Bibliografie tematiche / Pseudomonas aeruginosa

Letteratura scientifica selezionata sul tema "Pseudomonas aeruginosa"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 29 luglio 2024

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Articoli di riviste sul tema "Pseudomonas aeruginosa"

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FARRAG, SEHAM A., e ELMER H. MARTH. "Behavior of Listeria monocytogenes when Incubated Together with Pseudomonas Species in Tryptose Broth at 7 and 13°C". Journal of Food Protection 52, n. 8 (1 agosto 1989): 536–39. http://dx.doi.org/10.4315/0362-028x-52.8.536.

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Tryptose broth (TB) was inoculated with Listeria monocytogenes (strain Scott A or California), Pseudomonas aeruginosa, Pseudomonas flourescens, or a combination of L. monocytogenes plus Pseudomonas species, and incubated at 7 or 13°C for 8 weeks. McBride Listeria Agar was used to determine numbers of L. monocytogenes and Pseudomonas Isolation Agar to enumerate Pseudomonas species at 0, 7, 14, 28, 42, or 56 d. At 13°C, presence of P. fluorescens had a slight negative effect on growth of L. monocytogenes strain Scott A, and was somewhat detrimental to its survival during the extended incubation. Growth of L. monocytogenes strain California was retarded by presence of P. fluorescens although the maximum population achieved by the pathogen was greater in the presence rather than absence of the pseudomonad; the pseudomonad did have a negative effect on survival of the pathogen. At the same temperature, P. aeruginosa had a negative effect on survival of L. monocytogenes strain California, but had essentially no effect on the other strain of the pathogen. Neither strain of L. monocytogenes affected growth of P. fluorescens nor P. aeruginosa. At 13°C the pH of TB generally decreased when L. monocytogenes grew by itself but increased when either pseudomonad grew by itself or together with the pathogen. At 7°C, growth of both pseudomonads was minimal. Presence of non-growing cells of P. fluorescens retarded somewhat growth of both L. monocytogenes strains early during the incubation. P. aeruginosa had no detectable effect on either strain of L. monocytogenes. The pH of TB decreased when L. monocytogenes grew by itself or together with either pseudomonad, and remained unchanged in TB inoculated with either pseudomonad.
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Young, Heather, Bryan Knepper, Whitney Hernandez, Asaf Shor, Merribeth Bruntz, Chrystal Berg e Connie S. Price. "Pseudomonas aeruginosa". Journal of the American Podiatric Medical Association 105, n. 2 (1 marzo 2015): 125–29. http://dx.doi.org/10.7547/0003-0538-105.2.125.

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Background Pseudomonas aeruginosa has traditionally been considered a common pathogen in diabetic foot infection (DFI), yet the 2012 Infectious Diseases Society of America guideline for DFI states that “empiric therapy directed at P aeruginosa is usually unnecessary.” The objective of this study was to evaluate the frequency of P aeruginosa isolated from bone or tissue cultures from patients with DFI. Methods This study is a cross-sectional survey of diabetic patients presenting with a foot infection to an urban county hospital between July 1, 2012, and December 31, 2013. All of the patients had at least one debridement procedure during which tissue or bone cultures from operative or bedside debridements were obtained. The χ2 test and the t test of means were used to determine relationships between variables and the frequency of P aeruginosa in culture. Results The median number of bacteria isolated from DFI was two. Streptococcus spp and Staphylococcus aureus were the most commonly isolated organisms; P aeruginosa was isolated in only five of 112 patients (4.5%). The presence of P aeruginosa was not associated with the patient's age, glycosylated hemoglobin level, tobacco abuse, the presence of osteomyelitis, a prescription for antibiotic drugs in the preceding 3 months, or the type of operative procedure. Conclusions Pseudomonas aeruginosa was an infrequent isolate from DFI in this urban, underserved diabetic population. The presence of P aeruginosa was not associated with any measured risk factors. By introducing a clinical practice guideline, we hope to discourage frontline providers from using routine antipseudomonal antibiotic drugs for DFI.
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Weinberg, M. "Pseudomonas aeruginosa". Kazan medical journal 20, n. 5 (11 agosto 2021): 551. http://dx.doi.org/10.17816/kazmj76617.

