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  1. Article ; Online: In cold blood: a new way to achieve therapeutic cooling?

    Yenari, Midori A

    Science bulletin

    2023  Volume 68, Issue 23, Page(s) 2905–2906

    MeSH term(s) Body Temperature Regulation ; Skin Temperature ; Cold Temperature
    Language English
    Publishing date 2023-10-31
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2816140-3
    ISSN 2095-9281 ; 2095-9273
    ISSN (online) 2095-9281
    ISSN 2095-9273
    DOI 10.1016/j.scib.2023.10.036
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Microglia, the brain's double agent.

    Yenari, Midori A

    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

    2020  Volume 40, Issue 1_suppl, Page(s) S3–S5

    MeSH term(s) Brain/anatomy & histology ; Humans ; Microglia/physiology
    Language English
    Publishing date 2020-11-17
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 604628-9
    ISSN 1559-7016 ; 0271-678X
    ISSN (online) 1559-7016
    ISSN 0271-678X
    DOI 10.1177/0271678X20968993
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Clinical perspectives on ischemic stroke.

    Mizuma, Atsushi / Yenari, Midori A

    Experimental neurology

    2021  Volume 338, Page(s) 113599

    Abstract: Treatments for acute stroke have improved over the past years, but have largely been limited to revascularization strategies. The topic of neuroprotection, or strategies to limit brain tissue damage or even reverse it, has remained elusive. Thus, the ... ...

    Abstract Treatments for acute stroke have improved over the past years, but have largely been limited to revascularization strategies. The topic of neuroprotection, or strategies to limit brain tissue damage or even reverse it, has remained elusive. Thus, the clinical mainstays for stroke management have focused on prevention. The lack of clinical translation of neuroprotective therapies which have shown promise in the laboratory may, in part, be due to a historic inattention to comorbidities suffered by a majority of stroke patients. With the advent of more stroke models that include one or more relevant comorbidities, it may be possible to identify effective treatments that may translate into new treatments at the clinical level. In the meantime, we review comorbidities in stroke patients, modification of stroke risk factors and available acute stroke treatments in the clinic.
    MeSH term(s) Humans ; Ischemic Stroke
    Language English
    Publishing date 2021-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 207148-4
    ISSN 1090-2430 ; 0014-4886
    ISSN (online) 1090-2430
    ISSN 0014-4886
    DOI 10.1016/j.expneurol.2021.113599
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Therapeutic hypothermia for stroke: Unique challenges at the bedside.

    You, Je Sung / Kim, Jong Youl / Yenari, Midori A

    Frontiers in neurology

    2022  Volume 13, Page(s) 951586

    Abstract: Therapeutic hypothermia has shown promise as a means to improving neurological outcomes at several neurological conditions. At the clinical level, it has been shown to improve outcomes in comatose survivors of cardiac arrest and in neonatal hypoxic ... ...

    Abstract Therapeutic hypothermia has shown promise as a means to improving neurological outcomes at several neurological conditions. At the clinical level, it has been shown to improve outcomes in comatose survivors of cardiac arrest and in neonatal hypoxic ischemic encephalopathy, but has yet to be convincingly demonstrated in stroke. While numerous preclinical studies have shown benefit in stroke models, translating this to the clinical level has proven challenging. Major obstacles include cooling patients with typical stroke who are awake and breathing spontaneously but often have significant comorbidities. Solutions around these problems include selective brain cooling and cooling to lesser depths or avoiding hyperthermia. This review will cover the mechanisms of protection by therapeutic hypothermia, as well as recent progress made in selective brain cooling and the neuroprotective effects of only slightly lowering brain temperature. Therapeutic hypothermia for stroke has been shown to be feasible, but has yet to be definitively proven effective. There is clearly much work to be undertaken in this area.
    Language English
    Publishing date 2022-10-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2022.951586
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Temperature affects thrombolytic efficacy using rt-Pa and eptifibatide, an in vitro study: editorial commentary on Meunier et al., 2012.

