While 5 seconds afters hibernation doesn't sound like a lot, it does get annoying over time as a single YouTube video can cause it to go into hibernation. Is there any way to increase to start-up and wake-up process, or maybe even stop G Hub from hibernating?
In 2015, the Marine Board met with an advisory committee and marine law enforcement to study wakes. The advisory committee recommended changing the definition of slow -no wake so the rule can be more enforceable. After receiving public comments, the Board approved a new definition.
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I feel that also the dock owner needs to have a responsibility to a boater. There should be a certain courtesy to a boat passing by. Just the other day I witnessed a drift boat under oar power. The dock owner came out and screamed at the top of his lungs to slow down and quit making a wake The owners of a dock, before they put up there no wake sign need to be educated on what a wake is. I see this a lot on the tidle Rivers on the Oregon coast.
(a) No person shall operate a vessel in a manner where the speed and/or wake of the vessel may cause danger or injury to life or limb or damage to property.
(b) All vessels shall reduce speed to slow speed/no wake when passing:
(c) "Slow speed/No wake" as used in this section means the speed at which a vessel moves through the water and is able to maintain minimum headway in relation to the vessel or structure being passed and producing the minimum wake possible.
(d) State Police, on the recommendation of the Commission or on its own initiative, may designate a specific area not included in (b)1 through 6 above as a temporary slow speed/no wake area based on congestion, visibility, safety, or other good cause. All vessels moving through these areas shall reduce their speed to slow speed/no wake within a 200-foot radius of the sign or buoy, in addition to any restriction under (b) above.
(e) No person shall place, anchor, or construct any buoy that states or implies that an area is a "Slow Speed/No Wake" area except as provided in (a) through (d) above. The State Police may remove or have removed any such unauthorized buoy.
Slow waves of neuronal activity are a fundamental component of sleep that are proposed to have homeostatic and restorative functions. Despite this, their interaction with pathology is unclear and there is only indirect evidence of their presence during wakefulness. Using intracortical recordings from the temporal lobe of 25 patients with epilepsy, we demonstrate the existence of local wake slow waves (LoWS) with key features of sleep slow waves, including a down-state of neuronal firing. Consistent with a reduction in neuronal activity, LoWS were associated with slowed cognitive processing. However, we also found that LoWS showed signatures of a homeostatic relationship with interictal epileptiform discharges (IEDs): exhibiting progressive adaptation during the build-up of network excitability before an IED and reducing the impact of subsequent IEDs on network excitability. We therefore propose an epilepsy homeostasis hypothesis: that slow waves in epilepsy reduce aberrant activity at the price of transient cognitive impairment.
Like wakefulness4 and cognitive processing3,18, epileptic activity results in increased synaptic connectivity19,20,21 and metabolic need22. Consequently, the increased SWA observed during sleep after repetitive seizures has been interpreted as a compensatory mechanism17,23 which counteracts the increased local metabolic demand. However, this contrasts with the view that SWs occurring in pathological brain regions are detrimental24,25 or even pro-epileptic26 and there is currently no evidence for SW having a beneficial impact on epileptic activity. Furthermore, it is unclear whether such SWs might also appear during wakefulness, although this could constitute a mechanism to offset pathological activity, such as epileptiform discharges and seizures.
