Real-time Motion Generation and Data Augmentation for Grasping Moving Objects with Dynamic Speed and Position Changes

While deep learning enables real robots to perform complex tasks had been difficult to implement in the past, the challenge is the enormous amount of trial-and-error and motion teaching in a real environment. The manipulation of moving objects, due to their dynamic properties, requires learning a wide range of factors such as the object's position, movement speed, and grasping timing. We propose a data augmentation method for enabling a robot to grasp moving objects with different speeds and grasping timings at low cost. Specifically, the robot is taught to grasp an object moving at low speed using teleoperation, and multiple data with different speeds and grasping timings are generated by down-sampling and padding the robot sensor data in the time-series direction. By learning multiple sensor data in a time series, the robot can generate motions while adjusting the grasping timing for unlearned movement speeds and sudden speed changes. We have shown using a real robot that this data augmentation method facilitates learning the relationship between object position and velocity and enables the robot to perform robust grasping motions for unlearned positions and objects with dynamically changing positions and velocities

Suppression of osteoclastogenesis via α2-adrenergic receptors

The sympathetic nervous system is known to regulate osteoclast development. However, the involvement of α2-adrenergic receptors (α2-ARs) in osteoclastogenesis is not well understood. In the present study, their potential role in osteoclastogenesis was investigated. Guanabenz, clonidine and xylazine were used as agonists of α2-ARs, while yohimbine and idazoxan were employed as antagonists. Using RAW264.7 pre-osteoclast and primary bone marrow cells, the mRNA expression of the osteoclast-related genes nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), tartrate-resistant acid phosphatase (TRAP) and cathepsin K was evaluated following induction with receptor activator of nuclear factor κB ligand (RANKL). TRAP staining was also conducted to assess effects on osteoclastogenesis in mouse bone marrow cells in vitro. Administration of 5-20 µM guanabenz (P<0.01, for RANKL-only treatment), 20 µM clonidine (P<0.05, for RANKL-only treatment) and 20 µM xylazine (P<0.05, for RANKL-only treatment) attenuated RANKL-induced upregulation of NFATc1, TRAP and cathepsin K mRNA. Furthermore, the reductions in these mRNAs by 10 µM guanabenz and 20 µM clonidine in the presence of RANKL were attenuated by 20 µM yohimbine or idazoxan (P<0.05). The administration of 5-20 µM guanabenz (P<0.01, for RANKL-only treatment) and 10-20 µM clonidine (P<0.05, for RANKL-only treatment) also decreased the number of TRAP-positive multi-nucleated osteoclasts. Collectively, the present study demonstrates that α2-ARs may be involved in the regulation of osteoclastogenesis

The impact of crystal phase transition on the hardness and structure of kidney stones

The version of record of this article, first published in Urolithiasis, is available online at Publisher’s website: https://doi.org/10.1007/s00240-024-01556-5.Calcium oxalate kidney stones, the most prevalent type of kidney stones, undergo a multi-step process of crystal nucleation, growth, aggregation, and secondary transition. The secondary transition has been rather overlooked, and thus, the effects on the disease and the underlying mechanism remain unclear. Here, we show, by periodic micro-CT images of human kidney stones in an ex vivo incubation experiment, that the growth of porous aggregates of calcium oxalate dihydrate (COD) crystals triggers the hardening of the kidney stones that causes difficulty in lithotripsy of kidney stone disease in the secondary transition. This hardening was caused by the internal nucleation and growth of precise calcium oxalate monohydrate (COM) crystals from isolated urine in which the calcium oxalate concentrations decreased by the growth of COD in closed grain boundaries of COD aggregate kidney stones. Reducing the calcium oxalate concentrations in urine is regarded as a typical approach for avoiding the recurrence. However, our results revealed that the decrease of the concentrations in closed microenvironments conversely promotes the transition of the COD aggregates into hard COM aggregates. We anticipate that the suppression of the secondary transition has the potential to manage the deterioration of kidney stone disease

Evidence for Solution-Mediated Phase Transitions in Kidney Stones: Phase Transition Exacerbates Kidney Stone Disease

Maruyama M., Tanaka Y., Momma K., et al. Evidence for Solution-Mediated Phase Transitions in Kidney Stones: Phase Transition Exacerbates Kidney Stone Disease. Crystal Growth and Design 23, 4285 (2023); https://doi.org/10.1021/acs.cgd.3c00108.In this study, we investigated calcium oxalate (CaOx) kidney stones and showed direct evidence of the solution-mediated phase transition of calcium oxalate dihydrate (COD; the metastable phase) to calcium oxalate monohydrate (COM; the stable phase). We examined the crystal phases, crystal textures, and protein distributions within thin sections of calcium oxalate kidney stones. Observation with a polarized-light microscope showed that the outline of the mosaic texture, in which COM crystals are assembled in a mosaic pattern, roughly coincides with COD’s crystallographically stable face angles. Microfocus X-ray CT measurement captured the intermediate process of the phase transition, starting inside the COD single crystal and gradually transforming to COM crystals. In addition, the distribution of osteopontin and prothrombin fragment-1, common proteins contained in urine and visualized by multicolor fluorescence immunostaining, showed no apparent striations inside the COM single crystals with the mosaic texture, although the striation is apparent inside the COD single crystals. This is probably because the phase transition of mosaic-like COM occurred in a semiclosed system inside the COD single crystal, so the effect of periodic (day-night, seasonal, etc.) urinary protein concentration changes was small. On the other hand, striations were visible in concentrically laminated COM. This indicated that concentrically laminated COM formed in response to the changes in urinary protein concentrations. From the above, we conclude that the COD single crystals and the concentrically laminated COM seen in CaOx stones are primary structures, and the mosaic COM is a secondary structure that is a pseudomorph formed by the solution-mediated phase transition from COD single crystals

A switchable controlled-NOT gate in a spin-chain NMR quantum computer

A method of switching a controlled-NOT gate in a solid-stae NMR quantum computer is presented. Qubits of I=1/2 nuclear spins are placed periodically along a quantum spin chain (1-D antiferromagnet) having a singlet ground state with a finite spin gap to the lowest excited state caused by some quantum effect. Irradiation of a microwave tuned to the spin gap energy excites a packet of triplet magnons at a specific part of the chain where control and target qubits are involved. The packet switches on the Suhl-Nakamura interaction between the qubits, which serves as a controlled NOT gate. The qubit initialization is achieved by a qubit initializer consisting of semiconducting sheets attached to the spin chain, where spin polarizations created by the optical pumping method in the semiconductors are transferred to the spin chain. The scheme allows us to separate the initialization process from the computation, so that one can optimize the computation part without being restricted by the initialization scheme, which provides us with a wide selection of materials for a quantum computer.Comment: 8 pages, 5 figure