Objective:To compare the efficacy and safety between WangShiBaoChiWan and mosapride in the treatment of functional dyspepsia (FD).Methods:From September 2019 to September 2020, patients with postprandial fullness and early satiation who met the Rome Ⅳ criteria for FD diagnosis were enrolled from 15 hospitals, including the First Affiliated Hospital of Naval Medical University (Shanghai Changhai Hospital), Beijing Traditional Chinese Medicine Hospital Affiliated to Capital Medical College. The subjects were randomly divided into WangShiBaoChiWan (experimental) group and mosapride (control) group in the ratio of 1∶1. The treatment regimens were WangShiBaoChiWan+ mosapride simulator, WangShiBaoChiWan simulator+ mosapride, respectively with a treatment period of 2 weeks. The primary efficacy outcome was the improvement rates of main symptoms before and after treatment, the secondary efficacy primary efficacy outcome was the total clinical effective rate and the change of the single symptom score. And the safety indicator included adverse events. Independent sample t-test, paired t-test and chi-square test were used for statistical analysis. Results:A total of 251 FD patients were enrolled in the full analysis set, including 124 in the experimental group and 127 in the control group; 241 FD patients were in the per-protocol analysis set, including 117 in the experimental group and 124 in the control group. The analysis of per-protocol analysis set showed that the improvement rates of the main symptoms of the experimental group and the control group were (66±29)% and (60±30)%, respectively, and the difference was not statistically significant ( P>0.05). The improvement rate of the main symptoms of the experimental group reached 117% of that of the control group, which exceeded the expected non-inferiority standard of 80%. The total clinical effective rates of the experimental group and the control group were 76.07% (89/117) and 75.81% (94/124), respectively, and the difference was not statistically significant ( P>0.05). The results of full analysis set showed that the incidence of adverse events of the experimental group and the control group was 1.62% (2/124) and 1.57% (2/127), respectively, and the difference was not statistically significant ( P>0.05). There were no serious adverse events in the two groups. Conclusion:The improvement rate of the main symptoms of WangShiBaoChiWan is not inferior to that of mosapride in the treatment of FD, and it has good safety.

ObjectiveTo explore the differences of cognitive function in patients with treatment-resistant depression and drug-naive first-episode major depressive disorder， and to examine the relationship between severity of clinical symptoms and cognitive function， so as to provide references for prognosis improvement. MethodsFrom November 2016 to December 2019， 119 patients with drug-naive first-episode major depressive disorder and 82 patients with treatment-resistant depression in a hospital in Guangzhou were enrolled， meantime， another 71 healthy individuals recruited from the community were set as healthy control group. Clinical symptoms were assessed using Hamilton Depression Scale-17 item （HAMD-17） and Hamilton Anxiety Scale （HAMA）. Cognitive domains， including speed of processing， working memory， verbal learning and memory， and visual learning and memory were measured with the MATRICS Consensus Cognitive Battery （MCCB）. Multiple covariance analysis was used to compare the differences in cognitive function among three groups. Thereafter， partial correlation analysis was performed within patient groups to explore the relationship of HAMD-17/HAMA score with the four dimensions of MCCB. ResultsThe speed of processing， visual learning and memory scores of treatment-resistant depression group and drug-naive first-episode depression group were lower than those of healthy control group， and the working memory score of the treatment-resistant depression group was lower than that of the healthy control group， with statistical significance （P<0.05 or 0.01）. The speed of processing， visual learning and memory scores of treatment-resistant depression group were significantly lower than those of drug-naive first-episode depression group （P<0.05 or 0.01）. Partial correlation analysis within patient groups found that HAMD-17/HAMA total score had no correlation with the four dimensions of MCCB （P>0.05）. ConclusionCompared with drug-naive first-episode major depressive disorder patients and healthy controls， the impairments of speed of processing， visual learning and memory are more severe in patients with treatment-resistant depression. Moreover， the cognitive function impairment in patients with drug-naive first-episode major depressive disorder and treatment-resistant depression has no correlation with the severity of depressive and anxious symptoms.

