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We demonstrate chip-level integrated n-type metal–insulator–semiconductor field effect transistors with a sputtered molybdenum disulfide (MoS2) thin channel and titanium nitride top-gate electrode, all defined by optical lithography. The devices successfully exhibit a normally-off operation and the highest off-voltage. This is achieved by the single dielectric layer and forming gas annealing, which reduce the positive fixed charges in aluminum oxide (Al2O3) film and interface trap densities between the MoS2 and Al2O3 films, respectively. These normally-off MISFETs are suitable for internet-of-things edge devices with low energy consumption using two-dimensional materials in the future. [ABSTRACT FROM AUTHOR]

With the increasing fault rate on high-end supercomputers, the topic of fault tolerance has been gathering attention. To cope with this situation, various fault-tolerance techniques are under investigation; these include user-level, algorithm-based fault-tolerance techniques and parallel execution environments that enable jobs to continue following node failure. Even with these techniques, some programs with static load balancing, such as stencil computation, may underperform after a failure recovery. Even when spare nodes are present, they are not always substituted for failed nodes in an effective way. This article considers the questions of how spare nodes should be allocated, how to substitute them for faulty nodes, and how much the communication performance is affected by such a substitution. The third question stems from the modification of the rank mapping by node substitutions, which can incur additional message collisions. In a stencil computation, rank mapping is done in a straightforward way on a Cartesian network without incurring any message collisions. However, once a substitution has occurred, the optimal node-rank mapping may be destroyed. Therefore, these questions must be answered in a way that minimizes the degradation of communication performance. In this article, several spare node allocation and failed node substitution methods will be proposed, analyzed, and compared in terms of communication performance following the substitution. The proposed substitution methods are named sliding methods. The sliding methods are analyzed by using our developed simulation program and evaluated by using the K computer, Blue Gene/Q (BG/Q), and TSUBAME 2.5. It will be shown that when failures occur, the stencil communication performance on the K and BG/Q can be slowed around 10 times depending on the number of node failures. The barrier performance on the K can be cut in half. On BG/Q, barrier performance can be slowed by a factor of 10. Further, it will also be shown that almost no such communication performance degradation can be seen on TSUBAME 2.5. This is because TSUBAME 2.5 has an Infiniband network connected with a FatTree topology, while the K computer and BG/Q have dedicated Cartesian networks. Thus, the communication performance degradation depends on network characteristics. [ABSTRACT FROM AUTHOR]

Background: Kososan, a Kampo (traditional Japanese herbal) medicine, has been used for the therapy of depressive mood in humans. However, evidence for the antidepressant efficacy of kososan and potential mechanisms are lacking. Recently, it has been recognized that stress triggers neuroinflammation and suppresses adult neurogenesis, leading to depression and anxiety. Here, we examined whether kososan extract affected social behavior in mice exposed to chronic social defeat stress (CSDS), an animal model of prolonged psychosocial stress, and neuroinflammation induced by CSDS.Methods: In the CSDS paradigm, C57BL/6J mice were exposed to 10 min of social defeat stress from an aggressive CD-1 mouse for 10 consecutive days (days 1-10). Kososan extract (1.0 g/kg) was administered orally once daily for 12 days (days 1-12). On day 11, the social avoidance test was performed to examine depressive- and anxious-like behaviors. To characterize the impacts of kososan on neuroinflammation and adult neurogenesis, immunochemical analyses and ex vivo microglial stimulation assay with lipopolysaccharide (LPS) were performed on days 13-15.Results: Oral administration of kososan extract alleviated social avoidance, depression- and anxiety-like behaviors, caused by CSDS exposure. CSDS exposure resulted in neuroinflammation, as indicated by the increased accumulation of microglia, the resident immune cells of the brain, and their activation in the hippocampus, which was reversed to normal levels by treatment with kososan extract. Additionally, in ex vivo studies, CSDS exposure potentiated the microglial pro-inflammatory response to a subsequent LPS challenge, an effect that was also blunted by kososan extract treatment. Indeed, the modulatory effect of kososan extract on neuroinflammation appears to be due to a hippocampal increase in an anti-inflammatory phenotype of microglia while sparing an increased pro-inflammatory phenotype of microglia caused by CSDS. Moreover, reduced adult hippocampal neurogenesis in defeated mice was recovered by kososan extract treatment.Conclusions: Our findings suggest that kososan extract prevents a social avoidant behavior in socially defeated mice that is partially mediated by the downregulation of hippocampal neuroinflammation, presumably by the relative increased anti-inflammatory microglia and regulation of adult hippocampal neurogenesis. Our present study also provides novel evidence for the beneficial effects of kososan on depression/anxiety and the possible underlying mechanisms. [ABSTRACT FROM AUTHOR]