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Circulation. 2000;101:1767-1772

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(Circulation. 2000;101:1767.)
© 2000 American Heart Association, Inc.


Clinical Investigation and Reports

Plasma Concentration of Interleukin-6 and the Risk of Future Myocardial Infarction Among Apparently Healthy Men

Paul M. Ridker, MD; Nader Rifai, MD; Meir J. Stampfer, MD; Charles H. Hennekens, MD

From the Center for Cardiovascular Disease Prevention (P.M.R.) and the Divisions of Preventive Medicine (P.M.R., C.H.H.), Cardiovascular Diseases (P.M.R.), and the Channing Laboratory (M.J.S.), Brigham and Women’s Hospital; the Department of Ambulatory Care and Prevention (C.H.H.); and the Children’s Hospital Medical Center (N.R.), all at the Harvard Medical School, Boston, Mass.

Correspondence to Paul M. Ridker, MD, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail pridker{at}partners.org


*    Abstract
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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 prospective study involving 14 916 apparently healthy men, we measured baseline plasma concentration of IL-6 in 202 participants who subsequently developed myocardial infarction (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.


Key Words: myocardial infarction • risk factors • inflammation • epidemiology • cytokines


*    Introduction
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Interleukin (IL)-6 is a pleiotropic cytokine with a broad range of humoral and cellular immune effects relating to inflammation, host defense, and tissue injury.1 2 Produced in response to several factors, including infection, IL-1, interferon-{gamma}, and tumor necrosis factor,3 4 5 IL-6 is a central mediator of the acute-phase response and a primary determinant of hepatic production of C-reactive protein.6 7

Although elevated levels of IL-6 have been reported in some chronic inflammatory conditions,2 epidemiological data evaluating the potential role of IL-6 in early atherogenesis are sparse. However, experimental studies indicate that vascular endothelial and smooth muscle cells from normal and aneurysmal arteries produce IL-6,8 9 10 that IL-6 gene transcripts are expressed in human atherosclerotic lesions,11 12 and that IL-6 may have procoagulant effects.13 14 15 Furthermore, prospective studies of apparently healthy16 17 as well as high-risk18 19 20 individuals indicate that elevated levels of C-reactive protein, a potential surrogate for IL-6 activity,21 are associated with first coronary and cerebrovascular events. Finally, elevated levels of IL-6 and other acute-phase proteins have been reported among patients with acute coronary syndromes,22 23 24 25 even among those without overt plaque rupture or acute tissue trauma.26

On the basis of these data and the hypothesis that atherosclerosis fundamentally represents a chronic inflammatory disorder,27 28 we sought to determine whether plasma levels of IL-6 might be elevated among apparently healthy individuals at risk for future myocardial infarction. We further sought to determine whether any relationship between IL-6 and subsequent vascular risk was modified by other cardiovascular risk factors, including markers of chronic inflammation.


*    Methods
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We performed a prospective, nested, case-control study of IL-6 as a potential marker for future myocardial infarction among participants in the Physicians’ Health Study, a randomized, double-blind, placebo-controlled trial of aspirin (325 mg PO every other day) and ß-carotene (50 mg PO every other day) in the primary prevention of cardiovascular disease and cancer conducted among 22 071 US male physicians 40 to 84 years of age with no prior history of myocardial infarction, stroke, transient ischemic attack, or cancer.29 Before randomization, between August 1982 and December 1984, potential participants were asked to provide baseline blood samples, which were collected in EDTA and processed for long-term storage at -80°C. Of randomized study participants, 14 916 (68%) provided baseline plasma samples. At the time of blood collection, all study participants were taking active oral aspirin.

For cases of incident myocardial infarction reported during study follow-up, hospital records, death certificates, and autopsy reports were reviewed by a committee of physicians using standardized criteria to confirm or refute reported events. Reported myocardial infarction was confirmed if symptoms met World Health Organization criteria and the event was associated with increased concentrations of diagnostic cardiac enzymes or characteristic ECG changes. Deaths due to coronary disease were confirmed on the basis of autopsy reports, circumstances of death, symptom patterns, and a history of coronary disease. Silent myocardial infarctions were not included, because they could not be dated accurately.

Study participants who provided an adequate baseline plasma sample for analysis and who had a confirmed myocardial infarction during follow-up (cases) were each matched with 1 control subject. Controls were study participants who also provided adequate baseline plasma samples and who remained free of reported vascular disease during follow-up. Controls were randomly selected from study participants who met the matching criteria of age (±1 year), length of study follow-up (6-month intervals), and smoking status (past smoker, current smoker, or never smoked). With these criteria, 202 cases and 202 matched controls were evaluated in this analysis.

Stored plasma obtained at baseline from each case and control subject was thawed and assayed for IL-6 by use of a commercially available ELISA (R&D Systems). In pilot data based on these frozen plasma samples, coefficients of variation ranged between 5% and 11%, and repeat determinations on the same plasma sample were highly correlated (r=0.93, P<0.001). Blood specimens were analyzed in blinded pairs, with the position of the case specimen varied at random within pairs to reduce the possibility of systematic bias and minimize interassay variability. Methods used to evaluate baseline lipid parameters, homocysteine, fibrinogen, C-reactive protein, and tissue-type plasminogen activator have been described elsewhere.16 30 31 32

Because IL-6 levels were skewed, median concentrations were computed, and the significance of any differences in median values between cases and controls was assessed by Wilcoxon rank-sum test. We used logistic regression analysis, conditioned on the matching variables of age and smoking, to determine relative risks of future myocardial infarction after dividing the study sample into quartiles of IL-6 based on the distribution of the control values. Adjusted estimates of risk were obtained with multivariate models that additionally controlled for body-mass index; history of diabetes, hypertension, or hyperlipidemia; parental history of premature atherosclerosis; and randomized treatment assignment. Stratified analyses were performed in low-risk subgroups and by duration of follow-up. All probability values are 2-tailed, and all CIs were computed at the 95% level.


