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351 results on '"Curb, J D"'

13. TRIAD: A Multicenter Study of Managed Care and Diabetes Quality of Care, Costs, and Outcomes

Author

NARAYAN, K. M., SELBY, J. V., MANGIONE, C. M., HERMAN, W. H., SAFFORD, M. M., MARRERO, D. G., CURB, J. D., and COWAN, D. N.

Subjects
Diabetes -- Research, Health
Abstract

Effective treatments improve the health status of people with diabetes. However, the utilization of such treatments remains sub-optimal in all settings including managed care, which is a rapidly growing mode [...]

Published
2000

14. Statin use and risk of haemorrhagic stroke in a community-based cohort of postmenopausal women: an observational study from the Women's Health Initiative

Author

Salmoirago-Blotcher, E., primary, Hovey, K. M., additional, Andrews, C. A., additional, Robinson, J. G., additional, Johnson, K. C., additional, Wassertheil-Smoller, S., additional, Crawford, S., additional, Qi, L., additional, Martin, L. W., additional, Ockene, J., additional, Manson, J. E., additional, Nabel, E., additional, Rossouw, J., additional, Ludlam, S., additional, McGowan, J., additional, Ford, L., additional, Geller, N., additional, Prentice, R., additional, Anderson, G., additional, LaCroix, A., additional, Kooperberg, C. L., additional, Patterson, R. E., additional, McTiernan, A., additional, Stein, E., additional, Cummings, S., additional, Rajkovic, A., additional, Eaton, C. B., additional, Phillips, L., additional, Beresford, S., additional, Chlebowski, R., additional, Michael, Y., additional, Caan, B., additional, Kotchen, J. M., additional, Howard, B. V., additional, Van Horn, L., additional, Black, H., additional, Stefanick, M. L., additional, Lane, D., additional, Jackson, R., additional, Lewis, C. E., additional, Thomson, C. A., additional, Wactawski-Wende, J., additional, Robbins, J., additional, Hubbell, F. A., additional, Nathan, L., additional, Langer, R. D., additional, Gass, M., additional, Limacher, M., additional, Curb, J. D., additional, Wallace, R., additional, Lasser, N., additional, O'Sullivan, M. J., additional, Margolis, K., additional, Brunner, R., additional, Heiss, G., additional, Kuller, L., additional, Brzyski, R., additional, Sarto, G. E., additional, Vitolins, M., additional, Simon, M., additional, and Shumaker, S., additional

Published
2015
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15. Admixture mapping of quantitative trait loci for blood lipids in African-Americans

Author

Tang, H., Quertermous, T., Lewis, C. E., Risch, N. J., Curb, J. D., North, K., Boerwinkle, E., Zhu, X., Basu, A., and Mosley, T. H.

Subjects
lipids (amino acids, peptides, and proteins)
Abstract

Blood lipid levels, including low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG), are highly heritable traits and major risk factors for atherosclerotic cardiovascular disease (CVD). Using individual ancestry estimates at marker locations across the genome, we present a novel quantitative admixture mapping analysis of all three lipid traits in a large sample of African-Americans from the Family Blood Pressure Program. Regression analysis was performed with both total and marker-location-specific European ancestry as explanatory variables, along with demographic covariates. Robust permutation analysis was used to assess statistical significance. Overall European ancestry was significantly correlated with HDL-C (negatively) and TG (positively), but not with LDL-C. We found strong evidence for a novel locus underlying HDL-C on chromosome 8q, which correlated negatively with European ancestry (P = .0014); the same location also showed positive correlation of European ancestry with TG levels. A region on chromosome 14q also showed significant negative correlation between HDL-C levels and European ancestry. On chromosome 15q, a suggestive negative correlation of European ancestry with TG and positive correlation with HDL-C was observed. Results with LDL-C were less significant overall. We also found significant evidence for genome-wide ancestry effects underlying the joint distribution of HDL-C and TG, not fully explained by the locus on chromosome 8. Our results are consistent with a genetic contribution to and may explain the healthier HDL-C and TG profiles found in Blacks versus Whites. The identified regions provide locations for follow-up studies of genetic variants underlying lipid variation in African-Americans and possibly other populations.

