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Recent Developments on ALICE (Accelerators and Lasers In Combined Experiments) at Daresbury Laboratory
Progress made in ALICE (Accelerators and Lasers In Combined Experiments) commissioning and a summary of the latest experimental results are presented in this paper. After an extensive work on beam loading effects in SC RF linac (booster) and linac cavities conditioning, ALICE can now operate in full energy recovery mode at the bunch charge of 40pC, the beam energy of 30MeV and train lengths of up to 100us. This improved operation of the machine resulted in generation of coherently enhanced broadband THz radiation with the energy of several tens of uJ per pulse and in successful demonstration of the Compton Backscattering x-ray source experiment. The next steps in the ALICE scientific programme are commissioning of the IR FEL and start of the research on the first non-scaling FFAG accelerator EMMA. Results from both projects will be also reported
Selective protection by hsp 70 against cytotoxic drug-, but not Fas-induced T-cell apoptosis
The phenomenon of heat-shock (HS) protection to many cytotoxic insults has previously been described; however, the specific molecular mechanism underlying this HS-mediated protection remains undefined. To gain insight into this protective mechanism, heat-shocked Jurkat T cells were treated with a range of cytotoxic agents. Those against which HS conferred protection (camptothecin and actinomycin D) were compared with agents against which HS showed no protective effect (anti-Fas monoclonal antibody (mAb)). Reactive oxygen species (ROS) production was found to be an event common to apoptosis induced by camptothecin and actinomycin D, whereas Fas-mediated apoptosis was shown to occur via a ROS-independent mechanism. The selective protection observed against these agents was found to be mimicked by pretreatment with antioxidant compounds. Furthermore, this antioxidant protection appears to be occurring downstream of ROS production. Experiments were extended using heat-shock protein (hsp) 70 gene-transfected Jurkat T cells to confirm that the protective effects observed were caused by hsp 70 synthesis rather than any other cellular response to HS. Bcl-2 expression levels were also examined to determine whether any correlation existed between Bcl-2- and hsp 70-mediated protection