Matsumoto University

Purpose This study addresses the disconnect between how authorities present heritage and how people experience it by testing sensory mapping as a method to bridge theoretical considerations of the ecosystem approach with on-ground heritage practices. Focusing on Yanaka, Tokyo's historic district facing urban change, this research explores how sensory ethnography can reveal everyday heritage values that differ from authorized heritage discourse. Design/methodology/approach Fourteen participants conducted a 2.5-h sensory mapping workshop on July 7th 2024. Each participant received an empty paper map and was randomly assigned a specific sensory category (sight, hearing, smell, touch, taste) and urban morphological element (following Lynch's framework). Participants walked freely through and Yanaka, marking their sensory experiences and documenting them through photographs and recordings. Routes were compared with official heritage tour paths to identify convergences and divergences. Findings While participant routes showed some overlap with official tours, significant divergences emerged, particularly in residential areas. Hebi-michi (snake alley) and the Kayaba Coffee area emerged as unexpected sensory hotspots. Remarkably, sensory experiences triggered personal memories, with one participant recalling nostalgic moments from their hometown, suggesting heritage experiences transcend physical boundaries. Originality/value This represents the first sensory heritage mapping study in Yanesen, contributing a replicable methodology that connects ecosystem approaches with everyday heritage theory. The method offers heritage managers practical tools for understanding how people actually experience urban heritage, potentially informing more inclusive and accessible preservation strategies that acknowledge heritage as a living, sensory ecosystem.

The interplay of noncovalent interactions is a powerful tool for enhancing charge transport and device morphology in organic electronic systems. Organic semiconductors, characterized by aromatic rings, primarily rely on π-π stacking to form supramolecular structures. However, introducing additional noncovalent interactions, offers alternative routes for tuning aggregation and improving optoelectronic properties. Recently, backbone fluorination has become a powerful molecular design strategy to simultaneously boost charge transport and control the morphology of organic electronic devices. Here we explore the charge transport properties of a series of hydrogen-bonded quinquethiophene-rhodanine semiconductors featuring different fluorinated substituents that are remotely located from the conjugated backbone. By combining optical and vibrational spectroscopy, electrochemistry, microscopy and contactless microwave conductivity techniques, we establish clear correlations between the fluorination degree, supramolecular organization, and charge carrier dynamics. We demonstrate through this molecular design that even though the fluorinated moieties are not incorporated into the conjugated backbone or in the solubilizing alkyl tails, they play an essential role in the final charge transport properties. More importantly, our results provide general design guidelines for fluorinated 2 supramolecular semiconductors, and highlight fluorination in combination with H-bonding as an effective strategy for controlling multiscale structure-property relationships in organic electronic materials.

<bold>Background and Aim:</bold> The role of airway mucus plugging in asthma pathophysiology is well-established. However, its relationship with infectious episodes and type 2 inflammation remains unclear in refractory asthma with bronchiectasis. As part of the BEXAS study (Nomura N, et al. <italic>Respir Res</italic> 2022; 23: 365), this study aimed to clarify the association between mucus plugging, infectious episodes, and type 2 inflammation, with a specific focus on plug location. <bold>Methods:</bold> Patients with refractory asthma complicated by bronchiectasis, but not with allergic bronchopulmonary aspergillosis, were included, if they had high-resolution CT images suitable for mucus score evaluation. Mucus plugging was scored separately for bilateral upper and lower lobes, as well as for the total lung. Cluster analysis was performed using mucus scores in the upper and lower lobes and the number of lobes affected by bronchiolitis. <bold>Results:</bold> Forty-two patients were included, and three distinct clusters were identified. CL 1 (n = 14) was characterized by lower-lobe-dominant mucus plugs, the highest number of bronchiolitis-affected lobes, frequent detection of Pseudomonas, systemic corticosteroid-requiring exacerbations, and bronchopneumonia. This cluster also exhibited the lowest FeNO and %FEV1. CL 2 (n = 6) showed high mucus scores in both lower and upper lobes, along with the highest FeNO levels. CL 3 (n = 22) had the lowest mucus scores overall. The degree of bronchiectasis was comparable among the three clusters. <bold>Conclusions:</bold> Lower-lobe-dominant mucus plugs may reflect the severest phenotype, characterized by frequent bronchiolitis involvement and infectious episodes. The location of mucus plugs may be clinically important.

BackgroundWith aging, the canonical histone H3.1/3.2 in skeletal muscle is progressively replaced by the non-canonical variant H3.3. Although H3.3 is thought to be involved in age-related epigenetic regulation due to its role as a histone variant, its functional characteristics remain largely unknown. Serine 31 (S31) is a unique amino acid residue of H3.3 that undergoes phosphorylation. Therefore, the present study aimed to investigate the relationship between skeletal muscle aging and H3.3 phosphorylation at S31 (H3.3S31ph).ResultsWe first demonstrated that H3.3S31ph levels were significantly reduced in the tibialis anterior muscle of 75-wk-old mice compared to 8-wk-old mice. We then examined the effects of viral vector–mediated expression of wild-type H3.3 or a phosphorylation-mimicking H3.3 mutant (H3.3S31E) on gene responsiveness to acute exercise in aging skeletal muscle. In muscles expressing wild-type H3.3, which simulates epigenetic alterations observed during skeletal muscle aging, the transcriptional response to acute exercise was lost by 30 weeks post-treatment (60 weeks of age). In contrast, expression of H3.3S31E successfully rescued the gene responses to acute exercise. This rescue was accompanied by increased enrichment of H3K4me3 and H3K27me3 following acute exercise in the H3.3S31E group, whereas no such histone modification changes were observed in the wild-type H3.3 group. Additionally, robust involvement of exogenous H3.3 in exercise-related histone turnover was observed in the wild-type H3.3 group, but not in the H3.3S31E group, suggesting that phosphorylation at S31 limits the dynamic behavior of H3.3.ConclusionsImpaired transcriptional responsiveness to exercise in a simulated epigenetic aging model induced by exogenous H3.3 expression was rescued by the phosphorylation-mimicking H3.3S31E variant in middle-aged skeletal muscle. The findings of the present study demonstrate that H3.3S31ph plays a critical role in regulating the stability of H3.3 within chromatin.Supplementary InformationThe online version contains supplementary material available at 10.1186/s42826-025-00254-6.

We herein describe an autopsy case of acute-on-chronic liver failure (ACLF) in a patient with primary biliary cholangitis (PBC) that was triggered by an exacerbation of autoimmune hepatitis (AIH)-related features. A 62-year-old woman was diagnosed as having PBC 12 years prior and had been maintained on ursodeoxycholic acid. She presented with fatigue, and was found to have acute exacerbation of liver injury. Her liver function rapidly deteriorated. Upon transfer to our hospital, she exhibited marked hyperbilirubinemia, severe coagulopathy, and ascites, which fulfilled the ACLF diagnostic criteria of the Asian Pacific association for the study of the liver (APASL). Despite intensive treatment including plasma exchange, she died on day 15 of hospitalization. Autopsy revealed advanced hepatic fibrosis with lobular distortion, chronic non-suppurative destructive cholangitis, and loss of interlobular bile ducts, which were characteristic of PBC, along with centrilobular hepatic necrosis, bridging necrosis, bile ductular proliferation, and bile plugs that were suggestive of submassive hepatic necrosis. Interface hepatitis with plasma cell infiltration was also evident. These results indicated an overlap between chronic PBC and AIH exacerbation, leading to ACLF. Our findings highlight the importance of recognizing overlap features in autoimmune liver diseases for more timely interventions and better outcomes in these complex cases.