Belle II実験におけるB→Xsℓ+ℓ-過程の崩壊分岐比の測定

Tohoku University佐貫智行課

Tumor necrosis factor α (TNFα) induces pro-matrix metalloproteinase 9 production in human uterine cervical fibroblasts but interleukin 1 α antagonizes the inductive effect of TNFα

AbstractWe have examined the regulation of precursor of matrix metalloproteinase 9 (proMMP-9)/progelatinase B production by tumor necrosis factor α (TNFα) and interleukin 1α (IL-1α) using human uterine cervical fibroblasts. TNFα, but not IL-1α, induces the production of proMMP-9 in the cervical cells. IL-1α, however, suppresses the TNFα-induced proMMP-9 production. 12-O-tetradecanoylphorbol 13-acetate (TPA) also stimulates the cervical cells to produce proMMP-9, and IL-1α synergistically enhances its production. TNFα-induced proMMP-9 production is not mediated by protein kinase C (PKC), whereas the effect of IL-1α is through PKC. By contrast, proMMP-3/prostromelysin 1 is up-regulated by TNFα or TPA in the presence of IL-1α, whose modulation is PKC-dependent. The suppressive effect of IL-1α on the TNFα-induced proMMP-9 production is a new biological effect of IL-1 on MMP production

Interaction and Experience in Enactive Intelligence and Humanoid Robotics

We overview how sensorimotor experience can be operationalized for interaction scenarios in which humanoid robots acquire skills and linguistic behaviours via enacting a “form-of-life”’ in interaction games (following Wittgenstein) with humans. The enactive paradigm is introduced which provides a powerful framework for the construction of complex adaptive systems, based on interaction, habit, and experience. Enactive cognitive architectures (following insights of Varela, Thompson and Rosch) that we have developed support social learning and robot ontogeny by harnessing information-theoretic methods and raw uninterpreted sensorimotor experience to scaffold the acquisition of behaviours. The success criterion here is validation by the robot engaging in ongoing human-robot interaction with naive participants who, over the course of iterated interactions, shape the robot’s behavioural and linguistic development. Engagement in such interaction exhibiting aspects of purposeful, habitual recurring structure evidences the developed capability of the humanoid to enact language and interaction games as a successful participant

A SARM1-mitochondrial feedback loop drives neuropathogenesis in a Charcot-Marie-Tooth disease type 2A rat model

Charcot-Marie-Tooth disease type 2A (CMT2A) is an axonal neuropathy caused by mutations in the mitofusin 2 (MFN2) gene. MFN2 mutations result in profound mitochondrial abnormalities, but the mechanism underlying the axonal pathology is unknown. Sterile α and Toll/IL-1 receptor motif-containing 1 (SARM1), the central executioner of axon degeneration, can induce neuropathy and is activated by dysfunctional mitochondria. We tested the role of SARM1 in a rat model carrying a dominant CMT2A mutation (Mfn2H361Y) that exhibits progressive dying-back axonal degeneration, neuromuscular junction (NMJ) abnormalities, muscle atrophy, and mitochondrial abnormalities - all hallmarks of the human disease. We generated Sarm1-KO (Sarm1-/-) and Mfn2H361Y Sarm1 double-mutant rats and found that deletion of Sarm1 rescued axonal, synaptic, muscle, and functional phenotypes, demonstrating that SARM1 was responsible for much of the neuropathology in this model. Despite the presence of mutant MFN2 protein in these double-mutant rats, loss of SARM1 also dramatically suppressed many mitochondrial defects, including the number, size, and cristae density defects of synaptic mitochondria. This surprising finding indicates that dysfunctional mitochondria activated SARM1 and that activated SARM1 fed back on mitochondria to exacerbate the mitochondrial pathology. As such, this work identifies SARM1 inhibition as a therapeutic candidate for the treatment of CMT2A and other neurodegenerative diseases with prominent mitochondrial pathology

Dialogue Modelling and the Remit of Core Grammar

In confronting the challenge of providing formal models of dialogue, with its plethora of fragments and rich variation in modes of context-dependent construal, it might seem that linguists face two types of methodological choice: either (a) conversation employs dialogue-specific mechanisms, for which a grammar specific to such activity must be constructed; or (b) variation arises due to independent parsing/production systems which invoke a process-neutral grammar. However, as dialogue research continues to develop, there are intermediate possibilities, and in this paper we discuss the approach developed within Dynamic Syntax (DS, Kempson et al. 2001, Cann et al. 2005), a grammar framework within which, not only the parser, but indeed “syntax” itself are just a single mechanism allowing the progressive construction of semantic representations in context. Here we take as a case study the set of phenomena classifiable as clarifications, reformulations, fragment requests and corrections accompanied by extensions, and argue that though these may seem to be uniquely constitutive of dialogue, they are grounded in the mechanisms of apposition equivalently usable in monologue for presenting reformulations, extensions, self-corrections etc