Objective To analyze the risk factors of type 2 diabetes mellitus (T2DM) with metabolic-associated fatty liver disease (MAFLD) and explore their relationship with BMI management. Methods A retrospective analysis was conducted of 310 patients with type 2 diabetes who underwent physical examinations at the 363 hospital between March 2023 and March 2025. Among these patients, those with MAFLD were counted. The risk factors of T2DM with MAFLD were analyzed by logistic regression analysis. The relationship between T2DM with MAFLD and BMI management was explored by Spearman correlation coefficient analysis. Results Compared with the non-MAFLD group, the levels of alanine aminotransferase (ALT), fasting insulin (I₀), fasting blood glucose (G₀), BMI, triglyceride (TG), aspartate aminotransferase (AST), and serum uric acid (SUA) were higher while the level of high-density lipoprotein cholesterol (HDL-C) was lower in the MAFLD group (P<0.05). Logistic regression analysis showed that BMI, SUA, I₀, ALT, G₀, and BMI control scale score were risk factors of T2DM with MAFLD (P<0.05). The score of BMI control scale of patients in the MAFLD group was higher than that in the non-MAFLD group (P<0.05). Correlation analysis indicated that T2DM with MAFLD was negatively correlated with BMI management (P<0.05). Conclusion BMI, SUA, I₀, ALT, and G₀ are all risk factors of T2DM with MAFLD. BMI management is negatively correlated with T2DM with MAFLD. Patients with T2DM should control BMI and blood glucose to reduce the occurrence of MAFLD.

ObjectiveTo investigate the disruptive effects of perinatal exposure to the environmental endocrine disruptor bisphenol AF (BPAF) on hepatic lipid metabolism in prepubertal (postnatal day 21, PND21) male offspring rats, and to provide scientific evidence for assessing the obesogenic effect of BPAF. MethodsSprague-Dawley (SD) rats aged 8 weeks were used in this study. Pregnant rats were divided into BPAF dose groups (2, 10, 50 mg·kg⁻¹) and a vehicle control group (corn oil), with 6 confirmed pregnant females per group. Gavage administration started from gestational day 0 and continued until the end of lactation. At PND21, one male offspring per litter was randomly selected. Serum concentrations of glucose (GLU), triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), leptin (LEP), free fatty acid (FFA), as well as oxidative stress markers superoxide dismutase (SOD) and malondialdehyde (MDA), were measured. Pathological changes in liver and adipose tissues were evaluated, and the expression levels of genes related to hepatic lipid metabolism were measured. ResultsCompared to the vehicle control group, the 50 mg·kg⁻¹ group showed significantly increased serum LEP and MDA levels in male offspring (P<0.05), and significant upregulation of hepatic lipoprotein lipase (Lpl), fatty acid synthetase (Fas), and peroxisome proliferator-activated receptor γ (Pparg) gene expression (P<0.05). The 2 mg·kg⁻¹ group exhibited a significant increase in adipocyte length (P<0.05), while the 50 mg·kg⁻¹ group showed significant increases in both adipocyte area and length (P<0.05). No significant abnormalities were observed in liver histopathological examination. ConclusionPerinatal exposure to 50 mg·kg⁻¹ BPAF induced adipocyte hypertrophy, elevated leptin levels, upregulation of lipid synthesis gene expression, and enhanced oxidative stress in prepubertal male offspring, suggesting that BPAF may exert environmental obesogenic effects by disrupting lipid metabolism pathways.

