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2. Life expectancy associated with different ages at diagnosis of type 2 diabetes in high-income countries:23 million person-years of observation

Author

Sun, L., Best, L. G., Cooper, C., Bakker, S. J.L., Kavousi, M., Meyer, H. E., Thompson, S. G., Hunt, K. J., Bom, M. T., Kraft, P., Psaty, B. M., de Boer, R., Trompet, S., Tilly, M., Ikram, M. A., Dorr, M., Can, G., Geleijnse, M., Sun, L., Best, L. G., Cooper, C., Bakker, S. J.L., Kavousi, M., Meyer, H. E., Thompson, S. G., Hunt, K. J., Bom, M. T., Kraft, P., Psaty, B. M., de Boer, R., Trompet, S., Tilly, M., Ikram, M. A., Dorr, M., Can, G., and Geleijnse, M.

Abstract

Background:The prevalence of type 2 diabetes is increasing rapidly, particularly among younger age groups. Estimates suggest that people with diabetes die, on average, 6 years earlier than people without diabetes. We aimed to provide reliable estimates of the associations between age at diagnosis of diabetes and all-cause mortality, cause-specific mortality, and reductions in life expectancy. Methods:For this observational study, we conducted a combined analysis of individual-participant data from 19 high-income countries using two large-scale data sources: the Emerging Risk Factors Collaboration (96 cohorts, median baseline years 1961–2007, median latest follow-up years 1980–2013) and the UK Biobank (median baseline year 2006, median latest follow-up year 2020). We calculated age-adjusted and sex-adjusted hazard ratios (HRs) for all-cause mortality according to age at diagnosis of diabetes using data from 1 515 718 participants, in whom deaths were recorded during 23·1 million person-years of follow-up. We estimated cumulative survival by applying age-specific HRs to age-specific death rates from 2015 for the USA and the EU. Findings: For participants with diabetes, we observed a linear dose–response association between earlier age at diagnosis and higher risk of all-cause mortality compared with participants without diabetes. HRs were 2·69 (95% CI 2·43–2·97) when diagnosed at 30–39 years, 2·26 (2·08–2·45) at 40–49 years, 1·84 (1·72–1·97) at 50–59 years, 1·57 (1·47–1·67) at 60–69 years, and 1·39 (1·29–1·51) at 70 years and older. HRs per decade of earlier diagnosis were similar for men and women. Using death rates from the USA, a 50-year-old individual with diabetes died on average 14 years earlier when diagnosed aged 30 years, 10 years earlier when diagnosed aged 40 years, or 6 years earlier when diagnosed aged 50 years than an individual without diabetes. Using EU death rates, the corresponding estimates

Published
2023

6. Blood-based DNA methylation biomarkers for cumulative lead exposure: associations with cardiovascular disease incidence and mortality in the Strong Heart Study

Author

Gao, X., primary, Domingo-Relloso, A., additional, Colicino, E., additional, Cole, S. A., additional, Haack, K., additional, Best, L. G., additional, Umans, J. G., additional, Fallin, M. D., additional, Tellez-Plaza, M., additional, Baccarelli, A. A., additional, and Navas-Acien, A., additional

Published
2020
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10. Covariate-adjusted measures of discrimination for survival data

Author

White, Ian R, Rapsomaniki, Eleni, Wannamethee, S. G., Morris, R. W., Willeit, J., Willeit, P., Santer, P., Kiechl, S., Wald, N., Ebrahim, S., Lawlor, D. A., Gallacher, J., Yarnell, J. W. G., Ben Shlomo, Y., Casiglia, Edoardo, Tikhonoff, V., Sutherland, S. E., Nietert, P. J., Keil, J. E., Bachman, D. L., Psaty, B. M., Cushman, M., Nordestgaard, B. G., Tybjærg Hansen, A., Frikke Schmidt, R., Giampaoli, S., Palmieri, L., Panico, S., Pilotto, L., Vanuzzo, D., Simons, L. A., Friedlander, Y., Mccallum, J., Price, J. F., Mclachlan, S., Taylor, J. O., Guralnik, J. M., Wallace, R. B., Kohout, F. J., Cornoni Huntley, J. C., Blazer, D. G., Phillips, C. L., Wareham, N. J., Khaw, K. T., Brenner, H., Schöttker, B., Müller, H. T., Rothenbacher, D., Nissinen, A., Donfrancesco, C., Harald, K., Jousilahti, P. R., Vartiainen, E., Salomaa, V., D'Agostino, R. B., Wolf, P. A., Vasan, R. S., Daimon, M., Oizumi, T., Kayama, T., Kato, T., Chetrit, A., Dankner, R., Lubin, F., Welin, L., Svärdsudd, K., Eriksson, H., Lappas, G., Lissner, L., Mehlig, K., Björkelund, C., Nagel, D., Kiyohara, Y., Arima, H., Ninomiya, T., Hata, J., Rodriguez, B., Dekker, J. M., Nijpels, G., Stehouwer, C. D. A., Iso, H., Kitamura, A., Yamagishi, K., Noda, H., Goldbourt, U., Kauhanen, J., Salonen, J. T., Tuomainen, T. P., Meade, T. W., Destavola, B. L., Blokstra, A., Verschuren, W. M. M., de Boer, I. H., Folsom, A. R., Koenig, W., Meisinger, C., Peters, A., Bueno de Mesquita, H. B., Rosengren, A., Wilhelmsen, L., Kuller, L. H., Grandits, G., Cooper, J. A., Bauer, K. A., Davidson, K. W., Kirkland, S., Shaffer, J. A., Shimbo, D., Sato, S., Dullaart, R. P. F., Bakker, S. J. L., Gansevoort, R. T., Ducimetiere, P., Amouyel, P., Arveiler, D., Evans, A., Ferrières, J., Schulte, H., Assmann, G., Jukema, J. W., Westendorp, R. G. J., Sattar, N., Cantin, B., Lamarche, B., Després, J. P., Null, E. Barrett Connor, Wingard, D. L., Daniels, L. B., Gudnason, V., Aspelund, T., Trevisan, M., Hofman, A., Franco, O. H., Tunstall Pedoe, H., Tavendale, R., Lowe, G. D. O., Woodward, M., Howard, W. J., Howard, B. V., Zhang, Y., Best, L. G., Umans, J., Davey Smith, G., Onat, A., Nakagawa, H., Sakurai, M., Nakamura, K., Morikawa, Y., Njølstad, I., Mathiesen, E. B., Wilsgaard, T., Sundström, J., Gaziano, J. M., Ridker, P. M., Marmot, M., Clarke, R., Collins, R., Fletcher, A., Brunner, E., Shipley, M., Kivimaki, M., Buring, J., Rifai, N., Cook, N., Ford, I., Robertson, M., Marín Ibañez, A., Feskens, E. J. M., Geleijnse, J. M., MUMC+: HVC Pieken Maastricht Studie (9), Interne Geneeskunde, MUMC+: MA Interne Geneeskunde (3), RS: FHML non-thematic output, Apollo - University of Cambridge Repository, White, Ian R, Rapsomaniki, Eleni, and Panico, Salvatore

