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American journal of obstetrics and gynecology, ISSN 0002-9378, 2015, Volume 213, Issue 3, pp. 359.e1 - 359.e16
Journal Article
Neuron (Cambridge, Mass.), ISSN 0896-6273, 2003, Volume 40, Issue 3, pp. 485 - 499
The CNS is thought to develop from self-renewing stem cells that generate neurons, astrocytes, and oligodendrocytes. Other data, however, have suggested that... 
OLIGODENDROCYTE LINEAGE | PROGENITOR CELLS | TRANSCRIPTION FACTORS | GLIAL-RESTRICTED PRECURSORS | RAT CEREBRAL-CORTEX | SONIC HEDGEHOG | EMBRYONIC SPINAL-CORD | NEURAL-TUBE | CENTRAL-NERVOUS-SYSTEM | MAMMALIAN FOREBRAIN | NEUROSCIENCES | Immunohistochemistry | Green Fluorescent Proteins | O Antigens - metabolism | Embryo, Mammalian | Cell Count | Homeodomain Proteins - metabolism | Fibroblast Growth Factor 2 - pharmacology | Glial Fibrillary Acidic Protein - metabolism | Hedgehog Proteins | RNA, Messenger - biosynthesis | Time Factors | SOXE Transcription Factors | Neurons - metabolism | Basic Helix-Loop-Helix Transcription Factors | Receptor, Platelet-Derived Growth Factor alpha - metabolism | Enzyme Inhibitors - pharmacology | Proteoglycans - metabolism | Rats | Oligodendrocyte Transcription Factor 2 | Mice | Astrocytes - metabolism | Oligodendroglia - metabolism | Flow Cytometry - methods | Epithelial Cells - metabolism | Epithelial Cells - drug effects | PAX7 Transcription Factor | Carbocyanines - metabolism | DNA-Binding Proteins - metabolism | Dose-Response Relationship, Drug | Tubulin - metabolism | Transfection | Reverse Transcriptase Polymerase Chain Reaction - methods | beta-Galactosidase - metabolism | Fibroblast Growth Factor 2 - physiology | Bromodeoxyuridine - metabolism | Spinal Cord - cytology | Cell Differentiation - physiology | High Mobility Group Proteins - metabolism | Cells, Cultured | Zebrafish Proteins | Antigens - metabolism | Body Patterning - physiology | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Spinal Cord - embryology | Blotting, Northern | Animals | Cell Aggregation | Stem Cells - physiology | Trans-Activators - metabolism | Epidermal Growth Factor - pharmacology | In Vitro Techniques | Luminescent Proteins - metabolism | Spinal cord | Scholarships & fellowships | Neurosciences | Rodents | Stem cells | Experiments | Neurogenesis
Journal Article
Aging cell, ISSN 1474-9718, 2017, Volume 16, Issue 4, pp. 837 - 846
Summary Kallistatin, an endogenous protein, protects against vascular injury by inhibiting oxidative stress and inflammation in hypertensive rats and enhancing... 
sirtuin 1 | kallistatin | vascular senescence | aging | microRNA‐34a | oxidative stress | microRNA-34a | TISSUE KALLIKREIN INHIBITOR | MICRORNA-21 | SIRT1 | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | PROTECTIVE ROLE | INFLAMMATION | PROGENITOR-CELL SENESCENCE | ENDOTHELIAL-CELLS | BINDING-SITE | RENAL INJURY | Sirtuin 1 - metabolism | Diabetes Mellitus, Experimental - drug therapy | Endothelial Progenitor Cells - cytology | MicroRNAs - antagonists & inhibitors | Streptozocin | Humans | Diabetes Mellitus, Experimental - genetics | NADPH Oxidases - metabolism | Caenorhabditis elegans Proteins - metabolism | Cellular Senescence - drug effects | Male | MicroRNAs - metabolism | Sirtuin 1 - genetics | Telomerase - genetics | Plasminogen Activator Inhibitor 1 - metabolism | Superoxides - metabolism | beta-Galactosidase - metabolism | NADPH Oxidases - genetics | Telomerase - metabolism | Diabetes Mellitus, Experimental - chemically induced | Superoxides - antagonists & inhibitors | Nitric Oxide Synthase Type III - metabolism | Plasminogen Activator Inhibitor 1 - genetics | Diabetes Mellitus, Experimental - metabolism | Sirtuins - genetics | Endothelial Progenitor Cells - metabolism | Cellular Senescence - genetics | Caenorhabditis elegans - metabolism | Caenorhabditis elegans - genetics | Catalase - genetics | Endothelial Progenitor Cells - drug effects | Cells, Cultured | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Nitric Oxide Synthase Type III - genetics | Serpins - pharmacology | Catalase - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Animals | Caenorhabditis elegans - drug effects | Genistein - pharmacology | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Mice | MicroRNAs - genetics | beta-Galactosidase - genetics | Caenorhabditis elegans Proteins - genetics | Sirtuins - metabolism | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Gene expression | MicroRNA | Oxidative stress | Senescence | Genistein | INK4a protein | Kinases | NAD(P)H oxidase | Catalase | Rodents | Aging | Aorta | miRNA | Telomerase | Protein-tyrosine kinase | Tyrosine | Enzymes | Diabetes mellitus | p16 Protein | Superoxide | SIRT1 protein | Life span | Tumor necrosis factor | MicroRNAs | Stem cells | Nematodes | Diabetes | Original
Journal Article
Plant physiology (Bethesda), ISSN 1532-2548, 2015, Volume 169, Issue 3, pp. pp.00690.2015 - 2063
Journal Article
Scientific reports, ISSN 2045-2322, 03/2016, Volume 6, Issue 1, p. 23795
We characterized cerebral Oil Red O-positive lipid-laden cells (LLC) of aging mice evaluating their distribution, morphology, density, functional activities... 
ALZHEIMER-DISEASE | WHITE-MATTER | MICROGLIA | CORTEX | AGE-RELATED-CHANGES | MULTIDISCIPLINARY SCIENCES | NEURAL STEM | PROINFLAMMATORY CYTOKINES | SUBVENTRICULAR ZONE | AUTOPHAGY | ASTROCYTES | Tumor Necrosis Factor-alpha - metabolism | Glial Fibrillary Acidic Protein - genetics | Microglia - metabolism | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Cell Count | Tumor Necrosis Factor-alpha - genetics | Glial Fibrillary Acidic Protein - metabolism | Autophagy | Neurogenesis | Cerebral Cortex - metabolism | Meninges - metabolism | Cerebral Cortex - ultrastructure | Lipid Droplets - ultrastructure | Neurons - ultrastructure | beta-Galactosidase - metabolism | Female | S100 Calcium Binding Protein beta Subunit - genetics | Microfilament Proteins - metabolism | Neurons - metabolism | S100 Calcium Binding Protein beta Subunit - metabolism | Lipid Droplets - metabolism | Microfilament Proteins - genetics | Calcium-Binding Proteins - metabolism | Gene Expression | Astrocytes - ultrastructure | Phenotype | Animals | Perilipin-1 - genetics | Microglia - ultrastructure | Histocytochemistry | Beclin-1 - genetics | Mice | Mice, Inbred BALB C | Perilipin-1 - metabolism | beta-Galactosidase - genetics | Beclin-1 - metabolism | Meninges - ultrastructure | Aging - metabolism | Astrocytes - metabolism | Calcium-Binding Proteins - genetics | Senescence | Astrocytes | Glial fibrillary acidic protein | Cortex | Parenchyma | Blood vessels | Ventricles (cerebral) | Lipids | Inflammation | Neuronal-glial interactions | Microglia | Ependymal cells | Tumor necrosis factor | Neostriatum | Aging | Ventricle
Journal Article
Nature neuroscience, ISSN 1097-6256, 08/2011, Volume 14, Issue 8, pp. 1009 - 1016
Permanent damage to white matter tracts, comprising axons and myelinating oligodendrocytes, is an important component of brain injuries of the newborn that... 