*    Results
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Baseline characteristics of the study participants are shown in Table 1Down. Owing to matching, the distribution of age and smoking was identical for cases and controls. As expected in a prospective study of myocardial infarction, cases had higher baseline levels of total cholesterol and triglycerides, lower levels of HDL cholesterol, and a greater prevalence of hypertension and obesity than controls.


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Table 1. Baseline Characteristics of Study Participants

The overall frequency distribution of baseline IL-6 levels is presented in Figure 1Down. As shown, IL-6 levels ranged between 0.015 and 10.01 pg/mL in a pattern virtually identical to that expected from fresh blood samples obtained in otherwise healthy populations (0.01 to 11.5 pg/mL; data on file, R&D Systems, Minneapolis, Minn).



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Figure 1. Frequency distribution and cumulative frequency of baseline Il-6 levels among apparently healthy men participating in the Physicians’ Health Study.

Median plasma concentrations of IL-6 at baseline were significantly higher among men who went on to experience a first myocardial infarction than among men who remained free of reported cardiovascular disease during follow-up (1.81 versus 1.46 pg/mL; P=0.002). As shown in Table 2Down, these differences were present in the total cohort as well as in the low-risk subgroups of nonsmokers and those with no history of hypertension, hyperlipidemia, diabetes, or obesity or a family history of premature myocardial infarction (all P<=0.001).


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Table 2. Baseline Plasma Concentrations of IL-6 According to Case and Control Status

As shown in Table 3Down, the relative risk of first myocardial infarction increased with increasing quartiles of baseline IL-6 concentration (P for trend <0.001) such that men in the highest quartile at baseline had a relative risk 2.3 times higher than those in the lowest quartile (95% CI 1.3 to 4.3, P=0.005); overall, each quartile increase in baseline plasma concentration of IL-6 was associated with a statistically significant 38% increase in risk of future myocardial infarction (95% CI 15% to 66%, P=0.001).The relationship between baseline IL-6 level and risk of future myocardial infarction was not altered in analyses that adjusted for baseline differences in total cholesterol, HDL cholesterol, body mass index, blood pressure, diabetes, a family history of premature coronary artery disease, alcohol use, and exercise frequency (Table 3Down).


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Table 3. Crude and Adjusted Relative Risks of Future Myocardial Infarction Among Apparently Healthy Men According to Baseline Level of IL-6

Smokers had significantly higher median concentrations of IL-6 than did nonsmokers (2.23 versus 1.58 pg/mL; P<0.001). However, because we matched case and control subjects on smoking status, confounding by this factor was minimized. Moreover, in analyses limited to nonsmokers, the relationship between baseline level of IL-6 and subsequent risk remained highly significant such that the relative risks of future myocardial infarction from lowest to highest quartiles of IL-6 among nonsmokers were 1.0, 1.4, 2.5, and 2.6 (P for trend 0.001). As in the total cohort, these effects were minimally altered in analyses that adjusted for lipid and nonlipid risk factors (Table 3Up).

To assess whether the effect of baseline IL-6 levels on risk of future myocardial infarction varied over time, we stratified our analyses by months of follow-up. Statistically significant increases in risk were found to be associated with elevations of IL-6 in the first 2 years of follow-up (P=0.04), in years 2 to 4 (P=0.006), and in years 4 to 6 (P=0.02). As shown in Figure 2Down, the relative risk associated with each increasing quartile of baseline IL-6 level was stable over long periods of time, with no significant time trends noted.



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Figure 2. Relative risk of future myocardial infarction associated with each increasing quartile of baseline IL-6 concentration according to months of follow-up.

Log-normalized concentration of IL-6 was not correlated with total cholesterol (r=-0.01, P=0.9) or triglycerides (r=0.03, P=0.5) and was modestly correlated with HDL cholesterol (r=0.15, P=0.003). Modest correlations were also found between IL-6 and several nontraditional markers of vascular risk, including antigen level for tissue-type plasminogen activator (r=0.21, P=0.004), total plasma homocysteine (r=0.15, P=0.003), fibrinogen (r=0.24, P=0.002), and soluble intercellular adhesion molecule-1 (r=0.19, P=0.001). The strongest correlate of IL-6 in these data was log-normalized plasma concentration of C-reactive protein (r=0.43, P=0.001). However, the relationship between IL-6 and myocardial infarction remained statistically significant after controlling for this inflammatory marker. Specifically, in analyses that adjusted for baseline plasma concentration of C-reactive protein, a 44% increase in relative risk of future myocardial infarction was associated with each increasing quartile of IL-6 (95% CI 12% to 86%, P=0.005).

