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ELECTRONIC TUBE OSCILLATORSC + THERMIONIC VALVE OSCILLATORS (ELECTRICAL OSCILLATION TECHNOLOGY)
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We extend the two-dimensional model of drug use introduced in Behrens et al. [1999, 2000, 2002] by introducing two additional states that model in more detail newly initiated (“light”) users’ response to the drug experience. Those who dislike the drug quickly “quit” and briefly suppress initiation by others. Those who like the drug progress to ongoing (“moderate”) use, from which they may or may not escalate to “heavy” or dependent use. Initiation is spread contagiously by light and moderate users, but is moderated by the drug’s reputation, which is a function of the number of unhappy users (recent quitters + heavy users). The model reproduces recent prevalence data from the U.S. cocaine epidemic reasonably well, with one pronounced peak followed by decay toward a steady state. However, minor variation in parameter values yields both long-run periodicity with a period akin to the gap between the first U.S. cocaine epidemic (peak ~1910) and the current one (peak ~1980), as well as short-run periodicity akin to that observed in data on youthful use for a variety of substances. The combination of short- and long-run periodicity is reminiscent of the elliptical burstors described by Rubin and Terman [2002]. The existence of such complex behavior including cycles, quasi periodic solutions, and chaos is proven by means of bifurcation analysis.
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We extend the two-dimensional model of drug use introduced in Behrens et al. [1999, 2000, 2002] by introducing two additional states that model in more detail newly initiated (“light”) users’ response to the drug experience. Those who dislike the drug quickly “quit” and briefly suppress initiation by others. Those who like the drug progress to ongoing (“moderate”) use, from which they may or may not escalate to “heavy” or dependent use. Initiation is spread contagiously by light and moderate users, but is moderated by the drug’s reputation, which is a function of the number of unhappy users (recent quitters + heavy users). The model reproduces recent prevalence data from the U.S. cocaine epidemic reasonably well, with one pronounced peak followed by decay toward a steady state. However, minor variation in parameter values yields both long-run periodicity with a period akin to the gap between the first U.S. cocaine epidemic (peak ~1910) and the current one (peak ~1980), as well as short-run periodicity akin to that observed in data on youthful use for a variety of substances. The combination of short- and long-run periodicity is reminiscent of the elliptical burstors described by Rubin and Terman [2002]. The existence of such complex behavior including cycles, quasi periodic solutions, and chaos is proven by means of bifurcation analysis.
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HSOs in cardiomyocytes with blockade of the SR functions. (A) Top, left: epi-illumination image of a myocyte expressed with AcGFP in Z-disks. Fluo-8 was loaded into the myocyte, and 200μM ryanodine and 4μM thapsigargin were present. Laser center is indicated (closed red circle). The yellow arrow indicates the sarcomere used for the analysis. Top, right: time-dependent changes in temperature induced by IR laser irradiation for 10s (2nd irradiation; see Fig. S1B for data of 1st, 2nd and 3rd irradiations). Given the distance from the laser center, the temperature in the sarcomeres indicated by the yellow arrow in Top, left was estimated to be 40.8°C. Bottom, left: enlarged view of the graph (2–6s) showing the occurrence of HSOs. Note that HSOs were induced in a delayed fashion (∼1.5s after the onset of heating). Bottom, right: enlarged view of the graph showing HSOs at the steady-state. Note no periodic F.I. (i.e., [Ca2+]i) changes in any of the graphs, due to the presence of ryanodine and thapsigargin. (B) Effect of heating on peak SLs during HSOs. IR laser irradiation (for 10s each) was applied three times consecutively. Minimal and maximal SLs, obtained at the peak of shortening and lengthening, respectively. (C) Effect of heating on the amplitude of HSOs. Amplitude was defined as maximal SL (at the peak of lengthening) minus minimal SL (at the peak of shortening) [cf. (B)]. (D) Effect of heating on the frequency of HSOs. (E) Effect of heating on the sarcomere shortening velocity during HSOs. Velocity was calculated based on our previous study employing SL nanometry [13]. In (B), (C), (D) and (E), data obtained 1.5, 5 and 8.5s after the onset of heating (i.e., beginning, middle and end of heating) were analyzed for 2nd and 3rd heating. Due to time delay of the appearance of HSOs [see (A) and Fig. S1B], data obtained 4, 6.5 and 9s after the onset of heating (i.e., beginning, middle and end of heating) were analyzed for 1st heating. ∗P<0.05 compared with the corresponding value obtained in the beginning of heating. #P<0.05 compared with the corresponding value obtained in the middle of heating. †P<0.05 compared with the corresponding value during the 1st heating. ‡P<0.05 compared with the corresponding value during the 2nd heating. ... Temperature dependence of the occurrence of HSOs. (A) Top: relationship between the