医院医疗健康大数据中心的建设是一项系统工程,如何分步骤、科学、有效实施是亟需解决的现实问题.本文初步提出了综合医院多源异构健康体检数据平台建设方案,将包含有绝大多数临床诊疗数据类型的健康体检资料作为研究对象,探讨了健康体检数据平台建设目的 、整体框架,以及卫生信息标准、数据治理、数据质控、数据建模、数据应用等关键技术,可为建设医疗信息互联互通的医院"医疗健康大数据中心"提供技术储备.

Aim: To assess the effectiveness of antibiotic therapy against five indicator bacteria in a Chinese hospital using an index-based approach. Methods: The study population comprises 1031 patients who had one clinically significant bacterial isolate in 2008, 2010 and 2013. Drug resistance index (DRI) based on pathogens was calculated. Results: The adaptive DRIs for Klebsiella pneumoniae, Pseudomonas aeruginosa, Staphylococcus aureus decreased, while both adaptive and fixed DRIs for Acinetobacter spp. increased from 2008 to 2013. The adaptive DRIs for Escherichia coli increased from 2008 to 2013, while the fixed DRIs exhibited a decreasing trend. Conclusion: DRI could be used to demonstrate the changes of antimicrobial resistance and prescribing over time as a result of evolutionary processes and governmental regulatory interference.

Objective To compare the differences between two statistical methods for evaluating non-sensitivity of pathogenic bacteria to antimicrobial agents,and explore effect of non-consideration of clinical background on evalua-ting extent of bacterial resistance.Methods Data of Staphylococcus aureus and Acinetobacter spp .in a hospital in the first half year of 2008,2010 and 2013 were collected and conducted statistical analysis with two methods (me-thod 1 :based on all clinically isolated bacteria;method 2 :based on infection-related non-repetitive bacteria),two methods for evaluating bacterial non-sensitive rates to antimicrobial agents were compared.Results The non-sensi-tive rates of Acinetobacter spp .to various antimicrobial agents :statistical results by using method 1 were generally higher than those using method 2,absolute difference between two statistical methods was 10.46%-33.77%;the non-sensitive rates of Staphylococcus aureus to various antimicrobial agents :except compound sulfamethoxazole in 2010 and 2013(difference were 6.17% and 10.21 % respectively),penicillin G (difference was 3.86%),erythromy-cin (difference was 2.71 %),and azithromycin in 2013 (difference was 2.43%),statistical results by using method 1 were generally higher than those using method 2,absolute difference between two statistical methods was 0-18.04%.Conclusion There are deviation in the non-sensitive rates of bacterial strains to antimicrobial agents by using two different statistical methods,deviation is larger in Acinetobacter spp ..The resistance level might be incorrectly higher when evaluating the resistance status without considering clinical background of bacteria.

本文从门诊信息系统改造的目标和适应医保政策要求的实现等方面,就军队医院门诊系统适应医保需要改造的相关问题进行了探讨.

分析了传统PACS硬件平台的不足,提出了适用于大型医院新一代信息系统、高可用PACS系统的技术要求,设计实现了一个基于双机实时应用集群和虚拟化技术的高可用性PACS硬件平台.实际应用表明,该技术平台具有管理自动化程度高、故障恢复迅速、异地容灾、报表数据实时查询等技术优势,可满足大型医院新一代PACS系统建设的需求.

[目的]:设计实现适合大型医院的高可用、高可靠医院核心信息系统数据的备份恢复平台,保证医院核心信息系统的数据安全和业务连续性.[方法]:在综合分析该领域新技术的基础上,针对307医院实际情况和不同业务系统需求特性确定具体技术方案,利用Oracle RMAN进行数据库备份并通过TSM备份服务器完成到物理磁带库的离线备份,设计消息平台做备份的可靠性验证;使用虚拟化技术实现数据恢复及业务接管,同时利用Oracle Data Guard实现容错；制定针对不同业务系统的数据备份和恢复方案.[结果]:在307医院建立了一体化的HIS、PACS、LIS等核心系统数据备份恢复平台,并已上线运行,可以很好地满足实际应用需求.该方案可为其他大型医院建立类似平台提供设计参考.

探讨一套适合于三甲医院学科评估的方法,并介绍了学科评估辅助软件系统的设计、实现思路.使用软件辅助进行医院学科评估,提升了工作效率和效益.采用软件辅助进行学科评估,不仅便于评估方法的横向对比,也可以对历次评估结果进行纵向分析,能为管理者对学科建设决策提供更丰富的数据信息.

