Objective To explore the correlation of high-risk type HPV infection with mycoplasma,chlamydia infection in sterile female patients.Methods The cervical specimens from 524 sterile female patients in northwest area were performed the laboratory detection of high-risk type HPV,mycoplasma and chlamydia.The correlation among these 3 kinds of pathogen was analyzed.Results In 524 sterile female patients,the sequence of the infection rate of 3 kinds of pathogen from high to low was mycoplasma,high-risk type HPV and chlamydia.The positive rate of high-risk type HPV in the patients with simple mycoplasma positive,simple chlamydia positive and double positive of mycoplasma and chlamydia was significantly higher than that in the patients with myco-plasma and chlamydia negative,the difference had statistical significance(P <0.05).Conclusion Certain correlation exists between the high-risk type HPV infection with mycoplasma and the chlamydia infection in sterile female patients.So it is suggested that in the pathogenic microbiological detection,such patients in clinic need to simultaneously perform the high-risk type HPV detection in addition to completing the laboratory detection of mycoplasma and chlamydia.

Objective to establish an ethical assessment system in the admittance of the limitative medical technologies.Method:literature review and Delphi method are employed to adjust and set the structure,index numbers,and index weights of ethical assessment system of the limitative medical technologies.Result:An ethical assessment system in the admittance of the limitative medical technologies was established,which included 3 primary indices,11 secondary indices and 35 tertiary indices.There were 4 qualitative levels with different weights in tertiary indices,based on which the global grade and proposed-admittance criterion were obtained.Conclusion:Establishment of ethical assessment system in the admittance of the limitative medical technologies provides an ethical evidence for the assessment of clinical admittance of the limitative medical technologies with qualitative and quantitative approaches and class-setting evidence.

Objective To explore the clinical correlation of the variation of plasma homocysteine (HCY), melatonin (MLT) and ulceative colitis (UC). Methods The clinical data of 112 UC patients was collected, and 110 normal healthy persons as control. The level of plasma HCY and MLT was detected by high pressure liquid chromatography-fluorescence detection (HPLC-FD) method. The level of plasma folate ( FA) and vitamin B12 was detected by enzyme-linked immunosorbent assay (ELISA) method. The correlation of these four indexes and UC was analyzed. Results The serum level of HCY in UC patients was significantly higher than that in normal healthy persons [(11. 27± 7.26) μmol/L vs (8. 19±4. 81) μmol/L, P = 0. 000]. The serum level of MLT in UC patients was significantly lower than that in normal healthy persons [(49. 06 + 31. 40) pg/ml vs (64. 28±41. 16) pg/ml,P=0. 008]. The serum level of FA in UC patients was significantly lower than that in normal healthy persons [(7. 64 + 1.95) nmol/L vs (9. 14 + 1.23) nmol/L, P = 0. 005]. The serum level of vitamin B12 in UC patients was significantly lower than that in normal healthy persons [(108. 64 ±32. 22) pmol/L vs (112. 64±33. 33) pmol/L, P = 0. 004]. There was no correlation between plasma HCY, MLT and UC disease activity degree, range, disease duration, erythrocyte sedimentation rate (ESR), or C reactive protein (CRP) in UC patients. There was no significant correlation between MLT and HCY in UC patients. Conclusions The serum level of HCY is higher in UC patients than that in normal control, and MLT is lower than that in normal control. However there is no significant correlation between them.

Objective To investigate the effect and mechanism of anti-tumor necrosis factor (TNF)-α on the intestinal mucosal permeability in dextran sulfate sodium (DSS) induced colitis mice.Methods Eighteen C57BL/6J mice were evenly divided into healthy control group,model group and anti-TNF-α treated group.The mice of model group and anti-TNF-α treated group were fed with 5％DSS solution for 7 days.The mice of anti-TNF-α treated group were injected anti-TNF-α (5 mg/kg)intraperitoneally on the first and fourth day; control group and model group were substituted with equal volume saline injection.The mice were sacrificed at 7 days after modeling.The disease activity index (DAI) score was evaluated everyday.The intestinal permeability was examined by Evan′s blue (EB) method and FITC-dextran (FITC-D) method.The colon tissue was collected for observation under microscope and histological index (HI).The small intestinal tissues were examined under electron microscope.The 10％ homogenate of colon and intestinal mucosa was prepared,the activity of myeloperoxidase (MPO),the content of TNF-α and epithelial myosin light chain kinase (MLCK) concentration were determined with kits respectively.The expression of MLCK in intestinal mucosa was tested by Western blot assay.Single factor of variance between groups were analyzed.Results Compared with control group,the DAI of model group increased daily.Compared with model group,the DAI of anti-TNF-α treated group improved.In model group,mice intestinal epithelial cells junctional complex shortened and widened and the cell gap expanded.In anti-TNF-α treated group,the connection structure of mice intestinal epithelial cells was tighter.The activity of HI and MPO and the content of TNF-α of model group were higher than those of control group (P ＝ 0.008,0.006 and 0.001,respectively),all of those of anti-TNF-α treated group were lower than those of model group (P=0.004,0.008 and 0.005,respectively).The F value of three groups was 131.98,218.28 and 58.93,respectively.The contents of EB in mice intestinal wall and serum FITC-D of model group were higher than those of control group (P=0.003 and 0.010),and those of anti-TNF-α treated group were lower model group (P＝0.001 and 0.009).The F value of three groups was 69.36 and 17.96.The MLCK concentration in mice intestinal mucosa of model group [(71.10± 7.52) ng/g] was higher than that of control group [(18.56±9.92) ng/g,P＜0.01],that of anti-TNF-α treated group [(37.56±15.84) ng/g] was lower than model group (P=0.008),and the difference among these three groups was statistically significant (F＝ 17.23).The Western blot results indicated the expression of MLCK in intestinal mucosa of model group was higher than that of control group,and that of anti-TNF-α treated group was lower than model group.Conclusions Anti-TNF-α play an important role in improving colitis,and the intestinal mucosal permeability.The mechanism may be related with the regulation of MLCK expression.

