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Aging Cell, ISSN 1474-9718, 08/2015, Volume 14, Issue 4, pp. 644 - 658
The healthspan of mice is enhanced by killing senescent cells using a transgenic suicide gene. Achieving the same using small molecules would have a tremendous... 
dasatinib | plasminogen‐activated inhibitor | dependence receptors | quercetin | ephrins | 3K delta | p21 | Dasatinib | Dependence receptors | Ephrins | Plasminogen-activated inhibitor | Quercetin | PI3K delta | P21 | ENDOTHELIAL DYSFUNCTION | PLASMINOGEN-ACTIVATOR INHIBITOR-1 | EXPRESSION PROFILES | plasminogen-activated inhibitor | CELLULAR SENESCENCE | CANCER-THERAPY | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | LUNG-CANCER | SET ENRICHMENT ANALYSIS | GENE-EXPRESSION | IONIZING-RADIATION | TUMOR-GROWTH | Carotid Arteries - drug effects | Endonucleases - genetics | Plasminogen Activator Inhibitor 2 - genetics | Transcriptome | Gene Expression Profiling | Adipocytes - drug effects | Aging - genetics | Osteoporosis - metabolism | Ephrins - metabolism | Plasminogen Activator Inhibitor 2 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Osteoporosis - genetics | Intervertebral Disc - pathology | Fibroblasts - metabolism | Endothelial Cells - metabolism | Intervertebral Disc - chemistry | Fibroblasts - pathology | Mesenchymal Stem Cells - pathology | Mice, Knockout | Dasatinib - pharmacology | Osteoporosis - pathology | Ephrins - genetics | Fibroblasts - drug effects | Mice | Endothelial Cells - pathology | bcl-X Protein - metabolism | Aging - metabolism | Aging - drug effects | bcl-X Protein - genetics | Cellular Senescence - drug effects | Phosphatidylinositol 3-Kinases - metabolism | Endonucleases - metabolism | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Mesenchymal Stem Cells - drug effects | Mesenchymal Stem Cells - metabolism | Heart - physiopathology | Cellular Senescence - genetics | Osteoporosis - prevention & control | DNA-Binding Proteins - genetics | Adipocytes - pathology | Aging - pathology | Phosphatidylinositol 3-Kinases - genetics | Animals | Quercetin - pharmacology | Adipocytes - metabolism | Heart - drug effects | Carotid Arteries - pathology | Intervertebral Disc - drug effects | Drug Combinations | Endothelial Cells - drug effects | Original
Journal Article
Journal Article
Journal Article
Advanced Drug Delivery Reviews, ISSN 0169-409X, 05/2012, Volume 64, Issue 7, pp. 640 - 665
The blood–brain barrier (BBB) is a highly regulated and efficient barrier that provides a sanctuary to the brain. It is designed to regulate brain homeostasis... 
Nanoparticles | Drug delivery | Receptor-mediated transport | Liposomes | Pathological conditions | Cell-mediated transport | Blood–brain barrier | Blood-brain barrier | HUMAN INSULIN-RECEPTOR | PROTEIN-KINASE-C | MICROVESSEL ENDOTHELIAL-CELLS | FOCAL CEREBRAL-ISCHEMIA | CELL-PENETRATING PEPTIDES | NECROSIS-FACTOR-ALPHA | PLURONIC BLOCK-COPOLYMERS | IMMUNODEFICIENCY-VIRUS TYPE-1 | PHARMACOLOGY & PHARMACY | CENTRAL-NERVOUS-SYSTEM | TIGHT JUNCTION PERMEABILITY | Brain - drug effects | Brain - metabolism | Pharmaceutical Preparations - metabolism | Animals | Biological Transport, Active - physiology | Biological Transport, Active - drug effects | Humans | Drug Delivery Systems - trends | Pharmaceutical Preparations - administration & dosage | Blood-Brain Barrier - drug effects | Drug Delivery Systems - methods | Blood-Brain Barrier - metabolism | Drugs | Multiple sclerosis | Transferrin | Drug delivery systems | Glycosaminoglycans | Endothelial growth factors | Peptides | Tissue plasminogen activator | Immunoglobulin G | Low density lipoproteins | Lactoferrins | Anticoagulants (Medicine) | Biological response modifiers | Drug resistance | Muscle proteins | HIV (Viruses) | Polyols | Vehicles | Epidermal growth factor | Polyethylene glycol | Myosin | Protein kinases | Alzheimer's disease | Vascular endothelial growth factor | Adenosine triphosphate | Asylum, Right of | Tyrosine | Nitrogen oxide | Immunoglobulins | Albumin | Heat shock proteins | Apolipoproteins | Endothelium | Propylene | Cogeneration power plants | Analysis | Nitric oxide | Monoclonal antibodies | Ethylene oxide | Adenylic acid | Mitogens | Methods | Nanotechnology
Journal Article
Journal of Neurotrauma, ISSN 0897-7151, 07/2007, Volume 24, Issue 7, pp. 1132 - 1146
Traumatic brain injury (TBI) remains a major public health problem globally. Presently, there is no way to restore cognitive deficits caused by TBI. In this... 