Objective To identify the changes of DNA methylation profile in the process of malignant transformation of BEP2D cell induced by α particles.Methods The genomic DNAs were isolated from the malignant transformation BERP35T4 cells and immortalized human bronchial epithelial cell line BEP2D.Genomic DNAs were digested by MseI and ligated of PCR linkers.Methylated DNAs were digested by BstUI and amplified by PCR.The methylated DNA probes were prepared by labeling with Cy3 and Cy5 fluorescence dyes individually and hybridized to the methylation CpG-Island microarray.The hybridization results were scanned and analyzed.Intensity values were quality controlled and normalized.The normalized data were used to identify the differentially expressed genes based on a 1.5 fold difference of the expression level.Results There were 16 genes which showed changes of methylation level in malignant transformation BERP35T4 cells, 9 of them were hypermethylation and 7 were hypomethylation.These genes were including the SKIP gene, PPP3CC gene, MAP2K6 gene, KIR2DL1 gene, KIR2DL4 gene, KIR3DP1 gene, ZNF493 gene, ZNF100 gene, NKX2-5 gene, TFAP2D gene, DR1 gene, KCNJ16 gene, CCDC18 gene, FNBP1L gene, IRX4 gene, EPB41L3 gene, TCP10 gene and so on.Conclusions The DNA methylation might have effects on ionizing radiation drived tumorigenesis.

Despite the significance of oxidative damage in carcinogenesis, the molecular mechanisms that lead to increased susceptibility to oxidative stress are not well understood. We now report a link between loss of protection against oxidative damage and loss of function of PTEN, a highly mutated tumor suppressor gene in a variety of human tumors. Using two-dimensional gel electrophoresis, combined with Western and Northern blot analyses, we found that PTEN deficiency in mouse embryonic fibroblasts (MEFs) displays deregulated expression of several antioxidant enzymes. including peroxiredoxins 1, 2, 5, and 6 and Cu, Zn superoxide dismutase. In these Pten-deleted MEFs, the basal levels of reactive oxygen species (ROS) were increased, and both the basal level and the ROS-induced oxidative damage of DNA were increased, as evidenced by increased levels of hydrogen peroxide (H2O2), superoxide anion, 8-hydroxy-2'-deoxyguanosine, and DNA double-strand breaks. We further show that Pten deletion is correlated with resistance to H2O2-induced expression of several antioxidants. These findings suggest an essential role for PTEN in maintaining the normal redox state of mouse embryonic fibroblasts against oxidative damage. They also provide a molecular link between PTEN. whose inactivation is known to be involved in a variety of human tumors, and antioxidants, whose perturbation leads to oxidative damage of cells. (c) 2008 Elsevier Inc. All rights reserved.

Objective:To explore the potential molecular functions of pleiotrophin(PTN).Methods:The Arizona cancer center bioinformatics resources were used to perform bioinformatics analysis.The Ptn-related genes which identified from genomic-based cDNA microarray analysis were put to GO Terms analysis to classify genes based on gene ontology terms,and Pathway Miner analysis to classify and extract network of associated genes/proteins based on KEGG,BIOKARTA and GENMAPP resources.Results:Bioinformatics analysis revealed that in 370 Ptn significantly related genes,231 genes were present in GO Terms database and 105 genes were found in Pathway Miner database.According to GO Terms analysis,the distribution of these present genes was as follows,cellular component,31.83%;molecular function,35.34%;biological process,32.83%.According to Pathway Miner analysis,more than 100 pathways were associated with these genes,these pathways including cellular and regulatory process pathways and metabolism pathways.Conclusion:The bioinformatics analysis results manifested that PTN is an important cytokine which should be involved in immune and defense response,inflammatory response,cell proliferation and apoptosis regulation and so on.

Objective To study the effect of TGF-β1 on the activation of ERK MAPK in human bronchial epithelial BEP2D cells. Methods Western blot was employed to examine the time-dependent activation of ERK MAPK by TGF-β1. BEP2D cells were harvested after treatment of human bronchial epithelial cells with 2 ng/ml TGF-β1 for 0, 10, 30, 60, 120, 240 and 480 min, respectively. Fluorescent dye staining and flow cytometry were employed to assess the apoptosis of BEP2D cells treated with vehicle, or with 2ng/ml TGF-β1, or co-treated with 2ng/ml TGF-β1 and 5μM U0126. Proliferation of BEP2D cells treated with vehicle, or with 2ng/ml TGF-β1 or 5μM U0126, or co-treated with 2ng/ml TGF-β1 and 5μM U0126 was assayed with colony-forming test, respectively. Morphological observation was performed to observe the morphological changes in BEP2D cells treated with vehicle, or with 5ng/ml TGF-β1 or 5μM U0126, or co-treated with 5ng/ml TGF-β1 and 5μM U0126, respectively. Results TGF-β1 activated ERK MAPK in BEP2D cell. The maximal activation of ERK MAPK took place at 60min after stimulation with 2ng/ml TGF-β1. TGF-β1 treatment effectively inhibited cell proliferation, and induced their apoptosis and epithelial-mesenchymal transition. Pretreatment with U0126, an inhibitor of ERK MAPK, significantly enhanced the TGF-β1-mediated anti-proliferation and apoptosis effects, and inhibited the effect of epithelial-mesenchymal transition of TGF-β1 in BEP2D cells. Conclusion TGF-β1-induced phosphorylation of ERK MAPK may participate in BEP2D cell proliferation and apoptosis regulation.

