A simple model based on non-ambipolar radial transport and planar sheath physics is used to describe the generation of radial electric fields and currents in the scape-off layer of the Tokamak de Varennes (TdeV) during divertor plate biasing. In general, the calculated predictions compare favourably with TdeV results over a variety of plasma conditions and divertor magnetic configurations. Validated by the experiment, the model is used to study the scaling laws of perpendicular ion mobility and to test existing related theories. Finally, the model is proposed as a useful tool for the design and upgrade of biased divertors through optimization of the plate and throat geometry.
The most promising concept for deep fuelling a reactor is by the injection of compact toroid (CT) plasmoids. The first results showing CT fuelling of a tokamak plasma, without any adverse perturbation t o the tokamak discharge, are reported. The Compact Toroid Fueller (CTF) device was used to inject a CT-spheromak plasmoid into the TdeV tokamak. Following the CT penetration, the tokamak particle inventory increased by 16%, the loop voltage and the plasma current did not change, and there was no increase in magnetohydrodynamic (MHD) activity. The number of injected impurities was low and dominated by non-metallic elements. The plasma diamagnetic energy and the energy confinement time increased by more than 35%.
Nowadays, pain represents one of the most important societal burdens. Current treatments are, however, too often ineffective and/or accompanied by debilitating unwanted effects for patients dealing with chronic pain. Indeed, the prototypical opioid morphine, as many other strong analgesics, shows harmful unwanted effects including respiratory depression and constipation, and also produces tolerance, physical dependence, and addiction. The urgency to develop novel treatments against pain while minimizing adverse effects is therefore crucial. Over the years, the delta-opioid receptor (DOP) has emerged as a promising target for the development of new pain therapies. Indeed, targeting DOP to treat chronic pain represents a timely alternative to existing drugs, given the weak unwanted effects spectrum of DOP agonists. Here, we review the current knowledge supporting a role for DOP and its agonists for the treatment of pain. More specifically, we will focus on the cellular and subcellular localization of DOP in the nervous system. We will also discuss in further detail the molecular and cellular mechanisms involved in controlling the cellular trafficking of DOP, known to differ significantly from most G protein-coupled receptors. This review article will allow a better understanding of how DOP represents a promising target to develop new treatments for pain management as well as where we stand as of our ability to control its cellular trafficking and cell surface expression.
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