Objective To evaluate the efficacy and safety of intraoperative pleural irrigation with Nocardia rubra cell-wall skeleton (N-CWS) for reducing pleural effusion drainage after radical surgery for lung cancer. Methods A retrospective analysis was conducted on the clinical data of lung cancer patients who underwent lobectomy and mediastinal lymph node dissection at the First Affiliated Hospital of Xiamen University between December 2024 and May 2025. Patients were divided into a control group and an irrigation group based on the intraoperative use of N-CWS. Patients in the irrigation group received pleural irrigation with 800 μg of N-CWS diluted in 10 mL of normal saline. The following outcomes were compared between the two groups: pleural effusion drainage volume at 0-24 h, 24-48 h, and 48-72 h postoperatively, degree of air leak, chest tube duration, postoperative length of stay, and the incidence of adverse events (fever, chest pain, and nausea and vomiting). Results A total of 245 patients were included (97 males, 148 females) with a mean age of (61.28±6.26) years, with 205 in the control group and 40 in the irrigation group. Compared to the control group, the irrigation group showed significantly lower pleural effusion drainage volumes at 0-24 h, 24-48 h, and 48-72 h, as well as shorter chest tube duration and postoperative length of stay (all P<0.05). There was no statistical difference in the degree of postoperative air leak (P=0.661). No significant differences were observed between the two groups regarding the highest body temperature within 72 h post-surgery (P=0.130), fever grade (P=0.196), severity of chest pain (P=0.105), or the incidence of nausea and vomiting (P=0.376). Conclusion Intraoperative pleural irrigation with N-CWS in patients undergoing lobectomy and mediastinal lymph node dissection for lung cancer can significantly reduce postoperative pleural effusion drainage volume, shorten chest tube duration and length of hospital stay. The procedure is safe and feasible.

The diagnostic frequency of multiple pulmonary tumor nodules has increased significantly in clinical practice. Among patients with multiple pulmonary nodules, distinguishing between separate primary lung carcinomas and intrapulmonary metastases is critical for accurate tumor staging, therapeutic decision-making, and prognostic evaluation. The consensus document "Differentiating separate primary lung adenocarcinomas from intrapulmonary metastases with emphasis on pathological and molecular considerations: Recommendations from the International Association for the Study of Lung Cancer Pathology Committee" highlights the pivotal role of integrated pathological and molecular analyses in diagnosing and differentiating primary lung adenocarcinomas from intrapulmonary metastatic lesions. It further proposes a combined four-step histologic and molecular classification algorithm for addressing multiple pulmonary tumor nodules of adenocarcinoma histology, providing clinicians with enhanced diagnostic tools to refine staging accuracy, guide therapeutic strategies, and improve prognostic predictions for lung adenocarcinoma. Building on current advancements in global research, this article offers a comprehensive interpretation of the consensus recommendations.

Non-small cell lung cancer is one of the primary types of cancer that leads to brain metastases. Approximately 10% of patients with non-small cell lung cancer have brain metastases at the time of diagnosis, and 26%-53% of patients develop brain metastases during the progression of their disease. However, the underlying mechanisms of lung cancer brain metastasis have not been fully elucidated. With the continuous development of single-cell and spatial transcriptomics, the genomic and transcriptomic characteristics of lung cancer brain metastasis are gradually being revealed. In February 2025, the journal Nature Medicine published an article titled "Single-cell and spatial genomic landscape of non-small cell lung cancer brain metastases". This article aims to provide a brief interpretation of the paper for colleagues in research and clinical practice.

