20,204 research outputs found

    Unified Formalism for calculating Polarization, Magnetization, and more in a Periodic Insulator

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    In this paper, we propose a unified formalism, using Green's functions, to integrate out the electrons in an insulator under uniform electromagnetic fields. We derive a perturbative formula for the Green's function in the presence of uniform magnetic or electric fields. Applying the formula, we derive the formula for the polarization, the orbital magnetization, and the orbital magneto-polarizability, without assuming time reversal symmetry. Specifically, we realize that the terms linear in the electric field can only be expressed in terms of the Green's functions in one extra dimension. This observation directly leads to the result that the coefficient of the θ\theta term in any dimensions is given by a Wess-Zumino-Witten-type term, integrated in the extended space, interpolating between the original physical Brillouin zone and a trivial system, with the group element replaced by the Green's function. This generalizes an earlier result for the case of time reversal invariance [see Z. Wang, X.-L. Qi, and S.-C. Zhang, Phys. Rev. Lett. {\bf 105}, 256803 (2010)].Comment: 16 pages, 1 figure. The version accepted by PR

    Threshold Regression for Survival Analysis: Modeling Event Times by a Stochastic Process Reaching a Boundary

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    Many researchers have investigated first hitting times as models for survival data. First hitting times arise naturally in many types of stochastic processes, ranging from Wiener processes to Markov chains. In a survival context, the state of the underlying process represents the strength of an item or the health of an individual. The item fails or the individual experiences a clinical endpoint when the process reaches an adverse threshold state for the first time. The time scale can be calendar time or some other operational measure of degradation or disease progression. In many applications, the process is latent (i.e., unobservable). Threshold regression refers to first-hitting-time models with regression structures that accommodate covariate data. The parameters of the process, threshold state and time scale may depend on the covariates. This paper reviews aspects of this topic and discusses fruitful avenues for future research.Comment: Published at http://dx.doi.org/10.1214/088342306000000330 in the Statistical Science (http://www.imstat.org/sts/) by the Institute of Mathematical Statistics (http://www.imstat.org

    Increased risk for T cell autoreactivity to ß-cell antigens in the mice expressing the Avy obesity-associated gene.

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    There has been considerable debate as to whether obesity can act as an accelerator of type 1 diabetes (T1D). We assessed this possibility using transgenic mice (MIP-TF mice) whose ß-cells express enhanced green fluorescent protein (EGFP). Infecting these mice with EGFP-expressing murine herpes virus-68 (MHV68-EGFP) caused occasional transient elevation in their blood glucose, peri-insulitis, and Th1 responses to EGFP which did not spread to other ß-cell antigens. We hypothesized that obesity-related systemic inflammation and ß-cell stress could exacerbate the MHV68-EGFP-induced ß-cell autoreactivity. We crossed MIP-TF mice with Avy mice which develop obesity and provide models of metabolic disease alongside early stage T2D. Unlike their MIP-TF littermates, MHV68-EGFP-infected Avy/MIP-TF mice developed moderate intra-insulitis and transient hyperglycemia. MHV68-EGFP infection induced a more pronounced intra-insulitis in older, more obese, Avy/MIP-TF mice. Moreover, in MHV68-EGFP-infected Avy/MIP-TF mice, Th1 reactivity spread from EGFP to other ß-cell antigens. Thus, the spreading of autoreactivity among ß-cell antigens corresponded with the transition from peri-insulitis to intra-insulitis and occurred in obese Avy/MIP-TF mice but not lean MIP-TF mice. These observations are consistent with the notion that obesity-associated systemic inflammation and ß-cell stress lowers the threshold necessary for T cell autoreactivity to spread from EGFP to other ß-cell autoantigens
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