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Pennington, James E. "Pseudomonas aeruginosa". Infectious Disease Clinics of North America 4, n. 2 (giugno 1990): 259–70. http://dx.doi.org/10.1016/s0891-5520(20)30340-8.

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Hauser, Alan R. "Pseudomonas aeruginosa". American Journal of Respiratory and Critical Care Medicine 178, n. 5 (settembre 2008): 438–39. http://dx.doi.org/10.1164/rccm.200805-789ed.

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Wright, Gordon L. T. "Pseudomonas aeruginosa". Medical Journal of Australia 158, n. 3 (febbraio 1993): 214. http://dx.doi.org/10.5694/j.1326-5377.1993.tb121719.x.

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Chen, Xi, Benjamin S. Bleier, Daniel R. Lefebvre e Nahyoung Grace Lee. "Pseudomonas Aeruginosa". Ophthalmic Plastic and Reconstructive Surgery 32, n. 5 (2016): 374–77. http://dx.doi.org/10.1097/iop.0000000000000558.

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SHEFF, BARBARA. "Pseudomonas aeruginosa". Nursing 30, n. 5 (maggio 2000): 79. http://dx.doi.org/10.1097/00152193-200030050-00047.

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Cornaglia, G. "Pseudomonas aeruginosa". International Journal of Infectious Diseases 14 (marzo 2010): e24. http://dx.doi.org/10.1016/j.ijid.2010.02.1541.

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Besedin, O. M., S. O. Kosulnikov, L. M. Storubel, S. I. Karpenko, S. O. Tarnopolsky, K. V. Kravchenko, A. S. Kudryavtsev, K. O. Sinitsa, G. M. Pundik e L. I. Karpenko. "Infections caused by Pseudomonas aeruginosa isolates in patients of Surgical Infections Department". Modern medical technologies 41 part 1, n. 2 (6 aprile 2019): 56–60. http://dx.doi.org/10.34287/mmt.2(41).2019.11.

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The role of Pseudomonas aeruginosa isolates among the pathogens of surgical infection in purulent-septic surgery department for 2018 is determined. Investigated the antibiotic resistance of Pseudomonas aeruginosa hospital strains and the most effective antibiotics were investigated. Poly resistant in wound material were almost half of the cultures of Pseudomonas aeruginosa (19 strains, 45,2%). Carbapenem resistant Pseudomonas aeruginosa was found to be 47,1%. Of the aminoglycoside group antibiotics, Tobramycin (82,1%) showed the best sensitivity, Amikacin was sensitive in half of the microorganisms tested (55,0%). The sensitivity of cephalosporins ranged from 23,1% (Cefoperazone) to 40,5% (Ceftazidime). Even the use of the Sulbactam protective molecule did not improve the situation: 37,5% (Cefoperazone/ Sulbactam). For fluoroquinolones (Ciprofloxacin) sensitive third part of bacteria only. Piperacillin with Tazobactam, Fosfomycin, and Colistin E showed a high anti-pseudomonad efficacy. The use of anti-diarrhea bacteriophage was ineffective. Keywords: hospital strains, antibiotic resistance, Pseudomonas aeruginosa.
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Tesi sul tema "Pseudomonas aeruginosa"

