Radiotherapy is a crucial treatment modality for head and neck tumors. However, while effectively killing tumor cells, it significantly disrupts the homeostasis of the oral microecology, which is closely associated with various complications such as radiation-induced oral mucositis. Literature review indicates that as radiotherapy doses accumulate and treatment durations extend, the richness and diversity of the oral microbiota show a declining trend, with the genus Streptococcus decreasing most markedly. In contrast, radiotherapy selectively promotes the proliferation of bacterial phyla such as Proteobacteria and Bacteroidetes, which are rich in opportunistic pathogens. Mechanistically, radiotherapy activates the nuclear factor-kappa B pathway, triggering chronic inflammation and oxidative stress, damaging the epithelial barrier, suppressing local immunity, and causing damage to organs such as the salivary glands. It can also induce systemic diseases via the oral-gut axis, forming a multi-level, interconnected pathogenic network. In terms of interventions, treatment strategies including probiotics and prebiotics have shown promising efficacy against side effects such as radiation-induced oral mucositis. Saliva-based oral microbiota transplantation is an emerging strategy that is expected to become widely utilized for restoring oral microecological balance. Existing interventions provide preliminary pathways for clinical practice, but this field still faces several key scientific questions. The association between oral microecology and systemic diseases remains largely correlative, lacking causal evidence. Furthermore, critical parameters for oral microbiota transplantation, such as donor screening criteria, transplantation protocols, and long-term safety, are not yet well-defined. Therefore, future research should focus on conducting large-scale clinical trials to establish standardized protocols and safety evaluation systems for oral microecological interventions, and explore combined treatment therapies such as probiotics, prebiotics, and microbiota transplantation to advance the development of personalized precision modulation. These will enable more effective management of radiotherapy-induced oral microecological dysbiosis and improve treatment outcomes and quality of life for patients with head and neck tumors.

Background: This study was performed to characterize the incidence, costs, and risk factors associated with renal and cardiovascular adverse outcomes following primary percutaneous coronary intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI). Methods: Patients with STEMI who underwent pPCI using iso-osmolar contrast were enrolled at 39 centers. The incidence of acute kidney injury (AKI) and major adverse renal and cardiovascular events (MARCE) was analyzed, as well as inpatient costs. Logistic regression analysis was performed to identify risk factors. Results: Among 2,293 patients, the incidence of AKI and MARCE within 72 hours post-pPCI was 4.14% (n = 95) and 4.40% (n = 101), respectively. AKI and/or MARCE were associated with systolic blood pressure (AKI: odds ratio [OR], 1.009; 95% confidence interval [CI], 1.000–1.018), hypertension (AKI: OR, 1.815; 95% CI, 1.133–2.906; MARCE: OR, 1.760;95% CI, 1.118–2.769), anterior wall infarction (AKI: OR, 1.895; 95% CI, 1.196–3.004; MARCE:OR, 1.939; 95% CI, 1.240–3.032), Killip class (AKI: OR, 1.465; 95% CI, 1.117–1.922; MARCE:OR, 1.467; 95% CI, 1.131–1.903), and serum creatinine (SCr; MARCE: OR, 1.006; 95% CI, 1.000–1.012). Hospitalization costs for patients with STEMI who developed AKI or MARCE were significantly higher than for those without AKI (9,595 ± 5,795 vs. 8,279 ± 3,872 USD, P = 0.003) or without MARCE (9,890 ± 5,616 vs. 8,255 ± 3,859 USD, P < 0.001). Conclusions In patients with STEMI undergoing pPCI with iso-osmolar contrast, the incidence of AKI and MARCE was associated with higher hospitalization costs. Systolic blood pressure, hypertension, anterior wall infarction, Killip class, and SCr were identified as risk factors for these outcomes.

In the context of burgeoning economic trade, there has been a remarkable increase in the number of ships travelling between domestic and international ports. Inbound and outbound cargo ships, cruise liners, ferries, and other types of vessels have emerged as critical vehicles for the dispersal of vector organisms and the spread of infectious disease agents. Public health concerns associated with these vessels represent a significant threat to human welfare. In this paper, we comprehensively review the hazards posed by vector organisms on ships, the latest advances in prevention and control strategies, and proposes appropriate countermeasures. The aim is to provide effective guidance for the prevention and control of public health security issues caused by ship-borne vector organisms.

