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Large-scale experiments examining spherical-flame propagation of propane–air flames up to a diameter of 1.2m were performed. Throughout these experiments, the growth of the Darrieus–Landau instability was directly observed and detailed measurements show that the increase of flame velocity follows a pattern of self-similar oscillatory growth that has not been previously reported. These oscillations are found to be the result of periodic growth and saturation of a narrow range of length scales that follows each generation of cell formation. Based on these observations, a new method to estimate the fractal-acceleration exponent is proposed based on the amplitude and frequency of these oscillations. Comparisons between the fractal exponents derived by this method and a direct power law fit show reasonable agreement with one another, as well as with values reported by previous studies.
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Bidirectional higher frequency intraburst epileptiform activities have different onset locations compared to lower frequency activity. (A) Four field electrodes (Ch1–Ch4) placed along the septotemporal axis of the hippocampus (left inset) record two consecutive epileptiform bursts. The initial burst begins at the temporal region (dashed vertical line), while higher frequency oscillations emerge from the septal region (solid vertical lines). (B) Four field electrodes (Ch1–Ch4) placed along the septotemporal axis of the hippocampus (left inset) record two consecutive epileptiform bursts. The initial burst begins at the septal region (dashed vertical line), while higher frequency oscillations emerge from the temporal region (solid vertical lines). (C) Latency graph (single seizure) plotting the differences in the relative times of the higher frequency epileptiform activity across the four channels shows bidirectional activity of the intraburst activity. The origin of the lower frequency depolarization was superpositioned on the latency graph near their respective region of onset (solid horizontal line) and it can be seen that at certain timepoints during the seizure, the lower frequency burst originates at a different location than their corresponding higher frequency components (arrows). ... Optical visualization of late seizure bidirectionality. (A1) In a different preparation, the orientation of the hippocampus and the recording electrode in the imaging chamber are shown. The area visualized is in the boxed region. (A2) Field recording (E) of two late seizure bursts and their corresponding optical traces (O) extracted from six locations in the photodiode array (location color-coded in A1) lying along the septotemporal axis. (A3) Analysis of the event initiation as seen by the optical traces reveals that the first burst has a septal origin (○, expanded from panel A2) while the consequent burst has a temporal origin (⋄). (A4) Pseudo-colored multiframe display of the beginning of the epileptic bursts. Each row represents a consecutive event (right inset; start time = 0 to 6 ms, Δt = 3 ms). Silent time between events omitted for visualization. Bursts initiated at septal (○) and temporal (⋄) locations along the septotemporal axis (dashed region). (B1) In a different preparation, the orientation of the hippocampus and the recording electrode in the imaging chamber. Area visualized in boxed region. (B2) Field recording (E) of the imaged burst and its corresponding optical traces (O) extracted from six locations in the photodiode array lying along the septotemporal axis (location color-coded in panel B1). Peak detection analysis of the optical traces reveals a separate site of onset of the higher and lower frequency components. (B3) Pseudo-colored multiframe display of the lower (1) and higher (2, 3) frequency epileptic activity. The lower frequency depolarization (⋄) originates at a more temporal location than the consequent higher frequency intraburst activity (○). Each row represents a consecutive time period (right inset; start time = 0 to 4 ms, Δt = 2 ms). ... Disconnection experiments. (A) The septal half of the hippocampus disconnected from the temporal half demonstrates epileptogenicity, as shown by recurrent, spontaneous seizures. Two channels (S1, S2) recorded seizures from the septal pole, and the mid-tissue region. Epileptiform activity seen after 10 min in low-Mg2+ ACSF. (B) The temporal half of the hippocampus disconnected from the septal half demonstrates epileptogenicity, as shown by recurrent, spontaneous seizures. Two channels (T1, T2) recorded seizures from the temporal pole, and the mid-tissue region. After five recurrent seizures, LRDs evolve in both channels. (C and D) Latency graphs (S1–S2; T1–T2) of three seizures from the septal (C, from boxed region in A) and temporal (D, from boxed region in B) regions reveal bidirectional epileptiform activity in the tissue. (E and F) Overlay of the latency graphs of the initial lower frequency component (●) of the burst and the subsequent higher frequency activity (□) reveals different sites of onset within the same bursts from the isolated septal (E) and temporal half (F). Expanded graph (inset) illustrates more clearly the differential sites of onset between these events.... Optical imaging of the origin of both the higher and lower frequency events of an epileptic burst. The initial lower-frequency component of the burst originates near the temporal region (lower region), while the subsequent higher-frequency events originate near the septal region (upper region). The septal hippocampus is located at the top of the window. The time lapse covers a period of about 500 ms (QuickTime; 3.3 MB). ... Network oscillators
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Normalized transverse sphere oscillation frequency as a function of reduced velocity. Present results: +, Sphere dynamics; ◊, PIV. Literature: m⁎=7.87 (Van Hout et al., 2010): □ fN=2.65Hz (represents measured natural frequency in medium). ○ m⁎=0.76; ▵ m⁎=2.83 (Govardhan and Williamson, 1997).
