Infliximab attenuates early myocardial dysfunction after resuscitation in a swine cardiac arrest model. - Wikidata - awgldk - TriplyDB

Infliximab attenuates early myocardial dysfunction after resuscitation in a swine cardiac arrest model.

Infliximab attenuates early myocardial dysfunction after resuscitation in a swine cardiac arrest model.

http://www.wikidata.org/entity/Q33753939

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Myocardial Dysfunction and Shock after Cardiac Arrest Translating novel strategies for cardioprotection: the Hatter Workshop Recommendations.Adora2b signaling on bone marrow derived cells dampens myocardial ischemia-reperfusion injury.TNF-α blockade improves early post-resuscitation survival and hemodynamics in a swine model of ischemic ventricular fibrillation.Predicting the outcomes for out-of-hospital cardiac arrest patients using multiple biomarkers and suspension microarray assays Tumor necrosis factor α antagonism improves neurological recovery in murine intracerebral hemorrhage.Ischaemic/reperfusion injury: Role of infliximab A comparison of etanercept vs. infliximab for the treatment of post-arrest myocardial dysfunction in a swine model of ventricular fibrillation.

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Infliximab attenuates early myocardial dysfunction after resuscitation in a swine cardiac arrest model.

http://www.wikidata.org/entity/Q33753939

description

2010 nî lūn-bûn

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2010 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի ապրիլին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Infliximab attenuates early my ...... a swine cardiac arrest model.

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Infliximab attenuates early my ...... a swine cardiac arrest model.

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Infliximab attenuates early my ...... a swine cardiac arrest model.

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Infliximab attenuates early my ...... a swine cardiac arrest model.

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Critical Care Medicine

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Infliximab attenuates early my ...... a swine cardiac arrest model.

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James T Niemann

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John P Rosborough

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Quynh T Phan

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Scott G Filler

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P2860

Regional variation in out-of-hospital cardiac arrest incidence and outcome

Why immunomodulatory therapies have not worked in sepsis.

Cellular basis for the negative inotropic effects of tumor necrosis factor-alpha in the adult mammalian heart.

Interleukin 1 and tumor necrosis factor inhibit cardiac myocyte beta-adrenergic responsiveness

Negative inotropic mediators released from the heart after myocardial ischaemia-reperfusion.

Inflammatory mediators and reversible myocardial dysfunction.

Myocardial protection during resuscitation from cardiac arrest.

Genetic polymorphisms in sepsis and septic shock: role in prognosis and potential for therapy.

Understanding the inflammatory cytokine response in pneumonia and sepsis: results of the Genetic and Inflammatory Markers of Sepsis (GenIMS) Study.

Genetic determinants of the inflammatory response.

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1162-1167

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