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Artykuły w czasopismach na temat "Bordetella"

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Sebaihia, Mohammed, Andrew Preston, Duncan J. Maskell, Holly Kuzmiak, Terry D. Connell, Natalie D. King, Paul E. Orndorff i in. "Comparison of the Genome Sequence of the Poultry Pathogen Bordetella avium with Those of B. bronchiseptica, B. pertussis, and B. parapertussis Reveals Extensive Diversity in Surface Structures Associated with Host Interaction". Journal of Bacteriology 188, nr 16 (15.08.2006): 6002–15. http://dx.doi.org/10.1128/jb.01927-05.

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ABSTRACT Bordetella avium is a pathogen of poultry and is phylogenetically distinct from Bordetella bronchiseptica, Bordetella pertussis, and Bordetella parapertussis, which are other species in the Bordetella genus that infect mammals. In order to understand the evolutionary relatedness of Bordetella species and further the understanding of pathogenesis, we obtained the complete genome sequence of B. avium strain 197N, a pathogenic strain that has been extensively studied. With 3,732,255 base pairs of DNA and 3,417 predicted coding sequences, it has the smallest genome and gene complement of the sequenced bordetellae. In this study, the presence or absence of previously reported virulence factors from B. avium was confirmed, and the genetic bases for growth characteristics were elucidated. Over 1,100 genes present in B. avium but not in B. bronchiseptica were identified, and most were predicted to encode surface or secreted proteins that are likely to define an organism adapted to the avian rather than the mammalian respiratory tracts. These include genes coding for the synthesis of a polysaccharide capsule, hemagglutinins, a type I secretion system adjacent to two very large genes for secreted proteins, and unique genes for both lipopolysaccharide and fimbrial biogenesis. Three apparently complete prophages are also present. The BvgAS virulence regulatory system appears to have polymorphisms at a poly(C) tract that is involved in phase variation in other bordetellae. A number of putative iron-regulated outer membrane proteins were predicted from the sequence, and this regulation was confirmed experimentally for five of these.
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Allen, Andrew G., Tomoko Isobe i Duncan J. Maskell. "Identification and Cloning of waaF (rfaF) from Bordetella pertussis and Use To Generate Mutants ofBordetella spp. with Deep Rough Lipopolysaccharide". Journal of Bacteriology 180, nr 1 (1.01.1998): 35–40. http://dx.doi.org/10.1128/jb.180.1.35-40.1998.

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ABSTRACT A DNA locus from Bordetella pertussis capable of reconstituting lipopolysaccharide (LPS) O-antigen biosynthesis inSalmonella typhimurium SL3789 (rfaF511) has been isolated, by using selection with the antibiotic novobiocin. DNA within the locus encodes a protein with amino acid sequence similarity to heptosyltransferase II, encoded by waaF (previouslyrfaF) in other gram-negative bacteria. Mutation of this gene in B. pertussis, Bordetella parapertussis, and Bordetella bronchiseptica by allelic exchange generated bacteria with deep rough LPS phenotypes consistent with the proposed function of the gene as an inner core heptosyltransferase. These are the first LPS mutants generated in B. parapertussis andB. bronchiseptica and the first deep rough mutants of any of the bordetellae.
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López-Boado, Yolanda S., Laura M. Cobb i Rajendar Deora. "Bordetella bronchiseptica Flagellin Is a Proinflammatory Determinant for Airway Epithelial Cells". Infection and Immunity 73, nr 11 (listopad 2005): 7525–34. http://dx.doi.org/10.1128/iai.73.11.7525-7534.2005.

