Adult ; Cord Blood Stem Cell Transplantation ; adverse effects ; Cytomegalovirus ; Cytomegalovirus Infections ; complications ; Female ; Hemolysis ; Humans

Objective:This study has two objectives. One is to detect the methylation status of reversion-inducing cysteine-rich protein with Kazal motifs (RECK, a new tumor suppressor gene) gene promoter in primary laryngeal squamous cell carcinoma and nor-mal laryngeal mucosa. The other is to analyze the correlation between RECK gene methylation status and radiosensitivity in laryngeal squamous cell carcinoma. Methods:Methylation-specific polymerase chain reaction was used to detect the RECK gene methylation of 70 specimens of laryngeal squamous cell carcinoma and 15 normal tissues of laryngeal mucosa. The patients underwent six cycles of ra-diotherapy and were followed-up for 5 years. The correlation between RECK gene methylation status and radiosensitivity in laryngeal squamous cell carcinoma was analyzed. Results: After six cycles of radiotherapy, 47 patients (67.14%) showed sensitivity and 23 (32.86%) showed tolerance to radiotherapy. The methylation level of the RECK gene was lower in the radiation-sensitive group than in the nonradiation-sensitive group (P<0.05). The methylation level of the RECK gene was lower in the remission group than in the non-remission group. RECK gene methylation could increase the risk of cancer by approximately 5.010 times (OR=5.010, 95%CI:1.616-15.533). Conclusion:RECK gene promoter methylation in human laryngeal squamous cell carcinoma is an early event that is correlated with the patient's sensitivity to radiotherapy. Thus, the patient's sensitivity to radiation can be predicted by detecting the meth-ylation status of the RECK gene promoter.

Aged ; Aged, 80 and over ; Atrial Fibrillation ; blood ; Biomarkers ; blood ; Female ; Humans ; Male ; Middle Aged ; Natriuretic Peptide, Brain ; blood

Actins ; metabolism ; Adenocarcinoma ; pathology ; Adult ; Diagnosis, Differential ; Endometriosis ; pathology ; Epithelium ; pathology ; Female ; Gastrointestinal Stromal Tumors ; pathology ; Hamartoma ; metabolism ; pathology ; Humans ; Muscle, Smooth ; pathology ; Stomach Diseases ; metabolism ; pathology

Acupuncture Points ; Acupuncture Therapy ; Adolescent ; Adult ; Ankle Injuries ; therapy ; Female ; Humans ; Male ; Sprains and Strains ; therapy ; Treatment Outcome ; Young Adult

Objective To study whether p38 mitogen-activated protein kinases (p38MAPK) signal pathway were activated in the process of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) which then induces rheumatoid arthritis (RA) fibroblast-like synoviocyte (FLS) to synthesize matrix metalloproteinase-1 (MMP-1) and look for the relative mechanisms of how TWEAK was involved in the destruction of articular bones and cartilage. Methods RA FLS were primarily cultured and stimulated with TWEAK. FLS were pretreated with SB203580 or not. ELISA was used to detect the concentration of MMP-1 in cell-cultured supernatant. Western blotting was used to detect the expression of p-p38MAPK and P65 in RA FLS. Results TWEAK (100 ng/ml) could induce RA FIS to synthesize MMP-1. SB203580 could partially inhibite the expression of MMP-1 producted by RA FLS which was induced by TWEAK. TWEAK could make p38MAPK phosphorylated and increase the expression of P65 protein in the cell nucleus. Conclusion TWEAK induces RA FLS to synthesize MMP-1. In this process, p38MAPK signal transduction pathway is activated and then induce the expression of NF-κB.

