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Nygren, Erik. "A mouse model for direct evaluation of cholera vaccines /". Göteborg : Dept. of Microbiology and immunology, Institute of Biomedicine, The Sahlgrenska Academy at University of Gothenburg, 2009. http://hdl.handle.net/2077/19376.
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Moore, Sandra. "Dynamics of cholera epidemics in Haiti and Africa". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5505/document.
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Le cholera est une maladie diarrhéique aiguë due à la consommation d’eau ou d’aliments contaminés par des souches toxigéniques de Vibrio cholerae. Selon le “paradigme du choléra”, la maladie est provoquée par une exposition à un réservoir environnemental de V. cholerae avec des épidémies directement modulées par des facteurs environnementaux. Cependant, comme divers arguments plaident contre ce dogme, nous avons voulu élucider les mécanismes de la dynamique des épidémies de cholera dans trois foyers situés en Haïti, en République Démocratique du Congo (RDC) et en Afrique de l’Ouest. Nous avons associé une analyse temporo-spatiale des épidémies à une étude génétique des isolats de V. cholerae. En Haïti, nous avons cherché à savoir si les épidémies actuelles étaient dues à des souches toxigéniques de V. cholerae O1 durablement implantées dans l’environnement aquatique. En Afrique de l’Ouest, notre étude a révélé qu’Accra, la capitale du Ghana, était le principal foyer de choléra pour l’ensemble des pays d’Afrique de l’Ouest situés à l’Ouest du Nigeria. Le réseau d’eau d’Accra a probablement joué un rôle dans la propagation rapide de V. cholerae vers la majorité des quartiers de la ville. Les épidémies de choléra ont diffusé vers les autres pays sous la forme de vagues épidémiques et plusieurs épidémies ont été liées à la migration de populations à risque comme certains pêcheurs. En conclusion, notre réflexion globale sur les épidémies de choléra dans ces trois foyers distincts nous donne une vision cohérente des mécanismes d’émergence et de diffusion du choléraCholera is an acute diarrheal disease caused by consumption of water or food contaminated with toxigenic Vibrio cholerae. According to the "cholera paradigm", the disease is contracted by exposure to environmental reservoirs of V. cholerae, with outbreaks driven directly by climatic factors. However, as recent findings argue against this dogma, we aimed to elucidate the dynamics of cholera outbreaks in three global foci: Haiti, Democratic Republic of the Congo (DRC) and West Africa. We combined spatiotemporal analysis of epidemics with genetic assessment of V. cholerae isolates. In Haiti, we assessed whether outbreak re-emergence during the rainy season was due to toxigenic V. cholerae O1 strains that have settled into the aquatic environment. Instead, we found that the re-emergence of outbreaks was likely due to persisting outbreaks during the dry season that were insufficiently controlled, rather than an environmental reservoir of V. cholerae O1. In West Africa, our study revealed that Accra, Ghana was the hotspot of cholera in the entire region of West Africa, west of Nigeria. The Accra water network likely played a role in rapid diffusion of V. cholerae throughout the city. Cholera outbreaks spread from Accra into other countries in a wave-like fashion. Distinct outbreaks were linked via migration of at-risk populations, such as certain fishermen. In conclusion, our global reflection of cholera epidemics in these three distinct foci provides a coherent vision of the mechanisms of cholera emergence and diffusion
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Le, Roux Wouter Jacobus. "Population dynamics of Vibrio cholerae in the Vaal Barrage". Pretoria : [s.n.], 2005. http://upetd.up.ac.za/thesis/available/etd-02162007-175110.
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Falklind, Jerkérus Susanna. "Vibrio cholerae O139 : identification, characterization and vaccine strategies /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-696-0/.
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Occhino, Deborah Ann. "Vibrio cholerae iron transport : characterization of two tonB systems and components of a heme transport system /". Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.
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Zo, Young-Gun. "Phylogenomic and structural analyses of Vibrio cholerae populations and endemic cholera". College Park, Md. : University of Maryland, 2005. http://hdl.handle.net/1903/3090.
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Thesis (Ph. D.) -- University of Maryland, College Park, 2005.Thesis research directed by: Marine-Estuarine-Environmental Sciences. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Mann, Maretta Clare y n/a. "Sialylmimetics as Potential Inhibitors fo Vibrio Cholerae Sialidase". Griffith University. Institute for Glycomics, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20061006.083947.
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Cholera is an epidemic infectious diarrhoeal disease that for centuries has proven its frightening ability to cause rapid and widespread loss of human life. All symptoms associated with cholera are a result of rapid dehydration due to infection by pathogenic strains of the bacterium Vibrio cholerae. The damaging effects associated with cholera are mainly attributed to the toxin, which is secreted by the bacterium and infects cells lining the gastrointestinal tract. A sialidase, also secreted by the bacterium, is believed to facilitate toxin uptake by the gastrointestinal epithelium. V. cholerae sialidase is therefore a potential target for therapeutic intervention. A survey of the literature reveals that sialidases from different species share common features with respect to their structure, substrate specificity and catalytic mechanism. The unsaturated sialic acid, Neu5Ac2en, inhibits most exosialidases with a dissociation constant of inhibitor of -10-4 to-10-6 M and has frequently been used as a template in the design of more potent sialidase inhibitors. In the case of V. cholerae sialidase, there have been no inhibitors reported to date that are significantly more potent than Neu5Ac2en itself The present research aimed to develop a range of mimics of Neu5Ac2en, which contain various substituents to replace the C-6 glycerol side chain, as potential inhibitors of V cholerae sialidase. The x-ray crystal structure of V cholerae sialidase was used to explore potential interactions between active site residues and C-6 modified Neu5Ac2en mimetics of known inhibitory potency. Opportunities for interactions within the glycerol side chain pocket in the active site of V cholerae sialidase are discussed. A novel synthetic strategy was developed for the synthesis of a series of glucuronidebased Neu5Ac2en mimetics starting from readily available GIcNAc. This approach was employed for the preparation of Neu5Ac2en mimetics that contained an ether or thioether substituent as replacement of the glycerol side chain of Neu5Ac2en. Progress was also made towards the synthesis of a series of C-6 acylamino Neu5Ac2en mimetics. Analysis by 1H NMR spectroscopy showed that the acylamino derivatives adopted a half-chair conformation that was similar to the conformation of Neu5Ac2en but different to the conformation adopted by the ether and thioether derivatives prepared. The inhibitory activity of the C-6 ether and thioether Neu5Ac2en mimetics prepared was evaluated in vitro using an enzyme assay. It was found that most of the derivatives inhibited V. cholerae sialidase with a K1 of approximately 1O-4 M. The derivatives containing a hydrophobic side chain were found to be slightly more potent compared to derivatives with more hydrophilic side chains. A more detailed study of binding interactions between the C-6 thioether Neu5Ac2en mimetics and V cholerae sialdiase was carried out using STD 1H NMR spectroscopy and computational molecular modelling.
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Bougoudogo, Fiabou. "Contribution à l'étude de l'immunité protectrice contre le choléra : rôle des anticorps vibriocides reconnaissant le polysaccharide spécifique du lipopolysaccharide de "Vibrio cholerae" O:1". Paris 11, 1994. http://www.theses.fr/1994PA114831.
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Mitchell, Daniel David. "Cholera toxin inhibition and EpsF from its secretion system /". Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/9210.
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Jahan, Nasrin. "Structural studies of Vibrio cholerae quorum sensing proteins". Thesis, University of St Andrews, 2011. http://hdl.handle.net/10023/2565.
