***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: OBJECTIVES To inform the debate over whether human sleep can be chronically reduced without consequences , we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation . DESIGN The chronic sleep restriction experiment involved r and omization to one of three sleep doses ( 4 h , 6 h , or 8 h time in bed per night ) , which were maintained for 14 consecutive days . The total sleep deprivation experiment involved 3 nights without sleep ( 0 h time in bed ) . Each study also involved 3 baseline ( pre-deprivation ) days and 3 recovery days . SETTING Both experiments were conducted under st and ardized laboratory conditions with continuous behavioral , physiological and medical monitoring . PARTICIPANTS A total of n = 48 healthy adults ( ages 21 - 38 ) participated in the experiments . INTERVENTIONS Noctumal sleep periods were restricted to 8 h , 6 h or 4 h per day for 14 days , or to 0 h for 3 days . All other sleep was prohibited . RESULTS Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days result ed in significant cumulative , dose-dependent deficits in cognitive performance on all tasks . Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days , and did not significantly differentiate the 6 h and 4 h conditions . Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis -- displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights . Comparison of chronic sleep restriction to total sleep deprivation showed that the latter result ed in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost . A statistical model revealed that , regardless of the mode of sleep deprivation , lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h ( s.e . 0.73 h ) . CONCLUSIONS Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation , it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults . Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits , which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign . Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses , but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions . This suggests that sleep debt is perhaps best understood as result ing in additional wakefulness that has a neurobiological " cost " which accumulates over time STUDY OBJECTIVES To investigate whether sleep restriction therapy ( SRT ) is associated with reduced objective total sleep time ( TST ) , increased daytime somnolence , and impaired vigilance . DESIGN Within-subject , noncontrolled treatment investigation . SETTING Sleep research laboratory . PARTICIPANTS Sixteen patients [ 10 female , mean age = 47.1 ( 10.8 ) y ] with well-defined psychophysiological insomnia ( PI ) , reporting TST ≤ 6 h. INTERVENTIONS Patients were treated with single-component SRT over a 4-w protocol , sleeping in the laboratory for 2 nights prior to treatment initiation and for 3 nights ( SRT night 1 , 8 , 22 ) during the acute interventional phase . The psychomotor vigilance task ( PVT ) was completed at seven defined time points [ day 0 ( baseline ) , day 1,7,8,21,22 ( acute treatment ) and day 84 ( 3 mo ) ] . The Epworth Sleepiness Scale ( ESS ) was completed at baseline , w 1 - 4 , and 3 mo . MEASUREMENT AND RESULTS Subjective sleep outcomes and global insomnia severity significantly improved before and after SRT . There was , however , a robust decrease in PSG-defined TST during acute implementation of SRT , by an average of 91 min on night 1 , 78 min on night 8 , and 69 min on night 22 , relative to baseline ( P < 0.001 ; effect size range = 1.60 - 1.80 ) . During SRT , PVT lapses were significantly increased from baseline ( at three of five assessment points , all P < 0.05 ; effect size range = 0.69 - 0.78 ) , returning to baseline levels by 3 mo ( P = 0.43 ) . A similar pattern was observed for RT , with RTs slowing during acute treatment ( at four of five assessment points , all P < 0.05 ; effect size range = 0.57 - 0.89 ) and returning to pretreatment levels at 3 mo ( P = 0.78 ) . ESS scores were increased at w 1 , 2 , and 3 ( relative to baseline ; all P < 0.05 ) ; by 3 mo , sleepiness had returned to baseline ( normative ) levels ( P = 0.65 ) . CONCLUSION For the first time we show that acute sleep restriction therapy is associated with reduced objective total sleep time , increased daytime sleepiness , and objective performance impairment . Our data have important implication s for implementation guidelines around the safe and effective delivery of cognitive behavioral therapy for insomnia This study compared the accuracy of reporting adherence to sleep instructions in participants who were informed that adherence would be verified with an actigraph ( aware group ) to participants not informed the actigraph would be used to assess adherence ( unaware of group ) . Participants were college students ( N = 68 ) , who were screened for psychiatric or sleep disorders or extremes in circadian tendency . The UG had later actigraph estimates of bedtime than the AG , but the two groups did not differ on their self-report of adherence to the sleep rules . Only the UG had later actigraphic estimates of bedtimes that violated the sleep rules . These findings have implication s for the accuracy of sleep diary self-reports as well as for the use of actigraphs in studies requiring people to follow specific sleep schedule instructions BACKGROUND The folk belief that we should sleep 8 h seems to be incorrect . Numerous studies have shown that self-reported sleep longer than 7.5 h or shorter than 6.5 h predicts increased mortality risk . This study examined if prospect ively-determined objective sleep duration , as estimated by wrist actigraphy , was associated with mortality risks . METHODS From 1995 - 1999 , women averaging 67.6 years of age provided one-week actigraphic recordings .  