Rat | Neurogenesis | Spatial learning | Statins | CELLS | INTERCELLULAR-ADHESION MOLECULE-1 | rat | CONTROLLED CORTICAL IMPACT | MICE DEFICIENT | ADULT HIPPOCAMPUS | ACQUISITION | FACTOR EXPRESSION | spatial learning | NEUROSCIENCES | CLINICAL NEUROLOGY | ATORVASTATIN | STROKE | PLASMINOGEN-ACTIVATOR | statins | neurogenesis | CRITICAL CARE MEDICINE | Neuroprotective Agents - therapeutic use | Memory Disorders - physiopathology | Neovascularization, Physiologic - drug effects | Simvastatin - therapeutic use | Rats, Wistar | Recovery of Function - drug effects | Brain Injuries - drug therapy | Heptanoic Acids - therapeutic use | Nerve Regeneration - physiology | Nerve Degeneration - physiopathology | Neuronal Plasticity - drug effects | Male | Hippocampus - drug effects | Brain Injuries - physiopathology | Simvastatin - pharmacology | Dose-Response Relationship, Drug | Neuronal Plasticity - physiology | Neuroprotective Agents - pharmacology | Dentate Gyrus - drug effects | Neurons - physiology | Recovery of Function - physiology | Neurons - drug effects | Pyrroles - therapeutic use | Heptanoic Acids - pharmacology | Maze Learning - physiology | Rats | Treatment Outcome | Hippocampus - pathology | Maze Learning - drug effects | Atorvastatin Calcium | Neovascularization, Physiologic - physiology | Dentate Gyrus - cytology | Pyrroles - pharmacology | Animals | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Memory Disorders - drug therapy | Memory Disorders - etiology | Dentate Gyrus - physiology | Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use | Nerve Regeneration - drug effects | Stem Cells - drug effects | Stem Cells - physiology | Cell Proliferation - drug effects | Nerve Degeneration - etiology | Brain Injuries - pathology | Hippocampus - physiopathology | Nerve Degeneration - drug therapy | Neurology | Head injuries | Cognition & reasoning | Rodents | Brain damage | Trauma
Journal Article
American Journal of Pathology, The, ISSN 0002-9440, 2015, Volume 185, Issue 4, pp. 969 - 986
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 11/2016, Volume 36, Issue 11, pp. 2143 - 2151
APC (activated protein C), derived from the plasma protease zymogen, is antithrombotic and anti-inflammatory. In preclinical injury models, recombinant APC... 
neurogenesis | endothelial cells | anticoagulant | neurons | stroke | FOCAL ISCHEMIC-STROKE | TISSUE-PLASMINOGEN ACTIVATOR | REDUCED ANTICOAGULANT ACTIVITY | HIPPOCAMPAL-NEURONS | RECEPTOR 1 | ENDOTHELIAL-CELLS | COAGULATION-FACTOR VA | PERIPHERAL VASCULAR DISEASE | MICE | HEMATOLOGY | GLUTAMATE EXCITOTOXICITY | BRAIN | Neuroprotective Agents - therapeutic use | Recombinant Proteins - therapeutic use | Endothelial Protein C Receptor | Neurons - pathology | Reperfusion Injury - etiology | Receptor, PAR-1 - metabolism | Humans | Brain Ischemia - metabolism | Recombinant Proteins - adverse effects | Antigens, CD - metabolism | Brain - metabolism | Stroke - pathology | Intracranial Thrombosis - drug therapy | Neurogenesis - drug effects | Neurons - metabolism | Neuroprotective Agents - adverse effects | Neurons - drug effects | Reperfusion Injury - metabolism | Hemostasis - drug effects | Intracranial Thrombosis - pathology | Reperfusion Injury - pathology | Endothelial Cells - metabolism | Receptors, Cell Surface - agonists | Receptors, Cell Surface - metabolism | Stroke - drug therapy | Intracranial Thrombosis - metabolism | Brain - drug effects | Stroke - metabolism | Animals | Reperfusion Injury - prevention & control | Signal Transduction - drug effects | Brain Ischemia - drug therapy | Brain Ischemia - pathology | Brain - pathology | Endothelial Cells - pathology | Thrombolytic Therapy - adverse effects | Protein C - adverse effects | Protein C - therapeutic use | Endothelial Cells - drug effects | Receptor Cross-Talk - drug effects
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 06/2016, Volume 374, Issue 24, pp. 2313 - 2323
Journal Article