Objective To investigate the relationship of the location of nerve compression and different type of trigeminal neuralgia.Methods Twenty-one patients with typical trigeminal neuralgia and 16 patients with atypical trigeminal neuralgia were treated by micro-vascular decompression.The position of the responsible vessels was probed during operation.Results Compared with atypical trigeminal neuralgia group, the compression rate of trigeminal root entry/exit zone (REZ) in typical trigeminal neuralgia group was significantly higher(P<0.01).The compression rate of trigeminal REZ which oppressed by artery in typical trigeminal neuralgia group was significantly higher than that in atypical trigeminal neuralgia group ( P<0.01 ) .Conclusions The responsible vessels in typical trigeminal neuralgia patients is mostly located in the trigeminal REZ, and the responsible vessels is mostly not located in other location in the trigeminal REZ.The responsible vessels oppress REZ is closely related to types of trigeminal neuralgia.

AIM:In order to ensure the quality stability of Fructus Polygoni Orientalis,to study the determination method of the fingerprint of Fruetus Polygoni Orientalis and to establish the fingerprint of Fructus Polygoni Orientalis.METHODS:The HPLC assay was used to establish the fingerprint of Fructus Polygoni Orienlalis and 28 pieces of goods were compared.RESULTS:The fingerprint of Fructus Polygoni Orientalis with 7 common peaks was established.The relative retention time and the ranges of relative area of the common peaks were determined.CONCLUSION:The established fingerprint can be used for the quality control of Fructus Polygoni Orientalis.

Objective To investigate the effect of N-myc downstream regulated gene 2 (NDRG2) on the apoptosis of bladder cancer cells by regulating the signal transducer and activator of transcription 3(STAT3) signaling pathway.Methods The expression level of NDRG2 in human bladder cancer cell BIU-87 and immortalized cell SV-HUC-1 was detected by Western blot.NDRG2 over expression vector and empty vector control (pcDNA3.1),siRNA-NDRG2,siRNA control were transfected into BIU-87 cells.After transfected 48 h,the expression level of NDRG2,Cleaved caspase 3,STAT3,p-STAT3,JAK2,p-JAK2 were detected by Western blot,the cell proliferation and apoptosis were measured by MTT and flow cytometry.After adding inhibitor AG490 of 45 μmol/L in cultured BIU-87 cells,MTT assay was used to detect cell proliferation and flow cytometry was used to detect the cell apoptosis,Western blot to detect the expression level of Cleaved caspase 3,STAT3,p-STAT3,JAK2,p-JAK2.Results The expression level of NDRG2 in bladder cancer cells was higher than that in bladder epithelial cells.The cell survival rate of pcDNA3.1/NDRG2 group was lower than that of pcDNA3.1 group,the difference was statistically significant (P ＜ 0.01).The cell survival rate of siRNA-NDRG2 group was higher than that of siRNA control group (P＜ 0.01).The apoptosis rate of pcDNA3.1/NDRG2 group was higher than that of pcDNA3.1 group (P ＜ 0.01).The apoptosis rate of NDRG2 siRNA group was lower than that of siRNA control group (P ＜ 0.01).The level of p-STAT3 and p-JAK2 in pcDNA3.1/NDRG2 group was lower than that in pcDNA3.1 group (P＜ 0.01).The survival rate and apoptosis rate of BIU-87 cells cultured with AG490 were in agreement with the trend of pcDNA3.1/NDRG2 after transfection.Conclusions NDRG2 could promote the apoptosis of bladder cancer cells,and its mechanism may be related to STAT3 signaling pathway.

Objective:To prepare for mAb of progesterone receptor. It would provide support for the immunohistochemistry behind. Methods:Target gene connected together with a carrier by seamless cloning method. The target protein that expression by inducing was collected. And with cell fusion method , the monoclonal antibodies were preparation. Then the mAb were detected by IHC. Results: The mAb ( clone 7C7 ) was detected and it found positive for the breast, uterine fibroid tissue, showed negative in colorectal cancer tissue, smooth muscle tissue, the goal of the claim were achieve. Conclusion: Finally, we found the method that prepare for mAb was far beyond our imagination. The result of IHC on different samples about mAb(7C7)obtained compliance with an-ticipation. Study on the difference between the PR-A and PR-B had significance.