ObjectiveTo systematically screen and validate key immunogenic cell death （ICD）-related genes that play important roles in primary sjögren’s syndrome （pSS） using multi-omics data. MethodsGene expression profiles of pSS patients and healthy controls （GSE66795， 131pSS patients/29 healthy controls） were obtained from the Gene Expression Omnibus （GEO） database. Candidate genes were selected by intersecting these profiles with known ICD core gene sets and pSS-related targets. The CIBERSORT algorithm was used to analyze immune cell infiltration characteristics. Validation of gene expression was performed using transcriptomic data from sorted CD8⁺ T cell subsets （GSE93683）. Finally， labial gland tissues and peripheral blood samples from 10 pSS patients and 4 healthy controls were collected， and key genes were experimentally validated by reverse transcription quantitative polymerase chain reaction （RT-qPCR）. ResultsSeven intersecting genes from the ICD-differentially expressed genes （DEGs）-pSS intersection were identified ［caspase 1 （CASP1）， forkhead box P3 （FOXP3）， interferon-gamma （IFNG）， myeloid differentiation primary response 88 （MYD88）， toll-like receptor 7 （TLR7）， DExD/H-box helicase 58 （DDX58）， and interferon induced helicase C domain 1 （IFIH1）］. Immune infiltration analysis showed that in pSS labial gland tissues， the proportions of naïve B cells and dendritic cells significantly increased， while the proportions of resting NK cells and M0 macrophages decreased （P<0.05）. Transcriptomic data of CD8⁺T cell subsets indicated that IFIH1 expression was significantly elevated in central memory CD8⁺T cells （P<0.05）. RT-qPCR experimental validation revealed that DDX58， IFIH1， and CASP1 were significantly upregulated in both peripheral blood leukocytes and labial gland tissues of pSS patients （all P<0.05）， whereas IFNG expression increased in peripheral blood but decreased in labial gland tissues （P<0.05）. ConclusionThis study identified and confirmed DDX58， IFIH1， CASP1， and IFNG as key ICD-related genes in pSS through a combination of bioinformatics and experimental validation， providing new candidate targets for further understanding the immunopathological mechanisms of pSS.

Objective To explore the role of DNAJC5B in immunotherapy for esophageal squamous cell carcinoma (ESCC). Methods Using the ESCC dataset from The Cancer Genome Atlas (TCGA) database, genes correlated with DNAJC5B expression were identified through Pearson correlation analysis. Subsequently, Gene Ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed. Additionally, single-cell RNA sequencing (scRNA-seq) data were utilized to analyze the expression of DNAJC5B in different T-cell subsets. The prognostic value of DNAJC5B was evaluated using Kaplan-Meier survival curves, receiver operating characteristic curves, and Cox proportional hazards models. Results DNAJC5B was highly expressed in patients with advanced-stage ESCC, particularly in males. GO and KEGG analyses revealed a significant correlation between DNAJC5B expression and immune-related processes, such as the adaptive immune response and cell surface receptor signaling pathways. Single-cell analysis results indicated that DNAJC5B expression was positively correlated with immune function, with DNAJC5B predominantly accumulating in CD8+ T cells. Kaplan-Meier survival curves showed that the median survival time for patients with high DNAJC5B expression was 681 days, significantly shorter than the 1 361 days for patients with low expression (P<0.05). Furthermore, univariate and multivariate independent prognostic analyses demonstrated that DNAJC5B was an independent risk factor, with hazard ratios (HRs) of 3.577 and 4.114, respectively (both P<0.05). Conclusion DNAJC5B may play a crucial immunomodulatory role in ESCC, particularly in regulating CD8+ T-cell function and tumor immune escape. These findings support the potential of DNAJC5B as a biomarker for the treatment and prognostic assessment of ESCC.

