Robust Stochastic Bandit Algorithms under Probabilistic Unbounded Adversarial Attack

The multi-armed bandit formalism has been extensively studied under various attack models, in which an adversary can modify the reward revealed to the player. Previous studies focused on scenarios where the attack value either is bounded at each round or has a vanishing probability of occurrence. These models do not capture powerful adversaries that can catastrophically perturb the revealed reward. This paper investigates the attack model where an adversary attacks with a certain probability at each round, and its attack value can be arbitrary and unbounded if it attacks. Furthermore, the attack value does not necessarily follow a statistical distribution. We propose a novel sample median-based and exploration-aided UCB algorithm (called med-E-UCB) and a median-based $\epsilon$-greedy algorithm (called med-$\epsilon$-greedy). Both of these algorithms are provably robust to the aforementioned attack model. More specifically we show that both algorithms achieve $\mathcal{O}(\log T)$ pseudo-regret (i.e., the optimal regret without attacks). We also provide a high probability guarantee of $\mathcal{O}(\log T)$ regret with respect to random rewards and random occurrence of attacks. These bounds are achieved under arbitrary and unbounded reward perturbation as long as the attack probability does not exceed a certain constant threshold. We provide multiple synthetic simulations of the proposed algorithms to verify these claims and showcase the inability of existing techniques to achieve sublinear regret. We also provide experimental results of the algorithm operating in a cognitive radio setting using multiple software-defined radios.Comment: Published at AAAI'2

Tools for Prescreening the Most Active Sites on Ir and Rh Clusters toward C−H Bond Cleavage of Ethane: NBO Charges and Wiberg Bond Indexes

B3LYP calculations were carried out to study the insertion of iridium (Ir) and rhodium (Rh) clusters into a C−H bond of ethane, which is often the ratelimiting step of the catalytic cycle of oxidative dehydrogenation of ethane. Our previous research on Ir catalysis correlates the diffusivity of the lowest unoccupied molecular orbital of the Ir clusters and the relative activities of the various catalytic sites. The drawback of this research is that the molecular orbital visualization is qualitative rather than quantitative. Therefore, in this study on C−H bond activation by the Ir and Rh clusters, we conducted analyses of natural bond orbital (NBO) charges and Wiberg bond indexes (WBIs), both of which are not only quantitative but also independent of the basis sets. We found strong correlation between the NBO charges, the WBIs, and the relative activities of the various catalytic sites on the Ir and Rh clusters. Analyses of the NBO charges and the WBIs provide a fast and reliable means of prescreening the most active sites on the Ir and Rh clusters and potentially on other similar transition-metal clusters that activate the C−H bonds of ethane and other light alkanes

Genetic Knock-Down of Hdac3 Does Not Modify Disease-Related Phenotypes in a Mouse Model of Huntington's Disease

Huntington's disease (HD) is an autosomal dominant progressive neurodegenerative disorder caused by an expansion of a CAG/polyglutamine repeat for which there are no disease modifying treatments. In recent years, transcriptional dysregulation has emerged as a pathogenic process that appears early in disease progression and has been recapitulated across multiple HD models. Altered histone acetylation has been proposed to underlie this transcriptional dysregulation and histone deacetylase (HDAC) inhibitors, such as suberoylanilide hydroxamic acid (SAHA), have been shown to improve polyglutamine-dependent phenotypes in numerous HD models. However potent pan-HDAC inhibitors such as SAHA display toxic side-effects. To better understand the mechanism underlying this potential therapeutic benefit and to dissociate the beneficial and toxic effects of SAHA, we set out to identify the specific HDAC(s) involved in this process. For this purpose, we are exploring the effect of the genetic reduction of specific HDACs on HD-related phenotypes in the R6/2 mouse model of HD. The study presented here focuses on HDAC3, which, as a class I HDAC, is one of the preferred targets of SAHA and is directly involved in histone deacetylation. To evaluate a potential benefit of Hdac3 genetic reduction in R6/2, we generated a mouse carrying a critical deletion in the Hdac3 gene. We confirmed that the complete knock-out of Hdac3 is embryonic lethal. To test the effects of HDAC3 inhibition, we used Hdac3+/− heterozygotes to reduce nuclear HDAC3 levels in R6/2 mice. We found that Hdac3 knock-down does not ameliorate physiological or behavioural phenotypes and has no effect on molecular changes including dysregulated transcripts. We conclude that HDAC3 should not be considered as the major mediator of the beneficial effect induced by SAHA and other HDAC inhibitors in HD