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  1. Book: Purinergic regulation of respiratory diseases

    Picher, Maryse / Boucher, Richard C.

    (Subcellular Biochemistry ; 55)

    2011  

    Author's details Maryse Picher, ed.-in-chief ; Richard C. Boucher, ed
    Series title Subcellular Biochemistry ; 55
    Subcellular biochemistry
    Collection Subcellular biochemistry
    Language English
    Size XVII, 280 S. : Ill., graph. Darst.
    Publisher Springer
    Publishing place Dordrecht u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT016863142
    ISBN 978-94-007-1216-4 ; 9789400712171 ; 94-007-1216-2 ; 9400712170
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2011 A 2311 order for loan Magazin

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  2. Article: Mechanisms regulating airway nucleotides.

    Picher, Maryse

    Sub-cellular biochemistry

    2011  Volume 55, Page(s) 17–49

    Abstract: In the respiratory system, extracellular nucleotides and nucleosides serve as signaling molecules for a wide spectrum of biological functions regulating airway defenses against infection and toxic material. Their concentrations are controlled by a ... ...

    Abstract In the respiratory system, extracellular nucleotides and nucleosides serve as signaling molecules for a wide spectrum of biological functions regulating airway defenses against infection and toxic material. Their concentrations are controlled by a complex network of cell surface enzymes named ectonucleotidases. This highly integrated metabolic network combines the activities of three dephosphorylating ectonucleotidases, namely nucleoside triphosphate diphosphohydrolases (NTPDases), nucleotide pyrophosphatase/phosphodiesterases (NPPs) and alkaline phosphatases (APs). Extracellular nucleotides are also inter-converted by the transphosphorylating activities of ecto adenylate kinase (ectoAK) and nucleoside diphosphokinase (NDPK). Different cell types use specific combinations of ectonucleotidases to regulate local concentrations of P2 receptor agonists (ATP, UTP, ADP and UDP). In addition, they provide AMP for the activity of ecto 5'-nucleotidase (ecto 5'-NT; CD73), which produces the P1 receptor agonist: adenosine (ADO). Finally, mechanisms are in place to prevent the accumulation of airway ADO, namely adenosine deaminases and nucleoside transporters. This chapter reviews the properties of each enzyme and transporter, and the current knowledge on their distribution and regulation in the airways.
    MeSH term(s) Adenine Nucleotides/metabolism ; Animals ; Biological Transport ; Epithelial Cells/metabolism ; Humans ; Hydrolases/metabolism ; Hydrolysis ; Nucleotide Transport Proteins/metabolism ; Receptors, Purinergic/metabolism ; Respiratory Mucosa/metabolism ; Signal Transduction
    Chemical Substances Adenine Nucleotides ; Nucleotide Transport Proteins ; Receptors, Purinergic ; Hydrolases (EC 3.-)
    Language English
    Publishing date 2011
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 0306-0225 ; 0096-8757
    ISSN 0306-0225 ; 0096-8757
    DOI 10.1007/978-94-007-1217-1_2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book: Purinergic regulation of respiratory diseases

    Picher, Maryse

    (Subcellular biochemistry ; 55)

    2011  

    Author's details Maryse Picher ed.-in-chief
    Series title Subcellular biochemistry ; 55
    Keywords Cellular signal transduction ; Purines/Receptors ; Respiratory organs/Diseases
    Language English
    Size XVII, 280 S., Ill., graph. Darst.
    Publisher Springer
    Publishing place Dordrecht u.a.
    Document type Book
    ISBN 9789400712164 ; 9789400712171 ; 9400712162 ; 9400712170
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  4. Book: Purinergic regulation of respiratory diseases

    Picher, Maryse / Boucher, Richard C

    (Subcellular biochemistry ; v. 55)

