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  1. Book: Drug induced liver disease

    Kaplowitz, Neil / DeLeve, Laurie D.

    2013  

    Title variant Drug-induced liver disease
    Author's details Neil Kaplowitz ; Laurie D. Deleve
    Language English
    Size XXIV, 746 S. : Ill., graph. Darst., 28 cm
    Edition 3. ed.
    Publisher Elsevier ; Academic Press
    Publishing place Amsterdam u.a.
    Publishing country Netherlands
    Document type Book
    Note Includes bibliographical references and index
    HBZ-ID HT017697858
    ISBN 978-0-12-387817-5 ; 0-12-387817-9
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2013 A 1613 available for loan (reading room) Lesesaal EG

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  2. Book: Vascular liver disease

    DeLeve, Laurie D.

    mechanisms and management

    (Internal medicine)

    2011  

    Series title Internal medicine
    Language English
    Size XIV, 286 S. : Ill., graf. Darst., 51 schw.-w. Ill., 105 farb. Ill., 31 schw.-w. Tab.
    Publisher Springer
    Publishing place New York, NY
    Publishing country United States
    Document type Book
    HBZ-ID HT016788160
    ISBN 978-1-441-98326-8 ; 978-1-4419-8326-8 ; 1-4419-8326-0 ; 1-441-98326-0 ; 9781441983275 ; 1441983279
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2011 A 1588 order for loan Magazin

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  3. Article: Sinusoidal obstruction syndrome.

    Deleve, Laurie D

    Gastroenterology & hepatology

    2011  Volume 4, Issue 2, Page(s) 101–103

    Language English
    Publishing date 2011-08-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2386402-3
    ISSN 1554-7914
    ISSN 1554-7914
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6543: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 517: Show issues

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  4. Article ; Online: Liver sinusoidal endothelial cells in hepatic fibrosis.

    DeLeve, Laurie D

    Hepatology (Baltimore, Md.)

    2015  Volume 61, Issue 5, Page(s) 1740–1746

    Abstract: Capillarization, lack of liver sinusoidal endothelial cell (LSEC) fenestration, and formation of an organized basement membrane not only precedes fibrosis, but is also permissive for hepatic stellate cell activation and fibrosis. Thus, dysregulation of ... ...

    Abstract Capillarization, lack of liver sinusoidal endothelial cell (LSEC) fenestration, and formation of an organized basement membrane not only precedes fibrosis, but is also permissive for hepatic stellate cell activation and fibrosis. Thus, dysregulation of the LSEC phenotype is a critical step in the fibrotic process. Both a vascular endothelial growth factor (VEGF)-stimulated, nitric oxide (NO)-independent pathway and a VEGF-stimulated NO-dependent pathway are necessary to maintain the differentiated LSEC phenotype. The NO-dependent pathway is impaired in capillarization and activation of this pathway downstream from NO restores LSEC differentiation in vivo. Restoration of LSEC differentiation in vivo promotes HSC quiescence, enhances regression of fibrosis, and prevents progression of cirrhosis.
    MeSH term(s) Cell Differentiation ; Endothelial Cells ; Humans ; Liver Cirrhosis/pathology
    Language English
    Publishing date 2015-03-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.27376
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
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  5. Article ; Online: Sinusoids as Drivers of Liver Development: More Than Simple Chemistry.

    Maretti-Mira, Ana C / DeLeve, Laurie D

    Hepatology (Baltimore, Md.)

    2019  Volume 70, Issue 2, Page(s) 737–739

    MeSH term(s) Animals ; Capillaries/cytology ; Capillaries/physiology ; Endothelial Cells/physiology ; Hepatocyte Growth Factor/physiology ; Humans ; Liver/growth & development ; Mice ; Vascular Endothelial Growth Factor Receptor-3/physiology
    Chemical Substances Hepatocyte Growth Factor (67256-21-7) ; Vascular Endothelial Growth Factor Receptor-3 (EC 2.7.10.1)
    Language English
    Publishing date 2019-03-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.30524
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: Liver sinusoidal endothelial cells and liver regeneration.

    DeLeve, Laurie D

    The Journal of clinical investigation

    2013  Volume 123, Issue 5, Page(s) 1861–1866

    Abstract: Liver sinusoidal endothelial cells (LSECs) have long been noted to contribute to liver regeneration after liver injury. In normal liver, the major cellular source of HGF is the hepatic stellate cell, but after liver injury, HGF expression has been ... ...

