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Shock, ISSN 1073-2322, 08/2005, Volume 24, Issue 2, pp. 132 - 138
Journal Article
Critical Care Medicine, ISSN 0090-3493, 11/2016, Volume 44, Issue 11, pp. e1054 - e1066
Journal Article
Glia, ISSN 0894-1491, 10/2011, Volume 59, Issue 10, pp. 1489 - 1502
Activation of the unfolded protein response (UPR) is involved in the pathogenesis of numerous CNS myelin abnormalities; yet, its direct role in traumatic... 
spinal cord injury | locomoter activity | ER‐stress | white‐matter sparing | contusion | oligodendrocyte | White-matter sparing | Contusion | ER-stress | Oligodendrocyte | Spinal cord injury | Locomoter activity | TRANSCRIPTION FACTORS C/EBP | INDUCED APOPTOSIS | ER STRESS | XBP1 MESSENGER-RNA | NEUROSCIENCES | CELL-DEATH | IN-VITRO | UNFOLDED PROTEIN RESPONSE | INTERFERON-GAMMA | ADULT-RAT | white-matter sparing | GENE-TRANSCRIPTION | Oligodendroglia - metabolism | Caspase 3 - metabolism | Apoptosis - genetics | Endoplasmic Reticulum Stress - genetics | RNA, Messenger - metabolism | Spinal Cord Injuries - pathology | DNA-Binding Proteins - metabolism | Myelin Basic Protein - genetics | Basic Helix-Loop-Helix Transcription Factors - metabolism | Time Factors | Nerve Fibers, Myelinated - pathology | Up-Regulation - physiology | Caspase 3 - genetics | Eukaryotic Initiation Factor-2 - metabolism | Recovery of Function - physiology | Female | Disease Models, Animal | Nerve Fibers, Myelinated - metabolism | Basic Helix-Loop-Helix Transcription Factors - genetics | Myelin Basic Protein - metabolism | Spinal Cord Injuries - metabolism | Unfolded Protein Response - genetics | Mice, Inbred C57BL | Up-Regulation - genetics | Oligodendrocyte Transcription Factor 2 | Transcription Factor CHOP - deficiency | Nerve Tissue Proteins - genetics | Regulatory Factor X Transcription Factors | Mice, Knockout | Nerve Tissue Proteins - metabolism | Oligodendroglia - pathology | Transcription Factors - metabolism | Animals | Activating Transcription Factor 4 - metabolism | Analysis of Variance | Mice | Spinal Cord Injuries - physiopathology | Locomotion - physiology | Unfolded Protein Response - physiology | Endoplasmic Reticulum Stress - physiology | Animal models | Transcription | Astrocytes | Myelin | Neurons | Central nervous system | Homeostasis | Recovery of function | Defense mechanisms | Myelin basic protein | Stress | Infection | Locomotion | Protein folding | Oligodendrocytes | Evolution | Endoplasmic reticulum | Apoptosis
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2014, Volume 9, Issue 9, p. e109099
In humans, sensory abnormalities, including neuropathic pain, often result from traumatic spinal cord injury (SCI). SCI can induce cellular changes in the CNS,... 
PROMOTER ACTIVITY | NEUROPATHIC PAIN | CENTRAL SENSITIZATION | NOXIOUS-STIMULATION | DELTA-FOSB | GLUTAMATE TRANSPORTERS | MULTIDISCIPLINARY SCIENCES | DISEASE | RAT MODEL | C-FOS EXPRESSION | DEGENERATION | Neurons - pathology | Neuralgia - complications | Cell Proliferation | Spinal Cord Dorsal Horn - metabolism | Spinal Cord Injuries - complications | Astrocytes - pathology | Neuralgia - metabolism | Ki-67 Antigen - metabolism | Male | Spinal Cord Dorsal Horn - physiopathology | Glial Fibrillary Acidic Protein | Excitatory Amino Acid Transporter 2 - genetics | Neurons - metabolism | Neuralgia - physiopathology | Spinal Cord Dorsal Horn - injuries | Contusions - complications | Disease Models, Animal | Biomarkers - metabolism | Gene Expression | Hyperalgesia - metabolism | Spinal Cord Injuries - metabolism | Hyperalgesia - complications | Mice, Inbred C57BL | Contusions - metabolism | Proto-Oncogene Proteins c-fos - metabolism | Contusions - physiopathology | Mice, Transgenic | Excitatory Amino Acid Transporter 2 - metabolism | Nerve Tissue Proteins - genetics | Hyperalgesia - physiopathology | Nerve Tissue Proteins - metabolism | Animals | Ki-67 Antigen - genetics | Proto-Oncogene Proteins c-fos - genetics | Mice | Spinal Cord Injuries - physiopathology | Astrocytes - metabolism | Genetic engineering | Glutamate | Neurons | Intermediate filament proteins | Neurophysiology | Neurosciences | Spinal cord | Target recognition | Circuits | Central nervous system | Activation | Neuropathy | Spinal cord injury | Neuronal-glial interactions | Proteins | Pain | Rodents | Grip strength | Tactile | Injuries | Dorsal horn | Pain perception | Glial fibrillary acidic protein | Abnormalities | Transgenic mice | Excitability | Tactile stimuli | Gene expression | Molecular modelling | Spinal cord injuries | Glutamic acid transporter | Glutamatergic transmission | Aberration | Transporter
Journal Article
Neuron, ISSN 0896-6273, 09/2014, Volume 83, Issue 5, pp. 1098 - 1116
Macrophages and microglia can be polarized along a continuum toward a detrimental (M1) or a beneficial (M2) state in the injured CNS. Although phagocytosis of... 
