Robust Stackelberg Equilibria in Extensive-Form Games and Extension to Limited Lookahead

Stackelberg equilibria have become increasingly important as a solution concept in computational game theory, largely inspired by practical problems such as security settings. In practice, however, there is typically uncertainty regarding the model about the opponent. This paper is, to our knowledge, the first to investigate Stackelberg equilibria under uncertainty in extensive-form games, one of the broadest classes of game. We introduce robust Stackelberg equilibria, where the uncertainty is about the opponent's payoffs, as well as ones where the opponent has limited lookahead and the uncertainty is about the opponent's node evaluation function. We develop a new mixed-integer program for the deterministic limited-lookahead setting. We then extend the program to the robust setting for Stackelberg equilibrium under unlimited and under limited lookahead by the opponent. We show that for the specific case of interval uncertainty about the opponent's payoffs (or about the opponent's node evaluations in the case of limited lookahead), robust Stackelberg equilibria can be computed with a mixed-integer program that is of the same asymptotic size as that for the deterministic setting.Comment: Published at AAAI1

Novel Method for Analyzing Crack Growth in Polymeric Microtensile Specimens by In Situ Atomic Force Microscopy

In this paper a micro tensile test which allows the determination and observation of the crack growth behaviour in thin polymer layers is presented. The setup consists of micromanipulators and piezo actuators for straining the sample while an atomic force microscope (AFM) is used for scanning the crack tip area with high lateral resolution. The stress in the specimen is determined by an optical microscope for observation of the deflection of a force sensing beam. The material under investigation is an amorphous and strongly entangled thermoplastic polyimide which can be patterned photolithographically and is spin cast to form layers of 3μm thickness. The results show the potential of the setup to measure crack length, crack tip opening and nominal stress. The stress-crack length-diagram then allows to determine different stages during crack growt

Pengaruh Sosialisasi Perpajakan, Pengetahuan Perpajakan, dan Kualitas Pelayanan terhadap Kepatuhan Wajib Pajak dengan Kesadaran Wajib Pajak sebagai Variabel Intervening (Studi pada Kantor Pelayanan Pajak Pratama Pekanbaru Senapelan)

The purpose of this research are to analyze the influence of taxpayer socialization, taxpayer knowledge, and quality of service to taxpayer compliance, directly or indirectly, by usingtaxpayer awareness as an intervening variable.The sample of this research from of 100 correspondences who are as taxpayers listed in KPP Pratama Pekanbaru Senapelan.The method of sampling using convenience sampling. The data were analysed using the path analysis with SPSS version 19.0. The results of the research showed that the tax socialization did have effect to the tax awareness. Secondly, the tax knowledge did have effect to the tax awareness. Third, quality of service did have effect to the tax awareness.Fourth, the tax socialization did have effect tothe tax compliance. Fifth, the tax knowledge did have effect tothe tax compliance. Sixth, quality of service did have noteffect tothe tax compliance. Seventh, the tax awareness did have effect tothe tax compliance. Eighth, the tax awareness incapable as an intervening variable tax socialization to tax compliance. Ninth, the tax awareness incapable as an intervening variable tax knowledge to tax compliance. Tenth, the tax awareness able as an intervening variable quality of service to tax compliance

Neuroactivational and Behavioral Correlates of Psychosocial Stress-Induced Cocaine Seeking in Rats

