ObjectiveTo investigate the effects of comprehensive geriatric assessment (CGA) intervention on depression and anxiety in patients with benign prostatic hyperplasia (BPH).Methods90 patients with BPH (aged 65 years and over) from June 2009 to June 2010 were randomly assigned to control(n= 45) and CGA (n = 45) group.Control group received conventional therapy,while CGA group was given CGA and consultation therapy as well as conventional therapy.The scores of international were assayed and compared between two groups before and 6 months after treatment.ResultsThe scores of international prostate symptom score (IPSS),quality of life scale (QOLS),self-rating depression scale (SDS) and self-rating anxiety scale (SAS) in control (t= 11.0,5.84,7.08and 9.68,respectively) and CGA (t= 14.0,10.4,9.16 and 6.1,respectively)group 6 months after treatment reduced as compared with those before treatmen (all P ＜ 0.01).After 6 months of treatment,the scores of IPSS,QOLS,SDS and SAS in CGA group were lower than in control group (t= 4.25,5.55,3.45 and 2.88,respectively,all P＜0.01).ConclusionsCGA intervention can improve the quality of life in BPH patients and alleviate their depression and anxiety.

The lengths and depths of occlusal rest base slope were calcukted accurately when the inclinations of occlusal rest base were 10?,15?and 20?at 1/2, 1/3 and 1/4 crown width respectively. The data will be usefull in the process of removable denture design with computer and provide a suitable way for the preparation of tilt abutment.

Objective To investigate the association between CYP1A1 gene polymorphism and toxicities related to high-does methotrexate of childhood acute leukemia. Methods The SNPs were detected by reverse transcriptional (RT)-PCR-denaturing gradient gel elelctrphoresis combined with direct sequencing in 51 children with acute leukemia. Toxicities were collected thereby. Results Only one SNP,A4889G, was screened in CYP1A1. A4889G polymorphism was not associated with all the toxicities (P > 0.05). High-risk ALL children were more likely to increase the risk of thrombocytopenia compared with standard-risk ALL (P< 0.05). Conclusions CYP1A1 A4889G polymorphism may be not association with all toxicities after HD-MTX ,but the thrombocytopenia may be relevant to the risk degree of ALL children.

Objective To investigate the single nucleotide polymorphism(SNP)in the coding region in cyto-chrome P4501 A1 (CYP1A1)gene and to evaluate the contributions of SNPs to acute lymphocytic leukemia(ALL)and acute myeloid leukemia(AML)susceptibility in children.Methods One hundred and twenty -one(male 76,female 45)children with acute leukemia were selected from Department of Hematology in Shenzhen Children′s Hospital,Zuyi Medical College between January 2007 and January 201 4 as the case study group,and the average age was 4.42 years old.Case study group included 1 01 (male 65,female 36,average age 4.38 years old)ALL children (ALL group)and 20(male 1 1 ,female 9,average age 4.66 years old)AML children(AML group).A total of 1 1 6(male 74,female 42) children with respiratory tract infections on health examination during the same period were selected as the control group and the average age was 3.93 years old.SNPs in the coding region in CYP1A1 gene were detected by reverse transcrip-tional(RT)-PCR -denaturing gradient gel elelctrphoresis(DGGE)combined with direct sequencing in the case study group and the control group.Results Only one SNP,A4889G,was screened in the open reading frame (ORF)of CYP1A1 gene in Chinese Han children and the G allele frequency of CYP1A1 gene in the case group,ALL group,AML group and the control group were 31 .4%,32.2%,27.5% and 38.8%.The CYP1A1 A4889G AG and AG +GG geno-type were linked with decreased risk of AML(OR =0.31 ,95%CI:0.1 1 -0.87,P =0.02;OR =0.35,95%CI:0.1 4 -0.93,P =0.03)especially in boys with AML(OR =0.1 2,95%CI:0.03 -0.60,P =0.01 ;OR =0.1 6,95%CI:0.04 -0.65,P =0.01 ),but the CYP1A1 A4889G polymorphism was not associated with the risk of ALL(P >0.05). The CYP1A1 A4889G allele frequency and the distribution of genotypes were significantly different from those reported in America,India,Korea,Brazil and Iran(all P <0.05).Conclusions CYP1A1 A4889G polymorphism may be not as-sociated with susceptibility to ALL,but may decrease the risk of childhood AML especially in boys with AML.In addi-tion,it may exhibit an ethnic difference.

