***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 Interleukin-6 ( IL-6 ) plays a central role in inflammation and tissue injury . However , epidemiological data evaluating the role of IL-6 in atherogenesis are sparse . METHODS AND RESULTS In a prospect i ve study involving 14 916 apparently healthy men , we measured baseline plasma concentration of IL-6 in 202 participants who subsequently developed myocardial infa rct ion ( MI ) and in 202 study participants matched for age and smoking status who did not report vascular disease during a 6-year follow-up .  Median concentrations of IL-6 at baseline were higher among men who subsequently had an MI than among those who did not ( 1.81 versus 1 . 46 pg/mL ; P=0.002 ) . The risk of future MI increased with increasing quartiles of baseline IL-6 concentration ( P for trend < 0.001 ) such that men in the highest quartile at entry had a relative risk 2.3 times higher than those in the lowest quartile ( 95 % CI 1.3 to 4.3 , P=0.005 ) ; for each quartile increase in IL-6 , there was a 38 % increase in risk (P=0.001).This relationship remained significant after adjustment for other cardiovascular risk factors , was stable over long periods of follow-up , and was present in all low-risk subgroups , including nonsmokers . Although the strongest correlate of IL-6 in these data was C-reactive protein ( r=0.43 , P<0.001 ) , the relationship of IL-6 with subsequent risk remained after control for this factor ( P<0.001 ) . CONCLUSIONS In apparently healthy men , elevated levels of IL-6 are associated with increased risk of future MI . These data thus support a role for cytokine-mediated inflammation in the early stages of atherogenesis Background Significant regression of coronary and femoral atherosclerotic lesions has been documented by angiographic studies using aggressive lipid-lowering treatment . This study tested the applicability and effects of intensive physical exercise and low-fat diet on coronary morphology and myocardial perfusion in nonselected patients with stable angina pectoris . Methods and Results Patients were recruited after routine coronary angiography for stable angina pectoris ; they were r and omized to an  intervention group ( n = 56 ) and a  control group on “ usual care ” ( n = 57 ) . Treatment comprised intensive physical exercise in group training sessions ( minimum , 2 hr/wk ) , daily home exercise periods ( 20 min/d ) , and low-fat , low-cholesterol diet ( American Heart Association recommendation , phase 3 ) . No lipid-lowering agents were prescribed . After 12 months of participation , repeat coronary angiography was performed ; relative and minimal diameter reductions of coronary lesions were measured by digital image processing . Change in myocardial perfusion was assessed by 201TI scintigraphy . In patients participating in the intervention group , body weight decreased by 5 % ( p<0.001 ) , total cholesterol by 10 % ( p<0.001 ) , and triglycerides by 24 % ( p<0.001 ) ; high density lipoproteins increased by 3 % ( p = NS ) . Physical work capacity improved by 23 % ( p<0.0001 ) , and myocardial oxygen consumption , as estimated from maximal rate-pressure product , by 10 % , ( p<0.05 ) . Stress-induced myocardial ischemia decreased concurrently , indicating improvement of myocardial perfusion . Based on minimal lesion diameter , progression of coronary lesions was noted in nine patients ( 23 % ) , no change in 18 patients ( 45 % ) , and regression in 13 patients ( 32 % ) . In the control group , metabolic and hemodynamic variables remained essentially unchanged , whereas progression of coronary lesions was noted in 25 patients ( 48 % ) , no change in 18 patients ( 35 % ) , and regression in nine patients ( 17 % ) . These changes were significantly different from the intervention group ( p<0.05 ) . Conclusions In patients participating in regular physical exercise and low-fat diet , coronary artery disease progresses at a slower pace compared with a control group on usual care Alterations in circulating angiogenic cells ( CAC ) and endothelial progenitor cells ( EPC ) , known to contribute to endothelial repair , could explain the reversal of endothelial function in response to exercise training . Moreover , training-induced vascular remodeling might affect the acute response of EPC and CAC following a single exercise bout . We studied the impact of exercise training on CAC function and numbers of CD34+/KDR+ EPC in patients with chronic heart failure ( CHF ) and we assessed the effect of acute exercise on CAC and EPC in sedentary and trained patients . Twenty-one sedentary