***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 Persons with human immunodeficiency virus ( HIV ) infection are at risk for premature cardiovascular disease ( CVD ) . Predictors of atherosclerotic disease progression in contemporary patients have not been well described . METHODS Using data from a prospect i ve observational cohort of adults infected with HIV ( Study to Underst and the Natural History of HIV/AIDS in the Era of Effective Therapy ) , we assessed common carotid artery intima-media thickness ( CIMT ) at baseline and year 2 by ultrasound . We examined HIV-associated predictors of CIMT progression after adjusting for age , sex , race/ethnicity , body mass index , smoking , hypertension , diabetes , low-density lipoprotein cholesterol level , and baseline CIMT using linear regression . RESULTS Among 389 participants ( median age at baseline , 42 years ; male sex , 77 % ; median CD4 + cell count at baseline , 485 cells/mm³ ; 78 % receiving antiretroviral therapy ) , the median 2-year CIMT change was 0.016 mm ( interquartile range , -0.003 to 0.033 mm ; P < .001 ) . Lesser CIMT progression was associated with a suppressed viral load at baseline ( -0.009 mm change ; P = .015 ) and remaining virologically suppressed throughout follow-up ( -0.011 mm change ; P < .001 ) . After adjusting for additional risk factors and a suppressed viral load during follow-up , nonnucleoside reverse transcriptase inhibitor versus protease inhibitor exposure was associated with lesser CIMT progression ( -0.011 mm change ; P = .02 ) . CONCLUSIONS Suppressing HIV replication below clinical thresholds was associated with less progression of atherosclerosis . The proatherogenic mechanisms of HIV replication and the net CVD benefit of different antiretroviral drugs should be a focus of future research BACKGROUND Human immunodeficiency virus (HIV)-infected patients are at increased risk of cardiovascular disease , which may be related to chronic inflammation and endothelial dysfunction despite virological control with antiretroviral therapy . The relationship between carotid intima-media thickness ( IMT ) , a surrogate marker for cardiovascular disease , proinflammatory cytokines , and endothelial activation markers has not been fully explored in HIV-infected patients who are receiving antiretroviral therapy .  METHODS We conducted a prospect i ve , cross-sectional , observational study of treated HIV-infected patients and healthy control subjects to evaluate the relationship between carotid IMT , proinflammatory cytokines , endothelial activation biomarkers , and metabolic parameters in treated HIV-infected patients , compared with healthy control subjects . RESULTS We enrolled 73 HIV-infected patients and 21 control subjects .  Common carotid artery and internal carotid artery IMT measurements , as well as tumor necrosis factor-alpha , high-sensitivity C-reactive protein , interleukin-6 , myeloperoxidase , and soluble vascular cell adhesion molecule-1 levels were higher in the HIV-infected group . High-sensitivity C-reactive protein was the only biomarker that was positively correlated with carotid IMT in both groups . In the HIV-infected group , soluble vascular cell adhesion molecule-1 was positively correlated with all inflammatory cytokine levels . In multiple regression analysis , soluble vascular cell adhesion molecule-1 , myeloperoxidase , and tumor necrosis factor-alpha levels were all associated with internal carotid artery IMT in the HIV-infected group , whereas age was associated with both common carotid artery and internal carotid artery IMT . CONCLUSIONS Enhanced endothelial activation , inflammation , and increased carotid IMT occur in HIV-infected patients despite antiretroviral therapy . Inflammatory markers are associated with endothelial activation , and both are associated with internal carotid artery IMT , supporting a potential role of inflammation in endothelial activation and cardiovascular disease in HIV infection OBJECTIVE Combined antiretroviral therapy ( cART ) has significantly improved the survival rate and quality of life for HIV-infected