Evaluation of methods for extraction of the volitional EMG in dynamic hybrid muscle activation

BACKGROUND: Hybrid muscle activation is a modality used for muscle force enhancement, in which muscle contraction is generated from two different excitation sources: volitional and external, by means of electrical stimulation (ES). Under hybrid activation, the overall EMG signal is the combination of the volitional and ES-induced components. In this study, we developed a computational scheme to extract the volitional EMG envelope from the overall dynamic EMG signal, to serve as an input signal for control purposes, and for evaluation of muscle forces. METHODS: A "synthetic" database was created from in-vivo experiments on the Tibialis Anterior of the right foot to emulate hybrid EMG signals, including the volitional and induced components. The database was used to evaluate the results obtained from six signal processing schemes, including seven different modules for filtration, rectification and ES component removal. The schemes differed from each other by their module combinations, as follows: blocking window only, comb filter only, blocking window and comb filter, blocking window and peak envelope, comb filter and peak envelope and, finally, blocking window, comb filter and peak envelope. RESULTS AND CONCLUSION: The results showed that the scheme including all the modules led to an excellent approximation of the volitional EMG envelope, as extracted from the hybrid signal, and underlined the importance of the artifact blocking window module in the process. The results of this work have direct implications on the development of hybrid muscle activation rehabilitation systems for the enhancement of weakened muscles

Neural adaptations to electrical stimulation strength training

This review provides evidence for the hypothesis that electrostimulation strength training (EST) increases the force of a maximal voluntary contraction (MVC) through neural adaptations in healthy skeletal muscle. Although electrical stimulation and voluntary effort activate muscle differently, there is substantial evidence to suggest that EST modifies the excitability of specific neural paths and such adaptations contribute to the increases in MVC force. Similar to strength training with voluntary contractions, EST increases MVC force after only a few sessions with some changes in muscle biochemistry but without overt muscle hypertrophy. There is some mixed evidence for spinal neural adaptations in the form of an increase in the amplitude of the interpolated twitch and in the amplitude of the volitional wave, with less evidence for changes in spinal excitability. Cross-sectional and exercise studies also suggest that the barrage of sensory and nociceptive inputs acts at the cortical level and can modify the motor cortical output and interhemispheric paths. The data suggest that neural adaptations mediate initial increases in MVC force after short-term EST

Live and let die: regulatory mechanisms in Fas-mediated apoptosis

Activation of Fas receptor by Fas ligand causes caspase 8 activation and apoptosis in cells and is an important mechanism by which normal tissue homeostasis and function are maintained. Activation of caspase 8 is preceded by the formation of a death-inducing signalling complex (DISC), and a number of redundant mechanisms regulate DISC formation in vivo. Fas receptor is widely expressed in tissues, and dysfunction of the regulatory mechanisms in Fas receptor signalling has been reported in several diseases including autoimmune disease and cancer. This review aims to identify and discuss the various mechanisms employed by cells to alter their sensitivity to Fas-mediated apoptosis by regulating DISC formation. We also discuss a number of defects identified with Fas receptor signalling and the associated pathologies

Two new species of Trevathana (Crustacea, Cirripedia, Balanomorpha, Pyrgomatidae) from the Western Indian Ocean and French Polynesia

Two new species of the Pyrgomatid barnacle Trevathana are described: Trevathana synthesysae nov. sp., extracted from Plesiastrea versipora from the Indian Ocean Islands Réunion and Mauritius, and Trevathana isfae nov. sp. from a colony of Favia stelligera from French Polynesia, which, until recently, was terra incognita with regard to coral-inhabiting barnacles. The two new species are distinctive by their relatively broad scutum as compared to Trevathana dentatum, their prominent adductor ridge extending beyond the basal margin of the scutum, and their quadrangular tergum.</jats:p

Effect of toluene on Pseudomonas stutzeri ST-9 morphology: Plasmolysis, cell size and formation of outer membrane vesicles

IIsolated toluene-degrading Pseudomonas stutzeri ST-9 bacteria were grown in a minimal medium containing toluene (100 mg L-1) (MMT) or glucose (MMG) as the sole carbon source, with specific growth rates of 0.019 h-1 and 0.042 h-1, respectively. Scanning (SEM) as well as transmission (TEM) electron microscope analyses showed that the bacterial cells grown to mid log in the presence of toluene possess a plasmolysis space. TEM analysis revealed that bacterial cells that were grown in MMT were surrounded by an additional "material" with small vesicles in between. Membrane integrity was analyzed by leakage of 260 nm absorbing material and demonstrated only 7% and 8% leakage from cultures grown in MMT compared to MMG. X-ray microanalysis showed a 4.3-fold increase in Mg and a 3-fold increase in P compared to cells grown in MMG. FACS analysis indicated that the permeability of the membrane to propidium iodide was 12.6% and 19.6% when the cultures were grown in MMG and MMT, respectively. The bacterial cell length increased by 8.5%Âą0.1 and 17% Âą2 as measured using SEM images and FACS analysis, respectively. The results obtained in this research show that the presence of toluene led to morphology changes such as plasmolysis, cell size and formation of outer membrane vesicles. However, it does not cause significant damage to membrane integrity.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author