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The present study systematically compared the neural processing of tones, vowels, and consonants in Mandarin syllable perception for both first language (L1) and second language (L2) listeners. Using a passive oddball paradigm, we evaluated participants' syllable perception at a pre-attentive stage with mismatch negativity (MMN). Results confirmed that both L1 and L2 groups exhibited typical MMNs to consonant-, vowel-, and tone-deviant syllables due to their acoustic and/or phonological differences. Specifically, the L1 group exhibited similarly larger MMNs to the vowel- and tone-deviant syllables than to the consonant-deviant syllables, with vowels eliciting the earliest latencies, followed by tones, and consonants demonstrating the latest latencies. The L2 group exhibited graded MMN amplitudes and latencies across three deviation types, with vowels eliciting the strongest and earliest response, consonants an intermediate response, and tones the weakest and latest response. Group comparisons highlighted overall weakened and delayed MMNs for the L2 listeners than L1 listeners, in support of the reduced automaticity inherent in L2 perception. Taken together, our findings reveal the extent and efficiency of Mandarin sub-syllabic processing for both L1 and L2 listeners, and are particularly informative of the neural basis underlying the L2 tone-to-segmental disadvantage.

This study delves into the regulatory mechanism of TRERNA1 in ferroptosis of non-small cell lung cancer (NSCLC) cells. TRERNA1, KAT6A, and PIK3CA are abundantly expressed in NSCLC tissues and cells. TRERNA1 is negatively correlated with ACSL4 but positively correlated with GPX4. TRERNA1 knockdown inhibits cell proliferation and promotes ferroptosis. Mechanistically, TRERNA1 interacts with KAT6A protein to promote KAT6A expression and nuclear ectopy. KAT6A acetylates H3K23, which in turn enhances the binding of TRIM24 to H3K23ac. Therefore, TRIM24 acts as a transcriptional activator to activate the transcription of PIK3CA and inhibit ferroptosis. Overexpression of KAT6A or PIK3CA alleviateS the promoting effect of TRERNA1 knockdown on ferroptosis of NSCLC cells. In conclusion, TRERNA1 represses ferroptosis in NSCLC via the KAT6A/H3K23ac/TRIM24-PIK3CA pathway, representing a promising therapeutic strategy for NSCLC.

In this study, a Schiff base organic ligand (denoted as H2L) bearing specific substituents was prepared by an aldehyde-amine condensation reaction of o-phenylenediamine with 5-fluorosalicylaldehyde. On this basis, we further employed a solvothermal method to react the prepared H2L with zinc chloride in methanol as the reaction medium. After a coordination reaction process, a novel zinc complex crystal (1) with a trinuclear core structure was successfully prepared. Complex 1 was characterized by single-crystal X-ray diffraction, Hirshfeld surface analysis, FT-IR spectra, 1H/13C NMR, UV-Vis and fluorescence spectra. Single-crystal structure analysis indicates that the asymmetric unit is connected via intermolecular C-H···Cl/F hydrogen bonding to form a two-dimensional supramolecular, which is verified by the two-dimensional fingerprint plot. The analysis of the fluorescence spectra indicates that the zinc complex exhibits strong green fluorescence emission around 500 nm upon excitation at 365 nm. Zinc complex 1 possess unique fluorescent properties, providing experimental and theoretical support for the development of novel zinc complex fluorescent materials, while also expanding the application prospects of Schiff base complexes in the field of photoluminescent materials.

