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The objective of this paper is to investigate the possibility and efficacy of recurrent laryngeal nerve repair by transplantation of co-cultured Schwann cells and neural stem cells (NSCs) in laminin-chitosan-poly-lactic-co-glycolic acid (laminin-chitosan-PLGA) nerve conduits in rats. A laminin-chitosan-PLGA conduit was used in a rat recurrent laryngeal nerve transection model. The rat recurrent laryngeal nerve was dissected to generate a 5  mm defect. Then, a laminin-chitosan-PLGA nerve conduit with or without Schwann cells and NSCs in the lumen was transplanted into the defect. A total of 96 female rats were randomised into six groups: co-culture of NSCs and Schwann cells in the nerve conduit group (CO), Schwann cells only in the nerve conduit group (SC), neural stem cells only in the nerve conduit group (NSC-only), nerve conduit group (null), autologous nerve graft group (autograft) and sham operation group (sham). Regenerated nerves were evaluated by histological and functional assessment at 8 and 12 weeks after surgery. The diameter and area of the regenerated myelin sheath, as well as the secretion of brain-derived neurotrophic factor and glial cell-derived neurotrophic factor in laryngeal muscle or regenerated nerve tissue in the CO group, were significantly better than they were in the SC, NSC-only and null groups (all P values  <  0.05). Immunofluorescence showed that the CO group had significantly more neurofilament-200 immunoreactive and S-100 immunoreactive fibres than the SC, NSC-only and null groups (all P values  <  0.05). The performance of the CO groups and autograft groups was found to be similar by laryngoscopy. Arytenoid cartilage motion recovery in these two groups was significantly better than it was in the other groups (all P values  <  0.05). Our results indicated that co-culture of Schwann cells and NSCs in laminin-chitosan-PLGA conduits might promote injured nerve regeneration. This method might be a promising alternative for defective nerve repair.

Background Seismic analysis in marine geotechnical engineering is computationally intensive. Conventional methods for accounting for the influence of infinite water domains are often costly and time-consuming. Objective To propose a simplified anhydrous substructure model that significantly reduces computational cost while maintaining accuracy for efficient seismic analysis of ocean engineering sites. Methods The model employs the finite element method to discretize the seawater, saturated seabed, and bedrock as an integrated system. Its core innovations involve the precise derivation of the coupling interface condition between the water and the saturated medium, and the introduction of an exact artificial boundary to model the radiation damping effect of the infinite water domain. The seismic input, based on one-dimensional free-field response, is extended to the artificial boundaries of each medium layer via Snell's law to obtain equivalent seismic loads. Following this, and assuming water incompressibility, the expression for dynamic water pressure on the saturated medium surface is derived and incorporated into the global finite element equation as an added mass model. Results The proposed anhydrous substructure model achieves a significant improvement in computational efficiency while ensuring analytical accuracy. Conclusion The model's correctness and its applicability to sites with structures are verified through comparison with a full-domain model. It provides an efficient and reliable numerical tool for seismic analysis in ocean engineering that considers seawater effects, demonstrating considerable potential for future engineering applications.

The influenza virus induces cellular apoptosis during viral propagation, and controlling this virus-induced apoptosis process has been shown to have significant antiviral effects. The proapoptotic BH3-only protein Noxa is a strong inducer of apoptosis that can be activated by this virus, suggesting that Noxa has the potential as an anti-influenza target. To assess the value of Noxa as an antiviral target, we utilized CRISPR/Cas9 technology to produce a Noxa-knockout cell line. We found that the knockout of Noxa resulted in a dramatic reduction in the cytopathic effect induced by the influenza virus. Moreover, Noxa knockout decreased the expression of influenza viral proteins (NP, M2, HA, and NS2). In addition, Noxa deficiency triggered a complete autophagic flux to weaken influenza virus-induced autophagosome accumulation, indicating that Noxa may be a promising antiviral target for controlling influenza virus infections.

The white-striped longhorn beetle Batocera horsfieldi (Coleoptera: Cerambycidae) is a polyphagous wood-boring pest that causes substantial damage to the lumber industry. Moreover olfactory proteins are crucial components to function in related processes, but the B. horsfieldi genome is not readily available for olfactory proteins analysis. In the present study, developmental transcriptomes of larvae from the first instar to the prepupal stage, pupae, and adults (females and males) from emergence to mating were built by RNA sequencing to establish a genetic background that may help understand olfactory genes. Approximately 199 million clean reads were obtained and assembled into 171,664 transcripts, which were classified into 23,380, 26,511, 22,393, 30,270, and 87, 732 unigenes for larvae, pupae, females, males, and combined datasets, respectively. The unigenes were annotated against NCBI's non-redundant nucleotide and protein sequences, Swiss-Prot, Gene Ontology (GO), Pfam, Clusters of Eukaryotic Orthologous Groups (KOG), and KEGG Orthology (KO) databases. A total of 43,197 unigenes were annotated into 55 sub-categories under the three main GO categories; 25,237 unigenes were classified into 26 functional KOG categories, and 25,814 unigenes were classified into five functional KEGG Pathway categories. RSEM software identified 2,983, 3,097, 870, 2,437, 5,161, and 2,882 genes that were differentially expressed between larvae and males, larvae and pupae, larvae and females, males and females, males and pupae, and females and pupae, respectively. Among them, genes encoding seven candidate odorant binding proteins (OBPs) and three chemosensory proteins (CSPs) were identified. RT-PCR and RT-qPCR analyses showed that BhorOBP3, BhorCSP2, and BhorOBPC1/C3/C4 were highly expressed in the antenna of males, indicating these genes may may play key roles in foraging and host-orientation in B. horsfieldi. Our results provide valuable molecular information about the olfactory system in B. horsfieldi and will help guide future functional studies on olfactory genes.

