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PLoS ONE, ISSN 1932-6203, 08/2017, Volume 12, Issue 8, pp. e0182449 - e0182449
Chronic inflammation and oxidative stress are striking features of Duchenne muscular dystrophy disease. Diacerhein is an anthraquinone, which exhibits... 
SKELETAL-MUSCLE | OXIDATIVE STRESS | MULTIDISCIPLINARY SCIENCES | MOUSE | NITRIC-OXIDE | MUSCULAR-DYSTROPHY | TNF-ALPHA | OSTEOARTHRITIS | DAMAGE | PROGRESSION | PATHOPHYSIOLOGY | Necrosis - drug therapy | Diaphragm - drug effects | Muscular Dystrophy, Duchenne - drug therapy | Anthraquinones - therapeutic use | Male | Muscle, Skeletal - metabolism | Muscular Dystrophy, Duchenne - pathology | Phenotype | Animals | Muscular Dystrophy, Duchenne - physiopathology | Muscle, Skeletal - drug effects | Muscle, Skeletal - physiopathology | Mice, Inbred mdx | Female | Anthraquinones - pharmacology | Mice | Muscular Dystrophy, Duchenne - metabolism | Muscle, Skeletal - pathology | Oxidative Stress - drug effects | Care and treatment | Corticosteroids | Research | Tumor necrosis factor | Duchenne muscular dystrophy | Oxidative stress | Reactive oxygen species | Glucocorticoids | Immunoglobulin G | Lipid peroxidation | Inflammatory response | Biology | Arthritis | Macrophages | Nuclei | Muscular dystrophy | Antioxidants | Anthraquinone | Duchenne's muscular dystrophy | Interleukin 1 | Tumor necrosis factor-TNF | Physiology | Peroxidation | Stresses | Diaphragms | Cytokines | Inflammation | Prednisone | Patients | Stress | Musculoskeletal system | Neurology | Nitric oxide | Morphology | Myonecrosis | Dystrophy | Diaphragm | Index Medicus
Journal Article
Journal Article
2015, Second edition., ISBN 1451151691, 334
Stay up to date with the latest developments in your field with the highly-anticipated second edition of Age-Related Macular Degeneration. This comprehensive... 
Choroidal Neovascularization | Macular Degeneration | Retinal degeneration
eBook
Human Mutation, ISSN 1059-7794, 03/2017, Volume 38, Issue 3, pp. 279 - 288
We studied the structural effects of point mutations of a membrane protein that cause genetic disease. SLC4A11 is a membrane transport protein (OH − /H + /NH 3... 
congenital hereditary endothelial dystrophy (CHED), Fuchs endothelial dystrophy (FECD), corneal dystrophy | SLC4A11, homology modeling | SLC4A11 | corneal dystrophy | Fuchs endothelial dystrophy (FECD) | ANION-EXCHANGERS | homology modeling; congenital hereditary endothelial dystrophy (CHED) | NUCLEIC-ACIDS | SWISS-MODEL | HARBOYAN SYNDROME | PROTEIN STRUCTURES | HEREDITARY ENDOTHELIAL DYSTROPHY | STRUCTURE VALIDATION | EVOLUTIONARY CONSERVATION | GENETICS & HEREDITY | TRANSPORT FUNCTION | BLOOD-CELL BAND-3 | Antiporters - chemistry | Humans | Protein Multimerization | Corneal Dystrophies, Hereditary - genetics | Structure-Activity Relationship | Anion Transport Proteins - chemistry | Biological Transport | Protein Interaction Domains and Motifs - genetics | Antiporters - genetics | HEK293 Cells | Conserved Sequence | Protein Domains | Catalysis | Amino Acid Sequence | Gene Expression | Genetic Predisposition to Disease | Models, Molecular | Antiporters - metabolism | Corneal Dystrophies, Hereditary - metabolism | Anion Transport Proteins - metabolism | Alleles | Protein Conformation | Mutation | Anion Transport Proteins - genetics | Amino Acid Substitution | Genetic disorders | Gene mutations | Analysis | Crystals | Genetic aspects | Models | Structure | Glutamine | Endothelium | Proteins | Eye diseases | Cornea | Crystal structure | Homology | Cell surface | Membrane proteins | Pathogenicity | Packing | Corneal dystrophy | Dystrophy | Protein transport | Protein structure | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2008, Volume 105, Issue 49, pp. 19183 - 19187
The overlapping histological and biochemical features underlying the beneficial effect of deacetylase inhibitors and NO donors in dystrophic muscles suggest an... 
