357 research outputs found

    Don't Make Me Angry! A Psychophysiological Examination of the Anger–Performance Relationship in Intermediate and Elite Fencers

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    We aimed to identify the effect of state-anger on precision, speed, and power components of performance during fencing attacks. We conducted a laboratory-based, single-case research experiment to test the fine motor task performance of two experienced and two elite-level fencers under two emotional states: anger and emotion-neutral. We assessed anger via psychophysiological and self-report measures, and we induced anger via a brief imagery intervention. Through the use of an innovative design, which included multiple measures of change, we showed that anger had a consistent negative effect on precision but an inconsistent relationship with response time and muscle activity. The current research design and protocol offer a novel and in-depth method for examining the specific relationships between affective states, emotions, and the complexities that underpin performance. The specific effects of anger on performance were multifarious, complex, and inconsistent. Nonetheless, the results tend to indicate that anger facilitates reaction time and debilitates performance, and these effects were clearer for the most elite performers. The effects of anger on performance are clearly complex, so it would be rather premature to make any suggestions for future practice at this point. Nonetheless, the clearer findings with the elite fencers indicate that researchers will likely yield the most fruitful insights by examining the effects of emotion of performance in elite performers

    Alanyl-Glutamine Restores Tight Junction Organization after Disruption by a Conventional Peritoneal Dialysis Fluid

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    Understanding and targeting the molecular basis of peritoneal solute and protein transport is essential to improve peritoneal dialysis (PD) efficacy and patient outcome. Supplementation of PD fluids (PDF) with alanyl-glutamine (AlaGln) increased small solute transport and reduced peritoneal protein loss in a recent clinical trial. Transepithelial resistance and 10 kDa and 70 kDa dextran transport were measured in primary human endothelial cells (HUVEC) exposed to conventional acidic, glucose degradation products (GDP) containing PDF (CPDF) and to low GDP containing PDF (LPDF) with and without AlaGln. Zonula occludens-1 (ZO-1) and claudin-5 were quantified by Western blot and immunofluorescence and in mice exposed to saline and CPDF for 7 weeks by digital imaging analyses. Spatial clustering of ZO-1 molecules was assessed by single molecule localization microscopy. AlaGln increased transepithelial resistance, and in CPDF exposed HUVEC decreased dextran transport rates and preserved claudin-5 and ZO-1 abundance. Endothelial clustering of membrane bound ZO-1 was higher in CPDF supplemented with AlaGln. In mice, arteriolar endothelial claudin-5 was reduced in CPDF, but restored with AlaGln, while mesothelial claudin-5 abundance was unchanged. AlaGln supplementation seals the peritoneal endothelial barrier, and when supplemented to conventional PD fluid increases claudin-5 and ZO-1 abundance and clustering of ZO-1 in the endothelial cell membrane.This work is part of the IMPROVE-PD project that has received funding from the European Union’s Horizon 2020 Research and Innovation Programme under the Marie Sklodowska-Curie grant agreement number 812699. M.B. is funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)—Projektnummer 419826430. R.H. was supported by a research fellowship of the European Renal Association and European Dialysis and Transplant Association (ERA-EDTA). E.L. was supported by the ÚNKP-18-2 New National Excellence Program of the Ministry of Human Capacities, Hungary. E.L. and H.J. were supported by Jellinek-Harry scholarship. S.G.Z. acknowledges the Alexander von Humboldt Stiftung/Foundation for an Experienced Researcher Fellowship (2019–2021) and the International Peritoneal Dialysis Society (ISPD) for an International Cooperation Research Grant (2019–2021). C.P.S. has obtained funding from European Nephrology and Dialysis Institute (ENDI).Peer reviewe
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