ObjectiveTo investigate the potential mechanism of heat-sensitive moxibustion on chronic atrophic gastritis （CAG） through the phosphoinositide 3-kinase/protein kinase B （PI3K/Akt） signaling pathway. MethodsFifty-eight SD rats were randomly divided into blank group （n=14） and modeling group （n=44）. Rats in the blank group were fed routinely， while the rats in the modeling group received drinking water containing 1-methyl-3-nitro-1-nitrosoguanidine （MNNG） at a concentration of 140 μg/ml， combined with irregular fasting and feeding for 12 weeks to establish CAG model. After successful modeling， the rats were randomly divided into model group （n=10）， inhibitor group （n=10） and moxibustion group （n=20）. After 40 minutes of suspended moxibustion at "Zhongwan" （CV 12） daily， the rats in the moxibustion group were divided into heat-sensitive moxibustion group （n=10） and non-heat-sensitive moxibustion group （n=9） according to the change of tail temperature during moxibustion. The inhibitor group was bound for 40 minutes daily， and then administered with PI3K/Akt signaling pathway inhibitor， rapamycin solution， by gavage at a dose of 1 mg/kg. The model group received intragastric administration of 1 ml/kg normal saline after 40 minutes of restraint stress each day. All interventions were administered once daily for 28 consecutive days， while the blank group received no intervention. After the intervention finished， the body weight of rats in each group was compared. HE staining was used to observe the histopathological changes of gastric mucosa. The apoptosis-positive rate of gastric mucosal cells was detected by TUNEL assay. Immunohistochemistry was performed to determine the protein levels of matric metalloproteinase-7 （MMP7）， vascular endothelial growth factor A （VEGFA） and epidermal growth factor receptor （EGFR） in gastric mucosa. The mRNA expression levels of PI3K， Akt and mammalian target of rapamycin （mTOR） in gastric mucosal tissues were detected by qPCR. The protein levels of phosphorylated Akt （p-Akt） and phosphorylated mTOR （p-mTOR） in rat gastric mucosal tissues were measured by Western Blotting. ResultsCompared to the blank group， rats in all other groups exhibited decreased body weight， significantly increased gastric mucosal cell apoptosis-positive rates， elevated protein levels of MMP7， VEGFA and EGFR in gastric mucosa， increased mRNA expression levels of PI3K， Akt and mTOR， and enhanced protein expression levels of p-Akt and p-mTOR （P＜0.05 or P＜0.01）. Histopathological examination revealed thinning of the gastric mucosa， glandular disorganization and atrophy， accompanied by intestinal metaplasia.Compared to the model group， the heat-sensitive moxibustion group， the non-heat-sensitive moxibustion group and the inhibitor group all showed significant improvements in the above-mentioned indicators （P＜0.05 or P＜0.01）. Compared to the heat-sensitive moxibustion group， the non-heat-sensitive moxibustion group and the inhibitor group exhibited increased positive rates of gastric mucosal cell apoptosis； the non-heat-sensitive moxibustion group showed increased protein levels of MMP7， VEGFA and EGFR， as well as mRNA expression levels of PI3K， Akt and mTOR， and protein expressions of p-Akt and p-mTOR； the inhibitor group exhibited elevated protein expression level of EGFR （P＜0.05 or P＜0.01）. Histopathological examination showed that the gastric mucosal glands in the heat-sensitive moxibustion group were arranged more regularly， with an approximately normal structural appearance. ConclusionHeat-sensitive moxibustion can improve the body weight of CAG rats and repair gastric mucosal injury. Its therapeutic effects may be mediated by inhibiting excessive activation of gastric mucosal PI3K/Akt signaling pathway， thereby reducing gastric mucosal cell apoptosis.

