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Current methods for solving games embody a form of "procedural rationality" that invites logical analysis in its own right. This paper is a brief case study of Backward Induction for extensive games, replacing earlier static logical definitions by stepwise dynamic ones. We consider a number of analysis from recent years that look different conceptually, and find that they are all mathematically equivalent. This shows how an abstract logical perspective can bring out basic invariant structure in games. We then generalize this to an exploration of fixed-point logics on finite trees that best fit game-theoretic equilibria. We end with some open questions that suggest a broader program for merging current computational logics with notions and results from game theory. This paper is largely a program for opening up an area: an extended version of the technical results will be found in the forthcoming dissertation [26]. [ABSTRACT FROM AUTHOR]

Abstract: Current dynamic epistemic logics for analyzing effects of informational events often become cumbersome and opaque when common knowledge is added for groups of agents. Still, postconditions involving common knowledge are essential to successful multi-agent communication. We propose new systems that extend the epistemic base language with a new notion of ‘relativized common knowledge’, in such a way that the resulting full dynamic logic of information flow allows for a compositional analysis of all epistemic postconditions via perspicuous ‘reduction axioms’. We also show how such systems can deal with factual alteration, rather than just information change, making them cover a much wider range of realistic events. After a warm-up stage of analyzing logics for public announcements, our main technical results are expressivity and completeness theorems for a much richer logic that we call LCC. This is a dynamic epistemic logic whose static base is propositional dynamic logic (PDL), interpreted epistemically. This system is capable of expressing all model-shifting operations with finite action models, while providing a compositional analysis for a wide range of informational events. This makes LCC a serious candidate for a standard in dynamic epistemic logic, as we illustrate by analyzing some complex communication scenarios, including sending successive emails with both ‘cc’ and ‘bcc’ lines, and other private announcements to subgroups. Our proofs involve standard modal techniques, combined with a new application of Kleene’s Theorem on finite automata, as well as new Ehrenfeucht games of model comparison. [Copyright &y& Elsevier]

Discusses various concept related to logic. Discussion about verificationism and the Fitch paradox; Logic of learning; Puzzle of knowledge and ignorance.

• New Strategy in genotoxicology has been proposed (Adverse Outcome Pathway (AOP)). • Germ cells classification use in genotoxicology under Global Harmonized System (GHS) should re-discussed. • Quantitative genotoxicity, a new approach to assess risk assessment. The tests used and the general principles behind test strategies are now often over 30 years old. It may be time by now, given that our knowledge of genetic toxicology has improved and that we also technically are better able to investigate DNA damage making use of modern molecular biological techniques, to start thinking on a new test strategy. In the present paper, it is discussed that the time is there to consider a new approach for genotoxicity assessment of substances. A fit for all test strategy was discussed making use of the most recent technological methods and techniques. It was also indicated that in silico tools should be more accepted by regulatory institutes/bodies as supporting information to better conclude which tests should be required for each separate substance to demonstrate its genotoxic potency. Next to that there should be a good rationale for performing in vivo studies. Finally, the need for germ cell genotoxicity testing, essential when classification and labeling of substances is mandatory, was discussed. It was suggested to change the GHS for genotoxicity classification and labelling from in vivo tests in germ cells into in vivo tests in somatic cells. Quantitative genotoxicology was also discussed. It appeared that we are currently at a transition, where the science developing to justify carrying out human health risk assessments based on genetic toxicology data sets supported by mechanistic data and exposure data. However, implementation will take time, and acceptance will be supported through the development of numerous case studies. Major remaining questions are: is genetic damage a relevant endpoint in itself, or should the risk assessment be carried out on the apical endpoint of cancer and which genotoxic endpoint should be used to derive the point of departure (PoD) for the human exposure limit? [ABSTRACT FROM AUTHOR]

