Objective: To screen taurine upregulated gene 1 (TUG1), a long non-coding RNA (LncRNA) with highly specific differential expression, in plasma extracellular vesicles (EVs) from patients with non-small cell lung cancer (NSCLC), and to validate its clinical value as a diagnostic biomarker for NSCLC. Methods: LncRNA sequencing was performed on plasma EVs from 6 NSCLC patients and 6 healthy individuals. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression of LncRNA TUG1 in plasma EVs from 60 NSCLC patients, 60 healthy controls, and 93 patients for differential diagnosis (including small cell lung cancer, mediastinal lymphoma, etc.). The correlation between TUG1 expression and clinical characteristics of NSCLC was analyzed. The effect of TUG1 on the biological behavior of NSCLC cells was explored through in vitro cellular experiments, and the receiver operating characteristic (ROC) curve was used to evaluate its diagnostic efficacy. Results: Sequencing and qRT-PCR verification showed that TUG1 expression in plasma EVs of NSCLC patients was significantly higher than that in healthy individuals (P<0.01), and its expression in multiple NSCLC cell lines was higher than that in normal bronchial epithelial cells. Notably, TUG1 expression in plasma EVs of NSCLC patients decreased significantly after surgery (P<0.01). TUG1 expression was correlated with tumor size, distant metastasis, lymph node metastasis, and TNM stage (P<0.05 or P<0.01). Knockdown of TUG1 significantly inhibited the proliferation and migration abilities of H1299 cells (P<0.05 or P<0.01). ROC curve analysis showed that the area under the curve (AUC) of TUG1 for diagnosing NSCLC was 0.849 (specificity=0.83, sensitivity=0.86). When combined with carcino-embryonic antigen (CEA), the AUC was further improved to 0.882 (P<0.01). Conclusion: LncRNA TUG1 is highly expressed in plasma EVs of NSCLC patients and closely associated with tumor progression. It can serve as a novel diagnostic biomarker for NSCLC, and combined detection with CEA can enhance diagnostic efficacy.

Objective: To investigate the impact of bronchial ligation prior to bronchial division with a linear cutting stapler on the incidence of postoperative cough during videoassisted thoracoscopic lobectomy. Methods: A retrospective analysis was conducted on the clinical data of 235 patients who underwent lobectomy in the Department of Thoracic Surgery, Affiliated Hospital of Jiangsu University, from January 2022 to January 2024. Patients were divided into the bronchial ligation group (67 cases) and the conventional surgery group (97 cases) based on whether bronchial ligation was performed intraoperatively. Baseline characteristics, perioperative indicators, and postoperative complications were compared between the two groups. The Leicester cough questionnaire (LCQ) was used to assess postoperative quality of life, and univariate and multivariate Logistic regression analyses were performed to identify independent risk factors for postoperative cough. Results: No statistically significant differences were observed between the two groups in preoperative general conditions, anesthesia duration, operative time, number of lymph nodes dissected, intraoperative blood loss, number of patients transferred to the ICU, or postoperative hospital stay (P>0.05). The incidence of postoperative cough in the bronchial ligation group (16.4%) was significantly lower than that in the conventional surgery group (30.9%), with a statistically significant difference (P<0.05). There were no significant differences in the incidence of other postoperative complications (such as pulmonary infection and atelectasis) between the two groups (P>0.05). The LCQ quality of life scores in the bronchial ligation group at 1 and 2 months postoperatively were significantly better than those in the conventional surgery group (P<0.05). Multivariate Logistic regression analysis showed that prolonged anesthesia time, right lung operation, upper lobe tumor location, and conventional surgical approach were independent risk factors for postoperative cough (P<0.05). Conclusion: Bronchial ligation can reduce the incidence of postoperative cough after lobectomy.