Objective: To preliminary, explore the effect of small intestinal epithelial dendritic cells on the occurrence and development of nonalcoholic fatty liver disease in mice. Methods: Thirty-two (half male and half female) 4-week-old C57BL/6 mice were randomly divided into two groups. The mice were fed with normal diet (SD group) and high-fat diet (HFD group). Eight mice (half male and half female) were randomly killed from each group over the 14 and 20-weeks feeding period to observe their body weight, liver and small-intestine wet weight. Alanine aminotransferase, aspartate aminotransferase, blood glucose, high-density lipoprotein, low-density lipoprotein, total cholesterol and triglyceride were determined by eyeball blood samples. Pathological diagnosis and alcoholic fatty liver disease activity score were collected. The number of mice small intestinal dendritic cells was observed under a microscope. Statistical analysis was performed to compare two groups of independent samples with homogeneity test of variance, t test, and covariance analysis. Results: The body weight, liver wet weight, serum alanine aminotransferase and aspartate aminotransferase of mice in HFD group were significantly higher than those of control group at 20 weeks (P < 0.05), and the serum high density lipoprotein of mice in HFD group was significantly higher than that of SD group at 14 weeks (P < 0.05). At 14th weeks, the liver tissue of mice in HFD group had early pathological manifestations of hepatitis (fatty degeneration, punctate necrosis and balloon-like degeneration). Of which 87.5% (7/8) of them were diagnosed as non-alcoholic steatohepatitis or non-alcoholic fatty liver disease, while only a few mice in SD group had early pathological manifestations of hepatitis. At 20th weeks, all mice in HFD group were diagnosed with non-alcoholic steatohepatitis or non-alcoholic fatty liver disease, while none of the mice in SD group was diagnosed with non-alcoholic fatty liver disease. At both time points, the percentage of small intestinal dendritic cells in HFD group was significantly higher than that in SD group (14 weeks: 4.181 ± 4.314 vs. 15.099 ± 10.349; 20 weeks: 9.615 ± 8.267 vs. 32.839 ± 24.475, both P < 0.05). Statistical analysis combined with the alcoholic fatty liver disease activity score showed that there was no linear correlation between the two groups (regression coefficient was 20.196%). Conclusion The number and different staging of small intestinal dendritic cells in mice is associated with the occurrence and development of NAFLD.

Objective To investigate the expression and significance of myeloid cell leukemia-1 (Mcl-1 )gene and protein in Hepatocellular Carcinoma(HCC).Methods The expression of Mcl-1 was detected respectively by Reverse Transcription-Polymerase Chain Reaction (RT-PCR),Western blot and ENVISION immunohistochemistry in 20 HCC specimens,19 liver cirrhosis(LC)specimens,and 12 control ones.Their relationship with clinical and pathological characteristics of HCC was investigated.Results The expression of Mcl-1 mRNA in the control group,LC group and HCC group was 0.52±0.17, 3.46±1.7,3.65±2.93,respectively.The level in HCC and LC group was statistically different compared with the control group,respectively (t=7.925,5.334,P<0.05).The relative expression of Mcl-1 protein in LC group (0.51±0.35)and HCC group (0.75±0.36)were significantly higher than that in the control group (0.21±0.19)(t=5.526,6.355,P<0.05).The positive expression rate of Mcl-1 in HCC group was 55.00% (11/20),significantly higher than that in the con-trol group 33.33% (4/12)(t=7.835,P<0.05).The positive expression of Mcl-1 was related to tumor necrosis and TNM staging (χ2=4.201,P<0.05).Conclusion Mcl-1 gene and protein are differentially expressed in HCC,LC and the control, which may be involved in the occurrence,development and malignant transformation of HCC.

Background:Secondary lymphoid tissue chemokine( SLC)is involved in lymphoid homing and anti-tumor immune response,and has a chemotactic effect on intestinal lymphocytes. Several animal studies have shown that SLC is involved in the occurrence and development of ulcerative colitis( UC). Aims:To investigate the expression and significance of SLC in UC. Methods:Forty active UC patients from Dec. 2010 to Dec. 2012 at Affiliated Hospital of Nantong University were enrolled,and 20 healthy volunteers were served as controls. Expression of SLC in the colon mucosa was detected by immunohistochemistry,and its relationship with severity of UC was analyzed. Results:SLC was positively expressed in all UC patients,while was negatively or weakly positively expressed in controls. Expression of SLC in UC patients was significantly higher than that in controls(4. 16 ± 0. 78 vs. 0. 52 ± 0. 11,P<0. 05). Expression of SLC was correlated with the severity of involvement of UC. Conclusions:Expression of SLC participates in development and progress of UC. SLC may play an important role in the induction of local damage and pathological changes of UC.

