Objective:To investigate the correlation of neutrophil-to-albumin ratio (NAR) and glucose-to-lymphocyte ratio (GLR) with in-hospital death in patients with acute myocardial infarction (AMI).Methods:The clinical data of 2 657 patients with AMI from January 2017 to December 2022 in Xuanwu Hospital, Capital Medical University were retrospectively analyzed. Using receiver operating characteristic (ROC) curve to determine the optimal cutoff values of GLR and NAR (6.02 and 0.25) for predicting in-hospital mortality in patients with AMI, the patients were divided into high GLR group (GLR≥6.02, 768 cases) and low GLR group (GLR<6.02, 1 889 cases), high NAR group (NAR≥0.25, 547 cases) and low NAR group (NAR<0.25, 2 110 cases) according the optimal cutoff values. The baseline characteristics and occurrence of in-hospital major adverse cardiovascular events (MACE) were recorded. Multivariate Logistic regression was used to analyze the independent risk factors for in-hospital death in patients with AMI.Results:Among the 2 657 patients with AMI, 265 patients had in-hospital MACE (10.0%), and 50 patients (1.9%) died. The age, proportion of Killip≥ 2 grade, proportion of diabetes, proportion of myocardial infarction, proportion of cerebral infarction history, proportion of ST-elevation myocardial infarction (STEMI), thrombolysis in myocardial infarction clinical trial score (TIMI score), global registry of acute coronary event score (GRACE score), fibrinogen, fasting blood glucose, glycated hemoglobin, high-density lipoprotein cholesterol (HDL-C), cardiac troponin I (cTnI) peak, N-terminal B-type natriuretic peptide (NT-proBNP), hypersensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), NAR, GLR, neutrophil count, left ventricular end-diastolic diameter (LVEDD) in high GLR group were significantly higher than those in low GLR group, the proportion of males, body mass index (BMI), proportion of smoking history, proportion of non-ST elevation myocardial infarction (NSTEMI), albumin, estimated glomerular filtration rate (eGFR), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), lymphocyte count, monocyte count and left ventricular ejection fraction (LVEF) were significantly lower than those in low GLR group, and there were statistical differences ( P<0.01 or <0.05). The proportion of Killip≥2 grade, proportion of STEMI, TIMI score, GRACE score, fibrinogen, fasting blood glucose, TC, LDL-C, cTnI peak, hs-CRP, IL-6, NAR, GLR, white blood cell count, neutrophil count and monocyte count in high NAR group were significantly higher than those in low NAR group, the age, proportion of myocardial infarction history, proportion of NSTEMI, albumin, lymphocyte count, left atrial diameter (LAD) and LVEF were significantly lower than those in low NAR group, and there were statistical differences ( P<0.01 or <0.05). The incidences of in-hospital MACE, death, ventricular fibrillation or pulseless ventricular tachycardia, atrial fibrillation, cardiac arrest and bleeding in high GLR group were significant higher than those in low GLR group: 15.2% (117/768) vs. 7.8% (148/1 889), 4.6% (35/768) vs. 0.8% (15/1 889), 5.3% (41/768) vs. 2.9% (54/1 889), 6.9% (53/768) vs. 4.0% (75/1 889), 4.7% (36/768) vs. 1.4% (26/1 889) and 2.3% (18/768) vs. 0.7% (13/1 889), and there were statistical differences ( P<0.01); there was no statistical difference in the incidence of heart rupture between two groups ( P>0.05). The incidence of in-hospital MACE, death, ventricular fibrillation or pulseless ventricular tachycardia, cardiac arrest, cardiac rupture and bleeding in high NAR group were significantly higher than those in low NAR group: 16.6% (91/547) vs. 8.2% (174/2 110), 5.9% (32/547) vs. 0.9% (18/2 110), 8.0% (44/547) vs. 2.4% (51/2 110), 5.9% (32/547) vs. 1.4% (30/2 110), 1.6% (9/547) vs. 0.4% (9/2 110) and 2.4% (13/547) vs. 0.9% (18/2 110), and there were statistical differences ( P<0.01); there was no statistical difference in the incidence of atrial fibrillation between two groups ( P>0.05). Multivariate Logistic regression analysis result showed that the Killip 3 and 4 grades, high NAR, high GRACE score, high fasting glucose and low LVEF were independent risk factors for in-hospital death in patients with AMI ( OR = 3.827, 4.660, 3.779, 1.020, 1.095 and 0.962; 95% CI 1.158 to 12.649, 1.184 to 18.344, 1.856 to 7.649, 1.009 to 1.032, 1.027 to 1.167 and 0.932 to 0.993; P<0.05 or <0.01). Conclusions:The NAR can independently predict the risk of in-hospital death in patients with AMI.

