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  • Language mapping in patient 2. (A) Neurostimulation: Stimulation of two electrode pairs of the posterior frontal lobe (Ch 37 and 45; 45 and 46; denoted by pink boxes) resulted in pure speech arrest with maintained comprehension. Language function was not satisfactorily assessed in the following electrode sites, where neurostimulation induced positive auditory or sensorimotor responses and stimulation had to be prematurely terminated before completion of a question-and-answer trial. Stimulation of an electrode pair of the posterior temporal lobe (Ch 33 and 41; denoted by a red box) induced subjective perception of an annoying high-pitch-sound. Since the patient stated that she did not want to hear such annoying sounds any longer, we decided not to stimulate a neighboring electrode pair (Ch 34 and 42) on the superior temporal gyrus. Stimulation of an electrode pair in the inferior post- and pre-central gyri (Ch 43 and 44; denoted by a blue box) resulted in movement of the throat, and stimulation of a pair (Ch 51 and 59; denoted by a blue box) resulted in movement of lip. Electrical stimulation of electrode pairs (Ch 11 and 12; 13 and 14; 15 and 16; 17 and 25; 18 and 26; 52 and 60) resulted in either motor (blue) or sensory-motor mixed (blue-green) responses involving the right upper extremity. Following the surgical resection of the superior frontal gyrus including the tumor, no postoperative language deficits were noted. (B) ECoG time–frequency analysis time-locked to patient's vocalization: This analytic method was designed to evaluate sequential brain activation associated with comprehension, word retrieval, and vocalization. A time–frequency plot matrix was placed on each subdural electrode. High-frequency gamma-augmentation began to involve the superior temporal gyrus (Ch 34) at 1580 ms prior to the onset of patient's vocalization, the medial part of superior frontal gyrus (Ch 8) and the cingulate gyrus (Ch 4) at 610 ms prior to the onset of patient's vocalization, the inferior frontal gyrus (Ch 46) at 570 ms prior to the onset of patient's vocalization, the inferior post-central gyrus (Ch 43) at 550 ms prior to the patient's vocalization, the medial temporal lobe structure (Ch 67) at 510 ms prior to the patient's vocalization, and the superior temporal gyrus (Ch 34) at 20 ms prior to the onset of patient's vocalization. Channels 48 and 49 were not assessed due to artifacts. (C) ECoG time–frequency analysis time-locked to auditory questions: This analytic method was designed to evaluate brain activation associated with the initiation of auditory question. High-frequency gamma-augmentation began to involve the superior temporal gyrus (Ch 34) at 90 ms after the onset of auditory questions, the cingulate gyrus (Ch 4) at 1000 ms after the onset of auditory questions, the inferior post-central gyrus (Ch 43) at 1410 ms after the onset of auditory questions, and the superior temporal gyrus (Ch 34) at 1510 ms after the onset of auditory questions. ... Language mapping in patient 1. (A) ECoG time–frequency analysis time-locked to patient's vocalization: This analytic method was designed to evaluate sequential brain activation associated with comprehension, word retrieval, and vocalization. A time–frequency plot matrix was placed on each subdural electrode. High-frequency gamma-augmentation began to involve the superior temporal gyrus (Ch 36) at 1750 ms prior to the onset of patient's vocalization, the middle temporal gyrus (Ch 25 and 33) at 740 ms prior to the onset of patient's vocalization, the medial part of superior frontal gyrus (Ch 7 and 8) and the cingulate gyrus (Ch 3) at 700 ms prior to the onset of patient's vocalization, the inferior frontal gyrus (Ch 56) at 510 ms prior to the onset of patient's vocalization, the inferior pre- and post-central gyri (most prominently seen in Ch 54 and 69) at 470 ms prior to the patient's vocalization, the medial temporal lobe structure (Ch 9) at 70 ms prior to the patient's vocalization, and the superior temporal gyrus (Ch 36) at 70 ms after the onset of patient's vocalization. (B) ECoG time–frequency analysis time-locked to auditory questions: This analytic method was