Recent interest in spintronic applications has necessitated the study of magnetic materials in contact with semiconductor substrates; importantly, the structure and composition of these interfaces can influence both device functionality and the magnetic properties. Nanoscale ferromagnet/semiconductor structures are of particular interest. In this study, the interface structure between a monolayer of ferromagnetic magnetite (Fe3O4) nanoparticles and a GaAs substrate was studied using cross-sectional transmission electron microscopy techniques. It was found that a continuous amorphous oxide interface layer separates the nanoparticles from the GaAs substrate, and that iron diffused into the interface layer forming a compositional gradient. Electron energy-loss near-edge fine structures of the O K absorption edge revealed that the amorphous oxide is composed of c-Fe3O3 directly underneath the Fe3O4 nanoparticles, followed by a solid solution of Ga2O3 and FeO and mostly Ga2O3 when approaching the buckled oxide/substrate interface. Realspace density functional theory calculations of the dynamical form factor confirmed the experimental observations. The implication of the findings on the optimization of these structures for spin injection is discussed. [ABSTRACT FROM AUTHOR]

This workshop reviewed the current science to inform and recommend the best evidence-based approaches on the use of germ cell genotoxicity tests. The workshop questions and key outcomes were as follows. (1) Do genotoxicity and mutagenicity assays in somatic cells predict germ cell effects? Limited data suggest that somatic cell tests detect most germ cell mutagens, but there are strong concerns that dictate caution in drawing conclusions. (2) Should germ cell tests be done, and when? If there is evidence that a chemical or its metabolite(s) will not reach target germ cells or gonadal tissue, it is not necessary to conduct germ cell tests, notwithstanding somatic outcomes. However, it was recommended that negative somatic cell mutagens with clear evidence for gonadal exposure and evidence of toxicity in germ cells could be considered for germ cell mutagenicity testing. For somatic mutagens that are known to reach the gonadal compartments and expose germ cells, the chemical could be assumed to be a germ cell mutagen without further testing. Nevertheless, germ cell mutagenicity testing would be needed for quantitative risk assessment. (3) What new assays should be implemented and how? There is an immediate need for research on the application of whole genome sequencing in heritable mutation analysis in humans and animals, and integration of germ cell assays with somatic cell genotoxicity tests. Focus should be on environmental exposures that can cause de novo mutations, particularly newly recognized types of genomic changes. Mutational events, which may occur by exposure of germ cells during embryonic development, should also be investigated. Finally, where there are indications of germ cell toxicity in repeat dose or reproductive toxicology tests, consideration should be given to leveraging those studies to inform of possible germ cell genotoxicity. [ABSTRACT FROM AUTHOR]

Preconceptional paternal exposures may affect offspring's health, which cannot be explained by mutations in germ cells, but by persistent changes in the regulation of gene expression. Therefore, we investigated whether pre-conceptional paternal exposure to benzo[a]pyrene (B[a]P) could alter the offspring's phenotype. Male C57BL/6 mice were exposed to B[a]P by gavage for 6 weeks, 3x per week, and were crossed with unexposed BALB-c females 6 weeks after the final exposure. The offspring was kept under normal feeding conditions and was sacrificed at 3 weeks of age. Analysis of the liver proteome by 2D-gel electrophoresis and mass spectrometry indicated that proteins involved in mitochondrial function were significantly downregulated in the offspring of exposed fathers. This down-regulation of mitochondrial proteins was paralleled by a reduction in mitochondrial DNA copy number and reduced activity of citrate synthase and b-hydroxyacyl-CoA dehydrogenase, but in male offspring only. Surprisingly, analysis of hepatic mRNA expression revealed a male-specific up-regulation of the genes, whose proteins were downregulated, including Aldh2 and Ogg1. This discrepancy could be related to several selected microRNA (miRNA)'s that regulate the translation of these proteins; miRNA-122, miRNA-129-2-5p, and miRNA-1941 were upregulated in a gender-specific manner. Since mitochondria are thought to be a source of intracellular reactive oxygen species, we additionally assessed oxidatively-induced DNA damage. Both 8-hydroxy-deoxyguanosine and malondialdehyde-dG adduct levels were significantly reduced in male offspring of exposed fathers. In conclusion, we show that paternal exposure to B[a]P can regulate mitochondrial metabolism in offspring, which may have profound implications for our understanding of health and disease risk inherited from fathers. [ABSTRACT FROM AUTHOR]