Background Sepsis-Induced coagulopathy (SIC) is not only a common complication in the development process of sepsis but also related to poor prognosis of sepsis. We aimed to establish a machine learning (ML) model to predict the 28-day mortality risk of patients with SIC. Methods We collected data for model training from the Medical Information Mart for Intensive Care IV Database version 2.2 to establish the model. We extracted patient data from the First Affiliated Hospital of Wenzhou Medical University for the model’s external validation. We used Least Absolute Shrinkage and Selection Operator (LASSO) regression and logistic regression analysis to identify predictive factors for a 28-day mortality risk. Then, we built prognostic prediction models for SIC patients using multiple ML classification models. We evaluated predictive performance using Receiver Operating Characteristic (ROC) curves, calibration curves, and Decision Curve Analysis (DCA). We used Shapley Additive Explanations (SHAP) to interpret the models. Results We selected seventeen variables for model development, and the XGBoost model performed the best. The area under the curve (AUC) (95% CI) of the test set reached 0.840 (0.810–0.870), with an accuracy of 0.807, sensitivity of 0.836, and specificity of 0.798. The model also demonstrated excellent predictive performance in external validation, with an AUC (95% CI) of 0.864 (0.794–0.934). Conclusion We constructed an XGBoost model and provided model interpretability using the SHAP. This model provides a basis for assessing the 28-day mortality risk of patients with SIC, aiding in clinical decision support and the formulation of personalized treatment strategies.

Ultrasonic technology has drawn extensive interests for its great potential in marine antifouling applications. However, its effects on the adhesion behavior of marine fouling organisms on marine structures remain underexplored. This work investigated how ultrasonic treatment impacted the adhesion of Pseudoalteromonas on a gel-like marine epoxy primer. And the process parameters for ultrasonic treatment were optimized using response surface analysis with Design-Expert software 11. The results revealed that ultrasonic treatment disrupted the cellular structure of Pseudoalteromonas, causing the deformation and fragmentation of the cell membrane, leading to bacterial death. Additionally, ultrasonic treatment reduced the particle size and Zeta potential value of Pseudoalteromonas, which disrupted the stability of bacterial suspensions. It also increased the relative surface hydrophobicity of Pseudoalteromonas cells, resulting in a reduction in adhesion to the gel-like marine epoxy primer. This study demonstrated that ultrasonic treatment significantly disturbed the adhesion behavior of microorganisms like Pseudoalteromonas on the gel-like marine epoxy primer, which provided an effective approach for controlling marine biofouling.

Post-induction hypotension (PIH) is a common complication associated with anesthesia, particularly in high-risk groups, such as elderly, malnourished patients with multiple comorbidities undergoing thoracoscopic esophagectomy. The selection of induction agents plays a significant role in influencing hemodynamic stability. However, there is a lack of comprehensive comparative data regarding the impact of different opioid agents on PIH. This retrospective cohort study included 289 patients undergoing thoracoscopic esophagectomy, who received etomidate combined with either fentanyl (Fentanyl group) or remifentanil (Remifentanil group) for anesthesia induction. A logistic regression model was used to examine the association between the induction regimen and PIH. Confounding factors were adjusted using a directed acyclic graph, and least absolute shrinkage and selection operator (LASSO) regression was employed to select covariates, ensuring robustness of the primary outcome analysis. Hemodynamic changes in systolic blood pressure, mean arterial pressure, and heart rate during the first 15 min post-induction were analyzed using generalized estimating equations to account for correlated observations. Subgroup analyses were performed for key clinical subgroups. Among 289 patients analyzed, the incidence of PIH was significantly lower in the Remifentanil group compared to the Fentanyl group (23.7% vs. 42.3%, = 0.001; adjusted odds ratio (OR) = 0.42, 95% confidence interval (CI): 0.25-0.73). Sensitivity analysis using LASSO-selected covariates yielded consistent results (adjusted OR = 0.41, 95% CI: 0.22-0.69, = 0.001). Bradycardia occurred more frequently with remifentanil (11.9% vs. 4.5%, = 0.03), whereas post-intubation hypertension and phenylephrine use were higher in the fentanyl group. No significant differences were observed in cardiovascular complications or postoperative hospital stay. Subgroup analyses revealed no significant effect modification across age, hemoglobin, or albumin levels. Remifentanil was also associated with more stable hemodynamics, including attenuated systolic blood pressure decline and lower variability during the first 15 min post-induction. Remifentanil-based general anesthesia induction reduces the risk of PIH and enhances hemodynamic stability in patients undergoing thoracoscopic esophagectomy.