designed to evaluate brain activation associated with the initiation of auditory question. High-frequency gamma-augmentation began to involve the superior temporal gyrus (Ch 36) at 30 ms after the onset of auditory questions, the medial part of superior frontal gyrus (Ch 7 and 8) at 1050 ms after the onset of auditory questions, the middle temporal gyrus (Ch 25) at 1260 ms after the onset of auditory questions, and the inferior pre- and post-central gyri (most prominently seen in Ch 54 and 69) at 990 ms after the onset of auditory questions. ... Language mapping in patient 3. (A) Neurostimulation: Stimulation of two electrodes pairs on the occipital lobe resulted in visual symptoms (Ch 1 and 2; 49 and 50; denoted by light-blue boxes). Stimulation of an electrode pair of the inferior pre-central gyrus (Ch 105 and 113; denoted by a pink–blue box) induced speech arrest associated with throat movement. Stimulation of an electrode pair of the inferior post-central gyrus (Ch 106 and 114; denoted by a green box) resulted in tingling of teeth. Language function was not satisfactorily assessed in the following electrode sites, where neurostimulation induced positive motor responses and stimulation had to be prematurely terminated before completion of a question-and-answer trial. Stimulation of an electrode pair of the pre- and post-central gyrus (Ch 121 and 129; denoted by a blue box) resulted in movement of mouth. Stimulation of an electrode pair of the post-central gyrus (Ch 122 and 129; denoted by a blue box) resulted in movement of the thumb. Stimulation of a pair of the medial frontal region (Ch 6 and 7; denoted by a blue box) resulted in tonic extension of the bilateral upper extremities. (B) ECoG time–frequency analysis time-locked to patient's vocalization: This analytic method was designed to evaluate sequential brain activation associated with comprehension, word retrieval, and vocalization. No cortical activation represented as gamma-augmentation was observed in the superior temporal gyrus (Ch 93) during auditory questions. High-frequency gamma-augmentation began to involve the posterior inferior temporal gyrus (Ch 55) at 1220-ms prior to the onset of patient's vocalization, the inferior frontal gyrus (Ch 103) at 590-ms prior to the onset of patient's vocalization, and the inferior pre-central gyrus (Ch 129) immediately prior to the patient's vocalization. (C) ECoG time–frequency analysis time-locked to auditory questions: This analytic method was designed to evaluate brain activation associated with the initiation of auditory question. High-frequency gamma-augmentation began to involve the left superior temporal gyrus (Ch 93) at 70-ms after the onset of auditory questions, the posterior inferior temporal gyrus (Ch 55) at 1020-ms after the onset of auditory questions, and the inferior frontal gyrus (Ch 103) at 910-ms after the onset of auditory questions. The time–frequency matrixes for the entire subdural electrode sites are presented as supplementary data on the website. ... Simultaneous recording of ECoG and vocal sound waves in patient 1. (A) An example of ECoG trace suitable for quantitative analysis is shown with a low-frequency filter of 53-Hz and a high-frequency filter of 300-Hz. Vocal sound waves were simultaneously recorded with intracranial ECoG. The time-lock trigger was placed at the onset of patient's vocalization. (B) Vocal sound wave on Cool Edit Pro Software is shown, and this was used to visually and audibly aid in the manual determination of the onset of the patient's vocalization. ... In vivo animation of auditory-language-induced gamma-oscillations in patient 1. Gamma-augmentation (50 to 150 Hz) initially involved the posterior part of the superior temporal gyrus. At 600 ms prior to the onset of patient's vocalization, gamma-augmentation in that area gradually subsided, and began to involve the most posterior part of middle temporal gyrus, the inferior frontal gyrus and the medial superior frontal gyrus. Immediately prior to the onset of vocalization, gamma-augmentation began to involve the pre- and post-central gyri. At 70 ms after the onset of vocalization, gamma-augmentation began to involve the posterior part of the superior temporal gyrus.