Objective To evaluate the clinical usefulness of 99m Tc MIBI imaging for the diagnosis of breast malignancy.Methods 195 patients with a total of 204 breast lesions were divided into three groups to undergo 99m Tc MIBI imaging and the results were compared with pathology.20 cases with normal breast served as control.Abnormal density showed by 99m Tc MIBI imaging in the breast(10% higher than surrounding structure) was regarded as positive.Results Of 100 breast cancer lesions,positive feature appeared in 92.Twelve out of 70 benign breast lesions showed positive imaging.Six out of 34 breast occult lesions were with positive imaging, among them 3 were finally found with carcinoma.No positive imaging was found in the control group.The diagnostic accuracy,sensitivity,specificity,positive predictive value,negative predictive value of 99m Tc MIBI was 92 0%,91 8%,92%,86%, and 92%,respectively.Conclusions[WT5”BZ] 99m Tc MIBI imaging has high sensitivity and accuracy in the diagnosis of breast cancer and in the differentiation between benign and malignant breast lesions.

The microsoft DirectX technique is utilized to achieve the display of fast moving waveforms with high resolution and full screen in the environment of WindowsXP. The waveforms can move fluently under the resolution of 1280 x 1024 with the fastest speed of 1 m/s without any dither.
Signal Processing, Computer-Assisted ; Software

Objective To evaluate the endocrine glands derived VEGF (EG-VEGF) influence on growth, migration and apoptosis of pancreatic cancer cells MiaPaCa Ⅱ. Methods MiaPaCa Ⅱ were treated by 100,200 ng/ml EG-VEGF for 24, 48, 72, 96 h, and MTT assay was used to determine the proliferation; and cell scratch experiment was used to investigate the percentage of cell migration distance, flow cytometry was used to measure the apoptosis of the cancer cells. Results After MiaPaCa Ⅱ cells were treated by 0, 100,200 ng/ml EG-VEGF for 72 h, the proliferation of MiaPaCa Ⅱ was 0. 253 ± 0. 012 , 0. 374 ± 0.013,0. 383 ±0.015, respectively EG-VEGF could significantly promote the proliferation of MiaPaCa Ⅱ ( P ＜ 0. 05 ). After MiaPaCa Ⅱ cells were treated by 0, 100 ng/ml EG-VEGF for 24 h, the percentage of cell migration distance was (27.40 ± 3.45 ) % and ( 13.21 ±4.65 ) % ,respectively with statistical difference ( P ＜ 0.05 ), EG-VEGF could significantly promote the migration ability of MiaPaCa Ⅱ cells and inhibite the apoptosis. Conclusions After EG-VEGF treatment, the growth and migration ability of MiaPaCa Ⅱ cells increases, apoptosis decreases.

