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| 1 | Endogenous PPAR gamma mediates anti-inflammatory activity in murine is- chemia-reperfusion injury 显示文摘 | Nakajima A Wada K Miki H | 2001 | Gastroenterology2001，120，2： | 1 |
| 2 | Operative indications and neuroendoseopic management of symptomatic cysts of the septum pcllucidum 显示文摘 | Miki T Wada J Nakajima N | 2005 | Childs Nerv Syst2005，21，： | 1 |
| 3 | Monitoring and mathematical modeling of mitochondrial ATP in myotubes at single-cell level reveals two distinct population with different kinetics显示文摘Backgrounds ATP is the major energy source for myotube contraction,and is quickly produced to compensate ATP consumption and to maintain sufficient ATP level.ATP is consumed mainly in cytoplasm and produced in mitochondria during myotube contraction.To understand the mechanism of ATP homeostasis during myotube contraction,it is essential to monitor mitochondrial ATP at single-cell level,and examine how ATP is produced and consumed in mitochondria.Methods:We established C2C12 cell line stably expressing fluorescent probe of mitochondrial ATP,and induced differentiation into myotubes・We gave electric pulse stimulation to the differentiated myotubes,and measured mitochondrial ATP.We constructed mathematical model of mitochondrial ATP at single-cell level,and analyzed kinetic parameters of ATP production and consumption.Results:We performed hierarchical clustering analysis of time course of mitochondrial ATP,which resulted in two clusters.Cluster 1 showed strong transient increase,whereas cluster 2 showed weak transient increase.Mathematical modeling at single-cell level revealed that the ATP production rate of cluster 1 was larger than that of cluster 2,and that both regulatory pathways of ATP production and consumption of cluster 1 were faster than those of cluster 2.Cluster 1 showed larger mitochondrial mass than cluster 2,suggesting that cluster 1 shows the similar property of slow muscle fibers,and cluster 2 shows the similar property of fast muscle fibers.Conclusions Cluster 1 showed the stronger mitochondrial ATP increase by larger ATP production rate,but not smaller consumption.Cluster 1 might reflect the larger oxidative capacity of slow muscle fiber. | Naoki Matsuda Ken-ichi Hironaka Masashi Fujii Takumi Wada Katsuyuki Kunida Haruki Inoue Miki Eto Daisuke Hoshino Yasuro Furuichi Yasuko Manabe Nobuharu LFujii Hiroyuki Noji Hiromi Imamura Shinya Kuroda | 2020 | Quantitative Biology2020，8，3： | 1 |
| 4 | Endogenous PPAR γmediates anti-inflammatory activity in murine ischemia-reperfusion injury显示文摘 | NAKAJIMA A WADA K MIKI H | 2001 | Gastroenterology2001，120，： | 1 |
| 5 | Apg1p, a novel protein kinase required for the autophagic process in Saccharomyces cerevisiae显示文摘 | Akira Matsuura Miki Tsukada Yoh Wada Yoshinori Ohsumi | 1996 | Gene1996，，2： | 1 |
| 6 | Endogenous PPAR gamma mediates anti-inflammatory activity in murine ischemia-reperfusion injury显示文摘 | Nakajima A Wada K Miki H | 2001 | Gastroenterology2001，120，2： | 1 |
| 7 | Endoscopic transma-xillary reduction and balloon technique for blowout frac-tures of the orbital floor 显示文摘 | Miki T Wada J Haraoka J | 2004 | Minim Invasive Neurosurg2004，47，： | 1 |