    2011  

    Author's details Maryse Picher, editor-in-chief ; Richard C. Boucher, editor
    Series title Subcellular biochemistry ; v. 55
    Keywords Purines/Receptors. ; Cellular signal transduction. ; Respiratory organs. ; signal transduction ; respiratory system ; metabolism
    Language English
    Size xvii, 280 p. :, ill. (some col.), 24 cm.
    Publisher Springer Science + Business Media
    Publishing place Dordrecht ; New York
    Document type Book
    ISBN 9400712162 ; 9789400712164
    Database NAL-Catalogue (AGRICOLA)

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  5. Book: Purinergic regulation of respiratory diseases

    Picher, Maryse / Boucher, Richard C

    (Subcellular biochemistry, ; volume 55)

    2011  

    Author's details Maryse Picher, editor-in-chief ; Richard C. Boucher, editor
    Series title Subcellular biochemistry, ; volume 55
    MeSH term(s) Receptors, Purinergic ; Signal Transduction ; Respiratory Tract Diseases ; Respiratory System/metabolism
    Language English
    Size xvii, 280 pages :, illustrations (some color) ;, 24 cm.
    Document type Book
    ISBN 9789400712164 ; 9400712162 ; 9789400712171 ; 9400712170
    Database Catalogue of the US National Library of Medicine (NLM)

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  6. Book ; Online: Purinergic Regulation of Respiratory Diseases

    Picher, Maryse / Boucher, Richard C

    (Subcellular Biochemistry ; 55)

    2011  

    Abstract: The book contains contributions by leading figures in philosophy of mind and action, emotion theory, and phenomenology. As the focus of the volume is truly innovative we expect the book to sell well to both philosophers and scholars from neighboring ... ...

    Author's details edited by Maryse Picher, Richard C. Boucher
    Series title Subcellular Biochemistry ; 55
    Abstract The book contains contributions by leading figures in philosophy of mind and action, emotion theory, and phenomenology. As the focus of the volume is truly innovative we expect the book to sell well to both philosophers and scholars from neighboring fields such as social and cognitive science. The predominant view in analytic philosophy is that an ability for self-evaluation is constitutive for agency and intentionality. Until now, the debate is limited in two (possibly mutually related) ways: Firstly, self-evaluation is usually discussed in individual terms, and, as such, not sufficiently related to its social dimensions, secondly, self-evaluation is viewed as a matter of belief and desire, neglecting its affective and emotional aspects. The aim of the book is to fill these research lacunas and to investigate the question of how these two shortcomings of the received views are related.
    Keywords Emerging infectious diseases ; Medicine ; Metabolic diseases ; Pharmaceutical technology ; Pneumology ; Trauma ; Medizin / Gesundheit # Chirurgie ; Medizin / Gesundheit # Grundlagen / Nachschlagewerke ; Medizin / Gesundheit # Innere Medizin ; Medizin / Gesundheit # Pneumologie / HNO ; Medizin / Gesundheit # Sonstiges
    Language English
    Size Online-Ressource, v.: digital
    Publisher Springer Science+Business Media B.V
    Publishing place Dordrecht
    Document type Book ; Online
    Note Includes bibliographical references and index
    ISBN 9789400712164 ; 9789400712171 ; 9400712162 ; 9400712170
    DOI 10.1007/978-94-007-1217-1
    Database Former special subject collection: coastal and deep sea fishing

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  7. Article: Animal models of airway diseases.

    Thompson, Linda F / Picher, Maryse / Blackburn, Michael R

    Sub-cellular biochemistry

    2011  Volume 55, Page(s) 195–234

    Abstract: Over the past 20 years, the growing awareness that purinergic signaling events literally shape the immune and inflammatory responses to infection and allergic reactions warranted the development of animal models to assess their importance in vivo in ... ...