A prominent feature of cocaine abuse is a high risk of relapse even despite prolonged periods of abstinence. Psychosocial stress is thought to be a major contributor to the onset of cocaine craving and relapse in human substance abusers, yet most preclinical models of stress-induced relapse employ physical stressors (e.g., unpredictable footshock) or pharmacological stressors (e.g., yohimbine to elicit a drug seeking response) and do not rely upon psychosocial stress per se. Importantly, social stressors are well known to activate distinct neural circuits within the brain as compared to other stressors. It is therefore possible that currently available animal models of stress-induced drug relapse do not fully engage the neuroanatomical, neurochemical, and/or molecular substrates that are recruited specifically by psychosocial stressors to produce drug-seeking behavior. Social defeat stress has been proposed as an ethologically valid psychosocial stressor in rodents that more closely models the forms of psychosocial stress that precede relapse episodes in drug abusers. We previously developed a model of psychosocial stress-induced reinstatement in rats in which cocaine seeking is elicited via exposure to a cue signaling impending social defeat stress. Using this model, we discovered that predilection towards displaying active coping behaviors during prior social defeat stress exposures was positively correlated with levels of psychosocial stress-induced cocaine seeking. The present study aimed to expand upon these initial findings by assessing and comparing patterns of neural activation in key brain areas during stress induced cocaine seeking that is triggered by psychosocial or footshock stress predictive cues

N-acetylaspartate supports the energetic demands of developmental myelination via oligodendroglial aspartoacylase

Breakdown of neuro-glial N-acetyl-aspartate (NAA) metabolism results in the failure of developmental myelination, manifest in the congenital pediatric leukodystrophy Canavan disease caused by mutations to the sole NAA catabolizing enzyme aspartoacylase. Canavan disease is a major point of focus for efforts to define NAA function, with available evidence suggesting NAA serves as an acetyl donor for fatty acid synthesis during myelination. Elevated NAA is a diagnostic hallmark of Canavan disease, which contrasts with a broad spectrum of alternative neurodegenerative contexts in which levels of NAA are inversely proportional to pathological progression. Recently generated data in the nur7 mouse model of Canavan disease suggests loss of aspartoacylase function results in compromised energetic integrity prior to oligodendrocyte death, abnormalities in myelin content, spongiform degeneration, and motor deficit. The present study utilized a next-generation “oligotropic” adeno-associated virus vector (AAV-Olig001) to quantitatively assess the impact of aspartoacylase reconstitution on developmental myelination. AAV-Olig001-aspartoacylase promoted normalization of NAA, increased bioavailable acetyl-CoA, and restored energetic balance within a window of postnatal development preceding gross histopathology and deteriorating motor function. Long-term effects included increased oligodendrocyte numbers, a global increase in myelination, reversal of vacuolation, and rescue of motor function. Effects on brain energy observed following AAV-Olig001-aspartoacylase gene therapy are shown to be consistent with a metabolic profile observed in mild cases of Canavan disease, implicating NAA in the maintenance of energetic integrity during myelination via oligodendroglial aspartoacylase

Performance of laminated contact material Cu—Mo in open air AC low voltage contactors

In the paper performance of laminated contact material Cu—Mo when use in open air ac low voltage contactors is presented and discussed. On the basis of the investigated results conclusions on effective application of such material to replace silver based compositions are formulated.Представлены и обсуждаются эксплуатационные качества слоистого контактного материала Cu—Mo, используемого в низковольтных контакторах на открытом воздухе. По результатам исследований сформулированы рекомендации по эффективному применению такого материала взамен серебросодержащего.Представлено і обговорюються експлуатаційні властивості шаруватого контактного матеріалу Cu—Mo, який використовується в низьковольтних контакторах на відкритому повітрі. За результатами досліджень сформульо-вано рекомендації щодо ефективного застосування такого матеріалу замість срібловміщуючого

