The present study aimed to examine the correlation of D-dimer levels with the Child-Pugh and MELD scores, as well as to determine the predictive ability of D-dimer level for the in-hospital mortality of liver cirrhosis patients. All cirrhotic patients who were consecutively admitted to our hospital between January 2011 and June 2014, and underwent D-dimer tests on admission were retrospectively analyzed. Pearson's χ2 tests were employed to evaluate the correlations of D-dimer levels with Child-Pugh and MELD scores. In addition, receiver operating curve (ROC) analysis was employed to evaluate the specificity and sensitivity of D-dimer levels for predicting the in-hospital mortality. In total, 703 cirrhotic patients were included in the study, with an in-hospital mortality of 5.4% (38/703). The D-dimer levels were correlated with Child-Pugh (correlation coefficient, 0.219; P15 group compared with the MELD score <15 group. The area under the ROC of D-dimer levels for predicting the in-hospital mortality of liver cirrhosis was 0.729 (P<0.0001), while the best cut-off D-dimer value was 0.28 µg/ml with a sensitivity of 86.84% and a specificity of 49.17%. In conclusion, the D-dimer level is significantly associated with the degree of liver dysfunction. Therefore, D-dimer testing could be employed for the prognostic stratification of liver cirrhosis.

Background and aims: Severe acute pancreatitis (SAP) is potentially lethal. Considering the role of inflammation in the progression of acute pancreatitis (AP), this study aims to develop a model based on inflammatory indexes for identifying the presence of SAP. Methods: Overall, 253 patients with AP who were consecutively admitted between July 2018 and November 2020 were screened, of whom 60 had SAP. Systemic immune-inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), neutrophil-to-platelet ratio (NPR), systemic inflammation response index (SIRI), platelet-to-albumin ratio (PAR), C-reactive protein-to-albumin ratio (CAR), C-reactive protein-to-lymphocyte ratio (CLR), and triglyceride glucose (TyG) index were calculated. Multivariate logistic regression analyses were performed to identify independent risk factors of SAP. Then, inflammation-based models were established. Receiver operating characteristics (ROC) curve analyses were performed. Area under ROC curve (AUROC) was calculated. Results: Diabetes mellitus, fatty liver, high white blood cell count (WBC), C-reactive protein (CRP), red blood cell distribution width (RDW), procalcitonin (PCT), SII, NLR, NPR, CAR, CLR, and TyG index, and a low LMR were significantly associated with SAP. Considering the collinearity among these variables, 10 multivariate logistic regression analyses were separately performed. Finally, four independent inflammation-based models were established. Of them, the best one, which was calculated as follows: 1.204*fatty liver (yes = 1; no = 0) + 0.419*PCT + 0.005*CLR - 2.629, had an AUROC of 0.795 with a specificity of 73.4% and a sensitivity of 71.7%. Conclusion: The inflammation-based model consisting of fatty liver, PCT, and CLR has a good diagnostic performance for SAP.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers, partly due to its high level of drug resistance. β-Catenin is critical for drug resistance in pancreatic cancer, which occurs through multiple mechanisms. Here, we observed that miR-33a targeted the 3′UTR of β-catenin, inducing apoptosis and inhibiting the growth of human pancreatic cancer cells. Moreover, gemcitabine (GEM) treatment enhanced β-catenin expression by reducing miR-33a expression in a dose-dependent manner. GEM-resistant MiaPaCa-2^res cells with a low level of miR-33a expression and high level of β-catenin expression adopted spindle-shaped morphologies, similar to their morphologies during the epithelial-to-mesenchymal transition (EMT), and their normal morphologies were restored by miR-33a overexpression. Furthermore, miR-33a downregulated β-catenin nuclear translocation, decreasing the transcription of survivin, cyclin D1, and MDR-1, and the protein expression of slug, vimentin, and N-cadherin, thereby mediating sensitization to GEM. Thus, miR-33a might function as a tumor suppressor to downregulate β-catenin expression, affecting cell growth, apoptosis, the EMT, and GEM resistance.