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The spread of cholera is always associated with contaminated food or water and this is the reason this disease has been endemic in developing countries for centuries due to their lack of proper sanitation facilities and poor or no infrastructure for sewage systems. Cholera can spread quickly and sporadically after any natural disaster that destroys the sewage system or safe drinking water supply of both developed and undeveloped countries. In Southeast Asia in December 2004 and in Pakistan and Haiti 2010, cholera outbreaks followed the natural disasters; with most of the cholera victims being children. Although it is known that the best way to prevent cholera outbreak is the development of the infrastructure, provision of a safe drinking water supply and proper sanitation, this is a very long-term process, and most of the developing countries cannot afford such improvements. These situations can be made worse by natural disasters. Therefore there is a pressing need for the development of a cholera vaccine and there have been numerous research projects working towards this end for several decades. A few of them have been successful to date but because of the severe side effects and narrow range of protection, more effective and wider range vaccine development is still ongoing. In this study, crystallographic and enzymatic studies have been carried out on several novel proteins involved in the control of the production of the factors required for quorum sensing. Quorum sensing is a process in which bacterial cells communicate among themselves by the synthesis, release and detection of small chemical compounds called autoinducers. In this work, structural analysis was carried out on proteins involved in the synthesis and detection of the major autoinducer of Vibrio cholerae, named CAI-1. The crystal structure of CqsA involved in CAI-1 synthesis has been successfully solved and its enzymatic properties have been characterized. The structure of one domain of the cytoplasmic region of the CAI-1 receptor CqsS was also elucidated, and other domains were expressed. The crystal structure of another enzyme (VCA0859, an aldo-keto reductase) thought to have been involved in the synthesis of CAI-1 was also determined. Another protein named VCA0939 was also studied, due to its importance in biofilm development, and its ability to control quorum-sensing in an alternative pathway in the mutated version of pathogenic strains of V. cholerae that were responsible for the seventh cholera pandemic. The aim of this project was to understand the three dimensional structure of some proteins that are involved in quorum sensing and control of the expression of virulence genes for the pathogenesis of V. cholerae. Understanding the three dimensional structure of the proteins and the mode of autoinducer binding to its specific receptor could be highly valuable in the development of a chemical compound that could lead to the discovery of a novel drug with the ability to target cross species specification.
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Edwin, Aaron. "Structural and functional studies of the secreted metalloprotease PrtV from Vibrio cholerae". Doctoral thesis, Umeå universitet, Kemiska institutionen, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-84553.
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Cholera, an acute diarrheal diseases caused by the intestinal infection of the pathogenic bacterium Vibrio cholerae, continues to be a global killer in the world today. PrtV, a secreted zinc metalloprotease, is a potent cytotoxic virulence factor of V. cholerae. The 102 kDa full length multi-domain PrtV protein undergoes several N and C terminal modifications before being secreted as a 81 kDa pro-protein. The activation of the pro-protein is calcium dependent. The removal of calcium triggers auto-proteolysis to give a stable active protease with the catalytic zinc binding domain. The aim of the thesis was to study the structure and function of the PrtV protein. The results from paper I, identified the end product of the maturation of PrtV as the stable 37 kDa M6 active domain, and not a 55 kDa complex as reported earlier. Results also showed the this 37 kDa active M6 domain alone was sufficient for catalytic activity. A revised model for the maturation of PrtV was proposed. Individual domains were isolated from the PrtV protein by domain phasing methods. This included the N-terminal domain (residues 23-103), the PKD1 domain (residues 755-839), and a 25 kDa fragment (residues 589-839). The isolated domains were recombinantly over expressed as fusion proteins to increase expression and solubility. The PKD1 domain was purified to homogeneity and crystallized. The structure of the PKD1 domain reported in paper II, was solved by X-ray crystallography at an atomic resolution of 1.1 Å. From the structure, a previously unknown calcium binding site was identified at the N-terminal of the PKD1 domain. The structure also revealed two conformations for the PKD1 domain depending on free or bound calcium. From the structure, a function of the PKD1 domain as a protector of the cleavage site in the linker region between the M6 domain and the PKD1 domain in the presence of calcium was elucidated. A new model for the activation of PrtV was given. In paper III, the structure of the N-terminal domain solved by NMR spectroscopy was reported. The structure revealed two well defined helices but a third predicted helix was found to be unstructured.
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Saul-McBeth, Jessica. "Characterization of SipA, A Protein Important for Stress Responses in Vibrio cholerae". University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1544540466901883.
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O'Neal, Claire J. "Structural studies of the cholera toxin catalytic subunit /". Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/8592.
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Yáñez, Marissa Elena. "Structural and functional studies of minor pseudopilins from the type 2 secretion system of Vibrio cholerae /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8086.
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Rebaudet, Stanislas. "Etude dynamique des épidémies de choléra en Afrique et en Haïti et application à la mise en place de stratégies d'élimination". Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5055/document.
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Le choléra est une diarrhée hydrique sévère volontiers épidémique causée par des Vibrio cholerae O1 toxinogènes. Ses déterminants environnementaux ont donné naissance à un paradigme influent sur les stratégies de lutte, qui sont se sont avérées peu efficientes en Afrique comme en Haïti. Elles pourraient être améliorées par une meilleure compréhension de la dynamique des épidémies. La synthèse bibliographique des influences de l'environnement sur les épidémies de choléra en Afrique y montre les limites du paradigme environnemental. L'étude multidisciplinaire des origines de l'épidémie de choléra en Guinée en 2012 suggère fortement qu'elle fut importée par voie humaine depuis la Sierra Leone voisine. Une description spatio-temporelle du choléra au Mozambique démontre l'hétérogénéité de sa transmission et amène à questionner le concept d'endémicité du choléra. Depuis son importation en Haïti en octobre 2010, l'épidémie de choléra présente également une répartition spatiale et temporelle très hétérogène. Son importante rétractation en saison sèche et son absence d'enracinement significatif dans l'environnement laissent espérer la possibilité d'une élimination rapide à condition d'apporter une réponse ciblée à tous les foyers épidémiques du pays. Une stratégie d'élimination basée sur nos recommandations y est actuellement menée par le Ministère de la Santé, l'UNICEF et leurs partenaires. Après des résultats spectaculaires en 2013 et au premier semestre 2014, la situation s'est à nouveau dégradée pendant la saison des pluies. Une élimination du choléra dans saison sèche à venir demeure cependant réaliste si nous parvenons à convaincre et remobiliser les acteurs de terrainCholera is an epidemic acute watery diarrhea caused by toxigenic bacteria Vibrio cholerae O1. Its environment determinants have been at the source of a popular paradigm. Many recent control strategies have shown little efficiency in Africa or in Haiti, but they could be improved by a better comprehension of the epidemics dynamic. The bibliographic synthesis of environment influences on cholera in Africa highlights the limits of the environmental paradigm on this continent. A multidisciplinary study of the origin of cholera epidemic in Guinea in 2012 strongly suggests it was humanly imported from nearby Sierra Leone. A space-time description of cholera in Mozambique demonstrates heterogeneous transmission patterns and challenges the concept of cholera endemicity. Since its importation in Haiti in October 2010, cholera transmission also exhibits a marked spatio-temporal heterogeneity. Cholera important retraction during the dry season and its absence of significant establishment in the Haitian environment suggest it may be possible to rapidly eliminate cholera in the country, provided that every outbreak focus receives a targeted response. An elimination strategy based on our recommendations is currently implemented by Haitian Ministry of Health, UNICEF and their partners. After spectacular results in 2013 and during the first half of 2014, the situation has slowly deteriorated during the rainy season. However, cholera elimination during the coming dry season remains realistic provided that we succeed in persuading and remobilizing the partners present on the field
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Antonova, Elena S. "The regulatory network controlling natural competence for DNA uptake in Vibrio cholerae". Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/47626.
