Relevant bibliographies by topics / Aeruginosa

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Aeruginosa'

Author: Grafiati
Published: 4 June 2021
Last updated: 22 June 2024

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Journal articles on the topic "Aeruginosa"

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Zhang, Shulin, Bo Zhang, Kezhi Xing, Xiumei Zhang, Xiuping Tian, and Wei Dai. "Inhibitory effects of golden thread (Coptis chinensis) and berberine on Microcystis aeruginosa." Water Science and Technology 61, no. 3 (February 1, 2010): 763–69. http://dx.doi.org/10.2166/wst.2010.857.

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The effects of 40 Chinese herbs on Microcystis aeruginosa growth were monitored spectrophotometrically. Golden thread (Coptis chinensis) exhibited the best inhibitory effects. Cell density of M. aeruginosa decreased with the increasing concentrations of golden thread and the prolongation of exposure time. Decreases in protein content, carbohydrate content, and chlorophyll a content were observed in a golden thread concentration-dependent manner after 96 h exposure. Changes in cell density, protein content, carbohydrate content, and chlorophyll a content of M. aeruginosa exposed to berberine, the main component of golden thread, were also investigated. It was observed that berberine exhibited the same inhibitory effects on M. aeruginosa. The results suggested that golden thread could inhibit M. aeruginosas growth effectively, and berberine might be the main allelochemical implementing the inhibitory effects of golden thread.
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Gasink, Leanne B., Neil O. Fishman, Irving Nachamkin, Warren B. Bilker, and Ebbing Lautenbach. "Risk Factors for and Impact of Infection or Colonization With Aztreonam-Resistant Pseudomonas aeruginosa." Infection Control & Hospital Epidemiology 28, no. 10 (October 2007): 1175–80. http://dx.doi.org/10.1086/520740.

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Objective.To identify risk factors for infection or colonization with aztreonam-resistant Pseudomonas aeruginosa and examine the impact of this organism on mortality.Design.A case-control study was performed to identify risk factors for infection or colonization with aztreonam-resistant P. aeruginosa. A cohort study was subsequently performed to examine the impact of aztreonam resistance on outcomes.Setting.A tertiary referral center in southeastern Pennsylvania.Participants.Inpatients with a clinical culture positive for P. aeruginosa between January 1, 1999, and December 31, 2000.Results.Of 720 P. aeruginosa, isolates, 183 (25.4%) were aztreonam-resistant and 537 (74.6%) were aztreonam susceptible. In a multivariable model, prior fluoroquinolone use (adjusted odds ratio [aOR], 1.81 [95% confidence interval {CI}, 1.17-2.80]), prior use of an antianaerobic agent (aOR, 1.56 [95% CI, 1.06-2.29]), and renal insufficiency (aOR, 1.59 [95% CI, 1.10-2.29]) were associated with infection or colonization with aztreonam-resistant P. aeruginosa, while older age (aOR, 0.98 [95% CI, 0.97-0.99] per year of age) was negatively associated with infection or colonization with this organism. In-hospital mortality was higher among subjects infected or colonized with aztreonam-resistant P. aeruginosa, compared with those who were infected or colonized with aztreonam-susceptible P. aeruginos (25.7% vs 16.8%;P = .009), but in multivariable analysis, no significant association was found between infection or colonization with aztreonam-resistant P. aeruginosa and mortality.Conclusions.Curbing the use of fluoroquinolones and antimicrobials with antianaerobic activity may be an effective strategy to limit the emergence of aztreonam-resistant P. aeruginosa.
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Higgins, Gerard, Coral Fustero Torre, Jean Tyrrell, Paul McNally, Brian J. Harvey, and Valerie Urbach. "Lipoxin A4prevents tight junction disruption and delays the colonization of cystic fibrosis bronchial epithelial cells byPseudomonas aeruginosa." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 11 (June 1, 2016): L1053—L1061. http://dx.doi.org/10.1152/ajplung.00368.2015.

