3-1 est hypersensible à l'ABA, au sel et au mannitol tandis que la lignée de surexpression Gain-de-fonction présente un phénotype opposé. Cependant, les doubles mutants mapkkk17/18 ne présentent pas de phénotype de germination. D'autres analyses ont pu montrer que mkk3-1 est sensible à la sécheresse et au stress salin tandis que les lignées surexpresseures sont plus tolérantes. Le double mutant mapkkk17/18 est quant à lui seulement sensible au NaCl. Pris dans leur ensemble, ces résultats indiquent que MAPKKK17/MAPKKK18 et MKK3 forment un complexe régulant la réponse des plantes aux stress abiotiques selon une voie dépendantes de l'ABAAbiotic stresses are the principal cause of crop failure worldwide. Developing crop plants better able to withstand these stresses has assumed great importance especially in the context of current population growth and global climatic change. The phytohormone abscisic acid (ABA) regulates diverse cellular processes and transduces signals to protect plants from abiotic stresses. Among the molecular elements working in ABA signaling, the mitogen activated protein kinase (MAPK) cascades play important roles in regulating the signaling network. To date, however, only a handful of MAPKs have been identified and characterized in ABA signaling. I isolated 2 closely related Arabidopsis MEKK-like MAPKKKs, MAPKKK17 and MAPKKK18, whose transcript expressions were highly induced by ABA and abiotic stresses. In 2 ABA insensitive mutants, pyr1/pyl1/pyl2/pyl4 and hab1G246D, the ABA- and NaCl-dependent expression of MAPKKK17 and MAPKKK18 was strongly reduced, indicating that these 2 kinases act downstream of the core ABA signaling complex. Western blot analysis of transgenic plants that expressed either a PC2 or YFP tagged MAPKKK18 under endogenous promoter revealed that MAPKKK18 protein strongly accumulated in response to ABA treatment but not in response to other abiotic stresses. This data indicated that ABA is the major regulator of MAPKKK18 protein function.Using yeast-2-hybrid approach, I identified MKK3 as the downstream MAPKK interactor of MAPKKK17 and MAPKKK18, and confirmed these interactions via BiFC assays. In mesophyll protoplasts, MAPKKK17 and MAPKKK18 activated MKK3, indicating that these 2 genes encode functional kinases. To provide genetic evidence of their functions, I isolated T-DNA knockout mutants of these genes. Germination assays reveal that mkk3-1 mutant was hypersensitive to ABA, NaCl and Mannitol stress whereas the over-expression line was resistant. The double homozygous mutant of mapkkk17/18 was not affected in germination. Further analysis revealed that mkk3-1 seedlings were sensitive to NaCl and terminal drought whereas the over-expression lines were resistant. The mapkkk17/18 seedlings were susceptible to NaCl but not terminal drought. Taken together, these results suggest that MAPKKK17/MAPKKK18 and MKK3 form complexes to regulate plant responses to abiotic stress in an ABA-dependent manner
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Bernardo, Letizia. "IDENTIFICATION AND CHARACTERIZATION OF PROTEINS INVOLVED IN BIOTIC STRESS RESISTANCE OF CEREALS". Doctoral thesis, Università degli studi di Padova, 2010. http://hdl.handle.net/11577/3426966.
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Leaf rust is one of the most important diseases of barley (Hordeum vulgare) and is caused by the biotrophic fungal pathogen Puccinia hordei. The rust fungi penetrate barley leaves through stomata and colonize cells of the mesophyll, then growing systemically through the leaf vascular tissue.
The leaf rust resistance gene Rph15 is of outstanding interest for resistance breeding because it confers resistance to over 350 Puccinia hordei isolates collected from around the world (Weerasena et al. 2004).
Plant-pathogen interactions activate many cellular signalling processes and, most likely, changes on protein accumulation and phosphorylation pattern of proteins play a pivotal role in plant responses to biotic stress. In this work, a proteomic approach was undertaken to study changes in total proteins accumulation and protein phosphorylation pattern in response to the leaf rust pathogen infection in two barley near isogenic lines, Bowman and Rph15, which differ for the introgression of the leaf rust resistance gene Rph15. Two infection time points, 24 hours and four days, were considered for the analysis.
No statistically significant differences were identified at the early time point, 24 hours post infection, for total and phosphorylated proteins.
At four days after inoculation, total protein analysis led to the identification of twenty-one protein spots significantly up or down regulated with a fold-change equal or higher than two following pathogen infection. Most of down-regulated proteins were found in the Rph15 near-isogenic line while no significantly differential protein abundance was recovered in the susceptible line. Nineteen out of 21 protein spots were characterized by LC-MS/MS analysis and found to be involved in photosynthesis, sugar metabolism, energy balance and defence.
Phosphoproteomics analysis was performed at four day after inoculation. A phosphoprotein enrichment methodology based on MOAC (metal oxide affinity chromatography) was optimized for subsequent 2DE analyses.La ruggine fogliare è una delle malattie più importanti della coltura dell'orzo (Hordeum vulgare) ed è causata dal patogeno fungino biotrofo Puccinia hordei. Il fungo penetra attraverso gli stomi delle foglie dell’orzo e colonizza le cellule del mesofillo, crescendo poi per via sistemica nei tessuti vascolari della foglia. Il gene Rph15 di orzo è di considerevole importanza per il miglioramento genetico della resistenza in quanto conferisce resistenza a più di 350 isolati di P. hordei provenienti da tutto il mondo (Weerasena et al. 2004). L’interazione pianta-patogeno attiva numerosi processi di signalling cellulare e, molto probabilmente, l’accumulo delle proteine e i cambiamenti nel pattern di fosforilazione delle proteine giocano un ruolo centrale nella risposta della pianta in seguito a stress biotico. In questo lavoro, un approccio di tipo proteomico è stato intrapreso per studiare i cambiamenti nei pattern proteici totali e delle proteine fosforilate in seguito a risposta alla ruggine fogliare in due linee quasi isogeniche di orzo, Bowman e la linea Rph15, che differiscono per l’ introgressione del gene Rph15. Due tempi di infezione, 24 ore e quattro giorni, sono stati presi in considerazione per le analisi. Nessuna differenza statisticamente significativa è stata individuate nel primo tempo di infezione precoce, a 24 ore dopo l’inoculo, sia per quanto riguarda le proteine totali che per le proteine fosforilate. A 4 giorni dall’infezione, l’ analisi delle proteine totali ha consentito di identificare ventuno spot proteici significativamente up o down regolati in risposta all’ infezione con un fold-change almeno di 2. La maggior parte delle proteine down-regolate sono state trovate nel campione infettato della linea isogenica contenente il gene di resistenza Rph15, mentre non è stata riscontrata alcuna differenza statisticamente significativa nel pattern proteico della linea isogenica suscettibile. Diciannove dei 21 spot proteici sono stati caratterizzati mediante analisi LC-MS/MS e identificati essere implicati in processi come fotosintesi, metabolismo degli zuccheri, bilancio energetico e risposte di difesa. L’analisi del fosfoproteoma è stata condotta a quattro giorni dopo l’inoculo. Una tecnica di arricchimento in fosfoproteine basata su MOAC (cromatografia di affinità mediante ossidi metallici) che è stata ottimizzata per la successiva analisi 2DE.