Objective To investigate the role of CCCTC-binding factor(CTCF)in the development of oxaliplatin(OXA)-induced gastric cancer drug-tolerant cells(DTCs)and to preliminarily elucidate its underlying mechanisms.Methods The DTCs model of gastric cancer was established by treating MGC803 cells with OXA.Overexpression and knockdown of CTCF in MGC803 cells were performed to observe their effects on the formation of DTCs in gastric cancer.Additionally,Bcl2-like protein 1(BCL2L1)was knocked down in CTCF-overexpressing cells,and its impact on DTCs formation was evaluated.Flow cytometry was used to analyze the effects of varying CTCF/BCL2L1 expression levels on the apoptosis of gastric cancer cells under OXA treatment.Immunohistochemistry(IHC)was employed to detect the expression levels of CTCF/BCL2L1 in gastric cancer tissues,and the therapeutic outcomes of neoadjuvant chemotherapy in patients with different CTCF/BCL2L1 expression levels were assessed.Results Gastric cancer DTCs can be obtained following a regimen of continuous treatment of MGC803 cells with a specific concentration of oxaliplatin(OXA,1.5 μmol/L)for 5 days,followed by an additional 5-day culture period post-treatment cessation.The upregulation of CTCF has been shown to facilitate the formation of DTCs in gastric cancer,whereas its downregulation inhibits this process(P<0.05).In MGC803 gastric cancer cells,the expression level of BCL2L1 is positively correlated with that of CTCF.Knockdown of BCL2L1 in MGC803 cells overexpressing CTCF can reverse the pro-DTC formation effect of CTCF(P<0.05).Overexpression of CTCF confers resistance to OXA-induced apoptosis in gastric cancer cells,and this anti-apoptotic effect can be reversed by BCL2L1 knockdown in MGC803 cells overexpressing CTCF(P<0.05).In the tumor tissues of the majority of gastric cancer patients,the expression levels of BCL2L1 are positively correlated with those of CTCF,and the efficacy of neoadjuvant chemotherapy is notably reduced in patients with high expression of the CTCF/BCL2L1 axis compared to those with low expression(P<0.05).Conclusion CTCF promotes the formation of OXA-related gas-tric cancer DTCs by upregulating BCL2L1 expression and inhibiting apoptosis,making the CTCF/BCL2L1 axis a potential therapeutic target for DTCs in gastric cancer.

