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  1. AU=Molyneaux Phillip L.
  2. AU=Shimizu Kazuki
  3. AU=Pell Robert AU=Pell Robert
  4. AU="Aguiar, Liza"
  5. AU="Bahls, Christine"
  6. AU="Dongho Lee"
  7. AU=Houser Steven R.
  8. AU="Morgom M.M."
  9. AU="Jordana-Comajuncosa, Rosa"
  10. AU="Kaushansky, Alexis"
  11. AU="Bhatjiwale, Mohinish"
  12. AU="Velu, Chinavenmeni S"
  13. AU=Trayanova Natalia A
  14. AU=Jimeno-Gonzlez Silvia
  15. AU=Bussolino F
  16. AU="Almulla, Hanan"
  17. AU="Chen, Wenmei"
  18. AU=Zeng Weiqing

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  1. Artikel ; Online: The impact of hiatus hernia in hypersensitivity pneumonitis.

    Heriot, David A / Stock, Carmel J W / Mumtaz, Zain-Ul-Abideen / Jenkins, R Gisli / Chua, Felix / Molyneaux, Phillip L / Devaraj, Anand / Kouranos, Vasilis / Wells, Athol U / Renzoni, Elizabetta A / Padley, Simon P G / Desai, Sujal R / George, Peter M

    Respirology (Carlton, Vic.)

    2024  Band 29, Heft 5, Seite(n) 421–425

    Mesh-Begriff(e) Humans ; Hernia, Hiatal/complications ; Alveolitis, Extrinsic Allergic/diagnosis ; Alveolitis, Extrinsic Allergic/etiology ; Manometry
    Sprache Englisch
    Erscheinungsdatum 2024-03-13
    Erscheinungsland Australia
    Dokumenttyp Journal Article
    ZDB-ID 1435849-9
    ISSN 1440-1843 ; 1323-7799
    ISSN (online) 1440-1843
    ISSN 1323-7799
    DOI 10.1111/resp.14701
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Host-Microbial Interactions in Idiopathic Pulmonary Fibrosis.

    Molyneaux, Philip L / Willis-Owen, Saffron A G / Cox, Michael J / James, Phillip / Cowman, Steven / Loebinger, Michael / Blanchard, Andrew / Edwards, Lindsay M / Stock, Carmel / Daccord, Cécile / Renzoni, Elisabetta A / Wells, Athol U / Moffatt, Miriam F / Cookson, William O C / Maher, Toby M

    American journal of respiratory and critical care medicine

    2016  Band 195, Heft 12, Seite(n) 1640–1650

    Abstract: Rationale: Changes in the respiratory microbiome are associated with disease progression in idiopathic pulmonary fibrosis (IPF). The role of the host response to the respiratory microbiome remains unknown.: Objectives: To explore the host-microbial ... ...

    Abstract Rationale: Changes in the respiratory microbiome are associated with disease progression in idiopathic pulmonary fibrosis (IPF). The role of the host response to the respiratory microbiome remains unknown.
    Objectives: To explore the host-microbial interactions in IPF.
    Methods: Sixty patients diagnosed with IPF were prospectively enrolled together with 20 matched control subjects. Subjects underwent bronchoalveolar lavage (BAL), and peripheral whole blood was collected into PAXgene tubes for all subjects at baseline. For subjects with IPF, additional samples were taken at 1, 3, and 6 months and (if alive) 1 year. Gene expression profiles were generated using Affymetrix Human Gene 1.1 ST arrays.
    Measurements and main results: By network analysis of gene expression data, we identified two gene modules that strongly associated with a diagnosis of IPF, BAL bacterial burden (determined by 16S quantitative polymerase chain reaction), and specific microbial operational taxonomic units, as well as with lavage and peripheral blood neutrophilia. Genes within these modules that are involved in the host defense response include NLRC4, PGLYRP1, MMP9, and DEFA4. The modules also contain two genes encoding specific antimicrobial peptides (SLPI and CAMP). Many of these particular transcripts were associated with survival and showed longitudinal overexpression in subjects experiencing disease progression, further strengthening the relationship of the transcripts with disease.
    Conclusions: Integrated analysis of the host transcriptome and microbial signatures demonstrated an apparent host response to the presence of an altered or more abundant microbiome. These responses remained elevated in longitudinal follow-up, suggesting that the bacterial communities of the lower airways may act as persistent stimuli for repetitive alveolar injury in IPF.
    Mesh-Begriff(e) Aged ; Bronchoalveolar Lavage Fluid/microbiology ; Female ; Follow-Up Studies ; Host-Pathogen Interactions ; Humans ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/microbiology ; Male ; Microbiota ; Prospective Studies ; Transcriptome
    Sprache Englisch
    Erscheinungsdatum 2016-12-09
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.201607-1408OC
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: The role of bacteria in the pathogenesis and progression of idiopathic pulmonary fibrosis.

    Molyneaux, Phillip L / Cox, Michael J / Willis-Owen, Saffron A G / Mallia, Patrick / Russell, Kirsty E / Russell, Anne-Marie / Murphy, Elissa / Johnston, Sebastian L / Schwartz, David A / Wells, Athol U / Cookson, William O C / Maher, Toby M / Moffatt, Miriam F

    American journal of respiratory and critical care medicine

    2014  Band 190, Heft 8, Seite(n) 906–913

    Abstract: Rationale: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of diagnosis. Overt respiratory infection and immunosuppression carry a high morbidity and mortality, ...

