A peripancreatic vascular reconstruction can reveal the vascular anatomy, variations of peripancreatic vascular, and tumor-induced vascular changes; the application of the simulation surgery platform could reduce surgical trauma and decrease operative time.

Gastric cancer is the main leading cause of cancer-related death worldwide. The aberrant expression of paternally expressed gene 10 (PEG10) is involved in development of a range of cancers. However, the potential biological function and the underling mechanism of PEG10 in human gastric carcinoma are still unknown. Knocking down LncRNA PEG10 might represent a promising therapeutic strategy for the treatment of gastric cancer. The expression of PEG10, miR-3200, and AEG1 in human gastric carcinoma NCI-N87 cells were altered by cell transfection assay. Cell viability, migration, invasion, and apoptosis were determined by trypan blue exclusion, Transwell assay, and flow cytometric analysis, respectively. RNA and protein expression level of gene was analyzed by real-time PCR and Western blot. Luciferase reporter assay was conducted to determine the target gene of miR-3200. JNK and Wnt signal pathway protein expressions were tested by Western blot. The up-regulation of PEG10 was found in clinical samples. PEG10 knockdown effectively inhibited gastric carcinoma cell viability, migration, and invasion, but promoted cell apoptosis. This tumor-suppressing effect of PEG10 knockdown might be realized by up-regulating miR-3200 in vitro and in vivo. AEG1 was a direct target gene of miR-3200. Moreover, miR-3200 might suppress NCI-N87 cells by negative regulating AEG1. Up-regulating miR-3200 effectively blocked JNK and Wnt pathways likely via down-regulating AEG1. PEG10 knockdown played a carcinostatic role via up-regulating miR-3200 and further regulating AEG1 in gastric carcinoma cells, during which process, JNK pathway and Wnt pathway were blocked.

Pancreatic cancer (PC), highly malignant, is one of the most lethal cancers. Interferon-induced transmembrane protein 1 (IFITM1) has recently been regarded as a new molecular marker in human cancers. However, the role of IFITM1 in PC remains unclear. In this study, a short hairpin RNA (shRNA) was constructed to assess the effect of IFITM1 on PANC-1 and ASPC-1 cells. The level of IFITM1 was downregulated in cells transfected with shRNA targeting IFITM1 (sh-IFITM1). Silencing of IFITM1 significantly decreased cell viability, downregulated the level of Ki-67, arrested cell at G1/S phase, reduced the number of cells in S phase, and decreased cyclinD1, cyclinE, CDK2, and CDK4 levels. Moreover, Hoechst staining and Western blotting analysis showed that cell apoptosis was induced by IFITM1. IFITM1 knockdown suppressed the MAPK signaling pathway by downregulation of p-ERK, p-P38, and p-JNK levels. These findings suggested that IFITM1 could be considered a potential therapeutic target for PC.

Severe acute pancreatitis (SAP) presents with an aggressive clinical presentation and high lethality rate. Early prediction of the severity of acute pancreatitis will help physicians to further precise treatment and improve intervention. This study aims to construct a composite model that can predict SAP using inflammatory markers. 212 patients with acute pancreatitis enrolled from January 2018 to June 2020 were included in this study, basic parameters at admission and 24 h after hospitalization, and laboratory results such as inflammatory markers were collected. Pearson's test was used to analyze the correlation between heparin-binding protein (HBP), procalcitonin (PCT), and C-reactive protein (CRP). Risk factors affecting SAP were analyzed using multivariate logistic regression, inflammatory marker models were constructed, and subject operating curves were used to verify the discrimination of individual as well as inflammatory marker models and to find the optimal cut-off value based on the maximum Youden index. In the SAP group, the plasma levels of HBP, CRP, and PCT were 139.1 ± 74.8 ng/mL, 190.7 ± 106.3 mg/L and 46.3 ± 22.3 ng/mL, and 25.3 ± 16.0 ng/mL, 145.4 ± 67.9 mg/L and 27.9 ± 22.4 ng/mL in non-SAP patients, with a statistically significant difference between the two groups (P < 0.001), The Pearson correlation analysis showed a positive correlation between the three values of HBP, CRP, and PCT. The results of the multivariate logistic regression analysis showed that HBP (OR = 1.070 [1.044–1.098], P < 0.001), CRP (OR = 1.010 [1.004–1.016], P = 0.001), and PCT (OR = 1.030[1.007–1.053], P < 0.001) were risk factors for SAP, and the area under the curve of the HBP-CRP-PCT model was 0.963 (0.936–0.990). The HCP model, consisting of HBP, CRP, and PCT; is well differentiated and easy to use and can predict the risk of SAP in advance.

