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1. The interphalangeal joint of the thumb was driven through sinusoidal flexion-extension movements while electromyograms were recorded from over the flexor pollicis longus muscle. 2. When the subject relaxed his thumb the movement generated no detectable e.m.g. response. When, however, he exerted a voluntary flexing force electrical activity could be(More)
1. A method is described for driving the interphalangeal joint of the thumb through repeated sinusoidal flexion-extension movements, while immobilizing other joints of the wrist and hand.2. The joint met the sinusoidal movement with a force that fluctuated in an approximately sinusoidal manner. This paper is concerned with the relationship between the(More)
1. The upper limbs of normal subjects were immobilized in a way that allowed measurement of forces and movements at the thumb interphalangeal joint without significant movement elsewhere in the limb. 2. When the subject attempted to maintain a steady flexing force at the joint against a rigid stop, the actual force showed the irregular 8-11 Hz fluctuations(More)
The critical role of the neurofibromatosis 1 (NF1) gene as a tumour suppressor has been clearly demonstrated for malignancies arising in NF1 patients. However, little is known about the more common benign tumours, such as the pilocytic astrocytoma. Most NF1-associated astrocytomas are benign and clinically non-progressive, though aggressive tumours are(More)
Distributed stimulation of slow skeletal muscle has previously been used to produce smooth tetanic contractions at low stimulus rates. This involved distributed or interleaved stimulation of portions of the muscle with near equal tension contributions. Extending this to fast and mixed muscle encounters difficulties in getting and maintaining equal twitch(More)
1. Imposed sinusoids were used to assess the resistance to movement at the thumb interphalangeal joint.2. The resistance to high-frequency movements (> 12 Hz) increased when the subject exerted a large voluntary flexing force; this increase was attributable to a greater non-reflex resistance of the contracting flexor muscles. This resistance was essentially(More)
Glycogen storage disease type II (Pompe disease; MIM 232300) stems from the deficiency of acid alpha-glucosidase (GAA; acid maltase; EC 3.2.1.20), which primarily involves cardiac and skeletal muscles. An adeno-associated virus 2/8 (AAV2/8) vector containing the muscle creatine kinase (MCK) (CK1) reduced glycogen content by approximately 50% in the heart(More)
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