Pancreatic adenocarcinoma is a severe-invasive, early-metastasis and malignant neoplasm with latent pathogenesis, while its biological behaviors are the highlight of current tumor study.In present study,through reviewing the studies related to expression profile of pancreatic cancer up to now.This artical summarized the achievement, challenge and trend of development of expression profile in pancreatic cancer.In conclusion, exploring the mechanism of carcinogenesis and development of pancreatic cancer based on the breakthrough of expression-profiling studies and establishing ideal models of pancreatic cancer, will promote systemic diagnosis and treatments of pancreatic cancer and do favor to the prognosis of the patients.

Great changes in drug metabolizing enzyme (DME) expression occur in the fetus and child during development. Individual hepatic DME ontogeny can be categorized into one of three groups based on developmental trajectories.Some enzymes such as CYP3A7,are expressed at highest level in the fetus dur-ing the first trimester and either remain elevated or slightly de-crease during gestation,but are silenced or reduced to relatively low levels within one to two years after birth.SULT1 A1 is an ex-ample of the second group of DME.These enzymes are ex-pressed at relatively constant levels throughout gestation and into adulthood.CYP3A4 belongs to the third DME group .These en-zymes are expressed at negligible or low levels in the fetus.Sig-nificant increases in enzyme levels are exhibited within the first one to two years after birth.The epigenetic regulation refers to genomic modifications that do not involve changes in DNA se-quence and include DNA methylation,histone modifications, and non-coding RNAs.The epigenetic regulation mechanisms are responsible for the developmental expression of DME genes dur-ing liver maturation.This review will provide a summary of DME developmental expression profiles and reveal epigenetic mecha-nisms underlying variable drug metabolism and drug response. Thus,knowledge regarding DME ontogeny has permitted im-proved capability to predict drug disposition in pediatric pa-tients,which is crucial for improving drug dosing leading to opti-mal safety and efficacy in children.

Objective:To select the differentially expressed vascular smooth muscle cell(VSMC) apoptosis gene induced by icariin,glucose regulated protein 78(GRP78),to observe the expression of GRP78 in atherosclerosis tissue and to the elucidate the mechanism of anti-atherosclerosis of icariin.Methods:The model was established by using halfcystine in viro.The vascular smooth muscle cell was incubated with various concentrations of icariin for 48 hours.The apoptosis was detected by TUNEL assay.GRP78 gene was amplificated by PCR,recombinant plasmid were constructed,transfected into E.coli,positive clonings were selected and conf irmed by restriction endonucleas analysis,and sequence-ed.Tissue situ hybridization was used to observe the GRP78 expression in atherosclerosis tissue.Results:Icariin promoted obviously vascular smooth muscle cell apoptosis.Furthermore,the fragment,648bp,was similar to the gene of GRP78 from VSMC,and the expression level was signif icantly higher in high cholesterol group than in control nroup.Conclusions:The GRP78 plays a key role in inducing atherosclerotic lesions.The mechanism of anti-atherosclerosis of icariin might be partly due to promoting apoptosis of vascular smooth muscle cell.

AIM: To investigate the effect of curcumin on the binding activity of hepatic nuclear factor-kappa B(NF-?B) and the expression of peroxisome proliferator-activated receptor-?(PPAR-?) in rats with liver fibrosis induced by carbon tetrachoride. METHODS: A total of 60 clean male rats were randomly and averagely divided into group A,B,C,D,E and F.The rats in group A served as normal controls,while those in other five groups were injected subcutaneously 40% CCI_4 for seven weeks to induce the model of liver fibrosis.After seven weeks,the rats in group C,D,E,F were intragastrically administered with 50 mg/kg silibinin,100 mg/kg cur,200 mg/kg cur,400 mg/kg cur once per day for six weeks,respectively.HE staining was used to observe the pathological changes of liver tissues under light microscope,and immunohistochemistry and reverse transcriptase polymerase chain reaction(RT-PCR) were performed to detect the activity of NF-?B,PPAR-? and mRNA expression of PPAR-?.RESULTS: The inflammatory and fibrotic degrees were obviously alleviated in group C,D,and E compared with group B.The expression of NF-?B p65 was significantly decreased in liver tissue in group C,D and E,compared with model control group B(P