Published
2009
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16. Relationship of dietary linoleic acid to blood pressure. The International Study of Macro-Micronutrients and Blood Pressure Study [corrected]

Author

Miura, K., Stamler, J., Nakagawa, H., Elliott, P., Ueshima, H., Chan, Q., Brown, I. J., Tzoulaki, I., Saitoh, S., Dyer, A. R., Daviglus, M. L., Kesteloot, H., Okayama, A., Curb, J. D., Rodriguez, B. L., Elmer, P. J., Steffen, L. M., Robertson, C., and Zhao, L.

Subjects
Adult, Male, Blood Pressure Determination, Middle Aged, Sensitivity and Specificity, Blood Pressure/*drug effects, Hypertension/epidemiology/*physiopathology/prevention & control, Cross-Sectional Studies, Multivariate Analysis, Humans, Linoleic Acid/*administration & dosage, Multicenter Studies as Topic, Regression Analysis, Female, Micronutrients, Registries, Energy Intake, Probability
Abstract

Findings from observational and interventional studies on the relationship of dietary linoleic acid, the main dietary polyunsaturated fatty acid, with blood pressure have been inconsistent. The International Study of Macro-Micronutrients and Blood Pressure is an international cross-sectional epidemiological study of 4680 men and women ages 40 to 59 years from 17 population samples in China, Japan, United Kingdom, and United States. We report associations of linoleic acid intake of individuals with their blood pressure. Nutrient intake data were based on 4 in-depth multipass 24-hour dietary recalls per person and 2 timed 24-hour urine collections per person. Systolic and diastolic blood pressures were measured 8 times at 4 visits. With several models to control for possible confounders (dietary or other), linear regression analyses showed a nonsignificant inverse relationship of linoleic acid intake (percent kilocalories) to systolic and diastolic blood pressure for all of the participants. When analyzed for 2238 "nonintervened" individuals (not on a special diet, not consuming nutritional supplements, no diagnosed cardiovascular disease or diabetes, and not taking medication for high blood pressure, cardiovascular disease, or diabetes), the relationship was stronger. With adjustment for 14 variables, estimated systolic/diastolic blood pressure differences with 2-SD higher linoleic acid intake (3.77% kcal) were -1.42/-0.91 mm Hg (P

Published
2008

17. Multiethnic Meta-Analysis of Genome-Wide Association Studies in >100 000 Subjects Identifies 23 Fibrinogen-Associated Loci but No Strong Evidence of a Causal Association Between Circulating Fibrinogen and Cardiovascular Disease