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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. This work illuminates the simplicity with which a transcription regulatory network can exhibit a complex behavior and generate phenotypic diversity in a clonal population.
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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 RsmZ. These sRNAs sequester multiple copies of the RNA-binding protein RsmA, antagonising its function. The RsmA/CsrA proteins act as translational repressors by binding to the GGA-motifs in the untranslated region of target mRNAs and blocking ribosome binding. In this study, the biological function of RsmN, an RsmA homologue with a conserved RNA-binding pocket but a distinct protein folding, the predicted autoregulatory mechanism of RsmN, the nature of target transcripts of RsmN, and the cross-regulation between the two Rsm proteins were investigated. The positive control of proteolytic and elastinolytic activities and swarming motility by RsmN has been demonstrated using single and inducible double deletion mutants of rsmN. Furthermore, rsmN deletion increased microcolony formation during biofilm formation. Regulation by RsmN was most apparent in the absence of RsmA, when rsmN expression was induced via a multicopy plasmid and at temperatures lower than 37°C. The double deletion of rsmA and rsmN affected growth, diminished proteolytic and elastinolytic activities, triggered autolysis and led to the increased secretion of the type VI secretion system protein Hcp1. Moreover, the double deletion of rsmA and rsmN altered the colony morphology of P. aeruginosa. Mutagenesis of the functionally critical, conserved RNA-binding residue which is identified as Arg44 in RsmA and Arg62 in RsmN resulted in the loss of RsmN function. In a genome-wide analysis by RNASeq, target transcripts were co-purified with RsmN from 37°C and 34°C cultures of a wild-type strain expressing rsmN in multicopy numbers. RNASeq results indicated that small regulatory RNAs such as CrcZ, RsmY and RgsA are common targets of RsmN and RsmA, whereas PhrS is a target of RsmN only. Other common RsmA and RsmN targets included transcriptional regulators, heat shock proteins, proteases, starvation response proteins, components of the denitrification pathway, outer membrane proteins required for pore formation, type III and type VI secretion system proteins and RsmA. Transcripts of heat shock proteins, the tss operon genes and rsmA were enriched by RsmN at 37°C but not at 34°C whereas the lasB transcript was enriched by RsmN at 34°C but not at 37°C. Based on the list of common targets of RsmA and RsmN and the results obtained from phenotypic assays, induction of the lytic Pf4 prophage, accumulation of alkyl quinolone or c-di-GMP signalling molecules, imbalanced redox state, carbon starvation, increased membrane permeability, and aggregation of misfolded proteins are suggested as possible mechanisms triggering the excessive autolysis of the rsmNind ΔrsmA mutant under uninducing conditions. The data gathered so far suggests that rsmN is differentially expressed, with increased RsmN activity at temperatures below 37°C in comparison with RsmA, and, RsmA and RsmN collectively contribute to the regulation of secondary metabolite production, motility and microcolony formation in P. aeruginosa.
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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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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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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 D1] cells can be used as a model for normal macrophages. Of the four monoclonal antibodies directed against similar epitopes of protein F, the three IgGl monoclonal antibodies were substantially more opsonic than the one IgG2a isotype. P. aeruginosa cytotoxin and periplasmic contents caused a significant reduction in antibody-mediated phagocytosis of P. aeruginosa. Phagocytosis was restored upon pre-incubation with anti-cytotoxin serum. Both cytotoxin and periplasmic contents caused depolarization of the P388[sub D1] cell membrane, as demonstrated using a polarization-sensitive fluorescent probe. These data indicated that P. aeruginosa cytotoxin was localized in the periplasm and had the potential to inhibit macrophage-mediated phagocytosis, possibly by perturbing ion gradients across the macrophage plasma membrane. Monoclonal antibodies directed against protein F were also capable of enhancing phagocytosis of in vivo-grown P. aeruginosa. P. aeruginosa cells taken directly from the in vivo growth system were significantly more susceptible to macrophage phagocytosis than were the same cells after being washed in buffer. The phagocytosis-promoting factor could be isolated from the supernatant of in vivo-grown bacteria and was determined to be fibronectin. Data indicated that promotion by fibronectin of non-opsonic phagocytosis was mediated by direct activation of the macrophages. The tetrapeptide arginine-glycine-aspartate-serine in the eukaryotic cell binding domain of fibronectin was demonstrated to be the macrophage-activating region. Phagocytosis of a mutant P. aeruginosa strain lacking surface pili could not be enhanced by fibronectin. Furthermore, exogenously added Pseudomonas pili was capable of abrogating the enhanced phagocytosis of the wild type strain observed with fibronectin-activated macrophages. It was concluded that Pseudomonas pili were the bacterial ligands required for attachment to fibronectin-activated macrophages in the initial stages of non-opsonic phagocytosis.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate
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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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Libri sul tema "Pseudomonas aeruginosa"

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Filloux, Alain, e Juan-Luis Ramos, a cura di. Pseudomonas aeruginosa. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08491-1.

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Bertoni, Giovanni, e Silvia Ferrara, a cura di. Pseudomonas aeruginosa. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-3473-8.

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Niels, Høiby, a cura di. Pseudomonas aeruginosa infection. Basel: Karger, 1989.

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Mario, Campa, Bendinelli Mauro e Friedman Herman 1931-, a cura di. Pseudomonas aeruginosa as an opportunistic pathogen. New York: Plenum Press, 1993.

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Daly, Philip John. Permeability of pseudomonas aeruginosa. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1986.

