Objective To construct expression vectors of human ribosomal protein S 3(RPS3) and RPS3Ser209 mutant in orcler to investigate the effect of RPS3Ser209 mutant on NF-κB signaling pathway and DNA binding capacity .Methods The vector RPS3-myc was amplified by polymerase chain reaction ( PCR) from the human liver cDNA and subcloned into pcDNA-3.1myc-HisB.RPS3S209A represented mutant RPS3 expression vectors, in which the designated amino acid was mutated to an alanine residue .Dual luciferase reporter gene assay was used to detect the NF-κB transcription activity in HEK293 cells,immunofluorescence to detect RPS3 location, and EMSA to examine NF-κB DNA-binding activity.Results The expression vectors of RPS3-myc and RPS3S209A-myc were constructed.Compared with wild-type RPS3,the nucleus translocation, transactivation activity of NF-κB and DNA binding ability of RPS3S290A were reduced significantly .Conclu-sion The impact of RPS3 on NF-κB signaling pathway depend on its serine 209.

Objective Acute liver failure is one of the significant causes of death clinically.It is important to explore new serum markers of liver injury for early diagnosis and prognosis prediction of severe liver disease.Hepassocin ( HPS) is a liver-specific mitogenic growth factor.Our study is intended to investigate the correlation between HPS serum levels and the degree of liver injury.Methods Firstly, a mouse model of acute liver injury was constructed via intraperitoneally injection with different doses of CCl4 .Then the survival rate, alanine aminotransferase ( ALT) , aspartate aminotransferase ( AST) and the pathological changes in the liver were detected.Meanwhile, ELISA assay was performed to detect the serum level of HPS.In addition, the mRNA level and protein level of HPS were detected by real-time PCR and Western blotting, respectively.Results The mortality rate was increased and the liver damage was aggravated with the increase of the CCl4 dose.Besides, the ALT and AST levels were also increased in a dose-dependent manner.Additionally, the mRNA and protein levels of HPS were significantly up-regulated and closely related to the degree of the liver injury in the model. Conclusion HPS can be used as a new marker of liver injury in mice.

Objective To investigate the regulation of T cells in the process of liver regeneration using a model of mice after 70% liver resection.Methods We performed 70% hepatectomy in T-cell-deficient mice and control mice.The liver mass and body mass ratio, BrdU infiltration level, proliferating cell nuclear antigen (PCNA),expression of M phase marker protein p-HDAC3, and serum transaminase levels were measured.Results The recovery of liver mass and body mass ratio of thymus-deficient mice occurred significantly later than that of control mice.The peak time of BrdU infiltration levels and the expression of PCNA and p-HDAC3 in T-cell-deficient mice were later than in control mice, but the degree of liver injury was lower.Conclusion T cells are involved in the regulation of liver regeneration, and the absence of T cells delays the process of liver regeneration.

Objective To study the effect of E3 ubiquitin ligase RNF31 knockdown on nuclear factor-κB (NF-κB) pathway activation and cell apoptosis. Methods Human RNF31 siRNA sequences were cloned into the lentiviral vector pGreenPuro and transiently transfected in HEK293T cells to screen the most effective fragments, which were co-transfected along with the packaging plasmids PMD and SPA in 293T cells. The cell supernatant was collected at 24 h and 48 h after the transfection and the viral titers were determined with flow cytometry. Real-time PCR and Western blotting were used to evaluate the effect of RNF31 knockdown on the expression of NF-κB downstream target genes and IκBα activity; the changes of NF-κB pathway transcriptional activity were assessed with dual luciferase reporter gene. Hochest dying was used to examine the influence of RNF31 down-regulation on cell apoptosis. Results RNF31 knockdown mediated by the lentiviral vector pGreenPuro-RNF31 suppressed the transcriptional activity of NF-κB and the downstream target genes in HEK293 cells stimulated with TNF-α. RNF31 knockdown also resulted in suppression of NF-κB-stimulated expression of pIκBαand in increased apoptosis of cells stimulated with TNF-αfor 24 h. Conclusion RNF31 down-regulation inhibits NF-κB pathway activation induced by TNF-α.

