33 research outputs found

    Osiadłe ptaki. Urodzeni za granicą pracownicy polskich instytucji akademickich, 182 s.

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    Monografia wydana w koedycji z Wyższą Szkołą Informatyki i Zarządzania z siedzibą w Rzeszowie (ISBN 978-83-66364-43-1 [Dodaj do projektu Citavi wg ISBN] ).Książka analizuje doświadczenia życiowe urodzonych za granicą pracowników naukowych, dydaktycznych oraz naukowo-dydaktycznych, którzy osiedlili się i pracują w Polsce (...) Od strony metodologicznej oraz etycznej jest wręcz wzorcowym przykładem prowadzenia badań. (...) Studium stanowi doskonale napisaną i wnikliwą analizę doświadczeń pracowników zagranicznych. Znacząco poszerza naszą wiedzę na temat tej kategorii wysoko wykwalifikowanych migrantów. Książka podważa wiele zdroworozsądkowych przekonań i obiegowych sądów, a także zawiera praktyczne rekomendacje, które mogą stanowić podstawę do bardziej realistycznej polityki naukowej. (fragment recenzji prof. K. Jaskułowskiego

    Osiadłe ptaki : urodzeni za granicą pracownicy polskich instytucji akademickich

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    Publikacja powstała w ramach projektu pt. „Zagraniczni uczeni w Polsce: motywacje, trajektorie życiowe oraz potencjał naukowy” realizowanego w Wyższej Szkole Informatyki i Zarządzania w Rzeszowie.Publikacja sfinansowana w ramach programu Ministra Nauki i Szkolnictwa Wyższego pod nazwą DIALOG w latach 2017–2019.Kamil Łuczaj: Wyższa Szkoła Informatyki i Zarządzania z siedzibą w RzeszowieBeata Bielska: Uniwersytet Mikołaja Kopernika w ToruniuOlga Kurek‑Ochmańska: Wyższa Szkoła Informatyki i Zarządzania z siedzibą w RzeszowieJanusz Mucha: Komitet Badań nad Migracjami PANAbraham Martin, Auspurg Katrin, Hinz Thomas (2010) Migration Decisions Within Dual‑Earner Partnerships: A Test of Bargaining Theory, „Journal of Marriage and Family” Vol. 72, Issue 4: 876–892, dostępny: http://kops.uni‑konstanz.de/bitstream/handle/123456789/13321/Hinz.pdf?sequence=2&isAllowed=y [08.01.2020].Abramowicz Marta (2017) Sytuacja społeczna osób LGBTA w Polsce. 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    Digenic Alport Syndrome

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    Digenic Alport syndrome refers to the inheritance of pathogenic variants in COL4A5 plus COL4A3 or COL4A4 or in COL4A3 plus COL4A4. Where digenic Alport syndrome includes a pathogenic COL4A5 variant, the consequences depend on the sex of the affected individual, COL4A5 variant ?severity,? and the nature of the COL4A3 or COL4A4 change. A man with a pathogenic COL4A5 variant has all his collagen IV ?3?4?5-heterotrimers affected, and an additional COL4A3 or COL4A4 variant may not worsen disease. A woman with a pathogenic COL4A5 variant has on average 50% of her heterotrimers affected, which is increased to 75% with a further COL4A3 or COL4A4 variant and associated with a higher risk of proteinuria. In digenic Alport syndrome with pathogenic COL4A3 and COL4A4 variants, 75% of the heterotrimers are affected. The COL4A3 and COL4A4 genes occur head-to-head on chromosome 2, and inheritance is autosomal dominant when both variants affect the same chromosome (in cis) or recessive when they affect different chromosomes (in trans). This form of digenic disease results in increased proteinuria and a median age of kidney failure intermediate between autosomal dominant and autosomal recessive Alport syndrome. Previous guidelines have suggested that all pathogenic or likely pathogenic digenic variants should be identified and reported. Affected family members should be identified, treated, and discouraged from kidney donation. Inheritance within a family is easier to predict if the two variants are considered independently and if COL4A3 and COL4A4 variants are known to be inherited on the same or different chromosomes