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ABSTRACT Motility is an important virulence phenotype for many bacteria, and flagellin, the monomeric component of flagella, is a potent proinflammatory factor. Of the three Bordetella species, Bordetella pertussis and Bordetella parapertussis are nonmotile human pathogens, while Bordetella bronchiseptica expresses flagellin and causes disease in animals and immunocompromised human hosts. The BvgAS two-component signal transduction system regulates phenotypic-phase transition (Bvg+, Bvg−, and Bvgi) in bordetellae. The Bvg− phase of B. bronchiseptica is characterized by the expression of flagellin and the repression of adhesins and toxins necessary for the colonization of the respiratory tract. B. bronchiseptica naturally infects a variety of animal hosts and constitutes an excellent model to study Bordetella pathogenesis. Using in vitro coculture models of bacteria and human lung epithelial cells, we studied the effects of B. bronchiseptica flagellin on host defense responses. Our results show that B. bronchiseptica flagellin is a potent proinflammatory factor that induces chemokine, cytokine, and host defense gene expression. Furthermore, we investigated receptor specificity in the response to B. bronchiseptica flagellin. Our results show that B. bronchiseptica flagellin is able to signal effectively through both human and mouse Toll-like receptor 5.
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Parise, Gina, Meenu Mishra, Yoshikane Itoh, Tony Romeo i Rajendar Deora. "Role of a Putative Polysaccharide Locus in Bordetella Biofilm Development". Journal of Bacteriology 189, nr 3 (17.11.2006): 750–60. http://dx.doi.org/10.1128/jb.00953-06.

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ABSTRACT Bordetellae are gram-negative bacteria that colonize the respiratory tracts of animals and humans. We and others have recently shown that these bacteria are capable of living as sessile communities known as biofilms on a number of abiotic surfaces. During the biofilm mode of existence, bacteria produce one or more extracellular polymeric substances that function, in part, to hold the cells together and to a surface. There is little information on either the constituents of the biofilm matrix or the genetic basis of biofilm development by Bordetella spp. By utilizing immunoblot assays and by enzymatic hydrolysis using dispersin B (DspB), a glycosyl hydrolase that specifically cleaves the polysaccharide poly-β-1,6-N-acetyl-d-glucosamine (poly-β-1,6-GlcNAc), we provide evidence for the production of poly-β-1,6-GlcNAc by various Bordetella species (Bordetella bronchiseptica, B. pertussis, and B. parapertussis) and its role in their biofilm development. We have investigated the role of a Bordetella locus, here designated bpsABCD, in biofilm formation. The bps (Bordetella polysaccharide) locus is homologous to several bacterial loci that are required for the production of poly-β-1,6-GlcNAc and have been implicated in bacterial biofilm formation. By utilizing multiple microscopic techniques to analyze biofilm formation under both static and hydrodynamic conditions, we demonstrate that the bps locus, although not essential at the initial stages of biofilm formation, contributes to the stability and the maintenance of the complex architecture of Bordetella biofilms.
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Sloan, Gina Parise, Cheraton F. Love, Neelima Sukumar, Meenu Mishra i Rajendar Deora. "The Bordetella Bps Polysaccharide Is Critical for Biofilm Development in the Mouse Respiratory Tract". Journal of Bacteriology 189, nr 22 (22.06.2007): 8270–76. http://dx.doi.org/10.1128/jb.00785-07.

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ABSTRACT Bordetellae are respiratory pathogens that infect both humans and animals. Bordetella bronchiseptica establishes asymptomatic and long-term to life-long infections of animal nasopharynges. While the human pathogen Bordetella pertussis is the etiological agent of the acute disease whooping cough in infants and young children, it is now being increasingly isolated from the nasopharynges of vaccinated adolescents and adults who sometimes show milder symptoms, such as prolonged cough illness. Although it has been shown that Bordetella can form biofilms in vitro, nothing is known about its biofilm mode of existence in mammalian hosts. Using indirect immunofluorescence and scanning electron microscopy, we examined nasal tissues from mice infected with B. bronchiseptica. Our results demonstrate that a wild-type strain formed robust biofilms that were adherent to the nasal epithelium and displayed architectural attributes characteristic of a number of bacterial biofilms formed on inert surfaces. We have previously shown that the Bordetella Bps polysaccharide encoded by the bpsABCD locus is critical for the stability and maintenance of three-dimensional structures of biofilms. We show here that Bps is essential for the formation of efficient nasal biofilms and is required for the colonization of the nose. Our results document a biofilm lifestyle for Bordetella in mammalian respiratory tracts and highlight the essential role of the Bps polysaccharide in this process and in persistence of the nares.
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Williams, Corinne L., Robert Haines i Peggy A. Cotter. "Serendipitous Discovery of an Immunoglobulin-Binding Autotransporter in Bordetella Species". Infection and Immunity 76, nr 7 (21.04.2008): 2966–77. http://dx.doi.org/10.1128/iai.00323-08.

