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  1. Book ; Online: G Protein-Coupled Receptor Kinases (GRKs) and Beta-Arrestins: New Insights into Disease Regulators

    Hattori, Yuichi / Michel, Martin C.

    2020  

    Keywords Science: general issues ; Pharmacology ; GRK ; beta-arrestins ; cardiovascular ; inflammation ; cancer
    Size 1 electronic resource (182 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021230493
    ISBN 9782889635474 ; 2889635473
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book ; Online ; E-Book: Histamine and histamine receptors in health and disease

    Hattori, Yuichi / Seifert, Roland

    (Handbook of experimental pharmacology ; 241)

    2017  

    Author's details Yuichi Hattori, Roland Seifert editors
    Series title Handbook of experimental pharmacology ; 241
    Collection
    Keywords Histamine / physiology ; Receptors, Histamine / physiology ; Medicine ; Immunology ; Neurosciences ; Pharmacology ; Endocrinology ; Biochemistry
    Subject code 615
    Language English
    Size 1 Online-Ressource (viii, 363 Seiten), Illustrationen, Diagramme
    Publisher Springer
    Publishing place Cham
    Publishing country Switzerland
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT019659451
    ISBN 978-3-319-58194-1 ; 9783319581927 ; 3-319-58194-5 ; 3319581929
    DOI 10.1007/978-3-319-58194-1
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  3. Article ; Online: Challenging and target-based shifting strategies for heart failure treatment: An update from the last decades.

    Hattori, Yuichi / Hattori, Kohshi / Ishii, Kuniaki / Kobayashi, Masanobu

    Biochemical pharmacology

    2024  , Page(s) 116232

    Abstract: Heart failure (HF) is a major global health problem afflicting millions worldwide. Despite the significant advances in therapies and prevention, HF still carries very high morbidity and mortality, requiring enormous healthcare-related expenditure, and ... ...

    Abstract Heart failure (HF) is a major global health problem afflicting millions worldwide. Despite the significant advances in therapies and prevention, HF still carries very high morbidity and mortality, requiring enormous healthcare-related expenditure, and the search for new weapons goes on. Following initial treatment strategies targeting inotropism and congestion, attention has focused on offsetting the neurohormonal overactivation and three main therapies, including angiotensin-converting enzyme inhibitors or angiotensin II type 1 receptor antagonists, β-adrenoceptor antagonists, and mineralocorticoid receptor antagonists, have been the foundation of standard treatment for patients with HF. Recently, a paradigm shift, including angiotensin receptor-neprilysin inhibitor, sodium glucose co-transporter 2 inhibitor, and ivabradine, has been added. Moreover, soluble guanylate cyclase stimulator, elamipretide, and omecamtiv mecarbil have come out as a next-generation therapeutic agent for patients with HF. Although these pharmacologic therapies have been significantly successful in relieving symptoms, there is still no complete cure for HF. We may be currently entering a new era of treatment for HF with animal experiments and human clinical trials assessing the value of antibody-based immunotherapy and gene therapy as a novel therapeutic strategy. Such tempting therapies still have some challenges to be addressed but may become a weighty option for treatment of HF. This review article will compile the paradigm shifts in HF treatment over the past dozen years or so and illustrate current landscape of antibody-based immunotherapy and gene therapy as a new therapeutic algorithm for patients with HF.
    Language English
    Publishing date 2024-04-20
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2024.116232
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: [Preface].

    Matsuda, Naoyuki / Hattori, Yuichi

    Nihon yakurigaku zasshi. Folia pharmacologica Japonica

    2022  Volume 159, Issue 2, Page(s) 100

    Language Japanese
    Publishing date 2022-10-22
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 1097532-9
    ISSN 1347-8397 ; 0015-5691
    ISSN (online) 1347-8397
    ISSN 0015-5691
    DOI 10.1254/fpj.23031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Reflections on the 150th anniversary of Naunyn-Schmiedeberg's Archives of Pharmacology: past, challenges, and future.

    Hattori, Yuichi / Seifert, Roland

    Naunyn-Schmiedeberg's archives of pharmacology

    2022  Volume 396, Issue 1, Page(s) 1–3

    MeSH term(s) Anniversaries and Special Events
    Language English
    Publishing date 2022-11-03
    Publishing country Germany
    Document type Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 121471-8
    ISSN 1432-1912 ; 0028-1298
    ISSN (online) 1432-1912
    ISSN 0028-1298
    DOI 10.1007/s00210-022-02321-4
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  6. Article ; Online: Stattic ameliorates the cecal ligation and puncture-induced cardiac injury in septic mice via IL-6-gp130-STAT3 signaling pathway.

    Imbaby, Samar / Hattori, Yuichi

    Life sciences

    2023  Volume 330, Page(s) 122008

    Abstract: Aim: Sepsis-induced cardiac dysfunction is the leading cause of higher morbidity and mortality with poor prognosis in septic patients. Our recent previous investigation provides evidence of the hallmarks of signal transducer and activator of ... ...

