Background: Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57% of COPD patients) is generally not controlled in studies and could explain this discrepancy. This study aimed to specifically compare voluntary and stimulated activation levels in COPD patients with and without muscle weakness. Methods: Twenty-two patients with quadriceps weakness (COPD MW), 18 patients with preserved quadriceps strength (COPD NoMW) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VA peripheral) and transcranial magnetic (VA cortical) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions. Results: COPD MW exhibited lower VA cortical and lower MEP/Mmax compared with COPD NoMW (p < 0.05). Hmax/Mmax was not significantly different between groups (p = 0.25). Silent period duration was longer in the two groups of COPD patients compared with controls (p < 0.01). Interestingly, there were no significant differences between all COPD patients taken together and controls regarding VA cortical and MEP/Mmax. Conclusions: COPD patients with muscle weakness have reduced voluntary activation without altered spinal excitability. Corticospinal inhibition is higher in COPD regardless of muscle weakness. Therefore, reduced cortical excitability and a voluntary activation deficit from the motor cortex are the most likely cortical mechanisms implicated in COPD muscle weakness. The mechanisms responsible for cortical impairment and possible therapeutic interventions need to be addressed.
Hemibody movements are strongly considered as being under the control of the contralateral hemisphere of the cerebral cortex. However, some neuroimaging studies have found a bilateral activation of either the primary sensori-motor (SM1) areas or the rostral prefrontal cortex (PFC), during unimanual tasks. More than just bilateral, the activation of these areas was found to be symmetrical in some studies. However, the symmetrical response remains strongly controversial notably for handgrip force generations. We therefore aimed to examine the bilateral SM1 and rostral PFC area activations in response to graded submaximal force generation during a unilateral handgrip task. Fifteen healthy subjects performed 6 levels of force (ranging from 5 to 50% of MVC) during a handgrip task. We concomitantly measured the activation of bilateral SM1 and rostral PFC areas through near-infrared spectroscopy (NIRS) and the electromyographic (EMG) activity of the bilateral flexor digitorum superficialis (FDS) muscles. Symmetrical activation was found over the SM1 areas for all the investigated levels of force. At the highest level of force (i.e., 50% of MVC), the EMG of the passive FDS increased significantly and the ipsilateral rostral PFC activation was found more intense than the corresponding contralateral rostral PFC activation. We suggest that the visuo-guided control of force levels during a handgrip task requires the cross-talk from ipsi- to contralateral SM1 to cope for the relative complexity of the task, similar to that which occurs during complex sequential finger movement. We also propose alternative explanations for the observed symmetrical SM1 activation including (i) the ipsilateral corticospinal tract and (ii) interhemispheric inhibition (IHI) mechanism. The increase in EMG activity over the passive FDS could be associated with a release of IHI at 50% of MVC. Finally, our results suggest that the greater ipsilateral (right) rostral PFC activation may reflect the greater demand of attention required to control the motor output at high levels of force.
We compare forward and backward Raman scattering results on folded acoustical phonons in GaAs-AlAs superlattices with a detailed theoretical analysis of their dispersion properties and light scattering activity. By forward scattering, which involves phonons with a vanishing wave vector, we first get evidence of zone-center gaps, in quantitative agreement with the elastic model predictions. We also check the zone-center selection rules and conclusively prove the assignment of the light scattering on folded acoustical phonons to a modulated photoelastic (Brillouin) process. In backscattering experiments, one creates phonons with a finite wave-vector and the zone-center selection rules are relaxed. We quantitatively describe this phenomenon, and demonstrate that the backscattering intensities directly reflect the coupling between folded branches and the related zoneboundary gap magnitude.An excellent agreement between measured and calculated intensities is obtained. Finally we emphasize the great sensitivity of the gaps and intensities, contrary to the backscattering frequency shifts, to the supercell inner structure. This greatly enhances the interest of Raman scattering as a tool for characterizing periodic structures.
The behavior of boron incorporation into GaAs has been studied by x-ray photoelectron spectroscopy, x-ray diffraction, and atomic force microscopy. As the boron content of the film was increased, both the characteristic peak for the B 1s core level at 188 eV and As Auger transition (260 eV) could be detected by XPS. At 550–600 °C, single crystalline films could only be grown for x⩽0.06. Upon increasing the diborane flux in the gas phase, the film stoichiometry and the boron surface composition evolved rapidly towards a boron-rich subarsenide compound. This trend is followed by a clear degradation of the surface morphology and an increase in the surface roughness. A surface segregation of boron is suggested due to the high diborane vapor supersaturation needed during growth.
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