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The specialized proresolution lipid mediator lipoxin A4(LXA4) is abnormally produced in cystic fibrosis (CF) airways. LXA4increases the CF airway surface liquid height and stimulates airway epithelial repair and tight junction formation. We report here a protective effect of LXA4(1 nM) against tight junction disruption caused by Pseudomonas aeruginosa bacterial challenge together with a delaying action against bacterial invasion in CF airway epithelial cells from patients with CF and immortalized cell lines. Bacterial invasion and tight junction integrity were measured by gentamicin exclusion assays and confocal fluorescence microscopy in non-CF (NuLi-1) and CF (CuFi-1) bronchial epithelial cell lines and in primary CF cultures, grown under an air/liquid interface, exposed to either a clinical or laboratory strains of P. aeruginosa. LXA4delayed P. aeruginosa invasion and transepithelial migration in CF and normal bronchial epithelial cell cultures. These protective effects of LXA4were inhibited by the ALX/FPR2 lipoxin receptor antagonist BOC-2. LXA4prevented the reduction in mRNA biosynthesis and protein abundance of the tight junction protein ZO-1 and reduced tight junction disruption induced by P. aeruginsosa inoculation. In conclusion, LXA4plays a protective role in bronchial epithelium by stimulating tight junction repair and by delaying and reducing the invasion of CF bronchial epithelial cells by P. aeruginsosa.
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Chakraborty, Tamalika, Tushar Gupta, Nayana Verma, Zarin Parwez, Kaustav Deb, and Tamoghana Chakraborty. "PREVALENCE OF ANTIBIOTIC RESISTANCE IN PSEUDOMONAS AERUGINOSA." International Journal of Advanced Research 12, no. 01 (January 31, 2024): 1249–60. http://dx.doi.org/10.21474/ijar01/18243.

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One of the main bacteria responsible for hospital-acquired illnesses is Pseudomonas aeruginosa. Through chromosomal changes or the horizontal acquisition of resistant determinants, antibiotic resistance can be easily developed it. High-risk clones, like ST175, are spreading together with the rising frequency of extensively-drug-resistant (XDR) or multi-drug-resistant (MDR) P. aeruginosa isolates. MDR/XDR infections should be taken seriously since they can make it difficult to choose the best empirical and conclusive antimicrobial therapies. New avenues for the treatment of MDR/XDR P. aeruginosa infections have been opened by the introduction of powerful new antibiotics. Pseudomonas aeruginosa strains are known to withstand the majority of antibiotics by utilizing their high levels of intrinsic and acquired resistance mechanisms. Furthermore, recalcitrance and infection recurrence are caused by P. aeruginosas adaptive antibiotic resistance, a recently identified process that combines biofilm-mediated resistance and the development of multidrug-tolerant persister cells. There is a growing need for and interest in the research and development of alternative therapeutic approaches that offer fresh approaches to combat P. aeruginosa infections. Much recent research has documented various novel therapeutic methods that have proven pronouncedly effective in treating drug-resistant P. aeruginosa strains, but largely at the preclinical stages. This review focuses on the Prevalence of antibiotic resistance in Pseudomonas aeruginosaand also provides an overview of the characteristics of pseudomonas bacteria, various infections caused by them, the mechanism of antibiotic resistance, their clinical implications, Challenges in treatment, strategies for management and control, and future perspectives and research directions.
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Aidah Abd Al-doori, Awatef Saber Jasem, and Adnan F. AL-Azzawie. "Effects of Nd:Yag Laser on some virulence factor genes of Pseudomonas aeruginosa bacteria." Tikrit Journal of Pure Science 25, no. 2 (March 17, 2020): 86–92. http://dx.doi.org/10.25130/tjps.v25i2.240.