Osteoporosis (OP) is increasingly recognized as a disorder driven not only by endocrine and metabolic abnormalities but also by chronic low-grade inflammation and aging-related immune dysregulation. Neutrophil extracellular traps (NETs), web-like extracellular DNA-protein structures released by activated neutrophils, can act as structural inflammatory scaffolds that sustain sterile inflammation, oxidative injury, and microenvironmental imbalance. However, the mechanistic contribution and translational significance of NETs in osteoporosis remain incompletely integrated. This review aims to summarize the current evidence linking NET formation to bone remodeling imbalance in osteoporosis, with particular emphasis on osteoclast activation, osteoblast dysfunction, inflammaging, oxidative stress, ferroptosis, metabolic reprogramming, and potential NET-targeted therapeutic strategies. We reviewed recent studies concerning NET biology, osteoimmunology, inflammaging, and inflammation-associated osteoporosis. Based on these findings, we constructed an integrated "NETs-inflammation-bone remodeling imbalance" framework to explain how persistent NET accumulation may promote osteoclastogenesis, impair osteogenic differentiation, amplify inflammatory feedback loops, and reshape the bone microenvironment. We also discussed the potential clinical relevance of neutrophil-related inflammatory indicators and NET-specific biomarkers. Persistent NET formation and insufficient NET clearance under inflammaging conditions may contribute to a self-sustaining inflammatory-oxidative network in the bone microenvironment. NET-derived extracellular DNA, histones, neutrophil elastase, myeloperoxidase, and citrullinated proteins may activate pattern-recognition receptor pathways, including TLR4/NF-κB and potentially TLR9- and TLR2-related signaling, thereby enhancing RANKL-mediated osteoclastogenesis and suppressing osteoblast differentiation and survival. In parallel, NETs may amplify oxidative stress, disturb iron homeostasis, promote ferroptosis susceptibility, and induce metabolic reprogramming, collectively shifting bone remodeling toward bone resorption. Targeting NET formation, promoting NET degradation, or blocking NET-related inflammatory and oxidative signaling may provide new therapeutic opportunities for inflammation-driven osteoporosis. Nevertheless, the NETs-ferroptosis-metabolic reprogramming axis in osteoporosis should currently be regarded as a promising mechanistic framework that requires further experimental and clinical validation.

Thallium (Tl) is a toxic metal and priority pollutant, its soluble Tl levels in soil drive Tl accumulation in edible plants, posing health risks to gut microbiota via dietary exposure even at low doses. This study investigated Tl accumulation in sweet potatoes (4.45-32.87&#xa0;&#xb5;g/kg dry weight, 0.2442-1.7368&#xa0;&#xb5;g/kg wet weight) from soils (282.89-699.50&#xa0;&#xb5;g/kg) and its impact on a single pooled microbial community derived from fecal samples of three healthy adults (2 females, 1 male, 20-30&#xa0;years) using an in vitro digestion-colon fermentation model. Low-dose Tl exposure drove significant, dose- and time-dependent genus-level restructuring of the pooled microbial community (Kruskal-Wallis, P&#x2009;=&#x2009;0.001; PERMANOVA, P&#x2009;=&#x2009;0.001, R2&#x2009;=&#x2009;0.783-0.980), without altering phylum-level alpha diversity (Kruskal-Wallis, P&#x2009;>&#x2009;0.05), indicating compositional shifts rather than richness loss. Genus-level shifts included proliferation of harmful taxa (Escherichia_Shigella, Enterococcus) and reduction of beneficial taxa (Bacteroides, Prevotella, Akkermansia, Bifidobacterium, Blautia). Significant correlations (p&#x2009;<&#x2009;0.05, 0.6883&#x2009;<&#x2009;R2&#x2009;<&#x2009;0.9850) linked Tl content to Bacteroides, Prevotella, Escherichia_Shigella, and Enterococcus abundances. These findings demonstrate exposure-relevant microbiome shifts within this single pooled microbial community even at Tl concentrations below regulatory limits (300&#xa0;&#xb5;g/kg) via food chain transfer. However, as this in vitro model lacks host-microbe interactions (e.g., immune signaling, peristalsis) and the results reflect the response of one mixed inoculum from three donors rather than inter-individual variability, chronic in vivo studies are essential to validate these shifts and their metabolic and immune implications, informing soil-plant-human safety and public health strategies for low-dose dietary Tl exposure.

