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Purpose This study aimed to evaluate the dose–response relationship and survival outcomes of iodine-125 seed implantation in patients with advanced lung cancer, focusing on the impact of different dose levels on tumor control and patient prognosis. Methods A retrospective analysis was conducted on 49 patients with advanced lung cancer who underwent iodine-125 seed implantation between January 2017 and March 2021. The patients were divided based on postoperative D90 dose levels, and tumor control rates, including complete response (CR), partial response (PR), stable disease (SD), and progressive disease (PD), were assessed. The objective response rate (ORR) and disease control rate (DCR) were also evaluated. Survival analysis was performed to identify prognostic factors. Results The optimal D90 cutoff values for CR, ORR, and DCR were 136.46 Gy, 121.98 Gy, and 111.47 Gy, respectively. Higher D90 doses were significantly associated with improved tumor control rates ( P  < 0.05). The 3-year survival rate was 20.41%, with complete response (CR) and preoperative hemoglobin levels identified as independent prognostic factors for long-term survival. Conclusion Iodine-125 seed implantation demonstrates a clear dose–response relationship in advanced lung cancer, with higher D90 doses correlating with better tumor control. CR and hemoglobin levels are critical factors influencing long-term survival outcomes.

serotype 2 is a major pathogen of swine streptococcicosis, which result in serious economic loss worldwide. SS2 is an important zoonosis causing meningitis and even death in humans. Neutrophil extracellular traps (NETs) constitute a significant bactericidal strategy of innate immune. The battle between SS2 and NETs may account for the pathogenicity of SS2. However, the molecular mechanism underlying release of SS2-induced NETs remains unclear. In this study, SS2 was found to induce NETs within 2-4 h, and was dependent on reactive oxygen species (ROS) from NADPH oxidase. Moreover, SS2 could activate neutrophil p38 MAPK and ERK1/2. Blockage of p38 MAPK or ERK1/2 activation decreased SS2-induced NETs formation by 65 and 85%, respectively. In addition, NADPH oxidase derived ROS inhibition negatively affected phosphorylation of p38 MAPK and ERK1/2 in SS2 induced neutrophils. Both TLR2 and TLR4 were significantly up-regulated by SS2 infection in blood cells and neutrophils , which indicates these two receptors are involved in SS2 recognition. Blocking TLR4 signaling could further inhibit the activation of ERK1/2, but not p38 MAPK; however, TLR4 signaling inhibition reduced NETs formation induced by SS2. In conclusion, SS2 could be recognized by TLR2 and/or TLR4, initiating NETs formation signaling pathways in a NADPH oxidase derived ROS dependent manner. ROS will activate p38 MAPK and ERK1/2, which ultimately induces NETs formation.

Glaesserella parasuis ( G. parasuis ) is a commensal bacterium in the upper respiratory tract of pigs that can also cause the swine Glässer disease, which induces an intensive inflammatory response and results in significant economic losses to the swine industry worldwide. G. parasuis can cause disease through infection of the respiratory tract, resulting in systemic infection, but the mechanism is largely unknown. Recently we showed that Glaesserella parasuis serotype 4 (GPS4) increased swine tracheal epithelial barrier permeability, resulting in easier bacterial translocation. Tight junction proteins (TJ) play a crucial role in maintaining the integrity and impermeability of the epithelial barrier. GPS4 decreased the expression of the TJ ZO-1 and occludin in swine tracheal epithelial cells (STEC). Furthermore, the proinflammatory cytokines IL-6, IL-8 and TNF-α were significantly upregulated in GPS4-infected STEC, and both the MAPK and NF-κB signaling pathways were activated and contributed to the expression of TNF-α. We demonstrate that the production of proinflammatory cytokines, especially TNF-α, during GPS4 infection was involved in barrier dysfunction. Additionally, animal challenge experiments confirmed that GPS4 infection downregulated TJ in the lungs of piglets and induced a severe inflammatory response. In general, G. parasuis infection downregulated the expression of TJ and induced massive secretion of proinflammatory cytokines, resulting in epithelial barrier disruption and favoring bacterial infection. This study allowed us to better understand the mechanism by which G. parasuis crosses the respiratory tract of pigs.