OBJECTIVE: To investigate the predictive value of sphinor kinase 1 (sphk1), D-lactic acid, and intestinal fatty acid binding protein (I-FABP) for gastrointestinal injury in patients with sepsis. METHODS: A prospective observational study was conducted. Sixty-eight patients with sepsis and gastrointestinal dysfunction admitted to the department of critical care medicine of the First Affiliated Hospital of Baotou Medical College Inner Mongolia University of Science and Technology from May 2024 to March 2025 were enrolled (sepsis group), and they were divided into acute gastrointestinal injury (AGI) I-IV groups according to the definition and grading criteria of AGI proposed by the European Society of Intensive Care Medicine in 2012. Twenty non-sepsis patients without AGI admitted to the intensive care unit during the same period were enrolled as the control group (non-sepsis group). Within 30 minutes of patient enrollment, plasma sphk1, D-lactic acid, and I-FABP levels were determined by enzyme linked immunosorbent assay (ELISA). General data such as gender, age were recorded, and levels of procalcitonin (PCT), high-sensitivity C-reactive protein (hs-CRP), lactic acid (Lac), and acute physiology and chronic health evaluation II (APACHEII), sequential organ failure assessment (SOFA) were measured. Spearman method was used to analyze the correlation between sphk1, I-FABP, D-lactic acid and other indicators. The receiver operator characteristic curve (ROC curve) was used to evaluate the predictive value of sphk1, D-lactic acid, I-FABP, APACHEII score, and SOFA score for gastrointestinal injury in patients with sepsis. RESULTS: Among the 68 sepsis patients, 13 were classified as AGI grade I, 16 as AGI grade II, 23 as AGI grade III, and 16 had AGI grade IV. There were no statistically significant differences in gender, age, and abdominal infection rate among the groups. The SOFA score and APACHEII score of the sepsis group were significantly higher than those of the non-sepsis group; and the APACHEII score of the AGI IV group was significantly higher than that of the AGI I and AGI II groups. The levels of sphk1, D-lactic acid, I-FABP, PCT, Lac and hs-CRP in the sepsis group were significantly higher than those in the non-sepsis group, and each indicator gradually increased with the increase of AGI grade. Correlation analysis showed that plasma sphk1, D-lactic acid, and I-FABP in patients with sepsis-induced gastrointestinal injury were positively correlated with PCT, Lac, APACHEII score, and AGI grade (all P < 0.05), and sphk1 was positively correlated with I-FABP and D-lactic acid (r values were 0.773 and 0.782, respectively, both P < 0.05). ROC curve analysis showed that sphk1, D-lactic acid, I-FABP, APACHEII score, and SOFA score had high predictive value for gastrointestinal injury in patients with sepsis, with area under the curve (AUC) of 0.996, 0.987, 0.976, 0.901, and 0.934 (all P < 0.05). When the optimal cut-off value of sphk1 was 60.46 ng/L, the sensitivity and specificity were 95.6% and 100%, respectively; when the optimal cut-off value of D-lactic acid was 1 454.3 μg/L, the sensitivity and specificity were 95.6% and 100%, respectively; when the optimal cut-off value of I-FABP was 0.91 ng/L, the sensitivity and specificity were 95.6% and 100%, respectively; when the optimal cut-off value of APACHEII score was 14.5, the sensitivity and specificity were 80.9% and 85.0%, respectively; when the optimal cut-off value of SOFA score was 3.5, the sensitivity and specificity were 85.3% and 95.0%, respectively. CONCLUSIONS The levels of plasma sphk1, I-FABP, and D-lactic acid were significantly elevated in patients with sepsis and gastrointestinal injury. These indicators can serve as sensitive and relatively specific serological markers for early prediction of intestinal mucosal damage.
Humans ; Lactic Acid/blood* ; Fatty Acid-Binding Proteins/blood* ; Sepsis/complications* ; Prospective Studies ; Male ; Female ; Middle Aged ; Predictive Value of Tests ; Adult ; Aged ; Gastrointestinal Diseases/blood* ; Prognosis

OBJECTIVES: To propose a hypothesis that aloe-emodin may inhibit scar tissue fibrosis through thrombospondin-1(THBS1)-PI3K-Akt pathway. METHODS: By cultivating fibroblasts derived from scar tissue after cleft palate surgery in humans, aloe emodin of different concentrations (10, 20, 30, 40 and 50 μmol/L) was added to the cells which activity was detected. At the same time, transcriptome sequencing was performed on scar tissue and cells, and bioinformatics methods were used to explore potential targets and signaling pathways of scar tissue fibrosis. RESULTS: Aloe-emodin had a concentration dependent inhibitory effect on fibroblast proliferation,with the 40 μmol/L concentration group showing the most significant effect. The results of tissue and cell sequencing indicated that differentially expressed genes were significantly enriched in extracellular matrix-receptor interaction pathway, and shared a common differential gene which was THBS1. The ORA analysis results indicated that differentially expressed genes, including THBS1, were significantly enriched in the PI3K-Akt signaling pathway. CONCLUSIONS Aloe emodin may inhibit the PI3K-Akt pathway by downregulating THBS1, thereby reducing the proliferation activity of fibroblasts derived from postoperative palatal scar tissue.
Thrombospondin 1/genetics* ; Humans ; Signal Transduction/drug effects* ; Fibroblasts/cytology* ; Proto-Oncogene Proteins c-akt/metabolism* ; Fibrosis ; Phosphatidylinositol 3-Kinases/metabolism* ; Cicatrix/metabolism* ; Cell Proliferation/drug effects* ; Anthraquinones/pharmacology* ; Cells, Cultured