Background In the past century, postoperative pancreatic fistula (POPF) has been the major complication and cause of mortality after pancreaticoduodenectomy (PD). No one knows what exactly happens in the pancreatic stump after POPF. The hypothesis of this manuscript was to investigate changes that occur in the pancreatic stump. Methods Two patients who had previously undergone PD for malignant tumors subsequently underwent complete pancreatectomy for life-threatening abdominal bleeding in the context of POPF. The pancreatic stumps were pathologically analyzed. It’s hard to prove digestive reflux directly. But we found that we can use 16s rRNA gene sequencing to detect the distribution of bacteria in the jejunum, pancreatic head, and pancreatic stump. Results Inflammation is widespread in both patients' pancreatic stumps, including hematoma, edema, infiltration of inflammatory cells, scattered necrosis, and acinar-duct metaplasia (ADM). The whole pancreatic stump shows a proliferative state. Apoptosis decreases significantly or even disappears. The inflammation of the pancreatic stump shows a descending trend from the anastomosis to the tail. Simultaneously, we found a universal phenomenon: chemotaxis in the ductal system. Inflammatory cells penetrate the ducts formed by ADM and gather in the ducts. The bacteria from duodena are also discovered in the major part of the pancreatic stump. The bacterial distribution shows the same trend as inflammation. Conclusions Inflammation and ADM widely exist in the pancreatic stump with POPF after PD and show a descending trend from the anastomosis to the pancreatic tail. Digestive reflux through the pancreatic ductal system does happen during the pancreatic fistula. We could stop POPF if we eliminate the digestive reflux and reduce the inflammation in the pancreatic stump.

Background and Objectives: Postoperative pancreatic fistula (POPF) contributes to significant morbidity and mortality after pancreaticoduodenectomy (PD). However, the underlying mechanisms of POPF remain unclear. This study is to explore the pathology in the pancreatic stump and elucidates the mechanisms of POPF following PD. Methods: Pathological analysis and 16S rRNA gene sequencing were performed on the specimens obtained from the two patients who accepted complete pancreatectomy for grade C POPF after PD. In addition, a retrospective radiological analysis was conducted on a cohort of 125 consecutive patients who underwent PD to evaluate the inflammatory response in the pancreatic stump. Results: The presence of gradient inflammation and acinar-duct metaplasia (ADM) in the pancreatic stumps is ubiquitous. The incidence of apoptosis is markedly reduced in the pancreatic stump. Moreover, a significant accumulation of neutrophil-dominated inflammatory cells is detected in the ductal system. Notably, the ADM-formed duct is the site where the neutrophils transmigrate through the ductal wall. Additionally, the microbial evidence indicates that gut microbes migrate from the digestive tract. Radiological analysis proves that a gradient of pancreatitis exists in all cases after PD and reaches peak on the fourth postoperative day. Conclusions: Inflammation and digestive reflux exist in the pancreatic stump after PD. The underlying mechanisms of POPF are the high biochemical activity of the pancreas, mechanical injury, and digestive reflux.

AbstractObjectiveThe aim of this study was to investigate the expression of FXYD domain-containing ion transport regulator 6 (FXYD6) mRNA and protein in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) tissues with cirrhosis, the corresponding paracancerous tissues and the normal liver tissues, and to explore the clinical significance of FXYD6 expression in HBV-related HCC with cirrhosis.MethodsThe FXYD6 mRNA and protein were examined by semi-quantitative reverse transcription polymerase chain reaction and immunohistochemistry, respectively.ResultsThe FXYD6 mRNA in HBV-related HCC tissues was significantly higher than that in the cirrhosis tissues or that in the normal liver tissues. The positive expression rate of FXYD6 protein was statistically higher in HBV-related HCC tissues than that in HBV-related cirrhosis or that in normal liver tissues. There was no significant correlation between the expression of FXYD6 protein and gender, age, histological differentiation, tumor diameter, tumor number, integrity of tumor capsule or not and alpha fetoprotein (AFP) concentration in serum, but the protein expression was associated with microvascular invasion, pathological stage, and early recurrence after operation within 1 year.ConclusionFXYD6 might be involved in hepatocyte carcinogenesis and tumor progression in HBV-related HCC with cirrhosis and indicated a poor prognosis.

Background and Objectives: Postoperative pancreatic fistula (POPF) contributes to significant morbidity and mortality after pancreaticoduodenectomy (PD). However, the underlying mechanisms of POPF remain unclear. This study is to explore the pathology in the pancreatic stump and elucidates the mechanisms of POPF following PD. Methods: Pathological analysis and 16S rRNA gene sequencing were performed on the specimens obtained from the two patients who accepted complete pancreatectomy for grade C POPF after PD. In addition, a retrospective radiological analysis was conducted on a cohort of 125 consecutive patients who underwent PD to evaluate the inflammatory response in the pancreatic stump. Results: The presence of gradient inflammation and acinar-duct metaplasia (ADM) in the pancreatic stumps is ubiquitous. The incidence of apoptosis is markedly reduced in the pancreatic stump. Moreover, a significant accumulation of neutrophil-dominated inflammatory cells is detected in the ductal system. Notably, the ADM-formed duct is the site where the neutrophils transmigrate through the ductal wall. Additionally, the microbial evidence indicates that gut microbes migrate from the digestive tract. Radiological analysis proves that a gradient of pancreatitis exists in all cases after PD and reaches peak on the fourth postoperative day. Conclusions: Inflammation and digestive reflux exist in the pancreatic stump after PD. The underlying mechanisms of POPF are the high biochemical activity of the pancreas, mechanical injury, and digestive reflux.