CHF patients underwent 6-month exercise training  and were compared to a non-trained control group ( n = 17 ) and 10 healthy age-matched subjects . At baseline and follow-up , flow-mediated dilation was assessed and grade d exercise testing ( GXT ) was performed . Before and immediately after GXT , CAC migratory capacity was assessed in vitro and circulating CD34+/KDR+ EPC were quantified using flow cytometry . At baseline , CAC migration was significantly impaired in sedentary CHF patients but normalized acutely after GXT . Training corrected endothelial dysfunction , which coincided with a 77 % increase in CAC migration ( P = 0.0001 ) . Moreover , the GXT-induced improvement detected at baseline was no longer observed after training . Numbers of CD34+/KDR+ EPC increased following 6-month exercise training ( P = 0.021 ) , but were not affected by GXT , either prior or post-training . In conclusion , the present findings demonstrate for the first time that exercise training in CHF reverses CAC dysfunction and increases numbers of CD34+/KDR+ EPC , which is accompanied by improvement of peripheral endothelial function . The acute exercise-induced changes in CAC function wane with exercise training , suggesting that repetitive exercise bouts progressively lead to functional endothelial repair Background Coronary heart disease as well as major cardiovascular risk factors are associated with elevated levels of proinflammatory markers . There is , however , limited information about how changes in lifestyle improving the cardiovascular risk profile influence these levels . The aim of the study was to evaluate whether changes in lifestyle measures with special attention to physical activity , were associated with the levels of such markers . Design Coronary heart disease patients ( n = 197 ) were r and omized to either a comprehensive lifestyle intervention programme comprising regular physical activity , low fat diet and smoking cessation , or usual care with routine follow-up in the outpatient clinic for 6 months . An exercise test and fasting blood sample s analysed for soluble cell adhesion molecules , C reactive protein and pro-inflammatory cytokines were evaluated before and at the end of the study . Results Improved diet , physical performance and reduction in smoking were obtained in the intervention programme when compared with usual care patients , but no significant group differences in levels of inflammatory markers were observed . In the total population , however , physical performance significantly and inversely predicted levels of soluble cell adhesion molecule 1 , ( P>0.001 ) , C-reactive protein ( P>0.001 ) and interleukin-6 ( P=0.01 ) at 6 months . Smokers had elevated levels of soluble cell adhesion molecule 1 when compared with non-smokers ( P=0.011 ) . Conclusions We demonstrated that physical performance is inversely correlated with levels of pro-inflammatory markers in coronary heart disease patients , possibly retarding the process of atherosclerosis . No effect on inflammatory markers was obtained with a 6-month lifestyle intervention programme when compared with patients who received usual care follow-up . Eur J Cardiovasc Prev Rehabil 13:356 - 362 © 2006 The European Society of Background —C-reactive protein ( CRP ) and interleukin (IL)-6 are important risk factors for atherosclerosis and coronary heart disease . In the present study , we examined serum levels of CRP and IL-6 , IL-6 production by monocytes , and the effect of nasal continuous positive airway pressure ( nCPAP ) in patients with obstructive sleep apnea syndrome ( OSAS ) . Methods and Results —After polysomnography , venous blood was collected at 5 am from 30 patients with OSAS and 14 obese control subjects .  Serum levels of CRP and IL-6 and spontaneous production of IL-6 by monocytes were investigated . In addition , the effects of 1 month of nCPAP were studied in patients with moderate to severe OSAS .  