***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: Abstract Objective : Quantitation of glutathione ( GSH ) in the human brain in vivo using short echo time 1 H NMR spectroscopy is challenging because GSH resonances are not easily resolved . The main objective of this study was to vali date such quantitation in a clinical ly relevant population using the resolved GSH resonances provided by edited spectroscopy . A secondary objective was to compare several of the neurochemical concentrations quantified along with GSH using LCModel analysis of short echo time spectra in schizophrenia versus control . Material s and Methods :  GSH  was quantified at 4 T from short echo STEAM spectra and MEGA-PRESS edited spectra from identical volumes of interest ( anterior cingulate ) in ten volunteers .  Neurochemical profiles were quantified in nine controls and 13 medicated schizophrenic patients . Results : GSH concentrations as quantified using STEAM , 1.6 ± 0.4 μmol/g ( mean ± SD , n=10 ) , were within error of those quantified using edited spectra , 1.4 ± 0.4 μmol/g , and were not different ( p=0.4 ) . None of the neurochemical measurements reached sufficient statistical power to detect differences smaller than 10 % in schizophrenia versus control . As such , no differences were observed . Conclusions : Human brain GSH concentrations can be quantified in a clinical setting using short-echo time STEAM spectra at 4 T Rationale Lithium is an effective treatment for bipolar disorder , but safety issues complicate its clinical use . The antioxidant drug , ebselen , may be a possible lithium-mimetic based on its ability to inhibit inositol monophosphatase ( IMPase ) , an action which it shares with lithium . Objectives Our primary aim was to determine whether ebselen lowered levels of inositol in the human brain . We also assessed the effect of ebselen on other brain neurometabolites , including glutathione , glutamate , glutamine , and glutamate + glutamine ( Glx ) Methods Twenty healthy volunteers were tested on two occasions receiving either ebselen ( 3600 mg over 24 h ) or identical placebo in a double-blind , r and om-order , crossover design . Two hours after the final dose of ebselen/placebo , participants underwent proton magnetic resonance spectroscopy ( 1H MRS ) at 7 tesla ( T ) with voxels placed in the anterior cingulate and occipital cortex . Neurometabolite levels were calculated using an unsuppressed water signal as a reference and corrected for individual cerebrospinal fluid content in the voxel . Results Ebselen produced no effect on neurometabolite levels in the occipital cortex . In the anterior cingulate cortex , ebselen lowered concentrations of inositol ( p = 0.028 , Cohen ’s d = 0.60 ) as well as those of glutathione ( p = 0.033 , d = 0.58 ) , glutamine ( p = 0.024 , d = 0.62 ) , glutamate ( p = 0.01 , d = 0.73 ) , and Glx ( p = 0.001 , d = 1.0 ) . Conclusions The study suggests that ebselen produces a functional inhibition of IMPase in the human brain . The effect of ebselen to lower glutamate is consistent with its reported ability to inhibit the enzyme , glutaminase . Ebselen may have potential as a re purpose d treatment for bipolar disorder OBJECTIVES As life expectancy increases , the need to prevent major health disorders is clear . Depressive symptoms are common in older adults and are associated with cognitive decline and greater risk for transitioning to major depression . Oxidative stress may be implicated in the pathophysiology of major depression and can be measured in vivo using proton magnetic resonance spectroscopy via the neurometabolite glutathione ( GSH ) . Evidence suggests ω-3 fatty acid ( FA ) supplementation may prevent depression and directly affect GSH concentration . The aim of this study was to examine the effect of ω-3 FA supplementation on in vivo GSH concentration in older adults at risk for depression . METHODS Fifty-one older adults at risk for depression were r and omized to receive either four 1000-mg ω-3 FA supplements daily ( containing eicosapentaenoic acid 1200 mg plus docosahexaenoic acid 800 mg ) or placebo ( four 1000-mg paraffin oil placebo capsules daily ) for 12 wk . Participants underwent magnetic resonance spectroscopy , as well as medical , neuropsychological , and self-report assessment s at baseline and after 12 wk of supplementation . GSH was measured in the thalamus and calculated as a ratio to creatine . Depressive symptoms were measured using the Patient Health Question naire . RESULTS Compared with the group given the ω-3 FA supplements , the placebo group had greater change in the GSH-to-creatine ratio in the thalamus ( t = 2.00 ; P = 0.049 ) after the 12 wk intervention . This increase was in turn associated with a worsening of depressive symptoms ( r = 0.43 ; P = 0.043 ) . CONCLUSIONS Depressive symptom severity in older adults appears to be associated with increased brain levels of GSH , a key marker of oxidative stress . Importantly , ω-3 FA supplementation may attenuate oxidative stress mechanisms , thereby offering benefits for depression prevention Studies have proposed the involvement of oxidative stress and neuronal energy dysfunctions in the pathophysiology of bipolar disorder ( BD ) . This study evaluates plasma levels of the oxidative/energy metabolism markers , thiobarbituric acid reactive substances ( TBARS ) , superoxide dismutase ( SOD ) , catalase ( CAT ) , and neuron-specific enolase ( NSE ) during initial episodes of mania compared to controls in 75 subjects . Two groups of manic subjects ( unmedicated n=30 , and lithium-treated n=15 ) were age/gender matched with healthy controls ( n=30 ) .  