Objective: This study aims at assessing the potential benefits of observation of monocyte-to-albumin ratio (MAR) and neutrophil percentage-to-hemoglobin ratio (NPHR) in the detection of non-small cell lung cancer (NSCLC). Methods: This study retrospectively involved 195 NSCLC patients and 204 healthy volunteers. The correlations between the clinicopathological characteristics of NSCLC and the two ratios including MAR and NPHR were assessed. The diagnostic efficiency of NSCLC patients by MAR and NPHR, alone or in combination with carcinoembryonic antigen (CEA), was assessed by receiver operating characteristic (ROC) curve. The risk factors for NSCLC were analyzed with binary logistic regression. Results: Compared to healthy controls, the levels of MAR and NPHR in NSCLC patients were elevated. MAR and NPHR were related to clinicopathologic characteristics and increased significantly along with the progression of NSCLC. The area under the curve (AUC) for 95% confidence interval (95% CI) of MAR and NPHR in the diagnosis of NSCLC was 0.812 (0.769– 0.854) and 0.724 (0.675– 0.774), respectively. The combination of MAR, NPHR, and CEA achieved the highest diagnostic utility compared to each individually or combined markers (AUC, 0.86; 95% CI, 0.824– 0.896; sensitivity, 72.8%; specificity, 87.3%). Further analysis showed that MAR combined with NPHR presented the potential to detect early-stage (IA–IIB) NSCLC (AUC, 0.794; 95% CI, 0.743– 0.845; sensitivity, 55.1%; specificity, 87.7%). The result indicated that MAR and NPHR might be risk factors for NSCLC. Conclusion: MAR and NPHR could be novel and effective auxiliary indexes in the detection of NSCLC, especially when combined with CEA.

Lung cancer remains a leading cause of cancer-related deaths worldwide, necessitating innovative treatments. Tumor-associated macrophages (TAMs) are primary immunosuppressive effectors that foster tumor proliferation, angiogenesis, metastasis, and resistance to therapy. They are broadly categorized into proinflammatory M1 and tumor-promoting M2 phenotypes, with elevated M2 infiltration correlating with poor prognosis. Strategies aimed at inhibiting TAM recruitment, depleting TAMs, or reprogramming M2 to M1 are therefore highly promising. Key signaling pathways, such as CSF-1/CSF-1R, IL-4/IL-13–STAT6, TLRs, and CD47-SIRPα, regulate TAM polarization. Additionally, macrophage-based drug delivery systems permit targeted agent transport to hypoxic regions, enhancing therapy. Preclinical studies combining TAM-targeted therapies with chemotherapy or immune checkpoint inhibitors have yielded improved responses and prolonged survival. Several clinical trials have also reported benefits in previously unresponsive patients. Future work should clarify the roles of macrophage-derived exosomes, cytokines, and additional mediators in shaping the immunosuppressive tumor microenvironment. These insights will inform the design of next-generation drug carriers and optimize combination immunotherapies within precision medicine frameworks. Elucidating TAM phenotypes and their regulatory molecules remains central to developing novel strategies that curb tumor progression and ultimately improve outcomes in lung cancer. Importantly, macrophage-based immunomodulation may offer expanded treatment avenues.

Asthma is a common chronic inflammatory airway disease; however, whether microRNAs (miRs) could be used in the treatment of asthma remains unclear. The aim of the present study was to investigate the role of miR‑625‑5p in the inflammatory response of human bronchial epithelial cells (HBECs). Inflammation in the HBEC line, 16HBEC, was induced using different concentrations of lipopolysaccharide (LPS), which demonstrated that 1 µg/ml LPS was an appropriate concentration for further experiments. The association between protein kinase B2 (AKT2) and miR‑625‑5p was verified using a luciferase reporter assay. LPS was added to 16HBECs following the administration of miR‑625‑5p mimics or miR‑625‑5p inhibitors, and cells with silenced or overexpressed AKT2 levels. miR‑625‑5p was expressed at a high level in LPS‑activated 16HBECs. Overexpression of miR‑625‑5p inhibited interleukin (IL)‑6 and tumor necrosis factor (TNF)‑α secretion in 16HBECs. Inhibition of miR‑625‑5p enhanced LPS‑induced IL‑6 and TNF‑α secretion. miR‑625‑5p negatively regulated the expression of AKT2 in 16HBECs. A dual‑luciferase reporter assay system confirmed that miR‑625‑5p directly targeted the 3'untranslated region of AKT2. Transfection with a small interfering RNA against AKT2 inhibited inhibitor of κB phosphorylation. In brief, miR‑625‑5p may protect LPS‑induced HBECs by targeting AKT2 and inhibiting the nuclear factor‑κB signaling pathway. Therefore, miR‑625‑5p may function as an inhibitor of asthma airway inflammation in HBECs by targeting AKT2.