Nonlipid cardiovascular risk factors that correlated with IL-6 levels included age (r=0.15, P=0.002), systolic (r=0.27, P=0.001) and diastolic (r=0.21, P=0.001) blood pressure, and body mass index (r=0.26, P=0.001). As shown in Figure 3Down, median levels of IL-6 increased with increasing number of traditional risk factors (hypertension, hyperlipidemia, smoking, diabetes, age >60 years, family history, and body mass index >27.3 kg/m2) (P for trend 0.001). However, as shown in Tables 2Up and 3Up, adjustment for these factors had a minimal effect on the relationship between IL-6 levels and future risk of myocardial infarction. Alcohol consumption also appeared to affect IL-6 such that daily drinkers had significantly higher plasma levels than those who consumed alcohol on a less frequent basis (2.7 versus 2.9 pg/mL; P=0.001). By contrast, daily exercisers tended to have lower levels of IL-6 than those who exercised less frequently, although this association was not statistically significant (2.1 versus 2.3 pg/mL; P=0.2). As shown in our multivariate analyses, additional control for these factors had no effect on our overall results.



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Figure 3. Median baseline IL-6 levels according to number of traditional risk factors present (hypertension, hyperlipidemia, smoking, diabetes, age >60 years, family history, and body mass index >27.3 kg/m2).

We repeated these analyses for events that occurred before the termination of the randomized aspirin component of the Physicians’ Health Study. In this subgroup, as in the cohort as a whole, each increasing quartile of IL-6 was associated with an increased risk of subsequent myocardial infarction (P for trend 0.001) such that those with the highest levels at baseline had a relative risk 4.1 times higher than those with the lowest levels (95% CI 1.7 to 9.5, P=0.001). The highest risk was observed among those with elevated levels of IL-6 who were randomly assigned to placebo (relative risk 7.3, P=0.001). The reduction in risk of first myocardial infarction attributable to aspirin was similar for those with and without elevated levels of IL-6.


*    Discussion
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*Discussion
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These data indicate that baseline levels of the inflammatory cytokine IL-6 are significantly elevated among apparently healthy men at risk for future myocardial infarction. The relationship between IL-6 level and risk was not altered in analyses that adjusted for baseline differences in total cholesterol, HDL cholesterol, body mass index, blood pressure, diabetes, a family history of premature coronary artery disease, alcohol use, or exercise frequency; it was stable over the 6-year follow-up period and was present even among all low-risk subgroups evaluated, including nonsmokers.

Prior data evaluating the role of IL-6 among healthy individuals at risk for future coronary events are sparse. In the setting of acute ischemia, however, it has recently been shown that IL-6 levels increase with the acute-phase response and that these elevations may be a marker for plaque instability.24 25 26 However, because blood samples in the present study were collected at baseline, we can exclude the possibility that acute ischemia was a cause of IL-6 elevation in these data. Thus, if an enhanced inflammatory response is present among individuals with a propensity for acute plaque rupture,33 then our data indicate that such effects are present and can be clinically detected many years in advance of first myocardial infarction.

Elevated levels of IL-6 have previously been observed in several autoimmune disorders, including arthritis, Castleman syndrome, psoriasis, mesangial proliferative glomerulonephritis, and inflammatory bowel disease.2 In this regard, the current data provide support for the hypothesis that atherosclerosis represents, at least in part, a fundamentally inflammatory condition.27

The strongest correlates of IL-6 in these data were C-reactive protein and fibrinogen, a finding that would be expected because IL-6 is a primary stimulant for hepatic production of acute-phase proteins.6 7 In our data, the effects of IL-6 on subsequent risk remained statistically significant after we controlled for these latter factors. Thus, the current data also help to explain why several acute-phase proteins, such as C-reactive protein, serum amyloid A, albumin, and fibrinogen, have been associated with increased vascular risk.34

Limitations of these data should be considered. We relied on a single baseline blood sample and thus cannot take into account any variation of IL-6 that may occur over time. Furthermore, because our baseline blood samples were not obtained at a uniform time of day, our data may be limited by any diurnal variation in IL-6 that might exist, a potential issue because both glucocorticoids and catecholamines increase IL-6 levels, and the plasma half-life of IL-6 is <6 hours. It is important to recognize, however, that both of these potential limitations would tend to increase random misclassification in our data, an effect that, if anything, would lead to an underestimation of true effects. Finally, because our samples were stored at -80°C, we cannot exclude the possibility of protein degradation. Such an effect is unlikely, however, because the distribution of IL-6 in our study was quite similar to that observed in studies that used fresh blood samples. Furthermore, even if such an effect were present, it would not affect the validity of our results, because both case and control samples were handled identically and in a blinded fashion throughout the study. In addition, because all our study participants were taking oral aspirin at the time of blood sampling, any effect of this agent on IL-6 levels could not have affected our main results.35

Stimuli underlying IL-6 production in apparently healthy men at risk for future myocardial infarction are uncertain. It is possible, for example, that preclinical atherosclerosis is itself an inflammatory stimulus and that IL-6 is a marker rather than a cause of disease. On the other hand, because monocyte-derived macrophages are abundant in atherosclerotic plaque and IL-6 gene transcripts are expressed in human atheroma, it is also possible that increased IL-6 production from endothelium and vascular smooth muscle has direct effects on plaque proliferation and stability.27 28 IL-6 levels also increase with infection,1 2 36 and it has been hypothesized that infection might aggravate atherogenesis.37 In this cohort, however, baseline IgG titers directed against Chlamydia pneumoniae, Helicobacter pylori, herpes simplex virus, and cytomegalovirus were not associated with increased vascular risk or with increased levels of inflammatory markers.38 39

Together, these prospective epidemiological data support a fundamental role for cytokine-mediated inflammation in the early stages of atherogenesis, data that corroborate and extend the recent finding that IL-6 levels are associated with increased mortality in the elderly.40 As such, we believe these data support the possibility that anti-inflammatory therapies might provide a new approach to cardiovascular disease treatment and prevention.