    Protein kinase D at the Golgi controls NLRP3 inflammasome activation

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    The inflammasomes are multiprotein complexes sensing tissue damage and infectious agents to initiate innate immune responses. Different inflammasomes containing distinct sensor molecules exist. The NLRP3 inflammasome is unique as it detects a variety of danger signals. It has been reported that NLRP3 is recruited to mitochondria-associated endoplasmic reticulum membranes (MAMs) and is activated by MAM-derived effectors. Here, we show that in response to inflammasome activators, MAMs localize adjacent to Golgi membranes. Diacylglycerol (DAG) at the Golgi rapidly increases, recruiting protein kinase D (PKD), a key effector of DAG. Upon PKD inactivation, self-oligomerized NLRP3 is retained at MAMs adjacent to Golgi, blocking assembly of the active inflammasome. Importantly, phosphorylation of NLRP3 by PKD at the Golgi is sufficient to release NLRP3 from MAMs, resulting in assembly of the active inflammasome. Moreover, PKD inhibition prevents inflammasome autoactivation in peripheral blood mononuclear cells from patients carrying NLRP3 mutations. Hence, Golgi-mediated PKD signaling is required and sufficient for NLRP3 inflammasome activation.PMC558412

    Minimal information for studies of extracellular vesicles 2018 (MISEV2018):a position statement of the International Society for Extracellular Vesicles and update of the MISEV2014 guidelines

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    The last decade has seen a sharp increase in the number of scientific publications describing physiological and pathological functions of extracellular vesicles (EVs), a collective term covering various subtypes of cell-released, membranous structures, called exosomes, microvesicles, microparticles, ectosomes, oncosomes, apoptotic bodies, and many other names. However, specific issues arise when working with these entities, whose size and amount often make them difficult to obtain as relatively pure preparations, and to characterize properly. The International Society for Extracellular Vesicles (ISEV) proposed Minimal Information for Studies of Extracellular Vesicles (“MISEV”) guidelines for the field in 2014. We now update these “MISEV2014” guidelines based on evolution of the collective knowledge in the last four years. An important point to consider is that ascribing a specific function to EVs in general, or to subtypes of EVs, requires reporting of specific information beyond mere description of function in a crude, potentially contaminated, and heterogeneous preparation. For example, claims that exosomes are endowed with exquisite and specific activities remain difficult to support experimentally, given our still limited knowledge of their specific molecular machineries of biogenesis and release, as compared with other biophysically similar EVs. The MISEV2018 guidelines include tables and outlines of suggested protocols and steps to follow to document specific EV-associated functional activities. Finally, a checklist is provided with summaries of key points

    Le rôle de la protéine kinase D dans la fission mitochondriale lors de la mitose

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    Over the last two decades, multiple studies have uncovered and strengthen the implication of mitochondrial dynamics in cancer. During my thesis, I discovered an unanticipated role for the PKD kinase family in mitochondrial fission. Loss of PKD activity led to blockade of mitochondrial fission and resulted in a significant elongation of mitochondria by unopposed fusion. Mechanistically, we showed that PKDs regulated mitochondrial dynamics by activating the mitochondrial fission factor (MFF) through phosphorylation of multiple sites. MFF acts as a main receptor for the large GTPase DRP1, which constricts mitochondria, and it is critical for proper mitochondrial division. All three PKD family members could phosphorylate MFF. PKD-mediated MFF phosphorylation and mitochondrial fragmentation occurred specifically during mitosis. As MFF phosphorylation was found to be significantly upregulated in highly mitotic cancers, which was evidenced in several global phosphoproteome studies, the discovered PKD-MFF signaling axis regulating mitochondrial dynamics in mitosis could become an attractive therapeutic avenue for cancer treatment.Plusieurs études ont découvert et renforcé l'implication de la dynamique mitochondriale dans le cancer. J'ai découvert un rôle inattendu des protéines kinases de la famille PKD dans la fission mitochondriale. La perte de l'activité PKD a conduit à un blocage de la fission et a entraîné une élongation significative des mitochondries par fusion continue. D'un point de vue mécanique, nous avons montré que les protéines PKD régulent la dynamique mitochondriale en activant le facteur de fission mitochondrial (MFF) par phosphorylation de plusieurs sites. MFF agit comme un récepteur principal de la GTPase DRP1, qui resserre les mitochondries, et il est essentiel à une bonne division mitochondriale. Les trois membres de la famille PKD peuvent phosphoryler MFF. La phosphorylation de MFF est médiée par PKD et la fragmentation mitochondriale se produit pendant la mitose. Comme démontré dans études sur les phosphoprotéomes, la phosphorylation du MFF est augmentée dans les cancers très mitotiques. Ainsi, l'axe de signalisation PKD-MFF régulant la dynamique mitochondriale en mitose pourrait devenir une voie thérapeutique attrayante pour le traitement du cancer