    Abstract Aim: Sepsis-induced cardiac dysfunction is the leading cause of higher morbidity and mortality with poor prognosis in septic patients. Our recent previous investigation provides evidence of the hallmarks of signal transducer and activator of transcription3 (STAT3) activation in sepsis and targeting of STAT3 with Stattic, a small-molecule inhibitor of STAT3, has beneficial effects in various septic tissues. We investigated the possible cardioprotective effects of Stattic on cardiac inflammation and dysfunction in mice with cecal ligation and puncture (CLP)-induced sepsis.
    Main methods: A polymicrobial sepsis model was induced by CLP in mice and Stattic (25 mg/kg) was intraperitoneally given at one and twelve hours after CLP operation. The cecum was exposed in sham-control mice without CLP. After 18 h of surgery, electrocardiogram (ECG) for anaesthized mice was registered followed by collecting of samples of blood and tissues for bimolecular and histopathological assessments. Myeloperoxidase, a marker of neutrophil infiltration, was assessed immunohistochemically.
    Key findings: CLP profoundly impaired cardiac functions as evidenced by ECG changes in septic mice as well as elevation of cardiac enzymes, and inflammatory markers with myocardial histopathological and immunohistochemical alterations. While, Stattic markedly reversed the CLP-induced cardiac abnormalities and restored the cardiac function by its anti-inflammatory activities.
    Significance: Stattic treatment had potential beneficial effects against sepsis-induced cardiac inflammation, dysfunction and damage. Its cardioprotective effects were possibly attributed to its anti-inflammatory activities by targeting STAT3 and downregulation of IL-6 and gp130. Our investigations suggest that Stattic could be a promising target for management of cardiac sepsis and inflammation-related cardiac damage.
    MeSH term(s) Animals ; Mice ; Anti-Inflammatory Agents/pharmacology ; Cecum/surgery ; Cecum/injuries ; Cytokine Receptor gp130/metabolism ; Heart Injuries ; Inflammation/etiology ; Interleukin-6/metabolism ; Ligation/adverse effects ; Punctures/adverse effects ; Sepsis/drug therapy ; Signal Transduction
    Chemical Substances Anti-Inflammatory Agents ; Cytokine Receptor gp130 (133483-10-0) ; Interleukin-6 ; stattic
    Language English
    Publishing date 2023-08-05
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2023.122008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: [Role of histamine in sepsis-induced organ dysfunction: study using knockout mice of histamine-related genes].

    Hattori, Yuichi

    Nihon yakurigaku zasshi. Folia pharmacologica Japonica

    2018  Volume 152, Issue 1, Page(s) 10–15

    Abstract: Sepsis is the leading cause of death in critically ill patients, and its incidence continues to rise. Sepsis is now defined as life-threatening organ dysfunction due to a dysregulated host response to infection. Histamine assumes a critical role as a ... ...

    Abstract Sepsis is the leading cause of death in critically ill patients, and its incidence continues to rise. Sepsis is now defined as life-threatening organ dysfunction due to a dysregulated host response to infection. Histamine assumes a critical role as a major mediator of many pathologic disorders with inflammation and immune reactions. However, direct evidence has not been provided showing the involvement of histamine in the development of multiple organ dysfunction or failure in sepsis. We have found that sepsis-induced major end-organ (lung, liver, and kidney) injury is attenuated in histidine decarboxylase (HDC) gene knockout mice. H1/H2-receptor gene-double knockout mice apparently behave similar to HDC knockout mice in reducing sepsis-related pathologic changes. Here we provide an overview on the role of endogenous histamine as an aggregating mediator that could contribute to the development of major end-organ injury in sepsis.
    MeSH term(s) Animals ; Histamine/genetics ; Histidine Decarboxylase/genetics ; Mice ; Mice, Knockout ; Multiple Organ Failure/etiology ; Receptors, Histamine H1 ; Receptors, Histamine H2/genetics ; Sepsis/complications
    Chemical Substances Receptors, Histamine H1 ; Receptors, Histamine H2 ; Histamine (820484N8I3) ; Histidine Decarboxylase (EC 4.1.1.22)
    Language Japanese
    Publishing date 2018-07-11
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 1097532-9
    ISSN 1347-8397 ; 0015-5691
    ISSN (online) 1347-8397
    ISSN 0015-5691
    DOI 10.1254/fpj.152.10
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Synthesis of Azadioxa-Planar Triphenylboranes Bridged by Aryl- and Alkylimino Groups and Their Photophysical Properties.

    Kitamoto, Yuichi / Oda, Kazuma / Kita, Hiroshi / Hattori, Tetsutaro / Oi, Shuichi

    The Journal of organic chemistry

    2023  Volume 88, Issue 9, Page(s) 5852–5860

    Abstract: Heteroatom-bridged planar triphenylboranes, in which the three phenyl groups are bridged at ... ...

