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  1. Book: Sepsis

    Bastarache, Julie A.

    (Clinics in chest medicine ; volume 37, number 2 (June 2016))

    2016  

    Author's details editors Julie A. Bastarache, Eric J. Seeley
    Series title Clinics in chest medicine ; volume 37, number 2 (June 2016)
    Collection
    Language English
    Size xvi Seiten, Seite 166-387, Illustrationen
    Publisher Elsevier
    Publishing place Philadelphia, Pennsylvania
    Publishing country United States
    Document type Book
    HBZ-ID HT019068298
    ISBN 978-0-323-44611-2 ; 0-323-44611-6
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Se 805 -37,2- verfügbar in Königswinter Königswinter

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  2. Article ; Online: The future of sepsis research: time to think differently?

    Bastarache, Julie A

    American journal of physiology. Lung cellular and molecular physiology

    2020  Volume 319, Issue 3, Page(s) L523–L526

    MeSH term(s) Global Health ; Humans ; Lung ; Pulmonary Fibrosis ; Respiratory Distress Syndrome ; Sepsis/therapy
    Keywords covid19
    Language English
    Publishing date 2020-08-05
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00368.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Pulmonary Vasculopathy in COVID-19 Acute Respiratory Distress Syndrome: A Step Closer to the Full Picture.

    Kerchberger, V Eric / Bastarache, Julie A

    American journal of respiratory and critical care medicine

    2022  Volume 206, Issue 7, Page(s) 809–810

    MeSH term(s) COVID-19 ; Humans ; Lung/blood supply ; Respiratory Distress Syndrome/etiology ; Respiratory Distress Syndrome/therapy ; Vascular Diseases
    Language English
    Publishing date 2022-07-22
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.202205-1019ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Toxic effects of cell-free hemoglobin on the microvascular endothelium: implications for pulmonary and nonpulmonary organ dysfunction.

    Meegan, Jamie E / Bastarache, Julie A / Ware, Lorraine B

    American journal of physiology. Lung cellular and molecular physiology

    2021  Volume 321, Issue 2, Page(s) L429–L439

    Abstract: Levels of circulating cell-free hemoglobin are elevated during hemolytic and inflammatory diseases and contribute to organ dysfunction and severity of illness. Though several studies have investigated the contribution of hemoglobin to tissue injury, the ... ...

    Abstract Levels of circulating cell-free hemoglobin are elevated during hemolytic and inflammatory diseases and contribute to organ dysfunction and severity of illness. Though several studies have investigated the contribution of hemoglobin to tissue injury, the precise signaling mechanisms of hemoglobin-mediated endothelial dysfunction in the lung and other organs are not yet completely understood. The purpose of this review is to highlight the knowledge gained thus far and the need for further investigation regarding hemoglobin-mediated endothelial inflammation and injury to develop novel therapeutic strategies targeting the damaging effects of cell-free hemoglobin.
    MeSH term(s) Animals ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Hemoglobins/metabolism ; Hemolysis ; Humans ; Inflammation/metabolism ; Inflammation/pathology ; Lung/metabolism ; Lung/pathology ; Multiple Organ Failure/metabolism ; Multiple Organ Failure/pathology ; Multiple Organ Failure/therapy ; Vascular Diseases/metabolism ; Vascular Diseases/pathology ; Vascular Diseases/therapy
    Chemical Substances Hemoglobins
    Language English
    Publishing date 2021-05-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00018.2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Call for Papers: "In It for the Long Haul: Understanding the Lasting Impact of COVID-19 on Lung Health and Disease".

    Bartlett, Nathan W / Bastarache, Julie A / Kuebler, Wolfgang M / Schmidt, Eric P

    American journal of physiology. Lung cellular and molecular physiology

    2022  Volume 323, Issue 6, Page(s) L683–L684

    MeSH term(s) Humans ; COVID-19 ; Time Factors ; Lung
    Language English
    Publishing date 2022-11-08
    Publishing country United States
    Document type Editorial
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00352.2022
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  7. Article ; Online: Cleaving the Acute Respiratory Distress Syndrome into Treatable Traits: A Role for Caspase 1?

