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.

On law invariant coherent risk measures

Abstract: The idea of coherent risk measures has been introduced by Artzner, Delbaen, Eber and Heath [1] We think of a special class of coherent risk measures and give a characterization of it Let (Ω, ℱ, P) be a probability space We denote L ∞(Ω, ℱ, P) by L ∞ Following [1], we give the following definition

Learning by watching: extracting reusable task knowledge from visual observation of human performance

Abstract: A novel task instruction method for future intelligent robots is presented, In our method, a robot learns reusable task plans by watching a human perform assembly tasks. Functional units and working algorithms for visual recognition and analysis of human action sequences are presented. The overall system is model based and integrated at the symbolic level. Temporal segmentation of a continuous task performance into meaningful units and identification of each operation is processed in real time by concurrent recognition processes under active attention control. Dependency among assembly operations in the recognized action sequence is analyzed, which results in a hierarchical task plan describing the higher level structure of the task. In another workspace with a different initial state, the system re-instantiates and executes the task plan to accomplish an equivalent goal. The effectiveness of our method is supported by experimental results with block assembly tasks. >

Altered microtubule organization in small-calibre axons of mice lacking tau protein

Abstract: The tau gene encodes a protein (Tau) that is a major neuronal microtubule-associated protein localized mostly in axons. It has microtubule-binding and tubulin-polymerizing activity in vitro and is thought to make short crossbridges between axonal microtubules. Further, tau-transfected non-neuronal cells extend long axon-like processes in which microtubule bundles resembling those in axons are formed. In contrast, tau antisense oligonucleotides selectively suppress axonal elongation in cultured neurons. Thus tau is thought to be essential for neuronal cell morphogenesis, especially axonal elongation and maintenance. To test this hypothesis, we used gene targeting to produce mice lacking the tau gene. We show that the nervous system of tau-deficient mice appears to be normal immunohistologically. Furthermore, axonal elongation is not affected in cultured neurons. But in some small-calibre axons, microtubule stability is decreased and microtubule organization is significantly changed. We observed an increase in microtubule-associated protein 1A which may compensate for the functions of tau in large-calibre axons. Our results argue against the suggested role of tau in axonal elongation but confirm that it is crucial in the stabilization and organization of axonal microtubules in a certain type of axon.

System-level identification of transcriptional circuits underlying mammalian circadian clocks.

Abstract: Mammalian circadian clocks consist of complexly integrated regulatory loops, making it difficult to elucidate them without both the accurate measurement of system dynamics and the comprehensive identification of network circuits. Toward a system-level understanding of this transcriptional circuitry, we identified clock-controlled elements on 16 clock and clock-controlled genes in a comprehensive surveillance of evolutionarily conserved cis elements and measurement of their transcriptional dynamics. Here we report the roles of E/E' boxes, DBP/E4BP4 binding elements and RevErbA/ROR binding elements in nine, seven and six genes, respectively. Our results indicate that circadian transcriptional circuits are governed by two design principles: regulation of E/E' boxes and RevErbA/ROR binding elements follows a repressor-precedes-activator pattern, resulting in delayed transcriptional activity, whereas regulation of DBP/E4BP4 binding elements follows a repressor-antiphasic-to-activator mechanism, which generates high-amplitude transcriptional activity. Our analysis further suggests that regulation of E/E' boxes is a topological vulnerability in mammalian circadian clocks, a concept that has been functionally verified using in vitro phenotype assay systems.