ObjectiveTo investigate the potential mechanism of heat-sensitive moxibustion on chronic atrophic gastritis （CAG） through the phosphoinositide 3-kinase/protein kinase B （PI3K/Akt） signaling pathway. MethodsFifty-eight SD rats were randomly divided into blank group （n=14） and modeling group （n=44）. Rats in the blank group were fed routinely， while the rats in the modeling group received drinking water containing 1-methyl-3-nitro-1-nitrosoguanidine （MNNG） at a concentration of 140 μg/ml， combined with irregular fasting and feeding for 12 weeks to establish CAG model. After successful modeling， the rats were randomly divided into model group （n=10）， inhibitor group （n=10） and moxibustion group （n=20）. After 40 minutes of suspended moxibustion at "Zhongwan" （CV 12） daily， the rats in the moxibustion group were divided into heat-sensitive moxibustion group （n=10） and non-heat-sensitive moxibustion group （n=9） according to the change of tail temperature during moxibustion. The inhibitor group was bound for 40 minutes daily， and then administered with PI3K/Akt signaling pathway inhibitor， rapamycin solution， by gavage at a dose of 1 mg/kg. The model group received intragastric administration of 1 ml/kg normal saline after 40 minutes of restraint stress each day. All interventions were administered once daily for 28 consecutive days， while the blank group received no intervention. After the intervention finished， the body weight of rats in each group was compared. HE staining was used to observe the histopathological changes of gastric mucosa. The apoptosis-positive rate of gastric mucosal cells was detected by TUNEL assay. Immunohistochemistry was performed to determine the protein levels of matric metalloproteinase-7 （MMP7）， vascular endothelial growth factor A （VEGFA） and epidermal growth factor receptor （EGFR） in gastric mucosa. The mRNA expression levels of PI3K， Akt and mammalian target of rapamycin （mTOR） in gastric mucosal tissues were detected by qPCR. The protein levels of phosphorylated Akt （p-Akt） and phosphorylated mTOR （p-mTOR） in rat gastric mucosal tissues were measured by Western Blotting. ResultsCompared to the blank group， rats in all other groups exhibited decreased body weight， significantly increased gastric mucosal cell apoptosis-positive rates， elevated protein levels of MMP7， VEGFA and EGFR in gastric mucosa， increased mRNA expression levels of PI3K， Akt and mTOR， and enhanced protein expression levels of p-Akt and p-mTOR （P＜0.05 or P＜0.01）. Histopathological examination revealed thinning of the gastric mucosa， glandular disorganization and atrophy， accompanied by intestinal metaplasia.Compared to the model group， the heat-sensitive moxibustion group， the non-heat-sensitive moxibustion group and the inhibitor group all showed significant improvements in the above-mentioned indicators （P＜0.05 or P＜0.01）. Compared to the heat-sensitive moxibustion group， the non-heat-sensitive moxibustion group and the inhibitor group exhibited increased positive rates of gastric mucosal cell apoptosis； the non-heat-sensitive moxibustion group showed increased protein levels of MMP7， VEGFA and EGFR， as well as mRNA expression levels of PI3K， Akt and mTOR， and protein expressions of p-Akt and p-mTOR； the inhibitor group exhibited elevated protein expression level of EGFR （P＜0.05 or P＜0.01）. Histopathological examination showed that the gastric mucosal glands in the heat-sensitive moxibustion group were arranged more regularly， with an approximately normal structural appearance. ConclusionHeat-sensitive moxibustion can improve the body weight of CAG rats and repair gastric mucosal injury. Its therapeutic effects may be mediated by inhibiting excessive activation of gastric mucosal PI3K/Akt signaling pathway， thereby reducing gastric mucosal cell apoptosis.

ObjectiveTo explore the therapeutic effect of Xuebijing injection （XBJ） on severe acute pancreatitis induced acute lung injury （SAP-ALI） by regulating formyl peptide receptors （FPRs）/nucleotide-binding oligomerization domain-like receptor 3 （NLRP3） inflammatory pathway. MethodsSixty rats were randomly divided into a sham group， a SAP-ALI model group， low-， medium-， and high-dose XBJ groups （4， 8， and 12 mL·kg^-1）， and a positive drug （BOC2， 0.2 mg·kg^-1） group. For the sham group， the pancreas of rats was only gently flipped after laparotomy， and then the abdomen was closed， while for the remaining five groups， SAP-ALI rat models were established by retrograde injection of 5% sodium taurocholate （Na-Tc） via the biliopancreatic duct. XBJ and BOC2 were administered via intraperitoneal injection once daily for 3 d prior to modeling and 0.5 h after modeling. Blood was collected from the abdominal aorta 6 h after the completion of modeling， and the expression of interleukin （IL）-1β， IL-6， and tumor necrosis factor-α （TNF-α） in plasma was measured by enzyme-linked immunosorbent assay （ELISA）. The amount of ascites was measured， and the dry-wet weight ratios of pancreatic and lung tissue were determined. Pancreatic and lung tissue was taken for hematoxylin-eosin （HE） staining to observe pathological changes and then scored. The protein expression levels of FPR1， FPR2， and NLRP3 in lung tissue were detected by the immunohistochemical method. Western blot was used to detect the expression of FPR1， FPR2， and NLRP3 in lung tissue. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of FPR1， FPR2， and NLRP3 in lung tissue. ResultsCompared with the sham group， the SAP-ALI model group showed significantly decreased dry-wet weight ratio of lung tissue （P<0.01）， serious pathological changes of lung tissue， a significantly increased pathological score （P<0.01）， and significantly increased protein and mRNA expression levels of FPR1， FPR2， and NLRP3 in lung tissue （P<0.01）. After BOC2 intervention， the above detection indicators were significantly reversed （P<0.01）. After treatment with XBJ， the groups of different XBJ doses achieved results consistent with BOC2 intervention. ConclusionXBJ can effectively improve the inflammatory response of the lungs in SAP-ALI rats and reduce damage. The mechanism may be related to inhibiting the expression of FPRs and NLRP3 in lung tissue， which thereby reduces IL-1β and simultaneously antagonize the release of inflammatory factors IL-6 and TNF-α.

