Purpose To investigate the clinicopathological characteristics of the gastric oxyntic gland adenoma(GOGA).Methods We collected 18 samples of GOGA,histopathological features and immunohistochemical staining were assessed.Main features of pathological diagnosis,treatment methods and follow-up were retrospectively analyzed.Results There were 18 patients,including 9 females and 9 males,aged from 36 to 86 years old.The endoscopic im-age showed a flat lesion with whitish in color or a polypoid protrusions.The size ranged from 0.3 cm to 0.8 cm.Hema-toxylin and eosin staining showed irregular glandular structures in the mucosal lamina propria,with branched and anas-tomosed patterns.The tumour demonstrating composed of chief cells hyperplasia with mild nuclear atypia.All lesions were confined to the mucous lamina propria.There was no atrophic within the peripheral gastic mucosa.Immunohisto-chemical examination showed positive for Pepsinogen-Ⅰ and MUC6.Gene mutation were analyzed in 2 cases using next generation sequence technology,and no KRAS and GNAS mutation had been detected.Endoscopic surgical treatment was performed in 11 cases,and biopsy forceps removal was carried out in 7 cases.No recurrence or metastasis was ob-served during the follow-up period of 1 to 58 months.Conclusion GOGA is a rare lesion,and appears to behave bio-logically benign.A full understanding of its histological morphology and biological behavior can improve the diagnostic ability of clinincans,and facilitate further research in the future.

Objective To elucidate the regulatory mechanism of hepatocyte nuclear factor 1α(HNF1A)in inducing human embryonic stem cells(hESCs)towards insulin producing cells(IPCs)differentiation.Methods An optimized stepwise protocol was implemented to generate definitive endoderm-derived IPCs.Dynamic HNF1A expression patterns were systematically monitered by qRT-PCR and Western blot.In the third stage(S3)of differentiation,cells were subjected to lentiviral-mediated interventions:respectively HNF1A knockdown(si-HNF1A)with scramble control(si-NC),and HNF1A over expression(oe-HNF1A)with empty vector control(oe-NC).Quantitative analysis of pancreatic lineage markers was performed by qRT-PCR.Glucose stimulated insulin secretion(GSIS)was assessed using ELISA under low glucose(LG)and high glucose(HG)conditions.Results Both HNF1A mRNA and protein levels demonstrated stage-dependent elevation,reaching peak expression at S3 relative to S1(P<0.05).Genetic silencing of HNF1A significantly suppressed key β-cell markers such as Pancreatoduodenal homeobox protein 1,GluT2,Ins compared to controls(P<0.05).Conversely,HNF1A overexpression enhanced transcriptional activation of these markers.Ins secretion increased stimulated by HG than LG in si-NC group.Functional analysis revealed impaired GSIS in si-HNF1A compared with si-NC group(P<0.05),whereas oe-HNF1A cells exhibited augmented GSIS capacity.Conclusions HNF1A positively regulates the IPC differentiation in hESCs,which may play a vital role in potentiating glucose-responsive insulin secretion.

Liver metastasis is one of the most common pathways of malignant tumor dissemination and a leading cause of cancer-related mortality. With continuous advances in surgical techniques and equipment,improved systemic therapies,and the widespread adoption of multidisciplinary treatment strategies,the concept of oligometastasis—originally proposed by radiation oncologists to describe a transitional state between localized disease and widespread systemic metastasis—has been increasingly recognized and applied by surgical oncologists. This has led to the development of metastasis-directed surgical interventions that have yielded encouraging clinical outcomes. However,due to the heterogeneity of primary tumors and the liver′s unique anatomical and immunological characteristics,standardized diagnostic and therapeutic approaches for hepatic oligometastases have yet to be established. This review provides a systematic overview of the evolution of the oligometastatic concept and discusses recent surgical advances in managing liver oligometastases across various primary tumor types.

Objective:To explore the differences in clinical phenotype characteristics and auxiliary test results of Gerstmann-Str?ussler-Scheinker syndrome (GSS) patients in the same family with GSS carrying a P102L mutation in the PRNP gene. Methods:A family with GSS carrying a P102L mutation in the PRNP gene, which was identified and treated at the Department of Neurology, Xuanwu Hospital, Capital Medical University in January 2024 was collected. A comprehensive evaluation was conducted on the proband, including neuropsychological examination, imaging studies, electroencephalogram, cerebrospinal fluid (CSF) analysis, real-time quaking-induced conversion (RT-QuIC) assay of skin biopsy samples, and genetic testing. At the same time, a survey and analysis were conducted on the family members. Skin RT-QuIC, genetic testing and neuropsychological evaluation were performed on some of the family members. Results:Among the 4-generation members of the GSS family, there were 5 GSS patients, including the proband′s father, younger brother, uncle and cousin. The proband, her younger brother and cousin all carried the P102L mutation in the PRNP gene, and her son was a carrier of the P102L mutation in the PRNP gene. The proband was a 53 years old female, and had a typical GSS phenotype, with the initial symptom of ataxia. The CSF 14-3-3 protein was negative and there were no abnormalities observed on her brain magnetic resonance imaging. The skin and CSF RT-QuIC test results of the proband were both negative. The cousin of the proband had a typical GSS phenotype, and his skin RT-QuIC test result was negative. The younger brother of the proband had a GSS phenotype of Creutzfeldt-Jakob disease type, with the initial symptom of rapidly progressing dementia and a positive skin RT-QuIC test result. The first symptoms of the proband′s father and uncle were both ataxia, and they had passed away without undergoing genetic testing. The son of the proband was a carrier of the P102L mutation in the PRNP gene and had no clinical symptoms. Conclusion:Different family members in the same GSS family may exhibit different clinical phenotypes, and GSS with different phenotypes have differences in RT-QuIC results.

