Linear magnetoresistance caused by mobility fluctuations in n-doped Cd(3)As(2).

Cd(3)As(2) is a candidate three-dimensional Dirac semimetal which has exceedingly high mobility and nonsaturating linear magnetoresistance that may be relevant for future practical applications. We report magnetotransport and tunnel diode oscillation measurements on Cd(3)As(2), in magnetic fields up to 65 T and temperatures between 1.5 and 300 K. We find that the nonsaturating linear magnetoresistance persists up to 65 T and it is likely caused by disorder effects, as it scales with the high mobility rather than directly linked to Fermi surface changes even when approaching the quantum limit. From the observed quantum oscillations, we determine the bulk three-dimensional Fermi surface having signatures of Dirac behavior with a nontrivial Berry phase shift, very light effective quasiparticle masses, and clear deviations from the band-structure predictions. In very high fields we also detect signatures of large Zeeman spin splitting (g∼16).

Dichotomy between the Hole and Electron Behavior in Multiband Superconductor FeSe Probed by Ultrahigh Magnetic Fields.

Magnetoresistivity ρ(xx) and Hall resistivity ρ(xy) in ultrahigh magnetic fields up to 88 T are measured down to 0.15 K to clarify the multiband electronic structure in high-quality single crystals of superconducting FeSe. At low temperatures and high fields we observe quantum oscillations in both resistivity and the Hall effect, confirming the multiband Fermi surface with small volumes. We propose a novel approach to identify from magnetotransport measurements the sign of the charge carriers corresponding to a particular cyclotron orbit in a compensated metal. The observed significant differences in the relative amplitudes of the quantum oscillations between the ρ(xx) and ρ(xy) components, together with the positive sign of the high-field ρ(xy), reveal that the largest pocket should correspond to the hole band. The low-field magnetotransport data in the normal state suggest that, in addition to one hole and one almost compensated electron band, the orthorhombic phase of FeSe exhibits an additional tiny electron pocket with a high mobility.

Direct measurement of anergy of antigen-specific T cells following oral tolerance induction.

T cell tolerance induced by oral administration of Ag may be the result of either deletion or functional inactivation of Ag-specific T cells. OVA p(323-339)-specific TCR transgenic (Tg+) lymphocytes were transplanted into BALB/c recipients. Chimeric mice were fed OVA and subsequently challenged with the peptide in CFA. Tolerance was then assessed by measurement of lymph node (LN) cell proliferation in response to the peptide, and deletion was assessed by measuring the frequency Tg+ T cells by flow cytometry. Lymphocytes from chimeric mice fed OVA showed a dose-dependent decline in their proliferative response to the peptide in vitro, compared with immunized control mice that were not fed OVA. Calculation of proliferative potential per Tg+ cell demonstrates that nonresponsiveness due to feeding Ag results in the induction of anergy in the LN. In addition, analysis of intestinal intraepithelial lymphocytes following feeding of OVA did not show evidence of trafficking of LN T cells to the small intestine intraepithelial nor lamina propria compartments.

Elevated expression of Bcl-2 and Bcl-x by intestinal intraepithelial lymphocytes: resistance to apoptosis by glucocorticoids and irradiation.

Administration of glucocorticoids or exposure to ionizing radiation in vivo results in a rapid cell death of thymocytes. We report that murine small intestinal intraepithelial lymphocytes (IEL) are resistant to both steroid- and radiation-induced deletion. This is due to resistance to apoptosis, as evidenced by the absence of detectable apoptotic IEL nuclei in situ after in vivo glucocorticoid treatment. IEL express normal levels of glucocorticoid receptors and these receptors bind [3H]dexamethasone to equivalent levels as other lymphocyte populations. Thus, their survival is due to post-receptor signaling mechanisms. Many IEL express high levels of Bcl-2 and that of these Bcl-2high IEL are largely TCR gamma delta +. Those IEL that do express high levels of Bcl-2 are CD8 alpha + beta - CD4-. In addition, IEL express Bcl-x, another protein shown to be involved in the protection of cells from apoptotic signals. IEL represent the first lymphocyte population in vivo shown to have high levels of expression of both molecules, that otherwise occur only in activated lymphocytes in vitro. These data suggest that the Bcl-2+Bcl-x+ IEL are activated cells and not an effete population of cells necessarily destined to die. Also, the high levels of Bcl-2 and Bcl-x in this in vivo activated population supports the in vitro correlate of protection from activation-induced cell death.