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Inflammation and Glucose Sensors: Use of Dexamethasone to Extend Glucose Sensor Function and Life Span in Vivo

机译:炎症和葡萄糖传感器:使用地塞米松延长体内葡萄糖传感器的功能和寿命

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摘要

BackgroundIt has been generally accepted that the acute loss of sensor function is the consequence of sensor biofouling as a result of inflammation induced at sites of sensor implantation, as well as tissue trauma induced by the sensor and its implantation. Because anti-inflammatory therapies are used routinely to control inflammation in a wide variety of diseases, we hypothesized that anti-inflammatory therapy would likely extend glucose sensor function in vivo. To test this hypothesis, we utilized our recently developed mouse model of implantable glucose sensors and the potent anti-inflammatory steroid dexamethasone (DEX).
机译:背景技术已经普遍接受的是,传感器功能的急剧丧失是由于在传感器植入部位诱发的炎症以及由传感器及其植入引起的组织损伤导致的传感器生物污损的结果。由于抗炎疗法通常用于控制多种疾病中的炎症,因此我们假设抗炎疗法可能会扩展体内葡萄糖传感器的功能。为了验证这一假设,我们利用了我们最近开发的植入式葡萄糖传感器和强效抗炎类固醇地塞米松(DEX)的小鼠模型。

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