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Journal Article
Cell, ISSN 0092-8674, 06/2006, Volume 125, Issue 5, pp. 987 - 1001
Oxidative stress influences cell survival and homeostasis, but the mechanisms underlying the biological effects of oxidative stress remain to be elucidated.... 
TRANSCRIPTION FACTORS | FAT-BODY | NEURONAL SURVIVAL | CAENORHABDITIS-ELEGANS | HISTONE H2B | PHOSPHORYLATION | PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-CYCLE | STERILE-20 KINASE | PROMOTES APOPTOSIS | CELL BIOLOGY | Phosphorylation | Conserved Sequence - physiology | Active Transport, Cell Nucleus - physiology | Oxidative Stress - physiology | Caenorhabditis elegans Proteins - metabolism | Nerve Tissue Proteins - chemistry | Forkhead Transcription Factors - metabolism | Forkhead Transcription Factors - chemistry | Neurons - metabolism | Protein-Serine-Threonine Kinases - metabolism | Animals, Newborn | Protein Structure, Tertiary | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Cellular Senescence - physiology | Rats | Caenorhabditis elegans Proteins - isolation & purification | 14-3-3 Proteins - metabolism | Nerve Tissue Proteins - metabolism | Caenorhabditis elegans | Animals | Cell Death - physiology | Signal Transduction - physiology | Transcriptional Activation - physiology | Caenorhabditis elegans Proteins - genetics | Longevity - physiology | Evolution, Molecular | Genetic research | Oxidative stress | Genetic aspects | Research | Mammals | Cell death | Yuan (China) | Medical colleges | Neurosciences | Neurons | Stem cells | Protection and preservation | DNA binding proteins | Protein kinases | Index Medicus
Journal Article
Journal Article
Journal Article
Circulation, ISSN 0009-7322, 05/2010, Volume 121, Issue 18, pp. 2012 - 2022
Background-Whether alterations in mitochondrial morphology affect the susceptibility of the heart to ischemia/reperfusion injury is unknown. We hypothesized... 
Myocardial infarction | Cardiomyocytes | Hypoxia | Reperfusion | Ischemia | hypoxia | PERMEABILITY TRANSITION PORE | APOPTOSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | FUSION | myocardial infarction | REPERFUSION INJURY | DEATH | ischemia | cardiomyocytes | HL-1 CELLS | FLUCTUATIONS | MITOFUSIN-2 | PERIPHERAL VASCULAR DISEASE | DYSFUNCTION | HEMATOLOGY | reperfusion | Age Factors | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Male | Green Fluorescent Proteins - genetics | GTP Phosphohydrolases - antagonists & inhibitors | Mitochondria - ultrastructure | Mitochondrial Membranes - drug effects | Myocardial Reperfusion Injury - pathology | Transfection | Myocardial Reperfusion Injury - drug therapy | Quinazolinones - pharmacology | Cell Line | Myocytes, Cardiac - cytology | Mitochondrial Membranes - physiology | Mice, Inbred C57BL | Dynamins | Cardiotonic Agents - pharmacology | Microtubule-Associated Proteins - antagonists & inhibitors | Mitochondria - drug effects | Microscopy, Electron | Myocardial Reperfusion Injury - physiopathology | Microscopy, Confocal | Animals | GTP Phosphohydrolases - metabolism | Myocytes, Cardiac - drug effects | Cell Death - physiology | GTP Phosphohydrolases - genetics | Myocytes, Cardiac - physiology | Mitochondrial Membranes - ultrastructure | Mice | Membrane Fusion - physiology | Mitochondria - physiology | Index Medicus | Abridged Index Medicus
Journal Article
Neuropharmacology, ISSN 0028-3908, 04/2014, Volume 79, pp. 161 - 171
Ischemia induces blood–brain barrier (BBB) disruption by matrix metalloproteases (MMPs) activation, leading to neuronal cell death. Here, we show that... 
Matrix metalloprotease | Tight junction | Global ischemia | Blood–spinal cord barrier | Hippocampus | Blood-spinal cord barrier | TISSUE-PLASMINOGEN ACTIVATOR | FOCAL CEREBRAL-ISCHEMIA | NECROSIS-FACTOR-ALPHA | GENE KNOCK-OUT | FOREBRAIN ISCHEMIA | NEUROSCIENCES | MATRIX METALLOPROTEINASES | INTRACEREBRAL HEMORRHAGE | MATRIX-METALLOPROTEINASE-9 | PHARMACOLOGY & PHARMACY | SPINAL-CORD-INJURY | RAT-BRAIN | Capillary Permeability - physiology | Gene Expression - drug effects | Blood-Brain Barrier - physiopathology | Capillary Permeability - drug effects | Male | Hippocampus - drug effects | RNA, Messenger - metabolism | Occludin - metabolism | Matrix Metalloproteinase 9 - metabolism | Microglia - physiology | Neuroprotective Agents - pharmacology | Neurons - physiology | Cell Death - drug effects | Neurons - drug effects | Macrophages - physiology | Astrocytes - drug effects | Fluoxetine - pharmacology | Hippocampus - blood supply | Microglia - drug effects | Matrix Metalloproteinase 2 - metabolism | Brain Ischemia - physiopathology | Hippocampus - pathology | Mice, Inbred Strains | Blood-Brain Barrier - drug effects | Astrocytes - physiology | Animals | Cell Death - physiology | Brain Ischemia - drug therapy | Brain Ischemia - pathology | Macrophages - drug effects | Laminin - metabolism | Hippocampus - physiopathology | Prevention | Brain | Neurosciences | Ischemia | RNA | Proteases | Fluoxetine | Neurons | Memory | Permeability | Injuries | Index Medicus
Journal Article
Blood, ISSN 0006-4971, 12/2011, Volume 118, Issue 23, pp. 6141 - 6152
Journal Article
Trends in Neurosciences, ISSN 0166-2236, 2015, Volume 38, Issue 3, pp. 127 - 128
As we age, movements become slower and inconsistent and require more attention. These hallmarks of aging suggest a switch from predictive to reactive motor... 
Neurology | motor control | cerebellum | aging | Cerebellum | Aging | Motor control | M