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El, Khatib Nour. "Identification des mécanismes moléculaires et physiopathologiques impliqués dans la dystrophie facioscapulohumérale". Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT039.
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La dystrophie musculaire facioscapulohumérale (FSHD) est une maladie autosomique dominante, caractérisée par une faiblesse et une atrophie progressive de certains muscles squelettiques. La FSHD est liée à une répression inefficace de la région des macrosatellites D4Z4 sur le chromosome 4, entraînant l'expression inappropriée dans le muscle squelettique, d’un gène à double homeobox 4 (DUX4), et la dérégulation des gènes avoisinants. La surexpression de DUX4 est responsable du phénotype atrophié des myotubes FSHD et induit la dérégulation de gènes impliqués dans la réponse au stress oxydant. Malgré les avancés majeures dans la compréhension du locus morbide, les mécanismes exacts impliqués dans la FSHD ne sont pas totalement compris et aucun traitement curatif n’est disponible. Cependant, de nombreuses données montrent le rôle prépondérant du stress oxydant dans la FSHD. Récemment, nous avons caractérisé la présence d’un stress oxydant dans les biopsies musculaires et les prélèvements sanguins des patients atteints de FSHD. Nous avons démontré que ce stress est corrélé à une altération de la fonction musculaire chez ces patients et qu’une supplémentation en antioxydants adaptée améliore la fonction musculaire et réduit les dommages oxydatifs. Par ailleurs, nous avons démontré que les myoblastes dérivés des biopsies FSHD sont plus sensibles à des agents pro-oxydants et présentent des défauts de différenciation. L’objectif de nos travaux est de caractériser les mécanismes moléculaires impliqués dans la FSHD afin de faciliter la mise en place d’approches thérapeutiques. Ce projet de thèse original réunit à la fois une approche fondamentale et clinique.Grâce à la mise en place d’un nouveau modèle in vitro de culture primaire de myoblastes de patients atteints de FSHD, nous avons montré la présence d’un stress oxydant dans ces myoblastes corroborant les observations précédemment obtenues aux niveaux systémiques et musculaires chez ces patients. Par ailleurs, les traitements par des agents pro-oxydants (paraquat et peroxyde d'hydrogène) ont un effet différentiel sur l’expression des enzymes antioxydantes par rapport aux contrôles suggérant un défaut dans les mécanismes d'adaptation au stress oxydant chez les patients atteints de FSHD.D’autre part, afin d'améliorer les procédures de réadaptation pour les patients atteints de FSHD, nous avons proposé d'étudier la faisabilité, la sécurité et l'efficacité de l’entraînement de force par électrostimulation neuromusculaire (ESNM) pour contrer la faiblesse musculaire des quadriceps chez ces patients. Cette étude, en cours, semble être une stratégie de réhabilitation prometteuse pour les patients atteints de FSHD et n’a montré aucun effets indésirables jusqu’à présentFacioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant disease, characterized by progressive weakness and atrophy of specific skeletal muscles. FSHD is linked to an inefficient repeat-mediated epigenetic repression of the D4Z4 macrosatellite repeat array on chromosome 4, resulting in the unappropriated expression in skeletal muscle of the double homeobox 4 (DUX4) retrogene. DUX4 overexpression leads to atrophic myotubes phenotype and dysregulation of antioxidant genes. Despite major progress in the understanding of the genetic locus, exact mechanisms that lead to FSHD defects are not completely understood and no curative treatment is available. However, several lines of evidence have proposed oxidative stress and myogenesis defect as the major biological processes affected in FSHD. Recently, we characterized oxidative stress in skeletal muscle biopsies and blood samples from patients with FSHD. We demonstrated that oxidative stress is associated with reduced physical performance in patients with FSHD and that antioxidants adapted strategy was effective to reduce oxidative stress and maintain muscle functions. Furthermore, satellite cell-derived myoblasts from these patients were more susceptible to pro-oxidant agents than control myoblasts and showed a defect in differentiation. The originality of this project relies on creating a synergy between basic and clinical research. The major goal of this work is to identify molecular mechanisms involved in FSHD oxidative stress in order to identify therapeutic approaches.Using in vitro cell model of FSHD, recently developed and optimized in our team, we demonstrate the presence of oxidative stress in FSHD primary myoblast cultures that corroborates previous observations at systemic and muscular levels. Furthermore, treatments with different pro-oxidant agents (paraquat and hydrogen peroxide) have a differential effect on the expression of antioxidant enzymes compared to controls, suggesting a defect in the oxidative stress adaptive response in FSHD myoblasts.Furthermore, in order to improve rehabilitation procedures for patients affected with FSHD, we proposed to investigate the feasibility, safety, and effectiveness of neuromuscular electrostimulation (NMES) strength training to counteract quadriceps muscle weakness in these patients. This ongoing study appears to be a promising rehabilitation strategy and shows no adverse effect for patients with FSHD
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Ugur, Zafer. "Mass Spectroscopic Identification and Quantification of Protein Carbonyls". VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/386.
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It is well established that free radical mediated oxidative stress plays a critical role in aging and age-related diseases. Among the post-translational protein modifications, carbonylation has attracted a great deal of attention due to its irreversible and irreparable nature. Despite the fact that protein carbonylation is associated with a series of physiological and pathological processes, there are still issues to be clarified such as why certain proteins are more vulnerable to modification, what are the locations of the protein modifications, and how does the nature of the oxidant affect the preferred site of modification. In this study, we will seek an answer to these questions and examine the global effect of oxidative stress on protein abundance. The study embraces three distinct specific aims. In the first, methods are developed for identifying sites of protein carbonylation. In the second specific aim, these methods are used to identify carbonylaytion sites in model proteins subjected to chemical oxidants. In the third aim, the focus is on a model organism, C. elegans, subjected to paraquat-induced oxidative stress. This is exploratory work and mass spectrometry is used to assess the impact of oxidative stress on the mitochondrial proteome.
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Salvo, Eliana. "Identification and functional analysis of genes associated with oncogenesis". Doctoral thesis, Università di Catania, 2014. http://hdl.handle.net/10761/1491.