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The bacterial pathogen Vibrio cholerae is responsible for ongoing cholera outbreaks in Haiti and elsewhere. Association of V. cholerae with the human host is responsible for fatal disease, but the bacteria also reside as natural inhabitants of aquatic environments, commonly attaching as biofilms to chitinous surfaces of copepods and crabs. Prior studies in V. cholerae demonstrated that competence for genetic transformation, a mechanism of horizontal gene transfer (HGT), requires the TfoX regulator protein that is triggered by chitin, and the HapR transcription factor that is made in response to quorum sensing (QS) signals produced by V. cholerae and Vibrios. To define regulatory components connecting extracellular signals to natural competence, I first demonstrated that QS molecules produced by Vibrios within multi-species chitinous biofilms are required for DNA uptake by V. cholerae, confirming the critical role of QS signals in HGT. Second, I identified by transposon-mutagenesis a new positive regulator of competence, CytR (cytidine repressor), only studied prior in E. coli as a regulator of nucleoside scavenging. Specific mutations in V. cholerae CytR impaired expression of competence genes and halted DNA uptake; and the addition of exogenous cytidine had similar affects as predicted in E. coli. V. cholerae and other competent Vibrios encode TfoX, HapR, and CytR, although none of these regulators directly controls genes coding for the DNA uptake apparatus. Thus, these results have uncovered a regulatory network, likely used by many Vibrios, that contains additional factors linking several extracellular chemical molecules (cytidine, chitin, and QS signals) to DNA uptake. My study has begun to define a molecular mechanism by which both environment and genetics contribute to genome evolution for this important marine pathogen.
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Said, Bengu. "Vibrio cholerae non-O1 and V. mimicus in diarrhoeal disease : a study of virulence factors". Thesis, Open University, 1995. http://oro.open.ac.uk/57564/.
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Vely, Frédéric. "Préparation et caractérisation d'anticorps monoclonaux anti-"Vibrio cholerae" O:1. Contributions à l'étude des bases moléculaires de la vibriocidie et à l'amélioration du diagnostic". Paris 5, 1993. http://www.theses.fr/1993PA05P215.
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Caplet, Nathalie. "Cloning and characterisation of EpsD, a protein required for toxin secretion from Vibrio cholerae". Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302104.
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Kazaji, Dieudonne KA'ngweji. "Factors contributing to the prevalence of cholera during 2008 to 2009 in Vhembe District of Limpopo Province, South Africa". Thesis, University of Limpopo, 2015. http://hdl.handle.net/10386/1616.
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Thesis (MPH.) -- University of Limpopo, 2015Cholera is an acute enteric infection caused by the ingestion of bacterium Vibrio cholerae present in faecally contaminated water or food. Primarily linked to insufficient access to safe water and proper sanitation, its impact can be even more dramatic in areas where basic environmental infrastructures are disrupted or have been destroyed. The aim of the study was to investigate the factors contributing to the prevalence of cholera and the environmental risk factors associated with cholera in the Vhembe district of Limpopo province between 2008 and 2012. The objectives of the study were to identify environmental risk factors for cholera and to determine the number of cholera cases in the Vhembe district. The study used a quantitative, retrospective and cross-sectional research method. The records of 317 patients who met the study criteria were reviewed using an audit tool. The Statistical Package for Social Sciences (SPSS) version 22 was used to analyze the data. The results revealed that lack of adequate hygiene practices, limited access to safe drinking water, lack of safe food preparation and handling, and inadequate sanitation system are risk factors associated with cholera. The study recommends prevention, control of cholera outbreak and case management. Keywords: Cholera, outbreak, Vibrio cholerae 01 and 0139, Watery diarrhea (ricewater), Prevalence, Risk factors.
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Robb, Rhonda Rae. "Risk Factors for Pre-Post Monsoon Cholera Epidemics in Bangladesh from 1992-1994". PDXScholar, 2004. https://pdxscholar.library.pdx.edu/open_access_etds/1691.
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The primary objective of this thesis is to differentiate between the risk factors for pre-and post-monsoon cholera epidemics in rural Bangladesh by analyzing the complex interaction between select environmental, cultural/behavioral, and socioeconomic variables over space and time. In rural Bangladesh, cholera epidemics correspond with the annual monsoon: the first, and smallest, occurs between March and June, while the larger cholera peak occurs between September and December. The differences between the spatial and temporal patterns of seasonal cholera are analyzed, and the risk factors are calculated for pre-and post-monsoon cholera epidemics.
The theoretical approach that underlies this medical geographical study is disease ecology, which espouses that risk of disease is caused by an interaction between people and their environment. This thesis is structured around a holistic understanding that human-environment interactions are inseparable.
In Bangladesh, the monsoon season typically starts between May and June. The 1992 and 1993 cholera peaks occurred just before the monsoon in April and March respectively, while the 1994 cholera peak occurred between April and June. In 1992 and 1993 cholera incidence increased in the post-monsoon period, and peaked in October. The 1994 post-monsoon cholera peak occurred in November. There is a regular temporal pattern to cholera, as the peaks followed a seasonal pattern with the smaller epidemic occurring in the pre-monsoon period and the larger epidemic occurring in the post-monsoon period.
This study shows that there are different risks associated with pre-monsoon cholera epidemics and post-monsoon cholera epidemics. The two main risk factors associated with cholera incidence pre-monsoon were bari population (i.e., crowding) and a house located within the flood controlled area. These two variables were even more strongly associated with post-monsoon cholera incidence to a greater degree, along with a number of other variables including water use, sanitation practices, and socioeconomic status.
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Pieretti, Simone. "ToxT promoter recognition by ToxR transcription factor, a co-activator within the Vibrio cholerae virulence cascade". Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/396666.
