Objective Detecting the level of IDO and KYN in ulcerative colitis (UC) patients; using ROC curve to discuss their value in the diagnosis of patients with active UC. Methods 60 cases of UC group, 18 cases of dis-ease control group and 20 cases of healthy control group were included in the study. Immunohistochemical staining methods were used to detect the expression of IDO in colonic mucosa of UC, enzyme-linked immunosorbent (ELISA) methods were used to detect the serum levels of IDO, KYN and CRP, and the value with ROC curve method was analyzed. Results ① There was a positive correlation between IDO level and IDO expression (P<0.05). There was a positive correlation between KYN level and IDO expression (P<0.05). ②The levels of IDO and KYN in UC group were higher than those of disease control group and health control group (P<0.05). ③The levels of IDO and KYN in patients with active UC were significantly higher than that in patients with catabasis UC (P<0.01), and the levels increased with severity of inflammation. ④ The levels of IDO and KYN in active UC were positively related to disease activity and CRP levels (P<0.05). ⑤The IDO,KYN and CRP area under ROC curve were 0.976, 0.856 and 0.864;best cut-off point were 53.66 U/L, 2.34 nmol/L and 1.75 mg/ml;sensitiv-ity were 90.5%, 78.65% and 100.0%; specifity were 94.4%, 83.3% and 61.1%; Youden index were 0.839 2, 0.619 0 and 0.611 1. Conclusion The levels of IDO and KYN in serum can be used as an important index to judge the severity of UC. They have important value in the diagnosis of active UC . The value of IDO is higher than KYN and CRP.

Small ubiquitin-related modifier(SUMOylation)is a dynamic post-translational modification that maintains cardiac function and can protect against a hypertrophic response to cardiac pressure overload.However,the function of SUMOylation after myocardial infarction(MI)and the molecular details of heart cell responses to SUMO1 deficiency have not been determined.In this study,we demonstrated that SUMO1 protein was inconsistently abundant in different cell types and heart regions after MI.However,SUMO1 knockout significantly exacerbated systolic dysfunction and infarct size after myocardial injury.Single-nucleus RNA sequencing revealed the differential role of SUMO1 in regulating heart cells.Among cardiomyocytes,SUMO1 deletion increased the Nppa+Nppb+Ankrd1+cardiomyocyte subcluster pro-portion after MI.In addition,the conversion of fibroblasts to myofibroblasts subclusters was inhibited in SUMO1 knockout mice.Importantly,SUMO1 loss promoted proliferation of endothelial cell subsets with the ability to reconstitute neovascularization and expressed angiogenesis-related genes.Computational analysis of ligand/receptor interactions suggested putative pathways that mediate cardiomyocytes to endothelial cell communication in the myocardium.Mice preinjected with cardiomyocyte-specific AAV-SUMO1,but not the endothelial cell-specific form,and exhibited ameliorated cardiac remodeling following MI.Collectively,our results identified the role of SUMO1 in cardiomyocytes,fibroblasts,and endothelial cells after Ml.These findings provide new insights into SUMO1 involvement in the patho-genesis of MI and reveal novel therapeutic targets.