Effective image-guided and precisely controlled drug release remains a critical challenge in cancer therapy, particularly for overcoming drug resistance and minimizing systemic toxicity. Herein, we developed a multifunctional nanoplatform by co-encapsulating a newly engineered near-infrared (NIR)-absorbing semiconducting oligomer (TD19) and doxorubicin (DOX) into DSPE-PEG 5000 carriers. Benefiting from a donor–acceptor molecular design, TD19 exhibited a high extinction coefficient, extended π-conjugation, and superior photothermal conversion efficiency, which directly contributed to strong photoacoustic imaging (PAI) and photothermal therapy (PTT) performance. The resulting TD19/DOX nanoparticles (TD19/DOX-NPs) demonstrated dual-responsive drug release triggered by 808 nm laser irradiation and the acidic tumor microenvironment. In vitro, the nanoplatform enhanced cellular uptake, nuclear delivery of DOX, and synergistic apoptosis of breast cancer cells. In vivo, TD19/DOX-NPs achieved precise PAI-guided tumor localization, efficient tumor ablation (96.8% growth inhibition), and no observable acute systemic toxicity in the 4T1 mouse model. This study highlights the structure–function–therapeutic relationship of the designed semiconducting oligomer, linking its rational molecular engineering to chemo-photothermal synergy as a promising nanotheranostic candidate for breast cancer precision therapy. Graphical Abstract We have developed a nanosystem capable of co-delivering NIR-absorbing semiconducting polymer (TD19) and doxorubicin (DOX), which enables controlled drug release in response to dual stimuli (808-nm laser irradiation and acidic tumor microenvironment), thereby facilitating PAI-guided synergistic cancer therapy.

Background Host factors are required for Influenza virus infection and have great potential to become antiviral target. Objective Here we demonstrate the role of TNK2 in influenza virus infection. CRISPR/Cas9 induced TNK2 deletion in A549 cells. Methods CRISPR/Cas9-mediated deletion of TNK2. Western blotting and qPCR was used to measure the expression of TNK2 and other proteins. Results CRISPR/Cas9-mediated deletion of TNK2 decreased the replication of influenza virus and significantly inhibited the ex-pression of viral proteins and TNK2 inhibitors (XMD8-87 and AIM-100) reduced the expression of influenza M2, while over-expression of TNK2 weakened the resistance of TNK2-knockout cells to influenza virus infection. Furthermore, a decrease of nuclear import of IAV in the infected TNK2 mutant cells was observed in 3 h post-infection. Interestingly, TNK2 deletion enhanced the colocalization of LC3 with autophagic receptor p62 and led to the attenuation of influenza virus-caused accumulation of autophagosomes in TNK2 mutant cells. Further, confocal microscopy visualization result showed that influenza viral matrix 2 (M2) was colocalized with Lamp1 in the infected TNK2 mutant cells in early infection, while almost no colocalization between M2 and Lamp1 was observed in IAV-infected wild-type cells. Moreover, TNK2 depletion also affected the trafficking of early endosome and the movement of influenza viral NP and M2. Conclusion Our results identified TNK2 as a critical host factor for influenza viral M2 protein trafficking, suggesting that TNK2 will be an attractive target for the development of antivirals therapeutics.

Glaesserella parasuis (GPS) infection causes severe inflammatory disorder, resulting in lung injury. SIRT7 is an NAD + -dependent deacetylase known to regulate inflammatory responses, but its role in GPS infection remains unclear. Here we found that GPS infection increased SIRT7 expression and induced inflammatory responses. Deficiency of SIRT7 by CRISPR/Cas9 technology significantly inhibited GPS-induced cytopathic effects and inflammatory responses. In addition, RNA-seq analysis showed that differentially expressed genes(DEGs) induced by SIRT7 deficiency were enriched in biological processes such as cell proliferation, actin cytoskeleton formation, lipid synthesis, protein kinase activation regulation, and GTPase activity regulation. Functional enrichment analysis further indicated the involvement of these DEGs in tight junction pathway, PI3K-Akt signaling pathway, actin cytoskeleton regulation, cGMP-PKG signaling pathway, Hippo signaling pathway, and TNF signaling pathway. Finally, we identified some hub genes ( GNAI3 , GNAI1 , JAK1 , NDUFS8 , CYC1 ) related to oxidative phosphorylation. In summary, our results demonstrate that SIRT7 is pivotal for GPS-induced inflammatory responses, which represents a promising target resistant to GPS infection.