ObjectiveTo explore the therapeutic effect of Xuebijing injection （XBJ） on severe acute pancreatitis induced acute lung injury （SAP-ALI） by regulating formyl peptide receptors （FPRs）/nucleotide-binding oligomerization domain-like receptor 3 （NLRP3） inflammatory pathway. MethodsSixty rats were randomly divided into a sham group， a SAP-ALI model group， low-， medium-， and high-dose XBJ groups （4， 8， and 12 mL·kg^-1）， and a positive drug （BOC2， 0.2 mg·kg^-1） group. For the sham group， the pancreas of rats was only gently flipped after laparotomy， and then the abdomen was closed， while for the remaining five groups， SAP-ALI rat models were established by retrograde injection of 5% sodium taurocholate （Na-Tc） via the biliopancreatic duct. XBJ and BOC2 were administered via intraperitoneal injection once daily for 3 d prior to modeling and 0.5 h after modeling. Blood was collected from the abdominal aorta 6 h after the completion of modeling， and the expression of interleukin （IL）-1β， IL-6， and tumor necrosis factor-α （TNF-α） in plasma was measured by enzyme-linked immunosorbent assay （ELISA）. The amount of ascites was measured， and the dry-wet weight ratios of pancreatic and lung tissue were determined. Pancreatic and lung tissue was taken for hematoxylin-eosin （HE） staining to observe pathological changes and then scored. The protein expression levels of FPR1， FPR2， and NLRP3 in lung tissue were detected by the immunohistochemical method. Western blot was used to detect the expression of FPR1， FPR2， and NLRP3 in lung tissue. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of FPR1， FPR2， and NLRP3 in lung tissue. ResultsCompared with the sham group， the SAP-ALI model group showed significantly decreased dry-wet weight ratio of lung tissue （P<0.01）， serious pathological changes of lung tissue， a significantly increased pathological score （P<0.01）， and significantly increased protein and mRNA expression levels of FPR1， FPR2， and NLRP3 in lung tissue （P<0.01）. After BOC2 intervention， the above detection indicators were significantly reversed （P<0.01）. After treatment with XBJ， the groups of different XBJ doses achieved results consistent with BOC2 intervention. ConclusionXBJ can effectively improve the inflammatory response of the lungs in SAP-ALI rats and reduce damage. The mechanism may be related to inhibiting the expression of FPRs and NLRP3 in lung tissue， which thereby reduces IL-1β and simultaneously antagonize the release of inflammatory factors IL-6 and TNF-α.

Objective: To investigate the effects and mechanisms of Xuebijing injection (XBJ) on Chimeric antigen receptor-T (CAR-T) cell function and its therapeutic potential against CAR-T therapy-associated cytokine storms (CRS). Methods: Anti-CD19 CAR-T cells were established based on FMC63 antibodies. Different doses of XBJ (1 and 10 mg/mL) were added to the culture system. Untreated anti-CD19 CAR-T cells served as negative controls. After 48-h co-culture, the effects of XBJ on CAR-T cell function were assessed. Carboxyfluorescein diacetate succinimidyl ester staining was used to assess the effect of XBJ on CAR-T cell proliferation. Flow cytometry, luciferase reporter gene assays, and real time cellular analysis were employed to evaluate the effects of XBJ on CAR-T cell cytotoxicity in vitro. RNA-sequencing was performed to analyze the effects of XBJ on CAR-T cell gene expression. Network pharmacology predicted potential XBJ therapeutic targets for CRS, which were verified in a THP-1 macrophage inflammation model. Results: XBJ enhanced both the proliferation and tumor killing capacities of CAR-T cells. Transcriptome analysis showed that XBJ treatment affects multiple genes and pathways in CAR-T cells, with differential gene enrichment in multiple cell proliferation and growth factor pathways. Potential targets for CRS control by XBJ were predicted using network pharmacology, and the inhibitory effect of XBJ on the expression of relevant genes was verified using a macrophage model. Conclusion The results of this study indicate that XBJ can enhance the killing effect of CAR-T cells on tumor cells and that the mechanism is related to the regulation of T cell proliferation and activation. Moreover, XBJ inhibited excessive inflammation associated with CAR-T therapy. However, the current findings remain to be further validated through in vivo experiments.