Objective:To analyze a novel antigenic determinant of Homo sapiens CMTM1-v17 protein and prepare polyclonal antibody.Methods:By means of DNA recombination method, the C-terminal(The coding sequences of 118-149 residues) of CMTM1-v17 gene was inserted into pGEX-4T-2 vector. The recombinant plasmid was transformed into E.coli XL-1 Blue to express the fusion protein of GST/CMTM1-v17. The GST tag of the purified fusion protein was removed by enzymatic cleavage with thrombin. The polyclonal anti-CMTM1-v17 antibody were prepared by immunizing rabbits with the purified protein. Highly-specific, polyclonal anti-CMTM1-v17 antibodies was purified by affinity chromatographic column matrix coupled with antigen. The specificity of the anti-CMTM1-v17 antibody was identified by Western blot and immunohistochemistry.Results:The polyclonal antibody showed specific response to CMTM1-v17 by Western blot analysis and immunohistochemistry. These results suggested that the polyclonal antibody can be used for further studies of CMTM1-v17 function.Conclusion:A polyclonal anti-CMTM1-v17 antibody has been synthesized successfully.

Objective To investigate the mechanism of the radiosensitivity effect of Cox-2 gene in esophageal cancer.Methods Cox-2 specific siRNA was constructed and transfected to EC9706 cells to downregulate intracellular Cox-2 expression.The expressions of MMP-2,Bcl-2 mRNA,AKT and phosphorylated AKT proteins were assayed after radiation.Colony formation,cell proliferation,apoptosis and cell invasion in vitro were examined as well.One-way ANOVA method was used to analyze the data.Results Affter 2 and 4 Gy irradiation,a significant increase in the mRNA expression of Bcl-2 was observed in the Cox-2 up-regulation group (F =3.36,4.32,P ＜ 0.05).In the group of Cox-2 downregulation,the expression of MMP-2 mRNA was significantly reduced(F =3.86,8.09,P ＜ 0.05).Affter irradiation,a significant decreaseof Bcl-2 mRNA (F =3.73,5.64,P ＜ 0.05) as well as an increase of Bax(F =7.03,7.42,P ＜ 0.05) was detected,and the levels of total and phosphorylated AKT proteins had the highest level in the Cox-2 upregulation group and had the lowest level in the Cox-2 downregulation group.In the Cox-2 downregulation group,the apoptosis induction obviously increased with dose (F =317.40,P ＜ 0.05),and the proportion of cells in Go-G1 phase gradually increased but the proportion of cells in S and G2-M phases decreased,concomitant with the obvious suppression of cell proliferation,in addition,cell invasion was decreased.Conclusions Downregulation of intracellular Cox-2 mRNA expression,concomitant with subsequent downregulation of MMP-2 and Bcl-2 and upregulation of Bax,resulted in reduction of the invasion and metastatic capabilities of tumor cells,and induction of Go-G1 phase arrest and apoptosis.Downregulation of AKT and phosphorylated AKT (pAKT) protein expression might also interfere with the capability of the PI3K/Akt signal transduction pathway to resist radiotherapy.

Objective To assess the tolerance of elderly patients with esophageal carcinoma to chemoradiotherapy through.Methods A retrospective analysis of 596 elderly patients with esophageal carcinoma receiving chemoradiotherapy was conducted.Patients were divided into radiachemotherapy group and radiotherapy group,and according to age,patients were divided into four age groups (aged 70-74,75-79,80 80 and 85years and over).The tolerance to treatment was assessed by Charlson index.Results 185 patients completed chemoradiotherapy,113 patients reduced the dose of chemotherapy (reduction group),81 patients unfinished chemoradiotherapy (unfinished CRT group),160 patients completed radical radiotherapy alone (unfinished RT group),and 57 patients incompleted radiotherapy.Further analysis found that the tolerance to treatment in reduction group had significant differences between patients aged ≥ 75 years and ＜ 75 years (x2 =6.815,P=0.009),and between WIC ≥ 1 and ＜ 1(x2 =10.636,P=0.001); the tolerance to treatment in unfinished CRT group had significantly differences between aged ≥ 80 years and ＜80 years (x2 =63.842,P=0.000),and between WIC =0,1 and ≥ 2 (x2 =21.153,P=0.000).Conclusions Further age re-grouping and WIC assessment is necessary before treating esophageal cancer patients.Reduction of therapy dosage is more beneficial for patients aged ≥ 75 years and WIC≥1,and greater caution is required in chemotherapy for patients aged ≥ 80 years and WIC＞1.