The Golgi body, a core organelle in eukaryotic cells, plays a critical role in protein modification, sorting, vesicular transport, and serves as a key site for lipid synthesis and glycosylation. Glucose and lipid metabolism are central processes for cellular energy maintenance and biosynthesis, and are closely linked to Golgi function. Recent studies have revealed the extensive involvement of the Golgi body in regulating glucose and lipid metabolism, where maintaining its structural and functional homeostasis is crucial for normal physiological activity. Under various stress conditions such as acidosis, hypoxia, and nutrient deficiency, the Golgi body undergoes structural and functional disruption, leading to Golgi stress. This in turn activates specific signaling pathways, such as those mediated by the cAMP-responsive element binding protein 3 (CREB3) and proteoglycans, to alleviate Golgi stress and enhance Golgi function. Golgi stress contributes to glucose and lipid metabolic disorders by affecting the activity of insulin receptors, glucose transporters, and lipid metabolism-related enzymes. For example, Golgi stress triggers the cleavage and release of the active fragment of CREB3, which enters the nucleus and upregulates the transcription of ADP-ribosylation factor 4 (ARF4) and key gluconeogenic enzymes, including phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase). ARF4 promotes vesicle retrograde transport between the Golgi and endoplasmic reticulum, maintains secretory capacity, and enhances hepatic glucose output. This pathway is particularly active under high-fat or lipotoxic stress, leading to fasting hyperglycemia. When damaged Golgi components accumulate beyond a tolerable threshold, the cell initiates an autophagic response, selectively encapsulating the damaged Golgi into autophagosomes, which then fuse with lysosomes to form autolysosomes, leading to Golgiphagy. This process results in the degradation and clearance of damaged Golgi, thereby regulating Golgi quantity, quality, and function. Golgiphagy also plays a significant role in regulating glucose and lipid metabolism. For instance, under high-glucose conditions, autophagic flux may be suppressed, impairing the timely clearance and renewal of damaged Golgi, compromising its normal function, and further exacerbating glucose metabolism disorders. Additionally, Golgiphagy may participate in lipid degradation and influence lipid synthesis and transport. Research indicates that Golgi stress and Golgiphagy play important roles in glucose and lipid metabolism-related diseases. For example, the leucine zipper protein (LZIP) under Golgi stress conditions can promote hepatic steatosis. In mouse primary cells and human tissues, LZIP induces the expression of apolipoprotein A-IV (APOA4), which increases peripheral free fatty acid uptake, resulting in lipid accumulation in the liver and contributing to the development of fatty liver disease. This review systematically outlines the structure and function of the Golgi apparatus, the molecular regulatory mechanisms of Golgi stress and Golgiphagy, and their synergistic roles. It further elaborates on how Golgi stress and Golgiphagy participate in the regulation of glucose and lipid metabolism, discusses their clinical significance in related diseases such as diabetes, fatty liver disease, and obesity, and highlights potential novel therapeutic strategies from the perspective of Golgi-targeted medicine. Finally, this article addresses the challenges and future directions in Golgi-targeted interventions, aiming to advance the clinical translation of such strategies and foster breakthroughs in the treatment of glucose and lipid metabolism-related disorders.

The Golgi body, a core organelle in eukaryotic cells, plays a critical role in protein modification, sorting, vesicular transport, and serves as a key site for lipid synthesis and glycosylation. Glucose and lipid metabolism are central processes for cellular energy maintenance and biosynthesis, and are closely linked to Golgi function. Recent studies have revealed the extensive involvement of the Golgi body in regulating glucose and lipid metabolism, where maintaining its structural and functional homeostasis is crucial for normal physiological activity. Under various stress conditions such as acidosis, hypoxia, and nutrient deficiency, the Golgi body undergoes structural and functional disruption, leading to Golgi stress. This in turn activates specific signaling pathways, such as those mediated by the cAMP-responsive element binding protein 3 (CREB3) and proteoglycans, to alleviate Golgi stress and enhance Golgi function. Golgi stress contributes to glucose and lipid metabolic disorders by affecting the activity of insulin receptors, glucose transporters, and lipid metabolism-related enzymes. For example, Golgi stress triggers the cleavage and release of the active fragment of CREB3, which enters the nucleus and upregulates the transcription of ADP-ribosylation factor 4 (ARF4) and key gluconeogenic enzymes, including phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase). ARF4 promotes vesicle retrograde transport between the Golgi and endoplasmic reticulum, maintains secretory capacity, and enhances hepatic glucose output. This pathway is particularly active under high-fat or lipotoxic stress, leading to fasting hyperglycemia. When damaged Golgi components accumulate beyond a tolerable threshold, the cell initiates an autophagic response, selectively encapsulating the damaged Golgi into autophagosomes, which then fuse with lysosomes to form autolysosomes, leading to Golgiphagy. This process results in the degradation and clearance of damaged Golgi, thereby regulating Golgi quantity, quality, and function. Golgiphagy also plays a significant role in regulating glucose and lipid metabolism. For instance, under high-glucose conditions, autophagic flux may be suppressed, impairing the timely clearance and renewal of damaged Golgi, compromising its normal function, and further exacerbating glucose metabolism disorders. Additionally, Golgiphagy may participate in lipid degradation and influence lipid synthesis and transport. Research indicates that Golgi stress and Golgiphagy play important roles in glucose and lipid metabolism-related diseases. For example, the leucine zipper protein (LZIP) under Golgi stress conditions can promote hepatic steatosis. In mouse primary cells and human tissues, LZIP induces the expression of apolipoprotein A-IV (APOA4), which increases peripheral free fatty acid uptake, resulting in lipid accumulation in the liver and contributing to the development of fatty liver disease. This review systematically outlines the structure and function of the Golgi apparatus, the molecular regulatory mechanisms of Golgi stress and Golgiphagy, and their synergistic roles. It further elaborates on how Golgi stress and Golgiphagy participate in the regulation of glucose and lipid metabolism, discusses their clinical significance in related diseases such as diabetes, fatty liver disease, and obesity, and highlights potential novel therapeutic strategies from the perspective of Golgi-targeted medicine. Finally, this article addresses the challenges and future directions in Golgi-targeted interventions, aiming to advance the clinical translation of such strategies and foster breakthroughs in the treatment of glucose and lipid metabolism-related disorders.

Malignant tumors represent a major threat to global health. Conventional anti-tumor pharmacotherapy often encounters challenges such as drug resistance, highlighting an urgent need for the development of novel therapeutic strategies. Fatty acid synthase (FASN), the key enzyme catalyzing de novo fatty acid synthesis, is subject to precise regulation at multiple levels, including transcriptional control, various post-translational modifications such as ubiquitination and phosphorylation, as well as modulation by diverse signaling pathways. Recent studies have revealed that FASN is aberrantly overexpressed in various malignant tumors and is closely associated with tumor progression and poor patient prognosis. FASN is a homodimer composed of seven functional domains that catalyzes the NADPH-dependent condensation of acetyl-CoA and malonyl-CoA to generate saturated fatty acids, primarily palmitic acid. Its stability is regulated by multiple ubiquitin ligases and deubiquitinating enzymes. Additionally, FASN is subject to upstream regulation via neural precursor cell-expressed developmentally downregulated 8 (Nedd8) modification and the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway, thereby establishing a metabolic-signaling positive feedback loop. As a core executor of metabolic reprogramming, FASN promotes tumorigenesis through dual mechanisms. First, its fatty acid synthesis product, palmitate, participates in membrane phospholipid synthesis, lipid raft formation, and protein palmitoylation, thereby activating several key oncogenic signaling pathways, including PI3K/AKT/mTOR, wingless-type MMTV integration site family member (Wnt)/β‑catenin, and signal transducer and activator of transcription 3 (STAT3)/matrix metalloproteinase (MMP), leading to tumor development and progression. Second, FASN plays a pivotal role in modulating the anti-tumor functions of immune cells and remodeling the tumor immune microenvironment. Specifically, FASN enhances immune checkpoint inhibition by inducing programmed death-ligand 1 (PD-L1) palmitoylation, suppresses the activation of cytotoxic T lymphocytes and natural killer cells, and promotes the polarization of M2-type macrophages, consequently facilitating tumor immune evasion and malignant progression. Precisely due to its significant overexpression in tumor cells, its critical functional role, and its differential expression compared to normal cells, FASN has emerged as a highly promising target for anti-tumor drug development. Highly selective small-molecule inhibitors, notably represented by TVB-2640, have advanced to clinical trial stages and demonstrated favorable anti-tumor activity. Furthermore, the combination of FASN inhibitors with other chemotherapeutic agents or targeted drugs can overcome the limitations of monotherapy through synergistic effects or by resensitizing tumor cells to conventional drugs, achieving a “1+1>2” therapeutic outcome. With the advancement of modern traditional Chinese medicine (TCM), numerous active ingredients derived from TCM have been confirmed to exert anti-tumor effects by modulating FASN-related pathways. This integrated approach leverages the precision of Western medicine while simultaneously harnessing the holistic regulatory benefits of TCM to alleviate the side effects of radiotherapy and chemotherapy. Despite the promising prospects of FASN-targeted therapies, challenges remain, including tumor cell metabolic plasticity, tumor context-dependent responses, and heterogeneity. This review systematically summarizes the molecular structure, physiological functions, and mechanisms of FASN in tumorigenesis, as well as recent advances in targeted therapies. Future directions—including the precise identification of responsive patient populations using spatial transcriptomics, the development of novel combination regimens, and the active exploration of integrative strategies combining traditional Chinese and Western medicine—will facilitate the clinical translation of FASN-targeted therapies and open new avenues for improving the quality of life and prognosis of cancer patients.

