A Method of Experimentally Probing Transeverse Momentum Dependent Distributions

We calculate the double spin asymmetry A_LL(x, y, z, P_hT) of pi^0 production with the spectator model and the model based on the factorization ansatz. We also calculate the double spin asymmetry for the integration over the range of (x,y,z) for the setups of the experiments of COMPASS, HERMES, and JLab. We find that the results are characteristically dependent on the model used. Therefore, we suggest that the measurements of the double spin asymmetry provides a method of experimentally probing the transeverse momentum dependent distributions.Comment: 10 pages, 31 figure

A gap between hyponormality and subnormality for block Toeplitz operators

AbstractThis paper concerns a gap between hyponormality and subnormality for block Toeplitz operators. We show that there is no gap between 2-hyponormality and subnormality for a certain class of trigonometric block Toeplitz operators (e.g., its co-analytic outer coefficient is invertible). In addition we consider the extremal cases for the hyponormality of trigonometric block Toeplitz operators: in this case, hyponormality and normality coincide

Learning Transferable Adversarial Robust Representations via Multi-view Consistency

Despite the success on few-shot learning problems, most meta-learned models only focus on achieving good performance on clean examples and thus easily break down when given adversarially perturbed samples. While some recent works have shown that a combination of adversarial learning and meta-learning could enhance the robustness of a meta-learner against adversarial attacks, they fail to achieve generalizable adversarial robustness to unseen domains and tasks, which is the ultimate goal of meta-learning. To address this challenge, we propose a novel meta-adversarial multi-view representation learning framework with dual encoders. Specifically, we introduce the discrepancy across the two differently augmented samples of the same data instance by first updating the encoder parameters with them and further imposing a novel label-free adversarial attack to maximize their discrepancy. Then, we maximize the consistency across the views to learn transferable robust representations across domains and tasks. Through experimental validation on multiple benchmarks, we demonstrate the effectiveness of our framework on few-shot learning tasks from unseen domains, achieving over 10\% robust accuracy improvements against previous adversarial meta-learning baselines.Comment: *Equal contribution (Author ordering determined by coin flip). NeurIPS SafetyML workshop 2022, Under revie

Role of G{alpha}12 and G{alpha}13 as Novel Switches for the Activity of Nrf2, a Key Antioxidative Transcription Factor

G{alpha}12 and G{alpha}13 function as molecular regulators responding to extracellular stimuli. NF-E2-related factor 2 (Nrf2) is involved in a protective adaptive response to oxidative stress. This study investigated the regulation of Nrf2 by G{alpha}12 and G{alpha}13. A deficiency of G{alpha}12, but not of G{alpha}13, enhanced Nrf2 activity and target gene transactivation in embryo fibroblasts. In mice, G{alpha}12 knockout activated Nrf2 and thereby facilitated heme catabolism to bilirubin and its glucuronosyl conjugations. An oligonucleotide microarray demonstrated the transactivation of Nrf2 target genes by G{alpha}12 gene knockout. G{alpha}12 deficiency reduced Jun N-terminal protein kinase (JNK)-dependent Nrf2 ubiquitination required for proteasomal degradation, and so did G{alpha}13 deficiency. The absence of G{alpha}12, but not of G{alpha}13, increased protein kinase C {delta} (PKC {delta}) activation and the PKC {delta}-mediated serine phosphorylation of Nrf2. G{alpha}13 gene knockout or knockdown abrogated the Nrf2 phosphorylation induced by G{alpha}12 deficiency, suggesting that relief from G{alpha}12 repression leads to the G{alpha}13-mediated activation of Nrf2. Constitutive activation of G{alpha}13 promoted Nrf2 activity and target gene induction via Rho-mediated PKC {delta} activation, corroborating positive regulation by G{alpha}13. In summary, G{alpha}12 and G{alpha}13 transmit a JNK-dependent signal for Nrf2 ubiquitination, whereas G{alpha}13 regulates Rho-PKC {delta}-mediated Nrf2 phosphorylation, which is negatively balanced by G{alpha}12