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ABSTRACT We describe the serendipitous discovery of BatB, a classical-type Bordetella autotransporter (AT) protein with an ∼180-kDa passenger domain that remains noncovalently associated with the outer membrane. Like genes encoding all characterized protein virulence factors in Bordetella species, batB transcription is positively regulated by the master virulence regulatory system BvgAS. BatB is predicted to share similarity with immunoglobulin A (IgA) proteases, and we showed that BatB binds Ig in vitro. In vivo, a Bordetella bronchiseptica ΔbatB mutant was unable to overcome innate immune defenses and was cleared from the lower respiratory tracts of mice more rapidly than wild-type B. bronchiseptica. This defect was abrogated in SCID mice, suggesting that BatB functions to resist clearance during the first week postinoculation in a manner dependent on B- and T-cell-mediated activities. Taken together with the previous demonstration that polymorphonuclear neutrophils (PMN) are critical for the control of B. bronchiseptica in mice, our data support the hypothesis that BatB prevents nonspecific antibodies from facilitating PMN-mediated clearance during the first few days postinoculation. Neither of the strictly human-adapted Bordetella subspecies produces a fully functional BatB protein; nucleotide differences within the putative promoter region prevent batB transcription in Bordetella pertussis, and although expressed, the batB gene of human-derived Bordetella parapertussis (B. parapertussis hu) contains a large in-frame deletion relative to batB of B. bronchiseptica. Taken together, our data suggest that BatB played an important role in the evolution of virulence and host specificity among the mammalian-adapted bordetellae.
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Hegerle, N., A. S. Paris, D. Brun, G. Dore, E. Njamkepo, S. Guillot i N. Guiso. "Evolution of French Bordetella pertussis and Bordetella parapertussis isolates: increase of Bordetellae not expressing pertactin". Clinical Microbiology and Infection 18, nr 9 (wrzesień 2012): E340—E346. http://dx.doi.org/10.1111/j.1469-0691.2012.03925.x.

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Cummings, C. A., M. M. Brinig, P. W. Lepp, S. van de Pas i D. A. Relman. "Bordetella Species Are Distinguished by Patterns of Substantial Gene Loss and Host Adaptation". Journal of Bacteriology 186, nr 5 (1.03.2004): 1484–92. http://dx.doi.org/10.1128/jb.186.5.1484-1492.2004.

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ABSTRACT Pathogens of the bacterial genus Bordetella cause respiratory disease in humans and animals. Although virulence and host specificity vary across the genus, the genetic determinants of this diversity remain unidentified. To identify genes that may underlie key phenotypic differences between these species and clarify their evolutionary relationships, we performed a comparative analysis of genome content in 42 Bordetella strains by hybridization of genomic DNA to a microarray representing the genomes of three Bordetella species and by subtractive hybridization. Here we show that B. pertussis and B. parapertussis are predominantly differentiated from B. bronchiseptica by large, species-specific regions of difference, many of which encode or direct synthesis of surface structures, including lipopolysaccharide O antigen, which may be important determinants of host specificity. The species also exhibit sequence diversity at a number of surface protein-encoding loci, including the fimbrial major subunit gene, fim2. Gene loss, rather than gene acquisition, accompanied by the proliferation of transposons, has played a fundamental role in the evolution of the pathogenic bordetellae and may represent a conserved evolutionary mechanism among other groups of microbial pathogens.
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Spears, Patricia A., Louise M. Temple, David M. Miyamoto, Duncan J. Maskell i Paul E. Orndorff. "Unexpected Similarities between Bordetella avium and Other Pathogenic Bordetellae". Infection and Immunity 71, nr 5 (maj 2003): 2591–97. http://dx.doi.org/10.1128/iai.71.5.2591-2597.2003.

