Advanced mobile network monitoring and automated optimization methods

The operation of mobile networks is a complex task with the networks serving a large amount of subscribers with both voice and data services, containing extensive sets of elements, generating extensive amounts of measurement data and being controlled by a large amount of parameters. The objective of this thesis was to ease the operation of mobile networks by introducing advanced monitoring and automated optimization methods. In the monitoring domain the thesis introduced visualization and anomaly detection methods that were applied to detect intrusions, mal-functioning network elements and cluster network elements to do parameter optimization on network-element-cluster level. A key component in the monitoring methods was the Self-Organizing Map. In the automated optimization domain several rule-based Wideband CDMA radio access parameter optimization methods were introduced. The methods tackled automated optimization in areas such as admission control, handover control and mobile base station cell size setting. The results from test usage of the monitoring methods indicated good performance and simulations indicated that the automated optimization methods enable significant improvements in mobile network performance. The presented methods constitute promising feature candidates for the mobile network management system.reviewe

ADVANCED MOBILE NETWORK MONITORING AND AUTOMATED OPTIMIZATION METHODS

This report is downloadable at www.sal.hut.fi/Publications/r-index.html ISBN 951-22-8079-5 ISSN 0782-203

Proghrelin peptides: Desacyl ghrelin is a powerful inhibitor of acylated ghrelin, likely to impair physiological effects of acyl ghrelin but not of obestatin A study of pancreatic polypeptide secretion from mouse islets.

BACKGROUND: Proghrelin, produced by the ghrelin (A-like) cells of the gastric mucosa, gives rise to cleavage products, including desacyl ghrelin, acyl ghrelin and obestatin. The products are thought to be secreted concomitantly. In an earlier study we found acyl ghrelin and obestatin, but not desacyl ghrelin, to suppress the release of hormones from isolated islets of mouse and rat pancreas. RESULTS: Using isolated mouse pancreatic islets to study the suppression of the spontaneous secretion of pancreatic polypeptide (PP) by acyl ghrelin and obestatin, we determined the EC(50) values for the two peptides. For acyl ghrelin it was 2x10(-13)M (ranging from 1.7 to 2.8x10(-13)M), for obestatin it was 10(-13)M (ranging from 0.3 to 1.1x10(-13)M). The Hill coefficient (i.e. the midpoint slope) for the acyl ghrelin dose-response curve was 0.30 (ranging from 0.21 to 0.35); the corresponding value for obestatin was 0.35 (ranging from 0.21 to 0.35). The PP-releasing effect of acyl ghrelin, but not that of obestatin, was counteracted by desacyl ghrelin. The acyl ghrelin dose-response curve was shifted to the right in a parallel manner by increasing concentrations of desacyl ghrelin. A Schild plot was constructed with a slope of 0.78, giving an apparent pA(2) value of 14. CONCLUSIONS: The results favour the view that acyl ghrelin and obestatin suppress spontaneous PP secretion at physiologically relevant concentrations and that they act on separate receptors. However, we conclude also that desacyl ghrelin acts as a competitive, surmountable (and quite potent) inhibitor of acyl ghrelin. In view of the allegedly high circulating concentrations of desacyl ghrelin it is to be expected that the effect of acyl ghrelin - but not that of obestatin - will be impaired, in fact probably severely blunted by desacyl ghrelin, thereby compromising the functional significance of circulating acyl ghrelin. In addition, we suggest that isolated pancreatic islets are well suited for studies of receptors to acyl ghrelin and obestatin, and that suppression of PP secretion represents a convenient way to measure the effect of both these peptides