***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: Rationale and objective In animal and human studies , the neurotransmitter serotonin ( 5-hydroxytryptamine ; 5-HT ) has been implicated in mediating impulsiveness and aggression . To test the hypothesis that 5-HT modulates neuro-cognitive brain activation during inhibitory control , we examined the effect of acute tryptophan depletion ( ATD ) , a dietary challenge , which has been shown to decrease 5-HT synthesis in the brain , on functional brain activation during a go/no-go task . Methods Nine healthy , right-h and ed volunteers performed a rapid , event-related go/no-go task in two functional magnetic resonance imaging ( fMRI ) scanning sessions , 5 h after either a tryptophan-free or a balanced amino acid drink in a double-blind , sham depletion-controlled , counterbalanced , crossover design . The task required subjects to selectively execute or inhibit a motor response . Tryptophan depletion significantly lowered total plasma tryptophan concentration by 80 % , but did not significantly alter inhibitory performance or mood ratings . Results ATD significantly reduced right orbito-inferior prefrontal activation during the no-go condition , and increased activation in superior and medial temporal cortices . Conclusions These findings provide neuro-functional evidence of a serotonergic modulation of right inferior prefrontal during inhibitory motor control . The increased engagement of temporal brain regions may reflect compensatory mechanisms The dopamine D2 receptor ( DRD2 ) C957 T polymorphism CC genotype is associated with decreased striatal binding of DRD2 and executive function and working memory impairments in healthy adults . We investigated the relationships between C957 T and acute stress with behavioral phenotypes of impulsivity in 72 young adults r and omly allocated to either an acute psychosocial stress or relaxation induction condition . Homozygotes for 957C showed increased reward responsiveness after stress induction . They were also quicker when making immediate choices on the delay discounting task when stressed , compared with homozygotes who were not stressed . No effects were found for response inhibition , a dimension of impulsivity not related to extrinsic rewards . These data suggest that C957 T is associated with a reward-related impulsivity endophenotype in response to acute psychosocial stress . Future studies should examine whether the greater sensitivity of 957C homozygotes to the effects of stress is mediated through dopamine release In animal and human research , the neurotransmitter serotonin ( 5-HT ) has been implicated in inhibitory control . Using functional magnetic resonance imaging ( fMRI ) , the present study investigated the acute effects of pharmacological modulation of the serotonergic system on brain activation during response inhibition and re-engagement in healthy human volunteers . In a r and omized double-blind placebo-controlled cross-over design 14 men received either a single oral dose of the selective serotonin reuptake inhibitor ( SSRI ) escitalopram ( 10 mg ) or a placebo . At the time of the expected plasma peak concentration , participants performed a stop-change task during fMRI . Escitalopram did not affect behavioural performance , since the main effect did not reveal significant differences between reaction times of go- , stop- or change-trials . During successful response inhibition , escitalopram , however , was associated with enhanced brain activation in right prefrontal cortex , right supplementary/pre-motor and bilateral cingulate cortex , and subcortical regions . During inhibition failures , escitalopram also modulated a broad network of brain regions , including anterior cingulate , right parietal cortex , right orbitofrontal cortex , and areas in right temporal cortex and subcortical regions . During response re-engagement escitalopram increased brain activation in right inferior frontal gyrus and precuneus as well as in left middle temporal gyrus . The results implicate the involvement of 5-HT in neural regulation of response inhibition and re-engagement . This study also provides evidence that 5-HT affects both action restraint and action cancellation through modulation of activation of brain areas . The results support the view for a fronto-striatal circuitry for response inhibition in conjunction with serotonin The functional significance of the N2 in  go/no-go tasks  was investigated by comparing electrophysiological data obtained from two tasks : a  go/no-go task involving both response inhibition as well as response conflict monitoring , and a  go/GO task  associated with conflict monitoring only . No response was required to no-go stimuli , and a response with maximal force to GO stimuli . The relative frequency of the go stimuli ( 80 % vs. 50 % ) was varied . The N2 peaked on both no-go and GO trials , with larger amplitudes for both signals when presented in a context of frequent ( 80 % ) go signals . These results support the idea that the N2 reflects conflict monitoring not response inhibition In females , most genes on the X chromosome are generally assumed to be transcriptionally silenced on the inactive X as a result of X inactivation . However , particularly in humans , an increasing number of genes are known to " escape " X inactivation and are expressed from both the active ( Xa ) and inactive ( Xi ) X chromosomes ; such genes reflect different molecular and epigenetic responses to X inactivation and are c and i date s for phenotypes associated with X aneuploidy . To identify genes that escape X inactivation and to generate a first-generation X-inactivation profile of the X , we have evaluated the expression of 224 X-linked genes and expressed sequence tags by  reverse-transcription-PCR analysis of a panel of multiple independent mouse/human somatic cell hybrids containing a normal human Xi but no Xa . The result ing survey yields an initial X-inactivation profile that is estimated to represent approximately 10 % of all X-linked transcripts . Of the 224 transcripts tested here , 34 ( three of which are pseudoautosomal ) were expressed in as many as nine Xi hybrids and thus appear to escape inactivation . The genes that escape inactivation are distributed nonr and omly along the X ; 31 of 34 such transcripts map to Xp , implying that the two arms of the X are epigenetically and /or evolutionarily distinct and suggesting that genetic imbalance of Xp may be more severe clinical ly than imbalance of Xq . A complete X-inactivation profile will provide information relevant to clinical genetics and genetic counseling and should yield insight into the genomic and epigenetic organization of the X chromosome BACKGROUND Response inhibition is a prototypical executive function of considerable clinical relevance to psychiatry . Nevertheless , our underst and ing of its pharmacological modulation remains incomplete . METHODS We used a r and omized , double-blind , placebo-controlled , crossover design to examine the effect of an acute dose of methylpheni date ( MPH ) ( 30 mg ) , atomoxetine ( ATM ) ( 60 mg ) , citalopram ( CIT ) ( 30 mg ) , and placebo ( PLAC ) ( dextrose ) on the stop signal inhibition task in 24 healthy , right-h and ed men 18 - 35 years of age . Participants performed the task under each of the four drug conditions across four consecutive sessions . RESULTS Methylpheni date led to a reduction in both response time variability and stop-signal reaction time ( SSRT ) , indicating enhanced response inhibition compared with all other drug conditions . Crucially , the enhancement of response inhibition by MPH occurred without concomitant changes in overall response speed , arguing against a simple enhancement of processing speed . We found no significant differences between ATM and PLAC , CIT and PLAC , or ATM and CIT for either response time variability or SSRT . CONCLUSIONS An acute dose of MPH but not ATM or CIT was able to improve SSRT and reduce response time variability in non clinical participants . Improvements in response inhibition and response variability might underlie the reported clinical benefits of MPH in disorders such as attention-deficit/hyperactivity disorder Cognitive functions dependent on the prefrontal cortex , such as the ability to suppress behavior ( response inhibition ) and to learn from complex feedback ( probabilistic learning ) , play critical roles in activities of daily life . To what extent do different neurochemical systems modulate these two cognitive functions ? Here , using stop-signal and probabilistic learning tasks , we show a double dissociation for the involvement of noradrenaline and serotonin in human cognition . In healthy volunteers , inhibition of central noradrenaline reuptake improved response inhibition but had no effect on probabilistic learning , whereas inhibition of central serotonin reuptake impaired probabilistic learning with no effect on response inhibition 
    Output:
    
We find no evidence of significant associations between those polymorphisms and RI .
None of these polymorphisms showed a reliable association with response inhibition performance .