Objective To study the effect of E3 ubiquitin ligase RNF31 knockdown on nuclear factor-κB (NF-κB) pathway activation and cell apoptosis. Methods Human RNF31 siRNA sequences were cloned into the lentiviral vector pGreenPuro and transiently transfected in HEK293T cells to screen the most effective fragments, which were co-transfected along with the packaging plasmids PMD and SPA in 293T cells. The cell supernatant was collected at 24 h and 48 h after the transfection and the viral titers were determined with flow cytometry. Real-time PCR and Western blotting were used to evaluate the effect of RNF31 knockdown on the expression of NF-κB downstream target genes and IκBα activity; the changes of NF-κB pathway transcriptional activity were assessed with dual luciferase reporter gene. Hochest dying was used to examine the influence of RNF31 down-regulation on cell apoptosis. Results RNF31 knockdown mediated by the lentiviral vector pGreenPuro-RNF31 suppressed the transcriptional activity of NF-κB and the downstream target genes in HEK293 cells stimulated with TNF-α. RNF31 knockdown also resulted in suppression of NF-κB-stimulated expression of pIκBαand in increased apoptosis of cells stimulated with TNF-αfor 24 h. Conclusion RNF31 down-regulation inhibits NF-κB pathway activation induced by TNF-α.

Objective To study the effectiveness of pain management on sleep quality of patients after total hip arthroplasty( THA ).Methods 80 patients with unilateral total hip replacement were recruited and equal randomly divided into experimental group and control group by Excel.Each patient completed the preoperative the Pittsburgh Sleep Quality Index (PSQI) scale and visual analogue scale (VAS) to evaluate the sleep quality and pain after THA.In experimental group,oral analgesics were administrated routinely at the preoperative 48th and 24th hour and after operation,if the postoperative pain scale was larger than 3 point,extra analgesic was used.In control group,no analgesic was used pre-operation,and postoperative oral analgesics were administrated according to the requirement of the patients.Pain scale and PSQI scale were recorded at the postoperative 24 hours in both groups.Results The VAS pain score and PSQI at the postoperative 24 hours in experimental group were both significant lower than control group [(2.13 ± 1.28) vs (4.90 ± 1.38 ),( 1.83 ±0.84) vs ( 5.55 ± 1.40 ),respectively],the difference was statistically significant ( t =5.286,7.674,respectively ;P ＜ 0.01 ).Conclusions Standardization pain management after total hip replacement can relieve the postoperative pain and improve sleep quality; it is benefit for the early rehabilitation of the patients.

OBJECTIVETo study the effect of E3 ubiquitin ligase RNF31 knockdown on nuclear factor-κB (NF-κB) pathway activation and cell apoptosis.

METHODSHuman RNF31 siRNA sequences were cloned into the lentiviral vector pGreenPuro and transiently transfected in HEK293T cells to screen the most effective fragments, which were co-transfected along with the packaging plasmids PMD and SPA in 293T cells. The cell supernatant was collected at 24 h and 48 h after the transfection and the viral titers were determined with flow cytometry. Real-time PCR and Western blotting were used to evaluate the effect of RNF31 knockdown on the expression of NF-κB downstream target genes and IκBα activity; the changes of NF-κB pathway transcriptional activity were assessed with dual luciferase reporter gene. Hochest dying was used to examine the influence of RNF31 down-regulation on cell apoptosis.

RESULTSRNF31 knockdown mediated by the lentiviral vector pGreenPuro-RNF31 suppressed the transcriptional activity of NF-κB and the downstream target genes in HEK293 cells stimulated with TNF-α. RNF31 knockdown also resulted in suppression of NF-κB-stimulated expression of pIκBα and in increased apoptosis of cells stimulated with TNF-α for 24 h.

CONCLUSIONRNF31 down-regulation inhibits NF-κB pathway activation induced by TNF-α.

Apoptosis ; Down-Regulation ; Gene Expression Regulation ; Genetic Vectors ; HEK293 Cells ; Humans ; I-kappa B Proteins ; metabolism ; Lentivirus ; NF-KappaB Inhibitor alpha ; NF-kappa B ; metabolism ; RNA, Small Interfering ; Real-Time Polymerase Chain Reaction ; Signal Transduction ; Transfection ; Tumor Necrosis Factor-alpha ; pharmacology ; Ubiquitin-Protein Ligases ; genetics ; metabolism

OBJECTIVETo explore the effect and mechanism of ginsenoside Rg3 (Shenyi Capsule) on the postoperative life span of patients with non-small cell lung cancer (NSCLC).