[ ABSTRACT] AIM:To investigate the role of the Notch pathway in Toll-like receptor 4 ( TLR4 )-mediated in-flammatory response in renal ischemia reperfusion injury ( IRI) in rats.METHODS: A total of 75 male sprague-Dawley rats were randomly divided into sham operation group , IRI group and DAPT treatment group .Blood samples and the kid-neys were obtained at 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion .The concentrations of blood urea nitrogen ( BUN) and serum creatinine (Scr) were measured.The serum levels of tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) were detected by ELISA, and the expression of Notch1, TLR4 and NF-κB p65 in the renal tissues was assessed by im-munohistochemistry and Western blot .RESULTS: The serum levels of BUN, Scr, TNF-αand IL-6 in IRI group were markedly increased as compared with sham group (P<0.05).The protein levels of Notch1, TLR4 and NF-κB p65 in re-nal tubular epithelial cells in IRI group was significantly enhanced as compared with sham group ( P<0.05 ) .In DAPT group, the serum levels of BUN, Scr, TNF-αand IL-6 were significantly reduced compared with IRI group (P<0.05), and the protein levels of Notch1, TLR4 and NF-κB p65 were apparently less than those in IRI group (P<0.05).CON-CLUSION:Significant changes of renal function , a rise of serum inflammatory factor including TNF-αand IL-6 and en-hanced expression of Notch 1, TLR4 and NF-κB p65 in the renal tissue occurred in the rats with IRI .γ-Secretase inhibitor DAPT attenuates TLR4-mediated inflammatory response in the renal IRI through the inhibition of Notch 1 and down-regula-tion of NF-κB.

[ ABSTRACT] AIM:To investigate the expression of calprotectin ( CALP) in the rats with renal ischemia-reperfu-sion injury ( IRI) .METHODS:Male Sprague-Dawley rats were randomly divided into sham operation and IRI group ( n=25 in each group) .Blood samples and the kidneys were obtained at 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion.The pathological changes of the kidneys were observed.The serum concentrations of blood urea nitrogen ( BUN) and serum cre-atinine (SCr) were measured.The serum levels of CALP, tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) were detected by ELISA, and the expression of CALP, Toll-like receptor 4 ( TLR4) and NF-κB p65 in the renal tissues were de-termined by the methods of immunohistochemistry and Western blot.RESULTS: Different serial ischemia changes were observed in the renal tissues, mainly in the renal tubular epithelial cells and the mesenchyma, with the infiltration of in-flammatory cells.The serum levels of BUN, SCr, CALP, TNF-αand IL-6 in IRI group were markedly increased as com-pared with sham group (P<0.05).The protein expression of CALP, TLR4 and NF-κB p65 in the renal tubular epithelial cells in IRI group was greatly enhanced in comparison with that in sham group ( P<0.05) .CONCLUSION:The serum concentrations of CALP, TNF-αand IL-6, and the protein expression levels of CALP, TLR4 and NF-κB p65 in the renal tissue are significantly increased in the rats with IRI, suggesting that calprotectin plays an important role in the inflamma-tion in rats with IRI.