    Yenari, Midori A

    Therapeutic hypothermia and temperature management

    2013  Volume 2, Issue 4, Page(s) 166

    Language English
    Publishing date 2013-04-16
    Publishing country United States
    Document type Editorial
    ZDB-ID 2609342-X
    ISSN 2153-7933 ; 2153-7658
    ISSN (online) 2153-7933
    ISSN 2153-7658
    DOI 10.1089/ther.2012.0020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Sexual dimorphism in immune cell responses following stroke.

    Liu, Jialing / Sato, Yoshimichi / Falcone-Juengert, Jaime / Kurisu, Kota / Shi, Jian / Yenari, Midori A

    Neurobiology of disease

    2022  Volume 172, Page(s) 105836

    Abstract: Recent bodies of work in regard to stroke have revealed significant sex differences in terms of risk and outcome. While differences in sex hormones have been the focus of earlier research, the reasons for these differences are much more complex and ... ...

    Abstract Recent bodies of work in regard to stroke have revealed significant sex differences in terms of risk and outcome. While differences in sex hormones have been the focus of earlier research, the reasons for these differences are much more complex and require further identification. This review covers differences in sex related immune responses with a focus on differences in immune cell composition and function. While females are more susceptible to immune related diseases, they seem to have better outcomes from stroke at the experimental level with reduced pro-inflammatory responses. However, at the clinical level, the picture is much more complex with worse neurological outcomes from stroke. While the use of exogenous sex steroids can replicate some of these findings, it is apparent that many other factors are involved in the modulation of immune responses. As a result, more research is needed to better understand these differences and identify appropriate interventions and risk modification.
    MeSH term(s) Disease Susceptibility ; Female ; Humans ; Immunity ; Male ; Sex Characteristics ; Stroke
    Language English
    Publishing date 2022-08-03
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2022.105836
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Therapeutic hypothermia for ischemic stroke; pathophysiology and future promise.

    Kurisu, Kota / Yenari, Midori A

    Neuropharmacology

    2017  Volume 134, Issue Pt B, Page(s) 302–309

    Abstract: Therapeutic hypothermia, or cooling of the body or brain for the purposes of preserving organ viability, is one of the most robust neuroprotectants at both the preclinical and clinical levels. Although therapeutic hypothermia has been shown to improve ... ...

    Abstract Therapeutic hypothermia, or cooling of the body or brain for the purposes of preserving organ viability, is one of the most robust neuroprotectants at both the preclinical and clinical levels. Although therapeutic hypothermia has been shown to improve outcome from related clinical conditions, the significance in ischemic stroke is still under investigation. Numerous pre-clinical studies of therapeutic hypothermia has suggested optimal cooling conditions, such as depth, duration, and temporal therapeutic window for effective neuroprotection. Several studies have also explored mechanisms underlying the mechanisms of neuroprotection by therapeutic hypothermia. As such, it appears that cooling affects multiple aspects of brain pathophysiology, and regulates almost every pathway involved in the evolution of ischemic stroke. This multifaceted mechanism is thought to contribute to its strong neuroprotective effect. In order to carry out this therapy in optimal clinical settings, methodological and pathophysiological understanding is crucial. However, more investigation is still needed to better understand the underlying mechanisms of this intervention, and to overcome clinical barriers which seem to preclude the routine use therapeutic hypothermia in stroke. This article is part of the Special Issue entitled 'Cerebral Ischemia'.
    MeSH term(s) Animals ; Brain Ischemia/complications ; Humans ; Hypothermia, Induced/methods ; Hypothermia, Induced/trends ; Stroke/etiology ; Stroke/therapy
    Language English
    Publishing date 2017-08-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 218272-5
    ISSN 1873-7064 ; 0028-3908
    ISSN (online) 1873-7064
    ISSN 0028-3908
    DOI 10.1016/j.neuropharm.2017.08.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Anti-Inflammatory Targets for the Treatment of Reperfusion Injury in Stroke.

    Mizuma, Atsushi / Yenari, Midori A

    Frontiers in neurology

    2017  Volume 8, Page(s) 467

    Abstract: While the mainstay of acute stroke treatment includes revascularization via recombinant tissue plasminogen activator or mechanical thrombectomy, only a minority of stroke patients are eligible for treatment, as delayed treatment can lead to worsened ... ...

