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Rozprawy doktorskie na temat „Antibiogram of Pseudomonas Aeruginosa”

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Data publikacji: 3 czerwca 2025
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1

Santos, Adailton Pereira dos. "Perfil de rastreamento de resistência das Pseudomonas aeruginosa e acompanhamento da rotina educacional." Universidade Federal de Goiás, 2018. http://repositorio.bc.ufg.br/tede/handle/tede/8698.

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Magalhães, Mary Joyce Targino Lopes. "Caracterização fenotípica e similiaridade genética de Pseudomonas aeruginosa provenientes de efluentes hospitalares e água superficial do igarapé do Mindu/Manaus - AM." Universidade Federal do Amazonas - Universidade Federal do Pará, 2013. http://tede.ufam.edu.br/handle/tede/4538.

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Submitted by Geyciane Santos (geyciane_thamires@hotmail.com) on 2015-07-31T15:27:26Z No. of bitstreams: 1 Dissertação- Mary Joyce Targino Lopes Magalhães.pdf: 1466870 bytes, checksum: 3202ba13f65ece33fb3c071651d2a444 (MD5)<br>Approved for entry into archive by Divisão de Documentação/BC Biblioteca Central (ddbc@ufam.edu.br) on 2015-08-04T15:21:41Z (GMT) No. of bitstreams: 1 Dissertação- Mary Joyce Targino Lopes Magalhães.pdf: 1466870 bytes, checksum: 3202ba13f65ece33fb3c071651d2a444 (MD5)<br>Approved for entry into archive by Divisão de Documentação/BC Biblioteca Central (ddbc@ufam.edu.br)
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Barré, Catherine. ""Pseudomonas aeruginosa" : analyse épidémiologique des isolements dans un hôpital chirurgical spécialisé, étude de l'activité bactériostatique des antibiotiques, analyse en fonction des principaux phénotypes de résistance, apport à la lecture interprétative." Paris 5, 1995. http://www.theses.fr/1995PA05P012.

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Turner, Keith Holte. "Bistability in Pseudomonas aeruginosa." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10159.

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The opportunistic pathogen P. aeruginosa is a leading cause of hospital-accquired infections, and is also the primary cause of morbidity and mortality in patients with cystic fibrosis (CF). In this thesis, I describe the identification and characterization of a novel LysR-type transcription regulator (LTTR) of P. aeruginosa named BexR. I show that BexR exhibits reversible ON/OFF bistable expression, which leads to the bistable expression of several genes including one encoding a virulence factor. I present results suggesting that this bistable expression depends on positive feedback of BexR. T
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5

Silistre, Hazel. "Riboregulation in Pseudomonas aeruginosa." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/32634/.

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The opportunistic human pathogen Pseudomonas aeruginosa controls virulence, production of secondary metabolites, motility, biofilm formation, growth in anaerobic conditions, intracellular and intercellular signalling and the switch from an acute to a chronic mode of infection at the transcriptional and post-transcriptional levels by modulation of the Gac/Rsm system. Cell density-dependent signal accumulation and environmental stimulators such as pH changes and ion limitation activate the GacS/GacA two-component system which in turn triggers transcription of the small regulatory RNAs RsmY and R
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Daly, Philip J. "Permeability of pseudomonas aeruginosa." Thesis, Aston University, 1986. http://publications.aston.ac.uk/12458/.

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Kluftinger, Janet Louise. "Macrophage interaction with Pseudomonas aeruginosa." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29129.

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The interactions of macrophages with Pseudomonas aeruginosa were studied. Five monoclonal antibodies specific for porin protein F were tested for their ability to opsonize P. aeruginosa for complement-independent phagocytosis by unelicited mouse peritoneal macrophages, human peripheral blood monocytes and mouse macrophage cell line P388[sub D1]. All five antibodies significantly increased the level of bacterial uptake over that obtained with the non-opsonic controls. The relative effectiveness of the different antibodies was approximately the same in all cell types indicating that the P388[sub
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8

Giske, Christian G. "Carbapenem resistance in Pseudomonas aeruginosa /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-080-0/.

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Henrichfreise, Beate. "Antibiotika-Multiresistenz bei Pseudomonas aeruginosa." [S.l.] : [s.n.], 2006. http://www.gbv.de/dms/bs/toc/517839636.pdf.

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Seabra, Rita A. M. "Immune modulation by Pseudomonas aeruginosa." Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436865.

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Beatson, Scott. "Pseudomonas aeruginosa genomics and pathogenesis /." [St. Lucia, Qld.], 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16848.pdf.