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The aim of this study was to assess effects of the 532nm Nd-yag laser on the genes of Tox A, Exo S, and Opr L, of Pseudomonas aeruginosa (P. aeruginosa) bacteria isolated from clinical (wounds, burns, otitis media) and environmental (water, soil) samples. Clinical samples were collected from patients coming to Saladdin General Hospital from wound, burns and middle ear infections while environmental samples were extracted from water and soil for Saladdin General Hospital . Bacterial samples irradiated by Nd-Yag laser with wavelength of 532 nm using energies (300mj,500mj) with (15 and 25 sec) and genomic DNA were extracted from all samples after the diagnosis of P. aeruginosa bacteria depending on the macroscopic and biochemical examination, then the PCR technique was performed. The results have shown an impact on P. aeruginosa bacteria of Nd-Yag laser by comparing PCR results of treated samples with control (unexposed) as loss of normal bands. This indicates that the laser had a genetic effect on the P. aeruginosa bacteria. We conclude that the laser induces genetic changes in P. aeruginosa's DNA so that lasers can be used in treatment and sterilization for clinical and environmental . The PCR technique could be used as a biomarker study to determine the biological effects of radiation on bacteria.
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Ishida, Lilian Konno, Katsuhisa Ikeda, Noriko Tanno, Tomonori Takasaka, Kiyo Nishioka, and Yasuo Tanno. "Erythromycin Inhibits Adhesion of Pseudomonas Aeruginosa and Branhamella Catarrhalis to Human Nasal Epithelial Cells." American Journal of Rhinology 9, no. 1 (January 1995): 53–56. http://dx.doi.org/10.2500/105065895781874097.

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Ciliated epithelial cells were obtained from nasal polyps. Bacterial adherence to these cells was compared for the ability to bind Hemophilus influenzae, Pseudomonas aeruginosa, and Branhamella catarrhalis in the presence of 10–5 M erythromycin, which was comparable with a physiologically attainable concentration in the nasal secretion and the maxillary sinus mucosa. Quantification of bacterial adherence showed the strongest ability of P. aeruginosa to the cells. Erythromycin has an inhibitory effect on adherence of P. aeruginose and B. catarrhalis to the nasal epithelial cell. Our findings suggest that the reduced adherence to the host cell is one of the underlying mechanisms to account for efficacy of erythromycin treatment in respiratory disorders.
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Al-doori1, Aidah Abd, Awatef Saber Jasem1, and Adnan F. AL-Azzawie2. "Effects of Nd:Yag Laser on some virulence factor genes of Pseudomonas aeruginosa bacteria." Tikrit Journal of Pure Science 25, no. 2 (March 17, 2020): 86. http://dx.doi.org/10.25130/j.v25i2.962.

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The aim of this study was to assess effects of the 532nm Nd-yag laser on the genes of Tox A, Exo S, and Opr L, of Pseudomonas aeruginosa (P. aeruginosa) bacteria isolated from clinical (wounds, burns, otitis media) and environmental (water, soil) samples. Clinical samples were collected from patients coming to Saladdin General Hospital from wound, burns and middle ear infections while environmental samples were extracted from water and soil for Saladdin General Hospital . Bacterial samples irradiated by Nd-Yag laser with wavelength of 532 nm using energies (300mj,500mj) with (15 and 25 sec) and genomic DNA were extracted from all samples after the diagnosis of P. aeruginosa bacteria depending on the macroscopic and biochemical examination, then the PCR technique was performed. The results have shown an impact on P. aeruginosa bacteria of Nd-Yag laser by comparing PCR results of treated samples with control (unexposed) as loss of normal bands. This indicates that the laser had a genetic effect on the P. aeruginosa bacteria. We conclude that the laser induces genetic changes in P. aeruginosa's DNA so that lasers can be used in treatment and sterilization for clinical and environmental . The PCR technique could be used as a biomarker study to determine the biological effects of radiation on bacteria. http://dx.doi.org/10.25130/tjps.25.2020.034
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Young, Heather, Bryan Knepper, Whitney Hernandez, Asaf Shor, Merribeth Bruntz, Chrystal Berg, and Connie S. Price. "Pseudomonas aeruginosa." Journal of the American Podiatric Medical Association 105, no. 2 (March 1, 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, no. 5 (August 11, 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, no. 2 (June 1990): 259–70. http://dx.doi.org/10.1016/s0891-5520(20)30340-8.

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Dissertations / Theses on the topic "Aeruginosa"

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Daroch, Maurycy. "Oxidoreductases of Stropharia aeruginosa." Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539912.

