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.

Background: s/Aims: Sarcomatoid hepatocellular carcinoma (HCC) is a rare histological subtype of HCC characterized by extremely poor prognosis; however, its molecular characterization has not been elucidated. Methods: In this study, we conducted an integrated multiomics study of whole-exome sequencing, RNA-seq, spatial transcriptome, and immunohistochemical analyses of 28 paired sarcomatoid tumor components and conventional HCC components from 10 patients with sarcomatoid HCC, in order to identify frequently altered genes, infer the tumor subclonal architectures, track the genomic evolution, and delineate the transcriptional characteristics of sarcomatoid HCCs. Results: Our results showed that the sarcomatoid HCCs had poor prognosis. The sarcomatoid tumor components and the conventional HCC components were derived from common ancestors, mostly accessing similar mutational processes. Clonal phylogenies demonstrated branched tumor evolution during sarcomatoid HCC development and progression. TP53 mutation commonly occurred at tumor initiation, whereas ARID2 mutation often occurred later. Transcriptome analyses revealed the epithelial–mesenchymal transition (EMT) and hypoxic phenotype in sarcomatoid tumor components, which were confirmed by immunohistochemical staining. Moreover, we identified ARID2 mutations in 70% (7/10) of patients with sarcomatoid HCC but only 1–5% of patients with non-sarcomatoid HCC. Biofunctional investigations revealed that inactivating mutation of ARID2 contributes to HCC growth and metastasis and induces EMT in a hypoxic microenvironment. Conclusions We offer a comprehensive description of the molecular basis for sarcomatoid HCC, and identify genomic alteration (ARID2 mutation) together with the tumor microenvironment (hypoxic microenvironment), that may contribute to the formation of the sarcomatoid tumor component through EMT, leading to sarcomatoid HCC development and progression.

Objective To analyse the clinical efficacy and safety of acupuncture combined with intermittent catheterisation in treating postoperative urinary retention after radical surgery for cervical cancer,and provide reference for the clinical treatment of postoperative urinary retention.Methods A retrospective analysis was conducted based on the clinical data of patients who underwent radical hysterectomy for cervical cancer at Obstetrics and Gynecology Hospital,Fudan University,from Sept 2019 to Dec 2021 and subsequently developed urinary retention.The patients were treated with a combination of acupuncture and intermittent catheterization.We observed residual urine volume,duration of acupuncture treatment,and urinary tract infection status to evaluate the effectiveness and safety of the acupuncture combined with intermittent catheterization regimen.We examined the relationship between treatment duration and various factors such as age,pathological type,surgical-pathological staging,surgical method,pre-treatment catheter indwelling time,pre-treatment residual urine volume,presence or absence of postoperative radiotherapy and chemotherapy,pre-existing urinary tract infection,and whether ureteral stenting was performed,in order to analyze the factors affecting the treatment duration.Results A total of 156 patients were reviewed.After treatment,132 cases had a post-treatment residual urine volume<100 mL,7 cases had a volume of 100-200 mL,and 15 cases had a volume>200 mL.Two cases still had great difficulty in urination after treatment,resulting in an overall effectiveness rate of 89.1%.No significant adverse events occurred in the patients.The treatment duration ranged from 2 to 17 days,with an average treatment time of 6.2 days.The treatment duration was a correlated with the preoperative indwelling catheter duration,residual urine volume and postoperative radiotherapy.Conclusion Acupuncture combined with intermittent catheterisation in treating urinary retention after radical surgery for cervical cancer has good efficacy,short treatment time and no obvious adverse effects,and can be an option for treating postoperative urinary retention.

Aim To investigate the effect of Huangqi injection(HI)and Huangqi oral solution(HO)on cisplatin-induced nephrotoxicity(CIN)based on un-targeted metabolomics technology and the underlying mechanisms.Methods Sprague Dawley(SD)rats were randomly divided into the blank group,cisplatin(CDDP)model group,HI treatment group,and HO treatment group,then the CIN model was built with low dose multiple intraperitoneal injections of CDDP.Pre-liminary evaluation of the renal protective efficacy of HI and HO was performed by measuring serum creatinine(Scr),blood urea nitrogen(BUN),and organ indi-ces.Further screening and identification of potential biomarkers(PBs)related to CIN and HI/HO pharma-cological effects were attained through metabolomics studies of renal tissues,and pathway enrichment analy-sis was conducted.Results HI and HO significantly restored the abnormal increase in renal function indica-tors and abnormal decrease in organ indices caused by CDDP,as well as significantly improved the abnormal renal metabolic profile induced by CDDP,indicating that both HI and HO had good alleviating effects on CIN.HI significantly reversed 47 out of 54 CIN related PBs,mainly involving metabolic pathways such as glycerophospholipid metabolism,tryptophan metabo-lism,pantothenate and CoA biosynthesis;HO signifi-cantly reversed 18 out of 54 CIN related PBs,mainly involving metabolic pathways such as taurine and hypo-taurine metabolism,ascorbate and aldarate metabo-lism,pentose and glucuronate interconversions.Con-clusions Both HI and HO have significant alleviating effects on CIN.In the short term,HI salleviating effect is superior to that of HO.Overall,the mechanisms by which both alleviate CIN are mainly related to regula-ting lipid metabolism,amino acid metabolism.