Objective To investigate the effect of MRE11 on the proliferation and apoptosis of esophageal squamous cancer cells and its molecular mechanism. Methods MRE11 expression was downregulated by MRE11 siRNA transfection in esophageal squamous cancer cells. The AKT agonist SC79 (0, 0.1, 0.5, 1, 1.5, 1.8, 2 μg/ml) were used to treat cells with MRE11 inhibition for 24 h. Overexpression vector pcDNA.3.1-c-myc was constructed and co-transfected cells with MRE11 siRNA. Western blot method was used to detect the protein expressions of MRE11, p-AKT and c-myc in esophageal squamous cancer cells Ec9706 and TE-1. The Annexin-V FITC/PI kit was used to detect the apoptosis of Ec9706 and TE-1 cells; the activity of caspase-3 was detected by the Caspase-3 activity detection kit; the proliferation of Ec9706 and TE-1 cells was tested by the BrdU method. Results The protein expressions of MRE11 in Ec9706 and TE-1 cells were significantly increased, compared with human esophageal epithelial Het-1A cells. After MRE11 siRNA transfection, AKT phosphorylation and the protein expressions of MRE11 and c-myc were significantly decreased in esophageal squamous cancer cells. MRE11 inhibition significantly promoted the apoptosis and caspase-3 activity in Ec9706 and TE-1 cells, while inhibited the proliferation of Ec9706 and TE-1 cells. SC79 (1.5, 1.8 and 2 μg/ml) significantly increased AKT phosphorylation in MRE11-suppressed esophageal squamous cancer cells, and reversed the inhibitory effects of MRE11 inhibition on c-myc protein expression and cell proliferation and the promoting effect on cell apoptosis. Overexpression of c-myc inhibited the inhibitory effect of MRE11 down-regulation on cell proliferation and the promotion on caspase-3 activity. Conclusion MRE11 inhibition could effectively inhibit the proliferation of esophageal squamous cancer cells and promote cell apoptosis by regulating AKT and c-myc.

Objective: To evaluate the expression of leucine zipper tumor suppressor 2 (LZTS2) in human breast cancer tissues and cell lines, and to investigate the effects and mechanisms of LZTS2 over-expression on proliferation, invasion and epithelial-mesenchymal transition (EMT) of breast cancer cells. Methods: Fifty pairs of cancerous tissues and para-cancerous tissues resected from breast cancer patients in Department of Breast Surgery of Kaifeng Central Hospital from January, 2016 to December, 2016, as well as breast cancer cell lines (MCF-7, MDA-MB-231, MDA-MB-468) and normal mammary epithelial HBL-100 cells were collected for this study; and Real-time quantitative PCR (qPCR) and Western blotting were used to determine the mRNA and protein expressions of LZTS2 in collected tissues and cell lines. MCF-7 cells were transfected with pcDNA-LZTS2 or pcDNA3.1 (negative control) using lipofectamineTM 2000, and the protein expression of LZTS2 at 49-72 h after transfection was measured by Western blotting; Then, the effects of LZTS2 over-expression on proliferation, migration and invasion of MCF-7 cells were detected by MTT assay and Transwell assay, respectively; Furthermore, Western blotting was performed to detect the expressions of EMT associated proteins (Cyclin D1, Vimentin, Ncadherin, E-cadherin) and PI3K/AKT signaling pathways-related molecules. Results: The mRNA and protein expressions of LZTS2 were down-regulated in breast cancerous tissues and cell lines (MCF-7, MDA-MB-468 and MDA-MB-231) as compared with paired para-cancerous tissues or normal mammary epithelial HBL-100 cells (P<0.05 or P<0.01). Compared with and blank control or pcDNA3.1 group, the protein expression of LZTS2 in MCF-7 cells of pcDNA-LZTS2 group significantly increased (P<0.01), while the proliferation, migration and invasion of MCF-7 cells significantly reduced (P<0.05 or P<0.01). In addition, forced expression of LZTS2 significantly down-regulated the protein expressions of Cyclin D1, Vimentin and N-cadherin (P<0.05 or P<0.01) but up-regulated the expression of E-cadherin in MCF-7 cells (P<0.01), indicating LZTS2 over-expression suppressed PI3K / AKT signaling pathway through inhibiting the expression p-PI3K and p-AKT. Conclusion: The findings collectively demonstrated that the expression of LZTS2 was decreased in breast cancer, and over-expression of LZTS2 efficiently inhibited the proliferation, migration and invasion of breast cancer cells, which might be related with the suppression of PI3K/AKT signaling pathway involved in EMT.

Objective To understand the effect of teacher training to provide reference for teachers' teaching methods in the standardization of clinical resident training.Method The teachers carried out five days of teacher training.Teacher training adopted the method of theory teaching and group discussion.The main content of the training had a "daily rounds with teaching","the proper use of ORIME evaluation","feedback of sandwich type","a minute tutor teaching method","SOAP method to report cases".Before the training,100 residents were randomly selected to evaluate the teaching in teaching teachers through self-designed questionnaire.After the training,the questionnaire survey was conducted among 100 residents again.All data were statistically analyzed by SPSS 22.0.The measurement data were represented by (mean or + standard deviation),and the date were compared by t test.Results Residents believed that after the teacher training,teachers' teaching level improved (P＜0.05).The three aspects of "general and phased learning goals","training students' clinical thinking ability through questions","requiring students to report cases and give guidance and feedback" were the most obvious.The pre training score was (3.28 ± 0.92) (3.31 ± 1.12) (3.55 ± 0.85),and the corresponding score was after training (3.98 ±0.85) (4.19 ± 0.85) (4.11 ± 0.74).Conclusion From the comparison of the survey results before and after the residents,the teachers' teaching modes,skills and methods have been improved after receiving teachers' training.

