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Phase Delay (phase + delay)
Selected AbstractsMeasurement of atmospheric water vapour on the ground's surface by radio wavesHYDROLOGICAL PROCESSES, Issue 11 2001Tokuo Kishii Abstract Water vapour in the atmosphere and various meteorological phenomena are essential to the understanding of the mechanism of the water cycle. However, it is very difficult to observe water vapour in the atmosphere because the quantities are usually observed at a single point not over long intervals or in a specific plane or volume. Accordingly, the use of radio waves is considered to be necessary to observe water vapour. Radio waves can be transmitted over long intervals and across large areas, and generally speaking, the characteristics of radio waves change due to material in the atmosphere, especially water vapour. Usually absorption is used to observe the quantity of water vapour. But the relationship between absorption and the quantity of water vapour is not linear, so we try to utilize the phase difference between two radio waves as an alternative method. First, the relationship between the phase delay and the water vapour was induced by a physical equation and the resulting phase delay was found to be proportional to the quantity of water vapour. Furthermore, the phase difference between two separate points was observed by use of two radio waves in the field, specifically 84 GHz and 245 GHz. For reference and comparison, water vapour density in the atmosphere was simultaneously observed by meteorological observation. As a result, the density of the water vapour was found to be proportional to the phase difference between the two radio waves. The result also shows that this method is able to measure the diurnal changes in water vapour density in each season. Copyright © 2001 John Wiley & Sons, Ltd. [source] Fourier transformation of arterial Doppler waveforms of the lower extremityJOURNAL OF CLINICAL ULTRASOUND, Issue 6 2004Hong Gi Lee MD Abstract Purpose Although it is well known that the normal, triphasic pulsatile arterial Doppler waveform changes in shape as flow is impaired, interpretation of the waveform has largely been subjective. We aimed to describe the Doppler waveforms of the lower extremity objectively using Fourier transformation. Methods Sixty-eight zero-crossing detector arterial recordings from 25 lower extremities were grouped as follows: group 1, no ischemic symptoms with an ankle-brachial index (ABI) > 0.9 (n = 17, 8 limbs); group 2, no ischemic symptoms with ABI < 0.9 (n = 18, 5 limbs); group 3, symptoms of claudication (n = 19, 7 limbs); group 4, rest pain or tissue loss (n = 14, 5 limbs). The waveforms were Fourier transformed and their amplitudes and phases were compared up to the third harmonic (H3). Results Amplitudes of both the fundamental (H1) and second harmonic (H2) were predominant in group 1. In contrast, amplitudes of the H2 and H3 decreased with altered flow (p < 0.0001 for group 1 versus others). The phases of the H1 and H2 were delayed with altered flow (p < 0.05 for group 1 versus others). Phases of the H1 were different between group 2 and 4 (p < 0.05). The difference of phase between the H3 and H1 was shortened with altered flow (p < 0.05 for group 1 or 2 versus group 4). Multivariate analysis revealed that the relative amplitudes of the H2 and H3, the phases of the H1 and H2, and the relative phase of the H3 were significant discriminators among the groups. Conclusion Abnormal waveforms could be characterized by the predominant amplitude of the H1, phase delay of the H1 and H2, and shortening of the relative phase of the H3. These parameters may be useful in the evaluation of Doppler waveforms in patients with peripheral arterial disease. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:277,285, 2004 [source] Effect of stimulation of endogenous melatonin secretion during constant light exposure on 6-sulphatoxymelatonin rhythmicity in ratsJOURNAL OF PINEAL RESEARCH, Issue 1 2000D.J. Kennaway When light is presented unexpectedly at night to rats, melatonin production and secretion is acutely inhibited and the time of onset of production on the subsequent night is altered. In a series of experiments, we examined the effects of 6,12 hr light (200 lux) at night on melatonin metabolite excretion (6-sulphatoxymelatonin, aMT.6S). During the light exposure, we administered isoproterenol to stimulate endogenous production of melatonin by the pineal gland to determine if replacement of melatonin would block any phase shifting effects of the light. Exposure to 6 hr of light either during the first or second half of the night suppressed aMT.6S excretion during the light treatment and delayed the onset of melatonin secretion by 3.7±0.6 and 2.5±0.6 hr, respectively, compared to a change of 0.5±0.1 hr in animals maintained in darkness. Twelve hours light exposure (i.e. one night of continuous light) suppressed aMT.6S excretion completely and resulted in a delay in the onset the next night of 2.1±0.7 hr. When propranolol (10 mg/kg) was administered at 2-hr intervals during darkness, aMT.6S excretion was suppressed