***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: BACKGROUND The adverse effects of alcohol on brain function result , in part , from inflammatory processes . The sex-specific neuropsychiatric consequences and inflammatory status of active alcohol dependence and early remission from dependence have not been investigated . METHODS Neuropsychiatric symptoms , inflammatory factors , and liver enzymes were compared in a prospect i ve cohort study of adults with ( n=51 ) or without ( n=31 ) a current or recent history of alcohol dependence . RESULTS Neuropsychiatric profiles were similar in adults with current or recent alcohol dependence regardless of sex . In male and female participants measures of depression ( female p<0.05 , male p<0.001 ) , anxiety ( female p<0.001 , male p<0.001 ) , and memory complaints ( female p<0.001 , male p<0.05 ) were elevated , relative to non-dependent controls . Significant sex × alcohol dependence history interactions were observed for plasma levels of tissue inhibitor of metalloproteinase 1 ( TIMP-1 ) and brain derived neurotrophic factor ( BDNF ) , with women in the alcohol dependent group exhibiting increased levels of both analytes ( p<0.05 ) relative to controls . Positive correlations between TIMP-1 levels and measures of depression ( r2=0.35 , p<0.01 ) , anxiety ( r2=0.24 , p<0.05 ) and memory complaints ( r2=0.44 , p<0.01 ) were found in female , but not male , participants . CONCLUSIONS Though neuropsychiatric profiles were similar for men and women with current or recent alcohol dependence , plasma factors associated with increases in depression , anxiety , and memory impairment differed and support the need to tailor treatments based on sex Background : Minimal hepatic encephalopathy ( MHE ) is common in cirrhosis but its pathophysiologic basis remains undefined . We evaluated whether the presence of MHE was associated with severity of liver disease , ammonia levels or the presence of inflammation and assessed factors determining neuropsychological deterioration accompanying induction of hyperammonemia . Methods : Eighty four cirrhotics were studied . A neuropsychological test battery was performed and blood taken for ammonia , WCC , CRP , nitrate/nitrite , IL-6 and amino acids , before and after , induction of hyperammonemia by administration of a solution mimicking the amino acid composition of haemoglobin ( 60 ) or placebo ( 24 ) . Results : The presence and severity of MHE were independent of severity of liver disease and ammonia concentration but markers of inflammation were significantly higher in those with MHE compared with those without . Induction of hyperammonemia produced deterioration in one or more neuropsychological tests by ≥1 SD in 73.3 % . This was independent of the magnitude of change in plasma ammonia and severity of liver disease but was significantly greater in those with more marked inflammation . Conclusion : Our data show that inflammation is an important determinant of the presence and severity of MHE . The change in neuropsychological function following induced hyperammonemia is greater in those with more severe inflammation AIMS The aim of the study was to investigate factors hypothesized to influence the relapse process , with a focus on the role of self-efficacy , alcohol dependence and cognitive functioning . DESIGN The study was conducted in the context of a controlled trial of a relapse prevention programme . Subjects were assessed prior to treatment , at immediate conclusion of treatment and at 6- and 12-month follow-up . SETTING The study was conducted in an Alcohol Treatment Unit ( ATU ) in Scotl and . PARTICIPANTS Subjects were 60 male problem drinkers who were patients at the ATU . They were heavy drinkers , with corresponding high levels of alcohol dependence and alcohol-related harm . MEASUREMENTS The independent variables were  post-treatment self-efficacy , alcohol dependence , cognitive functioning , level of depression and alcohol consumption prior to admission to treatment . The dependent variables were post-treatment drinking behaviour and functioning and time to lapse and relapse . FINDINGS Although the methodology does not allow identification of causality , support was found for the hypothesis that post-treatment self-efficacy was an intervening variable between treatment and outcome . Higher post-treatment self-efficacy predicted better outcome at 6-month follow-up and was associated with a reduced risk of lapse and relapse over the 12-month follow-up . Poorer cognitive functioning was significantly associated with being categorized as a problem drinker at 6-month follow-up and with higher risk of a lapse over the 12-month follow-up . Level of alcohol dependence did not predict outcome . CONCLUSIONS It was concluded that post-treatment self-efficacy rating is a predictor of treatment outcome and time to lapse and relapse and that cognitive functioning is a predictor of treatment outcome and time to lapse 
    Output:
    
Main findings : Although literature on the role of inflammation in alcohol use-related cognitive deficiency remains scarce , current findings indicate that pro-inflammatory processes indeed result in exacerbation of several domains of cognitive deterioration .
Interestingly , microglia , the immune cells of the brain , appear to exert initial compensatory neuroprotective functionalities upon acute ethanol exposure while chronic alcohol intake seems to attenuate these responses and overall microglial activity .