Part agent that proposes maintenance actions for a part considering its life cycle

Part of: Seliger, Günther (Ed.): Innovative solutions : proceedings / 11th Global Conference on Sustainable Manufacturing, Berlin, Germany, 23rd - 25th September, 2013. - Berlin: Universitätsverlag der TU Berlin, 2013. - ISBN 978-3-7983-2609-5 (online). - http://nbn-resolving.de/urn:nbn:de:kobv:83-opus4-40276. - pp. 235–240.The transition from a consumption-oriented society to a reuse-based society is needed for the effective use of resources and environmental protection. However, it is difficult for a user to make appropriate decisions for maintenance of his/her parts because of the wide range of choices of action and the huge amount of information required. To support the user's decision and to promote the reuse of parts, we have developed a part agent system that manages information about individual parts throughout their life cycle. A part agent is a network agent that contains the information of its corresponding part and follows the movement of the part via the network throughout its life cycle. This paper describes a new mechanism of a part agent that proposes appropriate maintenance actions for the corresponding part by estimating its expected value, cost, and environmental load based on the predicted information about its life cycle

ムノウリョクシャ ニツイテ ノ ケンキュウ ノート クキ シュウゾウ ノ テツガク カラ

研究ノー

RacGAP α2-Chimaerin Function in Development Adjusts Cognitive Ability in Adulthood

SummaryA major concern in neuroscience is how cognitive ability in adulthood is affected and regulated by developmental mechanisms. The molecular bases of cognitive development are not well understood. We provide evidence for the involvement of the α2 isoform of Rac-specific guanosine triphosphatase (GTPase)-activating protein (RacGAP) α-chimaerin (chimerin) in this process. We generated and analyzed mice with global and conditional knockouts of α-chimaerin and its isoforms (α1-chimaerin and α2-chimaerin) and found that α-chimaerin plays a wide variety of roles in brain function and that the roles of α1-chimaerin and α2-chimaerin are distinct. Deletion of α2-chimaerin, but not α1-chimaerin, beginning during early development results in an increase in contextual fear learning in adult mice, whereas learning is not altered when α2-chimaerin is deleted only in adulthood. Our findings suggest that α2-chimaerin acts during development to establish normal cognitive ability in adulthood

Emerging roles of ARHGAP33 in intracellular trafficking of TrkB and pathophysiology of neuropsychiatric disorders

Intracellular trafficking of receptor proteins is essential for neurons to detect various extracellular factors during the formation and refinement of neural circuits. However, the precise mechanisms underlying the trafficking of neurotrophin receptors to synapses remain elusive. Here, we demonstrate that a brain-enriched sorting nexin, ARHGAP33, is a new type of regulator for the intracellular trafficking of TrkB, a high-affinity receptor for brain-derived neurotrophic factor. ARHGAP33 knockout (KO) mice exhibit reduced expression of synaptic TrkB, impaired spine development and neuropsychiatric disorder-related behavioural abnormalities. These deficits are rescued by specific pharmacological enhancement of TrkB signalling in ARHGAP33 KO mice. Mechanistically, ARHGAP33 interacts with SORT1 to cooperatively regulate TrkB trafficking. Human ARHGAP33 is associated with brain phenotypes and reduced SORT1 expression is found in patients with schizophrenia. We propose that ARHGAP33/SORT1-mediated TrkB trafficking is essential for synapse development and that the dysfunction of this mechanism may be a new molecular pathology of neuropsychiatric disorders