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Nature Medicine, ISSN 1078-8956, 02/2017, Volume 23, Issue 2, pp. 250 - 255
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2014, Volume 9, Issue 7, p. e103532
Journal Article
Neuron, ISSN 0896-6273, 06/2015, Volume 86, Issue 6, pp. 1393 - 1406
Human genetic studies have revealed an association between GTP cyclohydrolase 1 polymorphisms, which decrease tetrahydrobiopterin (BH4) levels, and reduced... 
RHEUMATOID-ARTHRITIS | GTP CYCLOHYDROLASE-I | SEPIAPTERIN REDUCTASE | INDUCED NOCICEPTION | NITRIC-OXIDE SYNTHASE | RAT-BRAIN | FEEDBACK REGULATORY PROTEIN | NERVE INJURY | NEUROSCIENCES | BLOOD-PRESSURE | MICE LACKING | Inflammation - chemically induced | Pain Threshold - physiology | Neuralgia - metabolism | Biopterin - analogs & derivatives | Biopterin - metabolism | Inflammation - metabolism | Sciatic Nerve - metabolism | Time Factors | Inflammation - drug therapy | Reaction Time - drug effects | Neuralgia - chemically induced | Pain Threshold - drug effects | Blood Pressure - drug effects | Sensory Receptor Cells - metabolism | Calcitonin Gene-Related Peptide - metabolism | Disease Models, Animal | Sulfasalazine - therapeutic use | Gene Expression Regulation - physiology | Alcohol Oxidoreductases - metabolism | Mice, Transgenic | Reaction Time - genetics | Enzyme Inhibitors - therapeutic use | Neuralgia - drug therapy | Gene Expression Regulation - drug effects | Macrophages - metabolism | Animals | Sensory Receptor Cells - drug effects | Anti-Inflammatory Agents, Non-Steroidal - therapeutic use | Macrophages - drug effects | Mice | Pain Measurement | GTP Cyclohydrolase - genetics | Genetic research | Care and treatment | Pain | Genetic polymorphisms | Neurophysiology | Enzymes | Genotype & phenotype | Analgesics | Neurons | Nitric oxide | Pain management | Behavior | Artificial chromosomes | Children & youth
Journal Article
Journal Article
Journal of Lipid Research, ISSN 0022-2275, 2017, Volume 58, Issue 2, pp. 386 - 392
Nonsteroidal anti-inflammatory drugs are the most widely used medicine to treat pain and inflammation, and to inhibit platelet function. Understanding the... 
Epigenetics | Histone deacetylase | Prostaglandins | Prostaglandin E | Smooth muscle cells | Vascular biology | ACETYLATION | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | vascular biology | histone deacetylase | CANCER | epigenetics | BLOOD-PRESSURE | prostaglandin E-2 | smooth muscle cells | HISTONE DEACETYLATION | INHIBITION | INFLAMMATION | prostaglandins | Transcription, Genetic - drug effects | Prostaglandin-E Synthases - biosynthesis | Dinoprostone - biosynthesis | Dinoprostone - genetics | Humans | Protein Processing, Post-Translational - genetics | E1A-Associated p300 Protein - genetics | Histone Deacetylase Inhibitors - administration & dosage | E1A-Associated p300 Protein - metabolism | Gene Expression Regulation - drug effects | Animals | Prostaglandin-E Synthases - genetics | Anti-Inflammatory Agents, Non-Steroidal - administration & dosage | Hydroxamic Acids - administration & dosage | Histone Deacetylase 1 - antagonists & inhibitors | Mice | Acetylation | Histones - metabolism | Histone Deacetylase 1 - genetics | Chromatin | Immunoprecipitation | Antiinflammatory agents | Transcription | Prostaglandin E2 | Smooth muscle | Event-related potentials | Inflammation | Gene expression | Arachidonic acid | Prostaglandin-E synthase | Heterochromatin | Pain | Acetyltransferase | prostaglandin E2
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2013, Volume 8, Issue 7, p. e70124
Background: The Sphingosine-1-phosphate (S1P) signaling pathway is known to influence pathophysiological processes within the brain and the synthetic S1P... 
