Co-morbid PD accounted for many of the associations of adolescent Axis I disorder with physical health over the ensuing two decades. Co-morbid adolescent Axis I disorder and PD represent a particularly high risk for physical health.

Aims/hypothesis Islet amyloid, formed by aggregation of human islet amyloid polypeptide (hIAPP), is associated with beta cell death in type 2 diabetes as well as in cultured and transplanted human islets. Impaired prohIAPP processing due to beta cell dysfunction is implicated in hIAPP aggregation. We examined whether the glucagon-like peptide-1 receptor (GLP-1R) agonist exenatide can restore impaired prohIAPP processing and reduce hIAPP aggregation in cultured human islets and preserve beta cell function/mass during culture conditions used in clinical islet transplantation. Methods Isolated human islets (n010 donors) were cultured with or without exenatide in normal or elevated glucose for 2 or 7 days. Beta cell apoptosis, proliferation, mass, function, cJUN N-terminal kinase (JNK) and protein kinase B (PKB) activation and amyloid formation were assessed. ProhIAPP, its intermediates and mature hIAPP were detected. Results Exenatide-treated islets had markedly lower JNK and caspase-3 activation and beta cell apoptosis, resulting in higher beta/alpha cell ratio and beta cell area than nontreated cultured islets. Exenatide improved beta cell function, manifested as higher insulin response to glucose and insulin content, compared with non-treated cultured islets. Phospho-PKB immunoreactivity was detectable in exenatide-treated but not untreated cultured islets. Islet culture caused impaired prohIAPP processing with decreased mature hIAPP and increased NH 2 -terminally unprocessed prohIAPP levels resulting in higher release of immature hIAPP. Exenatide restored prohIAPP processing and reduced hIAPP aggregation in cultured islets. Conclusions/interpretation Exenatide treatment enhances survival and function of cultured human islets and restores impaired prohIAPP processing in normal and elevated glucose conditions thereby reducing hIAPP aggregation. GLP-1R agonists may preserve beta cells in conditions associated with islet amyloid formation.

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Recent advances in signal processing techniques have enabled wireless networks to have multi-packet reception (MPR) capability at the physical layer, where it is possible to receive more than one packets when concurrent transmissions occur. In this paper, we propose a novel multi-reservation multiple access (MRMA) scheme for future wireless multimedia networks based on such an MPR channel model. MRMA can fully exploit the channel's MPR capacity while fulfilling the quality of service requirements of different multimedia traffic. Similar to many existing reservation protocols, MRMA guarantees (i) bounded access delay for real-time traffic by dropping packets not transmitted within the required delay bound, and (ii) satisfaction of the required packet loss ratio when applied in conjunction with a connection admission control method to limit the number of admitted traffic streams. MRMA further incorporates a priority control mechanism to differentiate guaranteed and besteffort services for real-time voice/video and connectionless data, respectively. Analytical and simulation results are presented to illustrate the effectiveness of MRMA in service differentiation and increasing the number of admitted traffic streams.