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From Gibbs–Shannon entropy and microscopic reversibility to entropy production, heat, and fluctuation theorems
This work provides a self-contained derivation of several fundamental results in stochastic thermodynamics, including the Jarzynski equality, Crooks fluctuation theorem, and the Clausius inequality. Although the principal theoretical conclusions are well established in the literature, the present approach departs from conventional formulations of stochastic entropy by employing a trajectory-independent probability density constructed as the marginal of the full path-space distribution. This construction establishes a direct connection between microscopic path statistics and macroscopic state probabilities, thereby providing a natural framework for quantifying the relative statistical weights of distinct dynamical histories leading to the same microstate. We demonstrate that entropy production and the fluctuation theorems emerge directly from the Gibbs inequality under the assumption of microscopic reversibility of trajectories along with the extension of the Gibbs–Shannon entropy to time-evolving ensembles. For reduced stochastic descriptions such as Langevin dynamics, the counterpart of microscopic reversibility is local detailed balance, which is inherited from the underlying time-reversal symmetry of the full system–reservoir dynamics and is the condition under which the present framework applies to effective open-system descriptions. We show that the change in microscopic entropy can be attributed to both underlying stochastic fluctuations and the statistical uncertainties inherent in thermodynamic ensembles. This dual perspective ensures that the average entropy production remains non-negative, providing a consistent microscopic basis for thermodynamic irreversibility through the statistical preference of forward over time-reversed trajectories. The connection between microscopic entropy flow and heat, as well as the subsequent derivation of the Clausius inequality and Jarzynski–Crooks relations, requires the additional assumption of an ideal thermal reservoir at a fixed temperature. While this formulation introduces no new physical or mathematical insights, it illuminates the universality of fluctuation theorems across diverse systems, offering a unified perspective that may serve a pedagogical purpose for those studying the statistical–mechanical foundations of non-equilibrium thermodynamics.
Phase 3 Trial of Oral Infigratinib in Children with Achondroplasia
Multidirectional strain-insensitive stretchable RF electronics
Abstract Stretchable radio-frequency (RF) electronics underpin emerging wearable systems for body-centric communication, continuous health monitoring, and wireless power transfer. However, on-body stretchable antennas undergo multidirectional in-plane strain during natural motion, which detunes resonance and destabilizes wireless links. Existing strain-insensitive designs are typically effective only along prescribed loading directions and often compromise radiation performance. Here, we establish a systematic directional mechano-electromagnetic analysis framework for resonant planar antennas and introduce a dual-port multidirectional strain-insensitive antenna (DP-MSiA), whereby strain-insensitive resonance (shift ≤ 40 MHz at 2.45 GHz) is achieved under up to 45% strain across diverse in-plane directions. Based on the stable resonance and high realized gain of the DP-MSiA, we demonstrate strain-insensitive wireless energy harvesting with rectifiers under in-plane strain of varying direction and magnitude, as well as a strain-robust on-body communication system that sustains stable multimodal health-data transmission during natural motion. Our work opens new opportunities for creating deformation-insensitive electronics and enables integrated functionalities in wearable and embodied systems.
Ecological multifunctionality of watersheds increases with tree species richness
Enhanced crystal-melt segregation within dynamic mush systems links silicic cumulates with caldera-forming eruptions
Abstract Supported by the mush model, the origin of crystal-poor, high-silica rhyolitic magmas (≥ 75 SiO₂ wt.%) is commonly linked to melt extraction in shallow, crystalline mushes, yet their complementary cumulates remain elusive in the upper crust. Here we present the “dynamic mush model” for the Campo Alegre-Corupá system (Brazil), combining textural analysis and thermodynamic modeling to show that high-silica melts formed through upper-crustal fractionation, leaving a granitic residue and feeding a caldera-forming eruption. Syenites and melasyenites represent their silicic-mafic cumulates, the syenites being formed at relatively low crystallinities (~16-33 of bulk vol.%) after extraction of large amounts of interstitial melts (~47-80 of liquid vol.%). In contrast to static models (extraction window ~50-70 vol.%), our results indicate early melt segregation in a dynamic reservoir. Alkali-feldspar crystals were size-selectively and hydraulically sorted by upward melt flow; aggregates were then formed at low crystallinities, supposedly via synneusis, enabling rapid sinking, and were repacked by recharge. This process, enhanced by relatively high magma fluxes, efficiently separated crystals from melt, explaining the origin of large-volume eruptible magmas in the upper crust. Our findings redefine mush evolution while underscoring the role of flow-driven crystal sorting (elutriation) in caldera-forming systems.
