This assay reviewed the feeding arteries of CHL and summarized the mechanism,technologic method and common embolization agent of interventional therapy,as well as its effect,indications,contraindications and complications.

Objective To compare the effects among 1A29, CsA and their combined use on rejection after liver transplantation and hepatocellular apoptosis in rats. Methods The stable rat model of liver transplantation was established. Rats of the same strain were employed as the control group. The effects of 1A29, CsA and their combined use on rejection after liver transplantation were determined in both groups. Meanwhile, the hepatocellular apoptosis was recorded and evaluated. Results No rejection was found between the rats of the same strain (SDSD), while different levels of rejection was seen between the rats of different strains (WistarSD). Biochemical test showed a significant increase in levels of enzyme spectrum and bile in the blood. An apparent pathological change due to rejection was also observed. CsA of optimal dose (10mg/kg) effectively suppressed the rejection while 1A29 of optimal dose did not. When used alone, CsA of sub-optimal dose had no effect on rejection. On the contrary, the combined use of CsA of sub-optimal dose and 1A29 of optimal dose could significantly inhibit the rejection. There was a marked increase of the hepatocellular apoptosis in the liver graft rejected by the recipient. However, the level of hepatocellular apoptosis showed no remarkable change in the liver graft without rejection due to use of immunosuppressors. Conclusions Hepatocellular apoptosis is closely related to rejection of the liver graft. The apoptosis is not significantly correlated to application of 1A29. The use of 1A29 can result in significant decrease in dose of CsA. Using 1A29 alone can not effectively inhibit the rejection after liver transplantation.

Objective To investigate miR-146a-Smad4 expression during ultraviolet A(UVA)-induced photoaging of human skin fibroblasts (HSFs), and to evaluate effects of up-regulation of miR-146a expression on its target gene Smad4 and cell photoaging. Methods HSFs were isolated from the prepuce, and subjected to primary culture and maintained up to 10th passage. Then, the HSFs were classified into 4 groups: blank control group receiving no treatment, UVA group irradiated with 10 J/cm2 UVA, miR-146a group transfected with a lentiviral vector expressing miR-146a, UVA+ miR-146a group transfected with the lentiviral vector expressing miR-146a followed by UVA radiation. Real time PCR was performed to measure miR-146a expression in HSFs in the UVA group on day 0, 3, 7 and 14 after UVA radiation.Fluorescence microscopy was carried out to estimate transfection efficiency on day 7 and 14 in the miR-146a group after transfection, and real time PCR was performed to quantify miR-146a expression in these cells. Methyl thiazolyl tetrazolium (MTT)assay was conducted to evaluate proliferative activity of HSFs, real time PCR to quantify mRNA expressions of photoaging-related genes p53, p21 and p16, and Western blot analysis to measure Smad4 protein expression in these cells. Statistical analysis was carried out by using repeated-measures analysis of variance and factorial design analysis of variance. Results Repeated-measures analysis of variance showed that the expression of miR-146a decreased over time in both the UVA group and blank control group(F = 213.840, P < 0.01), and significantly lower in the UVA group than in the blank control group (F = 52.55, P < 0.01), with the difference between the two groups increasing over time. After transfection with the lentiviral vector expressing miR-146a-Smad4, HSFs showed a strong fluorescence intensity of miR-146a. The expression level of miR-146a was significantly higher in the miR-146a group than in the blank control group on day 7 and 14 after transfection(10.31 ± 0.17 vs. 8.33 ± 0.13 on day 7, 9.65 ± 0.19 vs. 7.86 ± 0.11 on day 14, F =42.49, P < 0.01), but insignificantly different between day 7 and 14 in the miR-146a group (P > 0.05). Factorial design analysis of variance showed that UVA radiation had an inhibitory effect on the proliferative activity of HSFs (P < 0.01), which was significantly lower in the UVA group than in the blank control group(P < 0.01), and lower in the UVA + miR-146a group than in the miR-146a group (P < 0.01). The lentivirus-mediated up-regulation of miR-146a expression also affected cellular proliferative activity (P < 0.01), which was significantly higher in the UVA + miR-146a group than in the UVA group(P < 0.01), but insignificantly different between the miR-146a group and blank control group(P > 0.05). Real time PCR and Western blot analysis both revealed that UVA radiation could increase the expressions of p53, p21 and p16 mRNAs as well as Smad4 protein(all P < 0.01). Concretely speaking, the expressions of p53, p21, p16 mRNAs and Smad4 protein were all significantly higher in the UVA group than in the blank control group (all P < 0.01), and higher in the UVA +miR-146a group than in the miR-146a group (all P < 0.01), but significantly lower in the UVA + miR-146a group than in the UVA group (all P < 0.01), and insignificantly different between the blank control group and miR-146a group (all P >0.05). Conclusion The expression of miR-146a is inhibited in UVA-induced photoaged HSFs, and its up-regulation may counteract cell photoaging by suppressing Smad4 expression in, and promoting proliferation of, photoaged HSFs.