Objective:To investigate the correlation of neutrophil-to-albumin ratio (NAR) and glucose-to-lymphocyte ratio (GLR) with in-hospital death in patients with acute myocardial infarction (AMI).Methods:The clinical data of 2 657 patients with AMI from January 2017 to December 2022 in Xuanwu Hospital, Capital Medical University were retrospectively analyzed. Using receiver operating characteristic (ROC) curve to determine the optimal cutoff values of GLR and NAR (6.02 and 0.25) for predicting in-hospital mortality in patients with AMI, the patients were divided into high GLR group (GLR≥6.02, 768 cases) and low GLR group (GLR<6.02, 1 889 cases), high NAR group (NAR≥0.25, 547 cases) and low NAR group (NAR<0.25, 2 110 cases) according the optimal cutoff values. The baseline characteristics and occurrence of in-hospital major adverse cardiovascular events (MACE) were recorded. Multivariate Logistic regression was used to analyze the independent risk factors for in-hospital death in patients with AMI.Results:Among the 2 657 patients with AMI, 265 patients had in-hospital MACE (10.0%), and 50 patients (1.9%) died. The age, proportion of Killip≥ 2 grade, proportion of diabetes, proportion of myocardial infarction, proportion of cerebral infarction history, proportion of ST-elevation myocardial infarction (STEMI), thrombolysis in myocardial infarction clinical trial score (TIMI score), global registry of acute coronary event score (GRACE score), fibrinogen, fasting blood glucose, glycated hemoglobin, high-density lipoprotein cholesterol (HDL-C), cardiac troponin I (cTnI) peak, N-terminal B-type natriuretic peptide (NT-proBNP), hypersensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), NAR, GLR, neutrophil count, left ventricular end-diastolic diameter (LVEDD) in high GLR group were significantly higher than those in low GLR group, the proportion of males, body mass index (BMI), proportion of smoking history, proportion of non-ST elevation myocardial infarction (NSTEMI), albumin, estimated glomerular filtration rate (eGFR), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), lymphocyte count, monocyte count and left ventricular ejection fraction (LVEF) were significantly lower than those in low GLR group, and there were statistical differences ( P<0.01 or <0.05). The proportion of Killip≥2 grade, proportion of STEMI, TIMI score, GRACE score, fibrinogen, fasting blood glucose, TC, LDL-C, cTnI peak, hs-CRP, IL-6, NAR, GLR, white blood cell count, neutrophil count and monocyte count in high NAR group were significantly higher than those in low NAR group, the age, proportion of myocardial infarction history, proportion of NSTEMI, albumin, lymphocyte count, left atrial diameter (LAD) and LVEF were significantly lower than those in low NAR group, and there were statistical differences ( P<0.01 or <0.05). The incidences of in-hospital MACE, death, ventricular fibrillation or pulseless ventricular tachycardia, atrial fibrillation, cardiac arrest and bleeding in high GLR group were significant higher than those in low GLR group: 15.2% (117/768) vs. 7.8% (148/1 889), 4.6% (35/768) vs. 0.8% (15/1 889), 5.3% (41/768) vs. 2.9% (54/1 889), 6.9% (53/768) vs. 4.0% (75/1 889), 4.7% (36/768) vs. 1.4% (26/1 889) and 2.3% (18/768) vs. 0.7% (13/1 889), and there were statistical differences ( P<0.01); there was no statistical difference in the incidence of heart rupture between two groups ( P>0.05). The incidence of in-hospital MACE, death, ventricular fibrillation or pulseless ventricular tachycardia, cardiac arrest, cardiac rupture and bleeding in high NAR group were significantly higher than those in low NAR group: 16.6% (91/547) vs. 8.2% (174/2 110), 5.9% (32/547) vs. 0.9% (18/2 110), 8.0% (44/547) vs. 2.4% (51/2 110), 5.9% (32/547) vs. 1.4% (30/2 110), 1.6% (9/547) vs. 0.4% (9/2 110) and 2.4% (13/547) vs. 0.9% (18/2 110), and there were statistical differences ( P<0.01); there was no statistical difference in the incidence of atrial fibrillation between two groups ( P>0.05). Multivariate Logistic regression analysis result showed that the Killip 3 and 4 grades, high NAR, high GRACE score, high fasting glucose and low LVEF were independent risk factors for in-hospital death in patients with AMI ( OR = 3.827, 4.660, 3.779, 1.020, 1.095 and 0.962; 95% CI 1.158 to 12.649, 1.184 to 18.344, 1.856 to 7.649, 1.009 to 1.032, 1.027 to 1.167 and 0.932 to 0.993; P<0.05 or <0.01). Conclusions:The NAR can independently predict the risk of in-hospital death in patients with AMI.

