Statistical method for testing the neutral mutation hypothesis by DNA polymorphism.

Deposits of clastic carbonate-dominated (calciclastic) sedimentary slope systems in the rock record have been identified mostly as linearly-consistent carbonate apron deposits, even though most ancient clastic carbonate slope deposits fit the submarine fan systems better. Calciclastic submarine fans are consequently rarely described and are poorly understood. Subsequently, very little is known especially in mud-dominated calciclastic submarine fan systems. Presented in this study are a sedimentological core and petrographic characterisation of samples from eleven boreholes from the Lower Carboniferous of Bowland Basin (Northwest England) that reveals a >250 m thick calciturbidite complex deposited in a calciclastic submarine fan setting. Seven facies are recognised from core and thin section characterisation and are grouped into three carbonate turbidite sequences. They include: 1) Calciturbidites, comprising mostly of highto low-density, wavy-laminated bioclast-rich facies; 2) low-density densite mudstones which are characterised by planar laminated and unlaminated muddominated facies; and 3) Calcidebrites which are muddy or hyper-concentrated debrisflow deposits occurring as poorly-sorted, chaotic, mud-supported floatstones. These

Phd by thesis

WRITING GROUP MEMBERS Emelia J. Benjamin, MD, SCM, FAHA Michael J. Blaha, MD, MPH Stephanie E. Chiuve, ScD Mary Cushman, MD, MSc, FAHA Sandeep R. Das, MD, MPH, FAHA Rajat Deo, MD, MTR Sarah D. de Ferranti, MD, MPH James Floyd, MD, MS Myriam Fornage, PhD, FAHA Cathleen Gillespie, MS Carmen R. Isasi, MD, PhD, FAHA Monik C. Jiménez, ScD, SM Lori Chaffin Jordan, MD, PhD Suzanne E. Judd, PhD Daniel Lackland, DrPH, FAHA Judith H. Lichtman, PhD, MPH, FAHA Lynda Lisabeth, PhD, MPH, FAHA Simin Liu, MD, ScD, FAHA Chris T. Longenecker, MD Rachel H. Mackey, PhD, MPH, FAHA Kunihiro Matsushita, MD, PhD, FAHA Dariush Mozaffarian, MD, DrPH, FAHA Michael E. Mussolino, PhD, FAHA Khurram Nasir, MD, MPH, FAHA Robert W. Neumar, MD, PhD, FAHA Latha Palaniappan, MD, MS, FAHA Dilip K. Pandey, MBBS, MS, PhD, FAHA Ravi R. Thiagarajan, MD, MPH Mathew J. Reeves, PhD Matthew Ritchey, PT, DPT, OCS, MPH Carlos J. Rodriguez, MD, MPH, FAHA Gregory A. Roth, MD, MPH Wayne D. Rosamond, PhD, FAHA Comilla Sasson, MD, PhD, FAHA Amytis Towfighi, MD Connie W. Tsao, MD, MPH Melanie B. Turner, MPH Salim S. Virani, MD, PhD, FAHA Jenifer H. Voeks, PhD Joshua Z. Willey, MD, MS John T. Wilkins, MD Jason HY. Wu, MSc, PhD, FAHA Heather M. Alger, PhD Sally S. Wong, PhD, RD, CDN, FAHA Paul Muntner, PhD, MHSc On behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee Heart Disease and Stroke Statistics—2017 Update

Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association

Author(s): Writing Group Members; Mozaffarian, Dariush; Benjamin, Emelia J; Go, Alan S; Arnett, Donna K; Blaha, Michael J; Cushman, Mary; Das, Sandeep R; de Ferranti, Sarah; Despres, Jean-Pierre; Fullerton, Heather J; Howard, Virginia J; Huffman, Mark D; Isasi, Carmen R; Jimenez, Monik C; Judd, Suzanne E; Kissela, Brett M; Lichtman, Judith H; Lisabeth, Lynda D; Liu, Simin; Mackey, Rachel H; Magid, David J; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Muntner, Paul; Mussolino, Michael E; Nasir, Khurram; Neumar, Robert W; Nichol, Graham; Palaniappan, Latha; Pandey, Dilip K; Reeves, Mathew J; Rodriguez, Carlos J; Rosamond, Wayne; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Woo, Daniel; Yeh, Robert W; Turner, Melanie B; American Heart Association Statistics Committee; Stroke Statistics Subcommittee

Heart Disease and Stroke Statistics—2016 Update: A Report From the American Heart Association

Appendix I: List of Statistical Fact Sheets. URL: http://www.americanheart.org/presenter.jhtml?identifier=2007

We wish to thank Drs Brian Eigel and Michael Wolz for their valuable comments and contributions. We would like to acknowledge Tim Anderson and Tom Schneider for their editorial contributions and Karen Modesitt for her administrative assistance.

