PMC:2940021 / 37109-38147
Annnotations
0_colil
{"project":"0_colil","denotations":[{"id":"20422195-20047568-60992","span":{"begin":665,"end":667},"obj":"20047568"},{"id":"20422195-16931510-60993","span":{"begin":1030,"end":1032},"obj":"16931510"},{"id":"20422195-16775221-60994","span":{"begin":1034,"end":1036},"obj":"16775221"}],"text":"Muscle channelopathies and metabolic myopathies\nCompared to the increasing data regarding the diagnostic value of neuromuscular MRI in patients presenting with dystrophic myopathies or non-dystrophic congenital myopathies, data concerning MRI findings in muscle channelopathies or metabolic myopathies are rather limited. A recently published study focussed on patients with myotonia congenital type Becker, a non-dystrophic generalised myotonia caused by mutations in the muscle chloride gene. Although all patients presented with a severe disabling myotonia, no fatty degeneration or muscle oedema could be detected by using a whole-body high-field MRI protocol [67]. These findings suggest that conventional MRI techniques are less sensitive in the detection of changes in channelopathies. Recent experimental studies using 23Na-MRI instead of or in combination with 1H-MRI have shed some light on the muscle cell function and disease process in Na-channelopathies by demonstrating Na-accumulation during episodes of weakness [33, 68]."}
2_test
{"project":"2_test","denotations":[{"id":"20422195-20047568-29368076","span":{"begin":665,"end":667},"obj":"20047568"},{"id":"20422195-16931510-29368077","span":{"begin":1030,"end":1032},"obj":"16931510"},{"id":"20422195-16775221-29368078","span":{"begin":1034,"end":1036},"obj":"16775221"}],"text":"Muscle channelopathies and metabolic myopathies\nCompared to the increasing data regarding the diagnostic value of neuromuscular MRI in patients presenting with dystrophic myopathies or non-dystrophic congenital myopathies, data concerning MRI findings in muscle channelopathies or metabolic myopathies are rather limited. A recently published study focussed on patients with myotonia congenital type Becker, a non-dystrophic generalised myotonia caused by mutations in the muscle chloride gene. Although all patients presented with a severe disabling myotonia, no fatty degeneration or muscle oedema could be detected by using a whole-body high-field MRI protocol [67]. These findings suggest that conventional MRI techniques are less sensitive in the detection of changes in channelopathies. Recent experimental studies using 23Na-MRI instead of or in combination with 1H-MRI have shed some light on the muscle cell function and disease process in Na-channelopathies by demonstrating Na-accumulation during episodes of weakness [33, 68]."}
TEST0
{"project":"TEST0","denotations":[{"id":"20422195-170-176-60992","span":{"begin":665,"end":667},"obj":"[\"20047568\"]"},{"id":"20422195-237-243-60993","span":{"begin":1030,"end":1032},"obj":"[\"16931510\"]"},{"id":"20422195-234-240-60994","span":{"begin":1034,"end":1036},"obj":"[\"16775221\"]"}],"text":"Muscle channelopathies and metabolic myopathies\nCompared to the increasing data regarding the diagnostic value of neuromuscular MRI in patients presenting with dystrophic myopathies or non-dystrophic congenital myopathies, data concerning MRI findings in muscle channelopathies or metabolic myopathies are rather limited. A recently published study focussed on patients with myotonia congenital type Becker, a non-dystrophic generalised myotonia caused by mutations in the muscle chloride gene. Although all patients presented with a severe disabling myotonia, no fatty degeneration or muscle oedema could be detected by using a whole-body high-field MRI protocol [67]. These findings suggest that conventional MRI techniques are less sensitive in the detection of changes in channelopathies. Recent experimental studies using 23Na-MRI instead of or in combination with 1H-MRI have shed some light on the muscle cell function and disease process in Na-channelopathies by demonstrating Na-accumulation during episodes of weakness [33, 68]."}
MyTest
{"project":"MyTest","denotations":[{"id":"20422195-20047568-29368076","span":{"begin":665,"end":667},"obj":"20047568"},{"id":"20422195-16931510-29368077","span":{"begin":1030,"end":1032},"obj":"16931510"},{"id":"20422195-16775221-29368078","span":{"begin":1034,"end":1036},"obj":"16775221"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"Muscle channelopathies and metabolic myopathies\nCompared to the increasing data regarding the diagnostic value of neuromuscular MRI in patients presenting with dystrophic myopathies or non-dystrophic congenital myopathies, data concerning MRI findings in muscle channelopathies or metabolic myopathies are rather limited. A recently published study focussed on patients with myotonia congenital type Becker, a non-dystrophic generalised myotonia caused by mutations in the muscle chloride gene. Although all patients presented with a severe disabling myotonia, no fatty degeneration or muscle oedema could be detected by using a whole-body high-field MRI protocol [67]. These findings suggest that conventional MRI techniques are less sensitive in the detection of changes in channelopathies. Recent experimental studies using 23Na-MRI instead of or in combination with 1H-MRI have shed some light on the muscle cell function and disease process in Na-channelopathies by demonstrating Na-accumulation during episodes of weakness [33, 68]."}