Objective To investigate the association of glyoxalase Ⅰ (GLO1) gene polymorphisms with susceptibility to atherosclerotic cerebral infarction (ACI).Methods Single nucleotide polymorphisms (SNPs) rs1130534 and rs1049346 in the GLO1 gene were genotyped in 300 ACI patients and 300 healthy controls using the SNaPshot technique.Additionally,quantitative real-time PCR was employed to determine the GLO1 expression levels in 50 ACI patients and 50 healthy controls,respectively.Results In terms of the rs1049346 polymorphism,the respective frequencies of CC,CT and TT genotypes were 9.3％,42.7％ and 48.0％ in the ACI patients,and 14.0％,47.7％ and 38.3％ in the control group.The respective frequencies of C and T alleles were 30.7％ and 69.3％ in the ACI patients,and 37.8％ and 62.2％ in the control group.There were statistically significant differences in the genotype and allele frequencies of rs1049346 between the ACI patients and controls (genotype:x2 =6.877,P =0.032;allele:x2 =6.842,P=0.009).For rs1130534,the respective frequencies of AA,AT and TT genotypes were 52.0％,42.0％ and 6.0％ in the ACI patients,and 60.0％,33.7％ and 6.3％ in the control group.The respective frequencies of A and T alleles were 73.0％ and 27.0％ in the ACI patients,and 76.8％ and 23.2％ in the control group.However,no statistically significant differences were found in the distribution of genotypes or alleles of the rs1130534 SNP between the ACI patients and controls (all P ＞ 0.05).The results of haplotype analysis revealed that the frequencies of the A-T and T-T (rs1130534-rs1049346) haplotypes in the ACI patients were all significantly higher compared to the controls (42.3％ vs 39.0％,x2 =4.733,P =0.030;27.0％ vs 23.2％,x2 =5.699,P =0.017).Additionally,the GLO1 expression levels in the ACI patients were significantly lower than that in the healthy controls (Mann-Whitney U =911.5,P =0.020).Conclusion The results indicate that the rs1049346 polymorphism of GLO1 gene is associated with the susceptibility to ACI.

The FRAX (Fracture Risk Assessment Tool) calculator is an application of different clinical risk factors to predict the absolute risk of fracture.It is the model based on a series of data of evidence-based medical researches on fracture risk factors.FRAX is limited by a number of factors.However,it is a major achievement in terms of our understanding and measuring fracture risk.

Objective To evaluate the effect of chest backplate in treating multiple rib fractures in patients with focal abnormal breathing.Methods The clinical data of 36 patients with multiple rib fractures and focal abnormal breathing who were treated by Chrisofix chest backplate were analyzed.Results Thirtyfour patients were cured by chest backplate and other conservative treatments,and 2 patients underwent rib internal fixation surgery.The numeric rating scales scores before and after the application of the chest backplate were (8.1 ± 0.7) scores and (5.2 ± 0.5) scores respectively(P ＜ 0.01).Seven patients had skin blisters forming around the shield,which were cured by liquid extraction with a syringe and gauze covered with povidone iodine.No patients stopped treatment because of allergy.Conclusions Chest backplate is an effective,easy and inexpensive method for patient with multiple rib fractures and focal abnormal breathing who doesn't need exploratory thoracotomy.It is worthy to spread in clinical treatment.

Objective To investigate the value of ionic-contrast esophagogram in diagnosis of intrathoracic anastomotic leakage after oesophagectomy.Methods The data of 728 patients suffered esophagectomy were retrospectively collected.723 patients without clinical manifestations of anastomotic leakage were divided into group A(esophagogram before eating,n=465) and group B(non-esophagogram before eating,n=258).The incidence of anastomotic leakage was compared between the two groups.Results The discovery rates of anastomotic leakage in group A and B were 0.43%(2/465) and 0.78%(2/258),respectively,the difference was no statistically significant between the two group(P=0.55).The total incidence rates of anastomotic leakage in group A and B were 0.65%(3/465) and 0.78%(2/258),respectively,the difference was no statistically significant between the two groups(P=0.84).5 patients with clinically suspected anastomotic leakage,all had loculated pleural effusion,4 cases had fever,and 2 cases had abnormal chest drainage.Finally,4 cases(80%) were confirmed to be anastomotic leak by esophagogram.Conclusion Routine ionic-contrast esophagogram before eating do not improve intrathoracic anastomotic leakage detection rate after esophagectomy,but when patients have fever,loculated pleural effusion and abnormal chest drainage,esophagogram is necessary and can improve the detection rate of esophageal anastomotic leak.CT radiography may detect smaller anastomotic leakage than conventional esophagogram.

