Insulin resistance is a manifestation of glucose metabolism disorder secondary to pancreatic disease, and previous studies have shown that it is associated with inflammatory factors and tumor progression. This article reviews the mechanism and influence of insulin resistance in chronic pancreatitis and pancreatic cancer and points out that further research on insulin resistance can provide an effective basis for the prevention of chronic pancreatitis and the evaluation of the progression and prognosis of pancreatic cancer.

PurposeTraumatic pancreatitis which has a high mortality rate is likely to be misdiagnosed. This study aims to analyze the clinical manifestations and CT findings of traumatic pancreatitis, so as to improve its early diagnosis and treatment.Materials and Methods The clinical manifestations and CT images of 25 patients with traumatic pancreatitis confirmed by operation or post-treatment review were analyzed retrospectively. Pancreatic injuries were classified as superficial lesions (with the depth of trauma less than 50% of the thickness of pancreas) and deep lesions (with the depth of trauma more than 50% of the thickness of pancreas). The clinical manifestations, CT findings and the complicated organ injuries in these two types of pancreatic trauma were analyzed.Results Eight patients had superficial lesions, and 17 patients were with deep lesions. Nine patients had complicated organ injuries. Patients with deep lesions showed a more severe abdominal pain, nausea, vomiting, rebound tenderness and muscular tension than those patients with superficial lesions. The serum amylases increased in all the patients. Pancreatic-relevant complications including pancreas pseudocyst, pancreatic fluid leakage and peritonitis occurred in 7 patients who accepted a delayed operation. Three out of 8 patients with superficial pancreatic injuries were missed on plain CT scan in the first time. Among 17 patients with deep pancreatic trauma, 12 had incomplete laceration, 5 had complete laceration, and 1 was missed in the first time. The direct CT features of pancreatic trauma were focal abnormal attenuation and/or discontinuity in pancreatic parenchyma.Conclusion The clinical manifestations of patients with traumatic pancreatitis are complicated. The direct CT features of pancreatic trauma include heterogeneous density of pancreatic parenchyma and/or interruption. Trauma's depth is closely related to the main injury of pancreatic duct. It is worth to be aware of the indirect signs such as peripancreatic oozy and other viscera damages.

Objective:To study the relationship between pancreaticobiliary maljunction (PBM) with cholangiopancreatic diseases, and to evaluate the efficacy and safety using endoscopic therapy for PBM.Methods:The clinical data of 734 patients treated with ERCP at the Affiliated Hospital of Guizhou Medical University from May 2016 to April 2020 were analyzed retrospectively. Of 31 PBM patients who were finally included in this study, there were 23 patients with benign diseases and 8 patients with malignant diseases. Using the diameter of bile duct, these patients were divided into two groups: dilated bile duct group and the non-dilated bile duct group. The general characteristics of patients, incidences of cholangiopancreatic disease, endoscopic treatment, therapeutic efficacy and follow-up data were analyzed.Results:Of the 31 patients with PBM, 11 were males and 20 were females, aged (56.7±16.2) years. There were 4 patients with choledochal cyst (12.9%) and 6 patients with biliary cancer (19.4%). The incidences were significantly higher than those in non-PBM patients (0.9% and 5.3%, respectively, P<0.05). All 31 patients with PBM underwent endoscopic EST treatment, including 15 patients (48.4%) treated with endoscopic naso-biliary drainage (ENBD), 9 patients (29.0%) with endoscopic retrograde biliary drainage (ERBD), 4 patients (12.9%) with endoscopic papillary balloon dilatation (EPBD)+ ENBD, 1 patient (3.2%) with endoscopic metal biliary endoprothesis (EMBE)+ ENBD, 1 patient with ERBD+ endoscopic retrograde pancreatic drainage (3.2%), and 1 patient with EPBD+ ERBD+ EMBE (3.2%). The operative success rate was 100%. Serum AST, ALT, ALP, GGT, TBil and DBil levels of patients in the benign group and malignant group were significantly decreased postoperatively when compared with the preoperative levels (all P<0.05). One patient (3.2%) developed post ERCP pancreatitis. The preoperative and postoperative NRS scores of the patients in the benign group were 7(6, 8) points compared to 0 (0, 1) points, respectively ( P<0.05). All the 23 patients in the benign group were followed up for (25.13±12.90) months. There were no patients who were loss to follow-up. There was no malignant transformation. Three PMB patients with dilated bile ducts still had attacks of abdominal pain or jaundice. The symptoms of the remaining 20 patients were completely relieved, giving a treatment efficacious rate of 87.0% (20/23). Conclusions:PBM was closely related to choledochal cysts, biliary cancer and other diseases. Endoscopic treatment was efficacious and safe, and provided a safe and feasible treatment in preventing future cholangiopancreatic attacks.

ObjectiveTo investigate the effect of laminin subunit α3 （LAMA3） on the epithelial-mesenchymal transition （EMT）， invasion， and metastasis abilities of pancreatic cancer （PC）. MethodsA comprehensive analysis was performed for tumor- and EMT-related databases to identify the EMT genes associated with PC， especially LAMA3. The methods of qRT-PCR and Western blot were used to measure the expression level of LAMA3 in PC tissue and cell lines； immunofluorescence assay was used to determine the localization of LAMA3 in PANC-1 cells； Transwell assay was used to investigate the effect of LAMA3 on the invasion and migration abilities of PC cells. The t-test was used for comparison of continuous data between groups. ResultsThe analysis of the TCGA database identified 3 EMT-related oncogenes for PC， i.e.， LAMA3， AREG， and SDC1. The LASSO-Cox regression model showed that LAMA3 had the most significant impact on the prognosis of PC （risk score=0.256 1×LAMA3+0.043 1×SDC1+0.071 4×AREG）. The Cox model and nomogram showed that the high expression of LAMA3 was an independent risk factor for the poor prognosis of PC （hazard ratio=1.32， 95% confidence interval： 1.07‍ ‍—‍ 1.62， P<0.01）. Experimental results showed that there was a significant increase in the expression of LAMA3 in pancreatic cancer tissue compared with the normal pancreatic tissue. Compared with the HPDE cell line， there were varying degrees of increase in the expression of LAMA3 in pancreatic cancer AsPC-1， BxPC-3， PANC-1， MIA PaCa-2， and SW1990 cell lines， with the highest expression level in PANC-1 cells. The enrichment analysis showed that LAMA3 was associated with the biological processes and signaling pathways such as EMT， collagen metabolism， extracellular matrix degradation， the TGF-β pathway， and the PI3K pathway. After the knockdown of LAMA3， there were significant reductions in the expression levels of N-Cadherin， Vimentin， and Snail， while there was a significant increase in the expression level of E-Cadherin. Transwell assay showed that there were significant reductions in the invasion and migration abilities of PANC-1 cells after the knockdown of LAMA3. ConclusionLAMA3 is highly expressed in PC and can promote the EMT， invasion， and migration of PC cells， and therefore， LAMA3 may be used as a novel diagnostic marker and a new therapeutic target for PC.