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Journal Article
Blood, ISSN 0006-4971, 08/2017, Volume 130, Issue 5, pp. 643 - 654
Journal Article
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 02/2012, Volume 302, Issue 4, pp. C709 - C719
Zampell JC, Elhadad S, Avraham T, Weitman E, Aschen S, Yan A, Mehrara BJ. Toll-like receptor deficiency worsens inflammation and lymphedema after lymphatic... 
Endogenous danger signals | ISCHEMIA/REPERFUSION INJURY | ACTIVATION | PHYSIOLOGY | endogenous danger signals | MACROPHAGES | HMGB1 | GROUP BOX-1 PROTEIN | CELL BIOLOGY | SYSTEMIC INFLAMMATION | BREAST-CANCER | DANGER SIGNALS | EXPRESSION | WOUND REPAIR | Inflammation - pathology | Lymphedema - immunology | Toll-Like Receptor 2 - genetics | Transforming Growth Factor beta1 - metabolism | Glycoproteins - metabolism | Toll-Like Receptor 9 - genetics | Fibrosis - metabolism | Leukemic Infiltration - complications | Inflammation - complications | Signal Transduction - immunology | Toll-Like Receptor 2 - deficiency | Transforming Growth Factor beta1 - immunology | Inflammation - metabolism | Lymphatic Vessels - metabolism | Lymphangiogenesis - immunology | Toll-Like Receptor 4 - deficiency | Gene Deletion | Fibrosis - immunology | Gene Expression - immunology | Lymphatic Vessels - injuries | Female | Macrophages - immunology | Leukemic Infiltration - metabolism | Lymphedema - complications | Lymphedema - pathology | Collagen - immunology | Fibrosis - complications | Toll-Like Receptor 9 - deficiency | Lymphatic Vessels - immunology | Toll-Like Receptor 4 - genetics | Inflammation - immunology | Macrophages - cytology | Vascular Endothelial Growth Factor C - immunology | Immunity, Innate | Mice, Knockout | Collagen - metabolism | Glycoproteins - immunology | Macrophages - metabolism | Animals | Vascular Endothelial Growth Factor C - metabolism | Leukemic Infiltration - pathology | Mice | Fibrosis - pathology | Lymphangiogenesis - genetics | Lymphedema - metabolism | Care and treatment | Lymphedema | Patient outcomes | Toll-like receptors | Inflammation | Lymphatics | Research | Health aspects | Vascular Biology
Journal Article
Blood, ISSN 0006-4971, 05/2012, Volume 119, Issue 20, pp. 4698 - 4707
Journal Article
Journal Article
Journal of Pediatric Endocrinology and Metabolism, ISSN 0334-018X, 10/2013, Volume 26, Issue 9-10, pp. 967 - 970
Background: Adrenocorticotropic hormone (ACTH)dependent Cushing syndrome (CS) in the presence of leukemic central nervous system infiltration is very rare.... 
Leukemia inhibitory factor (LIF) | Acute lymphoblastic leukemia (ALL) | Cushing syndrome | Leukemic central nervous system infiltration | leukemia inhibitory factor (LIF) | INHIBITORY FACTOR LIF | DIAGNOSIS | acute lymphoblastic leukemia (ALL) | ADRENOCORTICAL DISEASE | CHILDHOOD | CHILDREN | HORMONE | ENDOCRINOLOGY & METABOLISM | CHRONIC LYMPHOCYTIC-LEUKEMIA | PEDIATRICS | SECRETION | leukemic central nervous system infiltration | PITUITARY-ADRENAL AXIS | EXPRESSION | Leukemia, B-Cell - metabolism | Recurrence | Blast Crisis - physiopathology | Blast Crisis - psychology | Humans | Child, Preschool | Cushing Syndrome - etiology | Cushing Syndrome - metabolism | Central Nervous System Neoplasms - secondary | Leukemia Inhibitory Factor - metabolism | Depression - etiology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy | Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism | Fatal Outcome | Female | Leukemia, B-Cell - drug therapy | Maintenance Chemotherapy | Central Nervous System Neoplasms - psychology | Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology | Weight Gain | Leukemic Infiltration - metabolism | Central Nervous System Neoplasms - physiopathology | Blast Crisis - pathology | Leukemic Infiltration - physiopathology | Leukemia, B-Cell - pathology | Cell Transformation, Neoplastic - metabolism | Disease Progression | Obesity, Abdominal - etiology | Central Nervous System Neoplasms - pathology | Models, Biological | Leukemic Infiltration - pathology | Blast Crisis - metabolism | Leukemic Infiltration - psychology
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 8, p. e22369
Laminin alpha 2 (LAMA2)-deficient congenital muscular dystrophy is a severe, early-onset disease caused by abnormal levels of laminin 211 in the basal lamina... 
