2,251 research outputs found
River archaeology – a new tool for historical hydrology
River archaeology is consisting of underwater research of the rivers themselves, and
also the archaeology of the valleys/floodplains with special interest in humanenvironmental
interactions (reconstructing space, environment, economy and society
on the basis of the material culture and traces of human impacts). As historical
hydrology is occupying similar questions from the hydrologist’s point of view, the
combination of different approaches offers fruitful cooperation for both disciplines.
The paper presents the type, nature and problems of archaeological record through
recent work in the Drava river basin
PoszttranszláciĂłs mĂłdosĂtások hatása a humán szĂvizom kontraktilitására = Analysis of the effects of posttranslational modifications on human cardiac muscle cell contraction
A kutatás cĂ©lja a poszttranszláciĂłs változások (kĂĽlönös tekintettel a protein kináz C (PKC) általi mĂłdosĂtásokra) hatásainak vizsgálata volt humán kamrai szĂvizomsejteken. EredmĂ©nyeink a PKC jelentĹ‘s szerepĂ©t mutatták ki a kontraktilis erĹ‘ megĹ‘rzĂ©sĂ©ben egĂ©szsĂ©ges, donor szĂvekben. Ennek mechanizmusakĂ©nt a PKCalfa transzlokáciĂłját igazoltuk a citoszolbĂłl a kontraktilis rendszerhez. A miofibrilláris rendszerben a PKCalfa Ca2+ koncentráciĂł fĂĽggĹ‘ kötĹ‘partnerekĂ©nt a vĂ©kony filamentális regulatĂłrikus fehĂ©jĂ©t, a troponin I-t azonosĂtottuk. Habár a PKC aktivitás szabályozása számos kĂsĂ©rletes szĂvelĂ©gtelensĂ©g modellben hasznosnak bizonyult, ezen eredmĂ©nyek terápiás alkalmazása komoly kihĂvást jelent, mert a PKC valamennyi szövetben expresszálĂłdik Ă©s számos folyamatot szabályoz. EredmĂ©nyeink arra utalnak, hogy a troponin I-PKC kölcsönhatás szabályozásával lehetĹ‘sĂ©g nyĂlhat a specifikusan a szĂvizom kontraktilis rendszerĂ©vel kölcsönhatĂł PKC aktivitásának moduláciĂłjára. További kĂsĂ©rletekben igazoltuk a fehĂ©rje oxidáciĂł kontraktilitás csökkentĹ‘ hatásait. A károsodás Ă©s a funkciĂłcsökkenĂ©s megfelelĹ‘en alkalmazott redukálĂłszerekkel reverzĂbilisen megfordĂthatĂłnak bizonyult. Ez a szĂv kontraktilitásának csökkenĂ©sĂ©vel járĂł kĂłrkĂ©pek (pl. szĂvinfarktus) esetĂ©n Ăşj terápiás lehetĹ‘sĂ©get jelenthet. Gazdasági szempontbĂłl a 4,8 milliĂł Ft-os támogatás segĂtsĂ©gĂ©vel 7 közlemĂ©ny publikálására kerĂĽlt sor, melyek összesĂtett impact faktora 33,92. | The goal of the proposal was to investigate the role of post-translational modifications (in particular the protein kinase C (PKC) mediated effects) on the contractility of human ventricular cardiomyocytes. Our results suggested a prominent role for PKCalpha in the maintainance of contractile force of healthy (donor) hearts. Further analysis revealed the translocation of PKCalpha from the cytosol to the contractile system, supporting its functional role. the thin filamental regulatory protein troponin I was identified as the myofibrillar protein resonsible for Ca2+ dependent PKCalpha binding. Although modulation of PKC is effective in various forms of heart diseases leading to decreased contractility, in vitro, pharmacologic targeting of PKC is challenging based on its ubiquitous expression and many physiological functions. Our data suggest, that regulation of troponin I - PKCalpha interaction may be a new therapeutic strategy to achieve PKC modulation specifically at the level of the contractile system of the heart. In addition, we found a significant deleterious effect of protein oxidation on the contractile force, which was reversible by reducing agents. Such conditions occur in myocardial infarction; therefore reducing agents may represent a new therapeutic tool to preserve cardiac contractile force. In the economical viewpoint, investment of 4.8 million HUF resulted in the publication of 7 articles with a cumulated impact factor of 33.92
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Greenways as Linear Components of Green Infrastructure in Rural Agricultural Landscapes of South-Western Slovakia