subjects , but it contributes to the development of metabolic complications including coronary artery disease ( CAD ) . Recent studies have reported that high plasma levels of the soluble receptor for advanced glycation end products ( sRAGE ) were associated with a lower incidence of CAD in non-HIV infected patients . However , there has been no report of an association of sRAGE and sub clinical carotid atherosclerosis in HIV-infected patients receiving cART . METHODS We examined the association of circulating sRAGE in HIV-infected patients  with carotid intima-media thickness ( IMT ) and other metabolic variables .  We prospect ively enrolled 76 HIV-infected patients receiving cART for ≥ 6 months . RESULTS sRAGE had a significantly negative correlation with body mass index ( r = -0.324 , p = 0.005 ) , waist-to-hip ratio ( r = -0.335 , p = 0.003 ) , systolic blood pressure ( BP ) ( r=-0.359 , p=0.002 ) , diastolic BP ( r = -0.343 , p = 0.004 ) , total cholesterol ( r = -0.240 , p = 0.037 ) , low-density lipoprotein-cholesterol ( r=-0.284 , p=0.024 ) , log(homeostasis model assessment of insulin resistance [ HOMA-IR ] ) ( r = -0.380 , p = 0.002 ) and carotid IMT including max-IMT and mean-IMT ( r = -0.358 , p = 0.001 and r = -0.329 , p = 0.004 , respectively ) . By the use of multiple stepwise regression analyses , systolic BP ( p=0.001 ) and log[HOMA-IR ] ( p = 0.001 ) remained significant independently . CONCLUSIONS These results suggest that sRAGE may have a protective effect against sub clinical atherosclerosis by preventing inflammatory responses mediated by the activation of cell surface RAGE in HIV-infected patients receiving cART BACKGROUND Marked changes in the prevalence of noncommunicable diseases such as obesity , diabetes , and cardiovascular disease have occurred in developed and developing countries in recent decades . The overarching aim of the study is to examine the relationship of societal influences on human lifestyle behaviors , cardiovascular risk factors , and incidence of chronic noncommunicable diseases . METHODS The Prospect i ve Urban Rural Epidemiology ( PURE ) study is a large-scale epidemiological study that plans to recruit approximately 140,000 individuals residing in > 600 communities in 17 low- , middle- , and high-income countries around the world . Individual data collection includes medical history , lifestyle behaviors ( physical activity and dietary profile ) , blood collection and storage for biochemistry and future genetic analysis , electrocardiogram , and anthropometric measures . In addition , detailed information is being collected with respect to 4 environmental domains of interest-the built environment , nutrition and associated food policy , psychosocial/socioeconomic factors , and tobacco environment . A minimum follow-up of 10 years is currently planned . RESULTS This report describes the design , justification , and methodology of the PURE study . The PURE study has been recruiting since 2002 and has enrolled 139,506 individuals by March 31 , 2009 . CONCLUSIONS The PURE study builds on the work and experience gained through conduct of the INTERHEART study . Its design and extensive data collection are geared toward addressing major questions on causation and development of the underlying determinants of cardiovascular disease in population s at varying stages of epidemiologic transition Rosiglitazone may be useful for the treatment of antiretroviral therapy-associated lipoatrophy , but an association with cardiovascular disease ( CVD ) has been question ed in diabetics . We evaluated rosiglitazone 's effect on surrogate markers of CVD in HIV-infected individuals with lipoatrophy . HIV(+ ) patients with lipoatrophy on thymidine-sparing regimens were r and omized to rosiglitazone vs. placebo for 48 weeks . We serially assessed carotid IMT , fasting metabolic profiles , tumor necrosis factor (TNF)-α , soluble receptors ( sTNFRI and II ) , interleukin (IL)-6 , high-sensitivity C-reactive protein ( hsCRP ) , myeloperoxidase ( MPO ) , and endothelial activation markers [ von Willebr and factor ( vWF ) , soluble intercellular