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ABSTRACT Bordetella avium causes an upper respiratory tract disease (bordetellosis) in avian species. Commercially raised turkeys are particularly susceptible. Like other pathogenic members of the genus Bordetella (B. pertussis and B. bronchiseptica) that infect mammals, B. avium binds preferentially to ciliated tracheal epithelial cells and produces similar signs of disease. These similarities prompted us to study bordetellosis in turkeys as a possible nonmammalian model for whooping cough, the exclusively human childhood disease caused by B. pertussis. One impediment to accepting such a host-pathogen model as relevant to the human situation is evidence suggesting that B. avium does not express a number of the factors known to be associated with virulence in the other two Bordetella species. Nevertheless, with signature-tagged mutagenesis, four avirulent mutants that had lesions in genes orthologous to those associated with virulence in B. pertussis and B. bronchiseptica (bvgS, fhaB, fhaC, and fimC) were identified. None of the four B. avium genes had been previously identified as encoding factors associated with virulence, and three of the insertions (in fhaB, bvgS, and fimC) were in genes or gene clusters inferred as being absent or incomplete in B. avium, based upon the lack of DNA sequence similarities in hybridization studies and/or the lack of immunological cross-reactivity of the putative products. We further found that the genotypic arrangements of most of the B. avium orthologues were very similar in all three Bordetella species. In vitro tests, including hemagglutination, tracheal ring binding, and serum sensitivity, helped further define the phenotypes conferred by the mutations. Our findings strengthen the connection between the causative agents and the pathogenesis of bordetellosis in all hosts and may help explain the striking similarities of the histopathologic characteristics of this upper airway disease in avian and mammalian species.
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Marr, Nico, Alina Tirsoaga, Didier Blanot, Rachel Fernandez i Martine Caroff. "Glucosamine Found as a Substituent of Both Phosphate Groups in Bordetella Lipid A Backbones: Role of a BvgAS-Activated ArnT Ortholog". Journal of Bacteriology 190, nr 12 (18.04.2008): 4281–90. http://dx.doi.org/10.1128/jb.01875-07.

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ABSTRACT Endotoxins are amphipathic lipopolysaccharides (LPSs), major constituents of the outer membrane of gram-negative bacteria. They consist of a lipid region, covalently linked to a core oligosaccharide, to which may be linked a repetitive glycosidic chain carrying antigenic determinants. Most of the biological activities of endotoxins have been associated with the lipid moiety of the molecule: unique to gram-negative bacteria, LPS is a ligand of the mammalian TLR4-MD2-CD14 pathogen recognition receptor complex. Lipid A preparations are often heterogeneous with respect to both the numbers and the lengths of fatty acids and the natures of substituents on the phosphate groups when present. The variants can significantly affect host immune responses. Nine species in the Bordetella genus have been described, and the fine LPS structures of seven of them have been published. In this report, lipids A from Bordetella pertussis Tohama I and B. bronchiseptica strain 4650 were further characterized and revealed to have a glucosamine substituting both lipid A phosphate groups of the diglucosamine backbone. These substitutions have not been previously described for bordetellae. Moreover, a B. pertussis transposon mutation that maps within a gene encoding a Bordetella ArnT (formerly PmrK) glycosyl transferase ortholog does not carry this substitution, thus providing a genetic basis for the modification. Reverse transcriptase PCR of this locus showed that it is Bvg regulated, suggesting that the ability of Bordetella to modify lipid A via this glucosamine modification is a potential virulence trait.
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Rozprawy doktorskie na temat "Bordetella"

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Ben, Hafsia Abdelhafidh. "Facteurs de virulence des bordetellae : le modèle de Bordetella parapertussis". Paris 11, 1991. http://www.theses.fr/1991PA114806.

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Phillips, Linda Jane. "Immunization against Bordetella pertussis". Thesis, Kansas State University, 1985. http://hdl.handle.net/2097/9871.

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Smith, Colin J. "Genetic studies with Bordetella pertussis". Thesis, University of Glasgow, 1986. http://theses.gla.ac.uk/1505/.

