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Author Affiliations: Departments of Cardiology (Dr Boekholdt), Vascular Medicine (Drs Arsenault and Kastelein), and Clinical Epidemiology and Biostatistics (Dr Zwinderman), Academic Medical Center, Amsterdam, the Netherlands; Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital, Boston, Massachusetts (Drs Mora and Ridker); Center of Preventive Medicine, Oslo University Hospital, Ulleval, and University of Oslo, Norway (Dr Pedersen); State University of New York Health Science Center, Brooklyn (Dr LaRosa); Baker Heart and Diabetes Research Institute, Melbourne, Australia (Dr Nestel); NHMRC Clinical Trials Centre, University of Sydney, Sydney, Australia (Dr Simes); School of Biomedicine, University of Manchester, Manchester, United Kingdom (Dr Durrington); Centre for Diabetes and Metabolic Medicine, Barts, and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom (Dr Hitman); Rosalind Franklin University of Medicine and Science, North Chicago, Illinois (Dr Welch); Global Pharmaceuticals Pfizer, New York, New York (Dr DeMicco); Touro University, Mare Island, California (Dr Clearfield); Department of Medicine, University of Texas Health Science Center, and VERDICT, South Texas Veterans Health Care System, San Antonio (Dr Downs); Medical Research Institute, University of Dundee, Dundee, United Kingdom (Dr Colhoun); Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia (Dr Tonkin); and Weill Cornell Medical College, New York, New York (Dr Gotto).
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Context The associations of low-density lipoprotein cholesterol (LDL-C), non–high-density lipoprotein cholesterol (non–HDL-C), and apolipoprotein B (apoB) levels with the risk of cardiovascular events among patients treated with statin therapy have not been reliably documented.
Objective To evaluate the relative strength of the associations of LDL-C, non–HDL-C, and apoB with cardiovascular risk among patients treated with statin therapy.
Design Meta-analysis of individual patient data from randomized controlled statin trials in which conventional lipids and apolipoproteins were determined in all study participants at baseline and at 1-year follow-up.
Data Sources Relevant trials were identified by a literature search updated through December 31, 2011. Investigators were contacted and individual patient data were requested and obtained for 62 154 patients enrolled in 8 trials published between 1994 and 2008.
Data Extraction Hazard ratios (HRs) and corresponding 95% CIs for risk of major cardiovascular events adjusted for established risk factors by 1-SD increase in LDL-C, non–HDL-C, and apoB.
Results Among 38 153 patients allocated to statin therapy, 158 fatal myocardial infarctions, 1678 nonfatal myocardial infarctions, 615 fatal events from other coronary artery disease, 2806 hospitalizations for unstable angina, and 1029 fatal or nonfatal strokes occurred during follow-up. The adjusted HRs for major cardiovascular events per 1-SD increase were 1.13 (95% CI, 1.10-1.17) for LDL-C, 1.16 (95% CI, 1.12-1.19) for non–HDL-C, and 1.14 (95% CI, 1.11-1.18) for apoB. These HRs were significantly higher for non–HDL-C than LDL-C (P = .002) and apoB (P = .02). There was no significant difference between apoB and LDL-C (P = .21).
Conclusion Among statin-treated patients, on-treatment levels of LDL-C, non–HDL-C, and apoB were each associated with risk of future major cardiovascular events, but the strength of this association was greater for non–HDL-C than for LDL-C and apoB.
Quiz Ref IDStatin therapy is the cornerstone of pharmacological therapy for the primary and secondary prevention of cardiovascular disease. All currently available guidelines state that low-density lipoprotein cholesterol (LDL-C) levels should be used as the primary target to initiate and titrate lipid-lowering therapy.1,2 However, trials investigating the efficacy of statin therapy have shown that the cardiovascular benefits of statins may go beyond their influence on LDL-C levels. Thus, LDL-C may not be the best lipid parameter to predict cardiovascular risk or to quantify the atheroprotective effect of statin therapy.3Quiz Ref IDExperimental evidence supports a more important role for apolipoprotein B (apoB) and apoB-containing lipoproteins than for LDL-C content in mediating atherogenesis. Lipoproteins containing apoB must first enter the arterial wall and undergo oxidative modification before they can contribute to atherogenesis. This modification affects the structure of the apoB molecule or the phospholipid membrane of these lipoproteins, yielding ligands for the scavenger receptors of macrophages in the arterial wall.4 Subsequently, cholesterol accumulation and crystallization in macrophage cytoplasm leads to the formation of foam cells and progression to atherosclerotic plaque.5
Several alternative lipid and apolipoprotein parameters have been proposed as alternatives for LDL-C, most prominently apoB and non–high-density lipoprotein cholesterol (non–HDL-C), both markers of the concentration of atherogenic apoB-containing lipoproteins. Several population-based studies have shown that these 2 parameters are more strongly associated with cardiovascular risk than LDL-C.6- 9 Similar observations have been reported in some statin trials, although less extensively.10- 12 Therefore, the role of lipid or apolipoprotein parameters other than LDL-C as targets for statin therapy remains debated and clinically relevant.
It was the objective of this meta-analysis to assess whether among statin-treated patients, non–HDL-C and apoB were more strongly associated with the risk of future cardiovascular events than LDL-C. The secondary objective was to explore whether non–HDL-C and apoB explained a larger proportion of the atheroprotective effects of statin therapy than LDL-C. These objectives were addressed by performing a meta-analysis of individual patient data from large randomized controlled statin trials.
The literature was searched to identify all randomized controlled trials (RCTs) that assigned study participants in at least 1 of the study groups to statin therapy. Trials in which total cholesterol, LDL-C, HDL-C, triglycerides, and apolipoproteins were measured at baseline and during statin therapy in the entire study population were selected. Trials with a mean follow-up for cardiovascular events shorter than 2 years and those including fewer than 1000 participants were excluded.
The literature search was undertaken in PubMed using the following search terms: statin, hydroxymethylglutaryl coenzyme A reductase inhibitor, simvastatin, lovastatin, fluvastatin, pravastatin, atorvastatin, rosuvastatin, cholesterol, apolipoprotein, coronary heart disease, coronary artery disease and cardiovascular disease. The results were limited to randomized trials and English language. The first search was performed on January 4, 2009, and the updated search until December 31, 2011, was performed on January 20, 2012. Two authors (B.J.A. and S.M.B.) independently screened all abstracts for randomized controlled trials fulfilling the inclusion criteria. If an abstract described a subanalysis of a potentially relevant trial, the original publication was traced. Results were compared and inconsistencies were resolved by consensus. Investigators were contacted and asked to provide individual patient data. The requested patient characteristics included sex, age, smoking status, body mass index, diabetes mellitus, systolic and diastolic blood pressure, fasting glucose, total cholesterol, LDL-C, HDL-C, triglycerides, and apolipoprotein A-I and B at baseline and at 1-year follow-up, study medication, and patient history of stable coronary artery disease, myocardial infarction, percutaneous coronary intervention, or coronary artery bypass grafting. The following outcomes (and time to event) were also collected: fatal and nonfatal myocardial infarction, fatal other coronary artery disease, hospitalization for unstable angina, fatal and nonfatal stroke, peripheral artery disease, and congestive heart failure. Data were harmonized into a pooled database and this database was independently validated against the original files. Quality of the included trials was assessed by the Delphi score.13 This meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and a checklist was provided at the time of manuscript submission.14
Lipid and apolipoprotein levels at baseline and at 1-year follow-up were obtained from the participating trials. For on-statin measurements, the 1-year time point was chosen because this was the first uniform time point when apolipoproteins were measured in all participating trials. Quiz Ref IDNon–HDL-C was calculated as total minus HDL-C. Cholesterol levels reported in mmol/L were converted to mg/dL by multiplying by 38.7, and triglycerides levels reported in mmol/L were converted to mg/dL by multiplying by 88.5. The primary disease outcome of this meta-analysis was time to first major cardiovascular event, which was defined as fatal or nonfatal myocardial infarction, fatal other coronary artery disease, hospitalization for unstable angina, and fatal or nonfatal stroke. Additional analyses were performed for the prediction of time to first major coronary events (fatal or nonfatal myocardial infarction, fatal other coronary artery disease, and hospitalization for unstable angina) and time to major cerebrovascular event (fatal or nonfatal stroke).
Baseline characteristics, levels of lipids and apolipoproteins at baseline and on-trial, as well as absolute changes and percentage changes between on-trial and baseline levels were calculated for each trial separately. The risk of major cardiovascular events, major coronary events, and major cerebrovascular events associated with on-statin lipid and apolipoprotein levels was quantified using Cox proportional hazards models. Study participants allocated to placebo were excluded. Analyses were performed for LDL-C, non–HDL-C, and apoB separately. Hazard ratios (HRs) and corresponding 95% CIs were calculated per 1-SD increase of the respective on-statin lipid or apolipoprotein; this was the principal outcome on which conclusions were based.
Similar analyses were performed for patients in the top quartile of the on-statin lipid or apolipoprotein distribution, using those in the bottom quartile as the reference standard. A trend test was used to test for linear trend across quartiles. Analyses were adjusted for sex, age, smoking (current vs not), diabetes mellitus, systolic blood pressure, and trial. Analyses were not additionally adjusted for prevalent coronary artery disease since all trials enrolled either 0% or 100% patients with prevalent disease, so adjustment for trial implies adjustment for prevalent coronary artery disease.
Analyses were performed for the outcomes major cardiovascular events, major coronary events, and major cerebrovascular events. Because the Cox proportional hazards models were based on identical populations and included LDL-C, non–HDL-C, or apoB in addition to identical covariates, they were highly correlated and not independent. Therefore the approach to test for a significant difference between 2 models should be to assess whether the 95% CI of the difference between 2 models excludes zero. Bootstrapping was therefore performed on the difference between log-transformed HR of the adjusted Cox regression models (both by 1-SD increase and for top vs bottom quartile) for non–HDL-C vs LDL-C, non–HDL-C vs apoB, and apoB vs LDL-C. This approach yields a mean difference and its 95% CI, and thus an estimate of the statistical significance of this difference. HRs were also calculated for 4 categories of statin-treated patients based on whether or not they reached the LDL-C target 100 mg/dL and the non–HDL-C target 130 mg/dL. Forest plots were constructed and interaction terms were calculated to assess whether adjusted HRs per 1-SD increase of each lipid or apolipoprotein parameter differed significantly between subgroups based on baseline characteristics, lipid levels, or trial.
