Generation and analysis of synthetic surface electromyography signals under varied muscle fiber type proportions and validation using recorded signals.

The magnitude and duration of muscle force production are influenced by the fiber type proportion. In this work, surface electromyography (sEMG) signals of muscles with varied fiber type proportions, are generated. For this, relevant components of existing models reported in various literature have been adopted. Also, a method to calculate the motor unit size factor is proposed. sEMG signals of adductor pollicis (AP) and triceps brachii (TB) muscles are simulated from the onset of force production to muscle fatigue state at various percentages of maximal voluntary contraction (MVC) values. The model is validated using signals recorded from these muscles using well-defined isometric exercise protocols. Root mean square and mean power spectral density values extracted from the simulated and recorded signals are found to increase for TB and decrease for AP with time. A linear variation of the features with %MVC values is obtained for simulated and experimental results. The Bland-Altman plot is used to analyze the agreement between simulated and experimental feature values. Good agreement is obtained for the feature values at various %MVCs. The mean endurance time calculated using the model is found to be comparable to that of the experimental value. This method can be used to generate sEMG signals of different muscles with varying fiber type ratios under various neuromuscular conditions.

IL-10 dependent suppression of type 1, type 2 and type 17 cytokines in active pulmonary tuberculosis.

BACKGROUND: Although Type 1 cytokine responses are considered protective in pulmonary tuberculosis (PTB), their role as well as those of Type 2, 17 and immunoregulatory cytokines in tuberculous lymphadenitis (TBL) and latent tuberculosis (LTB) have not been well studied. AIM AND METHODS: To identify cytokine responses associated with pulmonary tuberculosis (TB), TB lymphadenitits and latent TB, we examined mycobacterial antigen-specific immune responses of PTB, TBL and LTB individuals. More specifically, we examined ESAT-6 and CFP-10 induced Type 1, Type 2 and Type 17 cytokine production and their regulation using multiplex ELISA. RESULTS: PTB individuals exhibited a significantly lower baseline as well as antigen-specific production of Type 1 (IFNγ, TNFα and IL-2); Type 2 (IL-4) and Type 17 (IL-17A and IL-17F) cytokines in comparison to both TBL and LTB individuals. TBL individuals exhibited significantly lower antigen-specific IFNγ responses alone in comparison to LTB individuals. Although, IL-10 levels were not significantly higher, neutralization of IL-10 during antigen stimulation resulted in significantly enhanced production of IFNγ, IL-4 and IL-17A in PTB individuals, indicating that IL-10 mediates (at least partially) the suppression of cytokine responses in PTB. CONCLUSION: Pulmonary TB is characterized by an IL-10 dependent antigen-specific suppression of Type 1, Type 2 and Type 17 cytokines, reflecting an important association of these cytokines in the pathogenesis of active TB.