Objective:To investigate the expression of human epidermal growth factor receptor 4 (HER4) and metastasis-related protein (MMP-9) in human esophageal carcinoma tissues, and their relationship with clinicopathological features of the disease. Methods:Immunohistochemical Envision technique was applied to detect the expressions of HER4 and MMP-9 in 45 specimens of esophageal carcinoma tissues, paracancerous tissues and normal tissues. Statistical method was used to analyze the association of the positivity of HER4 with clinical pathological index and MMP-9 expression.Results:The positive rates of HER4 expression were 73.3%, 33.3%, and 2.2% in 45 specimens of esophageal carcinoma tissues, paracancerous tissues, and normal tissues, respectively. The expression of HER4 was correlated with TNM stage and lymph node metastasis (P<0.01), but not correlated with histological grade (P>0.05). The expression of MMP-9 correlated with T stage, invasion depth, TNM stage, and lymph node metastasis (P<0.05). Conclusion:The expression of HER4 is apparently different in esophageal carcinoma tissues, paracancerous tissues, and normal tissues. Its positive expression in esophageal carcinoma tissues is correlated with TNM stage and lymph node metastasis. The expression of MMP-9 in esophageal carcinoma tissues is correlated with the T stage, TNM staging, and lymph node metastasis. The positive expression of HER4 in esophageal carcinoma tissues is associated with the expressions of MMP-9.

Objective RNA interference refers to post-transcriptional gene silencing caused by double strands RNA.To investigate the effect of EGFR receptor on esophageal carcinoma,the expression vector of HER4 gene targeted small interfering RNA was constructed to observe its silencing effect in human esophageal carcinoma cell line Eca-109,in order to find a promising method for the gene therapy of this disease.Methods Two complementary oligo DNA strands targeting HER4 gene were designed and synthesized according to the principles of designing siRNA.After annealing,oligo DNAs were inserted into SUPER.neo+gfp vector,then enzyme digestion analysis and DNA sequencing were applied.After transfecting it into human esophageal carcinoma cell line,we detected the level of expression of HER4 gene through real-time quantitative PCR and Western Blot.Results The enzyme digestion analysis and DNA sequencing show that HER4 gene targeted small interfering RNA and its expression vector were constructed successfully,and after transfection,the expression of HER4 gene in esophageal carcinoma cell line was suppressed greatly.Conclusion HER4 gene targeted small interfering RNA and its expression vector were constructed successfully,and could decrease the expression of HER4 gene in Eca-109 cell line,which laid the foundation for the following experiment.

OBJECTIVETo study the effect of length of cervical anterior fusion on adjacent levels by Biomechanical test.

METHODSSix fresh-frozen human cervical specimens were used in this study. The specimens were tested in flexion, extension, bending and rotation on a spine 3D test system. The specimens were tested intact and then underwent a single-level anterior cervical discectomy and fusion (ACDF) at the C4-5 first, a double-level fusion at the C4-6, and finally extended to triple-level at the C4-7, Based on a hybrid test method. Changes in overall range of motion (ROM), segmental motion and facet joints pressure during flexion, extension, bending and rotation were measured and statistically analyzed.

RESULTSThe overall ROM of the entire spinal construct decreased progressively as the single-level fixation extending to 2-level and 3-level (P < 0.05). A progressive increase in ROM above (C3-4) the fused motion segment units (MSUs) was found during flexion, extension and bending (P < 0.05). In bending and extension, a same result was recorded on the average pressure and max pressure of C3-4 facet joints (P < 0.05).

CONCLUSIONSThis study has demonstrated that the biomechanics at adjacent levels to a cervical spine fusion are altered and that there was progressively increased adjacent segment motion and stress as a single-level ACDF extended to a 3-level fusion, which might lead to the acceleration of adjacent segment degeneration.

Biomechanical Phenomena ; Cadaver ; Cervical Vertebrae ; surgery ; Diskectomy ; methods ; Humans ; Range of Motion, Articular ; Rotation ; Spinal Fusion ; methods

Objective To investigate the mechanism of tea polyphenols(TP)for regulating NLRP3 inflammasomes and alleviating acute lung injury in septic mice.Methods Sixty C57BL/6 mice were randomly assigned into sham-operated,cecal ligation and puncture(CLP)and CLP+TP treatment groups,and survival of the mice was recorded after modeling in each group.The lung wet/dry weight ratio and myeloperoxidase(MPO)activity were determined,and lung injury of the mice was evaluated using HE staining and acute lung injury score.The expressions of IL-1β,TNF-α,IL-6,NLRP3,caspase-1 p10,ASC,MPO,and caspase-8 in the lung tissue were detected using ELISA,Western blotting,or immunohistochemical staining.MDA and H2O2 levels in the lungs were detected to evaluate the level of oxidative stress.Immunofluorescence assay was used to investigate the co-localization of NLRP3 and NOX4.Results The postoperative mortality rate at 72 h,lung wet/dry weight ratio,MPO level and acute lung injury scores were significantly lower in CLP+TP group than in CLP group(P<0.05).Treatment with TP significantly reduced the expressions of NLRP3-related inflammatory factors(P<0.05)and lowered MDA and H2O2 levels in the lung tissue of the septic mice(P<0.05).Immunofluorescence co-staining showed a lower level of NOX4 and NLRP3 co-localization in CLP+TP group than in CLP group.Conclusion TP inhibits NLRP3 inflammasome-associated inflammation to alleviate CLP-induced acute lung injury in mice through a regulatory mechanism that inhibits NOX4 expression and reduces oxidative stress in the lung tissue.

Objective To investigate the mechanism of tea polyphenols(TP)for regulating NLRP3 inflammasomes and alleviating acute lung injury in septic mice.Methods Sixty C57BL/6 mice were randomly assigned into sham-operated,cecal ligation and puncture(CLP)and CLP+TP treatment groups,and survival of the mice was recorded after modeling in each group.The lung wet/dry weight ratio and myeloperoxidase(MPO)activity were determined,and lung injury of the mice was evaluated using HE staining and acute lung injury score.The expressions of IL-1β,TNF-α,IL-6,NLRP3,caspase-1 p10,ASC,MPO,and caspase-8 in the lung tissue were detected using ELISA,Western blotting,or immunohistochemical staining.MDA and H2O2 levels in the lungs were detected to evaluate the level of oxidative stress.Immunofluorescence assay was used to investigate the co-localization of NLRP3 and NOX4.Results The postoperative mortality rate at 72 h,lung wet/dry weight ratio,MPO level and acute lung injury scores were significantly lower in CLP+TP group than in CLP group(P<0.05).Treatment with TP significantly reduced the expressions of NLRP3-related inflammatory factors(P<0.05)and lowered MDA and H2O2 levels in the lung tissue of the septic mice(P<0.05).Immunofluorescence co-staining showed a lower level of NOX4 and NLRP3 co-localization in CLP+TP group than in CLP group.Conclusion TP inhibits NLRP3 inflammasome-associated inflammation to alleviate CLP-induced acute lung injury in mice through a regulatory mechanism that inhibits NOX4 expression and reduces oxidative stress in the lung tissue.