The Role of the Age of Antiquity in the First Years of the Young Modern Greek State (1830-1850)

Egy újonnan létrejött állam ideológiájában milyen szerep jut a múltnak? Mennyire befolyásolja a jelen nyomorúságos állapotát az a tudat, hogy örököse egy dicsőített múltnak, utódja egy világcsodának? Merre tekint az újkori, frissen felszabadult görög egyén? Hogyan magyarazza meg a jelenkornak történelmi létét? És mire építi fel az újra alakult államát? Ezekre a kérdésekre próbálunk választ adni, különös tekintettel arra a szerepre, amelyet az ókori Görögország az újkori görög állam létrejöttében játszott. Hogyan illeszkedett be a kor történelmi útkeresésének folyamatába az ókori Görögország? Azokat a fő véleményeket összegezzük ezzel a történeti korral kapcsolatban, amelyek röviddel a „szakadatlan görög kontinuitás” ideológiai formációjának megfogalmazása előtt uralták a kor szellemi életét. Az ókori és az újkori görögség közötti harmónia feltételezése már a szabadságharc előtt létezett, de Ottó trónra lépésével és a bajor uralom kezdetével egyre nagyobb jelentőségre tett szert. Nem véletlen tehát, hogy Ottó uralkodása idején maga az állam is élénk érdeklődést mutatott az ókori görög kultúra iránt. A fentiek összegzéseként megállapíthatjuk, hogy a bajorok a német nyelvű területeken régóta meglévő, általános ókor iránti érdeklődésükből kiindulva ösztönzik és erősítik a görögöknek a saját ókori múltjuk felé fordulását. Az állam megerősödésével megalakul a Régészeti Hivatal és a Régészeti Társaság, valamint kezdetét veszi a Régészeti Lapok kiadása, továbbá királyi rendeletek sora lát napvilágot az ókori műemlékek megmentése, az ásatások biztosítása, valamint a neoklasszicista építészeti stílus uralkodóvá tétele érdekében. Ezek az intézkedések, valamint a főváros Nafplióból Athénba történő áthelyezése a korszellemet átható, a bajorok által támogatott és felerősített ókorimádattal együtt olyan szellemi hátteret hoztak létre, amelyben „az ókori világ a Görög Királyság jelenjének szerves részévé vált”

Impact of the influenza A(H1N1) 2009 pandemic to the 17-25 year age group and to the students of the Medical School, Aristotle University of Thessaloniki

Introduction: In 2009 a novel A(H1N1) influenza virus emerged and caused a pandemic. The scope of this study was to identify the impact of the pandemic to the 17-25 year age group and to normal University function.Methods: a) Epidemiological data was obtained from the National Influenza Center for northern Greece, regarding the 17-25 age group. b) Absence records from the first semester of 2008-2009 and 2009-2010 were obtained from the School of Medicine, Aristotle University of Thessaloniki and a questionnaire was given to 100 medical students.Results and discussion: a) Two pandemic waves were identified; the first was during weeks 27-35 and the second during weeks 43-52.Of the 4949 examined samples, 1632 were confirmed pandemic H1N1 2009 infections (33%), and 362 (22%) belonged to the 17-25 age group. Of the latest, 53% were male and 47% were female. Most infections belonging to this group were mild, and developed influenza like illness (ILI) symptoms. Only 19% developed pneumonia or other complications and 2 were fatal. 4% was vaccinated against influenza and 2% against S. pneumoniae. Only 7% received Tamiflu treatment. 9% noted a travel history related to their infection. b) The second wave was synchronous with the 1st University Semester. However, no statistical difference between absence levels during 2008-2009 and 2009-2010 was identified and no students had reported ILI symptoms.Conclusively, whereas the 17-25 age group was indeed of the mostly affected from the pandemic, it seems that unexpectedly there was no impact to normal University function

The Histological and Immunohistochemical Aspects of Bile Reflux in Patients with Gastroesophageal Reflux Disease

Introduction. The pathogenesis of GERD is strongly related with mixed acid and bile reflux. Benign and malignant esophageal and gastric lesions have been associated with synergetic activity between those parameters. Bile reflux causes reactive gastropathy evaluated with Bile Reflux Index (BRI). The aim was to investigate if the sequence: bile reflux-intestinal metaplasia-GERD-esophagitis, is associated with apoptotic/oncogenetic disturbances. Materials/Methods. Fifteen asymptomatic subjects and 53 GERD patients underwent gastroscopy with biopsies. The specimens examined histologically and immunohistochemically for p53, Ki-67, Bax, and Bcl-2. Results. Elevated BRI score detected in 47% (25/53) of patients with GERD and in 13% (2/15) of controls (P = 0.02). Severe esophageal lesions were significantly more common in BRI (+) patients (14/25) compared to BRI (−) ones (P = 0.0049). Immunohistochemical analysis did not show associations between BRI score and biomarker expression. Conclusions. Bile reflux gastropathy is associated with GERD severity, but not with oncogene expression or apoptotic discrepancies of the upper GI mucosa

