***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: The photopigment in the human eye that transduces light for circadian and neuroendocrine regulation , is unknown . The aim of this study was to establish an action spectrum for light-induced melatonin suppression that could help eluci date the ocular photoreceptor system for regulating the human pineal gl and . Subjects ( 37 females , 35 males , mean age of 24.5 ± 0.3 years ) were healthy and had normal color vision .  Full-field , monochromatic light exposures took place between 2:00 and 3:30 A.M. while subjects ' pupils were dilated . Blood sample s collected before and after light exposures were quantified for melatonin . Each subject was tested with at least seven different irradiances of one wavelength with a minimum of 1 week between each nighttime exposure . Nighttime melatonin suppression tests ( n = 627 ) were completed with wavelengths from 420 to 600 nm . The data were fit to eight univariant , sigmoidal fluence – response curves ( R2 = 0.81–0.95 ) . The action spectrum constructed from these data fit an opsin template ( R2 = 0.91 ) , which identifies 446–477 nm as the most potent wavelength region providing circadian input for regulating melatonin secretion . The results suggest that , in humans , a single photopigment may be primarily responsible for melatonin suppression , and its peak absorbance appears to be distinct from that of rod and cone cell photopigments for vision . The data also suggest that this new photopigment is retinaldehyde based . These findings suggest that there is a novel opsin photopigment in the human eye that mediates circadian photoreception The circadian pacemaker is differentially sensitive to the re setting effects of retinal light exposure , depending upon the circadian phase at which the light exposure occurs . Previously reported human phase response curves ( PRCs ) to single bright light exposures have employed small sample sizes , and were often based on relatively imprecise estimates of circadian phase and phase re setting . In the present study , 21 healthy , entrained subjects underwent pre- and post-stimulus constant routines ( CRs ) in dim light ( approximately 2 - 7 lx ) with maintained wakefulness in a semi-recumbent posture . The 6.7 h bright light exposure stimulus consisted of alternating 6 min fixed gaze ( approximately 10 000 lx ) and free gaze ( approximately 5000 - 9000 lx ) exposures . Light exposures were scheduled across the circadian cycle in different subjects so as to derive a PRC . Plasma melatonin was used to determine the phase of the onset , offset , and midpoint of the melatonin profiles during the CRs . Phase shifts were calculated as the difference in phase between the pre- and post-stimulus CRs . The result ant PRC of the midpoint of the melatonin rhythm revealed a characteristic type 1 PRC with a significant peak-to-trough amplitude of 5.02 h. Phase delays occurred when the light stimulus was centred prior to the critical phase at the core body temperature minimum , phase advances occurred when the light stimulus was centred after the critical phase , and no phase shift occurred at the critical phase . During the subjective day , no prolonged ' dead zone ' of photic insensitivity was apparent . Phase shifts derived using the melatonin onsets showed larger magnitudes than those derived from the melatonin offsets . These data provide a comprehensive characterization of the human PRC under highly controlled laboratory conditions Light strongly influences the circadian timing system in humans via non-image-forming photoreceptors in the retinal ganglion cells . Their spectral sensitivity is highest in the short-wavelength range of the visible light spectrum as demonstrated by melatonin suppression , circadian phase shifting , acute physiological responses , and subjective alertness . We tested the impact of short wavelength light ( 460 nm ) on sleep EEG power spectra and sleep architecture . We hypothesized that its acute action on sleep is similar in magnitude to reported effects for polychromatic light at higher intensities and stronger than longer wavelength light ( 550 nm ) . The  sleep EEGs  of eight young men were analyzed after 2-h evening exposure to blue ( 460 nm ) and green ( 550 nm ) light of equal photon densities ( 2.8 x 10(13 ) photons x cm(-2 ) x s(-1 ) ) and to dark ( 0 lux ) under constant posture conditions . The time course of EEG slow-wave activity ( SWA ; 0.75 - 4.5 Hz ) across sleep cycles after blue light at 460 nm was changed such that SWA was slightly reduced in the first and significantly increased during the third sleep cycle in parietal and occipital brain regions . Moreover , blue light significantly shortened rapid eye movement ( REM ) sleep duration during these two sleep cycles . Thus the light effects on the dynamics of SWA and REM sleep duration s were blue shifted relative to the three-cone visual photopic system probably mediated by the circadian , non-image-forming visual system . Our results can be interpreted in terms of an induction of a circadian phase delay and /or repercussions of a stronger alerting effect after blue light , persisting into the sleep episode OBJECTIVE We examined the effects of an advanced sleep/wake schedule and morning short wavelength ( blue ) light in 25 adults ( mean age±SD=21.8±3 years ; 13 women ) with late sleep schedules and sub clinical features of delayed sleep phase disorder ( DSPD ) . METHODS After a baseline week , participants kept individualized , fixed , advanced 7.5-h sleep schedules for 6days . Participants were r and omly assigned to groups to receive " blue " ( 470 nm , ∼225lux , n=12 ) or " dim " ( < 1lux , n=13 ) light for 1h after waking each day . Head-worn " Daysimeters " measured light exposure ; actigraphs and sleep diaries confirmed schedule compliance . Salivary dim light melatonin onset ( DLMO ) , self-reported sleep , and mood were examined with 2 × 2 ANOVA . RESULTS After 6days , both groups showed significant circadian phase advances , but morning blue light was not associated with larger phase shifts than dim-light exposure . The average DLMO advances ( mean±SD ) were 1.5±1.1h in the dim light group and 1.4±0.7h in the blue light group . CONCLUSIONS Adherence to a fixed advanced sleep/wake schedule result ed in significant circadian phase shifts in young adults with sub clinical DSPD with or without morning blue light exposure . Light/dark exposures associated with fixed early sleep schedules are sufficient to advance circadian phase in young adults Ocular exposure to early morning room light can significantly advance the timing of the human circadian pacemaker . The re setting response to such light has a non-linear relationship to illuminance . The dose-response relationship of the human circadian pacemaker to late evening light of dim to moderate intensity has not been well established . Twenty-three healthy young male and female volunteers took part in a 9 day protocol in which a single experimental light exposure6.5 h in duration was given in the early biological night . The effects of the light exposure on the endogenous circadian phase of the melatonin rhythm and the acute effects of the light exposure on plasma melatonin concentration were calculated . We demonstrate that humans are highly responsive to the phase-delaying effects of light during the early biological night and that both the phase re setting response to light and the acute suppressive effects of light on plasma melatonin follow a logistic dose-response curve , as do many circadian responses to light in mammals . Contrary to expectations , we found that half of the maximal phase-delaying response achieved in response to a single episode of evening bright light ( approximately 9000 lux ( lx ) ) can be obtained with just over 1 % of this light ( dim room light of approximately 100 lx ) . The same held true for the acute suppressive effects of light on plasma melatonin concentrations . This indicates that even small changes in ordinary light exposure during the late evening hours can significantly affect both plasma melatonin concentrations and the entrained phase of the human circadian pacemaker The study investigated the effect of bright blue-enriched versus blue-suppressed indoor light on sleep and wellbeing of healthy participants over 65 years . Twenty-nine participants in 20 private houses in a uniform settlement in Copenhagen were exposed to two light epochs of 3 weeks with blue-enriched ( 280 lux ) and 3 weeks blue-suppressed ( 240 lux ) indoor light or vice versa from 8 to 13 pm in a r and omized cross-over design . The first light epoch was in October , the second in November and the two light epochs were separated by one week . Participants were examined at baseline and at the end of each light epoch . The experimental indoor light was well tolerated by the majority of the participants . Sleep duration was 7.44 ( 95 % CI 7.14–7.74 ) hours during blue-enriched conditions and 7.31 ( 95 % CI 7.01–7.62 ) hours during blue-suppressed conditions ( p = 0.289 ) . Neither rest hours , chromatic pupillometry , nor saliva melatonin profile showed significant changes between blue-enriched and blue-suppressed epochs . Baseline Pittsburgh Sleep Quality Index ( PSQI ) was significantly worse in females ; 7.62 ( 95 % CI 5.13–10.0 ) versus 4.06 ( 95 % CI 2.64–5.49 ) in males , p = 0.009 . For females , PSQI improved significantly during blue-enriched light exposure ( p = 0.007 ) ; no significant changes were found for males . The subjective grading of indoor light quality doubled from participants habitual indoor light to the bright experimental light , while it was stable between light epochs , although there were clear differences between blue-enriched and blue-suppressed electrical light conditions imposed . Even though the study was carried out in the late autumn at northern latitude , the only significant difference in Actiwatch-measured