University of Tokyo

About: University of Tokyo is a education organization based out in Tokyo, Japan. It is known for research contribution in the topics: Population & Gene. The organization has 134564 authors who have published 337567 publications receiving 10178620 citations. The organization is also known as: Todai & Universitas Tociensis.

Spatial Modulation for Generalized MIMO: Challenges, Opportunities, and Implementation

Abstract: A key challenge of future mobile communication research is to strike an attractive compromise between wireless network's area spectral efficiency and energy efficiency. This necessitates a clean-slate approach to wireless system design, embracing the rich body of existing knowledge, especially on multiple-input-multiple-ouput (MIMO) technologies. This motivates the proposal of an emerging wireless communications concept conceived for single-radio-frequency (RF) large-scale MIMO communications, which is termed as SM. The concept of SM has established itself as a beneficial transmission paradigm, subsuming numerous members of the MIMO system family. The research of SM has reached sufficient maturity to motivate its comparison to state-of-the-art MIMO communications, as well as to inspire its application to other emerging wireless systems such as relay-aided, cooperative, small-cell, optical wireless, and power-efficient communications. Furthermore, it has received sufficient research attention to be implemented in testbeds, and it holds the promise of stimulating further vigorous interdisciplinary research in the years to come. This tutorial paper is intended to offer a comprehensive state-of-the-art survey on SM-MIMO research, to provide a critical appraisal of its potential advantages, and to promote the discussion of its beneficial application areas and their research challenges leading to the analysis of the technological issues associated with the implementation of SM-MIMO. The paper is concluded with the description of the world's first experimental activities in this vibrant research field.

Results of PMIP2 coupled simulations of the Mid-Holocene and Last Glacial Maximum - Part 1: experiments and large-scale features

Abstract: . A set of coupled ocean-atmosphere simulations using state of the art climate models is now available for the Last Glacial Maximum and the Mid-Holocene through the second phase of the Paleoclimate Modeling Intercomparison Project (PMIP2). This study presents the large-scale features of the simulated climates and compares the new model results to those of the atmospheric models from the first phase of the PMIP, for which sea surface temperature was prescribed or computed using simple slab ocean formulations. We consider the large-scale features of the climate change, pointing out some of the major differences between the different sets of experiments. We show in particular that systematic differences between PMIP1 and PMIP2 simulations are due to the interactive ocean, such as the amplification of the African monsoon at the Mid-Holocene or the change in precipitation in mid-latitudes at the LGM. Also the PMIP2 simulations are in general in better agreement with data than PMIP1 simulations.

The kinase TAK1 can activate the NIK-IκB as well as the MAP kinase cascade in the IL-1 signalling pathway

Abstract: Interleukin-1 (IL-1) is a proinflammatory cytokine that has several effects in the inflammation process When it binds to its cell-surface receptor, IL-1 initiates a signalling cascade that leads to activation of the transcription factor NF-kappaB and is relayed through the protein TRAF6 and a succession of kinase enzymes, including NF-kappaB-inducing kinase (NIK) and I kappaB kinases (IKKs) However, the molecular mechanism by which NIK is activated is not understood Here we show that the MAPKK kinase TAK1 acts upstream of NIK in the IL-1-activated signalling pathway and that TAK1 associates with TRAF6 during IL-1 signalling Stimulation of TAK1 causes activation of NF-kappaB, which is blocked by dominant-negative mutants of NIK, and an inactive TAK1 mutant prevents activation of NF-kappaB that is mediated by IL-1 but not by NIK Activated TAK1 phosphorylates NIK, which stimulates IKK-alpha activity Our results indicate that TAK1 links TRAF6 to the NIK-IKK cascade in the IL-1 signalling pathway

Long-term depression

Abstract: LTD has now been established as a synaptic plasticity specific to the cerebellum. Cellular and molecular mechanisms of LTD have been elucidated to some extent, but still a number of questions are left open. The most crucial question may concern its time course, as to how long the LTD lasts beyond the limit of the present maximum observation time of 3 hr, and whether and how it is eventually transformed to a permanent memory. Molecular mechanisms underlying LTD should be investigated further in respect to Ca2+ binding and storage, protein kinase C, phosphorylation of glutamate receptors, GTP proteins, etc. The ineffectiveness of mass field potentials in representing LTD makes such studies relatively difficult, and a hope for future development may be placed in reproduction of LTD in tissue cultured Purkinje cells or even in isolated glutamate receptors in a simplified form. The cerebellar neuronal network incorporating LTD as a memory element has been conceived as a simple perceptron-like (Albus 1971) or adaptive filter-like (Fujita 1982a) parallel processing computer. Such a neuronal computer incorporated in a reflex or a more complex movement system would endow the system with subtle capabilities of adaptation and learning. The scheme of the floccular control of the VOR closely resembles that of a self-tuning regulator, a type of adaptive control system. For cerebellar control of voluntary movements, however, another version of the adaptive control system, the model reference control system, seems to be more applicable (Ito 1986). This system continuously readjusts its dynamics by referring to errors derived through comparison of its performance with that of an internal model. It is important to note that a model for an unknown system can be built based on the same principle, by feeding errors derived from their comparison to adjust the model. It may thus be conceived that an internal model is built within the cerebellum in the manner of model reference adaptive control, and that an internal model so formed is utilized for adaptive control of movement. A recent simulation study successfully reproduced learning in formation of an arm trajectory based on these principles of model reference control (Kawato et al 1987). On the experimental side, however, the complex neural organization for control of locomotion, posture, and voluntary movements still eludes full elucidation. Nevertheless, evidence is accumulating to support the cerebellar learning hypothesis.(ABSTRACT TRUNCATED AT 400 WORDS)