Objective: To explore the effects of recombinant avirulent Newcastle disease virus La Sota strain expressing rabies virus glycoprotein (rL-RVG) on the polarization of murine macrophage RAW264.7 cells and to analyze the effect of polarized RAW264.7 cells on the viability of Lewis lung cancer cells. Methods: Murine macrophage RAW264.7 cells were divided into four groups: blank control group and rL-RVG groups at different multiplicities of infection(0.5, 1, 5 MOI); and the viability of RAW264.7 cells was assessed by using the CCK-8 assay. RAW264.7 cells were divided into three groups: RAW264.7-M0 type (complete media), RAW264.7-M1 type (induced by 1 μg/mL lipopolysaccharide +50 ng/mL IFN-γ), and RAW264.7-M2 type (induced by 20 ng/mL IL-4); and the morphological characteristics of these phenotypes were observed under phase-contrast microscopy. The protein expression levels of CD86 and Arg-1 were measured by immunofluorescence in four groups: Raw264.7-M1, Raw264.7-M2, rL-RVG+Raw264.7-M0, and rL-RVG+Raw264.7-M2. The mRNA expression levels of cytokines IL-4, IL-6, IL-10 and tumor necrosis factor-α (TNF-α) in the blank control group and rL-RVG groups were also assessed by qRT-PCR. Lewis lung cancer cells were co-cultured with conditioned media from the above groups and divided into four groups: blank control group and rL-RVG groups at different MOIs (0.5, 1, 5 MOI). The viability of Lewis lung cancer cells was evaluated by using the CCK-8 assay. Results: Compared with the blank control group, the cell proliferation rates in the 1, 5 MOI rL-RVG groups were significantly increased (both P<0.01). The morphological characteristics of Raw264.7-M0, M1 and M2 macrophages were round or oval, flat or irregular, and fibrous, elongated or spindle-shaped, respectively. Compared with RAW264.7-M0 type macrophages, the relative expression level of CD86 mRNA in RAW264.7-M1 type was significantly increased (P<0.01), and the relative expression level of Arg-1 mRNA in RAW264.7-M2 type was greatly increased (P<0.01). Compared with Raw264.7-M1 type, the relative fluorescence expression level of CD86 in rL-RVG+Raw264.7-M0 type was significantly increased (P<0.05); compared with Raw264.7-M2 type, the relative fluorescence expression level of CD86 in rL-RVG+Raw264.7-M2 type was significantly increased (P<0.05), and the relative fluorescence expression level of Arg-1 was significantly decreased (P<0.05). rL-RVG treatment led to an increase in the mRNA expressions of TNF-α and IL-6, while the mRNA expressions of IL-4 and IL-10 decreased. Compared with the blank control group, the viability of Lewis lung cancer cells in the 0.5, 1, and 5 MOI rL-RVG groups were significantly decreased (all P<0.01). Conclusion: rL-RVG could induce the polarization of RAW264.7 macrophages towards the M1 phenotype and subsequently inhibit the viability of Lewis lung cancer cells at MOIs ranging from 0.5 to 5.

Objective: To investigate the effects of cryoablation-derived necrotic fluid on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) A549 and H1299 cells, and to analyze its immune-related mechanisms. Methods: NSCLC A549 and H1299 cell lines were selected and divided into control groups (conventional culture) and necrotic fluid groups (supplemented with cryoablation-induced necrotic fluid). Cell proliferation was assessed by using CCK-8 assay, and apoptosis was detected by flow cytometry. Indirect co-culture systems were established by using human peripheral blood mononuclear cells (PBMCs) and two cell lines. The human tumor microenvironment research chip (AAH-CYT-G5) was employed to detect 80 immune-related proteins, followed by differential protein screening, clustering and GO/KEGG pathway enrichment analysis. Results: Compared with the control group, the cell proliferation rates of the A549 and H1299 cells in the necrosis fluid group were significantly decreased (P<0.05), and the cell apoptosis rates were markedly increased(P<0.05). The results of the coculture experiment showed that compared with the control group, 68 differentially expressed proteins of the two type cells were detected in A549 cells in the necrosis fluid group(P<0.05), with KEGG enrichment analysis identifying 76 pathways; for H1299 cells, 70 differentially expressed proteins were detected (P<0.05), with KEGG enrichment analysis identifying 74 pathways. The top 10 common differentially expressed proteins of the two type cells were GM-CSF, IP-10, NAP-2, SDF-1, FGF-6, IL-6, Osteopontin and fractalkine. Core pathways were identified as PI3K-Akt signaling, MAPK signaling, TNF signaling, JAK-STAT signaling, IL-17 signaling and Ras signaling. Conclusion: The lysate released by necrotic tumor cells after cryoablation could inhibit the proliferation of NSCLC A549 and H1299 cells and promote their apoptosis. It may exert anti-tumor effect by modulating immune-related proteins and key signaling pathways to influence the tumor immune microenvironment.