| 8 | Cause ofpost-trattmatic hydrocephalus because of traumatic aqueduct obstruction in two cases 显示文摘 | Miki T Nakajima N Wada J | 2006 | J Trauma2006，61，4： | 1 |
| 9 | Endogenous PPAR gamma mediates anti - inflammatory activity in murine ischemia - reperfusion injury 显示文摘 | Nakajima A Wada K Miki H | 2001 | Gastroenterology2001，12，： | 1 |
| 10 | Endogenous PPAR gamma mediates anti-inflammatory activity in murine ischemiareperfusion injury显示文摘 | Nakajima A Wada K Miki H | 2001 | Gastroenterology2001，120，2： | 1 |
| 11 | Endogenous PPARγ mediates anti-inflammatory activity in murine ischemia-reperfusion injury显示文摘 | Nakajima A Wada K Miki H | 2001 | Gastroenterology2001，120，： | 1 |
| 12 | WAVE/Scars in platelets显示文摘 | Oda A Miki H Wada I | 2005 | {H}Blood2005，，8： | 1 |
| 13 | Endogcnous PPAR gamma mediates anti-intlammatory activity in routine is- chemia repuriusion injury 显示文摘 | Nakajima A Wada K Miki H el al | 2001 | Gastroenterology2001，120，2： | 1 |
| 14 | Cause of post-traumatic hydrocephalus because of traumatic aqueduct obstruction in two cases显示文摘 | MIKI T NAKAJIMA N WADA J | 2006 | J Trauma2006，61，4： | 1 |
| 15 | Endogenous PPAR gammamediates anti - inflammtory activity in murine ischemia - reperfu-sion injury显示文摘 | Nakajima A Wada K Miki H ef a/ | 2001 | Gastroenterology2001，120，2： | 1 |
| 16 | Surface rendering-based virtual intraventrieular endoscopy: Retrospective feasibility study and com- parison to volume rendering-based approach 显示文摘 | Nakajima N Wada J Miki T | 2007 | Neuro Image2007，37，1： | 1 |
| 17 | Endogenous PPAR gamma mediates anti-inflammatory activity in murine ischemia-reperfusion injury显示文摘 | Nakajima A Wada K Miki H | 2001 | Gastroenterology2001，120，2： | 1 |
| 18 | Cause of post-traumatic hydrocephalus because of traumatic aqueduct obstruction in two cases显示文摘 | Miki T Nakajima N Wada J | 2006 | J Trauma2006，61，4： | 1 |
| 19 | Endogenous PPAR gamma mediates anti-inflammatory activity in murine ischemia-reperfusion injury显示文摘 | Nakajima A Wada K Miki H | 2001 | Gastroenterology2001，120，7： | 1 |
| 20 | Crystal structures of the TRIC trimeric intracellular cation channel orthologues显示文摘从 sarcoplasmic 蜂窝胃(SR ) 和 endoplasmic 蜂窝胃的 Ca 2+ 版本(嗯) 为肌肉收缩是关键的,细胞生长, apoptosis,学习并且记忆。trimeric 细胞内部的阳离子(TRIC ) 隧道最近作为平衡 SR 的阳离子隧道被识别并且嗯膜潜力,并且在 Ca 2+ 发信号和动态平衡被含有。这里我们在场处于关上的状态和原核生物、真核细胞的 TRIC 隧道的基于结构的功能的分析的原核生物的 TRIC 隧道的水晶结构。各更整齐的子单元由七 transmembrane (TM ) 组成有二的 helices 转换了重复区域。electrophysiological,揭示的生物化学、生物物理的分析 TRIC 隧道在每个子单元以内拥有一个进行离子的毛孔,并且更整齐的形成贡献蛋白质的稳定性。相称性地相关的 TM2 和 TM5 helices 是在保存 glycine 簇的 kinked,并且这些性变态为隧道活动是重要的。而且, TM2 和 TM5 helices 的性变态在每个子单元接口产生侧面的开窗术。出人意料地,这些侧面的开窗术与类脂化合物分子被占据。这研究为这个离子隧道总科的分子的机制提供结构、功能的框架。 | Go Kasuya Masahiro Hiraizumi Andres D Maturana Kaoru Kumazaki Yuichiro Fujiwara Keihong Liu Yoshiko Nakada-Nakura So Iwata Keisuke Tsukada Tomotaka Komori Sotaro Uemura Yuhei Goto Takanori Nakane Mizuki Takemoto Hideaki E Kato Keitaro Yamashita Miki Wada Koichi Ito Ryuichiro Ishitani Motoyuki Hattori Osamu Nureki | 2016 | Cell Research2016，26，12： | 0 |
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