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Pharmacological modulation of spontaneous Ca2+ oscillations and effects of altered extracellular ionic milieu in Fluo-4 loaded differentiating chondrocytes of 2-day-old HDC. Representative confocal line-scan images and time courses of Fluo-4 fluorescence intensities are shown; horizontal and vertical calibrations are the same for all traces in panels (A)–(D). Horizontal lines under traces show the duration of treatments with pharmacons or altered extracellular ionic milieu. Acquisition of line-scan images started immediately after changing the bath solution on the cultures. Prior to that, normal functions were detected on each culture. (A) Spontaneous Ca2+ oscillations in normal ([Ca2+]e=1.8mM) Tyrode's solution. (B) After the non-selective cation channel-mediated Ca2+ entry blocker LaCl3 (500μM) and the store-operated Ca2+ entry and Ca2+ release-activated Ca2+ (CRAC) channel blocker YM-58483 (1μM) were applied in normal ([Ca2+]e=1.8mM) Tyrode's, Ca2+ oscillations ceased, although irregular fluctuations in basal cytosolic Ca2+ concentration remained detectable. (C) When the SERCA-blocker CPA (10μM) was co-administered with 500μM LaCl3 and 1μM YM-58483 in 1.8mM [Ca2+]e, Ca2+ oscillations were totally eliminated. (D) 3min after changing the bath solution to Ca2+-free Tyrode's, periodic oscillations could not be detected. Line-scan diagrams on panels (A)–(D) are representative data out of 4 independent experiments. ... Pooled data of Ca2+ oscillations gathered from series of X–Y images acquired from random visual fields of Fluo-4 loaded HDC on culturing days 1 and 2 with Zeiss LIVE 5 Laser Scanning Confocal Microscope. (A) Ratio of oscillating cells and frequency of repetitive Ca2+ transients on days 1 and 2 of culturing. Numbers above bars indicate the number of oscillating cells compared to all cells recorded. (B) Amplitude and full time at half maximum (FTHM) of Ca2+ oscillations in differentiating cells of HDC on culturing days 1 and 2. For both panels (A) and (B), while calculating the parameters of Ca2+ oscillations, only oscillating cells with round, chondroblast-like morphology were considered. Measurements were carried out on cultures from 4 independent experiments. Data represent mean±standard error of the mean (SEM). Numbers in parentheses above bars indicate the number of cells measured. Asterisks (*) mark significant differences (*Poscillating cells in 1- and 2-day-old HDC. ... Spontaneous Ca2+ oscillations in cells of HDC on day 2 of culturing. Prior to measurements, cells were loaded with Fluo-4-AM for 30min Ca2+ oscillations were observed without agonist stimulation in Tyrode's solution containing 1.8mM Ca2+ at room temperature. (A) Series of X–Y images were recorded from random visual fields of chondrifying cultures with Zeiss LIVE 5 Laser Scanning Confocal Microscope. These four representative frames were acquired at 6.5, 18.3, 29.6 and 54.4s during measurements. Arrows indicate differentiating chondrocytes with repetitive intracellular Ca2+ oscillations. (B) Time course of fluorescence intensities of the cells marked with arrows in panel (A). Fluo-4 fluorescence intensity values normalised to baseline fluorescence (F/F0) are plotted vs. time. Wide ranges of frequency and amplitude of oscillating cells were observed. ... Pooled data of Ca2+ oscillations obtained from series of X–Y images acquired from Fluo-4 loaded HDC in response to various treatments. Measurements were carried out with Zeiss LIVE 5 Laser Scanning Confocal Microscope. A total number of 500 images were recorded at each time point for each visual field; frame acquisition rate was 10s−1. (A) Percentage of oscillating cells before treatment (control), and 1, 3 or 5min after the application of bath solution containing 10μM nifedipine, or 500μM LaCl3 and 1μM YM-58483. Values were normalised to the untreated cells measured at 0min (control), and then at 1, 3 and 5min. Numbers in parentheses above bars show the number of cells measured. (B) Amplitude of Ca2+ oscillations, normalised to values of untreated control cells. Numbers in parentheses above bars represent the number of oscillating cells measured. (C) Frequency of Ca2+ oscillations normalised to the control. Numbers in parentheses above bars show the number of cells measured. For panels (A)–(C), oscillating cells with round morphology in the same random visual field were recorded at all four time points. Differentiating cartilage colonies were only used for a single measurement series and then were discarded. Graphs represent pooled data of 3 