Objective To explore the significances of the endoscopic diagnosis for chronic atrophic and histological assessment gastritis (CAG). Method Five hundred patients with CAG were determined by gastroscopy and the samples of gastric mucosa were examined by the pathology. Results Among 500 cases of CAG by gastroscopy, 429 cases were similar with the pathologic results and the coincidence rate of diagnosis with endoscopy and pathology was 85.8%(429/500), 370 cases had a change of atrophic gastritis in cirumjacent mucosa. Conclusion The coincidence rate of diagnosis under endoscopy and pathology is quite good in CAG.

Objective To introduce the necessity of newly added examination and approval system. Methods The expatiation content of examination and approval system, process and the attention-getting problems of implementation were expounded. Results The new system is established, on the one hand it can be made evidence-based in the purchasing process and on the other hand it can be limited to same species and wash out inadaptable manufacture. Conclusion The newly added examination and approval system was built to meet the clinic need and conform to the standard of using equipment in hospital.

The purpose of inviting public bidding is to enhance the management of medical consumables and reduce the cost of medical treatment. The project contains three aspects: fixing of the bid products and bid methods, compilation of the bid documents, evaluation of the bid and results collection. The bid project should follow some principles such as publicity, equity and honesty.

ObjectiveTo detect the mechanism of the growth inhibition and apoptosis of human acute leukemia cell line U937 cells induced by honokiol.MethedsThe proliferation inhibition was detected by MTT method.Cell apoptosis was tested by Hoechst 33342 staining and flow cytometry with Annexin V/PI staining.RT-PCR was used to detect the mRNA expression of the apoptosis gene Bcl-2,Bax,Caspase 3,Caspase 8 and Caspase 9.ResultsThe inhibition effect of honokiol(5 μg/ml,48 h) on U937 cells proliferation could he observed,and the inhibition rate of 10 μg/ml honokiol on cell proliferation reached above 50％ (48 h).U937 cells proliferation could be completely inhibited for 120 h. U937 cells apoptosis rate reached 26.8％ (P ＜0.01)after being treated with 10 μg/ml honokiol.After being treated with 10 μg/ml honokiol for 48 h,the Bcl-2 gene expression in U937 cells was reduced (control group:0.33 ± 0.02,experimental group:0.14 ±0.01,P ＜ 0.01 ),and the Bax gene expression was elevated ( control group:0.1 ± 0.01,experimental group:0.87 ± 0.08,P ＜ 0.01 ).The gene expressions of Caspase 3 ( control group:0.48 ± 0.01,experimental group:0.87±0.06,P ＜0.01),Caspase 8(control group:0.23±0.02,experimental group:0.41 ±0.07,P ＜ 0.01 ) and Caspase 9 ( control group:0.44 ± 0.05,experimental group:0.76 ± 0.06,P ＜ 0.01 ) were all increased.The activity of Caspase-3 was 0.325 ±0.089,which was significantly higher than that of the control group ( P ＜0.01 ).ConclusionHonokiol can significantly inhibit the proliferation and induce cell apoptosis of human acute leukemia cell line U937 cells.The mechanism is related to the up-regulation of Bax and down-regulation of Bcl-2,and the endogenous and exogenous pathways are both inolved in the apoptosis process.

Objective To study the effect of PPARγ ligand troglitazone (TGZ) on invasion and metastasis of gastric cancer cells, and investigate the relationship of PPARγ ligand with gastric cancer.Methods The expression of PPARγ in gastric cancer cell line MGC803 were detected by immunofluorescence cytochemistry method. The effect of different density TGZ on proliferation activity and adhesion of gastric cancer cell were detected by MTT chromatometry. The effect of different ligands on invasion and metastasis of gastric cancer cell MGC803 were detected by invasion system in vitro. Results The expression of PPARγ mainly located in cell nucleus. TGZ inhibited the proliferation of gastric cancer cell, decreased cell adhesion, locomotory capacity and invasion to matrigel, which had time and dose-dependent relationship.When treatment with 0. 1,1.0 and 10μ mol/ L TGZ, inhibition ratio of invasion and metastasis of cell was 8.79% ,31.31% ,51.42% and 28.29% ,4. 27% ,59. 27% respectively, which had statistical significance compared with control group( P <0. 05). When treatment was 10μ mol/L TGZ, cell adhesion was 0. 32 ±0. 03, it was statistically significant higher than that in control group (0. 52 ± 0. 04, P < 0. 05 ). Conclusion Human gastric cancer cell line MGC803 expressed functional PPARγ protein. TGZ inhibited adhesion and invasion of MGC803 cell on ECM at different degree, the effect of combination of two ligands was evident, which mechanism of action needed to be further investigated.

Objective To identify the gene mutation of Chinese Charcot-Marie-Tooth (CMT) pedigrees and investigate the association of gene mutation to the clinical manifestations and electrophysiology,and the underlying mechanisms.Methods A total of 105 pedigrees with CMT in our hospital were enrolled from January,2007 to December 2013.The clinical features,CMT neuropathy score (CMTNS) and electrophysiological data were collected.Gene mutations were analyzed using multiplex ligation-dependent probe amplification (MLPA) and Sanger gene sequencing.Results We found 31 (29.5％) PMP22 duplication pedigrees,8 (7.6％) GJB1 mutation pedigrees,4 (3.8％) MFN2 mutation pedigrees,4 (3.8％) HSPB1 mutation pedigrees,3 (2.9％) MPZ mutation pedigrees and 1 (1.0％) PMP22 mutation pedigree.In Chinese Han population,the proportion of PMP22 duplication was relatively lower than that in western countries and manifested with classical clinical characteristics of CMT.Subjects with axonal CMT often presented with isolated lower extremity injury and with central nervous system involvement.Hereditary motor neuropathy might be underestimated in clinical setting and should be differentiated from motor neuron disease.Conclusions The gene frequency distribution in patients with CMT in Chinese Han population is different from that in patients from western countries.We should establish our own epidemiological data of CMT in Chinese Han population.

