糖尿病患者骨质疏松的发生源于骨代谢状态改变,与胰岛素、胰岛素样生长因子-1(IGF-1)的作用有关。此外,高血糖毒性刺激细胞分泌肿瘤坏死因子α(TNF-α)、巨噬细胞集落刺激因子(MCSF)、核因子κB受体活化因子配体(RANKL)、血管内皮生长因子-A(VEGF-A)等破骨源性细胞因子也发挥重要作用。

Osteoporosis in patients with diabetes mellitus originates from the alteration in bone metabolism , which is regulated by insulin and insulin-like growth factor-1 (IGF-1).In addition, the osteoclastogenic mediators, which are secreted by the stimulation of hyperglycemia toxicity , including TNF-α, macrophage colony stimulating factor ( MCSF) , receptor activator of nuclear factor-κB ligand ( RANKL) , and vascular endothelial growth factor A ( VEGF-A) , also play an important role in the progress of osteoporosis .

肿瘤相关巨噬细胞（ Tumor associate macrophages ，TAMs）是肿瘤的炎症微环境与肿瘤细胞间的重要信使。它是从血液中的单核细胞演变而来，主要通过集落刺激因子（ Colony -stimulating factor ， CSF）趋化至肿瘤组织中。本文简述了TAMs通过影响血管生成和淋巴管生成，抑制免疫，调节基质，与干细胞相互作用等方面促进肿瘤的进展。分析表明靶向于TAMs的治疗策略是未来治疗肿瘤的一个新方向。

Tumor associate macrophages ( TAMs) play a significant role in the interaction of tumor inflam-mative microenvironment and tumor cells .TAMs originate from monocytic precursors ,recruiting into tumor tissue by colony stimulating factor ( CSF) .This review summarized that TAMs promote tumor progression and metastasis though angiogenesis ,lymphogenesis , immunosuppression , matrix remodeling and affecting cancer stem cells .The article pointed that targeting TAMs is a new strategy for future tumor therapy .

探讨肿瘤相关巨噬细胞(tumor-associated macrophages,TAMs)对口腔鳞癌细胞基质金属蛋白酶(matrix metallproteinases,MMPs)表达以及其对口腔鳞癌细胞侵袭转移的影响。方法:用佛波脂(phorbol 12-myristate 13-acetate,PMA)和巨噬细胞集落刺激因子(macrophage colony-stimulating factor,M-CSF)刺激人单核/巨噬细胞株THP-1促其形成TAMs,收集其上清液作为TAMs条件培养基培养口腔鳞癌细胞,应用实时定量RT-PCR、Western blot方法检测TAMs条件培养基作用前后口腔鳞癌细胞MMPs表达的差异,应用Transwell侵袭实验检测口腔鳞癌细胞侵袭转移能力的差异。结果:THP-1细胞在PMA和MCSF作用后贴壁生长,分化成TAMs。口腔癌细胞在TAMs条件培养基作用48 h后,MMP-2、MMP-9、MMP-13 mRNA的表达水平显著增高,相同条件下蛋白质的表达水平也明显增高。TAMs条件培养基作用24 h后的口腔鳞癌细胞侵袭转移能力显著增强。结论:TAMs可以上调口腔鳞癌中MMPs的表达并促进其侵袭转移。

Objective:To explore the influence of tumor-associated macrophages (TAMs)on the expression of matrix metalloprotei-nases (MMPs)and the ability of invasion and metastasis of oral squamous cancer cells.Methods:We used phorbol 12-myristate 13-acetate (PMA)and macrophage colony-stimulating factor (M-CSF)to make THP-1 monocytes differentiate into TAMs,and then we col-lected the culture media of TAMs as condition medium (CM)to stimulate oral squamous cancer cells.Real-time RT-PCR and Western blot were applied to detect the expression of MMPs before and after stimulation of TAMs.The ability of invasion and metastasis of oral squamous cells was measured by Transwell assays.Results:When treated with PMA and M-CSF,THP-1 cells became attached,and differentiated into TAMs.Compared to control group,the expression of MMP-2,MMP-9,MMP-13 mRNA in experimental group were up-regulated when treated with TAMs CM for 48h.Protein level of MMP-2,MMP-9,MMP-13 was up-regulated accordingly.And stim-ula

目的 应用细胞因子抗体芯片(cytokine antibody chip,CAC)分析尘肺患者血清中细胞因子表达的变化.方法 采用CAC技术平台,测定12例尘肺患者和3例正常对照血清中60种细胞因子.结果 在尘肺患者血清中筛选到白细胞介素(IL-1α、-1β、-2、-4～16)、集落刺激因子(M-CSF)、干扰素(IFN-γ)、肿瘤坏死因子(TNF-α和TNF-β)、人骨形成蛋白6(BMP-6)、角蛋白细胞生长因子(FGF-7)、神经营养因子3(NT-3)和干细胞因子(SCF)等高表达的细胞因子,重组人(I-309)、单核细胞趋化蛋白(MCP-1、MCP-2、MCP-3、MCP-4)、巨噬细胞炎性蛋白(MIP-1-δ、MIP-3-α)等在尘肺患者血清中低表达的细胞因子.结论 尘肺患者血清中绝大部分细胞因子表达存在差异.

