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Background The proportion of patients with lung cancer complicated by atrial fibrillation (AF) is increasing. Identifying shared molecular targets between these two conditions may provide important prognostic insights for patients with comorbidities. Methods The GSE8569 and GSE41177 datasets were downloaded from the Gene Expression Omnibus (GEO) database. Differential expression analysis was performed using the limma package in R. Weighted gene co-expression network analysis (WGCNA) was conducted to identify significant gene modules. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, along with gene set enrichment analysis (GSEA), were used to explore biological functions. Clinical survival data for lung cancer were obtained from The Cancer Genome Atlas (TCGA), and receiver operating characteristic (ROC) analysis was conducted using the R package ROC (version 1.17.0.1). Results A total of 598 differentially expressed genes (DEGs) were identified. These DEGs were primarily enriched in cell proliferation, inflammatory responses, non-small cell lung cancer, the p53 signaling pathway, and the cell cycle. Three core genes (CYBB, ITGB2, FCER1G) were identified. Notably, CYBB was downregulated in lung cancer compared to normal tissue. Patients in the low-risk group had significantly better survival outcomes. Heatmap visualization showed that expression of CYBB decreased with increasing risk scores, suggesting a protective role. Conclusion CYBB expression may influence lung cancer prognosis and contribute to the pathogenesis of AF. Further research is needed to clarify CYBB’s role in patients with both conditions.

Background Heart failure (HF) and COVID-19 are distinct but serious conditions with overlapping features such as systemic inflammation and multiorgan involvement. Both may share underlying molecular mechanisms, but the common genetic contributors remain poorly understood. This study aimed to identify shared key genes involved in HF and COVID-19 using integrative bioinformatics analysis. Methods Two transcriptomic datasets GSE76701 (HF myocardial tissue) and GSE190496 (COVID-19 lung tissue)—were retrieved from the GEO database. Differentially expressed genes (DEGs) were identified using the limma package. Weighted gene co-expression network analysis (WGCNA) and protein–protein interaction (PPI) network analysis were used to identify hub genes. Functional enrichment (GO, KEGG, GSEA), immune infiltration (CIBERSORT), disease association (CTD), and miRNA prediction (TargetScan) analyses were also performed. Results A total of 511 overlapping DEGs were identified. Enrichment analyses revealed involvement of pathways such as mTOR, insulin, and thyroid hormone signaling. WGCNA and PPI network analysis identified five core genes, including RPS27A and PPP2R1A, both of which were significantly upregulated in HF and COVID-19 samples. Immune infiltration analysis revealed increased macrophage fractions. miRNA predictions suggested PPP2R1A is potentially regulated by miR-497-5p, miR-15b-5p, and miR-15a-5p. Conclusion RPS27A and PPP2R1A may serve as common molecular regulators in HF and COVID-19. These findings offer potential cross-disease biomarkers and therapeutic targets for conditions driven by inflammation and immune dysregulation.

Objective Enhanced recovery after surgery (ERAS) protocols help optimize inpatient care and minimize discomfort. This study was performed to explore the safety, feasibility, and clinical and social value of ERAS in pediatric gastrointestinal surgery. Methods This study included all children (n = 125) who underwent appendectomy, pyloromyotomy, transabdominal Soave’s procedure, Meckel’s diverticulum resection, or reduction of intussusception in our institution from January to September 2018. We compared surgical outcomes between children who underwent surgery under conventional perioperative regimens (control group, n = 57) and those who were treated with ERAS protocols (ERAS group, n = 68). Results There were no significant intergroup differences in demographic or surgical data. However, the bowel function recovery time, postoperative intravenous nutrition time, duration of postoperative hospital stay, and hospital costs were significantly lower in the ERAS group than control group. There was no significant intergroup difference in the complication rate. Conclusions Our results indicate that implementation of ERAS protocols is safe and feasible in pediatric gastrointestinal surgery. They can improve patient comfort, shorten the duration of the postoperative hospital stay, reduce hospital costs, and accelerate postoperative rehabilitation without increasing the risk of postoperative complications. Therefore, ERAS protocols deserve wider implementation and promotion.