Objective To explore the prevalence and clinical significance of metabolic disorder of lipids, glucose and uric acid at different fibrosis stages of patients with chronic hepatitis B (CHB).Methods From January 2006 to December 2014, 1 812 CHB patients in Department of Infectious Diseases, Shunde Hospital of Southern Medical University were retrospectively enrolled and analyzed.All biochemistry indexes were obtained by automatic biochemical instrument.Polymerase chain reaction was used for detecting serum hepatitis B virus (HBV) DNA, and particles immune detection kit was used for detecting hepatitis B e antigen (HBeAg).In statistical analyses, chi-square test, nonparametric test and Logistic analysis were used.Results The metabolic disorder prevalence in 1 812 CHB patients was as follows, 455 cases (25.1%) with decreased high density lipoprotein, 435 cases (24.0%) with increased uric acid, 342 cases (18.9%) with increased total cholesterol, 254 cases (14.0%) with increased triglyceride, 171 cases (9.4%) with decreased apolipoprotein A, 165 cases (9.1%) with increased apolipoprotein B, 162 cases (8.9%) with increased low density lipoprotein and 117 cases (6.5%) increased fasting blood glucose.Patients who had mild liver fibrosis tended to have metabolic disorders of uric acid (26.4%), total cholesterol (22.8%) and high density lipoprotein cholesterol (20.5%).Patients who had moderate liver fibrosis tended to have metabolic disorders of high density lipoprotein (27.2%) and uric acid (20.9%).Patients who had severe liver fibrosis tended to have metabolic disorders of high density lipoprotein (33.6%) and uric acid (22.2%).Multivariate Logistic regression analysis showed that inflammation activty (OR=17.31, 95% CI: 13.410-22.336, P=0.001), age (OR=1.019, 95%CI:1.005-1.035, P=0.010), sex (OR=1.497, 95% CI: 1.061-2.111, P=0.022), apolipoprotein A (OR=0.50, 95% CI: 0.281-0.892, P=0.019) and HBV DNA (OR=0.904, 95% CI: 0.858-0.952, P=0.001) may be independent predictors of moderate and severe liver fibrosis.Conclusions CHB patients with mild liver fibrosis tend to have metabolic disorders of uric acid, total cholesterol and high density lipoprotein cholesterol;patients with moderate liver fibrosis tend to have metabolic disorders of high density lipoprotein and uric acid;and patients with severe liver fibrosis tend to have metabolic disorders of high density lipoprotein and uric acid.

Objective To study the clinical and pathological features of hepatic steatosis in patients with chronic hepatitis B (CHB)based on a matched case-control study.Methods Cross-sectional study was carried out on CHB patients who received liver biopsy in the Department of Infectious Diseases, Shunde First People′s Hospital from January 2006 to December 2014.Clinical data of the patients were collected.A total of 216 matched pairs were created according to gender and age.The clinical and pathological feathers of both groups were compared and analyzed. Quantitative data with normal distribution were compared by t test and those with abnormal distribution were compared by nonparametric rank sum test of two- or multi-independent samples. Categorical data were compared by χ2 test. Results In matched pairs,rates of overweight/obesity were 84.2% in fatty liver group and 18.5 % in non-fatty liver group (χ2 =189.30,P =0.001 ),patients with high cholesterol in the two groups were 30.6% and 13.4%,respectively (χ2 =18.47,P =0.001 ),high triglycerides were 27.3% and 9.7%, respectively (χ2 =22.15 ,P =0.001),high low-density lipoprotein were 16.7% and 5 .6%,respectively (χ2 =13.50,P =0.001),high uric acid were 31 .0% and 15 .3%,respectively (χ2 =15 .04,P =0.001 ) and rates of alcohol history were 38.9% and 25 .9%,respectively (χ2 =8.08,P =0.001).The differences of hepatitis B virus (HBV)DNA and status of hepatitis B e antigen between the two groups were not statistically significant (both P >0.05 ).Compared to fatty liver group,rates of hepatic inflammation activity degree ≥ 3 (54.6% vs 37.5 %,χ2 = 12.75 ,P <0.01 )and fibrosis staging ≥ 3 (53.2% vs 41 .7%,χ2 =5 .80,P =0.016)in non-fatty liver group were both significantly higher.Conclusions CHB patients with overweight/obesity,high cholesterol,high triglycerides,high low-density lipoprotein,high uric acid and drinking history are more likely to develop hepatic steatosis.The inflammatory grade and fibrosis stage in non-fatty liver group are more serious than those in fatty liver group.

