Η Νομισματική Ένωση ως μορφή Ενισχυμένης Συνεργασίας στην Ευρωπαϊκή Ένωση

Αντικείμενο της παρούσας εργασίας αποτελεί η προσέγγιση των μηχανισμών της νομισματικής ένωσης και της ενισχυμένης εργασίας, ως δύο μηχανισμών ικανών να επιφέρουν διαφοροποιημένη ολοκλήρωση στους κόλπους της Ευρωπαϊκής Ένωσης, με σκοπό να εντοπιστούν οι ομοιότητες και οι διαφορές τους. Στο πρώτο μέρος της εργασίας παρουσιάζονται εκτενώς οι ευρεθείσες ομοιότητες των μηχανισμών, διακρίνοντας σε ομοιότητες που αφορούν αφενός το πεδίο εφαρμογής τους και αφετέρου το διαδικαστικό πλαίσιο λήψης αποφάσεων. Στο δεύτερο μέρος αντιστοίχως προσεγγίζονται οι ουσιώδεις διαφορές των μηχανισμών, οι οποίες αν και ολιγάριθμες, κρίνονται θεμελιώδεις και επαρκείς να αποτρέψουν τυχόν σύγχυση των υπό κρίση θεσμών. Η μεθοδολογία που χρησιμοποιήθηκε για την συγγραφή της εργασίας βασίζεται σε διμερές πλάνο, καθένα από τα μέρη της οποίας διαιρείται σε δύο κεφάλαια, τα οποία με την σειρά τους απαρτίζονται από δύο υποκεφάλαια. Σε πρώτο πάντα πεδίο εκτίθενται τα σχετικά με την νομισματική ένωση ευρήματα, ενώ σε δεύτερο ακολουθεί η προσέγγιση του μηχανισμού της ενισχυμένης συνεργασίας. Στην αφετηρία κάθε κεφαλαίου αναπτύσσεται εισαγωγική παράγραφος και κάθε κεφάλαιο φέρει το δικό του αυτοτελές συμπέρασμα. Από την μελέτη της εργασίας προκύπτει σαφώς το συμπέρασμα ότι οι υπό κρίση μηχανισμοί αν και φέρουν σημαντικές ομοιότητες τόσο στα ουσιαστικά όσο και στα διαδικαστικά χαρακτηριστικά τους, παραταύτα δεν δύνανται να ταυτιστούν, καθότι ελλοχεύουν μερικές πολυσήμαντες διαφοροποιήσεις στους μοχλούς ενεργοποίησής τους, αρκετές για να επιφέρουν αρνητικό αποτέλεσμα στην προσπάθεια εξομοίωσής τους.The subject of this dissertation is to touch upon the mechanisms of monetary union and enhanced cooperation, as mechanisms capable of bringing differentiated integration within the European Union in order that their similarities and differences will be identified. In the first part of this dissertation, the similarities of the mechanisms are outlined, distinguishing those between the scope and the procedural decision-making framework. The second part addresses the fundamental differences of the mechanisms, which are considered sufficient to prevent any confusion between the mechanisms in question. The methodology used for the drafting of the dissertation is based on a bilateral plan, consisting of two parts, as explained above, each of which is divided into two chapters, which are composed of two subchapters. In the first place, the findings on monetary union are outlined, followed by the development of enhanced co-operation. In the beginning of each chapter an introductory paragraph is developed and each chapter carries its own independent conclusion. Through the study of the dissertation it becomes evident that the mechanisms in question, although bearing significant similarities, can not be identified, since there are some variations of great value in their levers, which could have a negative effect on any assimilation effort

Adipose Tissue Lipolysis Is Upregulated in Lean and Obese Men During Acute Resistance Exercise

OBJECTIVE—To investigate the effect of acute resistance exercise on adipose tissue triacylglycerol lipase activity (TGLA) in lean and obese men

Recurrent Hypoglycaemia in a Patient with Metastatic Pancreatic Carcinoma

The patient's recurrent hypoglycaemia was found to be due to non-islet cell tumour hypoglycaemia

Isoflavone glycosides: Synthesis and evaluation as α-glucosidase inhibitors

On the basis of the structure of 4′,7,8-trihydroxyisoflavone 7-O-α-D-arabinofuranoside (namely A-76202, 1), a Rhodococcus metabolite showing potent inhibitory activities against the α-glucosidases of rat liver microsome (IC 50 = 0.46 ng/mL), 26 analogs, each with minor variations at the sugar moiety and the isoflavone A and B rings, were readily synthesized. Notably, a new and efficient method was developed for the divergent synthesis of the B-ring congeners of the isoflavone glycosides by using Suzuki-Miyaura coupling as the final step. Modifications at the sugar moiety and the isoflavone A ring significantly diminish the activity, whereas variations at the B ring are largely tolerated for retaining the potent α-glucosidase inhibitory activity. © Wiley-VCH Verlag GmbH & Co. KGaA, 2008.postprin

Disruption of fasting and post-load glucose homeostasis are largely independent and sustained by distinct and early major beta-cell function defects: a cross-sectional and longitudinal analysis of the relationship between insulin sensitivity and cardiovascular risk (RISC) study cohort

Background/aims: Uncertainty still exists on the earliest beta-cell defects at the bases of the type 2 diabetes. We assume that this depends on the inaccurate distinction between fasting and post-load glucose homeostasis and aim at providing a description of major beta-cell functions across the full physiologic spectrum of each condition. Methods: In 1320 non-diabetic individuals we performed an OGTT with insulin secretion modeling and a euglycemic insulin clamp, coupled in subgroups to glucose tracers and IVGTT; 1038 subjects underwent another OGTT after 3.5 years. Post-load glucose homeostasis was defined as mean plasma glucose above fasting levels (δOGTT). The analysis was performed by two-way ANCOVA. Results: Fasting plasma glucose (FPG) and δOGTT were weakly related variables (stβ = 0.12) as were their changes over time (r = −0.08). Disruption of FPG control was associated with an isolated and progressive decline (approaching 60%) of the sensitivity of the beta-cell to glucose values within the normal fasting range. Disruption of post-load glucose control was characterized by a progressive decline (approaching 60%) of the slope of the full beta-cell vs glucose dose-response curve and an early minor (30%) decline of potentiation. The acute dynamic beta-cell responses, neither per se nor in relation to the degree of insulin resistance appeared to play a relevant role in disruption of fasting or post-load homeostasis. Follow-up data qualitatively and quantitatively confirmed the results of the cross-sectional analysis. Conclusion: In normal subjects fasting and post-load glucose homeostasis are largely independent, and their disruption is sustained by different and specific beta-cell defects