throughout the night, but on the subsequent release into constant darkness the onset of excretion was not delayed (0.6±0.1 hr delay). Administration of isoproterenol (10 mg/kg) to animals in constant light, at the time of expected lights off (CT12), and 5 hr later (CT17) resulted in an increase in melatonin production and aMT.6S excretion that was similar in duration and amount to the control night. The stimulation of endogenous melatonin production failed to block the phase shifting effects of the light exposure and, in fact, appeared to potentiate the delay at least on the first night (4.2±0.9 hr). The timing of the release into constant darkness following the light treatment had an unexpected effect on melatonin production on the cycle after treatment. Thus, animals exposed to 12 hr light and released into darkness at the normal time of lights off as above had a delay of about 2 hr and excreted 71±18% of the aMT.6S excreted on a control night. Animals released into darkness at the expected time of lights on failed to excrete more than 20 pmol/hr (i.e. no onset of excretion could be determined) at any time on the first subjective night after light treatment, which was no different from the excretion during the light treatment. On the next subjective night, the onset was delayed as expected and the amount of aMT.6S produced was restored. Treatment with isoproterenol at CT12 and CT17 failed to affect either the amount of aMT.6S excreted on the first subjective night after light treatment or the phase delay on the second night after treatment. The failure to produce melatonin on the first subjective night after 12 hr light exposure and release into darkness at CTO was not due to failure at the level of the pineal gland since injection of isoproterenol at CT12 and CT17 on the first subjective night after light restored the normal amount of melatonin production. These results suggest that the absence of melatonin during light stimulation at night is not responsible for the phase delay in melatonin production and excretion on subsequent nights. The basis of the failure of the rats to commence melatonin production following 12 hr extended light exposure followed immediately by continuous darkness is not known. [source] Alterations in Circadian Rhythm Phase Shifting Ability in Rats Following Ethanol Exposure During the Third Trimester Brain Growth SpurtALCOHOLISM, Issue 5 2006Hiromi Sakata-Haga Background: Disruptions in sleep and feeding rhythms are among the consequences of prenatal alcohol exposure. Previously, we reported that ethanol exposure during the second trimester equivalent in rats produces long-lasting impairments in circadian system functioning. In the present study, we examined the effects of ethanol exposure during the third trimester equivalent brain growth spurt on the development of the circadian clock system. Methods: Sprague,Dawley male rat pups were exposed to 6.0 g/kg/d ethanol via an artificial rearing procedure on postnatal days (PD) 4 through 9 (EtOH). An artificially reared gastrostomized control group and a normally reared suckle control group were also included. At 10 to 12 weeks of age, wheel-running behavior was measured continuously under a 12-hour/12-hour light/dark (LD) cycle. Thereafter, subjects were exposed to a 6-hour phase delay of the LD cycle, and the ability to adjust to the new LD cycle was evaluated. Results: Before the phase delay, onset time of activity and acrophases of activity in all 3 groups were not significantly different from one another. After the 6-hour LD cycle delay, EtOH subjects were slower to adapt to the new cycle compared with both control groups, as measured by both activity onset and acrophase. Throughout the experiment, activity levels of EtOH subjects tended to be higher compared to both controls. Conclusions: These data demonstrate that ethanol exposure during the third trimester disrupts the ability to synchronize circadian rhythm to light cues. Disruptions in circadian regulation may cause abnormal behavioral rhythmicity, such as disrupted sleep and feeding patterns, as seen in individuals prenatally exposed to ethanol. [source] Disturbances in melatonin and core body temperature circadian rhythms after minimal invasive surgeryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2007I. Gögenur Background:, Sleep disturbances, fatigue and reduced general well-being frequently occur after minimal invasive surgery. The circadian rhythms of melatonin and core body temperature are central to the regulation of normal sleep. The aim of this study was to assess changes in these circadian rhythms after laparoscopic cholecystectomy. Methods:, Twelve women were studied before and after laparoscopic cholecystectomy. The major urinary melatonin metabolite, 6-sulphatoxymelatonin (aMT6s), and the core body temperature were measured for 1 day before and 1 day after surgery. The basal and maximum secretion of aMT6s were determined, as well as the timing and amplitude of aMT6s and the temperature rhythm. The patients' rest,activity and calculated sleep parameters were assessed by actigraphy. Results:, A significant delay