Subjects
Statistics and Probability, Male, Biometry, C-index, D-index, Discrimination, Analysis of Variance, Cardiovascular Diseases, Clinical Trials as Topic, Discriminant Analysis, Female, Humans, Middle Aged, Risk Factors, Survival Analysis, Medicine (all), Statistics, Probability and Uncertainty, 01 natural sciences, Article, Unit (housing), 010104 statistics & probability, 03 medical and health sciences, 0302 clinical medicine, Survival data, Cardiovascular Disease, Covariate, Statistics, 030212 general & internal medicine, 0101 mathematics, 10. No inequality, Prognostic models, Survival analysis, Medicine(all), Proportional hazards model, Risk Factor, General Medicine, Probability and Uncertainty, Discriminant Analysi, Demography, Human
Abstract

Discrimination statistics describe the ability of a survival model to assign higher risks to individuals who experience earlier events: examples are Harrell's C-index and Royston and Sauerbrei's D, which we call the D-index. Prognostic covariates whose distributions are controlled by the study design (e.g. age and sex) influence discrimination and can make it difficult to compare model discrimination between studies. Although covariate adjustment is a standard procedure for quantifying disease-risk factor associations, there are no covariate adjustment methods for discrimination statistics in censored survival data.To develop extensions of the C-index and D-index that describe the prognostic ability of a model adjusted for one or more covariate(s).We define a covariate-adjusted C-index and D-index for censored survival data, propose several estimators, and investigate their performance in simulation studies and in data from a large individual participant data meta-analysis, the Emerging Risk Factors Collaboration.The proposed methods perform well in simulations. In the Emerging Risk Factors Collaboration data, the age-adjusted C-index and D-index were substantially smaller than unadjusted values. The study-specific standard deviation of baseline age was strongly associated with the unadjusted C-index and D-index but not significantly associated with the age-adjusted indices.The proposed estimators improve meta-analysis comparisons, are easy to implement and give a more meaningful clinical interpretation.? 2014 The Author. Biometrical Journal published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Published
2015
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12. Cadmium body burden and increased blood pressure in middle-aged American Indians: the Strong Heart Study

Author

Franceschini, N, primary, Fry, R C, additional, Balakrishnan, P, additional, Navas-Acien, A, additional, Oliver-Williams, C, additional, Howard, A G, additional, Cole, S A, additional, Haack, K, additional, Lange, E M, additional, Howard, B V, additional, Best, L G, additional, Francesconi, K A, additional, Goessler, W, additional, Umans, J G, additional, and Tellez-Plaza, M, additional

Published
2016
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13. Covariate-adjusted measures of discrimination for survival data

