Objective To investigate the effect of intravenous omega-3 fish oil on the prognosis of patients with sepsis. Methods 1733 patients with sepsis were selected from the Department of Critical Care Medicine of Shenzhen People's Hospital from December 1, 2016 to June 30, 2019. According to the survival situation, these patients were divided into survival group(n=1351) and death group (n=382). The general information, infection site, complications, organ support measures and clinical outcomes were analyzed and compared between the two groups. Multivariate logistic regression and Kaplan-Meier survival analysis were performed to evaluate the effect of intravenous supplementation of omega-3 fish oil on the prognosis of patients with sepsis. Results There were significant differences in gender, age, pulmonary infection, abdominal infection, blood infection,complication, mechanical ventilation, renal replacement therapy and omega-3 fish oil intervention between survival group and death group (P<0.05). There was no significant difference in the proportion of biliary tract infection, urinary tract infection and other site infections between the two groups (P>0.05). Logistic regression analysis showed that men, old age, bloodstream infection,mechanical ventilation support, and renal replacement therapy were risk factors for the survival status of patients with sepsis within 90 days, and intravenous omega-3 fish oil supplementation was a protective factor for sepsis. Survival analysis results show that intravenous supplementation of omega-3 fish oil can improve the 90-day survival rate of patients with sepsis. Conclusion Omega-3 fish oil intervention can improve the prognosis of patients with sepsis, and the clinical application feasibility is high.

Healthy skeletal muscle has a certain capacity for regeneration. Muscle regenerative response mainly rely on the action of myogenic stem cells, other structures of muscle tissue are reconstructed with the support of vascular and neural networks.However, endogenous self-regeneration is severely impaired in large muscle injuries or under pathological condition. Consequently,tissue engineering approaches are a promising means to regenerate skeletal muscle. The latest domestic and international research progress of tissue engineering technology in repairing skeletal muscle injury has been reviewed in present paper.

The pathological mechanism of celiac disease is not completely clear, and environmental factors may trigger the occurrence of intestinal inflammatory response in genetic susceptible individuals. Recent researches indicated that, due to the coordinated action of multiple factors such as abnormal intestinal mucosal barrier function and intestinal microbial changes, the homeostasis of intestinal environment is imbalanced, which aggravates the severity of the disease. Gluten-free diet combined with probiotics and other drugs would regulate intestinal microbiota and be conducive to resume intestinal mucosal barrier function,thereafter effectively alleviate the clinical symptoms of patients. However, both the composition of intestinal flora and its role in pathogenesis of the disease needs further consideration. To explore the pathological mechanism of celiac disease and targeted treatment for those factors will become a new perspective for precise prevention and treatment of celiac disease.

Neutrophil extracellular trap (NETs) is a kind of DNA-based skeleton released by neutrophils to the outside of the cell, in which a variety of granular proteins, proteolytic enzymes, antibacterial peptides, and other network structures are embedded.In recent years, studies have confirmed that NETs are highly expressed in a variety of tumors, and tumor microenvironment (TME)is a special environment for tumor cell survival and development, including cellular and non-cellular components. This article mainly explains that TME can stimulate the formation of NETs, and NETs can also promote tumor proliferation, invasion and metastasis by affecting tumor cells, immune cells, endothelial cells, epithelial cells, fibroblasts and extracellular matrix in TME. Finally, the clinical application prospects of NETs as tumor markers and potential therapeutic targets are discussed.

Bone stress injuries (BSI) is the most common musculoskeletal injuries in military training injuries, including stress injuries of different degrees of bone microstructure (grade Ⅰ to Ⅲ) and end-stage stress fractures (grade Ⅳ). It related to factors such as the gender of the injured and the patients, endocrine hormones in the body, calcium content, body mass index, and lower extremity mechanical structure. It has the characteristics of hidden onset and easy to be ignored in the early stage, which lead to non-combat attrition and sharp increase in treatment expenditures. In this review, risk factors, diagnosis, treatment and prevention protocols for the BSI are concluded and discussed in detail by systematically reviewing these latest literatures published worldwide,which has been aimed at improving the early diagnosis of BSI and providing the theoretical basis for the establishment of "all-round BSI prevention and treatment system".

Pancreatic cancer is one of the malignant tumors of digestive system with high malignancy and poor prognosis,so is called the "king of cancer" since resulting in an extremely high mortality rate. The death cases account for more than 90% of new cases in 2020, and there is still a lack of better treatments for pancreatic cancer. Chimeric antigen receptor T cell (CAR-T)immunotherapy has achieved great success in hematological malignancies, with an overall remission rate reached more than 80%. At present, five CAR-T products have been approved by the US FDA for listing, which marks a new era of anti-cancer road. In recent years, many scientists have focused their attention on CAR-T therapy to treatment of pancreatic cancer and have made good progress.The recent progress was summarized in present article of CAR-T therapy in treatment of pancreatic cancer including the selection of CAR-T targets, existed early clinical research, safety assessment, existed problems and challenges, etc., aiming to provide new ideas for pancreatic cancer immunotherapy.