With the rapid spread of the novel coronavirus (COVID-19), a sustained global pandemic has emerged. Globally, the cumulative death toll is in the millions. The rising number of COVID-19 infections and deaths has severely impacted the lives of people worldwide, healthcare systems, and economic development. We conducted a retrospective analysis of the characteristics of COVID-19 patients. This analysis includes clinical features upon initial hospital admission, relevant laboratory test results, and imaging findings. We aimed to identify risk factors for severe illness and to construct a predictive model for assessing the risk of severe COVID-19. We collected and analyzed electronic medical records of confirmed COVID-19 patients admitted to the Affiliated Hospital of Jiangsu University (Zhenjiang, China) between December 18, 2022, and February 28, 2023. According to the WHO diagnostic criteria for the novel coronavirus, we divided the patients into two groups: severe and non-severe, and compared their clinical, laboratory, and imaging data. Logistic regression analysis, the least absolute shrinkage and selection operator (LASSO) regression, and receiver operating characteristic (ROC) curve analysis were used to identify the relevant risk factors for severe COVID-19 patients. Patients were divided into a training cohort and a validation cohort. A nomogram model was constructed using the “rms” package in R software. Among the 346 patients, the severe group exhibited significantly higher respiratory rates, breathlessness, altered consciousness, neutrophil-to-lymphocyte ratio (NLR), and lactate dehydrogenase (LDH) levels compared to the non-severe group. Imaging findings indicated that the severe group had a higher proportion of bilateral pulmonary inflammation and ground-glass opacities compared to the non-severe group. NLR and LDH were identified as independent risk factors for severe patients. The diagnostic performance was maximized when NLR, respiratory rate (RR), and LDH were combined. Based on the statistical analysis results, we developed a COVID-19 severity risk prediction model. The total score is calculated by adding up the scores for each of the twelve independent variables. By mapping the total score to the lowest scale, we can estimate the risk of COVID-19 severity. In addition, the calibration plots and DCA analysis showed that the nomogram had better discrimination power for predicting the severity of COVID-19. Our results showed that the development and validation of the predictive nomogram had good predictive value for severe COVID-19.

Asthma is a chronic inflammatory airway disease and the airway epithelium is involved in airway inflammation and innate immunity. However, whether circular RNA (circRNA) is involved in the pathogenesis of asthma remains unclear. The present study aimed to determine the functions and molecular mechanisms of circRNA targeting dehydrogenase E1 (circDHTKD1) in the inflammation response of human bronchial epithelial cells. BEAS‑2B cells were stimulated with lipopolysaccharide (LPS) to establish a model of in vitro airway inflammation. Cell viability was assessed using Cell Counting Kit‑8 assay. CircDHTKD1 was characterised by nucleocytoplasmic isolation and Sanger sequencing. The RNA expression levels of circDHTKD1, microRNA (miR)‑338‑3p and potential ERK pathway downstream genes were evaluated by reverse transcription‑quantitative polymerase chain reaction. Western blot analysis was performed to measure associated protein levels. The levels of inflammatory cytokines were detected by ELISA. The interaction between circDHTKD1 and miR‑338‑3p was confirmed by dual‑luciferase reporter assay. circDHTKD1 expression was significantly upregulated by LPS treatment, whereas miR‑338‑3p expression was decreased. Furthermore, circDHTKD1 directly targeted miR‑338‑3p, which negatively regulated expression of E26 transformation specific‑1 (ETS1). Inflammatory cytokine and ETS1 expression levels decreased following transfection with small interfering RNA targeting circDHTKD1 or miR‑338‑3p mimics. In addition, co‑transfection with miR‑338‑3p inhibitor reversed the effects caused by circDHTKD1 knockdown. The knockdown of ETS1 in LPS‑induced BEAS‑2B cells resulted in decreased cytokine production and inhibition of the ERK signalling pathway. Overall, these results suggested that the knockdown of circDHTKD1 alleviated the LPS‑induced production of inflammatory cytokines and activation of the ERK pathway in BEAS‑2B cells through the miR‑338‑3p/ETS1 axis. In summary, circDHTKD1 exacerbated LPS‑triggered inflammation responses in BEAS‑2B cells by regulating ETS1 expression by interacting with miR‑338‑3p, suggesting that circDHTKD1 may serve as a potential therapeutic target against asthma.

The present study aimed to evaluate the potential of the monocyte to red blood cell count ratio (MRR), the neutrophil to red blood cell count ratio (NRR), the lymphocyte to red blood cell count ratio (LRR) and the product of lymphocyte count and albumin concentration (LA) for the diagnosis of lung cancer. The cases of 216 patients with newly diagnosed lung cancer and 184 healthy volunteers were retrospectively analysed. The MRR and NRR were found to be higher in patients with lung cancer compared with those in healthy controls, while the LRR and LA were lower. The receiver operating characteristic curve analysis revealed that of the four markers, the MRR and LA yielded a higher area under the curve (AUC) (MRR: AUC, 0.810; 95% CI, 0.768‑0.847; and LA: AUC, 0.721; 95% CI, 0.674‑0.764). The combination of MRR, LA, carcinoembryonic antigen (CEA) and cytokeratin 19 fragment antigen 21‑1 (CYFRA21‑1) achieved the highest diagnostic value when compared with other single or combined markers (AUC, 0.882; 95% CI, 0.846‑0.912; sensitivity, 81.9%; specificity, 81.0%). As the disease progressed, the MRR tended to increase, while LA exhibited a decreasing trend. Binary logistic regression analysis revealed an increase in the MRR, as well as in CEA and CYFRA21‑1 concentrations, and a decrease in the LA, which could all be possible risk factors for lung cancer. Differences in the MRR and LA between patients with early stage (IA‑IIIA) lung cancer and healthy controls were observed. Further analysis revealed that the MRR also exhibited the potential to detect early stage (IA‑IIIA) lung cancer in the model. The present findings demonstrated that the MRR and LA may be used as auxiliary biomarkers for the diagnosis of lung cancer and could partly indicate disease progression.