Artificial satellites | Duchenne muscular dystrophy | Muscles | Small interfering RNA | Histones | Oxides | Muscular dystrophies | Pharmacology | Skeletal muscle | Myoblasts | Epigenetic | RECRUITMENT | COMPLEX | SKELETAL-MUSCLE MASS | FUSION | epigenetic | MULTIDISCIPLINARY SCIENCES | INDUCTION | MDX MICE | SYNTHASE | SIGNALING PATHWAY | GENE-EXPRESSION | skeletal muscle | FOLLISTATIN | Muscular Dystrophy, Animal - drug therapy | Epigenesis, Genetic | Muscle, Skeletal - cytology | Muscular Dystrophy, Animal - pathology | Repressor Proteins - antagonists & inhibitors | Mice, Inbred mdx | Muscular Dystrophy, Animal - metabolism | Myoblasts - cytology | Benzamides - pharmacology | Repressor Proteins - metabolism | Nitrogen - metabolism | Histone Deacetylases - genetics | Muscular Dystrophy, Duchenne - drug therapy | Mice, Inbred C57BL | Satellite Cells, Skeletal Muscle - cytology | Cells, Cultured | Enzyme Inhibitors - pharmacology | Repressor Proteins - genetics | Histone Deacetylase 2 | Histone Deacetylases - metabolism | Muscular Dystrophy, Duchenne - pathology | Satellite Cells, Skeletal Muscle - enzymology | Animals | Histone Deacetylase Inhibitors | Mice | Muscular Dystrophy, Duchenne - metabolism | Pyridines - pharmacology | RNA, Small Interfering | Nitric Oxide - metabolism | Myoblasts - enzymology | Musculoskeletal system | Biochemistry | Mutation | Gene expression | Rodents | Nitric oxide | Index Medicus | Biological Sciences
Journal Article
Muscle & Nerve, ISSN 0148-639X, 07/2013, Volume 48, Issue 1, pp. 55 - 67
Introduction: Glucocorticoid (GC) therapy in Duchenne muscular dystrophy (DMD) has altered disease progression, necessitating contemporary natural history... 
phenotype | quality of life/psychology | child/preschool | locomotion | muscular dystrophies/Duchenne/physiopathology | muscle strength/physiology | health status | muscular dystrophies/therapy | respiratory function tests | adolescent | follow‐up studies | adult | humans | male | muscular dystrophies/classification | Humans | Male | Follow-up studies | Child/preschool | Locomotion | Phenotype | Quality of life/psychology | Health status | Muscular dystrophies/Duchenne/physiopathology | Muscular dystrophies/therapy | Muscular dystrophies/classification | Adolescent | Adult | Muscle strength/physiology | Respiratory function tests | PROFILES | DESIGN | 6-MINUTE WALK TEST | RELIABILITY | CLINICAL NEUROLOGY | psychology | Duchenne | muscular dystrophies | PREDNISONE THERAPY | GAIT | therapy | physiology | MUSCULAR-DYSTROPHY | STRENGTH | classification | NEUROSCIENCES | muscle strength | follow-up studies | physiopathology | BOYS | preschool | STAR AMBULATORY ASSESSMENT | quality of life | child | Outcome Assessment (Health Care) - methods | Glucocorticoids - therapeutic use | Prospective Studies | Child, Preschool | Diagnostic Techniques, Neurological - standards | Muscular Dystrophy, Duchenne - epidemiology | Young Adult | Biomedical Research - methods | Clinical Trials as Topic - standards | Child | Cross-Sectional Studies | Muscular Dystrophy, Duchenne - drug therapy | Treatment Outcome | International Cooperation | Disease Progression | Outcome Assessment (Health Care) - standards | Clinical Trials as Topic - methods | Longitudinal Studies | Biomedical Research - standards | Cohort Studies | Muscle Strength - physiology | Muscular Dystrophy, Duchenne - diagnosis | Clinical trials | Medicine, Experimental | Medical research | Corticosteroids | Steroids | Index Medicus | Neurologi | Pediatrics | strength | Pediatrik | prednisone therapy | reliability | profiles | boys | 6-minute walk test | Neurology | protocol | children | muscular-dystrophy | star ambulatory assessment
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2015, Volume 10, Issue 9, pp. e0138254 - e0138254
Purpose To elucidate the reliability of MRI as a non-invasive tool for assessing in vivo muscle health and pathological amelioration in response to Losartan... 