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Lasry, Judith. "Les Pseudomonas aeruginosa dans l'environnement." Paris 5, 1998. http://www.theses.fr/1998PA05P233.

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Eschbach, Martin. "Molekulare Regulation und Biochemie des anaeroben Langzeitüberlebens von Pseudomonas aeruginosa." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971750645.

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Wiehlmann, Lutz. "Sequenzspezifizierte Transposonmutagenese (STM) in Pseudomonas aeruginosa." [S.l. : s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=96511211X.

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Juhas, Mario. "Global virulence regulators of Pseudomonas aeruginosa." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=974133221.

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Mettrick, Karla Adelle, and n/a. "Iron signalling pathways of Pseudomonas aeruginosa." University of Otago. Department of Biochemistry, 2008. http://adt.otago.ac.nz./public/adt-NZDU20081128.143145.

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The pathogenic bacterium Pseudomonas aeruginosa uses a variety of highly efficient chelating compounds (siderophores) to acquire sufficient iron for growth and virulence. These siderophores can either be endogenous or acquired from exogenous sources such as other bacteria or fungi. The transport of the endogenous siderophore pyoverdine activates a signal-transduction pathway that increases the synthesis of both the ferripyoverdine receptor protein (FpvA) and pyoverdine itself. Signal-transduction systems similar to this have three specific proteins involved: a receptor protein specific for one
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Léger, Jean-François. "Effects of chloramphenicol on Pseudomonas aeruginosa." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60549.

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The characteristics of the effects of chloramphenicol on Pseudomonas aeruginosa were examined. Resistant strains were easily isolated following a single passage in chloramphenicol at 150 $ mu$g/ml to 500 $ mu$g/ml. Drug detoxification or altered sensitivity of the target site could not be the mechanism of resistance. This resistance to chloramphenicol was correlated with the addition of an outer membrane protein with a molecular weight of 49 kDa and the loss of two outer membrane proteins, one with the molecular weight of 19 kDa and the other of about 10 kDa. The highly specific requirement of
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Wang, Chan-Ju. "Characterisation of azoreductases form pseudomonas aeruginosa." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531806.

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Hughes, M. A. "Transfer RNA genes in Pseudomonas aeruginosa." Thesis, University of Liverpool, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370854.

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Balasubramanian, Deepak. "Pseudomonas Aeruginosa AmpR Transcriptional Regulatory Network." FIU Digital Commons, 2013. http://digitalcommons.fiu.edu/etd/863.

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In Enterobacteriaceae, the transcriptional regulator AmpR, a member of the LysR family, regulates the expression of a chromosomal β-lactamase AmpC. The regulatory repertoire of AmpR is broader in Pseudomonas aeruginosa, an opportunistic pathogen responsible for numerous acute and chronic infections including cystic fibrosis. Previous studies showed that in addition to regulating ampC, P. aeruginosa AmpR regulates the sigma factor AlgT/U and production of some quorum sensing (QS)-regulated virulence factors. In order to better understand the ampR regulon, the transcriptional profiles generated
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Chen, Chun Chiang. "Rhamnolipid Production with Denitrifying Pseudomonas Aeruginosa." University of Akron / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=akron1236689824.

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Moore, Matthew Phillip. "Comparative genomics of Pseudomonas aeruginosa populations." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3021281/.

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Pseudomonas aeruginosa causes a wide range of infections, is often associated with antimicrobial resistance and is the primary cause of chronic lung infection in cystic fibrosis (CF) and the overall morbidity and mortality associated with the disease. As P. aeruginosa is an environmental bacterium that opportunistically infects CF patients most infecting lineages are distinct. The determination of common adaptive routes during infection is further complicated by within-lineage heterogeneity, multi-lineage infections and the emergence of transmissible strains. In order to better understand the
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Stacey, Sean D. "Regulating rsmA Expression in Pseudomonas aeruginosa." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etd/1232.

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Pseudomonas aeruginosa, a Gram-negative bacillus, commonly infects immunocompromised individuals and uses a variety of virulence factors to persist in these hosts. The posttranscriptional regulator, RsmA, plays a role in the expression of many virulence factors in P. aeruginosa. RsmA up regulates virulence factors used in colonizing hosts. However, regulation of rsmA is not well elucidated. Transposon mutagenesis was performed on P. aeruginosa containing a transcriptional rsmA-lacZ fusion to answer this question. Mutants were screened via β-galactosidase assay and transposon insertions identif
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O'Toole, Ann Marie. "Thermal deactivation of Pseudomonas aeruginosa biofilms." Thesis, University of Iowa, 2015. https://ir.uiowa.edu/etd/1715.

