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1. Full Text Myogenic Signaling of Phosphatidylinositol 3-Kinase Requires the Serine-Threonine Kinase Akt/Protein Kinase B
by Bing-Hua Jiang and Masahiro Aoki and Jenny Z. Zheng and Jian Li and Peter K. Vogt
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/1999, Volume 96, Issue 5, pp. 2077 - 2081
The oncogene p3k, coding for a constitutively active form of phosphatidylinositol 3-kinase (PI 3-kinase), strongly activates myogenic differentiation.... 
Memory interference | Chickens | Antibodies | Muscle development | Viruses | Cultured cells | Infections | Muscle fibers | Embryos | Myoblasts | Protein phosphorylation | Muscle-specific proteins | Transdominant negative mutant | SURVIVAL | TRANSLOCATION | APOPTOSIS | CELLS | PHOSPHORYLATION | BAD | MULTIDISCIPLINARY SCIENCES | protein phosphorylation | BETA-CATENIN | INSULIN | transdominant negative mutant | muscle-specific proteins | MOLECULAR-CLONING | DIFFERENTIATION | Proto-Oncogene Proteins - metabolism | Recombinant Proteins - metabolism | MyoD Protein - genetics | Cells, Cultured | Enzyme Inhibitors - pharmacology | Gene Expression Regulation | Morpholines - pharmacology | Myosin Heavy Chains - genetics | Phosphatidylinositol 3-Kinases - metabolism | Muscle, Skeletal - physiology | Muscle, Skeletal - cytology | Chick Embryo | Creatine Kinase - genetics | Muscle Proteins - genetics | Proto-Oncogene Proteins c-akt | Animals | Transfection | Phosphatidylinositol 3-Kinases - pharmacology | Desmin - genetics | Signal Transduction - physiology | Cell Differentiation | Chromones - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Phosphatidylinositol | Research | Cell differentiation | Protein kinases | Oncogenes | Proteins | Cellular biology | Genes | Index Medicus | Space life sciences | Biological Sciences
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2. Creatine kinase isoenzymes
: pathophysiology and clincial application
by Lang, Hermann
1981, ISBN 0387107142, xviii, 317
Myocardial infarction | Diagnostic use | Diagnosis | Creatine kinase | Isoenzymes
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3. Full Text Mitochondrial creatine kinase activity prevents reactive oxygen species generation: Antioxidant role of mitochondrial kinase-dependent ADP re-cycling activity
by Meyer, Laudiene Evangelista and Machado, Lilia Bender and Santiago, Ana Paula S. A and Da-Silva, Wagner Seixas and De Felice, Fernanda G and Holub, Oliver and Oliveira, Marcus F and Galina, Antonio
Journal of Biological Chemistry, ISSN 0021-9258, 12/2006, Volume 281, Issue 49, pp. 37361 - 37371
As recently demonstrated by our group (da-Silva, W. S., Gomez-Puyou, A., Gomez-Puyou, M. T., Moreno-Sanchez, R., De Felice, F. G., de Meis, L., Oliveira, M.... 
RAT SKELETAL-MUSCLE | ENZYME-ACTIVITIES | OXIDATIVE STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | HYDROGEN-PEROXIDE | ENERGY-METABOLISM | GLUCOSE-UPTAKE | HIPPOCAMPAL-NEURONS | HEART-MITOCHONDRIA | PERMEABILITY TRANSITION | CELL-DEATH | Creatine Kinase, Mitochondrial Form - metabolism | Reactive Oxygen Species - metabolism | Rats, Wistar | Antioxidants - metabolism | Cells, Cultured | Oxygen Consumption | Rats | Male | Mitochondria - metabolism | Substrate Cycling | Hydrogen Peroxide - metabolism | Brain - metabolism | Hyperglycemia - metabolism | Animals | Models, Biological | Creatine - metabolism | Membrane Potential, Mitochondrial | Phosphocreatine - metabolism | Adenosine Diphosphate - metabolism | In Vitro Techniques | Index Medicus
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4. Full Text Protective effect of urantide against ischemia–reperfusion injury via protein kinase C and phosphtidylinositol 3′-kinase – Akt pathway
by Zhang, Jun-Yan and Chen, Zhi-Wu and Yao, Hua
Canadian Journal of Physiology and Pharmacology, ISSN 0008-4212, 05/2012, Volume 90, Issue 5, pp. 637 - 645
Urantide is the most potent UT receptor antagonist compound found to date. Our previous studies have shown that it has cardioprotective effect against... 
