The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform
Charlotte J Sumner - One of the best experts on this subject based on the ideXlab platform.
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sustained improvement of spinal muscular atrophy mice treated with trichostatin a plus nutrition
Annals of Neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Marta Boschmarce, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients. Ann Neurol 2008; 64:465–470
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Sustained improvement of spinal muscular atrophy mice treated with trichostatin A plus nutrition.
Annals of neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Marta Bosch-marce, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients.
Heather L Narver - One of the best experts on this subject based on the ideXlab platform.
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sustained improvement of spinal muscular atrophy mice treated with trichostatin a plus nutrition
Annals of Neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Marta Boschmarce, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients. Ann Neurol 2008; 64:465–470
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Sustained improvement of spinal muscular atrophy mice treated with trichostatin A plus nutrition.
Annals of neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Marta Bosch-marce, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients.
Dong W Choe - One of the best experts on this subject based on the ideXlab platform.
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sustained improvement of spinal muscular atrophy mice treated with trichostatin a plus nutrition
Annals of Neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Marta Boschmarce, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients. Ann Neurol 2008; 64:465–470
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Sustained improvement of spinal muscular atrophy mice treated with trichostatin A plus nutrition.
Annals of neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Marta Bosch-marce, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients.
Lingling Kong - One of the best experts on this subject based on the ideXlab platform.
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sustained improvement of spinal muscular atrophy mice treated with trichostatin a plus nutrition
Annals of Neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Marta Boschmarce, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients. Ann Neurol 2008; 64:465–470
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Sustained improvement of spinal muscular atrophy mice treated with trichostatin A plus nutrition.
Annals of neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Marta Bosch-marce, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients.
Barrington G Burnett - One of the best experts on this subject based on the ideXlab platform.
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sustained improvement of spinal muscular atrophy mice treated with trichostatin a plus nutrition
Annals of Neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Marta Boschmarce, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients. Ann Neurol 2008; 64:465–470
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Sustained improvement of spinal muscular atrophy mice treated with trichostatin A plus nutrition.
Annals of neurology, 2008Co-Authors: Heather L Narver, Dong W Choe, Michael A Eckhaus, Addis A Taye, Lingling Kong, Barrington G Burnett, Marta Bosch-marce, Charlotte J SumnerAbstract:Early treatment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median survival of spinal muscular atrophy mice by 170%. Treated mice continued to gain weight, maintained stable motor function, and retained intact neuromuscular junctions long after trichostatin A was discontinued. In many cases, ultimate decline of mice appeared to result from Vascular Necrosis, raising the possibility that Vascular dysfunction is part of the clinical spectrum of severe spinal muscular atrophy. Early spinal muscular atrophy disease detection and treatment initiation combined with aggressive ancillary care may be integral to the optimization of histone deacetylase inhibitor treatment in human patients.
