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  1. Article ; Online: Is VITT really a HIT.

    Ruggeri, Zaverio M / Ruf, Wolfram

    Nature immunology

    2021  Volume 22, Issue 11, Page(s) 1352–1353

    MeSH term(s) COVID-19 ; Humans ; SARS-CoV-2
    Language English
    Publishing date 2021-10-22
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-021-01042-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5294: Show issues Location:
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    Zs.MG 42: Show issues

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  2. Book: Von Willebrand factor and the mechanisms of platelet function

    Ruggeri, Zaverio M.

    1998  

    Author's details Zaverio M. Ruggeri (ed.)
    Keywords Willebrand-Faktor ; Thrombozyt ; Rezeptor ; Gefäßkrankheit
    Subject Faktor VIII A ; Anti-bleeding factor ; Faktor-VIII-assoziiertes Antigen ; Ristocetin-Cofaktor ; Blutgerinnungsfaktor VIII A ; Angiologische Krankheit ; Angiopathie ; Blutgefäßkrankheit ; Gefäßerkrankung ; Blutgefäß ; Vaskulopathie ; Gefäßkrankheiten ; Blutplättchen ; Platelet ; Thrombozyten
    Language English
    Size 257 S. : Ill., graph. Darst.
    Publisher Springer
    Publishing place Berlin u.a.
    Document type Book
    Note Literaturangaben
    HBZ-ID HT009964175
    ISBN 3-540-64709-0 ; 978-3-540-64709-6
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    1999 A 1404 order for loan Magazin

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  3. Article ; Online: Platelet GPIb: sensing force and responding.

    Ruggeri, Zaverio M

    Blood

    2015  Volume 125, Issue 3, Page(s) 423–424

    MeSH term(s) Blood Platelets/metabolism ; Cell Membrane/metabolism ; Humans ; Platelet Adhesiveness ; Platelet Glycoprotein GPIb-IX Complex/metabolism ; Stress, Mechanical ; von Willebrand Factor/metabolism
    Chemical Substances Platelet Glycoprotein GPIb-IX Complex ; von Willebrand Factor
    Language English
    Publishing date 2015-01-15
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2014-12-610642
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book: Coagulation disorders

    Ruggeri, Zaverio M.

    (CLINICS IN HAEMATOLOGY ; 14,2)

    1985  

    Series title CLINICS IN HAEMATOLOGY ; 14,2
    Clinics in haematology
    Collection Clinics in haematology
    Keywords BLOOD COAGULATION DISORDERS
    Size S. 281 - 599
    Publisher Saunders
    Publishing place London
    Document type Book
    HBZ-ID HT002496066
    Database Catalogue ZB MED Medicine, Health

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    SE 128 -14,2- verfügbar in Königswinter Königswinter

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  5. Article ; Online: Arenaviral infection causes bleeding in mice due to reduced serotonin release from platelets.

    Aiolfi, Roberto / Sitia, Giovanni / Iannacone, Matteo / Brunetta, Ivan / Guidotti, Luca G / Ruggeri, Zaverio M

    Science signaling

    2022  Volume 15, Issue 722, Page(s) eabb0384

    Abstract: Bleeding correlates with disease severity in viral hemorrhagic fevers. We found that the increase in type I interferon (IFN-I) in mice caused by infection with the Armstrong strain of lymphocytic choriomeningitis virus (LCMV; an arenavirus) reduced the ... ...

    Abstract Bleeding correlates with disease severity in viral hemorrhagic fevers. We found that the increase in type I interferon (IFN-I) in mice caused by infection with the Armstrong strain of lymphocytic choriomeningitis virus (LCMV; an arenavirus) reduced the megakaryocytic expression of genes encoding enzymes involved in lipid biosynthesis (
    MeSH term(s) Animals ; Blood Platelets/metabolism ; Hemorrhage/metabolism ; Lymphocytic Choriomeningitis/genetics ; Lymphocytic Choriomeningitis/metabolism ; Lymphocytic choriomeningitis virus/genetics ; Mice ; Serotonin/metabolism
    Chemical Substances Serotonin (333DO1RDJY)
    Language English
    Publishing date 2022-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.abb0384
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Book ; Conference proceedings: Progress in vascular biology, hemostasis, and thrombosis

    Zimmerman, Theodore S. / Ruggeri, Zaverio M.