The principe of electrical impedance tomography(EIT)was described,and the research progress of EIT technology in the field of gesture recognition was reviewed from the aspects of hardware system and gesture recognition algorithm.The challenges of EIT technology applied in the field of gesture recognition were analyzed,and the future development trends were envisioned.[Chinese Medical Equipment Journal,2025,46(4):93-99]

The application of sensors to the monitoring of spinal morphology and motion was reviewed in terms of the research object and monitoring index.The present situation of the application of sensors was introduced,such as inertial sensor,stretchable strain sensor and electromagnetic sensor.The deficiencies of sensors applied to the monitoring of spinal morphology and motion were analyzed,and the future directions of the application were pointed out.[Chinese Medical Equipment Journal,2025,46(6):105-110]

Alzheimer's disease(AD)is a multifactorial condi-tion characterized by the accumulation of toxic proteins and asso-ciated neurodegeneration.AD is distinguished by the pathologi-cal aggregation of amyloid beta(Aβ)and Tau proteins.The in-teraction between Aβ and Tau can further induce neuroinflamma-tion,mitochondrial autophagy dysfunction,and endoplasmic retic-ulum stress,exacerbating synaptic damage and neuronal death.Neuronal cells are particularly susceptible to protein misfolding due to an imbalance between protein production and degrada-tion.The ubiquitin/26S proteasome system(UPS),a major pathway for protein degradation in eukaryotic cells,plays a cruci-al role in recognizing misfolded or damaged proteins within the nervous system.In UPS,the levels of ubiquitin are tightly regu-lated by both ubiquitin ligases(E3s)and deubiquitylases(DUBs).This article reviews the involvement and mechanisms of E3s and DUBs in the pathogenesis of AD,aiming to provide novel research strategies for its treatment.

Aim To explore the biological mechanism of ligustilide in the prevention and treatment of osteo-porosis by regulating H-type blood vessels,combined with animal experiments for verification,based on net-work pharmacology and molecular docking technology Methods The possible mechanism of ligustilide regu-lating H-type blood vessels to prevent osteoporosis was predicted by network pharmacology.Molecular docking technology was used to verify the binding ability of the core target EGFR to ligustilide.The rat model of osteo-porosis was established and divided into the sham group,model group,ligustilide high,medium and low dose(80,40,20 mg·kg-1)groups.The pathological changes of femur were observed by HE staining.The expressions of CD31,EMCN,OSX+and RUNX2+pro-tein in tibial metaphysis were detected by immunofluo-rescence.The expression of p-EGFR,p-PI3K and p-Akt protein was detected by Western blot.Results The results of network pharmacology showed that a total of 20 intersection targets were obtained.EGFR,PTGS2,ESR1 and ICAM1 were core targets,and mo-lecular docking showed that EGFR had a strong bind-ing ability with ligustilide.The signaling pathways of ligustilide in the prevention and treatment of osteoporo-sis by regulating the expression of H-type blood vessels were mainly enriched in PI3K-Akt,TNF,etc.Com-pared with the model group,ligustilide could signifi-cantly increase the number of trabecular bone and im-prove the destruction of bone microstructure.The ex-pression of CD31,EMCN,OSX+and RUNX2+signifi-cantly increased(P＜0.01,P＜0.05),the formation of H-type blood vessels were promoted,and the expres-sion of p-EGFR,p-PI3K and p-Akt significantly in-creased(P＜0.01,P＜0.05).Conclusions Ligusti-lide can increase the expression of H-type blood vessels in bone tissue of osteoporosis model rats,reduce the damage of bone trabecula and improve bone micro-structure effectively.EGFR-mediated PI3K/Akt signa-ling pathway may be the key way to exert its biological effects.

Objective To explore the clinical effect of 3D-printed interbody fusion cage applied in anterior cervical decompression and bone graft fusion for the treatment of cervical spondylotic myelopathy.Methods A total of 100 patients with cervical spondylotic myelopathy who underwent anterior cervical fusion surgery in our hospital from June 2020 to June 2023 were selected as the research subjects,they were randomly divided into the 3D group and the control group according to the random number table method,with 50 cases in each group.Patients in the 3D group were implanted with a 3D-printed interbody fusion cage which was made of microporous metal materials,while patients in the control group were implanted with intervertebral fusion cage which was made of polyetheretherketone material.The surgery-related indicators,cervical imaging parameters,cervical spinal cord function,cervical axial function and surgical complications of patients between the two groups were compared.Results There was no statistically significant difference in the operation time,intraoperative blood loss or length of hospital stay of patients between the two groups(P>0.05).The height of the cervical fusion segments and the Cobb angle of the fusion segments of patients in both groups at each time point after the operation were significantly increased compared with those before the operation(P<0.05).The height of the cervical fusion segments and the Cobb angle of the fusion segments of patients 1 month,3 months,and 6 months after the operation in the 3D group were all greater than those in the control group(P>0.05).The subjective symptom score and the total score of the Japanese orthopaedic association(JOA)of patients 6 months after the operation in the 3D group were higher than those in the control group(P<0.05).The cervical axial function of patients 6 months after the operation in the 3D group was better than that in the control group(P<0.05).The incidence of surgical complications in the 3D group was lower than that in the control group(P<0.05).Conclusion The use of 3D-printed interbody fusion cage during the anterior cervical decompression and bone graft fusion for patients with cervical spondylotic myelopathy can significantly improve the clinical symptoms of patients,achieve better cervical axial function,and have fewer complications.