***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: OBJECTIVE To test whether children and adolescents with co-occurring asthma and depression are at risk for elevated inflammation-concurrently and at the next assessment . STUDY DESIGN Up to 6 yearly assessment s per person from the prospect i ve , population -based Great Smoky Mountains Study ( N = 1420 ) were used , covering children in the community aged 10 - 16 years old .  High-sensitivity C-reactive protein ( CRP ) was assayed from annual bloodspot collection s and provided indicators of elevated inflammation at CRP > 1 , CRP > 2 , and CRP > 3 mg/L. Depression was assessed with the Child and Adolescent Psychiatric Assessment . Asthma was assessed using a form adapted from the Centers for Disease Control and Prevention National Health Interview Survey . RESULTS Controlling common covariates of CRP , the co-occurrence of asthma and depression predicted heightened CRP-concurrently and at the next assessment . In turn , elevated CRP was relatively stable from one assessment to the next . CONCLUSIONS The co-occurrence of asthma and depression in childhood poses a risk for substantially elevated inflammation concurrently and over time , which could contribute to pathophysiological processes involved in the development of additional chronic diseases and also to asthma -- related morbidity and mortality In 1998 , the American Heart Association convened Prevention Conference V to examine strategies for the identification of high-risk patients who need primary prevention . Among the strategies discussed was the measurement of markers of inflammation.1  The Conference concluded that “ many of these markers ( including inflammatory markers ) are not yet considered applicable for routine risk assessment because of : ( 1 ) lack of measurement st and ardization , ( 2 ) lack of consistency in epidemiological findings from prospect i ve studies with endpoints , and ( 3 ) lack of evidence that the novel marker adds to risk prediction over and above that already achievable through the use of established risk factors . ” The National Cholesterol Education Program Adult Treatment Panel III Guidelines identified these markers as emerging risk factors,1a which could be used as an optional risk factor measurement to adjust estimates of absolute risk obtained using st and ard risk factors . Since these publications , a large number of peer- review ed scientific reports have been published relating inflammatory markers to cardiovascular disease ( CVD ) . Several commercial assays for inflammatory markers have become available . As a consequence of the exp and ing research base and availability of assays , the number of inflammatory marker tests ordered by clinicians for CVD risk prediction has grown rapidly . Despite this , there has been no consensus from professional societies or governmental agencies as to how these assays of markers of inflammation should be used in clinical practice . On March 14 and 15 , 2002 , a workshop titled “ CDC/AHA Workshop on Inflammatory Markers and Cardiovascular Disease : Applications to Clinical and Public Health Practice ” was convened in Atlanta , Ga , to address these issues . The goals of this workshop were to determine which of the currently available tests should be used ; what results should be used to define high risk ; which patients should be tested ; and the indications for which the tests would be most useful . These The prevalence of depression may be affected by changes in psychiatric practice s and the availability of online mental health information in the past two decades . This study aim ed to evaluate the aggregate prevalence of  depression  in communities from different countries between 1994 and 2014 and to explore the variations in prevalence stratified by geographical , method ological and socio-economic factors . A total of 90 studies were identified and met the inclusion criteria ( n = 1,112,573 adults ) with 68 studies on single point prevalence , 9 studies on one-year prevalence , and 13 studies on lifetime prevalence of depression . A r and om-effects model meta- analysis that was performed to calculate the aggregate point , one-year and lifetime prevalence of depression calculated prevalences of 12.9 % , 7.2 % and 10.8 % respectively . Point prevalence of depression was significantly higher in women ( 14.4 % ) , countries with a medium human development index ( HDI ) ( 29.2 % ) , studies published from 2004 to 2014 ( 15.4 % ) and when using self-reporting instruments ( 17.3 % ) to assess depression . Heterogeneity was identified by meta-regression and subgroup analysis , and response rate , percentage of women and year of publication , respectively , were determined contribute to depression prevalence . This meta- analysis allows benchmarking of the prevalence of depression during the era when online health information emerged , facilitating future comparisons Major depression ( MD ) is associated with peripheral inflammation and increased cardiovascular risk . Regular physical exercise can have anti-inflammatory effects . The present study examined whether behavioral activation with exercise  affects inflammatory processes in MD . Ninety-eight patients with MD were r and omly assigned to cognitive-behavioral therapy ( CBT ) emphasizing exercise during behavioral activation ( CBT-E ) , CBT with pleasurable low-energy activities as an active control condition ( CBT-C ) or a passive waiting list control group ( WL )  . Plasma levels of C-reactive protein ( CRP ) , interleukin (IL)-6 , IL-10 , lipopolysaccharide (LPS)-stimulated IL-6 production , and blood immune cell counts were analyzed at baseline and weeks 8 ( post-behavioral activation ) and 16 ( post-treatment ) . Thirty non-depressed age- and sex-matched controls were included to examine potential immunological alterations  in MD at baseline . Patients with MD exhibited higher levels of CRP , higher neutrophil and monocyte counts , lower IL-10 levels and reduced LPS-stimulated IL-6 production compared to controls ( P<0.001−0.045 ) . Multilevel modeling indicated that CBT-E was associated with increased anti-inflammatory IL-10 at weeks 8 and 16 compared to CBT-C and WL ( P=0.004−0.018 ) . CBT-E did not significantly affect other immunological makers in the total sample . A subgroup analysis including patients with potentially higher cardiovascular risk ( CRP ⩾1 μg ml−1 ) indicated that CRP was reduced in CBT-E compared to CBT-C ( P<0.007 ) and marginally reduced compared to WL ( P<0.085 ) after week 16 . The present findings provide new insights into immunological effects of behavioral treatments against depression . Behavioral activation in conjunction with exercise may have the potential to reverse , in part , immunological alterations in MD CONTEXT Increased concentrations of inflammatory biomarkers predict antidepressant nonresponse , and inflammatory cytokines can sabotage and circumvent the mechanisms of action of conventional antidepressants . OBJECTIVES To determine whether inhibition of the inflammatory cytokine tumor necrosis factor ( TNF ) reduces depressive symptoms in patients with treatment-resistant depression and whether an increase in baseline plasma inflammatory biomarkers , including high-sensitivity C-reactive protein ( hs-CRP ) , TNF , and its soluble receptors , predicts treatment response . DESIGN Double-blind , placebo-controlled , r and omized clinical trial . SETTING Outpatient infusion center at Emory University in Atlanta , Georgia . PARTICIPANTS A total of 60 medically stable out patients with major depression who were either on a consistent antidepressant regimen ( n = 37 ) or medication-free ( n = 23 ) for 4 weeks or more and who were moderately resistant to treatment as determined by the Massachusetts General Hospital Staging method . INTERVENTIONS Three infusions of the TNF antagonist infliximab ( 5 mg/kg ) ( n = 30 ) or placebo ( n = 30 ) at baseline and weeks 2 and 6 of a 12-week trial . MAIN OUTCOME MEASURES The 17-item Hamilton Scale for Depression ( HAM-D ) scores . RESULTS No overall difference in change of HAM-D scores between treatment groups across time was found . However , there was a significant interaction between treatment , time , and log baseline hs-CRP concentration ( P = .01 ) , with change in HAM-D scores ( baseline to week 12 ) favoring infliximab-treated patients at a baseline hs-CRP concentration greater than 5 mg/L and favoring placebo-treated patients at a baseline hs-CRP concentration of 5 mg/L or less . Exploratory analyses focusing on patients with a baseline hs-CRP concentration greater than 5 mg/L revealed a treatment response ( ≥50 % reduction in HAM-D score at any point during treatment ) of 62 % ( 8 of 13 patients ) in infliximab-treated patients vs 33 % ( 3 of 9 patients ) in placebo-treated patients ( P = .19 ) . Baseline concentrations of TNF and its soluble receptors were significantly higher in infliximab-treated responders vs nonresponders ( P < .05 ) , and infliximab-treated responders exhibited significantly greater decreases in hs-CRP from baseline to week 12 