Despite the success of Multimodal Sentiment Analysis in ideal settings, real-world data corruption often leads to “variance explosion” in continuous latent spaces and “semantic drift” during teacher–student alignment. To overcome these challenges, we introduce Quantized and Distilled Robust Fusion (QDRF), a framework that replaces fragile continuous imputation with a Finite Scalar Quantization bottleneck to improve robustness against latent-space perturbations through a discrete semantic pivot. We further stabilize the system using an asymmetric Exponential Moving Average distillation framework that enforces dual alignment at both the feature and weight levels. Evaluated on CMU-MOSI, CMU-MOSEI, and CH-SIMS, QDRF achieves state-of-the-art or highly competitive performance on CMU-MOSEI and CH-SIMS, demonstrating that linguistic-prior-guided discrete representation learning is effective for robust sentiment prediction in incomplete data environments.
The inflammatory response in the cerebral cortex serves an important role in the progression of secondary injury following traumatic brain injury (TBI). The NLR family pyrin domain containing 3 (NLRP3) inflammasome is necessary for initiating inflammation and is involved in various central nervous system disorders. The aim of the present study was to investigate the neuroprotective effect of resveratrol and elucidate the underlying mechanisms of resveratrol associated regulation of the NLRP3 inflammasome in TBI. The results demonstrated that the activation of NLRP3, caspase‑1 and sirtuin 1 (SIRT1), enhanced the production of inflammatory cytokines and reactive oxygen species (ROS) following TBI. Administration of resveratrol alleviated the degree of TBI, as evidenced by the reduced neuron‑specific enolase (NSE) and brain water content (WBC). Resveratrol pretreatment also inhibited the activation of NLRP3 and caspase‑1, and reduced the production of inflammatory cytokines and ROS. In addition, resveratrol further promoted SIRT1 activation. Furthermore, the suppressing effect of resveratrol on the NLRP3 inflammasome and ROS was blocked by the SIRT1 inhibitor, sirtinol. The results revealed that the activation of the NLRP3 inflammasome and the subsequent inflammatory responses in the cerebral cortex were involved in the process of TBI. Resveratrol may attenuate the inflammatory response and relieve TBI by reducing ROS production and inhibiting NLRP3 activation. The effect of resveratrol on NLRP3 inflammasome and ROS may also be SIRT1 dependent.
The microgravity, radiation, and high-stress environment of space present unique challenges to astronauts’ physical and mental health. In this environment, interactions between the host and pathogens are altered, thereby increasing astronauts’ risk of endogenous viral infections. Notably, viral shedding detected during spaceflight does not necessarily indicate clinically significant disease, and the distinction between molecular reactivation, productive viral replication, and symptomatic infection must be carefully considered. This review aims to ensure mission success and enhance space biocapacity and biodefence by summarizing case studies and reactivation mechanisms of endogenous latent herpesviruses, the latest prevention and control strategies, and the challenges posed by host variability and antiviral efficacy in the space environment.
Intentional emotional contagion, the conscious transmission of emotions between individuals, has unclear neurobehavioral mechanisms in naturalistic dyadic communications. Experiment 1 demonstrated that conscious engagement enhanced sad emotional contagion between strangers. Using the fNIRS pseudo-hyperscanning technique, Experiment 2 showed a behavioral-neural dissociation in intentional sadness contagion: Behavioral findings revealed increased interpersonal intimacy and listener altruism. Neurocognitive findings demonstrated reduced activation in the left frontopolar cortex, bilateral dorsolateral prefrontal cortex (dlPFC), and angular/supramarginal gyri. While weaker interpersonal neural synchronization emerged between the speaker’s left frontopolar/dlPFC and listener’s right dlPFC. Mediation analysis indicated that intentional emotional contagion mediated emotional communication and self-other overlap, extending Emotions as Social Information Model. Findings suggest that intentional sadness contagion based on dyadic story sharing has an adaptive neurocognitive reorganization which facilitates prosocial behavior.
BACKGROUND:Coenzyme Q10 (CoQ10) is a key mitochondrial electron carrier and a widely used dietary supplement with potential neurological benefits. However, the mechanisms underlying its effect in ameliorating memory deficits caused by cerebellar injury are not fully understood. In this study, we investigated the effects of long-term CoQ10 supplementation on working memory and the underlying mechanisms. METHODS:Network pharmacology analysis was used to identify genetic targets of CoQ10 in cerebellar injury-related cognitive impairment. Purkinje cell (PC)-specific Drp1-deficient mice (PC-Drp1-/-) were generated to model mitochondrial dysfunction. Behavioral performance was evaluated using the eight-arm radial maze. Mitochondrial structure and respiratory chain complex levels were evaluated by morphological and biochemical assays. Molecular targets of CoQ10 were identified using integrated drug-target engagement approaches, and their functional relevance was tested by viral vector-mediated overexpression. RESULTS:The PC-Drp1-/- mice displayed progressive working memory impairment and decreased PC density, accompanied by disrupted mitochondrial morphology and reduced activities of electron transport chain complexes III-V. Long-term CoQ10 treatment significantly reduced working memory errors and preserved PC numbers in PC-Drp1-/- mice. Target engagement analyses identified cytochrome c oxidase assembly factor 6 (Coa6) as a direct binding target of CoQ10. Viral vector-mediated overexpression of Coa6 in PCs partially recapitulated the CoQ10-associated improvements in respiratory chain complex levels and working memory, whereas Coa6 knockdown attenuated these benefits. CONCLUSIONS:CoQ10 directly interacts with Coa6 to enhance mitochondrial respiratory chain function and preserve PC integrity in the context of Drp1 deficiency. Our findings suggest a promising mechanistic pathway for CoQ10-based intervention in memory deficits associated with mitochondrial dysfunction.