voie de signalisation | ischémie–reperfusion du myocarde | signaling pathway | PKC | urantide | PI3K–Akt | myocardial ischemia–reperfusion | Myocardial ischemia-reperfusion | Signaling pathway | Urantide | PI3K-Akt | ISOLATED RAT-HEART | ISCHEMIA/REPERFUSION INJURY | RECEPTOR GPR14 | ACTIVATION | PHYSIOLOGY | INCREASED EXPRESSION | HUMAN UROTENSIN-II | MYOCARDIAL-ISCHEMIA | MECHANISMS | myocardial ischemia-reperfusion | EPSILON | PHARMACOLOGY & PHARMACY | TISSUES | Urotensins - pharmacology | Male | Peptide Fragments - pharmacology | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - enzymology | Troponin I - blood | Myocardial Reperfusion Injury - pathology | Protein Kinase C - metabolism | Myocardium - metabolism | Myocardial Reperfusion Injury - drug therapy | Chromones - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Creatine Kinase - blood | Morpholines - pharmacology | Rats | Myocardium - pathology | Protein Kinase C - antagonists & inhibitors | Cardiotonic Agents - pharmacology | Rats, Sprague-Dawley | Benzophenanthridines - pharmacology | Animals | Signal Transduction - drug effects | L-Lactate Dehydrogenase - blood | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Proteins | Studies | Signal transduction | Physiology | Ischemia | Kinases | Index Medicus
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5. Full Text Cardiac-specific inhibition of kinase activity in calcium/calmodulin-dependent protein kinase kinase-β leads to accelerated left ventricular remodeling and heart failure after transverse aortic constriction in mice
by Watanabe, Shin and Horie, Takahiro and Nagao, Kazuya and Kuwabara, Yasuhide and Baba, Osamu and Nishi, Hitoo and Sowa, Naoya and Narazaki, Michiko and Matsuda, Tetsuya and Takemura, Genzou and Wada, Hiromichi and Hasegawa, Koji and Kimura, Takeshi and Ono, Koh
PLoS ONE, ISSN 1932-6203, 09/2014, Volume 9, Issue 9, pp. e108201 - e108201
Background: The mechanism of cardiac energy production against sustained pressure overload remains to be elucidated. Methods and Results: We generated... 
HYPERTROPHY | OXIDATIVE STRESS | RECEPTOR-GAMMA | MITOCHONDRIAL BIOGENESIS | PGC-1-ALPHA | CALMODULIN | GLUCOSE | MULTIDISCIPLINARY SCIENCES | ALPHA | CASCADE | MOLECULAR-CLONING | Up-Regulation | Phosphorylation | Mitochondria, Heart - metabolism | Heart Failure - physiopathology | Myosin Heavy Chains - genetics | Male | Adenosine Triphosphate | Ventricular Dysfunction, Left - genetics | Ventricular Remodeling - genetics | Mitochondria, Heart - genetics | Heart Failure - etiology | Heart Ventricles - pathology | Disease Models, Animal | Heart Failure - mortality | Promoter Regions, Genetic | Magnetic Resonance Spectroscopy | Signal Transduction | Gene Expression Regulation | Mice, Transgenic | Heart Failure - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Kinase - genetics | Ventricular Dysfunction, Left - physiopathology | Animals | Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism | Heart Ventricles - metabolism | Mice | Phosphates | Heart | Systems science | Calcium | Biosynthesis | Glucose | Kinases | Creatine | Magnetic resonance spectroscopy | Proteins | Morphogenesis | Mitochondria | Energy | Transgenic animals | Rodents | Calcium-binding protein | Myosin | Aorta | Ca2+/calmodulin-dependent protein kinase | Heart diseases | Informatics | Stretching | Calmodulin | Failure | Heart failure | Spectroscopy | Damage assessment | Adenosine monophosphate | AMP | Magnetic resonance | Transgenic mice | Phosphocreatine | Pressure | Medicine | Signaling | Adenosine kinase | Coronary vessels | Ventricle | Laboratory animals | Index Medicus
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6. Full Text The structure of lombricine kinase: Implications for phosphagen kinase conformational changes
by Bush, D. Jeffrey and Kirillova, Olga and Clark, Shawn A and Davulcu, Omar and Fabiola, Felcy and Xie, Qing and Somasundaram, Thayumanasamy and Ellington, W. Ross and Chapman, Michael S
Journal of Biological Chemistry, ISSN 0021-9258, 03/2011, Volume 286, Issue 11, pp. 9338 - 9350
Lombricine kinase is a member of the phosphagen kinase family and a homolog of creatine and arginine kinases, enzymes responsible for buffering cellular ATP... 