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Bacterial biofilm infection is a common (~ 2 to 4%) complication for recipients of surgically implanted medical devices. Due to the tremendous increase in antibiotic resistance when these bacteria enter the biofilm phenotype, present treatment requires explantation and replacement of the device, often with multiple surgeries and always with much longer patient recovery time. The specific objective of this study was to quantify the degree of biofilm deactivation from exposure to thermal shock for varying temperature and time durations. While extreme temperature (>150˚C) is routinely used to ste
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Kowalska, Karolina. "Formation of biofilm in Pseudomonas aeruginosa : molecular characterisation of the macromolecular complex Pel." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22003.

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Pseudomonas aeruginosa est une bactérie pathogène opportuniste qui peut développer deux modes d’infection. Les infections aigües sont associées à la production et à la sécrétion de toxines qui peuvent avoir un effet cytotoxique, alors que dans le contexte d’une infection chronique la bactérie a tendance à s’établir sous la forme d’un biofilm. Un biofilm est une population de microorganismes organisée en une communauté et attachée sur une surface. Cette surface peut être biotique ou abiotique. Les biofilms bactériens ont des caractéristiques intrinsèques qui les rendent plus résistants à des co
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Head, Nathaniel Edwards. "Regulation of biofilm formation of pseudomonas aeruginosa." Huntington, WV : [Marshall University Libraries], 2006. http://www.marshall.edu/etd/descript.asp?ref=663.

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Limpert, Anna Silke. "Functional genome analysis in Pseudomonas aeruginosa SG17M." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976191474.

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Fakhimi, Tatiana. "Sekundära metaboliters antibakteriella effekt mot Pseudomonas aeruginosa." Thesis, Umeå universitet, Farmakologi, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-146099.

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Handfield, Martin. "Expression génique in vivo chez Pseudomonas aeruginosa." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq25421.pdf.

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Meldrum, Allison J. "Regulation of pyoverdine biosynthesis in Pseudomonas aeruginosa." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ37969.pdf.

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Purevdorj-Gage, Boloroo. "Pseudomonas aeruginosa Biofilm Structure, Behavior and Hydrodynamics." Thesis, Montana State University, 2004. http://etd.lib.montana.edu/etd/2004/purevdorj-gage/Purevdorj-GageB1204.pdf.

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Biofilm formation by bacterial pathogens is an important factor in the progression and treatment of many infectious diseases. Biofilm structural development is a dynamic process dependent on many cellular and environmental parameters including Quorum Sensing (QS) and hydrodynamics. Since QS is dependent on a threshold autoinducer concentration, it was hypothesized that the flow dynamics in the bulk fluid surrounding the biofilm would play an important role in expression of QS and the genes that are under its control. In order to investigate the relative contribution of hydrodynamics and QS on
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Xu, Ruifang. "Spatial Growth Patterns of Pseudomonas aeruginosa Biofilms." Thesis, Montana State University, 2004. http://etd.lib.montana.edu/etd/2004/xu/XuR0805.pdf.

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Biofilms are less susceptible to antimicrobial action compared to their planktonic counterparts. The protective mechanisms are not fully understood. Physiological heterogeneity within biofilms is thought to contribute to the low susceptibility and was therefore studied. Expression of green fluorescent protein (GFP), induction of alkaline phosphatase (APase) by phosphate starvation, and the cell viability assay using the LIVE/DEAD BacLight bacterial viability stain were performed to visualize the spatial patterns of growth and viability within 5-d-old Pseudomonas aeruginosa biofilms. The capill
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Fu, Yinan. "Structure and dynamics of Pseudomonas aeruginosa ICP." Thesis, University of Glasgow, 2009. http://theses.gla.ac.uk/723/.

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Pseudomonas aeruginosa inhibitor of cysteine peptidases (PA-ICP) is a potent protein inhibitor of papain-like cysteine peptidases (CPs) identified in Pseudomonas aeruginosa, an opportunistic pathogenic bacteria that can cause severe infections in human. It belongs to the newly characterized natural CP inhibitors of the I42 family, designated the ICP family. The members of this family are present in some protozoa and bacterial pathogens. They can inhibit both parasite and mammalian CPs with high affinity and specificity. Whether the main biological function of the proteins in the pathogens is t
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Worrall, Kathryn E. "The role of MvaT in Pseudomonas aeruginosa." Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430524.

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Gifford, Danna R. "Population genetics of rifampicin-resistant Pseudomonas aeruginosa." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:044b9258-4f10-4e77-9ff6-aa4035cec33b.