    Abstract Liver sinusoidal endothelial cells (LSECs) have long been noted to contribute to liver regeneration after liver injury. In normal liver, the major cellular source of HGF is the hepatic stellate cell, but after liver injury, HGF expression has been thought to increase markedly in proliferating LSECs. However, emerging data suggest that even after injury, LSEC expression of HGF does not increase greatly. In contrast, bone marrow progenitor cells of LSECs (BM SPCs), which are rich in HGF, are recruited to the liver after injury. This Review examines liver regeneration from the perspective that BM SPCs that have been recruited to the liver, rather than mature LSECs, drive liver regeneration.
    MeSH term(s) Animals ; Bone Marrow Cells/cytology ; Cell Proliferation ; Endothelial Cells/cytology ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/cytology ; Humans ; Liver/cytology ; Liver/metabolism ; Liver Diseases/metabolism ; Liver Regeneration ; Rats ; Stem Cells/cytology ; Vascular Endothelial Growth Factor A/metabolism
    Chemical Substances Vascular Endothelial Growth Factor A ; Hepatocyte Growth Factor (67256-21-7)
    Language English
    Publishing date 2013-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI66025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ua VI Zs.184: Show issues Location:
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  7. Article ; Online: Liver Sinusoidal Endothelial Cell: An Update.

    DeLeve, Laurie D / Maretti-Mira, Ana C

    Seminars in liver disease

    2017  Volume 37, Issue 4, Page(s) 377–387

    Abstract: This update focuses on two main topics. First, recent developments in our understanding of liver sinusoidal endothelial cell (LSEC) function will be reviewed, specifically elimination of blood-borne waste, immunological function of LSECs, interaction of ... ...

    Abstract This update focuses on two main topics. First, recent developments in our understanding of liver sinusoidal endothelial cell (LSEC) function will be reviewed, specifically elimination of blood-borne waste, immunological function of LSECs, interaction of LSECs with liver metastases, LSECs and liver regeneration, and LSECs and hepatic fibrosis. Second, given the current emphasis on rigor and transparency in biomedical research, the update discusses the need for standardization of methods to demonstrate identity and purity of isolated LSECs, pitfalls in methods that might lead to a selection bias in the types of LSECs isolated, and questions about long-term culture of LSECs. Various surface markers used for immunomagnetic selection are reviewed.
    MeSH term(s) Animals ; Biomarkers/metabolism ; Capillaries/immunology ; Capillaries/metabolism ; Capillaries/pathology ; Cell Culture Techniques ; Cell Separation/methods ; Endothelial Cells/immunology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Humans ; Liver/blood supply ; Liver Diseases/immunology ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Phenotype ; Signal Transduction
    Chemical Substances Biomarkers
    Language English
    Publishing date 2017-12-22
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 603177-8
    ISSN 1098-8971 ; 0272-8087
    ISSN (online) 1098-8971
    ISSN 0272-8087
    DOI 10.1055/s-0037-1617455
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1752: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Liver Complications Following Treatment of Hematologic Malignancy With Anti-CD22-Calicheamicin (Inotuzumab Ozogamicin).

    McDonald, George B / Freston, James W / Boyer, James L / DeLeve, Laurie D

    Hepatology (Baltimore, Md.)

    2019  Volume 69, Issue 2, Page(s) 831–844

    Abstract: Treatment of hematological malignancy with antibody-drug conjugates (ADCs) may cause liver injury. ADCs deliver a toxic moiety into antigen-expressing tumor cells, but may also injure hepatic sinusoids (sinusoidal obstruction syndrome; SOS). We studied ... ...

    Abstract Treatment of hematological malignancy with antibody-drug conjugates (ADCs) may cause liver injury. ADCs deliver a toxic moiety into antigen-expressing tumor cells, but may also injure hepatic sinusoids (sinusoidal obstruction syndrome; SOS). We studied patients who received an anti-CD22/calicheamicin conjugate (inotuzumab ozogamicin; InO) to gain insight into mechanisms of sinusoidal injury, given that there are no CD22
    MeSH term(s) Antineoplastic Agents, Immunological/adverse effects ; Chemical and Drug Induced Liver Injury/etiology ; Gastroenterologists ; Hematopoietic Stem Cell Transplantation ; Hepatic Veno-Occlusive Disease/etiology ; Humans ; Inotuzumab Ozogamicin/adverse effects ; Lymphoma, Non-Hodgkin/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy
    Chemical Substances Antineoplastic Agents, Immunological ; Inotuzumab Ozogamicin (P93RUU11P7)
    Language English
    Publishing date 2019-01-18
    Publishing country United States
    Document type Clinical Trial, Phase III ; Journal Article ; Multicenter Study ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.30222
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  9. Article ; Online: Incomplete Differentiation of Engrafted Bone Marrow Endothelial Progenitor Cells Initiates Hepatic Fibrosis in the Rat.

    Maretti-Mira, Ana C / Wang, Xiangdong / Wang, Lei / DeLeve, Laurie D

    Hepatology (Baltimore, Md.)

    2019  Volume 69, Issue 3, Page(s) 1259–1272

    Abstract: Normal liver sinusoidal endothelial cells (LSECs) promote quiescence of hepatic stellate cells (HSCs). Prior to fibrosis, LSECs undergo capillarization, which is permissive for HSC activation, the proximate event in hepatic fibrosis. The aims of this ... ...

