***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 It has been suggested that the extract of gingko biloba ( EGb ) may enhance the efficiency of the classic antipsychotic haloperidol in patients with chronic schizophrenia , especially on positive symptoms , and reduce serum superoxide dismutase ( SOD ) levels . Therefore , we decided to evaluate the therapeutic effect of EGb and to examine the effect of it on the levels of antioxidant enzymes in schizophrenic patients on olanzapine treatment . We hypothesized that EGb would have the beneficial effects on schizophrenic symptoms and might cause reductions in antioxidant enzymes . The subjects were r and omly assigned to the two groups : olanzapine plus EGb  ( group I ) ( n=15 ) and olanzapine alone  ( group II ) ( n=14 ) . The patients were evaluated at baseline and at week 8 with respect to the Positive and Negative Syndrome Scale ( PANSS ) , serum SOD , catalase ( CAT ) , and glutathion peroxidase ( GPX ) levels . At baseline , no statistically significant difference regarding the mean total PANSS scores between treatment groups was found . At the evaluation of week 8 , a significant difference in mean Scale for the Assessment of Postive Symptoms ( SAPS ) scores but not in Scale for the Assessment of Negative Symptoms scores between groups was found . Total patients had statistically significant higher serum SOD , CAT and GPX levels compared to control groups at baseline . At 8 weeks , there were significant differences in the mean decrease in SOD and CAT levels but not in GPX levels between treatment groups . The changes in SOD and CAT levels were correlated with the change in SAPS in group I , but not in the group II . The present study supported the findings of the previous study demonstrating that EGb might enhance the efficiency of antipsychotic in patients with schizophrenia , particularly on positive symptoms of the disorder Abstract Biomarker-guided treatments are needed in psychiatry , and previous data suggest oxidative stress may be a target in schizophrenia . A previous add-on trial with the antioxidant N-acetylcysteine ( NAC ) led to negative symptom reductions in chronic patients . We aim to study NAC ’s impact on symptoms and neurocognition in early psychosis ( EP ) and to explore whether glutathione (GSH)/redox markers could represent valid biomarkers to guide treatment . In a double-blind , r and omized , placebo-controlled trial in 63 EP patients , we assessed the effect of NAC supplementation ( 2700 mg/day , 6 months ) on PANSS , neurocognition , and redox markers ( brain GSH [ GSHmPFC ] , blood cells GSH levels [ GSHBC ] , GSH peroxidase activity [ GPxBC ] ) . No changes in negative or positive symptoms or functional outcome were observed with NAC , but significant improvements were found in favor of NAC on neurocognition ( processing speed ) . NAC also led to increases of GSHmPFC by 23 % ( P = .005 ) and GSHBC by 19 % ( P = .05 ) . In patients with high-baseline GPxBC compared to low-baseline GPxBC , subgroup explorations revealed a link between changes of positive symptoms and changes of redox status with NAC . In conclusion , NAC supplementation in a limited sample of EP patients did not improve negative symptoms , which were at modest baseline levels . However , NAC led to some neurocognitive improvements and an increase in brain GSH levels , indicating good target engagement . Blood GPx activity , a redox peripheral index associated with brain GSH levels , could help identify a subgroup of patients who improve their positive symptoms with NAC . Thus , future trials with antioxidants in EP should consider biomarker-guided treatment Schizophrenia unfolds during the late period of brain maturation , while myelination is still continuing . In the present study , we used MRI and T2 relaxation analysis to measure the myelin water fraction in schizophrenia . In schizophrenia ( n=30 ) compared with healthy subjects ( n=27 ) , overall white matter showed 12 % lower myelin water fraction ( P=0.031 ) , with the most prominent effects on the left genu of the corpus callosum ( 36 % lower , P=0.002 ) . The left anterior genu was affected in both first-episode ( P=0.035 ) and chronic patients ( P=0.011 ) . In healthy subjects  , myelin water fraction in total white matter and in frontal white matter increased with age , and with years of education , indicating ongoing maturation . In patients with schizophrenia , neither relation was statistically significant . Post-mortem studies of anterior frontal cortex demonstrated less immunoreactivity of two oligodendrocyte-associated proteins in schizophrenia ( 2′,3′-cyclic nucleotide 3′-phosphodiesterase by 33 % , P=0.05 ; myelin-associated glycoprotein by 27 % , P=0.14 ) . Impaired myelination in schizophrenia could contribute to abnormalities of neural connectivity and persistent functional impairment in the illness OBJECTIVE Diverse electrophysiological abnormalities have been associated with schizophrenia , but the underlying causes remain elusive . We tested whether the altered oxidative stress in schizophrenia contributes to the electrophysiological abnormalities . METHODS We used an auditory oddball task to measure  mismatch negativity ( MMN ) and gamma b and response on 29 schizophrenia patients and 25 normal controls . Oxidative stress was assessed by monomeric glutathione ( GSH , reduced form ) and glutathione disulfide ( GSSG , oxidized form ) . RESULTS Patients had reduced MMN ( p=0.015 ) and reduced power of gamma b and responses at 21 - 40 Hz and 41 - 85 Hz ( all p<0.001 ) . GSH was significantly lower ( p<0.001 ) while % GSSG was higher ( p=0.023 ) in patients compared with controls . MMN was correlated with GSH in controls ; while 21 - 40 Hz responses were correlated with GSH in patients . Lower GSH and higher GSSG levels were associated with low community functioning ( p=0.018 ) . Multivariate mediation modeling showed that gamma b and at 21 - 40 Hz was a significant mediator for GSH effect on community functions . CONCLUSIONS High beta/low gamma range ( 21 - 40 Hz ) responses may be an intermediate biomarker indexing oxidative stress and its effect on clinical functions . SIGNIFICANCE