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  1. Article ; Online: Sickle particulars of microparticles.

    Kato, Gregory J

    Blood

    2020  Volume 136, Issue 2, Page(s) 154–155

    MeSH term(s) Anemia, Sickle Cell ; Cell-Derived Microparticles ; Endothelium ; Humans ; Hydroxyurea ; Plasma
    Chemical Substances Hydroxyurea (X6Q56QN5QC)
    Language English
    Publishing date 2020-07-08
    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.2020006303
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Sickle cells and sickle trait in thrombosis.

    Kato, Gregory J

    Blood

    2019  Volume 133, Issue 23, Page(s) 2463

    MeSH term(s) Anemia, Sickle Cell ; Erythrocyte Count ; Erythrocytes ; Humans ; Thrombosis
    Language English
    Publishing date 2019-06-06
    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.2019000694
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  3. Article ; Online: Sickle cell vasculopathy: vascular phenotype on fire!

    Kato, Gregory J

    The Journal of physiology

    2018  Volume 597, Issue 4, Page(s) 993–994

    MeSH term(s) Altitude ; Anemia, Sickle Cell ; Animals ; Exercise Tolerance ; Mice ; Phenotype ; Vascular Diseases
    Language English
    Publishing date 2018-08-03
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/JP276705
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  4. Article ; Online: Exercise training: a prescription for sickle-cell disease?

    Kato, Gregory J

    The Lancet. Haematology

    2018  Volume 5, Issue 11, Page(s) e502–e503

    MeSH term(s) Anemia, Sickle Cell/immunology ; Anemia, Sickle Cell/therapy ; Arteries/immunology ; Atherosclerosis/immunology ; Exercise ; Gastrointestinal Microbiome/immunology ; Humans ; Hyperplasia ; Immunity, Innate ; Inflammation/immunology ; Tunica Intima/pathology
    Language English
    Publishing date 2018-10-30
    Publishing country England
    Document type Journal Article
    ISSN 2352-3026
    ISSN (online) 2352-3026
    DOI 10.1016/S2352-3026(18)30178-9
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  5. Article ; Online: Low global arginine bioavailability: a common phenomenon in pulmonary hypertension.

    Hatabah, Dunia / De Marco, Teresa / McGlothlin, Dana P / Malloy, Mary / Reyes, Loretta Z / Korman, Rawan / Kato, Gregory J / Morris, Claudia R

    American journal of physiology. Lung cellular and molecular physiology

    2024  Volume 326, Issue 4, Page(s) L514–L515

    MeSH term(s) Humans ; Hypertension, Pulmonary ; Arginine/pharmacokinetics ; Biological Availability
    Chemical Substances Arginine (94ZLA3W45F)
    Language English
    Publishing date 2024-04-08
    Publishing country United States
    Document type Letter
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00026.2024
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    Zs.A 2749: Show issues Location:
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  6. Article ; Online: Molecular mechanisms of hepatic dysfunction in sickle cell disease: lessons from Townes mouse model.

    Pradhan-Sundd, Tirthadipa / Kato, Gregory J / Novelli, Enrico M

    American journal of physiology. Cell physiology

    2022  Volume 323, Issue 2, Page(s) C494–C504

    Abstract: Sickle cell disease (SCD) is an autosomal recessive genetic disorder that affects ∼100,000 Americans and millions of people worldwide. Erythrocyte sickling, vaso-occlusion, sterile inflammation, and hemolysis are the major pathophysiological pathways ... ...

    Abstract Sickle cell disease (SCD) is an autosomal recessive genetic disorder that affects ∼100,000 Americans and millions of people worldwide. Erythrocyte sickling, vaso-occlusion, sterile inflammation, and hemolysis are the major pathophysiological pathways leading to liver injury in SCD. Although hepatic dysfunction affects up to 10%-40% of patients with SCD, therapeutic approaches to prevent liver injury in SCD are not known, and the molecular mechanisms promoting progressive liver injury in SCD remain poorly understood. Animal models have been beneficial in bridging the gap between preclinical and translational research in SCD. Recent advances in methodology have allowed the development of several humanized animal models to address various aspects of SCD-related liver diseases. This review provides an overview of current knowledge of the molecular mechanisms and potential therapeutic options of SCD-associated liver dysfunction using the Townes mouse model.
    MeSH term(s) Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/drug therapy ; Anemia, Sickle Cell/genetics ; Animals ; Disease Models, Animal ; Erythrocytes/metabolism ; Hemolysis ; Humans ; Liver Diseases/genetics ; Mice
    Language English
    Publishing date 2022-06-27
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00175.2022
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  7. Article ; Online: Iron restriction in sickle cell disease: When less is more.