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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
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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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Books on the topic "Aeruginosa"

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

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Bertoni, Giovanni, and Silvia Ferrara, eds. 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, ed. Pseudomonas aeruginosa infection. Basel: Karger, 1989.

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

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1926-, Baltch Aldona L., and Smith Raymond P. 1946-, eds. Pseudomonas aeruginosa: Infections and treatment. New York: M. Dekker, 1994.

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Y, Homma J., ed. Pseudomonas aeruginosa in human diseases. Basel: Karger, 1991.

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

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Mario, Campa, Bendinelli Mauro, and Friedman Herman 1931-, eds. Pseudomonas aeruginosa as an opportunistic pathogen. New York: Plenum Press, 1993.

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Hauser, Alan R., and Jordi Rello, eds. Severe Infections Caused by Pseudomonas Aeruginosa. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0433-7.

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Campa, Mario, Mauro Bendinelli, and Herman Friedman, eds. Pseudomonas aeruginosa as an Opportunistic Pathogen. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3036-7.

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Book chapters on the topic "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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Lim, T. K. "Curcuma aeruginosa." In Edible Medicinal and Non-Medicinal Plants, 233–40. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26065-5_13.

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Paterson, David L., and 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, and 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, and 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, and 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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Pennington, J. E. "Pseudomonas aeruginosa immunization." In Recent Developments in Prophylactic Immunization, 74–85. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1067-6_5.

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Deretic, V. "Pseudomonas aeruginosa Infections." In Persistent Bacterial Infections, 305–26. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818104.ch15.

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Conference papers on the topic "Aeruginosa"

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Silva, Leidyanne Karolaine Barbosa da, Esaú Simões Da Silva, Rhana Cavalcanti Do Nascimento, and 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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Argyraki, A., M. Markvart, Anne Nielsen, T. Bjarnsholt, L. Bjørndal, and P. M. Petersen. "Comparison of UVB and UVC irradiation disinfection efficacies on Pseudomonas Aeruginosa (P. aeruginosa) biofilm." In SPIE Photonics Europe, edited by Jürgen Popp, Valery V. Tuchin, Dennis L. Matthews, and Francesco S. Pavone. SPIE, 2016. http://dx.doi.org/10.1117/12.2225597.

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Mahgoub, Yasmine, Rida Arif, and 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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Zeng, Xiaoxi, Xueduan Liu, Pei Jiang, Wen Li, and 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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Ito, Miu, and Yuichi Sugai. "Evaluation of the Potential of Foam Producing Microorganism Improving Heterogeneity of Permeability for Novel Microbial Foam EOR." In SPE Asia Pacific Oil & Gas Conference and Exhibition. SPE, 2022. http://dx.doi.org/10.2118/210696-ms.