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A RMD, mapping at the 6q26-27 region, which harbored a locus of senescence SEN6 was also implicated with tumorigenesis. One cDNA clone mapped within the RMD was recovered, it was a putative novel gene that encodes a protein without any homology with known sequences, named CATP (Cytomembrane-Associated Trafficking Protein). Modifications of its sequence across evolution, especially in Great Apes, were evaluated. Mutational analysis allowed to identify different alleles of the gene. Alleles were analyzed for association with some human pathologies. Functional analysis was performed in S. cerevisiae model, in order to clarify function of catp and the different effects of its alleles on yeast chronological lifespan. catp alleles affect yeast growth in distinguishable ways, moreover they showed different sensitivity to oxidative stress. So far a possible role of catp in senescence and/or tumorogenesis, throught ossidative stress responce and ROS level regulation, has been suggested.
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Brottsjö, Johan, i Marie Andersson. "Estetisk arbetskraft: negativ stress eller ökat välmående genom rollidentifikation". Thesis, Karlstads universitet, Avdelningen för företagsekonomi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-45405.
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Aesthetic labour means that a person with a certain physical aptitude is required. Previous researcher in this field has essentially been focusing on the business benefits from front-line employees as reinforcement to their image. Furthermore, researches have discussed how the employees experience the aesthetic requirements and have found negative effects. Motivation research have, on the other hand, shown that if a person can identify with the requirements it can create wellbeing, through the creation of role identification. Consequently, the research shows different effects of aesthetic requirements, which are this study’s starting point and the aesthetic labour will be illumine with motivations research. The purpose of this study is to illuminate aesthetic labour from a role identification perspective, to understand how the front-line employee is affected by the aesthetic requirements. In the theoretical framework the aesthetic labour will be explained and its negative effects, although also illumined by the research of motivation’s benefits. The method applied has a qualitative approach and the data has been collected by semi-structured interviews with seven employees in retail and the banking sector. The interviews have been transcribed and coded to enable interpretations of the data with the theoretical framework by categorizing and creating themes of the found phenomena. The result yielded four different levels on how the employees identified themselves in their role at work, which creates different reactions to behaviour (active identification, acknowledgment, acceptance and conflicting conciliation). In the discussion these levels where further developed in relation to and with the theoretical framework, concerning how result partially confirms previous research. Furthermore, the study’s findings in the field of aesthetic labour are discussed, which are that employees’ experience of aesthetic requirements is more complex and that additional levels of motivation in the role at work exists. The conclusion summarizes the main points of the study and outlines the study’s contribution of aesthetic labour, which is the understanding that additional levels of motivation in a role at work exists and that employees can be motivated without identification.
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Akter, Shamima. "Identification of common and unique stress responsive genes of Arabidopsis thaliana under different abiotic stress through RNA-Seq meta-analysis". Thesis, Virginia Tech, 2018. http://hdl.handle.net/10919/82036.
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Abiotic stress is a major constraint for crop productivity worldwide. To better understand the common biological mechanisms of abiotic stress responses in plants, we performed meta-analysis of 652 samples of RNA sequencing (RNA-Seq) data from 43 published abiotic stress experiments in Arabidopsis thaliana. These samples were categorized into eight different abiotic stresses including drought, heat, cold, salt, light and wounding. We developed a multi-step computational pipeline, which performs data downloading, preprocessing, read mapping, read counting and differential expression analyses for RNA-Seq data. We found that 5729 and 5062 genes are induced or repressed by only one type of abiotic stresses. There are only 18 and 12 genes that are induced or repressed by all stresses. The commonly induced genes are related to gene expression regulation by stress hormone abscisic acid. The commonly repressed genes are related to reduced growth and chloroplast activities. We compared stress responsive genes between any two types of stresses and found that heat and cold regulate similar set of genes. We also found that high light affects different set of genes than blue light and red light. Interestingly, ABA regulated genes are different from those regulated by other stresses. Finally, we found that membrane related genes are repressed by ABA, heat, cold and wounding but are up regulated by blue light and red light. The results from this work will be used to further characterize the gene regulatory networks underlying stress responsive genes in plants.Master of Science
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Schilirò, Elisabetta. "Stress proteins and identification of interacting partners in the resurrection plant Craterostigma plantagineum". [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=962336459.
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McLaughlin, Catherine A. "The role of identification in stress and well-being in burn care professionals". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ61468.pdf.
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Polato, Frederica. "Identification and characterisation of new genes important for p53- dependent, stress-induced apoptosis". Thesis, Open University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424595.
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Vieira, Natacha Cristiana dos Santos. "Identification of transcription factors regulating cork oak UNK1 gene during abiotic stress response". Master's thesis, ISA/UL, 2017. http://hdl.handle.net/10400.5/13961.
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Mestrado em Engenharia Agronómica - Protecção das Plantas - Instituto Superior de Agronomia - ULO sobreiro (Quercus suber L.) é uma árvore autóctone do Mediterrâneo que desempenha um papel-chave no seu ecossistema. A relevância económica da espécie, aliada ao seu declínio populacional, tanto devido a ameaças biológicas (ex.: P. cinnamomi), como abióticas (ex.: calor e secura), levaram a um acrescido interesse nesta árvore. Num projecto anterior (SuberStress) do laboratório de acolhimento foram selecionados 10 genes diferencialmente expressos em diferentes stresses aplicados separadamente, entre eles QsUNK1, de função desconhecida. Para a caracterização de QsUNK1 foram inicialmente determinadas as sequências genómica (2264pb com três intrões de 819, 486 e 506pb) e do promotor (identificados 1220pb). Por “Yeast-1-Hybrid” (Y1H) identificaram-se cinco potenciais factores de transcrição (TFs) por rastreio de uma biblioteca de cDNAs de stresse abiótico (calor e secura) com “baits” de levedura contendo parte do promotor (-797 a -260pb). Para a validação funcional deste gene utilizaram-se duas linhas descritas como mutantes no gene homólogo em Arabidopsis (AT3G55646). Plântulas de Arabidopsis (selvagens e mutantes) e plantas de sobreiro foram sujeitas a ensaios de calor, por choque ou aclimatação. Por análise da expressão em sobreiro, verificou-se indução de QsUNK1 em ambas as condições de stresse. Em Arabidopsis, AtUNK1 não revelou variações de expressão claras, pelo que o gene não está a ser silenciado. Igualmente não se confirmou o “knockout” nas duas linhas analisadas. Para validar a ligação TF-promotor e efectuar estudos funcionais, foram desenvolvidas linhas embriogénicas de sobreiro
N/A
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Bickel, Cory Lyn. "Identification of Genomic Regions Involved in Stress Responsiveness in Flax by Genetic Mapping". Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1301676557.
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Martini, Cecilia. "Identification and characterization of new virulence factors in Enterococcus faecalis". Caen, 2014. http://www.theses.fr/2014CAEN2064.