TBARS and antioxidant enzymes activity ( SOD and CAT ) were increased in unmedicated manic patients compared to controls . Conversely , plasma NSE levels were lower during mania than in the controls . In contrast , acute treatment with lithium showed a significant reduction in both SOD/CAT ratio and TBARS levels . These results suggest that initial manic episodes are associated with both increased oxidative stress parameters and activated antioxidant defenses , which may be related to dysfunctions on energy metabolism and neuroplasticity pathways . Antioxidant effects using lithium in mania were shown , and further studies are necessary to evaluate the potential role of these effects in the pathophysiology and therapeutics of BD A prospect i ve survey was conducted on 155 consecutive subjects with manic symptoms admitted to an inpatient psychiatric facility to identify possible reasons for rehospitalization . Approximately one third were previously hospitalized at the same facility within the past month . Over half ( 57 % ) of the sample were admitted because of aggressive episodes . On admission , 80 percent were receiving carbamazepine or lithium for a mood disorder , and 52.3 percent were receiving multiple medications , of which antipsychotics accounted for over half . Forty-four percent of the sample had comorbid substance use on admission , with marijuana and stimulants accounting for the majority of illicit drug use . Medication noncompliance in 64 percent , and identifiable psychosocial stressors in 55 percent , were also likely contributors to rehospitalization . The data highlights specific treatment issues in the care of patients with a manic component to their illness , and suggests the need for individualized discharge planning with careful followup and continual patient education to assist in the transition from inpatient to society Abstract There is evidence of derangement of oxidant and antioxidant defense systems in depression . The present study examined the effects of fluoxetine and citalopram , st and ard selective serotonin re-uptake inhibitors , on lipid peroxidation , superoxide dismutase ( SOD ) activity and ascorbic acid concentrations . For this , a prospect i ve open-labeled , r and omized design was utilized . Patients with major depression ( n = 62 ) were compared with age- and sex-matched healthy volunteers ( n = 40 ) . There was a significant increase in serum SOD , serum MDA and decrease in plasma ascorbic acid levels in patients of major depression as compared to control subjects . The trend reversed significantly after treatment with fluoxetine and citalopram . Results indicate a greater reduction in oxidative stress with citalopram than fluoxetine . The Hamilton Rating Scale for Depression ( HRSD ) score also improved with fluoxetine and citalopram treatment . These findings indicate that major depression is associated with increased levels of serum SOD , serum MDA and decreased levels of plasma ascorbic acid . Treatment with fluoxetine and citalopram reversed these biochemical parameters . This study can be used as a predictor of drug response by fluoxetine and citalopram in major depression There is strong evidence that oxygen free radicals may play an important role in the pathophysiology of schizophrenia . Impaired antioxidant defense and increased lipid peroxidation have been previously reported in drug-naïve , first episode and chronically medicated schizophrenic patients using typical neuroleptics . We measured serum SOD and TBARS in two groups of chronic medicated DSM-IV schizophrenic patients , under haloperidol ( n = 10 ) or clozapine ( n = 7 ) and a group of healthy controls ( n = 15 ) .  Serum SOD and TBARS were significantly higher ( p = 0.001 ) in schizophrenic patients ( 7.1 + /- 3.0 and 3.8 + /- 0.8 ) than in controls ( 4.0 + /- 1.6 and 2.5 + /- 0.7 ) . Among patients , serum TBARS was significantly higher ( p = 0.008 ) in those under clozapine ( 4.4 + /- 0.7 ) than in those under haloperidol treatment ( 3.4 + /- 0.7 ) . For SOD levels the difference between groups was not found . It is reasonable to argue that the difference found in TBARS levels might be due to the course of the disease , instead of medication . Further investigation on the role of oxidative tonus and lipid peroxidation in different schizophrenia subtypes and different outcome patterns in this disorder is warranted . Additionally it could also address questions concerning a possible oxidant/antioxidant imbalance in schizophrenia 
    Output:
    
RESULTS There is limited evidence showing altered brain glutathione concentration in mental disorders ; the best evidence suggests glutathione is decreased in depression , but is not altered in bipolar disorder .
CONCLUSIONS Analysis of the minimum effect size measurable in existing studies indicates that increased number of participants is required to measure subtle but possibly important differences and move the field forward