ObjectiveTo investigate the influencing factors for hepatocyte steatosis in patients with chronic hepatitis B (CHB) and the high-risk population by classification tree model analysis, and to establish a simple method to assess the risk of hepatocyte steatosis in CHB patients. MethodsThe clinical data and pathological results of the CHB patients who underwent liver biopsy in Department of Infectious Diseases, The First People's Hospital of Shunde, from January 2006 and December 2014 were collected. The classification tree model was applied to analyze the influencing factors for hepatocyte steatosis, and index value curve, misclassification matrix, and error of estimation were applied for overall evaluation of classification results of the classification tree model. ResultsThe influencing factors for hepatocyte steatosis in CHB patients were body mass index (BMI), total cholesterol, and low-density lipoprotein, and the most important factor was BMI. This classification tree model had a sensitivity of 84.3%, a specificity of 81.5%, an accuracy of 82.9%, and an error of estimation of 0.171, suggesting that this model was well fitted. ConclusionClassification tree model analysis shows that the pathogenesis of hepatocyte steatosis in CHB patients is closely related to the influencing factors BMI, total cholesterol, and low-density lipoprotein. A simple classification method is established based on these factors to evaluate the risk of hepatocyte steatosis in CHB patients. It is necessary to conduct further clinical studies to investigate the clinical value of this method.

Objective To investigate the treatment values of precise target delineation of chest MRI for lung cancer Methods From August 2011 to February 2015 , 45 non-small cell lung cancer patients were given chest CT scans and MRI scans before radiotherapy , and then active target tumor delineation , then related influencing factors were analyzed. Results All patients completed CT scans and MRI positioning. For patients that it was difficult to identify lung tissue lesions caused by lung cancer through CT , their MRI imaging showed high signal and the boundaries between the tumor and surrounding normal tissue became relatively clear. Meanwhile , 20 patients of borders were diagnosed by CT , while 25 by MRI; 36 patients with lymph node metastasis were diagnosed by CT while 40 by MRI. The difference was statistically significant (P<0.05). Univariate logistic regression analysis showed that pathological type and atelectasis were the influence factors for CT and MRI tumor target delineation differences (P<0.05), and multivariate logistic regression analysis showed the atelectasis was the main factor (P<0.05). Conclusion Compared with CT, breast MRI can precisely delineate target to improve the accuracy of target localization before radiotherapy. It can help determine lymph node metastasis and avoid the impact of atelectasis then ensure the accuracy of radiotherapy.

ObjectiveTo assess the efficacy and safety of Xuebijing injection for the treatment of severe acute pancreatitis (SAP).Methods An extensive search of related literatures from the Cochrane Library, EMBASE, China Biology Medicine (CBM), CNKI, VIP and Wanfang data up to March 2014 was performed. Randomized controlled trials (RCTs) regarding Xuebijing injection for the treatment of SAP were collected regardless of languages. Jadad scale was taken for quality evaluation of the included studies by two researchers. The patients in control group were given conventional treatment, and those of the Xuebijing group were given Xuebijing injection on the top of conventional treatment. The Cochrane Collaboration RevMan 5.2 software was used for data analysis regarding the effect of Xuebijing injection on the mortality, incidence of complication, effective rate, the length of stay in hospital, and the safety of the drug in patients with SAP.Results A total of 15 published reports meeting the inclusion criteria were enrolled. The methodological quality of the trials was low. Meta analysis showed that the mortality in Xuebijing group was significantly lower [odds ratio (OR) = 0.37, 95% confidence interval (95%CI) =0.17 - 0.77,P = 0.008], and the incidence of complication was also significantly decreased (OR = 0.26, 95%CI =0.14 - 0.45,P< 0.000 01) as compared with those of control group. The effective rate in Xuebijing group was significantly higher than that of the control group [relative risk (RR) = 0.85, 95%CI = 0.80-0.91,P< 0.000 01]. The length of stay in hospital in Xuebijing group was significantly shorter than that of the control group [mean difference (MD) = -5.28, 95%CI = -6.69 to -3.86,P< 0.000 01]. Adverse reactions of Xuebijing injection were reported in 2 studies. The adverse reaction in one study was headache and nausea, which were relieved by adjusting the speed of intravenous infusion, and mild rash was reported in another case, and it disappeared after the withdrawal of Xuebijing. Conclusions The currently available evidence shows that Xuebijing injection may have some therapeutic effect on SAP. Because of the low methodological quality of the included trials, multi-center and high-quality RCTs with large sample sizes are needed to provide stronger evidence.