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RSG Performance Group

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Waves Complete 9.6 [2017.03.16] [HOT]

Figure 2. Comparison of atmospheric variables recorded from the R/P FLIP (shades of red) and the SV2 Wave Glider Kelvin (shades of blue) during the LCDRI2017 experiment. (A) Wind speed Uz (left axis, solid lines) and wind direction (right axis, dots). (B) Wind stress u* measured using the eddy-covariance technique on the R/P FLIP and using Charnock's relationship on the Wave Glider. (C) Atmospheric temperature (left axis, solid lines) and relative humidity (right axis, dots). (D) Atmospheric pressure. For all panels, variables are expressed at the height they were measured, i.e., 1 m above the surface layer for the Wave Glider and 8.3 m above the mean sea level for the R/P FLIP. In (C), gaps in the Wave Glider data correspond to measurements that were discarded because they were associated with periods of high wind and waves when the Wave Glider was subject to frequent capsizes, leading to abnormal values of the atmospheric temperature and relative humidity.

Waves Complete 9.6 [2017.03.16]

Figure 11. Ten-hours evolution of (A) the short-wave solar radiation SWR, (B) the true wind speed TWS, (C) the wave field spectrogram, and (D) the water temperature during LCDRI2017 starting at 0830 PDT 24 March 2017. Solar radiation was measured from the R/P FLIP while wind, waves, and water temperatures were measured by the SV2 Wave Glider Kelvin. In the morning when the wind was low, the heat from the incoming solar radiation was stored in a very thin layer beneath the interface. As soon as the wind increased, short wind-waves developed leading to enhanced mixing through direct mechanisms such as wave breaking or via indirect mechanisms such as Langmuir circulation. The surface heat content was then quickly mixed downward, leading to an increase of the water temperature throughout the ocean mixed layer.

Although inducing sleep-like EEG slow waves [23], propofol recently have been demonstrated to significantly change the sleep architecture with increase inN3 sleep and total abolishment of rapid-eye-movement (REM) in health humans [24, 25]. Opioids use, whether acute (when used to provide sedation or sedative) or chronic, have been shown to disturb the sleep pattern [26]. For example, some studies have shown that morphine significantly altered sleep architecture with increase of N2 sleep and reduction of slow wave sleep (SWS) in health humans [27, 28]. REM and SWS are generally associated with the restorative processes in the body (especially the energy restoration) [29]. Therefore, we presume that the reduction of REM and SWS might be the most possible reasons that sedative patients showed subjective impaired sleep quality 1 week after diagnostic UGE.


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