学术论文作者机构规范文档构建

以中国生物医学文献数据库为基础,面向基于学术论文开展机构检索、分析与评价相关知识服务需要,对学术论文作者机构名称规范目标与内容、体系结构与组织方式以及构建过程与实现策略进行研究、实践总结。     

The relationship between levels of salivary and serum interleukin-6 and oral lichen planus: A systematic review and meta-analysis

Background

The relationship between levels of salivary and serum interleukin (IL)-6 and oral lichen planus (OLP) is not understood fully. The authors conducted a systematic review and meta-analysis to compare levels of salivary and serum IL-6 among people with OLP and healthy control participants.

三种中文期刊数据库 收录医学文献的比较研究

对<中国生物医学文献数据库>、<中国期刊全文数据库>和<中文科技期刊数据库>等三种期刊数据库收录的医学文献总量和抽样文献进行了对比研究.结果显示,<中国生物医学文献数据库>的收录范围和覆盖面更大一些,其他两个数据库也有其优势和特点.     

CBM在线文献分析功能探讨

以“文献计量学”为主题词实施检索,从作者、出版时间、发文机构、来源期刊、主题等方面介绍CBM的在线文献分析功能,探讨存在的不足并提出改进建议,包括提高数据标引规范性、增加数据清洗功能等方面。     

Phosphorylation of CARMA1 by HPK1 is critical for NF-κB activation in T cells

Activation of the NF-κB pathway in T cells is required for induction of an adaptive immune response. Hematopoietic progenitor kinase (HPK1) is an important proximal mediator of T-cell receptor (TCR)-induced NF-κB activation. Knock-down of HPK1 abrogates TCR-induced IKKβ and NF-κB activation, whereas active HPK1 leads to increased IKKβ activity in T cells. Yet, the precise molecular mechanism of this process remains elusive. Here, we show that HPK1-mediated NF-κB activation is dependent on the adaptor protein CARMA1. HPK1 interacts with CARMA1 in a TCR stimulation-dependent manner and phosphorylates the linker region of CARMA1. Interestingly, the putative HPK1 phosphorylation sites in CARMA1 are different from known PKCθ consensus sites. Mutations of residues S549, S551, and S552 in CARMA1 abrogated phosphorylation of a CARMA1-linker construct by HPK1 in vitro. In addition, CARMA1 S551A or S5549A/S551A point mutants failed to restore HPK1-mediated and TCR-mediated NF-κB activation and IL-2 expression in CARMA1-deficient T cells. Thus, we identify HPK1 as a kinase specific for CARMA1 and suggest HPK1-mediated phosphorylation of CARMA1 as an additional regulatory mechanism tuning the NF-κB response upon TCR stimulation.     

松质骨基质作为细胞载体应用于牙周组织工程的实验研究

目的 研究评价松质骨基质(CBM)作为细胞载体应用于牙周组织工程的可行性及意义。方法 将体外培养的犬自体牙周膜细胞(PDLCs)接种到CBM三维支架上,扫描电镜观察PDLCs在CBM支架上的生长、附着情况;同时,将PDLCs/CBM复合植入动物牙周组织缺损,以空白组及仅植入CBM组为对照组,术后8周观察评价其牙周组织的再生情况。结果 扫描电镜显示PDLCs在CBM上伸展充分,生长旺盛,而CBM具有良好的多孔网状结构。动物实验结果可见PDLCs/CBM复合植入组较对照组有更多的新生牙骨质、新生牙周膜和新生牙槽骨生成,缺损处牙周组织几近完全再生,且未见上皮长入。结论 CBM可作为细胞载体用于牙周组织工程研究,有望用作牙周组织工程的支架材料。     

基于OM与CBM的医疗设备维修决策研究

本文基于医院医疗设备工作对象的特殊性与维修人力资源的匮乏性,针对医疗设备维修的时效性、可靠性和安全性三个要素,从理论上比较了机会维修策略（OM）与视情维修策略（CBM）的优缺点,结合＂P—F＂曲线,分析医疗设备维修的故障类型、现场要求和维修难度,对医疗设备的维修策略选择进行了研究和探讨,以期达到医疗设备维修的最优化。     

CBM数据库在医药卫生科技项目查新咨询中的应用研究

对中国生物医学文献数据库(CBM)检索途径做了简要概述,从预检索、优化关键词、文献对比分析、撰写查新结论等方面,介绍该数据库在医药卫生科技项目查新咨询工作中的应用,并对数据库的发展提出建议。     

Irradiated human endothelial progenitor cells induce bystander killing in human non-small cell lung and pancreatic cancer cells

Purpose To investigate whether irradiated human endothelial progenitor cells (hEPC) could induce bystander killing in the A549 non-small cell lung cancer (NSCLC) cells and help explain the improved radiation-induced tumor cures observed in A549 tumor xenografts co-injected with hEPC.

Materials and methods We investigated whether co-injection of CBM3 hEPC with A549 NSCLC cells would alter tumor xenograft growth rate or tumor cure after a single dose of 0 or 5?Gy of X-rays. We then utilized dual chamber Transwell dishes, to test whether medium from irradiated CBM3 and CBM4 hEPC would induce bystander cell killing in A549 cells, and as an additional control, in human pancreatic cancer MIA PaCa-2 cells. The CBM3 and CBM4 hEPC were plated into the upper Transwell chamber and the A549 or MIA PaCa-2 cells were plated in the lower Transwell chamber. The top inserts with the CBM3 or CBM4 hEPC cells were subsequently removed, irradiated, and then placed back into the Transwell dish for 3?h to allow for diffusion of any potential bystander factors from the irradiated hEPC in the upper chamber through the permeable membrane to the unirradiated cancer cells in the lower chamber. After the 3?h incubation, the cancer cells were re-plated for clonogenic survival.

Results We found that co-injection of CBM3 hEPC with A549 NSCLC cells significantly increased the tumor growth rate compared to A549 cells alone, but paradoxically also increased A549 tumor cure after a single dose of 5?Gy of X-rays (p?CBM3 and CBM4 hEPC induced significant bystander killing and decreased the surviving fraction of A549 and MIA PaCa-2 cells to 0.46 (46%)?±?0.22 and 0.74?±?0.07 (74%) respectively (p?p?p?Conclusions These data provide evidence that irradiated hEPC can induce strong bystander killing in A549 and MIA PaCa-2 human cancer cells and that this bystander killing is mediated by the cytokines TNF-α and TGF-β.