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Arachidonic acid-derived prostaglandins not only contribute to the development of inflammation as intercellular pro-inflammatory mediators, but also promote the excitability of the peripheral somatosensory system, contributing to pain exacerbation. Peripheral tissues undergo many forms of diseases that are frequently accompanied by inflammation. The somatosensory nerves innervating the inflamed areas experience heightened excitability and generate and transmit pain signals. Extensive studies have been carried out to elucidate how prostaglandins play their roles for such signaling at the cellular and molecular levels. Here, we briefly summarize the roles of arachidonic acid-derived prostaglandins, focusing on four prostaglandins and one thromboxane, particularly in terms of their actions on afferent nociceptors. We discuss the biosynthesis of the prostaglandins, their specific action sites, the pathological alteration of the expression levels of related proteins, the neuronal outcomes of receptor stimulation, their correlation with behavioral nociception, and the pharmacological efficacy of their regulators. This overview will help to a better understanding of the pathological roles that prostaglandins play in the somatosensory system and to a finding of critical molecular contributors to normalizing pain.

Although guest-filled carbon nanotube yarns provide record performance as torsional and tensile artificialmuscles, they are expensive, and only part of themuscle effectively contributes to actuation. We describe a muscle type that provides higher performance, in which the guest that drives actuation is a sheath on a twisted or coiled core that can be an inexpensive yarn. This change from guest-filled to sheath-run artificial muscles increases the maximum work capacity by factors of 1.70 to 2.15 for tensile muscles driven electrothermally or by vapor absorption. A sheath-run electrochemical muscle generates 1.98 watts per gram of average contractile power—40 times that for human muscle and 9.0 times that of the highest power alternative electrochemical muscle. Theory predicts the observed performance advantages of sheath-run muscles.

The orphan nuclear receptor Nurr1 is critical for the development, maintenance and protection of midbrain dopaminergic (mDA) neurons. Here we show that prostaglandin E1 (PGE1) and its dehydrated metabolite, PGA1, directly interact with the ligand-binding domain (LBD) of Nurr1 and stimulate its transcriptional function. We also report the crystallographic structure of Nurr1-LBD bound to PGA1 at 2.05 Å resolution. PGA1 couples covalently to Nurr1-LBD by forming a Michael adduct with Cys566, and induces notable conformational changes, including a 21° shift of the activation function-2 helix (H12) away from the protein core. Furthermore, PGE1/PGA1 exhibit neuroprotective effects in a Nurr1-dependent manner, prominently enhance expression of Nurr1 target genes in mDA neurons and improve motor deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse models of Parkinson’s disease. Based on these results, we propose that PGE1/PGA1 represent native ligands of Nurr1 and can exert neuroprotective effects on mDA neurons, via activation of Nurr1’s transcriptional function. Prostaglandins PGE1 and PGA1 have neuroprotective effects by enhancing the transcriptional activity of Nurr1 by directly binding to its ligand-binding domain and upregulating their target genes implicated in Parkinson’s disease.

Self-powered sensor technologies are receiving increasing attention owing to their ability to operate independently without the need for external batteries or power supplies. This autonomy enables continuous and real-time monitoring in various applications. Carbon nanotubes (CNTs) are particularly promising as electrode materials and energy-harvesting components, owing to their excellent electrical conductivity, mechanical robustness, and tunable surface properties. This review provides a concise overview and critical perspectives on recent progress in CNT-based self-powered sensors, focusing on their structural designs, operating mechanisms, and application areas. The sensors are classified according to their practical application environments, including environmental, wearable, and implantable applications, rather than by their energy-harvesting mechanisms or detection targets. Furthermore, current critical challenges, such as durability, scalable fabrication, and in vivo validation, which must be solved to achieve fully autonomous CNT-based sensors for healthcare and environmental monitoring, are discussed. This review underscores the pivotal role of CNT-based self-powered sensors in driving next-generation autonomous monitoring technologies and offers insights for the implementation of such sensors in practical biomedical and environmental applications.