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Cholera is an acute diarrheal infection caused by the bacterium Vibrio cholerae. An estimated 2.9 million of cases and about 100000 cholera deaths occur annually all over the world. Upon ingestion of the V. cholerae, the bacterium travels to small intestine where it colonizes and produces the cholera toxin. Cholera toxin raises intracellular cyclic AMP and leads to chloride secretion and the subsequent secretory diarrhoea. Cholera toxin production is regulated through the master virulence regulator ToxT. Trascriptional activation of toxT is activated by membrane-localized ToxR, in association with another membrane protein named TcpP. Both ToxR and TcpP work as a two-component regulatory system merged in single proteins: they receive an external signal through its periplasmic C-terminal domain and bind to the toxT promoter by their cytoplasmic N-terminal domains. This project thesis aims at characterizing part of the system by studying ToxR-DNA complexes, since two ToxR molecules are supposed to bind the promoter to recruit TcpP and hence the RNA polymerase for transcription activation. Using X-ray crystallography, we have solved the structure of three complexes of the ToxR DNA binding domain with 20-bp, 40-bp and 25-bp oligonucleotides at 2.0 A, 2.6 A and 3.2 A resolution, respectively. According to the three structures, ToxR is able to bind to an extensive region of the toxT promoter that goes from the position -97 to the position -45. Considering an integrated model of the three structures, there are four ToxR molecules binding the toxT promoter: two molecules bind the DNA in tandem, one molecule binds the ToxR degenerate box and the last one is binding what is supposed to be the TcpP binding site. The structure determination of the three complexes is important to define with more accuracy the ToxR binding site in the toxT promoter. This site is characterized by eleven bases with a high A-T rich region sequence followed by a CATA/CATG/TGTA box, where the last two bases perform direct and specific contacts with the protein. In the three structures, ToxR shows a winged helix-turn-helix (w-HTH) fold. The wing interacts with the minor groove in an A-T rich region sequence while the recognition helix enters in the major groove at the region with a sequence corresponding to a CATA box. We have compared ToxR with the other w-HTH family proteins and we have found a new structural element, the secondary wing, which displays interactions with the DNA. We have analyzed the protein-DNA contacts in the three structures, and also the protein-protein interactions in the ToxR-DNA40 structure, thus validating the data published on ToxR defective mutations. Finally, we put forward a model of toxT promoter activation at molecular level, based on our crystal structures and on what is known in literature and from our collaborators. We propose that ToxR acts as co-activator in the first steps of toxT transcription activation at different levels. First, it would capture the DNA and hold it close to the cytoplasmic membrane, since both ToxR and TcpP are membrane proteins. Second, it would play a key-role in relieving H-NS from the toxT promoter: H-NS binds the DNA and transcription is repressed, but ToxR is able to replace it in a region that goes from the position -97 to the position -45. Third, ToxR would not be recruiting the RNA polymerase directly, but creating the suitable conditions for the action of TcpP. ToxR recruits TcpP probably through a hand-holding mechanism since one of the ToxR binding site is very close to the TcpP's binding site.El cólera es una infección diarreica aguda causada por la bacteria Vibrio cholerae. La producción de la toxina colérica se controla a través del regulador maestro de virulencia ToxT, cuya activación se lleva a cabo por las proteínas de membrana ToxR y TcpP. Este proyecto de tesis tiene como objetivo el estudio de los complejos formados por ToxR junto con el ADN, dado que se conoce que ToxR se une al promotor toxT para reclutar TcpP y consecuentemente la ARN polimerasa, produciendo la activación de la transcripción. Mediante cristalografía de rayos X hemos resuelto la estructura de tres complejos del dominio de unión a ADN de ToxR con oligonucleótidos de 20, 40 y 25 pares de bases a resoluciones de 2.0 A, 2.6 A y 3.2 A, respectivamente. De acuerdo con las tres estructuras, ToxR es capaz de unirse a una amplia región del promotor toxT que se expande desde la posición -97 hasta la posición -45. Teniendo en cuenta el modelo integrado de las tres estructuras, cuatro moléculas de ToxR se unen al promotor toxT en tándem e invertidas. En las tres estructuras, ToxR muestra un tipo de plegamiento winged helix-turn-helix (w-HTH). El ala (wing) interactúa con el surco menor del ADN, mientras que la hélice de reconocimiento penetra en el surco mayor. Comparando ToxR con el resto de proteínas de la familia w-HTH, hemos encontrado un nuevo elemento estructural, el ala secundaria (secondary wing), que interacciona con el ADN. La determinación de la estructura de los tres complejos es importante para definir con mayor precisión el sitio de unión de ToxR en el promotor toxT. Este sitio se caracteriza por once bases con una secuencia rica en A-T seguida de una caja CATA/CATG/TGTA, donde las dos últimas bases contactan directamente y específicamente con la proteína. Proponemos que ToxR actuaría como co-activador de la transcripción de toxT a diferentes niveles: (i) podría ser responsable de capturar el ADN y mantenerlo cerca de la membrana citoplasmática, (ii) podría jugar un papel clave en el desplazamiento de H-NS, (iii) podría reclutar TcpP y estabilizar su interacción con el promotor.
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Monteiro, Sandra Maria Nunes. "Efficacy of glutamine, peptides and vitamins A and E supplementation on diarrheal disease induced by methotrexate and cholera toxin: improvement of intestinal barrier function". Universidade Federal do CearÃ, 2004. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=596.
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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel SuperiorA desnutriÃÃo, desidrataÃÃo e agentes antineoplÃsicos, tais como o metotrexato (MTX), sÃo imediatos causadores das doenÃas diarrÃicas. Objetivando investigar a mucosite intestinal (MI) induzida por MTX, a eficÃcia das soluÃÃes de reidrataÃÃo oral (SRO) acrescidas com glutamina (Gln), alanilglutamina (Ala-Gln), Hyprol 4107 (HYP) e hyfoama (HYFO) utilizou-se a perfusÃo intestinal. E para a suplementaÃÃo com vitaminas A (VITA) e E (VITE), Gln e peptÃdeos, utilizou-se as avaliaÃÃes morfomÃtricas, metabÃlicas e a de permeabilidade intestinal [(teste lactulose/manitol (L/M)], em camundongos (n=344) e em coelhos (n=72). A mucosite intestinal por MTX (2,75 mg/kg/24h s.c., durante 3 dias) foi validada em camundongos, atravÃs da constataÃÃo do quadro diarrÃico e do prejuÃzo no estado nutricional (-1.89Â0,52 g) estabelecido apÃs o 3o dia de tratamento. A anÃlise morfomÃtrica demonstrou achatamento de vilos (364,8Â19.9 mm) e hiperplasia de criptas (251Â19.2 mm) intestinais com aumento do nÃmero de apoptoses (7.48Â1, 23/cripta), no duodeno e no jejuno. A taxa L/M no grupo MTX foi maior c que no controle (0,35). A perfusÃo intestinal com toxina da cÃlera aumentou a secreÃÃo de Na+ (-12,8Â1.4 mEq/g/min), Cl- (-12,9Â4,6 mEq/g/min) e de Ãgua (-0,02 Â0,04 ml/g/min). As SRO acrescidas de Gln e peptÃdeos, restauram este efeito secretÃrio. A suplementaÃÃo de Gln e peptÃdeos, VITA e VITE, melhoram o ganho ponderal, a ingestÃo de raÃÃo, as alteraÃÃes morfolÃgicas e a apoptose, no modelo de mucosite intestinal. Nenhuma alteraÃÃo foi observada no padrÃo de mitoses nas criptas intestinais, apÃs o 3o dia de tratamento com MTX. A suplementaÃÃo nutricional reduziu na mucosite, a elevaÃÃo das taxas de L/M (0,35 para 0,73) nas vias paracelular e transcelular. Nossos resultados sugerem que, o restabelecimento da barreira morfofuncional, induzido pela suplementaÃÃo, foi obtido atravÃs de um aumento do transporte de cÃtions (Na+ e K+) na mucosa, do fornecimento de substrato energÃtico para o enterÃcito, inibiÃÃo da apoptose (0,25Â0,05), de cÃlulas indiferenciadas incremento no potencial redox e reduÃÃo da peroxidaÃÃo lipÃdica das cÃlulas intestinais diferenciadas. EntÃo sugerimos que o uso de SRO acrescidas de Gln e peptÃdeos podem prevenir a desnutriÃÃo e reduzir as doenÃas diarrÃicas, e a suplementaÃÃo com VITE e VITA melhorar a morfo fisiologia da barreira intestinal
A desnutriÃÃo, desidrataÃÃo e agentes antineoplÃsicos, tais como o metotrexato (MTX), sÃo imediatos causadores das doenÃas diarrÃicas. Objetivando investigar a mucosite intestinal (MI) induzida por MTX, a eficÃcia das soluÃÃes de reidrataÃÃo oral (SRO) acrescidas com glutamina (Gln), alanilglutamina (Ala-Gln), Hyprol 4107 (HYP) e hyfoama (HYFO) utilizou-se a perfusÃo intestinal. E para a suplementaÃÃo com vitaminas A (VITA) e E (VITE), Gln e peptÃdeos, utilizou-se as avaliaÃÃes morfomÃtricas, metabÃlicas e a de permeabilidade intestinal [(teste lactulose/manitol (L/M)], em camundongos (n=344) e em coelhos (n=72). A mucosite intestinal por MTX (2,75 mg/kg/24h s.c., durante 3 dias) foi validada em camundongos, atravÃs da constataÃÃo do quadro diarrÃico e do prejuÃzo no estado nutricional (-1.89Â 0,52 g) estabelecido apÃs o 3o dia de tratamento. A anÃlise morfomÃtrica demonstrou achatamento de vilos (364,8Â 19.9 Âm) e hiperplasia de criptas (251Â 19.2 Âm) intestinais com aumento do nÃmero de apoptoses (7.48Â 1, 23/cripta), no duodeno e no jejuno. A taxa L/M no grupo MTX foi maior c que no controle (0,35). A perfusÃo intestinal com toxina da cÃlera aumentou a secreÃÃo de Na+ (-12,8Â 1.4 ÂEq/g/min), Cl- (-12,9Â 4,6 ÂEq/g/min) e de Ãgua (-0,02 Â 0,04 ml/g/min). As SRO acrescidas de Gln e peptÃdeos, restauram este efeito secretÃrio. A suplementaÃÃo de Gln e peptÃdeos, VITA e VITE, melhoram o ganho ponderal, a ingestÃo de raÃÃo, as alteraÃÃes morfolÃgicas e a apoptose, no modelo de mucosite intestinal. Nenhuma alteraÃÃo foi observada no padrÃo de mitoses nas criptas intestinais, apÃs o 3o dia de tratamento com MTX. A suplementaÃÃo nutricional reduziu na mucosite, a elevaÃÃo das taxas de L/M (0,35 para 0,73) nas vias paracelular e transcelular. Nossos resultados sugerem que, o restabelecimento da barreira morfofuncional, induzido pela suplementaÃÃo, foi obtido atravÃs de um aumento do transporte de cÃtions (Na+ e K+) na mucosa, do fornecimento de substrato energÃtico para o enterÃcito, inibiÃÃo da apoptose (0,25Â 0,05), de cÃlulas indiferenciadas incremento no potencial redox e reduÃÃo da peroxidaÃÃo lipÃdica das cÃlulas intestinais diferenciadas. EntÃo sugerimos que o uso de SRO acrescidas de Gln e peptÃdeos podem prevenir a desnutriÃÃo e reduzir as doenÃas diarrÃicas, e a suplementaÃÃo com VITE e VITA melhorar a morfo fisiologia da barreira intestinal
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Bedenbaugh, Crystal M. "Development of ganglioside-based assays for the identification of botulinum and cholera toxins utilizing an evanescent wave biosensor". [Tampa, Fla] : University of South Florida, 2006. http://purl.fcla.edu/usf/dc/et/SFE0001617.
