EdgeAP: Enabling Edge Computing on Wireless Access Points

With the rise of the Internet of Things (IoT) leading to an explosion in the number of internet-connected devices, the current cloud computing paradigm is approaching its limits. Moving data back and forth between its origin and a far-away data center leads to issues regarding privacy, latency, and energy consumption. Edge computing, which instead processes data as close to its origin as possible, oers a promising solution to the pitfalls of cloud computing. Our proof-of-concept edge computing platform, EdgeAP, is a programmable platform for the delivery of applications on wireless access points. Use cases of the platform will be demonstrated via an example application. Additionally, the viability of edge computing on wireless access points will be thoroughly evaluated

Novel Pharmacologic Targeting of Tight Junctions and Focal Adhesions in Prostate Cancer Cells

Cancer cell resistance to anoikis driven by aberrant signaling sustained by the tumor microenvironment confers high invasive potential and therapeutic resistance. We recently generated a novel lead quinazoline-based Doxazosin® derivative, DZ-50, which impairs tumor growth and metastasis via anoikis. Genome-wide analysis in the human prostate cancer cell line DU-145 identified primary downregulated targets of DZ-50, including genes involved in focal adhesion integrity (fibronectin, integrin-α6 and talin), tight junction formation (claudin-11) as well as insulin growth factor binding protein 3 (IGFBP-3) and the angiogenesis modulator thrombospondin 1 (TSP-1). Confocal microscopy demonstrated structural disruption of both focal adhesions and tight junctions by the downregulation of these gene targets, resulting in decreased cell survival, migration and adhesion to extracellular matrix (ECM) components in two androgen-independent human prostate cancer cell lines, PC-3 and DU-145. Stabilization of cell-ECM interactions by overexpression of talin-1 and/or exposing cells to a fibronectin-rich environment mitigated the effect of DZ-50. Loss of expression of the intracellular focal adhesion signaling effectors talin-1 and integrin linked kinase (ILK) sensitized human prostate cancer to anoikis. Our findings suggest that DZ-50 exerts its antitumor effect by targeting the key functional intercellular interactions, focal adhesions and tight junctions, supporting the therapeutic significance of this agent for the treatment of advanced prostate cancer

Beta 1, Beta 2 and Beta 3 Adrenergic Receptor Gene Polymorphisms in a Southeastern European Population

Genetic polymorphisms in β1-, β2- and β3-adrenergic receptors (β-ARs) have been associated with chronic non-communicable disorders, such as cardiovascular diseases, asthma, chronic obstructive pulmonary disease (COPD) and obesity, as well as β-agonists and antagonists response and toxicity. The purpose of this study was to determine the frequency distribution of ADRB1 genetic variants Ser49Gly and Arg389Gly, ADRB2 variants Gly16Arg and Gln27Glu, ADRB3 variant Trp64Arg in a Southeastern European Caucasian (SEC) population sample and to establish a comparison with existing data from other human populations. A sample of 431 men and 590 women volunteered to participate in this genotyping analysis after anonymization and de-identification. Real Time PCR (Melting Curve Analysis) followed DNA extraction from buccal swabs and statistical analysis of the results was performed. The allele frequencies in the SEC population were Ser49 (90.3%), Arg389 (69.49%), Gly16 (61.61%), Gln27 (65.72%), and Trp64 (94.52%), while a Hardy-Weinberg Equilibrium (HWE) was detected in the population studied. Comparisons for the Ser49Gly, Gln27Glu, and Trp64Arg allele distributions demonstrated significant differences between SEC and the European group. European subgroups comparisons showed that allele distributions were similar for four of the five SNPs between SEC and Southwestern European Caucasians (SWC), while they were quite distinct from the Northwestern European Caucasians (NWC). These data underline the importance of interethnic variability of β-ARs genetic polymorphisms

Sorafenib decreases proliferation and induces apoptosis of prostate cancer cells by inhibition of the androgen receptor and Akt signaling pathways

