Introducing a new hazard and exposure atlas for European winter storms.

Winter storms are one of the riskiest natural hazards in Europe. They are often assessed either from a climatology perspective or the exposed land use type. However, for accurate storm protection management, analyzing compatible wind speed and land use data at the highest spatiotemporally accuracy is critical. Thus, the study goals were (1) modeling wind speed for the 27 most extreme winter storm events from 1993 to 2022 at high spatial resolution (250 m × 250 m) and (2) defining and developing new and representative storm hazard and storm exposure indices for forested area, built-up area, and population. The winter storm event-related wind speed was modeled using a least-squares boosting approach based on ERA5 reanalysis data and 1730 wind speed measurement sites from the integrated surface global hourly meteorological dataset. In combination with temporally variable population density, built-up area, and forested area grids, the storm exposure indices for the European NUTS3 regions were calculated. The coefficient of determination of the median of the modeled wind speed fields is 0.73 for an independent subset of measurement sites. The wind speed maps reveal the uniqueness of the winter storm events. Each storm only affects parts of Europe. The study also emphasizes the relevance of distinguishing between storm hazard and storm exposure. The exposure of built-up areas to winter storms has increased considerably in recent years. This example underlines that storm exposure is not temporally constant but depends on the development of wind speed and land use. Decision-makers can apply the results of this study to evaluate and improve the effectiveness of storm protection measures. The developed storm exposures indices enable a sector- and location-specific evaluation with high precision.

Later growth onsets or reduced growth rates: What characterises legacy effects at the tree-ring level in conifers after the severe 2018 drought?

Severe drought events negatively affect tree growth and often cause legacy effects, expressed by smaller tree rings in the post-drought recovery years. While the pattern of reduced tree-ring widths is frequently described the processes underlying such legacy effects, i.e., whether it is due to shorter growth periods or lower growth rates, remains unclear and is investigated in this study. To elucidate these post-drought effects, we examined radial stem growth dynamics monitored with precision band-dendrometers on 144 Douglas fir, Norway spruce and silver fir sample trees distributed along four elevational gradients in the Black Forest (Southwest Germany) during the post-drought years 2019 and 2020. Growth onset of all investigated species occurred between 11 and 24 days significantly earlier in 2020 compared to 2019. Modelling growth onset based on chilling and forcing units and taking the study year into account explained 88-98 % of the variance in the growth onset data. The highly significant effect of the study year (p < 0.001) led to the conclusion, that other factors than the prevailing site conditions (chilling and forcing units) must have triggered the earlier growth onset in 2020. On the other hand, for Douglas fir growth rates were significantly higher in 2020 compared to 2019 (2.9 µm d-1) and marginally significantly higher for silver fir (1.3 µm d-1), underlining the explanatory power of growth rate on recovery processes in general and suggesting that Douglas fir copes better with droughts, as it recovered faster. Growth dynamics at the beginning of the year showed limited growth for earlier growth onsets, which, however, could not explain the difference between the investigated years. Our results provide evidence that legacy effects of drought events are expressed by a delayed growth onset and a reduced growth rate in the post-drought year and that Douglas fir has a superior recovery potential.

Energy expenditure during sleep, sleep deprivation and sleep following sleep deprivation in adult humans.

Sleep has been proposed to be a physiological adaptation to conserve energy, but little research has examined this proposed function of sleep in humans. We quantified effects of sleep, sleep deprivation and recovery sleep on whole-body total daily energy expenditure (EE) and on EE during the habitual day and nighttime. We also determined effects of sleep stage during baseline and recovery sleep on EE. Seven healthy participants aged 22 ± 5 years (mean ± s.d.) maintained ∼8 h per night sleep schedules for 1 week before the study and consumed a weight-maintenance diet for 3 days prior to and during the laboratory protocol. Following a habituation night, subjects lived in a whole-room indirect calorimeter for 3 days. The first 24 h served as baseline ­ 16 h wakefulness, 8 h scheduled sleep ­ and this was followed by 40 h sleep deprivation and 8 h scheduled recovery sleep. Findings show that, compared to baseline, 24 h EE was significantly increased by ∼7% during the first 24 h of sleep deprivation and was significantly decreased by ∼5% during recovery, which included hours awake 25-40 and 8 h recovery sleep. During the night time, EE was significantly increased by ∼32% on the sleep deprivation night and significantly decreased by ∼4% during recovery sleep compared to baseline. Small differences in EE were observed among sleep stages, but wakefulness during the sleep episode was associated with increased energy expenditure. These findings provide support for the hypothesis that sleep conserves energy and that sleep deprivation increases total daily EE in humans.