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Spangenberg, Claudia. Sequenzdiversität von Pseudomonas aeruginosa. [s.l.]: [s.n.], 1997.

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G, Döring, Holder Ian Alan e Botzenhart K, a cura di. Basic research and clinical aspects of Pseudomonas aeruginosa. Basel: Karger, 1987.

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Fursova, P. V. Limitirui︠u︡shchie resursy i sostav soobshchestva bakteriĭ: Ėksperimenty i modelʹnyĭ analiz. Moskva: GEOS, 2008.

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B, Fick Robert, a cura di. Pseudomonas aeruginosa, the opportunist: Pathogenesis and disease. Boca Raton: CRC Press, 1993.

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Y, Homma J., a cura di. Pseudomonas aeruginosa in human diseases. Basel: Karger, 1991.

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Capitoli di libri sul tema "Pseudomonas aeruginosa"

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Lefebvre, Cedric W., Jay P. Babich, James H. Grendell, James H. Grendell, John E. Heffner, Ronan Thibault, Claude Pichard et al. "Pseudomonas aeruginosa". In Encyclopedia of Intensive Care Medicine, 1868–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_95.

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Paterson, David L., e Baek-Nam Kim. "Pseudomonas aeruginosa". In Antimicrobial Drug Resistance, 811–17. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-595-8_9.

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Anuj, Snehal, e David M. Whiley. "Pseudomonas aeruginosa". In PCR for Clinical Microbiology, 191–95. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9039-3_24.

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Gronthoud, Firza Alexander. "Pseudomonas aeruginosa". In Practical Clinical Microbiology and Infectious Diseases, 378–82. First edition. | Boca Raton : CRC Press, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9781315194080-5-4.

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Panayidou, Stavria, e Yiorgos Apidianakis. "Pseudomonas aeruginosa". In Laboratory Models for Foodborne Infections, 373–89. Boca Raton : CRC Press/Taylor & Francis, 2017. | Series: Food microbiology series: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120089-25.

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Poole, Keith. "Pseudomonas aeruginosa". In Frontiers in Antimicrobial Resistance, 355–66. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817572.ch26.

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Liu, Junyan, Ruirui Xu, Zerong Lu, Guangchao Yu e Zhenbo Xu. "Pseudomonas aeruginosa". In Molecular Typing in Bacterial Infections, Volume II, 147–68. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-83217-9_8.

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Lam, Joseph S., Mauricia Matewish e Karen K. H. Poon. "Lipopolysaccharides of Pseudomonas aeruginosa". In Pseudomonas, 3–51. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9088-4_1.

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Cohen, Taylor S., Dane Parker e Alice Prince. "Pseudomonas aeruginosa Host Immune Evasion". In Pseudomonas, 3–23. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9555-5_1.

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Temple, Louise M., Andrew E. Sage, Herbert P. Schweizer e Paul V. Phibbs. "Carbohydrate Catabolism in Pseudomonas aeruginosa". In Pseudomonas, 35–72. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0120-0_2.

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Atti di convegni sul tema "Pseudomonas aeruginosa"

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Silva, Leidyanne Karolaine Barbosa da, Esaú Simões Da Silva, Rhana Cavalcanti Do Nascimento e Maria Joanellys dos Santos Lima. "RESISTÊNCIA ANTIMICROBIANA DE PSEUDOMONAS AERUGINOSA EM AMBIENTE HOSPITALAR". In Anais do II Congresso Brasileiro de Saúde On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1971.