Objective To investigate the therapeutic effects and safety of beraprost sodium on vascular endothelial dysfunction in elderly patients with lower extremity arteriosclerotic occlusive disease (LEAOD).Methods A total of 80 patients with LEAOD were randomly divided into 2 groups:the treatment group and the control group (n=40 each group).All patients were treated with conventional antihypertensive,antidiabetic,hypolipidemic,antiplatelet drug therapy and non-drug therapy such as smoking cessation,foot care.In addition,patients in the treatment group received 40 μg oral beraprost sodium at a dose of 120 μg/day,3 times/day for 30 days.The changes in symptoms,vital signs,the function of liver and kidney,hemorheology,and serum nitric oxide (NO)were observed before and after the treatment.Results No adverse reactions happened among all patients.After 30 days treatment,there was a significant difference in the total efficacy between the treatment and control groups (80％ vs.35％,x2 =19.60,P＜0.01).The levels of plasma viscosity,erythrocyte aggregation index and serum NO in the control group were (1.70±0.19) mpas.s,5.69±1.08,(43.86±5.20) μmol/L,respectively before the treatment and (1.36±0.14) mpas.s,3.23±0.67,(56.84 ± 7.05) μmol/L,respectively after the treatment.The levels of plasma viscosity,erythrocyte aggregation index and serum NO in the treatment group were (1.71 ±0.18) mpas.s,5.70±1.04,(44.24±5.40) μmol/L,respectively before the treatment and (1.10±0.12) mpas.s,2.80 ±0.52,(64.00±8.15) μmol/L,respectively after the treatment.Compared with pretreatment,the levels of plasma viscosity and erythrocyte aggregation index in the two groups were significantly decreased and serum NO level was increased after the treatment (t=9.07,12.17,17.85,15.76,9.38,12.78,respectively,all P＜0.05).Compared with the control group,the levels of plasma viscosity and erythrocyte aggregation index in the treatment group were significantly decreased and serum NO level was increased (t =8.91,3.27,4.21,all P＜0.05).Conclusions The oral beraprost sodium can effectively and safely improve the hemorheologic and endothelial function in elderly patients with LEAOD.

Objective To investigate the anti-apoptosis effects of EG-VEGF on pancreatic cancer cell MiaPaCa and its molecular mechanism. Methods The cells were treated with 50, 100, 200 ng/ml EG-VEGF. Flow cytometry was used to determine the apoptosis. The expression of p42/44MAPK, STAT3 protein and the phosphorylation, and anti-apoptosis protein Mcl-1 was evaluated by Western blot. Non-specific G protein-coupled receptor antagonist PTX, Rsa/ERK signal transduction blockade PD98059, JAK/STAT3 signal transduction blockade AG490 were used to treat the cells for 1 h, and the change of Mcl-1 protein was observed. Results After treated with 50 ng/ml EG-VEGF, the apoptosis rate of MiaPaCa was decreased from (28.4 ±4.6)% to (13.21 ±4.65)% (P<0.05) ; the phosphorylation of p42/44MAPK increased by 1.735 ± 0.019 folds; the phosphorylation of STAT3 increased by 21.810 ± 0.052 folds; the expression of Mcl-1 protein increased by 3.460 ±0.002 folds when compared with that of control group,and the difference was statistically significant (P < 0.05 ). But the degree of phosphorylation and the expression of Mcl-1 were not further increased with 100, 200 ng/ml EG VEGF treatment. After PTX pre-treatment, the increase of Mcl-1 protein expression was completely inhibited, and after PD98059, AG490 pre-treatment, the increase of Mcl-1 expression was inhibited to 52% and 68%. Conclusions EG-VEGF can inhibit MiaPaCa cell from apoptosis,and the mechanism may be related with activation of Ras MAPK and JAK STAT3 signal transduction pathway and up-regulation of Mcl-1.