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  • Evolution of ξ(t)/π in the phase space difference for a CPG with N=4 oscillators and P=3 patterns ξ11=(π,0,0), ξ22=(0,π,0) and ξ43=(0,0,π). ... Schematic representation of the model. The model has three main blocks: the central pattern generator CPG, the CPG–robot interface and the virtual robot. The CPG has a pacemaker ψ, a number of P stored patterns ξk with phase instants τk, where k=1,…,P, and a retrieval network with N phase oscillators. We consider three external inputs from the environment to the system: I1(t) and I2(t) to the CPG, and, I3(t) to the interface CPG–robot. ... Phase oscillators
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  • Relative variation of the particle volume fraction of the electronanofluidized bed as a function of the peak field strength E0 for different humidity conditions of the fluidizing air. Electric field oscillation frequency and superficial gas velocity are fixed to 20Hz and vg=2.7cm/s, respectively. In the case of the humidified air, the bed was previously subjected to a fixed superficial gas velocity vg=0.7cm/s for periods of time of 30min and 55min, respectively (indicated). ... Relative variation of the particle volume fraction of the electronanofluidized bed as a function of the field strength for three different waveform types. Top: Data is shown as a function of the peak field strength E0. Bottom: Data is shown as a function of the root-mean-squared field strength Erms (Erms=E0 for square wave, Erms=E0/2 for sine wave, Erms=E0/3 for triangular wave). Electric field oscillation frequency and superficial gas velocity are fixed to 20Hz and vg=2.7cm/s, respectively. The inset is a log–log plot of the data, where the solid line shows E2 behavior. ... Relative variation of the particle volume fraction of the electronanofluidized bed as a function of the superficial gas velocity. Electric field oscillation frequency and strength are fixed to 500Hz and E0=1.25kV/m (square wave), respectively. The lines are predicted curves by the model. Solid line: complex-agglomerate charge Q∗∗0=1.9×10−14C. Dotted line: Q∗∗0=1×10−14C. Dashed line: Q∗∗0=3×10−14C. ... Relative variation of the particle volume fraction of the electronanofluidized bed as a function of the oscillation frequency of the alternating electric field. Peak field strength is fixed to 1.25kV/cm. Data is shown for three different values of the superficial gas velocity vg (indicated). Inset: Photographs of the electronanofluidized bed at 1Hz (left) and 20Hz (right).
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  • Mapping table of the small-signal model in frequency domain. ... Demonstration of pin chasing grinding in an oscillating grinding machine. ... Oscillating grinding machine
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  • The experimental results of response frequency as a function of different velocities and for different plates fluttering motion. ... Response frequency of flow induced rotation versus vortex shedding frequency. ... Natural frequency... (a)Time series for the rotation of the hinged flat plate about the vertical axis submitted to a uniform current (Re=1.26×105), and (b) the respective frequency domain response.
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  • ECoG frequency alteration induced by a seizure and subsequent administration of midazolam in patient 1. Forty subdural electrodes on the left frontal lobe (33 on the lateral surface and 7 on the medial surface), 17 electrodes on the left parietal lobe (14 on the lateral surface and 3 on the medial surface), and 16 electrodes on the left temporal lobe (12 on the temporal neocortex and 4 on the medial temporal region) were included in further analyses. An electrographic seizure occurred in the epilepsy monitoring unit, when the patient had verbal communication with a physician. The seizure discharges (red arrows in [C] and [D]) were characterized by paroxysmal rhythmic discharges at alpha and sigma range, followed by rhythmic spike-and-wave discharges arising from the left superior frontal cortex overlying the tumor; the seizure discharge was slowly propagated to the adjacent left frontal neocortex. During this seizure event, the patient continued to communicate with the physician appropriately and denied having an epileptic seizure. Neither tremor nor clonic movement of the body was noted. Intravenous boluses of midazolam (0.1mg/kg) were given twice to abort the ongoing electrographic seizure and to reduce the risk of generalized tonic–clonic seizure. The seizure discharge lasted 10min. Quantitative assessment of ECoG amplitude spectra showed that the seizure discharge was initially characterized by focal augmentation of alpha and sigma amplitudes in the seizure focus followed by amplitude augmentation of widespread frequency bands as the seizure progressed. The seizure offset was characterized by sweep subsidence of amplitudes of all eight frequency bands but delta band in the seizure focus. The non-epileptic brain region distant from the seizure focus (i.e.: the inferior-frontal region, parietal lobe, temporal neocortex as well as the medial temporal lobe structure) showed gradual augmentation of sigma-oscillations (best shown by a blue arrowhead in [E]) with a waxing and waning pattern. [F–I] show z-score maps (standard deviation score maps) of ECoG spectral amplitudes. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.) ... In-vivo animation of spectral amplitudes altered by a seizure and subsequent administration of midazolam in patient 2. An electrographic seizure was associated with augmentation of widespread frequency bands in the left medial temporal lobe region. The seizure offset was associated with subsidence of such amplitude augmentation in the left medial temporal lobe region. Following administration of midazolam, gradual sigma-augmentation was noted in the widespread region (including both medial temporal lobe structures) with a waxing and waning pattern. SD: standard deviation score also known as z-score. ... Gamma-oscillations... ECoG frequency alteration induced by a seizure and subsequent administration of midazolam in patient 2. Twenty-six subdural electrodes on the right frontal lobe, 15 electrodes on the right parietal lobe, 46 electrodes on the right temporal lobe (39 on the temporal neocortex and 7 on the medial temporal region), 8 electrodes on the right occipital lobe, and 10 electrodes on the left temporal lobe (4 on the temporal neocortex and 6 on the medial temporal region) were included in further analyses. An electrographic seizure occurred in the epilepsy monitoring unit, when the patient was asleep. The seizure discharges (denoted by a red arrow in [C]) were characterized by paroxysmal rhythmic discharges involving alpha and sigma bands, followed by rhythmic spike-and-wave discharges arising from the left medial temporal region; the seizure discharge was slowly propagated to the adjacent left temporal lobe region. During this seizure event, the patient did not show clinical changes. Neither tremor nor clonic movement of the body was noted. This seizure was considered as simple partial seizure, since no alteration of consciousness was noted when another electrographic seizure event showing a similar ECoG finding occurred during awake state. An intravenous bolus of midazolam (0.1mg/kg) was given in order to abort the ongoing electrographic seizure. The seizure discharge lasted 40s. Quantitative assessment of ECoG amplitude spectra showed that the seizure discharge was initially characterized by focal augmentation of alpha and sigma amplitudes in the seizure focus followed by amplitude augmentation of widespread frequency bands as the seizure progressed. Following the seizure offset, the non-epileptic brain region distant from the seizure focus showed gradual augmentation of sigma-oscillations (denoted by blue arrowheads in [D]) with a waxing and waning pattern. [E–G] show z-score maps (standard deviation score maps) of ECoG spectral amplitudes. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.) ... ECoG frequency alteration induced by sedation using midazolam and subsequent general anesthesia induction in patient 3. Thirty-seven subdural electrodes on the left frontal lobe (31 on the lateral surface and 6 on the medial surface), 33 electrodes on the left parietal lobe (27 on the lateral surface and 6 on the medial surface), 26 electrodes on the left temporal lobe (20 on the temporal neocortex and 6 on the medial temporal region), 4 electrodes on the left medial occipital region, 7 electrodes on the right medial frontal region, 3 electrodes on the right medial parietal region, and 2 electrodes on the right medial occipital region were included in further analyses. An intravenous bolus of midazolam (0.03mg/kg) was given in order to provide sedation prior to induction of general anesthesia. Prior to the administration of propofol, significant augmentation of sigma amplitudes was noted in the left medial temporal region (denoted by blue arrowheads in [C]). Two and a half minutes after administration of midazolam, general anesthesia was induced using an intravenous bolus of propofol (2.5mg/kg); sweep reduction in the amplitudes of all eight frequency bands was noted in the entire electrode sites. Visual assessment of ECoG recording showed electrical silence lasting for 60s [D]. Subsequently, ECoG recording showed a burst-suppression pattern characterized by waxing and waning of ECoG amplitudes of all frequency bands (see Video S3). [E–G] show z-score maps (standard deviation score maps) of ECoG spectral amplitudes. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.) ... In-vivo animation of spectral amplitudes altered by a seizure and subsequent administration of midazolam in patient 1. An electrographic seizure was associated with augmentation of widespread frequency bands (including the sigma band) in the left superior frontal region. Augmentation of low-frequency (32–64Hz), high-frequency (64–100Hz) and very high-frequency gamma-oscillations (100–200Hz) was noted in the presumed seizure focus in the left superior frontal gyrus. The seizure offset was associated with subsidence of such amplitude augmentation in the left superior frontal region. Following administration of midazolam, gradual sigma-augmentation was noted in the widespread region (including the medial temporal lobe structures) with a waxing and waning pattern. SD: standard deviation score also known as z-score.