total blue light exposure was from 8 to 9 am , because contributions from blue-enriched , bright indoor light were superseded by contributions from daylight Significance The use of light-emitting electronic devices for reading , communication , and entertainment has greatly increased recently . We found that the use of these devices before bedtime prolongs the time it takes to fall asleep , delays the circadian clock , suppresses levels of the sleep-promoting hormone melatonin , reduces the amount and delays the timing of REM sleep , and reduces alertness the following morning . Use of light-emitting devices immediately before bedtime also increases alertness at that time , which may lead users to delay bedtime at home . Overall , we found that the use of portable light-emitting devices immediately before bedtime has biological effects that may perpetuate sleep deficiency and disrupt circadian rhythms , both of which can have adverse impacts on performance , health , and safety . In the past 50 y , there has been a decline in average sleep duration and quality , with adverse consequences on general health . A representative survey of 1,508 American adults recently revealed that 90 % of Americans used some type of electronics at least a few nights per week within 1 h before bedtime . Mounting evidence from countries around the world shows the negative impact of such technology use on sleep . This negative impact on sleep may be due to the short-wavelength – enriched light emitted by these electronic devices , given that artificial-light exposure has been shown experimentally to produce alerting effects , suppress melatonin , and phase-shift the biological clock . A few reports have shown that these devices suppress melatonin levels , but little is known about the effects on circadian phase or the following sleep episode , exposing a substantial gap in our knowledge of how this increasingly popular technology affects sleep . Here we compare the biological effects of reading an electronic book on a light-emitting device ( LE-eBook ) with reading a printed book in the hours before bedtime . Participants reading an LE-eBook took longer to fall asleep and had reduced evening sleepiness , reduced melatonin secretion , later timing of their circadian clock , and reduced next-morning alertness than when reading a printed book . These results demonstrate that evening exposure to an LE-eBook phase-delays the circadian clock , acutely suppresses melatonin , and has important implication s for underst and ing the impact of such technologies on sleep , performance , health , and safety Background Light exposure can cascade numerous effects on the human circadian process via the non-imaging forming system , whose spectral relevance is highest in the short-wavelength range . Here we investigated if commercially available compact fluorescent lamps with different colour temperatures can impact on alertness and cognitive performance . Methods Sixteen healthy young men were studied in a balanced cross-over design with light exposure of 3 different light setting s ( compact fluorescent lamps with light of 40 lux at 6500 K and at 2500 K and inc and escent lamps of 40 lux at 3000 K ) during 2 h in the evening . Results Exposure to light at 6500 K induced greater melatonin suppression , together with enhanced subjective alertness , well-being and visual comfort . With respect to cognitive performance , light at 6500 K led to significantly faster reaction times in tasks associated with sustained attention ( Psychomotor Vigilance and GO/NOGO Task ) , but not in tasks associated with executive function ( Paced Visual Serial Addition Task ) . This cognitive improvement was strongly related with attenuated salivary melatonin levels , particularly for the light condition at 6500 K . Conclusions Our findings suggest that the sensitivity of the human alerting and cognitive response to polychromatic light at levels as low as 40 lux , is blue-shifted relative to the three-cone visual photopic system . Thus , the selection of commercially available compact fluorescent lights with different colour temperatures significantly impacts on circadian physiology and cognitive performance at home and in the workplace Light in the short wavelength range 
    Output:
    
The melatonin concentration recovered rather rapidly , within 15 min from cessation of the exposure , suggesting a short-term or simultaneous impact of light exposure on the melatonin secretion .
Melatonin secretion and suppression were reduced with age , but the light-induced circadian phase advance was not impaired with age .
Light exposure in the evening , at night and in the morning affected the circadian phase of melatonin levels .
In addition , even the longest wavelengths ( 631 nm , red ) and intermittent light exposures induced circadian re setting responses , and exposure to low light levels ( 5 - 10 lux ) at night when sleeping with eyes closed induced a circadian response .