Objective To investigate the effect of epidermal growth factor (EGF) on the expression of Matrix metalloproteinase-9 (MMP-9) and the signalling pathways involved in the trophoblast cell line JEG-3. Methods The JEG-3 trophoblast cell line was used in this study. (1) JEG-3 cells were cultured with various concentrations of EGF (0, 1, 10,20 ng/ml) for 24 hours and the expression of MMP-9 was tested by western blotting and reverse transcription PCR (RT-PCR). (2) Western blotting and RT-PCR were also used to investigate the expression of MMP-9 expression after incubation for 0,4,12 and 24 hours with EGF treatment (10 ng/ml) in JEG-3 cells. (3) According to the different added ingredients, JEG-3 cells were divided into some groups: control group (without EGF), EGF group (exposure to l0ng/ml EGF),EGF + inhibitors group (exposure to 10 ng/ml EGF +20 ng/ml SB203580 or exposure to 10 ng/ml EGF + 10ng/ml U0126) inhibitors group (exposure to 20 ng/ml SB203580 or exposure to 10 ng/ml U0126). Western blotting were used to investigate the expression levels of MMP-9, nuclear factor kappa B (NF-kB) ,p38MAPK, phospho-p38MAPK (p-p38MAPK) , extracellular -signal regulated kinase (ERK) and phospho-ERK (p-ERK) protein in JEG-3 cells after incubation for 24 hours. Results (1) The profiles of MMP-9mRNA were increased by various concentrations of EGF (0, 1 , 10, 20 ng/ml) in JEG-3 cells after 24hculture. The expression of MMP-9 mRNA in JEG-3 cells exposure at 1 ng/ml of EGF (0. 567 ±0. 056) , 10ng/ml of EGF (1. 392 ±0. 133) , 20 ng/ml of EGF (1. 971 ±0. 067) were significantly higher respectively (P <0. 05) , compared with 0 ng/ml of EGF treatment (0. 166 ±0. 015). Similarly, MMP-9 mRNAs were also increased with the increasing incubation time. Compared to EGF (10 ng/ml) stimulation for 0 h (0.253 ±0.044), the MMP-9 mRNA profiles were 0. 470 ±0. 026, 1.061 ±0. 115, 1. 453 ±0. 180 for 4,12 and 24 hours, respectively (P < 0. 05). (2) In accordance to the mRNA profiles, the expression of MMP-9 protein was also increased by different concentrations of EGF (0,1, 10, 20 ng/ml) in JEG-3 cells after 24 h-culture. The abundance of MMP-9 protein in the three groups was 0. 043 ±0. 012, 0. 085 ±0. 008, 0. 142 ±0. 015, with a significantly higher expression, compared with 0 ng/ml of EGF treatment (0. 004 ±0.001, P < 0.05) respectively. Similarly, MMP-9 proteins were also increased with the increasing incubation time. Compared to EGF(10 ng/ml) stimulation for 0 h (0. 030 ±0. 009) , the profiles of MMP-9 protein were 0. 137 ± 0. 010, 0. 240 ± 0. 010, 1.240 ±0.061 for 4, 12 and 24 hours, respectively (P < 0.05). (3) Both p38MAPK and ERK signalling pathways were activated by EGF in JEG-3 cells. The expression of p-p38MAPK was significantly higher (without or with 10 ng/ml EGF, 234. 1 ± 4. 1 vs.260. 9 ± 2. 5 , P < 0. 05) , however, the p38 MAPK inhibitor SB203580 markedly suppressed the increase in p-p38MAPK content induced by EGF(227. 9 ±2. 4 vs. 260. 9 ±2. 5, P<0. 05). Similarly, the expression of p-ERK was significantly higher with EGF treatment (812. 2 ±3. 5) vs. without EGF group (453.4±5.8) (P <0. 05) , while the ERK inhibitor U0126 significantly inhibited the increased p-ERK content in response to EGF treatment (71. 0 ± 1. 2 vs. 812. 2 ± 3. 5, P < 0. 05) . (4) The p38MAPK inhibitor SB203580 significantly reduced the expression of EGF-induced MMP-9 (0. 645 ± 0. 270 vs. 1. 476 ± 0. 452, P < 0. 05)and NF-kB (0.530 ± 0.026 vs. 0.959 ± 0. 017, P < 0. 05) . (5) The ERK inhibitor U0126 also significantly reduced the expression of EGF-induced MMP-9 (0. 623 ±0. 030 vs. 2. 112 ±0. 056, P <0. 05)and NF-kB (0. 325 ± 0. 082 vs. 0. 939 ± 0. 153, P < 0. 05). Conclusion EGF induced the expression of MMP-9 in a time and dose-dependant manner in JEG-3 cells. EGF enhanced MMP-9 expression through the activation of p38MAPK and ERK signalling pathways in JEG-3 cells.