Mobility: a double-edged sword for HSPA networks

This paper presents an empirical study on the performance of mobile High Speed Packet Access (HSPA, a 3.5G cellular standard) networks in Hong Kong via extensive field tests. Our study, from the viewpoint of end users, covers virtually all possible mobile scenarios in urban areas, including subways, trains, off-shore ferries and city buses. We have confirmed that mobility has largely negative impacts on the performance of HSPA networks, as fast-changing wireless environment causes serious service deterioration or even interruption. Meanwhile our field experiment results have shown unexpected new findings and thereby exposed new features of the mobile HSPA networks, which contradict commonly held views. We surprisingly find out that mobility can improve fairness of bandwidth sharing among users and traffic flows. Also the triggering and final results of handoffs in mobile HSPA networks are unpredictable and often inappropriate, thus calling for fast reacting fallover mechanisms. We have conducted in-depth research to furnish detailed analysis and explanations to what we have observed. We conclude that mobility is a double-edged sword for HSPA networks. To the best of our knowledge, this is the first public report on a large scale empirical study on the performance of commercial mobile HSPA networks

Local anaesthetic bupivacaine induced ovarian and prostate cancer apoptotic cell death and underlying mechanisms in vitro

Retrospective studies indicate that the use of regional anesthesia can reduce cancer recurrence after surgery which could be due to ranging from immune function preservation to direct molecular mechanisms. This study was to investigate the effects of bupivacaine on ovarian and prostate cancer cell biology and the underlying molecular mechanisms. Cell viability, proliferation and migration of ovarian carcinoma (SKOV-3) and prostate carcinoma (PC-3) were examined following treatment with bupivacaine. Cleaved caspase 3, 8 and 9, and GSK-3β, pGSK-3β(tyr216) and pGSK-3β(ser9) expression were assessed by immunofluorescence. FAS ligand neutralization, caspase and GSK-3 inhibitors and GSK-3β siRNA were applied to further explore underlying mechanisms. Clinically relevant concentrations of bupivacaine reduced cell viability and inhibited cellular proliferation and migration in both cell lines. Caspase 8 and 9 inhibition generated partial cell death reversal in SKOV-3, whilst only caspase 9 was effective in PC-3. Bupivacaine increased the phosphorylation of GSK-3β(Tyr216) in SKOV-3 but without measurable effect in PC3. GSK-3β inhibition and siRNA gene knockdown decreased bupivacaine induced cell death in SKOV-3 but not in PC3. Our data suggests that bupivacaine has direct ‘anti-cancer’ properties through the activation of intrinsic and extrinsic apoptotic pathways in ovarian cancer but only the intrinsic pathway in prostate cancer