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Éva Katona

Researcher at University of Debrecen

Publications -  128
Citations -  3634

Éva Katona is an academic researcher from University of Debrecen. The author has contributed to research in topics: Factor XIII & Fibrinogen. The author has an hindex of 30, co-authored 121 publications receiving 3270 citations. Previous affiliations of Éva Katona include University of Helsinki & Carol Davila University of Medicine and Pharmacy.

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Effect of a Novel Free Radical Scavenger, Edaravone (MCI-186), on Acute Brain Infarction

TL;DR: Edaravone represents a neuroprotective agent which is potentially useful for treating acute ischemic stroke, since it can exert significant effects on functional outcome as compared with placebo.
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Factor XIII: a coagulation factor with multiple plasmatic and cellular functions.

TL;DR: The role of FXIII in maintaining pregnancy, its contribution to the wound healing process, and its proangiogenic function are reviewed in details.
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The involvement of blood coagulation factor XIII in fibrinolysis and thrombosis.

TL;DR: This review focuses on the biochemical and clinical aspects of the involvement of FXIII in fibrinolysis and thrombosis and the polymorphisms in the FXIII subunit genes have stirred a lot of interest.
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Val34Leu polymorphism of plasma factor XIII: biochemistry and epidemiology in familial thrombophilia.

TL;DR: It was demonstrated that the intracellular stability and the plasma concentration of FXIII of different Val34Leu genotypes are identical, which suggests that there is no difference in the rate of synthesis and externalization of wild-type and mutant FXIII-A, and faster activation of the Leu34 allele hardly could be associated with its presumed protective effect against venous thrombosis.
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Mechanical loading stimulates chondrogenesis via the PKA/CREB-Sox9 and PP2A pathways in chicken micromass cultures.

TL;DR: The results indicate that proper mechanical stimuli augment in vitro cartilage formation via promoting both differentiation and matrix production of chondrogenic cells, and the opposing regulation of the PKA/CREB-Sox9 and the PP2A signalling pathways is crucial in this phenomenon.