*    Acknowledgments
 
This study was supported by funding from the National Heart, Lung, and Blood Institute (HL58755) and by an Established Investigator Award from the American Heart Association (Dr Ridker).

Received September 23, 1999; revision received November 3, 1999; accepted November 15, 1999.


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*References
 
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Depression and C-Reactive Protein: Population-Based Health 2000 Study
Psychosom Med, May 1, 2009; 71(4): 423 - 430.
[Abstract] [Full Text] [PDF]


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Arterioscler. Thromb. Vasc. Bio.Home page
M. L.E. MacDonald, M. van Eck, R. B. Hildebrand, B. W.C. Wong, N. Bissada, P. Ruddle, A. Kontush, H. Hussein, M. A. Pouladi, M. J. Chapman, et al.
Despite Antiatherogenic Metabolic Characteristics, SCD1-Deficient Mice Have Increased Inflammation and Atherosclerosis
Arterioscler. Thromb. Vasc. Biol., March 1, 2009; 29(3): 341 - 347.
[Abstract] [Full Text] [PDF]


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Clin. Chem.Home page
P. M Ridker
C-Reactive Protein: Eighty Years from Discovery to Emergence as a Major Risk Marker for Cardiovascular Disease
Clin. Chem., February 1, 2009; 55(2): 209 - 215.
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Rheumatology (Oxford)Home page
V. F. Panoulas, K. M. J. Douglas, J. P. Smith, A. Stavropoulos-Kalinoglou, G. S. Metsios, P. Nightingale, and G. D. Kitas
Transforming growth factor-{beta}1 869T/C, but not interleukin-6 -174G/C, polymorphism associates with hypertension in rheumatoid arthritis
Rheumatology, February 1, 2009; 48(2): 113 - 118.
[Abstract] [Full Text] [PDF]


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Am J EpidemiolHome page
J. A. Hyder, M. A. Allison, N. Wong, A. Papa, T. F. Lang, C. Sirlin, S. M. Gapstur, P. Ouyang, J. J. Carr, and M. H. Criqui
Association of Coronary Artery and Aortic Calcium With Lumbar Bone Density: The MESA Abdominal Aortic Calcium Study
Am. J. Epidemiol., January 15, 2009; 169(2): 186 - 194.
[Abstract] [Full Text] [PDF]


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Arterioscler. Thromb. Vasc. Bio.Home page
W. Peeters, W.E. Hellings, D.P.V. de Kleijn, J.P.P.M. de Vries, F.L. Moll, A. Vink, and G. Pasterkamp
Carotid Atherosclerotic Plaques Stabilize After Stroke: Insights Into the Natural Process of Atherosclerotic Plaque Stabilization
Arterioscler. Thromb. Vasc. Biol., January 1, 2009; 29(1): 128 - 133.
[Abstract] [Full Text] [PDF]


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CirculationHome page
D. S. Frankel, J. B. Meigs, J. M. Massaro, P. W.F. Wilson, C. J. O'Donnell, R. B. D'Agostino, and G. H. Tofler
Von Willebrand Factor, Type 2 Diabetes Mellitus, and Risk of Cardiovascular Disease: The Framingham Offspring Study
Circulation, December 9, 2008; 118(24): 2533 - 2539.
[Abstract] [Full Text] [PDF]


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The OncologistHome page
G. Mantovani, C. Madeddu, C. Cadeddu, M. Dessi, A. Piras, E. Massa, R. Serpe, G. Antoni, and G. Mercuro
Persistence, Up to 18 Months of Follow-Up, of Epirubicin-Induced Myocardial Dysfunction Detected Early by Serial Tissue Doppler Echocardiography: Correlation with Inflammatory and Oxidative Stress Markers
Oncologist, December 1, 2008; 13(12): 1296 - 1305.
[Abstract] [Full Text] [PDF]


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Br. J. Sports. Med.Home page
P Borrione, M Rizzo, A Spaccamiglio, R A Salvo, A Dovio, A Termine, A Parisi, F Fagnani, A Angeli, and F Pigozzi
Sport-related hyperhomocysteinaemia: a putative marker of muscular demand to be noted for cardiovascular risk
Br. J. Sports Med., November 1, 2008; 42(11): 894 - 900.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
S. S. Martin, A. Qasim, and M. P. Reilly
Leptin Resistance: A Possible Interface of Inflammation and Metabolism in Obesity-Related Cardiovascular Disease
J. Am. Coll. Cardiol., October 7, 2008; 52(15): 1201 - 1210.
[Abstract] [Full Text] [PDF]


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Biol Res NursHome page
H. Fukuda, T. Ichinose, T. Kusama, A. Yoshidome, K. Anndow, N. Akiyoshi, and T. Shibamoto
The Relationship Between Job Stress and Urinary Cytokines in Healthy Nurses: A Cross-Sectional Study
Biol Res Nurs, October 1, 2008; 10(2): 183 - 191.
[Abstract] [PDF]


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Psychosom. Med.Home page
P. G. Surtees, N. W. J. Wainwright, S. M. Boekholdt, R. N. Luben, N. J. Wareham, and K.-T. Khaw
Major Depression, C-Reactive Protein, and Incident Ischemic Heart Disease in Healthy Men and Women
Psychosom Med, October 1, 2008; 70(8): 850 - 855.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Renal Physiol.Home page
E. I. Boesen, J. M. Sasser, M. A. Saleh, W. A. Potter, M. Woods, T. D. Warner, J. S. Pollock, and D. M. Pollock
Interleukin-1{beta}, but not interleukin-6, enhances renal and systemic endothelin production in vivo
Am J Physiol Renal Physiol, August 1, 2008; 295(2): F446 - F453.
[Abstract] [Full Text] [PDF]