in the timing of aMT6s rhythm was observed after surgery [median (range) peak time of aMT6s: after surgery, 05:49 h (02:57,08:23 h); before surgery, 04:32 h (02:18,06:49 h); P, 0.05]. The amplitude of the aMT6s rhythm was also significantly decreased after surgery [after surgery, 7.1 ng aMT6s/mg creatinine (1,15.9 ng); before surgery, 13.2 ng aMT6s/mg creatinine (2.9,22.7 ng); P, 0.005]. There was almost a12-h phase delay of the core body temperature rhythm after surgery [peak time: before surgery, 17:39 h (15:17,22:06 h); after surgery, 05:14 h (03:24,21:43 h); P, 0.01]. Conclusions:, Following laparoscopic cholecystectomy, there was a delay in the timing of the aMT6s rhythm and a decreased evening decline in the temperature rhythm. [source] 3D models of radiatively driven colliding winds in massive O + O star binaries , III.MONTHLY NOTICES OF THE ROYAL ASTRONOMICAL SOCIETY, Issue 4 2010Thermal X-ray emission ABSTRACT The X-ray emission from the wind,wind collision in short-period massive O + O star binaries is investigated. The emission is calculated from 3D hydrodynamical models which incorporate gravity, the driving of the winds, orbital motion of the stars and radiative cooling of the shocked plasma. Changes in the amount of stellar occultation and circumstellar attenuation introduce phase-dependent X-ray variability in systems with circular orbits, while strong variations in the intrinsic emission also occur in systems with eccentric orbits. The X-ray emission in eccentric systems can display strong hysteresis, with the emission softer after periastron than at corresponding orbital phases prior to periastron, reflecting the physical state of the shocked plasma at these times. Our simulated X-ray light curves bear many similarities to observed light curves. In systems with circular orbits the light curves show two minima per orbit, which are identical (although not symmetric) if the winds are identical. The maxima in the light curves are produced near quadrature, with a phase delay introduced due to the aberration and curvature of the wind collision region. Circular systems with unequal winds produce minima of different depths and duration. In systems with eccentric orbits the maxima in the light curves may show a very sharp peak (depending on the orientation of the observer), followed by a precipitous drop due to absorption and/or cooling. We show that the rise to maximum does not necessarily follow a 1/dsep law. Our models further demonstrate that the effective circumstellar column can be highly energy dependent. Therefore, spectral fits which assume energy-independent column(s) are overly simplified and may compromise the interpretation of observed data. To better understand observational analyses of such systems we apply Chandra and Suzaku response files, plus Poisson noise, to the spectra calculated from our simulations and fit these using standard xspec models. We find that the recovered temperatures from two- or three-temperature mekal fits are comparable to those from fits to the emission from real systems with similar stellar and orbital parameters/nature. We also find that when the global abundance is thawed in the spectral fits, subsolar values are exclusively returned, despite the calculations using solar values as input. This highlights the problem of fitting oversimplified models to data, and of course is of wider significance than just the work presented here. Further insight into the nature of the stellar winds and the wind,wind collision region in particular systems will require dedicated hydrodynamical modelling, the results of which will follow in due course. [source] Resetting the brain clock: time course and localization of mPER1 and mPER2 protein expression in suprachiasmatic nuclei during phase shiftsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2004Lily Yan Abstract The mechanism whereby brief light pulses reset the mammalian circadian clock involves acute Per gene induction. In a previous study we investigated light-induced expression of mPer1 and mPer2 mRNA in the suprachiasmatic nuclei (SCN), with the aim of understanding the relationship between gene expression and behavioural phase shifts. In the present study, we examine the protein products of mPer1 and mPer2 genes in the core and shell region of SCN for 34 h following a phase-shifting light pulse, in order to further explore the molecular mechanism of photic entrainment. The results indicate that, during the delay zone of the phase response curve, while endogenous levels of mPER1 and mPER2 protein are falling, a light pulse produces an increase in the expression of both proteins. In contrast, during the advance zone of the phase response curve, while levels of endogenous mPER1 and mPER2 proteins are rising, a light pulse results in a further increase in mPER1 but not mPER2 protein. The regional distribution of mPER1 and mPER2 protein in the SCN follows the same pattern as their respective mRNAs, with mPER1 expression in the shell region of SCN correlated with phase advances and mPER2 in the shell region correlated with phase delays. [source] The Mammalian Circadian Clock Exhibits