Liver fibrosis is a common complication of diabetes. Due to the crucial role of HSCs in the pathogenesis of hepatic fibrosis, they are considered a key target in anti-fibrosis research. We designed this experiment to investigate the effects of liraglutide on the proliferation of rat hepatic stellate cells under high glucose conditions and its relationship with the extracellular regulated protein kinases (ERK) signaling pathway. Rat hepatic stellate cells were randomly assigned to five groups: the normal glucose control group, the high glucose control group, the high osmotic group, the high glucose + liraglutide group (referred to as the liraglutide group), and the high glucose + inhibitor group referred to as the inhibitor group). The five groups of cells were cultured for 48 h before proceeding with the subsequent procedures. First, the ELISA method was employed to quantitatively measure the concentration of type I collagen in the supernatant from the rat hepatic stellate cell culture. Subsequently, RT-PCR was utilized to assess the expression level of ERK mRNA in the rat hepatic stellate cells. Finally, Western blot analysis was performed to detect the expression of ERK and phosphorylated ERK (p-ERK) proteins. The proliferation of rat HSCs was significantly increased in the high glucose group compared to the normal glucose group ( P  < 0.05). In the liraglutide group, after 48 h of treatment, cell proliferation was reduced relative to the high glucose group ( P  < 0.05), although it remained higher than that of the normal glucose group ( P  < 0.05) and the inhibitor group ( P  < 0.05). No statistically significant difference in proliferation was observed between the hypertonic group and the normal glucose control group ( P  > 0.05). Comparison of Type I Collagen Content: There was no significant change in Type I collagen content in the hypertonic group compared to the control group ( P  > 0.05). However, a significant increase in Type I collagen content was observed in the high glucose group ( P  < 0.05). Both the liraglutide group and the inhibitor group exhibited a significant decrease in Type I collagen content compared to the high glucose group ( P  < 0.05). Furthermore, the Type I collagen content in the inhibitor group was lower than that in the liraglutide group ( P  < 0.05). Comparison of ERK mRNA Expression Levels: Compared to the control group, the hyperosmolar group exhibited no significant change in ERK mRNA expression ( P  > 0.05). In contrast, the high glucose group significantly increased ERK mRNA expression ( P  < 0.05). Both the inhibitor group and the liraglutide group showed significantly lower ERK mRNA expression levels compared to the high glucose group ( P  < 0.05), with the inhibitor group presenting lower expression than the liraglutide group ( P  < 0.05). P-ERK Expression Results: When compared to the control group, the hyperosmolar group displayed no significant change in p-ERK expression ( P  > 0.05). The high glucose group, however, exhibited a significant increase in p-ERK expression ( P  < 0.05). Both the liraglutide group and the inhibitor group had significantly reduced p-ERK expression compared to the high glucose group ( P  < 0.05), with the inhibitor group showing a further reduction in p-ERK expression relative to the liraglutide group ( P  < 0.05). Hyperglycemia promotes the proliferation of rat hepatic stellate cells. Liraglutide inhibits the proliferation of HSCs in high glucose conditions by inhibiting the ERK signaling pathway.

Objective Atherosclerosis (AS) is a life-threatening disease in aging populations worldwide. However, the molecular and gene regulation mechanisms of AS are still unclear. This study aimed to identify gene expression differences between atheroma plaques and normal tissues in humans. Methods The expression profiling dataset GSE43292 was obtained from the Gene Expression Omnibus (GEO) dataset. The differentially expressed genes (DEGs) were identified between the atheroma plaques and normal tissues via GEO2R, and functional annotation of the DEGs was performed by GSEA. STRING and MCODE plug-in of Cytoscape were used to construct a protein–protein interaction (PPI) network and analyze hub genes. Finally, quantitative polymerase chain reaction (qPCR) was performed to verify the hub genes. Results Overall, 134 DEGs were screened. Functional annotation demonstrated that these DEGs were mainly enriched in sphingolipid metabolism, apoptosis, lysosome, and more. Six hub genes were identified from the PPI network: ITGAX, CCR1, IL1RN, CXCL10, CD163, and MMP9. qPCR analysis suggested that the relative expression levels of the six hub genes were significantly higher in AS samples. Conclusions We used bioinformatics to identify six hub genes: ITGAX, CCR1, IL1RN, CXCL10, CD163, and MMP9. These hub genes are potential promising diagnostic and therapeutic targets for AS.

Atrial fibrillation (AF) is the most common type of persistent arrhythmia. Although its incidence has been increasing, the pathogenesis of AF in stroke remains unclear. In this study, a total of 30 participants were recruited, including 10 controls, 10 patients with AF and 10 patients with AF and stroke (AF + STROKE). Differentially expressed genes (DEGs) were identified, and functional annotation of DEGs, comparative toxicogenomic database analysis associated with cardiovascular diseases, and predictions of miRNAs of hub genes were performed. Using RT‐qPCR, biological process and support vector machine neural networks, numerous DEGs were found to be related to AF. HBG1, SNCA and GYPB were found to be upregulated in the AF group. Higher expression of hub genes in AF and AF + STROKE groups was detected via RT‐PCR. Upon training the biological process neural network of SNCA and GYPB for HBG1, only small differences were detected. Based on the support vector machine, the predicted value of SNCA and GYPB for HBG1 was 0.9893. Expression of the hub genes of HBG1, SNCA and GYPB might therefore be significantly correlated to AF. These genes are involved in the incidence of AF complicated by stroke, and may serve as targets for early diagnosis and treatment.