Objective To investigate the expression of galectin-3 in pancreatic cancer cell and its effect on the proliferation and invasion of SW1990.Methods Immunocytochemistry and semi-quantitative RT-PCR was used to detect the expression of galectin-3 protein and mRNA in SW1990,PANC1 and ASPC-1 cell lines.Galectin-3 mono-antibody of different concentrations ( 1,2,3,5 μg/ml) was used to treat SW1990 cells for 24,48,72 h,CCK-8 kits were used to detect the proliferation in SW1990 cells; Transwell chamber was used to study the invasion in SW1990.Results Expression of galectin-3 protein and mRNA was present in SW1990,PANC1,and ASPC-1.Galectin 3 mono-antibody inhibited the proliferation and number of invasive cells in a dose and time dependant manner.The inhibitory rates at 72 h were 19.8％,29.9％ and 42.7％ in 2,3,5 μg/ml galectin 3 mono-antibody groups,the difference among them and control group was statistically significant ( P ＜ 0.05 ).The inhibite rate of permeating membrane cells in 3 μg/ml galectin-3 mono antibody was 37.1％,the difference between this group and control group was statistically significant (P ＜0.05 ).ConcLusions Galectin-3 is highly expressed in pancreatic cancer cells.Galectin-3 antibody can inhibit the proliferation and migration capability of SW1990 cells.

Objective To investigate the dynamic expressions of CXCL11 and its role in the pathogenesis of acute necrotizing pancreatitis (ANP).Methods Forty-eight SD rats were randomly divided into control group and ANP group,with 24 rats in each group.ANP model was induced by retrograde injection of 4％ sodium taurocholate (1 ml/kg body weight) into the biliary and pancreatic duct.The rats were sacrificed at 1,3,6,12 hours.Serum level of amylase was determined,pathological changes in pancreatic tissue were routinely observed and scored.The expression of CXCL11 mRNA and proteon in pancreas was measured by fluorescence quantitative polymerase chain reaction and immunohistochemical method.The serum levels of CXCL11 were measured by enzyme-linked immunoadsorbent assay.Results The serum levels of amylase in ANP rats were significantly higher than those in control group [(6153 ± 355)U/L vs (185 ± 32)U/L at 6 h,P ＜0.05],pathological changes in pancreatre tisues were more significant in ANP rats,and the pathological score was significantly higher than that in control group [(9.00 ± 0.63) vs (0.33 ± 0.12) points at 6 h,P ＜ 0.05] ; the expressions of CXCL11 mRNA and protein in pancreatic tissue were significantly increased than those in control group (3.13 ± 0.43 vs 0.99 ± 0.24,2.76 ± 0.27 vs 0.33 ± 0.12 at 6 h,P ＜ 0.05).The serum level of CXCL11 was significantly higher than that in control group [(112.1 ± 14.2)ng/L vs (56.8 ±4.3) ng/L at 6 h,P ＜0.05)].Conclusions CXCL11 is an early inflammatory mediator in acute pancreatitis,and involved in the pathogenesis of ANP in rats.

Objective To investigate the relationship between expression of nuclear factor kappa B p65 ( NF-κB p65) and hippocampal neuronal apoptosis in acute necrotizing pancreatitis (ANP) rats with brain injury. Methods Sixty-four SD rats were randomized into normal saline group (NS) and ANP group. The ANP rat model was induced by retrograde injection of 4% sodium taurocholate into the pancreaticobiliary duct of SD rats. Nissle stain was used to detect the brain injury. Neuronal apoptosis was determined by TUNEL.NF-κB p65 expression was detected by immunohistochemistry and RT-PCR. Results Hippocampal neuron was absent, karyopyknosis, unclear nucleolus and decreased Nissl bodies were found, the injuries was aggravated with time. The apoptosis index at the 3, 6 and 12 h in ANP group was 10.63 ±0.24, 21.02±0.25, 17.12±0.36, respectively, while they were 0.33±0.19,0.71±0.67, 0.45 ± 0. 33 in NS group, and the difference was statistically significant ( P ＜ 0. 01 ). The expressions of NF-κB p65 mRNA were 0. 63 ± 0.05,1.05 ±0.06,0.92 ±0.05, which were significantly higher than those in the NS group (0.11 ±0.01,0.12±0.01,0.08±0.01,P＜0.05).The chatge of expression of NF±κB p65 protein was consistent with that of NF-κB p65 mRNA. Conclusions The brain injury of ANP rats was highly correlated with neuronal apoptosis at the early and middle phase of ANP, and its mechanism may be related with NF-κB p65 activation.