Objective To explore the relationship between intestinal flora imbalance and pulmonary function in patients with chronic obstructive pulmonary disease (COPD), and to analyze the related influencing factors. Methods A total of 310 patients with COPD who were admitted to Air Force Military Medical University Tangdu Hospital from June 2022 to December 2024 were retrospectively analyzed. Based on intestinal flora status, the enrolled patients were classified into imbalance group (n=83) and non-imbalance group (n=227). Logistic regression analysis was conducted to analyze the independent related factors of intestinal flora imbalance in COPD patients. Based on the above factors, a prediction model was constructed, and ROC curve analysis model was applied to analyze the predictive value of the model on intestinal flora imbalance. Results Logistic regression analysis revealed that age, IL-6, albumin, pulmonary function, long-term bed rest and long-term use of antibiotics were related to intestinal flora imbalance in COPD patients (all P<0.05). ROC results of the Logistic prediction model showed that the area under the curve, sensitivity, specificity and 95%CI were 0.961, 0.880, 0.996 and 0.932-0.989 respectively. Conclusion The intestinal flora imbalance in patients with COPD is closely related to lung function, age, inflammatory status, nutritional indicators, activity ability and antibiotic use.

With the continuous deepening of the concept of precision diagnosis and treatment for lung cancer, how to achieve higher efficiency and accuracy in the screening, diagnosis, and treatment pathways in clinical practice has become an important issue that urgently needs to be overcome. The current clinical difficulty lies in the fact that despite continuous advancements in imaging and molecular diagnostic technologies, there are still limitations in manual efficiency and subjective experience when it comes to massive data analysis and multi-scale feature extraction. Artificial intelligence (AI), especially algorithm systems based on deep learning, is an innovative technology capable of deeply empowering medical big data. This method utilizes algorithms such as convolutional neural networks, combined with radiomics, pathomics, and multi-modal data fusion analysis, demonstrating immense potential in early precise detection and benign-malignant differentiation of pulmonary nodules, digital pathological subtype recognition and non-invasive prediction of driver genes, precise 3D surgical planning and automatic delineation of radiotherapy target volumes, as well as dynamic risk warning during follow-up. This innovative technology provides a brand-new solution for realizing intelligent and individualized lung cancer diagnosis and treatment models. This consensus, based on the latest evidence from evidence-based medicine and combined with the development trends in the AI field and real-world clinical needs, was ultimately formed by gathering the consensus opinions of multidisciplinary experts in radiology, pathology, thoracic surgery, and other fields. The main content covers the application specifications of AI in the three core scenarios of lung cancer screening, diagnosis, and treatment, the technical standards for data collection and algorithm validation, as well as the ethical and regulatory challenges faced at the current stage. It aims to clarify the applicable boundaries of AI as a clinical auxiliary decision support tool, providing scientific guidance and standardized exploration directions for peers currently engaged in or planning to carry out AI-assisted clinical diagnosis, treatment, and translation of lung cancer.

Objective To analyze the predictive value of different obesity indicators on acute cerebral infarction in patients with transient ischemic attack (TIA). Methods A total of 310 patients with TIA admitted to Tangdu Hospital of Air Force Medical University from March 2022 to September 2025 were selected and classified into non-event group (276 cases) and cerebral infarction group (34 cases) based on acute cerebral infarction within 90 days. The basic data and obesity-related indicators [body mass index (BMI), waist-to-hip ratio, body adiposity index (BAI), conicity index (C-index) and a body shape index (ABSI were compared. Multivariate logistic regression analysis was utilized to screen the independent influencing factors. Receiver operating characteristic (ROC) curve was drawn to analyze the predictive efficiency. Results The age, proportions of concurrent hypertension and concurrent diabetes mellitus, ABCD2 score, waist-to-hip ratio, ABSI, C-index, BMI and BAI in the cerebral infarction group were older or higher than those in the non-event group, and the symptoms duration was longer (P<0.05). The above indicators were all related factors for acute cerebral infarction in patients with TIA within 90 days (P<0.05), and ABSI and ABCD² score were independent influencing factors (P<0.05). The prediction model was manifested as Logit (P)=− 4.205 + 0.482 × ABCD² score + 1.120 × ABSI × 100. ABSI and ABCD2 score had predictive value on the occurrence of acute cerebral infarction (P<0.05), and the predictive efficiency of combined model was higher than that of single indicator (P<0.05). Conclusion Among different obesity indicators, ABSI has the highest value on predicting recent acute cerebral infarction in TIA. The prediction model based on ABSI and ABCD2 score exhibits the best predictive efficiency.