Objective To investigate whether 17β-estradiol (E2) can stimulate the proliferation,migration,and secretion of trefoil factor family 1 (TFF1) in papillary thyroid cancer K-1 cells and explore the molecular mechanisms.Methods ELISA was used to detect the content of TFF1 in the supernatant of K-1 cells after the treatment of E2,propylpyrazoletriol (PPT,ERα agonist) or diarylpropionitrile (DPN,ERβ agonist).The expression of ERα and ERβ in the untreated cells was measured by Western blotting.ERα siRNA and ERβ siRNA by RNA interference were designed and synthesized,and the change of TFF1 was measured by ELISA again after the transfection.The interaction between TFF1 promoter and ER was evaluated by chromatin immunoprecipitation analysis (CHiP).The proliferation and migration were detected in the K-1 cells after E2 treatment by MTT assay and Transwell chamber test respectively.Festults After E2 treatment,the TFF1 content in the supernatant of K-1 cells was increased gradually,reached peak at 24 h,and then declined slowly.PPT treatment enhanced the secretion of TFF1 but DPN decreased it in the K-1 cells.Transfection of ERα siRNA obliterated the inductive effect of E2 on the secretion of TFF1,but that of ERβ siRNA increased the inductive effect in the K-1 cells.Western blotting showed that the expression level of ERα was higher than that of ERβ in the K-1 cells.ChIP results confirmed that ERα protein was bound to the promoter of TFF1 gene in K-1 cells.E2 treatment promoted cell proliferation and improved cell migration in the K-1 cells.Conclusion E2 induces the expression and secretion of TFF1 in K-1 cells through ERα-dependent manner,and thus promotes the proliferation and migration of the cells.

Objective To study the levels of soluble thrombomodulin (sTM)in patients with acute coronary syndrome (ACS) and evaluate its clinical significance. Method Measured the sTM levels with enzyme linked immunosorbent assay, and described the characteristics of coronary arteriography, risk factors of coronary heart disease, and adverse events in a case-control study of 48 ACS patients (ACS group)and 10 normal people (control group). Results The level of sTM in ACS group was (3.67±1.71) μg/L, and (2.34±0.43)μg/L in control group (P<0.05). The level of sTM in the patients of risk factors or impaired vessels number more than 2 increased significantly than those in the patients of risk factors or impaired vessols number inferior or equal to 2, (4.93±2.76) μg/Lvs (3.13±0.81) μg/L, P<0.05, (4.60± 2.83) μg/L vs (2.91±0.23) μg/L, P < 0.05 respectively. The incidence of cardiac events in the patients of sTM more than 3.2 μg/L (70.0%)was higher significantly than that in the patients of sTM inferior or equal to 3.2 μg/L(35.7%), P< 0.05. Conclusions The levels of sTM are valuable markers to evaluate the impaired degree and scope of endothelial cells in ACS. They are also associated with the number of risk factors, and useful in predicting the extent and prognosis of the disease.

