***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: Emotion  regulation ( ER ) has become a relevant construct to underst and ing paranoia . While the ER strategy called expressive suppression ( e.g. , poker face ) may foster state paranoia by increasing arousal , another strategy called re appraisal ( e.g. , changing the perspective on situations ) may reduce negative emotions and state paranoia when adaptively used . However , if re appraisal fails , this could increase paranoia . The aim of this study was to test the proposed effects of the ER strategies on state paranoia in the socially stressful situation of being excluded in paranoia-prone individuals . We conducted an experimental online study with N=116 participants who were r and omized to a social inclusion or an exclusion condition using a virtual Cyberball ball-tossing game .  They completed question naires on paranoia proneness and habitual ER strategies . Before and after the Cyberball task , participants rated their level of state paranoia . The impact of habitual ER strategies , paranoia proneness , and social stress on changes in state paranoia was investigated using linear regression analysis . The three-way interaction of social stress , paranoia proneness , and habitual re appraisal use significantly predicted state paranoia , t(114)=2.62 , p=0.010 . The decomposition of the interaction term revealed that in the social stress condition , the impact of re appraisal on state paranoia was moderated by the level paranoia proneness . Specifically , in high paranoia-prone individuals the use of re appraisal predicted higher state paranoia . The findings regarding habitual use of suppression were not significant . Although re appraisal is generally considered a functional strategy , its use in distressing social situations seems to be impaired in persons with higher paranoia proneness . A working model of emotion dysregulation in delusions is presented and possible implication s for cognitive therapy of psychosis are discussed OBJECTIVE This longitudinal , prospect i ve study examined the relationship between childhood sexual abuse and later sleep problems in adolescence while taking into account cooccurring psychopathology that is closely related to sleep disruption [ e.g. , depression and posttraumatic stress disorder ( PTSD ) ] . METHOD Sleep disturbances in 147 females ( 78 sexually abused ; 69 comparison ) were assessed 10 years after disclosure of substantiated abuse . The follow-up protocol included self-report questions regarding typical sleeping patterns and sleep disturbances as well as measures of depression , PTSD , and lifetime victimization histories . RESULTS Sleep disturbances correlated significantly with both depression and PTSD . Hierarchical regression analysis showed that sexually abused participants reported significantly greater rates of sleep disturbances than comparison participants above and beyond depression and PTSD . Sleep disturbances were related to revictimization rates independent of sexual abuse , depression , and PTSD . CONCLUSIONS Assessment s of sleep disturbances should be integrated into st and ard of care for adolescents who have experienced sexual abuse STUDY OBJECTIVES To investigate sleep 's effect in the immediate aftermath of experiencing an analog trauma in the laboratory on reducing intrusive emotional memory formation . METHODS Sixty-five healthy women were exposed to an experimental laboratory trauma . They viewed a neutral and a trauma film in the laboratory and were r and omly allocated to either a group that slept following film viewing or a group that remained awake . Sleep was recorded with electroencephalogram  in a subgroup of participants in the sleep group . All participants recorded intrusive memories in the week following the film . RESULTS The sleep group experienced fewer and less distressing intrusive trauma memories compared to the wake group . These effects were particularly evident toward the end of the week . Duration spent in stage N2 as opposed to light N1 sleep , a higher number of fast parietal sleep spindles and a lower rapid eye movement sleep density predicted intrusion frequency . CONCLUSIONS Our results have clinical implication s and set the ground for early-intervention sleep studies following trauma and prevention of chronic posttrauma disorders Abstract Our view is that insomnia may be a causal factor in the occurrence of psychotic experiences such as paranoia and hallucinations . However , the causal relationship is not established . The aim of the study was to investigate the causal role of insomnia in psychotic experiences via a sleep restriction manipulation . The study was a within-subjects crossover design that included a planned mediation analysis . Sixty-eight non clinical volunteers underwent a sleep loss condition ( restricted to 4 h sleep for 3 nights ) and a control condition ( st and ard sleep ) in r and omized order in 2 consecutive weeks , with a weekend washout period . Psychotic experiences ( paranoia , hallucinations , gr and iosity , and cognitive disorganization ) and c and i date mediating variables ( negative affect and related processes , working memory , decision making , and perceptual