Author

White, Ian R., Rapsomaniki, Eleni, Wannamethee, S. G., Morris, R. W., Willeit, J., Willeit, P., Santer, P., Kiechl, S., Wald, N., Ebrahim, S., Lawlor, D. A., Gallacher, J., Yarnell, J. W G, Ben-Shlomo, Y., Casiglia, E., Tikhonoff, V., Sutherland, S. E., Nietert, P. J., Keil, J. E., Bachman, D. L., Psaty, B. M., Cushman, M., Nordestgaard, B. G., Tybjærg-Hansen, A., Frikke-Schmidt, R., Giampaoli, S., Palmieri, L., Panico, S., Pilotto, L., Vanuzzo, D., Simons, L. A., Friedlander, Y., McCallum, J., Price, J. F., McLachlan, S., Taylor, J. O., Guralnik, J. M., Wallace, R. B., Kohout, F. J., Cornoni-Huntley, J. C., Blazer, D. G., Phillips, C. L., Wareham, N. J., Khaw, K. T., Brenner, H., Schöttker, B., Müller, H. T., Rothenbacher, D., Nissinen, A., Donfrancesco, C., Harald, K., Jousilahti, P. R., Vartiainen, E., Salomaa, V., D'Agostino, R. B., Wolf, P. A., Vasan, R. S., Daimon, M., Oizumi, T., Kayama, T., Kato, T., Chetrit, A., Dankner, R., Lubin, F., Welin, L., Svärdsudd, K., Eriksson, H., Lappas, G., Lissner, L., Mehlig, K., Björkelund, C., Nagel, D., Kiyohara, Y., Arima, H., Ninomiya, T., Hata, J., Rodriguez, B., Dekker, J. M., Nijpels, G., Stehouwer, C. D A, Iso, H., Kitamura, A., Yamagishi, K., Noda, H., Goldbourt, U., Kauhanen, J., Salonen, J. T., Tuomainen, T. P., Meade, T. W., DeStavola, B. L., Blokstra, A., Verschuren, W. M M, de Boer, I. H., Folsom, A. R., Koenig, W., Meisinger, C., Peters, A., Bueno-de-Mesquita, H. B., Rosengren, A., Wilhelmsen, L., Kuller, L. H., Grandits, G., Cooper, J. A., Bauer, K. A., Davidson, K. W., Kirkland, S., Shaffer, J. A., Shimbo, D., Sato, S., Dullaart, R. P F, Bakker, S. J L, Gansevoort, R. T., Ducimetiere, P., Amouyel, P., Arveiler, D., Evans, A., Ferrières, J., Schulte, H., Assmann, G., Jukema, J. W., Westendorp, R. G J, Sattar, N., Cantin, B., Lamarche, B., Després, J. P., E.Barrett-Connor, Wingard, D. L., Daniels, L. B., Gudnason, V., Aspelund, T., Trevisan, M., Hofman, A., Franco, O. H., Tunstall-Pedoe, H., Tavendale, R., Lowe, G. D O, Woodward, M., Howard, W. J., Howard, B. V., Zhang, Y., Best, L. G., Umans, J., Davey-Smith, G., Onat, A., Nakagawa, H., Sakurai, M., Nakamura, K., Morikawa, Y., Njølstad, I., Mathiesen, E. B., Wilsgaard, T., Sundström, J., Gaziano, J. M., Ridker, P. M., Marmot, M., Clarke, R., Collins, R., Fletcher, A., Brunner, E., Shipley, M., Kivimaki, M., Buring, J., Rifai, N., Cook, N., Ford, I., Robertson, M., Marín Ibañez, A., Feskens, E. J M, Geleijnse, J. M., White, Ian R., Rapsomaniki, Eleni, Wannamethee, S. G., Morris, R. W., Willeit, J., Willeit, P., Santer, P., Kiechl, S., Wald, N., Ebrahim, S., Lawlor, D. A., Gallacher, J., Yarnell, J. W G, Ben-Shlomo, Y., Casiglia, E., Tikhonoff, V., Sutherland, S. E., Nietert, P. J., Keil, J. E., Bachman, D. L., Psaty, B. M., Cushman, M., Nordestgaard, B. G., Tybjærg-Hansen, A., Frikke-Schmidt, R., Giampaoli, S., Palmieri, L., Panico, S., Pilotto, L., Vanuzzo, D., Simons, L. A., Friedlander, Y., McCallum, J., Price, J. F., McLachlan, S., Taylor, J. O., Guralnik, J. M., Wallace, R. B., Kohout, F. J., Cornoni-Huntley, J. C., Blazer, D. G., Phillips, C. L., Wareham, N. J., Khaw, K. T., Brenner, H., Schöttker, B., Müller, H. T., Rothenbacher, D., Nissinen, A., Donfrancesco, C., Harald, K., Jousilahti, P. R., Vartiainen, E., Salomaa, V., D'Agostino, R. B., Wolf, P. A., Vasan, R. S., Daimon, M., Oizumi, T., Kayama, T., Kato, T., Chetrit, A., Dankner, R., Lubin, F., Welin, L., Svärdsudd, K., Eriksson, H., Lappas, G., Lissner, L., Mehlig, K., Björkelund, C., Nagel, D., Kiyohara, Y., Arima, H., Ninomiya, T., Hata, J., Rodriguez, B., Dekker, J. M., Nijpels, G., Stehouwer, C. D A, Iso, H., Kitamura, A., Yamagishi, K., Noda, H., Goldbourt, U., Kauhanen, J., Salonen, J. T., Tuomainen, T. P., Meade, T. W., DeStavola, B. L., Blokstra, A., Verschuren, W. M M, de Boer, I. H., Folsom, A. R., Koenig, W., Meisinger, C., Peters, A., Bueno-de-Mesquita, H. B., Rosengren, A., Wilhelmsen, L., Kuller, L. H., Grandits, G., Cooper, J. A., Bauer, K. A., Davidson, K. W., Kirkland, S., Shaffer, J. A., Shimbo, D., Sato, S., Dullaart, R. P F, Bakker, S. J L, Gansevoort, R. T., Ducimetiere, P., Amouyel, P., Arveiler, D., Evans, A., Ferrières, J., Schulte, H., Assmann, G., Jukema, J. W., Westendorp, R. G J, Sattar, N., Cantin, B., Lamarche, B., Després, J. P., E.Barrett-Connor, Wingard, D. L., Daniels, L. B., Gudnason, V., Aspelund, T., Trevisan, M., Hofman, A., Franco, O. H., Tunstall-Pedoe, H., Tavendale, R., Lowe, G. D O, Woodward, M., Howard, W. J., Howard, B. V., Zhang, Y., Best, L. G., Umans, J., Davey-Smith, G., Onat, A., Nakagawa, H., Sakurai, M., Nakamura, K., Morikawa, Y., Njølstad, I., Mathiesen, E. B., Wilsgaard, T., Sundström, J., Gaziano, J. M., Ridker, P. M., Marmot, M., Clarke, R., Collins, R., Fletcher, A., Brunner, E., Shipley, M., Kivimaki, M., Buring, J., Rifai, N., Cook, N., Ford, I., Robertson, M., Marín Ibañez, A., Feskens, E. J M, and Geleijnse, J. M.