Objective To investigate the role of p38MAPK in the differentiation of murine osteoblasts, and to observe the expressions of receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG). Methods The calvarial osteoblasts of newborn BALB/c mice were cultured in MEM medium containing 10% NCS. Raloxifene (10~(-7) mol/L) and 17β-estradiol (10~(-8) mol/L) were added respectively when cells reached 70%-80% confluence combined with or without 5 μmol/L SB202190, an inhibitor of p38MAPK. The osteoblasts alkaline phosphatase activity assays were performed 72 hours later using PNPP method, and mRNA levels of alkaliphosphatase (ALP), OPG and RANKL were determined by RT-PCR. Results 17β-estradiol and raloxifene increased ALP activity and ALP mRNA level in osteoblasts in vitro which were blocked by p38MAPK inhibitor.The mRNA levels of RANKL and OPG were up-regulated by 17β-estradiol and raloxifene while the ratio of OPG/RANKL kept constant. SB202190 (5 μmol/L) inhibited the highly expressed RANKL and OPG in osteoblasts, and obviously decreased the ratio of OPG/RANKL. Conclusions p38MAPK inhibition blocked the differentiation of osteoblasts and decreased the up-regulated OPG and RANKL expressions in osteoblasts significantly (P<0.05).

Objective To assess the effectiveness and safety of hyperthermia combined with chemotherapy(HCT)compared with chemotherapy (CT)for ovarian cancer. Methods Related literatures were searched by two independent investigators from the following electronic databases:PubMed,Cochrane Library,EMbase,VIP,WanFang Data,CNKI and CBM.Then the meta?analysis was performed by using RevMan 5.3 software. Results A total of 10 RCTs involving 546 patients were included. The results of Meta?analysis showed that the HCT group was superior to the CT group in the effective rate,tumor control rate,effective rate of CA125,ascites control rate and PD,with significant differences(P<0.05). There was no significant difference in the improvement rate of life quality and the incidences of myelosuppression,severe myelosuppression,severe nausea and vomiting,severe constipation and diarrhea,liver and renal damage(P>0.05). Conclusion Compared with CT,HCT can significantly increase short?term curative effect,ameliorate the quality of life,and it does not increase the incidence of adverse reactions. HCT is worthy of clinical applica?tion.

Objective To explore the expression of matrix metalloproteinase-14(MMP-14)protein in the human stomach carcinoma tissues and its correlation with carcinoma invasiveness and metastasis.Methods The MMP-14 protein expression was detected by immunohistochemistry in 59 cases of stomach carcinoma tissues (observation group)and 20 cases of normal stomach tissues (control group,the adjacent normal tissues from the tumor margin of 5 cm confirmed by pathology),and its correlation with the clinically pathological parameters was analyzed.The expression characteristics of MMP-14 among various TNM stages of stom-ach carcinoma were also analyzed.Results The positive rate of MMP-14 expression was 50.85%(30/59)in the observation group and 5.00% (1/20)in the control group,the positive rate of the observation group was significantly higher than that of the control group (P <0.01);the expression level of MMP-14 was correlated with the differentiation degree,regional lymph node metastasis degree,invasion depth,lymphatic invasion and TNM stage,which showing the statistical difference(P < 0.01);the expression of MMP-14 protein was up-regulated and showed the transferring trend from cytoplasm to cellular membrane along with the progres-sion of TNM stage.Conclusion The overexpression of MMP-14 protein exists in stomach carcinoma tissues,which contributing to the invasion and metastasis of stomach carcinoma cells.