independent experiments, measuring random visual fields of 5 colonies for each treatment. Asterisks (*) mark significant differences (*P<0.05) between parameters of treated vs. control cells at respective time points. ... Refined model showing known components of Ca2+ homeostasis and signalling pathways that modulate Ca2+ oscillations in developing chondrocytes. Ca2+ can enter the cell via voltage-operated Ca2+ channels (VOCCs), P2X4 purinergic receptors, NMDA receptors or TRP channels; changes in resting membrane potential are mediated by voltage-gated K+ channels. ATP is secreted to the extracellular space via putative connexin 43 hemichannels. Activation of G-protein coupled P2Y purinergic receptors cause Ca2+-release from the endoplasmic reticulum (ER) via inositol-1,4,5-trisphosphate receptors (IP3R). Depletion of the Ca2+ stores cause aggregation of stromal interaction molecules (STIM1/STIM2), which are the Ca2+ sensors of the ER and trigger the opening of the store-operated Orai1 channels. Reuptake of Ca2+ to the ER is mediated by the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) and the Na+–Ca2+ exchanger (NCX). See text for details.
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Frequency response and optimal output power. (a) Peak-to-peak voltage and (b) output current of the Hy-TENG versus various vibration frequencies. Straight lines represents the half of maximum value. Both the output voltage and the current show resonance at 5Hz, and the FWHM of the output voltage and current are 22Hz and 250Hz, respectively. (c) Dependence of the output voltage and current at various load resistances. (d) Instantaneous output power density and average power of the Hy-TENG versus various load resistances.
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Simulation of nuclear movement. (A) Schematic diagram illustrating the microtubule-mediated nuclear movement in a fission yeast cell. Vn and ωn are the translational and rotational velocities of the nucleus, respectively. R is the nuclear radius and θi (−πfrequencies used in the simulations are indicated (0.2min−1, 0.4min−1, and 0.6min−1), and error bars represent SD. (E) Probability distributions of the peak amplitudes of the translational displacements of the nucleus from model predictions and experimental measurements. Experimental datasets were obtained from Fig. 2E. The values of the rescue and catastrophe frequencies used in the simulations are indicated, and error bars represent SD.
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A time course of glutamate-induced GFP-PKCγ translocation versus a time course of Ca2+ signals in hippocampal astrocytes. (a) The time course analysis of repetitive GFP-PKCγ translocations (green trace) compared to the time course of intracellular Ca2+ oscillations measured with Ca2+ Crimson (red trace) resulting from the addition of 100 μM glutamate (final concentration). These dual measurements were made by rapidly switching between TIRF-excited GFP images (excitation: 488 nm) and epifluorescence-excited Ca2+ Crimson images (excitation: 568 nm). The images shown in Figure 1 represent the GFP-PKCγ fluorescence in the basal condition (Figure 1a) and during maximal translocation (Figure 1b). The time points when the images were taken are marked in the GFP-PKCγ trace. The relative fluorescence intensity represented by both traces was measured in the circular region marked in Figure 1. The maximum change in the relative fluorescence intensity was 1.2 for the GFP-PKCγ trace and 0.2 for the calcium trace. (b) The time course of intracellular Ca2+ concentration changes induced by glutamate (100 μM) in two astrocytes loaded with the Ca2+ fluorescent dye Fluo-3AM and analyzed by confocal microscopy. The oscillatory pattern shown was seen in 6 out of 14 experiments, with single transients and plateaus observed in the other experiments. The maximum change in relative fluorescence intensity was 1.5 ... Glutamate-induced oscillating translocation of DAG binding C1 domains. (a) Glutamate stimulation (1 mM) induced a marked plasma membrane translocation of the tandem DAG binding C1 domains of PKCδ (GFP-C12δ). The left and right panels show images taken before and after maximal translocation occurred. (b) The oscillating time course of the GFP-C12δ fluorescence intensity change in the two astrocytes shown in (a). The calibration bar represents 5 μm. Similar oscillations were observed in 9 out of 21 experiments. The maximum change in relative fluorescence intensity was 0.3. (c) The time course of plasma membrane translocation of a single DAG binding