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Gruaz-Guyon, Anne. "Reponse anticorps et protection locale induites par des immunogenes synthetiques selectionnes dans la sequence de la toxine cholerique : immunisation systemique et orale". Paris 6, 1987. http://www.theses.fr/1987PA066409.
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Proposition d'une sequence immunogenique devant contenir des tetrapeptides absents de proteines de l'hote (ou presentant peu d'homologie avec les sequences contenues dans les banques de donnees) en association avec les sequences capables de reconnaitre les antigenes du complexe majeur d'histocompatibilite
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Chow, Ka-hang. "Molecular characterization of RTX toxin of vibrio cholerae causing epidemics". Click to view the E-thesis via HKUTO, 2001. http://sunzi.lib.hku.hk/hkuto/record/B42575898.
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Fonseca, Ana Glória Rodrigues Sanches da. "Seroprevalência de cólera em área endémica : estudo". Master's thesis, Faculdade de Ciências Médicas. Universidade Nova de Lisboa, 2007. http://hdl.handle.net/10362/4842.
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Ao longo da história, a cólera tem assolado populações sob a forma de epidemias e pandemias com elevada morbimortalidade, que condicionam o desenvolvimento das regiões atingidas (120.000 óbitos estimados por ano a nível mundial). Em 2001, 94% (173.359 casos) dos casos de cólera foram notificados no continente africano (OMS). A cidade da Beira é considerada área de endemo-epidemicidade de cólera.
Na cidade da Beira foi realizado um estudo de seroprevalência de cólera (serogrupo O1), em período inter-epidémico, através do doseamento de anticorpos vibriocida, numa amostra de conveniência de 136 indivíduos adultos sem história de vacinação prévia contra a cólera. Obteve-se uma seroprevalência de 2,2%, que não pode ser extrapolada para a população em geral. Ambas as estirpes do serogrupo O1 (Inaba e Ogawa) foram identificadas.
A metodologia utilizada é exequível em regiões com suporte laboratorial básico e pode ter interesse como ferramenta de vigilância epidemiológica da cólera na cidade da Beira, dado que a seroprevalência em anticorpos vibriocida traduz a imunidade de grupo da população. A monitorização da seroprevalência pode contribuir para orientar as estratégias de intervenção no sentido do controlo da cólera, nomeadamente na implementação de uma campanha de vacinação.
De facto, tendo em conta o impacto da cólera na população e as limitações da estratégia existente, urge equacionar de forma objectiva o papel da vacinação oral na estratégia de controlo da cólera na cidade da Beira.
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Guidolin, Angelo. "Molecular biology of "Vibrio cholerae" bacteriophage CP-T1 and its host interactions". Title page, contents and abstract only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phg948.pdf.
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Chow, Ka-hang y 周嘉恆. "Molecular characterization of RTX toxin of vibrio cholerae causing epidemics". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B42575898.
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Purins, Leanne Roslyn. "Molecular characterisation of the transcriptional activator, HLYU, of Vibrio cholerae O1 /". Title page, abstract and table of contents only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09php9857.pdf.
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Thesis (Ph.D.)--University of Adelaide, School of Molecular and Biomedical Science , Discipline of Microbiology and Immunology, 2005."May, 2004" Includes corrigenda. includes bibliographical references (leaves 118-156).
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Navarro, Romain. "Etude structurale par RMN de la protéine TolAIII impliquée dans le mécanisme d'infection de Vibrio cholerae par le bactériophage CTXphi". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4079.
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Vibrio cholerae acquiert les gènes de la toxine cholérique suite à l’infection par le phage CTXphi et devient par la suite une bactérie pathogène. L'infection se déroule en deux étapes : une interaction entre le pilus TCP et le domaine pIIIN2ctx, puis la formation du complexe TolAIIIV.c/pIIIN1ctx. Cette seconde étape est l’étape limitante de l’infection. L’objectif général de ma thèse a été d’étudier les forces motrices associées à cette étape.1) J’ai étudié les mécanismes moléculaires associés à la spécificité phage/bactérie en ciblant les interactions électrostatiques et le feuillet intermoléculaire par RMN et double hybride bactérien.2) J’ai résolu la structure de TolAIIIV.c libre par RMN. La comparaison des structures de cette protéine à l’état libre et liée ont permis de mettre en évidence un changement conformationnel et de proposer un mécanisme moléculaire d’ajustement induit. De plus, l’étude de la flexibilité de la protéine par RMN à haute pression (HP) a montré l’importance de la cavité interne de la protéine TolAIII pour favoriser l’ajustement induit lors de la formation du complexe TolAIIIV.c/pIIIN1CTX.3) J’ai vérifié si l’ajustement induit observé précédemment était lié à la présence de cette cavité d’une manière générale chez les protéines TolAIII. Une étude de dispersion de relaxation et de RMN à HP de la protéine TolAIIIE.c a permis de vérifier l’importance de cette cavité pour le mécanisme d’ajustement induit essentiel à cette famille de protéine. De plus, nous avons corrélée la flexibilité particulière de la protéine TolAIIIE.c à la présence d’une boucle qui lui confère une certaines flexibilité nécessaires pour interagir avec plusieurs partenairesVibrio cholerae becomes a pathogen after CTXphi phage infection. The phagic infection is a wo step mechanism: first TCP pilus binds to pIIIN2ctx, then TolAIIIV.c binds to pIIIN1ctx. The second step is essential for the acquisition of genes of cholera toxins leading to cholera disease. The main goal of my thesis is to study the driving forces associated to the phage infection.First, I studied the molecular mechanism associated to phage/bacteria specificity targeting electrostatic bonds and hydrophobic interactions within the intermolecular sheet. These experiments use NMR and bacterial two hybrids methods. Our results show that electrostatic bonds are essential for the complex formation.Second, I solved the solution structure of TolAIIIV.c using NMR. The comparison of the structures of free and bound states of TolAIIIV.c, shows an associate conformational change and lead us to propose a model for the molecular mechanism of the induced fit. Then the study of the TolAIII flexibility, using high pressure NMR shows the importance of TolAIII cavity to promote the induced fit during TolAIIIV.c/pIIIN1ctx complex formation.Finally, we wanted to show if the induced fit is correlated to the presence of cavity in TolAIII family. A study using NMR relaxation dispersion and high-pressure NMR experiments on TolAIIIE.c shows the importance of this cavity for the induced fit. The presence of a loop at the top of the N-terminal helix in TolAIIIE.c leads to the protein to have several conformations necessary to interact with many partners
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Cofie, Daniel Quarcoopome Guthrie Rufus K. "Effect of chitin on Vibrio cholerae /". See options below, 1988. http://proquest.umi.com/pqdweb?did=746612041&sid=1&Fmt=2&clientId=68716&RQT=309&VName=PQD.