目的 研究转化生长因子-β1(TGF-β1)在永生化人支气管上皮细胞BEP2D信号转导中MAPK家族ERK通路的激活情况及其引起的细胞增殖、凋亡和形态学的改变.方法 用Western blot方法检测TGF-β1对ERK的活化特点;用荧光染料染色分析和流式细胞术检测TGF-β1引起ERK活化时细胞的凋亡变化;用细胞克隆形成率分析TGF-β1引起ERK活化时细胞的增殖情况;观察TGF-β1引起ERK活化时细胞的形态改变.结果 TGF-β1可在短时间内激活ERK1/2,1h达峰值,然后逐渐减弱;TGF-β1诱导BEP2D细胞凋亡,抑制其增殖,使其体积和间距增大;用U0126抑制ERK通路,能促进TGF-β1对细胞在凋亡、增殖方面的作用,但抑制其对细胞形态的影响.结论 TGF-β1诱导的ERK1/2的磷酸化在调节BEP2D细胞的增殖和凋亡间的平衡方面起着重要作用.

Objective:To explore the change of gene expression profiles in Pten-/-MEF241 cells,in which the secretion of growth factor pleiotrophin(Ptn) was inhibited by the Ptn-specific siRNA and normal Pten-/-MEF241 cells using cDNA microarray.Methods:The total RNAs were isolated from the Ptn-inhibited Pten-/-MEF241 cells and normal Pten-/-MEF241 cells.Total RNAs were purified and subjected to reverse transcription into first-strand cDNA.The cDNA probes were prepared by labeling with Cy3 and Cy5 fluorescence dyes individually and hybridized to the Agilent rat oligo microarray containing approximately 22392 rat genes.Differential expression genes were analyzed using Aglient Feature Extraction software.Results:Expression of 240 genes was up-regulated by two-fold in the Ptn-inhibited Pten-/-MEF241 cells,while expression of 129 genes was down-regulated by 0.5 time.Conclusion:The difference of gene expression profiles between the Ptn-inhibied Pten-/-MEF241 cells and normal Pten-/-MEF241 cells was suceessfully analyzed by cDNA microarray.

To investigate the function of Smad4 in ERK/MAPK signaling pathway in human bronchial epithelial BEP2D cells, siRNAs were designed to specifically target Smad4 in BEP2D cells, siRNA transfection and western blots were performed to examine the phosphorylation levels of ERK and MEK. The results showed that Smad4 gene silencing leads to the phosphorylation level of MEK1 but not ERK decreased. After stimulation with TGF-#beta#1, phosphorylation levels of both ERK and MEK are decreased and lower than the control cells. The results demonstrated that Smad4 is participating in the activation of the ERK/MAPK signaling by TGF-#beta#1.

To investigate the function of Smad4 in ERK/MAPK signaling pathway in human bronchial epithelial BEP2D cells. siRNAs were designed to specifically target Smad4 in BEP2D cells. siRNA transfection and western blots were performed to examine the phosphorylation levels of ERK and MEK. The results showed that Smad4 gene silencing leads to the phosphorylation level of MEK1 but not ERK decreased. After stimulation with TGF-β1, phosphorylation levels of both ERK and MEK are decreased and lower than the control cells. The results demonstrated that Smad4 is participating in the activation of the ERK/MAPK signaling by TGF-β1.

Objective To investigate the mechanism of TGF-β on the phosphorylation of extracellular signal-regulated kinase ERK or p44/42 in human bronchial epithelial BEP2D cells. Methods siRNAs were designed to specifically target TβRⅡ and Smad7 of BEP2D cells. siRNA transfection and Western blot were performed to examine the phosphorylation of ERK. Results Smad7 gene silencing leads to the phosphorylation level of ERK decreased. When expression of TβRⅡ and Smad7 was knock-down at the same time TGF-β1-induced phosphorylation level of ERK is decreased further and lower than the control cells. Conclusions TGF-β1 activate ERK/MAPK signaling in a TβRⅡ and Smad7 dependent manner.