C1 domain from PKCγ (GFP-C1Aγ) measured in parallel with cytosolic Ca2+ oscillations after glutamate stimulation (1 mM). The GFP and the Ca2+ Crimson fluorescent recordings were performed as described in Figure 2a. In 4 out of 8 experiments, the GFP-C1Aγ showed a similar oscillating pattern, with each translocation event being preceded by a Ca2+ spike. The maximum change in relative fluorescence intensity was 0.2 for the GFP-C1Aγ trace and 0.2 for the calcium trace ... Periodic PKC activation as a negative feedback mechanism that supports the generation of astrocyte Ca2+ oscillations and waves. A proposed model of the positive and negative feedback mechanisms that control baseline Ca2+ spiking, Ca2+ oscillations, and waves. The two positive feedbacks that participate in the upstroke of each Ca2+ transient are shown on the left. DAG and IP3 are both expected to oscillate in this model, with each increase in IP3 and DAG being driven by Ca2+ activation of PLC. As shown in the schematic view on the right, periodic desensitization of the GPCR pathway by cPKC is then expected to support the termination of each Ca2+ spike by phosphorylating the GPCR, PLC, and other upstream signaling proteins. The same cPKC-mediated phosphorylation events would then generate a prolonged downregulation with a recovery rate that defines the time period (frequency) when the subsequent Ca2+ spike is triggered ... The effect of the expression of the tandem DAG binding domains of PKCδ (C12δ) on shape and duration of Ca2+ oscillations. Parallel measurements of GFP-C12δ translocation and Ca2+ signals in an astrocyte that exhibited slow baseline Ca2+ spikes. This type of slow Ca2+ transient was not observed in astrocytes in the absence of C1 domain expression. The two superimposed traces in the upper panel show a comparison of the time courses of Ca2+ spikes and repetitive plasma membrane translocation of GFP-C12δ after stimulation with 100 μM glutamate. The magnified view in the lower panel shows that the translocation of the C1 domain is delayed by a few seconds and that the GFP-C12δ translocation is triggered only after reaching a threshold in Ca2+ concentration. The maximum change in relative fluorescence intensity was 1.3 for the GFP-C12δ trace and 0.45 for the calcium trace
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IR spectra of zeolite LTA external surface using both (a) Morse Potential and (b) Harmonic Oscillator to simulate the OH bond stretch.
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Oscillating Water Column... Water elevation into the converter (wave gauge 4) for free oscillation test. Natural frequency found are 0.91±0.03s-1 for laboratory test (plain line) and 0.91±0.04s-1 for simulation (dashed line).
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Experiments on a robotic fish controlled by the general CPG controller. The robotic fish starts with forward swimming in sinusoidal oscillation form, and then transforms to turning right in sinusoidal oscillation form, and then transforms to turning right in sawtooth oscillation form, and at last transforms to backward swimming in oscillation form. All the transformations are quickly and quite smooth. ... 1initialization2repeat3if locomotion pattern transition4 then Update CPG control parameters5 if Oscillating form need change6 then Calculate corresponding ϕi and ϕ̇i7 else Update amplitude ri and its derivative ri̇8 Update offset xi and its derivative xi̇9 Update phase ϕi and its derivative ϕ̇i10 Update output angle θi11 if min(ϕi)≥2π12 then ϕi←ϕi−2π13 until Received “stop control” from the up computer by wireless communication.... A typical CPG network with three oscillators. The inputs are the amplitudes Ri, the offsets Xi, phase differences φij, frequency ω and oscillating switching signal σ. The outputs are the angles of the joints θi. (i,j=1,2,3, and i≠j ). ... Snapshot sequence of transition from turning right with sawtooth-wave like oscillation to swimming backward in sinusoidal oscillation. The time step is 0.2s. ... Snapshot sequence of fish turning right with sawtooth-wave like oscillation. The time step is 0.2s. ... 3D animation of a robotic fish controlled by the general CPG controller. The robotic fish starts with forward swimming in sinusoidal oscillation form, and then transforms to turning right in sinusoidal oscillation form, and then transforms to turning right in sawtooth oscillation form, and at last transforms to backward swimming in oscillation form. All the transformations are quickly and quite smooth.
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