Lifeline Australia Inc provides a free 24 hour telephone counselling and referral service to all Australians. The trained telephone counsellors of the service record information on many of their calls in Lifeline's Client Service Management Information System (CSMIS). This paper presents a descriptive summary of a national CSMIS data set, which was compiled during a three month period in 2003. The CSMIS data provided a clear national profile of the callers to the service. The results of this study support the hypothesis that callers are generally seeking social support from the service. The discussion explores the implications of this finding for Lifeline and other generalist counselling and referral services and their capacity to offer suicide intervention to the community.
The effects of cAMP-dependent protein kinase A and protein kinase C on cell-cell communication have been examined in primary ovarian granulosa cells microinjected with purified components of these two regulatory cascades. These cells possess connexin43 (alpha 1)-type gap junctions, and are well-coupled electrotonically and as judged by the cell-to-cell transfer of fluorescent dye. Within 2-3 min after injection of the protein kinase A inhibitor (PKI) communication was sharply reduced or ceased, but resumed in about 3 min with the injection of the protein kinase A catalytic subunit. A similar resumption also occurred in PKI-injected cells after exposure to follicle stimulating hormone. Microinjection of the protein kinase C inhibitor protein caused a transient cessation of communication that spontaneously returned within 15-20 min. Treatment of cells with activators of protein kinase C, TPA or OAG for 60 min caused a significant reduction in communication that could be restored within 2-5 min by the subsequent injection of either the protein kinase C inhibitor or the protein kinase A catalytic subunit. With a longer exposure to either protein kinase C activator communication could not be restored and this appeared to be related to the absence of aggregates of connexin43 in membrane as detected immunologically. In cells injected with alkaline phosphatase communication stopped but returned either spontaneously within 20 min or within 2-3 min of injecting the cell with either the protein kinase A catalytic subunit or with protein kinase C. When untreated cells were injected with protein kinase C communication diminished or ceased within 5 min. Collectively these results demonstrate that cell-cell communication is regulated by both protein kinase A and C, but in a complex interrelated manner, quite likely by multiple phosphorylation of proteins within or regulating connexin-43 containing gap junctions.
SummaryBackground: Paclitaxel-eluting stents inhibit restenosis; however, this technology has drawbacks (e.g., stent thrombosis, requirement for long-term antiplatelet therapy, and cost-particularly for patients with multivessel disease). Systemic treatment with a novel 130-nm, albumin-bound particle form of paclitaxel (nabpaclitaxel) has been shown to reduce restenosis in animals.Hypothesis: This study was designed to establish the safety and optimal dose of systemic nab-paclitaxel for reducing in-stent restenosis in humans. If well tolerated, systemic nab-paclitaxel may be used with any available bare-metal stent and at potentially lower cost than drugeluting stents.Methods: Patients received nab-paclitaxel 10, 30, 70, or 100 mg/m 2 intravenously after stenting of a single de novo lesion 3 mm in diameter. Study endpoints included safety and major adverse cardiac events (MACE) at 2 and 6 months.Results: Data were obtained for all 23 enrolled patients (mean age 66 ± 10 years, 74% men, 26% with diabetes). No significant adverse events (AE) were attributable to nab-paclitaxel at 10 or 30 mg/m 2 . Moderate neutropenia,
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