FUNCTIONAL INTERACTION | MULTIPLE-SCLEROSIS | CNS REMYELINATION | MYELINATION | SIGNALING PATHWAY | TRANSCRIPTION | DIFFERENTIATION | BETA-CATENIN | NEUROSCIENCES | WHITE-MATTER INJURY | NEGATIVE REGULATOR | Humans | Ki-67 Antigen - metabolism | Male | Brain Injuries - metabolism | Wnt Proteins - metabolism | Oligodendroglia - drug effects | Hypoxia-Ischemia, Brain - therapy | Infant, Newborn | Organ Culture Techniques | Disease Models, Animal | Animals, Newborn | Basic Helix-Loop-Helix Transcription Factors - genetics | Mice, Transgenic | Oligodendrocyte Transcription Factor 2 | Brain Injuries - therapy | Multiple Sclerosis - therapy | Myelin Proteins - genetics | beta Catenin - metabolism | Heterocyclic Compounds, 3-Ring - therapeutic use | Spinal Cord - physiology | Axin Protein | Mice | Myelin Sheath - ultrastructure | beta-Galactosidase - genetics | Cerebellum - ultrastructure | Myelin Proteins - metabolism | Corpus Callosum - metabolism | Spinal Cord - drug effects | Heterocyclic Compounds, 3-Ring - pharmacology | Myelin Proteins - therapeutic use | Cerebellum - drug effects | Myelin Sheath - drug effects | Hypoxia-Ischemia, Brain - pathology | Cerebral Cortex - cytology | Cytoskeletal Proteins - deficiency | Dose-Response Relationship, Drug | Oligodendroglia - physiology | Wnt Proteins - genetics | beta-Galactosidase - metabolism | Adult | Cytoskeletal Proteins - metabolism | Female | Demyelinating Diseases - chemically induced | Demyelinating Diseases - pathology | Neurons - drug effects | Cell Differentiation - physiology | Hypoxia-Ischemia, Brain - metabolism | Microscopy, Electron, Transmission | Myelin Sheath - pathology | Gene Expression Regulation - genetics | Cerebellum - metabolism | Cells, Cultured | Gene Expression Regulation - physiology | Corpus Callosum - drug effects | Nerve Tissue Proteins - genetics | beta Catenin - genetics | Multiple Sclerosis - complications | Nerve Tissue Proteins - metabolism | Animals | Cell Differentiation - drug effects | Multiple Sclerosis - pathology | Stem Cells - drug effects | Brain Injuries - etiology | Lysophosphatidylcholines - toxicity | Postmortem Changes | Infants (Newborn) | Brain | Care and treatment | Physiological aspects | Research | Binding proteins | Health aspects | Injuries
Journal Article
Nature neuroscience, ISSN 1546-1726, 2004, Volume 7, Issue 11, pp. 1233 - 1241
Establishing the cellular identity in vivo of adult multipotent neural progenitors is fundamental to understanding their biology. We used two transgenic... 
SITE-SPECIFIC RECOMBINATION | NEURAL STEM-CELLS | RADIAL GLIAL-CELLS | FIBRILLARY ACIDIC PROTEIN | IN-VIVO | CENTRAL-NERVOUS-SYSTEM | SUBVENTRICULAR ZONE | MAMMALIAN FOREBRAIN | NEUROSCIENCES | INTERMEDIATE-FILAMENT PROTEIN | TRANSGENIC MICE | Glial Fibrillary Acidic Protein - genetics | Microtubule-Associated Proteins - metabolism | Phosphopyruvate Hydratase - metabolism | Prosencephalon - physiology | Olfactory Bulb - metabolism | Hippocampus - drug effects | Glial Fibrillary Acidic Protein - metabolism | Prosencephalon - drug effects | Tubulin - metabolism | Neurons - physiology | beta-Galactosidase - metabolism | Ganciclovir - pharmacology | Integrases - metabolism | Bromodeoxyuridine - metabolism | Neural Cell Adhesion Molecule L1 - metabolism | Cell Differentiation - physiology | Olfactory Bulb - cytology | Green Fluorescent Proteins - metabolism | Thymidine Kinase - genetics | Neuroglia - physiology | Sialic Acids - metabolism | Gene Expression Regulation - physiology | Cell Size | Mice, Transgenic | Neuropeptides - metabolism | Hippocampus - cytology | Gene Expression Regulation - drug effects | Immunohistochemistry - methods | Hippocampus - metabolism | Animals | Cell Count - methods | Analysis of Variance | Cell Differentiation - drug effects | Prosencephalon - cytology | Stem Cells - drug effects | Stem Cells - physiology | Mice | Olfactory Bulb - drug effects | Physiological aspects | Brain | Cellular proteins | Research | Neurons
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 01/2009, Volume 29, Issue 2, pp. 529 - 542
.... Reactive oxygen species (ROS) generated by the mitochondrial metabolism have been postulated to be the central source of molecular damages and imbalance between levels of intracellular ROS and antioxidant defenses... 