Published
2015

14. Covariate-adjusted measures of discrimination for survival data

Author

AIOS Psychiatrie, Public Health Epidemiologie, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, MS MDL 1, Cancer, Affectieve & Psychotische Med., White, Ian R., Rapsomaniki, Eleni, Wannamethee, S. G., Morris, R. W., Willeit, J., Willeit, P., Santer, P., Kiechl, S., Wald, N., Ebrahim, S., Lawlor, D. A., Gallacher, J., Yarnell, J. W G, Ben-Shlomo, Y., Casiglia, E., Tikhonoff, V., Sutherland, S. E., Nietert, P. J., Keil, J. E., Bachman, D. L., Psaty, B. M., Cushman, M., Nordestgaard, B. G., Tybjærg-Hansen, A., Frikke-Schmidt, R., Giampaoli, S., Palmieri, L., Panico, S., Pilotto, L., Vanuzzo, D., Simons, L. A., Friedlander, Y., McCallum, J., Price, J. F., McLachlan, S., Taylor, J. O., Guralnik, J. M., Wallace, R. B., Kohout, F. J., Cornoni-Huntley, J. C., Blazer, D. G., Phillips, C. L., Wareham, N. J., Khaw, K. T., Brenner, H., Schöttker, B., Müller, H. T., Rothenbacher, D., Nissinen, A., Donfrancesco, C., Harald, K., Jousilahti, P. R., Vartiainen, E., Salomaa, V., D'Agostino, R. B., Wolf, P. A., Vasan, R. S., Daimon, M., Oizumi, T., Kayama, T., Kato, T., Chetrit, A., Dankner, R., Lubin, F., Welin, L., Svärdsudd, K., Eriksson, H., Lappas, G., Lissner, L., Mehlig, K., Björkelund, C., Nagel, D., Kiyohara, Y., Arima, H., Ninomiya, T., Hata, J., Rodriguez, B., Dekker, J. M., Nijpels, G., Stehouwer, C. D A, Iso, H., Kitamura, A., Yamagishi, K., Noda, H., Goldbourt, U., Kauhanen, J., Salonen, J. T., Tuomainen, T. P., Meade, T. W., DeStavola, B. L., Blokstra, A., Verschuren, W. M M, de Boer, I. H., Folsom, A. R., Koenig, W., Meisinger, C., Peters, A., Bueno-de-Mesquita, H. B., Rosengren, A., Wilhelmsen, L., Kuller, L. H., Grandits, G., Cooper, J. A., Bauer, K. A., Davidson, K. W., Kirkland, S., Shaffer, J. A., Shimbo, D., Sato, S., Dullaart, R. P F, Bakker, S. J L, Gansevoort, R. T., Ducimetiere, P., Amouyel, P., Arveiler, D., Evans, A., Ferrières, J., Schulte, H., Assmann, G., Jukema, J. W., Westendorp, R. G J, Sattar, N., Cantin, B., Lamarche, B., Després, J. P., E.Barrett-Connor, Wingard, D. L., Daniels, L. B., Gudnason, V., Aspelund, T., Trevisan, M., Hofman, A., Franco, O. H., Tunstall-Pedoe, H., Tavendale, R., Lowe, G. D O, Woodward, M., Howard, W. J., Howard, B. V., Zhang, Y., Best, L. G., Umans, J., Davey-Smith, G., Onat, A., Nakagawa, H., Sakurai, M., Nakamura, K., Morikawa, Y., Njølstad, I., Mathiesen, E. B., Wilsgaard, T., Sundström, J., Gaziano, J. M., Ridker, P. M., Marmot, M., Clarke, R., Collins, R., Fletcher, A., Brunner, E., Shipley, M., Kivimaki, M., Buring, J., Rifai, N., Cook, N., Ford, I., Robertson, M., Marín Ibañez, A., Feskens, E. J M, Geleijnse, J. M., AIOS Psychiatrie, Public Health Epidemiologie, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, MS MDL 1, Cancer, Affectieve & Psychotische Med., White, Ian R., Rapsomaniki, Eleni, Wannamethee, S. G., Morris, R. W., Willeit, J., Willeit, P., Santer, P., Kiechl, S., Wald, N., Ebrahim, S., Lawlor, D. A., Gallacher, J., Yarnell, J. W