AIM:To investigate the effects of Kuntai capsule combined with stem cell therapy on oxidative stress damage in rats with premature ovarian failure(POF),focusing on the Nrf2-ARE signaling pathway.METHODS:Bone marrow mesenchymal stem cells(BMSCs)from Sprague-Dawley rats were cultured from primary to third generation.Female Sprague-Dawley rats were selected,and mesenchymal stem cells were isolated.A POF rat model was established through intraperitoneal injection of cyclic phosphamide,and the model was randomly divided into five groups:POF group,Kuntai group,stem cell group,combination group,and combination+Brusatol group.Normal rats injected with physio-logical saline served as the control group,with 10 rats in each group.After the intervention,changes in body weight and ovarian index were analyzed.Serum levels of estrogen indicators[luteinizing hormone(LH),follicle-stimulating hormone(FSH),serum estradiol(E2),and anti-Müllerian hormone(AMH)]and oxidative stress markers[malondialdehyde(MDA),glutathione(GSH),and superoxide dismutase(SOD)]were measured.Ovarian tissue was isolated for histologi-cal examination using HE staining and for expression analysis of anti-apoptotic BCL-2 and pro-apoptotic BAX mRNA via RT-qPCR.Western blot analysis was conducted to assess the expression of Nrf2 and heme oxygenase-1(HO-1)proteins.RESULTS:Compared to the control group,the POF group exhibited fewer mature follicles and disorganized ovarian mor-phology,along with significantly reduced body weight gain,ovarian index,E2,AMH,SOD and GSH levels,BCL-2 mRNA,and Nrf2 and HO-1 protein expression.Conversely,LH,FSH,MDA levels,and BAX mRNA expression were significantly increased(P＜0.05).In comparison to the POF group,the Kuntai group,stem cell group,and combination group showed improved ovarian morphology,with the combination group demonstrating the most significant improvement.In these groups,body weight gain,ovarian index,E2,AMH,SOD,GSH levels,BCL-2 mRNA,and Nrf2 and HO-1 pro-tein expression were markedly increased,while LH,FSH,MDA levels,and BAX mRNA expression were notably de-creased,with significant statistical differences observed between the combination group and the Kuntai and stem cell groups(P＜0.05).In contrast,the combination+Brusatol group exhibited a reduction in mature follicles and disrupted follicular structure compared to the combination group,along with decreased body weight gain,ovarian index,E2,AMH,SOD and GSH levels,BCL-2 mRNA,and Nrf2 and HO-1 protein expression,while LH,FSH and MDA levels,and BAX mRNA expression were significantly increased(P＜0.05).CONCLUSION:The combination of Kuntai capsule and stem cell therapy effectively mitigates oxidative stress damage in POF rats,potentially through the activation of the Nrf2-ARE signaling pathway.

Inflammatory response is a common feature of many acute and chronic diseases,which involves in activation of various cell types.Similar to tumor cells,inflammatory response is regulated by glucose metabolic reprogramming.Cells involved in pro-inflammatory response,such as M1 macrophages,Th1 and Th17 lymphocytes,must generate energy rapidly through glycolysis transformed by glucose metabolic reprogramming to promote inflammation,while cells involved in immune regulation and anti-inflam-matory response,such as regulatory T cells and M2 macrophages,preferentially use fatty acid oxidation and oxidative phosphorylation as a main source for energy production.This article systematically reviews the role of glucose metabolic reprogramming in different stages of inflammatory response,as well as the various molecular mechanisms of glucose metabolic reprogramming in inflammatory response,including activation or inhibition of signaling pathways,epigenetic regulation,post-transcriptional regulation and post-translational modification,which aims to provide a reference for exploring the specific regulatory mechanisms of glucose metabolic reprogramming on inflammatory response and the therapeutic targets of inflammatory-related diseases.