Μελέτη της δομής και λειτουργίας της πρωτεΐνης HURP στη μιτωτική διαίρεση

HURP protein (Hepatoma Up-Regulated protein) is a RanGTP regulated protein, originally identified inXenopus egg extracts, acting in complex with TPX2, XMAP215, Eg5 and Aurora A. HURP isa MAP that localizes to kt-MTs and is required for proper mitotic spindle assembly. HURP interactingpartners in mammalian cells, however, remained unknown.In this study, we describe the identification of a novel partner of HURP, CHD4 (ChromodomainHelicase DNA binding protein 4) a chromatin remodeling ATPase and a catalytic subunit of the NuRD(Nucleosome remodeling and histone Deacetylase) complex that was recently identified as a RanGTPdependentMAP.Our studies, in mammalian cells, showed that during mitosis CHD4 dissociated from mitoticchromosomes and localized to the spindle, indicating a new role of CHD4 in spindle assembly. Tobetter understand the function of CHD4, we performed RNA interference studies. Depletion of CHD4induced defects in spindle assembly and chromosome alignment in early mitosis, leading tochromosome missegregation. Furthermore, loss of CHD4 affected K-fiber stability by reducingsignificantly the quantity of kt-MTs, which are essential for chromosome biorientation and segregation.Upon CHD4 depletion, HURP’s localization was altered, loosing its preference for kt-MTs, indicatingthat CHD4 might regulate HURP’s localization. Finally, from in vitro and in vivo experiments we foundthat CHD4 is associated with the mitotic kinase Aurora A and the MAP TPX2, describing a newcomplex in mammalian cells.Η πρωτεΐνη HURP (Hepatoma Up-Regulated protein) έχει αναγνωριστεί ως παράγονταςσυναρμολόγησης της ατράκτου (SAF) που ρυθμίζεται από τη RanGTP. Αρχικά βρέθηκε σε μιτωτικάεκχυλίσματα αυγών Xenopus laevis, σε σύμπλοκο με τις TPX2, XMAP215, Eg5 και Aurora A. Η HURPπροσδένεται στους μικροσωληνίσκους, εντοπίζεται κυρίως στους μικροσωληνίσκους των κινητοχώρωνκαι είναι απαραίτητη για την σωστή συναρμολόγηση της μιτωτικής ατράκτου. Παρόλο αυτά, πρωτεΐνεςπου αλληλεπιδρούν με τη HURP σε ανθρώπινα κύτταρα παραμένουν άγνωστες.Σε αυτή τη μελέτη περιγράφουμε την αναγνώριση μίας νέας πρωτεΐνης που αλληλεπιδρά με τη HURP,τη CHD4 (Chromodomain Helicase DNA binding protein 4) μία ATPάση της αναδιαμόρφωσης τηςχρωματίνης και καταλυτική υπομονάδα του συμπλόκου αποκετυλασών που ευθύνεται για τηναναδιαμόρφωση του νουκλεοσώματος (Nucleosome remodeling and histone Deacetylase - NuRD).Πρόσφατα η πρωτεΐνη CHD4 αναγνωρίστηκε ως πρωτεΐνη που προσδένεται στους μικροσωληνίσκουςκαι ρυθμίζεται από την RanGTP.Οι μελέτες μας σε ανθρώπινα κύτταρα έδειξαν ότι η CHD4 κατά τη μίτωση απελευθερώνεται από ταμιτωτικά χρωμοσώματα και εντοπίζεται στην άτρακτο, υποδεικνύοντας ένα καινούριο ρόλο της CHD4στη συναρμολόγηση της ατράκτου. Για να κατανοήσουμε τη λειτουργία της CHD4 πραγματοποιήσαμεμελέτες απαλοιφής της CHD4 με την τεχνική της αποσιώπισης γονιδίου με siRNA. Μείωση της CHD4προκαλεί βλάβες στη συναρμολόγηση της μιτωτικής ατράκτου και στη στοίχιση των χρωμοσωμάτωνστις αρχές της μίτωσης, οδηγώντας σε ανώμαλο διαχωρισμό των χρωμοσωμάτων. Επιπλέον, ηαπώλεια της CHD4 επηρρεάζει τη σταθερότητα των K-fibers μειώνοντας σημαντικά την ποσότητα των μικροσωληνίσκων των κινητοχώρων. Μετά την απαλοιφή της CHD4, ο εντοπισμός της HURP βρέθηκενα αλλάζει, χάνοντας την προτίμησή της για τους μικροσωληνίσκους, των κινητοχώρων,υποδεικνύοντας την πιθανή ρύθμιση του εντοπισμού της HURP από την CHD4. Τέλος από in vitro καιin vivo πειράματα, βρήκαμε ότι η CHD4 αλληλεπιδρά με τη μιτωτική κινάση Aurora A και την πρωτεΐνηTPX2 που συνδέεται με μικροσωληνίσκους, δημιουργώντας ένα καινούριο σύμπλοκο σημαντικό για τηλειτουργία της μιτωτικής ατράκτου στα κύτταρα θηλαστικών