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Dans cette étude, nous nous sommes focalisés sur l'identification et la caractérisation de nouveaux facteurs de virulence chez Enterococcus faecalis. SlyA est un régulateur transcriptionnel impliqué dans la virulence, la persistance dans les reins et le foie, ainsi que dans la survie à l'intérieur des macrophages. Nous avons recherché les conditions de stress susceptibles d’affecter la transcription du gène slyA. Parmi plusieurs contraintes testées, nous avons montré que les sels biliaires induisaient l'expression de slyA. Des études transcriptomiques avaient suggéré que SlyA pouvait être un répresseur de l'expression de facteurs de virulence. Ainsi, parmi les gènes surexprimés dans le mutant ΔslyA, un ou plusieurs pourraient être impliqués dans le phénotype «d’hyper-virulence» observé pour le mutant. Ainsi, EF_3001 (renommé pmvE) apparaît comme un candidat intéressant. Nous avons en effet montré qu’il joue un rôle dans la virulence, ainsi que sa persistance dans l'intérieur de l'hôte. De plus, il apparait que PmvE est important pour la croissance d’E. Faecalis en présence de polyamines et qu‘elle est capable d’interagir avec la putrescine. Nous avons également mis en évidence deux nouvelles protéines de surface impliquées dans l'adhésion et la colonisation. La première, EfbA, contribuant probablement à un tropisme accru pour les cellules de rein et qui joue un rôle dans les infections urinaires. La seconde, CspR, est une protéine de choc froid capable de se lier à l’ARN et qui peut être localisée à la surface des cellules. Outre son implication dans la réponse à de basses températures, CspR est également impliquée dans la survie à long terme et la virulenceIn this study, we focused on the identification and characterization of new virulence factor in E. Faecalis. SlyA is a transcriptional regulator, involved in the virulence, persistence in mouse kidneys and liver, and survival inside peritoneal macrophages. We attempt to find stress conditions that affect the transcription of slyA. Among several stresses tested we found that bile salts induced expression of slyA. In addition, transcriptomic results performed to identify SlyA-regulated genes suggested that SlyA could be a repressor for the expression of virulence factors. It is then tempting to speculate that among genes overexpressed in the ΔslyA mutant, one or more could play a role in the more virulent phenotype observed for the mutant. Then, EF_3001 (renamed pmvE) may be an interesting candidate. We found that PmvE plays a role in the virulence of E. Faecalis as well as in its persistence inside the host. In addition, PmvE was important for growth in presence of polyamines and that it was able to interact with putrescine. Bacterial adherence is an important step in the process of disease that facilitates colonization in the host. We characterized two new surface proteins, involved in the adherence and colonization. The first one, EfbA, localized on the enterococcal cell surface, probably contributing to an increased tropism for the kidney for the bacteria, and which has a role in UTIs. The second, CspR, is cold shock RNA binding protein located in both the cytoplasm and the surface of E. Faecalis. In addition to its involvement in the cold-shock response and in the long-term survival, CspR plays a role in the virulence of E. Faecalis
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Jonavičienė, Kristina. "Genetic diversity of Phleum spp. and identification of genes involved in water stress response". Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2012. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2011~D_20120508_105857-18465.
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Genetic material of Lithuanian origin varieties, breeding lines and wild ecotypes representing P. pratense, P. bertolonii and P. phleoides species were studied for the most important agro-morphological and feeding value indicators as well as at the genetic level employing different biochemical–molecular markers. The water stress experiment clearly demonstrated the existence of different levels of water stress response in Phleum species, suggesting that P. phleoides might have evolved under conditions of limited water availability. “Blind” mapping by HRM was used successfully to map water stress response genes of timothy in the perennial ryegrass mapping population. In total, 12 putative water stress response genes were mapped in seven perennial ryegrass linkage groups.Pasitelkus agromorfologinius, kokybės ir biocheminius – molekulinius metodus ištirtos lietuviškos kilmės pašarinių, žemaūgių bei stepinių motiejukų veislės, selekcinės linijos bei laukiniai ekotipai. Fiziologiniai sausros atsparumo tyrimų rezultatai įrodė, kad stepiniai motiejukai turi geriau išvystytą atsparumo sausrai mechanizmą. Pirmą kartą motiejukuose aptikti ekspresuojami atsparumo sausrai kandidatiniai genai HRM metodu sužymėti daugiametės svidrės genolapyje.
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He, Jia. "Identification and Characterization of Metal Uptake Loci in Porphyromonas gingivalis". Available to VCU users at :, 2007. http://hdl.handle.net/10156/1263.
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Pope, Simon Alexander Samuel. "The analysis and identification of urinary metabolites of vitamin E in man using mass spectrometry and chemical synthesis". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247078.
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Vitamin E (a-tocopherol) is the major lipid soluble antioxidant in vivo and is important for maintaining the integrity of cell membranes. Oxidative stress, defined as an imbalance between oxidants and antioxidants, has been implicated in the aetiology of numerous diseases. There is, therefore, interest in establishing methods to measure oxidative stress. It has been suggested that metabolites of vitamin E such as atocopheronolactone (a-TL), with an oxidised chroman ring, may be an indicator of in vivo oxidative stress and that the carboxyethyl-hydroxychromans (CEHCs), with a shortened phytyl side chain, may provide a measure of adequate or excess vitamin E status. However, doubts have been raised about the authenticity of a-TL since a-CEHC has been shown to be artefactually oxidised to a-TL in many of the procedures described. In the course of the current study a relatively simple method using gas chromatographymass spectrometry (GC-MS) was developed which allowed the reproducible measurement of a wide range of deconjugated vitamin E metabolites in urine. This method was used to study the urinary metabolites produced by normal subjects before and after supplementation with vitamin E. The CEHCs were confirmed as the major urinary metabolites of vitamin E, a-TL was detected and a novel group of metabolites, the carboxymethylbutyl-hydroxychromans (CMBHCs), was also tentatively identified. A range of conjugated (sulphated and glucuronidated) and free metabolites of vitamin E were synthesised chemically and used to a) confirm the identity of (x-CMBHC, b) provide standards for GC-MS and tandem mass spectrometry, c) elucidate the mechanism of artefactual oxidation and to develop new methods for the precise measurement of endogenously produced a-TL and d) investigate the type of conjugation of the various metabolites of vitamin E in human urine.
36
Boudsocq, Marie. "Identification de protéines kinases activées par des contraintes osmotiques chez Arabidopsis thaliana : étude des familles AtSK et SnRK2". Paris 11, 2005. http://www.theses.fr/2005PA112008.
