Background and aims:Noninvasive assessments play a crucial role in ruling out high-risk esophageal varices(HREV)in cirrhotic patients.However,the value of sound touch elastography(STE)in predicting HREV has not been comprehensively investigated.Therefore,this study aimed to establish prediction models based on liver and spleen stiffness measurements obtained by STE and provide assessment strategies and cutoff values tailored for different clinical situations.Methods:This prospective study included cirrhotic patients who underwent esophagogastroduodeno-scopy(EGD).Liver and spleen stiffness measurements by STE were performed within six months of EGD examination.Various prediction models and their corresponding cutoff values were established for different clinical situations,incorporating spleen diameter and laboratory parameters.Results:A total of 154 cirrhotic patients were included in the study and stratified into training(n=119)and validation(n=35)sets.Multivariable analysis revealed platelet,spleen diameter and spleen stiffness measurement as independent predictors of HREV.The model incorporating spleen stiffness measurement,platelet,and spleen diameter demonstrated superior performance in predicting HREV,yielding an area under the receiver operating characteristic curve(AUC)of 0.878 and 0.853 in the training set and validation set,respectively.Application of this model for screening cirrhotic patients could avoid EGDs in 39.7％(27/68)and 35.3％(6/17)of patients in the training and validation sets,respectively.Conclusions:Liver and spleen stiffness measurements obtained through STE are valuable for predicting HREV in cirrhotic patients.The developed prediction models and their corresponding cutoff values provide tailored solutions for various clinical situations,thereby effectively reducing the need for un-necessary endoscopies.

The transcription factor nuclear factor kappa B (NF-B) is activated in hepatocytes in the pathogenesis of hepatic steatosis. However, the action mechanism of NF-B remains to be established in the hepatic steatosis. In this study, the subunit of NF-B was found to promote the hepatic steatosis through regulation of histone deacetylase 1 (HDAC1) in hepatocytes. The activity was supported by the phenotypes of knockout (-KO) mice and knockout (-KO) mice. Hepatic steatosis was reduced in the -KO mice, but not in the -KO mice. The reduction was a result of inhibition of HDAC1 activity in the -KO cells. Knockdown of gene led to suppression of hepatocyte steatosis in HepG2 cells. A decrease in sterol-regulatory element binding protein 1c (SREBP1c) protein was observed in the liver of -KO mice and in cell with knockdown. The decrease was associated with an increase in succinylation of SREBP1c protein. The study suggests that stabilizes HDAC1 to support the SREBP1c activity in hepatic steatosis in the pathophysiological condition. Interruption of this novel pathway in the -KO, but not the -KO mice, may account for the difference in hepatic phenotypes in the two lines of transgenic mice.