BACKGROUND:Based on variational principle and weighting technology of three-dimensional finite element method, human teeth with a complex morphology can be modeled, which helps to understand the stress distribution of dental hard tissue and prosthesis during the dynamic repair process. OBJECTIVE:To comprehensively analyze the three-dimensional finite element studies concerning biomechanics of dental prostheses, focusing on the effects of metal crown, porcelain thickness, root canal preparation and fil ing on the tooth stress. METHODS:A computer-based search of PubMed (1993-04/2012-09), China Academic Journal Network Publishing Database (2001-2008), and VIP (2001-2008) was performed by the first author to retrieve articles concerning the effects of metal crown, porcelain thickness, root canal preparation and fil ing on the tooth stress. The keywords were“porcelain-fused-to-metal, finite element method, stress analysis, root canal”in English and Chinese. Articles with repetitive contents or meta-analysis were ruled out. Then 40 articles were suitable for further analysis.RESULTS AND CONCLUSION:Finite element method has important significance to establish high-fidelity and high-accuracy models in oral medicine, thereby providing effective biomechanical information for the root canal treatment and post-treatment repair. Scholars continue to explore the stress distribution of dental prostheses during chewing. This review summarizes the stress changes of post and core crowns, supporting reference for further research. Three-dimensional finite element method can be used to build nonlinear three-dimensional finite element models with anisotropic biomechanical characteristics, and can gradual yimprove the transition from static analysis to a dynamic analysis, truly achieving accurate simulation of oral biology and dental morphology as wel as chewing function of the teeth.

Objective To investigate the expression of Polo-like kinase 1 in renal clear cell carcinoma and tissue adjacent to carcinoma;impact of BI2536 on the cell proliferation of renal clear cell carcinoma A498 cell line.Methods We select 12 cases of renal cancer Specimens of randical surgery between January 2013 and December 2014.The study included 7 male patients and 5 female patients,whose age ranged from 41 to 68 years(mean 49 years).Tumors were single and the location of tumor included 5 in left kidney,7 in right kidney.The size of renal tumor ranged from 2.1 to 6.3 cm.All patients did not have radiotherapy and chemotherapy preoperative who have no local and distant matastasis.The pathological results demonstrated renal clear cell carcinoma in 12 cases.At the same time,we collect the tissue 2 centimeters away as control,which pathological results demonstrated normal tissue.The expression of PLK1 was detected by western bloting in tissues from 12 cases of renal clear cell carcinoma and tissue adjacent to carcinoma and quantitative analysis was made.Cell proliferation of A498 cell line at the different concentrations of BI2536 were assayed by flow cytometry (0,20,40,60μg/L).Results The expression of PLK1 in renal clear cell carcinoma tissue are 0.74 ±0.2 and 0.21 ±0.13.The carcinoma tissue is higher than tissue adjacent to carcinoma (P =0.02).BI2536 act on A498 after 48 hours,the A498 cell number were arrested at G2/M phase at 0μg/L,20μg/L,40μg/L and 60μg/L were (10.28 ± 0.47) ％,(14.35 ± 0.85) ％,(20.49 ± 0.78) ％ and (23.90 ± 0.54) ％,respectively.The A498 cell number were arrested at G2/M phase increase when we incearse the concentrations of BI2536 at 48 hours (P ＜ 0.05).Conclusions The higher expression of PLK1 in renal clear cell carcinoma and the proliferation of the renal clear carcinoma cell can be repressed by BI2536 both reveal PLK1 may be used as the molecular maker and therapeutics target of renal clear cell carcinoma.

Objective To evaluate the effect of different densities of830nm laser irradiation on genetic damages in mice cells.Methods 100Kunming mice were randomly divided into micronuleus groups and sperm group,as well as control group.Mice thymus glands and spleens were irradiated with an830nm semiconductor laser,30mW for5minutes or20minutes each day in vitro,and the micronuclei of polychromatic erythrocytes in sternum bone marrow and rate of abnormal sperm produced were determined.Results Laser irradiation induced deformed sperm(? 2 =111.747,P=0.000),while higher dose(20min per day)laser irradiation increased the micronuclei of polychromatic erythrocytes in sternum bone marrow.There was statistical significance in the difference between the rates of abnormal sperm and micronuclei in sternum bone marrow caused by irradiation on thymus and spleen(? 2 =27.395,P=0.000)and there was dosage effect.The spleen was the more sensitive.Conclusion Laser irradiation at830nm might have a genetic damages to mice cells.Attention should be paid to the potential hazardous effects induced by semiconductor laser irradiation.

Objective To investigate the biological effect of wild p16 gene on senescence of human keloid fibroblasts (HKFb) and discuss the feasibility of gene therapy on keloid. Methods Firstly, the HKFb was transfected with pcDNA3-p16 and the positive clones selected by G418. Then, the fibroblast changes were investigated by determining growth curve, cycle profile and ultrastructure of the transfected HKFb. Meanwhile, morphological changes of the transfected HKFb were identified by senescence associated-?-galactosidase staining. Results After HKFb was transfected by p16, the morphology of HKFb changed obviously from the third passage on. The cell proliferation was inhibited markedly and the cell cycle profile analysis showed that about 96.7% cells were trapped in stage G1. The electroscopic analysis of HKFb also showed that the lysosomes were overloaded. Senescence associated-?-galactosidase staining identified the senescence of HKFb. Conclusions The wild p16 gene can induce the HKFb into senescence in advance, as may provide experimental basis for gene therapy on human keloid.