Lawrence Hayward
Affiliations: | Neurology | Univ Mass Worcester, Worcester, MA, United States |
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"Lawrence Hayward"Mean distance: 15.86 (cluster 6) | S | N | B | C | P |
Parents
Sign in to add mentor| Stephen C. Cannon | post-doc | 1992-1995 | Harvard Medical School and Massachusetts General Hospital |
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Publications
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| Guo D, Daman K, Chen JJ, et al. (2022) iMyoblasts for ex vivo and in vivo investigations of human myogenesis and disease modeling. Elife. 11 |
| Khogali S, Lucas B, Ammar T, et al. (2015) Physiological basis for muscle stiffness and weakness in a knock-in M1592V mouse model of hyperkalemic periodic paralysis. Physiological Reports. 3 |
| Ammar T, Lin W, Higgins A, et al. (2015) Understanding the physiology of the asymptomatic diaphragm of the M1592V hyperkalemic periodic paralysis mouse. The Journal of General Physiology. 146: 509-25 |
| Lucas B, Ammar T, Khogali S, et al. (2014) Contractile abnormalities of mouse muscles expressing hyperkalemic periodic paralysis mutant NaV1.4 channels do not correlate with Na+ influx or channel content. Physiological Genomics. 46: 385-97 |
| Renaud JM, Hayward LJ. (2012) Lessons learned from muscle fatigue: implications for treatment of patients with hyperkalemic periodic paralysis. Recent Patents On Biotechnology. 6: 184-91 |
| Clausen T, Nielsen OB, Clausen JD, et al. (2011) Na+,K+-pump stimulation improves contractility in isolated muscles of mice with hyperkalemic periodic paralysis. The Journal of General Physiology. 138: 117-30 |
| Hayward LJ, Kim JS, Lee MY, et al. (2008) Targeted mutation of mouse skeletal muscle sodium channel produces myotonia and potassium-sensitive weakness. The Journal of Clinical Investigation. 118: 1437-49 |
| Hayward LJ, Sandoval GM, Cannon SC. (1999) Defective slow inactivation of sodium channels contributes to familial periodic paralysis. Neurology. 52: 1447-53 |
| Andreu AL, Bruno C, Shanske S, et al. (1998) Missense mutation in the mtDNA cytochrome b gene in a patient with myopathy. Neurology. 51: 1444-7 |
| Green DS, Hayward LJ, George AL, et al. (1997) A proposed mutation, Val781Ile, associated with hyperkalemic periodic paralysis and cardiac dysrhythmia is a benign polymorphism. Annals of Neurology. 42: 253-6 |