***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 A family history of type 2 diabetes ( T2D ) confers a high risk of developing the disease , independent of that due to other common risk factors . Postpr and ial state is a pro-inflammatory condition associated with a transiently impaired endothelial function ; an increased oxidative stress is considered as a mediator of such effects in T2D . We evaluated the short-term effect of a lipid meal on markers of early vascular damage in subjects at risk of developing T2D . A total of thirty-two healthy volunteers , divided according to the presence ( FHD+ ) or absence ( FHD - ) of a family history of T2D , underwent a fatty meal test . We measured the monocyte mRNA expressions of IL-6 , IL-8 and IL-1β , and IL-6 , soluble CD40 lig and ( sCD40L ) , vascular cellular adhesion molecule-1 ( VCAM-1 ) , intracellular adhesion molecule-1 ( ICAM-1 ) and nitrotyrosine plasma concentrations at baseline and in the post-meal phase , relating them to the lipid profile and other biochemical parameters . The basal expression of the cytokines did not differ in FHD - and FHD+ subjects ; neither was it modified by the meal ingestion . IL-6 and sCD40L plasma levels , similar in the two groups in the fasting state , did not vary after the meal . VCAM-1 and ICAM-1 increased in FHD+ subjects but not in FHD - subjects . Nitrotyrosine , similar between the FHD - and FHD+ subjects at baseline , increased more in FHD+ subjects than in FHD - subjects after the meal . In conclusion , the presence of a familial history of T2D confers an abnormal endothelial activation after an oral lipid meal , coupled with an increased oxidative stress , supporting the hypothesis of an early endothelial dysfunction already present in healthy individuals prone to develop T2D BACKGROUND Among apparently healthy men , elevated levels of C-reactive protein ( CRP ) , a marker for systemic inflammation , predict risk of myocardial infa rct ion and thromboembolic stroke . Whether increased levels of CRP are also associated with the development of symptomatic peripheral arterial disease ( PAD ) is unknown . METHODS AND RESULTS Using a prospect i ve , nested , case-control design , we measured baseline levels of CRP in 144 apparently healthy men participating in the Physicians ' Health Study who subsequently developed symptomatic PAD ( intermittent claudication or need for revascularization ) and in an equal number of control subjects matched on the basis of age and smoking habit who remained free of vascular disease during a follow-up period of 60 months .  Median CRP levels at baseline were significantly higher among those who subsequently developed PAD ( 1.34 versus 0.99 mg/L ; P=.04 ) . Furthermore , the risks of developing PAD increased significantly with each increasing quartile of baseline CRP concentration such that relative risks of PAD from lowest ( referent ) to highest quartile of CRP were 1.0 , 1.3 , 2.0 , and 2.1 ( Ptrend=.02 ) . Compared with those with no clinical evidence of disease , the subgroup of case patients who required revascularization had the highest baseline CRP levels ( median= 1.75 mg/L ; P= .04 ) ; relative risks from lowest to highest quartile of CRP for this end point were 1.0 , 1.8 , 3.8 , and 4.1 ( Ptrend=.02 ) . Risk estimates were similar after additional control for body mass index , hypercholesterolemia , hypertension , diabetes , and a family history of premature atherosclerosis . CONCLUSIONS These prospect i ve data indicate that among apparently healthy men , baseline levels of CRP predict future risk of developing symptomatic PAD and thus provide further support for the hypothesis that chronic inflammation is important in the pathogenesis of atherothrombosis A high-fat meal ( HFM ) induces an increase in blood lipids ( postpr and ial lipemia ; PPL ) , systemic inflammation , and acute airway inflammation . While acute exercise has been shown to have anti-inflammatory and lipid-lowering effects , it is unknown whether exercise prior to an HFM will translate to reduced airway inflammation post-HFM . Our purpose was to determine the effects of an acute bout of exercise on airway inflammation post-HFM and to identify whether any protective effect of exercise on airway inflammation was associated with a reduction in PPL or systemic inflammation . In a r and omized cross-over study , 12 healthy , 18- to 29-year-old men ( age , 23.0 ± 3.2 years ; height , 178.9 ± 5.5 cm ; weight , 78.5 ± 11.7 kg ) consumed an HFM ( 1 g fat/1 kg body weight ) 12 h following exercise ( EX ; 60 min at 60 % maximal oxygen uptake ) or without exercise ( CON ) . Fractional exhaled nitric oxide ( FENO ; measure of airway inflammation ) , triglycerides ( TG ) , and inflammatory markers ( high-sensitivity C-reactive protein , tumor-necrosis factor-alpha , and interleukin-6 ) were measured while fasted at 2 h and 4 h post-HFM . FENO increased over time ( 2 h : CON , p = 0.001 ; EX , p = 0.002 , but not by condition ( p = 0.991 ) . TG significantly increased 2 and 4 h post-HFM ( p < 0.001 ) , but was not significant between conditions ( p = 0.256 ) . Inflammatory markers did not significantly increase by time or condition ( p > 0.05 ) . There were no relationships between FENO and TG or systemic inflammatory markers for any time point or condition ( p > 0.05 ) . In summary , an acute bout of moderate-intensity exercise performed 12 h prior to an HFM did not change postpr and ial airway inflammation or lipemia in healthy , 18- to 29-year-old men Soy isoflavones may impede atherogenic processes associated with cardiovascular disease . Research suggests that the postpr and ial generation of TG-rich remnants contributes to the development of atherosclerosis . The purpose of the current study was to determine if 39 g soy ( 85 mg aglycone isoflavones , treatment ) compared with 40 g milk protein ( 0 mg aglycone isoflavones , control ) in combination with a high-fat meal can modify postpr and ial , atherogenic-associated events and biomarkers for oxidative stress , inflammation , and thrombosis .  