The proportion of the treatment effect of the statin intervention (either statin vs placebo or high-dose vs usual-dose statin) that was explained by LDL-C, non–HDL-C, or apoB was calculated as previously described.12 Bootstrapping was performed on the difference between the proportions of treatment effect explained by non–HDL-C vs LDL-C, non–HDL-C vs apoB, and apoB vs LDL-C.
Statistical heterogeneity across studies was quantified using the Cochran Q statistic and I2 statistic. The I2 statistic is derived from the Q statistic ([Q − df /Q ]*100) and provides a measure of the proportion of the overall variation attributable to between-study heterogeneity.15 The potential for publication bias was addressed by drawing funnel plots and visual assessment. Proportionality of hazards over time was graphically checked by plotting the cumulative hazards over time for all quartiles against each other. This was done for LDL-C, non–HDL-C, and apoB separately. A P value of less than .05 was considered statistically significant. Bootstrapping was performed in R. All other statistical analyses were performed using SPSS (version 17.0).
The literature search yielded a total of 1643 potentially relevant abstracts (eFigure). The large majority of articles were excluded because they were not primary reports on an RCT fulfilling the inclusion criteria.
We identified 28 potentially relevant RCTs. A total of 17 were excluded because apolipoprotein levels were not measured. One RCT was excluded because apolipoprotein levels were not measured during statin therapy, and 2 additional RCTs were excluded because apolipoproteins were measured in only a subset. A total of 8 trials fulfilled all inclusion criteria: the Scandinavian Simvastatin Survival Study (4S),16 the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS-TexCAPS),17 the Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) trial,18 the Collaborative Atorvastatin Diabetes Study (CARDS),19 the Treating to New Targets (TNT) trial,20 the Incremental Decrease in Endpoints through Aggressive Lipid Lowering (IDEAL) trial,21 the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial,22 and the Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER).23 Individual patient data were obtained from all 8 trials. Study characteristics of these 8 trials are presented in eTable 1.
Trials were of high quality with a median Delphi score of 9 (range 6-9). Heterogeneity between trials with regard to the association with risk of major cardiovascular events was low for LDL-C (Q = 6.94, P = .43, I2 = 0), non–HDL-C (Q = 6.05, P = .53, I2 = 0) and apoB (Q = 9.55, P = .22, I2 = 26%). Visual assessment of funnel plots suggested bias, although it is unlikely that this was publication bias since the primary objective of our meta-analysis was different from the primary objective of the included trials (statin efficacy). Bias was based on the fact that the associations between all 3 lipid parameters and risk of cardiovascular events were stronger in 2 trials contributing low numbers of events (AFCAPS-TexCAPS, JUPITER), which may have been related to their inclusion criteria. The proportionality assumptions were satisfied.
Data were available from 62 154 study participants of the 8 included trials. Baseline characteristics are presented in eTable 2. Levels of lipids and apolipoproteins at baseline and at 1-year on trial, as well as the absolute changes and percentage changes between baseline and on-trial levels for each trial separately are presented in eTable 3. A total of 38 153 study participants were randomized to a statin group and had a complete set of lipid and apolipoprotein levels during statin treatment available. Among these individuals, a total of 158 (0.4%) developed a fatal myocardial infarction and 1678 (4.4%) developed a non-fatal myocardial infarction during follow-up. Fatal other coronary artery disease occurred in 615 study participants (1.6%) and fatal or nonfatal stroke occurred in 1029 study participants (2.7%). A total of 2806 participants (7.4%) were hospitalized for unstable angina. A total of 6286 major cardiovascular events occurred in 5387 study participants (event rate 14.1%). Of these, 4577 experienced 1 event, 728 experienced 2 events, 75 experienced 3 events, and 7 experienced 4 events.
All studied lipid and apolipoprotein parameters were statistically significantly associated with the risk of major cardiovascular events. The HRs per 1-SD increase in LDL-C (32 mg/dL), non–HDL-C (36 mg/dL), and apoB (27 mg/dL) were 1.13 (95% CI, 1.10-1.17), 1.16 (95% CI, 1.12-1.19) and 1.14 (95% CI, 1.11-1.18), respectively (Table 1). Patients in the top quartile of the LDL-C distribution had an HR of 1.26 (95% CI, 1.14-1.39) compared with those in the bottom quartile. Associations were stronger for non–HDL-C (HR, 1.42; 95% CI, 1.29-1.56) and for apoB (HR, 1.33; 95% CI, 1.22-1.45) (P for linear trend across quartiles <.001 for each). Bootstrap analyses showed that the difference between LDL-C and non–HDL-C in predicting the risk of major cardiovascular events per 1-SD increase was statistically significant (P = .002). The difference between non–HDL-C and apoB was also statistically significant (P = .02), whereas the difference between LDL-C and apoB was not statistically significant (P = .21). Analyses for the major coronary events outcome showed similar associations as for major cardiovascular events (eTable 4). Associations with risk of major cerebrovascular events were not as strong.
Subgroup analyses showed that the associations between lipid or apolipoprotein parameters and risk of major cardiovascular events did not have statistically significant difference between primary and secondary prevention trials (P for interaction >.78 for each; Figure 1). The strength of the associations with LDL-C, non–HDL-C, or apoB also did not differ between clinically relevant subgroups, including those with vs without diabetes mellitus, hypertriglyceridemia, and low HDL-C (P for interaction >.10 for each). There was also no overall statistically significant difference between the individual trials (P for interaction >.26 for each; Figure 2).
Data markers indicate hazard ratios for risk of major cardiovascular events per 1-SD increase of the lipid or apolipoprotein and 95% CIs. Dashed line indicates point estimate for all participants combined. All interaction terms were by presence or absence of the listed characteristics and were nonsignificant. BMI indicates body mass index; CHD, coronary heart disease; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; and TG, triglyceride.
Data markers indicate hazard ratios (HRs) for risk of major cardiovascular events per 1-SD increase of on-statin low-density lipoprotein cholesterol (LDL-C), non–high-density lipoprotein cholesterol (non–HDL-C), or apolipoprotein B (apoB) and 95% CIs. For placebo-controlled trials, data from the placebo group were not used in this analysis. Dashed line indicates point estimate for all participants combined. All interaction terms by study were nonsignificant.
In Figure 3, HRs for the risk of major cardiovascular events are presented for 4 patient categories divided by the LDL-C target of 100 mg/dL and the non–HDL-C target of 130 mg/dL. Statin-treated patients reaching the non–HDL-C target but not the LDL-C target had an HR of 1.01 (95% CI, 0.92-1.12; P = .85) compared with those reaching both targets. Patients reaching the LDL-C target but not the non–HDL-C target had an HR of 1.32 (95% CI, 1.17-1.50; P < .001).
Data markers indicate hazard ratios (HRs) and 95% CIs for risk of major cardiovascular events. Results are shown for 4 categories of statin-treated patients based on whether or not they reached the low-density lipoprotein cholesterol (LDL-C) target of 100 mg/dL and the non–high-density lipoprotein cholesterol (non–HDL-C) target of 130 mg/dL. HRs were adjusted for sex, age, smoking, diabetes, systolic blood pressure, and trial.
The proportions of the treatment effect of the respective trial interventions (either statin vs placebo or high-dose vs moderate-dose statin therapy) that are explained by changes in LDL-C, non–HDL-C, and apoB are shown in Table 2. Statin-induced changes in LDL-C levels explained 50% of the effect of statin treatment, whereas non–HDL-C explained 64% and apoB explained 54%. The proportion of treatment effect explained by non–HDL-C was larger than by LDL-C (P < .001) and by apoB (P = .007). The proportion of treatment effect explained did not differ between LDL-C and apoB (P = .44).
Quiz Ref IDWe performed a meta-analysis to determine the association between on-statin LDL-C, non–HDL-C, and apoB and risk of future cardiovascular events. The main finding of this study is that among statin-treated patients, non–HDL-C had a stronger association with risk of major cardiovascular events than LDL-C and apoB. Changes in non–HDL-C also explained a larger proportion of the atheroprotective effect of statin intervention than did LDL-C and apoB.
The predictive value of different lipid and apolipoprotein parameters has been a topic of debate for decades. As early as 1980, Sniderman et al24 suggested that apoB levels were more closely associated with the presence of coronary atherosclerosis compared with either LDL-C levels or triglyceride levels. The strong predictive value of apoB was confirmed in the apolipoprotein-related mortality risk (AMORIS) study,25 which included more than 175 000 individuals. Although LDL-C was not measured by established methods in AMORIS, it was shown to correlate well with LDL-C as quantified by conventional methods in a subgroup. The INTERHEART study26 has shown that the association between deciles of apoB and risk of first myocardial infarction was stronger than for non–HDL-C, but these 2 parameters were not compared with LDL-C. Another important limitation of INTERHEART resides in its cross-sectional design. A recent large-scale meta-analysis on individual patient data from 68 prospective studies showed that the HRs for risk of coronary artery disease were similar for non–HDL-C and apoB.9 These parameters were not compared with LDL-C as calculated by the Friedewald formula, as is commonly used in prospective studies and in clinical practice. More recently, another meta-analysis, which used study level data and a different set of inclusion criteria, addressed the same question. This meta-analysis concluded that apoB was superior to non–HDL-C and that both were superior to LDL-C as a predictor of cardiovascular risk.27