    Determinants of risk management on the example of selected farms

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    W pracy podjęto zagadnienie zarządzania ryzykiem w gospodarstwie rolnym. Celem badań było zaprezentowanie opinii wybranej grupy rolników na temat występującego w rolnictwie ryzyka, a także przedstawienie propozycji udoskonalenia zarządzania w kierunku minimalizowania ryzyka. Metodą badawczą niezbędną do uzyskania wyników był sondaż diagnostyczny, a jako narzędzie badawcze posłużył kwestionariusz ankietowy. Badania przeprowadzone zostały w grupie 40 osób zarządzających lub pracujących w gospodarstwach rolnych. Niewłaściwe zarządzanie ryzykiem doprowadziło do pogorszenia sytuacji gospodarstw. Znaczny odsetek badanych (58,82%), którzy nie posiadali wiedzy na temat możliwości zarządzania ryzykiem uznali prowadzenie gospodarstw rolnych za nieopłacalne, natomiast wśród respondentów znających możliwości zarządzania ryzykiem 21,74% stwierdziło nieopłacalność prowadzenia gospodarstwa. Wyniki badań mogą posłużyć do wprowadzenia zmian w niewłaściwym zarządzaniu ryzykiem w gospodarstwach rolnych. Ukazanie problemu powinno umożliwić wdrożenie szkoleń lub pomocy rolnikom w tematyce dotyczącej zapobiegania powstawaniu ryzyka lub przeciwdziałania jego skutkom. Doprowadzić to może w konsekwencji do poprawy funkcjonowania gospodarstw, zwiększenia bezpieczeństwa i stabilności, jak i również zmniejszenia stopnia narażenia związanego w występującym ryzykiem.This paper has been dedicated the risk management on farms. The aim of this paper was to present the opinion of a selected group of farmers on the subject concerning risk occurring in agriculture as well as to show a proposal to improve management in order to minimize risk. The research method required to raise the results, was the diagnostic survey and there has been used the questionnaire as a research tool. The research was carried out in a group of 40 managers or working on farms. Improper risk management has led to situation’s deterioration in agriculture. Significant percent of respondents (58,82%), those did not have knowledge about risk management recognized that farm keeping is unprofitable, while among respondents familiar with risk management (21,74%), recognized farm keeping as a unprofitable. Results of research can be used to make changes in improperly risk management in farms. Showing of the problem should allow the implementation of trainings or help the farmers in subject of prevention of risk or counteraction with its impact. That can consequently lead to improve the functioning of farms, improve the safety and stability and decrease level of expose related to occurring risk

    Design and synthesis of 4,5,6,7\u2010tetrahydro\u20101H\u20101,2\u2010diazepin\u20107\u2010one derivatives as a new series of Phosphodiesterase 4 (PDE4) inhibitors

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    Phosphodiesterase 4 (PDE4) inhibitors have attractive therapeutic potential in respiratory, inflammatory, metabolic and CNS disorders. The present work details the design, chemical exploration and biological profile of a novel PDE4 inhibitor chemotype. A diazepinone ring was identified as an under-represented heterocyclic system fulfilling a set of PDE4 structure-based design hypotheses. Rapid exploration of the structure activity relationships for the series was enabled by robust and scalable two/three-steps parallel chemistry protocols. The resulting compounds demonstrated PDE4 inhibitory activity in cell free and cell-based assays comparable to the Zardaverine control used, suggesting potential avenues for their further development

    Histone malonylation is regulated by SIRT5 and KAT2A

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    Summary: The posttranslational modification lysine malonylation is found in many proteins, including histones. However, it remains unclear whether histone malonylation is regulated or functionally relevant. Here, we report that availability of malonyl-co-enzyme A (malonyl-CoA), an endogenous malonyl donor, affects lysine malonylation, and that the deacylase SIRT5 selectively reduces malonylation of histones. To determine if histone malonylation is enzymatically catalyzed, we knocked down each of the 22 lysine acetyltransferases (KATs) to test their malonyltransferase potential. KAT2A knockdown in particular reduced histone malonylation levels. By mass spectrometry, H2B_K5 was highly malonylated and regulated by SIRT5 in mouse brain and liver. Acetyl-CoA carboxylase (ACC), the malonyl-CoA producing enzyme, was partly localized in the nucleolus, and histone malonylation increased nucleolar area and ribosomal RNA expression. Levels of global lysine malonylation and ACC expression were higher in older mouse brains than younger mice. These experiments highlight the role of histone malonylation in ribosomal gene expression
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