No abstract

The ATLAS barrel toroid magnet is a large air-core toroid that provides the magnetic field needed for the ATLAS muon spectrometer. The barrel toroid structure, named warm structure, holds the eight superconducting coils evenly positioned around the beam axis with an outer diameter of 20 m. The warm structure supports not only the coils but also muon detectors, services and access for the ATLAS experiment.The warm structure withstands about 1400 tons of weight and strong magnetic forces. Physics performance of the muon detectors, and the fact that many design aspects of the toroid and of other related sub-system of the ATLAS experiment are intertwined, impose stringent requirements on the warm structure design. Extensive finite element analyses have been carried out to achieve the final design. Manufacturing feasibilities and facilities have been taken into account.This paper gives an overview on the design and manufacturing of the ATLAS Barrel Toroid Warm Structure.Index Terms-Finite element analysis, manufacturing, mechanical engineering.

Altered cytochromes P450 enzymes (CYP) and P-glycoprotein transporter (P-gp) activity may explain variabilities in drug response. In this study, we analyzed four years of phenotypic assessments of CYP/P-gp activities to optimize pharmacotherapy in psychiatry. A low-dose probe cocktail was administered to evaluate CYP1A2, 2B6, 2D6, 2C9, 2C19, 3A4, and P-gp activities using the probe/metabolite concentration ratio in blood or the AUC. A therapeutic adjustment was suggested depending on the phenotyping results. From January 2017 to June 2021, we performed 32 phenotypings, 10 for adverse drug reaction, 6 for non-response, and 16 for both reasons. Depending on the CYP/P-gp evaluated, only 23% to 56% of patients had normal activity. Activity was decreased in up to 57% and increased in up to 60% of cases, depending on the CYP/P-gp evaluated. In 11/32 cases (34%), the therapeutic problem was attributable to the patient’s metabolic profile. In 10/32 cases (31%), phenotyping excluded the metabolic profile as the cause of the therapeutic problem. For all ten individuals for which we had follow-up information, phenotyping allowed us to clearly state or clearly exclude the metabolic profile as a possible cause of therapeutic failure. Among them, seven showed a clinical improvement after dosage adaptation, or drug or pharmacological class switching. Our study confirmed the interest of CYP and P-gp phenotyping for therapeutic optimization in psychiatry.