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Stroher, Vive Horst. "Serotype conversion in Vibrio cholerae 01 /". Title page, contents and abstract only, 1992. http://web4.library.adelaide.edu.au/theses/09PH/09phs919.pdf.
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Ogierman, Monica A. "Molecular characterisation of the fungus Corynespora cassicola /". Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09pho344.pdf.
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Mutreja, Ankur. "The origins and evolution of Vibro cholerae O1 E1 Tor". Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648490.
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Sheikh, Md Arif. "Structural biology of Vibrio cholerae pathogenicity factors". Thesis, St Andrews, 2009. http://hdl.handle.net/10023/696.
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Focareta, Tony. "The extracellular DNase(s) of vibrio cholerae /". Title page, abstract and table of contents only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09phf652.pdf.
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Sharma, Dharam Pal. "Non-lipopolysaccharide protective antigens of Vibrio cholerae /". Title page, abstract and contents only, 1990. http://web4.library.adelaide.edu.au/theses/09PH/09phs5314.pdf.
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Findlay, Gordon. "Biogenesis of virulence factors in Vibrio cholerae". Thesis, University of Kent, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294636.
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Berg, Thorsten. "Virulenzregulationskaskade und Chitobiose-Metabolismus in Vibrio cholerae". Doctoral thesis, kostenfrei, 2008. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2008/2829/.
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Cherubin, Patrick. "The Anti-toxin Properties of Grape Seed Phenolic Compounds". Master's thesis, University of Central Florida, 2014. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/6254.
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Corynebacterium diphtheriae, Pseudomonas aeruginosa, Ricinus communis, Shigella dysentariae, and Vibrio cholerae produce AB toxins which share the same basic structural characteristics: a catalytic A subunit attached to a cell-binding B subunit. All AB toxins have cytosolic targets despite an initial extracellular location. AB toxins use different methods to reach the cytosol and have different effects on the target cell. Broad-spectrum inhibitors against these toxins are therefore hard to develop because they use different surface receptors, entry mechanisms, enzyme activities, and cytosolic targets.
We have found that grape seed extract provides resistance to five different AB toxins: diphtheria toxin (DT), P. aeruginosa exotoxin A (ETA), ricin, Shiga toxin, and cholera toxin (CT). To identify individual compounds in grape seed extract that are capable of inhibiting the activities of these AB toxins, we screened twenty common phenolic compounds of grape seed extract for anti-toxin properties. Three compounds inhibited DT, four inhibited ETA, one inhibited ricin, and twelve inhibited CT. Additional studies were performed to determine the mechanism of inhibition against CT. Two compounds inhibited CT binding to the cell surface and even stripped bound CT off the plasma membrane of a target cell. Two other compounds inhibited the enzymatic activity of CT. We have thus identified individual toxin inhibitors from grape seed extract and some of their mechanisms of inhibition against CT. This work will help to formulate a defined mixture of phenolic compounds that could potentially be used as a therapeutic against a broad range of AB toxins.M.S.
Masters
Molecular Biology and Microbiology
Medicine
Biotechnology
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Ha, Thi Quyen y Duy Khang Dinh. "The changes in antigenic components of Vibrio cholerae strains isolated in Vietnam". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-190840.
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Whole cells of Vibrio cholerare serotype Inaba and serotype Ogawa (strains I389 and O395) were injected into rabbits to obtain antiserum. The antiserums were used for immune reaction with antigenic components of 25 strains of V.cholerae isolated from five provinces of Vietnam and the two standard strains I389 and O395 by Western-blot technique. Analysis of immune hybrid results showed that there were 11 antigenic components with molecular weights approximately 79kDa, 62kDa, 52kDa, 45kDa, 42kDa, 38kDa, 35kDa, 31kDa, 26kDa, 23kDa and 20kDa. In which the antigens of 45kDa, 42kDa, 31kDa and 20kDa were similar to OmpT, OmpS, Omp-31kDa and TcpA that have been considered as vaccine-candidate antigens. Among 25 V.cholerae strains, there were 6 antigenic components in common including 79kDa, 62kDa, 45kDa, 35kDa, 31kDa and 20kDa. 23/25 strains contained 42kDa antigen; 5/25 strains contained 38kDa and 23kDa antigens; 11/25 had 26kDa antigen. In addition, 7/25 strains contained antigens identical to V.cholerae I389 serotype Inaba; 6/25 strains contained antigens of I389 and O395; 12/25 strains had changes of antigenic components. These changes were actually the lack of antigens, not appearing new antigens. These results are considered as basis for researches about immune response and prevention of cholera diseaseToàn bộ tế bào của các chủng Vibrio cholerare typ huyết thanh Inaba và typ huyết thanh Ogawa (chủng I389 và O395) được sử dụng để gây miễn dịch trên thỏ để thu kháng huyết thanh. Các kháng huyết thanh được dùng để thực hiện phản ứng miễn dịch với các thành phần kháng nguyên của 25 chủng V.cholerae phân lập từ 5 tỉnh thành của Việt Nam và hai chủng chuẩn I389 và O395 bằng kỹ thuật Western-blot. Phân tích kết quả lai miễn dịch cho thấy, có tổng số 11 thành phần kháng nguyên có kích thước khoảng 79kDa, 62kDa, 52kDa, 45kDa, 42kDa, 38kDa, 35kDa, 31kDa, 26kDa, 23kDa và 20kDa. Các kháng nguyên này chủ yếu là các protein màng ngoài (Omp) và kháng nguyên lông (TcpA). Trong đó các kháng nguyên 45kDa, 42kDa, 31kDa và 20kDa trùng với các kháng nguyên OmpS, OmpT, Omp-31kDa và TcpA được xem là những kháng nguyên dự tuyển vacxin tả. Có 6 kháng nguyên chung giữa 25 chủng với kích thước 79kDa, 62kDa, 45kDa, 35kDa, 31kDa và 20kDa. 7/25 chủng có các kháng nguyên giống với kháng nguyên của chủng V. cholerae I389 typ huyết thanh Inaba; 6/25 chủng có các kháng nguyên giống với kháng nguyên của cả hai chủng V.cholerae I389 và O395; 12/25 chủng có sự biến đổi thành phần kháng nguyên. Tuy nhiên, sự biến đổi này thực chất là sự thiếu hụt chứ không phải là sự xuất hiện các thành phần kháng nguyên mới. Các kết quả nghiên cứu này có thể được xem là nền tảng ban đầu cho các nghiên cứu về miễn dịch và dự phòng bệnh tả
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Midonet, Caroline. "Mécanisme d'intégration du phage TLC dans le génome de Vibrio cholerae". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS314/document.
