Design within uncertainty: Gathering, generative process, and unexpected event

This thesis aims to explore design within uncertainty. Our worlds are ongoingly formed within an interdependent web of relationships, and thus design cannot intentionally create better futures. Rather, the thesis argues that what is required in design is to engage with uncertainty and thus to foster unexpected events, exploring the way to do so. Reviewing the participatory design context, this thesis clarified two approaches to discussing uncertainty. The first generative approach has involved actors in specific uncertainty like darkness together and elicited unintentional emotions to depict the generative dimension of uncertainty. Second, The emergent approach focuses on everyday settings such as communities. In this approach, design means cultivating environments and relationships, and then, involved actors relate to each other and generate unexpected events. This thesis follows the emergent approach while adopting the methodological attitude of the generative approach. Also, to explore uncertainty, this thesis classified it into three aspects: a gathering, a relationship in which heterogeneous actors flow; generative processes, in which actors encounter and generate something; and unexpected events that emerge from them. Based on it, this thesis questions what a gathering is, how generative processes foster unexpected events, and how design can be involved with uncertainty. In the study, first, I compare ten gatherings to articulate the features of a gathering. Then, I examine one specific gathering, the Shared Houses, to explore generative processes by reconstructing four episodes that occurred, such as a radio and a crowdfunding project. The study revealed multiple aspects of uncertainty. First, in a gathering, heterogeneous actors intricately flow and blur definitions of a gathering. Then, generative processes are those collectively formed among human and non-human actors, and intentions and capabilities are shared in these processes. In addition, behind them, actors surrender their vulnerabilities to others and accept to be transformed, and I argued that this relationship of vulnerability elicits others’ interventions and contributes to the emanation of unexpected events. Finally, I argued design within uncertainty. It consists of four ways: 1) situating uncertainty by blurring a definition of a gathering, 2) inviting heterogeneous actors, 3) surrendering designers’ vulnerabilities and letting go of their intentions, and lastly, 4) ongoingly practicing in uncertainty and reacting to others to encourage generative processes. This design is a mundane, long-term engagement and also requires the ceaseless engagement of other actors. And this thesis claims that this constant engagement with uncertainty can cultivate possibilities of unexpected events

Heteroatom doping enables hydrogen spillover via H⁺/e⁻ diffusion pathways on a non-reducible metal oxide

Shun K., Mori K., Kidawara T., et al. Heteroatom doping enables hydrogen spillover via H⁺/e⁻ diffusion pathways on a non-reducible metal oxide. Nature Communications 15, 6403 (2024); https://doi.org/10.1038/S41467-024-50217-Z.Hydrogen spillover, the simultaneous diffusion of protons (H⁺) and electrons (e⁻) is considered to be applicable to ubiquitous technologies related to hydrogen but limited to over reducible metal oxides. The present work demonstrates that a non-reducible MgO with heteroatom Al dopants (Al–MgO) allows hydrogen spillover in the same way as reducible metal oxides. Furthermore, a H⁺ storage capacity of this material owing to hydrogen spillover is more than three times greater than those of various standard metal oxides based on H⁺ transport channels within its bulk region. Atomic hydrogen diffuses over the non-reducible Al–MgO produces active H⁺-e⁻ pairs, as also occurs on reducible metal oxides, to enhance the catalytic performance of Ni during CO2 hydrogenation. The H⁺ and e⁻ diffusion pathways generated by the heteroatom Al doping are disentangled based on systematic characterizations and calculations. This work provides a new strategy for designing functional materials intended to hydrogen spillover for diverse applications in a future hydrogen-based society