STATE ANALOG COMPLEX | ANGSTROM RESOLUTION | EFFECT SPECTROSCOPY TRNOESY | SUBSTRATE-SPECIFICITY | MOLECULAR REPLACEMENT | ACTIVE-SITE | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUSCLE CREATINE-KINASE | NUCLEOTIDE CONFORMATIONS | ARGININE KINASE | Catalytic Domain | Protein Structure, Secondary | Models, Molecular | Phosphotransferases (Nitrogenous Group Acceptor) - metabolism | Crystallography, X-Ray | Phosphotransferases (Nitrogenous Group Acceptor) - chemistry | Adenosine Diphosphate - chemistry | Annelida - enzymology | Animals | Adenosine Triphosphate - metabolism | Computer Simulation | Nuclear Magnetic Resonance, Biomolecular | Adenosine Diphosphate - metabolism | Adenosine Triphosphate - chemistry | Index Medicus | Enzyme Structure | Arginine Kinase | Protein Structure and Folding | Crystal Structure | Creatine Kinase | Protein Structure | Creatine | Crystallography
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7. Full Text Activity of Selumetinib in Neurofibromatosis Type 1–Related Plexiform Neurofibromas
by Dombi, Eva and Baldwin, Andrea and Marcus, Leigh J and Fisher, Michael J and Weiss, Brian and Kim, AeRang and Whitcomb, Patricia and Martin, Staci and Aschbacher-Smith, Lindsey E and Rizvi, Tilat A and Wu, Jianqiang and Ershler, Rachel and Wolters, Pamela and Therrien, Janet and Glod, John and Belasco, Jean B and Schorry, Elizabeth and Brofferio, Alessandra and Starosta, Amy J and Gillespie, Andrea and Doyle, Austin L and Ratner, Nancy and Widemann, Brigitte C
The New England Journal of Medicine, ISSN 0028-4793, 12/2016, Volume 375, Issue 26, pp. 2550 - 2560
Plexiform neurofibroma is a complication of the NF1 mutation in neurofibromatosis that results in overactivity of the RAS pathway. Selumetinib, a... 
YOUNG-ADULTS | MEDICINE, GENERAL & INTERNAL | MEK INHIBITION | SOLID TUMORS | CLINICAL-TRIALS | TUMOR-SUPPRESSOR | FARNESYLTRANSFERASE INHIBITOR TIPIFARNIB | HYPERACTIVE RAS | CANCER | CONSORTIUM PHASE-II | CHILDREN | Neurofibroma, Plexiform - diagnostic imaging | Protein Kinase Inhibitors - pharmacokinetics | Humans | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Benzimidazoles - pharmacokinetics | Child, Preschool | Male | Protein Kinase Inhibitors - adverse effects | Neurofibroma, Plexiform - drug therapy | Disease Progression | Magnetic Resonance Imaging | Protein Kinase Inhibitors - administration & dosage | Animals | Benzimidazoles - administration & dosage | Neurofibromatosis 1 - drug therapy | Adolescent | Female | Mice | Benzimidazoles - adverse effects | Child | Disease Models, Animal | Drugs | Care and treatment | Usage | Neurofibromatosis | Extracellular signal-regulated kinases | Dosage and administration | Diagnosis | Research | Pediatrics | Creatine kinase | Plexiform neurofibroma | Clinical trials | MAP kinase | Creatine | Kinases | Recklinghausen's disease | Children & youth | Pain | Magnetic resonance imaging | Protein kinase | Children | Pharmacokinetics | Drug therapy | Tumors | Index Medicus | Abridged Index Medicus
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8. Full Text AMP Kinase Is Required for Mitochondrial Biogenesis in Skeletal Muscle in Response to Chronic Energy Deprivation
by Haihong Zong and Jian Ming Ren and Lawrence H. Young and Marc Pypaert and James Mu and Morris J. Birnbaum and Gerald I. Shulman
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2002, Volume 99, Issue 25, pp. 15983 - 15987
Mitochondrial biogenesis is a critical adaptation to chronic energy deprivation, yet the signaling mechanisms responsible for this response are poorly... 