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Lewandowski, Anna Zofia. "Antigenic variation in Bordetella pertussis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ60480.pdf.

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Sidey, Fiona M. "Metabolic effects of Bordetella pertussis". Thesis, University of Strathclyde, 1987. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=20352.

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The present work confirmed that B. pertussis infection or pertussis toxin produce hypoglycaemia in mice. The hypoglycaemia was associated with hyperinsulinaemia, and both were abolished by destruction of the pancreatic β cells with alloxan. Impaired glucose counterregulatory mechanisms may also contribute to pertussis-induced hypoglycaemia, as the hypoglycaemic action of insulin was prolonged in pertussis infected mice. On the other hand, impaired responsiveness to lower doses of insulin was found. Pertussis-induced hyperinsulinaemia had two components. First, the increase in serum insulin in response to food intake was both greater and more prolonged in pertussis-infected mice. Second, infected or pertussis toxin-treated animals, unlike controls, showed a marked increase in serum insulin in response to certain stresses, such as ether, histamine, anoxia and 2-deoxyglucose. However, other stresses (LPS, cold and hypoxia) did not cause hyperinsulinaemia in pertussis infected mice. Stress-induced hyperinsulinaemia was also seen in normal mice receiving the a2- adrenoceptor blocking drug idazoxan. Stress-induced hyperinsulinaemia in a2 adrenoceptor blocked mice, but not in pertussis-treated mice, was prevented by β adrenoceptor blockade using propranolol. Adrenal demedullation or ganglionic blockade (using hexamethonium) in normal mice also allowed stress induced hyperinsulinaemia. Thus, adrenal medullary catecholamines may normally serve to prevent stress induced hyperinsulinaemia, which becomes unmasked when they are absent or when their action is prevented. Stress-induced hyperinsulinaemia in pertussis treated mice was unlikely to involve autonomic, cholinergic oropioid mechanisms as it was not blocked by hexamethonium, atropine or naloxone. Human infants with pertussis showed no hypoglycaemia compared with non-pertussis controls, although their plasma insulin concentrations were slightly but significantly raised. It remains possible that hyperinsulinaemia with resultant profound hypoglycaemia might occur in susceptible patients following exposure to pertussis-toxin (either during the disease or following vaccination).
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Ladant, Daniel. "L'adenyl cyclase de bordetella pertussis". Paris 7, 1989. http://www.theses.fr/1989PA077200.

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Bordetella pertussis, l'agent de la coqueluche secrete une adenyl cyclase qui constitue l'un des principaux facteurs de virulence de cet organisme. Cet enzyme bacterien presente l'originalite d'etre active par la calmoduline, une proteine regulatrice eucaryote. Nous avons purifie l'adenyl cyclase a l'homogeneite; elle possede l'activite specifique la plus elevee connue pour cette classe d'enzymes. Elle est constituee d'une chaine polypeptidique de 43-50 kilodaltons qui fixe une molecule de calmoduline avec une grande affinite. Par proteolyse limitee du complexe adenyl cyclase/calmoduline, nous avons identifie, dans la molecule d'adenyl cyclase, deux domaines d'interaction avec la calmoduline. Le clonage du gene de l'adenyl cyclase de b. Pertussis nous a permis d'etudier et de caracteriser la proteine exprimee chez e. Coli. La determination de la sequence nucleotidique du gene a revele l'existence d'une phase ouverte de 1706 acides amines: l'adenyl cyclase se situe dans la partie n-terminale; la partie c-terminale presente une homologie de sequence avec l'hemolysine d'e. Coli. Ces donnees suggerent que l'adenyl cyclase pourrait etre synthetisee sous forme d'un precurseur commun, adenyl cyclase-hemolysine. Un tel precurseur, d'un poids moleculaire apparent de 200 kilodaltons a ete identifie dans les souches virulentes de b. Pertussis; nous avons montre que, dans certaines conditions de culture, cette forme d'adenyl cyclase de 200 kilodaltons peut etre secretee par b. Pertussis sans proteolyse. Enfin, nous avons mis en evidence une parente antigenique entre les adenyl cyclases calmoduline-dependantes de b. Pertussis et de cerveau de rat. L'hypothese d'une origine evolutive commune pour ces deux enzymes est ainsi serieusement etayee
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Keidel, Kristina [Verfasser], i Roy [Akademischer Betreuer] Gross. "Charakterisierung des Hfq-Regulons in Bordetella pertussis und Bordetella bronchiseptica / Kristina Keidel. Betreuer: Roy Gross". Würzburg : Universitätsbibliothek der Universität Würzburg, 2011. http://d-nb.info/1018612696/34.

