ObjectiveTo investigate the role of local pancreatectomy for benign and low-grade malignant pancreatic tumors.MethodThe clinical data of 45 patients with benign and low-grade malignant pancreatic tumors who underwent local pancreatectomy from January 2014 to June 2019 in Union Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology were analyzed.ResultsForty-five patients underwent the local enucleation or resection with negative margin. The pathological results showed that there were 17 cases of solid pseudopapilloma, 5 cases of mucinous cystadenoma, 4 cases of serous cystadenoma, 10 cases of islet cell tumor, 5 cases of nonfunctional neuroendocrine tumor, 4 cases of congenital cyst. There were 6 cases of head of pancreas, 26 cases of body of pancreas, 8 cases of tail of pancreas, 5 cases of uncinate process. The tumor was 1.2 to 9.0 cm in diameter with an average of 3.2 cm. Among them, the diameter was more than 5.0 cm in 9 cases. The incidence of pancreatic fistula after operation was 57.8%, 65.4% was grade A fistula, 34.6% was grade B fistula, and no grade C fistula occurred. The incidence of abdominal infection was 13.3%, incidence of abdominal hemorrhage was 6.7%. There was no secondary diabetes mellitus and pancreatic endo- and exocrine dysfunction, and no death case.ConclusionsPancreatic enucleation for benign and low-grade malignant pancreatic tumors after strict preoperative evaluation can effectively preserve the pancreatic endocrine function of patients. Although the incidence of pancreatic fistula is high, it is mostly biochemical fistula, and the incidence of serious complications is low.
ObjectiveTo understand the molecular mechanism of ferroptosis and its research progress and future prospects in pancreatic cancer. MethodThe relevant literature on the molecular mechanism of ferroptosis and its basic and clinical application in the occurrence and development of pancreatic cancer was retrievaled and reviewed. ResultsFerroptosis was a non-apoptotic form of cell death that depended on iron aggregation, and its molecular biological features included iron ion overload, reactive oxygen species accumulation, lipid peroxidation, and so on. Ferroptosis was closely related to cell metabolism, and the imbalance of ferroptosis caused by abnormal metabolism also existed during the tumorigenesis and progression of pancreatic cancer, which in turn triggered the abnormal proliferation of pancreatic cancer cells and leaded to their progression. By regulating the key molecular signaling pathways of ferroptosis, it was expected to find new drug targets and therapeutic pathways for pancreatic cancer treatment. The results of ferroptosis-related studies so far had shown the potential for future translational research in the field of pancreatic cancer treatment. ConclusionsThe mechanism of ferroptosis is of great value in pancreatic cancer research. At present, there are still many uncharted areas in the study of ferroptosis, and the molecular mechanisms involved are still poorly understood. In the future, as the study of ferroptosis continues, it is expected to provide new ideas for pancreatic cancer treatment and discover new targets for drug development.
ObjectiveTo conclude the current status and research progress on the pathological mechanism, development and management of pancreatic cancer-associated diseases and provide evidence for intervention of such diseases.MethodThe relevant literatures were reviewed, and the research progress on pancreatic cancer-associated diseases were summarized.ResultsThere are many types of pancreatic cancer-associated diseases, and common diseases included pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasm, mucinous cystic neoplasm, diabetes, and chronic pancreatitis. Although management and following-up about this kind of diseases remain controversial, the basic consensus has been reached.ConclusionAdequate follow-up is required for patients with pancreatic cancer-associated disease, individualized interventions should be taken if necessary.
Objective To observe the expression of GdCl3 on Toll-like receptors （TLRs） of RAW264.7 from murine macrophage cell line induced by lipopolysaccharide (LPS) stimulation. Methods Cells were divided into 3 groups: blank group, LPS group and GdCl3 group. And these cells dyed by goat anti-mouse TLR2/4 poly-antibody and anti-goat IgG labelled with fluorescein isothiocyanate (FITC). The synthesis of TLR2/4 protein were determined by flow cytometry (FCM) analysis and reverse transcription polymerase chain reaction (RT-PCR) analyzed their gene expression. Cell supernatants were taken to measure TNF-α production following the ELISA (enzyme-linked immunosorbent assay) protocol. Results The expressions of TLR2/4 protein and mRNA in GdCl3 group under action of different concentration of GdCl3〔TLR2/4 protein, 200 μmol/L: (70.2±1.28）％/(66.7±2.59)％, 400 μmol/L: (64.9±1.43)％/(60.4±1.25)％, 2 000 μmol/L: (47.4±0.98)％/(32.1±0.74)％; TLR2/4 mRNA (the value of absorbance), 200 μmol/L: (76.42±2.76)/(101.72±3.14), 400 μmol/L: (75.60±3.76)/(89.65±5.17), 2 000 μmol/L: (64.22±4.67)/(78.44±4.88)〕 were significantly lower than those of in LPS group 〔TLR2/4 protein: (94.4±1.76)％/(95.7±0.87)％, P＜0.01; TLR2/4 mRNA: (127.64±3.25)/(119.82±5.59), P＜0.05, P＜0.01〕. The expression of TNF-α in GdCl3 group under action of different concentration of GdCl3〔200 μmol/L: (2 540±77) pg/ml, 400 μmol/L: (2 041±106) pg/ml, 2 000 μmol/L: (1 020±220) pg/ml〕 was also significantly lower that that of in LPS group 〔(4 688±127) pg/ml, P＜0.01)〕. Conclusion GdCl3 significantly inhibits TLR expression and secretion of TNF-α under the condition of LPS stimulation in vivo.
【Abstract】Objective To observe the synthesis of TLR2 protein and its mRNA expression in Kupffer cells (KCs) and sinusoidal endothelial cells(SECs).Methods Thirty-two BALB/c mice divided into two groups (operation group and false operation group) were used to prepare the model of partial hepatic ischemia/reperfusion (I/R) injury. After injury KCs and SECs were isolated with twosteps situ perfusion technique. And these cells were dyed by rat anti-mouse TLR2 IgG and anti-rat IgG2b labeled with flurescein isothiocyanate (FITC). The sysnthesis of TLR2 protein were determined by flow cytometric (FCM) analysis and real time reverse transcription polymerase chain reaction (Real-Time RT-PCR) analysis for gene expression.Results As for KCs: TLR2 expression was significant higher in operation group, compared with false operation group 〔protein expression: （9.19±1.07）% vs （1.52±0.21）%, P＜0.01; gene expression: 0.54±0.77 vs 2.62±2.19, P＜0.05〕. But there were no significant differences with expression in SECs. Conclusion Synthesis of TLR2 protein and its gene expression increased in KCs in the mouse partial hepatic ischemia-reperfusion injury.