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Eur Respir JHome page
N. Burioka, S. Koyanagi, M. Endo, M. Takata, Y. Fukuoka, M. Miyata, K. Takeda, H. Chikumi, S. Ohdo, and E. Shimizu
Clock gene dysfunction in patients with obstructive sleep apnoea syndrome
Eur. Respir. J., July 1, 2008; 32(1): 105 - 112.
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Infect. Immun.Home page
Y. Koizumi, T. Kurita-Ochiai, S. Oguchi, and M. Yamamoto
Nasal Immunization with Porphyromonas gingivalis Outer Membrane Protein Decreases P. gingivalis-Induced Atherosclerosis and Inflammation in Spontaneously Hyperlipidemic Mice
Infect. Immun., July 1, 2008; 76(7): 2958 - 2965.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
E. Tamagawa, N. Bai, K. Morimoto, C. Gray, T. Mui, K. Yatera, X. Zhang, L. Xing, Y. Li, I. Laher, et al.
Particulate matter exposure induces persistent lung inflammation and endothelial dysfunction
Am J Physiol Lung Cell Mol Physiol, July 1, 2008; 295(1): L79 - L85.
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Psychosom. Med.Home page
K. L. Petersen, A. L. Marsland, J. Flory, E. Votruba-Drzal, M. F. Muldoon, and S. B. Manuck
Community Socioeconomic Status is Associated With Circulating Interleukin-6 and C-Reactive Protein
Psychosom Med, July 1, 2008; 70(6): 646 - 652.
[Abstract] [Full Text] [PDF]


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StrokeHome page
M. Fornage, Y. A. Chiang, E. S. O'Meara, B. M. Psaty, A. P. Reiner, D. S. Siscovick, R. P. Tracy, and W.T. Longstreth Jr
Biomarkers of Inflammation and MRI-Defined Small Vessel Disease of the Brain: The Cardiovascular Health Study
Stroke, July 1, 2008; 39(7): 1952 - 1959.
[Abstract] [Full Text] [PDF]


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J. Nutr.Home page
C. T. Damsgaard, H. Frokiaer, A. D. Andersen, and L. Lauritzen
Fish Oil in Combination with High or Low Intakes of Linoleic Acid Lowers Plasma Triacylglycerols but Does Not Affect Other Cardiovascular Risk Markers in Healthy Men
J. Nutr., June 1, 2008; 138(6): 1061 - 1066.
[Abstract] [Full Text] [PDF]


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HeartHome page
A Malarstig, P Eriksson, A Hamsten, B Lindahl, L Wallentin, and A Siegbahn
Raised interleukin-10 is an indicator of poor outcome and enhanced systemic inflammation in patients with acute coronary syndrome
Heart, June 1, 2008; 94(6): 724 - 729.
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Am. J. Respir. Crit. Care Med.Home page
S. Yende, G. D'Angelo, J. A. Kellum, L. Weissfeld, J. Fine, R. D. Welch, L. Kong, M. Carter, D. C. Angus, and for the GenIMS Investigators
Inflammatory Markers at Hospital Discharge Predict Subsequent Mortality after Pneumonia and Sepsis
Am. J. Respir. Crit. Care Med., June 1, 2008; 177(11): 1242 - 1247.
[Abstract] [Full Text] [PDF]


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Clin. Chem.Home page
A. J. P. Smith, F. D'Aiuto, J. Palmen, J. A. Cooper, J. Samuel, S. Thompson, J. Sanders, N. Donos, L. Nibali, D. Brull, et al.
Association of Serum Interleukin-6 Concentration with a Functional IL6 -6331T>C Polymorphism
Clin. Chem., May 1, 2008; 54(5): 841 - 850.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. E. Lang, E. S. Williams, J. P. Mizgerd, and S. A. Shore
Effect of obesity on pulmonary inflammation induced by acute ozone exposure: role of interleukin-6
Am J Physiol Lung Cell Mol Physiol, May 1, 2008; 294(5): L1013 - L1020.
[Abstract] [Full Text] [PDF]


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Eur Heart JHome page
I. Tzoulaki, M.-R. Jarvelin, A.-L. Hartikainen, M. Leinonen, A. Pouta, M. Paldanius, A. Ruokonen, D. Canoy, U. Sovio, P. Saikku, et al.
Size at birth, weight gain over the life course, and low-grade inflammation in young adulthood: northern Finland 1966 birth cohort study
Eur. Heart J., April 9, 2008; (2008) ehn105v1.
[Abstract] [Full Text] [PDF]


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Am J EpidemiolHome page
L. Gallicchio, H. Chang, D. K. Christo, L. Thuita, H.-Y. Huang, P. Strickland, I. Ruczinski, S. C. Hoffman, and K. J. Helzlsouer
Single Nucleotide Polymorphisms in Inflammation-related Genes and Mortality in a Community-based Cohort in Washington County, Maryland
Am. J. Epidemiol., April 1, 2008; 167(7): 807 - 813.
[Abstract] [Full Text] [PDF]