Antihormonal and chemotherapy are standard treatments for nonorgan-confined prostate cancer. The effectivity of these therapies is limited and the development of alternative approaches is necessary. In the present study, we report on the use of the multikinase inhibitor sorafenib in a panel of prostate cancer cell lines and their derivatives which mimic endocrine and chemotherapy resistance. 3H-thymidine incorporation assays revealed that sorafenib causes a dose-dependent inhibition of proliferation of all cell lines associated with downregulation of cyclin-dependent kinase 2 and cyclin D1 expression. Apoptosis was induced at 2 μM of sorafenib in androgen-sensitive cells, whereas a higher dose of the drug was needed in castration-resistant cell lines. Sorafenib stimulated apoptosis in prostate cancer cell lines through downregulation of myeloid cell leukemia-1 (MCL-1) expression and Akt phosphorylation. Although concentrations of sorafenib required for the antitumor effect in therapy-resistant sublines were higher than those needed in parental cells, the drug showed efficacy in cells which became resistant to bicalutamide and docetaxel respectively. Most interestingly, we show that sorafenib has an inhibitory effect on androgen receptor (AR) and prostate-specific antigen expression. In cells in which AR expression was downregulated by short interfering RNA, the treatment with sorafenib increased apoptosis in an additive manner. In summary, the results of the present study indicate that there is a potential to use sorafenib in prostate cancers as an adjuvant therapy option to current androgen ablation treatments, but also in progressed prostate cancers that become unresponsive to standard therapies

The mechanical response of talin

Talin, a force-bearing cytoplasmic adapter essential for integrin-mediated cell adhesion, links the actin cytoskeleton to integrin-based cell–extracellular matrix adhesions at the plasma membrane. Its C-terminal rod domain, which contains 13 helical bundles, plays important roles in mechanosensing during cell adhesion and spreading. However, how the structural stability and transition kinetics of the 13 helical bundles of talin are utilized in the diverse talin-dependent mechanosensing processes remains poorly understood. Here we report the force-dependent unfolding and refolding kinetics of all talin rod domains. Using experimentally determined kinetics parameters, we determined the dynamics of force fluctuation during stretching of talin under physiologically relevant pulling speeds and experimentally measured extension fluctuation trajectories. Our results reveal that force-dependent stochastic unfolding and refolding of talin rod domains make talin a very effective force buffer that sets a physiological force range of only a few pNs in the talin-mediated force transmission pathway

Talin2-mediated traction force drives matrix degradation and cell invasion

Talin binds to ?-integrin tails to activate integrins, regulating cell migration, invasion and metastasis. There are two talin genes, TLN1 and TLN2, encoding talin1 and talin2, respectively. Talin1 regulates focal adhesion dynamics, cell migration and invasion, whereas the biological function of talin2 is not clear and, indeed, talin2 has been presumed to function redundantly with talin1. Here, we show that talin2 has a much stronger binding to ?-integrin tails than talin1. Replacement of talin2 Ser339 with Cys significantly decreased its binding to ?1-integrin tails to a level comparable to that of talin1. Talin2 localizes at invadopodia and is indispensable for the generation of traction force and invadopodium-mediated matrix degradation. Ablation of talin2 suppressed traction force generation and invadopodia formation, which were restored by re-expressing talin2 but not talin1. Furthermore, re-expression of wild-type talin2 (but not talin2S339C) in talin2-depleted cells rescued development of traction force and invadopodia. These results suggest that a strong interaction of talin2 with integrins is required to generate traction, which in turn drives invadopodium-mediated matrix degradation, which is key to cancer cell invasion

A method to improve mobile terminal positioning accuracy by exploiting historical data