Objective To investigate the effects of cathepsin B (CTSB) down-regulation on pyroptosis of lung tissue in mice with sepsis-induced acute lung injury. Methods Thirty SPF healthy male C57BL/6 mice were randomly divided into three groups: sham group (n=6), sepsis group (n=15), and sepsis plus CTSB inhibitor CA-074 group (sepsis+CA-074 group, n=9).Sepsis was induced by cecal ligation and puncture (CLP). Except for cecal ligation and perforation, other operations in the sham group were the same as those in sepsis group. 10 mg/kg CA-074 was intraperitoneally injected in sepsis+CA-074 group at 15 min after CLP. The mice were sacrificed 24 h after CLP. Bronchoalveolar lavage fluid (BALF) was collected for measurement of the white blood cell count and IL-18 and IL-1β concentrations with ELISA. Lung tissues were obtained for the determination of lung injury score, wet/dry lung weight ratio, the expressions of caveolin-1, MCPIP1, CTSB, caspase-1, and GSDMD mRNA (by RT-PCR), as well as the protein expressions of CTSB, caspase-1, and GSDMD (by Western blotting). Results The mice in sham group were normal throughout the observation period, and the 24 h survival rate after the operation was 100.0%. The sepsis mice showed obvious symptoms such as piloerection, dilatory, anorexia, and apathy, and these symptoms were improved in sepsis+CA-074 group.The 24 h survival rate after surgery in the two groups was 40.0% and 66.7%, respectively. Compared with sham group, the count of leukocytes and the expression of IL-18 and IL-1β in BALF were significantly increased, the wet/dry lung weight ratio and lung injury score were increased, the expression of caveolin-1 mRNA was up-regulated, the expression of MCPIP1 mRNA was down-regulated, and the expressions of CTSB, caspase-1, and GSDMD were up-regulated in the sepsis group (P<0.05). Compared with sepsis group, the count of leukocytes and the expressions of inflammatory factors were decreased, the wet/dry lung weight ratio and lung injury score were decreased, the expression of caveolin-1 mRNA was down-regulated, the expression of MCPIP1 mRNA was up-regulated, proteins associated with pyroptosis were significantly decreased, and the protein expression of CTSB was decreased in sepsis+CA-074 group (P<0.05). However, there was no significant change in the parameter of CTSB mRNA between the sepsis and sepsis+CA-074 groups (P=0.973). Conclusion Increased CTSB expression occurs in lung tissue with sepsis-induced acute lung injury, and inhibition of CTSB may alleviate sepsis-induced acute lung injury by suppressing pyroptosis.

Objective To observe the effect and significance of TRIM33 gene on proliferation and migration of human gastric cancer cell SGC-7901. Methods The expression of TRIM33 in normal gastric mucosa and gastric cancer tissues and its relationship with clinicopathological features and prognosis were analyzed through TCGA and TIMER databases. Human gastric cancer cell line SGC-7901 was either untreated [negative control (NC) group] or transfected with a control vector (vector group) or transfected with vector carries si-TRIM33 (si-TRIM33 group). The downregulation of TRIM33 was validated using Western blotting.Further, the CCK-8 assay and plate clone formation assay were performed to detect cell proliferation ability. The scratch healing assay and Transwell assay were employed to test cell proliferation and migration ability. The expression of epithelial-mesenchymal transition (EMT) related proteins was tested by Western blotting. The correlation between TRIM33 expression and immune cell infiltration was analyzed through the TIMER database. Results The expression level of TRIM33 in gastric cancer was significantly higher than that in normal tissues, related to age, gender, tumor stage and lymph node metastasis (P<0.05). Cell experiment showed that SGC-7901 cells with low expression of TRIM33 showed enhanced migration, decreased EMT-related protein E-Cadherin, and significantly increased vimentin and N-Cadherin (P<0.05). TIMER database analysis showed that TRIM33 mRNA level positively correlated with the expression of CD4⁺ T cells, CD8⁺ T cells, B cells, centrioles, macrophages and natural killer cells (P<0.05), and positively correlated with M2 macrophages, CD8⁺ T cells, centrioles and gene markers of natural killer cells CD163, CXCL9, ITGAM, KIR3DL2 expression (P<0.05). Conclusion Downregulation of TRIM33 can promote the progression of gastric cancer, which is related to the poor prognosis of patients. The mechanism may be related to enhancing the migration characteristics of gastric cancer cells by regulating the infiltration of immune cells.