Survival could be estimated from follow-up continuing until 2009 for 444 of the women , with an average of 10.5 years before censoring . Multivariate age-stratified Cox regression models were controlled for history of hypertension , diabetes , myocardial infa rct ion , cancer , and major depression . RESULTS Adjusted survival functions estimated 61 % survival ( 54 - 69 % , 95 % C.I. ) for those with sleep less than 300 min and 78 % survival ( 73 - 85 % , 95 % C.I. ) for those with actigraphic sleep longer than 390 min , as compared with survival of 90 % ( 85 - 94 % , 95 % C.I. ) for those with sleep of 300 - 390 min . Time-in-bed , sleep efficiency and the timing of melatonin metabolite excretion were also significant mortality risk factors . CONCLUSION This study confirms a U-shaped relationship between survival and actigraphically measured sleep duration s , with the optimal objective sleep duration being shorter than the self-report optimums . People who sleep five or six hours may be reassured . Further studies are needed to identify any modifiable factors for this mortality and possible approaches to prevention Background : Insomnia is a prevalent health complaint that is often difficult to evaluate reliably . There is an important need for brief and valid assessment tools to assist practitioners in the clinical evaluation of insomnia complaints . Objective : This paper reports on the clinical validation of the  Insomnia Severity Index ( ISI )  as a brief screening measure of insomnia and as an outcome measure in treatment research . The psychometric properties ( internal consistency , concurrent validity , factor structure ) of the ISI were evaluated in two sample s of insomnia patients . Methods : The first study examined the internal consistency and concurrent validity of the ISI  in 145 patients evaluated for insomnia at a sleep disorders clinic . Data from the ISI were compared to those of a sleep diary measure . In the second study , the concurrent validity of the  ISI  was evaluated in a sample of 78 older patients who participated in a r and omized-controlled trial of behavioral and pharmacological therapies for insomnia . Change scores on the  ISI  over time were compared with those obtained from sleep diaries and polysomnography .  Comparisons were also made between ISI scores obtained from patients , significant others , and clinicians . Results : The results of Study 1 showed that the  ISI  has adequate internal consistency and is a reliable self-report measure to evaluate perceived sleep difficulties . The results from Study 2 also indicated that the ISI is a valid and sensitive measure to detect changes in perceived sleep difficulties with treatment . In addition , there is a close convergence between scores obtained from the ISI patient 's version and those from the clinician 's and significant other 's versions . Conclusions : The present findings indicate that the ISI is a reliable and valid instrument to quantify perceived insomnia severity . The ISI is likely to be a clinical ly useful tool as a screening device or as an outcome measure in insomnia treatment research STUDY OBJECTIVES This study examined the effects of bright light exposure , as compared to dim light , on daytime subjective sleepiness , incidences of slow eye movements ( SEMs ) , and psychomotor vigilance task ( PVT ) performance following 2 nights of sleep restriction . DESIGN The study had a mixed factorial design with 2 independent variables : light condition ( bright light , 1,000 lux ; dim light , < 5 lux ) and time of day . The dependent variables were subjective sleepiness , PVT performance , incidences of SEMs , and salivary melatonin levels . SETTING Sleep research laboratory at Monash University . PARTICIPANTS Sixteen healthy adults ( 10 women and 6 men ) aged 18 to 35 years ( mean age 25 years , 3 months ) . INTERVENTIONS Following 2 nights of sleep restriction ( 5 hours each night ) , participants were exposed to modified constant routine conditions . Eight participants were exposed to bright light from noon until 5:00 pm . Outside the bright light exposure period ( 9:00 am to noon , 5:00 pm to 9:00 pm ) light levels were maintained at less than 5 lux . A second group of 8 participants served as controls for the bright light exposure and were exposed to dim light throughout the entire protocol . MEASUREMENTS AND RESULTS Bright light exposure reduced subjective sleepiness , decreased SEMs , and improved PVT performance compared to dim light . Bright lights had no effect on salivary melatonin . A significant positive correlation between PVT reaction times and subjective sleepiness was observed for both groups . Changes in SEMs did not correlate significantly with either subjective sleepiness or PVT performance . CONCLUSIONS Daytime bright light exposure can reduce the impact of sleep loss on sleepiness levels and performance , as compared to dim light . These effects appear to be mediated by mechanisms that are separate from melatonin suppression . The results may assist in the development of treatments for daytime sleepiness 
    Output:
    
We found  sleep diaries , polysomnography ( PSG ) , and clinical screening examinations  to be widely used with both control subjects and insomnia participants .
However , there are differences between research groups in the precise definitions applied to the components of normal sleep .