Wiley Acta Medica Okayama 1351-5101 20 5 2013 A novel familial prion disease causing pan-autonomic-sensory neuropathy and cognitive impairment e67 e69 EN Kosuke Matsuzono Yoshio Ikeda Department of Neurology, Okayama University Graduate School of Medicine and Dentistry Wentao Liu Tomoko Kurata Department of Neurology, Okayama University Graduate School of Medicine and Dentistry Shoko Deguchi Kentaro Deguchi Department of Neurology, Okayama University Graduate School of Medicine and Dentistry Koji Abe Department of Neurology, Okayama University Graduate School of Medicine and Dentistry No potential conflict of interest relevant to this article was reported.

Acta Medica Okayama 1554-8627 6 8 2010 In vivo imaging of autophagy in a mouse stroke model 1107 1114 EN FengFeng Tian Kentaro Deguchi Toru Yamashita Yasuyuki Ohta Nobutoshi Morimoto Jingwei Shang Xuemei Zhang Ning Liu Yoshio Ikeda Tohru Matsuura Koji Abe Recent studies have suggested that autophagy is involved in a neural death pathway following cerebral ischemia. In vivo detection of autophagy could be important for evaluating ischemic neural cell damage for human stroke patients. Using novel green fluorescent protein (GFP)-fused microtubule-associated protein 1 light chain 3 (LC3) transgenic (Tg) mice, in vivo imaging of autophagy was performed at 1, 3 and 6 d after 60 min transient middle cerebral artery occlusion (tMCAO). Ex vivo imaging of autophagy, testing of the autophagy inhibitor 3-methyladenine (3-MA), estern blot analysis, immunohistochemistry, terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) and fluorescent analyses were performed on brain sections following tMCAO. In vivo fluorescent signals were detected above the ischemic hemisphere through the skull bone at 1, 3 and 6 d after tMCAO, with a peak at 1 d. Similar results were obtained with ex vivo fluorescence imaging. western blot analysis revealed maximum LC3-I and LC3-II expression at 1 d after tMCAO and fluorescence immunohistochemistry demonstrated that GFP-LC3-positive cells were primarily neuronal, not astroglial or microglial, cells. The number of GFP-LC3/TUNEL double-positive cells was greater in the peri-ischemic area than in the core. These results provided evidence of in vivo autophagy detection, with a peak at 1 d, in a live animal model following cerebral ischemia. This novel technique could be valuable for monitoring autophagic processes in vivo in live stroke patients, as well as for clarifying the detailed role of autophagy in the ischemic brain, as well as in other neurological diseases. No potential conflict of interest relevant to this article was reported.

岡山医学会 Acta Medica Okayama 0030-1558 123 3 2011 神経内科領域の難治性疾患診療 227 230 EN Yoshio Ikeda Koji Abe No potential conflict of interest relevant to this article was reported.