Reconsidering urban development: the role of local self-organized groups in urban open green space upgrade

In the city of Thessaloniki, the co-creation of ‘an inclusive city’, which will ‘empower citizens and community-led projects... and enable co- creation in open and public spaces’, appears as one of the four main goals of the Resilience Strategy of the city, ‘Thessaloniki 2030’, published in 2017. Within this frame, and in conjunction with the need of open green spaces that Thessaloniki has, this paper is an attempt to identify and highlight the contribution of design self-organized groups to the upgrade of the urban environment of the city of Thessaloniki. This study focuses on the design team of Ev Zin (Ευ Ζην), an initiative of a group of students from the School of Spatial Planning and Development, Faculty of Engineering, Aristotle University of Thessaloniki, Greece. Aristotle’s University main campus occupies a large area within the city of Thessaloniki. This campus, particularly its various open spaces appear to be in a general degraded state, frequently used for delinquent activities. A group of students decided to act and to focus on the upgrade of the open green spaces of the campus, starting from a specific green space, situated at a focal point/crossroads within the campus. These students formed the Ev Zin group. This paper will be, hence, discussing the conditions that led to the degradation of the campus and the area around it, the formation of this team and its development, but more importantly the efforts of the Ev Zin group towards the upgrading of the campus, as well as the mobilization that these efforts have created, particularly concerning the principal formal stakeholders, mainly the Aristotle University’s authorities and the Attiko Metro authorities, the company constructing the underground stations at the university

Study of the genetic alterations of the thyroid cancer in Greece

The MAP kinase (RAS/RAF/MEK/ERK) signaling pathway is directly implicated in the modulation of the Thyroid cancer. In the present study we investigated the molecular genetics of this signaling pathway in Greek patients with follicular cell origin thyroid carcinoma. In addition, an attempt was made to relate the presence, if any, of genetic alterations with the diagnosis and prognosis of Thyroid cancer. Our material constituted 100 paraffin blocks from the files of the 1st Department of Pathology, Medical School, University of Athens, Greece, as well as, 26 fresh tissues taken directly from thyroid carcinomas. Paraffin sections were prepared from the paraffin blocks, in order to perform DNA extraction and immunohistochemistry. DNA and RNA were also extracted from the fresh tissue. In addition, 13 thyroid cancer cell lines were used comparatively. The presence of the RET/PTC 1,2,3 rearrangements, as well as the presence of BRAF, EGFR, MET and NTRK 1,2,3 mutations was detected with the use of PCR, RT-PCR, Southern Blotting, and Direct Sequencing. The phenotypic evaluation was performed with the immunohistochemical study of phospho-MET, phospho-EGFR, BRAF, MEK, phospho-MEK, ERK, and phospho-ERK. RET/PTC 2,3 rearrangements were detected in 7,7%, were as BRAFV600E mutation in 26,5%. No association was detected between the presence of BRAFV600E mutation and the four parameters studied (age and sex of the patients, the disease stage, and the prognostic groups). In addition, 2 new point mutations (S695G and V834M) (2,9%) and 4 silent mutations (15,9%) were detected in the egfr gene. The study of the met gene revealed only a silent mutation in 84,4%. The immunohistochemical study revealed the expression of BRAF protein in 74%, the expression of phospho-EGFR protein in 24% and the expression of phospho-MET in 55%. An association was observed between the increased expression of phospho-EGFR, phospho-MEK, nuclear phospho-p42/44ERK, and total p42/44ERK and the high disease stage (stages III, IV). The genetic alterations observed in the present study (especially the RET/PTC rearrangements and the BRAFV600E mutation) are detected in quite low levels compared to that observed in other populations. They have not been proven to be the major modus of activation in the Greek population harbouring Thyroid cancer. The need of further study of the molecular genetics of the Thyroid cancer in this population is mandatory.Το μονοπάτι RAS/RAF/MEK/ERK παίζει καταλυτικό ρόλο στη διαμόρφωση του θυλακιοκυτταρικού καρκινώματος. Στην παρούσα μελέτη ερευνήθηκε το σηματοδοτικό αυτό μονοπάτι σε Έλληνες ασθενείς με θυλακιοκυτταρικό θυρεοειδικό καρκίνωμα. Διερευνήθηκε η παρουσία γενετικών αλλοιώσεων και πραγματοποιήθηκε συσχετισμός τους με κλινικοπαθολογοανατομικές παραμέτρους και κατ’ επέκταση με τη διάγνωση και την πρόγνωση. Η μελέτη έγινε σε υλικό εγκλεισμένο σε κύβους παραφίνης, καθώς και σε νωπό υλικό. Έγινε επιλογή 100 περιστατικών θυλακιοκυτταρικών καρκινωμάτων από το αρχείο του Α΄ Εργαστηρίου Παθολογικής Ανατομικής της Ιατρικής Σχολής Αθηνών. Συγχρόνως, έγινε επιλογή φρέσκου ιστού από όγκο 26 ασθενών με θυλακιοκυτταρικό καρκίνωμα θυρεοειδούς. Από το αρχειακό υλικό κοπήκαν τομές για απομόνωση DNA καθώς και για ανοσοϊστοχημεία. Από τον φρέσκο ιστό αφαιρέθηκε τμήμα, από το οποίο πραγματοποιήθηκε απομόνωση DNA και RNA. Επιπλέον, συγκριτικά χρησιμοποιήθηκαν 13 θυλακιοκυτταρικές θυρεοειδικές καρκινικές κυτταρικές σειρές από τις οποίες έγινε επίσης απομόνωση DNA και RNA. Ακολούθησε η ανίχνευση RET/PTC1/2/3 ανασυνδιασμών και μεταλλάξεων στα γονίδια των BRAF, EGFR, MET, και NTRK1,2,3 με τις μοριακές μεθόδους PCR, RT-PCR, Southern Blotting και Direct Sequencing. Η φαινοτυπική μελέτη επικεντρώθηκε στην ανοσοϊστοχημική μελέτη των phospho-MET, phospho-EGFR, BRAF, MEK, phospho-MEK, ERK, και phospho-ERK. Οι ανασυνδυασμοί RET/PTC 2,3 ανιχνεύτηκαν σε ποσοστό 7,7%, ενώ η BRAFV600E σε ποσοστό 26,5%. Δεν παρατηρήθηκε καμία στατιστικά σημαντική σχέση της παρουσίας της V600E με τις κλινικοπαθολογικές παραμέτρους (ηλικία και φύλο ασθενών, στάδιο καρκινώματος και προγνωστικές ομάδες). Επιπλέον, ανιχνεύτηκαν δύο νέες σημειακές μεταλλάξεις (S695G και V834M) (2,9%) και τέσσερις επίσης νέες σιωπηρές μεταλλάξεις (15,9%) στο γονίδιο egfr. Στο γονίδιο met παρατηρήθηκε μόνο μια σιωπηρή μετάλλαξη σε ποσοστό 84,4%. Η ανοσοϊστοχημική μελέτη κατέδειξε έντονη την παρουσία της πρωτεΐνης BRAF (74%), ενώ σε χαμηλότερα ποσοστά ανιχνεύτηκαν οι phospho-EGFR (24%) και phospho-MET (55%). Στατιστικά σημαντική συσχέτιση παρατηρήθηκε ανάμεσα στην αυξημένη έκφραση των phospho-EGFR, phospho-MEK, phospho-p42/44ERK στον πυρήνα, και total p42/44ERK και το υψηλό στάδιο των καρκινωμάτων. Τα ποσοστά των παρατηρούμενων γονιδιακών αλλοιώσεων είναι χαμηλά σε σχέση με άλλους πληθυσμούς, ενώ δεν φαίνεται να αποτελούν το κυρίαρχο χαρακτηριστικό του καρκινώματος αυτού στον Ελληνικό πληθυσμό. Η ανάγκη για περαιτέρω μελέτη είναι εμφανής