    Bos, Lieuwe D J / Bastarache, Julie A

    American journal of respiratory and critical care medicine

    2021  Volume 204, Issue 1, Page(s) 6–7

    MeSH term(s) Caspase 1 ; Humans ; Phenotype ; Respiratory Distress Syndrome/therapy
    Chemical Substances Caspase 1 (EC 3.4.22.36)
    Language English
    Publishing date 2021-07-27
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.202102-0479ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: NET Gain for Sepsis Research: A New Approach to Assess Neutrophil Function in Patients.

    Meegan, Jamie E / Bastarache, Julie A

    American journal of respiratory and critical care medicine

    2019  Volume 200, Issue 7, Page(s) 798–799

    MeSH term(s) Animals ; Critical Illness ; Disseminated Intravascular Coagulation ; Extracellular Traps ; Humans ; Neutrophils ; Sepsis
    Language English
    Publishing date 2019-06-18
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.201905-1074ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Eyes wide open on bronchial aeration in acute respiratory distress syndrome.

    Jabaudon, Matthieu / Bastarache, Julie A / Ware, Lorraine B

    Anaesthesia, critical care & pain medicine

    2020  Volume 39, Issue 2, Page(s) 191–192

    MeSH term(s) Humans ; Lung ; Positive-Pressure Respiration ; Respiratory Distress Syndrome/therapy
    Language English
    Publishing date 2020-03-04
    Publishing country France
    Document type Editorial
    ISSN 2352-5568
    ISSN (online) 2352-5568
    DOI 10.1016/j.accpm.2020.03.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Cell-free hemoglobin-mediated human lung microvascular endothelial barrier dysfunction is not mediated by cell death.

    Tomasek, Toria / Ware, Lorraine B / Bastarache, Julie A / Meegan, Jamie E

    Biochemical and biophysical research communications

    2021  Volume 556, Page(s) 199–206

    Abstract: Circulating cell-free hemoglobin (CFH) contributes to endothelial injury in several inflammatory and hemolytic conditions. We and others have shown that CFH causes increased endothelial permeability, but the precise mechanisms of CFH-mediated endothelial ...

    Abstract Circulating cell-free hemoglobin (CFH) contributes to endothelial injury in several inflammatory and hemolytic conditions. We and others have shown that CFH causes increased endothelial permeability, but the precise mechanisms of CFH-mediated endothelial barrier dysfunction are not fully understood. Based on our previous study in a mouse model of sepsis demonstrating that CFH increased apoptosis in the lung, we hypothesized that CFH causes endothelial barrier dysfunction through this cell death mechanism. We first confirmed that CFH causes human lung microvascular barrier dysfunction in vitro that can be prevented by the hemoglobin scavenger, haptoglobin. While CFH caused a small but significant decrease in cell viability measured by the membrane impermeable DNA dye Draq7 in human lung microvascular endothelial cells, CFH did not increase apoptosis as measured by TUNEL staining or Western blot for cleaved caspase-3. Moreover, inhibitors of apoptosis (Z-VAD-FMK), necrosis (IM-54), necroptosis (necrostatin-1), ferroptosis (ferrostatin-1), or autophagy (3-methyladenine) did not prevent CFH-mediated endothelial barrier dysfunction. We conclude that although CFH may cause a modest decrease in cell viability over time, cell death does not contribute to CFH-mediated lung microvascular endothelial barrier dysfunction.
    MeSH term(s) Apoptosis ; Cells, Cultured ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Haptoglobins/metabolism ; Hemoglobins/metabolism ; Humans ; Lung/blood supply ; Microcirculation ; Time Factors
    Chemical Substances Haptoglobins ; Hemoglobins
    Language English
    Publishing date 2021-04-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2021.03.161
    Database MEDical Literature Analysis and Retrieval System OnLINE

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