Immunotherapy has become a primary treatment for advanced non-small cell lung cancer (NSCLC), although drug resistance is inevitable. Radiotherapy enhances immunotherapy efficacy, particularly in early to mid-stage NSCLC. However, the synergistic effects of radiotherapy and immunotherapy in advanced NSCLC remain controversial. We retrospectively analyzed data from 141 stage IV NSCLC patients treated with first-line immunotherapy or chemoimmunotherapy at Hangzhou Cancer Hospital. Patients were divided into groups receiving radiotherapy combined with immunotherapy versus immunotherapy alone. Progression-free survival (PFS) and overall survival (OS) were evaluated using the Cox regression method. Subgroup Cox regression analyses were performed to optimize the combination regimens. The combined therapy group showed longer PFS (16.9 vs. 8.49 months, HR 0.57, p&#x2009;=&#x2009;0.006) and OS (69.93 vs. 24.62 months, HR 0.60, p&#x2009;=&#x2009;0.04). Subgroup analysis indicated that non-squamous NSCLC patients without immunotherapy rechallenge benefited most. Radiotherapy added to immunotherapy in lung or brain metastases showed a trend toward improved PFS (lung: 19.34 vs. 6.03 months, HR 0.62, p&#x2009;=&#x2009;0.30; brain: 22.72 vs. 7.80 months, HR 0.59, p&#x2009;=&#x2009;0.29). Concurrent (HR 0.41, p&#x2009;=&#x2009;0.02) or consolidation radiotherapy (HR 0.32, p&#x2009;=&#x2009;0.003) during immunotherapy offered greater PFS benefits than symptom-relief radiotherapy. Both stereotactic body radiotherapy and conventional radiotherapy yielded similar survival outcomes. Incidence of grade 3 or higher pneumonia post-lung-radiotherapy was 3.45%. Our study highlights the synergistic efficacy of combining radiotherapy with immunotherapy in advanced NSCLC. Optimizing patient selection, targeting specific sites, effective timing, and tailored radiotherapy regimens significantly improved PFS and OS, providing crucial insights for enhancing clinical outcomes in advanced NSCLC.

The occurrence and progression of autoimmune diseases (AIDs) result from the combined effects of genetic susceptibility, immune response defects, and environmental triggers. Among these, microorganisms, as key environmental factors, have been widely hypothesized to play a role in initiating AIDs, but the exact causal relationship remains to be demonstrated. This review aims to deeply explore the core role of specific microbial infections in triggering AIDs by integrating evidence from three dimensions: epidemiological investigations, clinical studies, and animal model research. We focused on analyzing nine AIDs, including Guillain-Barr&#xe9; syndrome, systemic lupus erythematosus, and rheumatoid arthritis, and confirmed that specific pathogens such as Campylobacter jejuni, Epstein-Barr virus, and Porphyromonas gingivalis can induce corresponding autoimmune pathological damage in susceptible individuals through mechanisms including molecular mimicry and bystander activation. Nevertheless, the field still faces important gaps that caused the chain from mechanism association to clinical application to break.This review integrates existing evidence and demonstrates that microbial infections are one of the important triggers for AIDS. It provides a new theoretical basis and direction for mechanistic research, risk early warning, and targeted intervention of related diseases.

Interleukin-2 (IL-2) is a multifunctional cytokine that plays a central role in the proliferation, differentiation, and function of regulatory T cells (Tregs), effector T cells, and natural killer (NK) cells. Given the immunomodulatory properties of IL-2, high-dose IL-2 has been approved for the treatment of metastatic renal cell carcinoma and melanoma, making it the first cytokine-based immunotherapy to achieve clinical translation. However, the extremely short half-life in vivo, significant systemic toxicity, and immune suppression mediated by the preferential activation of Tregs severely limit its clinical application and therapeutic efficacy. In recent years, with a deeper understanding of the composition and distribution of IL-2 receptor subunits and their downstream signaling pathways, protein engineering research aimed at improving the therapeutic index of IL-2 has become increasingly active. This article reviews the structural-functional relationships of IL-2 and its receptor complexes, summarizes engineering strategies for IL-2 variants, and examines IL-2 delivery systems designed to achieve selective targeting of effector cells in cancer immunotherapy. These approaches have made progress in mitigating IL-2-induced systemic toxicity, providing a design basis for the development of safer and more effective IL-2 therapies.

To assess how perfusion interval relates to myocardial injury and whether this is modified by aortic cross-clamp duration in minimally invasive mitral valve surgery. We retrospectively analysed 556 patients receiving blood-enriched modified del Nido cardioplegia. The primary exposure and outcome were longest perfusion interval and base-10 logarithm-transformed peak cardiac troponin I within 48&#x2009;hours. Analyses included multivariable regression, interaction and subgroup analysis, restricted cubic splines, sensitivity analysis, and logistic regression. Longer perfusion intervals were initially associated with higher cardiac troponin I (regression coefficient 0.0097, 95% confidence interval 0.0035-0.0159; P&#x2009;=&#x2009;0.002). This association disappeared after adjustment for factors including aortic cross-clamp time and number of perfusions (regression coefficient -0.0006, 95% confidence interval -0.0109-0.0097; P&#x2009;=&#x2009;0.913). Aortic cross-clamp time remained independently associated with cardiac troponin I (regression coefficient 0.0099, 95% confidence interval 0.0013-0.0185; P&#x2009;=&#x2009;0.024). In patients with prolonged aortic cross-clamp time, exploratory analysis suggested a non-linear increase beyond 80&#x2009;min. In patients with aortic cross-clamp time of 90&#x2009;min or less, perfusion interval was not clearly associated with peak cardiac troponin I. No significant associations were found with the composite of adverse events. The association between perfusion interval and myocardial injury depended on aortic cross-clamp duration. Single-dose blood-enriched modified del Nido cardioplegia appeared adequate when aortic cross-clamp time was 90&#x2009;min or less. Longer intervals in prolonged procedures may matter, but the 80-minute threshold remains exploratory. These findings support a context-dependent myocardial protection strategy.