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Abstract The foam improves heterogeneity of permeability in oil reservoir and contributes to enhancing oil recovery. Both surfactant and gas are alternatingly injected into oil reservoir in foam EOR, therefore, it has several challenges: high cost of surfactant, formation of precipitation with bivalent cations, adsorption of surfactant on reservoir rock, etc. This study proposes the microbial foam EOR which overcomes those challenges by having microorganism generate foam in-situ. We have found an ability of a microorganism belonging to Pseudomonas aeruginosa to generate foam under anaerobic conditions. This study investigated the source materials constructing the foam and capacity of the foam to improve the heterogeneity of the permeability. The challenges of our study are the reproducibility of the foam generation and the foam stability. This study therefore examined the source materials of the foam to understand the mechanisms of the foam generation. We focused on protein, which has been suggested as a possible component of the foam in our previous studies, and examined the relationship between the amount of foam generated by P. aeruginosa and the concentration of protein in its culture solution. As a result, a positive correlation was found between them. This result indicates that the foam generated by P. aeruginosa is composed of the protein produced by the microorganism. Next, the performance of the foam decreasing permeability of high permeability porous media was evaluated through sand pack flooding experiment. P. aeruginosa was injected into a sand pack and cultivated in-situ. The post-flush water was injected into the sand pack after three days’ in-situ cultivation to measure the permeability. As a result, the permeability of the sand pack was successfully decreased to half after the cultivation. The permeability of a sand pack in which P. aeruginosa was injected with culture medium and in-situ cultivated was successfully decreased to half of initial. The efflux of bacterial cells of P. aeruginosa was detected after injecting 1.3 pore volumes of postflush water, which shows that the postflush water flowed through areas other than the area where P. aeruginosa grew and produced the foam. These results indicate that the foam produced in-situ by P. aeruginosa is effective for improving the heterogeneity of permeability in oil reservoir. This EOR can be operated at low cost without expensive chemicals. Because the foam produced by P. aeruginosa is induced by proteins, the precipitation will not be formed in oil reservoir. The stability of protein-induced foam is higher than that of surfactant-induced foam in the presence of oil or high saline conditions. The microbial foam EOR therefore has high potential improving the heterogeneity of permeability in oil reservoir more effectively than the conventional foam EOR.
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MATTER, Ikhlas Ramadan, Alaa Hussein ALMOLA, and Aisha W. ALOMARI. "EFFECT OF IRAQI DESERT TRUFFLE AND SOME TYPE OF HONEY AGAINST SOME BACTERIA." In III.International Scientific Congress of Pure,Appliedand Technological Sciences. Rimar Academy, 2021. http://dx.doi.org/10.47832/minarcongress3-8.

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The present study is interested in studying the effect of some natural nutrients on some types of bacteria , especially truffle and honey as food and nutritional value in our ancient parents. A water extract was prepared from the fruits of the black truffle and then studied the effect of this extract against Enterococcus faecalis, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Staphylococcus aureus. The results showed that the water extract had a clear inhibitory effect on all the bacteria except P. aeruginosa, which showed resistance to the extract. The study also examined the effect of five types of honey in the crude (non-diluted) and diluted form 1: 1 (v: v) obtained from home honey bee, mountain honey, pine honey, grape leaves honey and German honey against the isolates under study. In the our study were showed that the types of honey have a broad and diversity of inhibition against microorganisms under study ,The raw Germany honey (non-diluted) showed high inhibition of P. aeruginosaas 25 mm inhibition zone .In comparison, the same type of honey showed 17 mm inhibition zone against S. aureus when diluted it ,while P.aeruginosa were showed resistance .The results showed that pine tree honey was the best honey used in the study. It showed a clear inhibitory effect on all the isolates used in the test in the crude and dilution form (1:1) without any resistance from any of the isolates. Key words: Truffle, Water extract, Antibacterial, Pathogenic Bacterial.
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Liimatta, K., S. A. Riquelme, C. Lozano, P. J. Planet, Y. Saenz, A. C. Uhlemann, and A. S. Prince. "Metabolic Reprogramming Drives P. Aeruginosa Airway Infection." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6158.

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Alzubaidy, Mohanad W. Mahdi, Asmaa M. Salih Almohaidi, Ammar Ahmed Sultan, and 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, and 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, and 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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Reports on the topic "Aeruginosa"

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

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Sauer, Karin. Regulation of Initial Attachment of P. aeruginosa. Fort Belvoir, VA: Defense Technical Information Center, December 2010. http://dx.doi.org/10.21236/ada545997.

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Schnider, Shirley. The biological properties of Pseudomonas aeruginosa bacteriophage 7V. Portland State University Library, January 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, January 2000. http://dx.doi.org/10.15760/etd.2139.

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

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

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Borisova, Dayana, Tanya Strateva, Tsvetelina Paunova-Krasteva, Ivan Mitov, and 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, August 2018. http://dx.doi.org/10.7546/crabs.2018.08.05.

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Bigaud, Mariah A., and 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, April 2017. http://dx.doi.org/10.22186/jyi.32.4.25-29.

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Feng, XinYu, and 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, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0092.

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Petrova, Atanaska, Tsvetelina Borisova, Yana Feodorova, Irina Stanimirova, Tsonka Miteva-Katrandzhieva, Michael Petrov, and 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, December 2018. http://dx.doi.org/10.7546/crabs.2018.12.15.

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