Greenways are important linking elements of green infrastructure systems in rural cultural landscapes. Their significance markedly increases in agricultural landscapes, since green networks and systems are very often limited to linear structures in this particular type of landscape. Greenways can therefore be crucial green infrastructure components in intensively farmed arable-land matrixes. The uniqueness of the presented research consists in the focus on sustainability and resilience benefits provided by greenways in agricultural landscapes. Greenways and green infrastructure improve the overall environmental resilience of farmed landscapes towards climate change and extreme environmental events, such as long lasting drought and erosion of fertile topsoil by strong wind or rainstorms. Moreover, it facilitates and enhances wildlife migration in the landscape and increases the overall landscape and species biodiversity. All these positive environmental benefits lead to more sustainable agricultural landscapes. Additionally, greenways, thanks to their linear spatial structure, surface compactness and multifunctionality, do not threaten the food system resilience of the landscape
A humán myocardium kontraktilis fehérjéinek oxidációja és annak mechanikai következményei = The mechanical consequence of contractile protein oxidation in the human myocardium
MegfigyelĂ©seink szerint a szĂvelĂ©gtelensĂ©g elĹ‘rehaladott stádiumaiban a kontraktilis fehĂ©rjĂ©k Ca2+-Ă©rzĂ©kenysĂ©ge fokozĂłdik, mely leginkább a troponin I fehĂ©rjĂ©k alul-foszforforiláltságával fĂĽgghet össze. Amennyiben a funkciĂłzavar diastolĂ©s komponenssel is rendelkezik, Ăşgy a csökkent miofilemantáris fehĂ©rjefoszforiláciĂł a szarkomer titin nevű ĂłriásfehĂ©rjĂ©jĂ©t is Ă©rintheti, ezáltal fokozva a szĂvizomsejtek passzĂv feszĂĽlĂ©sĂ©t. Ezeket az eltĂ©rĂ©seket a nitro-oxidatĂv stressz fokozĂłdásával járĂł állapotokban további fehĂ©rjekárosodások egĂ©szĂthetik ki. In vitro teszt körĂĽlmĂ©nyek között a szĂvizomfehĂ©rjĂ©k szulfhidril csoportjainak (SH) ditiodipiridin segĂtsĂ©gĂ©vel lĂ©trehozott oxidáciĂłja, a tirozin oldalláncok peroxinitrit segĂtsĂ©gĂ©vel kiváltott nitráciĂłja, vagy karboniláciĂłja a szĂvizomsejtek Ca2+-ra adott válaszadĂł-kĂ©pessĂ©gĂ©t egyaránt csökkentik. A szarkomerek mechanikai funkciĂłjának változásit azonban ezekben az esetekben más Ă©s más fehĂ©rjĂ©k idĂ©zik elĹ‘. MĂg a szarkomerfehĂ©rjĂ©k nitráciĂłja elsĹ‘sorban strukturális változásokat eredmĂ©nyez, addig az SH-oxidáciĂł Ă©s a fehĂ©rjekarboniláciĂł a kontraktilis fehĂ©rjerendszer működĂ©sĂ©nek szabályozását károsĂtja. Ă–sszessĂ©gĂ©ben, a szĂvbetegsĂ©gek során a kontraktilis erĹ‘ Ca2+-Ă©rzĂ©kenysĂ©gĂ©nek növekedĂ©se vagy csökkenĂ©se a szakomert alkotĂł fehĂ©rjĂ©k egymáshoz viszonyĂtott hierarchikus rendszerĂ©tĹ‘l Ă©s a fehĂ©rjekárosodások egymásra gyakorolt hatásaitĂłl fĂĽgghetnek. Ez magyarázhatja azt is, hogy infarktuson átesett egerek (fokozott fehĂ©jekarboniláciĂłjával járĂł) szĂvelĂ©gtelensĂ©gĂ©ben, dacára a troponin I hipofoszforiláciĂłjának, a kontraktilis erĹ‘ Ca2+-Ă©rzĂ©kenysĂ©gĂ©nek csökkenĂ©se alakul ki. | Our results suggest that at progressed stages of heart failure beta-adrenergic down-regulation is accompanied by an increase in the Ca2+-sensitivity of force production mainly because of troponin I hypophosphorylation. In cases of diastolic dysfunction myofilament hypophosphorylation involves the giant sarcomeric protein titin, thereby increasing the passive stiffness of cardiomyocytes. These protein alterations might be complemented by additional ones during conditions leading to nitro-oxidative stress. Under in vitro test conditions selective oxidation of sulfhydryl groups (SH) by dithiodipyridine, nitration of tyrosine residues by peroxynitrite, or protein carbonylation all decrease the Ca2+-responsiveness of force production in permeabilized cardiomyocytes. However, the sarcomeric proteins affected by these insults and the mechanisms by which they evoke sarcomeric dysfunctions are divergent. Our results suggested predominant structural alterations of the sarcomere following protein nitration, while SH-oxidation or protein carbonylation were associated with changes in the fine regulation of sarcomeric function. Collectively, the direction of change in the Ca2+-sensitivity of force production may depend on the hierarchy of sarcomeric protein alterations and on their interactions in the diseased heart. For example, in a postischemic murine model of heart failure (with increased protein carbonylation) we found a decreased Ca2+-sensitivity of force production in cardiomyocytes at the infarcted zone despite troponin I hypophosphorylation
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