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Berlin Brandenburg

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  • 1
    Language: English
    In: The Journal of infectious diseases, 15 March 2011, Vol.203(6), pp.880-8
    Description: Superinfections from Staphylococcus aureus following influenza are an increasing concern. We assessed several laboratory and clinical strains in a mouse coinfection model with influenza virus. A methicillin-resistant USA300 clone and several recent clinical strains from patients with necrotizing pneumonia caused high mortality following influenza virus infection in mice. Both viral and bacterial lung titers were enhanced during coinfections compared with single infections. However, differences in titers did not correspond with differences in disease outcomes in a comparison of superinfections from a highly pathogenic strain with those from a poorly pathogenic strain. These strains did differ, however, in expression of Panton-Valentine leukocidin and in the degree of inflammatory lung damage each engendered. The viral cytotoxin PB1-F2 contributed to the negative outcomes. These data suggest that additional study of specific bacterial virulence factors involved in the pathogenesis of inflammation and lung damage during coinfections is needed.
    Keywords: Influenza A Virus -- Pathogenicity ; Influenza, Human -- Complications ; Pneumonia, Staphylococcal -- Microbiology ; Staphylococcus Aureus -- Pathogenicity ; Superinfection -- Microbiology
    ISSN: 00221899
    E-ISSN: 1537-6613
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  • 2
    In: Epilepsia, August 2012, Vol.53(8), pp.e161-e165
    Description: Autosomal dominant mutations and in the GABA receptor α1 subunit are associated with human absence epilepsy and juvenile myoclonic epilepsy, respectively. Because these mutations substantially reduce α1 subunit protein expression in vitro, it was hypothesized that they produce epilepsy by causing α1 subunit haploinsufficiency. However, in a mixed background strain of mice, α1 subunit deletion does not reduce viability or cause visually apparent seizures; the effects of α1 subunit deletion on electroencephalography (EEG) waveforms were not investigated. Here, we determined the effects of α1 subunit loss on viability, EEG spike‐wave discharges and seizures in congenic C57BL/6J and DBA/2J mice. Deletion of α1 subunit caused strain‐ and sex‐dependent reductions in viability. Heterozygous mice experienced EEG discharges and absence‐like seizures within both background strains, and exhibited a sex‐dependent effect on the discharges and viability in the C57BL/6J strain. These findings suggest that α1 subunit haploinsufficiency can produce epilepsy and may be a major mechanism by which the and mutations cause these epilepsy syndromes.
    Keywords: Generalized ; Inhibition ; Electroencephalogram ; Electromyography ; Ethosuximide
    ISSN: 0013-9580
    E-ISSN: 1528-1167
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  • 3
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 2012, Vol.109(38), pp.15389-15394
    Description: Conditional mutations are essential for determining the stage- and tissue-specific functions of genes. Here we achieve conditional mutagenesis in zebrafish using FT1, a gene-trap cassette that can be stably inverted by both Cre and Flp recombinases. We demonstrate that intronic insertions in the gene-trapping orientation severely disrupt the expression of the host gene, whereas intronic insertions in the neutral orientation do not significantly affect host gene expression. Cre- and Flp-mediated recombination switches the orientation of the gene-trap cassette, permitting conditional rescue in one orientation and conditional knockout in the other. To illustrate the utility of this system we analyzed the functional consequence of intronic FT1 insertion in supv3l1 , a gene encoding a mitochondrial RNA helicase. Global supv311 mutants have impaired mitochondrial function, embryonic lethality, and agenesis of the liver. Conditional rescue of supv311 expression in hepatocytes specifically corrected the liver defects. To test whether the liver function of supv311 is required for viability we used Flp-mediated recombination in the germline to generate a neutral allele at the locus. Subsequently, tissue-specific expression of Cre conditionally inactivated the targeted locus. Hepatocyte-specific inactivation of supv311 caused liver degeneration, growth retardation, and juvenile lethality, a phenotype that was less severe than the global disruption of supv311 . Thus, supv311 is required in multiple tissues for organismal viability. Our mutagenesis approach is very efficient and could be used to generate conditional alleles throughout the zebrafish genome. Furthermore, because FT1 is based on the promiscuous Tol2 transposon, it should be applicable to many organisms. ; p. 15389-15394.