Comparison of sustained attention assessed by auditory and visual psychomotor vigilance tasks prior to and during sleep deprivation.

To date, no detailed examination of the pattern of change in reaction time performance for different sensory modalities has been conducted across the circadian cycle during sleep deprivation. Therefore, we compared sustained auditory and visual attention performance during 40h of sleep deprivation assessing multiple metrics of auditory and visual psychomotor vigilance tasks (PVT). Forty healthy participants (14 women) aged 30.8±8.6years were studied. Subjects were scheduled for an ∼8h sleep schedule at home prior to three-six laboratory baseline days with an 8 h sleep schedule followed by 40h sleep deprivation. Visual and auditory PVTs were 10min in duration, and were administered every 2h during sleep deprivation. Data were analysed with mixed-model anova. Sleep deprivation and circadian phase increased response time, lapses, anticipations, standard deviation of response times and time on task decrements for visual and auditory PVTs. In general, auditory vigilance was faster and less variable than visual vigilance, with larger differences between auditory and visual PVT during sleep deprivation versus baseline. Failures to respond to stimuli within 10s were four times more likely to occur to visual versus auditory stimuli. Our findings highlight that lapses during sleep deprivation are more than just long responses due to eye closure or visual distraction. Furthermore, our findings imply that the general pattern of change in attention during sleep deprivation (e.g. circadian variation, response slowing, lapsing and anticipations, time on task decrements and state instability) is similar among sensory-motor behavioral response modalities.

The microglia response to electrical overstimulation of the retina imaged under a transparent stimulus electrode.

Objective.We investigated using the morphological response of retinal microglia as indicators of tissue damage from electrical overstimulation by imaging them through an optically transparent stimulus electrode.Approach.To track the microglia, we used a transgenic mouse where the microglia expressed a water soluble green fluorescent protein. The clear stimulus electrode was placed epiretinally on the inner limiting membrane and the microglia layers were imaged using time-lapse confocal microscopy. We examined how the microglia responded both temporally and spatially to local overstimulation of the retinal tissue. Using confocal microscope vertical image stacks, the microglia under the electrode were imaged at 2.5 min intervals. The retina was overstimulated for a 5 min period using 1 ms 749µC cm-2ph-1biphasic current pulses and changes in the microglia morphology were followed for 1 h post stimulation. After the imaging period, a label for cellular damage was applied to the retina.Main results.The microglia response to overstimulation depended on their spatial location relative to the electrode lumen and could result in three different morphological responses. Some microglia were severely injured and became a series of immotile ball-like fluorescent processes. Other microglia survived, and reacted rapidly to the injury by extending filopodia oriented toward the damage zone. This response was seen in inner retinal microglia outside the stimulus electrode edge. A third effect, seen with the deeper outer microglia under the electrode, was a fading of their fluorescent image which appeared to be due to optical scatter caused by overstimulation-induced retinal edema.Significance.The microglial morphological responses to electrical overstimulation injury occur rapidly and can show both direct and indirect effects of the stimulus electrode injury. The microglia injury pattern closely follows models of the electric field distribution under thinly insulated disc electrodes.

Effects of caffeine on the human circadian clock in vivo and in vitro.

Caffeine's wakefulness-promoting and sleep-disrupting effects are well established, yet whether caffeine affects human circadian timing is unknown. We show that evening caffeine consumption delays the human circadian melatonin rhythm in vivo and that chronic application of caffeine lengthens the circadian period of molecular oscillations in vitro, primarily with an adenosine receptor/cyclic adenosine monophosphate (AMP)-dependent mechanism. In a double-blind, placebo-controlled, ~49-day long, within-subject study, we found that consumption of a caffeine dose equivalent to that in a double espresso 3 hours before habitual bedtime induced a ~40-min phase delay of the circadian melatonin rhythm in humans. This magnitude of delay was nearly half of the magnitude of the phase-delaying response induced by exposure to 3 hours of evening bright light (~3000 lux, ~7 W/m(2)) that began at habitual bedtime. Furthermore, using human osteosarcoma U2OS cells expressing clock gene luciferase reporters, we found a dose-dependent lengthening of the circadian period by caffeine. By pharmacological dissection and small interfering RNA knockdown, we established that perturbation of adenosine receptor signaling, but not ryanodine receptor or phosphodiesterase activity, was sufficient to account for caffeine's effects on cellular timekeeping. We also used a cyclic AMP biosensor to show that caffeine increased cyclic AMP levels, indicating that caffeine influenced a core component of the cellular circadian clock. Together, our findings demonstrate that caffeine influences human circadian timing, showing one way that the world's most widely consumed psychoactive drug affects human physiology.