Drug development is a complex and lengthy process, and drug-disease association prediction aims to significantly improve research efficiency and success rates by precisely identifying potential associations. However, existing methods for drug-disease association prediction still face limitations in feature representation, feature integration, and generalization capabilities. To address these challenges, we propose a novel model named AMFGNN (Adaptive Multi-View Fusion Graph Neural Network). This model leverages an adaptive graph neural network and a graph attention network to extract drug features and disease features, respectively. These features are then used as the initial representations of nodes in the drug-disease association network to enable efficient information fusion. Additionally, the model incorporates a contrastive learning mechanism, which enhances the similarity and differentiation between drugs and diseases through cross-view contrastive learning, thereby improving the accuracy of association prediction. Furthermore, a Kolmogorov-Arnold network is employed to perform weighted fusion of various final features, optimizing prediction performance. AMFGNN demonstrates a significant advantage in predictive performance, achieving an average AUC value of 0.9453, which reflects the model's high accuracy in prediction. Cross-validation results across multiple datasets indicate that AMFGNN outperforms seven advanced drug-disease association prediction methods. Additionally, case studies on Hepatoblastoma, asthma and Alzheimer's disease further confirm the model's effectiveness and potential value in real-world applications.

Among the most common types of brain tumor, gliomas are the most aggressive and have the poorest prognosis. Dolichyl-diphosphooligosaccharide protein glycosyltransferase non-catalytic subunit (DDOST) encodes a component of the oligosaccharide transferase complex and is related to the N-glycosylation of proteins. The role of DDOST in gliomas, however, is not yet known. First, we performed a pan cancer analysis of DDOST in the TCGA cohort. The expression of DDOST was compared between glioma and normal brain tissues in the GEO and Chinese Glioma Genome Atlas (CGGA) databases. In order to explore the role of DDOST in glioma, we analyze the impact of DDOST on the prognosis of glioma patients, with the CGGA 325 dataset as a test set and the CGGA 693 dataset as a validation set. Immunohistochemistry was performed on tissue microarrays to examine whether DDOST has an impact on glioma patient survival. Next, using single-cell sequencing analysis, GSEA, immune infiltration analysis, and mutation analysis, we explored how DDOST affected the glioma tumor microenvironment. Finally, we evaluated the clinical significance of DDOST for glioma treatment by constructing nomograms and decision curve analysis (DCA) curves. We found that DDOST was overexpressed in patients with high grade, IDH wild type, 1p19q non-codel and MGMT un-methylated, which was associated with poor prognosis. Patients with high levels of DDOST, regardless of their clinical characteristics, had a worse prognosis. Immunohistochemical analysis confirmed the results of the above bioinformatics analysis. Mechanistic analysis revealed that DDOST was closely associated with the glioma microenvironment and negatively related to tumor-infiltrating B cells and CD4+ T cells and positively related to CAFs and tumor-associated macrophages. In conclusion, these findings suggested that DDOST mediated the immunosuppressive microenvironment of gliomas and could be an important biomarker in diagnosing and treating gliomas.

Background Primary intraosseous cavernous hemangiomas (PICHs) of the skull are extremely rare. To date, diffuse cranial hemangioma of skull has not been reported. In cancer patients, it is often misdiagnosed as metastasis. Case presentation Here, we presented a case of a 50-year-old female patient suffering from slightly headache who received breast cancer modified radical mastectomy in 2004, computed tomography and magnetic resonance imaging findings revealed abnormal lesions of diffuse skull which were misdiagnosed as skull metastasis, and the relevant literatures were also reviewed. Conclusions Diffuse cavernous hemangioma of the skull is exceedingly rare, and imaging data are not typical. The condition is often misdiagnosed, and pathological evaluation is necessary and important. In cases where the mass cannot be completely removed by surgery, radiotherapy could be beneficial.

Aberrant DNA methylation of tumor suppressor genes is a common event in the development and progression of gastric cancer (GC). Our previous study showed NDRG1, which could suppress cell invasion and migration, was frequently down-regulated by DNA methylation of its promoter in GC. To analyze the relationship between the expression and DNA methylation of NDRG1 and DNA methyltransferase (DNMT) family. We performed a comprehensive comparison analysis using 407 patients including sequencing analysis data of GC from TCGA. NDRG1 was down-regulated in GC, and was negatively correlative to DNMT1 (r = -0.11, = 0.03), DNMT3A (r = -0.10, = 0.01), DNMT3B (r = -0.01, = 0.88), respectively, whereas the DNA methylation of NDRG1 was positively correlative to DNMT family (DNMT1 r = 0.20, < 0.01; DNMT3A r = 0.26, < 0.001; DNMT3B r = 0.03, = 0.57, respectively). NDRG1 expression was significantly inverse correlated with invasion depth ( = 0.023), but DNMT1 was significantly positive correlated with invasion depth ( = 0.049). DNMT3B was significantly correlated with the degree of tumor cell differentiation ( = 0.030). However, there was no association between the expression of DNMT3A and clinicopathological features. The KM plotter showed that NDRG1 (HR = 0.95, 95% CI [0.8-1.12], = 0.53) and DNMT1 (HR = 1.04, 95% CI [0.88-1.23], = 0.67) had no association with prognosis of GC patients, while, DNMT3A ( = 0.0064) and DNMT3B ( = 0.00025) displayed significantly association. But the overall survival of high expression of NDRG1 tended to be prolonged. These data suggest that down-regulation of NDRG1expression in GC may be due to its promoter DNA methylation DNMT family. The demethylating agent maybe a potential target drug for GC patients.