Aging | Antioxidant | Bmi1 | Neuronal cell death | ROS | p53 | antioxidant | OXIDATIVE-STRESS | ACTIVATION | PROTECTION | TRANSCRIPTION | NEURODEGENERATION | SUPPRESSION | NEUROSCIENCES | neuronal cell death | INTRACELLULAR AMYLOID-BETA | SENESCENCE | aging | DYSFUNCTION | EXPRESSION | Cell Proliferation | Reactive Oxygen Species - metabolism | Age Factors | Embryo, Mammalian | Microtubule-Associated Proteins - metabolism | Homeodomain Proteins - metabolism | Peroxiredoxins - metabolism | Cell Survival - genetics | Apoptosis - genetics | Phosphopyruvate Hydratase - metabolism | Glial Fibrillary Acidic Protein - metabolism | Cerebral Cortex - cytology | Tumor Suppressor Protein p53 - genetics | Peroxiredoxins - genetics | Nuclear Proteins - deficiency | beta-Galactosidase - metabolism | Neurons - metabolism | Neurons - drug effects | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Gene Expression Regulation - genetics | Mice, Inbred C57BL | Cells, Cultured | Hydrogen Peroxide - pharmacology | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | PAX6 Transcription Factor | Proto-Oncogene Proteins - deficiency | Mice, Knockout | Neurotoxins - pharmacology | Animals | Polycomb Repressive Complex 1 | Analysis of Variance | Eye Proteins - metabolism | Mice | Histones - metabolism | Lipid Peroxidation - genetics | Paired Box Transcription Factors - metabolism | Index Medicus
Journal Article
PloS one, ISSN 1932-6203, 2011, Volume 6, Issue 8, p. e23367
Background: Recent studies have demonstrated that activation of autophagy increases the lifespan of organisms from yeast to flies. In contrast to the lifespan... 
LIFE-SPAN EXTENSION | PATHOGENESIS | OXIDATIVE STRESS | INHIBITION | DISRUPTION | MULTIDISCIPLINARY SCIENCES | GENES | RESISTANCE | MITOCHONDRIAL DYSFUNCTION | SUPPRESSION | CELL BIOLOGY | Reactive Oxygen Species - metabolism | TOR Serine-Threonine Kinases - metabolism | Sequestosome-1 Protein | Humans | Cellular Senescence - drug effects | Male | Autophagy - physiology | Phosphoproteins - metabolism | Fibroblasts - ultrastructure | Tumor Suppressor Protein p53 - genetics | Small Ubiquitin-Related Modifier Proteins - genetics | Toluene - analogs & derivatives | RNA Interference | Time Factors | beta-Galactosidase - metabolism | Autophagy - genetics | Toluene - pharmacology | Child | Fibroblasts - metabolism | Autophagy-Related Protein 12 | Cellular Senescence - genetics | Ubiquitin-Activating Enzymes - genetics | Lysosome-Associated Membrane Glycoproteins - metabolism | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Benzothiazoles - pharmacology | Small Ubiquitin-Related Modifier Proteins - metabolism | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Cellular Senescence - physiology | Signal Transduction - genetics | Microscopy, Electron | Ubiquitin-Activating Enzymes - metabolism | Blotting, Western | Autophagy-Related Protein 7 | Acetylcysteine - pharmacology | Lysosome-Associated Membrane Glycoproteins - genetics | Signal Transduction - physiology | Fibroblasts - cytology | Primary Cell Culture | Adaptor Proteins, Signal Transducing - metabolism | Lysosomal-Associated Membrane Protein 2 | Acetylcysteine | Tumor proteins | Genetic translation | Cells | Protein binding | TOR protein | Huntingtons disease | Senescence | Phosphorylation | Yeast | p53 Protein | Impairment | Galactosidase | Viruses | Homology | Activation | Biochemistry | Autophagy | Fibroblasts | Aging | Oxygen | Cytokines | LAMP-2 protein | Translation initiation | Rapamycin | Ribosomal protein S6 | siRNA | Mammals | Membrane proteins | Medicine | Life span | Morphology | Initiation factor eIF-4E | Molecular biology | Alzheimers disease | Phagocytosis | Apoptosis
Journal Article
Journal Article