In contrast to the extensive literature on the predictive value of lipids and apolipoproteins in population studies, the body of evidence on statin-treated patients is more limited. Investigators of the AFCAPS-TexCAPS trial10 were the first to report that among patients treated with statin therapy, apoB may be a more accurate predictor of risk of major cardiovascular events than LDL-C. Our results suggest that the association in AFCAPS-TexCAPS was somewhat stronger than in the other participating trials (although not significantly), which may have been caused by the fact that the inclusion criteria of AFCAPS-TexCAPS differed substantially from those of other trials. A subanalysis of the LIPID trial12 confirmed that apoB was more strongly associated with cardiovascular risk than LDL-C, but non–HDL-C was not evaluated in that analysis. A combined analysis of the TNT and IDEAL trials11 also confirmed a stronger predictive value of both apoB and non–HDL-C compared with LDL-C. A subanalysis of CARDS also reported that LDL-C was inferior to apoB and non–HDL-C but concluded that apoB was the most consistent goal for statin therapy.28 In JUPITER,29 on-treatment concentrations of non–HDL-C and apoB were comparable with LDL-C in the prediction of residual risk. In summary, our observations in statin-treated patients extend prior results from large population-based studies showing that non–HDL-C is more strongly associated with risk of future major cardiovascular events than LDL-C, but we did not find evidence that apoB performed better than non–HDL-C or LDL-C. We found no evidence that the predictive power of these 3 parameters differed between subgroups based on other characteristics such as diabetes mellitus or hypertriglyceridemia.
In participating trials, HDL-C was measured in the supernatant after heparin-manganese precipitation of apoB-containing lipoproteins according to the protocol of the Centers for Disease Control and Prevention.30 This is important to recognize in extrapolating the results of our meta-analysis to clinical practice because many clinical laboratories do not currently use this method to measure HDL-C.31 Rather, they use homogeneous methods that can be fully automated. Although the majority of these assays perform reasonably well and generally meet the National Cholesterol Education Program criteria for precision, accuracy, and total error, some assays show discrepant results compared with reference methods. This means that the use of HDL-C as measured in clinical practice could result in the calculation of non–HDL-C, which may not provide an index of cardiovascular risk as accurate as that in clinical trials. Nevertheless, given the fact that HDL-C is used to calculate LDL-C as well, these limitations similarly apply to LDL-C. Quiz Ref IDConversely, the standardized methods for the measurement of apoB used in statin trials are similar to those that can be used in clinical laboratories. Implementation of apoB assays in routine clinical practice is suboptimal but this is not due to the quality of the assays but due to the limited attention given in clinical guidelines. Thus, the final rating on the comparative accuracy of the methods used to measure apoB and non–HDL-C in clinical practice may therefore depend on other information. Such a conclusion should consider not just biological and statistical evidence, but also financial, logistic, and feasibility arguments.
Several aspects of the design of this meta-analysis warrant comment. An important strength is the availability of individual patient data, which enabled individual-level patient analyses—a more appropriate and accurate option than study-level analyses. A limitation is the fact that the participating trials had different inclusion criteria. The different distributions across trials of baseline characteristics, and lipid levels in particular, may have affected the results of our meta-analysis. In addition, outcome definitions may have differed slightly between trials. Subgroup analyses, however, showed that the associations did not differ significantly between trials. It should also be noted that the results are based on patients included in trials and that these results cannot necessarily be extrapolated to patients in routine clinical practice. Another limitation is the use of on-statin lipid and apolipoprotein levels measured at 1-year follow-up. This time point was chosen because it was the first uniform time point when lipids and apolipoproteins were measured in all participating trials. Therefore, fatal cardiovascular events occurring in the first year of therapy are not accounted for in this analysis.
In conclusion, among statin-treated patients, levels of LDL-C, non–HDL-C, and apoB were each strongly associated with the risk of major cardiovascular events, but non–HDL-C was more strongly associated than LDL-C and apoB. Given the fact that many other arguments for the clinical applicability of non–HDL-C and LDL-C are identical, non–HDL-C may be a more appropriate target for statin therapy than LDL-C.
Corresponding Author: John J. P. Kastelein, MD, PhD, Department of Vascular Medicine, Academic Medical Center, Meibergdreef 9, 1105 AZ, Amsterdam, the Netherlands (firstname.lastname@example.com).
Author Contributions: Drs Boekholdt and Kastelein had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Boekholdt, Kastelein.
Acquisition of data: Pedersen, LaRosa, Nestel, Simes, Durrington, Hitman, Welch, DeMicco, Clearfield, Downs, Tonkin, Colhoun, Gotto, Ridker, Kastelein.
Analysis and interpretation of data: Boekholdt, Arsenault, Mora, Pedersen, LaRosa, Nestel, Simes, Durrington, Hitman, Welch, DeMicco, Zwinderman, Clearfield, Downs, Tonkin, Colhoun, Gotto, Ridker, Kastelein.
Drafting of the manuscript: Boekholdt, Arsenault, Kastelein.
Critical revision of the manuscript for important intellectual content: Mora, Pedersen, LaRosa, Nestel, Simes, Durrington, Hitman, Welch, DeMicco, Clearfield, Downs, Tonkin, Colhoun, Gotto, Ridker.
Statistical analysis: Boekholdt, Arsenault, Zwinderman.
Administrative, technical, or material support: DeMicco, Kastelein.
Study supervision: Boekholdt, Kastelein.
Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Drs Boekholdt and Arsenault report receipt of consultancy fees from Pfizer. Dr Mora reports receipt of research grant support through her institution from Merck Sharpe & Dohme and AstraZeneca; consultancy fees from Pfizer and Quest Diagnostics; lecture honoraria from AstraZeneca and Abbott; and travel accommodations/meeting expenses from Pfizer. Dr Pedersen reports receipt of research grant support and lecture fees from Pfizer. Dr LaRosa reports receipt of consultancy fees from Pfizer and Amgen; and travel expenses from Pfizer. Dr Nestel reports serving as a board member for AstraZeneca and Merck Sharpe & Dohme; receipt of consultancy fees from AstraZeneca; lecture honoraria from Merck Sharpe & Dohme; and travel expenses from AstraZeneca and Merck Sharpe & Dohme. Dr Durrington reports provision of consulting services to Hoffman-La Roche; delivering lectures or serving on the speakers bureau for Pfizer; and receipt of royalties from Hodder Arnold Health Press. Dr Hitman reports receipt of lecture fees and travel expenses from Pfizer; provision of consulting services on advisory panels to GlaxoSmithKline, Merck Sharpe & Dohme, Eli Lilly, and Novo Nordisk; receipt of a grant from Eli Lilly; and delivering lectures or serving on the speakers bureau for GlaxoSmithKline, Takeda, and Merck Sharpe & Dohme. Dr Welch reports receipt of a grant, consulting fees, travel support, payment for writing or manuscript review, and provision of writing assistance, medicines, equipment, or administrative support from Pfizer; and provision of consultancy services to Edwards, MAP, and NuPathe. Dr Demicco reports having stock/stock options with and being a full-time employee of Pfizer. Dr Clearfield reports provision of consulting services on advisory committees to Merck Sharpe & Dohme and AstraZeneca. Dr Tonkin reports receipt of consultancy fees from Amgen, AstraZeneca, CSL, Boehringer-Ingelheim, and Pfizer; delivering lectures or serving on the speakers bureau for AstraZeneca, CSL, Merck Sharpe & Dohme, Boehringer-Ingelheim, Novartis, and Roche; and having stock/stock options with CSL and Sonic Health Care. Dr Colhoun reports receipt of research grant support through the EU Innovative Medicines Initiative from Roche, Pfizer, Eli Lilly, Boehringer-Ingelheim, sanofi-aventis, and AstraZeneca; consultancy fees from Pfizer, sanofi-aventis, Novartis, and Eli Lilly; stocks from Roche; and lecture honoraria and travel expenses from Pfizer. Dr Gotto reports serving on the board of directors for Aegerion Pharmaceuticals and Arisaph Pharmaceuticals; being a member of advisory boards for DuPont and Vatera Capital; and receiving consultancy fees from AstraZeneca, Kowa, and Merck Sharpe & Dohme. Dr Ridker reports receipt of research grant funding from Novartis and AstraZeneca; serving as a consultant to ISIS, Vascular Biogenics, Merck Sharpe & Dohme, Abbott, and Boerringer-Ingelheim; board membership with Merck Sharpe & Dohme; receipt of a grant or pending grant to his institution from Amgen; and being listed as a coinventor on patents held by the Brigham and Women's Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease and diabetes that have been licensed to AstraZeneca and Siemens. Dr Kastelein reports receipt of lecture honoraria from Merck Sharpe & Dohme, Roche, Novartis, ISIS, Genzyme, Pfizer, Kowa, and AstraZeneca. Drs Simes, Zwinderman, and Downs reported no conflicts of interest.
Funding/Support: This study was not supported by any funding. The contributing trials were funded by their respective sponsors.
Role of the Sponsors: The sponsors of the contributing trials provided the requested data. They did not play any role in the statistical analysis, interpretation of the data, writing of the manuscript, or the decision to submit the manuscript.
Disclaimer: The views expressed in this article are those of the authors and do not necessarily reflect the position or policy of the Department of Veterans Affairs or the United States government.
This article was corrected for errors on March 29, 2012.
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text:
FORT WORTH -- You've probably heard stories of people tracking down and recovering missing smartphones -- this is not that story.
This is about what smartphones can do to someone who steals, or maybe just fails to return one.
I kept monitoring it on GPS, and it kept moving around, said Scott Ellison, pointing to a computer screen map with a pin showing the last location of his phone. Eventually, it stopped moving in a neighborhood.
The device was lost by or stolen from Ellison's daughter Wednesday at a Target store on Overton Ridge Boulevard in south Fort Worth.
Ellison, a former Air Force navigator, tracked it through a Google app called Latitude to houses on Natalie Drive and Ashridge Road.
When I first started looking for it, it showed up in the backyard of this house, he said, showing precisely where the phone was.
He called it repeatedly, but no one answered.
Then he found an app that let him operate the phone remotely.
An application called Android Lost, he said.
He used it to set off alarms to get the attention of whoever had it. He could tell they were using it, and recorded the numbers called. Ellison activated the microphone, and was able to record people talking as they watched TV. One man made a possible drug reference. Then Ellison started taking photos, which were fed back to his laptop.
The people with the phone took a spy into their lives that can record intimate, even incriminating behavior.
Ellison sent them a verbal warning, and offered a $50 reward. They seemed startled and puzzled when the phone suddenly announced in a computerized voice, this is not your phone and I want my phone back.
Scott Ellison said police told him there wasn't much they could do to get his phone back, so eventually he just shut it down.
He's annoyed.
But people who steal smartphones perhaps should be paranoid.