Objective To evaluate the effects of ulinastatin on renal ischemia-reperfusion injury in patients undergoing operation on aorta with deep hypothermic circulatory arrest (DHCA ) .Methods Thirty patients ,aged 30-50 yr ,of ASA physical status Ⅲ or Ⅳ (NYHA Ⅱ or Ⅲ) ,scheduled for elective operation on aorta with DHCA ,were randomly divided into 2 groups ( n=15 each) using a random number table :control group (group C ) and ulinastatin group (group U ) .In group U ,ulinastatin 20 000 U/kg was infused via the central vein at 500-1 000 U·kg-1 ·min-1 from the time immediately after tracheal intubation until 10 min before ascending aortic cross-clamping .In group C ,the equal volume of normal saline was infused instead of ulinastatin .At 5 min before the beginning of DHCA (T1 ) and 15 min after the end of DHCA (T2 ) ,blood samples were taken from the extracorporeal circulation for determination of polymorphonuclear leukocyte counts , and plasma levels of intercellular adhesion molecule-1 , tumor necrosis factor-α, iterleukin-6 (IL-6 ) IL-8 , IL-10 , malondialdehyde , myeloperoxidase ,atrial natriuretic peptide ,cystatin C ,and creatinine .Results The polymorphonuclear leukocyte counts and plasma levels of intercellular adhesion molecule-1 , tumor necrosis factor-α, IL-6 , IL-8 , malondialdehyde , myeloperoxidase , cystatin C , and creatinine were significantly lower , and the plasma concentrations of IL-10 and atrial natriuretic peptide were higher in group U than in group C ( P< 0.05 ) . Conclusion Ulinastatin can attenuate renal ischemia-reperfusion injury in patients undergoing operation on aorta with DHCA and inhibition of inflammatory responses is involved in the mechanism .

Objective To evaluate the role of Fas/FasL signaling pathway in ulinastatin postconditioning-induced attenuation of apoptosis in the myocardial cells of patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty patients of both sexes,aged 21-59 yr,of ASA physical status Ⅱ or Ⅲ (NYHA class Ⅱ or Ⅲ),scheduled for elective cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each):control group (group C),and ulinastatin postconditioning group (group U).In group U,ulinastatin 10 000 U/kg was perfused via the aortic root at 4 000-5 000 U·kg-1 ·min-1 starting from 5 min before aortic unclamping.In group C,the equal volume of normal saline was infused instead of ulinastatin.Myocardial specimens were taken from the right auricle at 45 min after aortic unclamping for determination of Fas,Fas ligand (FasL),caspase-8,Bcl-2 and Bax expression and cell apoptosis.The ratio of Bcl-2 expression to/Bax expression (Bcl-2/Bax) and apoptotic index were calculated.Results Fas,FasL,caspase-8 and Bax expression and apoptotic index were significantly lower,and Bcl-2 expression and Bcl-2/Bax were higher in group U than in group C.Conclusion Ulinastatin postconditioning attenuates apoptosis in the myocardial cells through inhibiting Fas/FasL signaling pathway in the patients undergoing cardiac valve replacement with CPB.

Objective To investigate the role of phosphatidylinositol 3-kinase (PI3K)/protein-serine-threonine kinases (Akt) signal pathway in ulinastatin postconditioning-induced attenuation of apoptosis in myocardial cells in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty NYHA class and ASA physical status Ⅱ or Ⅲ patients of both sexes,aged 21-59 yr,scheduled for cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each):normal saline control group (group C) and ulinastatin postconditioning group (group U).In group U,ulinastatin 10 000 U/kg was perfused via the aortic root at 4000-5000 U· kg-1 · min-1 starting from 5 min before aortic unclamping.In group C,the equal volume of normal saline was given instead of ulinastatin.Myocardial specimens were taken from the right auricle at 45 min after aortic unclamping for determination of the expression of Akt,phosphorylated Akt (p-Akt),cytochrome c,caspase-9,Bcl-2 and Bax,and cell apoptosis.Bcl-2/Bax ratio and apoptotic index were calculated.Results The expression of p-Akt and Bcl-2 and Bcl-2/Bax ratio were significantly higher,and the expression of cytochrome c,caspase-9 and Bax and apoptotic index were lower in group U than in group C (P ＜ 0.05).Conclusion Ulinastatin postconditioning attenuates apoptosis in myocardial cells in patients undergoing cardiac valve replacement with CPB through activating PI3K/Akt signal pathway.