Fifteen healthy men ( 20–47 yr ) participated in a double-blind cross-over meal-challenge study occurring on two nonconsecutive days . The study meals consisted of two high-fat apple muffins consumed with either a soy or milk shake ( 229 mL , 41 % fat , 41 % carbohydrate , and 18 % protein ) . Blood sample s were obtained at base-line ( fasted ) and hours two , four , and six postpr and ial . Plasma TG significantly increased in both treatment and control meal challenges compared with baseline . There were no significant differences ( P>0.05 ) between treatment ( soy ) and control ( milk ) for ex vivo copper-induced LDL oxidation , serum C-reactive protein , serum interleukin-6 ( IL-6 ) , serum fibrinogen , or plasma lipids ( total cholesterol , HDL , LDL , TG ) . IL-6-concentrations significantly decreased as a function of time during either meal challenge ( P=0.005 ) . These data suggest that consumption of soy or milk protein in conjunction with a high-fat meal does not acutely modify postpr and ial oxidative stress , inflammation , or plasma lipid concentrations in young , healthy men Postpr and ial lipemia impairs insulin sensitivity and triggers the pro-inflammatory state which may lead to the progression of cardiovascular diseases . A r and omized , crossover single-blind study ( n = 10 healthy men ) was design ed to compare the effects of a high-fat load ( 50 g fat ) , rich in palmitic acid from both plant ( palm olein ) or animal source ( lard ) versus an oleic acid-rich fat ( virgin olive oil ) on lipemia , plasma glucose , insulin and adipocytokines . Serum triacylglycerol ( TAG ) concentrations were significantly lower after the lard meal than after the olive oil and palm olein meals ( meal effect P = 0.003 ; time effect P < 0.001 ) . The greater reduction in the plasma non-esterified free fatty acids levels in the lard group compared to the olive oil meal was mirrored by the changes observed for serum TAG levels ( P < 0.05 ) . The magnitude of response for plasma glucose , insulin and adipocytokines [ interleukin-6 ( IL-6 ) , tumor necrosis factor-α ( TNF-α ) , interleukin-1β ( IL-1β ) and leptin ] were not altered by the type of dietary fats . A significant difference in plasma IL-1β was found over time following the three high fat loads ( time effect P = 0.036 ) . The physical characteristics and changes in TAG structure of lard may contribute to the smaller increase in postpr and ial lipemia compared with palm olein . A high fat load but not the type of fats influences concentrations of plasma IL-1β over time but had no effect on other pro-inflammatory markers tested in the postpr and ial state Contrary to other long chain saturated fatty acids ( SFA ) , fats high in stearic acid do not raise plasma cholesterol concentrations , however , a slight elevation in inflammatory markers , plasma fibrinogen and interleukin-6 ( IL-6 ) , has been observed in the fasting state . The effect of stearic acid on inflammation in the postpr and ial state has not yet been reported . We conducted a single blind crossover , r and omized , postpr and ial study to compare the effects of a fat load of cocoa butter high in stearic acid and olive oil in ten healthy women . The test meals contained 1 g of fat per kg body weight ( mean 62 g ) . Blood sample s were collected at 0 ( fasting ) , 4 and 6 h. Both diets result ed in a significant increase in serum triacylglycerol ( TAG ) concentration over time ( P = 0.003 ) and a decrease in serum IL-6 concentration after 4 h followed by an increase to post absorptive values after 6 h ( P < 0.001 ) ; whereas serum high sensitivity C-reactive protein ( hsCRP ) concentration was not affected . There was no difference between diets in effects on serum TAG , hsCRP and IL-6 concentrations and no association between postpr and ial lipemia and inflammatory markers . High intake of dietary fats increase postpr and ial serum TAG , however , may not affect inflammatory markers postpr and ially . Thus , fat rich in stearic acid does not seem to increase postpr and ial inflammation BACKGROUND Previous studies on diet and coronary heart disease ( CHD ) focused primarily on individual nutrients or foods . OBJECTIVE We examined whether overall dietary patterns derived from a food-frequency question naire ( FFQ ) predict  risk of CHD in men . DESIGN This was a prospect i ve cohort study of 44875 men aged 40 - 75 y without diagnosed cardiovascular disease or cancer at baseline in 1986 . RESULTS During 8 y of follow-up , we documented 1089 cases of CHD 
    Output:
    
We assert that the findings of this systematic review on markers of inflammation in the postpr and ial period will considerably aid in informing future research and advancing clinical knowledge