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Paula A. Zacharowski

Researcher at Queen Mary University of London

Publications -  15
Citations -  725

Paula A. Zacharowski is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: Reperfusion injury & Sepsis. The author has an hindex of 11, co-authored 15 publications receiving 684 citations.

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The fibrin-derived peptide Bβ 15-42 protects the myocardium against ischemia-reperfusion injury

TL;DR: In this article, a fibrin-derived peptide, Bbeta15-42, was shown to reduce leukocyte infiltration, infarct size and subsequent scar formation in acute or chronic rat models of myocardial ischemia-reperfusion injury.
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Toll-like receptor 4 plays a crucial role in the immune–adrenal response to systemic inflammatory response syndrome

TL;DR: It is demonstrated that TLR-4 is a key mediator in the crosstalks between the innate immune system and the endocrine stress response and could contribute to the underlying mechanisms of impaired adrenal stress response in patients with bacterial sepsis.
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Impaired adrenal stress response in Toll-like receptor 2-deficient mice.

TL;DR: It is demonstrated that TLR-2 deficiency in mice is associated with reduced plasma corticosterone levels and marked cellular alterations in adrenocortical tissue, and a link between the innate immune system and the endocrine stress response is demonstrated.
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Fibrin(ogen) and its fragments in the pathophysiology and treatment of myocardial infarction.

TL;DR: The pathogenesis of reperfusion injury is summarized, detailing the role of fibrin(ogen) and its derivatives, and a new concept for fibrIn derivatives as potential targets for reperfusions therapy is introduced.
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Preconditioning by toll-like receptor 2 agonist Pam3CSK4 reduces CXCL1-dependent leukocyte recruitment in murine myocardial ischemia/reperfusion injury.

TL;DR: Testing whether preconditioning with a toll-like receptor (TLR) 2 agonist protects against myocardial ischemia and reperfusion by interfering with chemokine CXCL1 release from cardiomyocytes found that preconditioning by Pam3CSK4 reduced infarct size and troponin T release and resulted in an improved cardiac function.