distance from the laser center and ΔT in spontaneously beating myocytes, showing whether or not HSOs were induced by heat pulses. Myocytes were set on the microscopic system at the initial temperature of 25°C, and the heat pulse was given for 10s. The values of ΔT that induced HSOs are shown in orange, and those at which HSOs were not observed are shown in gray. The lowest and highest end of the temperature range for HSOs are shown in blue and red triangles, respectively. Bottom: temperature dependence of the state of sarcomeres in neonatal myocytes, i.e., spontaneous beating without HSOs (green) or spontaneous beating with HSOs (yellow), or contraction [with no oscillations (red)]. Cell numbers are indicated on left. Of the total 16 myocytes tested, four myocytes (#13–16) did not exhibit HSOs (one even at 41.5°C). Note that the lowest temperatures at which HSOs occur in various myocytes are likely lower than those shown in this graph (Table 2). (B) Top: same as in (A) top in non-beating myocytes, showing whether or not HSOs were induced by heat pulses. As in (A), myocytes were set on the microscopic system at the initial temperature of 25°C, and the heat pulse was given for 10s. The values of ΔT that induced HSOs are shown in orange, and those at which HSOs were not observed are shown in gray. The lowest and highest end of the temperature range for HSOs are shown in blue and red triangles, respectively. Bottom: temperature dependence of the state of sarcomeres in neonatal myocytes, either relaxation (green), HSOs (yellow) or contraction [with no oscillations (red)]. Cell numbers are indicated on left. Of the total 8 myocytes tested, one myocyte (#5) did not exhibit relaxation, presumably because the lowest temperature at which observation started was relatively high (i.e., 40.6°C). ... Summary of maximal and minimal temperatures for HSOs in beating and non-beating myocytes. Tmax (Tmin), maximal (minimal) temperature at which HSOs were observed in the experiments of Fig. 3. Note that the real Tmin value may be even lower than the value (∼38.6°C) in this table and hence closer to the body temperature of rat neonates [22] in beating myocytes, because in all myocytes showing HSOs, the oscillations were already induced at the lowest temperatures (37–40°C; see Fig. 3A) given. ΔT, Tmax minus Tmin. n, 12 and 8 for beating and non-beating myocytes, respectively. ... HSOs in spontaneously beating cardiomyocytes. (A) Epi-illumination image of a myocyte expressed with AcGFP in Z-disks. Fluo-8 loaded into the myocyte. Laser center is indicated (closed red circle). A yellow arrow indicates the sarcomere for the analysis in (C). (B) Top: changes in temperature induced by IR laser irradiation for 10s. Bottom: relationship of the distance from laser center and ΔT. Given the distance from the laser center, the temperature in the sarcomeres, indicated by the yellow arrow in (A), was estimated to be 39.7°C. (C) Left, top: time-dependent changes in SL and F.I. in the myocyte in (A) upon IR laser irradiation (2nd irradiation; see Fig. S1A for data of 1st and 2nd irradiations). F.I. was obtained from the whole myocyte in the view window. Heat pulse was given for 10s, i.e., from 3 to 13s (in gray). Due to the temperature sensitivity of fluorescence [23], F.I. was decreased (or increased) as heat pulse was given (or ceased). Left, bottom: enlarged view of the graph showing SL on top from 6 to 10s. HSOs are clearly seen coexisting with [Ca2+]i-dependent spontaneous beating. Right, top: FFT analysis for the changes in F.I. from 4.7 to 12.5s. Right, bottom: same as in Right, top for the changes in SL. Note that while only one peak is present for F.I., two different components, i.e., slow and fast components, are seen for SL (with the former corresponding to that for F.I.; see arrows). (D) Left: effects of IR laser irradiations on the frequency of Ca2+ transient. Closed red circles with error bars, average values; open circles in various colors without error bars, individual data. ∗Pfrequency of HSOs. Closed black circles with error bars, average values; open circles in various colors without error bars, individual data. The HSO frequency was not significantly changed during the course of heating (both 1st and 2nd heating). Data obtained 1.5, 5 and 8.5s after the onset of heating were analyzed. n=24 (12 cells). ... Summary of the effects of heating on the cross-bridge attachment rate and the properties of HSOs. Our mathematical model predicts that heating increases amplitude and decreases frequency via an increase in the attachment rate constant of cross-bridges, α. Arrows, directions of change. See [19,20] for details of our model.
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optoelectronic oscillator
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high frequency oscillations... Grand average topographical maps of log10 spectral power of high frequency activity in boys with autism and typically developing boys and scalp distribution of between-group differences (Mann-Whitney U-test). High spectral power at prefrontal, mid-temporal and occipital electrode positions is explained by strong contribution of miogenic artifacts. Boys with autism have significantly higher spectral power at the electrode positions distant from the sources of miogenic artefacts.
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