subset: commoncrawl


text:
Women's Soccer Snake Bitten 4-1 by Moccasins in Sunday Matinee
October 9, 2011
MISENHEIMER, N.C. A pair of goals in each half was plenty for Florida Southern during a 4-1 victory over Pfeiffer University in non-conference womens soccer action on Sunday afternoon. Morgan Sammons (Lithia, FL) put home two of the four for the Mocs as they improve to 7-3-1 overall. The loss snaps a brief two-game win streak for the Lady Falcons as they fall to 5-7.
Sammons started the day with her second of the year in the 32 minute as Alex Hoover (West Palm Beach, FL) and Hanna Jansson (Vasteras, SWEDEN) connected with Sammons for a 1-0 visitors lead. Just under three minutes later, Alyssa Wombwell (Grand Blanc, MI) netted her team-leading sixth of the year to knot the contest at one with a rocket from outside the 18-yard box put into the top left corner of the cage. To end the first half of scoring, Jansson deposited her first of the season from 25 yards out to put the Mocs up 2-1 at the break.
Out of the intermission, Sammons converted on her second of the day, third of the year, just 3:44 in as Kara Moore (Flemming Island, FL) delivered a pass over to Sammonds who sent her shot inside the left post for a two-goal lead. Insurance, in the form of Moores fourth of the year, came in the 67th minute.
Florida Southern held a 22-10 shots advantage overall, 13-4 on cage. Martina Tangen Billing (Uppsala, SWEDEN) made one save in her first half of action while Erin Moseley (Jacksonville, FL) made two in the second. Jamie Alcala (Fredericksburg, VA) turned away nine shots on the afternoon for Pfeiffer.
The Lady Falcons will re-enter Conference Carolinas play on Wednesday hosting St. Andrews for a 2:00 p.m. matchup. Live stats will be available through http://www.gofalconsports.com.


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Man builds opry house for those who love music
A variety of musical guests perform on the second Saturday of each month at the Tula Opry which was a 30-year dream of Rusty Pinion. See the grand ol' opry in Tula in today's Oxford Living. (April 15, 2011, Page 1B)


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HOW TO REGISTER A CHILD OR ADULT INTO A CAMP OR PROGRAM: In order to register your child or another adult into a camp or program, they must be added to your Account. Once your participants are associated with your account, you will be able to register them into the age-appropriate camp or program of your choice.
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The shoe was beatiful. I love it.
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Worn only once so far and by the end of the work day my toes were NUMB. I'm hoping that wearing them more will loosen the leather and make them more comfortable in that area. But never-the-less, it is a very attractive shoe on.
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Winners of our customer rewards giveaway contest will be announced through our newsletter.
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|The Active Women's Leopard Sock features a cheetah inspiration design with contrasting color at the heel and toe, an Active embroidery at the footbed. Introduce some color to your feet and enjoy the comfort of these sweet socks! 68% Cotton, 28% Polyester, 2% Nylon, 2% Spandex


text: Mike FaheyProfileFollowUnfollow Mike FaheyFiled to: Blip My little pony: friendship is magic Gameloft Hasbro ios Android Kotakumobile 11/09/12 1:55pmEditDelete Invite manuallyPromoteXDismissXUndismissBlock for kotakuHideShare to KinjaShare to FacebookShare to PinterestShare to TwitterGo to permalink The My Little Pony game, released yesterday for iOS, is now available on Android. Go launch trailer! 46Reply 46Discuss


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At Melissa & Doug we strive to produce the highest-quality educational toys for children. From puzzles to puppets, plush to play food, magnetic activities, music and more, Melissa & Doug is one of the leading designers and manufacturers of educational toys and children's products. Started in 1988 in their garage, Melissa & Doug has something for everyone, with over 2,000 unique and exciting products for children of all ages.
Skill Building: 5 Ways to Promote a Happy Team-Sports Activity
June 6, 2012 by melissaanddoug
Filed Under: By Age, Health & Wellness, Older Kids (12+), Parenting & Family, Preschoolers (3-4 years), Skill Building Tips, Skill Building Tips, Tweens (5-12) Tagged With: fun for kids, groups, Kids, Melissa & Doug, parenting articles, playing, sports, teams