Mobile terminal positioning and tracking has attracted the interest of mobile communications industry as it enables the provision of a wide variety of commercial applications and emergency services. This dissertation deals with the issue of improving the accuracy of existing terminal positioning techniques allowing at the same time the tracking of mobile terminals. The proposed innovative method called STAMP (Statistical Terminal Assisted Mobile Positioning) relies on the terminals’ ability to measure, collect and store a set of location related network parameters while in idle mode operation. At the initiation phase of a Location Based Service (LBS) the whole set of stored data (that corresponds to the current and previous positions) is statistically processed so as to increase the accuracy of the terminal position estimation. Part of the research focuses on the functional operation of the method and the definition of the architecture that enables its implementation (at both the terminal and network side) based on various factors such as the applicability to existing networks, terminals and positioning techniques as well as its expandability. At the same time, the design parameters, which affect the performance of the method when applied to positioning techniques that are based on signal strength measurements, are identified and analysed. The performance of the suggested method is analysed through simulations while its efficiency is demonstrated through experiments in a commercial GSM network for the Enhanced Cell Global Identity technique. The proposed method provides significant improvement in the positioning accuracy (while at the same time reduces the positioning error variance) and allows the tracking of mobile terminals. The deployment costs of STAMP are considered reasonable as it requires only additional software at the terminal and the network side, while it is applicable to every existing mobile positioning technique and every wireless access network.Η διδακτορική διατριβή επικεντρώνεται στο γενικότερο πρόβλημα του προσδιορισμού της θέσης ενός κινητού τερματικού. Πιο συγκεκριμένα προτείνεται και αναλύεται μια καινοτόμος μέθοδος με το όνομα STAMP (Statistical Terminal Assisted Mobile Positioning), η οποία στοχεύει στην αύξηση της ακρίβειας προσδιορισμού (με ταυτόχρονη μείωση της μεταβλητότητας του σφάλματος) που επιτυγχάνουν οι διαθέσιμες τεχνικές που εφαρμόζονται στα δίκτυα κινητών επικοινωνιών καθώς και την εκτίμηση της τροχιάς κίνησης κινητών τερματικών. Η μέθοδος που προτείνεται αξιοποιεί την ικανότητα του τερματικού να συλλέγει τις κατάλληλες μετρήσεις δικτύου στο οποίο είναι συνδεδεμένο (τις οποίες λαμβάνει συνεχώς ως μέρος της τυπικής του λειτουργίας) όταν βρίσκεται σε κατάσταση ηρεμίας. Στην περίπτωση έναρξης μιας Υπηρεσίας Θέσης, όταν δηλαδή ζητηθεί το στίγμα του τερματικού από μια εφαρμογή, τα δεδομένα (αλληλουχία μετρήσεων) που έχουν συλλεχθεί αποστέλλονται στον εξυπηρετητή προσδιορισμού θέσης, όπου και υφίστανται στατιστική επεξεργασία. Μέρος της έρευνας εστιάζεται στο μηχανισμό λειτουργίας και στον καθορισμό της αρχιτεκτονικής υλοποίησης της μεθόδου που υπαγορεύεται από παράγοντες όπως η εφαρμοσιμότητα της σε διαφορετικά δίκτυα, τερματικές συσκευές και σε πολλαπλές τεχνικές εντοπισμού, η ευκολία υλοποίησης και η επεκτασιμότητα της. Συγχρόνως, αναγνωρίζονται και αναλύονται οι σχεδιαστικές παράμετροι που επηρεάζουν την επίδοση της μεθόδου ενώ αναλύεται η επάρκεια της για τεχνικές που στηρίζονται στη λαμβανόμενη στάθμη σήματος. Όπως αποδεικνύεται με βάση εξομοιώσεις αλλά και πειραματικά δεδομένα από εμπορικό δίκτυο GSM, η προτεινόμενη μέθοδος οδηγεί σε πολύ αισιόδοξα αποτελέσματα, κυρίως ως προς την αύξηση της μέσης ακρίβειας προσδιορισμού της θέσης για τερματικά που βρίσκονται σε κίνηση. Στην περίπτωση ακίνητων τερματικών η μέθοδος STAMP βοηθάει κυρίως στην μείωση της μεταβλητότητας του σφάλματος. Το κόστος υλοποίησης της μεθόδου είναι οριακό καθώς δεν απαιτεί επιπρόσθετο εξοπλισμό παρά μόνο λογισμικό στο τερματικό και στο δίκτυο ενώ δύναται να εφαρμοστεί σε οποιαδήποτε τεχνική εντοπισμού ή δίκτυο κινητών επικοινωνιών