@article {662, title = {Echocardiographic features of the right heart in sleep-disordered breathing: the Framingham Heart Study.}, journal = {Am J Respir Crit Care Med}, volume = {164}, year = {2001}, month = {2001 Sep 15}, pages = {933-8}, abstract = {

The effect of sleep-disordered breathing (SDB) on right heart structure and function is controversial. Studies of patients referred for evaluation of possible sleep apnea have yielded conflicting results, and the impact of SDB on the right heart has not been investigated in the general population. We examined the echocardiographic features of subjects with SDB at the Framingham Heart Study site of the Sleep Heart Health Study. Of 1,001 polysomnography subjects, 90 with SDB defined as a respiratory disturbance index (RDI) score > 90th percentile (mean RDI = 42) were compared with 90 low-RDI subjects (mean RDI = 5) matched for age, sex, and body mass index. Right heart measurements, made without knowledge of clinical status, were compared between groups. The majority of the subjects were male (74\%). After multivariable adjustment, right ventricle (RV) wall thickness was significantly greater (p = 0.005) in subjects with SDB (0.78 +/- 0.02 cm) than in the low-RDI subjects (0.68 +/- 0.02 cm). Right atrial dimensions, RV dimensions, and RV systolic function were not found to be significantly different between subjects with SDB and the low-RDI subjects. We conclude that in this community-based study of SDB and right heart echocardiographic features, RV wall thickness was increased in subjects with SDB. Whether the RV hypertrophy observed in persons with SDB is associated with increased morbidity and mortality remains unknown.

}, keywords = {Adult, Age Factors, Aged, Cohort Studies, Cross-Sectional Studies, Data Interpretation, Statistical, Echocardiography, Female, Forced Expiratory Volume, Humans, Hypertrophy, Right Ventricular, Linear Models, Male, Middle Aged, Obesity, Observer Variation, Polysomnography, Prospective Studies, Sex Factors, Sleep Apnea Syndromes, Ventricular Function, Right, Vital Capacity}, issn = {1073-449X}, doi = {10.1164/ajrccm.164.6.2001092}, author = {Guidry, U C and Mendes, L A and Evans, J C and Levy, D and O{\textquoteright}Connor, G T and Larson, M G and Gottlieb, D J and Benjamin, E J} } @article {1079, title = {Systematically missing confounders in individual participant data meta-analysis of observational cohort studies.}, journal = {Stat Med}, volume = {28}, year = {2009}, month = {2009 Apr 15}, pages = {1218-37}, abstract = {

One difficulty in performing meta-analyses of observational cohort studies is that the availability of confounders may vary between cohorts, so that some cohorts provide fully adjusted analyses while others only provide partially adjusted analyses. Commonly, analyses of the association between an exposure and disease either are restricted to cohorts with full confounder information, or use all cohorts but do not fully adjust for confounding. We propose using a bivariate random-effects meta-analysis model to use information from all available cohorts while still adjusting for all the potential confounders. Our method uses both the fully adjusted and the partially adjusted estimated effects in the cohorts with full confounder information, together with an estimate of their within-cohort correlation. The method is applied to estimate the association between fibrinogen level and coronary heart disease incidence using data from 154,012 participants in 31 cohorts

}, keywords = {Cohort Studies, Computer Simulation, Coronary Disease, Data Interpretation, Statistical, Female, Fibrinogen, Humans, Male, Meta-Analysis as Topic, Models, Statistical}, issn = {0277-6715}, doi = {10.1002/sim.3540}, author = {Jackson, Dan and White, Ian and Kostis, J B and Wilson, A C and Folsom, A R and Wu, K and Chambless, L and Benderly, M and Goldbourt, U and Willeit, J and Kiechl, S and Yarnell, J W G and Sweetnam, P M and Elwood, P C and Cushman, M and Psaty, B M and Tracy, R P and Tybjaerg-Hansen, A and Haverkate, F and de Maat, M P M and Thompson, S G and Fowkes, F G R and Lee, A J and Smith, F B and Salomaa, V and Harald, K and Rasi, V and Vahtera, E and Jousilahti, P and D{\textquoteright}Agostino, R and Kannel, W B and Wilson, P W F and Tofler, G and Levy, D and Marchioli, R and Valagussa, F and Rosengren, A and Wilhelmsen, L and Lappas, G and Eriksson, H and Cremer, P and Nagel, D and Curb, J D and Rodriguez, B and Yano, K and Salonen, J T and Nyyss{\"o}nen, K and Tuomainen, T-P and Hedblad, B and Engstrom, G and Berglund, G and Loewel, H and Koenig, W and Hense, H W and Meade, T W and Cooper, J A and De Stavola, B and Knottenbelt, C and Miller, G J and Cooper, J A and Bauer, K A and Rosenberg, R D and Sato, S and Kitamura, A and Naito, Y and Iso, H and Salomaa, V and Harald, K and Rasi, V and Vahtera, E and Jousilahti, P and Palosuo, T and Ducimetiere, P and Amouyel, P and Arveiler, D and Evans, A E and Ferrieres, J and Juhan-Vague, I and Bingham, A and Schulte, H and Assmann, G and Cantin, B and Lamarche, B and Despr{\'e}s, J-P and Dagenais, G R and Tunstall-Pedoe, H and Lowe, G D O and Woodward, M and Ben-Shlomo, Y and Davey Smith, G and Palmieri, V and Yeh, J L and Meade, T W and Rudnicka, A and Brennan, P and Knottenbelt, C and Cooper, J A and Ridker, P and Rodeghiero, F and Tosetto, A and Shepherd, J and Lowe, G D O and Ford, I and Robertson, M and Brunner, E and Shipley, M and Feskens, E J M and Di Angelantonio, E and Kaptoge, S and Lewington, S and Lowe, G D O and Sarwar, N and Thompson, S G and Walker, M and Watson, S and White, I R and Wood, A M and Danesh, J} } @article {7375, title = {A DNA methylation biomarker of alcohol consumption.}, journal = {Mol Psychiatry}, year = {2016}, month = {2016 Nov 15}, abstract = {