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Dans des cultures cellulaires et des plantules d'Arabidopsis thaliana, l'hyperosmoiarité active 4 protéines kinases calcium-indépendantes n'appartenant pas à la famille MAPK. L'identification des familles de kinases impliquées a été entreprise en utilisant 2 anticorps famille-spécifiques dirigés chacun contre l'une des 2 familles candidates : les AtSK (Arabidopsis thaliana Shaggy-like kinase) et les SnRK2 (sucrose non-fermenting 1-related protein kinase 2). Des analyses de western-blot ont montré que les 2 anticorps reconnaissaient spécifiquement les 10 protéines de la famille contre laquelle ils ont été dirigés. Des expériences d'immunoprécipitation suivies d'activité kinase ont montré que les stress hyperosmotiques activaient au moins une AtSK et 4 SnRK2. Les poids moléculaires des SnRK2 immunoprécipitées correspondent à ceux des kinases activées et visualisées dans les extraits bruts, indiquant qu'il s'agit des mêmes protéines. L'identification moléculaire de ces protéines SnRK2 a ensuite été entreprise par expression transitoire en protoplastes. Toutes les kinases de la famille excepté SnRK2-9 sont activées par l'hyperosmolarité et la salinité, indiquant un rôle important de la famille SnRK2 dans la signalisation osmotique. En revanche, le froid n'active aucune des protéines SnRK2 et l'acide abscissique n'en active que 5. Ainsi, la signalisation osmotique impliquant les protéines SnRK2 pourrait emprunter deux voies de transduction, l'une ABA-dépendante et l'autre ABA-indépendante. Enfin, la recherche d'éléments de transduction en amont des SnRK2 a montré que les 9 kinases étaient activées par phosphorylation et de façon indépendante du calcium extracellulaireHyperosmotic stresses activate four calcium-independent protein kinases which do not belong to the MAPK family, in Arabidopsis thaliana cell suspensions. Similar activation profiles were also observed in seedlings exposed to hyperosmolarity. The identification of the involved kinase families was investigated using family-specific antibodies raised against two candidate families: the Arabidopsis thaliana Shaggy-like kinases (AtSK) and the sucrose non-fermenting 1-related protein kinases 2 (SnRK2). Immunoblot analyses performed on recombinant proteins showed that the two antibodies were able to specifically recognize the ten members of their family. Using immunoprecipitation followed by kinase assay, hyperosmolarity was shown to activate at least one AtSK and four SnRK2 proteins. Molecular masses of the immunoprecipitated SnRK2 proteins corresponded to those of the activated proteins visualized in crude extracts, indicating that they are the same kinases. Molecular identification of the activated SnRK2 was investigated by transient expression assays in Arabidopsis protoplasts. All SnRK2 except SnRK2-9 were activated by both hyperosmotic and saline stresses, indicating an important role of the SnRK2 family in osmotic signaling. In contrast, cold treatment did not activate any of the SnRK2 and abscisic acid only activated five of them. Thus, osmotic signaling involving SnRK2 proteins could imply one ABA-dependent and one ABA-independent pathways. Finally, research for SnRK2 upstream elements indicated that the nine SnRK2 kinases were hyperosmottcally activated by phosphorylation and independently of extracellular calcium
37
Turki, Ahmed. "Identification des mécanismes physiopathologiques de la dystrophie facioscapulohumérale : rôle de la mitochondrie et du stress oxydant". Thesis, Montpellier 1, 2012. http://www.theses.fr/2012MON1T024.
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La dystrophie facioscapulohumérale (FSHD) est une dystrophie musculaire autosomique dominante, dégénérative et progressive. Les traitements élaborés jusqu'à présent n'ont pas réussi à améliorer le quotidien des patients FSHD. Plusieurs études se sont focalisées sur les mécanismes moléculaires de cette pathologie, néanmoins plusieurs d'entre elles sont contradictoires. La vision actuelle de la FSHD est celle d'une pathologie due à un mécanisme épigénétique complexe et les mécanismes moléculaires responsables de cette pathologie sont encore mal connus. Plusieurs analyses comparatives des profils d'expression des ARNm et des protéines de muscles de patients atteints de FSHD et de contrôles ont permis de montrer que plusieurs gènes impliqués dans le stress oxydant sont dérégulés de façon spécifique dans les muscles FSHD. Nos travaux ont permis de montrer dans la FSHD, aussi bien au niveau systémique, musculaire et cellulaire (cultures primaires musculaires) une augmentation des dommages oxydatifs qui se traduisent par une augmentation des peroxydes lipidiques et protéines oxydées, associés à une altération des défenses antioxydantes. Ce stress oxydant dans les biopsies musculaires et cultures primaires musculaires est associé à un dysfonctionnement mitochondrial. Des analyses plus fines sur l'action des espèces réactives de l'oxygène et leurs sources pourraient contribuer à une meilleure compréhension des bases physiopathologiques de la FSHD et permettre la sélection de thérapeutiques adaptées aux anomalies des patients FSHDFacioscapulohumeral muscular dystrophy (FSHD) is an autosomal inherited muscular dystrophy. Actually no treatment led to improve the quality of life. Many studies have been focused on the molecular mechanisms of this disease, several of them were contradictory. The present view of the FSHD seems to be due to a complex epigenetic mechanism. Actually, no gene has been identified. Several comparative studies permit the identification of many genes involved in oxidative stress, deregulated in FSHD myoblasts and biopsies in comparison to healthy ones. Analysis of oxidative stress markers show that patients with FSHD present increased oxidative damage in blood as well as in biopsy muscle and muscular primary cell culture associated with altered antioxidant enzyme defenses. Oxidative stress is also associated with mitochondrial dysfunction. Complementary studies focusing in pathway of reactive oxygen species would contribute to a better understanding of pathophysiological bases of FSHD in order to establish a very helpful therapeutics for FSHD patients
38
Tarek, El-bashiti. "Trehalose Metabolism In Wheat And Identification Of Trehalose Metabolizing Enzymes Under Abiotic Stress Conditions". Phd thesis, METU, 2003. http://etd.lib.metu.edu.tr/upload/3/1102482/index.pdf.
