机译:增强的兴奋耦合Ca 2 + sup>进入诱导NFAT的核易位,并促进中枢核心疾病患者肌管中IL-6的释放
Department of Anesthesia and|Department of Biomedicine, Basel University Hospital, 4031 Basel, Switzerland,|Dipartimento di Medicina Sperimentale e Diagnostica, sez Patologia Generale, University of Ferrara, Ferrara, Italy,;
Department of Anesthesia and|Department of Biomedicine, Basel University Hospital, 4031 Basel, Switzerland,;
Unité de Neuropédiatrie CHUV - BH11, 1011 Lausanne, Switzerland,;
Department of Anesthesia and|Department of Biomedicine, Basel University Hospital, 4031 Basel, Switzerland,;
Department of Anesthesia and|Department of Biomedicine, Basel University Hospital, 4031 Basel, Switzerland,;
Department of Anesthesia and|Department of Biomedicine, Basel University Hospital, 4031 Basel, Switzerland,;
Department of Neuropediatrics, University Children's Hospital, Basel, Switzerland,|Department of Neurology, Basel University Hospital, 4031 Basel, Switzerland,;
Institut de Myo;
机译:增强的兴奋耦合Ca 2 + sup>进入诱导NFAT的核易位,并促进中枢核心疾病患者肌管中IL-6的释放
机译:增强的激发耦合的Ca(2+)进入诱导NFAT的核易位,并有助于从患有中枢核心疾病的患者的肌管中释放IL-6。
机译:丹特罗减弱了表达恶性高热突变R163C的肌管中增强的兴奋耦合钙进入。
机译:丹特罗减弱了表达恶性高热突变R163C的肌管中增强的兴奋耦合钙的输入。
机译:增强的兴奋耦合Ca2 +进入诱导NFAT的核易位,并促进患有中枢核心疾病的患者肌管中IL-6的释放