Objective: To investigate the effects of extracellular matrix (ECM) protein SVEP1 on lipolysis and thermogenesis in adipocytes. Methods: The RNA-seq database of abdominal subcutaneous adipose tissue (SAT) of 236 normal and obese individuals constructed previously was used to analyze the correlation between SVEP1 expression level and body mass index (BMI), fat mass, fat percentage and waist circumference. 3T3-L1 preadipocytes and human stromal vascular fraction (SVF) cells were differentiated into mature adipocytes respectively. The expression of Svep1 in adipocytes stimulated by rosiglitazone and Forskolin was detected by realtime quantitative PCR (qRT-PCR). Based on the Pearson correlation coefficient (r>0.4, P<0.05) between RPKM values of SVEP1 and other genes in the RNA-seq database of human SAT, co-expressed gene set was screened and KEGG enrichment analysis was performed. Svep1 was knocked down in mouse primary adipocytes by lentivirus-mediated shRNA. qRT-PCR and Western blotting were used to assess the expression of thermogenic genes and proteins in adipocytes. Glycerol detection kit was used to detect the level of lipolysis stimulated by isoproterenol (ISO), and Western blotting was used to detect the phosphorylation level of lipolysis-related proteins. Results: The expression level of SVEP1 in human abdominal SAT was positively correlated with obesity related indicators (BMI, fat mass, fat percentage and waist circumference). Cold stimulation could down-regulate Svep1 transcription level in brown and beige adipocytes in mice. The transcription level of Svep1 was down-regulated in mature 3T3-L1 adipocytes and human adipocytes when stimulated by Rosi or Forskolin. KEGG enrichment analysis showed that Svep1 co-expressed gene set was enriched in the regulation of lipolysis and insulin resistance related pathways. Svep1 knockdown could significantly promote ISO-stimulated lipolysis in mouse white adipocytes and increase the expression of thermogenic genes (Ucp1, Dio2, Pgc1α, Elovl3 and Cidea) in mouse beige adipocytes. Conclusion: This study demonstrated an association between Svep1 expression and adipocyte function, and it may be implicated that Svep1 might be involved in obesity-related adipose tissue dysfunction and contribute to the development and progression of obesity.

Objective: To investigate the expression and significance of SET domain containing lysine methyltransferase 5 (SETD5) in ovrian cancer tissues and cell lines. Methods: The correlation between SETD5 mRNA expression and the prognosis of patients with ovarian cancer was analyzed by Kaplan-Meier survival curves based on public database. Immunohistochemical staining was used to detect the expression level of SETD5 in 88 cases of ovarian cancer tissues and 8 cases of normal ovarian tissues. Western blotting was used to detect the expression levels of SETD5 in ovarian granulosa cells KGN, ovarian endometrioid adenocarcinoma cells A2780, ovarian serous adenocarcinoma cells SKOV3, epithelial ovarian cancer cells Hey A8 and ovarian serous adenocarcinoma cells ES-2. The SKOV3 cell line of ovarian serous adenocarcinoma was selected to construct a stable overexpression cell line of SETD5, and two SETD5-targeting shRNAs were used to construct a stable knockdown cell line of ovarian endometrioid adenocarcinoma A2780 cell line. The migration ability of SKOV3 and A2780 cells was detected by Transwell and wound healing assays, and the proliferation ability of SKOV3 and A2780 cells was detected by cell counting and CCK-8 assay. Results: The Kaplan-Meier survival analysis curves showed that high expression of SETD5 mRNA was associated with shortened progression-free survival and overall survival in patients with ovarian cancer. The immunohistochemical results of tissue microarray showed that the positive expression rate of SETD5 protein in ovarian cancer tissues was significantly higher than that in normal ovarian tissues (χ²=7.308, P=0.007). The expression level of SETD5 was significantly correlated with the tumor diameter (P=0.003), T stage (P=0.017), and FIGO stage (P=0.012) of patients with ovarian cancer. The results of in vitro functional experiments showed that overexpression of SETD5 significantly promoted the proliferation and migration ability of SKOV3 cells, while knockdown of SETD5 significantly inhibited the proliferation and migration of A2780 cells. Conclusion: SETD5 is highly expressed in human ovarian cancer tissues as well as SKOV3 and A2780 cells, and is associated with the prognosis of patients, promotes the proliferation and migration of ovarian cancer cells.