Disclosures 



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# Summary {#article-title-2}

Each year, the American Heart Association, in conjunction with the Centers for Disease Control and Prevention, the National Institutes of Health, and other government agencies, brings together the most up-to-date statistics on heart disease, stroke, other vascular diseases, and their risk factors and presents them in its Heart Disease and Stroke Statistical Update. The Statistical Update is a valuable resource for researchers, clinicians, healthcare policy makers, media professionals, the lay public, and many others who seek the best national data available on disease …

Heart Disease and Stroke Statistics—2010 Update A Report From the American Heart Association

Heart failure (HF) is a complex clinical syndrome hallmarked by an inability to match cardiac output with metabolic demand, resulting in exercise intolerance. HF is increasingly prevalent in an aging population and accounts for substantial burden of health care costs and morbidity. Because many of the central and peripheral mechanisms of HF respond favorably to exercise training, its role in HF treatment is becoming established. The role of habitual physical activity in the primary prevention of HF is less clear; however, available evidence is supportive. This article reviews recently published studies on exercise training and usual physical activity in HF treatment and prevention, discusses potential mechanisms, and suggests areas where further research is needed.

Physical Activity in the Treatment and Prevention of Heart Failure: An Update.

Meniscal Degeneration is Prognostic of Destabilzing Meniscal Tear and Accelerated Knee Osteoarthritis: Data from the Osteoarthritis Initiative.

To the Edi1M': Dr. Katemdahl s letter discusses some important issues related to the utilization of metaanalysis as a useful analytic tool in medicine. In my article the meta-analysis used for estimating a summary \"measure of effect\" was not that of physical inactivity and coronary heart disease (CHD), which had been performed in 1987 by Powell, et al.1 and more fonnally in 1990 by Berlin and Colditz,2 but rather was the study of the independent or multivariate relation of physical inactivity and CHD. Both of the former meta-analyses performed quality estimates using a scoring system of o to 6 in Powell, et al. and 0 to 32 in Berlin and Colditz based upon the measure of activity, the measure of outcome, and the epidemiologic methods. The 12 studies included in my meta-analysis received scores from 4 to 6 on Powell, et al.s scale and 18 to 26 using Berlin and Colditzs scale. These were not included in the description of the studies for the sake of brevity, as the reasons for inclusion were outlined in the Methods section in paragraphs 2 and 3. Only studies that used easily standardized hard endpoints and adjusted for confounders of age, smoking, lipids, and blood pressure were utilized in my analysis. Additional exclusions were studies that assessed cardiovascular fitness (attribute) and not physical inactivity (behavior). It is for this reason that only 12 out of the 75 studies were included, and all had quality scores near the highest categories established by Powell, et al. and Berlin and Colditz. The term historical cohort used to define the studies by Dr. Ralph Paffenbar~r, including the San Francisco longshoremen stud? and Harvard alumni study,4 refers to the fact that these two studies used job classification and mail surveys, respectively, to define physical inactivity in a previously established cohort. They certainly included a control group of unexposed individuals and used the same criteria for evaluating dependent and independent variables in both groups. Perhaps Dr. Katerndahl is confusing case series with historical cohort studies. These two studies3•4 are considered critical studies in our understanding the relation of physical inactivity and CHD, because the San Francisco longshoremen showed an apparent threshold effect, and the Harvard alumni study showed an effect not only on CHD mortality, but also on total mortality. It seems unwise to have had left out these important studies from my analysis. Of more than 7S articles reviewed, 14 studies met the standardS of evidence described above and evaluated the independent relation of physical inactivity and CHD. Two studies (Health Insurance PlanS and British civil servants~ listed in Table 1 used stratification to analyze confounding and thus could not be included in the weighted summary measure used in my meta-analysis and were therefore not included in Figure 1. Lists of the other 61 references are available in the bibliographies of Powell, et al. and Berlin and Colditz for 53 references and in Part IT of this review regarding cardiovascular fitness and secondary prevention trials. I will be glad to make these available upon request to the interested reader .. Dr. Katerndahl's concern about the possibility of publication bias needs further comment. While this is an important concern of meta-analysis in general, it is unlikely that unpublished studies related to the multivariate relation of physical inactivity and CHD were as problematic as he has suggested. First, this review follows that of Berlin, et aI., who attempted to find unpublished data. Second, I reviewed the manuscript with several \"content experts\" in both cardiovascular epidemiology and exercise sciencesports medicine who were unaware of any other unpublished materials. Since the submission of metaanalysis at least four additional publications related to physical inactivity and CHD have been published. The Adventist mortality study7 showed a decreased mortality with physical activity but did not take into account lipids in its multiple variable analysis. The Alameda County study8 showed benefit to physical activity in all age groups but only accounted for smoking and body mass index in its adjustments. The MRFIT 10.5-year mortality follow-up study9 showed essentially identical results as those it had published previously and were included in my original meta-analysis. The Dubbo study,IO while showing a beneficial effect of physical activity using the \"soft endpoint\" of any CHD, did not show a protective effect using a definite hard endpoint of myocardial infarction. The funnel graph depicted by Dr. Katerndahl shows nicely the fact alluded to in my manuscript that the more precise studies with larger sample sizes generally show measures of effect closer to 1 (null hypothesis) than those studies that were less precise and therefore with smaller sample sizes. The relation between sample size and the width of the confidence interval comes from the fact that the standard error of the relative risk is inversely related to the sample size. This fact can be seen visually by reviewing Figure 1 of my original manuscript and recognizing that those studies with the smallest 9S percent confidence intervals are closer to 1, whereas those with the greatest relative risks have large confidence intervals. It is for this reason that the often quoted median relative risk of 1.9 for physical inactivity based upon the review of Powell, et al. is spurious and that the relative risk of 1.37 derived from my weighted estimate accounting for sample size is a better estimate of the true independent relative risk of physical inactivity. Charles B. Eaton, M.D. Memorial Hospital of Rhode Island Pawtucket

