The paper reports an experimental study on AC loss characteristics of a YBCO coated tape conductor carrying AC transport current in AC external magnetic field. In the experiment we electrically measured total losses that were transport current losses plus magnetization losses in AC external magnetic fields perpendicular to the tape surfaces. The transport current losses were measured by a four terminal method and the magnetization losses by a method using a pick-up coil. To measure the total losses electrically we need to pay proper attentions to prevent electromagnetic coupling between the sample currents and the external magnetic fields and to suppress inductive voltage in signals from the pick-up coil and voltage taps. The total losses were purely hysteretic for the amplitude of the external field up to 20 mT and the peak transport current up to the critical current. The loss characteristics can be explained by a theory based on the Bean model if the dependence of the critical current on the external magnetic field is taken into consideration.

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Appropriate T cell responses are controlled by strict balance between activatory and inhibitory pathways downstream of TCR. Although mice or humans with impaired TCR signaling develop autoimmunity, the precise molecular mechanisms linking reduced TCR signaling to autoimmunity are not fully understood. Engagement of TCR activates Ca2+ signaling mainly through store-operated Ca2+ entry activated by stromal interaction molecule (Stim) 1 and Stim2. Despite defective T cell activation, mice deficient in both Stim1 and Stim2 in T cells (conditional double knockout [cDKO]) developed lymphoproliferative disorders and skin inflammation with a concomitant increase in serum IgG1 and IgE levels. In cDKO mice, follicular helper T (Tfh) cells were dramatically increased in number, and they produced IL-4 spontaneously. These inflammatory symptoms were abolished by the deletion of IL-4 in cDKO mice. Tfh development and inflammatory symptoms in cDKO mice were abrogated by further deletion of NFAT2 in T cells. These findings suggest that Tfh cells spontaneously developed in the absence of Ca2+ signaling and caused unregulated type 2 responses.