Author

Sabater-Lleal, M., Huang, J., Chasman, D., Naitza, S., Dehghan, A., Johnson, A. D., Teumer, A., Reiner, A. P., Folkersen, L., Basu, S., Rudnicka, A. R., Trompet, S., Malarstig, A., Baumert, J., Bis, J. C., Guo, X., Hottenga, J. J., Shin, S.-Y., Lopez, L. M., Lahti, J., Tanaka, T., Yanek, L. R., Oudot-Mellakh, T., Wilson, J. F., Navarro, P., Huffman, J. E., Zemunik, T., Redline, S., Mehra, R., Pulanic, D., Rudan, I., Wright, A. F., Kolcic, I., Polasek, O., Wild, S. H., Campbell, H., Curb, J. D., Wallace, R., Liu, S., Eaton, C. B., Becker, D. M., Becker, L. C., Bandinelli, S., Raikkonen, K., Widen, E., Palotie, A., Fornage, M., Green, D., Gross, M., Davies, G., Harris, S. E., Liewald, D. C., Starr, J. M., Williams, F. M. K., Grant, P. J., Spector, T. D., Strawbridge, R. J., Silveira, A., Sennblad, B., Rivadeneira, F., Uitterlinden, A. G., Franco, O. H., Hofman, A., van Dongen, J., Willemsen, G., Boomsma, D. I., Yao, J., Swords Jenny, N., Haritunians, T., McKnight, B., Lumley, T., Taylor, K. D., Rotter, J. I., Psaty, B. M., Peters, A., Gieger, C., Illig, T., Grotevendt, A., Homuth, G., Volzke, H., Kocher, T., Goel, A., Franzosi, M. G., Seedorf, U., Clarke, R., Steri, M., Tarasov, K. V., Sanna, S., Schlessinger, D., Stott, D. J., Sattar, N., Buckley, B. M., Rumley, A., Lowe, G. D., McArdle, W. L., Chen, M.-H., Tofler, G. H., Song, J., Boerwinkle, E., Folsom, A. R., Rose, L. M., Franco-Cereceda, A., Teichert, M., Ikram, M. A., Mosley, T. H., Bevan, S., Dichgans, M., Rothwell, P. M., Sudlow, C. L. M., Hopewell, J. C., Chambers, J. C., Saleheen, D., Kooner, J. S., Danesh, J., Nelson, C. P., Erdmann, J., Reilly, M. P., Kathiresan, S., Schunkert, H., Morange, P.-E., Ferrucci, L., Eriksson, J. G., Jacobs, D., Deary, I. J., Soranzo, N., Witteman, J. C. M., de Geus, E. J. C., Tracy, R. P., Hayward, C., Koenig, W., Cucca, F., Jukema, J. W., Eriksson, P., Seshadri, S., Markus, H. S., Watkins, H., Samani, N. J., Wallaschofski, H., Smith, N. L., Tregouet, D., Ridker, P. M., Tang, W., Strachan, D. P., Hamsten, A., O'Donnell, C. J., Jankowski, Janusz, Sabater-Lleal, M., Huang, J., Chasman, D., Naitza, S., Dehghan, A., Johnson, A. D., Teumer, A., Reiner, A. P., Folkersen, L., Basu, S., Rudnicka, A. R., Trompet, S., Malarstig, A., Baumert, J., Bis, J. C., Guo, X., Hottenga, J. J., Shin, S.-Y., Lopez, L. M., Lahti, J., Tanaka, T., Yanek, L. R., Oudot-Mellakh, T., Wilson, J. F., Navarro, P., Huffman, J. E., Zemunik, T., Redline, S., Mehra, R., Pulanic, D., Rudan, I., Wright, A. F., Kolcic, I., Polasek, O., Wild, S. H., Campbell, H., Curb, J. D., Wallace, R., Liu, S., Eaton, C. B., Becker, D. M., Becker, L. C., Bandinelli, S., Raikkonen, K., Widen, E., Palotie, A., Fornage, M., Green, D., Gross, M., Davies, G., Harris, S. E., Liewald, D. C., Starr, J. M., Williams, F. M. K., Grant, P. J., Spector, T. D., Strawbridge, R. J., Silveira, A., Sennblad, B., Rivadeneira, F., Uitterlinden, A. G., Franco, O. H., Hofman, A., van Dongen, J., Willemsen, G., Boomsma, D. I., Yao, J., Swords Jenny, N., Haritunians, T., McKnight, B., Lumley, T., Taylor, K. D., Rotter, J. I., Psaty, B. M., Peters, A., Gieger, C., Illig, T., Grotevendt, A., Homuth, G., Volzke, H., Kocher, T., Goel, A., Franzosi, M. G., Seedorf, U., Clarke, R., Steri, M., Tarasov, K. V., Sanna, S., Schlessinger, D., Stott, D. J., Sattar, N., Buckley, B. M., Rumley, A., Lowe, G. D., McArdle, W. L., Chen, M.-H., Tofler, G. H., Song, J., Boerwinkle, E., Folsom, A. R., Rose, L. M., Franco-Cereceda, A., Teichert, M., Ikram, M. A., Mosley, T. H., Bevan, S., Dichgans, M., Rothwell, P. M., Sudlow, C. L. M., Hopewell, J. C., Chambers, J. C., Saleheen, D., Kooner, J. S., Danesh, J., Nelson, C. P., Erdmann, J., Reilly, M. P., Kathiresan, S., Schunkert, H., Morange, P.-E., Ferrucci, L., Eriksson, J. G., Jacobs, D., Deary, I. J., Soranzo, N., Witteman, J. C. M., de Geus, E. J. C., Tracy, R. P., Hayward, C., Koenig, W., Cucca, F., Jukema, J. W., Eriksson, P., Seshadri, S., Markus, H. S., Watkins, H., Samani, N. J., Wallaschofski, H., Smith, N. L., Tregouet, D., Ridker, P. M., Tang, W., Strachan, D. P., Hamsten, A., O'Donnell, C. J., and Jankowski, Janusz

