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Object-related accidents among older adults often result from inadequately designed furniture and fixtures that do not accommodate age-related changes. However, technologies for quantitatively capturing how furniture and fixtures assist the body in daily life remain limited. This study addresses this gap by introducing a portable, non-disruptive system that measures and visualizes how humans interact with environmental objects, particularly during transitional movements such as standing, turning, or reaching. The system integrates wearable force sensors, motion capture gloves, RGB-D cameras, and LiDAR-based environmental scanning to generate spatial maps of body-applied forces, overlaid onto point cloud representations of actual living environments. Through home-based experiments involving 13 older adults aged 69–86 across nine households, the system effectively identified object-specific support interactions with specific furniture (e.g., doorframes, shelves) and enabled a three-dimensional comparative analysis across different spaces, including living rooms, entryways, and bedrooms. The visualization captured essential spatial features—such as contact height and positional context—without altering the existing environment. This study presents a novel methodology for evaluating life environments from a life-centric perspective and offers insights for the inclusive design of everyday objects and spaces to support safe and independent aging in place.

Abstract Palmoplantar pustulosis (PPP) is a chronic inflammatory skin disorder affecting the palms and soles. In rare cases, severe patients develop acute extra-palmoplantar lesions often accompanied by arthralgia. Such cases with extensive symptoms often necessitate systemic treatments with variable efficacy and potential side effects. Apremilast, known for its broad immune response modulation, presents promise as a therapeutic option for severe PPP with joint and extra-palmoplantar lesions. This case highlights apremilast as a potential systemic treatment for such cases with minimal side effects. Rare cases of severe palmoplantar pustulosis with rapidly developing extra-palmoplantar lesions and joint pain have been treated by immunosuppressants with variable efficacy and side effects from prolonged treatment. Our case was successfully treated with apremilast, which suggests apremilast as a potential systemic treatment for such cases.

This manuscript presents a rare case report of a patient with severe idiopathic aplastic anaemia who developed multiple subcutaneous abscesses by Corynebacterium amycolatum. The report aims to elucidate the growing significance of Corynebacterium species as pivotal pathogens in individuals with compromised immune systems. Abstract Corynebacterium amycolatum is a part of the normal skin flora and has been underestimated as a pathogen. However, in recent years, the species has gained recognition as an important pathogen causing severe infections, particularly in immunocompromised patients. Nevertheless, identifying these organisms at the species level is difficult in routine clinical microbiology, leading to limited knowledge of their clinical manifestations in infectious diseases. In this study, we report a rare case of multiple subcutaneous abscesses in a patient with severe neutropenia, wherein C.amycolatum was identified as the causative organism through genotyping tests. This case highlights the importance of this organism as an aetiological agent of severe skin infections in patients with compromised immune systems.

Atopic dermatitis (AD) is a skin disease exhibiting clinical and molecular heterogeneity, thereby jeopardizing the development of personalized treatments. Here we pursue a cross-sectional and longitudinal cohort analysis of 951 whole-skin samples, employing an unsupervised decomposition analysis to link gene expression profiles to disease severity, six distinct skin phenotypes, and blood cytokines representative of given endotypes. Specifically, type 2 and type 17 responses are associated with major skin phenotypes such as erythema and induration, while type 1 response is upregulated in lichen amyloidosis of AD patients. Longitudinal analysis of patients treated with dupilumab finds sustained gene signatures related to type 17 response in lesional skin and upregulated transcription factors in non-lesional skin of patients with poor treatment outcomes. Lastly, several extracellular matrix organization-associated genes are correlated with clinical severity and treatment response to dupilumab. Our findings thus provide potential skin and blood biomarkers for assessing endotypes and therapeutic responses in AD to pave the way for personalized medicine. Atopic dermatitis (AD) with complex manifestations and genetic associations. Here the author profile the transcriptome of 951 skin samples from patients with AD to link skin phenotypes, clinical severity, and efficacy of dupilumab treatment to specific types of immune responses and gene features to serve clues for personalized medicine.