Objective Domestic research institutions and researchers have established a wide variety of animal disease models and accumulated a wealth of specialized, distinctive, and targeted atlas data during the model development process. These atlas data are of great value for development and application. Therefore, it is necessary to develop a professional and complete digital atlas database platform for animal models, which can achieve the open sharing of animal model atlas data and the integration and optimization of atlas resources related to disease animal models held by relevant domestic institutions. Methods Based on the B/S architecture, the authors' institution built a digital atlas database of animal models, using Java as the main development language and Oracle database system along with related auxiliary tools. The database platform ran in a Linux environment and could be accessed by users through a web browser. At present, the data on this platform mainly came from the atlas resources submitted by animal model resource units within Guangdong Province. Results In August 2024, a digital atlas database platform for animal models was constructed based on the classification structure of three dimensions: systemic diseases, animal species, and resource units. This platform provided functions such as collection, management, retrieval, and viewing of atlas data. As of January 2025, four resource units had submitted 61 atlas data entries of animal models to the platform, totalling 610 data items. Conclusion The animal model digital atlas database platform has been constructed and put into preliminary use. Although the amount of data on the platform is still limited, it is capable of integrating and openly sharing animal model atlas data. It is believed that with the continuous enrichment of atlas data in the future, this platform is expected to provide important data support for the development of laboratory animal science and comparative medicine research, thereby promoting the efficient utilization of scientific research resources.

Objective Domestic research institutions and researchers have established a wide variety of animal disease models and accumulated a wealth of specialized, distinctive, and targeted atlas data during the model development process. These atlas data are of great value for development and application. Therefore, it is necessary to develop a professional and complete digital atlas database platform for animal models, which can achieve the open sharing of animal model atlas data and the integration and optimization of atlas resources related to disease animal models held by relevant domestic institutions. Methods Based on the B/S architecture, the authors' institution built a digital atlas database of animal models, using Java as the main development language and Oracle database system along with related auxiliary tools. The database platform ran in a Linux environment and could be accessed by users through a web browser. At present, the data on this platform mainly came from the atlas resources submitted by animal model resource units within Guangdong Province. Results In August 2024, a digital atlas database platform for animal models was constructed based on the classification structure of three dimensions: systemic diseases, animal species, and resource units. This platform provided functions such as collection, management, retrieval, and viewing of atlas data. As of January 2025, four resource units had submitted 61 atlas data entries of animal models to the platform, totalling 610 data items. Conclusion The animal model digital atlas database platform has been constructed and put into preliminary use. Although the amount of data on the platform is still limited, it is capable of integrating and openly sharing animal model atlas data. It is believed that with the continuous enrichment of atlas data in the future, this platform is expected to provide important data support for the development of laboratory animal science and comparative medicine research, thereby promoting the efficient utilization of scientific research resources.

As a third major discipline on par with internal medicine and surgery,interventional radiology is one of the key branches of modern medicine.The unique practicality and innovation of interventional radiology make it play an irreplaceable role in the diagnosis and treatment of diseases.In recent years,with the rapid development of technology and the updating of educational concepts,the teaching mode of interventional radiology is facing new challenges and opportunities.This article combines the clinical training methods adopted by interventional physicians in Europe and Germany,integrates imaging,anatomy and pathology teaching,strengthens the foundation,uses virtual reality(VR),augmented reality(AR)technology,and simulation training to enhance the practical ability of medical students.At the same time,with the help of online education platforms,the innovative methods and optimization strategies such as personalized learning program are implemented,which can greatly improve the teaching effectiveness of interventional radiology and provide useful references for teaching reform in this field.