Allogeneic haemopoietic stem cell transplantation (allo-HSCT)-related nephrotic syndrome is a rare complication, recognized as a clinical manifestation of chronic graft versus host disease (GVHD). T cell dysfunction is thought to play a significant role in the pathogenesis of allo-HSCT-related nephrotic syndrome, but the precise mechanism remains unclear. This paper reported a case of X-linked adrenoleukodystrophy (X-ALD) who had good control of the disease after allo-HSCT, but developed proteinuria and progressed to nephrotic syndrome after immunosuppressive therapy was tapered. Kidney biopsy revealed secondary membranous nephropathy, which responded well to treatment with glucocorticoids and tacrolimus. Limited literature exist on allo-HSCT-related nephrotic syndrome in children. This study provides a comprehensive summary of its mechanism, clinical features, pathology, diagnosis,and treatment, offering valuable insights for diagnosing and managing allo-HSCT-related nephrotic syndrome in pediatric patients.

Objective To construct the evaluation index system of DRG implementation effect from the interests of medical insurance,hospitals and patients,and provide evaluation tools for medical insurance departments to grasp the actual operation effect of DRG.Methods The evaluation index system is constructed initially through literature re-view,and then Delphi method is used to conduct two rounds of expert consultation.According to the concentration degree and coordination degree of expert opinions,the index system is selected and modified,and the final evalua-tion index system is constructed.Results The positive coefficients of experts in the two rounds of expert consultation were 73%and 82%respectively,and the average authority coefficient of experts was 0.78.In the second round of consultation,the Kendell's W coefficients of the importance,data availability and sensitivity of the evaluation index were 0.517,0.437 and 0.472 respectively(P＜0.001).Finally,the evaluation index system of DRG implementation effect includes 3 first-level indicators,9 second-level indicators and 29 third-level indicators.Conclusion The evalua-tion index system of DRG implementation effect has high enthusiasm of experts,good authority,coordination and concentration of experts,which can be used to evaluate the sustainability of medical insurance fund,the service out-put of medical institutions and the rights and interests of patients in DRG pilot areas.

Objective:To investigate the molecular markers involved in death related to acute myocardial infarction (AMI) and provide new targets for early intervention.Methods:Consecutive patients who hospitalized in department of cardiology, Xuanwu Hospital, Capital Medical University from January 2017 to December 2021 and diagnosed with AMI were enrolled. The clinical factors and markers associated with in-hospital death after AMI were analyzed. In addition, patients diagnosed with AMI hospitalized in department of cardiology, Xuanwu Hospital, Capital Medical University from September 2022 to April 2023 were enrolled. We prospectively analyzed the plasma protein of death related to AMI via Olink Precision Proteomics based on proximity extension assay (PEA) technology.Results:In the retrospective study, 2 325 patients with AMI were analyzed, including 75 patients in the in-hospital death group and 2 250 subjects in the survival group. The overall mortality rate during hospitalization was 3.23% (75/2325). The patients in the death group were older: 72 (64, 80) years vs. 63 (55, 71) years. And Interleukin-6 (IL-6), hypersensitive C-reactive protein (Hs-CRP), leukocyte counts and neutrophil counts were markedly higher in the death group than those in the survival group: 69.0 (26.7, 136.6) ng/L vs. 18.2 (9.4, 36.5) ng/L, 45.7 (28.7, 50.5) mg/L vs. 5.5 (2.0, 17.2) mg/L, 12.0 (9.8, 14.1) ×10 9/L vs. 8.9 (7.2, 11.2) × 10 9/L, 9.8 (7.8, 12.1) ×10 9/L vs. 6.5(4.7, 8.8) ×10 9/L ( P<0.01). In this prospective study, 86 patients with AMI were analyzed. 61 proteins including Insulin-like growth factor-binding protein 1, 2 (IGFBP-1, IGFBP-2), Chitotriosidase-1 (CHIT1), Complement component C1q receptor (CD93) were independently associated with in-hospital death related to AMI ( P<0.05). The differential proteins were mainly enriched in inflammatory response, cell adhesion, cytokine signaling pathway and apoptosis. Moreover, 22 proteins including Urokinase plasminogen activator surface receptor (U-PAR), Trefoil factor 3 (TFF3), Perlecan (PLC), Growth differentiation factor 15 (GDF-15), Junctional adhesion molecule A (JAM-A) were plotted according to a logistic regression model, and the area under the curve (AUC) was more than 0.9, showing the high accuracy in predicting in-hospital death after AMI. Conclusions:Molecular markers of the inflammatory response, cell adhesion, cell growth and apoptosis might be involved in death related to AMI, which provides new targets for early intervention.