G, Ben-Shlomo, Y., Casiglia, E., Tikhonoff, V., Sutherland, S. E., Nietert, P. J., Keil, J. E., Bachman, D. L., Psaty, B. M., Cushman, M., Nordestgaard, B. G., Tybjærg-Hansen, A., Frikke-Schmidt, R., Giampaoli, S., Palmieri, L., Panico, S., Pilotto, L., Vanuzzo, D., Simons, L. A., Friedlander, Y., McCallum, J., Price, J. F., McLachlan, S., Taylor, J. O., Guralnik, J. M., Wallace, R. B., Kohout, F. J., Cornoni-Huntley, J. C., Blazer, D. G., Phillips, C. L., Wareham, N. J., Khaw, K. T., Brenner, H., Schöttker, B., Müller, H. T., Rothenbacher, D., Nissinen, A., Donfrancesco, C., Harald, K., Jousilahti, P. R., Vartiainen, E., Salomaa, V., D'Agostino, R. B., Wolf, P. A., Vasan, R. S., Daimon, M., Oizumi, T., Kayama, T., Kato, T., Chetrit, A., Dankner, R., Lubin, F., Welin, L., Svärdsudd, K., Eriksson, H., Lappas, G., Lissner, L., Mehlig, K., Björkelund, C., Nagel, D., Kiyohara, Y., Arima, H., Ninomiya, T., Hata, J., Rodriguez, B., Dekker, J. M., Nijpels, G., Stehouwer, C. D A, Iso, H., Kitamura, A., Yamagishi, K., Noda, H., Goldbourt, U., Kauhanen, J., Salonen, J. T., Tuomainen, T. P., Meade, T. W., DeStavola, B. L., Blokstra, A., Verschuren, W. M M, de Boer, I. H., Folsom, A. R., Koenig, W., Meisinger, C., Peters, A., Bueno-de-Mesquita, H. B., Rosengren, A., Wilhelmsen, L., Kuller, L. H., Grandits, G., Cooper, J. A., Bauer, K. A., Davidson, K. W., Kirkland, S., Shaffer, J. A., Shimbo, D., Sato, S., Dullaart, R. P F, Bakker, S. J L, Gansevoort, R. T., Ducimetiere, P., Amouyel, P., Arveiler, D., Evans, A., Ferrières, J., Schulte, H., Assmann, G., Jukema, J. W., Westendorp, R. G J, Sattar, N., Cantin, B., Lamarche, B., Després, J. P., E.Barrett-Connor, Wingard, D. L., Daniels, L. B., Gudnason, V., Aspelund, T., Trevisan, M., Hofman, A., Franco, O. H., Tunstall-Pedoe, H., Tavendale, R., Lowe, G. D O, Woodward, M., Howard, W. J., Howard, B. V., Zhang, Y., Best, L. G., Umans, J., Davey-Smith, G., Onat, A., Nakagawa, H., Sakurai, M., Nakamura, K., Morikawa, Y., Njølstad, I., Mathiesen, E. B., Wilsgaard, T., Sundström, J., Gaziano, J. M., Ridker, P. M., Marmot, M., Clarke, R., Collins, R., Fletcher, A., Brunner, E., Shipley, M., Kivimaki, M., Buring, J., Rifai, N., Cook, N., Ford, I., Robertson, M., Marín Ibañez, A., Feskens, E. J M, and Geleijnse, J. M.

Published
2015

15. Genome-wide linkage scan for plasma high density lipoprotein cholesterol, apolipoprotein A-1 and triglyceride variation among American Indian populations: the Strong Heart Family Study

Author

Howard, B V, Diego, V P, Lee, E T, Almasy, L, Goring, H H H, Best, L G, Shara, N M, Li, X, MacCluer, J W, Fabsitz, R R, North, K. E, Cole, S A, Monda, K L, Laston, S, and Haack, K

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

Recent studies have identified chromosomal regions linked to variation in high density lipoprotein cholesterol (HDL-C), apolipoprotein A-1 (Apo A-1) and triglyceride (TG), although results have been inconsistent and previous studies of American Indian populations are limited

Published
2009
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16. Sex-specific interaction between APOE genotype and carbohydrate intake affects plasma HDL-C levels: the Strong Heart Family Study

Author

Howard, B. V., MacCluer, J. W., Mosher, M. J., North, K. E., Best, L. G., Lee, E. T., Lange, L. A., and Fabsitz, R. R.