is an important zoonotic agent for humans and various animals. A recombinase-aided amplification (RAA) assay was developed for detecting . RAA can be performed in a closed tube at 39°C within 30 min. The detection limit was 10.6 copies of the plasmid DNA per reaction. No positive signals for other pathogens were detected. The coincidence rate of RAA and conventional PCR was 95.24% (20/21) and 100% (96/96) for positive and negative samples, respectively. The established RAA assay is a simple, rapid, highly sensitive, and specific method for detecting

A meta‐analysis study to assess the effect of possible risk factors for pharyngocutaneous fistula (PCF) after total laryngectomy of laryngeal carcinoma. A comprehensive literature examination till January 2023 was implemented and 1794 linked studies were appraised. The picked studies contained 3140 subjects with total laryngectomy of laryngeal carcinomas in the picked studies' baseline, 760 of them were PCF, and 2380 were no PCF. Odds ratio (OR) in addition to 95% confidence intervals (CIs) were used to calculate the consequence of possible risk factors for PCF after total laryngectomy of laryngeal carcinomas and surgical wound infection after total laryngectomy of laryngeal carcinoma by the dichotomous and continuous styles and a fixed or random model. The PCF had a significantly higher surgical wound infection (OR, 6.34; 95% CI, 1.89–21.27, P = .003) compared with the no PCF in total laryngectomy of laryngeal carcinomas. The smoking (OR, 1.73; 95% CI, 1.15–2.61, P = .008), and preoperative radiation (OR, 1.90; 95% CI, 1.37–2.65, P < .001) had significantly higher PCF as a risk factor in total laryngectomy of laryngeal carcinomas. The preoperative radiation had a significantly lower spontaneous PCF closure (OR, 0.33; 95% CI, 0.14–0.79, P = .01) compared with the no preoperative radiation in total laryngectomy of laryngeal carcinomas. However, the neck dissection (OR, 1.34; 95% CI, 0.75–2.38, P = .32), and alcohol intake (OR, 1.95; 95% CI, 0.76–5.05, P = .17), had no significant effect on PCF in total laryngectomy of the PCF had a significantly higher surgical wound infection, and preoperative radiation had a significantly lower spontaneous PCF closure in total laryngectomy of laryngeal carcinomas. Smoking and preoperative radiation were shown to be risk factors for PCF, however, neck dissection and alcohol intake were not shown to be risk factors for PCF in total laryngectomy of laryngeal carcinomas. Although precautions should be taken when commerce with the consequences because some of the picked studies for this meta‐analysis was with low sample sizes.

BackgroundGastric cancer (GC) is the fifth most common malignancy worldwide and the third leading cause of cancer-related mortality. In recent years, SAMD14 has been studied in various malignant cancers; however, little is known about the exact mechanisms of SAMD14 involvement in carcinogenesis and malignant progression.Methods60 paired GC-normal gastric tissues were evaluated for their SAMD14 mRNA expression in relation to SAMD14 gene promoter methylation. GC patient survival was assessed by Kaplan–Meier analyses and a Cox’s proportional hazard model was employed for multivariate analyses.ResultsSAMD14 expression was significantly inversely correlated with the Borrmann type (P = 0.017), lymph node metastasis (P = 0.006) and tumor-node-metastasis (TNM) stage (P = 0.033). Methylation-specific PCR (MSP) revealed hyper-methylation of the SAMD14 promoter in 56.7% (34/60) of the primary GC tissues tested and in 10% (6/60) of matched non-malignant tissues. The SAMD14 promoter methylation status was also related to pathological differentiation, Borrmann type, TNM stage and lymph node metastasis. The results showed SAMD14 expression was significantly downregulated in Borrmann type, lymph node metastasis and TNM stage, which showed significantly higher methylation. SAMD14 promoter hyper-methylation was significantly associated with a poor prognosis and could serve as an independent marker for survival using multivariate Cox regression analysis.ConclusionsOur results indicated that promoter methylation was a key mechanism contributing to the downregulation of SAMD14 in GC. SAMD14 may be an epigenetically silenced tumor suppressor gene, and hyper-methylation of the SAMD14 promoter may serve as a biomarker to predict the clinical outcome of GC.