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Department Of Animal Husbandry Faculty Of Agriculture Tohoku University | 論文
- On a Role of the Endotoxin-Inactivating Agent in the Inactivation of Bacterial Endotoxin
- STUDIES ON THE PULLORUM DISEASE I. SOME CONSIDERATIONS OF THE CONTROL OF THE PULLORUM DISEASE IN A FIELD WITH THE RAPID WHOLE BLOOD AGGLUTINATION
- Effects of the Endotoxin-Inactivating Agent on the Biological Properties of Bacterial Endotoxin
- On an Opsonic Function of the Endotoxin-Inactlvating Agent
- Effects of Mouse Tissue Extracts on Bacterial Endotoxin
- Purification and Characteristics of an Endotoxin-Inactivating Agent
- Functional Analysis after Auto Iris Pigment Epithelial Cell Transplantation in Patients with Age-Related Macular Degeneration
- OE-076 Oxidative Stress Induce Myocardial Atrophy by Modulating Nuclear Translocation of FoxO1 Transcriptional Factor(Heart failure, basic(01)(M),Oral Presentation(English),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)
- PE-380 Combined Treatment of Angiotensin Receptor Blocker and HMG-CoA Reductase Inhibitor Improves Cardiac Dysfunction Synergistically in Dahl Rats(Cardiovascular pharmacology, basic/clinical-3, The 71st Annual Scientific Meeting of the Japanese Circulati
- FRS-071 Premature Senescence can be Induced by Oxidative Stress via PML-p53 Acetylation Pathway in Cardiomyocytes(Heart Failure Research (M) FRS15,Featured Research Session,The 70th Anniversary Annual Scientific Meeting of the Japanese Circulation Society
- CC Chemokine Receptor-1 Antagonist Inhibits the Development of Experimental Autoimmune Myocarditis through Induction of T Cell Anergy (Infection/Inflammation/Immunity 4 (H), The 69th Annual Scientific Meeting of the Japanese Circulation Society)
- The Subcellular Localization of Cyclin A Regulates Apoptosis of Cardiomyocytes Induced by Doxorubicin(Heart Failure, Basic 4 (M), The 69th Annual Scientific Meeting of the Japanese Circulation Society)
- Senescence-like Alterations by Oxidative Stress is Novel Mechanism of Cardiomyocyte Dysfunction(Heart Failure, Basic 4 (M), The 69th Annual Scientific Meeting of the Japanese Circulation Society)
- HMG-CoA Reductase Inhibitor Prevents Angiotensin-II-induced Cardiac Hypertrophy through Inhibition of CyclinD1 Expression via Rho Kinase(Cardiovascular Pharmacology, Basic/Clinical 1 (H), The 69th Annual Scientific Meeting of the Japanese Circulation Soci
- OE-277 HMG-CoA Reductase Inhibitor Pevents Agiotensinll-Induced Cardiac Hypertrophy through Inhibition of CyclinD1 Expression via Rho kinase.(Cardiovascular Pharmacology, Basic/Clinical 1 (H) : OE34)(Oral Presentation (English))
- Overexpression of ATF3 Inhibits Doxorubicin-Induced Apoptosis through Downregulation of p53 Transcription in Cardiac Myocytes
- Endogenous Nitric Oxide Inhibits Hypoxia-Reoxygenation-lnduced Myocardial Apoptosis with the Modulation of Cyclin A-Associated Kinase Activity
- Cyclin A / cdk2 kinase activity regulates apoptosis of cardiomyocytes induced by doxorubicin
- Nitric Oxide Inhibits Ischemia-Reperfusion-induced Myocardial Apoptosis by Suppression of Cyclin A-associated Kinase Activity
- Effects of Adrenaline Dose on Plasma Insulin and Glucagon Concentrations in the Hen
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