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GOYARD, SOPHIE. "Regulation de l'adenylcyclase de bordetella pertussis". Paris 6, 1993. http://www.theses.fr/1993PA066107.

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B. Pertussis, agent pathogene de la coqueluche, produit de nombreux facteurs de virulence dont la toxine adenylcyclase. Cet enzyme est active par une proteine eucaryote, la calmoduline ; particularite partagee avec une autre adenylcyclase bacterienne, celle de b. Anthracis, agent du charbon. Ces deux adenylcyclases comportent un motif peptidique hautement conserve que nous avons caracterise comme faisant partie du site catalytique de ces deux enzymes. Des anticorps diriges contre ce motif conserve nous ont permis de preciser une parente immunologique entre les deux adenylcyclases bacteriennes calmoduline-dependantes et la sous-unite catalytique de l'adenylcyclase de cerveau de rat. Chez b. Pertussis, l'expression des genes codant pour les facteurs de virulence est regulee de facon coordonnee en reponse a des signaux de l'environnement par les produits du locus bvg. Nous avons etudie la regulation du gene de l'adenylcyclase, cyaa chez e. Coli et chez b. Pertussis. Nous avons montre que le promoteur du gene cyaa n'est pas active chez e. Coli par les produits du locus bvg introduit en trans. Afin de mieux comprendre la regulation de ce promoteur, nous avons entrepris sa caracterisation et determine les regions impliquees dans son activation soit par deletion, soit par mutagenese. Ceci nous a egalement permis d'isoler des mutations conduisant a l'expression constitutive du gene cyaa, aussi bien chez e. Coli que chez b. Pertussis. L'ensemble des nos resultats suggere l'existence de sites multiples et d'une regulation complexe necessitant la presence de differentes proteines
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Al-Turkestany, Ismail M. A. "Interaction of Bordetella bronchiseptica and different Bordetella factors with sheep bone marrow mast cells and other cell types". Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440331.

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Adams, Toni Elizabeth. "Bordetella bronchiseptica dermonecrotic toxin, purification and characterisation". Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29723.

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Dermonecrotic toxin (DNT) is produced by all the Bordetella species, and DNT from B. bronchiseptica is considered to be an important virulence factor in turbinate atrophy of pigs.;Recombinant DNT (rDNT) was purified by sonication, ion-exchange and hydroxylapatite chromatography. Other methods for the purification of wild-type DNT and rDNT, including preparative isoelectric focusing and hydrophobic chromatography, were investigated in detail.;Partially pure preparations of rDNT contained a 145 kDa protein band and were cytotoxic to embryonic bovine lung (EBL) cells. Partially pure rDNT induced the formation of actin stress fibres and focal adhesions in Swiss 3T3 cells. In addition, rDNT stimulated DNA synthesis in quiescent Swiss 3T3 cells but prevented cell proliferation, resulting in binucleated cells. Recombinant DNT has been shown to directly modify the small GTP-binding protein, Rho, (Pullinger, unpublished), which regulates the cell cytoskeleton. Results from this thesis indicate that rDNT causes the assembly of actin stress fibres and focal adhesion possibly by direct activation of the Rho protein.;Partially purified rDNT with a site-directed mutation in a putative nucleotide-binding motif did not induce cytoskeletal rearrangements and did not stimulate DNA synthesis in Swiss 3T3 cells. This suggests that the nucleotide-binding motif is essential for activity.;Two lines of evidence indicate that the toxin is internalised in the endosomal/lysosomal compartment: i) stimulation of DNA synthesis by transient exposure of Swiss 3T3 cells to rDNT, and ii) blocking of rDNT-induced DNA synthesis with methylamine.;Three monoclonal antibodies (mAbs) were produced against B. bronchiseptica DNT. These mAbs recognised rDNT and B. pertussis DNT, but none neutralised the cytotoxic activity of DNT on EBL cells.;The partial purification of rDNT and characterisation of its biological effects provide valuable information for further studies of the toxin, including analysis of its enzymatic mode of action and its role in infection. Also, DNT may prove to be a useful tool for analysis of cell responses involving the important signalling molecule, Rho.
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Książki na temat "Bordetella"