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An Invitation to Amazement
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Cut-Off Time Restrictions
Gift card redemptions for Amaluna tickets must be made at least 2 hours prior to the desired show date and time.
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The children's discount applies to children 2 to 12 years old. Children under 2 years old are permitted to attend for free, but must remain seated on a parent's lap at all times.
Children are not permitted to be left unattended on the site of Cirque du Soleil. Tickets purchased for children must have an adult seated beside.
The student discount applies to individuals 13 years old and over with a valid student I.D. (includes College and University student I.D.). The senior discount applies to individuals 65 years old and up. Student and senior discounts are available for weekday performances only (Tuesday to Thursday, and Friday at 4:00 p.m.).
Show Duration
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The California State retention regulations require that the original medical records accumulated during the Hospital's operation are maintained. Records will be maintained until November, 2021.
Temple Community Hospital has entered into a legal arrangement whereby Iron Mountain will not only store the medical records, but will also provide release of information services.
Many former patients will need to obtain copies of their records, and Iron Mountain has established a procedure to comply with these requests.
The medical records have been moved to an Iron Mountain facility. In order for Iron Mountain to provide copies of medical records to patients, or a recipient designated by them, Iron Mountain requires an authorization signed by the patient or their legal representative.
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By Amber Goodhand – Radar Reporter
Juror number 3 is Jennifer Ford, a 32-year-old nurse in-training at St. Petersburg College, who said that acquitting Anthony of the murder charges in the death of her 2-year-old daughter Caylee in no way means that she believes Anthony is innocent.
"I did not say she was innocent," Ford told Nightline anchor Terry Moran Wednesday. "I just said there was not enough evidence. If you cannot prove what the crime was, you cannot determine what the punishment should be."
PHOTOS: Graphic Crime Scene Pictures Introduced Into Evidence
The stunning verdict was delivered Tuesday when the jury of 12 found Anthony, 25, not guilty aggravated manslaughter and aggravated child abuse.
"I'm not saying I believe the defense," Ford said. "Obviously, it wasn't proven so I'm not taking that and speculating at all. But it's easier for me logically to get from point A to point B" in considering the defense's arguments.
Watch the video on RadarOnline.com
Ford said the prosecution "didn't even paint a picture for me to consider" in terms of how Casey could have killed her child.
Asked about Casey's actions following her daughter's death — not reporting it for more than 30 days, partying in that time, and lying to investigators — Ford said that "bad behavior is not enough to prove a crime."
PHOTOS: Casey Anthony Laughs In Court
Ford said Casey's father George Anthony "did not help the state's case," due to his testimony coming off as "dishonest" and "evasive."
She said the fact that he seemingly switched allegiances from the defense to the prosecution during the trial further damaged his credibility.
"I don't know if he had anything to do with it, but I think that he was there," she said. "He and Casey have something."
PHOTOS: Casey Anthony's Secret Wild Life
Ford admitted it didn't feel good letting Anthony walk: "It was a horrible decision to have to make, but I had to do it based on the law. "
She said that the death penalty implications further weighed on her decision to cast a "not guilty" vote.
"You have to prove it … or else I'm a murderer too, and I'm not any better."
Ford said jury members didn't speak to the media right away "because we were sick to our stomach to get that verdict.
"We were crying and not just the women. It was emotional and we weren't ready. We wanted to do it with integrity and not contribute to the sensationalism of the trial."
But despite the emotional toll this trial took on the jury, Ford said they tried to stay positive.
PHOTOS: Celebs Involved In Murder
"They picked a great bunch of people, such high integrity," Ford said. "And there was high morale. We all joked.
"We are like a big group of cousins."
While there's been controversy over Anthony's acquittal, she was found guilty on four counts of lying to law enforcement officers, but is expected to be released following her sentencing on Thursday, as she's already spent nearly three years in custody.
Alternate Juror: I Would Have Freed Casey, Too
Casey Anthony Trial: Tears & Laughter During Closing Arguments


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text: ""; ?> Sayn I Love You by Moffatts - guitar chords, guitar tabs and lyrics - chordie guitar tabs, guitar chords and lyrics Login username: password: register 5 popular songs Hotel California Eagles Losing My Religion R.E.M Fields Of Gold Police Free Fallin Tom Petty Turn The Page Bob Seeger Artists Songs Public booksPublic My songbookSongbook ResourcesDiv Forum Browse artists: A B C D E F G H I J K L M N O P Q R S T U V W X Y Z # -first letter-A B C D E F G H I J K L M N O P Q R S T U V W X Y Z # return to normal Sayn I Love You Moffatts variations - click chord images Transpose chords: -5 semitones -4 semitones -3 semitones -2 semitones -1 semitone None +1 semitone +2 semitones +3 semitones +4 semitones +5 semitones +6 semitones Tuning: Guitar Guitar (left) 5-string Banjo Plectrum Banjo Tenor Banjo Baritone Ukulele Ukulele (C-tuning) Ukulele (D-tuning) Mandolin Cool service: View: Size: Normal Lyrics only Chords only Full screen A A A auto-scroll print chopro 1 2 3 4 5 6 7 8 9 stop Hotkey: alt-# Thanks for detecting errors in the layout. This will help us improve the service. Reload to close this box. Rating: Layout: Currently 0/5 Stars. Currently 0/5 Stars. 1 2 3 4 5 Accuracy: Currently 3.1/5 Stars. Currently 3.1/5 Stars. 1 2 3 4 5 click stars to rate Songbook: Login to add this song to your songbook Original version: Sayn I Love You Chords by Moffatts Support the artistPreview/buy this songMSN MusicWhy this non-profit ad? IMPORTANT: The song above is NOT stored on the Chordie server. The original song is hosted at www.guitaretab.com. Chordie works as a search engine and provides on-the-fly formating. Chordie does not index songs against artists/composers will. To remove this song please click here. login to add comments/video/corrections play their songs - buy their music - support the artists copyright © 2011 chordie guitar chords


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B.C.'s Olympic cauldron will be relit during Sochi Games
Vancouver's Olympic flame will flare again on the last day of the Sochi Winter Olympics, if not before, says the minister responsible.
Transportation and Infrastructure Minister Todd Stone said Wednesday the plan by PavCo, the corporation in charge of the downtown convention centre, is to light the natural gas-fired flames on the last day. But he has inquired of PavCo whether it can be done earlier.
"It could cost a couple of hundred thousand dollars to light it through the entire Olympics," Stone told reporters at the B.C. legislature.
He said one option would be to look for private sector sponsorship to light up the symbol of the 2010 Olympics.
"The reality is that British Columbians want to celebrate," Stone said. "We're right up there at the top of the medal standings, and a lot of those athletes are British Columbians."
CTV reported Wednesday afternoon that the cauldron will be lit tonight.
Community Events, May 2015
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Browse the print edition page by page, including stories and ads.
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Medical Baseline
Get Help With Life-Support Equipment
If you or someone who lives with you full-time has a medical condition that requires electricity-powered life support equipment, you may be eligible to receive additional baseline allocation. Certification by a doctor is required.
Medical Baseline program offers an additional year-round baseline allocation of 16.5 kWh per day in addition to your applicable seasonal baseline and the baseline for your region. You can apply for additional kWh if you have a hardship case and need more.
Eligibility for Medical Baseline
To be eligible for Medical Baseline, you or someone who lives with you full-time must require use of a medical life-support device or piece of equipment. Life support devices utilize mechanical or artificial means to sustain, restore or replace a vital function.
You or a full-time resident can also be a paraplegic, hemiplegic, quadriplegic, multiple sclerosis or scleraderma patient, or have a life-threatening illness or compromised immune system.View Hide
Life-Support Devices Include:
- Aerosol Tent
- Pressure Pad
- Apnea Monitor
- Pressure Pump
- Compressor / Concentrator
- Respirator (all types)
- Electronic Nerve Stimulator
- Suction Machine
- Oxygen Generator
- Ultrasonic Nebulizer
- Electrostatic Nebulizer
- Inhalation Pulmonary Pressure
- Breather Machine (IPPB)
- Iron Lung
- Dialysis Machine
- Hemodialysis Machine
- Motorized Wheelchair/Scooter
- Left Ventricular Assist Device (LVAD)
- Air Mattress/Hospital Bed
- Total Artificial Heart (TAH-t)
- The Vest/Airway Clearance System
- Pulse Oximeter/Monitor
- Infusion Pump
Emergencies and Rotating Power Outages
If the California Independent System Operator (CAISO) declares a Stage 3 Emergency and requires power reduction, SCE will automatically contact Medical Baseline customers with a pre-recorded telephone message.
The message warns of the strong likelihood of a rotating power outage, and recommends that you take any necessary emergency precautions. Because SCE could only receive 10 minutes' notice, Medical Baseline customers may not hear about the outage before it occurs.
If you or someone living with you has a health condition placing them at increased health risk when outdoor temperatures reach extreme levels, you are also eligible for advance notification during rotating power outages.
Sign up for Rotating Outage Advance Notice


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Special Guests
Featured Performer: Jennifer Holliday
For more than three decades, Tony Award-winner Jennifer Holliday has wowed audiences with her soulful voice. She first brought them to their feet with her show-stopping performance of "And I'm Telling You, I'm Not Going" in the Broadway musical "Dreamgirls." Since then, she has shared the recording studio with Barbra Streisand, Luther Vandross, Michael Jackson and Paul Simon, and performed around the world with leading symphonies including the Boston Pops.
Host & Founding Honorary Chair: Joey McIntyre
Mass. Eye and Ear is pleased to once again welcome performer Joey McIntyre. As parents of a child with severe hearing loss, Joey and his wife, Barrett, are passionate about the mission of Mass. Eye and Ear and have been ardent supporters of Sense-ation! and the Curing Kids Fund since its launch in 2010.
Joey became an icon as part of the pop phenomenon New Kids on the Block, selling more than 80 million albums worldwide. Joey's six solo albums and his vast stage and screen resumé, ranging from a successful stint in the Broadway production of "Wicked" to this fall's new set-in-Boston CBS series, "The McCarthys," display his versatility as a performer.