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Introdução: Pseudomonas aeruginosa é uma bactéria gram negativa que causa principalmente pneumonias, a mesma está associada a grande parte das infecções intra-hospitalares que podem ocorrer em um período de 48h após a entrada na unidade de saúde, ou até 10 dias após a alta médica. Raramente causa problemas em pacientes saudáveis, entretanto, é uma das responsáveis por morbidade e mortalidade nos imunocomprometidos, como os portadores de fibrose cística. Objetivo: Este trabalho possui como objetivo realizar uma breve revisão sobre a resistência da P. aeruginosa a antimicrobianos em ambiente hospitalar. Métodos: Foi feito um estudo literário nos idiomas inglês, espanhol e português, nas bases de dados: Pubmed, BDTD e ScienceDirect, utilizando os descritores “Pseudomonas aeruginosa”, “Mortalidade Hospitalar”, “Farmacorresistência Bacteriana Múltipla”, durante o período de 2019 a 2021. Resultado: A P. aeruginosas é conhecida coma uma bactéria super-resistente a diversos antimicrobianos e o seu genoma é considerado relativamente grande (5.5 a 7 Mbp) quando comparado a Escherichia coli e Mycobacterium tuberculosis, o que pode ser justificado pela existência de genes como MP, VIM, OXA, MexAB-OprM, MexCD-OprJ, MexEF-OprN e MexXY-OprM que codificam proteínas que oferecem resistência a antimicrobianos como a classe de β-lactâmicos e aminoglicosídeos. Pacientes de Unidade de Terapia Intensiva estão mais propensos a contrair a bactéria, no Brasil o número de infecções causadas por P. aeruginosas resistente chega a 36,6%, sendo o seu fenótipo mucoide um fator importante para a virulência, a produção de muco através da P. aeruginosa forma um biofilme que oferece resistência aos fármacos, e dificulta a ação natural do sistema imunológico. Com a alta resistência, uma ação bastante eficaz para o tratamento dessa bacteriose seria a utilização de bacteriófagos líticos específicos, que são vírus que infectam a bactéria causando lise celular, representando assim, uma ótima alternativa biológica para o tratamento desta infecção. Conclusão: A alta resistência da P. aeruginosa no ambiente hospitalar é uma causa preocupante para os profissionais de saúde, uma vez que as terapias conhecidas para tratamento dessa bactéria não são capazes de acompanhar a evolução da mesma, sendo assim se faz necessário mais estudos de desenvolvimento de terapias inovadoras para o combate dessa bacteriose.
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Zeng, Xiaoxi, Xueduan Liu, Pei Jiang, Wen Li e Jianxin Tang. "Cadmium Removal by Pseudomonas aeruginosa E1". In 2009 International Conference on Energy and Environment Technology. IEEE, 2009. http://dx.doi.org/10.1109/iceet.2009.351.

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Mahgoub, Yasmine, Rida Arif e Susu Zughaier. "Pyocyanin pigment from Pseudomonas aeruginosa modulates innate immune defenses in macrophages". In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0137.

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Background: Pseudomonas aeruginosa is a well-known opportunistic pathogen. The gram-negative bacillus, commonly associated with hospital-acquired infections, utilizes the host’s impaired immune responses to establish infection. Of its many virulence factors, pyocyanin is essential for P. aeruginosa to establish its full infectivity. Macrophages act as sentinels of the innate immune system, as well as play other roles in homeostasis, tissue remodeling, and bridging between the innate and adaptive immune systems. Aim: This study aimed to investigate the effects of pyocyanin on macrophage innate immune defenses by assessing the function of macrophages treated with pyocyanin and TLR ligands. Phagocytosis of opsonized zymosan, LPS-induced nitric oxide release and cytokine release were used as measures of functional responses. Results: This study found that pyocyanin inhibited phagocytosis-induced ROS release in a dose-dependent manner and reduced nitric oxide release from macrophages induced with P. aeruginosa LPS. In addition, pyocyanin modulated cytokines and chemokines release from macrophages exposed to P. aeruginosa LPS in a dose-dependent manner. Pyocyanin significantly enhanced IL-1β release as well as several chemokines. Therefore, pyocyanin facilitates Pseudomonas aeruginosa to persevere in the immunocompromised host through modulating macrophage’s innate immune defenses. Conclusion: Pyocyanin inhibits macrophage functional defense responses to facilitate Pseudomonas aeruginosa infection.
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Alzubaidy, Mohanad W. Mahdi, Asmaa M. Salih Almohaidi, Ammar Ahmed Sultan e Sana M. H. AL-Shimmary. "Virulence gene of Pseudomonas aeruginosa with nanoparticle". In XIAMEN-CUSTIPEN WORKSHOP ON THE EQUATION OF STATE OF DENSE NEUTRON-RICH MATTER IN THE ERA OF GRAVITATIONAL WAVE ASTRONOMY. AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5116966.

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Stanley, G. L., B. Chan, I. Ott, E. Mayo, Z. M. Harris, Y. Sun, B. Hu, G. Rajagopalan, P. Turner e J. L. Koff. "Bacteriophage Therapy Decreases Pseudomonas Aeruginosa Lung Inflammation". In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2977.

