Objective To construct a prognostic model of lung adenocarcinoma(LUAD)based on m5C modification-related genes and to explore its clinical value.Methods Based on the LUAD data in TCGA,GSE30219,GSE31210,and GSE50081 cohorts,prognosis-related m5C modification-related genes were screened,and the prognostic model was constructed by using univariate Cox,Lasso,and multivariate Cox regression analyses.Kaplan-Meier curve,ROC curve,and Cox regression were used to observe the robustness and prognostic performance of the model.The correlation between the prognostic model and clinico-pathologic features was further explored.Results A prognostic model consisting of eight m5C modifi-cation-related genes,including CDK1,CDKN1A,NOP2,RRM2,TCL6,TLR8,TRDMT1,and YTHDF2,was constructed.Risk score was an independent risk factor for the prognosis of patients with LUAD,and it is combined with age,T stage,and N stage to constitute a nomogram which can accurately predict the prognosis of patients.The infiltration of macrophages and CD4+/CD8+T cells was significantly reduced in high-risk patients.The risk score in LUAD tissues was significantly higher than that in normal tissues and was positively correlated with T stage and N stage.The risk score of smoking and EGFR wild-type patients was higher than that of non-smoking and EGFR-mutant patients.Conclusion The prognostic model constructed based on m5C modification-related genes has shown good accuracy and stability in predicting the prognosis of patients with LUAD,and it is closely related to clinical features,driver gene mutations,and immune infiltration,which can provide a potential basis for the treatment and prognostic assessment of LUAD.

Objective To construct a prognostic model of lung adenocarcinoma(LUAD)based on m5C modification-related genes and to explore its clinical value.Methods Based on the LUAD data in TCGA,GSE30219,GSE31210,and GSE50081 cohorts,prognosis-related m5C modification-related genes were screened,and the prognostic model was constructed by using univariate Cox,Lasso,and multivariate Cox regression analyses.Kaplan-Meier curve,ROC curve,and Cox regression were used to observe the robustness and prognostic performance of the model.The correlation between the prognostic model and clinico-pathologic features was further explored.Results A prognostic model consisting of eight m5C modifi-cation-related genes,including CDK1,CDKN1A,NOP2,RRM2,TCL6,TLR8,TRDMT1,and YTHDF2,was constructed.Risk score was an independent risk factor for the prognosis of patients with LUAD,and it is combined with age,T stage,and N stage to constitute a nomogram which can accurately predict the prognosis of patients.The infiltration of macrophages and CD4+/CD8+T cells was significantly reduced in high-risk patients.The risk score in LUAD tissues was significantly higher than that in normal tissues and was positively correlated with T stage and N stage.The risk score of smoking and EGFR wild-type patients was higher than that of non-smoking and EGFR-mutant patients.Conclusion The prognostic model constructed based on m5C modification-related genes has shown good accuracy and stability in predicting the prognosis of patients with LUAD,and it is closely related to clinical features,driver gene mutations,and immune infiltration,which can provide a potential basis for the treatment and prognostic assessment of LUAD.

Objective: To investigate the effects of 1, 25-dihydroxy vitamin D₃[1, 25(OH)₂D₃] on food allergy(FA) in mice and its mechanism. Methods: A total of 40 BALB/c mice were randomly divided into 5 groups, 8 in each group, including control group (group C) and FA model group (FA group), according to the dose of 1, 25(OH)₂D₃ intervention, the mice of the FA group were divided into FA₀ group (0), FA_l group [10 μg/(kg·d)], FA_m group [50 μg/(kg·d)] and FA_h group[100 μg/(kg·d)]. Egg albumin was used to establish a food allergy model, with different doses of 1, 25(OH)₂D₃ for gastric intervention, and the control group was replaced by 9 g/L saline.The serum levels of ovalbumin-immunoglobulin E(OVA-IgE), interleukin(IL)-9 and IL-17 of mice were measured by using enzyme linked immunosorbent assay after the last excitation, and HE staining and histopathological examination were carried out in the small intestine of mice. Results: Compared with group C, FA₀ group and FA_h group small intestinal mucosa in mice had different degrees of damage, partial peeling off, structure disorder, villi epithelial cell focal falls peeling off, necrosis, lamina propria edema, congestion, a large number of inflammatory cells infiltration, low but the FA_l group and FA_m group had light mucosa damage, intestinal epithelial basically intact, with integrity, no congestion, edema, and inflammatory cells infiltration to a lesser degree.The mean concentrations of serum IgE, IL-9 and IL-17 in different groups were statistically significant (F=40.770, 9.530, 5.624, all P<0.05). Compared with the FA₀ group [(41.87±3.19) ng/L], the OVA-IgE of the FA_l group [(22.71±4.77) ng/L] and the FA_m group [(16.34±2.81) ng/L] were significantly reduced (t=5.533, 11.835, all P<0.01), but there was no significant difference between the FA_h group [(36.29±6.52) ng/L] (t=1.673, P>0.05). Compared with the FA₀ group [(161.77±50.44) ng/L], the IL-9 levels of the FA_l group [(94.29±18.79) ng/L] and the FA_m group[(84.45±30.88) ng/L] were significantly lower (t=3.267, 3.366, all P<0.01), while that of the FA_h group [(36.29±6.52) ng/L] was not significantly lower (t=0.777, P>0.05). Compared with FA₀ group [(81.55±29.37) ng/L], IL-17 levels of FA_h group [(133.58±47.05) ng/L] was significantly increased (t=2.653, P<0.05), while IL-17 level of FA_l group [(79.41±25.15) ng/L] and FA_m group [(58.81±26.00) ng/L] were lower than that of FA₀ group [(81.55±29.37) ng/L], but the difference was not statistically significant (t=0.154, 1.640, all P>0.05). Conclusions Low, medium dose of 1, 25(OH)₂D₃ supplements can inhibit mice food allergies, but high doses of 1, 25(OH)₂D₃ improve performance in mice food allergies, and 1, 25(OH)₂D₃′s influence on the secretion of IL-9 is one that influences mechanism of food allergy.