ObjectiveTo investigate the mechanism by which Tianxiang pills （TXP） alleviates myocardial cell pyroptosis in the rat model of myocardial ischemia/reperfusion （I/R） injury through modulating the reactive oxygen species （ROS）/cysteinyl aspartate-specific proteinase-1 （Caspase-1）/gasdermin D （GSDMD） signaling pathway. MethodsA total of 54 SPF-grade adult male Sprague-Dawley rats were randomized into six groups （n=9）： sham （thoracotomy only without ligation）， I/R （left anterior descending coronary artery ligation for 30 min followed by reperfusion）， NAC （positive control， N-acetylcysteine， 150 mg·kg^-1， by gavage）， low-dose Tianxiang pills （TXP-L， 2.5 g·kg^-1， by gavage）］， medium-dose Tianxiang pills （TXP-M， 5 g·kg^-1， by gavage）， and high-dose Tianxiang pills （TXP-H， 10 g·kg^-1， by gavage）. The fluorescent probe method was employed to measure the ROS level. Biochemical assay kits were employed to determine the Caspase-1 activity， superoxide dismutase （SOD） activity， malondialdehyde （MDA） content， and glutathione peroxidase （GSH-Px） activity. Myocardial infarct size was assessed by 2，3，5-triphenyltetrazolium chloride （TTC） staining. Western blot analysis was performed to evaluate the expression levels of proteins in the ROS/Caspase-1/GSDMD pathway， including GSDMD， cleaved Caspase-1/Caspase-1 ratio， the N-terminal domain of GSDMD （GSDMD-N）， and the p22-phox subunit of the reduced nicotinamide adenine dinucleotide phosphate （NADPH） oxidase complex. Enzyme-linked immunosorbent assay （ELISA） was utilized to determine the concentration of interleukin-1β （IL-1β）. Transmission electron microscopy （TEM） was employed to observe mitochondrial structure and to score the degree of mitochondrial swelling. ResultsCompared with the Sham group， the I/R group exhibited elevated the levels of ROS， Caspase-1 activity， GSDMD expression， IL-1β concentration， MDA content， infarct area， mitochondrial swelling score， cleaved Caspase-1/Caspase-1， GSDMD-N， and p22phox and decreased activities of SOD and GSH-Px （P<0.05）. Compared with the I/R group， NAC and different doses of TXP significantly reduced the ROS level， Caspase-1 activity， GSDMD expression， IL-1β concentration， MDA content， infarct area， and mitochondrial swelling score. Moreover， they downregulated the expression of cleaved Caspase-1/Caspase-1， GSDMD-N， and p22phox and increased the activities of SOD and GSH-Px （P<0.05）. Furthermore， TXP exerted effects on ROS， MDA， SOD， GSH-Px， Caspase-1 activity， GSDMD expression， IL-1β concentration， cleaved Caspase-1/Caspase-1， GSDMD-N， p22phox， infarct area， and mitochondrial swelling score in a dose-dependent manner （P<0.05）. ConclusionTianxiang pills alleviates myocardial I/R injury by mitigating oxidative stress and cell pyroptosis through the inhibition of the ROS/Caspase-1/GSDMD signaling pathway.

Objective To investigate the status of job crafting, change fatigue, and organizational silence among clinical nurses, and to examine the mediating role of organizational silence in the relationship between change fatigue and job crafting. Methods A total of 500 clinical nurses from a tertiary grade A hospital in Shaanxi Province were selected as study participants using the convenience sampling method. The level of job crafting, change fatigue, and organizational silence was assessed using the Job Crafting Scale, Change Fatigue Scale, and Organizational Silence Scale, and the mediating effect of organizational silence between change fatigue and job crafting was examined by the Bootstrap method among clinical nurses. Results The mean scores of job crafting, change fatigue, and organizational silence among clinical nurses were (59.0±11.7), (22.9±5.6), and (81.3±8.5), respectively. Multiple linear regression analysis showed that higher education level, longer working years, and more severe change fatigue were associated with higher job crafting scores among clinical nurses (all P<0.05). A higher level of organizational silence was related to lower job crafting scores (P<0.01). Mediation analysis showed that organizational silence was negatively associated with both change fatigue and job crafting among clinical nurses (all P<0.01), while change fatigue was positively associated with job crafting (P<0.01). Organizational silence partially mediated the relationship between change fatigue and job crafting. The direct effect of change fatigue on job crafting was 0.26, and the indirect effect of organizational silence was 0.70, accounting for 72.8% of the total effect. Conclusion Organizational silence mediates the relationship between change fatigue and job crafting. Reducing organizational silence may help enhance the level of job crafting among nurses.