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Mumford & Sons Biography & News
Mumford & Sons Details
|Official site
About Mumford & Sons
Mumford & Sons set to release new album
It looks like 2015 will be a pretty busy year for Mumford & Sons.
All the way back on December 2013, the band's bassist Ted Dwane, said that the band would be meeting to write new music in the winter of 2014. By July, Ben Lovett confirmed that the band was recording its third studio album in London.
Mumford & Sons worked on at least a handful of new songs at Eastcote Studios in Kensal Town, west London, the same studio where they recorded their debut album "Sigh No More." It was rumored that the band was also working with James Ford, the producer for Arctic Monkeys and HAIM. Ultimately, they confirmed they were aiming for a release date in early 2015, but so far have not yet announced a date.
Also on the calendar for this year is a penciled-in date at the 2015 Bonnaroo Music Festival, which will take place in Manchester, Tennessee between June 11-14th. The alt-rockers will be joined by iconic piano man Billy Joel and EDM superstar Deadmau5. Overall, the festival will feature 125 musical acts and nearly two dozen comedians on 12 different stages.
More than 80,000 people are expected at this year's Bonnaroo, which will also feature well-known contemporary acts like Florence + the Machine, Robert Plant, Kendrick Lamar, My Morning Jacket and many more.
Dwane, Lovett, Winston Marshall and Marcus Mumford have all been confirmed for Bonnaroo, and will hopefully be playing a few cuts off that much anticipated third studio album. Let's also hope this is just the first in a number of new concert dates for the band this year.
Gentlemen of the Road (Updated 9/19/2013)
Mumford & Sons are "Gentlemen of the Road." Or at least that's what they'll have you believe. The band's tour in support of the album "Babel" commenced at the end of 2012 and has continued through 2013.
Stops among the "Gentlemen of the Road" tour included two shows on June 8 & 9, 2013 at the Austin 360 Amphitheater in Austin, Texas. Those shows went off without a hitch, but the very next day bassist Ted Dwane checked himself into a hospital, where doctors found a blood clot on the surface of his brain. He underwent surgery, and Mumford & Sons canceled the rest of its "Summer Stampede," including a performance at the 2013 Bonnaroo Music Festival and returned to the UK. Dwane's surgery was a success, and his recovery went smoothly enough that the band managed to headline the Glastonbury Festival.
One of the great parts of Mumford & Sons' summer was the 2013 Stopover towns. Back in February they were announced as Lewes (UK), Simcoe (ON), Troy (OH), Guthrie (OK) and St. Augustine (FL). That last stop, especially, had a major financial impact, filling bed and breakfasts, motels and hotels in an area known for its September slow period. Even more, it has changed the discussion in St. Augustine about bringing major cultural events to town for years to come.
Of all the press to come out of the summer for the band, there are a few things that may surprise you. One was actor Jake Gyllenhaal's tale of traveling with Mumford & Sons before they were famous, living a hobo-lifestyle and even playing in the band. The other was the band's abrupt exit from Atlanta's Clermont Lounge in late September, though media reports vary on whether they were kicked out or simply asked to leave for violating one of the club's policies.
Mumford & Sons about to go electric? (Updated December 26, 2012)
When Mumford & Sons caused a stir at the end of 2012, it wasn't for their folk, or for their rock. Instead, the English quartet, which has featured everything from acoustic guitars to accordions and mandolins, raised eyebrows for telling Style magazine it would begin to explore the electronic side of music on their next album.
A 12-time Grammy nominated outfit, the band has battled through the explosion of electronic dance music – especially in the United States. Still, a use of synthesizers would mark a dramatic shift in style for the band, which exploded with its debut album "Sigh No More" in 2009, and saw its sophomore effort, "Babel," become the fastest selling album of 2012 in the UK, and the biggest selling debut in 2012 in the U.S.
The band consists of lead singer Marcus Mumford, Ben Lovett, Winston Marshall and Ted Dwane.
Between them are an eclectic mix of instruments, including banjo and resonator guitar, and vocals honed in small to moderate venues in both the UK and the US. Their lead single, "Little Lion Man," received generous critical praise, with Dave Barry of XFM calling it his 'favorite track of the year.' When the band earned Grammy Award nominations for Best New Artist and Best Rock Song after its release, they knew they'd hit the big time.
Mumford & Sons continue to grow in popularity and has done well with "Babel," which was the second biggest bow of 2012 behind Taylor Swift's "Red." It scored six more Grammy nominations, including Album of the Year and Best Americana Album. Still, the band is already back to work on new music. Their 2013 East Coast tour includes stops in Boston, New York and Fairfax, Virginia.
Mumford & Sons Announce More Summer Tour Dates
Update 4/13 In addition to the "Gentlemen of the Road Stopover" dates, Mumford & Sons have announced additional shows for the summer months. They'll begin on June 2 at Coney Island in Brooklyn, followed by gigs in Boston, Chicago and Calgary. You can also catch them on the festival circuit with a slot at this year's…Read more
Mumford & Sons Ticket PricesFind Tickets
Past 12 Months
$146Average Price
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Cost for Upcoming Mumford & Sons Shows
$92Average Price
$144 - 2,159Listing RangeIn Secondary Market
Past Tour Dates for Mumford & Sons
Mumford & Sons Tour Dates 2015
date city state venue 06/02/2015 Brooklyn NY MCU Park
Mumford & Sons Tour Dates 2013
date city state venue 09/20/2013 Bonner Springs KS Cricket Wireless Amphitheater - KS 09/18/2013 Dallas TX Gexa Energy Pavilion 09/17/2013 The Woodlands TX The Cynthia Woods Mitchell Pavilion 09/16/2013 New Orleans LA Mardi Gras World 09/13/2013 St. Augustine FL Francis Field 09/13/2013 St. Augustine FL Francis Field 09/11/2013 Simpsonville SC Charter Amphitheatre at Heritage Park 09/10/2013 Atlanta GA Centennial Olympic Park 09/09/2013 Pelham AL Oak Mountain Amphitheatre 09/06/2013 Guthrie OK Cottonwood Flats 09/06/2013 Guthrie OK Cottonwood Flats 09/06/2013 Guthrie OK Cottonwood Flats 09/04/2013 Saint Paul MN Xcel Energy Center 09/03/2013 Milwaukee WI Marcus Amphitheater 09/02/2013 Noblesville IN Klipsch Music Center 08/31/2013 Troy OH Troy Memorial Stadium 08/30/2013 Troy OH Troy Memorial Stadium 08/29/2013 Burgettstown PA First Niagara Pavilion 08/28/2013 Queens NY Forest Hills Stadium 08/26/2013 Toronto ON Molson Canadian Amphitheatre 08/23/2013 Simcoe ON Norfolk County Fairgrounds 08/23/2013 Simcoe ON Norfolk County Fairgrounds 08/04/2013 Montreal QC Parc Jean-Drapeau 08/03/2013 Chicago IL Grant Park 08/03/2013 Chicago IL Grant Park 08/02/2013 Montreal QC Parc Jean-Drapeau 08/02/2013 Montreal QC Parc Jean-Drapeau 08/02/2013 Chicago IL Grant Park 07/30/2013 Tokyo 13 STUDIO COAST 07/20/2013 Lewes Sxe The Convent Field 07/19/2013 Lewes Sxe The Convent Field 07/18/2013 London London The Garage 07/14/2013 Dublin D Phoenix Park 07/14/2013 Kinross ?? Balado Airfield 07/12/2013 Kinross ?? Balado Airfield 07/12/2013 Kinross Pkn Balado Park 07/11/2013 Kinross Pkn Balado Park 07/06/2013 London Lnd Queen Elizabeth Olympic Park 06/26/2013 Pilton Som Worthy Farm 06/20/2013 Telluride CO Telluride Town Park 06/20/2013 Telluride CO Telluride Town Park 06/17/2013 Bonner Springs KS Cricket Wireless Amphitheater - KS 06/15/2013 Manchester TN Manchester Farm 06/13/2013 Manchester TN Manchester Farm 06/13/2013 New Orleans LA Mardi Gras World 06/12/2013 The Woodlands TX The Cynthia Woods Mitchell Pavilion 06/11/2013 Dallas TX Gexa Energy Pavilion 06/09/2013 Austin TX Austin360 Amphitheater 06/08/2013 Austin TX Austin360 Amphitheater 06/06/2013 Taos NM Kit Carson Park 06/05/2013 Phoenix AZ Ak-Chin Pavilion 06/03/2013 Chula Vista CA Sleep Train Amphitheatre 06/02/2013 San Bernardino CA San Manuel Amphitheater 05/31/2013 Berkeley CA Greek Theatre - Berkeley 05/30/2013 Berkeley CA Greek Theatre - Berkeley 05/29/2013 Berkeley CA Greek Theatre - Berkeley 05/27/2013 Portland OR Moda Center 05/26/2013 George WA Gorge Amphitheatre 05/26/2013 George WA Gorge Amphitheatre 05/24/2013 Surrey BC Holland Park 05/24/2013 George WA Gorge Amphitheatre 05/22/2013 Edmonton AB Rexall Place 05/21/2013 Calgary AB Scotiabank Saddledome 04/11/2013 Oslo 03 Sentrum Scene 04/10/2013 Stockholm Sto Annexet 04/08/2013 Copenhagen Danish Capital Regio Vega House Of Music 04/04/2013 Hamburg HH Alsterdorfer Sporthalle 04/03/2013 Dusseldorf NW Mitsubishi Electric Halle 04/02/2013 Berlin BE Velodrom 03/30/2013 Amsterdam A Ziggo Dome 03/28/2013 Antwerpen Vlg Lotto Arena 03/27/2013 Esch-sur-Alzette L Rockhal 03/26/2013 Paris Ile Le Trianon 03/21/2013 Madrid Mad La Riviera 03/20/2013 Barcelona Cat Palau Sant Jordi 03/19/2013 Toulouse Mid Le Bikini 03/16/2013 Rome Laz Atlantico Live 03/14/2013 Milan CA Alcatraz 03/12/2013 Bern BE Festhalle Bea Bern Expo 03/07/2013 Vienna 9 Gasometer 03/06/2013 Prague Praha Lucerna Music Bar 02/17/2013 Camden NJ Susquehanna Bank Center 02/16/2013 Camden NJ Susquehanna Bank Center 02/14/2013 Fairfax VA Patriot Center 02/13/2013 Fairfax VA Patriot Center 02/12/2013 Brooklyn NY Barclays Center 02/06/2013 Brooklyn NY Barclays Center 02/05/2013 Boston MA TD Garden
Mumford & Sons Tour Dates 2012
date city state venue 12/18/2012 London The O2 12/16/2012 Dublin D The O2 - Dublin 12/15/2012 Belfast Ant Odyssey Arena 12/15/2012 Belfast Ant Odyssey Arena 12/13/2012 Cardiff Cardiff Motorpoint Arena Cardiff 12/11/2012 London The O2 12/10/2012 Manchester Lancashire Manchester Arena 12/10/2012 Manchester Lancashire Manchester Arena 12/08/2012 Nottingham Nottinghamshire Capital FM Arena Nottingham 12/07/2012 Birmingham Warwickshire Genting Arena 12/05/2012 Glasgow Glasgow City SECC 12/05/2012 Glasgow Glasgow City SECC 12/04/2012 Newcastle Upon Tyne T & W Metro Radio Arena 11/27/2012 Llandudno Cwy Venue Cymru 11/26/2012 Carlisle Cma Carlisle Sands Centre 11/25/2012 Dundee Ans Caird Hall 11/23/2012 Ipswich Suffolk Ipswich Regent Theatre 11/22/2012 Portsmouth Hampshire Portsmouth Guildhall 11/21/2012 Torquay Dev Princess Theatre 11/12/2012 Los Angeles CA Hollywood Bowl 11/10/2012 Los Angeles CA Hollywood Bowl 11/06/2012 Christchurch Horncastle Arena 11/05/2012 Wellington Wellington Town Hall 11/04/2012 Wellington Wellington Town Hall 11/02/2012 Auckland Auk Vector Arena 10/29/2012 Townsville City Qld Townsville Entertainment and Convention Centre 10/26/2012 Canberra Act National Convention Centre, Canberra 10/25/2012 Melbourne Vic Rod Laver Arena 10/23/2012 Glenorchy Tas Derwent Entertainment Centre 10/20/2012 Dungog Nsw Dungog Showgrounds 10/18/2012 Sydney New South Wales Sydney Entertainment Centre 10/17/2012 Brisbane Qld Riverstage Brisbane 10/15/2012 Hindmarsh SA Adelaide Entertainment Centre 10/13/2012 Perth WA Belvoir Amphitheatre 10/12/2012 Perth WA Belvoir Amphitheatre 09/01/2012 Aspen CO Jazz Aspen Snowmass 09/01/2012 London London Roundhouse 08/29/2012 Morrison CO Red Rocks Amphitheatre 08/28/2012 Morrison CO Red Rocks Amphitheatre 08/25/2012 Monterey CA Monterey Fairgrounds 08/21/2012 Laramie WY Gryphon Theatre 08/20/2012 Lincoln NE Pinewood Bowl Theater 08/18/2012 Dixon IL Page Park 08/17/2012 Dixon IL Page Park 08/16/2012 Chicago IL Chicago Theatre 08/14/2012 Columbus OH Lifestyle Communities Pavilion 08/13/2012 Louisville KY Louisville Waterfront Park 08/11/2012 Bristol VA Downtown Bristol 08/09/2012 Portsmouth VA nTelos Wireless Pavilion 08/07/2012 Canandaigua NY Constellation Brands Performing Arts Center 08/06/2012 Providence RI Providence Performing Arts Center 08/04/2012 Portland ME Eastern Promenade 08/01/2012 Hoboken NJ Pier A 03/08/2012 Nashville TN Ryman Auditorium 03/07/2012 Nashville TN Ryman Auditorium 03/06/2012 Nashville TN Ryman Auditorium 03/04/2012 New York NY Radio City Music Hall
Mumford & Sons Tour Dates 2011
date city state venue 12/11/2011 Universal City CA Gibson Amphitheatre 12/09/2011 Oakland CA Oracle Arena 12/07/2011 Seattle WA Key Arena 12/06/2011 Portland OR Moda Center 10/27/2011 Montreal QC Bell Centre 10/26/2011 Hamilton ON FirstOntario Centre 10/25/2011 Toronto ON Air Canada Centre 10/23/2011 Mountain View CA Shoreline Amphitheatre 10/22/2011 Mountain View CA Shoreline Amphitheatre 06/19/2011 Telluride CO Telluride Town Park 06/18/2011 Telluride CO Sheridan Opera House 06/16/2011 Telluride CO Telluride Town Park 06/16/2011 Denver CO Fillmore Auditorium 06/15/2011 Denver CO Fillmore Auditorium 06/12/2011 Atlanta GA Fox Theatre 06/09/2011 Manchester TN Manchester Farm 06/09/2011 Columbia MD Merriweather Post Pavilion 06/08/2011 Raleigh NC Red Hat Amphitheater 06/07/2011 Asheville NC U.S. Cellular Center 06/05/2011 Saint Louis MO The Pageant 06/03/2011 Kansas City MO City Market 05/01/2011 Memphis TN Tom Lee Park 04/30/2011 Memphis TN Tom Lee Park 04/29/2011 Memphis TN Tom Lee Park 04/27/2011 New Orleans LA Woldenberg Park 04/21/2011 Oakland CA Middle Harbor Shoreline Park 04/18/2011 Santa Barbara CA Santa Barbara Bowl 04/16/2011 Indio CA Empire Polo Field 04/15/2011 Indio CA Empire Polo Field
Mumford & Sons Tour Dates 2010
date city state venue 11/16/2010 New York NY Terminal 5 11/15/2010 New York NY Terminal 5 11/13/2010 Toronto ON Sound Academy 11/12/2010 Montreal PQ Le National 11/11/2010 Boston MA House of Blues Boston 11/09/2010 Philadelphia PA Electric Factory 11/08/2010 Knoxville TN The Valarium 11/07/2010 Atlanta GA Buckhead Theatre 11/05/2010 New Orleans LA Republic New Orleans 11/04/2010 Dallas TX House of Blues Dallas 11/03/2010 Austin TX Stubbs Waller Creek Amphitheatre 11/03/2010 Austin TX Stubbs BarBQ 11/01/2010 Nashville TN War Memorial Auditorium 10/31/2010 Chicago IL Vic Theatre 10/31/2010 Chicago IL Riviera Theatre 10/30/2010 Milwaukee WI Pabst Theater 10/29/2010 Minneapolis MN First Avenue 10/27/2010 Denver CO Ogden Theatre 10/25/2010 Boulder CO Glenn Miller Ballroom 10/24/2010 Seattle WA Moore Theatre 10/24/2010 Seattle WA Paramount Theatre 10/23/2010 Vancouver BC Vogue Theatre 10/22/2010 Portland OR Crystal Ballroom 10/20/2010 San Francisco CA The Warfield 10/18/2010 Los Angeles CA Hollywood Palladium 06/20/2010 Telluride CO Telluride Town Park 06/16/2010 Kansas City MO The Record Bar 06/14/2010 Bloomington IN Bluebird Nightclub 06/10/2010 Dallas TX House of Blues Dallas 06/09/2010 Austin TX Antone's 06/09/2010 Austin TX La Zona Rosa 06/07/2010 Phoenix AZ Rhythm Room 06/06/2010 Solana Beach CA Belly Up Tavern 06/04/2010 Los Angeles CA Fonda Theatre 06/04/2010 Los Angeles CA The Fonda Theatre 06/03/2010 Los Angeles CA The Fonda Theatre 06/03/2010 San Francisco CA Great American Music Hall 06/02/2010 San Francisco CA Slims 05/31/2010 Portland OR Aladdin Theater 05/30/2010 Vancouver BC 560 Club 05/25/2010 Minneapolis MN Varsity Theater 05/24/2010 Chicago IL Lincoln Hall 05/22/2010 Columbus OH Wexner Mershon Auditorium 05/21/2010 Cleveland OH Beachland Ballroom 05/20/2010 Washington DC 9:30 Club 05/18/2010 New York NY Webster Hall 05/17/2010 Brooklyn NY Music Hall of Williamsburg 05/16/2010 Philadelphia PA Fillmore at the TLA 05/14/2010 Cambridge MA The Middle East 02/18/2010 New York NY Bowery Ballroom 02/15/2010 Toronto ON Lee's Palace


