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.

This study investigated the infection status,drug resistance,and molecular characteristics of Shiga toxin-producing Escherichia coli(STEC)in domestic goats in Chengkou county,Chongqing.In August 2023,283 fecal samples were collected from households in Chengkou county.After enrichment with EC broth and inoculation onto selective media,samples that tested positive for stx1/stx2 were selected for further isolation.The positive strains were investigated with antimicrobial susceptibility testing and whole genome sequencing.According to the whole genomic sequences,the stx subtypes,serotypes,multi-locus sequence types,virulence genes,drug resistance genes,and phylogenetic relationships of the STEC strains were analyzed.Forty-six strains of STEC were isolated from 283 goat fecal samples,thus resulting in a detection rate of 16.25%.The 46 STEC strains were categorized into 12 O∶H serotypes,among which O76∶H19 and O8∶H7 predominated,each represented by 9 strains.Five STEC strains were identified as serotype O157∶H7.The 46 STEC strains were categorized into 11 sequence types(STs),among which ST675 and ST196 predominated,each represented by nine strains,accounting for a 19.57%proportion.The strains were categorized into 7 stx subtypes,among which stx1c(26/46,56.52%),followed by stx2k(9/46,19.57%)predominated.All nine Stx2k-STEC strains were identified as serotype O8∶H7 and sequence type ST196.In antimicrobial susceptibility testing,2 STEC strains were resistant to ampicillin,one strain was resistant to ampicillin/sulbactam,one strain was resistant to cefazolin,and one strain was resistant to cefoxitin.Nine Stx2k-STEC strains were found to carry the beta-lactam resistance gene blaEC-18.Antimicrobial sensitivity tests revealed that the nine Stx2k-STEC strains were sensitive to all 15 tested antibiotics.Moreover,phylogenetic analysis indicated that the 9 Stx2k-STEC strains were remarkably similar but showed high genetic diversity with respect to that of the Stx2k-STEC strains isolated from other regions in China.Goatsare an important animal reservoir for STEC in theChengkou district of Chongqing,and novel sequence type Stx2k-STEC strains distinct from those found in other regions of China were identified in this region.

Aim To explore the mechanism of hispidu-lin in the treatment of cervical cancer by using network pharmacology and molecular docking methods and veri-fy it by in vitro experiments.Methods Cervical canc-er HeLa and SiHa cells were cultivated in vitro,and CCK-8 assay,cloning assay,scratch assay,transwell as-say,and flow cytometry were used to detect the effects of hispidulin on cell proliferation,migration,invasion,and apoptosis.SwissTarget Prediction was used to ob-tain predicted targets for hispidulin.Potential targets for cervical cancer were screened in GeneCards disease database.R software Venn package was used to obtain the intersection target genes of hispidulin and cervical cancer,STRING website and Cytoscape software were used to obtain protein-protein interaction(PPI)net-work,and the core targets were screened.The GEIPA data analysis platform was employed to analyze the dif-ferential gene expression levels of core targets in cervi-cal cancer.Gene Ontology(GO)and Kyoto Encyclo-pedia of Genes and Genomes(KEGG)enrichment a-nalysis were performed,and molecular docking was car-ried out on key targets.Western blot was used to detect the regulatory effects of hispidulin on the expression of key proteins PI3K,p-Akt,as well as core target pro-teins MMP9 and RARP1 in the PI3K/Akt signaling pathway.Results Cell experiments showed that after treatment with hispidulin,the proliferation and colony formation abilities of HeLa and SiHa cells significantly decreased in a concentration-and time-dependent man-ner.At the same time,the lateral and longitudinal mi-gration and invasion abilities of HeLa cells decreased,and the level of apoptosis significantly increased.A to-tal of 87 intersection targets between hispidulin and cervical cancer were obtained,and eight core targets,namely,Akt1,EGFR,SRC,ESR1,PTGS2,GSK3β,MMP9,and PARP1,were selected based on the degree values in network topology analysis.KEGG enrichment screening identified PI3K/Akt signaling pathway,canc-er pathway,and other signaling pathways.The molecu-lar docking results showed that hispidulin had strong affinity activity with AktⅠ,P13K,MMP9,and RARP1.Western blot results showed downregulation of PI3K,p-Akt expression,as well as MMP9 and RARP1 expres-sion.Conclusions Hispidulin can inhibit the prolif-eration,migration,invasion,and promote apoptosis of cervical cancer cells by downregulating the PI3K/Akt signaling pathway and the expression of MMP9 and RARP1.

Owing to the insidious onset and limited awareness of early screening,many patients with esophageal squamous cell carcinoma(ESCC)are diagnosed at an advanced stage.Immunochemotherapy is the current standard first-line treatment for advanced ESCC;however,survival outcomes remain suboptimal.Radiotherapy,with its precise local control and potential immunomodulatory effects,is anticipated to act synergistically with immunochemotherapy,offering a novel direction for overcoming survival limitations.This review systematically sum-marizes the progress in the use of radiotherapy as a first-line treatment for advanced ESCC and discusses the synergistic mechanisms,clinical applications,and challenges associated with its combination with immunochemotherapy.

