Platelets as modulators of neuro-inflammation in the ischaemic brain (B06)

在这里，先进的成像技术与转基因小鼠模型和药理学工具一起是获得血小板免疫细胞相关并发症的机制洞察的关键。我们发现，血小板分泌是在缺血/再灌注（I/R）损伤的血管界面有害的细胞相互作用的重要介质。接下来，我们研究了血小板在大血管闭塞过程中对半影组织损失的作用，以及与再灌注后早期以及脑静脉（窦）血栓形成过程中的关键分子和细胞相互作用的比较。

Here, advanced imaging techniques together with transgenic mouse models and pharmacological tools are key to gain mechanistic insight into platelet-immune cell relevant complications. We found that platelet secretion is an important mediator of detrimental cellular interactions at the vascular interface during ischaemia/reperfusion (I/R) injury. Next, we study the role of platelets for penumbral tissue loss during large vascular occlusion, and the key molecular and cellular interactions in comparison with those in the early phase after reperfusion as well as during cerebral venous (sinus) thrombosis.