Levels of CRP and IL-6 were significantly higher in patients with OSAS than in obese control subjects ( CRP P < 0.001 , IL-6 P < 0.05 ) . IL-6 production by monocytes was also higher in patients with OSAS than in obese control subjects ( P < 0.01 ) . In patients with OSAS , the primary factors influencing levels of CRP were severity of OSAS and body mass index and those influencing levels of IL-6 were body mass index and nocturnal hypoxia . nCPAP significantly decreased levels of both CRP ( P < 0.0001 ) and IL-6 ( P < 0.001 ) and spontaneous IL-6 production by monocytes ( P < 0.01 ) . Conclusions —Levels of CRP and IL-6 and spontaneous production of IL-6 by monocytes are elevated in patients with OSAS but are decreased by nCPAP . Therefore , OSAS is associated with increased risks for cardiovascular morbidity and mortality , and nCPAP may be useful for decreasing these risks Background Obesity is characterized by chronic mild inflammation and may influence the risk and progression of cancer . Purpose The current study is an exploratory analysis of the effect of a weight loss intervention that emphasized increased physical activity on inflammatory cytokines ( tumor necrosis factor-α [ TNF-α ] , interleukin-6 [ IL-6 ] , interleukin-8 [ IL-8 ] , and vascular endothelial growth factor [ VEGF ] ) at the end of the 16-week intervention period in overweight breast cancer survivors . Methods Study participants averaged 56 years of age ( N = 68 ) . Intervention participants ( n = 44 vs. 24 controls ) participated in a cognitive behavioral therapy-based weight management program as part of an exploratory r and omized trial . The intervention incorporated strategies to promote increased physical activity and diet modification . Baseline and 16-week data included height , weight , body composition , physical activity level , and biomarkers IL-6 , IL-8 , TNF-α , and VEGF . Results Weight loss was significantly greater in the intervention group than controls ( −5.7 [ 3.5 ] vs. 0.2 [ 4.1 ] kg , P < 0.001 ) . Paired t tests noted favorable changes in physical activity level ( P < 0.001 intervention , P = 0.70 control ) , marginally lower IL-6 levels ( P = 0.06 intervention , P = 0.25 control ) at 16 weeks for participants in the intervention group , and lower TNF-α levels for participants in the intervention ( P < 0.05 ) and control groups ( P < 0.001 ) . Increased physical activity was associated with favorable changes in IL-6 for participants in the intervention group ( R2 = 0.18 ; P < 0.03 ) . Conclusion Favorable changes in cytokine levels were observed in association with weight loss in this exploratory study with overweight breast cancer survivors BACKGROUND The purpose of this study was to determine the effects of systemic exercise training on endothelium-mediated arteriolar vasodilation of the lower limb and its relation to exercise capacity in chronic heart failure ( CHF ) . Endothelial dysfunction is a key feature of CHF , contributing to increased peripheral vasoconstriction and impaired exercise capacity . Local h and grip exercise has previously been shown to enhance endothelium-dependent vasodilation in conduit and resistance vessels in CHF . METHODS AND RESULTS Twenty patients were prospect ively r and omized to a training group ( n=10 , left ventricular ejection fraction [ LVEF ] 24+/-4 % ) or a control group ( n=10 , LVEF 23+/-3 % ) . At baseline and after 6 months , peak flow velocity was measured in the left femoral artery using a Doppler wire ; vessel diameter was determined by quantitative angiography . Peripheral blood flow was calculated from average peak velocity ( APV ) and arterial cross-sectional area . After exercise training , nitroglycerin-induced endothelium-independent vasodilation remained unaltered ( 271 % versus 281 % , P = NS ) . Peripheral blood flow improved significantly in response to 90 microg/min acetylcholine by 203 % ( from 152+/-79 to 461+/-104 mL/min , P<0.05 versus control group ) and the inhibiting effect of L-NMMA increased by 174 % ( from -46+/-25 to -126+/-19 mL/min , P<0.05 versus control group ) . Peak oxygen uptake increased by 26 % ( P<0.01 versus control group ) . The increase in peak oxygen uptake was correlated with the endothelium-dependent change in peripheral blood flow ( r=0.64 , P<0 . 005 ) . CONCLUSIONS Regular physical exercise improves both basal 
    Output:
    
Aerobic exercise decreased the adhesion molecules , vascular cell adhesion molecule-1 ( VCAM-1 ) and intercellular adhesion molecule-1 ( ICAM-1 ) ( moderate and high evidence , respectively ) , while effects of PA on E- and P-selectin were inconclusive .
PA decreases C-reactive protein ( CRP ) ( high evidence ) .
The angiogenic actors , endothelial progenitor cells ( EPCs ) are increased ( high evidence ) and VEGF is decreased ( moderate evidence ) by PA .
The effect of PA on these factors seems to depend on the type and duration of exercise intervention and patient factors , such as presence of ischemia .
As presented in this review , there is a high level of evidence that physical activity positively affects key players in atherosclerosis development .
These effects could partly explain the scientifically proven anti-atherogenic effects of PA , and do have important clinical implication