Objective To investigate the anti-tumor effect and mechanism of curcumin in pancreatic cancer (PC). Methods Smad4 and Jab1 expressions were detected by immunohistochemistry in tumor tissues and pericarcinomatous tis?sue from 35 PC cases, and the correlation of Smad4 and Jab1 were analyzed based on the percentage of positive staining in?tissues from 21 random selected PC cases. The effect of curcumin on expressions of tumor suppressors p53, Smad4 and cell cycle inhibitor p27 were examined by Western Blotting after human pancreatic cancer cell line PANC-1 were divided into PANC-1 control group (no treatments were given) and PANC-1 curcumin group (treated with cell culture medium containing 10μmol/L curcumin). The effect of curcumin on expressions of combination of β-TrCP1 and Smad4 was examined by Co-Immunoprecipitation after human embryonic kidney cell line 293T were divided into 293T control group (no treatments were given), 293T curcumin group (treated with cell culture medium containing 10μmol/L curcumin) and 293T Jab1 group (trans?fected by HA-Jab1 plasmid). Results Compared with expressions in pericarcinomatous tissues, Smad4 was down regulated while the expression of Jab1 was upregulated in PC tissues (P<0.01), and the expression of Smad4 was negatively correlated with the expression of Jab1 (n=21, r=-0.71, P=0.007). After treated with curcumin, the protein expression of p53, Smad4 and p27 was increased in PANC1 cell, and the protein expression of the combination ofβ-TrCP1 and Smad4 was decreased in 293T cell (P<0.05). After transfected by HA-Jab1 plasmid, the protein expression of the combination ofβ-TrCP1 and Smad4 was increased in 293T cell (P<0.05). Conclusion Curcumin may have suppression effect of PC through increasing the protein expression of p53, Smad4 and p27, and the mechanism of Smad4 upregulation may be related with the inhibition of Smad4 ubiquitination process, while Jab1 may be also involved in Smad4 degradation through ubiquitination.

Objective To investigate the effects of cyclooxygenase-2 inhibitor celecoxib on proliferation , invasion and migration of human pancreatic cancer cell line PANC-1 and then determine the optimal concentration of cele-coxib and the most suitable application time .Methods Human pancreatic cancer cell line PANC-1 was treated with diverse concentrations of celecoxib (20,60,100 μmol/L) for different durations (24,48,72 h).Cell prolifer-ation, invasion and migration capabilities were measured by MTT colorimetry , Transwell invasion assay , and scratch assay respectively .Results The proliferation capability of PANC-1 cell was reduced by celecoxib in a con-centration-and time-dependent manner ( P <0.05 ) .In addition , the invasion and migration capabilities were decreased by celecoxib in a concentration-dependent manner(P<0.01).Conclusions Celecoxib attenuates the proliferation of human pancreatic cancer cell line PANC-1 in a concentration-and time-dependent manner .Cele-coxib attenuates the invasion and migration in a concentration-dependent manner .

Objective To discuss some problems about current learning objectives for the speciality of clinical medicine in China,including the concepts,the decision-making systems and value-orientation,and to provide the reference for stipulating the learning objectives in future. Methods The objectives of some Chinese medical universities were collected from their websites.Some medical educators were consulted about their feelings about these learning objectives,and also were asked to identify their own objectives. Results Medical educators failed to distinguish their own objectives,and there were four main problems in current learning objectives: generalization,similarity and lack of individuality,difficulty in guide the curricula and teaching,and setting up too high object. Conclusion The learning objectives in clinical medicine should reflect both specialty characteristic and university individuality,so they should be drawn up by teachers,students and educatirnal administrators,moreover their value orientation should be eligible standard,not excellence.

To study the regulation of androgen receptor (AR) expression in human prostate cancer LNCaP cells by triptolide (TP) and the possible mechanism, by using qRT-PCR and Western blot, the AR mRNA and protein levels in TP treated LNCaP cells were detected, and the AR protein level in TP and NF-κB inhibitor treated LNCaP cells was also detected; a series of pGL3-AR promoter reporter gene vectors were built using restriction-free cloning method, and the vectors were employed to investigate the effects of TP on the transcriptional activity of AR promoter in LNCaP cells; the upstream proteins which may play regulatory roles were detected using western blot assay. After treated LNCaP cells with TP for 48 h, AR mRNA and protein expressions decreased with increasing TP concentration. The expression of AR target gene PART1 and prostate specific antigen (PSA) was also downregulated by TP treatment; a series of pGL3-AR promoter reporter vectors were constructed and validated by sequencing and luciferase activity; the results of dual luciferase reporter assay showed that TP downregulated AR at the transcriptional level; PI3K/AKT/NF-κB pathway which is associated with AR promoter activity was drowregulated by TP. In conclusion, our results demonstrated that the transcriptional activity of AR in LNCAP cells was downregulated by TP, and PI3K/AKT/NF-κB pathway may be involved in the regulation mechanism.