OBJECTIVE To investigate the effects of dexborneol on the pharmacokinetic parameters of edaravone in rats under the pathological condition of cerebral ischemic stroke （CIS）.METHODS Twenty male SD rats were randomly divided into the edaravone group and the Edaravone and dexborneol concentrated solution for injection （EDB injection） group， with 10 rats in each group. A middle cerebral artery occlusion （MCAO） rat model was established using the modified Longa suture method. Within 5 min of ischemia-reperfusion， the corresponding drug solutions were injected via the tail vein at a dose of 2.5 mg/kg （calculated by edaravone）. Blood samples were collected from the orbital venous plexus at 0.08， 0.5， 1， 3， 6， 18， and 24 h after injection. With carbamazepine as the internal standard， the plasma concentration of edaravone was determined by ultra-performance liquid chromatography-tandem mass spectrometry （UPLC-MS/MS） method. Pharmacokinetic parameters were calculated using DAS software and compared between the two groups.RESULTS Compared with the edaravone group， the peak concentration （ c max ） of edaravone in the EDB injection group was significantly increased （ P ＜0.05）， while no statistically significant differences were observed in the half life， time to peak， clearance， or area under curve （ P ＞0.05）.CONCLUSIONS Under the pathological condition of CIS， dexborneol can increase the c max of edaravone in the plasma of model rats， but has no significant effect on the systemic exposure or clearance of edaravone.

ObjectiveTo screen and identify uridine diphosphate （UDP）-rhamnose synthase （RHM） genes from Ornithogalum saundersiae and verify their UDP-rhamnose （UDP-Rha） biosynthetic functions， thereby providing reliable candidate genes for the efficient biosynthesis of neohesperidin and other rhamnoside natural products. MethodsBased on previously reported plant RHM sequences， two candidate RHM genes， OsRHM1 and OsRHM2， were identified from O. saundersiae through transcriptome screening and sequence alignment. The two genes were cloned and subjected to bioinformatics analysis and multiple sequence alignment. An in vitro RHM-Cm1，2RhaT cascade reaction was established， and the ability of OsRHM1 and OsRHM2 to catalyze the conversion of UDP-glucose （UDP-Glc） to UDP-Rha was evaluated based on neohesperidin production. Real-time fluorescence quantitative polymerase chain reaction PCR （Real-time PCR） was performed to analyze the relative expression levels of the two genes in roots， bulbs， and leaves. ResultsThe open reading frame （ORF） of OsRHM1 was 2 076 bp and encoded 692 amino acids， with a predicted protein molecular mass of 77.97 kDa and a theoretical isoelectric point of 7.25. The ORF of OsRHM2 was 2 019 bp and encoded 673 amino acids， with a predicted protein molecular mass of 75.82 kDa and a theoretical isoelectric point of 7.24. Multiple sequence alignment showed that OsRHM1 and OsRHM2 contained the typical conserved motifs GxxGxxG/A and YxxxK of the plant RHM family and shared high amino acid sequence identity with previously reported RHMs. The in vitro cascade reaction demonstrated that both OsRHM1 and OsRHM2 were capable of catalyzing the conversion of UDP-Glc to UDP-Rha. The neohesperidin production in the OsRHM2 cascade reaction system was approximately 2.58-fold that in the OsRHM1 system. Real-time PCR analysis showed that the relative expression levels of OsRHM1 and OsRHM2 were higher in roots than in bulbs and leaves. ConclusionOsRHM2 exhibited a relatively high capacity for UDP-Rha supply and may serve as a candidate enzyme resource for the subsequent biosynthesis of rhamnoside natural products and the construction of UDP-Rha supply systems.

