Le traitement du signal en électromyographie: mise au point

Automatic analysis of electromyography (EMG) signals, first operated in 1950 with analogic machines, steeply expanded from 1980 when fast computers and worthwhile programs became available. On-line measurement of response area and latency, averaging of low amplitude waves, fast sorting of motor unit potential shape parameters, computation of the “jitter” between two muscle fibers, turns/amplitude and spectral analysis of interferential pattern records, are some examples of programs currently offered in modern EMG machines. Other techniques are still reserved for research purposes: scanning EMG, decomposition of nerve and muscle compound potentials, measurement of the threshold and firing rate of motor units, trace analysis using tracking models. Finally, the credit for artificial intelligence systems (knowledge based systems, fuzzy logic, neuronal networks) is still not clearly stated.     

Fas receptor expression on B-lineage cells

Mice homozygous for the lpr mutation have B and T cell defects and develop autoantibodies, suggesting that lpr plays a role in their genesis. The lpr defect has been identified as a mutation in the apoptosis-associated Fas receptor (FasR) gene. To begin to define the role of FasR in B cells, we have surveyed FasR expression on B-lineage cells from early progenitors in the bone marrow through their maturation in the periphery. Contrary to some reports, we found that FasR is expressed on B cells at all stages of their development and is highest on germinal center B cells. FasR is not expressed on lpr/lpr-derived cells. These data are consistent with the idea that lpr/lpr mice have an intrinsic B cell defect that may be manifested in developing as well as peripheral B cells. An unexpected finding is that B-1 (CD5) B cells do not constitutively express FasR: FasR becomes detectable on B-1 B cells only after activation.     

Cardiovascular effects of caffeine and nifedipine

Because caffeine and nifedipine may have opposing effects on intracellular calcium concentration, a possible interaction between these agents on blood pressure and heart rate was examined. With a randomized, double-blind, crossover design, 10 normal, caffeine-abstaining subjects received caffeine, 300 mg, or placebo followed by nifedipine, 10 mg, or placebo. Caffeine increased blood pressure, whereas nifedipine reduced it and caused a reflex increase in heart rate. With caffeine pretreatment, nifedipine decreased blood pressure significantly more than with placebo pretreatment. However, nifedipine reduced blood pressure to the same absolute level on both the caffeine and placebo pretreatment days. The reflex increase in heart rate after nifedipine was not affected by prior caffeine or placebo administration. Caffeine pretreatment does not alter the cardiovascular responses to nifedipine but the pressor effect of caffeine is completely reversed by subsequent nifedipine administration.