    (Annals of the New York Academy of Sciences ; 614)

    1991  

    Event/congress Theodore S. Zimmerman Memorial Conference (1990, LaJollaCalif.)
    Author's details Theodore S. Zimmerman Memorial Conference, [held at La Jolla, California on February 28 - March 3, 1990]. Ed. by Zaverio M. Ruggeri
    Series title Annals of the New York Academy of Sciences ; 614
    Collection
    Keywords Blood Coagulation / congresses ; Blood Coagulation Disorders / congresses ; Hemostasis / congresses ; Thrombosis / congresses ; Koagulopathie ; Blutstillung ; Physiologische Chemie ; Blutgefäß ; Thrombose ; Blutgerinnung
    Subject Gerinnung ; Blutkoagulation ; Blood coagulation ; Thrombosen ; Hämostase ; Gefäß ; Blutgefäße ; Gefäße ; Ader ; Adern ; Chemische Physiologie ; Biochemische Medizin ; Medizinische Biochemie ; Blutgerinnungsstörung ; Coagulopathy ; Gerinnungsstörung
    Language English
    Size XI, 313 S. : Ill., graph. Darst.
    Publishing place New York, NY
    Publishing country United States
    Document type Book ; Conference proceedings
    HBZ-ID HT003812088
    ISBN 0-89766-645-3 ; 0-89766-646-1 ; 978-0-89766-645-9 ; 978-0-89766-646-6
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Se 110 -614- verfügbar in Königswinter Königswinter

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  7. Article ; Online: 14-3-3 proteins in platelet biology and glycoprotein Ib-IX signaling.

    Chen, Yunfeng / Ruggeri, Zaverio M / Du, Xiaoping

    Blood

    2018  Volume 131, Issue 22, Page(s) 2436–2448

    Abstract: Members of the 14-3-3 family of proteins function as adapters/modulators that recognize phosphoserine/phosphothreonine-based binding motifs in many intracellular proteins and play fundamental roles in signal transduction pathways of eukaryotic cells. In ... ...

    Abstract Members of the 14-3-3 family of proteins function as adapters/modulators that recognize phosphoserine/phosphothreonine-based binding motifs in many intracellular proteins and play fundamental roles in signal transduction pathways of eukaryotic cells. In platelets, 14-3-3 plays a wide range of regulatory roles in phosphorylation-dependent signaling pathways, including G-protein signaling, cAMP signaling, agonist-induced phosphatidylserine exposure, and regulation of mitochondrial function. In particular, 14-3-3 interacts with several phosphoserine-dependent binding sites in the major platelet adhesion receptor, the glycoprotein Ib-IX complex (GPIb-IX), regulating its interaction with von Willebrand factor (VWF) and mediating VWF/GPIb-IX-dependent mechanosignal transduction, leading to platelet activation. The interaction of 14-3-3 with GPIb-IX also plays a critical role in enabling the platelet response to low concentrations of thrombin through cooperative signaling mediated by protease-activated receptors and GPIb-IX. The various functions of 14-3-3 in platelets suggest that it is a possible target for the treatment of thrombosis and inflammation.
    MeSH term(s) 14-3-3 Proteins/metabolism ; Animals ; Blood Coagulation ; Blood Platelets/cytology ; Blood Platelets/metabolism ; Humans ; Phosphorylation ; Platelet Activation ; Platelet Glycoprotein GPIb-IX Complex/metabolism ; Protein Binding ; Signal Transduction ; von Willebrand Factor/metabolism
    Chemical Substances 14-3-3 Proteins ; Platelet Glycoprotein GPIb-IX Complex ; von Willebrand Factor
    Language English
    Publishing date 2018-04-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2017-09-742650
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The impact of aberrant von Willebrand factor-GPIbα interaction on megakaryopoiesis and platelets in humanized type 2B von Willebrand disease model mouse.