processing ) were assessed before and after each condition . Actigraphy verified an average sleep duration of 5 h 15 min in the sleep loss condition , vs 6 h 58 min in the control condition . After the sleep loss condition , relative to the control condition , participants reported significant increases in paranoia , hallucinations , and cognitive disorganization , with no significant changes in gr and iosity . The sleep loss condition was also associated with significant increases in negative affect , negative self and other cognitions , worry , and working memory impairment . Mediation analyses indicated that changes in psychotic experiences were mediated by changes in negative affect and related processes , but not memory impairment . The overall conclusion is that insomnia has a causal role in the occurrence of certain psychotic experiences , and that a key route is via negative affect Summary Background Sleep difficulties might be a contributory causal factor in the occurrence of mental health problems . If this is true , improving sleep should benefit psychological health . We aim ed to determine whether treating insomnia leads to a reduction in paranoia and hallucinations . Methods We did this single-blind , r and omised controlled trial ( OASIS ) at 26 UK universities . University students with insomnia were r and omly assigned ( 1:1 ) with simple r and omisation to receive digital cognitive behavioural therapy ( CBT ) for insomnia or usual care , and the research team were masked to the treatment . Online assessment s took place at weeks 0 , 3 , 10 ( end of therapy ) , and 22 . The primary outcome measures were for insomnia , paranoia , and hallucinatory experiences . We did intention-to-treat analyses . The trial is registered with the IS RCT N registry , number IS RCT N61272251 . Findings Between March 5 , 2015 , and Feb 17 , 2016 , we r and omly assigned 3755 participants to receive digital CBT for insomnia ( n=1891 ) or usual practice ( n=1864 ) . Compared with usual practice , the sleep intervention at 10 weeks reduced insomnia ( adjusted difference 4·78 , 95 % CI 4·29 to 5·26 , Cohen 's d=1·11 ; p<0·0001 ) , paranoia ( −2·22 , −2·98 to −1·45 , Cohen 's d=0·19 ; p<0·0001 ) , and hallucinations ( −1·58 , −1·98 to −1·18 , Cohen 's d=0·24 ; p<0·0001 ) . Insomnia was a mediator of change in paranoia and hallucinations . No adverse events were reported . Interpretation To our knowledge , this is the largest r and omised controlled trial of a psychological intervention for a mental health problem . It provides strong evidence that insomnia is a causal factor in the occurrence of psychotic experiences and other mental health problems . Whether the results generalise beyond a student population requires testing . The treatment of disrupted sleep might require a higher priority in mental health provision . Funding Wellcome Trust Sleep disturbance is common in schizophrenia , but its role in predicting functioning and psychotic symptoms has yet to be rigorously examined . The purpose of this study was to conduct a prospect i ve , high-resolution examination of the relationship between nightly sleep and next-day functioning and psychotic symptoms in people with a diagnosis of schizophrenia .  Experience sampling methodology was integrated with actigraphy and sleep diaries across 7 days in 22 patients with a diagnosis of schizophrenia . Momentary assessment s of mood , psychotic symptoms , and functioning were gathered at 5 points each day following pseudor and om schedules . Multilevel modeling was performed to evaluate the links between variables . Objective and subjective sleep disturbance predicted reduced next-day functioning , which remained significant after controlling for psychotic symptom severity . Increased sleep fragmentation and reduced subjective and objective sleep efficiency predicted greater next-day auditory hallucinations , whereas increased objective sleep fragmentation and reduced subjective sleep quality predicted greater paranoia and delusions of control . Negative affect on awakening mediated a proportion of these relationships ( range : 17.9 - 57.3 % ) . For the first time , we show that sleep disturbance is a predictor of next-day impaired functioning and psychotic symptom severity in people with a diagnosis of schizophrenia . Therefore , interventions targeting sleep may have the potential to directly and indirectly enhance functional and symptomatic recovery in those experiencing psychosis . ( PsycINFO Data base STUDY OBJECTIVES In schizophrenia there is a dramatic reduction of sleep spindles that predicts deficient sleep-dependent memory consolidation . Eszopiclone ( Lunesta ) , a non-benzodiazepine hypnotic , acts on γ-aminobutyric acid ( GABA ) neurons in the thalamic reticular nucleus where spindles are generated . We investigated whether eszopiclone could increase spindles and thereby improve memory consolidation in schizophrenia . DESIGN In a double-blind design , patients were r and omly assigned to receive either placebo or 3 mg of eszopiclone . Patients completed Baseline and Treatment visits , each consisting of two consecutive nights of polysomnography . On the second night of each visit , patients were trained on the  