***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: We conducted a prospect i ve , nested , case-control study of inflammatory markers as predictors of  type 2 diabetes among 32,826 women who provided blood sample s in 1989 through 1990 in the Nurses ' Health Study . Among women free of diabetes , cardiovascular disease , or cancer at baseline , 737 had developed diabetes by 2000 . Control women ( n = 785 ) were selected matched on age , fasting status , race , and BMI for cases in the top BMI decile . Baseline levels of tumor necrosis factor (TNF)-alpha receptor 2 , interleukin (IL)-6 , and C-reactive protein ( CRP ) were significantly higher among case than control subjects ( all P < /= 0.001 ) . After adjusting for BMI and other lifestyle factors , all three biomarkers significantly predicted diabetes risk ; the odds ratios ( ORs ) comparing extreme quintiles were 1.64 ( 95 % CI 1.10 - 2.45 ) for TNF-alphaR2 , 1.91 ( 1.27 - 2.86 ) for IL-6 , and 4.36 ( 2.80 - 6.80 ) for CRP ( P for trend < 0.001 for all biomarkers ) . In a multivariate model simultaneously including the three biomarkers , only CRP levels were significantly associated with risk of diabetes ( OR comparing extreme quintiles of CRP = 3.99 , P for trend < 0.001 ) . These data support the role of inflammation in the pathogenesis of type 2 diabetes . Elevated CRP levels are a strong independent predictor of type 2 diabetes and may mediate associations of TNF-alphaR2 and IL-6 with type 2 diabetes BACKGROUND Increased levels of the inflammatory biomarker high-sensitivity C-reactive protein predict cardiovascular events . Since statins lower levels of high-sensitivity C-reactive protein as well as cholesterol , we hypothesized that people with elevated high-sensitivity C-reactive protein levels but without hyperlipidemia might benefit from statin treatment . METHODS We r and omly assigned 17,802 apparently healthy men and women with low-density lipoprotein ( LDL ) cholesterol levels of less than 130 mg per deciliter ( 3.4 mmol per liter ) and high-sensitivity C-reactive protein levels of 2.0 mg per liter or higher to rosuvastatin , 20 mg daily , or placebo and followed them for the occurrence of the combined primary end point of myocardial infa rct ion , stroke , arterial revascularization , hospitalization for unstable angina , or death from cardiovascular causes . RESULTS The trial was stopped after a median follow-up of 1.9 years ( maximum , 5.0 ) . Rosuvastatin reduced LDL cholesterol levels by 50 % and high-sensitivity C-reactive protein levels by 37 % . The rates of the primary end point were 0.77 and 1.36 per 100 person-years of follow-up in the rosuvastatin and placebo groups , respectively ( hazard ratio for rosuvastatin , 0.56 ; 95 % confidence interval [ CI ] , 0.46 to 0.69 ; P<0.00001 ) , with corresponding rates of 0.17 and 0.37 for myocardial infa rct ion ( hazard ratio , 0.46 ; 95 % CI , 0.30 to 0.70 ; P=0.0002 ) , 0.18 and 0.34 for stroke ( hazard ratio , 0.52 ; 95 % CI , 0.34 to 0.79 ; P=0.002 ) , 0.41 and 0.77 for revascularization or unstable angina ( hazard ratio , 0.53 ; 95 % CI , 0.40 to 0.70 ; P<0.00001 ) , 0.45 and 0.85 for the combined end point of myocardial infa rct ion , stroke , or death from cardiovascular causes ( hazard ratio , 0.53 ; 95 % CI , 0.40 to 0.69 ; P<0.00001 ) , and 1.00 and 1.25 for death from any cause ( hazard ratio , 0.80 ; 95 % CI , 0.67 to 0.97 ; P=0.02 ) . Consistent effects were observed in all subgroups evaluated . The rosuvastatin group did not have a significant increase in myopathy or cancer but did have a higher incidence of physician-reported diabetes . CONCLUSIONS In this trial of apparently healthy persons without hyperlipidemia but with elevated high-sensitivity C-reactive protein levels , rosuvastatin significantly reduced the incidence of major cardiovascular events . ( Clinical Trials.gov number , NCT00239681 . 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 BACKGROUND Since inflammation is believed to have a role in the pathogenesis of cardiovascular events , measurement of markers of inflammation has been proposed as a method to improve the prediction of the risk of these events . METHODS We conducted a prospect i ve , nested case-control study among 28,263 apparently healthy postmenopausal women over a mean follow-up period of three years to assess the risk of cardiovascular events associated with base-line levels of markers of inflammation . The markers included high-sensitivity C-reactive protein ( hs-CRP ) , serum amyloid A , interleukin-6 , and soluble intercellular adhesion molecule type 1 ( sICAM-1 ) . We also studied homocysteine and a variety of lipid and lipoprotein measurements .  