    Keywords: Transposons ; Alleles ; Liver Function ; Juveniles ; Mitochondrial Rna ; Loci ; Phenotype ; Rna Helicases ; Hepatocytes ; Growth Retardation ; Mutants ; Danio Rerio ; Germ Cells ; Viability ; Mutagenesis ; Liver ; Gene Expression ; Tissues
    ISSN: 0027-8424
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  • 4
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 09 August 2016, Vol.113(32), pp.E4662-70
    Description: Tregs are essential for maintaining peripheral tolerance, and thus targeting these cells may aid in the treatment of autoimmunity and cancer by enhancing or reducing suppressive functions, respectively. Before these cells can be harnessed for therapeutic purposes, it is necessary to understand how they maintain tolerance under physiologically relevant conditions. We now report that transcription factor Kruppel-like factor 2 (KLF2) controls naive Treg migration patterns via regulation of homeostatic and inflammatory homing receptors, and that in its absence KLF2-deficient Tregs are unable to migrate efficiently to secondary lymphoid organs (SLOs). Diminished Treg trafficking to SLOs is sufficient to initiate autoimmunity, indicating that SLOs are a primary site for maintaining peripheral tolerance under homeostatic conditions. Disease severity correlates with impaired Treg recruitment to SLOs and, conversely, promotion of Tregs into these tissues can ameliorate autoimmunity. Moreover, stabilizing KLF2 expression within the Treg compartment enhances peripheral tolerance by diverting these suppressive cells from tertiary tissues into SLOs. Taken together, these results demonstrate that peripheral tolerance is enhanced or diminished through modulation of Treg trafficking to SLOs, a process that can be controlled by adjusting KLF2 protein levels.
    Keywords: Klf2 ; Treg Migration ; Autoimmunity ; Peripheral Tolerance ; Regulatory T Cell ; Immune Tolerance ; Kruppel-Like Transcription Factors -- Physiology ; T-Lymphocytes, Regulatory -- Physiology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 5
    Language: English
    In: Antimicrobial Agents and Chemotherapy, 2011, Vol. 55(5), p.2276
    Description: Alternate therapies are needed for treatment of secondary bacterial pneumonia following influenza. The immunomodulatory peptide P4 has shown promise in mouse models of primary pneumococcal infection. Mice infected with influenza virus and then challenged with Streptococcus pneumoniae were treated with a combination of P4 peptide and intravenous immune globulin. Survival was improved from 20% to 80% in treated mice relative to controls. Clinical cure correlated with increased clearance of bacteria and decreased lung consolidation. Greater trafficking of professional phagocytic cells to the site of pneumococcal infection coupled with enhanced opsonophagocytosis as manifest by decreased surface display of Fcγ receptors (FcγR) on neutrophils and macrophages were associated with P4 peptide treatment. This suggests that the mechanism of action for improved clearance of bacteria engendered by P4 is through improved uptake by phagocytes mediated by IgG Fc-Fcγ receptor interactions following antibody-mediated opsonophagocytosis of bacteria. Antibody-based therapies, when coupled with immune modulators, such as P4 peptide, may be an effective tool together with antibiotics in our armamentarium against severe pneumonia.