motor sequence task ( MST )  at bedtime and tested the following morning . SETTING Academic research center . PARTICIPANTS Twenty-one chronic , medicated schizophrenia out patients . MEASUREMENTS AND RESULTS We compared the effects of two nights of eszopiclone vs. placebo on stage 2 sleep spindles and overnight changes in MST performance . Eszopiclone increased the number and density of spindles over baseline levels significantly more than placebo , but did not significantly enhance overnight MST improvement . In the combined eszopiclone and placebo groups , spindle number and density predicted overnight MST improvement . CONCLUSION Eszopiclone significantly increased sleep spindles , which correlated with overnight motor sequence task improvement . These findings provide partial support for the hypothesis that the spindle deficit in schizophrenia impairs sleep-dependent memory consolidation and may be ameliorated by eszopiclone . Larger sample s may be needed to detect a significant effect on memory . Given the general role of sleep spindles in cognition , they offer a promising novel potential target for treating cognitive deficits in schizophrenia STUDY OBJECTIVES We studied the effects of sleep deprivation on executive functions using a task battery which included a modified Sternberg task , a probed recall task , and a phonemic verbal fluency task . These tasks were selected because they allow dissociation of some important executive processes from non-executive components of cognition . DESIGN Subjects were r and omized to a total sleep deprivation condition or a  control condition . Performance on the executive functions task battery was assessed at baseline , after 51 h of total sleep deprivation ( or no sleep deprivation in the control group ) , and following 2 nights of recovery sleep , at fixed time of day ( 11:00 ) . Performance was also measured repeatedly throughout the experiment on a control task battery , for which the effects of total sleep deprivation had been documented in previously published studies . SETTING Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring . PARTICIPANTS Twenty-three healthy adults ( age range 22 - 38 y ; 11 women ) . Twelve subjects were r and omized to the sleep deprivation condition ; the others were  controls  . RESULTS Performance on the control task battery was considerably de grade d during sleep deprivation . Overall performance on the modified Sternberg task also showed impairment during sleep deprivation , as compared to baseline and recovery and compared to controls . However , two dissociated components of executive functioning on this task -- working memory scanning efficiency and resistance to proactive interference -- were maintained at levels equivalent to baseline . On the probed recall task , resistance to proactive interference was also preserved . Executive aspects of performance on the phonemic verbal fluency task showed improvement during sleep deprivation , as did overall performance on this task . CONCLUSION Sleep deprivation affected distinct components of cognitive processing differentially . Dissociated non-executive components of cognition in executive functions tasks were de grade d by sleep deprivation , as was control task performance . However , the executive functions of working memory scanning efficiency and resistance to proactive interference were not significantly affected by sleep deprivation , nor were dissociated executive processes of phonemic verbal fluency performance . These results challenge the prevailing view that executive functions are especially vulnerable to sleep loss . Our findings also question the idea that impairment due to sleep deprivation is generic to cognitive processes subserved by attention Current antipsychotic medications fail to satisfactorily reduce negative and cognitive symptoms and produce many unwanted side effects , necessitating the development of new compounds . Cross-species , experimental behavioural model systems can be valuable to inform the development of such drugs . The aim of the current study was to further test the hypothesis that controlled sleep deprivation is a safe and effective model system for psychosis when combined with oculomotor biomarkers of schizophrenia . Using a r and omized counterbalanced within-subjects design , we investigated the effects of 1 night of total sleep deprivation in 32 healthy participants on smooth pursuit eye movements ( SPEM ) , prosaccades ( PS ) , antisaccades 
    Output:
    
Results showed that insomnia was associated with all individual psychotic‐like , dissociative and hypomanic experiences review ed ( effect size range : small‐to‐large ) .
Parasomnias were associated with all psychotic‐like experiences ; however , there was evidence of variation in magnitude between individual experiences .
An eveningness chronotype was associated with dissociative and hypomanic experiences , and circadian dysrhythmia was found alongside hypomania but not the other experiences review ed .
Finally , experimental sleep manipulation studies revealed a potential causal link between sleep loss and psychotic‐like and dissociative experiences , although size and consistency of effects varied by specific experience .