Okamoto Ryuji | Department Of Cardiology And Nephrology Mie University Graduate School Of Medicine

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概要

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著作論文

Overexpression of Myosin Phosphatase Reduces Ca2+ Sensitivity of Contraction and Impairs Cardiac Function
Left Ventricular Chamber Stiffness Does not Reflect Candesartan-Dependent Prevention of Myocardial Fibrosis in Canine Heart Failure with Non-ACE Pathway
Synergistic Effect of Combination with ACE Inhibitor and Angiotensin II Receptor Antagonist on Cardiac Structure and Function in Heart Failure
PJ-798 Randomized Comparison of Ticlopidine versus Cilostazol for Antiplatelet Therapy after Sirolimus-Eluting Stent Implantation(Thromboembolism/Antithrombotic therapy/Thrombolysis-5 (H) PJ141,Poster Session (Japanese),The 70th Anniversary Annual Scienti
MYPT2 Functions as a Regulatory Subunit of Cardiac MP, which Modulates Ca^ Sensitization of Contraction and LV Function in vivo(Gene Therapy/Genetic Engineering (IHD), The 69th Annual Scientific Meeting of the Japanese Circulation Society)
Critical Role of Rho/Rho-kinase Pathway for C-reactive Protein-induced Plasminogen Activator Inhibitor-1 Expression in Bovine Aortic Endothelial Cells(Atherosclerosis, Basic 1 (IHD), The 69th Annual Scientific Meeting of the Japanese Circulation Society)
PJ-358 Characterization of Cardiac Myosin Phosphatase(Molecular Biology, Myocardium 1 (M) : PJ60)(Poster Session (Japanese))
PJ-075 Cardiac Myosin Phosphatase Could Modulate LV Function(Genetics/Genetically Engineered Models 1 (H) : PJ13)(Poster Session (Japanese))
Functional Role of Endogenous Bradykinin on Congestive Heart Failure with Combined Angiotensin II Receptor Antagonism and Angiotensin-Converting Enzyme Inhibition
Aorto-Coronary Dissection During Angioplasty in a Patient With Myxedema
Acute Myocardial Infarction in a Patient With Anomalous Left Coronary Artery Origin and Primary Antiphospholipid Syndrome
Overexpression of Myosin Phosphatase Reduces Ca^ Sensitivity of Contraction and Impairs Cardiac Function
FRS-081 Activation of Small G protein RhoA Is Essential for Branching Morphogenesis in Endothelial Cell through Rho-kinase Independent Pathway.(NO and Cardiovascular System (H) : FRS10)(Featured Research Session (English))
RhoA Activation in Vascular Smooth Muscle Cells from Stroke-Prone Spontaneously Hypertensive Rats
Big Mitogen-Activated Protein Kinase : A New Player in Vascular Remodeling
Unitary-Model-Operator Approach to Nuclear Many-Body Problem. II : Three-Body-Cluster Effects on Properties of ^O : Nuclear Physics
Activation of RhoA Is Responsible for Hypertension
Stromal Cell-Derived Factor-1α (SDF-1α), Another Angiogenic Cytokine Activating PI3K/AKT/ENOS Pathway, Elevates in Plasmaof Mouse Myocardial Infarction Model
Cardiac Myosin Phosphatase Could Be a Rho/Rho-Kinase Signaling Target in Heart
RhoA/Rho-Kinase Signaling in Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rat
Unitary-Model-Operator Approach to Nuclear Many-Body Problem. I : The Ground-State and One-Body Energies of ^O : Nuclear Physics

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