Background Social frailty has not been comprehensively studied in China. Our objective is to investigate the prevalence of social frailty among the older population in China, as well as identify relevant factors and urban-rural differences. Methods We obtained data from the Fourth Sample Survey of the Aged Population in Urban and Rural China (SSAPUR) database. The study employed a multistage, stratified, cluster-sampling method, recruiting a total of 224,142 adults aged 60 years or older. Participants were interviewed to gather demographic data and information on family, health and medical conditions, health care service status, living environment conditions, social participation, protected rights status, spiritual and cultural life, and health. Social frailty was assessed using the HALFE Social Frailty Index. A score of three or above indicated social frailty. Results We analyzed a total of 222,179 cases, and the overall prevalence of social frailty was found to be 15.2%. The highest prevalence was observed among participants aged 75–79 years (18.0%). The prevalence of social frailty was higher in rural older populations compared to urban older populations (19.9% in rural vs. 10.9% in urban, P < 0.0001). In urban areas, women had a higher prevalence than men (11.7% in women vs. 9.9% in men, P < 0.0001), while in rural areas, men had a higher prevalence than women (20.6% in men vs. 19.2% in women, P < 0.0001). Multivariate regression analysis revealed that living in a rural/urban environment (OR 1.789, 95% CI 1.742–1.837), absence of a spouse/spousal presence (OR 4.874, 95% CI 4.743–5.009), self-assessed unhealthy/health status (OR 1.696, 95% CI 1.633–1.761), and housing dissatisfaction/satisfaction (OR 2.303, 95% CI 2.233–2.376) were all significantly associated with social frailty. Conclusions Using the HALFE social frailty index, we found a prevalence of 15.2% among older people in China, with the highest prevalence observed in the 75–79 age group. Social frailty was more prevalent in rural areas than in urban areas. Various factors, including spousal presence, housing satisfaction, health status, and urban-rural residential differences, were significantly associated with social frailty. These findings highlight the modifiable and non-modifiable factors that contribute to social frailty among older individuals in China.

Background Diabetic carotid atherosclerosis is a prevalent vascular disease in individuals with diabetes mellitus, imposing a significant global burden. A lesser-known risk factor for the development of diabetes and its associated atherosclerosis is sleep disturbance. Obstructive Sleep Apnea Syndrome has been confirmed by many studies to affect atherosclerosis, but the mechanism of other nonobstructive sleep disorders such as the number of awakenings on atherosclerosis is still unclear. This study aims to investigate the relationship between sleep patterns and carotid atherosclerosis in diabetic patients. Methods Experiments were designed, and Huawei Band 9 bracelets were utilized to monitor the sleep patterns of patients. Specific sleep indicators such as number of nighttime awakenings, time taken to fall asleep, waking time, duration of deep sleep, duration of shallow sleep, rapid eye movement (REM) duration, and sleep breathing quality were recorded. Carotid artery ultrasound was performed to assess the severity of carotid atherosclerosis in all patients, followed by statistical analysis to examine the correlation between sleep parameters and carotid atherosclerosis grades in diabetic individuals. Results Spearman correlation analysis revealed that age, duration of hypertension, number of nighttime awakenings, proportion of shallow sleep, average duration of shallow sleep per night, hypertension severity, years of smoking, and duration of diabetes were identified as risk factors for diabetic carotid atherosclerosis. Ordinal logistic regression analysis showed that diabetic carotid atherosclerosis was more severe in patients with a sleep score of less than 76 compared to those with a score greater than or equal to 76 (OR = 2.497, 95%CI 1.034–6.032). Patients with a shallow sleep duration of greater than or equal to 5.4 h had a higher grade of diabetic carotid atherosclerosis than those with a duration of less than 5.4 h (OR = 6.475, 95%CI 1.573–26.656), and patients with more than 4 awakenings had more severe diabetic carotid atherosclerosis than those with less than 4 awakenings at night (OR = 2.933, 95%CI 1.035–8.314). The degree of carotid atherosclerosis in diabetic patients over 60 years old is higher than that in diabetic patients under or equal to 60 years old (odds ratio = 4.019, 95% confidence interval: 0.496–2.285). ( P  < 0.05, Table  3 , Fig.  4 ). The results of the multivariate ordinal logistic model showed that compared to patients with a shallow sleep duration of less than 5.4 h, patients with a duration of greater than or equal to 5.4 h had higher grades of diabetic carotid atherosclerosis (OR = 4.50, 95% CI 1.010–20.045) ( P  < 0.05). Conclusions Prolonged periods of shallow sleep are associated with diabetic carotid atherosclerosis. Clinical trial Account number ChiCTR2300069928.