cell adhesion molecules-1 ( sICAM-1 ) , and vascular cell adhesion molecules-1 ( sVCAM-1 ) ] . Seventy-one subjects enrolled : 17 % were female and 51%were white . Baseline characteristics were similar between groups except for higher total cholesterol in the placebo group ( p = 0.04 ) . At 48 weeks , common carotid artery ( CCA ) IMT changed significantly ( p ≤ 0.05 ) within but not between the groups ( p = 0.36 ) : the median ( IQR ) increase was 0.10 ( 0.05 , 0.25 ) mm and 0.15 ( 0 , 0.25 ) mm in the rosiglitazone and placebo groups , respectively . hsCRP , sTNFRI and II , sVCAM-1 , and vWF changed significantly ( p ≤ 0.02 ) within but not between groups . Total cholesterol increased significantly in the rosiglitazone group ( p = 0.008 ) . In our study of virologically controlled subjects with lipoatrophy , rosiglitazone did not independently increase carotid IMT , endothelial activation , and inflammatory cytokines Chronic HIV infection is associated with increased risk of cardiovascular disease ( CVD ) , including in patients with virological suppression . Persistent innate immune activation may contribute to the development of CVD via activation of monocytes in these patients . We investigated whether changes in monocyte phenotype predict sub clinical atherosclerosis in virologically suppressed HIV-positive individuals with low cardiovascular risk . We enroled 51 virologically suppressed HIV-positive individuals not receiving protease inhibitors or statins and 49 age-matched uninfected controls in this study .  Carotid artery intima-media thickness ( cIMT ) was used as a surrogate marker for CVD , and traditional risk factors , including Framingham risk scores , were recorded . Markers of monocyte activation ( CD14 , CD16 , CCR2 , CX3CR1 , CD38 , HLA-DR and CD11b ) were measured in whole-blood sample s by flow cytometry . Associations were assessed using univariate and multivariate median regressions . Median cIMT was similar between HIV-positive and HIV-negative participants ( P=0.3 ) , although HIV-positive patients had significantly higher Framingham risk score ( P=0.009 ) and systemic inflammation . Expression of two monocyte markers , CD11b and CX3CR1 , independently predicted carotid artery thickness in HIV-positive individuals after controlling for Framingham risk score ( P=0.025 and 0.015 , respectively ) . These markers were not predictive of carotid artery thickening in controls . Our study indicates that monocyte surface markers may serve as novel predictors of CVD in HIV-positive individuals and is consistent with an important role for monocyte activation in the progression of HIV-related cardiovascular pathology BACKGROUND The relationships between soluble CD14 ( sCD14 ) , endotoxin ( lipopolysaccharide [ LPS ] ) , and progression of atherosclerosis have not been defined in human immunodeficiency virus ( HIV ) infection . METHODS We retrospectively assessed  serum sCD14 and LPS levels of 91 subjects in a prospect i ve 3-year study of carotid artery intima-media thickness ( CIMT ) ( AIDS Clinical Trials Group [ ACTG ] 5078 ) , where subjects were enrolled as risk factor-controlled triads of HIV-uninfected ( n = 36 ) and HIV-infected individuals with ( n = 29 ) or without ( n = 26 ) protease inhibitor (PI)-based therapy for ≥2 years . The primary end point was the yearly rate of change of CIMT ( ΔCIMT ) . RESULTS In multivariate analysis of the HIV-infected subjects , each 1 µg/mL above the mean of baseline serum sCD14 corresponded to an additional 1.52 µm/y ( 95 % confidence interval , .07 - 2.98 ; P = .04 ) in the ΔCIMT . Every 100 pg/mL above the mean of baseline serum LPS corresponded to an additional 0.49 µm/y ( 95 % confidence interval , .18-.81 ; P = .003 ) in the ΔCIMT . However , in univariate 
    Output:
    
CRP , IL-6 and soluble vascular cell adhesion molecule ( sVCAM-1 ) were the most studied markers in relation to CIMT .
None of the inflammatory markers showed an association with CIMT .
Interpretation This review showed a relation between some inflammatory markers and CVD , however , no consistent relation is observed for CIMT .