DENDRITIC SPINES | MATRIX METALLOPROTEINASES | AREA | MULTIDISCIPLINARY SCIENCES | FOCAL CEREBRAL-ISCHEMIA | SPHINGOSINE-1-PHOSPHATE | SPINAL-CORD-INJURY | BRAIN | ENDOTHELIAL GROWTH-FACTOR | SPHINGOSINE 1-PHOSPHATE | PLASTICITY | Intracranial Thrombosis - complications | Gene Expression - drug effects | Recovery of Function - drug effects | Astrocytes - pathology | Male | Gliosis - physiopathology | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - genetics | Stroke - physiopathology | Cerebral Cortex - metabolism | Cerebral Cortex - physiopathology | Time Factors | Immunosuppressive Agents - metabolism | Post-Synaptic Density - drug effects | Sphingosine - metabolism | Aldehyde-Lyases - genetics | Cerebral Cortex - drug effects | Gliosis - prevention & control | Immunosuppressive Agents - pharmacology | Propylene Glycols - pharmacology | Stroke - prevention & control | Mice, Inbred C57BL | Propylene Glycols - metabolism | Fingolimod Hydrochloride | Treatment Outcome | Reverse Transcriptase Polymerase Chain Reaction | Sphingosine - pharmacology | Sphingosine - analogs & derivatives | Stroke - etiology | Animals | Convalescence | Aldehyde-Lyases - metabolism | Mice | Phosphates | Vascular endothelial growth factor | Analysis | Sphingosine | Neuroprotection | Brain | Neurosciences | Animal models | Neuropathology | Recovery of function | Clinical trials | Biochemistry | Sphingosine 1-phosphate | Angiogenesis | Signal transduction | Spectrometry | Toxicology | Stroke | Cortex | Pharmacology | Metabolism | Neurotrophic factors | Neurology | Signaling | Brain research | Gliosis | FTY720 | Laboratory animals | Immunofluorescence | Synapses
Journal Article
Journal Article
EMBO Molecular Medicine, ISSN 1757-4676, 11/2014, Volume 6, Issue 11, pp. 1398 - 1422
R‐flurbiprofen is the non‐cyclooxygenase inhibiting R‐enantiomer of the non‐steroidal anti‐inflammatory drug flurbiprofen, which was assessed as a remedy for... 
regulatory T cells | pain | endocannabinoids | multiple sclerosis | optic neuritis | Multiple sclerosis | Pain | Regulatory T cells | Optic neuritis | Endocannabinoids | MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | EFFLUX TRANSPORTER | MULTIPLE-SCLEROSIS | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | DISEASE | ACTIVATED-RECEPTOR-GAMMA | RESISTANCE | ESTROGEN | CENTRAL-NERVOUS-SYSTEM | BETA LIGAND | T-Lymphocyte Subsets - immunology | Optic Nerve - pathology | Flurbiprofen - therapeutic use | Encephalomyelitis, Autoimmune, Experimental - drug therapy | Treatment Outcome | Prostaglandins - cerebrospinal fluid | Animals | Anti-Inflammatory Agents, Non-Steroidal - therapeutic use | Spinal Cord - pathology | Brain - pathology | Female | Mice | Disease Models, Animal | Endocannabinoids - blood | Multiple Sclerosis - drug therapy | Encephalomyelitis | Anti-inflammatory drugs | Analysis | T cells | Enantiomers | Alzheimer's disease | Flurbiprofen | Spinal cord | Peptides | Toxicity | Lymphocytes T | Experiments | Prostaglandin endoperoxide synthase | CTLA-4 protein | Cell activation | Prostaglandins | Cannabinoids | Lymphocytes | CD25 antigen | Foxp3 protein | Paralysis | Drug dosages | Pain perception | Optic nerve | Neurodegenerative diseases | Myelin | Immunoregulation | Cortex | Inflammation | Experimental allergic encephalomyelitis | Microglia | CD4 antigen | Disease prevention | Alzheimers disease | Prostate cancer | Index Medicus
Journal Article