Physical Activity and Coronary Heart Disease–Reply–I

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=INTEMED&articleId=411096&pdfFileName=ilt1023-4-2.pdf

Estrogen and Heart Disease: Alternatives to a Paradigm in Crisis—Reply

Background: Prospective epidemiologic data on the association between vitamin D and all-cause and cause-specific mortality are limited. Objective: This study aimed to determine whether 25-hydroxyvitamin D [25(OH)D] concentrations were prospectively and independently associated with cardiovascular disease (CVD), cancer, and all-cause mortality in postmenopausal women. Design: A substudy in 2429 postmenopausal women within the Women’s Health Initiative (WHI) with measured baseline 25(OH) D concentrations were followed for 10 y for death from CVD, cancer, and all-cause mortality. Proportional hazards models were performed to evaluate quartiles of month-adjusted 25(OH)D concentrations, with adjustment for potential confounders. Sequential model building and analysis for multiplicative interaction were performed to evaluate the effects of central adiposity on the association of low 25(OH)D with all-cause mortality. Results: Of the 2429 women, 224 deaths occurred, with 79 deaths from CVD and 62 deaths from cancer. Multivariate-adjusted HRs that compared quartiles 1 (lowest) to 4 (highest) of 25(OH)D for all-cause mortality (HR: 1.25; 95% CI: 0.80, 1.95), CVD mortality (HR: 1.27; 95% CI: 0.81, 1.99), and cancer mortality (HR: 1.39; 95% CI: 0.88, 2.19) were not significant. There was a potential interaction (P = 0.08) between abdominal obesity and low 25(OH)D concentrations that showed an increased risk of the lowest quartile of 25(OH)D concentrations (HR: 1.85; 95% CI: 1.00, 3.44) with increased mortality in women with a normal waist circumference but no increased risk in women with abdominal obesity (HR: 0.96; 95% CI: 0.52, 1.76). Conclusion: Body fat distribution may play an important role in the modulation of the effect of low vitamin D concentrations on health. This trial was registered at clinicaltrials.gov as NCT 00000611. Am J Clin Nutr doi: 10.3945/ajcn.111.017715.

Charles B. Eaton

Papers

Physical Activity in the Treatment and Prevention of Heart Failure: An Update.

Meniscal Degeneration is Prognostic of Destabilzing Meniscal Tear and Accelerated Knee Osteoarthritis: Data from the Osteoarthritis Initiative.

Physical Activity and Coronary Heart Disease–Reply–I

Estrogen and Heart Disease: Alternatives to a Paradigm in Crisis—Reply

Prospective association of vitamin D concentrations with mortality in postmenopausal women: results from the Women's Health