FIBROSIS | SKELETAL-MUSCLE | LOSARTAN | REGENERATION | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | MICE | DAMAGE | Fibrosis - drug therapy | Reproducibility of Results | Muscular Dystrophies - metabolism | Muscular Dystrophies, Limb-Girdle - diet therapy | Muscular Dystrophy, Animal - drug therapy | Losartan - pharmacology | Muscular Dystrophies - drug therapy | Magnetic Resonance Imaging - methods | Muscle, Skeletal - metabolism | Fibrosis - metabolism | Muscular Dystrophies - pathology | Angiotensin II Type 1 Receptor Blockers - pharmacology | Muscular Dystrophy, Animal - pathology | Animals | Muscular Dystrophies, Limb-Girdle - metabolism | Muscle, Skeletal - drug effects | Muscular Dystrophy, Animal - metabolism | Mice | Fibrosis - pathology | Laminin - metabolism | Muscle, Skeletal - pathology | Muscular Dystrophies, Limb-Girdle - pathology | Disease Models, Animal | Physiological aspects | Laminin | Magnetic resonance imaging | Gene expression | Muscular dystrophy | Angiotensin | Health sciences | Nuclear magnetic resonance--NMR | Genomics | Insulin-like growth factors | Signal transduction | Mac1 protein | Rodents | Spectrum analysis | Reliability analysis | Physiology | Angiotensin II | Edema | Congenital diseases | Muscles | Inflammation | Pathology | Musculoskeletal system | Fibrosis | Diabetes | Mutation | Dystrophy | Laboratory animals | Index Medicus | Nuclear magnetic resonance | NMR
Journal Article
Molecular Therapy, ISSN 1525-0016, 04/2018, Volume 26, Issue 4, pp. 1093 - 1108
Duchenne muscular dystrophy (DMD) is a lethal muscle-wasting disease currently without cure. We investigated the use of the PiggyBac transposon for full-length... 
transposon vectors | cell therapy | Duchenne muscular dystrophy | dystrophin | muscular dystrophies | muscle fatigue | mesoangioblasts | MORPHOLINOS | MEDICINE, RESEARCH & EXPERIMENTAL | GENETIC CORRECTION | STEM-CELLS | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | MOUSE MODEL | MUSCLE FUNCTION | GENETICS & HEREDITY | MICE | EXPRESSION | DELIVERY | Cell- and Tissue-Based Therapy - methods | Male | Transplantation, Autologous | Myoblasts - transplantation | Myoblasts - metabolism | Muscular Dystrophy, Duchenne - physiopathology | Mice, Inbred mdx | Muscular Dystrophy, Duchenne - therapy | Transgenes | Gene Order | Genes, Reporter | Disease Models, Animal | Cell Line | Gene Transfer Techniques | Gene Expression | Muscular Dystrophy, Duchenne - pathology | Gene Dosage | Mice, SCID | DNA Transposable Elements | Genetic Vectors - genetics | Phenotype | Animals | Dystrophin - genetics | Fluorescent Antibody Technique | Mice | Muscular Dystrophy, Duchenne - genetics | Atomic force microscopy | Satellite cells | Genomes | Transplantation | Muscular dystrophy | Genotype & phenotype | Duchenne's muscular dystrophy | Conflicts of interest | Dystrophin | Expression vectors | Autografts | Transposons | Silicon nitride | Artificial chromosomes | Vectors (Biology) | Progenitor cells | Musculoskeletal system | Plasmids | Stem cells | Monoclonal antibodies | Mutation | Dystrophy | Gene therapy | Gene mapping | Cell migration | Index Medicus | Original
Journal Article