Objective To investigate the interventional effect of anwulignan on pulmonary fibrosis and the underlying mechanism. Methods Sixty-five male ICR mice were randomly divided into control group, bleomycin (BLM) model group, anwuzhisu low dose group (1 mg/kg), anwuzhisu high dose group (4 mg/kg) and N-acetylcysteine group (150 mg/kg), with 13 mice in each group. Mouse pulmonary fibrosis model was induced by intratracheal perfusion of 5 mg/kg BLM. The serum and lung tissues were collected, and the pathological changes of lung tissues were observed by HE staining and Masson trichrome staining; serum oxidative stress index and hydroxyproline (HYP) content in lung tissue were measured by kit; the expression level of iron death pathway related genes was detected by Western blotting and qRT-PCR. Take the logarithmic growth phase HFL-1 cells, (1) set the control group and anwuzhisu administration group (0.3125, 0.625, 1.25, 2.5, 5, 10, 20,40, 80 μmol/L), and CCK-8 method was used to detect the toxic effect of anwuzhi on HFL-1 cells. (2) Set the control group, transforming growth factor (TGF)-β₁ model group, anwuzhisu low dose group (5 μmol/L) and anwuzhisu high dose group(10 μmol/L), with TGF-β₁ induced pulmonary fibrosis cell model. The oxidative stress index and reactive oxygen species(ROS) level were measured by kit; the expression level of iron death pathway related genes was detected by Western blotting and qRT-PCR. Results HE staining, Masson trichrome staining and the increase of HYP content indicated that the BLM-induced pulmonary fibrosis model was successfully constructed, and the pulmonary fibrosis phenotype was significantly improved after the administration of anwulignan. CCK-8 assay showed that the concentration of anwulignan <20 μmol/L had no significant effect on the proliferation activity of HFL-1 cells (P>0.05). Compared with model group, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and the levels of glutathione (GSH) in lung tissues of mice and HFL-1 cells were significantly increased after the administration of anwulignan, while the levels of malondialdehyde(MDA) were significantly decreased (P<0.01 or P<0.001). Compared with TGF-β₁ model group, 10 μmol/L anwulignan could decrease the level of ROS in HFL-1 cells (P<0.01). Western blotting and qRT-PCR results showed that anwulignan could significantly up-regulate the expressions of ferroptosis pathway related genes in lung tissues of mice and HFL-1 cells including glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11) and transferrin (TF), and significantly down-regulate the expression of transferrin receptor 1 (TFR1) (P<0.05, P<0.01 or P<0.001). Conclusion Anwulignan can improve pulmonary fibrosis by inhibiting oxidative stress and ferroptosis, laying a foundation for the development of clinical drugs for pulmonary fibrosis.

Objective To identify the clinicopathologic factors influencing the prognosis of the patients with distal cholangiocarcinoma (dCCA) after radical pancreatoduodenectomy (PD). Methods Retrospectively analyze the clinical data of 231 dCCA post-PD cases in Peking University First Hospital from January 2005 to January 2015. The clinicopathologic parameters were analyzed using univariate and multivariate Cox regression models and Kaplan-Meier method. Results The 1-year, 3-year and 5-year survival rates of the 231 post-PD dCCA patients were 86.6%, 55.0% and 34.6% respectively. Univariate Cox regression analysis showed that the primary tumor invasion depth (T stage) (P=0.000), lymph node metastasis (N stage) (P=0.001), AJCC stage(P=0.000), total number of dissected lymph nodes (P=0.038), metastasis lymph node ratio (P=0.001), vascular tumor thrombus(P=0.001), nerve invasion (P=0.001) and pathological type (P=0.002) were related to the prognosis of patients with dCCA after PD. Multivariate Cox regression analysis showed that the higher degree of lymph node metastasis (P=0.001), total number of lymph nodes dissected ≤10 (P=0.029), positive vascular tumor thrombus (P=0.007), positive nerve invasion (P=0.001) and low differentiation of pathological type (P=0.029) were independent risk factors for poor prognosis of patients with dCCA after PD.Kaplan-Meier analysis showed that the degree of lymph node metastasis, total number of dissected lymph nodes, vascular tumor thrombus, nerve invasion, and pathological type could affect the overall survival (OS) of patients with dCCA after pD (P<0.005), but whether adjuvant chemotherapy or not had no significant effect on OS of positive lymph node metastasis patients with dCCA after PD (P>0.05). Conclusion The higher degree of lymph node metastasis, total number of lymph nodes dissected less than 10, vascular tumor thrombus, nerve invasion and low differentiation of pathological type are considered as the independent poor prognostic factors of post-PD dCCA patients.