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1. 虚血後（虚血性）の急性尿細管壊死において考え得る予防および治療 possible prevention and therapy of postischemic ischemic acute tubular necrosis
2. 虚血後（虚血性）の急性尿細管壊死の発症および病因 pathogenesis and etiology of postischemic ischemic acute tubular necrosis
3. ドーパミンの腎臓作用 renal actions of dopamine
4. 腎臓の同種移植片機能不全の鑑別診断 differential diagnosis of renal allograft dysfunction
5. 急性腎障害（急性腎不全）における腎前性疾患および急性尿細管壊死の病因および診断 etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury acute renal failure

English Journal

Translating thyroid hormone effects into clinical practice: the relevance of thyroid hormone receptor α1 in cardiac repair.

Pantos C1, Mourouzis I.
Heart failure reviews.Heart Fail Rev.2015 May;20(3):273-82. doi: 10.1007/s10741-014-9465-4.
Thyroid hormone (TH) appears to have a critical role in cardiac repair after injury beyond its role in development and metabolism homeostasis. This unique action is due to the fact that TH effect on the heart is shown to be differentiated depending on its administration on injured or healthy myocard
PMID 25501869

Blockade of P2X7 receptors or pannexin-1 channels similarly attenuates postischemic damage.

Cisneros-Mejorado A1, Gottlieb M2, Cavaliere F3, Magnus T4, Koch-Nolte F5, Scemes E6, Pérez-Samartín A3, Matute C3.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.J Cereb Blood Flow Metab.2015 May;35(5):843-50. doi: 10.1038/jcbfm.2014.262. Epub 2015 Jan 21.
The role of P2X7 receptors and pannexin-1 channels in ischemic damage remains controversial. Here, we analyzed their contribution to postanoxic depolarization after ischemia in cultured neurons and in brain slices. We observed that pharmacological blockade of P2X7 receptors or pannexin-1 channels de
PMID 25605289

Ruling out pyridine dinucleotides as true TRPM2 channel activators reveals novel direct agonist ADP-ribose-2'-phosphate.

Tóth B1, Iordanov I1, Csanády L2.
The Journal of general physiology.J Gen Physiol.2015 May;145(5):419-30. doi: 10.1085/jgp.201511377.
Transient receptor potential melastatin 2 (TRPM2), a Ca(2+)-permeable cation channel implicated in postischemic neuronal cell death, leukocyte activation, and insulin secretion, is activated by intracellular ADP ribose (ADPR). In addition, the pyridine dinucleotides nicotinamide-adenine-dinucleotide
PMID 25918360

吉田耕太郎
金沢大学十全医学会雑誌 122(2), 31-34, 2013-06
… Endothelial PI3K-C2α deficiency in vivo suppressed postischemic and tumor angiogenesis and diminished vascular barrier function with a greatly augmented susceptibility to anaphylaxis and a higher incidence of dissecting aortic aneurysm formation in response to angiotensin II infusion. …
NAID 120005324081

松尾(池田) 由理
YAKUGAKU ZASSHI 133(9), 947-954, 2013
… Although augmented prostaglandin E2 (PGE2) accumulation has been demonstrated at the lesion sites of rodent ischemia models, the role of postischemic PGE2 in neuronal survival has remained obscure. … In mPGES-1 knockout (KO) mice, in which the postischemic PGE2 production in the cortex was completely absent, the ischemic injuries were less severe compared to those in wild-type (WT) mice. …
NAID 130003361986

Endothelial PI3K-C2α, a class II PI3K, has an essential role in angiogenesis and vascular barrier function

Yoshioka Kazuaki,Yoshida Kotaro,Cui Hong,Wakayama Tomohiko,Takuwa Noriko,Okamoto Yasuo,Du Wa,Qi Xun,Asanuma Ken,Sugihara Kazushi,Aki Sho,Miyazawa Hidekazu,Biswas Kuntal,Nagakura Chisa,Ueno Masaya,Iseki Shoichi,Schwartz Robert J.,Okamoto Hiroshi,Sasaki Takehiko,Matsui Osamu,Asano Masahide,Adams Ralf H.,Takakura Nobuyuki,Takuwa Yoh
Nature Medicine 18(10), 1560-1569, 2012-10
… Endothelial PI3K-C2α deficiency in vivo suppressed postischemic and tumor angiogenesis and diminished vascular barrier function with a greatly augmented susceptibility to anaphylaxis and a higher incidence of dissecting aortic aneurysm formation in response to angiotensin II infusion. …
NAID 120004966617