SKELETAL-MUSCLE | INFLAMMATORY MYOPATHY | ACTIVATION | MULTIDISCIPLINARY SCIENCES | DISEASE | TOLL-LIKE RECEPTORS | GENE-EXPRESSION | LIMB-GIRDLE | NF-KAPPA-B | MEROSIN DEFICIENCY | ONSET | Muscular Dystrophy, Animal - genetics | Leukemic Infiltration - genetics | Membrane Glycoproteins - metabolism | Immunity, Innate - genetics | Toll-Like Receptor 9 - genetics | Proto-Oncogene Proteins c-bcl-2 - metabolism | Mice, Mutant Strains | Toll-Like Receptor 6 - genetics | Muscular Dystrophy, Animal - metabolism | In Situ Nick-End Labeling | Leukemic Infiltration - metabolism | Toll-Like Receptor 6 - metabolism | Toll-Like Receptor 7 - genetics | Muscular Dystrophy, Animal - immunology | Toll-Like Receptor 7 - metabolism | Mice, Inbred C57BL | Toll-Like Receptor 4 - genetics | Reverse Transcriptase Polymerase Chain Reaction | Toll-Like Receptor 4 - metabolism | Blotting, Western | Membrane Glycoproteins - genetics | Immunity, Innate - immunology | Animals | Leukemic Infiltration - immunology | Toll-Like Receptor 8 - genetics | Mice | Toll-Like Receptor 9 - metabolism | Proto-Oncogene Proteins c-bcl-2 - genetics | Toll-Like Receptor 8 - metabolism | Genetic engineering | Inflammation | Laminin | RNA | Muscular dystrophy | Apoptosis | Regulators | Biomedical research | Disease | Bcl-2 protein | Pathogenesis | Transgenic | Effector cells | Animal diseases | mRNA | Autophagy | Proteins | Receptors | Toll-like receptors | Basal lamina | Degeneration | Stress response | Immune system | Heparan sulfate | Neuromuscular diseases | Immune response | MyoD protein | TLR7 protein | Congenital diseases | Cell survival | Cytokines | Leukocytes (eosinophilic) | Muscles | TLR4 protein | Gene expression | Survival | TLR9 protein | Pathology | Cell death | Ligands | Muscle function | Infiltration | Dystrophy | Endoplasmic reticulum | Eosinophils
Journal Article
European Journal of Neuroscience, ISSN 0953-816X, 02/2012, Volume 35, Issue 4, pp. 562 - 571
Although multiple sclerosis (MS) has traditionally been considered to be an inflammatory disease, recent evidence has brought neurodegeneration into the... 
