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.

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.

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.

This article reports the diagnosis and treatment course of a patient with granulomatosis with polyangiitis (GPA) complicated with Kennedy disease (KD). The patient presented with headache, purulent and bloody rhinorrhea, ocular pain, decreased hearing and vision, multiple nodular erythema with ulcers on both lower extremities, and lower limb weakness. Chest imaging revealed a nodule with cavity formation in the right lung, and cytoplasmic anti-neutrophil cytoplasmic antibody (c-ANCA) and proteinase 3-antineutrophil cytoplasmic antibody (PR3-ANCA) were positive. The patient was initially diagnosed with granulomatosis with polyangiitis. After treatment with glucocorticoids and cyclophosphamide, the vasculitis-related symptoms were relieved while lower limb weakness got worse. Genetic testing identified 50 CAG repeats in exon 1 of the androgen receptor (AR) gene, and the final diagnosis was GPA complicated with KD. After rehabilitation therapy, the patient′s lower limb weakness improved. Methylprednisolone combined with leflunomide was administered for maintenance treatment, and the condition remained stable during long-term follow-up.

With the extensive application of low-dose ionizing radiation (LDIR) in medicine, aerospace, and other fields, the potential for exposure among the general population and occupationally exposed workers has increased, raising growing public health concerns regarding its possible effects on cognitive function. Current occupational and environmental radiation protection frameworks are primarily established based on cancer risk estimates derived from epidemiological evidence under high-dose exposure and extrapolation across dose ranges, whereas evidence regarding non-cancer outcomes, including potential cognitive effects of LDIR, remains limited and inconsistent, and the underlying neurobiological mechanisms have not been fully elucidated. This review summarized recent advances in research on the effects of LDIR on cognitive function and the associated neural mechanisms. Existing evidence indicates that LDIR may adversely affect cognitive domains including spatial memory and object recognition memory under certain exposure conditions, with potential mechanisms involving alterations in synaptic plasticity, microglia activation, neurodevelopmental processes, epigenetic regulation, and DNA damage and repair pathways. In contrast, studies using pathological models, including stroke and neurodegenerative diseases, have reported potential protective effects of LDIR, which may be mediated by attenuation of oxidative stress, neuroinflammation and activation of endogenous repair pathways. This indicates that LDIR has both damaging and protective effects on brain function; a deeper understanding of its patterns and mechanisms can provide a scientific basis for establishing occupational and environmental radiation protection standards. Furthermore, re-examining the LDIR risk assessment system may also offer new insights into exploring the therapeutic potential of LDIR for brain diseases.

Objective:To evaluate the prognostic value of droplet digital PCR(ddPCR)in conjunction with multiparametric flow cytometry(MFC)for measurable residual disease(MRD)detection in predicting relapse risk in patients with acute myeloid leukemia(AML).Methods:In this retrospective cohort study,we have analyzed 78 newly diagnosed patients with AML who underwent combined MRD monitoring using MFC and ddPCR at The Affiliated Hospital of Hebei University(January 2018-January 2025).Clinical outcomes-including MRD negativity rates,cumulative incidence of relapse(CIR),relapse-free survival(RFS),and overall survival(OS)-were systematically evaluated.Prognostic discrim-ination between the MRD-negative and MRD-positive subgroups was compared across standalone and combined detection approaches.Results:With a median follow-up of 17 months(range:2.4-86.7)and a median of one mutation tracked per patient(range:1-3),both MFC-MRD and ddPCR-MRD negative subgroups demonstrated superior 2-year RFS compared with MRD-positive counterparts.Notably,com-bined MFC/ddPCR monitoring enhanced prognostic discrimination,with MRD-negative patients achieving significantly prolonged 2-year RFS compared with MRD-positive patients.MFC-MRD negativity independently predicted improved 2-year OS.Conclusion:ddPCR-based multi-gene MRD profiling provides significant independent prognostic value in patients with AML.The synergistic application of MFC and ddPCR enables superior predictive accuracy for relapse risk and survival outcomes,supporting its integration into standardized MRD monitoring protocols.

Objective:To investigate the relevant data on radiation dose in interventional radiodiagnosis and radiology of adults in Beijing and to provide a basis for establishing relevant diagnostic reference levels (DRLs) in this region.Methods:A total of 30 medical institutions in Beijing were surveyed, covering interventional radiodiagnosis and radiology surgeries for coronary artery, structural heart diseases, permanent cardiac pacemaker implantation, electrophysiological study and radiofrequency ablation, nervous systems, abdominal systems, and the blood vessels of the lower limbs. The primary parameters investigated included the air kerma area product ( PKA) and incident air kerma ( Ka, r). The 75 th percentiles of radiation dose were considered DRLs, which were analyzed at both the overall and individual medical institution levels. Results:A total of 3 331 cases of the abovementioned radiodiagnosis and radiology surgeries were collected. The DRLs (i.e., PKA and Ka, r) of various diagnostic examinations were 37.87 Gy·cm 2 and 509.00 mGy for coronary artery, 9.34 Gy·cm 2 and 48.00 mGy for electrophysiological study and radiofrequency ablation, 218.50 Gy·cm 2 and 901.70 mGy for nervous systems, 81.00 Gy·cm 2 and 302.20 mGy for the abdominal system, and 83.37 Gy·cm 2 and 214.69 mGy for the blood vessels of the lower limbs. In contrast, the DRLs (i.e., PKA and Ka, r) for interventional radiodiagnosis and radiology were determined at 135.00 Gy·cm 2 and 1 897.58 mGy for coronary artery, 26.91 Gy·cm 2 and 172.30 mGy for structural heart diseases, 27.77 Gy·cm 2 and 87.75 mGy for permanent cardiac pacemaker implantation, 34.46 Gy·cm 2 and 247.00 mGy for electrophysiological study and radiofrequency ablation, 214.36 Gy·cm 2 and 1 282.80 mGy for the nervous system, 196.64 Gy·cm 2 and 875.71 mGy for abdominal system, and 108.25 Gy·cm 2 and 523.25 mGy for the blood vessels of the lower limbs. Conclusions:The DRLs of radiation dose in interventional radiodiagnosis and radiology in Beijing were determined through a survey and statistic analysis. These findings suggest that for certain interventional procedures, the optimized radiation protection should be enhanced.

N6-methyladenosine (m6A) modification, as a widespread and high-profile type of epigenetic modification, can dynamically and reversibly regulate the whole process of RNA metabolism. This modification governs RNA stability, splicing, and translation via m6A regulators, which are categorized as Writers, Erasers, and Readers. m6A modification also plays a critical role in the development of tumors. Disruptions in the homeostasis of m6A modification levels lead to dysregulation of m6A regulators. Consequently, these dysregulated regulators modulate the proliferation, migration, and invasion of tumor cells and interfere with the normal functions of suppressor genes and oncogenes. This article aims to comprehensively elucidate the specific regulatory impacts of m6A modification on tumor-related gene expression. It focuses on the regulatory mechanisms of m6A modification on mRNA stability. Additionally, it explores the influence of m6A on the molecular translation of key signaling pathways. Moreover, it investigates the indirect regulatory effects mediated by non-coding RNAs (ncRNAs), etc. The intention is to offer a novel analysis of the pathogenesis of cancer at a new level, and also provide a theoretical basis for finding new effective treatment methods.