太陽光中のUVA/UVBの比率の季節差がDNA損傷（6-４）型光産物のDewar型光産物への光異性化の効率に影響を及ぼす

The UVA and UVB components of sunlight can produce three classes of bipyrimidine DNA photolesions [cyclobutane pyrimidine dimers (CPDs), pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) and related Dewar valence isomers (DewarPPs)]. The UVA/UVB ratio of sunlight is high in winter and low in summer in the Northern Hemisphere. Since UVB radiation produces 6-4PPs and UVA radiation converts them into DewarPPs through photoisomerization, it is expected that there may be differences in the photoisomerization of 6-4PPs between summer and winter, although that has never been documented. To determine that, isolated DNA was exposed to natural sunlight for 8 h in late summer and in winter, and absolute levels of the three classes of photolesions were quantified using calibrated ELISAs. It was found that sunlight produces CPDs and 6-4PPs in DNA at a ratio of about 9:1 and converts approximately 80% of 6-4PPs into DewarPPs within 3 h. Moreover, photoisomerization is more efficient in winter than in late summer after sunlight irradiation for the same duration, at similar solar UV doses and with the same induction level of CPDs. These results demonstrate that seasonal differences in the UVA/UVB ratio influence the efficiency of the photoisomerization of 6-4PPs into DewarPPs.博士（医学）・甲第775号・令和3年3月15日© 2020 The Authors. Photochemistry and Photobiology published by Wiley Periodicals LLC on behalf of American Society for Photobiology. This is an open access article under the terms of the Creative Commons Attribution License(https://creativecommons.org/licenses/by/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited

Differential determinants of physical daily activities in frail and nonfrail community-dwelling older adults

AbstractBackground/PurposeThe purpose of this study was to determine whether or not daily activities determined by average daily steps are associated with age, gender, body mass index, fear of falling, and physical functions (locomotive function, balance function, and muscle power) in community-dwelling nonfrail and frail older adults.MethodsThis is a cross-sectional study conducted in community-dwelling older adults in Japan. Based on the Timed Up and Go (TUG) test, 629 elderly adults were divided into two groups: 515 were grouped to nonfrail elderly (TUG time less than 13.5 seconds, mean age 77.0±7.2 years) and 114 to frail elderly (TUG time of 13.5 seconds or more, mean age 76.1±7.5 years). Daily physical activities were determined by average daily steps measured by pedometer and four other physical function tests (10-m walk test, single-leg standing, functional reach, and five-chair stand test) were performed along with the assessment of fear of falling.ResultsStepwise regression analysis revealed that age, gender, 10-m walk test, and single-leg standing were significant and independent determinants of the average step counts in the nonfrail elderly (R2=0.282, p<0.001), whereas fear of falling was the only significant and independent determinant of the average step counts in the frail elderly (R2=0.119, p<0.001).ConclusionThese results indicate that differential factors may be related to daily activities depending on the level of frailty in community-dwelling older adults

Pathophysiological Role of TRPM2 in Age-Related Cognitive Impairment in Mice

Aging causes various functional changes, including cognitive impairment and inflammatory responses in the brain. Transient receptor potential melastatin 2 (TRPM2), a Ca2+-permeable channel expressed abundantly in immune cells, exacerbates inflammatory responses. Previously, we reported that TRPM2 on resident microglia plays a critical role in exacerbating inflammation, white matter injury, and cognitive impairment during chronic cerebral hypoperfusion; however, the physiological or pathophysiological role of TRPM2 during age-associated inflammatory responses remains unclear. Therefore, we examined the effects of TRPM2 deletion in young (2–3 months) and older (12–24 months) mice. Compared with young wild-type (WT) mice, middle-aged (12–16 months) WT mice showed working and cognitive memory dysfunction and aged (20–24 months) WT mice exhibited impaired spatial memory. However, these characteristics were not seen in TRPM2 knockout (TRPM2-KO) mice. Consistent with the finding of cognitive impairment, aged WT mice exhibited white matter injury and hippocampal damage and an increase in the number of Iba1-positive cells and amounts of pro-inflammatory cytokines in the brain; these characteristics were not seen in TRPM2-KO mice. These findings suggest that TRPM2 plays a critical role in exacerbating inflammatory responses and cognitive dysfunction during aging

Topographic map reorganization in cat area 17 after early monocular retinal lesions