Energy deprivation | Phosphates | Biological Sciences | Sodium | Transgenic animals | Grade point average | Muscles | Actins | Gene expression regulation | Creatine | Skeletal muscle | MP-activated protein kinase | Calcium/calmodulin-dependent protein kinase IV | β-guanidinopropionic acid | Peroxisome proliferator-activated γ receptor coactivator-1α | ACTIVATED PROTEIN-KINASE | NUCLEAR | MULTIDISCIPLINARY SCIENCES | GLUCOSE-TRANSPORT | ACETYL-COA CARBOXYLASE | AMP-activated protein kinase | AMINOLEVULINATE SYNTHASE EXPRESSION | CONTRACTILE ACTIVITY | calcium/calmodulin-dependent protein kinase IV | FATTY-ACID OXIDATION | ELECTRICAL-STIMULATION | peroxisome proliferator-activated gamma receptor coactivator-1 alpha | IN-VIVO | GENE-EXPRESSION | beta-guanidinopropionic acid | Propionates - pharmacology | Calcium-Calmodulin-Dependent Protein Kinase Type 4 | Guanidines - pharmacology | Muscle Proteins - deficiency | Genes, Dominant | Muscle, Skeletal - drug effects | Calcium-Calmodulin-Dependent Protein Kinases - biosynthesis | Enzyme Induction - drug effects | Mitochondria, Muscle - physiology | Adenylate Kinase - physiology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 | Muscle Proteins - physiology | Muscle, Skeletal - enzymology | Calcium-Calmodulin-Dependent Protein Kinases - genetics | Muscle, Skeletal - ultrastructure | Mice, Transgenic | Transcription Factors - biosynthesis | Transcription Factors - genetics | Adenylate Kinase - deficiency | Gene Expression Regulation - drug effects | Muscle Proteins - genetics | Animals | Adenine Nucleotides - metabolism | Mice | Phosphocreatine - metabolism | Adenylate Kinase - genetics | Energy Metabolism - drug effects | Physiological aspects | Energy metabolism | Bioenergetics | Proteins | Fatigue | Biochemistry | Mutation | Muscular system | Index Medicus | calmodulin-dependent protein kinase IV | calcium | peroxisome proliferator-activated γ receptor coactivator-1α
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9. Full Text Inhibition of JNK mitochondrial localization and signaling is protective against ischemia/reperfusion injury in rats
by Chambers, Jeremy W and Pachori, Alok and Howard, Shannon and Iqbal, Sarah and LoGrasso, Philip V
Journal of Biological Chemistry, ISSN 0021-9258, 02/2013, Volume 288, Issue 6, pp. 4000 - 4011
To build upon recent findings that mitochondrial JNK signaling is inhibited by selectively blocking the interaction between JNK and Sab, we utilized a... 
APOPTOSIS | ACTIVATION | PYRUVATE-DEHYDROGENASE ACTIVITY | PROTEIN | PATHWAY | BIOENERGETICS | BIOCHEMISTRY & MOLECULAR BIOLOGY | N-TERMINAL KINASE | REPERFUSION | DEATH | IDENTIFICATION | Reactive Oxygen Species - metabolism | Mitochondria, Heart - pathology | Creatine Kinase, MB Form - metabolism | Humans | Mitochondrial Proteins - genetics | Protein Transport - drug effects | Myocardial Reperfusion Injury - enzymology | MAP Kinase Signaling System | Myocytes, Cardiac - enzymology | Myocardial Reperfusion Injury - pathology | MAP Kinase Kinase 4 - metabolism | Mitochondrial Proteins - metabolism | Cell Death | Muscle Proteins - metabolism | MAP Kinase Kinase 4 - antagonists & inhibitors | Mitochondria, Heart - genetics | Myocardial Reperfusion Injury - genetics | Creatine Kinase, MB Form - genetics | Cell Line | Mitochondria, Heart - enzymology | Rats | Rats, Sprague-Dawley | Protein Transport - genetics | Creatine Kinase - genetics | Muscle Proteins - genetics | Myocytes, Cardiac - pathology | Animals | Creatine Kinase - metabolism | Protein Kinase Inhibitors - pharmacology | Index Medicus | Enzyme Inhibitors | Mitochondria | Signal Transduction | Ischemia | c-Jun N-terminal Kinase (JNK)
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10. Full Text Estrogen-related receptor α regulates skeletal myocyte differentiation via modulation of the ERK MAP kinase pathway
by Jennifer Murray and Janice M. Huss
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 09/2011, Volume 301, Issue 3, pp. 630 - 645
Myocyte differentiation involves complex interactions between signal transduction pathways and transcription factors. The estrogen-related receptors (ERRs)... 