    Abstract Over the past 20 years, the growing awareness that purinergic signaling events literally shape the immune and inflammatory responses to infection and allergic reactions warranted the development of animal models to assess their importance in vivo in acute lung injury and chronic airway diseases. The pioneer work conducted with the adenosine deaminase (ADA)-deficient mouse provided irrefutable evidence that excess adenosine (ADO) accumulating in the lungs of asthmatic patients, constitutes a powerful mediator of disease severity. These original studies launched the development of murine strains for the two major ectonucleotidases responsible for the generation of airway ADO from ATP release: CD39 and CD73. The dramatic acute lung injury and chronic lung complications, manifested by these knockout mice in response to allergens and endotoxin, demonstrated the critical importance of regulating the availability of ATP and ADO for their receptors. Therapeutic targets are currently evaluated using knockout mice and agonists/antagonists for each ADO receptor (A(1)R, A(2A)R, A(2B)R, and A(3)R) and the predominant ATP receptors (P2Y(2)R and P2X(7)R). This chapter provides an in-depth description of each in vivo study, and a critical view of the therapeutic potentials for the treatment of airway diseases.
    MeSH term(s) Animals ; Disease Models, Animal ; Genetic Predisposition to Disease ; Humans ; Lung Diseases/genetics ; Lung Diseases/metabolism ; Mice ; Mice, Transgenic ; Phenotype ; Purines/metabolism ; Receptors, Purinergic/genetics ; Receptors, Purinergic/metabolism ; Signal Transduction
    Chemical Substances Purines ; Receptors, Purinergic
    Keywords covid19
    Language English
    Publishing date 2011-05-12
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 0306-0225 ; 0096-8757
    ISSN 0306-0225 ; 0096-8757
    DOI 10.1007/978-94-007-1217-1_8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Therapeutic applications.

    Tilley, Stephen / Volmer, Jon / Picher, Maryse

    Sub-cellular biochemistry

    2011  Volume 55, Page(s) 235–276

    Abstract: The current treatments offered to patients with chronic respiratory diseases are being re-evaluated based on the loss of potency during long-term treatments or because they only provide significant clinical benefits to a subset of the patient population. ...

    Abstract The current treatments offered to patients with chronic respiratory diseases are being re-evaluated based on the loss of potency during long-term treatments or because they only provide significant clinical benefits to a subset of the patient population. For instance, glucocorticoids are considered the most effective anti-inflammatory therapies for chronic inflammatory and immune diseases, such as asthma. But they are relatively ineffective in asthmatic smokers, and patients with chronic obstructive pulmonary disease (COPD) or cystic fibrosis (CF). As such, the pharmaceutical industry is exploring new therapeutic approaches to address all major respiratory diseases. The previous chapters demonstrated the widespread influence of purinergic signaling on all pulmonary functions and defense mechanisms. In Chap. 8, we described animal studies which highlighted the critical role of aberrant purinergic activities in the development and maintenance of chronic airway diseases. This last chapter covers all clinical and pharmaceutical applications currently developed based on purinergic receptor agonists and antagonists. We use the information acquired in the previous chapters on purinergic signaling and lung functions to scrutinize the preclinical and clinical data, and to realign the efforts of the pharmaceutical industry.
    MeSH term(s) Animals ; Biomarkers/metabolism ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Humans ; Lung Diseases/diagnosis ; Lung Diseases/drug therapy ; Lung Diseases/metabolism ; Lung Diseases/physiopathology ; Molecular Targeted Therapy ; Predictive Value of Tests ; Purinergic Agonists/therapeutic use ; Purinergic Antagonists/therapeutic use ; Purines/metabolism ; Receptors, Purinergic/drug effects ; Receptors, Purinergic/metabolism ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/physiopathology ; Signal Transduction/drug effects
    Chemical Substances Biomarkers ; Purinergic Agonists ; Purinergic Antagonists ; Purines ; Receptors, Purinergic
    Keywords covid19
    Language English
    Publishing date 2011-04-06
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 0306-0225 ; 0096-8757
    ISSN 0306-0225 ; 0096-8757
    DOI 10.1007/978-94-007-1217-1_9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Regulation of airway nucleotides in chronic lung diseases.

    Esther, Charles R / Alexis, Neil E / Picher, Maryse

    Sub-cellular biochemistry

    2011  Volume 55, Page(s) 75–93

    Abstract: The physiological relevance of the purinergic signaling network for airway defenses is emerging through cumulating reports of abnormal ATP and adenosine (ADO) levels in the airway secretions of patients with asthma, chronic pulmonary obstructive diseases, ...