Here, using intracranial macro- and micro- electrode recordings from the temporal lobe of people with focal, pharmacoresistant epilepsy, we demonstrate the presence of highly local wake slow waves (LoWS) that recapitulate the core features of sleep slow waves, including the associated down-state of neuronal spiking activity. Importantly, LoWS are isolated, discrete events that do not correlate with overall delta power, indicating that they are distinct from the focal slowing / delta oscillations typically associated with brain lesions and epilepsy in particular27. We hypothesized that these LoWS could serve a homeostatic purpose by normalizing neuronal activity to prevent epileptic discharges, mirroring the function of sleep SWs which correct the excessive neuronal excitability accumulated during wakefulness that translates into high sleep pressure (i.e., sleep homeostasis6). If LoWS do serve a homeostatic function, then they should exhibit two key features: first, responding to increases in network excitability that precede interictal epileptiform discharges (IEDs); and second, reducing abnormal activity linked with IEDs. In line with this hypothesis, we observed that progressive increases in neuronal activity (estimated by high-gamma (HG) power) before IEDs are accompanied by an increase of the slope and amplitude of LoWS, analogous to the response of sleep SW to increased sleep pressure13,15. Moreover, we found that a longer delay since the last LoWS is associated with higher HG power during IEDs, suggesting that any protective function of LoWS dissipates with time. Lastly, we found that a higher rate of LoWS during an associative memory task was associated with longer reaction times (RT), supporting the prediction5 that the substantial modulation of neuronal activity during SWs12,28 impacts cognitive processing. Together, our findings indicate that temporal lobe LoWS with key features of sleep SW dynamically respond to changes in network excitability, reduce aberrant activity associated with IEDs, and impact on cognition. We therefore propose that LoWS represent a homeostatic process that comes at the cost of transient cognitive impairment.
In sum, these findings reveal the existence of SW during wakefulness that recapitulate the distinctive features of sleep SW, including a down-state of neuronal activity. We demonstrate that these SWs are distinct from and not the result of sporadic increases in delta power that can occur as a result of lesions or within epileptogenic foci. Although evidence supports a restorative function of SW during sleep10,11, it was previously unknown whether such beneficial activity could occur during wakefulness under pathological conditions. Here, we provide evidence of changes in LoWS properties (slope and amplitude) before IEDs that reproduce the changes of sleep SW under high homeostatic sleep pressure13,15. We further show that the closer an IED is to the preceding LoWS, the lower the associated network excitability (measured by HG power). We therefore propose that LoWS operate as key components of epilepsy homeostasis38, mirroring the well-known sleep homeostasis regulated by sleep SWs6. This is further supported by the negative correlation between LoWS rate and IED rate, which suggests that IEDs occur more frequently in patients with fewer protective LoWS. Lastly, we observed that these beneficial effects are associated with a negative effect on cognitive processing, with slower RTs in an associative memory task, consistent with the impact of SW on neuronal activity5.
SWs have traditionally been considered to be specific to, and almost exclusively studied during sleep4,6,10,12,15,18,29,39,40, whilst evidence of slow wave activity during wakefulness has only recently been described25,41,42. Those studies of wake SWs have made use of sleep-deprived animals43, humans under sleep pressure undergoing scalp EEG recordings41, stimulation of cortical regions surrounding focal brain injury24, or thermocoagulation of clinically-defined brain areas25. However, typical slow waves with an associated neuronal down-state have not previously been described in awake humans, and it was unknown whether this core feature of sleep SW occurred during wakefulness. Indeed, the identification of neuronal down-states has been recognized as particularly challenging in awake humans, since these periods are expected to be very short44. Hence, LoWS might previously have been overlooked, but could be particularly important in the context of brain pathology24,25,43. Nonetheless, our results are based on wake SW with a particularly high amplitude, detected by an algorithm similar to that used by Frauscher et al.26, in order to distinguish SW from background noise. It thus remains unclear if the effects we observe generalize to all (including lower amplitude) SWs.
We followed the same procedure as described above. For this dataset, however, we did not manually curate identified SWs to remove potential post-IED waves or artefacts for three reasons: (1) this dataset presents only traces from presumably healthy brain regions, including the lack of IEDs31, (2) we did not want to introduce a bias in the removal of waves across states of vigilance (it is not possible to be blinded to the vigilance state, since many more waves were detected during NREM 3 than wakefulness) and (3) it was simply not conceivable to visually inspect all identified waves in this very large dataset. Besides wakefulness, the MNI Open iEEG Atlas also comprises data during NREM 2, NREM 3 and REM sleep. Since the data are presented in a bipolar montage, we included waves with both negative and positive polarities in these analyses.
If I do it one try after another, it is pretty instantaneous. However, if I take a break or just use it as I would normally use in a real life situation I can feel this lag. Especially during night if I wake up and want to check it. Maybe it has to do with the battery optimization/stand by mode of the apps. It takes a fraction to wake up. ff782bc1db