Organ size is a key phenotypic trait linking plant structure, physiological function, and ecological adaptation. The epiphytic orchid genus Dendrobium comprises highly diversified species adapted to heterogeneous canopy microhabitats, where water and nutrients are scarce and unpredictable. It has evolved two specialized organs, water-storing pseudobulbs and absorptive succulent roots that are critical for epiphytic survival. However, their central role in drought adaptation, interspecific anatomical variation and the drivers of organ size remain poorly understood. Here, we quantified 7 pseudobulb and 13 root traits across 37 Dendrobium species, using phylogenetic independent contrasts to explore the relationships among traits. All traits exhibited considerable interspecific variation, with pseudobulbs showing greater trait lability than roots, reflecting diversified water-use strategies under epiphytic pressure. Weak phylogenetic signals across traits indicate environmental selection dominates anatomical diversification. Pseudobulb radius correlated strongly with parenchyma area and vascular bundle traits, regardless of phylogenetic correction, but not with epidermis thickness after phylogenetic correction. Root radius was associated closely with cortex, velamen, and vascular bundle traits across analyses, but not with exodermis thickness after phylogenetic correction. Functionally analogous traits (pseudobulb radius vs. root radius; pseudobulb vascular bundle area vs. root vascular bundle area and root exodermis area; pseudobulb parenchyma area vs. root cortex thickness, velamen area, and velamen cell area) between pseudobulbs and roots were consistently and positively correlated, revealing coordinated water-use strategies across organs. Dendrobium organ size is determined by tissue-level adaptive architecture. Pseudobulb size depends primarily on water-storage parenchyma, while root size is tightly linked to absorptive velamen. The species-level variation, driven mainly by environmental selection, underscores diversified hydraulic strategies in epiphytic orchids. Coordinated trait association between pseudobulb and root traits reflects adaptive integration of storage and absorption organs, a key evolutionary strategy for epiphytic survival. These findings highlight the fundamental role of cell and tissue dimensions in shaping orchid organ morphology.

Transcription factors (TFs) are key drivers of tumorigenesis because of their crucial role in regulating aberrant gene expression. They contribute to tumor cell proliferation, invasion, and migration and play a pivotal role in enabling tumors to evade immune detection. In the tumor immune microenvironment (TIME), TFs reprogram tumor-infiltrating immune cells to exert pro-tumor and anti-tumor effects. In this review, we have proposed a novel, mechanism-driven classification of TFs, categorizing them into direct-acting, trans-cellular coordinated, and dual-role TFs. We have investigated the roles of direct-acting TFs in regulating CD8+ T cell exhaustion, maintaining CD8+ T cell effector functions, influencing regulatory T cell infiltration and epigenetic modifications, modulating the polarization and infiltration of tumor-associated macrophages, and promoting pro-tumor or anti-tumor properties of natural killer cells, dendritic cells and Myeloid-derived suppressor cells. In addition, we have emphasized the trans-cellular coordinated TFs that serve as bridges, facilitating cooperation among different immune cells to remodel the TIME. Finally, we have highlighted dual-role TFs that exhibit opposing functions dictated by distinct isoforms, splice variants, or post-translational modifications. Additionally, we highlight emerging pharmacological strategies targeting TFs, emphasizing their clinical potential to reverse TIME immunosuppression and synergize with immune checkpoint inhibitors. With an enhanced understanding of the molecular mechanisms underlying tumorimmune system interactions within the TIME, next-generation therapeutic strategies targeting TFs can be developed.