Prion-like domain mutations in hnRNPs cause multisystem proteinopathy and ALS

Summary Algorithms designed to identify canonical yeast prions predict that ~250 human proteins, including several RNA-binding proteins associated with neurodegenerative disease, harbor a distinctive prion-like domain (PrLD) enriched in uncharged polar amino acids and glycine. PrLDs in RNA-binding proteins are essential for the assembly of ribonucleoprotein granules. However, the interplay between human PrLD function and disease is not understood. Here, we define pathogenic mutations in PrLDs of hnRNPA2/B1 and hnRNPA1 in families with inherited degeneration affecting muscle, brain, motor neuron and bone, and a case of familial ALS. Wild-type hnRNPA2 and hnRNPA1 display an intrinsic tendency to assemble into self-seeding fibrils, which is exacerbated by the disease mutations. Indeed, the pathogenic mutations strengthen a ‘steric zipper’ motif in the PrLD, which accelerates formation of self-seeding fibrils that cross-seed polymerization of wild-type hnRNP. Importantly, the disease mutations promote excess incorporation of hnRNPA2 and hnRNPA1 into stress granules and drive the formation of cytoplasmic inclusions in animal models that recapitulate the human pathology. Thus, dysregulated polymerization caused by a potent mutant ‘steric zipper’ motif in a PrLD can initiate degenerative disease. Related proteins with PrLDs must be considered candidates for initiating and perhaps propagating proteinopathies of muscle, brain, motor neuron and bone

Networked T Cell Death following Macrophage Infection by Mycobacterium tuberculosis

<div><h3>Background</h3><p>Depletion of T cells following infection by <em>Mycobacterium tuberculosis</em> (Mtb) impairs disease resolution, and interferes with clinical test performance that relies on cell-mediated immunity. A number of mechanisms contribute to this T cell suppression, such as activation-induced death and trafficking of T cells out of the peripheral circulation and into the diseased lungs. The extent to which Mtb infection of human macrophages affects T cell viability however, is not well characterised.</p> <h3>Methodology/Principal Findings</h3><p>We found that lymphopenia (<1.5×10⁹ cells/l) was prevalent among culture-positive tuberculosis patients, and lymphocyte counts significantly improved post-therapy. We previously reported that Mtb-infected human macrophages resulted in death of infected and uninfected bystander macrophages. In the current study, we sought to examine the influence of infected human alveolar macrophages on T cells. We infected primary human alveolar macrophages (the primary host cell for Mtb) or PMA-differentiated THP-1 cells with Mtb H37Ra, then prepared cell-free supernatants. The supernatants of Mtb-infected macrophages caused dose-dependent, caspase-dependent, T cell apoptosis. This toxic effect of infected macrophage secreted factors did not require TNF-α or Fas. The supernatant cytotoxic signal(s) were heat-labile and greater than 50 kDa in molecular size. Although ESAT-6 was toxic to T cells, other Mtb-secreted factors tested did not influence T cell viability; nor did macrophage-free Mtb bacilli or broth from Mtb cultures. Furthermore, supernatants from <em>Mycobacterium bovis</em> Bacille de Calmette et Guerin (BCG)- infected macrophages also elicited T cell death suggesting that ESAT-6 itself, although cytotoxic, was not the principal mediator of T cell death in our system.</p> <h3>Conclusions</h3><p>Mtb-Infected macrophages secrete heat-labile factors that are toxic to T cells, and may contribute to the immunosuppression seen in tuberculosis as well as interfere with microbial eradication in the granuloma.</p> </div

Evaluating the role of pathogenic dementia variants in posterior cortical atrophy

Posterior cortical atrophy (PCA) is an understudied visual impairment syndrome most often due to “posterior Alzheimer's disease (AD)” pathology. Case studies detected mutations in PSEN1, PSEN2, GRN, MAPT, and PRNP in subjects with clinical PCA. To detect the frequency and spectrum of mutations in known dementia genes in PCA, we screened 124 European-American subjects with clinical PCA (n = 67) or posterior AD neuropathology (n = 57) for variants in genes implicated in AD, frontotemporal dementia, and prion disease using NeuroX, a customized exome array. Frequencies in PCA of the variants annotated as pathogenic or potentially pathogenic were compared against ∼4300 European-American population controls from the NHLBI Exome Sequencing Project. We identified 2 rare variants not previously reported in PCA, TREM2 Arg47His, and PSEN2 Ser130Leu. No other pathogenic or potentially pathogenic variants were detected in the screened dementia genes. In this first systematic variant screen of a PCA cohort, we report 2 rare mutations in TREM2 and PSEN2, validate our previously reported APOE ε4 association, and demonstrate the utility of NeuroX