An Integrated System for Urban Parks Touring and Management

Urban parks are important recreational spaces of environmental interest for citizens and city visitors. Targeted and attractive promotion of these areas can help develop alternative forms of “green tourism” and increase environmental awareness among citizens, which is particularly important and vital for the future of the planet. New technologies are a key tool for improving the experience of touring urban parks, as they can make the tour much more attractive by highlighting interesting information about the flora and fauna of the park, as well as various other points of interest. This paper presents an integrated system based on augmented reality, artificial intelligence, and data analytics methodologies, comprising both mobile and web applications, focusing on urban parks touring and management, respectively. Through the mobile app for the park visitors, an attractive, interactive touring environment is created which highlights the environmental and historical interest of those areas. At the same time, the web applications for the park managers receive and analyze visitor data to help improve the visitor experience and the overall quality of the park. Finally, the developed integrated system is evaluated to ensure that it meets all user requirements and that its usability and functional components satisfy both groups of potential users, i.e., park visitors and park managers

Neutrophil extracellular traps regulate IL-1 beta-mediated inflammation in familial Mediterranean fever

Objective Inflammatory attacks of familial Mediterranean fever (FMF) are characterised by circulation and influx of high number of polymorphonuclear neutrophils (PMN) in the affected sites and profound therapeutic effect of IL-1 beta inhibitors. We investigated the role of neutrophil extracellular traps (NET) in the pathogenesis of FMF, and their involvement in IL-1 beta production. Methods Blood samples were obtained from six FMF patients during remissions and from three patients during attacks. NET formation and NET components were studied by fluorescence techniques, immunobloting and MPO-DNA complex ELISA. Results PMNs from patients released NETs decorated with IL-1 beta during disease attacks. On the other hand, PMNs from patients during remission were resistant to inflammatory stimuli that induce NET release in PMNs from control subjects. Lower basal autophagy levels were identified in PMNs during remission, while induction of autophagy facilitated NET release, suggesting that autophagy is involved in the regulation of NET release. During the resolution of attacks, inhibition of NET formation by negative feedback mechanism was also observed. The anti-inflammatory agents, colchicine and DNAse I, inhibited IL-1 beta production in PMNs and IL-1 beta activity in NETs, respectively. Conclusions We suggest two additive events for triggering the FMF attack; the production of IL-1 beta by PMNs and its release through NETs. At the same time NETs, homeostatically, downregulate further NETosis, facilitating the resolution of attack. Compensatorly, lower basal autophagy of PMNs may protect from crises by attenuating the release of pro-inflammatory NETs

Prospective study of the incidence and risk factors of postsplenectomy thrombosis of the portal, mesenteric, and splenic veins

Hypothesis: Splenectomy is recognized as a cause of portal, mesenteric, and splenic vein thrombosis. The exact incidence of the complication and its predisposing factors are not known. Design: Prospective observational cohort study. The median follow-up time of the patients was 22.6 months. Setting: University surgical clinic in a teaching hospital Patients: A total of 147 consecutive patients who underwent splenectomy in a 4-year period were enrolled in the study. Interventions: Preoperative and postoperative evaluation included ultrasonography with color Doppler flow imaging of the portal system, results of blood coagulation tests, fibrinogen levels, D-dimer levels, and complete blood counts. Operative sheets were recorded and reviewed. When portal system thrombosis (PST) was diagnosed, a complete control for acquired and congenital thrombophilia disorders was obtained. Main Outcome Measures: Primary end points of the study were the assessment of the incidence of postsplenectomy PST and the identification of risk factors for its occurrence. Results: Portal system thrombosis occurred in 7 (4.79%) of 146 patients who underwent splenectomy. The age, sex, type or length of the operation, and use of preoperative and postoperative thromboprophylaxis with low molecular weight heparin did not prove to be significant factors in the occurrence of PST. Platelet count of more than 650 X 10(3)/mu L and greater spleen weight (> 650 g) was associated with the development of PST (P=.01, P=.03). Normal D-dimer levels on diagnosis of the complication showed a negative predictive value of 98%. Two of the affected patients were diagnosed with thrombophilia disorders. In a median follow-up period of 22.6 months, no other case of PST was recorded. Conclusions: Postsplenectomy PST occurs in approximately 5% of patients. Possible risk factors are thrombocytosis, splenomegaly, and congenital thrombophilia disorders