Objective To investigate the role of wild-type XPD in SMMC-7721 hepatoma cells,its re-lationship with wild-type p53.CDK7 and c-myc.And the apoptosis mechanism of SMMC-7721 hepatoma cells.Methotis We inserted the human length XPD into the pEGFP-N2 plasmid vector which expresses the green fluorescence protein(GFP).And the pEGFP-N2 and pEGFP-N2-XPD were transfected into SMMC-7721 hepa-toma cell lines stably.Cel lines for omparison were matched on the sanle genetic background and passage.The expression of wild-type XPD,CDK7,p53,c-myc waft detected by RT-PCR,Westem blot.Cell growth wag detet-ed by MTT FCM wag employed for examining the cell cycle and apoptosis of the transfected SMMC-7721 hepa-toms cells.Results ①SMMC-7721-pEGFP-N2-xPD and SMMC-7721-pEGFP-N2 express the green fluores-cence protein which could be detected under the immunoffuorescence microscope.②RT-PCR The relative ex-\pression of p53 mRNA,XPD mRNA in the SMMC-7721,SMMC-7721-pEGFP-N2 and SMMC-7721-pEGFP-N2-XPD,the relative expression of p53 mRNA,XPD mRNA in the SMMC-7721-pEGFP-N2-XPD was signifiantly higher than other two oontrols(P<0.01).Othewise,the relative expression of CDK7 mRNA,c-myc mRNA Wag signifi-antlv lower than other two oontrols(P<0.01),the difference of two controls was not signifiant(P>0.05). ③Western blot The relative expression of p53,XPD protein was signifiantly higher than other two oontrols (P<0.01).Othewise,the relative expression of CDK7,c-Myc protein was signifiantly lower than other two oontrols(P0.05).④MTT The ressuh showedthat the proliferative ability of SMMC-7721-pEGFP-N2-XPD was much more descreaged than other two oontrols (P<0.05),the other two oontrols were not different(P>0.05).⑤FCM Wild-type XPD gene could change the cell8 and induce apoptitise in vitro though the result of FCM.Conclusions The pEGFP-N2 and pEGFP-N2-XPD were transfected into SMMC-7721hepatoma cell lines stably,wild-type XPD could decreaSe the expres-sion of CDK7,c-myc and increase the expression of p53.Wild-type.XPD could inhibit the activity of cell growth and change cell cycle,as well as induce cell apoptosis in SMMC-7721 hepatoma cell line in vitro.

The purpose of this study is to investigate the effects of intravenous tetrandrine (Tet) on the outcome of myocardial ischemia and reperfusion. Tet 4mg- kg-1 iv significantly reduced arrhythmias resulting from a coronary artery ligation and reperfusion. It is suggested that Tet may be a prospective anti-arrhythmic drug in ischemic heart disease.

Objective To evaluate the effect of preoperative aescuven forte tablets in the prevention of procedure for prolapse and hemorrhoids(PPH) complications.Methods One hundred and seventy-nine patients underwent PPH in the Erlonglu Hospital of Beijing from June 2013 to June 2014 were divided into postoperative aescuven forte tablets group (n =90) and preoperative aescuven forte tablets group (n =89).The postoperative pain,bleeding,retention of urine,anal swelling,length of stay in hospital and recurrence were compared between the two groups.Results The incidence of postoperative pain,bleeding,retention of urine,anal swelling were lower than in the preoperative aescuven forte tablets group (pain after operations rate:7.9％ (7/89) vs.20.0％ (18/90),x2 =5.484,P＜ 0.05;Wound bleeding:0 vs.6.7 ％ (6/90),P =0.026;retention of urine:9.0％ (8/89) vs.20.0％(18/90),x2 =4.370,P＜0.05;anal swelling:1.1％(1/89) vs.8.9％(8/90),P=0.035),and length of stay in hospital was shorter(11.9±3.9) d vs.(13.3 ±5.0) d,t=3.134,P＜0.05).There was no recurrence both of two groups follow up for more than 2 months.Conclusion Preoperative oral aescuven forte tablets of 2 h can reduce PPH complications and worthy of popularization and application.

OBJECTIVETo observe the synergistic effects of paclitaxel and gemcitabine on prostate cancer cell line PC-3 in vitro.

METHODSCell morphology, MTU, flow cytometer and immunocytochemical method were used to observe the effects of 10(-6), 10(-7), 10(-8) mol/L paclitaxel and 10(-7), 10(-8), 10(-9) mol/L gemcitabine on prostate cancer cell line PC-3 by single or synergistic administration for 48 hours in vitro.

RESULTSGemcitabine above 10(-8) mol/L enhanced the growth suppression [suppression ratio > or = (50.8 +/- 4.2)%, P < 0.05] and apoptosis [apoptosis ratio > or = (22.9 +/- 2.3)%, P < 0.05] and down-regulation of the expression of cyclin D1 [expression ratio < or = (9.6 +/- 1.6)%, P < 0.01] induced by paclitaxel above 10(-7) mol/L in PC-3 cells. Gemcitabine changed the ratio of G2/M cell arrest induced by paclitaxel from (70.3 +/- 9.7)% to (38.2 +/- 4.2)%, and reversed the G2/M arrest partially (P < 0.01).

CONCLUSIONPaclitaxel and gemcitabine can enhance the growth suppression and apoptosis induced by paclitaxel in a synergistic way. They show great potential in the treatment of androgen-independent carcinoma of the prostate.

Antimetabolites, Antineoplastic ; pharmacology ; Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Deoxycytidine ; analogs & derivatives ; pharmacology ; Dose-Response Relationship, Drug ; Down-Regulation ; Drug Synergism ; Flow Cytometry ; Humans ; Male ; Paclitaxel ; pharmacology ; Prostatic Neoplasms ; pathology