Electrophysiological abnormalities and associated clinical functional changes may in part be associated with heightened oxidative stress in schizophrenia The objective of this study is to evaluate the effects of a diet with goat milk fat supplemented with physical training on markers of oxidative stress in the brain and anxiety behavior in rats . Adult male rats were r and omly divided into six groups ( n = 10 per group ) : control sedentary ( CON ) and exercised ( CON-EX ) groups , goat milk fat sedentary ( GM ) and exercised ( GM-EX ) groups , goat milk fat enriched with CLA sedentary ( GM-CLA ) and exercised ( GM-CLA-EX ) groups . The exercised groups were su bmi tted to treadmill running during four weeks . Anxiety parameters were evaluated with the open field ( OF ) and elevated plus maze ( EPM ) tests . Malondialdehyde ( MDA ) and glutathione ( GSH ) levels were measured in the brain . Compared to the CON and GM groups , the GM-CLA group ( p < 0.05 ) , in which the animals were treated with goat milk fat with an increased CLA content , showed higher rearing . All exercised animals presented an increase in grooming when compared to sedentary animals . The number of entries in the open arms and time spent in the open arms was higher in sedentary groups ( p < 0.05 ) . MDA levels in the brain were lower in the GM group when compared to those in the CON group ( p < 0.05 ) . MDA increased in exercised animals ( p < 0.05 ) . GM and GM-CLA groups showed a significant elevation in the GSH levels in the brain . Goat milk fat , however , showed a potential effect on the reduction of oxidative stress , which was associated with a reduction in anxiety behavior . However , this beneficial effect was reversed when exercise was involved Dysregulation of free radical metabolism as reflected by abnormal erythrocyte activities of three critical enzymes of the antioxidant defense system ( AODS ) , i.e. superoxide dismutase ( SOD ) , glutathione peroxidase ( GSH-Px ) and catalase ( CAT ) , has been reported in schizophrenic patients . The present study examined the effects of haloperidol , a st and ard antipsychotic agent , on the AODS enzymes , using a within-subject , repeated- measures , on-off haloperidol treatment design . The mean drug free period was 40 days . At baseline , there were no significant differences for all three enzymes between patients and age and sex-matched normal volunteers . During the drug-free condition , SOD activity , but not GSH-Px and CAT activities , was significantly higher relative to normal control subjects . However , within-subjects both SOD and GSH-Px activities , but not CAT activity , were higher in the drug-free condition compared to the treatment condition . No significant correlation was observed between SOD activity and plasma haloperidol ( or daily haloperidol dose ) levels . Smoking status , as assessed by the cotinine level , was unrelated to enzyme activities . In addition , none of the major AODS enzymes showed significant differences between relapsed and clinical ly stable patients . These findings suggest that haloperidol may not have direct regulatory effect on AODS enzyme activities and that SOD and GSH-Px activities may change in response to other factors such as change in symptom severity OBJECTIVES To develop and vali date a new risk-of-bias tool for nonr and omized studies ( NRSs ) . STUDY DESIGN AND SETTING We developed the Risk of Bias Assessment Tool for Nonr and omized Studies ( RoBANS ) . A validation process with 39 NRSs examined the reliability ( interrater agreement ) , validity ( the degree of correlation between the overall assessment s of RoBANS and Method ological Index for Nonr and omized Studies [ MINORS ] , obtained by plotting the overall risk of bias relative to effect size and funding source ) , face validity with eight experts , and completion time for the RoBANS approach . RESULTS RoBANS contains six domains : the selection of participants , confounding variables , the measurement of exposure , the blinding of the outcome assessment s , incomplete outcome data , and selective outcome reporting . The interrater agreement of the RoBANS tool except the measurement of exposure and selective outcome reporting domains ranged from fair to substantial . There was a moderate correlation between the overall risks of bias determined using RoBANS and MINORS . The observed differences in effect sizes and funding sources among the assessed studies were not correlated with the overall risk of bias in these studies . The mean time required to complete RoBANS was approximately 10 min . The external experts who were interviewed evaluated RoBANS as a " fair " assessment tool . CONCLUSIONS RoBANS shows moderate reliability , promising feasibility , and validity . The further refinement of this tool and larger validation studies are required Oxidative stress may be a contributing factor in the etiopathophysiology of schizophrenia , which may be exacerbated by the treatment with antipsychotics with pro-oxidant properties . Increased levels of S100 B are associated with neurodegenerative disorders , including schizophrenia . The aim of the present study was to investigate the role of oxidative cell damage in the pathogenesis of schizophrenia . Forty patients who fully met the fourth Diagnostic and Statistical Manual of Mental Disorders criteria for schizophrenia and 35 healthy control subjects were included in the study .  Serum S100 B level was determined to investigate brain damage . Plasma malondialdehyde ( MDA ) levels and susceptibility of red blood cell ( RBC ) to oxidation were determined to investigate the oxidative status and plasma vitamin E , vitamin C , serum total carotenoid levels and total antioxidant capacity and RBC superoxide dismutase ( SOD ) and whole blood glutathione peroxidase activities were measured to investigate the antioxidative 
    Output:
    
Patients with schizophrenia had lower levels of both glutathione and total glutathione and decreased activity of glutathione peroxidase compared to controls .
Conclusions : Our findings suggested that there may be glutathione deficits and abnormalities in the glutathione redox cycle in patients with schizophrenia .