Objective To investigate the changes in expression of serum cytokines in patients with pneumoconiosis using cytokine antibody chips (CACs).Methods The CAC technology was applied to measure the serum levels of 60 cytokines in 12 patients with pneumoconiosis and 3 normal controls.Results In the patients with pneumoconiosis,the highly expressed serum cytokines included interleukin (IL)-1α,IL-1β,IL-2,ILs 4-16,macrophage colony-stimulating factor,interferon-γ,tumor necrosis factor (TNF)-α,TNF-β,human bone morphogenetic protein-6,fibroblast growth factor-7,neurotrophin-3,and stem cell factor,and the lowly expressed serum cytokines included recombinant human I-309,monocyte chemoattractant protein (MCP) -1,MCP-2,MCP-3,MCP-4,macrophage inflammatory protein (MIP)-1-δ,and MIP-3-α.Conclusion Patients with pneumoconiosis have changes in the expression of most serum cytokines.

背景：以往的研究多采用长骨机械分离法获得破骨细胞，破骨细胞为终末分化细胞，无法进一步增殖和传代。因此目前常用骨髓细胞诱导培养法和RAW264.7细胞诱导培养法获得大量的破骨细胞以满足实验需要。 目的：探讨细胞核因子κB受体活化因子配体诱导破骨细胞前体细胞分化为成熟破骨细胞的最佳方法。 方法：分离小鼠骨髓细胞后添加核因子κB 受体活化因子配体与巨噬细胞集落刺激因子共同诱导或者取RAW264.7细胞单独加入核因子κB受体活化因子配体诱导破骨细胞的形成；分别给予不同浓度的核因子κB受体活化因子配体，观察生成破骨细胞的数量，评价核因子κB受体活化因子配体与破骨细胞生成的量效关系；采用膜联蛋白V-FITC联合PI染色进行流式细胞术分析破骨细胞形成过程中单核巨噬细胞的凋亡情况。 结果与结论：当核因子κB受体活化因子配体浓度为10μg/L时，破骨细胞形成数量最多的时间点在第六至七天；而核因子κB受体活化因子配体浓度为100μg/L时，高峰期出现在第四至五天。破骨细胞的形成数量随着核因子κB受体活化因子配体刺激浓度升高而增加，呈浓度依赖性，50μg/L的核因子κB受体活化因子配体是破骨细胞形成数量与浓度关系曲线的转折点，高于150μg/L以后破骨细胞形成数量的增幅明显放缓。核因子κB受体活化因子配体即能诱导单核巨噬细胞形成破骨细胞又可以促进其凋亡，通过破骨细胞计数比较发现在同一浓度(104/cm2)接种单核巨噬细胞后以30μg/L的核因子κB受体活化因子配体诱导后，平均每单位核因子κB受体活化因子配体所获得的破骨细胞数量最多。提示骨髓细胞或RAW264.7细胞诱导破骨细胞的培养方法皆简单可行，细胞接种的最佳浓度为104/cm2；核因子κB受体活化因子配体的适宜刺激浓度为30-50μg/L。

BACKGROUND:Previous studies have applied long-bone mechanical separation method to obtain osteoclasts, which are terminal y differentiated cells and cannot further proliferate. Therefore a large number of osteoclasts can be harvested with bone marrow cells inducing culture method and RAW264.7 cells inducing culture method to meet clinical requirements. OBJECTIVE:To investigate the optimal method of receptor activator of nuclear factor kappa-B ligand (RANKL) induced osteoclast precursors to differentiate into mature osteoclasts. METHODS:After bone marrow cells were isolated from mouse, RANKL and macrophage colony stimulating factor were added into the medium together, or RAW264.7 cells were cultured with RANKL to induce osteoclasts. The osteoclast precursors were treated with different concentrations of RANKL to observe the number of generated osteoclasts and evaluate the dose-effect relationship between RANKL and osteoclastogenesis.Annexin V-FITC and propidium iodide staining were used