Objective To evaluate the applicated value of color Doppler ultrasonography (CDUS) and CR molybdenum target in the diagnosis of breast nodules.Methods Comparative analysis of 87 patients with breast nodules diagnosed by CDUS and CR molybdenum target were contrasted with postoperative pathology.Results 47 cases of 78 patients with breast nodules were benign lesions.39 cases were correctly diagnosed by CR molybdenum target,41 cases were correctly diagnosed by CDUS,and 44 cases were correctly diagnosed by CR molybdenum target and CDUS.Contrasted with postoperative pathology,the accuracy rates of breast disease diagnosed were 82.5％,75.0％ and 95.0％ diagnosed by CR molybdenum target,CDUS,CR molybdenum target and CDUS.Conclusion There is no significant statistical difference between CR molybdenum target and CDUS in the diagnosis of benign breast nodules.The accuracy rate of breast disease diagnosed by CR molybdenum target and CDUS is better than that diagnosed by CR molybdenum target or CDUS only.The two co-diagnosis are benefit to raise the accuracy rate of breast nodules.

4 mm in diameter, re-operations of ESWL were required until no stones were detected. Results All the patients presented a good tolerability to the treatment and left for home by themselves. With exception of 1 case of failed lithotripsy, the ESWL was successfully accomplished in the rest of 17 cases after receiving 3~9 times of treatment. One or two times of hematuria occurred in 66 times of treatment (66/77, 85.7%). A “stone terrace”, 1.9~5.2 cm in length, was found in 5 cases, 4 of which were cured by re-operation of ESWL and 1 of which underwent ureteroscopic removal of stones. Conclusions Low-energy extracorporeal shock wave lithotripsy is a safe and effective option for patients with renal staghorn calculi.

Objective To analyze the influence of peptidimer-c on the gene expression profiling of K562 cells and investigate the mechanism of peptidimer-c inducing the apoptosis and inhibiting proliferation of K562cells.Methods Trypan blue staining technique was performed for counting the number of living K562 cells treated with peptidimer-c.The ultrastructure changes of K562 cells treated with peptidimer-c was observed under transmission electron microscope.The Human U133 Plus 3.0 gene chips were used to detect the differentially expressed genes of K562 cells treated with peptidimer-c.Reverse transcription PCR was conducted to confirm some genes identified by gene chips.Results Peptidimer-c could induce the apoptosis and inhibit the proliferation of K562 cells.Peptidimer-c caused widely changes of the gene expression profiles of K562 cells.The chip data suggested that there were 529 differentially expressed genes,of which 455 genes were up-regulated and 74 genes were down-regulated.The relevant apoptotic genes were down-regulated markedly,including JUN,AXUD1,TNFRSF10B,etc.Fifteen of the differentially expressed genes were detected by RT-PCR,which was consistent with the chip data.Conclusion Peptidimer-c may induce aooptosis of K562 cells by activating the TNF/TNFR family and the JUN family.

AIM:To study the effcts of caspase recruitment domain membrane-associated guanylate kinase protein 3 (CARMA3) knockdown on the growth, migration and invasion of human colonic carcinoma HCT116 cells and to analyze the mechanism.METHODS:A colonic carcinoma cell line with CARMA3 over-expression was selected.The CARMA3 gene in the HCT116 cells was knocked down by lentivirus technique.After screening by puromycin, the stably-transfected HCT116-shCARMA3 cell line was constructed.CARMA3 expression at mRNA and protein levels was detected by real-time PCR and Western blot,respectively.The cell proliferation was analyzed by WST-1 assay and RTCA S16 system.The colony formation ability was measured by colony-forming assay.The cell cycle was analyzed by flow cytometry.The cell morphological changes were observed under microscope.The abilities of migration and invasion in vitro were observed by wound healing assay and Transwell assay.The changes of related molecules were determined by Western blot to explore the mechanism.RESULTS:The expression of CARMA3 at mRNA and protein levels in the HCT116 cells was the highest in the 4 colonic carcinoma cell lines.HCT116-shCARMA3 cells with stably-silenced CARMA3 gene were successfully established.Among them, HCT116-shCARMA3-93 cells showed the greatest inhibition of CARMA3 at mRNA and protein levels.Therefore,HCT116-shCARMA3-93 cells were chosen as the cell model.Compared with control group, the morphological changes of the HCT116-shCARMA3-93 cells had epithelial-mesenchymal transition (EMT) reversion.The abilities of proliferation, colony formation, migration and invasion in the HCT116-shCARMA3-93 cells were obviously suppressed (P<0.01).G0 /G1 phase proportion was increased and S phase proportion was correspondingly decreased (P<0.05).Bcl10 and NF-κB were down-regulated, and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1)showed no change.Cyclin D1 was decreased obviously and cyclin A declined slightly.Metastasis-related mar-kers matrix metalloproteinase (MMP)-2 and MMP-9 were reduced,MMP-7 remained unchanged, while tissue inhibitor of metalloproteinase(TIMP)-1 and TIMP-2 were up-regulated.Furthermore, EMT-associated molecule E-cadherin was increased, while N-cadherin, Snail, Slug and Twist were decreased to some extent.CONCLUSION:CARMA3 has an impact on the growth,migration and invasion of colonic carcinoma cell line, which is possibly related to NF-κB signaling pathway to change cell cycle and metastasis-related markers and to regulate EMT.

