Michael J. McKenna
Massachusetts Eye and Ear Infirmary
372 Papers
2.4K Citations
Michael J. McKenna is an academic researcher from Massachusetts Eye and Ear Infirmary. The author has contributed to research in topics: Medicine & Skeletal muscle. The author has an hindex of 70, co-authored 356 publications. Previous affiliations of Michael J. McKenna include Charles Stark Draper Laboratory & University of Melbourne.
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Papers
Neural processing of emotional faces requires attention
TL;DR: Functional magnetic resonance imaging was used to measure activation in regions that responded differentially to faces with emotional expressions compared with neutral faces, and the modulation of these responses by attention was measured, using a competing task with a high attentional load.
1.2K
The physiological load imposed on basketball players during competition
TL;DR: It is concluded that the physiological requirements of men's basketball are high, placing considerable demands on the cardiovascular and metabolic capacities of players.
746
Validation of a Patient‐Graded Instrument for Facial Nerve Paralysis: The FaCE Scale
Jeffrey B. Kahn,Richard E Gliklich,K. Paul Boyev,Mph Michael G. Stewart Md,Ralph Metson,Michael J. McKenna +5 more
TL;DR: A patient‐based instrument to measure both facial impairment and disability, the Facial Clinimetric Evaluation (FaCE) Scale is developed and validated.
369
Mutations in a novel cochlear gene cause DFNA9, a human nonsyndromic deafness with vestibular dysfunction
Nahid G. Robertson,L Lu,Stefan Heller,Saumil N. Merchant,Roland D. Eavey,Michael J. McKenna,Joseph B. Nadol,Richard T. Miyamoto,Fred H. Linthicum,J F Lubianca Neto,A. J. Hudspeth,Christine E. Seidman,Cynthia C. Morton,Jonathan G. Seidman +13 more
TL;DR: Three missense mutations in human COCH (previously described as Coch5b2), a novel cochlear gene, are reported in three unrelated kindreds with DFNA9, an autosomal dominant, nonsyndromic, progressive sensorineural hearing loss with vestibular pathology.
349
Muscle K+, Na+, and Cl disturbances and Na+-K+ pump inactivation: implications for fatigue.
TL;DR: During intense contraction some Na(+)-K(+) pumps are inactivated and together with further ionic disturbances, likely precipitate muscle fatigue, and less severe local ionic changes can also augment subtetanic force, suggesting that they may potentiate muscle contractility early in exercise.
285