Objective To investigate the expressions of PGE2 and COX-2 between colorectal cancer tissue and normal colorectal mucosa tissue,and its relation to clinical pathology and significance.Methods 115 colon cancerous tissues and 69 normal colon tissues were collected in our hospital from Jan 2010 to Sept 2011.Immunohistochemistry was used to detect the PGE2 and COX-2 expression in both of the colorectal cancer and normal tissues.Results Positive expressions of PGE2 and COX-2 were 87.8％ (101/115) and 80.9％ (93/115) in the colorectal cancer tissue,and 8.7％ (6/69),21.7％ (15/69) in normal colorectal mucosa tissue respectively (x2 =110.96,62.194,all P ＜ 0.05).Expressions of PGE2 and COX-2 were closely associated with,tumor invasion,differentiation,lymph node metastasis and TNM stage (P ＜ 0.05).The Spearman rank correlation analysis indicated that the PGE2 and COX-2 expressions in tissues were closely correlated (r =0.987,P ＜ 0.05).Survival rate of the patients in both negative expressions of PGE2 and COX-2 (63.6％) were higher than that of both positive expressions (37.8％,P ＜ 0.05).Conclusion High PGE2 and COX-2 expressions in colorectal cancer tissues predicts poor patients' survival.

OBJECTIVETo explore the effect of colon cancer cell-derived interleukin-1α on the migration and proliferation of human umbilical vein endothelial cells as well as the role of IL-1α and IL-1ra in the angiogenesis process.

METHODSWestern blot was used to detect the expression of IL-1α and IL-1R1 protein in the colon cancer cell lines with different liver metastatic potential. We also examined how IL-1α and IL-1ra influence the proliferation and migration of umbilical vascular endothelial cells assessed by PreMix WST-1 assay and migration assay, respectively. Double layer culture technique was used to detect the effect of IL-1α on the proliferation and migration of vascular endothelial cells and the effect of IL-1ra on the vascular endothelial cells.

RESULTSWestern blot analysis showed that IL-1α protein was only detected in highly metastatic colon cancer HT-29 and WiDr cells, but not in the lowly metastatic CaCo-2 and CoLo320 cells.Migration assay showed that there were significant differences in the number of penetrated cells between the control (17.9±3.6) and 1 ng/ml rIL-1α group (23.2±4.2), 10 ng/ml rIL-1α group (31.7±4.5), and 100 ng/ml rIL-1α group (38.6±4.9), showing that it was positively correlated with the increasing concentration of rIL-1α (P<0.01 for all). The proliferation assay showed that the absorbance values were 1.37±0.18 in the control group, and 1.79±0.14 in the 1 ng/ml rIL-1α group, 2.14±0.17 in the 10 ng/ml rIL-1α group, and 2.21±0.23 in the 100 ng/ml rIL-1α group, showing a positive correlation with the increasing concentration of rIL-1α(P<0.01 for all). IL-1ra significantly inhibited the proliferation and migration of vascular endothelial cells (P<0.01). The levels of VEGF protein were (1.697±0.072) ng/ml, (3.507±0.064)ng/ml and (4.139±0.039)ng/ml in the control, HUVECs+ IL-1α and HUVECs+ HT-29 co-culture system groups, respectively, showing a significant difference between the control and HUVECs+ 10 pg/ml rIL-1α groups and between the control and HUVECs+ HT-29 groups (P<0.01 for both).

CONCLUSIONSOur findings indicate that colon cancer cell-derived IL-1α plays an important role in the liver metastasis of colon cancer through increased VEGF level of the colon cancer cells and enhanced vascular endothelial cells proliferation, migration and angiogenesis, while IL-1ra can suppress the effect of IL-1α and inhibit the angiogenesis in colon cancer.

Blotting, Western ; Caco-2 Cells ; Cell Line, Tumor ; Cell Movement ; physiology ; Cell Proliferation ; physiology ; Coculture Techniques ; Colonic Neoplasms ; blood supply ; metabolism ; pathology ; Human Umbilical Vein Endothelial Cells ; cytology ; Humans ; Interleukin 1 Receptor Antagonist Protein ; metabolism ; physiology ; Interleukin-1alpha ; metabolism ; physiology ; Liver Neoplasms ; secondary ; Neovascularization, Pathologic ; etiology