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Trehalose (α
-D-glucopyranosyl-1,1-&
#945
-D-glucopyranoside) is a non reducing disaccharide of glucose that occurs in a large variety of organisms, ranging from bacteria to invertebrate animals, where it serves as an energy source or stress protectant. Until recently, only few plant species, mainly desiccation tolerant &
#8216
resurrection&
#8217
plants, were considered to synthesize trehalose. Although most plant species do not appear to accumulate easily detectable amounts of trehalose, the discovery of genes for trehalose biosynthesis in Arabidopsis and in a range of crop plants suggests that the ability to synthesize trehalose is widely distributed in the plant kingdom. In this study, three wheat cultivars (Triticum aestivum L.) Tosun, Bolal (stress tolerant) and Ç
akmak (stress sensitive) were analysed for the presence of trehalose. Using gas chromatography-mass spectrometry (GC-MS) analysis, trehalose was unambiguously identified in extracts from seeds and seedlings of three different wheat cultivars (Bolal, Tosun and Ç
akmak). The trehalose amount was quantified by high performance liquid chromatography connected with refractory index detector. Effects of drought and salt stress on trehalose contents of wheat cultivars were studied at seedling level and trehalose analysis was achieved both on shoot and root tissues. It was found that trehalose had accumulated under salt and drought stress conditions in all wheat cultivars. The highest trehalose accumulation was detected in roots of Bolal cultivar under drought stress condition. Furthermore, trehalose metabolizing enzymes
trehalose-6-phosphate synthase (TPS) and trehalase enzyme activities were measured in roots and shoots of Bolal and Ç
akmak cultivars under control, salt and drought stress conditions. The most interesting results that we found that TPS activity sharply increased under stress conditions. The activity of TPS in roots under drought stress condition was the highest and reached to 3-4 times of its activity under control condition. The increase in the activity of TPS showed parallelism with trehalose accumulation under stress condition. Trehalase activity in Bolal cultivar decreased under both salt and drought stress conditions, however there was no significant change in trehalase activity of Ç
akmak variety.
39
Pirot, Pierre. "Identification and characterization of the endoplasmic reticulum (ER)-stress pathways in pancreatic beta-cells". Doctoral thesis, Universite Libre de Bruxelles, 2007. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210623.
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The endoplasmic reticulum (ER) is the organelle responsible for synthesis and folding of secreted and membranous protein and lipid biosynthesis. It also functions as one of the main cellular calcium stores. Pancreatic beta-cells evolved to produce and secrete insulin upon demand in order to regulate blood glucose homeostasis. In response to increases in serum glucose, insulin synthesis represents nearly 50% of the total protein biosynthesis by beta-cells. This poses an enormous burden on the ER, rendering beta-cells vulnerable to agents that perturb ER function. Alterations of ER homeostasis lead to accumulation of misfolded proteins and activation of an adaptive response named the unfolded protein response (UPR). The UPR is transduced via 3 ER transmembrane proteins, namely PERK, IRE-1 and ATF6. The signaling cascades activated downstream of these proteins: a) induce expression of ER resident chaperones and protein foldases. Increasing the protein folding capacity of the ER; b) attenuate general protein translations which avoids overloading the stressed ER with new proteins; c) upregulate ER-associated degradation (ERAD) genes, which decreases the unfolded protein load of the ER. In severe cases, failure by the UPR to solve the ER stress leads to apoptosis. The mechanisms linking ER stress to apoptosis are still poorly understood, but potential mediators include the transcription factors Chop and ATF3, pro-apoptotic members of the Bcl-2 familly, the caspase 12 and the kinase JNK. Accumulating evidence suggest that ER stress contributes to beta-cell apoptosis in both type 1 and type 2 diabetes. Type 1 diabetes is characterized by a severe insulin deficiency resulting from chronic and progressive destruction of pancreatic beta-cells by the immune system. During this autoimmune assault, beta-cells are exposed to cytokines secreted by the immune cells infiltrating the pancreatic islets. Our group has previously shown that the pro-inflamatory cytokines interleukin-1beta (IL1-beta and interferon-gamma (IFN-gamma), via nitric oxide (NO) formation, downregulate expression and function of the ER Ca2+ pump SERCA2. This depletes beta-cell ER Ca2+ stores, leading to ER stress and apoptosis. Of note, IL1-beta alone triggers ER stress but does not induce beta-cell death, while IFN-gamma neither causes ER stress nor induces beta-cell death. Together, these cytokines cause beta-cell apoptosis but the mechanisms behind this synergistic effect were unknown.
Type 2 diabetes is characterized by both peripheral resistance to insulin, usually as a result of obesity, and deficient insulin secretion secondary to beta cell failure. Obese patients have high levels of circulating free fatty acids (FFA) and several studies have shown that the FFA palmitate induces ER stress and beta-cell apoptosis.
In the present work we initially established an experimental model to specifically activate the ER stress response in pancreatic beta-cells. For this purpose, insulinoma cells (INS-1E) or primary rat beta-cells were exposed to the reversible chemical SERCA pump blocker cyclopiazonic acid (CPA). Dose-response and time course experiments determined the best conditions to induce a marked ER stress without excessive cell death (<25%).
The first goal of the work was to understand the synergistic effects of IL1-beta and IFN-gamma leading to pancreatic beta-cell apoptosis. Our group previously observed, by microarray analysis of primary beta-cells, that IFN-gamma down-regulates mRNAs encoding for some ER chaperones. Against this background, our hypothesis was that IFN-gamma aggravates beta-cell ER stress by decreasing the ability of these cells to mount an adequate UPR. To test this hypothesis, we investigated whether IFN-gamma pre-treatment augments CPA-induced ER stress and beta cell death. The results obtained indicated that IFN-gamma pre-treatment potentiates CPA-induced apoptosis in INS-1E and primary beta-cells. This effect was specific for IFN-gamma since neither IL1-beta nor a low dose CPA pre-treatment potentiated CPA-induced apoptosis in INS-1E cells. These effects of IFN-gamma were mediated via the down regulation of genes involved in beta cell defense against ER stress, including the ER chaperones BiP, Orp150 and Grp94 as well as Sec61, a component of the ERAD pathway. This had functional consequences as evidenced by a decreased basal and CPA-induced activity of a reporter construct for the unfolded protein response element (UPRE) and augmented expression of the pro-apoptotic transcription factor Chop.
We next investigated the molecular regulation of the Chop gene in INS-1E cells in response to several pro-apoptotic and ER stress inducing agents, namely cytokines (IL1-beta and IFN-gamma), palmitate, or CPA. Detailed mutagenesis studies of the Chop promoter showed differential regulation of Chop transcription by these compounds. While cytokines (via NO production)- and palmitate-induced Chop expression was mediated via a C/EBP-ATF composite and AP-1 binding sites, CPA induction required the C/EBP-ATF site and the ER stress response element (ERSE). Cytokines, palmitate and CPA induced ATF4 protein expression and further binding to the C/EBP-ATF composite site, as shown by Western blot and EMSA experiments. There was also formation of distinct AP-1 dimers and binding to the AP-1 site after exposure to cytokines or palmitate.
\
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished
40
Meves, Alexander [Verfasser]. "Identification and Characterization of Stress-Activated Signaling Networks in Human Primary Keratinocytes / Alexander Meves". Aachen : Shaker, 2004. http://d-nb.info/1181603315/34.