Abstract: Ultrathin films of nickel deposited onto (100) Si substrates were found to form kinetically constrained multilayered interface structures characterized by structural and compositional gradients. The presence of a native SiO2 on the substrate surface in tandem with thickness-dependent intrinsic stress of the metal film limits the solid-state reaction between Ni and Si. A roughly 6.5nm thick Ni film on top of the native oxide was observed regardless of the initial nominal film thickness of either 5 or 15nm. The thickness of the silicide layer that formed by Ni diffusion into the Si substrate, however, scales with the nominal film thickness. Cross-sectional in situ annealing experiments in the transmission electron microscope elucidate the kinetics of interface transformation towards thermodynamic equilibrium. Two competing mechanisms are active during thermal annealing: thermally activated diffusion of Ni through the native oxide layer and subsequent transformation of the observed compositional gradient into a thick reaction layer of NiSi2 with an epitaxial orientation relationship to the Si substrate; and, secondly, metal film dispersion and subsequent formation of faceted Ni islands on top of the native oxide layer. [Copyright &y& Elsevier]

Abstract: Nanoscratch tests have been conducted at room temperature on M-plane sapphire under a ramp loading condition from 100μN to 200mN along a scratch length of 200μm at a scratch velocity of 1μms−1 using a Berkovich nanoindenter XPS system in scratch mode. Plastic deformation features, including short shaving scratch debris, linear surface features along the scratch groove, pile-up, and fish-bone features, indicating a stick–slip mechanism, and brittle deformation features, i.e. microcracking, chipping and tearing, were observed by optical, scanning electron, and atomic force microscopy. Applying the focused ion beam (FIB) technique, site-specific cross-sectional transmission electron microscopy further revealed nanoscratch-induced deformation behavior. Basal twinning was observed in the region below the scratch. The evolution of plastic deformation mechanisms can be summarized as lattice disorder, dislocation loops, stacking faults, dislocation glide and then basal twin formation. The observed features were rationalized using elastic and residual stress field calculations. [Copyright &y& Elsevier]

Transgenic animal models are powerful tools for developing a more detailed understanding on the roles of specific genes in biological pathways and systems. Applications of these models have been made within the field of toxicology, most notably for the screening of mutagenic and carcinogenic potential and for the characterization of toxic mechanisms of action. It has long been a goal of research toxicologists to use the data from these models to refine hazard identification and characterization to better inform human health risk assessments. This review provides an overview on the applications of transgenic animal models in the assessment of mutagenicity and carcinogenicity, their use as reporter systems, and as tools for understanding the roles of xenobiotic-metabolizing enzymes and biological receptors in the etiology of chemical toxicity. Perspectives are also shared on the future outlook for these models in toxicology and risk assessment and how transgenic technologies are likely to be an integral tool for toxicity testing in the 21st century. [ABSTRACT FROM AUTHOR]

Background: Previously we found that Rad54/Rad54B cells are more sensitive towards mitomycin C (MMC) as compared to wild-type (WT) cells. This difference in sensitivity was absent upon exposure to other clastogens like bleomycin (BLM) and γ-radiation. In order to get further insight into possible underlying mechanisms, gene expression changes in WT and Rad54/Rad54B MEFs (mouse embryonic fibroblasts) after exposure to the clastogens MMC and BLM were investigated. Exposures of these cells to mutagens (N-ac-AAF and ENU) and vehicle were taken as controls. Results: Most exposures resulted in an induction of DNA damage signaling and apoptosis genes and a reduced expression of cell division genes in cells of both genotypes. As expected, responses to N-ac-AAF were very similar in both genotypes. ENU exposure did not lead to significant gene expression changes in cells of both genotypes, presumably due to its short half-life. Gene expression responses to clastogens, however, showed a genotypedependent effect for BLM and MMC. MMC treated Rad54/Rad54B MEFs showed no induction of p53-signaling, DNA damage response and apoptosis as seen for all the other treatments. Conclusion: These data support our finding that different types of clastogens exist and that responses to these types depend on the DNA repair status of the cells. [ABSTRACT FROM AUTHOR]