PROINFLAMMATORY CYTOKINE | IMMUNE-SYSTEM | COLONY-STIMULATING FACTOR | MIGRATION INHIBITORY FACTOR | CONTUSION INJURY | IN-VIVO | MONOCYTE-DERIVED MACROPHAGES | GENE-EXPRESSION | NECROSIS-FACTOR-ALPHA | NEUROSCIENCES | ALTERNATIVE ACTIVATION | Tumor Necrosis Factor-alpha - metabolism | Macrophages - transplantation | Microglia - metabolism | Protein-Serine-Threonine Kinases - deficiency | Tumor Necrosis Factor-alpha - genetics | Green Fluorescent Proteins - genetics | Cytoprotection - physiology | Myelin Sheath - metabolism | Spinal Cord Injuries - pathology | Intracellular Signaling Peptides and Proteins - deficiency | Time Factors | Cytoprotection - drug effects | Iron - pharmacology | Cytokines - genetics | Intracellular Signaling Peptides and Proteins - genetics | Intracellular Fluid - metabolism | Disease Models, Animal | Macrophages - physiology | Green Fluorescent Proteins - metabolism | Cytokines - metabolism | Gene Expression Regulation - genetics | Mice, Inbred C57BL | Protein-Serine-Threonine Kinases - genetics | Spinal Cord Injuries - surgery | Mice, Transgenic | Iron - metabolism | Phenotype | Animals | Cytoprotection - genetics | Spinal Cord Injuries - immunology | Mice | Apoptosis | Spinal cord injuries | Genetic aspects | Macrophages | Tumor necrosis factor | Genotype & phenotype | Cytokines | Rodents | Cytotoxicity | Kinases | Chemokines | Immune system
Journal Article
International Journal of Molecular Sciences, ISSN 1661-6596, 06/2014, Volume 15, Issue 7, pp. 11275 - 11293
Journal Article
Journal Article
Journal of Cerebral Blood Flow & Metabolism, ISSN 0271-678X, 8/2013, Volume 33, Issue 8, pp. 1182 - 1189
The role of tumor necrosis factor (TNF) and its receptors after traumatic brain injury (TBI) remains unclear. We evaluated the effects of genetic deletion of... 
traumatic brain injury | apoptosis | tumor necrosis factor | inflammation | microglia | pathophysiology | ACTIVATION | CONTUSION VOLUME | CONTROLLED CORTICAL IMPACT | ISCHEMIA | NEUROSCIENCES | FACTOR-ALPHA | CELL-DEATH | CLOSED-HEAD INJURY | BCL-2 | ENDOCRINOLOGY & METABOLISM | MICE | TNF-ALPHA | HEMATOLOGY | Immunohistochemistry | Tumor Necrosis Factor-alpha - metabolism | Microglia - metabolism | Tumor Necrosis Factor Decoy Receptors - genetics | Tumor Necrosis Factor-alpha - genetics | Cerebral Cortex - pathology | Male | Brain Injuries - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | Psychomotor Performance - physiology | Cerebral Cortex - metabolism | RNA, Messenger - biosynthesis | Cell Death - genetics | Receptors, Tumor Necrosis Factor, Type II - metabolism | Gene Deletion | Apoptosis Regulatory Proteins - genetics | In Situ Nick-End Labeling | Receptors, Tumor Necrosis Factor - metabolism | Mice, Inbred C57BL | RNA, Messenger - genetics | Brain Injuries - genetics | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Tumor Necrosis Factor Decoy Receptors - metabolism | Mice, Knockout | Macrophages - metabolism | Algorithms | Animals | Apoptosis Regulatory Proteins - physiology | Mice | DNA Damage | Brain Injuries - pathology | Original
Journal Article
Cytotherapy, ISSN 1465-3249, 2011, Volume 13, Issue 7, pp. 873 - 887
Abstract Background aims Bone marrow stromal cells (BMSC) have been shown to provide neuroprotection after transplantation into the injured central nervous... 
Advanced Basic Science | Other | red nucleus | retrograde degeneration | spinal cord trauma | bone marrow | mesenchymal stromal cells | transplantation | Bone marrow | Mesenchymal stromal cells | Retrograde degeneration | Red nucleus | Transplantation | Spinal cord trauma | MEDICINE, RESEARCH & EXPERIMENTAL | FUNCTIONAL RECOVERY | NERVOUS-SYSTEM | STEM-CELLS | ISCHEMIC BOUNDARY ZONE | NEUROTROPHIC FACTOR | AXONAL REGENERATION | OLFACTORY ENSHEATHING GLIA | CELL & TISSUE ENGINEERING | CELL BIOLOGY | TRAUMATIC BRAIN-INJURY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | CONTUSION INJURY | HEMATOLOGY | AXOTOMIZED RUBROSPINAL NEURONS | Neuroprotective Agents | Stromal Cells - transplantation | Cell Proliferation | Cervical Vertebrae - injuries | Neurons - cytology | Vascular Endothelial Growth Factor A - metabolism | Bone Marrow Transplantation - methods | Schwann Cells - cytology | Spinal Cord Injuries - pathology | Neuroglia - cytology | Female | Brain-Derived Neurotrophic Factor - metabolism | Cell Differentiation | Neurons - metabolism | Calcitonin Gene-Related Peptide - metabolism | Green Fluorescent Proteins - metabolism | Spinal Cord Injuries - metabolism | Bone Marrow Cells - cytology | Cells, Cultured | Axons - metabolism | Mesenchymal Stromal Cells - metabolism | Rats | Schwann Cells - metabolism | Nerve Regeneration | Rats, Sprague-Dawley | Red Nucleus - cytology | Red Nucleus - metabolism | Animals | Neurotrophin 3 - metabolism | Bone Marrow Cells - metabolism | Stromal Cells - cytology
Journal Article
Journal Article