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  • Out of phase oscillations... Detailed view of the mode amplitudes during the rotating oscillations for Model C. ... Initial growth of oscillations for Model C after an artificial perturbation was introduced at a simulation time of 1s. ... Detailed view of the mode amplitudes during the rotating oscillations for Model B. ... Progression of the radial power during the out-of-phase oscillations of the simulated turbine trip event for Model E. ... Parameters calculated for Model B during the stable limit cycle oscillations.
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  • (a) The logarithmic MSE values of the estimated IF obtained by NSFTT with different frequency bands for different noise levels and (b) the comparison of IF estimation between NSTFT, STFT, and WTSST. ... (a) The NSTFT representation for the 4th and 5th harmonic of the vibration signal and the extracted IF based on NSTFT representation, (b) the extracted IF of the 4th harmonic, and (c) the spectrum of its oscillation part. ... Instantaneous frequency... Nonlinear squeezing time–frequency transform... Time–frequency analysis
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  • Cross-frequency coupling... Raw signals in pre and post-injection period (0–15min after administration) of 10mg/kg of ketamine. Raw and decomposed traces into predominant frequency bands of LFPs recorded from the motor cortex of a representative animal. Ketamine increases the amplitude of low-gamma (LG), high-gamma (HG) and high frequency oscillations (HFO) bands. Note the coincidence of phasic increases in the amplitude of the HFOs and the valley of the delta oscillations, mainly during the post-ketamine period. ... High-gamma and high frequency oscillations are phase-locked to delta–theta oscillations. (A) Example of the evolution of the CFC for the Cx of a representative animal. Comodulograms computed across the five different periods analyzed (upper panels) show that in basal condition, delta activity mainly modulates HG oscillations (−15 to 0min); then ketamine produces a shift in the modulation frequency to theta values (0–15min) together with an increase in HFO and HG modulation. By the end of the recording, theta frequency shifts again to delta and modulation goes back to basal. These effects, together with the preferred phase of coupling can be observed by computing the average of the energy of oscillatory activity from 20 to 200Hz using the troughs of the slow oscillations as a trigger (lower panel). (B) Distribution of preferred phases of coupling is consistent for all the time segments. Rows show the normalized amplitude for HFO and HG respectively. Ketamine does not change the preferred phase over time which peaks at the troughs of delta–theta activity. ... Between-structure HFO synchronization is increased by the effect of ketamine. Time–frequency maps representing the ERCoh (A) and PLV (B) between the motor cortex and CPU using the Cx delta–theta phase trough time points as trigger for the analysis (see methods) of a representative animal. In basal condition (−15 to 0min, left column) and for the HG band, phasic events of interaction between structures are detected only for specific phases (the troughs) of the delta wave (superimposed white traces). After ketamine administration interactions in the HFO band are greatly increased (45–60min, right column). Similar results are obtained when choosing the activity of the second structure to set the trigger (data not shown). ... Ketamine alters intra-site phase-to-amplitude CFC patterns. (A) Time-course of CFC patterns (grand average across all the animals) for pre and post-injection periods. The comodulograms show coupling interactions between the phase of the activity in the delta–theta range and the amplitudes of HG and HFO activities. During the basal period CFC at HG and HFO bands exist. After ketamine administration, a shift in the modulating (phase) frequency occurs; changing from delta (basal) to theta (first post-ketamine periods) and again to delta (last recording segment) and MI is greatly increased for HFO and HG. (B) MI values for all the structures and time segments.
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  • A study of the plane Poiseuille flow of a micellar aqueous solution of cetylpyridinium chloride 100mM and sodium salicylate 60mM was performed in this work. The experiments were run at 27.5°C under controlled pressure using a transparent flow cell, where simultaneous measurements of transmitted light intensity, pressure drop and flow rate were performed in order to asses the flow stability. Particle image velocimetry (PIV) was also used to analyze the flow kinematics upstream of the contraction. Different regimes were observed in the flow curve, including shear banding and spurt. In the high shear rate branch the flow became unstable and was composed by asymmetric shear bands of structured and isotropic fluid, which oscillated with respect to the zero-shear stress plane. Symmetric lip vortices were observed to grow upstream of the contraction, and then to oscillate and decrease their average length under unstable flow. The shear bands downstream of the contraction oscillated in the same way as upstream vortices, with a frequency that increased along with the flow rate. Finally, the oscillating flow upstream of the contraction produced jets or spurts of highly oriented material followed by recoiling, akin to those reported in the melt fracture regime of polymers.
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