The lack of reliable measures of alcohol intake is a major obstacle to the diagnosis and treatment of alcohol-related diseases. Epigenetic modifications such as DNA methylation may provide novel biomarkers of alcohol use. To examine this possibility, we performed an epigenome-wide association study of methylation of cytosine-phosphate-guanine dinucleotide (CpG) sites in relation to alcohol intake in 13 population-based cohorts (ntotal=13 317; 54\% women; mean age across cohorts 42-76 years) using whole blood (9643 European and 2423 African ancestries) or monocyte-derived DNA (588 European, 263 African and 400 Hispanic ancestry) samples. We performed meta-analysis and variable selection in whole-blood samples of people of European ancestry (n=6926) and identified 144 CpGs that provided substantial discrimination (area under the curve=0.90-0.99) for current heavy alcohol intake (⩾42 g per day in men and ⩾28 g per day in women) in four replication cohorts. The ancestry-stratified meta-analysis in whole blood identified 328 (9643 European ancestry samples) and 165 (2423 African ancestry samples) alcohol-related CpGs at Bonferroni-adjusted P<1 {\texttimes} 10(-7). Analysis of the monocyte-derived DNA (n=1251) identified 62 alcohol-related CpGs at P<1 {\texttimes} 10(-7). In whole-blood samples of people of European ancestry, we detected differential methylation in two neurotransmitter receptor genes, the γ-Aminobutyric acid-A receptor delta and γ-aminobutyric acid B receptor subunit 1; their differential methylation was associated with expression levels of a number of genes involved in immune function. In conclusion, we have identified a robust alcohol-related DNA methylation signature and shown the potential utility of DNA methylation as a clinically useful diagnostic test to detect current heavy alcohol consumption.Molecular Psychiatry advance online publication, 15 November 2016; doi:10.1038/mp.2016.192.

}, issn = {1476-5578}, doi = {10.1038/mp.2016.192}, author = {Liu, C and Marioni, R E and Hedman, {\r A} K and Pfeiffer, L and Tsai, P-C and Reynolds, L M and Just, A C and Duan, Q and Boer, C G and Tanaka, T and Elks, C E and Aslibekyan, S and Brody, J A and K{\"u}hnel, B and Herder, C and Almli, L M and Zhi, D and Wang, Y and Huan, T and Yao, C and Mendelson, M M and Joehanes, R and Liang, L and Love, S-A and Guan, W and Shah, S and McRae, A F and Kretschmer, A and Prokisch, H and Strauch, K and Peters, A and Visscher, P M and Wray, N R and Guo, X and Wiggins, K L and Smith, A K and Binder, E B and Ressler, K J and Irvin, M R and Absher, D M and Hernandez, D and Ferrucci, L and Bandinelli, S and Lohman, K and Ding, J and Trevisi, L and Gustafsson, S and Sandling, J H and Stolk, L and Uitterlinden, A G and Yet, I and Castillo-Fernandez, J E and Spector, T D and Schwartz, J D and Vokonas, P and Lind, L and Li, Y and Fornage, M and Arnett, D K and Wareham, N J and Sotoodehnia, N and Ong, K K and van Meurs, J B J and Conneely, K N and Baccarelli, A A and Deary, I J and Bell, J T and North, K E and Liu, Y and Waldenberger, M and London, S J and Ingelsson, E and Levy, D} }