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Thank you, M. That is so elegant and concise.
People can be haunted by all sorts of spirits. We have on the one hand, people haunted by the Holy Spirit, and those on the other hand haunted by the "spirit of the times" (Zeitgeist). People want to be haunted. We know how that happens. In the end, all it turns out to be is laziness.
Atkins said it best. Theology obfuscates. It may be that post-structuralism is theology's new best friend. The only way either of them can proceed is by not ruling anything out.
Obviously, if theology was able to rule anything out, there would only be one world religion. The first thing that post-structuralism fails miserably to question in its questioning of knowledge is itself.
It is worth noting in passing that there is only one scientific method. Burt Voorhees, for one, is sometimes frustrated by this, but he, too, is a bit haunted by the ghost of Aristotle.
Saying that there is only one scientific method makes it sound as if that method were cast in stone and is eternal, immutable, in essence,... divine. In fact, we know that there are a variety of methods in different sciences (after all, not everybody in science is a condensed matter physicist) and that "scientific method", to the extent that the term refers to the body of procedures that are carried out in the pursuit of science, is something that has evolved over time. It seems that you are saying here that this evolution has stopped—I would respectfully disagree.


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(UK) The Telegraph Article: "Why watching classical music through Google Glass is a waste of time" (By Ivan Hewett 13 Aug 2014)
From a recent article in The Telegraph, a news article extolling the virtues (or not) of the use of Google Glass technology in music performances. While perhaps not be best of medium to view and hear a performance, but, as one commentator suggests, a way by which to augment the performance with such options as extra performance notes or even translations of libretto, etc. You be the judge ...
(UK) Summer with Shakespeare Family fun in Stratford-upon-Avon until 31 August
From the latest newsletter from the Shakespeare Trust
"There's still plenty of time to make the most of the Summer holidays at Shakespeare's family homes! ...
(UK) The Guardian News Article: " Dutch conductor Frans Brüggen has died aged 79"
EarlyMusicNews.org joins the early music world in commemorating the death and contribution of Mr. Frans Brüggen to the early music movement. He will be sorely missed by all of us. For more information of his passing, visit (UK) The Guardian website.
(UK) Four countertenors : Handel Rinaldo Glyndebourne
" ...For their first revival of the production, Glyndebourne brought back conductor Olivier Dantone, and assembled a cast which showcased the modern counter-tenor revival by including a total of four in the cast. . Unusually for a modern performance of a Handel opera, all the male characters were played by men ...
(AT) 5th International Singing Competition for Baroque Opera Pietro Antonio Cesti (16–21 Aug 2014)
As with previous years, the singing competition will take place during the "Innsbruck Festival of Early Music"
"The International Singing Competition for Baroque Opera Pietro Antonio Cesti will take place in Innsbruck for the fifth time. Named after the Italian composer Pietro Antonio Cesti, who turned Innsbruck into a centre for the Italian opera north of the Alps in the mid-17th century, young singers from all over the world with a special talent and training will compete in the varied field that is the baroque opera for participation in the final concert on 21 August. ... "
(AT) 38th Innsbruck Festival of Early Music (17-31 Aug 2014)
If you are in the region of Innsbruck, you may want to consider attending some of the concerts at this year's Innsbruck Festival of Early Music.
"The stars were favourable for music in 1685: Johann Sebastian Bach, George Frederic Handel and Domenico Scarlatti were born. The three bright stars that shone over the baroque era are the focus of the 2014 Innsbruck Festival. Presenting masterpieces from the opera, the church, the concert hall and the chamber. To round off the picture, there will also be music by the father figures and teachers of Bach, Handel and Scarlatti, by friends and contemporaries as well as by their sons' generation. ...
(DE) 23rd Festival of Ancient Music Knechtsteden 2014 (19-28 Sep 2014)
A recent reminder from the organisers of the "Festival Alte Musik Knechtsteden" (DE), reminding us that if in the area of Knechtsteden, consider the upcoming Festival concert lineups and symposium dates. (Read on) ...
(CA) Nota Bene Baroque Players: End of Successful 2013-2014 Concert Season
With the end of its 2013-2014 Nota Bene Baroque Players (NBBP) Concert Season, the NBBP Organization has proven itself resilient at re-inventing itself and offering it's audience a new and more dynamic approach to performances and community services.
Having reached a low in performance appearances in previous years (3 performances per year), the NBBP Organization undertook a closer look at its potential as the Region of Waterloo's (Ontario Canada) early music orchestra with the result being of a staggering expanded performance schedule of 14 concerts, as well as a number of NBBP-led initiatives. This past 2013-2014 season consisted of performances with a long list of luminaries such as, not only of the Nota Bene Baroque Players (NBBPlayers) but also the birth of its newly formed choir Nota Bene Baroque Singers (NBBSingers) and invited soloists of famed recognition such as: Michael Schade, Daniel Taylor, Agnes Zsigovics, Sean Watson, Baroque trumpetist John Thiessen, organist/harpsichordist Jan Overduin, conductor Howard Dyck (with concertmaster, Baroque violin Julie Baumgartel) as well as up and coming stars Anthea Conway-White Baroque flute and Victoria Melik Baroque violin.
(UK) From Lufthansa to London Festival of Baroque Music
(from a recent Lufthansa newsletter)
The following is a note sent to all subscribers to the previously called "Lufthansa Festival of Baroque Music" encouraging people to re-subscribe to the new newsletter from the rebranded "London Festival of Baroque Music"
"As you may be aware, after 30 years of sponsorship Lufthansa German Airlines has decided to reallocate its philanthropic support to other endeavours. ...
(NL) Brilliant Classics (Record Lable): "C.P.E. Bach: Keyboard Symphonies"
"A curious and unsatisfying reduction of huge music for tiny forces? By no means. These are not, after all, symphonies in the way that Beethoven, let alone Mahler, understood the term, but breezy three-movement affairs which had lately sprung out of an operatic context and were enjoying a new and independent life through the always-unpredictable idiom of C.P.E., who wrote eight such works between 1741 and 1762. Most of them began as symphonies for strings, with wind parts added later when Bach's orchestra was enlarged. ...
Composer : Carl Philipp Emanuel Bach
Artist: Andrea Chezzi harpsichord
Instrument: Alberto Colzani (2000), after Goermans-Taskin (Russel Collection of Edimburgh, 1764-1783)
Release: April 2014
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|The Huf Japanese Speckle 5 Panel features a woven label at the front with metal eyelets at the sides and an adjustable nylon closure at the backside.


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Trim and tone those trouble spots with the Inner & Outer Thigh Machine. Do both abductor/adductor exercises from one seated position. 5 range of motion adjustments accommodate users of all sizes. A lumbar supported adjustable back pad, swiveling knee pads and no cable change design provide the quality, comfort and ease of use necessary to achieve great results.
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Golf Takes Home Fifth Place at 2014 Trojan Invitational
April 8, 2014
GOLDSBORO, N.C. – The 2014 Trojan Invitational came to a conclusion today at Walnut Creek Country Club. Pfeiffer finished the tournament in fifth place as they shot a 33 over par 609.
Limestone finished atop the team leaderboard as they turned in a team score of four over par 580.
Individually, Matthew Reid of Belmont Abbey finished first with a score of seven under par 137.
Pfeiffer was paced by David Weinberger who posted a score of eight over par 152. Weinberger was coming off his career best tournament finish where he tied for 16th. He finished tied for 17th in the Trojan Invitational as he carries his strong performance into the conference tournament April 12.
C.J. Dreyfuss turned in a career performance as he finished tied for 17th as well with a score of eight over par.
Nathan Bull also turned in a strong performance, as he placed tied for 23rd with a score of nine over par 153.
Though the tournament was a co-ed tournament, Pfeiffer only sent three female golfers to compete in the women's individual tournament.
Stefania Valgeirsdottir paced the way for the Falcons on the women's side as she finished in lone position of eighth place. This was Valgeirsdottir's best finish in her career as she turned in a score of 10 over par 154.
The Falcons look to carry the strong individual play, as they will be competing in the first round of the Conference Carolinas Tournament on Saturday, April 12.


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I searched so long for a opportunity where i can edit sourcecode with a friend or a co-worker together - collaborative editing.
I found Gobby, Bespin (Skywriter) by Mozilla, Cloud9 IDE (at this time not public - only beta) and so on, but its either not in the cloud (Online) or its not for collaborative editing.
What i seach for is for example http://jsfiddle.net/ for collaborative editing.
Does anybody know a way / website for this?