Neither discrete peripheral retinal lesions nor the normal optic disk produces obvious holes in one\u27s percept of the world because the visual brain appears to perceptually fill in these blind spots. Where in the visual brain or how this filling in occurs is not well understood. A prevailing hypothesis states that topographic map of visual cortex reorganizes after retinal lesions, which sews up the hole in the topographic map representing the deprived area of cortex (cortical scotoma) and may lead to perceptual filling in. Since the map reorganization does not typically occur unless retinotopically matched lesions are made in both eyes, we investigated the conditions in which monocular retinal lesions can induce comparable map reorganization. We found that following monocular retinal lesions, deprived neurons in cat area 17 can acquire new receptive fields if the lesion occurred relatively early in life (8 weeks of age) and the lesioned cats experienced a substantial period of recovery (\u3e3 years). Quantitative determination of the monocular and binocular response properties of reactivated units indicated that responses to the lesioned eye for such neurons were remarkably robust, and that the receptive-field properties for the two eyes were generally similar. Moreover, excitatory or inhibitory binocular interactions were found in the majority of experimental units when the two eyes were activated together. These results are consistent with the hypothesis that map reorganization after monocular retinal lesions require experience-dependent plasticity and may be involved in the perceptual filling in of blind spots due to retinal lesions early in life

TRPM2 exacerbates central nervous system inflammation in experimental autoimmune encephalomyelitis by increasing production of CXCL2 chemokines

多発性硬化症の新たな病態増悪機構を解明 --TRPM2を介したケモカイン産生が神経炎症の増悪に至る好中球の浸潤を引き起こす--. 京都大学プレスリリース. 2018-09-13.Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS) characterized by demyelination and axonal injury. Current therapies that mainly target lymphocytes do not fully meet clinical need due to the risk of severe side effects and lack of efficacy against progressive MS. Evidence suggests that MS is associated with CNS inflammation, although the underlying molecular mechanism is poorly understood. Transient receptor potential melastatin 2 (TRPM2), a Ca²⁺-permeable nonselective cation channel, is expressed at high levels in the brain and by immune cells, including monocyte lineage cells. Here, we show that TRPM2 plays a pathological role in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Knockout or pharmacological inhibition of TRPM2 inhibited progression of EAE, and TRPM2-knockout (TRPM2-KO) mice showed lower activation of Iba1-immunopositive monocyte lineage cells and neutrophil infiltration of the CNS than wild-type (WT) mice. Moreover, CXCL2 production in TRPM2-KO mice was significantly reduced at Day 14 although the severity of EAE was the same as that in WT mice at that time point. In addition, we used bone marrow chimeric mice to show that TRPM2 expressed by CNS-infiltrating macrophages contributes to progression of EAE. Since CXCL2 induces migration of neutrophils, these results indicate that reduced expression of CXCL2 in the CNS suppresses neutrophil infiltration and slows progression of EAE in TRPM2-KO mice. Together, the results suggest that TRPM2 plays an important role in progression of EAE pathology and shed light on its putative role as a therapeutic target for MS. SIGNIFICANCE STATEMENT: Current therapies for multiple sclerosis (MS), which mainly target lymphocytes, carry the risk of severe side effects and lack efficacy against the progressive form of the disease. Here, we found that the transient receptor potential melastatin 2 (TRPM2) channel, abundantly expressed in CNS-infiltrating macrophages, plays a crucial role in development of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. EAE progression was suppressed by knockout or pharmacological inhibition of TRPM2; this was attributed to a reduction in CXCL2 chemokine production by CNS-infiltrating macrophages in TRPM2-knockout mice, resulting in suppression of neutrophil infiltration into the CNS. These results reveal an important role of TRPM2 in the pathogenesis of EAE and shed light on its potential as a therapeutic target

Texture analysis of myopathy

Given the recent technological advent of muscle ultrasound (US), classification of various myopathic conditions could be possible, especially by mathematical analysis of muscular fine structure called texture analysis. We prospectively enrolled patients with three neuromuscular conditions and their lower leg US images were quantitatively analyzed by texture analysis and machine learning methodology in the following subjects : Inclusion body myositis (IBM) [N=11] ; myotonic dystrophy type 1 (DM1) [N=19] ; polymyositis/dermatomyositis (PM-DM) [N=21]. Although three-group analysis achieved up to 58.8% accuracy, two-group analysis of IBM plus PM-DM versus DM1 showed 78.4% accuracy. Despite the small number of subjects, texture analysis of muscle US followed by machine learning might be expected to be useful in identifying myopathic conditions