Safety and outcomes following hybrid balloon and balloon-only procedures using a multifunction, multisinus balloon dilation tool.

BACKGROUND: A multicenter prospective study was conducted to assess the safety and sustained effectiveness of a new instrument possessing multifunctionality as an ostium seeker, suction-irrigator, and malleable balloon-dilator indicated for treating multiple sinuses. METHODS: Endoscopic balloon-only and hybrid-balloon procedures involving dilation of the frontal recesses, maxillary ostia, and/or sphenoid sinus ostia were performed in 175 patients. One-month follow-up was required for all patients. The first 50 patients enrolled also consented to a 1-year follow-up. Complications and sinus symptom severity were assessed at the 1-month visit. Symptom severity and ostial patency of the treated sinuses were evaluated at the 1-year visit. RESULTS: A total of 497 balloon dilations (279 frontal, 138 sphenoid, and 80 maxillary) were attempted in 175 patients. Over 96% (479/497) of the attempted sinus dilations were successfully completed, while 18 dilations were converted to traditional dissection due to an inability to access or dilate the targeted anatomy. Two (1.1%) nonserious adverse events were reported following hybrid-balloon dilation and both were unrelated to the device or the procedure. Forty-four of 50 patients in the extended follow-up cohort completed the 1-year follow-up. Sinus symptom improvement in this group improved significantly from an average severity of 1.9 ± 1.1 to 0.8 ± 0.7 (p < 0.0001) and 1-year ostial patency was 91.6% (76/83). One revision surgery (2.3%) was performed. CONCLUSION: These results indicate that a multifunctional, malleable, balloon-dilating device can be safely and successfully used to treat multiple sinuses with sustained ostial patency and symptom improvement for at least 1 year.

Combination of light and melatonin time cues for phase advancing the human circadian clock.

STUDY OBJECTIVES: Photic and non-photic stimuli have been shown to shift the phase of the human circadian clock. We examined how photic and non-photic time cues may be combined by the human circadian system by assessing the phase advancing effects of one evening dose of exogenous melatonin, alone and in combination with one session of morning bright light exposure. DESIGN: Randomized placebo-controlled double-blind circadian protocol. The effects of four conditions, dim light (∼1.9 lux, ∼0.6 Watts/m(2))-placebo, dim light-melatonin (5 mg), bright light (∼3000 lux, ∼7 Watts/m(2))-placebo, and bright light-melatonin on circadian phase was assessed by the change in the salivary dim light melatonin onset (DLMO) prior to and following treatment under constant routine conditions. Melatonin or placebo was administered 5.75 h prior to habitual bedtime and 3 h of bright light exposure started 1 h prior to habitual wake time. SETTING: Sleep and chronobiology laboratory environment free of time cues. PARTICIPANTS: Thirty-six healthy participants (18 females) aged 22 ± 4 y (mean ± SD). RESULTS: Morning bright light combined with early evening exogenous melatonin induced a greater phase advance of the DLMO than either treatment alone. Bright light alone and melatonin alone induced similar phase advances. CONCLUSION: Information from light and melatonin appear to be combined by the human circadian clock. The ability to combine circadian time cues has important implications for understanding fundamental physiological principles of the human circadian timing system. Knowledge of such principles is important for designing effective countermeasures for phase-shifting the human circadian clock to adapt to jet lag, shift work, and for designing effective treatments for circadian sleep-wakefulness disorders.

Acute effects of bright light exposure on cortisol levels.

Multisynaptic neural and endocrine pathways from the suprachiasmatic nucleus of the hypothalamus have been hypothesized to communicate circadian and photic information to the adrenal glands. In humans, light exposure has been reported to have no effect, increase, or decrease cortisol levels. These inconsistent findings in humans may be related to differences among studies including the intensity (approximately 500 to 5500 lux), duration (15 min to 4 h), and circadian phase of light exposure. The authors assessed the influence of exposure to bright light on cortisol levels in humans during the rising and descending phases of the circadian rhythm of cortisol, that is, when cortisol levels are high. Twenty healthy men and women were studied using a within-subject research design. Subjects were studied in an environment free of time cues for 9 to 10 days. Subjects received a 6.7-h exposure of bright light (approximately 10,000 lux; equivalent to ambient light intensity just after sunrise or just before sunset) or dim light (approximately 3 lux; equivalent to candle light) during the biological night and morning. Bright light exposure significantly reduced plasma cortisol levels at both circadian phases studied, whereas dim light exposure had little effect on cortisol levels. The finding of an acute suppressive effect of bright light exposure on cortisol levels supports the existence of a mechanism by which photic information can acutely influence the human adrenal glands.