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JCOHome page
A. H. Miller, S. Ancoli-Israel, J. E. Bower, L. Capuron, and M. R. Irwin
Neuroendocrine-Immune Mechanisms of Behavioral Comorbidities in Patients With Cancer
J. Clin. Oncol., February 20, 2008; 26(6): 971 - 982.
[Abstract] [Full Text] [PDF]


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Psychosom. Med.Home page
J. C. Stewart, D. Janicki-Deverts, M. F. Muldoon, and T. W. Kamarck
Depressive Symptoms Moderate the Influence of Hostility on Serum Interleukin-6 and C-Reactive Protein
Psychosom Med, February 1, 2008; 70(2): 197 - 204.
[Abstract] [Full Text] [PDF]


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CirculationHome page
J. Dai, A. H. Miller, J. D. Bremner, J. Goldberg, L. Jones, L. Shallenberger, R. Buckham, N. V. Murrah, E. Veledar, P. W. Wilson, et al.
Adherence to the Mediterranean Diet Is Inversely Associated With Circulating Interleukin-6 Among Middle-Aged Men: A Twin Study
Circulation, January 15, 2008; 117(2): 169 - 175.
[Abstract] [Full Text] [PDF]


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Arterioscler. Thromb. Vasc. Bio.Home page
J. G. Schneider, Y. Zhu, T. Coleman, and C. F. Semenkovich
Macrophage 3 Integrin Suppresses Hyperlipidemia-Induced Inflammation by Modulating TNF{alpha} Expression
Arterioscler. Thromb. Vasc. Biol., December 1, 2007; 27(12): 2699 - 2706.
[Abstract] [Full Text] [PDF]


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Arterioscler. Thromb. Vasc. Bio.Home page
L. I. Schrader, D. A. Kinzenbaw, A. W. Johnson, F. M. Faraci, and S. P. Didion
IL-6 Deficiency Protects Against Angiotensin II Induced Endothelial Dysfunction and Hypertrophy
Arterioscler. Thromb. Vasc. Biol., December 1, 2007; 27(12): 2576 - 2581.
[Abstract] [Full Text] [PDF]


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DiabetesHome page
L. Qi, N. Rifai, and F. B. Hu
Interleukin-6 Receptor Gene Variations, Plasma Interleukin-6 Levels, and Type 2 Diabetes in U.S. Women
Diabetes, December 1, 2007; 56(12): 3075 - 3081.
[Abstract] [Full Text] [PDF]


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JNMHome page
L. G. Spagnoli, E. Bonanno, G. Sangiorgi, and A. Mauriello
Role of Inflammation in Atherosclerosis
J. Nucl. Med., November 1, 2007; 48(11): 1800 - 1815.
[Abstract] [Full Text] [PDF]


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StrokeHome page
A. R. Tso, J. G. Merino, and S. Warach
Interleukin-6 174G/C Polymorphism and Ischemic Stroke: A Systematic Review
Stroke, November 1, 2007; 38(11): 3070 - 3075.
[Abstract] [Full Text] [PDF]


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Exp. Biol. Med.Home page
J. l. Sullivan
Macrophage Iron, Hepcidin, and Atherosclerotic Plaque Stability
Experimental Biology and Medicine, September 1, 2007; 232(8): 1014 - 1020.
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ChestHome page
H. Allayee, J. Hartiala, W. Lee, M. Mehrabian, C. G. Irvin, D. V. Conti, and J. J. Lima
The Effect of Montelukast and Low-Dose Theophylline on Cardiovascular Disease Risk Factors in Asthmatics
Chest, September 1, 2007; 132(3): 868 - 874.
[Abstract] [Full Text] [PDF]


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The OncologistHome page
G. Mercuro, C. Cadeddu, A. Piras, M. Dessi, C. Madeddu, M. Deidda, R. Serpe, E. Massa, and G. Mantovani
Early Epirubicin-Induced Myocardial Dysfunction Revealed by Serial Tissue Doppler Echocardiography: Correlation with Inflammatory and Oxidative Stress Markers
Oncologist, September 1, 2007; 12(9): 1124 - 1133.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Heart Circ. Physiol.Home page
E. I. Boesen and D. M. Pollock
Effect of chronic IL-6 infusion on acute pressor responses to vasoconstrictors in mice
Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1745 - H1749.
[Abstract] [Full Text] [PDF]


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Eur J EndocrinolHome page
J-M Gonzalez-Clemente, C Vilardell, M Broch, A Megia, A Caixas, O Gimenez-Palop, C Richart, I Simon, A Martinez-Riquelme, J Arroyo, et al.
Lower heart rate variability is associated with higher plasma concentrations of IL-6 in type 1 diabetes
Eur. J. Endocrinol., July 1, 2007; 157(1): 31 - 38.
[Abstract] [Full Text] [PDF]


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ChestHome page
K. Tomoda, M. Yoshikawa, T. Itoh, S. Tamaki, A. Fukuoka, K. Komeda, and H. Kimura
Elevated Circulating Plasma Adiponectin in Underweight Patients With COPD
Chest, July 1, 2007; 132(1): 135 - 140.
[Abstract] [Full Text] [PDF]


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Am. J. Clin. Nutr.Home page
J. A Nettleton, L. M Steffen, M. B Schulze, N. S Jenny, R G. Barr, A. G Bertoni, and D. R Jacobs Jr
Associations between markers of subclinical atherosclerosis and dietary patterns derived by principal components analysis and reduced rank regression in the Multi-Ethnic Study of Atherosclerosis (MESA)
Am. J. Clinical Nutrition, June 1, 2007; 85(6): 1615 - 1625.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Endocrinol. Metab.Home page
P. C. Geiger, C. Hancock, D. C. Wright, D.-H. Han, and J. O. Holloszy
IL-6 increases muscle insulin sensitivity only at superphysiological levels
Am J Physiol Endocrinol Metab, June 1, 2007; 292(6): E1842 - E1846.
[Abstract] [Full Text] [PDF]