Objective To study the effects of extracellular-signal regulated kinase mitogenactivated protein kinase (ERK-MAPK) signaling pathway inhibition on histone phosphorylation and the related gene expression in human colorectal cancer cells.Methods Two human colorectal cancer cell lines (SW1116 and HCT116) were cultured and treated with gradient(0,20,40/μmol/L) doses of ERK-MAPK signaling pathway inhibitor U0126.Cell viability was determined by cell counting kit 8 (CCK-8) assay.Cell cycle distribution was assessed by flow cytometry.The expression levels of histone H3 kinases including ribosomal S6 serine-threonine kinase (RSK-2) and mitogen-and stressactivated protein kinase 1 and 2 (MSK1 and MSK2),and the levels of histone H3 (Ser10) phosphorylation and c-Fos protein were detected using Western blotting.Results Treatment of these two human colorectal cancer cell lines with ERK-MAPK inhibitor resulted in a time and dose-dependent inhibition of cell proliferation significantly. Proliferation rate of HCT116 was reduced to 47% at 72 hours after 40/μmol/L U0126 treatment. Cell cycle analysis showed that the percentage of phase G0/G1 cells significantly increased (P<0. 01) and the percentage of phase S cells decreased (P<0.01) after treatment with ERK-MAPK inhibitor. The expression of MSK1 and RSK2 reduced obviously in both of human colorectal cancer cell lines treated with U0126, which resulted in a 28% and 40% reduction of levels of MSK1 and RSK2 as compared with control HCT116 cells respectively,while no detectable change in the expression of MSK2 was found. Consistent with this, the expression level of histone H3 (ser10) phosphorylation was markedly down-regulated by ERK-MAPK inhibitor, and the related protein c-Fos expression decreased accordantly. Conclusions Decreased ERK-MAPK signaling pathway may reduce histone H3 (Ser10) phosphorylation via suppression of the activity of histone H3 kinase including MSK1 and RSK2, but not MSK2, consequently decrease the expression of c-Fos protein, which results in the inhibition of colorectal cancer cells proliferation.

Objective To investigate the effect of folic acid on the DNA methylation of tumorrelated genes promoters in healthy human peripheral blood mononuclear cells(PBMC). Methods Ten healthy volunteers were divided into two groups, and were randomized to receive either 5 mg folic acid (n=5)or placebo(n = 5) , one time per day for 3 months. The serum folic acid concentration was detected with chemiluminescence enzyme immunoassay kit before and after the intervention. The methylation statuses of five tumor-related genes promoter, including oncogenes c-myc, c-Ha-ras,tumor suppressor genes p16INK4A, E-cadherin and mismatch repair gene hMLH1 in PBMC were detected by bisufite sequencing. Results After folic acid intervention, the level of serum folic acid increased significantly in intervention group (t= -4. 739,P<0. 05) , however no significant difference in control group. After three-month folic acid intervention, the level of methylation of oncogene c-myc promoter increased from 4%, 3. 3%, 4. 1% before intervention, one week after intervention, one month after intervention respectively to 8%(t= -4. 079,P<0. 05), while no significant change in placebo taken group. Before and after the folic acid intervention, there was no significant difference of DNA methylation of other tumor-related genes promoter, including c-Ha-ras、E-cadherin、p16INK4Aand hMLH1. Conclusion Folic acid intervention can up-regulate DNA methylation of oncogene c-myc promoter, but can not affect the promoter methylation status of tumor suppressor genes E-cadherin,p16INK4Aand hMLH1.