Orphan nuclear receptors | Gene regulation | Skeletal muscle | Mitogen-activated protein kinases | SIGNALING PATHWAYS | PHYSIOLOGY | MITOCHONDRIAL BIOGENESIS | NUCLEAR RECEPTORS | PROLIFERATOR-ACTIVATED RECEPTOR | OXIDATIVE-METABOLISM | MUSCLE CELL-DIFFERENTIATION | CELL BIOLOGY | CYTOCHROME-C-OXIDASE | gene regulation | mitogen-activated protein kinases | GENE-EXPRESSION | COACTIVATOR-1-ALPHA PGC-1-ALPHA | skeletal muscle | TRANSCRIPTIONAL COREPRESSOR RIP140 | orphan nuclear receptors | MAP Kinase Signaling System - physiology | Protein Binding - genetics | Receptors, Estrogen - metabolism | Gene Expression - genetics | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Myosin Heavy Chains - genetics | Myogenin - genetics | Receptors, Estrogen - deficiency | Mitogen-Activated Protein Kinase Kinases - metabolism | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Myoblasts, Skeletal - metabolism | Dual Specificity Phosphatase 1 - genetics | Butadienes - pharmacology | Transduction, Genetic | Receptors, Estrogen - antagonists & inhibitors | Creatine Kinase, Mitochondrial Form - genetics | Mitochondria - pathology | Mice, Knockout | Muscle Proteins - genetics | Muscle Fibers, Skeletal - cytology | Mice | Transcription Factors | Kinetics | Troponin I - metabolism | Muscle Fibers, Skeletal - enzymology | Gene Expression - drug effects | Nitriles - pharmacology | Extracellular Signal-Regulated MAP Kinases - metabolism | Muscle Fibers, Skeletal - drug effects | Muscle Fibers, Skeletal - metabolism | Sarcomeres - pathology | Myoblasts, Skeletal - cytology | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Troponin I - genetics | Muscle Proteins - metabolism | Trans-Activators - genetics | Flavonoids - pharmacology | Cell Differentiation - physiology | Receptors, Estrogen - genetics | Mice, Inbred C57BL | Muscle Development - physiology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Up-Regulation - genetics | Mitochondria - metabolism | Myoblasts, Skeletal - enzymology | Up-Regulation - drug effects | Animals | MAP Kinase Signaling System - drug effects | Muscle Development - drug effects | Cell Differentiation - drug effects | Dual Specificity Phosphatase 1 - metabolism | Trans-Activators - metabolism | Thiazoles - pharmacology | Myoblasts, Skeletal - drug effects | Phosphorylation | Transcription factors | Myotubes | MEK inhibitors | Extracellular signal-regulated kinase | MAP kinase | Regulatory sequences | Myocytes | Gene expression | MAP kinase phosphatase | Signal transduction | Mitochondria | Energy resources | Differentiation | Electron transport | myogenesis | PGC-1 protein | Sarcomeres | Index Medicus | Muscle Cell Biology and Cell Motility
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11. Full Text Death following creatine kinase-MB elevation after coronary intervention: Identification of an early risk period: Importance of creatine kinase-MB level, completeness of revascularization, ventricular function, and probable benefit of statin therapy
by Ellis, Stephen G and Chew, Derek and Chan, Albert and Whitlow, Patrick L and Schneider, Jakob P and Topol, Eric J
Circulation, ISSN 0009-7322, 09/2002, Volume 106, Issue 10, pp. 1205 - 1210
Background-Creatine kinase (CK)-MB elevation after percutaneous coronary intervention (PCI) has been associated with subsequent cardiac death. The patients at... 
Myocardial infarction | Proteins | Angioplasty | SURVIVAL | MULTIVESSEL DISEASE | CARDIAC & CARDIOVASCULAR SYSTEMS | proteins | myocardial infarction | PERCUTANEOUS INTERVENTION | PERIPHERAL VASCULAR DISEASE | ENZYME ELEVATION | HEMATOLOGY | angioplasty | Myocardial Infarction - diagnosis | Myocardial Infarction - mortality | Follow-Up Studies | Ventricular Function, Left | Humans | Risk Factors | Male | Survival Rate | Treatment Outcome | Angioplasty, Balloon, Coronary | Myocardial Infarction - therapy | Creatine Kinase - biosynthesis | Creatine Kinase, MB Form | Time Factors | Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use | Female | Aged | Isoenzymes - biosynthesis | Myocardial Infarction - enzymology | Index Medicus | Abridged Index Medicus
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12. Full Text Upregulation of Na+,Cl--Coupled Betaine/ γ-Amino-Butyric Acid Transporter BGT1 by Tau Tubulin Kinase 2
by Almilaji, Ahmad and Munoz, Carlos and Hosseinzadeh, Zohreh and Lang, Florian
Cellular Physiology and Biochemistry, ISSN 1015-8987, 09/2013, Volume 32, Issue 2, pp. 334 - 343
Background/Aims: The serine/threonine kinase Tau-tubulin-kinase 2 (TTBK2) is expressed in various tissues including kidney, liver and brain. Loss of function... 