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AMERICAN JOURNAL OF LIFESTYLE MEDICINEHome page
M. G. Flynn, B. K. McFarlin, and M. M. Markofski
State of the Art Reviews: The Anti-Inflammatory Actions of Exercise Training
American Journal of Lifestyle Medicine, May 1, 2007; 1(3): 220 - 235.
[Abstract] [PDF]


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ChestHome page
D. G. Yanbaeva, M. A. Dentener, E. C. Creutzberg, G. Wesseling, and E. F. M. Wouters
Systemic Effects of Smoking
Chest, May 1, 2007; 131(5): 1557 - 1566.
[Abstract] [Full Text] [PDF]


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CirculationHome page
I. Tzoulaki, G. D. Murray, A. J. Lee, A. Rumley, G. D.O. Lowe, and F. G. R. Fowkes
Relative Value of Inflammatory, Hemostatic, and Rheological Factors for Incident Myocardial Infarction and Stroke: The Edinburgh Artery Study
Circulation, April 24, 2007; 115(16): 2119 - 2127.
[Abstract] [Full Text] [PDF]


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HypertensionHome page
H. D. Sesso, L. Wang, J. E. Buring, P. M Ridker, and J. M. Gaziano
Comparison of Interleukin-6 and C-Reactive Protein for the Risk of Developing Hypertension in Women
Hypertension, February 1, 2007; 49(2): 304 - 310.
[Abstract] [Full Text] [PDF]


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Arterioscler. Thromb. Vasc. Bio.Home page
W. Koenig and N. Khuseyinova
Biomarkers of Atherosclerotic Plaque Instability and Rupture
Arterioscler. Thromb. Vasc. Biol., January 1, 2007; 27(1): 15 - 26.
[Abstract] [Full Text] [PDF]


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Br J AnaesthHome page
G. M. Howard-Alpe, J. W. Sear, and P. Foex
Methods of detecting atherosclerosis in non-cardiac surgical patients; the role of biochemical markers
Br. J. Anaesth., December 1, 2006; 97(6): 758 - 769.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
P. Libby and P. M. Ridker
Inflammation and Atherothrombosis: From Population Biology and Bench Research to Clinical Practice
J. Am. Coll. Cardiol., October 27, 2006; 48(9_Suppl_A): A33 - A46.
[Abstract] [Full Text] [PDF]


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Journal of the American Dental AssociationHome page
R. T. Demmer and M. Desvarieux
Periodontal infections and cardiovascular disease: The heart of the matter
J Am Dent Assoc, October 1, 2006; 137(suppl_2): 14S - 20S.
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J Am Coll CardiolHome page
D. Giugliano, A. Ceriello, and K. Esposito
The Effects of Diet on Inflammation: Emphasis on the Metabolic Syndrome
J. Am. Coll. Cardiol., August 15, 2006; 48(4): 677 - 685.
[Abstract] [Full Text] [PDF]


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ChestHome page
P. Joppa, D. Petrasova, B. Stancak, and R. Tkacova
Systemic Inflammation in Patients With COPD and Pulmonary Hypertension.
Chest, August 1, 2006; 130(2): 326 - 333.
[Abstract] [Full Text] [PDF]


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CirculationHome page
S. Blankenberg, M. J. McQueen, M. Smieja, J. Pogue, C. Balion, E. Lonn, H. J. Rupprecht, C. Bickel, L. Tiret, F. Cambien, et al.
Comparative Impact of Multiple Biomarkers and N-Terminal Pro-Brain Natriuretic Peptide in the Context of Conventional Risk Factors for the Prediction of Recurrent Cardiovascular Events in the Heart Outcomes Prevention Evaluation (HOPE) Study
Circulation, July 18, 2006; 114(3): 201 - 208.
[Abstract] [Full Text] [PDF]


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Eur Heart JHome page
F. M.A.C. Martens, T. J. Rabelink, J. op 't Roodt, E. J.P. de Koning, and F. L.J. Visseren
TNF-{alpha} induces endothelial dysfunction in diabetic adults, an effect reversible by the PPAR-{gamma} agonist pioglitazone
Eur. Heart J., July 1, 2006; 27(13): 1605 - 1609.
[Abstract] [Full Text] [PDF]


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Clin. Chem.Home page
A. M. Gori, F. Sofi, A. M. Corsi, A. Gazzini, I. Sestini, F. Lauretani, S. Bandinelli, G. F. Gensini, L. Ferrucci, and R. Abbate
Predictors of Vitamin B6 and Folate Concentrations in Older Persons: The InCHIANTI Study
Clin. Chem., July 1, 2006; 52(7): 1318 - 1324.
[Abstract] [Full Text] [PDF]


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Cardiovasc ResHome page
E. Paffen and M. P.M. deMaat
C-reactive protein in atherosclerosis: A causal factor?
Cardiovasc Res, July 1, 2006; 71(1): 30 - 39.
[Abstract] [Full Text] [PDF]