Cardiovascular events were defined as death from coronary heart disease , nonfatal myocardial infa rct ion or stroke , or the need for coronary-revascularization procedures . RESULTS Of the 12 markers measured , hs-CRP was the strongest univariate predictor of the risk of cardiovascular events ; the relative risk of events for women in the highest as compared with the lowest quartile for this marker was 4.4 ( 95 percent confidence interval , 2.2 to 8.9 ) . Other markers significantly associated with the risk of cardiovascular events were serum amyloid A ( relative risk for the highest as compared with the lowest quartile , 3.0 ) , sICAM-1 ( 2.6 ) , interleukin-6 ( 2.2 ) , homocysteine ( 2.0 ) , total cholesterol ( 2.4 ) , LDL cholesterol ( 2.4 ) , apolipoprotein B-100 ( 3.4 ) , HDL cholesterol ( 0.3 ) , and the ratio of total cholesterol to HDL cholesterol ( 3.4 ) . Prediction models that incorporated markers of inflammation in addition to lipids were significantly better at predicting risk than models based on lipid levels alone ( P<0.001 ) . The levels of hs-CRP and serum amyloid A were significant predictors of risk even in the subgroup of women with LDL cholesterol levels below 130 mg per deciliter ( 3.4 mmol per liter ) , the target for primary prevention established by the National Cholesterol Education Program . In multivariate analyses , the only plasma markers that independently predicted risk were hs-CRP ( relative risk for the highest as compared with the lowest quartile , 1.5 ; 95 percent confidence interval , 1.1 to 2.1 ) and the ratio of total cholesterol to HDL cholesterol ( relative risk , 1.4 ; 95 percent confidence interval , 1.1 to 1.9 ) . CONCLUSIONS The addition of the measurement of C-reactive protein to screening based on lipid levels may provide an improved method of identifying persons at risk for cardiovascular events BACKGROUND Statins lower the levels of low-density lipoprotein ( LDL ) cholesterol and C-reactive protein ( CRP ) . Whether this latter property affects clinical outcomes is unknown . METHODS We evaluated relationships between the LDL cholesterol and CRP levels achieved after treatment with 80 mg of atorvastatin or 40 mg of pravastatin per day and the risk of recurrent myocardial infa rct ion or death from coronary causes among 3745 patients with acute coronary syndromes . RESULTS Patients in whom statin therapy result ed in LDL cholesterol levels  of less than 70 mg per deciliter ( 1.8 mmol per liter ) had lower event rates than those with higher levels ( 2.7 vs. 4.0 events per 100 person-years , P=0.008 ) . However , a virtually identical difference was observed between those who had CRP levels of less than 2 mg per liter after statin therapy and those who had higher levels ( 2.8 vs. 3.9 events per 100 person-years , P=0.006 ) , an effect present at all levels of LDL cholesterol achieved . For patients with post-treatment LDL cholesterol levels  of more than 70 mg per deciliter , the rates of recurrent events were 4.6 per 100 person-years among those with CRP levels of more than 2 mg per liter and 3.2 events per 100 person-years among those with CRP levels of less than 2 mg per liter ; the respective rates among those with LDL cholesterol levels of less than 70 mg per deciliter were 3.1 and 2.4 events per 100 person-years ( P<0.001 ) . Although atorvastatin was more likely than pravastatin to result in low levels of LDL cholesterol and CRP , meeting these targets was more important in determining the outcomes than was the specific choice of therapy . Patients who had LDL cholesterol levels of less than 70 mg per deciliter and CRP levels of less than 1 mg per liter after statin therapy had the lowest rate of recurrent events ( 1.9 per 100 person-years ) . CONCLUSIONS Patients who have low CRP levels after statin therapy  have better clinical outcomes than those with higher CRP levels , regardless of the result ant level of LDL cholesterol . Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol BACKGROUND Maternal periodontal disease has been associated with an increased risk of  preterm birth and low birth weight .  We studied the effect of nonsurgical periodontal treatment on preterm birth . METHODS We r and omly assigned women between 13 and 17 weeks of gestation to undergo  scaling and root planing either before 21 weeks ( 413 patients in the treatment group ) or after delivery ( 410 patients in the control group ) . Patients in the treatment group also underwent monthly tooth polishing and received instruction in oral hygiene . The gestational age at the end of pregnancy was the prespecified primary outcome . Secondary outcomes were birth weight and the proportion of infants who were small for gestational age . RESULTS In the follow-up analysis , preterm birth ( before 37 weeks of gestation ) occurred in 49 of 407 women ( 12.0 % ) in the treatment group ( result ing in 44 live births ) and in 52 of 405 women ( 12.8 % ) in the control group ( result ing in 38 live births ) . Although periodontal treatment improved periodontitis measures ( P<0.001 ) , it did not significantly alter the risk of preterm delivery ( P=0.70 ; hazard ratio for treatment group vs. control group , 0.93 ; 95 % confidence interval [ CI ] , 0.63 to 1.37 ) . There were no significant differences between the treatment and control groups in birth weight ( 3 
    Output:
    
Anti-infective periodontal treatment results in short-term modest reductions in systemic CRP