Serotonergic psychedelics (SP) are increasingly used in clinical research and naturalistic settings, but their psychotic-like side effects, including persisting perceptual abnormalities (PPAs), are poorly understood. Psychosis-associated hallucinations are associated with susceptibility to conditioned hallucinations and computationally-estimated overweighting of perceptual expectations, or priors. However, SPs are widely argued to reduce prior weighting. We surveyed 186 naturalistic SP users on prior SP use, SP-associated PPA history, and current PPAs. Participants completed the visual conditioned hallucinations (VCH) task, in which conditioning induces perception of absent stimuli. Behavioral data were used to fit parameters of a computational model to estimate latent states driving percepts and responses. Past and current PPAs were associated with younger age at first use and higher SP doses, lower visual thresholds, higher VCH rate and confidence, and reduced sensory discrimination. Among model parameters, however, only reduced decision precision tracked both measures and mediated the dose-PPA relationship; relative prior weighting rose equivocally, as expected when priors and sensory evidence gain precision together. SP-related PPAs may therefore arise from a noisy visual system biased toward detection, in which priors act as templates that convert sensory noise into expected percepts. These findings may point to a tractable model for how psychotic-like perception emerges.

Intracerebral hemorrhage (ICH) is associated with substantial morbidity and mortality, and early hematoma expansion (HE), defined as an increase in hematoma volume on follow-up imaging, is a major determinant of early neurological deterioration and poor outcomes. Accurate, hyperacute prediction of HE is critical for guiding precise interventions, such as intensive blood pressure management and surgical evacuation. This narrative review examines the progression of prediction models from univariate predictors to systems incorporating artificial intelligence (AI), with particular attention to risk factors, model validation, and clinical translation. We further examine the validation status of current prediction models and the methodological and practical barriers to their clinical implementation. We review the progression from established independent predictors, such as the CT angiography (CTA) spot sign (SpS) and non-contrast CT (NCCT) island sign (IS), to multivariable clinical scoring systems, radiomics-based machine learning (ML) approaches, and deep learning (DL) models, while also discussing emerging generative architectures. Furthermore, major clinical trials evaluating strategies to limit HE are reviewed. Finally, the current challenges and future prospects of predictive models of HE are also elucidated.

Potassium (K) is a key nutrient for increasing yield, improving quality, and enhancing stress resistance in wax gourd (Benincasa hispida). However, the phenotypic, physiological, ecological, and molecular adaptation mechanisms of wax gourd under different K levels remain poorly understood. In this study, a field experiment was conducted with three treatments, i.e., K deficiency (K0), moderate K (300 kg K2O hm[-2], K300), and excessive K (500 kg K2O hm[-2], K500), to evaluate the effects of K fertilization on the morphology, physiology, and transcriptomics of wax gourd. Results showed that compared with K300, K0 and K500 reduced wax gourd yield by 25.22% and 10.38%, respectively. Fruit soluble sugar, soluble protein, titratable acidity, vitamin C, and dry matter content were all significantly decreased under K0 treatment. Both K0 and K500 damaged chloroplast ultrastructure, induced stomatal closure, and reduced photosynthetic efficiency. Under K0, the activities of Rubisco, sucrose phosphate synthase (SPS), and ADP-glucose pyrophosphorylase (AGPase) decreased by 50.79%-60.30%, 58.75%-61.11%, and 51.20%-54.00%, respectively, while photosynthetic K-use efficiency (PKUE) and K accumulation decreased by 1.54%-22.70% and 25.67%-65.95%. Collectively, K deficiency exacerbated yield and quality reduction by inhibiting photosynthesis and K[+] uptake/utilization. Transcriptomic analysis revealed that under K deficiency, genes associated with photosynthesis, photosynthetic antenna proteins, nitrogen metabolism, and starch and sucrose metabolism were downregulated, whereas genes associated with antioxidant enzyme activity and plant hormone signal transduction (ABA and CTK) were upregulated. Under excess K, genes encoding various transporters, as well as those involved in starch and sucrose metabolism, were downregulated. In conclusion, among the tested K levels, K300 (300 kg K2O hm[-2]) showed the best overall performance in wax gourd cultivation, contributing to synergistic improvements in yield, quality, and fertilizer efficiency. This study offers both theoretical insights and practical guidance for elucidating K-stress response mechanisms and for optimizing K-fertilizer strategies in wax gourd.

Pathogenic microbes deploy secreted effectors to subvert host immunity and physiology across kingdom boundaries, yet the molecular mechanisms that maintain effector competence during this transition remain poorly defined. Here, we identify MrNIS1, an effector from the insect-pathogenic fungus Metarhizium robertsii whose stability and secretion are governed by K24 acetylation through physical association with the acetyltransferase MrKAT1 and the deacetylase MrSIR2. Once inside the insect, MrNIS1 acts as a dual-targeting effector to disrupt distinct physiological pathways. It binds the serine protease SPS to block prophenoloxidase activation, thereby suppressing melanization-based immunity. MrNIS1 interacts with the evolutionarily conserved cholesterol transporter ERP, disrupting ecdysteroid biosynthesis and leading to impaired larval growth and cuticle synthesis. This MrNIS1-ERP interaction is functionally conserved across Lepidoptera, Coleoptera, and Diptera. Furthermore, heterologous expression in Beauveria bassiana demonstrates that the KAT1/SIR2 regulatory system is conserved across fungal species, where MrNIS1 acts as a portable virulence module to significantly enhance pathogen efficacy. Our findings reveal that lysine acetylation serves as a molecular switch that preserves effector competence during cross-kingdom transit, enabling the simultaneous targeting of multiple host physiological processes. These results elucidate a conserved strategy of fungal pathogenesis and identify potential targets for the improvement of microbial biocontrol agents.

