***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 
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    ***EXAMPLES*** 
    Input: BACKGROUND Although the underlying pathology is initially confined to the lungs , the associated emotional responses to chronic obstructive pulmonary disease ( COPD ) contribute greatly to the result ing morbidity . The objective of this study was to examine the effect of an antidepressant drug on disease-specific quality of life in patients with end-stage COPD who present significant depressive symptoms . METHODS We conducted a 12-week , r and omized double-blind placebo-controlled trial of Paroxetine in which quality of life measured by the Chronic Respiratory Question naire ( CRQ ) , an evaluative COPD -specific quality -of-life question naire , was the primary outcome . RESULTS 23 patients were r and omized and 15 completed the trial ( 8 on Paroxetine ; 7 on placebo ) . In the per- protocol analysis , we observed statistically and clinical ly significant improvements favoring the active treatment in 2 of the 4 domains of the CRQ : emotional function ( adjusted mean difference : 1.1 ; 95 % confidence interval [ CI ] : 0.0 - 2.2 ) and mastery ( difference : 1.1 ; CI : 0.4 - 1.8 ) . Dyspnea and fatigue improved , but to an extent that did not reach statistical significance . In the intention-to-treat analysis , none of the differences in CRQ scores was significant . Paroxetine was not associated to any worsening of respiratory symptoms . CONCLUSIONS The results of this small r and omized trial indicated that patients with end-stage COPD may benefit from antidepressant drug therapy when significant depressive symptoms are present . This study underlined the difficulties in conducting experimental studies in frail and elderly patients with COPD Chronic obstructive pulmonary disease ( COPD ) affects over 16 million people in the United States and is a major cause of disability and death worldwide . Its prevalence and mortality are increasing disproportionately among the elderly , women , African-Americans , persons of lower socioeconomic status , and the population s of developing countries in which tobacco is aggressively marketed . In contrast to other major chronic diseases such as heart disease and cancer , medical treatments for COPD have not made decisive inroads into its morbidity or death rates over the last 20 years , result ing in continuing efforts to reduce disability in patients with established disease . Depression is a source of increased disability in COPD , and , as in other chronically ill patient population s , is often unrecognized and untreated in the primary and specialty care sectors . Nearly half of all patients experience some depressive symptoms and at least one-fifth have had one or more major depressive episodes , frequently of long duration . Evidence from r and omized controlled trials supports the thesis that patients with mild depression improve with multidisciplinary rehabilitation , whereas patients with major depression may require specific pharmacotherapy to achieve significant improvement in mood disorder and day-to-day function . In addition to its impact on disability , depression may contribute indirectly to the etiology and progression of COPD through its relationship to addictive smoking . Mood disorder in adolescence and early adulthood contributes to early smoking and failure to quit , even after the onset of respiratory disease in later life . Patients with a history of major depression are more likely to fail in smoking cessation programs and to develop a major depressive episode when they do stop . This relationship calls for psychiatrically informed intervention models to improve long-term abstinence rates . The functional impairments associated with COPD are themselves potential promoters of depressive morbidity and chronicity , acting through complex causal pathways . Progressive hypoxia due to respiratory insufficiency leads to structural brain changes and neurocognitive deficits that impair day-to-day function and reduce adaptive potential ;  and oxygen therapy , as now practice d , offers minimal neurocognitive and mood benefits to most patients . Limited data from studies of experimental hypoxia in animals suggest that relatively mild lack of oxygen impairs the function and plasticity of critical neurotransmitter systems implicated in both cognition and mood , although current practice st and ards withhold oxygen therapy until late in the course of disease when the damaging effects of hypoxia on the brain have become well established . Neuropsychiatric approaches to the prevention , delay , and treatment of brain dysfunction should be a primary objective of research to improve patient outcomes . A comprehensive relational model that links pulmonary disease , hypoxia , neurocognitive