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  1. Book: Chemokines in the lung

    Strieter, Robert M.

    (Lung biology in health and disease ; 172)

    2003  

    Author's details ed. by Robert M. Strieter
    Series title Lung biology in health and disease ; 172
    Collection
    Keywords Lung Diseases / immunology ; Chemokines / immunology ; Leukocytes / immunology ; Chemotaxis, Leukocyte ; Inflammation ; Lungenkrankheit ; Chemokine
    Subject Lungenerkrankung
    Language English
    Size XVIII, 399 S. : Ill., graph. Darst.
    Publisher Dekker
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT013554838
    ISBN 0-8247-0858-X ; 978-0-8247-0858-0
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    2003 A 2297 order for loan Magazin

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  2. Article ; Online: Systemic Fibrocyte Levels and Keloid Expression of the Chemoattractant CXCL12 Are Upregulated Compared With Patients With Normal Scar.

    Campbell, Chris A / Burdick, Marie D / Strieter, Robert M

    Annals of plastic surgery

    2021  Volume 87, Issue 2, Page(s) 150–155

    Abstract: Background: Fibrocytes are bone marrow mesenchymal precursors with a surface phenotype compatible with leukocytes, fibroblasts, and hematopoietic progenitors that have been shown to traffic to wound healing sites in response to described chemokine ... ...

    Abstract Background: Fibrocytes are bone marrow mesenchymal precursors with a surface phenotype compatible with leukocytes, fibroblasts, and hematopoietic progenitors that have been shown to traffic to wound healing sites in response to described chemokine pathways. Keloids are focal fibrotic responses to cutaneous trauma characterized by disordered collagen, which may be associated with elevated systemic fibrocyte levels and/or wound bed chemokine expression.
    Methods: Blood specimens from patients with longstanding keloids and those who form grossly normal scars were assayed by fluorescence activated cell sorting analysis for fibrocytes (CD45+, Col I+). The expression of the fibrocyte chemotactic cell surface marker CXCR4, intracellular markers of fibroblast differentiation (pSMAD2/3), and plasma levels of the CXCR4 cognate CXCL12 were compared. Keloid specimens and grossly normal scars were excised, and local expression of CXCL12 was assayed.
    Results: Keloid-forming patients demonstrated a significantly greater number of circulating fibrocytes (17.4 × 105 cells/mL) than control patients (1.01 × 105 cells/mL, P = 0.004). The absolute number of fibrocytes expressing CXCR4 was significantly greater (P = 0.012) in keloid-forming patients. Systemic CXCL12 levels were insignificantly greater in keloid-forming patients than controls. Keloid specimens had significantly greater CXCL12 expression (529.3 pg/mL) than normal scar (undetectable).
    Conclusions: Systemic fibrocyte levels and the CXCR4/CXCL12 biologic axis responsible for fibrocyte trafficking to areas of regional fibrosis were both upregulated in patients who form keloids compared with controls. Keloids persistently expressed CXLC12, which serves both as the main chemoattractant for fibrocytes and a downstream mediator for local inflammation, suggesting a role for this biologic axis in keloid formation and possibly recurrence.
    MeSH term(s) Cell Differentiation ; Chemokine CXCL12 ; Chemotactic Factors ; Cicatrix ; Fibroblasts/pathology ; Fibrosis ; Humans ; Keloid/pathology
    Chemical Substances CXCL12 protein, human ; Chemokine CXCL12 ; Chemotactic Factors
    Language English
    Publishing date 2021-06-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 423835-7
    ISSN 1536-3708 ; 0148-7043
    ISSN (online) 1536-3708
    ISSN 0148-7043
    DOI 10.1097/SAP.0000000000002929
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book: Chemokines in disease

    Koch, Alisa E. / Strieter, Robert M.

    (Medical intelligence unit)

    1996  

    Author's details Alisa E. Koch ; Robert M. Strieter
    Series title Medical intelligence unit
    Keywords Chemokines / physiology ; Chemotaxis, Leukocyte / physiology ; Inflammation / immunology ; Chemokine ; Pathophysiologie
    Subject Pathologische Physiologie ; Physiologische Pathologie ; Physiopathologie
    Language English
    Size 215 S. : Ill., graph. Darst.
    Publisher Springer u.a.
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    Note Literaturangaben
    HBZ-ID HT007436050
    ISBN 3-540-61354-4 ; 0-412-11411-9 ; 1-57059-365-5 ; 978-3-540-61354-1 ; 978-0-412-11411-3 ; 978-1-57059-365-9
    Database Catalogue ZB MED Medicine, Health

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  4. Article ; Online: Out of the shadows: CXC chemokines in promoting aberrant lung cancer angiogenesis.