EAE | neurodegeneration | mitochondria | multiple sclerosis | neuroprotective | p66 isoform of ShcA | Neuroprotective | Mitochondria | Multiple sclerosis | P66 isoform of ShcA | Neurodegeneration | LIFE-SPAN | OXIDATIVE STRESS | REDOX ENZYME | SPINAL-CORD | NEUROSCIENCES | CELL-DEATH | MITOCHONDRIAL PERMEABILITY TRANSITION | CYCLOPHILIN-D | AXONAL DEGENERATION | PORE | ANIMAL-MODEL | Optic Nerve - pathology | Shc Signaling Adaptor Proteins - metabolism | Cell Proliferation | Spinal Cord - metabolism | Cyclophilins - deficiency | Cerebral Cortex - cytology | Spinal Cord - ultrastructure | Neurons - ultrastructure | Encephalomyelitis, Autoimmune, Experimental - chemically induced | Nerve Fibers, Myelinated - pathology | Spinal Cord - pathology | T-Lymphocytes - drug effects | Axons - ultrastructure | Freund's Adjuvant - adverse effects | Optic Nerve - immunology | Neurons - metabolism | Encephalomyelitis, Autoimmune, Experimental - genetics | Disease Models, Animal | Leukemic Infiltration - metabolism | Microscopy, Electron, Transmission | Encephalomyelitis, Autoimmune, Experimental - pathology | Cytokines - metabolism | Mice, Inbred C57BL | Cells, Cultured | Hydrogen Peroxide - pharmacology | Myelin-Oligodendrocyte Glycoprotein | Glycoproteins - adverse effects | Optic Nerve - ultrastructure | Mice, Knockout | Spinal Cord - immunology | Animals | Src Homology 2 Domain-Containing, Transforming Protein 1 | Axons - pathology | Encephalomyelitis, Autoimmune, Experimental - prevention & control | Leukemic Infiltration - drug therapy | T-Lymphocytes - immunology | Mice | Peptide Fragments - adverse effects | Shc Signaling Adaptor Proteins - deficiency | Optic Nerve - metabolism | Enzymes | Cell death | Analysis | Mitochondrial DNA | Paralysis | Permeability | Cells | Neuroprotection | Oxidative stress | Animal models | Reactive oxygen species | Spinal cord | Mitochondrial permeability transition pore | Nervous system | Optics | Calcium (mitochondrial) | Experimental allergic encephalomyelitis | Inflammatory diseases | Cell activation | Nerves | Axon guidance
Journal Article
Neuroscience, ISSN 0306-4522, 2003, Volume 121, Issue 3, pp. 619 - 628
Previous studies in a mouse model of neonatal excitotoxic brain damage mimicking the brain lesions in human cerebral palsy showed microglial activation within... 
macrophage | ibotenate | minocycline | N-methyl- d-aspartate | PBS | PCNA | SAP | Saporin | DAB | P | Ibotenate | Phosphate buffer saline | Proliferating cell nuclear antigen | Minocycline | NMDA | Postnatal day | N-methyl-D-aspartate | Diaminobenzidine | Macrophage | RISK-FACTORS | PERIVENTRICULAR WHITE-MATTER | NEUROSCIENCES | LESIONS | ISCHEMIC-INJURY | MOUSE MODEL | TETRACYCLINE | CEREBRAL-PALSY | CELL | MONONUCLEAR PHAGOCYTES | Immunohistochemistry | Neuroprotective Agents - therapeutic use | Brain | Leukocyte Common Antigens - metabolism | Brain Injuries - drug therapy | Minocycline - pharmacology | Cell Count | Cerebral Palsy - metabolism | Cerebral Cortex - pathology | Macrophage-1 Antigen - immunology | Brain Injuries - metabolism | Dose-Response Relationship, Drug | Leukocyte Common Antigens - immunology | Lectins - metabolism | Drug Interactions | Time Factors | Cell Death | Microglia - pathology | Macrophage-1 Antigen - metabolism | Cerebral Cortex - drug effects | Disease Models, Animal | Animals, Newborn | Leukemic Infiltration - metabolism | Cerebral Palsy - pathology | Microglia - drug effects | Neurons | Brain Injuries - chemically induced | Antirheumatic Agents | Glycoproteins | Ibotenic Acid | Animals | Staining and Labeling | Anti-Bacterial Agents - pharmacology | Chloroquine - administration & dosage | Mice | Proliferating Cell Nuclear Antigen - metabolism | Brain Injuries - pathology
Journal Article