Atopic dermatitis (AD) is a skin disease that is heterogeneous both in terms of clinical manifestations and molecular profiles. It is increasingly recognized that AD is a systemic rather than a local disease and should be assessed in the context of whole-body pathophysiology. Here we show, via integrated RNA-sequencing of skin tissue and peripheral blood mononuclear cell (PBMC) samples along with clinical data from 115 AD patients and 14 matched healthy controls, that specific clinical presentations associate with matching differential molecular signatures. We establish a regression model based on transcriptome modules identified in weighted gene co-expression network analysis to extract molecular features associated with detailed clinical phenotypes of AD. The two main, qualitatively differential skin manifestations of AD, erythema and papulation are distinguished by differential immunological signatures. We further apply the regression model to a longitudinal dataset of 30 AD patients for personalized monitoring, highlighting patient heterogeneity in disease trajectories. The longitudinal features of blood tests and PBMC transcriptome modules identify three patient clusters which are aligned with clinical severity and reflect treatment history. Our approach thus serves as a framework for effective clinical investigation to gain a holistic view on the pathophysiology of complex human diseases. Atopic dermatitis is an inflammatory skin disease featuring systemic involvement. Here authors show that the two major clinical manifestations of the disease, erythema and papulation, are distinguished by differential interplay between local skin and systemic immunity, uncovered by integrated transcriptomics.

Pulmonary arterial hypertension (PAH) remains a disease with poor prognosis; thus, a new mechanism for PAH treatment is necessary. Circulating nerve growth factor receptor (Ngfr)-positive cells in peripheral blood mononuclear cells are associated with disease severity and the prognosis of PAH patients; however, the role of Ngfr in PAH is unknown. In this study, we evaluated the function of Ngfr using Ngfr gene-deletion (Ngfr−/−) mice. To elucidate the role of Ngfr in pulmonary hypertension (PH), we used Ngfr−/− mice that were exposed to chronic hypoxic conditions (10% O2) for 3 weeks. The development of hypoxia-induced PH was accelerated in Ngfr−/− mice compared to littermate controls. In contrast, the reconstitution of bone marrow (BM) in Ngfr−/− mice transplanted with wild-type BM cells improved PH. Notably, the exacerbation of PH in Ngfr−/− mice was accompanied by the upregulation of pulmonary vascular remodeling-related genes in lung tissue. In a hypoxia-induced PH model, Ngfr gene deletion resulted in PH exacerbation. This suggests that Ngfr may be a key molecule involved in the pathogenesis of PAH.

Selenoprotein P (SeP), a liver-derived secretory protein, functions as a selenium supply protein in the body. SeP has been reported to be associated with insulin resistance in humans through serial analysis of gene expression. Recently, SeP has been found to inhibit vascular endothelial growth factor-stimulated cell proliferation in human umbilical vein endothelial cells, and impair angiogenesis in a mouse hind limb model. In this study, the role of SeP in ischemia/reperfusion (I/R) injury has been investigated. SeP knockout (KO) and littermate wild-type (WT) mice were subjected to 30 min of myocardial ischemia followed by 24 h of reperfusion. The myocardial infarct area/area at risk (IA/AAR), evaluated using Evans blue (EB) and 2,3,5-triphenyltetrazolium chloride (TTC) staining, was significantly smaller in SeP KO mice than in WT mice. The number of terminal de-oxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive nuclei was significantly lower in SeP KO mice than in WT mice. In addition, caspase-3 activation was reduced in SeP KO mice compared to that in WT mice. Furthermore, phosphoinositide 3-kinase/Akt and Erk levels were examined for the reperfusion injury salvage kinase (RISK) pathway. Interestingly, SeP KO significantly increased the phosphorylation of IGF-1, Akt, and Erk compared to that in WT mice after I/R. Finally, I/R-induced myocardial IA/AAR was significantly increased in SeP KO mice overexpressing SeP in the liver compared to other SeP KO mice. These results, together, suggest that inhibition of SeP protects the heart from I/R injury through upregulation of the RISK pathway.