Objective To explore the influencing factors of cognitive impairment in non-dialysis patients with chronic kidney disease(CKD).Methods A total of 60 hospitalized non-dialysis patients with CKD in the Department of Nephrology of Northern Jiangsu People's Hospital Affiliated to Yangzhou University from September 2022 to September 2023 were enrolled as research objects.According to the estimated glomerular filtration rate(eGFR),they were divided into stage 1 to 2 of CKD group[eGFR ≥60 mL/(min·1.73 m2)]with 23 cases,the stage 3 of CKD group[eGFR 30～＜60 mL/(min·1.73 m2)]with 20 cases,and stage 4 to 5 of CKD group[eGFR＜30 mL/(min·1.73 m2)]with 17 cases.The Montreal Cognitive Assessment Scale(MoCA)was used to evaluate the cognitive function of the patients.Basic data and common clinical laboratory in-dicators on hospital admission were collected to analyze the differences in cognitive function levels under different renal function statuses and to explore the influencing factors of cognitive impairment.Results The incidence rates of cognitive impairment in the stage 1 to 2 of CKD group,stage 3 of CKD group,and stage 4 to 5 of CKD group were 47.8％,85.0％,and 94.1％respectively,the median MoCA scored 26,24 and 20 respectively,with statistically significant between-group differ-ences(P＜0.05).Cognitive function was significantly negatively correlated with age(r=-0.634,P＜0.001),blood urea nitrogen(BUN)(r=-0.574,P＜0.001),serum creatinine(Cr)(r=-0.417,P＜0.001),cystatin C(Cys-C)(r=-0.327,P=0.011),serum β2-microglobulin(β2-MG)(r=-0.259,P=0.046),and N-terminal pro-brain natriuretic peptide(NT-proBNP)(r=-0.474,P＜0.001),and was significantly positively correlated with hemoglobin(HB)(r=0.401,P=0.001)and eGFR(r=0.485,P＜0.001).Multivariate Logistic regression analysis showed that age(P=0.006)and NT-proBNP(P=0.041)were influencing factors of cognitive im-pairment in non-dialysis patients with CKD.Receiver operating characteristic(ROC)curve analysis showed that the area under the curve(AUC),sensitivity,and specificity of age for prediction were 0.860,0.864 and 0.812 respectively,the AUC,sensitivity,and specificity of NT-proBNP for pre-diction were 0.808,0.795 and 0.875 respectively,and the combined prediction of age and NT-proBNP had an AUC,sensitivity,and specificity of 0.893,0.955,and 0.750,respectively.Conclusion As renal function deteriorates,the incidence rate and severity of cognitive impairment in non-dialysis patients with CKD tend to increase.Advanced age,renal function deterioration,high NT-proBNP level,and anemia are associated with the occurrence of cognitive impairment in non-di-alysis patients with CKD,among which age and NT-proBNP are influencing factors for cognitive im-pairment.

Objective To explore the regulatory mechanism of NFE2L2/KEAP1 in alveolar bone repair induced by periodontitis.Methods A rat periodontitis model was established and divided into four groups:Control group(n=6);Periodontitis model group(n=6);Periodontitis+lentivirus empty vector group(n=6);Periodontitis+NFE2L2 overexpression plasmid group(n=6).Histopathological changes in each group were observed using HE staining.TRAP staining was used to detect osteoclast positivity,while ELISA was employed to measure inflammatory cytokine levels in tissues.Immunofluorescence and qPCR were used to detect NFE2L2 expression,and western blot was used to assess the expression of osteogenic proteins ALPL2,RUNX2,and COL1.Primary periodontal ligament cells(hPDLCs)were cultured,and cells were transfected to overexpress NFE2L2 and KEAP1.The cells were divided into six groups:Normal group;Model group;pcDNA-NC group;pcDNA-NFE2L2 group;pc-NFE2L2+pcDNA-NC group;pc-NFE2L2+pcDNA-KEAP1 group.A cellular model was established,and the morphology of primary hPDLCs was observed under a microscope.Cell proliferation was assessed using CCK-8.Osteogenic mineralization was observed using alizarin red staining,and western blot was used to detect osteogenic proteins and autophagy markers.Cell migration was observed using a scratch assay.Results(1)After model induction,redness,swelling of the gums,extensive inflammatory infiltration,and alveolar bone resorption were observed,confirming successful model establishment.Partial tissue recovery occurred after NFE2L2 overexpression via lentivirus.(2)After model induction,osteoclast positivity increased,confirming successful model establishment.Overexpression of NFE2L2 reduced osteoclast positivity(P<0.001).(3)After model induction,levels of IL-1β,IL-10,and TNF-α were significantly higher than in the normal group(P<0.05),confirming successful model establishment.Transfection with NFE2L2 lentivirus reduced inflammatory cytokine levels(P<0.0001).After model induction,osteogenic protein expression decreased compared to the normal group,but overexpression of NFE2L2 increased osteogenic protein expression(P<0.05).(5)LPS treatment significantly reduced cell viability,while NFE2L2 overexpression enhanced it(P<0.0001).(6)LPS treatment reduced calcified nodules,while NFE2L2 overexpression increased them.Addition of pcDNA-KEAP1 reduced mineralized nodules.(7)LPS treatment decreased osteogenic protein expression,while NFE2L2 overexpression increased it.However,addition of pcDNA-KEAP1 reduced osteogenic protein expression(P<0.05).(8)LPS treatment reduced cell migration,whereas NFE2L2 overexpression enhanced it(P<0.0001).(9)Expression of autophagy markers decreased after LPS treatment,but increased after transfection with NFE2L2 plasmid.However,addition of pcDNA-KEAP1 reduced the expression of autophagy markers(P<0.05).Conclusion This study identified the regulatory role of NFE2L2/KEAP1 in periodontitis,providing a scientific basis for the treatment of periodontitis.