Four weeks after SD diabetic rats were induced by streptozotocin,skin thickness was obviously reduced with obscure multilayer epithelium features.Moreover,the thickness of epidermic layers in diabetic rat skin was significantly thinner than that ofnornlal rat skin at the eighth week[(0.016±0.006 vs 0.041±0.007)mm,P<0.01].The percentage of G2/M phase cells in epidermic layers of diabetic group was significantly lower than that in the normal group.At the twelfth week,skin microangiopathy was easily detected in the diabetic group.The blood levels of advanced glycation end products(AGEs)and malonialdehyde were significantly increased and glutathione decreased in diabetic rats compared with control rats(aU P<0.01),along with the increased contents of local glucose and AGEs in the skin of diabetic rats.These results suggest that the local accumulation of glucose and AGEs seems to be one of the important mechanisms in the pathogenesis of diabetic skin lesions.

Objective To investigate the clinical significance of WDHD1 protein expression in esophageal squamous cell carcinoma.Methods The expression of WDHD1 protein in esophageal squamous cell carcinoma,adenocarcinoma of esophagus and normal esophagus tissues by immunohistochemical MaxVision was detected.Results The expression of WDHD1 protein in the tissues of esophageal squamous cell carcinoma was significantly higher than that in the normal esophagus tissues and adenocarcinoma of esophagus (15.68 ± 3.01 vs.3.89 ± 2.98 and 4.66 ± 2.46)(P ＜ 0.05),there was no significant between normal esophagus tissues and adenocarcinoma of esophagus (P ＞ 0.05).The expression of WDHD 1 protein in the tissues of esophageal squamous cell carcinoma,high-middle differentiation tissues was higher than poorly differentiation,TNM stage Ⅲ + Ⅳ stage was higher than Ⅰ + Ⅱ stage,depth of invasion T3 + T4 was higher than T1 + T2,with lymph node metastasis tissue was higher than without,differences was statistically significant (P ＜0.05).Conclusions The higher expression of WDHD1 protein is the marker of high invasive and low histological grade of esophageal squamous cell carcinoma,and WDHD1 in esophageal squamous cell carcinomas may play an important role in development.

AIM:To evaluate complement activation in patients with all forms of acute coronary syndromes(ACS)and to examine the relationship between the degree of complement activation and myocardial injury.METHODS:The subjects were divided into 2 groups:110 ACS patients(group ACS)and 18 healthy persons(group control).One hundred and ten patients with ACS were divided into 3 sub-group:51 patients with ST-segment elevated myocardial infarction(STEMI),28 patients with non-ST-segment elevated myocardial infarction(NSTEMI)and 31 patients with unstable angina(UA).Complement 3(C3),complement 4(C4),troponin T(TnT)as well as creatine kinase MB(CK-MB)were evaluated.RESULTS:Plasma C3 and C4 peak levels were significantly higher in patients with STEMI [(1 525?302)mg/L and(423?123)mg/L] and NSTEMI [(1 516?289)mg/L and(396?68)mg/L] than those in patients with UA [(1 275?172)mg/L and(356?91)mg/L] and the control subjects [(1 072?196)mg/L and(182?73)mg/L](P

To investigate the relationship of the expression of vascular endothelial growth factor (VEGF) and C-myc with the occurrence, development and metastasis of gallbladder carcinoma, the expression levels of VEGF and C-myc in gallbladder carcinoma tissue (n = 30) and in normal gallbladder tissue (n = 20) were examined by immunochemistry. Results show that the positive rates of VEGF and C-myc in gallbladder carcinoma tissue were 80% and 63.3% respectively, and 45% and 25% respectively in normal gallbladder tissue. The positive rates of VEGF and C-myc were significantly higher in gallbladder carcinoma than in normal gallbladder tissue. The expression of VEGF and C-myc in gallbladder carcinoma related to the metastasis of gallbladder carcinoma. VEGF and C-myc play important roles in the occurrence, development and metastasis of gallbladder carcinoma.
Adult ; Aged ; Endothelial Growth Factors ; biosynthesis ; physiology ; Female ; Gallbladder Neoplasms ; metabolism ; pathology ; Humans ; Intercellular Signaling Peptides and Proteins ; biosynthesis ; physiology ; Lymphokines ; biosynthesis ; physiology ; Male ; Middle Aged ; Neoplasm Metastasis ; Proto-Oncogene Proteins c-myc ; biosynthesis ; physiology ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors