The critical role of ocular-infiltrating macrophages in the development of choroidal neovascularization

Choroidal neovascularization (CNV) is directly related to visual loss in some eye diseases, such as age-related macular degeneration. Although several human histological studies have suggested the participation of macrophages in CNV formation, the precise mechanisms are still not fully understood. In this study, we elucidated the role of ocular-infiltrating macrophages in experimental CNV using CCR2 knockout (KO) mice, wild-type mice, and C57BL/6 (B6) mice. CCR2 is the receptor of monocyte chemoattractant protein-1, and the number of infiltrating macrophage and the area of CNV were significantly reduced in CCR2 KO mice. Enriched ocular-infiltrating macrophages from B6 mice actually showed angiogenic ability in a dorsal air sac assay. Moreover, their expression of class II, CD40, B7-1 and B7-2 molecules, and the mRNA for potential angiogenic factors, such as vascular endothelial growth factor, basic fibroblast growth factor, and tumor necrosis factor alpha, was also observed. Collectively, we conclude that ocular-infiltrating macrophages play an important role in CNV generation.     

Self-assembled biomimetic monolayers using phospholipid-containing disulfides

Several phospholipid-based disulfide molecules were synthesized and attached onto the gold-coated silicon wafer using the self-assembling method. The syntheses of these surface-modifying agents were conducted by introducing bromoethylphosphorate (PBr), phosphorylcholine (PC) or phosphorylethanolamine (PE) groups on the terminals of a dialkyl disulfide. After disulfides adsorption onto gold substrate surfaces, the composition, the film thickness, and the conformational order of self-assembled monolayer surfaces were explored and discussed in detail based on reflection-absorption infrared spectroscopy, contact angle measurement, Auger electron spectroscopy, X-ray photoelectron spectroscopy, and so on. The monolayer having the PBr end group could also be converted to a PC surface by treating with trimethylamine. The model functional surfaces of Au-SC11-PC, -PE, -PBr, -OH or corresponding mixed layers were used to mimic biomembrane surfaces. The monolayer having PC groups was found to reduce fibrinogen adsorption as evaluated from protein adsorption experiments using quartz crystal microbalance. It also showed relatively low platelet adherence compare to the glass, PBr and PE surfaces. The cell viability test also revealed that the PC surface displayed lower cytotoxicity than other surfaces.     

NOD小鼠胸腺细胞TCR介导的信号通路缺陷

目的 进一步研究NOD小鼠T细胞应答改变机理。方法 用抗TCR抗体、ConA激活NOD小鼠胸腺细胞，分析TCR介导的信号通路的水平。结果 与Balb／c小鼠胸腺细胞相比，抗TCR抗体诱导的增殖应答较弱，与年龄及NOD胸腺CD4^ CD8^-和CD4^-CD8^ SP细胞有关；rIL-2能部分恢复对TCR抗体应答的缺乏。NOD小鼠对PMA IONO和PMA anti—TCR-mAb应答正常，但对anti-TCRmAb IONO应答缺乏。结论 与年龄有关的NOD小鼠胸腺细胞对TCR抗体应答的缺乏与T细胞激活时上游PKC信号通路的缺乏有关。     

单侧外周伤害性刺激诱发大鼠脊髓中转录因子CREB的双侧磷酸化(英文)

c AMP反应成分结合蛋白 (c AMP response elem ent-binding protein,CREB)是一种转录因子 ,它在磷酸化之后可调节靶基因的转录。 CREB在 13 3位置的丝氨酸的磷酸化 ,与脊髓中伤害性传入的处理有关 ,本文作者等用特殊抗体对此进行了免疫细胞化学研究。在正常大鼠 ,虽然几乎所有脊髓神经元的核中都可见 CREB的轻度着色 ,但磷酸化的 CREB仅见于双侧腰段脊髓的 ～ 层 (75± 15 vs60± 18)和 层 (9± 3 )。用福尔马林注射引起一侧后脚掌出现炎症时 ,可在双侧腰段脊髓看到磷酸化CREB细胞核的快速 (小于 5 min)和节段性的显著增多 ;它们主要分布在双侧背角表层 ～ 层 (2 5 4± 2 0 vs 2 62± 2 3 )、 层(115± 13 )和双侧 ～ 层 (3 46± 2 0 vs3 2 8± 2 6) ;而在对照和炎症组大鼠的胸段脊髓中均未见磷酸化 CREB的增加。在注射CFA诱发一侧炎症或切断一侧坐骨神经的实验组大鼠 ,也可看到至少延续到第三天的强而双侧性的 CREB的磷酸化。这种由一侧后肢伤害性传入引致腰段脊髓中镜像式双侧 CREB磷酸化的出现 ,与一般看到的损伤传入只在同侧脊髓背角引起某些神经化学改变的结果不同 ,可能是人神经损伤后或在实验动物中出现对侧镜像式疼痛过敏现象的基础     

钴60放射法制备免疫功能抑制大鼠模型

目的通过系统的钴60放射计划,对大鼠免疫功能抑制的合适剂量进行评估,为干细胞移植研究提供合适的的动物模型。方法SD大鼠随机分为12.5Gy、10Gy、7.5Gy、5Gy4个剂量组,10只/组。计算放射后2个月的死亡率。检测白细胞数量,评价各剂量组动物的白细胞参考值范围。结合死亡率和白细胞参考值范围,确定合适的放射剂量。通过对外周血中性粒细胞(PMN)吞噬实验和外周血白细胞移行抑制实验(MIT),对细胞免疫功能进行检测。结果行12.5Gy照射的大鼠,3d内全部死亡;10Gy放射后的大鼠在1个月内全部死亡;7.5Gy照射的大鼠2个月内死亡1只;5Gy照射的大鼠没有死亡情况发生。设定95%作为可信区间,计算白细胞数量参考值范围(109个/L),未放疗组:16.978+1.96×6.46;5Gy放疗组:4.93+1.96×0.72;7.5Gy放疗组:2.313+1.96×0.782;10Gy放疗组:1.03+1.96×0.507。t检验表明,随着放疗剂量的增加,各实验组的白细胞数量显著减少。对于细胞免疫功能的检测,外周血中性粒细胞(PMN)吞噬实验结果表明,机体全身免疫功能降低;外周血白细胞移行抑制实验(MIT)表明,机体T细胞免疫功能降低。结论7.5Gy可以一定程度上抑制大鼠的免疫功能,为合适的放疗剂量。