ABSTRACT Chronic obstructive pulmonary disease (COPD) is a devastating condition characterized by airflow limitation, inflammation, and structural lung damage. Metabolic dysregulation is recognized as a critical feature, but the key metabolic drivers remain unclear. This study identifies transaldolase1 (TALDO1) as a previously unrecognized metabolic regulator in cigarette smoke (CS)‐induced COPD pathogenesis. TALDO1 is markedly upregulated in airway epithelial cells by CS exposure. Elevated TALDO1 promotes mitochondrial dysfunction, whereas its genetic knockdown attenuates CS‐induced lung function decline and pulmonary inflammation. Mechanistically, TALDO1 activation redirects tryptophan metabolism toward the kynurenine pathway, leading to L‐kynurenine accumulation. Genetic or pharmacological inhibition of this pathway significantly alleviates mitochondrial damage, while L‐kynurenine supplementation exacerbates injury. Treatment with the IDO inhibitor Epacadostat ameliorates CS‐induced lung impairment and inflammation in vivo. These findings define a TALDO1‐kynurenine‐mitochondrial injury axis linking airway epithelial metabolic reprogramming to COPD, providing translational evidence for targeting this pathway as a therapeutic strategy.
ABSTRACT Human experience is inherently rich and multisensory, composed of intertwined visual, auditory, and kinesthetic feedback. Digital media capture only its audiovisual dimensions, omitting its mechanosensory dimensions. While full‐body (kinesthetic) haptic feedback can enrich media, no general method exists for deriving structured motion from heterogeneous signals and combining it with the audiovisual content for rendering. The Experience Filter maps multimedia signals into structured motion trajectories through a common pipeline of modality‐specific feature extraction followed by a modality‐agnostic shared encoding, recombining them into a synchronized multisensory experience: each signal is reduced to a shared descriptor space – signal intensity, dominant spectral feature, and distance from neutral axis – then mapped to a trajectory via a fixed, deterministic, training‐free encoding. Because this encoding space is hardware‐independent, the motion can be retargeted to robotic platforms of arbitrary degrees of freedom and morphology. A feature‐sensitivity analysis shows that the descriptor axes are independent and the encoding‐space topology follows from the chosen descriptors rather than being fixed. The framework is demonstrated on real‐world music and images, producing continuous, synchronized image‐audio‐motion experiences without manual authoring. The Experience Filter thus provides an analytical mapping from multimedia signals to combined image‐audio‐motion rendering, enabling expressive, user‐adjustable experience across robotic platforms.
ABSTRACT Host innate immunity is a major barrier to microbial infection and often limits the efficacy of biological and chemical pest‐control agents. While microbial immunosuppressive effectors have been described, whether quorum‐sensing systems coordinate virulence and immune suppression during host infection remains largely unknown. We demonstrated that the PlcR‐PapR quorum‐sensing system acts as a master regulator that promotes both processes (virulence and immune suppression) to enhance Bacillus thuringiensis (Bt) pathogenicity. During infection, PlcR‐PapR signaling induces production of the heptapeptide PapR 7 , which activates expression of patatin‐like protein PisP, a previously uncharacterized and widely conserved protein. PisP suppresses host immunity by inhibiting nuclear translocation of the transcription factor DAF‐16, thereby attenuating the expression of antimicrobial defense genes. Consistent with this mechanism, Bt strains overexpressing pisP display enhanced virulence against both nematodes and insect hosts. Importantly, exogenous PisP markedly potentiates the activity of Bt Cry5Ba toxin and several commercial chemical insecticides, enabling effective pest control at reduced doses. Together, these findings reveal a quorum‐sensing‐controlled mechanism that links virulence regulation to immune suppression during Bt infection and identify PisP as a conserved Bt‐encoded immunosuppressive effector with strong potential as a bio‐adjuvant for improving the efficacy and sustainability of biological and chemical pest‐management strategies.
ABSTRACT The rapid advancement of wearable electronics places ever‐increasing demands on the electrical and mechanical properties of materials. Cellulose offers renewability, low cost, and high durability for green wearables, but its weak electron‐donating ability and poor charge‐transport efficiency limit triboelectric performance. Interfacial mismatch between the electrode and triboelectric layers also induces charge dissipation, further aggravating this problem. Inspired by the Janus structure found in sea urchin spines, a gradient‐integrated triboelectric material (MWCNT/T‐CNFs) was fabricated via vacuum‐assisted layer‐by‐layer filtration. The resulting gradient electric field forms a highly compatible interface between the triboelectric layer and the electrode layer, providing a low‐impedance path that effectively suppresses charge dissipation. Consequently, the material achieves a surface charge density of 20.5 nC cm −2 (931.8% that of pure T‐CNFs) and excellent cycling stability (8044 cycles). The integrated interface offers strong adhesion, far outperforming conventional electrode tapes, while the gradient design alleviates stress concentration, yielding a tensile strength of 126.33 MPa and toughness of 9.11 MJ m −3 (535.9% that of pure T‐CNFs). The material also exhibits good water stability and high‐temperature resistance. This study addresses the key limitations of low surface charge density and interfacial mismatch in cellulose materials, providing a solid foundation for interface design in wearable electronics.
ABSTRACT Metabolic reprogramming and immune evasion are critical drivers of hepatocellular carcinoma (HCC) progression and therapeutic resistance, yet the upstream regulators linking these processes remain poorly understood. Here, we identify adipogenesis‐associated secreted signaling protein (ADISSP) as a previously unrecognized oncogenic regulator in HBV‐related HCC. ADISSP was markedly upregulated in HCC tissues and associated with poor prognosis, while its inhibition suppressed tumor progression in vitro and in vivo. Mechanistically, ADISSP interacted with PPP1CA to sustain NF‐κB activation, resulting in transcriptional induction of SLC16A3 and CCL20. The ADISSP/SLC16A3 axis promoted glycolytic adaptation and lactate‐mediated STAT3 activation, thereby driving macrophage M2 polarization, whereas CCL20 facilitated macrophage recruitment. Together, these pathways established an immunosuppressive tumor microenvironment characterized by enhanced M2 macrophage infiltration and impaired antitumor immunity. More important, targeting ADISSP markedly enhanced the therapeutic efficacy of anti‐PD‐1 plus lenvatinib in HCC. Collectively, our findings identify ADISSP as a central regulator integrating metabolic reprogramming and immune suppression through the PPP1CA/NF‐κB axis and highlight ADISSP as a potential therapeutic target for increasing immunotherapy sensitivity in HCC.