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Gonzalez, Marquez Humberto. "Réponse au stress acide chez Streptococcus thermophilus : purification, identification et caractérisation d'une protéine surexprimée". Nancy 1, 1997. http://docnum.univ-lorraine.fr/public/SCD_T_1997_0018_GONZALEZ_MARQUEZ.pdf.
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Streptococcus thermophilus a suivi différentes pressions de sélection (stress) lors des protocoles de fabrication ; par exemple, les montées et descentes de la température et l'acidification du milieu. Dans ce travail, nous mettons en évidence, dans un premier temps, que Streptococcus thermophilus PB18 surexprime une protéine de masse moléculaire apparente de 16 kDa quand elle arrive en phase stationnaire de croissance en milieu M17 (lactose 20g/l, pH≤5). Nous avons également observé que cette protéine est surexprimée quand la croissance est arrêtée brusquement par addition d'acide lactique exogène, afin d'obtenir un pH inferieur à 5,0. Des études d'électrophorèse bidimensionnelle ont montré que cette protéine correspond à une famille de 4 spots protéiques dont le point isoélectrique est compris entre 5 et 5,5 unités de pH. Dans un second temps, les extrémités N-terminales des deux spots principaux obtenus en électrophorèse bidimensionnelle ont été séquencées. Les séquences se sont révélées identiques entre elles. La comparaison de la séquence avec les banques de données a permis de montrer l'identité avec la séquence d'une protéine hypothétique de la souche japonaise de S. Thermophilus No. 29 codée par le plasmide de 3,5 Kb, pST1. Enfin, nous avons mis au point un protocole de purification qui nous a permis de l'obtenir avec une haute homogénéité relative. Le protocole présente quatre étapes de purification : 1) précipitation des protéines au sulfate d'ammonium, 2) chromatographie d'échange anionique, 3) chromatographie de phase inverse et 4) chromatographie de phase inverse isocratique. La séquence putative de la protéine de 16 kDa a été vérifiée par dégradation d'Edman et par spectrométrie de masse des fragments d'hydrolyse enzymatique. Une étude comparative des séquences a montré que la protéine de 16 kDa serait homologue à des protéines de choc thermique de Classe I chez les végétaux, et plus spécifiquement à la famille des Hsp20. Ceci est la troisième petite protéine de choc thermique de Classe I décrite pour des bactéries après la Hsp 18 de Clostridium acetobutylicum et son homologue de Lactobacillus delbrueckii.
42
Rezaïki, Lahcen. "Métabolisme respiratoire chez Lactococcus lactis dans un environnement oxydant et identification de composants de la chaîne respiratoire". Paris 11, 2004. http://www.theses.fr/2004PA112133.
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Lactococcus lactis est tres utilisee dans l'industrie agroalimentaire. A cette fin elle a ete principalement etudiee pour ses capacites fermentaire. Le dogme des bacteries lactiques exclusivement fermentaire est caduque depuis qu'il a ete montre que l. Lactis est capable d'adopter un metabolisme respiratoire en presence d'heme exogene et d'oxygene. Dans ces conditions un doublement de la biomasse, une augmentation du ph et la survie largement augmentee, sont observees par rapport a un metabolisme fermentaire. Mon projet de these s'est focalise sur le metabolisme respiratoire de l. Lactis et s'est articule autour de deux axes : identifier et caracteriser les composes de la chaine respiratoire et comprendre les raisons de la meilleure survie. Nous avons mis en evidence par mutagenese ciblee le role des menaquinones dans le processus de transfert d'electrons a la cytochrome oxydase ainsi que son implication dans la production d'ion superoxyde et de reduction du fer extracellulaire. Les nadh deshydrogenases noxa et noxb semblent impliquees en partie dans ce processus. La cytochrome bd oxydase deja identifiee pour sa fonction en tant que seule terminale oxydase a ete confirmee par nos mutants cyda et cydb obtenus lors de la mutagenese aleatoire. La mise en place du metabolisme respiratoire permet a l. Lactis de survivre plus longtemps, notamment grace a une diminution de l'environnement oxydant cytoplasmique et l'augmentation du ph. L'environnement cree par l'activite respiratoire augmente egalement la survie des bacteries fermentaires, presentes dans le meme milieuLactococcus lactis is mainly used in the food industry, and has been mainly studied for its capacities to ferment sugar sources. Recently our laboratory discovered that l. Lactis are capable of a respiration metabolism when exogenous heme and oxygen are present in the medium. Respiration growth results in improved biomass, higher ph and a striking increased long term survival compared to fermentation metabolism. My thesis project was focused on the respiratory metabolism of l. Lactis, and principally addressed two objectives : the identification of respiratory chain components, and clarification of the factors that associate improved survival with respiration growth. We showed by mutagenesis that menaquinones function to assure electron transfer to cytochrome oxidase. We also demonstrate a role of menaquinones in generating superoxyde species, and in extracellular iron reduction. Our results suggest that nadh dehydrogenase noxa and noxb may be acting as electron donors for the respiration chain. The role of cytochrome bd oxidase, already known for its function as the only terminal oxidase in l. Lactis, was confirmed by our mutants cyda and cydb obtained by a random mutagenesis approach. Our results indicate that greater l. Lactis survival after respiration metabolism (compared to aeration growth in the absence of hème) is associated with, and likely due to a decrease in cytoplasmic oxidative stress and an increase of ph. The environment created by respiratory chain activity also improve the long term survival of fermenting bacteria present in the same medium
43
Thornton, Elizabeth Claire. "Identification and characterisation of a novel β subunit of AMP-activated protein kinase". Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312986.
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Holbrook, Eric. "Identification and Characterization of Histoplasma capsulatum extracellular proteins and their roles in virulence". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1353964000.
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TUVERI, ROSSANA. "Identification & characterization of natural and synthetic compounds as new anticancer agents". Doctoral thesis, Università degli Studi di Cagliari, 2016. http://hdl.handle.net/11584/266770.
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This thesis collects the work I have done during the three-year PhD Course. During my first
year I have started a path that has allowed me to acquire different techniques devoted to set up
and maintain primary cell cultures and cancer derived cell lines as well as to evaluate the
cytotoxicity of potential novel synthetic inhibitors of human cancer cells. Part of the second and
all the third year was spent at the University of Cape Town, South Africa, in the laboratory of
prof. Ariel Katz under the supervision of proff. Roger Hunter and Catherine H. Kaschula
investigating the anticancer activity of Z-ajoene, a garlic compound.
Overall, the main aim of all the my research project was to identify and characterize natural or
synthetic compounds as new antineoplastic agents. The results obtained are divided according
to the research topics addressed:
Anticancer activity of new Phenanthroline compounds (Part I);
The garlic compound Z-ajoene as anticancer agents (Part II).