    Kanaji, Sachiko / Morodomi, Yosuke / Weiler, Hartmut / Zarpellon, Alessandro / Montgomery, Robert R / Ruggeri, Zaverio M / Kanaji, Taisuke

    Haematologica

    2022  Volume 107, Issue 9, Page(s) 2133–2143

    Abstract: Type 2B von Willebrand disease (VWD) is caused by gain-of-function mutations in von Willebrand factor (VWF). Increased VWF affinity for GPIba results in loss of high molecular weight multimers and enhanced platelet clearance, both contributing to the ... ...

    Abstract Type 2B von Willebrand disease (VWD) is caused by gain-of-function mutations in von Willebrand factor (VWF). Increased VWF affinity for GPIba results in loss of high molecular weight multimers and enhanced platelet clearance, both contributing to the bleeding phenotype. Severity of the symptoms vary among type 2B VWD patients, with some developing thrombocytopenia only under stress conditions. Efforts have been made to study underlying pathophysiology for platelet abnormalities, but animal studies have been limited because of species specificity in the VWF-GPIba interaction. Here, we generated a severe form of type 2B VWD (p.V1316M) knockin mice in the context of human VWF exon 28 (encoding A1 and A2 domains) and crossed them with human GPIba transgenic strain. Heterozygous mutant mice recapitulated the phenotype of type 2B VWD in autosomal dominant manner and presented severe macrothrombocytopenia. Of note, platelets remaining in the circulation had extracytoplasmic GPIba shed-off from the cell surface. Reciprocal bone marrow transplantation determined mutant VWF produced from endothelial cells as the major cause of the platelet phenotype in type 2B VWD mice. Moreover, altered megakaryocyte maturation in the bone marrow and enhanced extramedullary megakaryopoiesis in the spleen were observed. Interestingly, injection of anti-VWF A1 blocking antibody (NMC-4) not only ameliorated platelet count and GPIba expression, but also reversed MK ploidy shift. In conclusion, we present a type 2B VWD mouse model with humanized VWF-GPIba interaction which demonstrated direct influence of aberrant VWF-GPIba binding on megakaryocytes.
    MeSH term(s) Animals ; Blood Platelets/metabolism ; Endothelial Cells/metabolism ; Humans ; Mice ; Platelet Glycoprotein GPIb-IX Complex/metabolism ; Thrombocytopenia/metabolism ; von Willebrand Disease, Type 2/genetics ; von Willebrand Diseases/metabolism ; von Willebrand Factor/genetics ; von Willebrand Factor/metabolism
    Chemical Substances Platelet Glycoprotein GPIb-IX Complex ; adhesion receptor ; von Willebrand Factor
    Language English
    Publishing date 2022-09-01
    Publishing country Italy
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2021.280561
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Platelet adhesion under flow.

    Ruggeri, Zaverio M

    Microcirculation (New York, N.Y. : 1994)

    2008  Volume 16, Issue 1, Page(s) 58–83

    Abstract: Platelet-adhesive mechanisms play a well-defined role in hemostasis and thrombosis, but evidence continues to emerge for a relevant contribution to other pathophysiological processes, including inflammation, immune-mediated responses to microbial and ... ...