Objective : To explore the general information，clinical features，imaging findings and outcome of pa- tients with drug-induced cholestatic． Methods : The clinical data of patients diagnosed as cholestatic drug-induced liver injury in recent 5 years were analyzed retrospectively，and followed up for at least 6 months. Results : There were 105 patients with drug-induced cholestatic liver injury in the hospital，the median age was 55 years old (54. 3% male) ，most of them had no specific clinical symptoms ; there were nearly 80 kinds of drugs involved，the top three were traditional Chinese medicine (34. 3% ) ，antineoplastic drugs (22. 9% ) and antibiotics ( 10. 5% ) . Among the 49 patients with magnetic resonance cholangiopancreatography ( MRCP) ，7 ( 14. 3% ) had sclerosing cholangitis-like changes ; most of the patients were combined with multiple liver-protecting and enzyme-lowering drugs ; there were 53 cured (50. 5% ) ，41 improved (39. 0% ) ，7 uncured (6. 7% ) ，and 4 died (3. 8% ) among 105 patients，and the total effective rate was 89. 5%． Conclusion Drug-induced cholestatic liver injury mainly oc- curs in elderly patients，involving many kinds of drugs，mainly traditional Chinese medicine．Drugs can also cause changes similar to sclerosing cholangitis，so drug-induced liver injury (DILI) should be used as one of the differen- tial diagnosis of cholestasis and abnormal cholangiography．Liver disease and the number of drugs have no effect on the prognosis of the patients，while low Roussel Uclaf causality assessment method (RUCAM) score and hemoglobin count，short hospitalization time and high white blood cell count are poor prognostic factors.

OBJECTIVETo investigate the effects of polyunsaturated fatty acids (PUFA) ω-3 and ω-6, and their middle metabolites PGE2 and PGE3 on angiogenesis formation of gastric cancer, and to explore associated mechanism.

METHODSThe effects of ω-3, ω-6, PGE2, PGE3 on the proliferation and migration of human umbilical vein endothelial cell (HUVEC) were measured by proliferation and migration assay respectively. The angiogenesis assay in vivo was used to measure the effects of ω-3, ω-6, PGE2 and PGE3 on neovascularization. In all the assays, groups without ω-3, ω-6, PGE2 and PGE3 were designed as the control.

RESULTSWith the increased concentration of ω-6 from 1 μmol/L to 10 μmol/L, the proliferation ability of HUVECs enhanced, and the number of migration cells also increased from 28.2±3.0 to 32.8±2.1, which was higher than control group (21.2±3.2) respectively (both P<0.05). With the increased concentration of ω-3 from 1 μmol/L to 10 μmol/L, the proliferation ability of HUVECs was inhibited, and the number of migration cells decreased from 15.8±2.0 to 11.0±2.1, which was lower than control group (22.1±3.0) respectively (both P<0.05). In the angiogenesis assay, compared with control group (standard number: 43 721±4 654), the angiogenesis ability of HUVECs was significantly enhanced by ω-6 in concentration-dependent manner (1 μmol/L group: 63 238±4 795, 10 μmol/L group: 78 166±6 123, all P<0.01). Meanwhile, with the increased concentration of ω-3 from 1 μmol/L to 10 μmol/L, the angiogenesis ability was significantly decreased from 30 129±3 102 to 20 012±1 541(all P<0.01). The proliferation and migration ability of HUVECs were significantly promoted by ω-6 metabolites PGE2 (P<0.05) in a concentration-dependent manner. In contrast, ω-3 metabolites PGE3 significantly inhibited the proliferation and migration ability of HUVECs in a concentration-dependent manner (all P<0.05). After rofecoxib (a COX-2 specific inhibitor) inhibited the expression of COX-2, the expression level of PGE2 was significantly decreased in a dose-dependent manner. In co-culture system, whose gastric cancer cells expressed positive COX-2, ω-6 could increase angiogenesis of gastric cancer cells(P<0.01), but ω-3 could inhibit such angiogenesis(P<0.01). In co-culture system, whose gastric cancer cells did not express COX-2, ω-3 could inhibit the angiogenesis of gastric cancer cells (P<0.05), but ω-6 had no effect on angiogenesis.

CONCLUSIONSThe PUFA ω-6 can enhance the angiogenesis via the promotion of proliferation and migration of HUVECs, and COX-2 and PGE2 may play an important role in this process, whereas, the ω-3 can inhibit the angiogenesis through its middle metabolites PGE3 to inhibit the proliferation and migration of HUVECs. Results of this experiment may provide a new approach to inhibit and prevent the spread of gastric cancer.

Alprostadil ; analogs & derivatives ; pharmacology ; Angiogenesis Inducing Agents ; metabolism ; pharmacology ; Angiogenesis Inhibitors ; pharmacology ; Cell Count ; methods ; Cell Line, Tumor ; drug effects ; physiology ; Cell Migration Assays ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Coculture Techniques ; Cyclooxygenase 2 ; pharmacology ; Dinoprostone ; metabolism ; pharmacology ; Fatty Acids, Omega-3 ; pharmacology ; Fatty Acids, Omega-6 ; metabolism ; pharmacology ; Fatty Acids, Unsaturated ; pharmacology ; Human Umbilical Vein Endothelial Cells ; drug effects ; physiology ; Humans ; Lactones ; pharmacology ; Neovascularization, Pathologic ; physiopathology ; Stomach Neoplasms ; physiopathology ; Sulfones ; pharmacology