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W Alston

Publications and source records attributed to W Alston.

14 recordsLinked to original sources
PubMed1981

Inaccuracy in automated measurement of hematocrit and corpuscular indices in the presence of severe hyperglycemia.

Because we recently observed two patients with severe diabetic hyperglycemia and spuriously elevated electronically determined hematocrit and mean corpuscular volume (MCV), we investigated the effect of hyperglycemia on two popular automated hematology systems, the Coulter S and Ortho ELT-8. Marked hyperglycemia (blood glucose 800--2000 mg/dl) caused consistent overestimation of the electronically determined MCV compared to that derived from a simultaneous spun microhematocrit. The resultant overestimation and underestimation, respectively, of the derived values for hematocrit and mean corpuscular hemoglobin concentration may be clinically misleading. The mechanism of MCV elevation in hyperglycemia appears to be swelling of hyperosmolar glucose "loaded" erythrocytes when diluted into "isotonic" counting medium. This effect is readily circumvented by determination of a spun microhematocrit.

Autoanalysis↗
PubMed1967

Motor activity following the silent period in human muscle.

1. When a muscle is unloaded during voluntary contraction, there is normally a silent period in the electromyogram. The silence is terminated by a sudden return of muscle action potentials.2. In order to investigate the mechanism of the terminal motor volley, the unloading reflex was studied in six human subjects. The independent variables were the initial muscular force, the inertia of the limb and the amount of motion permitted. The dependent variables were the size and latency of the terminal volley.3. During isometric contraction, the amplitude of the surface-recorded muscle action potentials increased monotonically with increasing muscular tension.4. The action potentials were significantly larger during the terminal volley than during the period before unloading.5. When acceleration of the limb was reduced by increasing the inertia, the terminal volley was decreased in size, but the latency was not affected.6. When movement was interrupted by a mechanical block, the latency of the terminal volley was reduced, but the size was not affected.7. The results suggest that the terminal motor volley is not the result of a decrease in Renshaw feed-back or in autogenetic inhibition.8. The motor volley must be regulated by proprioceptive feed-back, because it is affected by the velocity and displacement of the limb.9. The muscle frequently responded within 20 msec after motion of the limb was blocked. Hence it appears that the mechanism involves a spinal reflex.10. Because the motor discharge occurs while the muscle is shortening, it cannot be an ordinary stretch reflex. If the discharge is attributed to spindle afferent driving, one must assume that the gamma motor neurones are active during the silent period.11. The authors postulate a fusimotor reflex, which is driven by afferent impulses from the moving limb and excites the alpha motoneurones by way of the ;gamma loop'.

Action Potentials↗