    Abstract While the mainstay of acute stroke treatment includes revascularization via recombinant tissue plasminogen activator or mechanical thrombectomy, only a minority of stroke patients are eligible for treatment, as delayed treatment can lead to worsened outcome. This worsened outcome at the experimental level has been attributed to an entity known as reperfusion injury (R/I). R/I is occurred when revascularization is delayed after critical brain and vascular injury has occurred, so that when oxygenated blood is restored, ischemic damage is increased, rather than decreased. R/I can increase lesion size and also worsen blood barrier breakdown and lead to brain edema and hemorrhage. A major mechanism underlying R/I is that of poststroke inflammation. The poststroke immune response consists of the aberrant activation of glial cell, infiltration of peripheral leukocytes, and the release of damage-associated molecular pattern (DAMP) molecules elaborated by ischemic cells of the brain. Inflammatory mediators involved in this response include cytokines, chemokines, adhesion molecules, and several immune molecule effectors such as matrix metalloproteinases-9, inducible nitric oxide synthase, nitric oxide, and reactive oxygen species. Several experimental studies over the years have characterized these molecules and have shown that their inhibition improves neurological outcome. Yet, numerous clinical studies failed to demonstrate any positive outcomes in stroke patients. However, many of these clinical trials were carried out before the routine use of revascularization therapies. In this review, we cover mechanisms of inflammation involved in R/I, therapeutic targets, and relevant experimental and clinical studies, which might stimulate renewed interest in designing clinical trials to specifically target R/I. We propose that by targeting anti-inflammatory targets in R/I as a combined therapy, it may be possible to further improve outcomes from pharmacological thrombolysis or mechanical thrombectomy.
    Language English
    Publishing date 2017-09-07
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2017.00467
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  9. Article ; Online: Targeting Reperfusion Injury in the Age of Mechanical Thrombectomy.

    Mizuma, Atsushi / You, Je Sung / Yenari, Midori A

    Stroke

    2018  Volume 49, Issue 7, Page(s) 1796–1802

    MeSH term(s) Brain Ischemia/surgery ; Humans ; Reperfusion Injury/etiology ; Reperfusion Injury/prevention & control ; Thrombectomy/adverse effects ; Thrombectomy/methods ; Treatment Outcome
    Language English
    Publishing date 2018-05-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 80381-9
    ISSN 1524-4628 ; 0039-2499 ; 0749-7954
    ISSN (online) 1524-4628
    ISSN 0039-2499 ; 0749-7954
    DOI 10.1161/STROKEAHA.117.017286
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Heat shock protein signaling in brain ischemia and injury.

    Kim, Jong Youl / Kim, Ji Won / Yenari, Midori A

    Neuroscience letters

    2019  Volume 715, Page(s) 134642

    Abstract: Heat shock proteins (HSPs) are chaperones that catalyze the refolding of denatured proteins. In addition to their ability to prevent protein denaturation and aggregation, the HSPs have also been shown to modulate many signaling pathways. Among HSPs, the ... ...

    Abstract Heat shock proteins (HSPs) are chaperones that catalyze the refolding of denatured proteins. In addition to their ability to prevent protein denaturation and aggregation, the HSPs have also been shown to modulate many signaling pathways. Among HSPs, the inducible 70 kDa HSP (HSP70) has especially been shown to improve neurological outcome in experimental models of brain ischemia and injury. HSP70 can modulate various aspects of the programmed cell death pathways and inflammation. This review will focus on potential mechanisms of the neuroprotective effects of HSP70 in stroke and brain trauma models. We also comment on potential ways in which HSP70 could be translated into clinical therapies.
    MeSH term(s) Animals ; Apoptosis/physiology ; Brain Injuries/physiopathology ; Brain Ischemia/physiopathology ; HSP70 Heat-Shock Proteins/physiology ; Humans ; Neuroprotection/physiology
    Chemical Substances HSP70 Heat-Shock Proteins
    Language English
    Publishing date 2019-11-20
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2019.134642
    Database MEDical Literature Analysis and Retrieval System OnLINE

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