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La plupart des bactéries ont un unique chromosome circulaire. Lors de la réplication de l’ADN, la circularité lie topologiquement les deux chromatides sœurs résultant de la réplication (caténanes et dimères). Ces liens topologiques doivent être résolus afin de permettre une bonne ségrégation de l’information génétique entre les deux cellules filles au cours de la division cellulaire. Les bactéries possèdent une machinerie très conservée: les recombinases à tyrosines XerC et XerD, capables de résoudre les dimères et une partie des caténanes, en catalysant un crossover au site spécifique dif situé dans la région Ter du chromosome. Lors de ce processus elles réalisent successivement deux échanges de brins. La réaction Xer est spatio-temporellement contrôlée par une protéine du divisome: FtsK. FtsK est une translocase qui pompe l’ADN à travers le septum de division. Lorsqu’elle rencontre une synapse constituée de deux sites dif chargés de XerC et XerD, elle active la catalyse de XerD pour initier le premier échange de brins. Dans un second temps XerC catalyse un second échange de brins indépendamment de FtsK. A ce jour le mécanisme d’activation de XerD n’est pas bien compris. Certains éléments mobiles résolvent leur états multimériques (tels que les plasmides) ou intègrent leur génome dans celui de leur hôte en détournant les recombinases XerCD. On parle d’IMEXs (integrative Mobile Element using Xer). Les éléments mobiles étudiés avant ma thèse utilisaient tous des voies de recombinaison initiées par la catalyse de XerC et ne nécessitant pas l’activation de XerD. Au cours de ma thèse j’ai étudié dans un premier temps le mécanisme d’intégration / excision d’une nouvelle classe d’IMEXs en utilisant comme modèle le phage TLCphi de Vibrio cholerae, la bactérie responsable du choléra. Par des approches de génétique j’ai démontré que TLCphi utilise une voie de recombinaison initiée par la catalyse de XerD et indépendante de FtsK. Mes travaux ont également montré que l’excision du phage participe à l’évolution des souches pandémiques de V.cholerae. Dans une seconde partie, j’ai identifié un facteur phagique qui permet à TLCphi de contourner le contrôle de FtsK sur l’activation de XerD. Ce facteur était une protéine de fonction inconnue présentant un domaine HTH et un domaine DUF3653. Ce dernier est retrouvé dans de nombreux IMEXs. Par des approches de biologie moléculaire j’ai étudié le mécanisme d’action de cette protéine. J’ai reproduit la réaction de recombinaison in vitro et démontré qu’elle active XerD en interagissant directement avec elle. Enfin dans un troisième temps, nous nous sommes intéressés aux disparités observées entre la recombinaison Xer chez E.coli et V.cholerae. En particulier, la recombinaison Xer semble agir seulement sur les dimères chez E.coli alors qu’elle est active également sur les monomères chez V.cholerae. Nous avons démontré que ces divergences de comportement ne viennent pas des Xer elles-mêmes, ni de leurs propriétés d'activations par FtsK. Elles résultent des différentes chorégraphies de ségrégation des chromosomes entre ces deux bactéries et dépendent également des vitesses de croissanceMost of bacteria have a single circular chromosome. During replication of DNA, this circularity can lead to two sister chromatids topologically linked (catenanes and dimers). These topological links have to be solved in order to allow good segregation of genetic information between the two daughter cells during cell division. Bacteria possess a highly conserved machinery: the tyrosine recombinases XerC XerD that are capable to resolve dimers and some catenanes, by catalyzing a crossover at the specific site dif located in the Ter region of the chromosome. During this process they realize two sequentialstrand exchanges.The Xer reaction is spatiotemporally controlled by a protein of the divisome: FtsK. FtsK is a pump that translocates DNA through the septum of division. When FtsK meets a synapse that consists of two dif loaded by XerC and XerD, it activates XerD catalysis that initiates first strand exchange. Secondly XerC catalyzes a second strand exchange independently of FtsK. To date the activation mechanism of XerD is not well understood. Some mobile elements solve their multimeric states (like plasmids) or integrate their genome into the chromosome of their host by using XerCD recombinases. Such integrative elements are named IMEXs (Integrative Mobile Element using Xer). The mobile elements studied before my thesis all used recombination pathways initiated by catalysis of XerC and not requiring activation of XerD .During my PhD I studied at first the integration mechanism / excision of a new class IMEXs using as a model the TLC phage Vibrio cholerae, the bacterium responsible for cholera. By genetic approaches I demonstrated that TLCphi uses a recombination pathway initiated by XerD catalysis and independently of FtsK. My work has also shown that the phage excision participates in the evolution of pandemic strains of V. cholerae. In the second part, I identified a phage factor that allows TLC to bypass the activation of XerD by FtsK. This factor was a protein of unknown function with a HTH domain and a DUF3653 domain. DUF3653 are found in many IMEXs. Using molecular biology approaches, I studied the mechanism of action of this protein. I reproduced the recombination reaction in vitro and demonstrated that this factor activates XerD by directly interacting with it. Finally, we were interested to study disparities between Xer recombination in E.coli and V.cholerae. In particular, the Xer recombination seems to act only on dimers in E.coli while it is also active on monomers in V.cholerae. We have demonstrated that these differences in behaviors do not come from Xer themselves or their activation by FtsK. They result from different choreographies of chromosome segregation between these two bacteria and are also dependent on growth rates
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Yam, Wing-cheong. "Molecular epidemiology of enterotoxigenic escherichia coli and vibrio cholerae in Hong Kong /". [Hong Kong : University of Hong Kong], 1990. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12966381.
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Ha, Thi Quyen y Duy Khang Dinh. "The changes in antigenic components of Vibrio cholerae strains isolated in Vietnam: Research article". Technische Universität Dresden, 2014. https://tud.qucosa.de/id/qucosa%3A29114.
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Whole cells of Vibrio cholerare serotype Inaba and serotype Ogawa (strains I389 and O395) were injected into rabbits to obtain antiserum. The antiserums were used for immune reaction with antigenic components of 25 strains of V.cholerae isolated from five provinces of Vietnam and the two standard strains I389 and O395 by Western-blot technique. Analysis of immune hybrid results showed that there were 11 antigenic components with molecular weights approximately 79kDa, 62kDa, 52kDa, 45kDa, 42kDa, 38kDa, 35kDa, 31kDa, 26kDa, 23kDa and 20kDa. In which the antigens of 45kDa, 42kDa, 31kDa and 20kDa were similar to OmpT, OmpS, Omp-31kDa and TcpA that have been considered as vaccine-candidate antigens. Among 25 V.cholerae strains, there were 6 antigenic components in common including 79kDa, 62kDa, 45kDa, 35kDa, 31kDa and 20kDa. 23/25 strains contained 42kDa antigen; 5/25 strains contained 38kDa and 23kDa antigens; 11/25 had 26kDa antigen. In addition, 7/25 strains contained antigens identical to V.cholerae I389 serotype Inaba; 6/25 strains contained antigens of I389 and O395; 12/25 strains had changes of antigenic components. These changes were actually the lack of antigens, not appearing new antigens. These results are considered as basis for researches about immune response and prevention of cholera disease.Toàn bộ tế bào của các chủng Vibrio cholerare typ huyết thanh Inaba và typ huyết thanh Ogawa (chủng I389 và O395) được sử dụng để gây miễn dịch trên thỏ để thu kháng huyết thanh. Các kháng huyết thanh được dùng để thực hiện phản ứng miễn dịch với các thành phần kháng nguyên của 25 chủng V.cholerae phân lập từ 5 tỉnh thành của Việt Nam và hai chủng chuẩn I389 và O395 bằng kỹ thuật Western-blot. Phân tích kết quả lai miễn dịch cho thấy, có tổng số 11 thành phần kháng nguyên có kích thước khoảng 79kDa, 62kDa, 52kDa, 45kDa, 42kDa, 38kDa, 35kDa, 31kDa, 26kDa, 23kDa và 20kDa. Các kháng nguyên này chủ yếu là các protein màng ngoài (Omp) và kháng nguyên lông (TcpA). Trong đó các kháng nguyên 45kDa, 42kDa, 31kDa và 20kDa trùng với các kháng nguyên OmpS, OmpT, Omp-31kDa và TcpA được xem là những kháng nguyên dự tuyển vacxin tả. Có 6 kháng nguyên chung giữa 25 chủng với kích thước 79kDa, 62kDa, 45kDa, 35kDa, 31kDa và 20kDa. 7/25 chủng có các kháng nguyên giống với kháng nguyên của chủng V. cholerae I389 typ huyết thanh Inaba; 6/25 chủng có các kháng nguyên giống với kháng nguyên của cả hai chủng V.cholerae I389 và O395; 12/25 chủng có sự biến đổi thành phần kháng nguyên. Tuy nhiên, sự biến đổi này thực chất là sự thiếu hụt chứ không phải là sự xuất hiện các thành phần kháng nguyên mới. Các kết quả nghiên cứu này có thể được xem là nền tảng ban đầu cho các nghiên cứu về miễn dịch và dự phòng bệnh tả.