Artificial muscles translate the biological principles of motion into soft, adaptive, and multifunctional actuation. This review accordingly highlights research into natural actuation strategies, such as skeletal muscles, muscular hydrostats, spider silk, and plant turgor systems, to reveal the principles underlying energy conversion and deformation control. Building on these insights, polymer-based artificial muscles based on these principles, including pneumatic muscles, dielectric elastomers, and ionic electroactive systems, are described and their capabilities for efficient contraction, bending, and twisting with tunable stiffness and responsiveness are summarized. Furthermore, the abilities of carbon nanotube composites and twisted yarns to amplify nanoscale dimensional changes through hierarchical helical architectures and achieve power and work densities comparable to those of natural muscle are discussed. Finally, the integration of these actuators into soft robotic systems is explored through biomimetic locomotion and manipulation systems ranging from jellyfish-inspired swimmers to octopus-like grippers, gecko-adhesive manipulators, and beetle-inspired flapping wings. Despite rapid progress in the development of artificial muscles, challenges remain in achieving long-term durability, energy efficiency, integrated sensing, and closed-loop control. Therefore, future research should focus on developing intelligent muscular systems that combine actuation, perception, and self-healing to advance progress toward realizing autonomous, lifelike machines that embody the organizational principles of living systems.

A hallmark of cancer cells is the metabolic switch from oxidative phosphorylation (OXPHOS) to glycolysis, a phenomenon referred to as the ‘Warburg effect’, which is also observed in primed human pluripotent stem cells (hPSCs). Here, we report that downregulation of SIRT2 and upregulation of SIRT1 is a molecular signature of primed hPSCs and that SIRT2 critically regulates metabolic reprogramming during induced pluripotency by targeting glycolytic enzymes including aldolase, glyceraldehyde-3-phosphate dehydrogenase, phosphoglycerate kinase, and enolase. Remarkably, knockdown of SIRT2 in human fibroblasts resulted in significantly decreased OXPHOS and increased glycolysis. In addition, we found that miR-200c-5p specifically targets SIRT2, downregulating its expression. Furthermore, SIRT2 overexpression in hPSCs significantly affected energy metabolism, altering stem cell functions such as pluripotent differentiation properties. Taken together, our results identify the miR-200c–SIRT2 axis as a key regulator of metabolic reprogramming (Warburg-like effect), via regulation of glycolytic enzymes, during human induced pluripotency and pluripotent stem cell function. Cha et al.  show that SIRT2 suppression by miR-200c enhances acetylation levels and enzymatic activities of glycolytic enzymes and contributes to metabolic reprogramming of human induced pluripotent stem cells and human embryonic stem cells.

Axillary odor is a malodor produced by bacterial metabolism near the apocrine glands, which often causes discomfort in an individual's daily life and social interactions. A deodorant is a personal care product designed to alleviate or mask body odor. Currently, most deodorants contain antimicrobial chemicals and fragrances for odor management; however, direct application to the underarm skin can result in irritation or sensitivity. Therefore, there is a growing interest in technologies that enable disinfection and odor control without the antiperspirants or perfumes. The cold atmospheric plasma temporally generates reactive radicals that can eliminate bacteria and surrounding odors. In this study, cultured Staphylococcus hominis and Corynebacterium xerosis , the causative bacteria of axillary bromhidrosis, were killed after 90% plasma exposure for 3 min. Moreover, the electronic nose system indicated a significant reduction of approximately 51% in 3-hydroxy-3-methylhexanoic acid and approximately 34% in 3-methyl-3-sulfanylhexan-1-ol, the primary components of axillary odor, following a 5-min plasma exposure. These results support the dual function of our deodorant in eliminating bacteria and axillary odors without the chemical agents. Therefore, cold atmospheric plasma-applied deodorant devices have great potential for the treatment and management of axillary odors as a non-contact approach without chemical use in daily life.