    Abstract The physiological relevance of the purinergic signaling network for airway defenses is emerging through cumulating reports of abnormal ATP and adenosine (ADO) levels in the airway secretions of patients with asthma, chronic pulmonary obstructive diseases, cystic fibrosis and idiopathic pulmonary fibrosis. The consequences for airway defenses range from abnormal clearance responses to the destruction of lung tissue by excessive inflammation. This chapter reviews the challenges of assessing airway purines in human subjects, and identifies the general trend in aberrant airway composition. Most diseases are associated with an accumulation of ATP and/or ADO in bronchoalveolar lavage, sputum or exhaled breadth condensate. Intriguing is the case of cystic fibrosis patients, which do not accumulate airway ADO, but its precursor, AMP. This observation launched the investigation of ectonucleotidases as target proteins for the correction of airway purine levels in chronic respiratory diseases. This chapter exposes the extensive rearrangement of the enzymatic network taking place in diseased airways, and identifies signaling pathways likely involved in the aberrant regulation of the airway purines.
    MeSH term(s) Adenosine/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Chronic Disease ; Epithelial Cells/metabolism ; Humans ; Lung Diseases/metabolism ; Nucleotides/metabolism ; Respiratory Mucosa/metabolism
    Chemical Substances Nucleotides ; Adenosine Triphosphate (8L70Q75FXE) ; Adenosine (K72T3FS567)
    Language English
    Publishing date 2011
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 0306-0225 ; 0096-8757
    ISSN 0306-0225 ; 0096-8757
    DOI 10.1007/978-94-007-1217-1_4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: E-NTPDases in human airways: Regulation and relevance for chronic lung diseases.

    Burch, Lauranell H / Picher, Maryse

    Purinergic signalling

    2006  Volume 2, Issue 2, Page(s) 399–408

    Abstract: Chronic obstructive lung diseases are characterized by the inability to prevent bacterial infection and a gradual loss of lung function caused by recurrent inflammatory responses. In the past decade, numerous studies have demonstrated the importance of ... ...

    Abstract Chronic obstructive lung diseases are characterized by the inability to prevent bacterial infection and a gradual loss of lung function caused by recurrent inflammatory responses. In the past decade, numerous studies have demonstrated the importance of nucleotide-mediated bacterial clearance. Their interaction with P2 receptors on airway epithelia provides a rapid 'on-and-off' signal stimulating mucus secretion, cilia beating activity and surface hydration. On the other hand, abnormally high ATP levels resulting from damaged epithelia and bacterial lysis may cause lung edema and exacerbate inflammatory responses. Airway ATP concentrations are regulated by ecto nucleoside triphosphate diphosphohydrolases (E-NTPDases) which are expressed on the mucosal surface and catalyze the sequential dephosphorylation of nucleoside triphosphates to nucleoside monophosphates (ATP --> ADP --> AMP). The common bacterial product, Pseudomonas aeruginosa lipopolysaccharide (LPS), induces an acute reduction in azide-sensitive E-NTPDase activities, followed by a sustained increase in activity as well as NTPDase 1 and NTPDase 3 expression. Accordingly, chronic lung diseases, including cystic fibrosis (CF) and primary ciliary dyskinesia, are characterized by higher rates of nucleotide elimination, azide-sensitive E-NTPDase activities and expression. This review integrates the biphasic regulation of airway E-NTPDases with the function of purine signaling in lung diseases. During acute insults, a transient reduction in E-NTPDase activities may be beneficial to stimulate ATP-mediated bacterial clearance. In chronic lung diseases, elevating E-NTPDase activities may represent an attempt to prevent P2 receptor desensitization and nucleotide-mediated lung damage.
    Language English
    Publishing date 2006-05-30
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2172143-9
    ISSN 1573-9546 ; 1573-9538
    ISSN (online) 1573-9546
    ISSN 1573-9538
    DOI 10.1007/s11302-006-9001-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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