Purpose To investigate the clinicopathological characteristics of the gastric oxyntic gland adenoma(GOGA).Methods We collected 18 samples of GOGA,histopathological features and immunohistochemical staining were assessed.Main features of pathological diagnosis,treatment methods and follow-up were retrospectively analyzed.Results There were 18 patients,including 9 females and 9 males,aged from 36 to 86 years old.The endoscopic im-age showed a flat lesion with whitish in color or a polypoid protrusions.The size ranged from 0.3 cm to 0.8 cm.Hema-toxylin and eosin staining showed irregular glandular structures in the mucosal lamina propria,with branched and anas-tomosed patterns.The tumour demonstrating composed of chief cells hyperplasia with mild nuclear atypia.All lesions were confined to the mucous lamina propria.There was no atrophic within the peripheral gastic mucosa.Immunohisto-chemical examination showed positive for Pepsinogen-Ⅰ and MUC6.Gene mutation were analyzed in 2 cases using next generation sequence technology,and no KRAS and GNAS mutation had been detected.Endoscopic surgical treatment was performed in 11 cases,and biopsy forceps removal was carried out in 7 cases.No recurrence or metastasis was ob-served during the follow-up period of 1 to 58 months.Conclusion GOGA is a rare lesion,and appears to behave bio-logically benign.A full understanding of its histological morphology and biological behavior can improve the diagnostic ability of clinincans,and facilitate further research in the future.

Objective To elucidate the regulatory mechanism of hepatocyte nuclear factor 1α(HNF1A)in inducing human embryonic stem cells(hESCs)towards insulin producing cells(IPCs)differentiation.Methods An optimized stepwise protocol was implemented to generate definitive endoderm-derived IPCs.Dynamic HNF1A expression patterns were systematically monitered by qRT-PCR and Western blot.In the third stage(S3)of differentiation,cells were subjected to lentiviral-mediated interventions:respectively HNF1A knockdown(si-HNF1A)with scramble control(si-NC),and HNF1A over expression(oe-HNF1A)with empty vector control(oe-NC).Quantitative analysis of pancreatic lineage markers was performed by qRT-PCR.Glucose stimulated insulin secretion(GSIS)was assessed using ELISA under low glucose(LG)and high glucose(HG)conditions.Results Both HNF1A mRNA and protein levels demonstrated stage-dependent elevation,reaching peak expression at S3 relative to S1(P<0.05).Genetic silencing of HNF1A significantly suppressed key β-cell markers such as Pancreatoduodenal homeobox protein 1,GluT2,Ins compared to controls(P<0.05).Conversely,HNF1A overexpression enhanced transcriptional activation of these markers.Ins secretion increased stimulated by HG than LG in si-NC group.Functional analysis revealed impaired GSIS in si-HNF1A compared with si-NC group(P<0.05),whereas oe-HNF1A cells exhibited augmented GSIS capacity.Conclusions HNF1A positively regulates the IPC differentiation in hESCs,which may play a vital role in potentiating glucose-responsive insulin secretion.

Objective:To explore the differences in clinical phenotype characteristics and auxiliary test results of Gerstmann-Str?ussler-Scheinker syndrome (GSS) patients in the same family with GSS carrying a P102L mutation in the PRNP gene. Methods:A family with GSS carrying a P102L mutation in the PRNP gene, which was identified and treated at the Department of Neurology, Xuanwu Hospital, Capital Medical University in January 2024 was collected. A comprehensive evaluation was conducted on the proband, including neuropsychological examination, imaging studies, electroencephalogram, cerebrospinal fluid (CSF) analysis, real-time quaking-induced conversion (RT-QuIC) assay of skin biopsy samples, and genetic testing. At the same time, a survey and analysis were conducted on the family members. Skin RT-QuIC, genetic testing and neuropsychological evaluation were performed on some of the family members. Results:Among the 4-generation members of the GSS family, there were 5 GSS patients, including the proband′s father, younger brother, uncle and cousin. The proband, her younger brother and cousin all carried the P102L mutation in the PRNP gene, and her son was a carrier of the P102L mutation in the PRNP gene. The proband was a 53 years old female, and had a typical GSS phenotype, with the initial symptom of ataxia. The CSF 14-3-3 protein was negative and there were no abnormalities observed on her brain magnetic resonance imaging. The skin and CSF RT-QuIC test results of the proband were both negative. The cousin of the proband had a typical GSS phenotype, and his skin RT-QuIC test result was negative. The younger brother of the proband had a GSS phenotype of Creutzfeldt-Jakob disease type, with the initial symptom of rapidly progressing dementia and a positive skin RT-QuIC test result. The first symptoms of the proband′s father and uncle were both ataxia, and they had passed away without undergoing genetic testing. The son of the proband was a carrier of the P102L mutation in the PRNP gene and had no clinical symptoms. Conclusion:Different family members in the same GSS family may exhibit different clinical phenotypes, and GSS with different phenotypes have differences in RT-QuIC results.