Objective:To investigate the molecular markers involved in death related to acute myocardial infarction (AMI) and provide new targets for early intervention.Methods:Consecutive patients who hospitalized in department of cardiology, Xuanwu Hospital, Capital Medical University from January 2017 to December 2021 and diagnosed with AMI were enrolled. The clinical factors and markers associated with in-hospital death after AMI were analyzed. In addition, patients diagnosed with AMI hospitalized in department of cardiology, Xuanwu Hospital, Capital Medical University from September 2022 to April 2023 were enrolled. We prospectively analyzed the plasma protein of death related to AMI via Olink Precision Proteomics based on proximity extension assay (PEA) technology.Results:In the retrospective study, 2 325 patients with AMI were analyzed, including 75 patients in the in-hospital death group and 2 250 subjects in the survival group. The overall mortality rate during hospitalization was 3.23% (75/2325). The patients in the death group were older: 72 (64, 80) years vs. 63 (55, 71) years. And Interleukin-6 (IL-6), hypersensitive C-reactive protein (Hs-CRP), leukocyte counts and neutrophil counts were markedly higher in the death group than those in the survival group: 69.0 (26.7, 136.6) ng/L vs. 18.2 (9.4, 36.5) ng/L, 45.7 (28.7, 50.5) mg/L vs. 5.5 (2.0, 17.2) mg/L, 12.0 (9.8, 14.1) ×10 9/L vs. 8.9 (7.2, 11.2) × 10 9/L, 9.8 (7.8, 12.1) ×10 9/L vs. 6.5(4.7, 8.8) ×10 9/L ( P<0.01). In this prospective study, 86 patients with AMI were analyzed. 61 proteins including Insulin-like growth factor-binding protein 1, 2 (IGFBP-1, IGFBP-2), Chitotriosidase-1 (CHIT1), Complement component C1q receptor (CD93) were independently associated with in-hospital death related to AMI ( P<0.05). The differential proteins were mainly enriched in inflammatory response, cell adhesion, cytokine signaling pathway and apoptosis. Moreover, 22 proteins including Urokinase plasminogen activator surface receptor (U-PAR), Trefoil factor 3 (TFF3), Perlecan (PLC), Growth differentiation factor 15 (GDF-15), Junctional adhesion molecule A (JAM-A) were plotted according to a logistic regression model, and the area under the curve (AUC) was more than 0.9, showing the high accuracy in predicting in-hospital death after AMI. Conclusions:Molecular markers of the inflammatory response, cell adhesion, cell growth and apoptosis might be involved in death related to AMI, which provides new targets for early intervention.