Objective To investigate changes of N-methyl-D-aspartic acid receptor 2B(NR2B) level and calcium/calmodulin-dependent protein kinase Ⅱ(CaMK Ⅱ) activities in the hippocampus of vascular dementia(VD) rats and the intervention effects of Memantine.Methods The VD rat models were established by permanent,bilateral occlusion of the common carotid arteries.The rats were randomly divided into VD group and Memantine-treated group.At 4,8,12,16 weeks after operation,the water maze test was performed to detect the ability of learning and memory of the rats.The changes of NR2B level were measured by RT-PCR.The changes of the CaMK Ⅱ activities were determined by incorporation of 32P into histone.The resoults were compared with the sham-operated group.Results Compared with the sham-operated group,the ability of learning and memory of VD group rats at each time point after operation decreased significantly(all P

Objective To recognize hereditary IgM glomerulopathy. Methods Three patients with hereditary IgM glomerulopathy were report first time in China. Genealogic investigation and light, immunofluorescence and electron microscopy were performed. Literatures concerned were reviewed. Results Kidney biopsies from three patients all revealed diffuse mesangial proliferative glomerulonephritis with intense IgM and C3 deposits. These siblings might be suffering from a hitherto undescribed clinico-pathological entity. Genealogic investigation enabled us to discover 10 additional affected members with clinical glomerulonephritis in the kindred of the family. The clinical picture was that of hematuria and/or proteinuria, meanwhile one patient died of uremia. Conclusion Genetic factors may be involved in the mechanism of IgM nephropathy .

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.

Objective To evaluate the role of multi-slice computed tomography (MSCT) in the diagnosis of pulmonary sequestration.Methods MSCT scans of 18 cases of pulmonary sequestration proved by surgery and pathology were reviewed.All cases underwent plain and contrast enhanced CT scanning,and retrospective reconstruction was made.Various reconstruction techniques in displaying the pulmonary sequestration and associated malformation were evaluated.Results Anomalous systemic arterial supply was discovered by transverse CT images in 12 cases.The reconstructed images using multiple methods showed the aberrant artery more clearly in all cases,including 6 cases in which the abnormalities were not confirmed by transverse CT.Drainage vein was revealed in 13 cases and lung heteroplasia with other malformation was demonstrated in 14 cases.Volume rendering (VR) reconstruction is the optimal choice for displaying the abnormal vessels and airway.Conclusion Enhanced MSCT with image post-processing can show the abnormal artery and vein of the pulmonary sequestration and the associated malformation,so it is the first choice in diagnosing pulmonary sequestration in pediatric population.

Objective α?Asarone has the effect of relieving cough and asthma as well as sedative, hypnotic and anticonvul?sive function. Our study was designed to explore the effects of apoptosis induced by α? Asarone on human esophageal carcinoma Eca?109 cell line as well as the expression levels of GADD153 and Smac mRNA. Methods Human esophageal carcinoma Eca?109 cells were cultured in vitro, which were divided into blank control group, 5?FU group( 500μg/mL) andα?Asarone group of different dosages ( 25,50,100μg/mL) . After cultivation, MTT method and Annexin V?PI were used to measure cell proliferation rate and apoptosis rate. Expression levels of GADD153 and Smac protein and mRNA were detected by western blotting and real? time quantitative PCR. Results Compared with blank control group, the cell proliferation rates in other groups decreased significantly (P<0.01), and cell apoptosis rate increased significantly ( P<0.01) . Compared with blank control group, the expression levels of GADD153 and Smac pro?tein and mRNA in other groups increased significantly( P<0.05) . Conclusion α? Asarone can inhibit cell proliferation and induce the apoptosis of human esophageal carcinoma Eca?109 by regulating the expression levels of GADD153 and Smac gene.

AIM: To select differentially the expressed gene,glucose regulated protein 78(GRP78),to observe the expression of GRP78 in atherosclerosis tissue and to elucidate the mechanism for anti-atherosclerosis of puerarin.METHODS: The model was established by using homocysteinemia in vitro.The vascular endothelial cells were incubated with various concentrations of puerarin(10 -7 mol/L,10 -6 mol/L,10 -5 mol/L) for 48 h.The apoptosis rate was detected by flow cytometry using Annexin/PI-staining.GRP78 gene was amplificated by PCR.These differentially expressed fragments were cloned,selected,confirmed,and sequenced.Digoxigenin-labeled DNA Probe and cholesterol-rich rabit model were prepared,GRP78 mRNA was determined by in situ hybridization in atherosclerotic lesions and normal tissue.RESULTS: Three concentrtions of puerarin significantly inhibited the apoptosis of endothelial cells.The early apoptosis rate was decreased magnificently in a dose dependent manner compared with that of HCY group (P