The successful correction of lens aberrations in scanning transmission electron microscopy has allowed an improvement in resolution by a factor of two in just a few years. The benefits for materials research are far greater than a factor of two might imply, because enhanced resolution also brings enhanced image contrast, and therefore a vast increase in sensitivity to single atoms, both for imaging and electron energy loss spectroscopy. In addition, aberration correction enables simultaneous, aberration-corrected, Z-contrast and phase contrast imaging, and brings a depth resolution at the nanometer level. It becomes possible to focus directly on features at different depths in the specimen thickness, and three-dimensional information can be extracted with single atom sensitivity. In conjunction with density functional and elasticity theory, these advances provide a new level of insight into the atomistic origins of materials properties. Several examples are discussed that illustrate the potential for applications, including the segregation of rare earth elements to grain boundaries in Si3N4 ceramics, the quantitative analysis of strain-induced growth phenomena in semiconductor quantum wells, the explanation of the enhanced thermal stability of La-doped γ-alumina as a catalyst support, and the origin of the remarkable catalytic activity of Au nanoparticles. [ABSTRACT FROM AUTHOR]

Abstract: The synthesis of alternating poly(amide urethane)s 5a–d was performed in three steps using ε-caprolactone, diamines, and diphenyl carbonate as starting materials. The microstructure and nature of the end groups of the poly(amide urethane)s were determined by means of 1H NMR spectroscopy, which reveals an alternating sequence of amide and urethane linkages in a linear chain with hydroxy and phenyl urethane end groups. The molecular weight and polydispersity of the polymers obtained (, ) were determined by means of gel permeation chromatography. The thermal properties determined by means of DSC show that the poly(amide urethane)s 5a–d are semicrystalline materials having one or two endothermic transitions similar to the poly(amide urethane)s 10a–d prepared from ε-caprolactam, amino alcohols, and diphenyl carbonate. Thermogravimetric analysis of poly(amide urethane)s 5a–b shows a single step decomposition, while poly(amide urethane)s 10a–c decompose in two steps indicating that different degradation mechanisms are operating. [Copyright &y& Elsevier]

The nucleotide excision repair (NER) pathway comprises two sub-pathways, transcription coupled repair (TCR) and global genome repair (GGR). To establish the importance of these separate sub-pathways in tumor suppression, we exposed mice deficient for either TCR (Csb), GGR (Xpc) or both (Xpa) to 300ppm 2-acetylaminofluorene (in feed, ad libitum) in a unique comparative exposure experiment. We found that cancer proneness was directly linked to a defect in the GGR pathway of NER as both Xpa and Xpc mice developed significantly more liver tumors upon 2-AAF exposure than wild type or Csb mice. In contrast, a defect in TCR appeared to act tumor suppressive, leading to a lower hepatocellular tumor response in Xpa mice (tumor incidence of 25%) as compared to Xpc mice (53% tumor-bearing mice). The link between deficient GGR and tumor proneness was most pronounced in the liver, but this phenomenon was also found in the urinary bladder. As tumor induction by 2-AAF appeared almost exclusively dependent on a defect in GGR, we examined whether gene mutation induction in the non-transcribed lacZ locus could reliably predict tumor risk. Interestingly, however, short-term 2-AAF exposure induced lacZ mutant levels in Csb mice almost as high as those found in Xpa or Xpc mice. This indicates that lacZ mutant frequencies are not correlated with a specific DNA repair defect and eventual tumor outcome, at least not in the experimental design presented here. [Copyright &y& Elsevier]

Alternating poly(amide urethane)s from #x03B5;-caprolactam, amino alcohols H2N–(CH2)x–OH (x=2–6), and diphenyl carbonate were prepared by polycondensation of α-hydroxy-ω-O-phenylurethanes 4a-e. The degree of oligomerization was adjusted by the conversion. Oligomers with two or three O-phenylurethane end groups and predetermined molecular weight were prepared by polycondensation of the α-hydroxy-ω-O-phenylurethanes 4a-e in the presence of comonomers with O-phenylurethane end groups in a given concentration. In order to prepare oligomers with hydroxyl and carboxyl groups at both chain ends suitable for coupling reactions, chain analogous reactions were performed with amino acids and amino alcohols. The microstructure of the polymers and the nature of end groups was determined by means of 1H NMR spectroscopy and the molecular weights were determined by means of gel permeation chromatography. The poly(amide urethane)s 5a-e prepared are semicrystalline materials with melting points between 150 and 200 °C. [Copyright &y& Elsevier]