Original Paper | Electrophysiology | Kinase | Neurodegeneration | Osmolyte transporter | RAT-LIVER | CELL-VOLUME REGULATION | MDCK CELLS | PHYSIOLOGY | PROTEIN-KINASE | TAURINE-TRANSPORTER | FUNCTIONAL-CHARACTERIZATION | CELL BIOLOGY | CREATINE DEFICIENCY SYNDROMES | PHOSPHORYLATES-TAU | ORGANIC OSMOLYTE TRANSPORT | HYPERTONIC STRESS | Recombinant Proteins - metabolism | Xenopus | Up-Regulation | Oocytes - metabolism | gamma-Aminobutyric Acid - metabolism | Humans | Protein-Serine-Threonine Kinases - genetics | Recombinant Proteins - genetics | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Protein-Serine-Threonine Kinases - metabolism | Sodium Chloride - chemistry | Index Medicus
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13. Creatine and creatine kinase in health and disease
by Salomons, Gajja S and Wyss, Markus
2007, Subcellular biochemistry, ISBN 9781402064869, Volume 46., xvii, 351
A number of beneficial health effects have been ascribed to oral creatine supplementation. Creatine may even improve memory and intelligence. This book... 
pharmacokinetics | Creatine | Creatine kinase | Therapeutic use | biosynthesis | Human Genetics | Quality of Life Research | Neurology | Medical Biochemistry | Medicine & Public Health
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14. Full Text Long-Term Outcomes of Non-ST-Elevation Myocardial Infarction Without Creatine Kinase Elevation　― The J-MINUET Study
by Ishihara, Masaharu and Nakao, Koichi and Ozaki, Yukio and Kimura, Kazuo and Ako, Junya and Noguchi, Teruo and Fujino, Masashi and Yasuda, Satoshi and Suwa, Satoru and Fujimoto, Kazuteru and Nakama, Yasuharu and Morita, Takashi and Shimizu, Wataru and Saito, Yoshihiko and Hirohata, Atsushi and Morita, Yasuhiro and Inoue, Teruo and Okamura, Atsunori and Uematsu, Masaaki and Hirata, Kazuhito and Tanabe, Kengo and Shibata, Yoshisato and Owa, Mafumi and Tsujita, Kenichi and Funayama, Hiroshi and Kokubu, Nobuaki and Kozuma, Ken and Tobaru, Tetsuya and Oshima, Shigeru and Nakai, Michikazu and Nishimura, Kunihiro and Miyamoto, Yoshihiro and Ogawa, Hisao and J-MINUET Investigators and on behalf of J-MINUET Investigators
Circulation Journal, ISSN 1346-9843, 2017, Volume 81, Issue 7, pp. 958 - 965
Background:According to troponin-based criteria of myocardial infarction (MI), patients without elevation of creatine kinase (CK), formerly classified as... 
Myocardial infarction | Cardiac troponin | Prognosis | Multicenter registry | Creatine kinase | MORTALITY | POPULATION | CARDIAC & CARDIOVASCULAR SYSTEMS | MANAGEMENT | PLAQUES | TRENDS | PERCUTANEOUS CORONARY INTERVENTION | UNIVERSAL DEFINITION | DISEASE | UNSTABLE ANGINA | REGISTRY | Myocardial Infarction - blood | Myocardial Infarction - mortality | Prospective Studies | Creatine Kinase - blood | Follow-Up Studies | Humans | Middle Aged | Male | Survival Rate | Heart Failure - blood | Stroke - blood | Disease-Free Survival | Heart Failure - therapy | Myocardial Infarction - complications | Myocardial Infarction - therapy | Stroke - etiology | Time Factors | Aged, 80 and over | Female | Aged | Stroke - mortality | Heart Failure - etiology | Stroke - therapy | Heart Failure - mortality | Index Medicus
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