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Antibiotic resistance is generally associated with a cost in terms of reduced competitive fitness in the absence of antibiotics. Despite this 'cost of resistance', the cessation of antibiotic treatment does not result in significant reductions in the prevalence of resistance. The maintenance of resistance, in spite of the costs, has been attributed to the rarity of reversion mutations, relative to compensatory mutations at other loci in the genome. However, the large size of bacteria populations, and the potential for migration, suggest that reversion mutations should occasionally be introduce
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Crescente, Vincenzo. "Azoreductases : genes and proteins in Pseudomonas aeruginosa." Thesis, Kingston University, 2015. http://eprints.kingston.ac.uk/36328/.

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Pseudomonas aeruginosa is one of the primary causes of opportunistic infections in humans and it is associated with both acute and chronic infections in immunocompromised individuals. This bacterium is extremely resistant to many antibiotics, making the treatments against this pathogen often unsuccessful. Azoreductases, a family of enzymes involved in the reduction of azo compounds and quinones, are found in many bacterial species including P. aeruginosa. Although the enzymatic activity of three of these enzymes has been extensively characterized, their physiological role remains unclear. In t
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Davies, Emily. "The role of prophages in Pseudomonas aeruginosa." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2034639/.

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Pseudomonas aeruginosa is a common opportunistic respiratory pathogen of individuals with cystic fibrosis (CF), capable of establishing chronic infections in which the bacterial population undergoes extensive phenotypic and genetic diversification. The Liverpool Epidemic Strain (LES) is a widespread hypervirulent and transmissible strain that is capable of superinfection and is linked to increased morbidity and mortality, relative to other P. aeruginosa strains. The LES has six prophages (LESφ1-6) within its genome, of which three are essential to the competitiveness of this strain. Temperate
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Bhamra, Amrat. "Pathogenesis of Pseudomonas aeruginosa in leukaemic patients." Thesis, University of Surrey, 1993. http://epubs.surrey.ac.uk/843880/.

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The incidence of production and biological activity of various extracellular factors of Pseudomonas aeruginosa from leukaemic and non-leukaemic patients were investigated. A panel of 157 isolates was constructed from blood of leukaemic (Group I), and other body sites of the same patients (Group II), and from various specimens of non-leukaemic patients (Group III). Most strains produced pyocyanin. Cross infection between patients was not a significant problem. The incidence of protease production was high (94%) and there was no significant quantitative difference between strains. Protease produ
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Saulnier, Joëlle. "Activités enzymatiques de l'élastase de Pseudomonas aeruginosa." Lyon 1, 1989. http://www.theses.fr/1989LYO10107.

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Pseudomonas aeruginosa est une bacterie pathogene qui est responsable de nombreuses infections graves. Il a ete demontre que l'elastase secretee par la bacterie contribue a la pathogenicite de celle-ci mais son role exact n'a pas ete clairement elucide. C'est pourquoi nous avons entrepris d'etudier quelques unes de ses proprietes tant structurales qu'enzymatiques. Apres des rappels bibliographiques et la presentation des materiels et methodes utilises, nous avons expose nos resultats: 1) les vitesses initiales d'elastolyse d'elastines bovine et humaine par l'elastase ont ete mesurees par la me
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Vareechon, Chairut Charles. "Host-Pathogen Interaction in Pseudomonas aeruginosa Infection." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1499427972888735.

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ANDRIEU, LAURENCE. "Caracterisation d'une alginate lyase de pseudomonas aeruginosa." Paris 11, 1995. http://www.theses.fr/1995PA112264.

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Pseudomonas aeruginosa est une bacterie pathogene opportuniste pouvant entrainer des infections graves, surtout au niveau des poumons des malades atteints de mucoviscidose. Sous l'effet de facteurs environnementaux, les bacteries vont produire des exopolysaccharides, les alginates, facteur important de la virulence de la bacterie. Les alginates sont des polymeres d'acides d-mannuronique et l-guluronique en liaison 1-4. Ils sont hydrolyses par un enzyme specifique, l'alginate lyase, qui catalyse une reaction de -elimination entre deux residus d-mannurosyl ou l-gulurosyl. Une activite alginolyti
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Wilton, Alison Jane. "Iron-regulated surface antigens of Pseudomonas aeruginosa." Thesis, Aston University, 1989. http://publications.aston.ac.uk/12564/.

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Baretto, Bernadette J. "Studies on survival of Pseudomonas aeruginosa 6750." Thesis, Aston University, 1996. http://publications.aston.ac.uk/11046/.