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International Symposium on Pertussis (6th 1990 Bethesda, Md.). Proceedings of the Sixth International Symposium on Pertussis. Bethesda, Md: DHHS, US PHS, Food and Drug Administration, 1990.

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Workshop on Acellular Pertussis Vaccines (1986 Bethesda, Md.). Workshop on Acellular Pertussis Vaccines: Transcript of a workshop sponsored by the Interagency Group to Monitor Vaccine Development, Production, and Usage : September 22-24, 1986, Holiday Inn, Bethesda, Maryland. [Bethesda, Md.?]: U.S. Dept. of Health and Human Services, Public Health Service, 1987.

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Peter, Williamson. Characterisation of Bordetella pertussis antigens and production of human recombinant antibodies to these antigens. Manchester: University of Manchester, 1996.

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International Symposium on Pertussis (6th 1990 Bethesda, Md.). Abstrasts and program [of] Sixth International Symposium on Pertussis [held at] Jack Masur Auditorium, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland, September 26-28, 1990. Bethesda, Md: Dept. of Health and Human Services, United States Public Health Service, Food and Drug Administration, 1990.

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C, Wardlaw A., i Parton Roger, red. Pathogenesis and immunity in pertussis. Chichester: Wiley, 1988.

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Center for Biologics Evaluation and Research (U.S.), red. Proceedings of the Sixth International Symposium on Pertussis, Jack Masur Auditorium, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland, September 26-28, 1990. Bethesda, Md: Dept. of Health and Human Services, United States Public Health Service, Food and Drug Administration, 1990.

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T, Perkins F., International Association of Biological Standardization. i World Health Organization, red. Proceedings of the Fourth International Symposium on Pertussis: A joint meeting of the International Association of Biological Standardization and the World Health Organization held at the Executive Board room of the World Health Organization, Geneva, Switzerland 25.-27. Sept. 1984. Basel: S. Karger, 1985.

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Kokuritsu Yobō Eisei Kenkyūjo (Japan) i International Association of Biological Standardization., red. International Symposium on Pertussis, Evaluation, and Research on Acellular Pertussis Vaccines: Proceedings of a symposium supported by the National Institute of Health, Tokyo, and the International Association of Biological Standardization : held at the Teijin Institute of Education and Training, Shizuoka, Japan, September 14-15, 1990. Basel: Karger, 1991.

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Bordetella: Molecular Microbiology. Taylor & Francis, 2007.

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Cherry, James D., i Tod J. Merkel. Whooping Cough Due to Bordetella Pertussis and Other Bordetella Subspecies. Springer, 2019.

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Części książek na temat "Bordetella"

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Register, K., i E. Harvill. "Bordetella". W Pathogenesis of Bacterial Infections in Animals, 411–27. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9780470958209.ch21.

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von König, Carl Heinz Wirsing, i Marion Riffelmann. "Bordetella". W Medizinische Mikrobiologie und Infektiologie, 379–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-662-61385-6_35.

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von König, C. H. Wirsing, i M. Riffelmann. "Bordetella". W Springer-Lehrbuch, 292–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-24167-3_34.

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König, Carl Heinz Wirsing von, i Marion Riffelmann. "Bordetella". W Lexikon der Infektionskrankheiten des Menschen, 96–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-39026-8_132.