    Abstract Normal liver sinusoidal endothelial cells (LSECs) promote quiescence of hepatic stellate cells (HSCs). Prior to fibrosis, LSECs undergo capillarization, which is permissive for HSC activation, the proximate event in hepatic fibrosis. The aims of this study were to elucidate the nature of and mechanisms leading to capillarization and to determine how LSECs promote HSC quiescence and why "capillarized LSECs" lose control of HSC activation. The contribution of bone marrow (BM) endothelial progenitor cells to capillarization was identified using rats transplanted with transgenic enhanced green fluorescent protein-positive BM. Shotgun proteomics and informatics were used to identify the LSEC mediator that maintains HSC quiescence. The study shows that capillarization is due to repair of injured LSECs by BM endothelial progenitors that engraft but fail to fully mature. Lack of maturation of BM-derived LSECs is due to cell autonomous pathways that inhibit the nitric oxide pathway. We identify heparin binding epidermal growth factor-like growth factor (HB-EGF) as the signal that maintains HSC quiescence and show that immature LSECs are unable to shed HB-EGF from the cytosolic membrane. Conclusion: Chronic liver injury can recruit BM progenitors of LSECs that engraft and fail to fully differentiate, which creates an environment that is permissive for hepatic fibrosis; elucidation of these early events in the fibrotic process will provide targets for treatment of hepatic fibrosis.
    MeSH term(s) Animals ; Cell Differentiation ; Endothelial Progenitor Cells/cytology ; Endothelial Progenitor Cells/transplantation ; Liver Cirrhosis/etiology ; Male ; Rats ; Rats, Inbred Lew
    Language English
    Publishing date 2019-02-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.30227
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
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  10. Article ; Online: VEGF-sdf1 recruitment of CXCR7+ bone marrow progenitors of liver sinusoidal endothelial cells promotes rat liver regeneration.

    DeLeve, Laurie D / Wang, Xiangdong / Wang, Lei

    American journal of physiology. Gastrointestinal and liver physiology

    2016  Volume 310, Issue 9, Page(s) G739–46

    Abstract: In liver injury, recruitment of bone marrow (BM) progenitors of liver sinusoidal endothelial cells (sprocs) is necessary for normal liver regeneration. Hepatic vascular endothelial growth factor (VEGF) is a central regulator of the recruitment process. ... ...

    Abstract In liver injury, recruitment of bone marrow (BM) progenitors of liver sinusoidal endothelial cells (sprocs) is necessary for normal liver regeneration. Hepatic vascular endothelial growth factor (VEGF) is a central regulator of the recruitment process. We examine whether stromal cell-derived factor 1 [sdf1, or CXC ligand 12 (CXCL12)] acts downstream from VEGF to mediate recruitment of BM sprocs, what the sdf1 receptor type [CXC receptor (CXCR)-4 or CXCR7] is on sprocs, and whether sdf1 signaling is required for normal liver regeneration. Studies were performed in the rat partial hepatectomy model. Tracking studies of BM sprocs were performed in wild-type Lewis rats that had undergone BM transplantation from transgenic enhanced green fluorescent protein-positive Lewis rats. Knockdown studies were performed using antisense oligonucleotides (ASOs). Expression of sdf1 doubles in liver and liver sinusoidal endothelial cells (LSECs) after partial hepatectomy. Upregulation of sdf1 expression increases proliferation of sprocs in the BM, mobilization of CXCR7(+) BM sprocs to the circulation, and engraftment of CXCR7(+) BM sprocs in the liver and promotes liver regeneration. Knockdown of hepatic VEGF with ASOs decreases hepatic sdf1 expression and plasma sdf1 levels. When the effect of VEGF knockdown on sdf1 is offset by infusion of sdf1, VEGF knockdown-induced impairment of BM sproc recruitment after partial hepatectomy is completely attenuated and liver regeneration is normalized. These data demonstrate that the VEGF-sdf1 pathway regulates recruitment of CXCR7(+) BM sprocs to the hepatic sinusoid after partial hepatectomy and is required for normal liver regeneration.
    MeSH term(s) Animals ; Bone Marrow Transplantation ; Cells, Cultured ; Chemokine CXCL12/genetics ; Chemokine CXCL12/metabolism ; Endothelial Progenitor Cells/metabolism ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Liver/blood supply ; Liver/cytology ; Liver/metabolism ; Liver/physiology ; Liver Regeneration ; Male ; Rats ; Rats, Inbred Lew ; Receptors, CXCR/metabolism ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism
    Chemical Substances Ackr3 protein, rat ; CXCL12 protein, rat ; Chemokine CXCL12 ; Receptors, CXCR ; Vascular Endothelial Growth Factor A
    Language English
    Publishing date 2016-03-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603840-2
    ISSN 1522-1547 ; 0193-1857
    ISSN (online) 1522-1547
    ISSN 0193-1857
    DOI 10.1152/ajpgi.00056.2016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.89: Show issues Location:
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