Targeting macrophage ferritin heavy chain mitigates ferroptosis and lung injury in experimental acute respiratory distress syndrome
Abstract Ferritin, composed of heavy chain (FTH1) and light chain (FTL) subunits, is a key intracellular iron storage protein, but the origin and biological role of extracellular ferritin (ex-ferritin) remain poorly understood. Elevated serum ex-ferritin is associated with worse outcomes in acute respiratory distress syndrome (ARDS). Here, we show that both FTH1 and FTL are significantly enriched in the serum, blood monocytes, and alveolar macrophages (AM) of individuals with ARDS, findings we replicate in a murine hyperoxia-induced acute lung injury model. Myeloid-specific FTH1 ( Fth1 ΔLysM ) deletion attenuates lung injury, and is associated with reduced macrophage ferroptosis, altered airway inflammatory responses, lower extracellular iron and compensatory secretion of FTL-ex-ferritin. While pharmacologic ferroptosis inhibition prior to hyperoxia had no effect, transplantation of FTL-ex-ferritin-enriched bronchoalveolar lavage fluid conferred protection from lung injury. These findings identify macrophage ferritin metabolism and ex-ferritin secretion as critical regulators of lung injury, offering new insights into the pathobiology of ARDS.
Metal-center electron affinity modulates multicolor electrochromism in 2D conjugated metal-organic frameworks
Bispecific antibody engineered extracellular vesicles redirect T cells to prevent postoperative epidural fibrosis
Abstract Epidural fibrosis (EF) is a frequent and debilitating complication that impairs recovery following spinal surgery, yet effective targeted therapies are lacking. Here we observe enrichment of FAP⁺ fibroblasts at surgical sites in patients after laminectomy. To therapeutically target this subset, we develop bispecific antibody–decorated extracellular vesicles (BsAb EVs), which redirect endogenous T cells to eliminate FAP⁺ fibroblasts in situ. In a preclinical model, BsAb EVs selectively eliminate pathogenic fibroblasts, reduce fibrotic collagen accumulation, and prevent the development of postoperative epidural fibrosis without detectable systemic toxicity under the tested conditions. Single-cell RNA sequencing reveals that FAP⁺ fibroblasts represent a transcriptionally distinct subset from α-SMA⁺ myofibroblasts, characterized by enhanced extracellular matrix remodeling and TGF-β production. Together, these findings highlight a critical stromal subset in EF pathogenesis and position BsAb EVs as a promising immunotherapeutic strategy for targeting pathogenic stromal cells in fibrotic and tissue-remodeling disorders.
NAD+ modulates mitochondrial vulnerability in MERTK-associated models of retinitis pigmentosa
Development and validation of a multiancestry and multitrait polygenic risk score for lung cancer
Splenic macrophage-B cell axis drives systemic autoimmune-like pathology in Cerebral Malaria
Hierarchical self-assembly of atomically precise Au6 nanoclusters into fibrillar superstructures with collective optical properties
Highly robust molecular information carriers for traceability of plastic materials
Plasmonic nanocomposite helices for weather-adaptive LiDAR function
No cloning of quantum ensembles
Volcanic eruptions caused weakening AMOC during the preindustrial past millennium
Structural basis for multivitamin recognition and transport by human SMVT
Multiple human transgenes prolong survival of triple-carbohydrate knockout porcine kidney xenografts in nonhuman primates
Systemic atopy and upper-airway disease define susceptibility to incident asthma after COVID-19 in Korea
Abstract Incident asthma is an important respiratory sequela after COVID-19, but it is unclear which allergic phenotypes amplify risk. Using a linked nationwide Korean database of 3,987,182 individuals with confirmed severe acute respiratory syndrome coronavirus 2 infection, we compare claims-based incident asthma in those with pre-existing systemic atopy and/or upper-airway disease (allergic rhinitis, chronic rhinosinusitis, atopic dermatitis or food allergy) versus those without after 1:1 propensity score matching. During follow-up to 31 December 2022, participants with pre-existing disease have higher asthma incidence than matched controls (3.55 vs 2.13 per 1,000 person-years), with a hazard ratio of 1.66 (95% confidence interval 1.58–1.75). Asthma risk is elevated for each condition and increases with greater disease burden. These findings show that pre-existing allergic and upper-airway phenotypes stratify post-COVID incident asthma risk on a national scale, supporting targeted surveillance in high-risk subgroups.