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Lindmark, Barbro. "Modulators of Vibrio cholerae predator interaction and virulence". Doctoral thesis, Umeå universitet, Molekylärbiologi (Medicinska fakulteten), 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-30211.
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Vibrio cholerae, the causal agent of cholera typically encodes two critical virulence factors: cholera toxin (CT), which is primarily responsible for the diarrhoeal purge, and toxin-co-regulated pilus (TCP), an essential colonisation factor. Nontoxigenic strains expressing TCP can efficiently acquire the CT gene through lysogenic conversion with CTXΦ, a filamentous phage that encodes CT and uses TCP as a receptor. V. cholerae is a Gram-negative bacterium and a natural inhabitant of estuarine and coastal waters throughout both temperate and tropical regions of the world. In the aquatic environment, V. cholerae encounters several environmental stresses, such as change in salinity, UV stress, nutrient limitation, temperature fluctuations, viral infections and protozoan predation. To fully understand the pathogenic and virulence potential of V. cholerae, knowledge is required of its interactions with, not only human, but also environmental factors. By using the nematode Caenorhabditis elegans as host model, we were able to identify a previously uncharacterised protein, the extracellular protease PrtV. PrtV was shown to be required for the killing of. elegans and also necessary for survival from grazing by the ciliate Tetrahymena pyriformis and the flagellate Cafeteria roenbergensis. The PrtV protein, which belongs to a M6 family of metallopeptidases was cloned and purified for further characterisations. The purified PrtV was cytotoxic against the human intestinal cell line HCT8. By using human blood plasma, fibrinogen, fibronectin and plasminogen were identified as candidate substrates for the PrtV protease. Outer membrane vesicles (OMVs) are released to the surroundings by most Gram-negative bacteria through “bulging and pinching” of the outer membrane. OMVs have been shown to contain many virulence factors important in pathogenesis. Therefore, we investigated the association of PrtV with OMVs. PrtV was not associated with OMVs from the wild type O1 strain. In contrast, in an LPS mutant lacking two sugar chains in the core oligosaccharide PrtV was found to be associated with the OMVs. The OMV-associated PrtV was shown to be proteolytically and cytotoxically active. V. cholerae strains are grouped into >200 serogroups. Only the O1 and O139 serogroups have been associated with pandemic cholera, a severe diarrhoeal disease. All other serogroups are collectively referred to as non-O1 non-O139 V. cholerae. Non-O1 non-O139 V. cholerae can cause gastroenteritis and extraintestinal infections, but unlike O1 and O139 strains of V. cholerae, little is known about the virulence gene content and their potential to become human pathogens. We analysed clinical and environmental non-O1 non-O139 isolates for their putative virulence traits. None of them carry the genes encoding CT or the TCP, but other putative virulence factors were present in these isolates. The incidence of serum resistance was found to vary considerably and was independent of encapsulation. Three strains were strongly serum-resistant, and these same strains could also kill C. elegans.
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Wennberg, Aina Charlotte. "PCR-detection of Vibrio cholerae in ballast water". Thesis, Norwegian University of Science and Technology, Department of Biotechnology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-6883.
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Yu, Jan. "Pathways facilitating enterotoxin biogenesis in Vibro cholerae". Thesis, University of Kent, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240131.
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Franzon, Vicki L. "Haemagglutinins of Vibrio cholerae : molecular characterization of the mannose-fucose resistant haemagglutinin (MFRHA) /". Title page, abstract and contents only, 1988. http://web4.library.adelaide.edu.au/theses/09PH/09phf837.pdf.
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David, Ariane. "Chorégraphie de ségrégation des deux chromosomes de Vibrio cholerae". Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-00921394.
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L'objectif de cette thèse est de définir la chorégraphie de ségrégation des deux chromosomes circulaires de Vibrio cholerae, c'est à dire le positionnement de l'information génétique au cours de la croissance de la cellule, ainsi que les mécanismes dirigeant ces ségrégations. Il a longtemps été supposé que les bactéries étaient trop petites pour avoir une organisation intra-cellulaire, et le manque de techniques appropriées ne permettait pas d'infirmer cette hypothèse. Or la taille des chromosomes comparée à celle de la bactérie impose une compaction et aujourd'hui, de nouvelles techniques de microscopie et d'analyse génétique permettent d'affirmer que les chromosomes bactériens étudiés jusqu'à maintenant ont tous une organisation et une chorégraphie de ségrégation précises et différentes selon les espèces. Toutes les espèces étudiées à ce jour ont un chromosome circulaire unique : la réplication du chromosome commence à une origine unique bidirectionnelle, les deux fourches de réplication se déplacent le long des deux bras de réplication (ou réplichores) et finissent la réplication au terminus, diamétralement à l'opposée de l'origine de réplication sur la carte du chromosome. Peu d'espèces ont été étudiées, et Vibrio cholerae émerge progressivement comme un nouveau modèle : son génome est réparti sur deux chromosomes, et la chorégraphie de plusieurs chromosomes dans une cellule n'a jamais été décrite. De plus, cette espèce semble être au croisement évolutif entre Caulobacter crescentus et Escherichia coli : Vibrio cholerae a d'une part une morphologie en croissant, des systèmes de partition aux origines et un positionnement de l'origine du chromosome I, semblables à C. crescentus, et d'autre part un système de compaction du terminus et un set de gènes impliqués dans la maintenance du chromosome ayant co-évolué, qu'on ne retrouve que dans peu d'espèces proches d'E. coli. Une autre caractéristique intéressante de V. cholerae est que le chromosome II semble avoir été acquis récemment et n'est donc peut être pas gouverné par les mêmes mécanismes que le chromosome I, comme en témoignent le positionnement de son origine et son terminus, inédits pour des chromosomes bactériens. Parmi les Vibrios (environ 60 espèces principalement retrouvées dans les environnements aquatiques), certaines espèces sont des pathogènes dévastateurs pour les poissons, le corail, les crustacés ou les fruits de mer. Mais la plus documentée est Vibrio cholerae, car elle provoque chez l'Humain une maladie provoquée par l'ingestion d'eau contaminée qui peut être mortelle si le patient n'est pas réhydraté à temps. Bien que facilement traitable, le choléra fait encore de nombreuses victimes dans les pays en développement où les structures de santé et les règles d'hygiène font parfois défaut. Ainsi l'étude de Vibrio cholerae présente un intérêt médical, mais également par extension aux autres Vibrios, un intérêt environnemental non négligeable.