To evaluate the diagnostic value of multislice spiral computed tomography (MSCT) in differentiating pancreatic acinar cell carcinoma (PACC) from pancreatic ductal adenocarcinoma (PDAC). The clinical, pathological, and imaging data of 17 patients with pathologically confirmed PACC and 62 patients with PDAC were retrospectively analyzed. Quantitative variables were compared between groups using the independent samples t-test or the Mann-Whitney U test, as appropriate. Qualitative variables were compared using the Pearson's chi-square test or Fisher's exact test. Variables showing statistical significance in univariate analysis were entered into multivariate logistic regression analysis to identify independent predictors for distinguishing PACC from PDAC. Diagnostic performance was assessed using receiver operating characteristic curve analysis, with calculation of the area under the curve (AUC), sensitivity, specificity, positive predictive value, negative predictive value, and accuracy. Univariate analysis demonstrated significant differences between the two groups in tumor shape, margin, pancreatic atrophy, pancreatic duct transection, maximum tumor diameter, CT attenuation values, and enhancement ratios in the pancreatic parenchymal, portal venous, and delayed phases, all of which showed statistically significant differences. Multivariate logistic regression analysis identified tumor margin, pancreatic duct transection, pancreatic parenchymal phase CT attenuation value as independent predictors for distinguishing PACC from PDAC. The combined diagnostic model incorporating these variables achieved the highest diagnostic performance, with an AUC of 0.968. The model demonstrated a sensitivity of 94.1%, specificity of 88.7%, accuracy of 89.9%, positive predictive value of 69.5%, and negative predictive value of 98.2%. Tumor margin, pancreatic duct transection, and pancreatic parenchymal phase CT attenuation value are significant imaging features for differentiating PACC from PDAC. A combined diagnostic model integrating these imaging features provides excellent diagnostic performance and may aid in improving preoperative differential diagnosis.

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Early adolescence represents a developmental period marked by increased vulnerability to loneliness and meaninglessness. Although theoretical frameworks posit reciprocal associations between loneliness and life meaning, longitudinal research examining their developmental trends and reciprocal associations has been limited. A total of 3825 Chinese junior high school students (47.5% girls; Mage = 12.36, SD&#x2009;=&#x2009;0.50) participated in this five-wave longitudinal study, among whom 39.9% were only children and 80.7% came from middle-class families, with other demographic details presented later. The results showed that loneliness increased slowly in the first semester of seventh grade, rose sharply in the next semester, and grew steadily in eighth grade. Adolescents' presence of meaning dropped sharply in the seventh-grade second semester, with slow declines continuing afterward. Parallel process latent growth modeling indicated that a faster increase in loneliness was associated with a greater decline in the presence of meaning. And random intercept cross-lagged modeling revealed that higher loneliness predicted lower subsequent the presence of meaning, whereas stronger the presence of meaning predicted reduced later loneliness, indicating co-development and bidirectional links in early adolescence.

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With escalating global health challenges, triclocarban (TCC) contamination has reemerged as a critical ecological threat, especially in wetland ecosystems. Yet, the mechanisms by which arbuscular mycorrhizal fungi (AMF) regulate plant root resistance and the rhizosphere environment under TCC exposure remain poorly understood. Here, we established an AMF-Phragmites communis symbiotic system and conducted TCC exposure experiments. Our results demonstrated that TCC exposure significantly inhibited mycorrhizal colonization, root morphology, and the antioxidant system of P. communis. Specifically, under the 5&#xa0;mg kg-&#x2009;1 soil TCC exposure, arbuscule abundance decreased by 3.53-fold, root total length declined to 1011.13&#xa0;cm, and the integrated biomarker response index value of the antioxidant system dropped to 0.25. In contrast, arbuscular mycorrhizal (AM) symbiosis promoted root morphological and physiological growth. Transcriptome analysis revealed that AM symbiosis upregulated genes encoding key enzymes in the Mitogen-Activated Protein Kinase (MAPK) signaling pathway (e.g., MAPKKK and MAPK family members), whereas TCC exposure downregulated their expressions. Furthermore, in the rhizosphere soil, the composition and structure of microbial communities were distinctly influenced by AM symbiosis and TCC exposure. Compared to AM symbiosis, which upregulated soil metabolites associated with metabolism, TCC exposure downregulated soil metabolites across multiple functional categories, including metabolism, environmental information processing, and cellular processes. This research broadens our understanding of how AM symbiosis enhances the resistance of P. communis and maintains the stability of the rhizosphere environment under TCC exposure, and evidences the potential of AMF application in improving the purification capacity of wetland systems.