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Am. J. Clin. Nutr.Home page
J. A Nettleton, L. M Steffen, E. J Mayer-Davis, N. S Jenny, R. Jiang, D. M Herrington, and D. R Jacobs Jr
Dietary patterns are associated with biochemical markers of inflammation and endothelial activation in the Multi-Ethnic Study of Atherosclerosis (MESA)
Am. J. Clinical Nutrition, June 1, 2006; 83(6): 1369 - 1379.
[Abstract] [Full Text] [PDF]


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Diabetes CareHome page
C. Langenberg, J. Bergstrom, C. Scheidt-Nave, J. Pfeilschifter, and E. Barrett-Connor
Cardiovascular Death and the Metabolic Syndrome: Role of adiposity-signaling hormones and inflammatory markers.
Diabetes Care, June 1, 2006; 29(6): 1363 - 1369.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Endocrinol. Metab.Home page
T. T. Antunes, A. Gagnon, B. Chen, F. Pacini, T. J. Smith, and A. Sorisky
Interleukin-6 release from human abdominal adipose cells is regulated by thyroid-stimulating hormone: effect of adipocyte differentiation and anatomic depot
Am J Physiol Endocrinol Metab, June 1, 2006; 290(6): E1140 - E1144.
[Abstract] [Full Text] [PDF]


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CirculationHome page
R. S. Vasan
Biomarkers of Cardiovascular Disease: Molecular Basis and Practical Considerations
Circulation, May 16, 2006; 113(19): 2335 - 2362.
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ANGIOLOGYHome page
A. Ziakas, S. Gavrilidis, G. Giannoglou, E. Souliou, K. Gemitzis, D. Kalampalika, M. A. Vayona, I. Pidonia, G. Parharidis, and G. Louridas
In-Hospital and Long-Term Prognostic Value of Fibrinogen, CRP, and IL-6 Levels in Patients with Acute Myocardial Infarction Treated with Thrombolysis
Angiology, May 1, 2006; 57(3): 283 - 293.
[Abstract] [PDF]


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Arch Intern MedHome page
L. E. Bernstein, J. Berry, S. Kim, B. Canavan, and S. K. Grinspoon
Effects of Etanercept in Patients With the Metabolic Syndrome.
Arch Intern Med, April 24, 2006; 166(8): 902 - 908.
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Am. J. Clin. Nutr.Home page
S. E Kasim-Karakas, A. Tsodikov, U. Singh, and I. Jialal
Responses of inflammatory markers to a low-fat, high-carbohydrate diet: effects of energy intake.
Am. J. Clinical Nutrition, April 1, 2006; 83(4): 774 - 779.
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Physiol. Rev.Home page
A. Tedgui and Z. Mallat
Cytokines in Atherosclerosis: Pathogenic and Regulatory Pathways
Physiol Rev, April 1, 2006; 86(2): 515 - 581.
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Psychosom. Med.Home page
J. M. McCaffery, N. Frasure-Smith, M.-P. Dube, P. Theroux, G. A. Rouleau, Q. Duan, and F. Lesperance
Common genetic vulnerability to depressive symptoms and coronary artery disease: a review and development of candidate genes related to inflammation and serotonin.
Psychosom Med, March 1, 2006; 68(2): 187 - 200.
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J. Am. Soc. Nephrol.Home page
Y. Liu, Y. Berthier-Schaad, M. D. Fallin, N. E. Fink, R. P. Tracy, M. J. Klag, M. W. Smith, and J. Coresh
IL-6 Haplotypes, Inflammation, and Risk for Cardiovascular Disease in a Multiethnic Dialysis Cohort
J. Am. Soc. Nephrol., March 1, 2006; 17(3): 863 - 870.
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Am. J. Physiol. Heart Circ. Physiol.Home page
D. L. Lee, L. C. Sturgis, H. Labazi, J. B. Osborne Jr., C. Fleming, J. S. Pollock, M. Manhiani, J. D. Imig, and M. W. Brands
Angiotensin II hypertension is attenuated in interleukin-6 knockout mice
Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H935 - H940.
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Am. J. Respir. Crit. Care Med.Home page
R. Ruckerl, A. Ibald-Mulli, W. Koenig, A. Schneider, G. Woelke, J. Cyrys, J. Heinrich, V. Marder, M. Frampton, H. E. Wichmann, et al.
Air Pollution and Markers of Inflammation and Coagulation in Patients with Coronary Heart Disease
Am. J. Respir. Crit. Care Med., February 15, 2006; 173(4): 432 - 441.
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CMAJHome page
K. W.J. Lee, J. S. Hill, K. R. Walley, and J. J. Frohlich
Relative value of multiple plasma biomarkers as risk factors for coronary artery disease and death in an angiography cohort.
Can. Med. Assoc. J., February 14, 2006; 174(4): 461 - 466.
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Am. J. Clin. Nutr.Home page
P. Libby
Inflammation and cardiovascular disease mechanisms
Am. J. Clinical Nutrition, February 1, 2006; 83(2): 456S - 460S.
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Am. J. Clin. Nutr.Home page
A. S Greenberg and M. S Obin
Obesity and the role of adipose tissue in inflammation and metabolism
Am. J. Clinical Nutrition, February 1, 2006; 83(2): 461S - 465S.
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J. Clin. Pathol.Home page
M Libra, S S Signorelli, Y Bevelacqua, P M Navolanic, V Bevelacqua, J Polesel, R Talamini, F Stivala, M C Mazzarino, and G Malaponte
Analysis of G(-174)C IL-6 polymorphism and plasma concentrations of inflammatory markers in patients with type 2 diabetes and peripheral arterial disease
J. Clin. Pathol., February 1, 2006; 59(2): 211 - 215.
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