impairment , and structural brain disease with depression provides a useful framework for the design of such studies . The near-term research agenda should include three components : ( 1 ) practical methods for improving physician and patient recognition of depression and neurocognitive impairment as targets for intervention ; ( 2 ) additional trials of st and ard antidepressant treatment approaches for both major and minor depression ; and ( 3 ) tests of the hypothesis that late-onset depression in patients with COPD is a marker for the presence of neurocognitive deficits and structural brain changes . The long-range research agenda must aim at preventive interventions design ed to forestall brain deterioration . Controlled clinical trials of supplemental oxygen in patients with mild hypoxia and minimal cognitive deficits are needed to determine whether early treatment can reverse or moderate decline , reduce the incidence and chronicity of depression , and improve response to antidepressant treatment . Novel neuroprotective therapies such as antioxidant supplementation and modulation of monoaminergic neurotransmission , coupled with overall improvements in long-term respiratory disease management that minimize episodes of increased systemic oxidative stress , should be considered for multisite trials design ed to define optimal treatment and prevention Buspirone is an anxiolytic agent that appears to have no sedative effects . The aim of this study was to assess the effects of buspirone on breathlessness and exercise tolerance in patients with chronic airway obstruction . Sixteen patients , age 56.9 + /- 17.0 ; forced expiratory volume in 1 s ( FEV1 ) 1.15 + /- 0.42 l ; FEV1/forced vital capacity ( FVC ) 50.7 + /- 15.0 % ; PaCO2 42.2 + /- 5.5 mm Hg ; and PaO2 57.6 + /- 10 mm Hg , underwent a 6-min walking test , an incremental cycle ergometer test , an incremental treadmill walking test with self- assessment of dyspnea on Borg 's scale during exercise and an assessment of respiratory drive  ( P 0.1 ) , timing [ inspiration time (TI)/total breathing time ( Ttot ) ] , PaO2 , PaCO2 , FVC , FEV1 , following oral administration for 14 days of placebo or buspirone ( 20 mg daily ) in a double-blind , cross-over r and omized way . We also used the symptom check list-90-R for the assessment of subjective complaints and symptomatic behavior . A significant improvement in anxiety , depression and obsessive symptoms and complaints was noted after buspirone treatment . The P 0.1 , TI/Ttot , arterial blood gases and respiratory mechanics did not change after drug treatment . There was an improvement in exercise tolerance and in the sensation of dyspnea during the buspirone period . Thus , as given in this study , oral buspirone has therapeutic potential in the treatment of dyspnea in patients with chronic lung disease Over the ensuing seven months she had three more clinical relapses , each accompanied by reappearance in the stools of either the organism or its cytotoxin , or both . Each improvement after vancomycin ( eight to 14-daycourses ) was accompanied by disappearance of the organism . At one point she was given cholestyramine , but she was unable to tolerate it . Her illness was punctuated by malnutrition and episodes of heart failure . She was given no other antibiotics . After the sixth relapse maintenance treatment with oral vancomycin 125 mg eight-hourly was begun . With this regimen diarrhoea was controlled and stools over the next 10 weeks remained negative for C difficile and its cytotoxin . There was no adverse reaction to vancomycin throughout Although recent epidemiologic studies have established that patients with chronic medical illness and depressed mood are more disabled than euthymic patients , detailed data on the benefits and risks of antidepressant treatment in medically high-risk patients have been slow to accumulate . The authors have examined multiple outcome indicators in patients with disabling chronic obstructive pulmonary disease and comorbid depression . Thirty patients completed a 12-week , r and omized controlled trial of nortriptyline . Nortriptyline was clearly superior to placebo for treatment of depression . Nortriptyline treatment was accompanied by marked improvements in anxiety , certain respiratory symptoms , overall physical comfort , and day-to-day function ;  placebo effects were negligible . Physiological measures reflecting pulmonary insufficiency were generally unaffected by treatment . These data provide impetus for renewed efforts to improve recognition and treatment of mood disorders in even severely disabled medical patients There is controversy as to whether effects on mood play a role in mediating the response to corticosteroids in chronic obstructive pulmonary disease ( COPD ) . If alterations in mood are important , it is conceivable that psychotropic drugs such as mianserin might produce similar responses to prednisolone in patients with COPD .Twelve patients age 62.5 y , with FEV1 29 % of predicted and < 15 % reversibility to salbutamol completed a r and omised , double-blind crossover study . After an initial three week placebo run-in period patients received three weeks of prednisolone 40 mg daily or mianserin 60–90 mg daily with an intervening three week placebo washout period . Full respiratory function tests , bicycle ergometry and 6 minute walks were performed before and after the run-in and at the end of each period . Psychological and functional assessment s were also made at each visit . Prednisolone significantly increased FVC , maximum ventilation ( VEmax ) and maximum heart rate ( HRmax ) compared with placebo , with mean for the difference of 0.251 , 2.561 · min−1 and 12 beats · min−1 respectively . FVC , maximum oxygen uptake ( VO2max ) and HRmax were also significantly increased with prednisolone compared with mianserin . Anxiety scores were significantly lower with prednisolone compared with placebo . In contrast , mianserin had no significant effects on lung function , exercise or psychological parameters compared with placebo . The improvements in ventilation , exercise and anxiety scores following treatment with prednisolone were not reproduced by mianserin , suggesting that the effects of prednisolone in COPD are unlikely to be due to alterations in mood The objective of this study was to determine if buspirone would alleviate anxiety and improve exercise tolerance of anxious patients with chronic airflow obstruction ( CAO ) . Eleven male patients with mild to moderate anxiety and CAO completed this study comparing buspirone , 10 to 20 mg given three times a day , with placebo . Patients were evaluated with State Trait Anxiety Inventory , spirometry , 12-min walk , incremental exercise  on a  cycle ergometer  to symptom limitation and measurement of dyspnea with a modified Borg scale at exercise levels and the end of each 2 min on 12-min walk . There were no significant differences in anxiety scores , work load , maximum oxygen consumption per minute , maximum expired volume per minute , PETCO2 , PETO2 , 12-min walking distance or dyspnea scores after 6 weeks of buspirone or placebo therapy . We conclude that administration of buspirone has no significant effect on anxiety levels , exercise capabilities or PETO2 or PETCO2 in patients with CAO and mild anxiety The aim of this study was to determine whether treating concomitant depression improves quality of life and exercise tolerance in COPD patients . Out- patients with moderate to severe , stable COPD completed Hospital Anxiety-Depression ( HAD ) and General Health question naires . A psychiatrist interviewed those with high scores . In a r and omised , double-blind fashion , 28 depressed COPD patients took a selective serotonin re-uptake inhibitor , Paroxetine 20 mg daily , or matched placebo for 6 weeks . Subsequently , all patients took un-blinded Paroxetine for 3 months . From these question naires , 35 % of 135 patients had significant depression , but this was confirmed by psychiatric interview in only 21 % . Throughout the study , there were no changes in laboratory lung function nor in home peak flow . Six weeks ' treatment produced no significant differences between placebo and treatment group in either depression , quality of life scores or 6-minute walking distances , although overall improvements in depression , correlated with increases in walking distance . Three months of un-blinded treatment , significantly improved depression scores ( self-complete HAD , Beck 's Depression and psychiatrist-completed Montgomery-Asberg scores ) , walking distances ( 369 to 427 m , p = 0.0003 ) and St. George 's Respiratory Question naire Total Scores ( 65 to 58 , p = 0.033 ) . Although self-complete question naires over-diagnose depression , the condition is nevertheless common in patients with moderately severe COPD . Six weeks of antidepressants is insufficient to improve either depression , quality of life or exercise tolerance . However , our study suggests that a longer course of treatment may be effective and that improvements in depression are associated with improvements in exercise tolerance . A larger , double blind study with a longer treatment period is indicated During each of two six-week treatment periods , 12 depressed out patients with chronic obstructive pulmonary disease received increasing doses of doxepin hydrochloride or a placebo as tolerated . The mean maximal doses of doxepin hydrochloride and placebo were 105 and 
    Output:
    
Due to the sub-optimal quality of the trials and statistically non-significant results , it is not possible to draw any conclusions for treatment .