Objective To evaluate the effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Eighty New York Heart Association (NYHA) class Ⅱ or Ⅲ patients of both sexes,aged 21-59 years,scheduled for cardiac valve replacement with CPB,were randomly divided into four groups (n =20 each):normal saline control group (group C),ulinastatin preconditioning group (group U1),ulinastatin postconditioning group (group U2) and ulinastatin preconditioning plus postconditioning group (group U3).In group U1,uinastatin 20000 U/kg was infused via the central vein at 500-1000 U·kg-1 · min-1 after endotracheal intubation until 10 minutes before blocking the ascending aorta.In group U2,ulinastatin 10000 U/kg was infused via the aortic root at 4000-5000 U· kg-1 · min-1 at 5-7 minutes before opening the aorta.In group U3,ulinastatin preconditioning and postconditioning were performed as described in groups U1 and U2.In group C,the same volume of normal saline was infused instead of ulinastatin.Blood samples were taken from the radial artery at 10 minutes before blocking the ascending aorta,40 minutes after blocking the ascending aorta,45 minutes after opening the aorta and at the end of operation for determination of plasma concentrations of tumor necrosis factor-alpha (TNF-α) and soluble tumor necrosis factor receptor 1 (sTNF-R1).Myocardial tissues were obtained from the right atrial appendage at 45 minutes after opening the aorta for determination of the expression of TNF-α,bcl-2,bax,caspase-3,and apoptosis.The bcl-2/bax ratio and apoptotic index were calculated.Results Plasma concentrations of TNF-α and sTNF-R1 and the expression of TNF-α,bax,caspase-3 and apoptotic index were lower and the expression of bcl-2 and bcl-2/bax ratio were higher in groups U1,U2 and U3 than in group C and they were lower in group U3 than in groups U1 and U2 (P ＜ 0.05).Conclusion Ulinastatin postconditioning can inhibit myocardial apoptosis in patients undergoing cardiac valve replacement with CPB,and the efficacy of combination of ulinastatin preconditioning and postconditioning is stronger than that of ulinastatin postconditioning.The mechanism is involved in balancing the expression of bax and bcl-2 and down-regulating the expression of TNF-α and its receptor.

Objective To assess the association of metabolic syndrome (MetS) and low-level high density lipoprotein-cholesterol (HDL-C) with the invasion of prostate cancer (PCa) in the patients after radical prostatectomy (RP). Methods We collected and analyzed the data of 232 PCa patients treated with RP for prospective multicenter clinical study.The MetS was assessed according to NCEP-ATP Ⅲ.Patients were divided into MetS group and non-MetS group.Locally advanced PCa was defined as a pT-stage≥3.ISUP Gleason grading system (GS) were used for pathological grading.Logistic regression analyses assessed the association of MetS and its components with pathological data. Results MetS was an independent risk factor for GS≥8 after RP.Low HDL-C level was associated with locally advanced PCa.The risks of adverse pathological features increased with the number of MetS components. Conclusion Low HDL-C level and 4 or more MetS components are associated with higher risk of adverse pathological features of PCa.

Objective To evaluate the effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Eighty NYHA class Ⅱ or Ⅲ patients of both sexes,aged 21-59,scheduled for cardiac valve replacement with CPB,were randomly divided into 4 groups ( n =20 each):normal saline control group ( group C ),ulinastatin preconditioning group ( group U1 ),ulinastatin postconditioning group (group U2 ) and ulinastatin preconditioning plus postconditioning group(group U3 ).In group U1,uinastatin 20 000U/kg was infused via central vein at 500-1000 U·kg-1 ·min-1 from after tracheal intubation until 10 min before ascending aortic cross-clamping.In group U2,ulinastatin 10 000 U/kg was perfused via aortic root at 4000-5000 U· kg-1 · min-1 at 5-7 min before aortic unclamping.In group U3,ulinastatin preconditioning and postconditioning were performed as described in groups U1 and U2.In group C same volume normal saline was infused instead of ulinastatin.Blood samples were taken from radial artery at 10 min before ascending aortic cross-clamping,40 min after ascending aortic cross-clamping,45 min after aortic unclamping and the end of operation for determination of plasma concentrations of TNF-α and soluble tumor necrosis factor receptor 1 (sTNF-R1).Myocardial tissues were obtained from right atrial appendage at 45 min after aortic unclamping for determination the expression of TNF-d,Bcl-2,Bax and caspase-3 and apoptosis.The Bcl-2/Bax ratio and apoptotic index were calculated.Results Plasma concentrations of TNF-α and sTNF-R1 and the expression of TNF-α,Bax,caspase-3 and apoptotic index were lower,the expression of Bcl-2 and Bcl-2/Bax ratio were higher in groups U1,U2 and U3 thah group C and in group U3 than groups U1,U2 ( P ＜ 0.05 ).Conclusion Ulinastatin postconditioning can inhibit myocardial apoptosis in patients undergoing cardiac valve replacement with CPB,and efficacy of combination of ulinastatin preconditioning and postconditioning is stronger than that of ulinastatin postconditioning.The mechanism is involved in balancing the expression of Bax and Bcl-2 and down-regulating the expression of TNF-α and its receptor.