    Abstract Rationale: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of diagnosis. Overt respiratory infection and immunosuppression carry a high morbidity and mortality, and polymorphisms in genes related to epithelial integrity and host defense predispose to IPF.
    Objectives: To investigate the role of bacteria in the pathogenesis and progression of IPF.
    Methods: We prospectively enrolled patients diagnosed with IPF according to international criteria together with healthy smokers, nonsmokers, and subjects with moderate chronic obstructive pulmonary disease as control subjects. Subjects underwent bronchoalveolar lavage (BAL), from which genomic DNA was isolated. The V3-V5 region of the bacterial 16S rRNA gene was amplified, allowing quantification of bacterial load and identification of communities by 16S rRNA quantitative polymerase chain reaction and pyrosequencing.
    Measurements and main results: Sixty-five patients with IPF had double the burden of bacteria in BAL fluid compared with 44 control subjects. Baseline bacterial burden predicted the rate of decline in lung volume and risk of death and associated independently with the rs35705950 polymorphism of the MUC5B mucin gene, a proven host susceptibility factor for IPF. Sequencing yielded 912,883 high-quality reads from all subjects. We identified Haemophilus, Streptococcus, Neisseria, and Veillonella spp. to be more abundant in cases than control subjects. Regression analyses indicated that these specific operational taxonomic units as well as bacterial burden associated independently with IPF.
    Conclusions: IPF is characterized by an increased bacterial burden in BAL that predicts decline in lung function and death. Trials of antimicrobial therapy are needed to determine if microbial burden is pathogenic in the disease.
    Mesh-Begriff(e) Aged ; Bacteria/isolation & purification ; Bacterial Load ; Bronchoalveolar Lavage ; Bronchoalveolar Lavage Fluid/microbiology ; Bronchoscopy ; Case-Control Studies ; DNA, Bacterial/analysis ; Disease Progression ; Female ; Genetic Markers ; Genotyping Techniques ; Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/microbiology ; Idiopathic Pulmonary Fibrosis/mortality ; Idiopathic Pulmonary Fibrosis/physiopathology ; Logistic Models ; Male ; Microbiota ; Middle Aged ; Mucin-5B/genetics ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Prospective Studies ; Sequence Analysis, DNA
    Chemische Substanzen DNA, Bacterial ; Genetic Markers ; MUC5B protein, human ; Mucin-5B
    Sprache Englisch
    Erscheinungsdatum 2014-09-03
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.201403-0541OC
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Identification, synthesis and SAR of amino substituted pyrido[3,2b]pyrazinones as potent and selective PDE5 inhibitors.

    Owen, Dafydd R / Walker, John K / Jon Jacobsen, E / Freskos, John N / Hughes, Robert O / Brown, David L / Bell, Andrew S / Brown, David G / Phillips, Christopher / Mischke, Brent V / Molyneaux, John M / Fobian, Yvette M / Heasley, Steve E / Moon, Joseph B / Stallings, William C / Joseph Rogier, D / Fox, David N A / Palmer, Michael J / Ringer, Tracy /
    Rodriquez-Lens, Margarita / Cubbage, Jerry W / Blevis-Bal, Radhika M / Benson, Alan G / Acker, Brad A / Maddux, Todd M / Tollefson, Michael B / Bond, Brian R / Macinnes, Alan / Yu, Yung

    Bioorganic & medicinal chemistry letters

    2009  Band 19, Heft 15, Seite(n) 4088–4091

    Abstract: A new class of potent and selective PDE5 inhibitors is disclosed. Guided by X-ray crystallographic data, optimization of an HTS lead led to the discovery of a series of 2-aryl, (N8)-alkyl substituted-6-aminosubstituted pyrido[3,2b]pyrazinones which show ... ...

    Abstract A new class of potent and selective PDE5 inhibitors is disclosed. Guided by X-ray crystallographic data, optimization of an HTS lead led to the discovery of a series of 2-aryl, (N8)-alkyl substituted-6-aminosubstituted pyrido[3,2b]pyrazinones which show potent inhibition of the PDE5 enzyme. Synthetic details and some structure-activity relationships are also presented.
    Mesh-Begriff(e) Animals ; Catalytic Domain ; Chemistry, Pharmaceutical/methods ; Crystallography, X-Ray/methods ; Cyclic Nucleotide Phosphodiesterases, Type 5/chemistry ; Cyclic Nucleotide Phosphodiesterases, Type 6/antagonists & inhibitors ; Cyclic Nucleotide Phosphodiesterases, Type 6/chemistry ; Drug Design ; Humans ; Hydrogen-Ion Concentration ; Inhibitory Concentration 50 ; Phosphodiesterase 5 Inhibitors ; Phosphodiesterase Inhibitors/chemical synthesis ; Phosphodiesterase Inhibitors/pharmacology ; Phosphoric Diester Hydrolases/chemistry ; Protein Structure, Tertiary ; Pyrazines/chemical synthesis ; Pyrazines/pharmacology ; Rats ; Structure-Activity Relationship
    Chemische Substanzen Phosphodiesterase 5 Inhibitors ; Phosphodiesterase Inhibitors ; Pyrazines ; Phosphoric Diester Hydrolases (EC 3.1.4.-) ; Cyclic Nucleotide Phosphodiesterases, Type 5 (EC 3.1.4.35) ; Cyclic Nucleotide Phosphodiesterases, Type 6 (EC 3.1.4.35) ; PDE11A protein, human (EC 3.1.4.35)
    Sprache Englisch
    Erscheinungsdatum 2009-08-01
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1063195-1
    ISSN 1464-3405 ; 0960-894X
    ISSN (online) 1464-3405
    ISSN 0960-894X
    DOI 10.1016/j.bmcl.2009.06.012
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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