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Brickman, Timothy J., Carin K. Vanderpool i Sandra K. Armstrong. "Bordetella". W Iron Transport in Bacteria, 311–28. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816544.ch20.

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Wirsing von König, C. H., i M. Riffelmann. "Bordetella". W Springer-Lehrbuch, 287–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-48678-8_34.

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Sammels, Leanne. "Bordetella pertussis and Bordetella parapertussis". W PCR for Clinical Microbiology, 119–23. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9039-3_9.

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Stechenberg, Barbara. "Bordetella pertussis". W The Neurological Manifestations of Pediatric Infectious Diseases and Immunodeficiency Syndromes, 215–18. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-391-2_16.

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Valsamakis, Alexandra, i Christina Newman. "Bordetella pertussis". W Diagnostic Molecular Pathology in Practice, 299–305. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19677-5_37.

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Vogel, Frederick R. "Bordetella pertussis". W Pulmonary Infections and Immunity, 149–57. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-1063-9_9.

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Streszczenia konferencji na temat "Bordetella"

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Chan, N., P. J. Sloane i P. A. Eder. "Bordetella Bronchiseptica: A Phantom Menace?" W American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3026.

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Matsuda, T. "Early Diagnosis for Bordetella Pertussis and Bordetella Parapertussis Infection With Pertussis Antibody IgM, IgA, and IgM/IgA Ratio". W American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a1311.

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Matsuda, T. "Kanpo Medicine (Japanese Traditional Medicine) Could Terminate Coughing Induced by Bordetella Pertussis and Bordetella Parapertussis Infection Within 2 Weeks". W 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.a3908.

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Matsuda, T. "Early Detection of Bordetella Pertussis and Bordetella Parapertussis Infection with Pertussis Antibody Ig-M, Ig-A, and IgM/IgA Ratio". W 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.a6161.

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Schiavoni, Ilaria, Pasqualina Leone i Giorgio Fedele. "Investigating the mechanisms of Bordetella pertussis-induced airway inflammation." W ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4632.

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Cambuy, Diego, Fernanda Freitas, Érica Scheidegger, Érica Fonseca, Flávio Silva i Ana Vicente. "Coqueluche no Brasil: caracterização de linhagem de Bordetella pertussis pós-vacinal". W I Seminário Anual Científico e Tecnológico em Imunobiológicos. Instituto de Tecnologia em Imunobiológicos, 2013. http://dx.doi.org/10.35259/isi.sact.2013_28705.

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Silva, Flávio, Luiz Pinto, Alexandre Saisse, Luciano Gomes i Salvatore De Simone. "Bordetella pertussis: mapeamento e caracterização dos epitopos da toxina pertussis e pertactina". W I Seminário Anual Científico e Tecnológico em Imunobiológicos. Instituto de Tecnologia em Imunobiológicos, 2013. http://dx.doi.org/10.35259/isi.sact.2013_28799.

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Shimizu, Kenichiro, Ken Kikuchi, Masayuki Otsuka i Keiichi Hiramatsu. "Microbiological Features Of Emergent Increase Of Quinolone-Resistant Strains Of Bordetella Pertussis". W 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.a6086.

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de la Rosa, Carlos, Ranjit Prakash, Peter A. Tilley, Julie D. Fox i Karan V. I. S. Kaler. "Integrated Microfluidic Systems for Sample Preparation and Detection of Respiratory Pathogen Bordetella pertussis". W 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4353796.

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Mukherjee, Piyali, Brigitte Cheuvart, Nathalie Baudson, Monique Dodet, Elisa Turriani, Lauriane Harrington, Nadia Meyer, Simona Rondini, Laura Taddei i Peter Van Den Steen. "Late Breaking Abstract - Seroprevalence of Bordetella pertussis in chronic obstructive pulmonary disease (COPD) patients". W ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4927.

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Raporty organizacyjne na temat "Bordetella"

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McDonough, E. A., C. P. Barrozo, K. L. Russell i D. Metzgar. A Multiplex PCR for Detection of Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella pneumophila, and Bordetella pertussis in Clinical Specimens. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2005. http://dx.doi.org/10.21236/ada432554.

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