    Strieter, Robert M

    Cancer prevention research (Philadelphia, Pa.)

    2009  Volume 1, Issue 5, Page(s) 305–307

    MeSH term(s) Carcinoma, Non-Small-Cell Lung/blood supply ; Carcinoma, Non-Small-Cell Lung/pathology ; Chemokines, CXC/physiology ; Humans ; Lung Neoplasms/blood supply ; Lung Neoplasms/pathology ; Models, Biological ; Neovascularization, Pathologic/etiology ; Signal Transduction/physiology
    Chemical Substances Chemokines, CXC
    Language English
    Publishing date 2009-01-08
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 2434717-6
    ISSN 1940-6215 ; 1940-6207
    ISSN (online) 1940-6215
    ISSN 1940-6207
    DOI 10.1158/1940-6207.CAPR-08-0168
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: What differentiates normal lung repair and fibrosis? Inflammation, resolution of repair, and fibrosis.

    Strieter, Robert M

    Proceedings of the American Thoracic Society

    2008  Volume 5, Issue 3, Page(s) 305–310

    Abstract: There has been ongoing controversy related to what differentiates normal lung repair and fibrosis. For example, the current prevailing concept has been that idiopathic forms of pulmonary fibrosis are due only to epithelial injury in response to some ... ...

    Abstract There has been ongoing controversy related to what differentiates normal lung repair and fibrosis. For example, the current prevailing concept has been that idiopathic forms of pulmonary fibrosis are due only to epithelial injury in response to some unknown cause that results in persistent evolving fibrosis without preceding inflammation. This concept would suggest that the lung responds to injury in a different manner than other organs, such as the liver, kidney, and heart. However, that would seem to contradict known established pathological concepts. To address this controversy, concepts were presented as follows: (1) loss of basement membrane integrity is critical in determining the "point of no return," and contributes to the inability to reestablish normal lung architecture with promotion of fibrosis; (2) loss of epithelial cells, endothelial cells, and basement membrane integrity in usual interstitial pneumonia associated with idiopathic pulmonary fibrosis leads to destroyed lung architecture and perpetual fibrosis; (3) transforming growth factor-beta is necessary, but not entirely sufficient, to promote permanent fibrosis; (4) persistent injury/antigen/irritant is critical for the propagation of fibrosis; (5) idiopathic pulmonary fibrosis is an example of a process related to the persistence of an "antigen(s)," chronic inflammation, and fibrosis; and (6) unique cells are critical cellular players in the regulation of fibrosis. In keeping with the theme of the Aspen Lung Conference, it is hoped that more questions are raised than answered in this presentation, in support of the continued need for research in this area to address these important concepts.
    MeSH term(s) Basement Membrane/injuries ; Basement Membrane/physiopathology ; Endothelial Cells ; Humans ; Inflammation ; Lung/physiology ; Lung Diseases, Interstitial/immunology ; Lung Diseases, Interstitial/physiopathology ; Macrophages, Alveolar ; Pulmonary Fibrosis/etiology ; Pulmonary Fibrosis/physiopathology ; Respiratory Distress Syndrome/complications ; Respiratory Distress Syndrome/physiopathology ; Respiratory Mucosa/physiopathology ; Transforming Growth Factor beta/immunology ; Wound Healing/physiology
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2008-04-09
    Publishing country United States
    Document type Address ; Research Support, N.I.H., Extramural
    ZDB-ID 2132421-9
    ISSN 1943-5665 ; 1546-3222
    ISSN (online) 1943-5665
    ISSN 1546-3222
    DOI 10.1513/pats.200710-160DR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Fibrocytes and the pathogenesis of diffuse parenchymal lung disease.

    Mehrad, Borna / Strieter, Robert M

    Fibrogenesis & tissue repair

    2012  Volume 5, Issue Suppl 1, Page(s) S22

    Abstract: Fibrosis is fundamental to the pathogenesis of many chronic lung diseases, including some lung infections, airway diseases such as bronchiectasis and asthma, and most of the diffuse parenchymal lung diseases. Idiopathic pulmonary fibrosis, the ... ...