Objective To investigate the effects of two inhibitors of arachidonic acid metabolic pathway (5-cyclooxygenase blockade MK886 and COX 2 blockade celecoxib) on growth and VEGF mRNA expression of human pancreatic cancer cell SW1990.MethodsPancreatic cancer cells SW1990 were cultured with different concentrations of MK886,celecoxib,MK886 and celecoxib,then the cell proliferation was detected by using CCK-8,BLT1 mRNA,PGE2 mRNA and VEGF mRNA expressions were determined by RTPCR.ResultsAfter 10 μmol/L MK886 or 20 mmol/L celecoxib treatment for 24 h,the growth of SW1990 was greatly suppressed ( 1.80 ±0.06 vs 1.65 ±0.10,2.04 ±0.03 vs 1.86 ±0.02,P ＜0.01 ),and the growth suppression of SW1990 cells was increased accompanying the raised concentration of MK886 or celecoxib.After both MK886 and celecoxib treatment for 12 h,the growth of SW 1990 cells was much obviously suppressed (1.72 ±0.05 vs 1.52 ±0.05,P ＜0.01 ).After celecoxib treatment for 48 h,the BLT1 mRNA,PGE2 mRNA and VEGFmRNA expressions were not significantly changed,but the expressions of PGE2 mRNA were significantly decreased ( P ＜ 0.05 ).After MK886 or MK886 + celecoxib treatment,the expressions of BLT1 mRNA,VEGF mRNA were significantly decreased ( P ＜ 0.05 ),but the expressions of PGE2 mRNA were not significantly changed when compared to control group.ConclusionsTwo metabolic pathways of arachidonic acid have a close relation with occurrence and proliferation of pancreatic cancer,when both of the pathways were blocked,the proliferation of the pancreatic cancer cell was suppressed obviously.

ObjectiveTo describe the novel variants of the Smqnr family of quinolone resistance genes and their distribution in clinical isolates of Stenotrophomonas maltophilia, and investigate the relationship between Smqnr and quinolone resistance. MethodsThe identification of 442 strains of Stenotrophomonas maltophilia were performed by VITEK automated identification and susceptibility. Minimum inhibitoryconcentrationsof tigecycline,chloramphenicol,ceftazidime,compoundsulfamethoxazole,ticarcillin/clavulanic acid, levofloxacin and moxifloxacin against Stenotrophomonas maltophilia were detected by standard agar dilution method. Full length of Smqnr gene was amplified by polymerase chain reaction (PCR) and sequenced. DNAMAN software was used to compare the sequence divergence and construct the genealogical tree to analyze the phylogenetic relationships of Smqnr family. Results Stenotrophomonas maltophilia was resistant to the 7 kinds of clinical antibiotics in various extent ( from 5％ to 50％ ). Levofloxacin showed s good antibacterial activity with the resistance rate of 6. 11％ (27/442), nevertheless the best was moxifloxacin with the resistance rate of 5. 88％ (25/442). Smqnr gene was detected in 114 of 442 strains of Stenotrophomonas maltophilia[25.79％ (114/442)], including 11 known genes and 20 novel variants of the Smqnr genes ( Smqnr28-47 ) which was caused by several genes mutation changing the translation of 219 amino acids. The gene detection rate of resistant, intermediate and sensitive strains was 42. 30％ (11/26), 34. 37％ (11/32) and 23.95％ (92/384), respectively. The Smqnr gene harbored the highest detection rote (37. 78％ ) in the sensitive strains of Stenotrophomonas maltophilia with minimal inhibitory concentration of 0. 125 μg/ml. Conclusions The gene coding region of Smqnr is highly polymorphic and the novel variants of Smqnr gene are caused by several genes mutation changing the translation of 219 amino acids. Smqnr gene in Stenotrophomonas maltophilia has a high detection rate and different distribution.