Midori A. Yenari
San Francisco VA Medical Center
193 Papers
2.4K Citations
Midori A. Yenari is an academic researcher from San Francisco VA Medical Center. The author has contributed to research in topics: Medicine & Neuroprotection. The author has an hindex of 72, co-authored 185 publications. Previous affiliations of Midori A. Yenari include Veterans Health Administration & United States Department of Veterans Affairs.
Chat about Author
Papers
Safety of heparin in acute ischemic stroke
TL;DR: In the authors' view, the most interesting findings of this study are that hemorrhagic clinical worsening was unrelated to estimates of brain hemorrhage during heparin therapy.
Models of poststroke depression and assessments of core depressive symptoms in rodents: How to choose?
Xi Tao,Wanlin Yang,Shuzhen Zhu,Rongfang Que,Chujuan Liu,Tao Fan,Jia Wang,Danheng Mo,Zhuohua Zhang,Jieqiong Tan,Kunlin Jin,Midori A. Yenari,Tao Song,Qing Wang +13 more
TL;DR: The characteristics of the different models of PSD are discussed and comment on the advantages and disadvantages of each model, drawing from research on model innovation.
Therapeutic Hypothermia for Brain Ischemia Where Have We Come and Where Do We Go
TL;DR: The state of therapeutic hypothermia in ischemic and hemorrhagic stroke and an outlook for its role in stroke therapy are reviewed.
Reconsidering Neuroprotection in the Reperfusion Era
TL;DR: Two future neuroprotective approaches will require preclinical studies that anticipate novel clinical trial designs and trials that will be organized and evaluated differently than past monotherapy neuroprotection trials.
Microglial Calcium Release-Activated Calcium Channel Inhibition Improves Outcome from Experimental Traumatic Brain Injury and Microglia-Induced Neuronal Death.
Atsushi Mizuma,Jong Youl Kim,Jong Youl Kim,Rachid Kacimi,Kenneth A. Stauderman,Michael J. Dunn,Sudarshan Hebbar,Midori A. Yenari +7 more
TL;DR: Male C57/BL6 mice exposed to experimental brain trauma and treated with CM-EX-137 had decreased lesion size, brain hemorrhage, and improved neurological deficits with decreased microglial activation, iNOS and Orai1 and STIM1 levels, suggesting a novel anti-inflammatory approach for managing acute brain injury.