210 research outputs found

    László Barkóczi (1919–2017)

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    THE FATE AND RECONSTRUCTION OF A ROMAN MOSAIC FLOOR AT PÉCS = EGY PÉCSI RÓMAI MOZAIKPADLÓ SORSA ÉS REKONSTRUKCIÓJA

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    In Pécs due to the continuous development of the town throughout many centuries, there are only few sites where the remains of the Roman town can be excavated and even fewer remains come to light undisturbed. Some archaeological monuments have already been disappeared for good, others are situated under streets and houses unavailable for any archaeological research. In many cases it is not easy to follow what happened to the finds and remains. The mosaic floor that was found in 1841 during the building of a house at 6 Káptalan Street and a Roman burial chamber, observed during canalization in 1927 belong to this category. Some researchers still consider these as they were parts of the same early Christian building. Some authors made mistakes or misinterpreted the sources, because they relied on old, short and inaccurate descriptions of the finds. Either they were not aware of the sources or did not read them carefully. Therefore there are many different opinions in the publications often contradicting each other. Also, the lack of drawings and documentation added to the difficulties of later research, just like the inaccurate observations in some previous publications. In 2011 when we made the illustrations to Pécs Története (History of Pécs town), Volume I, it became evident, that the reconstruction of the mosaics, published in 1984, and the interpretation of the archaeological remains found in 1927 were inaccurate. These Roman remains did not come to light in the same time yet they are connected to each other in so many ways. We have started our research with the examination of both the written sources and the actual archaeological material. Later we have researched the different opinions of earlier publications and only after that were we in the position - with the help of few survived drawings and photos - to re-evaluate the remains and to make an attemp to reconstruct what they might have looked like in Roman times. Our recent research on the finds from 1841 and 1927 started in 2011, when we made a presentation about them for the archaeology PhD students of the University of Pécs for the first time. In accordance with the topic of the semester first we gave an account of our ongoing research regarding the actual size of the mosaics and the location and identification of Burial Chamber X that came to light in 1927. We have also presented the new, amended reconstruction of the mosaics and some of the corrections we have made. We have published our finished research about the building and the mosaics on the 10th of December 2013 at the Morsa Archaelogica Conference in Pécs. We hope that this article helps to answer the questions that emerged or were left unanswered so far about the mosaics and the archaeological remains found in 1927

    Modulation of Leukocyte Behavior by an Inflamed Extracellular Matrix

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    Inflammation is a response of the immune system to foreign insult or physical damage. Various cellular and humoral components of the immune system are recruited from the vascular system and are translocated through endothelium, and into extracellular matrix (ECM) compartments of inflamed tissues. This translocation is orchestrated by various types of accessory signals, in the form of soluble or complexed molecules, which evoke remarkable transitions in leukocyte activities. Recruited inflammatory cells give rise to mechanisms of migration, including the secretion of enzymes and other pro-inflammatory mediators and the alteration of their adhesive contacts with the ECM. Hence, migrating cells secrete enzymes, chemokines, and cytokines which interact with the ECM, and thereby, provide the cells with intrinsic signals for coordinating their responses. Resultant products of enzymatic modifications to the ECM microenvironment, such as cytokine- and ECM-derived molecules, may be also part of a cell-signaling mechanism that provides leukocytes with information about the nature of their inflammatory activity; such a mechanism may give the immune system data that can be cognitively interpreted for consequential activities. This article reviews the findings that support this notion and describe the dynamic interactions between participants of the inflammatory processes

    2-Amino-5-bromo­pyridine–benzoic acid (1/1)

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    In the title adduct, C5H5BrN2·C7H6O2, the carboxyl group of the benzoic acid mol­ecule is twisted away from the attached ring by 12.97 (11)°. The 2-amino-5-bromo­pyridine mol­ecules inter­act with the carboxylic group of neighbouring benzoic acid mol­ecules through N—H⋯O and O—H⋯N hydrogen bonds, forming cyclic R 2 2(8) hydrogen-bonded motifs and linking the mol­ecules into a two-dimensional network lying parallel to (100). The crystal structure is further stabilized by weak C—H⋯O hydrogen bonds

    2-Amino-5-bromo­pyridinium trifluoro­acetate

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    In the title compound, C5H6BrN2 +·C2F3O2 −, the F atoms of the anion are disordered over two sets of sites, with occupancies of 0.59 (2):0.41 (2). In the crystal structure, the anions and cations are linked into a two-dimensional network parallel to (100) by N—H⋯O and C—H⋯O hydrogen bonds. Within this network, the N—H⋯O hydrogen bonds generate R 2 2(8) ring motifs

    2-Amino-5-bromo­pyridinium hydrogen succinate

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    In the title compound, C5H6BrN2 +·C4H5O4 −, the pyridine N atom of the 2-amino-5-bromo­pyridine mol­ecule is protonated. The protonated N atom and the amino group are linked via N—H⋯O hydrogen bonds to the carboxyl­ate O atoms of the singly deprotonated succinate anion. The hydrogen succinate anions are linked via O—H⋯O hydrogen bonds. A weak inter­molecular C—H⋯O hydrogen bond is also observed

    Modification of MCF-10A Cells with Pioglitazone and Serum-Rich Growth Medium Increases Soluble Factors in the Conditioned Medium, Likely Reducing BT-474 Cell Growth

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    In the present study, we aimed to preincubate MCF-10A cells with pioglitazone and/or serum-rich growth media and to determine adhesive and non-adhesive interactions of the preincubated MCF-10A cells with BT-474 cells. For this purpose, the MCF-10A cells were preincubated with pioglitazone and/or serum-rich growth media, at appropriate concentrations, for 1 week. The MCF-10A cells preincubated with pioglitazone and/or serum-rich growth media were then co-cultured adhesively and non-adhesively with BT-474 cells for another week. Co-culture of BT-474 cells with the preincubated MCF-10A cells, both adhesively and non-adhesively, reduced the growth of the cancer cells. The inhibitory effect of the preincubated MCF-10A cells against the growth of BT-474 cells was likely produced by increasing levels of soluble factors secreted by the preincubated MCF-10A cells into the conditioned medium, as immunoassayed by ELISA. However, only an elevated level of a soluble factor distinguished the conditioned medium collected from the MCF-10A cells preincubated with pioglitazone and serum-rich growth medium than that with pioglitazone alone. This finding was further confirmed by the induction of the soluble factor transcript expression in the preincubated MCF-10A cells, as determined using real-time PCR, for the above phenomenon. Furthermore, modification of the MCF-10A cells through preincubation did not change the morphology of the cells, indicating that the preincubated cells may potentially be injected into mammary fat pads to reduce cancer growth in patients or to be used for others cell-mediated therapy
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