Acute Tolerance to EthanolALCOHOLISM, Issue 12 2009Rebecca A. Prosser Background:, Tolerance to ethanol is observed over a variety of time courses, from minutes to days. Acute tolerance, which develops over 5 to 60 minutes, has been observed for both behavioral and neurophysiological variables and may involve changes in signaling through NMDA, GABA, or other receptors. Previous work has shown that both acute and chronic ethanol treatments modulate photic and nonphotic phase resetting of the mammalian circadian clock located in the suprachiasmatic nucleus (SCN). Although not specifically tested, the data thus far do not point to the development of chronic tolerance to the modulatory effects of ethanol. Here we investigated whether acute tolerance the ethanol occurs with respect to in vitro phase modulation of the SCN clock. Methods:, Mouse brain slices containing the SCN were pretreated with ethanol for varying lengths of time, followed by treatment concurrent with either glutamate or the serotonin agonist, 8-hydroxy-DPAT (DPAT). The phase of the SCN circadian clock was assessed the following day through extracellular recordings of SCN neuronal activity. SCN neuronal activity normally peaks during mid-day, and this rhythm can be shifted by treatment with either glutamate or DPAT. Results:, While concurrent treatment of SCN-containing brain slices with ethanol and glutamate blocks glutamate-induced phase delays of the SCN clock, pretreating the slices with ethanol for ,15 minutes prevents this inhibition. Likewise, while concurrent treatment with ethanol and DPAT enhances DPAT-induced phase advances of the SCN clock, pretreating the slices with ethanol for ,30 minutes prevents this enhancement. Conclusions:, Both the inhibiting and enhancing effects of ethanol on in vitro SCN clock phase resetting show acute tolerance. Additional experiments are needed to determine whether more slowly developing forms of tolerance also occur with respect to the SCN circadian clock. [source] Developmental Alcohol Exposure Alters Light-Induced Phase Shifts of the Circadian Activity Rhythm in RatsALCOHOLISM, Issue 7 2004Yuhua Z. Farnell Background: Developmental alcohol (EtOH) exposure produces long-term changes in the photic regulation of rat circadian behavior. Because entrainment of circadian rhythms to 24-hr light/dark cycles is mediated by phase shifting or resetting the clock mechanism, we examined whether developmental EtOH exposure also alters the phase-shifting effects of light pulses on the rat activity rhythm. Methods: Artificially reared Sprague-Dawley rat pups were exposed to EtOH (4.5 g/kg/day) or an isocaloric milk formula (gastrostomy control; GC) on postnatal days 4 to 9. At 2 months of age, rats from the EtOH, GC, and suckle control groups were housed individually, and wheel-running behavior was continuously recorded first in a 12-hr light/12-hr dark photoperiod for 10 to 14 days and thereafter in constant darkness (DD). Once the activity rhythm was observed to stably free-run in DD for at least 14 days, animals were exposed to a 15-min light pulse at either 2 or 10 hr after the onset of activity [i.e., circadian time (CT) 14 or 22, respectively], because light exposure at these times induces maximal phase delays or advances of the rat activity rhythm. Results: EtOH-treated rats were distinguished by robust increases in their phase-shifting responses to light. In the suckle control and GC groups, light pulses shifted the activity rhythm as expected, inducing phase delays of approximately 2 hr at CT 14 and advances of similar amplitude at CT 22. In contrast, the same light stimulus produced phase delays at CT 14 and advances at CT 22 of longer than 3 hr in EtOH-treated rats. The mean phase delay at CT 14 and advance at CT 22 in EtOH rats were significantly greater (p < 0.05) than the light-induced shifts observed in control animals. Conclusions: The data indicate that developmental EtOH exposure alters the phase-shifting responses of the rat activity rhythm to light. This finding, coupled with changes in the circadian period and light/dark entrainment observed in EtOH-treated rats, suggests that developmental EtOH exposure may permanently alter the clock mechanism in the suprachiasmatic nucleus and its regulation of circadian behavior. [source] Measuring the spin up of the accreting millisecond pulsar XTE J1751,305MONTHLY NOTICES OF THE ROYAL ASTRONOMICAL SOCIETY, Issue 1 2008A. Papitto ABSTRACT We perform a timing analysis on RXTE data of the accreting millisecond pulsar XTE J1751,305 observed during the 2002 April outburst. After having corrected for Doppler effects on the pulse phases due to the orbital motion of the source, we performed a timing analysis on the phase delays, which gives, for the first time for this source, an estimate of the average spin frequency derivative . We discuss the torque resulting from the spin-up of the neutron star deriving a dynamical estimate of the mass accretion rate and comparing it with the one obtained from X-ray flux. Constraints on the distance to the source are discussed, leading to a lower limit of , 6.7 kpc. [source] | |||||||||||||