Abstract

Background—Estimates of the heritability of plasma fibrinogen concentration, an established predictor of cardiovascular disease, range from 34% to 50%. Genetic variants so far identified by genome-wide association studies explain only a small proportion (<2%) of its variation. Methods and Results—We conducted a meta-analysis of 28 genome-wide association studies including >90 000 subjects of European ancestry, the first genome-wide association meta-analysis of fibrinogen levels in 7 studies in blacks totaling 8289 samples, and a genome-wide association study in Hispanics totaling 1366 samples. Evaluation for association of single-nucleotide polymorphisms with clinical outcomes included a total of 40 695 cases and 85 582 controls for coronary artery disease, 4752 cases and 24 030 controls for stroke, and 3208 cases and 46 167 controls for venous thromboembolism. Overall, we identified 24 genome-wide significant (P<5×10−8) independent signals in 23 loci, including 15 novel associations, together accounting for 3.7% of plasma fibrinogen variation. Gene-set enrichment analysis highlighted key roles in fibrinogen regulation for the 3 structural fibrinogen genes and pathways related to inflammation, adipocytokines, and thyrotrophin-releasing hormone signaling. Whereas lead single-nucleotide polymorphisms in a few loci were significantly associated with coronary artery disease, the combined effect of all 24 fibrinogen-associated lead single-nucleotide polymorphisms was not significant for coronary artery disease, stroke, or venous thromboembolism. Conclusions—We identify 23 robustly associated fibrinogen loci, 15 of which are new. Clinical outcome analysis of these loci does not support a causal relationship between circulating levels of fibrinogen and coronary artery disease, stroke, or venous thromboembolism.

Published
2013

19. Physical Activity Assessment: Biomarkers and Self-Report of Activity-Related Energy Expenditure in the WHI

Author

Neuhouser, M. L., primary, Di, C., additional, Tinker, L. F., additional, Thomson, C., additional, Sternfeld, B., additional, Mossavar-Rahmani, Y., additional, Stefanick, M. L., additional, Sims, S., additional, Curb, J. D., additional, Lamonte, M., additional, Seguin, R., additional, Johnson, K. C., additional, and Prentice, R. L., additional

Published
2013
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28. Coronary Artery Calcification in Japanese Men in Japan and Hawaii

Author

Abbott, R. D., primary, Ueshima, H., additional, Rodriguez, B. L., additional, Kadowaki, T., additional, Masaki, K. H., additional, Willcox, B. J., additional, Sekikawa, A., additional, Kuller, L. H., additional, Edmundowicz, D., additional, Shin, C., additional, Kashiwagi, A., additional, Nakamura, Y., additional, El-Saed, A., additional, Okamura, T., additional, White, R., additional, and Curb, J. D., additional

Published
2007
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29. Serum estradiol and risk of stroke in elderly men

Author

Abbott, R. D., primary, Launer, L. J., additional, Rodriguez, B. L., additional, Ross, G. W., additional, Wilson, P.W.F., additional, Masaki, K. H., additional, Strozyk, D., additional, Curb, J. D., additional, Yano, K., additional, Popper, J. S., additional, and Petrovitch, H., additional

Published
2007
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38. Midlife adiposity and the future risk of Parkinson's disease

Author

Abbott, R. D., primary, Ross, G. W., additional, White, L. R., additional, Nelson, J. S., additional, Masaki, K. H., additional, Tanner, C. M., additional, Curb, J. D., additional, Blanchette, P. L., additional, Popper, J. S., additional, and Petrovitch, H., additional

Published
2002
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39. Effects of Diets High in Palmitoleic Acid on Serum Lipid Levels and Metabolism

Author

HAWAII UNIV AT MANOA HONOLULU, Curb, J. D., HAWAII UNIV AT MANOA HONOLULU, and Curb, J. D.

Abstract

Using a controlled, crossover design feeding study, each of 30 healthy individuals (15 males and 15 females) aged 18 to 53 years, were fed, in random order, a tree nut based mono-unsaturated fat diet (MONO) (37% Kcal fat); an American Heart Association Step 1 diet (AHA) (30% Kcal fat); and a high saturated fat 'typical American' diet (AMERICAN) (37% Kcal fat). Mean and (standard deviation) for total Cholesterol at the end of the AMERICAN was 201.2 mg/dl (30.4). That for the AHA and the MONO diets was 193.1 (34.5) and 191.3 (32.6) mg/dl. HDL was 55.3 (7.6), 52.0 (8.2) and 52.8 (8.2). Triglycerides were 77.5 (32.7), 83.6 (32.6) and 70.4 (26.0). In all cases the values after AHA and MONO diets had similar positive effects on lipids when compared to an AMERICAN diet. In an absorption study involving 6 males, the dietary fats in a nut oil based diet, as reflected by the rise in serum triglycerides, were more available than those using ground or whole nuts. None of the diets had a glycemic effect. These results suggest that high monounsaturated fat diets which incorporate nuts could be part of a healthy energy diet for combat troops.

Published
1996

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