The Rho/Rho-kinase pathway plays an important role in many cardiovascular diseases such as hypertension, atherosclerosis, heart failure, and myocardial infarction. Although previous studies have shown that Rho-kinase inhibitors reduce ischemia/reperfusion (I/R) injury and cytokine production, the role of Rho-kinase in leukocytes during I/R injury is not well understood. Mice were subjected to 30-min ischemia and reperfusion. Rho-kinase activity was significantly greater in leukocytes subjected to myocardial I/R compared to the sham-operated mice. Administration of fasudil, a Rho-kinase inhibitor, significantly reduced the I/R-induced expression of the proinflammatory cytokines interleukin (IL)-6, C-C motif chemoattractant ligand 2 (CCL2), and tumor necrosis factor (TNF)-α, in leukocytes, compared with saline as the vehicle. Furthermore, fasudil decreased I/R-induced myocardial infarction/area at risk (IA) and I/R-induced leukocyte infiltration in the myocardium. Interestingly, IA in fasudil-administered mice with leukocyte depletion was similar to that in fasudil-administered mice. I/R also resulted in remarkable increases in the mRNA expression levels of the proinflammatory cytokines TNF-α, IL-6, and CCL2 in the heart. Inhibition of Rho-kinase activation in leukocytes has an important role in fasudil-induced cardioprotective effects. Hence, inhibition of Rho-kinase may be an additional therapeutic intervention for the treatment of acute coronary syndrome.

Fatty acid binding protein 4 (FABP4) is highly expressed in adipocytes. Lipolysis, caused by an elevated adrenergic input, has been suggested to contribute to elevated serum FABP4 levels in patients with cardiovascular diseases. However, the relationship between the serum FABP4 and efferent sympathetic nerve activity remains poorly understood. Twenty‐one healthy subjects (average age, 29.1 years; 15 men) performed an isometric handgrip (HG) exercise at 30% of the maximal voluntary contraction until they were fatigued. The beat‐by‐beat heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were recorded. Blood samples were collected at rest and at the time of peak fatigue. The MSNA, HR, and systolic BP were significantly increased by the HG exercise (all, p < 0.05). MSNA was obtained from 14 patients. The change in the FABP4 on HG exercise was significantly correlated with the change in MSNA (bursts/100 heartbeats) (R = 0.808, p < 0.001) but not with changes in other parameters, which might, in part, reflect an association of efferent sympathetic drive with FABP4. Meanwhile, resting FABP4 levels were not associated with any parameters including MSNA, in healthy individuals. Future studies on patients with elevated sympathetic activity are warranted to examine the relationship further.

Product accidents often occur due to poorly designed products that do not consider age-related functional changes. This study focuses on the inadequate ‘body-supporting properties’ of everyday products, which are recognized as a critical factor affecting independent living and fall prevention. To address this issue, we developed a portable system that measures and visualizes the vector fields of the hands’ body support, and we evaluated the body-supporting ability of everyday products in the home. A study was conducted to measure body-supporting movements using the developed system in 9 houses with 13 participants aged 69 to 86 years. The results of the study identified daily activities that involve body-supporting movements, such as putting on and taking off shoes and clothes, sitting and standing up, etc. The study also identified various everyday products, such as tables, footrests, fusuma (sliding doors or partitions used in traditional Japanese architecture), windows, TV racks, etc., that generate body-supporting forces. By using the proposed system to measure hand forces at multiple points, it is possible to investigate how the hands are used to hold everyday products and interact with the environment in daily life, as well as the direction in which force is applied to support the body. For example, research has shown that a body-supporting force of as little as 4 N in the horizontal direction is sufficient to maintain horizontal balance. This finding underscores the importance of considering body support in everyday environments for older people and provides valuable insights for future design improvements.