Objective: In ovarian cancer (OvCa), tumor cell high glucocorticoid receptor (GR) has been associated with poor patient prognosis. In vitro, GR activation inhibits chemotherapyinduced OvCa cell death in association with transcriptional upregulation of genes encoding anti-apoptotic proteins. A recent randomized phase II study demonstrated improvement in progression-free survival (PFS) for heavily pre-treated OvCa patients randomized to receive therapy with a selective GR modulator (SGRM) plus chemotherapy compared to chemotherapy alone. We hypothesized that SGRM therapy would improve carboplatin response in OvCa patient-derived xenograft (PDX). Methods: Six high-grade serous (HGS) OvCa PDX models expressing GR mRNA (NR3C1) and protein were treated with chemotherapy +/− SGRM. Tumor size was measured longitudinally by peritoneal transcutaneous ultrasonography. Results: One of the 6 GR-positive PDX models showed a significant improvement in PFS with the addition of a SGRM. Interestingly, the single model with an improved PFS was least carboplatin sensitive. Possible explanations for the modest SGRM activity include the high carboplatin sensitivity of 5 of the PDX tumors and the potential that SGRMs activate the tumor invasive immune cells in patients (absent from immunocompromised mice). The level of tumor GR protein expression alone appears insufficient for predicting SGRM response. Conclusion The significant improvement in PFS shown in 1 of the 6 models after treatment with a SGRM plus chemotherapy underscores the need to determine predictive biomarkers for SGRM therapy in HGS OvCa and to better identify patient subgroups that are most likely to benefit from adding GR modulation to chemotherapy.

Objective The mouse autologous tumor model H22 is more valuable for tumor immunological-related research.This paper aims to establish mouse hepatic tumor cell line(H22-luc2-tdT)that stably express the tan-dem-dimer tomato(tdTomato)and luciferase genes.Establish an in vivo imaging model of cell line derived trans-planted tumors.Methods Using transplanted H22 tumor tissue,primary culture and continuous passage in vitro were performed to establish a continuous cell line.Cell proliferation,chromosome analysis,organoid culture,tumorigenicity,HE and ICH of aFP,CK7,CK15 were performed to charaterize the cell line.Then the luc2-tdT plasmid was transfected into H22 cells of P22,flow cytometry and in vitro/in vivo imaging were employed to screen and verify fluorescence expression.Mycoplasma detection and species verification of the established cell lines were performed.Results The H22 cells had been continuously passaged over 50 times.The cells of passsge 22(P22)were transplanted subcutaneously and intraperitoneally into C57 and Kunming mice,with a 100%tumor formation.The HE morphology of subcutaneous transplanted tumor were consistent with the original tumor.CK+/AFP+proved that it was of liver cancer origin.The H22 cells were hypo-triploid with a modal number of 40-44 chromosomes and telocentromeres,verifing its mouse origin.The latent phase for in vitro growth of H22 lasted from d0 to d3,while the exponential phaes d3 to d5,and reach plateou at d6.Successful transfection of H22 cells with the luc2-tdT were observed with in vitro/in vivo 100%fluorescence positivity,thus named H22-luc2-tdT.The transplanted tumor tissue of H22 cells could be primarily cultured to form organoids.The detection of Mycoplasma was negative,and its mouse origin confirmed by PCR.Conclusions H22 and H22-luc2-tdT cell lines are established and characterized,which can be used for the establishment and application of in vitro and in vivo liver cancer research and metastatic cell tracking.These cell lines are deposited at and can obtain from the National Biomedical Cell Resource Center(http://www.cellresource.cn).

Objective To investigate the differences of perineuronal net(PNN)and parvalbumin(PV)-positive neuron distribution across specific brain regions between young and aged mice.Methods Brains from young(45 days)and aged(350 days)mice(n=4 per group)were fixed with 4％paraformaldehyde,sectioned(50 μm)using a vibratome,and stained with Wisteria floribunda agglutinin(WFA)and PV immunofluorescence.Quantitative analyses of PNN-positive and PV-positive neurons,along with PNN encapsulation of PV-positive neurons,were performed in the anterior cingulate cortex(ACC),somatosensory cortex barrel field layer 4(S1BF L4),striatum(STR),and hippocampal CA2 region.Results Aged mice exhibited no significant changes in PNN-positive or PV-positive neuron counts in ACC,S1BF L4,or STR compared to young mice,but showed significantly increased PNN encapsulation of PV-positive neurons.In hippocampal CA2,PNN-positive neurons increased significantly without PV-positive neuron alterations.Conclusion The differences in PNN-PV neuron interactions and PNN density exist in specific brain regions of young and aged mice.