    Abstract Heteroatom-bridged planar triphenylboranes, in which the three phenyl groups are bridged at the
    Language English
    Publishing date 2023-04-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 123490-0
    ISSN 1520-6904 ; 0022-3263
    ISSN (online) 1520-6904
    ISSN 0022-3263
    DOI 10.1021/acs.joc.3c00275
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: [Vascular hyperpermeable molecules potentially contributing to the development of pulmonary edema in sepsis-associated ARDS].

    Hattori, Kohshi / Matsuda, Naoyuki / Hattori, Yuichi

    Nihon yakurigaku zasshi. Folia pharmacologica Japonica

    2022  Volume 157, Issue 4, Page(s) 226–231

    Abstract: The acute respiratory distress syndrome (ARDS) is an important cause of respiratory failure in critically ill patients and may become a life-threatening condition where inflammation of the lungs may begin in one lung but eventually affects both, leading ... ...

    Abstract The acute respiratory distress syndrome (ARDS) is an important cause of respiratory failure in critically ill patients and may become a life-threatening condition where inflammation of the lungs may begin in one lung but eventually affects both, leading to damage to the alveoli and surrounding small blood vessels. ARDS is particularly characterized by noncardiogenic pulmonary edema caused by an increase in pulmonary capillary permeability. Several clinical disorders can precipitate in ARDS, including pneumonia, sepsis, aspiration of gastric contents, and major trauma. The most common cause of ARDS is sepsis, which is a serious and widespread infection of the bloodstream and is now defined as life-threatening organ dysfunction due to a dysregulated reponse of the host to infection. In sepsis, a number of vascular hyperpermeable factors, such as histamine, nitric oxide, thromboxane A
    MeSH term(s) Humans ; Lung ; Pulmonary Edema/etiology ; Respiratory Distress Syndrome/etiology ; Sepsis/complications ; Vascular Endothelial Growth Factor A
    Chemical Substances Vascular Endothelial Growth Factor A
    Language Japanese
    Publishing date 2022-03-01
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 1097532-9
    ISSN 1347-8397 ; 0015-5691
    ISSN (online) 1347-8397
    ISSN 0015-5691
    DOI 10.1254/fpj.22013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Stattic ameliorates the cecal ligation and puncture-induced cardiac injury in septic mice via IL-6-gp130-STAT3 signaling pathway

    Imbaby, Samar / Hattori, Yuichi

    Life Sciences. 2023 Oct., v. 330 p.122008-

    2023  

    Abstract: Sepsis-induced cardiac dysfunction is the leading cause of higher morbidity and mortality with poor prognosis in septic patients. Our recent previous investigation provides evidence of the hallmarks of signal transducer and activator of transcription3 ( ... ...

    Abstract Sepsis-induced cardiac dysfunction is the leading cause of higher morbidity and mortality with poor prognosis in septic patients. Our recent previous investigation provides evidence of the hallmarks of signal transducer and activator of transcription3 (STAT3) activation in sepsis and targeting of STAT3 with Stattic, a small-molecule inhibitor of STAT3, has beneficial effects in various septic tissues. We investigated the possible cardioprotective effects of Stattic on cardiac inflammation and dysfunction in mice with cecal ligation and puncture (CLP)-induced sepsis. A polymicrobial sepsis model was induced by CLP in mice and Stattic (25 mg/kg) was intraperitoneally given at one and twelve hours after CLP operation. The cecum was exposed in sham-control mice without CLP. After 18 h of surgery, electrocardiogram (ECG) for anaesthized mice was registered followed by collecting of samples of blood and tissues for bimolecular and histopathological assessments. Myeloperoxidase, a marker of neutrophil infiltration, was assessed immunohistochemically. CLP profoundly impaired cardiac functions as evidenced by ECG changes in septic mice as well as elevation of cardiac enzymes, and inflammatory markers with myocardial histopathological and immunohistochemical alterations. While, Stattic markedly reversed the CLP-induced cardiac abnormalities and restored the cardiac function by its anti-inflammatory activities. Stattic treatment had potential beneficial effects against sepsis-induced cardiac inflammation, dysfunction and damage. Its cardioprotective effects were possibly attributed to its anti-inflammatory activities by targeting STAT3 and downregulation of IL-6 and gp130. Our investigations suggest that Stattic could be a promising target for management of cardiac sepsis and inflammation-related cardiac damage.
    Keywords cardiac output ; cecum ; electrocardiography ; histopathology ; immunohistochemistry ; inflammation ; interleukin-6 ; models ; morbidity ; mortality ; myeloperoxidase ; neutrophils ; prognosis ; signal transduction ; surgery ; Stattic ; STAT3 inhibitor ; Sepsis ; ECG ; Cardiac inflammation, STAT3
    Language English
    Dates of publication 2023-10
    Publishing place Elsevier Inc.
    Document type Article ; Online
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2023.122008
    Database NAL-Catalogue (AGRICOLA)

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