    Keywords: Immunoglobulins, Intravenous -- Therapeutic Use ; Pneumonia, Pneumococcal -- Drug Therapy;
    ISSN: 0066-4804
    ISSN: 00664804
    E-ISSN: 10986596
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  • 6
    Language: English
    In: Science, 28 May 2010, Vol.328(5982), pp.1103-1103
    Keywords: 〈bold〉LETTERS〈/bold〉
    ISSN: 00368075
    E-ISSN: 10959203
    Source: Archival Journals (JSTOR)
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  • 7
    Language: English
    In: Science, 28 May 2010, Vol.328(5982), pp.1103-1103
    Keywords: Biological sciences -- Biology -- Zoology ; Biological sciences -- Biology -- Zoology ; Health sciences -- Medical sciences -- Medical research ; Biological sciences -- Biology -- Zoology ; Biological sciences -- Biology -- Zoology ; Philosophy -- Applied philosophy -- Philosophy of science ; Applied sciences -- Research methods -- Modeling
    ISSN: 00368075
    E-ISSN: 10959203
    Source: Archival Journals (JSTOR)
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  • 8
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 18 September 2012, Vol.109(38), pp.15389-94
    Description: Conditional mutations are essential for determining the stage- and tissue-specific functions of genes. Here we achieve conditional mutagenesis in zebrafish using FT1, a gene-trap cassette that can be stably inverted by both Cre and Flp recombinases. We demonstrate that intronic insertions in the gene-trapping orientation severely disrupt the expression of the host gene, whereas intronic insertions in the neutral orientation do not significantly affect host gene expression. Cre- and Flp-mediated recombination switches the orientation of the gene-trap cassette, permitting conditional rescue in one orientation and conditional knockout in the other. To illustrate the utility of this system we analyzed the functional consequence of intronic FT1 insertion in supv3l1, a gene encoding a mitochondrial RNA helicase. Global supv311 mutants have impaired mitochondrial function, embryonic lethality, and agenesis of the liver. Conditional rescue of supv311 expression in hepatocytes specifically corrected the liver defects. To test whether the liver function of supv311 is required for viability we used Flp-mediated recombination in the germline to generate a neutral allele at the locus. Subsequently, tissue-specific expression of Cre conditionally inactivated the targeted locus. Hepatocyte-specific inactivation of supv311 caused liver degeneration, growth retardation, and juvenile lethality, a phenotype that was less severe than the global disruption of supv311. Thus, supv311 is required in multiple tissues for organismal viability. Our mutagenesis approach is very efficient and could be used to generate conditional alleles throughout the zebrafish genome. Furthermore, because FT1 is based on the promiscuous Tol2 transposon, it should be applicable to many organisms.
    Keywords: Zebrafish -- Genetics
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 9
    Language: English
    In: The Journal of infectious diseases, 15 October 2010, Vol.202(8), pp.1287-95
    Description: The role of respiratory viruses in the transmission of Streptococcus pneumoniae is poorly understood. Key questions, such as which serotypes are most fit for transmission and disease and whether influenza virus alters these parameters in a serotype-specific manner, have not been adequately studied. In a novel model of transmission in ferrets, we demonstrated that pneumococcal transmission and disease were enhanced if donors had previously been infected with influenza virus. Bacterial titers in nasal wash, the incidence of mucosal and invasive disease, and the percentage of contacts that were infected all increased. In contact ferrets, viral infection increased their susceptibility to S. pneumoniae acquisition both in terms of the percentage infected and the distance over which they could acquire infection. These influenza-mediated effects on colonization, transmission, and disease were dependent on the pneumococcal strain. Overall, these data argue that the relationship between respiratory viral infections, acquisition of pneumococci, and development of disease in humans needs further study to be better understood.
    Keywords: Ferrets ; Host-Pathogen Interactions ; Influenza A Virus -- Immunology ; Orthomyxoviridae Infections -- Immunology ; Pneumococcal Infections -- Immunology ; Streptococcus Pneumoniae -- Physiology
    ISSN: 00221899
    E-ISSN: 1537-6613
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  • 10
    Language: English
    In: The Journal of Allergy and Clinical Immunology, February 2017, Vol.139(2), pp.AB375-AB375
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jaci.2016.12.896 Byline: Melissa H. Bloodworth (1), Kelli L. Boyd (1), Lisa M. Rogers (2), David M. Aronoff (2), Stokes Peebles (3) Author Affiliation: (1) Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (2) Division of Infectious Diseases, Vanderbilt University, Nashville, TN (3) Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University, Nashville, TN Article Note: (miscellaneous) L2
    Keywords: Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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