    Abstract Fibrosis is fundamental to the pathogenesis of many chronic lung diseases, including some lung infections, airway diseases such as bronchiectasis and asthma, and most of the diffuse parenchymal lung diseases. Idiopathic pulmonary fibrosis, the prototypical fibrotic lung disease, is amongst the most common diffuse parenchymal lung diseases and is characterized by progressive decline in lung function and premature death from respiratory failure. The clinical management of patients with this illness is hampered by our current inability to predict clinical deterioration and lack of an effective therapy. Fibrocytes are a population of bone marrow-derived circulating progenitor cells that home to injured tissues and differentiate into fibroblasts and myofibroblasts, thus contributing to scar formation. We summarize the evidence supporting the role of these cells in the pathogenesis of fibrotic lung diseases.
    Language English
    Publishing date 2012-06-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 2460211-5
    ISSN 1755-1536
    ISSN 1755-1536
    DOI 10.1186/1755-1536-5-S1-S22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Masters of angiogenesis.

    Strieter, Robert M

    Nature medicine

    2005  Volume 11, Issue 9, Page(s) 925–927

    MeSH term(s) Animals ; Gene Expression Regulation, Neoplastic ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; NF-kappa B/physiology ; Neoplasms/blood supply ; Neovascularization, Pathologic/physiopathology ; Transcription Factors/physiology
    Chemical Substances HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; NF-kappa B ; Transcription Factors
    Language English
    Publishing date 2005-09
    Publishing country United States
    Document type Comment ; News
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm0905-925
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Pathogenesis and natural history of usual interstitial pneumonia: the whole story or the last chapter of a long novel.

    Strieter, Robert M

    Chest

    2005  Volume 128, Issue 5 Suppl 1, Page(s) 526S–532S

    Abstract: Idiopathic pulmonary fibrosis (IPF)/usual interstitial pneumonia (UIP) is not well-understood. Current explanations of the natural history and pathogenesis of IPF/UIP are controversial, and ongoing research continues to investigate multiple hypotheses. A ...

    Abstract Idiopathic pulmonary fibrosis (IPF)/usual interstitial pneumonia (UIP) is not well-understood. Current explanations of the natural history and pathogenesis of IPF/UIP are controversial, and ongoing research continues to investigate multiple hypotheses. A complete understanding of the natural history of IPF could potentially help to identify different mechanisms that are operative at the early, intermediate, and end stages of the disease. This knowledge could lead to the development of more effective therapeutic interventions that target stage-specific aberrant pathways involved in IPF/UIP pathogenesis.
    MeSH term(s) Chemokines, CXC/physiology ; Disease Progression ; Epithelial Cells/pathology ; Extracellular Matrix/metabolism ; Fibroblast Growth Factor 2/physiology ; Fibroblasts/metabolism ; Gene Expression ; Humans ; Lung Diseases, Interstitial/classification ; Lung Diseases, Interstitial/diagnostic imaging ; Lung Diseases, Interstitial/pathology ; Lung Diseases, Interstitial/physiopathology ; Neovascularization, Pathologic/physiopathology ; Oligonucleotide Array Sequence Analysis ; Pulmonary Fibrosis/pathology ; Tomography, X-Ray Computed/methods
    Chemical Substances Chemokines, CXC ; Fibroblast Growth Factor 2 (103107-01-3)
    Language English
    Publishing date 2005-11
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1378/chest.128.5_suppl_1.526S
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Mastering innate immunity.

    Strieter, Robert M

    Nature medicine

    2003  Volume 9, Issue 5, Page(s) 512–513

    MeSH term(s) Adenosine Triphosphate/metabolism ; Animals ; Energy Metabolism ; Glycolysis ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; Immunity, Innate ; Transcription Factors/physiology
    Chemical Substances HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Transcription Factors ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2003-05
    Publishing country United States
    Document type News
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm0503-512
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  10. Article: To clot or not to clot, that is the question in pulmonary fibrosis.

    Strieter, Robert M

    American journal of respiratory and critical care medicine

    2003  Volume 167, Issue 12, Page(s) 1589–1590

    MeSH term(s) Bronchoalveolar Lavage Fluid/chemistry ; Bronchoalveolar Lavage Fluid/immunology ; Fibrinolysis/drug effects ; Fibrinolysis/immunology ; Humans ; Immunotherapy ; Inflammation ; Lung Diseases, Interstitial/drug therapy ; Lung Diseases, Interstitial/immunology ; Protein C/antagonists & inhibitors ; Protein C/immunology ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/immunology ; Thrombin/drug effects ; Thrombin/immunology
    Chemical Substances Protein C ; Thrombin (EC 3.4.21.5)
    Language English
    Publishing date 2003-06-15
    Publishing country United States
    Document type Comment ; Editorial ; Review
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 1073-449X ; 0003-0805
    ISSN (online) 1535-4970
    ISSN 1073-449X ; 0003-0805
    DOI 10.1164/rccm.2303007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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