This review summarizes recent advances in neoadjuvant immunotherapy for advanced gastric cancer.Through literature search in PubMed,Web of Science,and CNKI databases from 2020 to 2023,we systematically analyzed the mechanisms,clinical applications,and bio-marker research.Programmed death-1(PD-1)inhibitors combined with chemotherapy significantly improve patient outcomes,while mi-crosatellite instability(MSI),programmed death-ligand 1(PD-L1)expression,and tumor mutational burden(TMB)have been identified as important predictive biomarkers.Multi-omics analysis shows great potential in identifying optimal responders,with pyroptosis-related gene scoring system(PRS)positively correlating with anti-tumor immune infiltration.Metabolic reprogramming and epigenetic regulation in the tumor microenvironment play key roles in immune evasion,while emerging targets such as Claudin 18.2 and combination targeting strategies further enhance therapeutic efficacy.Despite significant progress,precise patient selection and overcoming resistance mechan-isms remain major challenges.Future research should focus on biomarker validation,personalized treatment strategy development,tumor microenvironment dynamic analysis,and novel combination therapy exploration to improve clinical outcomes.

Objective To observe the ultrasonic manifestations of abdominal pregnancy.Methods Ultrasonic and clinical data of 18 pregnant woman with abdominal pregnancy diagnosed by operation and pathology were retrospectively analyzed.Results Among 15 cases in first trimester,no preoperative ultrasonic diagnosis of abdominal pregnancy was obtained.Ultrasound showed no gestational sac in uterine cavity but mass in pelvic cavity,which located in the adnexal region in 8 cases,in the front and the post of uterus each in 2 cases,while in the adnexal region and the front of uterus in 1 case,in the post of the cervix in 1 case,and closed to uterine wall in 1 case,without obvious tubal echo around mass in all 15 cases.There were 2 cases of abdominal pregnancy in the second trimester,which were first diagnosed with ultrasound at 13+6 weeks and 21 weeks,with gestational sac located on the left side of uterus and behind the uterus,respectively.One case of abdominal pregnancy in the third trimester was first diagnosed with ultrasound at 35 4 weeks,with gestational sac located on the right side of uterus.Ultrasonic manifestations of the above three cases all showed gestational sac located outside the uterus without myometrium wrapping around the gestational sac nor placenta implanted in uterus,while echoes of fluid accumulation were detected around fetus.The ultrasonic diagnosis rate of abdominal pregnancy was 16.67％(3/18).Conclusion In the first trimester,if the ectopic pregnancy mass was large or the gestational sac located adjacent to the cervix,anterior or posterior to uterus and on the uterine wall,also no fallopian tube-like echo around the mass,the possibility of abdominal pregnancy should be considered.Ultrasonic manifestations of abdominal pregnancy in the second and third trimester present as gestational sac outside uterine cavity without wrapping uterine muscle layer around,no placenta implantation in uterine cavity,as well as echoes of fluid accumulation around fetus.Transabdominal combined with transvaginal ultrasound could improve diagnostic rate of abdominal pregnancy.