Studies referring to the Part have been carried out at the University of Cagliari and were
focalized on the evaluation of new Cu(II) -phenanthroline complexes as a potent antineoplastic
agents against various solid and suspension tumours. The [Cu(1,10-phenanthrolin
-5,6-diol)2(OH2)](ClO4)2 complex appears to be the most potent compound against human
leukemia, prostate and lung cancer cell lines. The results obtained on the biological activity of
this class of compounds, providing valuable information for the design of new anticancer drugs,
have been published in the Journal of Inorganic Biochemistry (2014).
As for the Part II of my research, I focused on the mechanisms underlying the anti-tumoral
activity of garlic compound Z-ajoene on human triple –negative breast cancer cells. The results
indicate that Z-ajoene localizes in the ER of MDA-MB-231 cells where it activates the unfolded
protein response (UPR) and ER stress. These findings have been published in the Molecular
Carcinogenesis journal (2015)
Moreover, immunofluorescence studies support the concept that the Z-ajoene main target is a
ER-resident chaperon protein (PDI), whose functional alteration may well be the cause of the
cytotoxic effect. Another molecular target of Z-ajoene is the cytoskeleton protein Vimentin.
Z-ajoene interacts with Vimentin through a S–thiolation causing the disruption of Vimentin
filaments and therefore an alteration of the cell morphology. Given that Vimentin is known to
participate to the early stage of the metastatic process, I also investigated the potential effect of
Z-ajoene at non-cytotoxic concentrations in a specific cell assay and found that it effectively
inhibits cell migration, both in the absence and presence of a chemotactic agent. The metastatic
inhibition induced by Z-ajoene seems caused by modification of several signaling pathways as
expression of Axl and Src proteins, and phosphorylation of β–catenin were changed. Although
following inhibition of cell migration, a reduction of Vimentin expression was to be expected,
Z-ajoene treatment surprisingly induced an upregulation of Vimentin. We interpreted this result
as a consequence of Z-ajoene binding to Vimentin which unable this protein to perform its
physiologic functions (manuscripts in preparation).
Altogether, the data of my in vitro study indicate that Z-ajoene is a promising chemotherapeutic
agent simultaneously acting on different molecular targets, also able to affect the metastatic
process in cells derived from highly invasive breast tumors. Due to its potential use in the clinic,
preclinical evaluation in xenograft mouse models of cancer are ongoing.
46
Azizi, Samir Lalla Amina. "Identification et caractérisation de nouveaux gènes de réponse au stress induit par la pancréatite aiguë". Université Joseph Fourier (Grenoble), 2003. http://www.theses.fr/2003GRE18002.
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L'approche systématique et la technique des micropuces à ADN, nous a permis de montrer que parmi 8000 gènes analysés, 239 présentent une expression différente entre le pancréas sain et le pancréas au cours de la pancréatite : 107 gènes étaient sur-exprimés et 132 gènes étaient sous-exprimés. Parmi ces gènes, 96 correspondaient à des gènes non répertoriés auparavant. Dans le but d'identifier de nouveaux mécanismes de défense cellulaire, nous avons caractérisé deux nouveaux gènes. Le premier gène code une protéine de 49 kDa, appelé PIP 49 (Pancreatitis Induced Protein). Il s'agit d'une protéine transmembranaire jouant probablement le rôle d'un récepteur. Le deuxième gène code un transcrit d'environ 5Kb. Il répond à différents stimuli. Nous l'avons appelé SIP (Stress Induced Protein). SIP subit un épissage altérnatif qui génère deux transcrits qui codent deux protéines de 18 et 27 kDa de localisation nucléaire. L'expression de SIP est dépendante du gène suppresseur de tumeur TP53. SIP est renommée en TP53INP1 (TP53 Induced Nuclear Protein 1). TP53INP1 est capable à son tour de réguler l'activité transactivatrice de p53 et la sur-expression de ses deux isoformes induit l'arrêt du cycle cellulaire et l'apoptose. Des études sur les mécanismes d'action de TP53INP1 ont montré que la protéine interagit physiquement avec p53 ainsi qu'avec la kinase HIPK2, et que ces 3 protéines sont localisées dans les mêmes structures intranucléaires appelées CN-PML.
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BALDI, GIORGIO. "IDENTIFICATION AND CHARACTERIZATION OF STRESSED REPLICATION FORK INTERMEDIATES". Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/609359.
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The DNA replication machinery encounters a number of obstacles while duplicating the genome, which put the replicative apparatus under stress. Cells have developed a number of mechanisms to overcome replication stress sources. However, in the presence of chronic stress, or after loss of key factors that help to deal with this stress, a range of deleterious events can occur. One of the main pathways implicated in DNA damage sensing and response is DNA damage checkpoint. When DNA replication fork progression is blocked, checkpoint activation ensures structural stability of the replisome components avoiding fork collapse and promoting, when possible, fast resumption of DNA replication. One of the hallmarks of replication stress is the accumulation single-stranded DNA at the replication forks. Here we used Atomic Force microscopy (AFM) and Electron Microscopy (EM)-based approaches to provide a detailed characterization of DNA lesions arising in the presence of replication stress imposed by interference with DNA polymerase activity in Xenopus laevis egg extract. We identified a number of intermediates induced by DNA polymerase inhibition, including replication forks containing ssDNA gaps and reversed forks (RVFs). Importantly, we directly correlated the presence and the length of ssDNA gaps at the replication fork junctions with the onset RVFs. Significantly, we identified one possible source of ssDNA gap accumulation at forks by showing that homologous recombination protein Rad51 is required for optimal function of Polymerase-alpha at stressed replication forks. To fulfill this function, Rad5/Pol-alpha interaction is likely to be important for stalled fork resumption. We also provided evidence that replication fork intermediates with persistent ssDNA gaps are converted into RVFs by Smarcal1 translocase, showing that this enzyme is among the most important fork remodelers that can trigger fork reversal upon fork stalling. We also showed that RVFs can trigger extensive Mre11 dependent DNA degradation upon replication stress in the absence of functional Rad51. Finally, we provided mechanistic insights into checkpoint regulation of RVFs levels through ATR, Smarcal1 and Rad51 regulation. Overall this provides structural and molecular insights into the metabolisms of replication forks under stressful conditions.
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Alino-Wilcockson, David Paul. "A study of underachievement in a middle school : identification, measurement, perspectives and change". Thesis, De Montfort University, 1999. http://hdl.handle.net/2086/7984.
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Mukhopadhyay, Suman. "Identification and characterization of genes that protect Escherichia coli from hydrogen peroxide mediated oxidative stress". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0018/NQ30161.pdf.
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Scharf, Sebastian [Verfasser], i Mathias [Akademischer Betreuer] Schmidt. "Identification of novel molecular factors involved in individual stress vulnerability / Sebastian Scharf. Betreuer: Mathias Schmidt". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1029040397/34.
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