机译:体内动物中风模型
Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine">(1);
Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine">(1);
Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine">(1);
Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine">(1);
Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine">(1);
Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine">(1);
Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine">(1);
Department of Neurology University of British Columbia">(2);
Department of Restorative Neurosurgery Kanazawa University Graduate School of Medical Science">(3);
Department of Neurological Surgery Okayama University Graduate School of Medicine">(4);
Department of Neurological Surgery Okayama University Graduate School of Medicine">(4);
Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine">(1);
Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine">(1);
Cerebral ischemia; Animals; Basic research; Translational; Clinical application;
机译:III型mGlu受体激动剂ACPT-1在缺血性中风动物模型中的神经保护潜力:体外和体内研究
机译:在动物模型中新的非侵入性连续心室中风量监测系统的体内验证
机译:在动物模型中新的非侵入性连续心室中风量监测系统的体内验证
机译:抑制中风后对正的半球:审查一些积木的专注于动物模型
机译:雌激素对中风老年动物模型的影响。
机译:在体内动物行程模型中:啮齿动物和非人类灵长类动物模型的理由
机译:全身性(S)-roscovitine的延迟治疗提供了神经保护作用,并在动物卒中模型中抑制了体内CDK5活性的增加。