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Skoric, Billy, Anne-Marie F. Gibson, Rosemary Carzino, Jo Harrison, Kay Ramsay, Timothy Kidd, Scott Bell e Sarath C. Ranganathan. "Geographical Differences In Acquisition Of Pseudomonas Aeruginosa". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2470.

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Dunn, M., G. J. Beltran Ale, R. Steuart, J. Thomson, E. Hysinger, C. Hart, A. de Alarcon e D. Benscoter. "Pseudomonas Aeruginosa Cultures in Pediatric Tracheostomy Patients". In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7168.

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8

Lobo, Leonard J., Clair Doerschuk e Jessica Martin. "Clearance Of Pseudomonas Aeruginosa From The Lungs". In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1792.

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9

Akbar, A., D. AL-Otaibi, H. Drobiova, C. Obwekue e E. Al-Saleh. "Occurrence of Pseudomonas aeruginosa in Kuwait environment". In GEO-ENVIRONMENT 2008. Southampton, UK: WIT Press, 2008. http://dx.doi.org/10.2495/geo080061.

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VORONINA, O. L., E. I. AKSENOVA, N. E. SHARAPOVA, M. S. KUNDA, N. N. SEMENOV, A. N. RYZHOVA e N. A. ZIGANGIROVA. "THE DIVERSITY OF CLINICAL PSEUDOMONAS AERUGINOSA STRAINS". In 5TH MOSCOW INTERNATIONAL CONFERENCE "MOLECULAR PHYLOGENETICSAND BIODIVERSITY BIOBANKING". TORUS PRESS, 2018. http://dx.doi.org/10.30826/molphy2018-39.

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Rapporti di organizzazioni sul tema "Pseudomonas aeruginosa"

1

Lewis, Kim. Genetics of Persister Formation in Pseudomonas aeruginosa. Fort Belvoir, VA: Defense Technical Information Center, dicembre 2012. http://dx.doi.org/10.21236/ada580295.

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2

Schnider, Shirley. The biological properties of Pseudomonas aeruginosa bacteriophage 7V. Portland State University Library, gennaio 2000. http://dx.doi.org/10.15760/etd.771.

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Benson, Deanne. A study of RNA bacteriophage 7s infection of Pseudomonas aeruginosa. Portland State University Library, gennaio 2000. http://dx.doi.org/10.15760/etd.2139.

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4

McFarland, Lynne. Purification and properties of lysozyme from Pseudomonas aeruginosa bacteriophage 7v. Portland State University Library, gennaio 2000. http://dx.doi.org/10.15760/etd.2982.

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5

Avedovech, Richard. Nutritional requirements for protease production by Pseudomonas aeruginosa, Ps-1C. Portland State University Library, gennaio 2000. http://dx.doi.org/10.15760/etd.629.

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6

Borisova, Dayana, Tanya Strateva, Tsvetelina Paunova-Krasteva, Ivan Mitov e Stoyanka Stoitsova. Phenotypic Investigation of Paired Pseudomonas aeruginosa Strains Isolated from Cystic Fibrosis Patients Prior- and Post-tobramycin Treatment. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, agosto 2018. http://dx.doi.org/10.7546/crabs.2018.08.05.

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Bigaud, Mariah A., e Anna Kam-Ha Yeung-Cheung. The in vitro Studies of the Inhibitory Effect of Green Tea (Camellia sinensis) on Pseudomonas aeruginosa Treated Contact Lenses. Journal of Young Investigators, aprile 2017. http://dx.doi.org/10.22186/jyi.32.4.25-29.

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8

Feng, XinYu, e YuLan Zeng. Effects of Pseudomonas aeruginosa infection on the prognosis of patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, aprile 2021. http://dx.doi.org/10.37766/inplasy2021.4.0092.

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9

Petrova, Atanaska, Tsvetelina Borisova, Yana Feodorova, Irina Stanimirova, Tsonka Miteva-Katrandzhieva, Michael Petrov e Marianna Murdjeva. Analysis of OprD Receptor in Carbapenem Resistant Clinical Isolates Pseudomonas aeruginosa and Interplay between the Expression of Main Efflux Pumps and Intrinsic AmpC. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, dicembre 2018. http://dx.doi.org/10.7546/crabs.2018.12.15.

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