This paper presents a method based on inverse kinematics with task specification for online human to humanoid motion imitation. We particularly focus on the problem of lifting and placing feet on the floor during the motion, allowing change of support during stepping or locomotion. The approach avoids the use of motion primitives that limit the robot motions to what had been learned. A direct transposition of movements is generated, allowing the robot to move freely in space as the human model does, at a velocity close to the reference one. The approach is validated on the humanoid robot NAO and shows very promising results for the use of online motion imitation.
We present the current status of geo-neutrino measurements and their implications for radiogenic heating in the mantle. Earth models predict di erent levels of radiogenic heating and, therefore, di erent geo-neutrino fluxes from the mantle. Seismic tomography reveals features in the deep mantle possibly correlated with radiogenic heating and causing spatial variations in the mantle geo-neutrino flux at the Earth surface. An ocean-based observatory o ers the greatest sensitivity to the mantle flux and potential for resolving Earth models and mantle features. Refinements to estimates of the geo-neutrino flux from continental crust reduce uncertainty in measurements of the mantle flux, especially measurements from land-based observatories. These refinements enable the resolution of Earth models using the combined measurements from multiple continental observatories.
Existing methods for security risk analysis typically estimate time, cost, or likelihood of success of attack steps. When the threat environment changes, such values have to be updated as well. However, the estimated values reflect both system properties and attacker properties: the time required for an attack step depends on attacker skill as well as the strength of a particular system component. In the TRESPASS project, we propose the separation of attacker and system properties. By doing so, we enable “plug-and-play” attacker profiles: profiles of adversaries that are independent of system properties, and thus can be re- used in the same or different organisation to compare risk in case of different attacker profiles. We demonstrate its application in the framework of attack trees, as well as our new concept of attack navigators.
Consider the question whether a cyber security investment is cost-effective. The result will depend on the expected frequency of attacks. Contrary to what is referred to as threat event frequencies or hazard rates in safety risk management, frequencies of targeted attacks are not independent from system design, due to the strategic behaviour of attackers. Although there are risk assessment methods that deal with strategic attackers, these do not provide expected frequencies as outputs, making it impossible to integrate those in existing (safety) risk management practices. To overcome this problem, we propose to extend the FAIR (Factor Analysis of Information Risk) framework to support malicious, targeted attacks. Our approach is based on (1) a clear separation of system vulnerability and environmental threat event frequencies, and (2) deriving threat event frequencies from attacker resources and attacker strategies rather than estimating them directly, drawing upon work in adversarial risk analysis. This approach constitutes an innovative way to quantify expected attack frequencies as a component of (information) security metrics for investment decisions.
Mutations of spliceosome components are common in myeloid neoplasms. One of the affected genes, PRPF8, encodes the most evolutionarily conserved spliceosomal protein. We identified either recurrent somatic PRPF8 mutations or hemizygous deletions in 15/447 and 24/450 cases, respectively. Fifty percent of PRPF8 mutant and del(17p) cases were found in AML and conveyed poor prognosis. PRPF8 defects correlated with increased myeloblasts and ring sideroblasts in cases without SF3B1 mutations. Knockdown of PRPF8 in K562 and CD34+ primary bone marrow cells increased proliferative capacity. Whole-RNA deep sequencing of primary cells from patients with PRPF8 abnormalities demonstrated consistent missplicing defects. In yeast models, homologous mutations introduced into Prp8 abrogated a block experimentally produced in the second step of the RNA splicing process, suggesting that the mutants have defects in proof-reading functions. In sum, the exploration of clinical and functional consequences suggests that PRPF8 is a novel leukemogenic gene in myeloid neoplasms with a distinct phenotype likely manifested through aberrant splicing.
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