METHODSThe prospective, randomized, controlled method was adopted. One hundred and thirty-three patients with NSCLC were randomly assigned to 3 groups: Shenyi Capsule group (43 cases), combined therapy group (Shenyi Capsule plus chemotherapy, 46 cases), and chemotherapy group (44 cases). The survival rates, immune function and the correlation between vascular endothelial growth factor (VEGF) expression and clinical effect were analyzed in the three groups.

RESULTS(1) The 1-year survival rate in the Shenyi group, the combined group and the chemotherapy group was 76.7% (33/43), 82.6% (38/46), and 79.5% (35/44), respectively; the 2-year survival rate was 67.4% (29/43), 71.7% (33/46), and 70.5% (31/44), respectively; and the 3-year survival rate was 46.5% (20/43), 54.3% (25/46), and 47.7% (21/44), respectively. There was no significant difference among the 3 groups (P>0.05). (2) NK cells were increased to different degrees and the ratio of CD4/CD8 was normal in the Shenyi Capsule group and the combined group, while the ratio of CD4/CD8 was disproportional in the chemotherapy group. (3) In the chemotherapy group, the 3-year survival rate was lower in patients with positive expression of VEGF than in patients with negative expression (37.0% vs 64.7%, chi2=17.9, P<0.01), but no signifi cant statistical difference was shown in the other two groups (53.6% vs 55.6%, P>0.05; 44.4% vs 50.0%, P>0.05).

CONCLUSIONShenyi Capsule, especially in combination with chemotherapy, can improve the life span of patients with NSCLC after operation. The mechanism might be correlated with improving the immune function and anti-tumor angiogenesis

Adult ; Aged ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; immunology ; mortality ; Female ; Ginsenosides ; adverse effects ; pharmacology ; therapeutic use ; Humans ; Lung Neoplasms ; drug therapy ; immunology ; mortality ; Male ; Middle Aged ; Prospective Studies ; Survival Rate ; Vascular Endothelial Growth Factor A ; analysis

Objective To compare the efficacy and safety of oxcarba-zepine and carbamazepine for primary trigeminal neuralgia management.Methods Cochrane library, PubMed, Medline, CBMdisc, CNKI and Wanfang Data were searched to collect the randomized controlled studies that compared the efficacy and safety of oxcarbazepine and carbamazepine in treating primary trigeminal neuralgia.Reference list of each primary study was hand -searched.Two reviewers independently screened the literatures, extracted data, assessed risks of bias and then did cross -checking.RevMan 5.2 software was used for Meta -analysis.Results Eighteen studies ( 1465 participants ) were included.Results of Meta -analysis showed that oxcarbazepine was more effective than carbama-zepine [RR=1.09,95%CI (1.02,1.16), P<0.05].Comparisons of VAS before and after 2 and 4 weeks of treatment were not significantly different between two groups , while comparisons of VAS before and after the 8weeks of treatment favored oxcarbazepine.Oxcarbazepine was asso-ciated with a lower incidence of adverse drug reaction than carbamazepine [RR=0.50,95%CI(0.39,0.63),P<0.001].The influence of repor-ting bias is small.Conclusion Compared with carbamazepine , oxcarba-zepine is not inferior in efficacy but superior in safety in treating primary trigeminal neuralgia.

BACKGROUNDCan single-agent maintenance therapy be considered as an ideal strategy for non-small cell lung cancer (NSCLC) treatment to achieve prolonged survival and tolerated toxicity? A systematic review and meta-analysis was performed to elucidate this issue.

METHODSThe electronic databases were searched for RCTs comparing single-agent maintenance therapy with placebo, best support care or observation. The required data for estimation of response, survival and toxicity were extracted from the publications and the combined data were calculated.

RESULTSEleven RCTs involving 3686 patients were identified. We found a statistically significant higher probability of tumor response for patients with maintenance therapy versus control patients (OR: 2.80, 95%CI: 2.15 - 3.64). Patients receiving maintenance therapy had significantly longer progression-free survival (PFS) (HR: 0.67, 95%CI: 0.62 - 0.71) and overall survival (OS) (HR: 0.84, 95%CI: 0.78 - 0.90). However, maintenance therapy was associated with more severe toxicities (OR: 6.45, 95%CI: 4.61 - 9.01).

CONCLUSIONIn patients with advanced NSCLC, the use of single-agent maintenance therapy is associated with higher response rate and significantly prolongs PFS and OS despite of the risk of additional toxicity.

Antineoplastic Agents ; adverse effects ; therapeutic use ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; mortality ; Disease-Free Survival ; Humans ; Lung Neoplasms ; drug therapy ; mortality ; Publication Bias