Subjects
nutritional and metabolic diseases, lipids (amino acids, peptides, and proteins)
Abstract

Low plasma levels of high-density lipoprotein cholesterol (HDL-C) are identified as a risk factor for cardiovascular disease (CVD). Sexual dimorphism, however, is widely reported in both HDL-C and CVD, with the underlying explanations of these sexual differences not fully understood. HDL-C is a complex trait influenced by both genes and dietary factors. Here we examine evidence for a sex-specific effect of APOE and the macronutrient carbohydrate on HDL-C, triglycerides (TG) and apoprotein A-1 (ApoA-1) in a sample of 326 male and 423 female participants of the Strong Heart Family Study (SHFS). Using general estimating equations in SAS to account for kinship correlations, stratifying by sex, and adjusting for age, body mass index (BMI) and SHS center, we examine the relationship between APOE genotype and carbohydrate intake on circulating levels of HDL-C, TG, and ApoA-1 through a series of carbohydrate-by-sex interactions and stratified analyses. APOE-by-carbohydrate intake shows significant sex-specific effects. All males had similar decreases in HDL-C levels associated with increased carbohydrate intake. However, only those females with APOE-4 alleles showed significantly lower HDL-C levels as their percent of carbohydrate intake increased, while no association was noted between carbohydrate intake and HDL-C in those females without an APOE-4 allele. These findings demonstrate the importance of understanding sex differences in gene-by-nutrient interaction when examining the complex architecture of HDL-C variation.

Published
2008
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17. Linkage analysis of LDL cholesterol in American Indian populations: the Strong Heart Family Study

Author

Laston, S., Almasy, L., Fabsitz, R. R., Göring, H. H.H., Diego, V. P., Lee, E. T., Best, L. G., Cantu, T., MacCluer, J. W., Cole, S. A., North, K. E., and Howard, B. V.

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

Previous studies have demonstrated that low density lipoprotein cholesterol (LDL-C) concentration is influenced by both genes and environment. Although rare genetic variants associated with Mendelian causes of increased LDL-C are known, only one common genetic variant has been identified, the apolipoprotein E gene (

Published
2006
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18. Bivariate genetic association of KIAA1797 with heart rate in American Indians: the Strong Heart Family Study

Author

Melton, P. E., primary, Rutherford, S., additional, Voruganti, V. S., additional, Goring, H. H. H., additional, Laston, S., additional, Haack, K., additional, Comuzzie, A. G., additional, Dyer, T. D., additional, Johnson, M. P., additional, Kent, J. W., additional, Curran, J. E., additional, Moses, E. K., additional, Blangero, J., additional, Barac, A., additional, Lee, E. T., additional, Best, L. G., additional, Fabsitz, R. R., additional, Devereux, R. B., additional, Okin, P. M., additional, Bella, J. N., additional, Broeckel, U., additional, Howard, B. V., additional, MacCluer, J. W., additional, Cole, S. A., additional, and Almasy, L., additional

Published
2010
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23. Linkage analysis of LDL cholesterol in American Indian populations: the Strong Heart Family Study

Author

North, K. E., Göring, H. H. H., Cole, S. A., Diego, V. P., Almasy, L., Laston, S., Cantu, T., Howard, B. V., Lee, E. T., Best, L. G., Fabsitz, R. R., and MacCluer, J. W.

Abstract

Previous studies have demonstrated that low density lipoprotein cholesterol (LDL-C) concentration is influenced by both genes and environment. Although rare genetic variants associated with Mendelian causes of increased LDL-C are known, only one common genetic variant has been identified, the apolipoprotein E gene (APOE). In an attempt to localize quantitative trait loci (QTLs) influencing LDL-C, we conducted a genome-wide linkage scan of LDL-C in participants of the Strong Heart Family Study (SHFS). Nine hundred eighty men and women, age 18 years or older, in 32 extended families at three centers (in Arizona, Oklahoma, and North and South Dakota) were phenotyped for LDL-C concentration and other risk factors. Using a variance component approach and the program SOLAR, and after accounting for the effects of covariates, we detected a QTL influencing LDL-C on chromosome 19, nearest marker D19S888 at 19q13.41 [logarithm of odds (LOD) = 4.3] in the sample from the Dakotas. This region on chromosome 19 includes many possible candidate genes, including the APOE/C1/C4/C2 gene cluster. In follow-up association analyses, no significant evidence for an association was detected with the APOE*ε2 and APOE*ε4 alleles (P = 0.76 and P = 0.53, respectively). Suggestive evidence of linkage to LDL-C was detected on chromosomes 3q, 4q, 7p, 9q, 10p, 14q, and 17q. These linkage signals overlap positive findings for lipid-related traits and harbor plausible candidate genes for LDL-C.

Published
2006

24. Myocardial mechano-energetic efficiency and insulin resistance in non-diabetic members of the Strong Heart Study cohort

Author

Costantino Mancusi, Mary J. Roman, Elisa T. Lee, Wenyu Wang, Richard B. Devereux, Lyle G. Best, Ying Zhang, Barbara V. Howard, Giovanni de Simone, Mancusi, C., De Simone, G., Best, L. G., Wang, W., Zhang, Y., Roman, M. J., Lee, E. T., Howard, B. V., and Devereux, R. B.