Objective To discuss the mechanism of the streaking artifact of Star-volumetric interpolated body examination(Star-VIBE)sequence and the influence of phase coding on it.Methods Twenty-six volunteers underwent many times Star-VIBE sequences scanning with different phase coding(320,640,960,1 280,1 600).The severity of streaking artifact of images in different phase cod-ing groups was evaluated qualitatively.The signal-to-noise ratio(SNR)of muscle,thyroid and contrast-enhanced artery,contrast-to-noise ratio(CNR)between soft tissues,and CNR between muscle and contrast-enhanced artery of the images in different phase coding groups were evaluated quantitatively.Results In qualitative evaluation,with the number of phase coding increased,the streaking artifact decreased(H=83.022,P＜0.005).In quantitative evaluation,SNRmuscle,SNRthyroid,SNRcontrast-enhanced artery and CNRcontrast-enhanced gradually increased with the increase of phase coding number(SNRmuscle:F=6.913,P＜0.005;SNRthyroid:F=3.930,P=0.005;SNRcontrast-enhanced artery:F=6.980,P＜0.005;CNRcontrast-enhanced:F=6.482,P＜0.005),while CNRsoft tissue showed no statistical difference(F=1.114,P=0.339).Conclusion There is streaking artifact on the image of the Star-VIBE sequence,which can be reduced by increas-ing the number of phase coding appropriately.The most suitable phase coding is 960.

Objective To explore the application value of fractional anisotropy(FA)analysis of RGB component transformation in different directions of fibers in substantia nigra in Parkinson's disease(PD).Methods There were 35 cases of PD and 37 cases of normal control group.After being performed by brain diffusion tensor imaging(DTI)scanning,the sequence was imported into 3DSlicense 5.6.0,and the diffusion module was used to implement pseudo color mapping based on FA,locate and segment substantia nigra,and use the substantia nigra mask as the tracking starting point.After forming tracing,fibers were imported into DTIANALYSIS 1.51,converting the RGB components into FA values for analysis,and visualized the analysis result.At the same time,fiber length,fiber density,and segmented FA point cloud percentage were compared.Results Compared with the normal group,the length of substantia nigra fibers in the PD group was shorter[(95.14±19.85)mm vs(115.99±21.39)mm,P＜0.01],and there was a statistical difference between the two groups.There was no statistical difference in fiber density[(0.07±0.05)/mm3 vs(0.10±0.12)/mm3,P＞0.05]between control group and PD group.The percentage of FA segment point clouds in the PD group was lower than that in the normal group at 0.9-1,but the principal component characteristics of the point cloud ratios in each FA segment were not significant.Conclusion Based on the transformation of RGB components into FA analysis,the length,density,and FA values of substantia nigra nerve fibers in PD patients can be quantified and visualized,providing a basis for the study of PD neural pathways.

Objective This study aimed to provide an effective scientific basis for prevention and control of cockroaches on aircrafts by identifying cockroach-carried pathogens,and assess the insecticidal efficacy of gel bait mediated cockroach control on aircrafts,to provide technical guidance for aircraft disinsection.Methods Cassette-trapping was used to trap cockroaches,and the carried pathogens were detected using bacterial cultivation techniques.The gel bait mediated killing rate was calculated after 1,7,and 30 d by field application of gel bait.Results A total of 411 cockroaches were captured,and all were identified as Blattella germanica.26 strains of pathogenic bacteria were isolated from the trapped cockroaches.The killing rates of cockroaches were 58.8％-96.3％with 1-30 day application of gel bait.Statistically significant differences were observed in cockroach killing rates on different days(χ2=58.95,P<0.01).Conclusions B.germanica carry a large variety of pathogenic bacteria and opportunistic pathogens and are thus important infectious disease carriers.Gel bait agents have proven to be very effective against cockroaches on aircrafts.

Rheumatoid arthritis(RA)is a chronic autoimmune disease of unknown etiology that can cause joint destruction and deformity.As a small molecule cytokine,the chemokine C-X-C motif chemokine ligand 12(CXCL12)regulates the pathogenesis of rheumatoid arthritis by binding to the specific receptor CXC chemokine receptor 4(CXCR4).Therefore,based on the bio-logical characteristics of CXCL12 and CXCR4,this paper intro-duces the pathogenesis of CXCL12/CXCR4 in RA and summari-zes the progress in RA-related research,with the aim of providing clinical value for understanding the pathogenesis of RA and de-veloping novel therapeutic targets.

Objective To investigate the mechanism of Ginkgo biloba extracts(GB)in the treatment of cerebral ischemia-reperfusion(CIR)injury based on network pharmacology and animal experiments.Methods The intersection targets of CIR and GB were obtained from TCMSP,GeneCards and other databases.Cytoscape software and Metascape database were used to analyze and map the related targets.The model of transient middle cerebral arterial occlusion(t-MCAO)was constructed in mice by suture method,and the effects of GB on the neurological function of mice after t-MCAO were observed by the neurological deficit score and Morris water maze test.HE staining was used to observe the pathological structural changes of neuron in the hippocampus of mice,and Western blot was used to verify the signal pathways screened by network pharmacology.Results Network pharmacology predicted that GB contained 33 active ingredients,and 116 potential targets of GB in treatment of CIR included Caspase3,Bax,etc.In addition,GB may play a protective role through signaling pathways such as PI3K-Akt and AMPK.Animal experiments showed that GB treatment could significantly improve the neural function and learning spatial memory ability of mice,alleviate the brain histopathological injury,and activate p-Akt/Akt signaling pathway.Conclusion GB has the characteristics of multi-target and multi-pathways therapy for CIR,which may reduce neuronal apoptosis by activating the p-Akt/Akt signaling pathway.