    Abstract Platelet-adhesive mechanisms play a well-defined role in hemostasis and thrombosis, but evidence continues to emerge for a relevant contribution to other pathophysiological processes, including inflammation, immune-mediated responses to microbial and viral pathogens, and cancer metastasis. Hemostasis and thrombosis are related aspects of the response to vascular injury, but the former protects from bleeding after trauma, while the latter is a disease mechanism. In either situation, adhesive interactions mediated by specific membrane receptors support the initial attachment of single platelets to cellular and extracellular matrix constituents of the vessel wall and tissues. In the subsequent steps of thrombus growth and stabilization, adhesive interactions mediate platelet-to-platelet cohesion (i.e., aggregation) and anchoring to the fibrin clot. A key functional aspect of platelets is their ability to circulate in a quiescent state surveying the integrity of the inner vascular surface, coupled to a prompt reaction wherever alterations are detected. In many respects, therefore, platelet adhesion to vascular wall structures, to one another, or to other blood cells are facets of the same fundamental biological process. The adaptation of platelet-adhesive functions to the effects of blood flow is the main focus of this review.
    MeSH term(s) Animals ; Blood Coagulation/immunology ; Blood Flow Velocity ; Blood Platelets/immunology ; Blood Vessels/immunology ; Extracellular Matrix/immunology ; Hemorrhage/immunology ; Humans ; Platelet Adhesiveness/immunology ; Platelet Aggregation/immunology ; Thrombosis/immunology
    Language English
    Publishing date 2008-11-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1217758-1
    ISSN 1549-8719 ; 1073-9688
    ISSN (online) 1549-8719
    ISSN 1073-9688
    DOI 10.1080/10739680802651477
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Mechanisms of anti-GPIbα antibody-induced thrombocytopenia in mice.

    Morodomi, Yosuke / Kanaji, Sachiko / Won, Eric / Ruggeri, Zaverio M / Kanaji, Taisuke

    Blood

    2020  Volume 135, Issue 25, Page(s) 2292–2301

    Abstract: Immune thrombocytopenia (ITP) is an acquired bleeding disorder characterized by antibody-mediated platelet destruction. Different mechanisms have been suggested to explain accelerated platelet clearance and impaired thrombopoiesis, but the ... ...

    Abstract Immune thrombocytopenia (ITP) is an acquired bleeding disorder characterized by antibody-mediated platelet destruction. Different mechanisms have been suggested to explain accelerated platelet clearance and impaired thrombopoiesis, but the pathophysiology of ITP has yet to be fully delineated. In this study, we tested 2 mouse models of immune-mediated thrombocytopenia using the rat anti-mouse GPIbα monoclonal antibody 5A7, generated in our laboratory. After a single IV administration of high-dose (2 mg/kg) 5A7, opsonized platelets were rapidly cleared from the circulation into the spleen and liver; this was associated with rapid upregulation of thrombopoietin (TPO) messenger RNA. In contrast, subcutaneous administration of low-dose 5A7 (0.08-0.16 mg/kg) every 3 days gradually lowered the platelet count; in this case, opsonized platelets were observed only in the spleen, and TPO levels remained unaltered. Interestingly, in both models, the 5A7 antibody was found on the surface of, as well as internalized to, bone marrow megakaryocytes. Consequently, platelets generated in the chronic phase of repeated subcutaneous 5A7 administration model showed reduced GPIbα membrane expression on their surface. Our findings indicate that evaluation of platelet surface GPIbα relative to platelet size may be a useful marker to support the diagnosis of anti-GPIbα antibody-induced ITP.
    MeSH term(s) Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/toxicity ; Antigen-Antibody Reactions ; Blood Platelets/immunology ; Disease Models, Animal ; Injections, Intravenous ; Injections, Subcutaneous ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Opsonin Proteins/immunology ; Platelet Aggregation/immunology ; Platelet Glycoprotein GPIb-IX Complex/antagonists & inhibitors ; Platelet Glycoprotein GPIb-IX Complex/immunology ; Purpura, Thrombocytopenic, Idiopathic/etiology ; Purpura, Thrombocytopenic, Idiopathic/immunology ; RNA, Messenger/biosynthesis ; Rats ; Spleen/pathology ; Thrombopoietin/biosynthesis ; Thrombopoietin/genetics ; Up-Regulation
    Chemical Substances Antibodies, Monoclonal ; Opsonin Proteins ; Platelet Glycoprotein GPIb-IX Complex ; RNA, Messenger ; adhesion receptor ; Thrombopoietin (9014-42-0)
    Language English
    Publishing date 2020-03-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2019003770
    Database MEDical Literature Analysis and Retrieval System OnLINE

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