Objective: To analyze the risk factors associated with coronary slow flow (CSF) and construct a clinical predictive model. Methods: From January 2018 to December 2023, patients who underwent coronary angiography (CAG) at the Affiliated People′s Hospital of Jiangsu University and the First People′s Hospital of Lianyungang were retrospectively selected. Among them, 201 patients with coronary artery stenosis ≤40% and evidence of CSF on CAG were included in the observation group. Meanwhile, 153 patients with coronary artery stenosis ≤40% but without CSF during the same period were enrolled as the control group. General clinical characteristics, echocardiographic data, complete blood count, biochemical parameters, and inflammatory markers were collected and compared between the two groups. Least Absolute Shrinkage and Selection Operator (LASSO) regression was employed to preliminarily select candidate variables. Multivariate logistic regression was then performed to identify independent risk factors associated with CSF. A nomogram prediction model was constructed using R software, and a corresponding nomogram was generated. The model′s discriminative ability, calibration, and clinical utility were assessed using the receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA), respectively. Results: LASSO regression identified hypertension, smoking, hemoglobin, high-density lipoprotein cholesterol (HDL-C), triglyceride-glucose (TyG) index, platelet-to-lymphocyte ratio (PLR), and left ventricular enddiastolic diameter (LVEDD) as relevant features for predicting CSF. Multivariate logistic regression analysis demonstrated that hypertension, smoking, elevated TyG index, elevated PLR, and increased LVEDD were independent risk factors for CSF, while increased HDL-C levels were found to be a protective factor. Based on these variables, a nomogram prediction model was constructed. The area under the ROC curve (AUC) was 0.793 (95% CI: 0.747-0.838), indicating good discrimination. The calibration curve and Hosmer-Lemeshow goodness-of-fit test (P=0.151) showed good agreement between predicted and observed outcomes. Additionally, the DCA curve demonstrated favorable clinical applicability of the model, indicating its potential to provide clinical benefit. Conclusion: Hypertension, smoking, elevated TyG index, elevated PLR, and increased LVEDD are independent risk factors for CSF, while increased HDL-C serves as a protective factor. The predictive model based on these factors exerts good performance in predicting the occurrence of CSF.

Objective: Screening and identifying of core genes in clear cell renal cell carcinoma (ccRCC) based on bioinformatics analysis techniques to search for novel biomarkers for the diagnosis of ccRCC and therapeutic targets. Methods: Differentially expressed genes (DEGs) between ccRCC samples and normal kidney samples were obtained from three datasets (including GSE100666, GSE168845, and GSE96574) using the GEO2R tool; DAVID online tool was used to annotate the intersection DEGs of these three datasets with GO and KEGG functions; A protein interaction network of these intersecting DEGs was constructed using the STRING website, and then the core genes through the CytoHubba plugin in Cytoscape software were determined; The expression of core genes in ccRCC were verified using data from Oncomine and TIMER 2.0 databases, the relationship between core genes and the survival of ccRCC patients were further analysed using GEPIA database, and also the relationship between core genes and immune cell infiltration were further analysed using TIMER 2.0 database. Results: A total of 189 DEGs were screened, which involve various biological functions and pathways such as tumor growth regulation. Ten DEGs were identified as core genes, includingPTPRC, CTLA4, CCR5, CXCL9, GZMB, CD27, CXCL13, IDO1, LCP2, and CASR . The expression analysis results of GEO dataset, Oncomine, and TIMER database all showed that compared with normal samples, the expression of CASR in ccRCC was significantly reduced, while the expression of the other 9 core genes was significantly increased. Survival analysis showed that CTLA4, CXCL13, and CASR were associated with overall survival in ccRCC patients, while CXCL13 and CASR were associated with disease-free survival in ccRCC patients. The TIMER 2.0 results indicated that upregulation of core gene expression was associated with immune cell infiltration in ccRCC. Conclusion: Ten core genes were identified that may be closely related to the pathogenesis of ccRCC, which may become new diagnostic markers and therapeutic targets for ccRCC.

Objective: To analyze the risk factors for major adverse cardiac events (MACE) following the treatment of coronary large vessel primary lesions with drugcoated balloon (DCB), and to construct a nomogram prediction model. Methods: A total of 271 patients who received DCB treatment for coronary large vessel primary lesions from January 2020 to August 2022 in Affiliated Hospital of Hebei University were selected as the study subjects. According to the occurrence of MACE after treatment, patients were divided into the MACE group and the non-MACE group. Clinical data, target vessel lesion characteristics, and procedural features were compared between the two groups. Variables with statistical significance in univariate analysis were further included in multivariate Logistic regression analysis to identify independent risk factors and to develop a predictive model for MACE after DCB treatment. Results: A total of 271 patients were included, among whom 64 cases (23.62%) were in the MACE group and 207 cases (76.38%) were in the non-MACE group. Significant differences were observed between the two groups in hypertension, diabetes mellitus, smoking history, low-density lipoprotein cholesterol (LDL-C), serum creatinine (SCr), and aspirin use (P<0.001). Regarding lesion and procedural characteristics, the incidence of acute myocardial infarction (AMI) and the degree of postoperative lesion stenosis differed significantly between groups (P<0.01). Multivariate Logistic regression analysis revealed that hypertension, diabetes mellitus, smoking history, elevated LDL-C, elevated SCr, AMI, and higher postoperative residual stenosis were independent risk factors for MACE (P<0.05), while aspirin use was a protective factor for MACE (P<0.001). The constructed nomogram model demonstrated strong predictive performance, with good calibration based on the Hosmer-Lemeshow test (P=0.181). The area under the receiver operating characteristic (AUC) curve was 0.912 (95%CI: 0.868-0.955), with a sensitivity of 81.2% and specificity of 90.3%. Conclusion: The developed nomogram model provides good predictive accuracy for MACE occurrence in the studied population.