Background Chronic diseases, such as heart disease, cancer, and diabetes, are the leading causes of death and disability. Loneliness is linked to a greater risk of chronic disease. However, the lack of loneliness may change this relationship. Methods The 4th Survey of the Aged Population in Urban and Rural China (SSAPUR) was performed. 222,179 people over 60 years old were recruited. Chronic disease was defined by self-reported tumble incidents using the fourth SSAPUR questionnaire. We found that the residuals were well normally distributed. Subsequently, we analyzed the association between each studied factor and chronic disease by univariate logistic regression analysis. Finally, we stratified the population by age, gender, and urban and rural. Results 77,448 individuals experienced loneliness, while 137,593 did not. Loneliness correlated significantly with urban-rural classification, age, and gender ( P  < 0.001). There was a significant association between chronic diseases and loneliness ( P  < 0.05). Compared to lonely individuals, those with low level of loneliness had a lower incidence of gastric diseases (OR = 0.752, 95% CI, 0.736–0.769, P  < 0.001), osteoarthritis (OR = 0.685, 95% CI, 0.673–0.697, P  < 0.001), chronic obstructive pulmonary disease (COPD) (OR = 0.678, 95% CI, 0.659–0.698, P  < 0.001), asthma (OR = 0.608, 95% CI, 0.583–0.633, P  < 0.001), malignant tumors (OR = 0.892, 95% CI, 0.822–0.968, P  = 0.006), and reproductive system diseases (OR = 0.871, 95% CI, 0.826–0.918, P  < 0.001). Conclusion In summary, loneliness is an important risk factor in the occurrence and development of chronic diseases in the elderly in China, and it has adverse effects on hypertension, stomach disease, cataract or glaucoma, osteoarthrosis, chronic lung disease, asthma, malignant tumor, and reproductive system diseases.

The WD‐repeat (WDR) family affects carcinogenesis, but its role in the immune microenvironment is poorly characterized. Although functional loss or gain of WDR6 does not markedly change in vitro proliferative and invasive capacity of HCC cells, its deficiency in hepa1‐6 cells drastically inhibits the growth and lung metastasis of orthotopically implanted tumors in immune‐competent C57BL/6J mice. Mechanistically, WDR6 targets tumor suppressor UVRAG to the CUL4A‐DDB1‐ROC1 E3 ubiquitin ligase complex through a unique WDxR motif and promotes its degradation. This upregulates chromatin accessibility at the TNFα locus by blocking autophagic degradation of p65, elevates intratumoral myeloid‐derived suppressor cell (MDSC) number, and reduces CD8 + T cell infiltration, thereby promoting HCC progression. These immunosuppressive effects are reversed by TNFα blockade. TNFα recruits NF‐κB to activate the transcription of WDR6 , establishing a WDR6‐TNFα loop. Clinically, the WDR6/UVRAG/NF‐κB pathway is hyperactivated in HCC, predicting a poor prognosis. Importantly, a WDxR‐like peptide disrupts the WDR6/UVRAG complex and enhances the efficiency of anti‐PD‐L1 against HCC with WDR6 dysregulation. Synopsis The WD‐repeat (WDR) family affects carcinogenesis, but its role in immune microenvironment is poorly characterized. This study reports the cellular and molecular effects of targeting WDR6 on HCC. Functional loss of WDR6 inhibited HCC growth and metastasis only in immune‐competent mice. Increased number of intra‐tumoral PMN‐MDSCs mediated by WDR6 activation was reversed by TNFα blockade. UVRAG degradation was enhanced by WDR6 via a WDxR motif, thereby leading to TNFα increase and PMN‐MDSC recruitment in HCC. Anti‐PD‐L1 immunotherapy efficiency was improved by a WDxR‐like peptide in HCC with WDR6 dysregulation. Graphical Abstract The WD‐repeat (WDR) family affects carcinogenesis, but its role in immune microenvironment is poorly characterized. This study reports the cellular and molecular effects of targeting WDR6 on HCC.