Subjects
Adult, Male, medicine.medical_specialty, lcsh:Diseases of the circulatory (Cardiovascular) system, Adolescent, Endocrinology, Diabetes and Metabolism, Heart Ventricles, 030209 endocrinology & metabolism, Blood Pressure, 030204 cardiovascular system & hematology, Models, Biological, Ventricular Function, Left, Myocardial metabolism, 03 medical and health sciences, Ventricular Dysfunction, Left, Young Adult, 0302 clinical medicine, Insulin resistance, Oxygen Consumption, Heart Rate, Risk Factors, Diabetes mellitus, Internal medicine, medicine, Humans, Mass index, Aged, Original Investigation, Aged, 80 and over, medicine.diagnostic_test, business.industry, Myocardium, Cardiac function, Stroke volume, Middle Aged, medicine.disease, Blood pressure, Echocardiography, lcsh:RC666-701, Population study, Female, Metabolic syndrome, Insulin Resistance, Cardiology and Cardiovascular Medicine, Lipid profile, business, Energy Metabolism
Abstract

Background Myocardial energetic efficiency (MEE), is a strong predictor of CV events in hypertensive patient and is reduced in patients with diabetes and metabolic syndrome. We hypothesized that severity of insulin resistance (by HOMA-IR) negatively influences MEE in participants from the Strong Heart Study (SHS). Methods We selected non-diabetic participants (n = 3128, 47 ± 17 years, 1807 women, 1447 obese, 870 hypertensive) free of cardiovascular (CV) disease, by merging two cohorts (Strong Heart Study and Strong Heart Family Study, age range 18–93). MEE was estimated as stroke work (SW = systolic blood pressure [SBP] × stroke volume [SV])/“double product” of SBP × heart rate (HR), as an estimate of O2 consumption, which can be simplified as SV/HR ratio and expressed in ml/sec. Due to the strong correlation, MEE was normalized by left ventricular (LV) mass (MEEi). Results Linear trend analyses showed that with increasing quartiles of HOMA-IR patients were older, more likely to be women, obese and hypertensive, with a trend toward a worse lipid profile (all p for trend Conclusions Severity of insulin resistance has significant and independent negative impact on myocardial mechano-energetic efficiency in nondiabetic individual from a population study of American Indians. Trial registration number NCT00005134, Name of registry: Strong Heart Study, URL of registry: https://clinicaltrials.gov/ct2/show/NCT00005134, Date of registration: May 25, 2000, Date of enrolment of the first participant to the trial: September 1988

Published
2019
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25. Plasminogen activator inhibitor-1 is associated with leukocyte telomere length in American Indians: findings from the Strong Heart Family Study.

Author

Peng H, Yeh F, Lin J, Best LG, Cole SA, Lee ET, Howard BV, and Zhao J

Subjects
Adult, Alcohol Drinking, Arizona ethnology, Blood Glucose analysis, Blood Pressure, Cross-Sectional Studies, Exercise, Female, Healthy Volunteers, Humans, Insulin blood, Kidney Function Tests, Life Style, Longitudinal Studies, Male, Middle Aged, North Dakota ethnology, Obesity complications, Oklahoma ethnology, Smoking, South Dakota ethnology, United States, Young Adult, Indians, North American, Leukocytes cytology, Plasminogen Activator Inhibitor 1 metabolism, Telomere ultrastructure
Abstract

Essentials Plasminogen activator inhibitor-1 (PAI-1) advanced cellular senescence in experiment studies. No population study exists on the association between PAI-1 and biological aging in American Indians. We found cross-sectional and longitudinal associations between higher PAI-1 and shorter telomere length. Our findings suggest a pathway linking PAI-1 with biological aging beyond metabolic factors., Summary: Background Plasminogen activator inhibitor-1 (PAI-1) promotes cellular aging both in vitro and in vivo. Telomere length is a marker of biological aging. Objectives To examine the cross-sectional and longitudinal associations between plasma PAI-1 and leukocyte telomere length in a large-scale epidemiological study of American Indians. Methods We measured leukocyte telomere length (LTL) and plasma PAI-1 in 2560 American Indians who were free of overt cardiovascular disease (CVD) and participated in the Strong Heart Family Study (SHFS) clinical examination in 2001-2003. LTL and PAI-1 were repeatedly measured in 475 participants who attended SHFS clinical visits in both 2001-2003 and 1998-1999. A generalized estimating equation model was used to examine the cross-sectional and longitudinal associations between PAI-1 and LTL, adjusting for known risk factors. Results A higher level of plasma PAI-1 was negatively associated with shorter age-adjusted LTL (β = -0.023; 95% CI, -0.034 to -0.013). This association was attenuated (β = -0.015; 95% CI, -0.029 to -0.002) after adjustments for demographics, study site, lifestyle (smoking, drinking and physical activity) and metabolic factors (obesity, blood pressure, fasting glucose, insulin, lipids and kidney function). Further adjustment for hsCRP did not change this association (β = -0.015; 95% CI, -0.029 to -0.001). Longitudinal analysis revealed that change in plasma PAI-1 was also inversely associated with change in LTL after adjusting for demographics, follow-up years, lifestyle factors, changes in metabolic factors, baseline levels of PAI-1 and LTL (β = -0.0005; 95% CI, -0.0009 to -0.0001). Conclusions A higher level of plasma PAI-1 was associated with shorter LTL in American Indians. This finding may suggest a potential role of PAI-1 in biological aging among American Indians., (© 2017 International Society on Thrombosis and Haemostasis.)

