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Версія від 13:52, 23 травня 2017, створена Drawer9parade (обговореннявнесок) (Створена сторінка: , Charlotte, NC, USA), bandpass filtered from DC to 50 Hz and referenced to the bilateral mastoids. Individual electrode impedance was set below 5 k��. The...)

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, Charlotte, NC, USA), bandpass filtered from DC to 50 Hz and referenced to the bilateral mastoids. Individual electrode impedance was set below 5 k��. The participants were provided with paired inspiratory occlusions of 150 ms each with a 500 ms inter-stimulus-interval. The paired stimuli were provided at the onset of inspiration randomly every 2�C4 breaths. The onset of occlusion was identified as the start of mouth pressure change (Labchart V7, ADInstruments Inc., Bella Vista, #MAO randurls[1|1|,|CHEM1|]# NSW, Australia). At least 100 paired occlusions were collected for data analysis in every participant. The trigger box was set up to send parallel markers to the Neuroscan 4.5 recording software (Compumedics Neuroscan Inc., Charlotte, NC, USA). The participants were instructed to keep breathing normally, rather than to stop breathing, during inspiratory occlusions, and to count the number of breaths they felt obstructed during the experiment. Data Analyses For offline analysis, the EEG epoch was defined and extracted from 200 ms before to 1000 ms after the respiratory occlusion, i.e., for S1 and S2 separately. The first 200 ms served as the baseline. The signals were corrected for ocular movement using a built-in algorithm of the analysis software (BrainVision Analyzer 2, Brain Products GmbH., Gilching, Germany) and further filtered between 1 and 50 Hz (12 dB/octave roll-off). The artifacts were defined when greater than 100 and 60 ��V, baseline to peak, for the four eye electrodes and all other electrodes, respectively. After the artifacts were extracted from the signals, the corresponding epochs were then averaged for S1 and S2 separately. The RREP N1 peak amplitudes for S1 and S2 were identified in a time window of 85�C135 ms after occlusion onset at cortical sites C3 and C4 and the S2/S1 ratios were calculated. Separate one-way analyses of variance (ANOVA) were performed to test for group differences in pulmonary function, non-respiratory parameters, and S2/S1 ratios. Based on our a priori hypothesis, the analyses for the N1 peaks were conducted with a one-tailed test. The critical p value was set at