The differential effects of inspiratory, expiratory, and combined resistive breathing on healthy lung

Combined resistive breathing (CRB) is the hallmark of obstructive airway disease pathophysiology. We have previously shown that severe inspiratory resistive breathing (IRB) induces acute lung injury in healthy rats. The role of expiratory resistance is unknown. The possibility of a load-dependent type of resistive breathing-induced lung injury also remains elusive. Our aim was to investigate the differential effects of IRB, expiratory resistive breathing (ERB), and CRB on healthy rat lung and establish the lowest loads required to induce injury. Anesthetized tracheostomized rats breathed through a two-way valve. Varying resistances were connected to the inspiratory, expiratory, or both ports, so that the peak inspiratory pressure (IRB) was 20%-40% or peak expiratory (ERB) was 40%-70% of maximum. CRB was assessed in inspiratory/expiratory pressures of 30%/50%, 40%/50%, and 40%/60% of maximum. Quietly breathing animals served as controls. At 6 hours, respiratory system mechanics were measured, and bronchoalveolar lavage was performed for measurement of cell and protein concentration. Lung tissue interleukin-6 and interleukin-1 beta levels were estimated, and a lung injury histological score was determined. ERB produced significant, load-independent neutrophilia, without mechanical or permeability derangements. IRB 30% was the lowest inspiratory load that provoked lung injury. CRB increased tissue elasticity, bronchoalveolar lavage total cell, macrophage and neutrophil counts, protein and cytokine levels, and lung injury score in a dose-dependent manner. In conclusion, CRB load dependently deranges mechanics, increases permeability, and induces inflammation in healthy rats. ERB is a putative inflammatory stimulus for the lung