Anomalous Transport in Sketched Nanostructures at the LaAlO3/SrTiO3 Interface

The oxide heterostructure LaAlO3/SrTiO3 supports a two-dimensional electron liquid with a variety of competing phases including magnetism, superconductivity and weak antilocalization due to Rashba spin-orbit coupling. Further confinement of this 2D electron liquid to the quasi-one-dimensional regime can provide insight into the underlying physics of this system and reveal new behavior. Here we describe magnetotransport experiments on narrow LaAlO3/SrTiO3 structures created by a conductive atomic force microscope lithography technique. Four-terminal local transport measurements on ~10-nm-wide Hall bar structures yield longitudinal resistances that are comparable to the resistance quantum h/e2 and independent of the channel length. Large nonlocal resistances (as large as 10^4 ohms) are observed in some but not all structures with separations between current and voltage that are large compared to the 2D mean-free path. The nonlocal transport is strongly suppressed by the onset of superconductivity below ~200 mK. The origin of these anomalous transport signatures is not understood, but may arise from coherent transport defined by strong spin-orbit coupling and/or magnetic interactions

Polyclonal B Cell Differentiation and Loss of Gastrointestinal Tract Germinal Centers in the Earliest Stages of HIV-1 Infection

BACKGROUND: The antibody response to HIV-1 does not appear in the plasma until approximately 2–5 weeks after transmission, and neutralizing antibodies to autologous HIV-1 generally do not become detectable until 12 weeks or more after transmission. Moreover, levels of HIV-1–specific antibodies decline on antiretroviral treatment. The mechanisms of this delay in the appearance of anti-HIV-1 antibodies and of their subsequent rapid decline are not known. While the effect of HIV-1 on depletion of gut CD4(+) T cells in acute HIV-1 infection is well described, we studied blood and tissue B cells soon after infection to determine the effect of early HIV-1 on these cells. METHODS AND FINDINGS: In human participants, we analyzed B cells in blood as early as 17 days after HIV-1 infection, and in terminal ileum inductive and effector microenvironments beginning at 47 days after infection. We found that HIV-1 infection rapidly induced polyclonal activation and terminal differentiation of B cells in blood and in gut-associated lymphoid tissue (GALT) B cells. The specificities of antibodies produced by GALT memory B cells in acute HIV-1 infection (AHI) included not only HIV-1–specific antibodies, but also influenza-specific and autoreactive antibodies, indicating very early onset of HIV-1–induced polyclonal B cell activation. Follicular damage or germinal center loss in terminal ileum Peyer's patches was seen with 88% of follicles exhibiting B or T cell apoptosis and follicular lysis. CONCLUSIONS: Early induction of polyclonal B cell differentiation, coupled with follicular damage and germinal center loss soon after HIV-1 infection, may explain both the high rate of decline in HIV-1–induced antibody responses and the delay in plasma antibody responses to HIV-1. Please see later in the article for Editors' Summar