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.

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.

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.