Objective To explore the correlation of anxiety and depression with social support among caregivers of children with mental retardation and major related influencing factors.Methods 64 mothers of children with mental retardation were investigated by using the questionnaires of SAS,SDS and SSRS.The results underwent analysis.Results The incidence of anxiety among mothers of children with mental retardation was 23.4％,the incidence of depression was 40.7％.Mothers had higher scores of SAS and SDS than the national norm.The total score of social support was(32.19±5.02),which was lower than the national norm.The anxiety and depression was negatively correlated with social support.The influencing factors of anxiety and depression of mothers were family income.Conclusions The anxiety and depression among mothers of children with mental retardation was evident,the social supports for those mothers were insufficient.Effective social support was propitious to abate the anxiety and depression and promote quality of life of those children with mental retardation and their mothers.

ObjectiveTo investigate the related factors which influencing endoscopists in the accuracy of diagnosis of chronic atrophic gastritis (CAG). Methods With retrospective analysis method,from January to December in 2009,10 765 chronic gastritis cases underwent endoscopy examination in Renji Hospital,school of medicine,Shanghai Jiaotong University were collected.The influence of congestion and exudation,gastric ulcer,bile reflux,gastric polyps and H.pylori infection under endoscopy on CAG endoscopic and pathological diagnosis was analyzed.ResultsThe percentage of histopathological diagnosed CAG was 69.41％,endoscopic diagnosed CAG was 54.27％. The coincidence rate was 62.30％.2575 cases were H.pylori positive (23.92％),the coincidence rate between endoscopic and histopathological diagnosis in H.pylori positivc cascs was 90％.of that of H.pylori negative cases (β=-0.1067,P＜0.05).The coincidence was positively related to age.For each 1 year increase in age,the coincidence rate increased by 0.01 time [OR=exp(0.00855)=1.01]; For each 10-year increase in age,the coincidence rate increased by 0.09 time [OR=exp(0.0855) =1.09].The coincidence rate was negatively related to congestion and exudation.The coincidence rate of CAG between endoscopic and histopathological diagnosis in cases with congestion and exudation was 40％ of that without congestion and exudation (β=-0.1067,P＜0.01).ConclusionCAG diagnosed under endoscopy was somewhat subjective and should be combined with histopathological analysis.The patients' age,H.pylori infection,congestion and exudation may have influence on the coincidence rate between endoscopic and histopathological diagnosis of CAG.

Objective To investigate the feasibility of using ultrasound‐mediated destruction of microbubbles ( US+ MB) to enhance the transplantation of endothelial progenitor cells ( EPCs) to confer chronic allograft vasculopathy (CAV) .Methods Bone marrow derived mononuclear cells were isolated and induced in vitro . The abdominal aorta transplantation was performed . Four groups were divided:control group without treatment (group A) ,injection with saline (group B) ,injection with EPCs (group C) ,group D ( US+MB+EPCs) was injected with EPCs and US was applied to MB prior to the infusion . All rats were killed during 8 weeks after transplantation to enable histological examination;SDF‐1α expression was detected by immunohistochemistry ,the expression of SDF‐1αand TNF‐αin the grafted aortas were detected with RT‐PCR . Results When 8 weeks after EPCs transplantation ,there was a significant improvement in aortic intima of Group D compared with Group B and C ,respectively ( P <0 .05) . In addition ,treatment of Group D significantly increased the expression of SDF‐1αand reduced the expression of TNF‐αin the grafted aortas . Conclusions US‐mediated MB destruction prior to EPCs transplantation into the grafted aortas can improves the effectiveness of endothelial repair and delay the progress of CAV .

AIM:To observe the expressions of cathepsin B (CB) and cystatin C (CC) in different stage of diabetic rats and to investigates their potential roles.METHODS:Sixty rats were divided into diabetes mellitus group induced by intravenous injection of streptozotocin (55 mg/kg) and normal group injected with citrate buffer. Ten rats were sacrificed respectively at the end of fourth week,eighth week and sixteenth week in both groups. 24 h urine excretion was collected in rats before sacrifice. The blood and the kidney were also collected. The mRNA and protein expressions of CB and CC in kidney were detected by real time PCR and immunohistochemical staining,respectively.RESULTS:At the end of eighth week,the expression of Ccr,24 h urinary protein excretion,CB,CC in diabetic rats increased significantly,compared to the results at the fourth week (P