    Castro, Oswaldo L / De Franceschi, Lucia / Ganz, Tomas / Kanter, Julie / Kato, Gregory J / Pasricha, Sant-Rayn / Rivella, Stefano / Wood, John C

    American journal of hematology

    2024  

    Abstract: Primum non nocere! Can iron deficiency, an abnormality that causes anemia, benefit people with sickle cell disease (SCD) who already have an anemia? The published literature we review appears to answer this question in the affirmative: basic science ... ...

    Abstract Primum non nocere! Can iron deficiency, an abnormality that causes anemia, benefit people with sickle cell disease (SCD) who already have an anemia? The published literature we review appears to answer this question in the affirmative: basic science considerations, animal model experiments, and noncontrolled clinical observations all suggest a therapeutic potential of iron restriction in SCD. This is because SCD's clinical manifestations are ultimately attributable to the polymerization of hemoglobin S (HbS), a process strongly influenced by intracellular HbS concentration. Even small decrements in HbS concentration greatly reduce polymerization, and iron deficiency lowers erythrocyte hemoglobin concentration. Thus, iron deficiency could improve SCD by changing its clinical features to those of a more benign anemia (i.e., a condition with fewer or no vaso-occlusive events). We propose that well-designed clinical studies be implemented to definitively determine whether iron restriction is a safe and effective option in SCD. These investigations are particularly timely now that pharmacologic agents are being developed, which may directly reduce red cell hemoglobin concentrations without the need for phlebotomies to deplete total body iron.
    Language English
    Publishing date 2024-02-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 196767-8
    ISSN 1096-8652 ; 0361-8609
    ISSN (online) 1096-8652
    ISSN 0361-8609
    DOI 10.1002/ajh.27267
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  8. Article ; Online: Defective nitric oxide metabolism in sickle cell disease.

    Kato, Gregory J

    Pediatric blood & cancer

    2015  Volume 62, Issue 3, Page(s) 373–374

    MeSH term(s) Anemia, Sickle Cell/metabolism ; Humans ; Nitric Oxide/metabolism
    Chemical Substances Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2015-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2131448-2
    ISSN 1545-5017 ; 1545-5009
    ISSN (online) 1545-5017
    ISSN 1545-5009
    DOI 10.1002/pbc.25297
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    Zs.A 1131: Show issues Location:
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  9. Article ; Online: New insights into sickle cell disease: mechanisms and investigational therapies.

    Kato, Gregory J

    Current opinion in hematology

    2016  Volume 23, Issue 3, Page(s) 224–232

    Abstract: Purpose of review: Sickle cell disease (SCD) afflicts millions worldwide. The simplicity of its single nucleotide mutation belies the biological and psychosocial complexity of the disease. Despite only a single approved drug specifically for the ... ...

    Abstract Purpose of review: Sickle cell disease (SCD) afflicts millions worldwide. The simplicity of its single nucleotide mutation belies the biological and psychosocial complexity of the disease. Despite only a single approved drug specifically for the treatment of SCD, new findings reviewed from 2015 provide the direction forward.
    Recent findings: The last year has provided a wealth of support for mechanisms affecting the red cell, hemolysis and vasculopathy, the innate immune system activation, blood cell and endothelial adhesiveness, central sensitization to pain, and chronic brain injury. The evidence supporting expanded use of hydroxyurea continues to mount. Many promising therapies are reaching clinical trial, including curative therapies, with more on the horizon.
    Summary: Evidence is compelling that the use of hydroxyurea must be expanded by clinicians to gain the full pleiotropic benefits of this approved drug. Clinicians must become aware that severe acute and chronic pain has a biological and neurologic basis, and the understanding of this basis is growing. Researchers are testing investigational therapies at an unprecedented pace in SCD, and partnership between patients, researchers, and the private sector provides the most rapid and productive way forward.
    MeSH term(s) Anemia, Sickle Cell/drug therapy ; Anemia, Sickle Cell/metabolism ; Humans ; Hydroxyurea/therapeutic use
    Chemical Substances Hydroxyurea (X6Q56QN5QC)
    Language English
    Publishing date 2016-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1153887-9
    ISSN 1531-7048 ; 1065-6251
    ISSN (online) 1531-7048
    ISSN 1065-6251
    DOI 10.1097/MOH.0000000000000241
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  10. Article ; Online: Identifying adolescent and young adult patients with sickle cell disease at highest risk of death.

    Gladwin, Mark T / Kato, Gregory J / Gordeuk, Victor R

    American journal of hematology

    2020  Volume 96, Issue 1, Page(s) 9–11

    MeSH term(s) Adolescent ; Anemia, Sickle Cell ; Child ; Cohort Studies ; Humans ; Young Adult
    Language English
    Publishing date 2020-11-06
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 196767-8
    ISSN 1096-8652 ; 0361-8609
    ISSN (online) 1096-8652
    ISSN 0361-8609
    DOI 10.1002/ajh.26035
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