Tokamak TCABR: Acquisition system, data analysis, and remote participation using MDSplus

Each plasma physics laboratory has a proprietary scheme to control and data acquisition system. Usually, it is different from one laboratory to another. It means that each laboratory has its own way to control the experiment and retrieving data from the database. Fusion research relies to a great extent on international collaboration and this private system makes it difficult to follow the work remotely. The TCABR data analysis and acquisition system has been upgraded to support a joint research programme using remote participation technologies. The choice of MDSplus (Model Driven System plus) is proved by the fact that it is widely utilized, and the scientists from different institutions may use the same system in different experiments in different tokamaks without the need to know how each system treats its acquisition system and data analysis. Another important point is the fact that the MDSplus has a library system that allows communication between different types of language (JAVA, Fortran, C, C++, Python) and programs such as MATLAB, IDL, OCTAVE. In the case of tokamak TCABR interfaces (object of this paper) between the system already in use and MDSplus were developed, instead of using the MDSplus at all stages, from the control, and data acquisition to the data analysis. This was done in the way to preserve a complex system already in operation and otherwise it would take a long time to migrate. This implementation also allows add new components using the MDSplus fully at all stages. (c) 2012 Elsevier B.V. All rights reserved.

Toll-like receptor 2/MyD88 signaling mediates zymosan-induced joint hypernociception in mice: Participation of TNF-alpha, IL-1 beta and CXCL1/KC

Arthritic pain is a serious health problem that affects a large number of patients. Toll-like receptors (TLRs) activation within the joints has been implicated in pathophysiology of arthritis. However, their role in the genesis of arthritic pain needs to be demonstrated. In the present study, it was addressed the participation of TLR2 and TLR4 and their adaptor molecule MyD88 in the genesis of joint hypernociception (a decrease in the nociceptive threshold) during zymosan-induced arthritis. Zymosan injected in the tibio-tarsal joint induced mechanical hypernociception in C57BL/6 wild type mice that was reduced in TLR2 and MyD88 null mice. On the other hand, zymosan-induced hypernociception was similar in C3H/HePas and C3H/Hej mice (TLR4 mutant mice). Zymosan-induced joint hypernociception was also reduced in TNFR1 null mice and in mice treated with IL-1 receptor antagonist or with an antagonist of CXCR1/2. Moreover, the joint production of TNF-alpha, IL-1 beta and CXCL1/KC by zymosan was dependent on TLR2/MyD88 signaling. Investigating the mechanisms by which TNF-alpha, IL-1 beta and CXCL1/KC mediate joint hypernociception, joint administration of these cytokines produced mechanical hypernociception, and they act in an interdependent manner. In last instance, their hypernociceptive effects were dependent on the production of hypernociceptive mediators, prostaglandins and sympathetic amines. These results indicate that in zymosan-induced experimental arthritis, TLR2/MyD88 is involved in the cascade of events of joint hypernociception through a mechanism dependent on cytokines and chemokines production. Thus, TLR2/MyD88 signaling might be a target for the development of novel drugs to control pain in arthritis. (C) 2011 Elsevier B.V. All rights reserved.