N6-methyladenosine(m6A)modification is considered to be the most common eukaryotic RNA modification.Under regulation of writers,erasers and readers,m6A mediates RNA transcription,nuclear export,splicing,translation and other processes.Innate immunity is body's first line of defense against pathogen invasion,and under stimulation of pathogens and foreign bodies,it rapidly produces non-specific protective response.Recent studies have found that m6A modification plays an important role in process of innate immunity,participating in regulation of innate immunity by targeting innate immune cells,affecting immune recognition,and regulating antiviral responses.This article reviews molecular mechanism of m6A modification and its progress in innate immunity,providing new ideas for treatment strategies of related diseases based on m6A modification.

AIM:To investigate the effects of Kuntai capsule combined with stem cell therapy on oxidative stress damage in rats with premature ovarian failure(POF),focusing on the Nrf2-ARE signaling pathway.METHODS:Bone marrow mesenchymal stem cells(BMSCs)from Sprague-Dawley rats were cultured from primary to third generation.Female Sprague-Dawley rats were selected,and mesenchymal stem cells were isolated.A POF rat model was established through intraperitoneal injection of cyclic phosphamide,and the model was randomly divided into five groups:POF group,Kuntai group,stem cell group,combination group,and combination+Brusatol group.Normal rats injected with physio-logical saline served as the control group,with 10 rats in each group.After the intervention,changes in body weight and ovarian index were analyzed.Serum levels of estrogen indicators[luteinizing hormone(LH),follicle-stimulating hormone(FSH),serum estradiol(E2),and anti-Müllerian hormone(AMH)]and oxidative stress markers[malondialdehyde(MDA),glutathione(GSH),and superoxide dismutase(SOD)]were measured.Ovarian tissue was isolated for histologi-cal examination using HE staining and for expression analysis of anti-apoptotic BCL-2 and pro-apoptotic BAX mRNA via RT-qPCR.Western blot analysis was conducted to assess the expression of Nrf2 and heme oxygenase-1(HO-1)proteins.RESULTS:Compared to the control group,the POF group exhibited fewer mature follicles and disorganized ovarian mor-phology,along with significantly reduced body weight gain,ovarian index,E2,AMH,SOD and GSH levels,BCL-2 mRNA,and Nrf2 and HO-1 protein expression.Conversely,LH,FSH,MDA levels,and BAX mRNA expression were significantly increased(P＜0.05).In comparison to the POF group,the Kuntai group,stem cell group,and combination group showed improved ovarian morphology,with the combination group demonstrating the most significant improvement.In these groups,body weight gain,ovarian index,E2,AMH,SOD,GSH levels,BCL-2 mRNA,and Nrf2 and HO-1 pro-tein expression were markedly increased,while LH,FSH,MDA levels,and BAX mRNA expression were notably de-creased,with significant statistical differences observed between the combination group and the Kuntai and stem cell groups(P＜0.05).In contrast,the combination+Brusatol group exhibited a reduction in mature follicles and disrupted follicular structure compared to the combination group,along with decreased body weight gain,ovarian index,E2,AMH,SOD and GSH levels,BCL-2 mRNA,and Nrf2 and HO-1 protein expression,while LH,FSH and MDA levels,and BAX mRNA expression were significantly increased(P＜0.05).CONCLUSION:The combination of Kuntai capsule and stem cell therapy effectively mitigates oxidative stress damage in POF rats,potentially through the activation of the Nrf2-ARE signaling pathway.

Inflammatory response is a common feature of many acute and chronic diseases,which involves in activation of various cell types.Similar to tumor cells,inflammatory response is regulated by glucose metabolic reprogramming.Cells involved in pro-inflammatory response,such as M1 macrophages,Th1 and Th17 lymphocytes,must generate energy rapidly through glycolysis transformed by glucose metabolic reprogramming to promote inflammation,while cells involved in immune regulation and anti-inflam-matory response,such as regulatory T cells and M2 macrophages,preferentially use fatty acid oxidation and oxidative phosphorylation as a main source for energy production.This article systematically reviews the role of glucose metabolic reprogramming in different stages of inflammatory response,as well as the various molecular mechanisms of glucose metabolic reprogramming in inflammatory response,including activation or inhibition of signaling pathways,epigenetic regulation,post-transcriptional regulation and post-translational modification,which aims to provide a reference for exploring the specific regulatory mechanisms of glucose metabolic reprogramming on inflammatory response and the therapeutic targets of inflammatory-related diseases.