Objective To construct the evaluation index system of DRG implementation effect from the interests of medical insurance,hospitals and patients,and provide evaluation tools for medical insurance departments to grasp the actual operation effect of DRG.Methods The evaluation index system is constructed initially through literature re-view,and then Delphi method is used to conduct two rounds of expert consultation.According to the concentration degree and coordination degree of expert opinions,the index system is selected and modified,and the final evalua-tion index system is constructed.Results The positive coefficients of experts in the two rounds of expert consultation were 73%and 82%respectively,and the average authority coefficient of experts was 0.78.In the second round of consultation,the Kendell's W coefficients of the importance,data availability and sensitivity of the evaluation index were 0.517,0.437 and 0.472 respectively(P＜0.001).Finally,the evaluation index system of DRG implementation effect includes 3 first-level indicators,9 second-level indicators and 29 third-level indicators.Conclusion The evalua-tion index system of DRG implementation effect has high enthusiasm of experts,good authority,coordination and concentration of experts,which can be used to evaluate the sustainability of medical insurance fund,the service out-put of medical institutions and the rights and interests of patients in DRG pilot areas.

Objective To investigate the role of CCCTC-binding factor(CTCF)in the development of oxaliplatin(OXA)-induced gastric cancer drug-tolerant cells(DTCs)and to preliminarily elucidate its underlying mechanisms.Methods The DTCs model of gastric cancer was established by treating MGC803 cells with OXA.Overexpression and knockdown of CTCF in MGC803 cells were performed to observe their effects on the formation of DTCs in gastric cancer.Additionally,Bcl2-like protein 1(BCL2L1)was knocked down in CTCF-overexpressing cells,and its impact on DTCs formation was evaluated.Flow cytometry was used to analyze the effects of varying CTCF/BCL2L1 expression levels on the apoptosis of gastric cancer cells under OXA treatment.Immunohistochemistry(IHC)was employed to detect the expression levels of CTCF/BCL2L1 in gastric cancer tissues,and the therapeutic outcomes of neoadjuvant chemotherapy in patients with different CTCF/BCL2L1 expression levels were assessed.Results Gastric cancer DTCs can be obtained following a regimen of continuous treatment of MGC803 cells with a specific concentration of oxaliplatin(OXA,1.5 μmol/L)for 5 days,followed by an additional 5-day culture period post-treatment cessation.The upregulation of CTCF has been shown to facilitate the formation of DTCs in gastric cancer,whereas its downregulation inhibits this process(P<0.05).In MGC803 gastric cancer cells,the expression level of BCL2L1 is positively correlated with that of CTCF.Knockdown of BCL2L1 in MGC803 cells overexpressing CTCF can reverse the pro-DTC formation effect of CTCF(P<0.05).Overexpression of CTCF confers resistance to OXA-induced apoptosis in gastric cancer cells,and this anti-apoptotic effect can be reversed by BCL2L1 knockdown in MGC803 cells overexpressing CTCF(P<0.05).In the tumor tissues of the majority of gastric cancer patients,the expression levels of BCL2L1 are positively correlated with those of CTCF,and the efficacy of neoadjuvant chemotherapy is notably reduced in patients with high expression of the CTCF/BCL2L1 axis compared to those with low expression(P<0.05).Conclusion CTCF promotes the formation of OXA-related gas-tric cancer DTCs by upregulating BCL2L1 expression and inhibiting apoptosis,making the CTCF/BCL2L1 axis a potential therapeutic target for DTCs in gastric cancer.

Allogeneic haemopoietic stem cell transplantation (allo-HSCT)-related nephrotic syndrome is a rare complication, recognized as a clinical manifestation of chronic graft versus host disease (GVHD). T cell dysfunction is thought to play a significant role in the pathogenesis of allo-HSCT-related nephrotic syndrome, but the precise mechanism remains unclear. This paper reported a case of X-linked adrenoleukodystrophy (X-ALD) who had good control of the disease after allo-HSCT, but developed proteinuria and progressed to nephrotic syndrome after immunosuppressive therapy was tapered. Kidney biopsy revealed secondary membranous nephropathy, which responded well to treatment with glucocorticoids and tacrolimus. Limited literature exist on allo-HSCT-related nephrotic syndrome in children. This study provides a comprehensive summary of its mechanism, clinical features, pathology, diagnosis,and treatment, offering valuable insights for diagnosing and managing allo-HSCT-related nephrotic syndrome in pediatric patients.