compared with placebo-treated responders ( P < .01 ) . Dropouts and adverse events were limited and did not differ between groups . CONCLUSIONS This proof-of-concept study suggests that TNF antagonism does not have generalized efficacy in treatment-resistant depression but may improve depressive symptoms in patients with high baseline inflammatory biomarkers . TRIAL REGISTRATION clinical trials.gov Identifier : NCT00463580 CONTEXT The association between depression and inflammation is inconsistent across research sample s. OBJECTIVE To test whether a history of childhood maltreatment could identify a subgroup of depressed individuals with elevated inflammation levels , thus helping to explain previous inconsistencies . DESIGN Prospect i ve longitudinal cohort study . SETTING New Zeal and . PARTICIPANTS A representative birth cohort of 1000 individuals was followed up to age 32 years as part of the Dunedin Multidisciplinary Health and Development Study . Study members were assessed for history of childhood maltreatment and current depression . MAIN OUTCOME MEASURES Inflammation was assessed using a clinical ly relevant categorical measure of high-sensitivity C-reactive protein ( > 3 mg/L ) and a dimensional inflammation factor indexing the shared variance of continuous measures of high-sensitivity C-reactive protein , fibrinogen , and white blood cells . RESULTS Although depression was associated with high levels of high-sensitivity C-reactive protein ( relative risk,1.45 ; 95 % confidence interval,1.06 - 1.99 ) , this association was significantly attenuated and no longer significant when the effect of childhood maltreatment was taken into account . Individuals with current depression and a history of childhood maltreatment were more likely to have high levels of high-sensitivity C-reactive protein compared with control subjects ( n = 27 ; relative risk , 2.07 ; 95 % confidence interval , 1.23 - 3.47 ) . In contrast , individuals with current depression only had a nonsignificant elevation in risk ( n = 109 ; relative risk , 1.40 ; 95 % confidence interval , 0.97 - 2.01 ) . Results were generalizable to the inflammation factor . The elevated inflammation levels in individuals who were both depressed and maltreated were not explained by correlated risk factors such as depression recurrence , low socioeconomic status in childhood or adulthood , poor health , or smoking . CONCLUSIONS A history of childhood maltreatment contributes to the co-occurrence of depression and inflammation . Information about experiences of childhood maltreatment may help to identify depressed individuals with elevated inflammation levels and , thus , at greater risk of cardiovascular disease OBJECTIVE Major depressive disorder has been linked with inflammatory processes , but it is unclear whether individual differences in levels of inflammatory biomarkers could help match patients to treatments that are most likely to be beneficial . The authors tested the hypothesis that C-reactive protein ( CRP ) , a commonly available marker of systemic inflammation , predicts differential response to escitalopram ( a serotonin reuptake inhibitor ) and nortriptyline ( a norepinephrine reuptake inhibitor ) . METHOD The hypothesis was tested in the Genome-Based Therapeutic Drugs for Depression ( GENDEP ) study , a multicenter open-label r and omized clinical trial . CRP was measured with a high-sensitivity method in serum sample s from 241 adult men and women with major depressive disorder r and omly allocated to 12-week treatment with escitalopram ( N=115 ) or nortriptyline ( N=126 ) . The primary outcome measure was the score on the Montgomery-Åsberg Depression Rating Scale ( MADRS ) , administered weekly . RESULTS CRP level at baseline differentially predicted treatment outcome with the two antidepressants ( CRP-drug interaction : β=3.27 , 95 % CI=1.65 , 4.89 ) . For patients with low levels of CRP ( < 1 mg/L ) , improvement on the MADRS score was 3 points higher with escitalopram than with nortriptyline . For patients with  higher CRP levels , improvement on the MADRS score was 3 points higher with nortriptyline than with escitalopram . CRP and its interaction with medication explained more than 10 % of individual-level variance in treatment outcome . CONCLUSIONS An easily accessible peripheral blood biomarker may contribute to improvement in outcomes of major depressive disorder by personalizing treatment choice I 
    Output:
    
These findings suggest that inflammation could be relevant to a large number of patients with depression