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The growth of Pseudomonas aeruginosa 6750 as a biofilm was investigated using a novel system based on that of Gilbert et al (1989). The aim was to test the effect of controlled growth of the organism on antibiotic susceptibility and examine the survival of the organism as a biofilm. During the investigations it became clear that, because of the increasing growth of P.aeruginosa and production of exopolysaccharide, a growth rate controlled monolayer could not be achieved and so the method was not used further. The data, however, showed that there was an increase in the smooth colony type of the
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Noguès, Aurélie. "Résistance adaptative aux polymyxines chez Pseudomonas aeruginosa." Thesis, Besançon, 2015. http://www.theses.fr/2015BESA3006.

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La résistance aux polymyxines chez P. aeruginosa résulte en partie de la modification du lipide A par addition de 4-amino-aL-arabinose (L-Ara4N), due à l'expression de l'opéron arnBCADTEF-ugD (arn), activée par au moins 6 systèmes de régulation à deux composants (S2C). Nous avons mis en évidence que P. aeruginosa était capable de s'adapter de manière transitoire à la présence de fortes concentrations de polymyxines (8 x CMI) aussi bien in vitro que in vivo dans un modèle murin d'infection pulmonaire aiguë. La délétion de l'opéron arn chez la souche sauvage n'a pas modifié la capacité d'adaptat
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Klebensberger, Janosch. "Detergent-induced cell aggregation in Pseudomonas aeruginosa." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:352-opus-26614.

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Damron, Frederick H. "Regulation of alginate production of Pseudomonas aeruginosa." [Huntington, WV : Marshall University Libraries], 2009. http://www.marshall.edu/etd/descript.asp?ref=999.

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Ferreira, Luciana Lobianco. "Estrutura clonal e multirresitência em Pseudomonas aeruginosa." reponame:Repositório Institucional da FIOCRUZ, 2005. https://www.arca.fiocruz.br/handle/icict/8542.

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Made available in DSpace on 2014-10-07T19:33:50Z (GMT). No. of bitstreams: 2 license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) 147.pdf: 1702752 bytes, checksum: 2ca15a3ffb097f591dfca56269551aba (MD5) Previous issue date: 2005<br>Fundação Oswaldo Cruz. Instituto Nacional de Controle de Qualidade em Saúde. Rio de Janeiro, RJ, Brasil.<br>O presente trabalho teve como principal objetivo avaliar a multirresistência e os fatores envolvidos na resistência aos carbapenemas, em 187 cepas de Pseudomonas aeruginosa oriundas de hospitais no Rio de Janeiro {3) e Mato Grosso do Sul
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Speaks, Tyler. "AlgR Directly Controls rsmA in Pseudomonas aeruginosa." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etd/2570.

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Pseudomonas aeruginosa is a bacterial pathogen that can infect any human tissue. The lungs of cystic fibrosis patients become chronically infected with Pseudomonas aeruginosa. Virulence factor gene expression is under elaborate regulatory control that remains poorly characterized. Understanding the regulatory hierarchy involved during infection is essential for identifying novel drug targets. RsmA is a post-transcriptional regulatory protein that controls expression of several virulence factors. Previous studies demonstrated alginate regulatory components AlgU and AlgR as regulators of rsmA ex
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Pandey, Sundar. "Novel Role of Pseudomonas Aeruginosa LptD Operon." FIU Digital Commons, 2018. https://digitalcommons.fiu.edu/etd/3734.

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Pseudomonas aeruginosais an opportunistic pathogen that infects cystic fibrosis (CF) patients contributing to their high morbidity and mortality. P. aeruginosaundergoes a phenotypic conversion in the CF lung, from nonmucoid to mucoid, by constitutively producing a polysaccharide called alginate. These mucoid strains often revert to nonmucoid in vitrodue to second-site suppressor mutations. We hypothesized that mapping these mutations would lead to the identification of novel genes involved in alginate production. In a previous study, a mucoid strain, PDO300 (PAOmucA22), was used to isolate sup
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Pesaresi, Alessandro. "Pseudomonas aeruginosa PA3859: From Structure to Function." Doctoral thesis, SISSA, 2005. http://hdl.handle.net/20.500.11767/4739.

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The aim of this work has been the structural and functional study of a putative carboxylesterase purified from P. aeruginosa, namely PA3859. The protein has been purified from the wild type and a preliminary biochemical charcterization was carried out. The PA3859 gene was then cloned and the recombinant protein was expressed in E. coli (Chapter 2). The recombinant PA3859 was successfully crystallized and its 3D crystal structure was determined (Chapter 3 and 4). Starting from the enzyme 3D structure, an approach involving in silico, in vitro and in vivo ass
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