The orphan nuclear receptor Nurr1 (also known as NR4A2) is critical for the development and maintenance of midbrain dopaminergic neurons, and is associated with Parkinson's disease. However, an association between Nurr1 and Alzheimer's disease (AD)‐related pathology has not previously been reported. Here, we provide evidence that Nurr1 is expressed in a neuron‐specific manner in AD‐related brain regions; specifically, it is selectively expressed in glutamatergic neurons in the subiculum and the cortex of both normal and AD brains. Based on Nurr1’s expression patterns, we investigated potential functional roles of Nurr1 in AD pathology. Nurr1 expression was examined in the hippocampus and cortex of AD mouse model and postmortem human AD subjects. In addition, we performed both gain‐of‐function and loss‐of‐function studies of Nurr1 and its pharmacological activation in 5XFAD mice. We found that knockdown of Nurr1 significantly aggravated AD pathology while its overexpression alleviated it, including effects on Aβ accumulation, neuroinflammation, and neurodegeneration. Importantly, 5XFAD mice treated with amodiaquine, a highly selective synthetic Nurr1 agonist, showed robust reduction in typical AD features including deposition of Aβ plaques, neuronal loss, microgliosis, and impairment of adult hippocampal neurogenesis, leading to significant improvement of cognitive impairment. These in vivo and in vitro findings suggest that Nurr1 critically regulates AD‐related pathophysiology and identify Nurr1 as a novel AD therapeutic target.

Olfactory perception depends on soluble proteins in the perireceptor environment that support odorant transport, mucosal protection, and tissue homeostasis. In insects, odorant-binding proteins (OBPs) in the sensillum lymph are indispensable for odor detection, whereas in humans the indispensability of OBPs (OBP2A/2B) remains unclear because they are inconsistently detected in nasal mucus. Consequently, it remains unclear whether other soluble proteins compensate for this function or how they contribute to odorant processing and signal transmission within the olfactory mucus. Accumulating evidence indicates that OBP-like lipocalins (LCN1, LCN2, LCN15) and apolipoprotein D, together with bactericidal/permeability-increasing (BPI)-fold proteins, act as major mediators of odorant solubilization, antimicrobial defense, oxidative stress regulation, and extracellular matrix (ECM) remodeling. Alterations in those proteins and ECM organization are linked to idiopathic and age-related smell loss, chronic rhinosinusitis, and neurodegenerative disorders, underscoring their broad relevance at the interface of chemosensation, mucosal defense, and brain health. Major unresolved issues include the functional indispensability of human OBPs, the receptor-specific contributions of OBP-like proteins, and the mechanistic relationships linking olfactory proteome remodeling, sensory signaling, and disease progression. This review provides an integrative overview of structural and mechanistic insights, highlights current controversies, and proposes future research directions, including receptor–protein mapping, integrated structural–functional studies, structural–functional analysis of OBP–ECM networks, and clinical validation of OBP-related biomarkers.

Salmonella is a major foodborne pathogen that causes salmonellosis, which is characterized by symptoms such as diarrhea, fever, and abdominal cramps. Existing methods for detecting Salmonella, such as culture plating, ELISA, and PCR, are accurate but time-consuming and unsuitable for on-site applications. In this study, we developed a rapid and sensitive electrochemical sensor using a molecularly imprinted polymer (MIP) to detect Salmonella typhimurium (S. typhimurium ) by targeting lipopolysaccharides (LPS). Polydopamine (PDA) was used as the polymer matrix because of its cost-efficiency and functional versatility. The sensor demonstrated high sensitivity and selectivity, with a detection limit of 10 CFU/mL and a linear response over the 10²–10⁸ CFU/mL range. The specificity of the sensor was validated against other gram-positive and gram-negative bacteria and showed no significant cross-reactivity. Furthermore, the sensor performed effectively in real food samples, including tap water, milk, and pork, without complex preprocessing. These results highlight the potential of the LPS-imprinted MIP sensor for practical on-site detection of S. typhimurium , improving food safety monitoring and preventing outbreaks in food-handling environments.