Published
2017
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26. Computer-assisted DREZ microcoagulation: posttraumatic spinal deafferentation pain.

Author

Edgar RE, Best LG, Quail PA, and Obert AD

Subjects
Catheter Ablation, Causalgia epidemiology, Causalgia etiology, Electrocoagulation adverse effects, Electrophysiology, Evaluation Studies as Topic, Follow-Up Studies, Humans, Laminectomy, Laser Coagulation, Microsurgery adverse effects, Prevalence, Causalgia surgery, Electrocoagulation methods, Microsurgery methods, Spinal Cord Injuries complications, Spinal Nerve Roots surgery, Therapy, Computer-Assisted
Abstract

Our data demonstrate that approximately 23-29% of standard dorsal root entry zone (DREZ) microcoagulation procedures fail to relieve pain due to inadequate thermal lesions and that approximately 39% fail due to insufficient superior extent of lesions. The remaining failures are related to inadequate lesion placement, improper selection of patients, and, rarely, posttraumatic spinal deafferentation pain resulting from other non-DREZ mechanisms. Computer-assisted DREZ microcoagulation is a satisfactory procedure to treat intractable posttraumatic spinal deafferentation pain, brachial plexus avulsion pain, and lumbosacral nerve root avulsion pain. In all these conditions we have identified areas of abnormal focal hyperactivity in the DREZ area. Perhaps this procedure can be applied to other central pain conditions if, using this technique, abnormal focal hyperactivity is demonstrated to be present.

Published
1993

27. Familial posterior helical ear pits and Wiedemann-Beckwith syndrome.

Author

Best LG

Subjects
Beckwith-Wiedemann Syndrome diagnostic imaging, Child, Child, Preschool, Female, Genes, Dominant genetics, Humans, Infant, Male, Osteopetrosis genetics, Pedigree, Radiography, Beckwith-Wiedemann Syndrome genetics, Ear, External abnormalities
Abstract

Multiple cases of posterior helical ear pits (PHEP) with apparent autosomal dominant inheritance in a very large family are reported. There are at least 2 cases of Wiedemann-Beckwith syndrome (WBS) within this family. Three other instances of familial PHEP and/or WBS are presented. An individual with a somewhat atypical osteopetrosis and PHEP is described. The previous literature of PHEP and the association with WBS is reviewed.

Published
1991
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28. Chromosome abnormality in Kallmann syndrome.

Author

Best LG, Wasdahl WA, Larson LM, and Sturlaugson J

Subjects
Adult, Bone and Bones abnormalities, Cells, Cultured, Humans, Karyotyping, Male, Olfactory Nerve abnormalities, Syndrome, Chromosomes, Human, Pair 12, Chromosomes, Human, Pair 7, Hypogonadism genetics, Olfaction Disorders genetics, Translocation, Genetic
Abstract

We report on an individual with Kallman syndrome (KS) and a balanced de novo translocation (7;12)(q22,q24). None of 6 full sibs, 3 half-sibs, or parents have KS or this chromosome translocation. This is the only known report of KS with a chromosome abnormality. This may represent a spurious association or genetic heterogeneity vis-a-vis the reported linkage of KS to the steroid sulphatase gene on the X chromosome. The pathophysiology and genetics of KS are discussed.

Published
1990
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29. Wiedemann-Beckwith syndrome: autosomal-dominant inheritance in a family.

Author

Best LG and Hoekstra RE

Subjects
Adult, Child, Female, Genotype, Gigantism complications, Hernia, Umbilical complications, Humans, Infant, Infant, Newborn, Macroglossia complications, Male, Pedigree, Phenotype, Syndrome, Chromosome Aberrations, Chromosome Disorders, Gigantism genetics, Hernia, Umbilical genetics, Macroglossia genetics
Abstract

We report four additional cases of Wiedemann-Beckwith syndrome (WBS): A mother, her brother, and two of her children (half-sibs). Theories of the genetic transmission of the WBS are reviewed. The trait in this family appears to be an autosomal-dominant with variable expressivity. A theory of delayed mutation of an unstable premutated gene is discussed and an interpretation and observations are offered which could alter slightly the expected pattern of inheritance. Eighty-eight other family members were screened for evidence of WBS and noteworthy findings are presented.

Published
1981
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32. Familial duodenal atresia: a report of two families and review.

Author

Best LG, Wiseman NE, and Chudley AE

Subjects
Consanguinity, Duodenal Obstruction surgery, Female, Genes, Recessive, Humans, Infant, Newborn, Intestinal Atresia surgery, Male, Pedigree, Recurrence, Duodenal Obstruction congenital, Intestinal Atresia genetics
Abstract

We report on 2 families with recurrence of uncomplicated duodenal atresia. The presence of consanguinity in one family, the frequent occurrence of consanguinity in parents of affected children previously reported, and the equal sex ratio suggest autosomal recessive inheritance.

Published
1989
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34. Cryosurgery for control of vertigo.

Author

Tabor JR, Best LG, and Metz MJ

Subjects
Adult, Female, Humans, Male, Meniere Disease surgery, Middle Aged, Cryosurgery, Ear, Inner surgery, Vertigo surgery
Published
1969

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