Objective: To explore the impact of pulmonary nodule spatial location on the number of resected subsegments and surgical outcomes in anatomic sublobar resection. Methods: A retrospective analysis was conducted on 157 patients with pulmonary nodules who underwent “nodule-centric, subsegment-as-unit” surgery at the Affiliated Hospital of Jiangsu University and Jiangsu Province Hospital between January 2016 and November 2020. Based on the surgical approach, patients were divided into four groups: single subsegmentectomy (28 cases), combined subsegmentectomy (42 cases), single segmentectomy (66 cases), and single segmentectomy combined with adjacent subsegmentectomy (21 cases). Preoperative, intraoperative, and postoperative data were compared among the four groups. Results: There were no perioperative deaths, with no recurrence or metastasis by the end of followup in March 2025. Univariate analysis showed significant differences among the four groups in terms of maximum radiographic diameter and transverse location (relationship to the intersegmental vein) (P=0.022, P<0.001, respectively). No significant differences were found in other baseline data such as gender, age, and smoking history (all P>0.05). For intrasegmental nodules with a diameter of 8-20 mm, multivariate logistic regression analysis indicated that, compared to single segmentectomy, the performance of single subsegmentectomy was closely associated with the nodule's depth position (OR=7.224, 95%CI: 1.084-48.132, P=0.041) and maximum radiographic diameter (OR=0.068, 95%CI: 0.009-0.503, P=0.008). Conclusion: The surgical strategy using the pulmonary subsegment as the anatomic unit is safe and feasible for treating ground-glass-opacity dominant pulmonary nodules. For intrasegmental pulmonary nodules with a diameter of 8-20 mm, the spatial location and diameter of the nodule are key factors influencing the number of pulmonary subsegments involved in the surgery.

Objective: To observe the clinical efficacy and safety of Keyin mixture in treating moderate-to-severe plaque psoriasis with blood-heat syndrome and preliminarily explore its intervention effects on the IL-23/Th17 cell axis. Methods: A total of 30 patients with moderate-to-severe plaque psoriasis and blood-heat syndrome who attended the Dermatology Department of Jiangyin Hospital of Traditional Chinese Medicine from January 2023 to March 2024 were enrolled as the study group, and 30 healthy volunteers were selected as the control group. The study group received oral Keyin mixture (30 mL per dose, three times daily) for 12 weeks. Psoriasis area and severity index (PASI) scores, body surface area (BSA) scores, and dermatology life quality index (DLQI) scores were compared before and after treatment in the study group. Serum levels of IL-17, IL-22, IL-23, IL-6, and TNF-α were measured in both groups before treatment and in the study group after treatment. Adverse reactions were recorded throughout the study. Results: After 12 weeks of treatment, the study group showed significant reductions in PASI, BSA, and DLQI scores compared to baseline (all P<0.01), with PASI 50 and PASI 75 response rates of 63.3% and 16.7%, respectively. Before treatment, serum levels of IL-17, IL-22, IL-6, IL-23, and TNF-α in the study group were significantly higher than those in the control group (all P<0.01). After 12 weeks of treatment, the serum levels of these cytokines in the study group were significantly decreased compared to pretreatment values (all P<0.01). No obvious adverse reactions were observed during treatment, and there were no significant abnormalities in blood routine, urine routine, liver function, or kidney function before and after treatment. Conclusion: Keyin mixture exhibits significant efficacy and good safety in the treatment of moderate-to-severe plaque psoriasis with blood-heat syndrome. Its therapeutic mechanism may involve suppressing the expression of IL-23/Th17 axis-related factors (IL-23, IL-22, IL-17, IL-6, TNF-α).