Abstract. Due to its effects on the atmospheric lifetime of methane, the burdens of tropospheric ozone and growth of secondary organic aerosol, isoprene is central among the biogenic compounds that need to be taken into account for assessment of anthropogenic air pollution-climate change interactions. Lack of process-understanding regarding leaf isoprene production as well as of suitable observations to constrain and evaluate regional or global simulation results add large uncertainties to past, present and future emissions estimates. Focusing on contemporary climate conditions, we compare three global isoprene models that differ in their representation of vegetation and isoprene emission algorithm. We specifically aim to investigate the between-and within model variation that is introduced by varying some of the models' main features, and to determine which spatial and/or temporal features are robust between models and different experimental set-ups. In their individual standard configurations, the models broadly agree with respect to the chief isoprene sources and emission seasonality, with maximum monthly emission rates around 20-25 Tg C, when averaged by 30-degree latitudinal bands. They also indicate relatively small (approximately 5 to 10 % around the mean) interannual variability of total global emissions. The models are sensitive to changes in one or more of their main model components and drivers (e.g., underlying vegetation fields, climate input) which can yield increases or decreases in total annual emisCorrespondence to: A. Arneth (almut.arneth@nateko.lu.se) sions of cumulatively by more than 30 %. Varying drivers also strongly alters the seasonal emission pattern. The variable response needs to be interpreted in view of the vegetation emission capacities, as well as diverging absolute and regional distribution of light, radiation and temperature, but the direction of the simulated emission changes was not as uniform as anticipated. Our results highlight the need for modellers to evaluate their implementations of isoprene emission models carefully when performing simulations that use nonstandard emission model configurations.

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Sleep patterns and endogenous melatonin profiles in 13 fragile X boys between the age of 4.7 and 11.0 years were compared to those of 8 age-matched, normal control boys. Parents recorded sleep patterns on a Sleep Diary Chart for 14 consecutive days. Twelve saliva samples were obtained from 8 fragile X participants and all of the controls over 48 hours for the assessment of salivary melatonin profiles. The results showed greater variability in total sleep time and difficulty in sleep maintenance in fragile X boys compared with the control participants. Nocturnal melatonin production, expressed as both peak level and area under the concentration-time curve between 20:00 h and 08:00 h, were found to be significantly larger in fragile X boys than in controls. Additionally, the mean of the minimum daytime melatonin levels recorded was significantly higher for the fragile X group. Elevated levels in some fragile X boys relative to the range seen in controls, occurring either during the day or at night, or in both segments of the secretory profile for some individuals, may be due in part to overactivity of the sympathetic nervous system. Alternative molecular mechanisms leading to changes in melatonin profiles in fragile X are also discussed.

Melatonin is a hormone released during darkness under the control of the hypothalamic circadian pacemaker. It has been shown that melatonin is suppressed by light as a function of intensity, with low levels of illumination producing small effects and more intense light greater, but not complete inhibition. The studies which lead to these conclusions administered light subsequent to the secretion pattern being well established. Light as low as 250 lux administered during the normal onset of secretion can reduce melatonin to below detectable levels. The onset of melatonin secretion was delayed for at least an hour during 250 lux exposure and did not rise until termination of light exposure (two hours after control melatonin onset) with higher illumination (500, 1000 and 2500 lux). This tentatively indicates that duration of the inhibition is intensity dependent. It is suggested that the experimental paradigm used in the present study may be a more realistic representation of the effect of normal light exposure (both natural and artificial) on the circadian system, and that findings may be pertinent to the aetiology of certain sleep onset insomnias, which would include delayed sleep phase syndrome (DSPS) and adaptation to shift work.

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Sleep patterns and endogenous melatonin profiles in 13 fragile X boys between the age of 4.7 and 11.0 years were compared to those of 8 age-matched, normal control boys. Parents recorded sleep patterns on a Sleep Diary Chart for 14 consecutive days. Twelve saliva samples were obtained from 8 fragile X participants and all of the controls over 48 hours for the assessment of salivary melatonin profiles. The results showed greater variability in total sleep time and difficulty in sleep maintenance in fragile X boys compared with the control participants. Nocturnal melatonin production, expressed as both peak level and area under the concentration-time curve between 20:00 h and 08:00 h, were found to be significantly larger in fragile X boys than in controls. Additionally, the mean of the minimum daytime melatonin levels recorded was significantly higher for the fragile X group. Elevated levels in some fragile X boys relative to the range seen in controls, occurring either during the day or at night, or in both segments of the secretory profile for some individuals, may be due in part to overactivity of the sympathetic nervous system. Alternative molecular mechanisms leading to changes in melatonin profiles in fragile X are also discussed.