Liver metastasis is one of the most common pathways of malignant tumor dissemination and a leading cause of cancer-related mortality. With continuous advances in surgical techniques and equipment,improved systemic therapies,and the widespread adoption of multidisciplinary treatment strategies,the concept of oligometastasis—originally proposed by radiation oncologists to describe a transitional state between localized disease and widespread systemic metastasis—has been increasingly recognized and applied by surgical oncologists. This has led to the development of metastasis-directed surgical interventions that have yielded encouraging clinical outcomes. However,due to the heterogeneity of primary tumors and the liver′s unique anatomical and immunological characteristics,standardized diagnostic and therapeutic approaches for hepatic oligometastases have yet to be established. This review provides a systematic overview of the evolution of the oligometastatic concept and discusses recent surgical advances in managing liver oligometastases across various primary tumor types.

Objective To explore the correlation of occurrence of major adverse cardiovascular events(MACE)with QRS-T angle,N-terminal pro-B-type natriuretic peptide(NT-proBNP)and fibrinogen(FIB)levels and platelet/lymphocyte ratio(PLR)in patients with acute myocardial in-farction(AMI)after percutaneous coronary intervention(PCI).Methods A retrospectively analy-sis was conducted on 98 AMI patients undergoing PCI in our department from May 2020 to June 2022.According to the occurrence of MACE or not,they were divided into MACE group(25 cases)and non-MACE group(73 cases).The general data and QRS-T angle,PLR,and Fib and NT-proBNP levels were compared between the two groups.Univariate logistic regression analysis and ROC curve analysis were used to analyze the influencing factors and predictive efficacy for MACE occurrence in AMI patients after PCI.Results Significantly larger QRS-T angle and PLR,and higher FIB and NT-proBNP levels were observed in the MACE group than the non-MACE group(P＜0.05,P＜0.01).Univariate logistic regression analysis showed that RS-T angle(OR=1.086,95％CI:1.043-1.131,P=0.000),PLR(OR=1.184,95％CI:1.102-1.272,P=0.000)and NT-proBNP level(OR=1.009,95％CI:1.004-1.014,P=0.000)were influencing factors for MACE occurrence in AMI patients after PCI.ROC curve analysis indicated that the AUC value of QRS-T angle,PLR and NT-proBNP level in predicting MACE after PCI in AMI patients was 0.822,0.870 and 0.907,with a sensitivity of 76.00％,76.00％and 84.00％,and a specificity of 72.60％,89.04％and 94.52％,respectively.Conclusion QRS-T angle,PLR and NT-proBNP are the influencing factors of MACE in AMI patients after PCI,and they have good predictive value.

Objective To explore the correlation of occurrence of major adverse cardiovascular events(MACE)with QRS-T angle,N-terminal pro-B-type natriuretic peptide(NT-proBNP)and fibrinogen(FIB)levels and platelet/lymphocyte ratio(PLR)in patients with acute myocardial in-farction(AMI)after percutaneous coronary intervention(PCI).Methods A retrospectively analy-sis was conducted on 98 AMI patients undergoing PCI in our department from May 2020 to June 2022.According to the occurrence of MACE or not,they were divided into MACE group(25 cases)and non-MACE group(73 cases).The general data and QRS-T angle,PLR,and Fib and NT-proBNP levels were compared between the two groups.Univariate logistic regression analysis and ROC curve analysis were used to analyze the influencing factors and predictive efficacy for MACE occurrence in AMI patients after PCI.Results Significantly larger QRS-T angle and PLR,and higher FIB and NT-proBNP levels were observed in the MACE group than the non-MACE group(P＜0.05,P＜0.01).Univariate logistic regression analysis showed that RS-T angle(OR=1.086,95％CI:1.043-1.131,P=0.000),PLR(OR=1.184,95％CI:1.102-1.272,P=0.000)and NT-proBNP level(OR=1.009,95％CI:1.004-1.014,P=0.000)were influencing factors for MACE occurrence in AMI patients after PCI.ROC curve analysis indicated that the AUC value of QRS-T angle,PLR and NT-proBNP level in predicting MACE after PCI in AMI patients was 0.822,0.870 and 0.907,with a sensitivity of 76.00％,76.00％and 84.00％,and a specificity of 72.60％,89.04％and 94.52％,respectively.Conclusion QRS-T angle,PLR and NT-proBNP are the influencing factors of MACE in AMI patients after PCI,and they have good predictive value.