Supraparticles (SPs) are secondary particles formed through nanoparticle self-assembly with porous architectures and bioinspired structural features suitable for drug delivery applications. Although binder-mediated structural control influences SP assembly, how different loaded drugs systematically alter amyloid nanofibril (ANF) and SP structures remains unclear. In this study, neutral, basic, and acidic model drugs-acetaminophen (ACP), fluconazole (FCZ), and proglumide (PGM), respectively-were incorporated into spray-dried SPs composed of silica nanoparticles (SiNPs) and ANFs to investigate the effects of drug properties on SP structure and release behavior. All drugs exhibited nearly 100% loading efficiency, and powder X-ray diffraction analysis revealed that they were in an amorphous state within the SPs. ACP- and FCZ-loaded SPs maintained their characteristic ANF-induced wrinkled morphology, whereas PGM-loaded SPs exhibited a pronounced loss of wrinkling at pH 2, indicating that acidic drugs can disrupt ANF-mediated assembly during SP formulation. Drug release studies further showed that ANFs suppressed the initial burst release and slowed the overall release by restricting diffusion pathways within the SP structures. This suppression was the most pronounced in PGM-loaded SPs, likely owing to drug retention within the assembled ANF domains. These findings demonstrate that drug acid-base properties critically modulate SP morphology and release behavior, highlighting the importance of drug-biomaterial interactions in designing SP-based delivery platforms.

Dysfunction of the ventral tegmental area (VTA) dopaminergic circuits is strongly implicated in the pathological progression of post-traumatic stress disorder (PTSD). Oxytocin (OXT) exerts robust stress-buffering effects, yet its direct neuromodulatory influence on VTA dopaminergic neurons under PTSD pathological conditions remains poorly defined. Here, we performed in vivo extracellular recordings to quantify spontaneous firing and burst activity in normal control and single prolonged stress (SPS)-induced PTSD model rats. Graded intracerebroventricular OXT infusions and OXTR antagonist pretreatment were used to characterize OXT-mediated neuronal modulation. Baseline spontaneous firing and burst rates were markedly suppressed in PTSD model rats; however, OXT elevated neuronal excitability in both cohorts, an effect nearly abolished by pretreatment with the selective OXTR antagonist L-371,257. Although absolute firing values remained persistently lower in PTSD model rats at baseline and following OXT administration, the relative fold increase in response to OXT was comparable to that observed in normal controls. These electrophysiological findings demonstrate that PTSD-like traumatic stress depresses baseline VTA dopaminergic activity, whereas the excitatory responsiveness of VTA dopaminergic neurons to exogenous OXT is largely preserved in PTSD model animals.

Adaptive survival requires flexibly choosing passive or active defenses as threat intensity varies. Many studies have described the execution of defensive behaviors, but the flexibility of mice to choose defensive strategies is poorly understood. Here, we demonstrate that auditory cues of different intensities (60 dB and 80 dB) elicit passive (freezing) and active (escape) defensive behaviors in mice, mimicking the flexibility to choose appropriate defensive behaviors when faced with varying degrees of threat. Single prolonged stress (SPS) mice exhibited dysregulated defensive behavior selection, showing a maladaptive tendency to freeze when facing imminent threats. Chemogenetic inhibition of the dorsal periaqueductal gray (dPAG) and ventrolateral periaqueductal gray (vlPAG) coordinates selective shifts in defensive behavior. These results imply that interactions between the dPAG and vlPAG may support flexible defensive strategy selection and influence behavioral output, highlighting PAG circuitry as a candidate target for improving adaptive responses in stress-related disorders.

CsSnI3-based perovskite light-emitting diodes (PeLEDs) show great potential in near-infrared (NIR) applications, yet device performance is limited by interfacial degradation at the acidic hole-transport layer (HTL) based on Poly(3,4-ethylenedioxythiophene):poly(styrene sulfonate) (PEDOT:PSS). Herein, a multifunctional guanidine derivative of N-(3-methoxy-phenyl)-guanidine (NMPG), is used to modify the buried interface between the CsSnI3 perovskite and the HTL. NMPG deprotonates the polystyrene sulfonic acid (PSSH) of PSS and reduces the acidity of PEDOT:PSS, while its methoxy and C═N groups coordinate with Sn[2+], effectively inhibiting Sn[2+] oxidation, passivating Sn (II) induced defects. This customized buried interface enables uniform and discrete growth of perovskite grain, improves charge injection balance, and enhances vertical compositional and optical homogeneity. As a result, the target PeLEDs achieve a competitive maximum external quantum efficiency (EQE) of 9.0% and a high average EQE of 8.4%, significantly outperforming the control device (EQEmax = 6.6%, EQEave = 5.5%). The target PeLEDs also demonstrate superior operational stability, with a T50 lifetime of 67.9 h, representing a 5-fold improvement compared to the control PeLEDs. This work reveals the pivotal role of buried interface chemistry and presents a viable molecular design strategy for achieving high-performance CsSnI3-based PeLEDs.