4&#x2011;Nitrophenol (4&#x2011;NP) pollution causes serious environmental risks. Traditional catalysts and surfactant&#x2011;modified metal foams suffer from insufficient active sites, poor stability and low catalytic efficiency, restricting their practical industrial applications. To solve these problems, this work develops a green, surfactant&#x2011;free one&#x2011;pot route to fabricate PdCu bimetallic foam catalysts with a unique 3D interwoven nanowire network, which effectively overcomes the above limitations. The catalyst is synthesized via room&#x2011;temperature reduction of Pd(NO3)2 and CuSO4 precursors by NaBH4, followed by water&#x2011;ethanol alternate washing and freeze&#x2011;drying. This fabrication method is simple, scalable and eco&#x2011;friendly without harsh synthetic conditions. Key structural and compositional advantages include: the 3D porous network reduces mass&#x2011;transfer resistance; surfactant&#x2011;free synthesis yields a clean catalyst surface to facilitate active site&#x2011;substrate interactions; ultrathin nanowires maximize exposed active sites; and Pd&#x2011;Cu electronic synergy decreases Pd consumption and optimizes electronic configuration for improved catalytic activity. Among as&#x2011;prepared catalysts, Pd3Cu1 exhibits the optimal performance, achieving complete 4&#x2011;NP reduction within 269&#xa0;s with a high apparent rate constant (Kapp&#x2009;=&#x2009;29.18&#x2009;&#xd7;&#x2009;10&#x2011;3&#xa0;s&#x2011;1) and TOF value of 2309&#xa0;h&#x2011;1, as well as good reusability after five consecutive cycles. This green synthetic strategy and structural merits offer a facile pathway to design high&#x2011;performance bimetallic catalysts for environmental remediation.

The 5-HT2A receptor (5-HT2AR) is a validated target in schizophrenia (SCZ); however, the therapeutic potential of repurposed drugs targeting this pathway remains underexplored. Here, we show that the antihistamine desloratadine (DLT) robustly ameliorates a full spectrum of SCZ-like behavioral deficits in an MK-801-induced male mouse model. Single-nucleus RNA sequencing (snRNA-seq) analysis revealed 5-HT2AR expression specifically within neuronal populations of the medial prefrontal cortex (mPFC). Mechanistically, these behavioral impairments were associated with a specific upregulation of 5-HT2AR in mPFC neurons-a molecular pathology reversed by DLT. Targeted overexpression of 5-HT2AR in mPFC neurons was sufficient to recapitulate the SCZ-like phenotypes, which are rescued by DLT, establishing a causal role for this receptor in disease pathology. Through integrated transcriptomic and biochemical analyses, we identified the PI3K/AKT/mTOR pathway as a key downstream effector of 5-HT2AR. We demonstrated that 5-HT2AR-mediated activation of this pathway drives neuroinflammation, apoptosis, and long-term potentiation impairments-effects that were effectively blocked by DLT. In a definitive pharmacological reversal experiment, activation of AKT with SC79 completely abrogated DLT's therapeutic efficacy, both behaviorally and molecularly. Collectively, our findings reveal that DLT exerts its therapeutic effects by suppressing a pathogenic feed-forward loop, wherein 5-HT2AR activates the PI3K/AKT/mTOR pathway, which may, in turn, sustain its own aberrant expression. This study provides a compelling rationale for repurposing desloratadine for SCZ and validates the 5-HT2AR-PI3K/AKT/mTOR signaling axis as a pivotal, druggable target for therapeutic intervention.

The South American tomato pinworm, Tuta absoluta (Lepidoptera: Gelechiidae), is a devastating invasive pest of tomato (Solanum lycopersicum). To evaluate candidate female-oriented semiochemicals, we examined the electroantennogram (EAG) activity of ten tomato-associated volatiles selected from previous reports. The compound 1-nonanol was selected as a candidate based on its relatively strong EAG activity and was subsequently assessed for its effects on olfaction, orientation, and oviposition. These findings indicate that 1-nonanol elicits female-biased attraction and stimulates oviposition under laboratory conditions. However, its ecological relevance within natural tomato volatile blends and its field performance require further validation before it can be developed as a female-oriented IPM component.