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您的检索式：作者名="Lars K. Poulsen"
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| 1 | 食物过敏的定义、流行性、诊断及治疗显示文摘食物过敏是异质性群体相关疾病,会通过一种或多种方式对多个器官造成影响。其反应的严重程度可从轻度的局部反应到全身性的过敏反应。从机制上来看,食物过敏是Th2细胞驱动的免疫紊乱疾病,食物特异性IgE是这种速发型不良反应的基础。过敏的部位和症状并不一定相同。食物过敏常会与自身免疫性(如乳糜泻)和非免疫性(如乳糖不耐受)的其他食物不良反应相混淆。为了正确诊断食物过敏,需要详细了解患者病史,检测特异性IgE,并进行经口激发试验来确诊。一些辅助因素(如运动、药物和酒精)有助于诱发食物过敏,会进一步增加诊断的复杂性。以食物提取物为基础的诊断试验并不能反映症状的严重程度,而检测单个食物致敏原IgE的新一代分子诊断技术,则能够为临床医生和患者提供可靠的症状严重程度依据。分子诊断还有助于确定食物过敏是直接源于对食物的暴露还是间接源于花粉过敏(交叉反应)。流行病学调查表明,桃过敏在欧洲主要是源于对桃的食用,而在中国则是源于对艾蒿花粉的初级致敏。但这两种情况都是由来自同一家族的致敏原分子介导的。流行病学调查深入揭示了食物过敏的病因、流行性及其所包含的风险因素,为预防食物过敏提供了循证策略。过去的十年中,食物过敏在发达国家盛行。经济发展和城市化进程都被认为会导致食物过敏流行性的增加,而且饮食习惯不同,过敏的食物也不同。目前,分子变态反应学和生物技术正在开发安全的免疫治疗方法,有望能够减轻日益加重的食物过敏负担。一种使用低致敏性突变重组分子的免疫疗法已经开始进行第一阶段临床试验的评估。食物致敏原名单的不断完善为转基因食品致敏性的评估提供了坚实基础。 | Ronald van Ree Lars K. Poulsen Gary WK Wong Barbara K. Ballmer-Weber 高中山 贾旭东 | 2015 | 中华预防医学杂志2015，49，1： | 28 |
| 2 | Signaling transduction pathways involved in basophil adhesion and histamine release显示文摘Background Little is known about basophil with respect to the different signaling transduction pathways involved in spontaneous, cytokine or anti-IgE induced adhesion and how this compares to IgE-dependent and IgE-independent mediator secretion. The purpose of the present study was to investigate the roles of β1 andβ2 integrins in basophil adhesion as well as hosphatidylinositol 3-kinase (PI3K), src-kinases and extracellular signal regulated kinase (ERK)1/2 in basophil adhesion and histamine release (HR). Methods Basophils (purity of 10%-50%) were preincubated with anti-CD29 or anti-CD18 blocking antibodies before used for adhesion study. Basophils were preincubated with the pharmacological inhibitors wortmannin, PP1, PD98059 before used for adhesion and HR study. Cell adherence to bovine serum albumin (BSA) or fibronectin (Fn) was monitored using cell associated histamine as a basophil marker and the histamine was measured by the glass fiber assay. Results Basophil spontaneous adhesion to Fn was inhibited by anti-CD29. Interleukin (IL)-3, granulocyte/macrophage colony stimulating factor (GM-CSF) induced adhesion to BSA was inhibited by anti-CD18. Wortmannin at 1 μmol/L and PP1 at 20 μmol/L strongly interfered with, whereas PD98059 at 50 μmol/L weakly inhibited basophil spontaneous adhesion to Fn. One μmol/L wortmannin strongly inhibited IL-3, IL-5, GM-CSF and anti-IgE induced adhesion to BSA. PP1 at 20 μmol/L partly inhibited anti-IgE induced adhesion. Fifty μmol/L PD98059 marginally inhibited IL-5, weakly inhibited anti-IgE, partly inhibited GM-CSF induced adhesion. Wortmannin, PP1 and PD98059 inhibited anti-IgE (1:100 or 1:1000) induced basophil HR in a dose dependent manner. They inhibited calcium ionophore A23187 (10 μmol/L, 5 μmol/L) induced basophil HR in a dose dependent manner, but to different extend with PP1 being the most efficient. Conclusions Basophil spontaneous adhesion to Fn is mediated by β1-integrins whereas cytokine induced adhesion to BSA is mediated by β2-integrins. PI3K, src-kinases and ERK1/2 play distinct signaling roles in basophil adhesion and HR. PI3K is the key player whileERK1/2 is the weakest participant. | SHA Quan Lars K. Poulsen Jens Gerwien NielsФdum Per Stahl Skov | 2006 | Chinese Medical Journal2006，，2： | 8 |
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