Search

Your search keyword '"Jang, K. L."' showing total 110 results
Start Over Author "Jang, K. L."
110 results on '"Jang, K. L."'

3. The CODATwins Project: The Current Status and Recent Findings of COllaborative Project of Development of Anthropometrical Measures in Twins

Author

Silventoinen, K., primary, Jelenkovic, A., additional, Yokoyama, Y., additional, Sund, R., additional, Sugawara, M., additional, Tanaka, M., additional, Matsumoto, S., additional, Bogl, L. H., additional, Freitas, D. L., additional, Maia, J. A., additional, Hjelmborg, J. v. B., additional, Aaltonen, S., additional, Piirtola, M., additional, Latvala, A., additional, Calais-Ferreira, L., additional, Oliveira, V. C., additional, Ferreira, P. H., additional, Ji, F., additional, Ning, F., additional, Pang, Z., additional, Ordoñana, J. R., additional, Sánchez-Romera, J. F., additional, Colodro-Conde, L., additional, Burt, S. A., additional, Klump, K. L., additional, Martin, N. G., additional, Medland, S. E., additional, Montgomery, G. W., additional, Kandler, C., additional, McAdams, T. A., additional, Eley, T. C., additional, Gregory, A. M., additional, Saudino, K. J., additional, Dubois, L., additional, Boivin, M., additional, Brendgen, M., additional, Dionne, G., additional, Vitaro, F., additional, Tarnoki, A. D., additional, Tarnoki, D. L., additional, Haworth, C. M. A., additional, Plomin, R., additional, Öncel, S. Y., additional, Aliev, F., additional, Medda, E., additional, Nisticò, L., additional, Toccaceli, V., additional, Craig, J. M., additional, Saffery, R., additional, Siribaddana, S. H., additional, Hotopf, M., additional, Sumathipala, A., additional, Rijsdijk, F., additional, Jeong, H.-U., additional, Spector, T., additional, Mangino, M., additional, Lachance, G., additional, Gatz, M., additional, Butler, D. A., additional, Gao, W., additional, Yu, C., additional, Li, L., additional, Bayasgalan, G., additional, Narandalai, D., additional, Harden, K. P., additional, Tucker-Drob, E. M., additional, Christensen, K., additional, Skytthe, A., additional, Kyvik, K. O., additional, Derom, C. A., additional, Vlietinck, R. F., additional, Loos, R. J. F., additional, Cozen, W., additional, Hwang, A. E., additional, Mack, T. M., additional, He, M., additional, Ding, X., additional, Silberg, J. L., additional, Maes, H. H., additional, Cutler, T. L., additional, Hopper, J. L., additional, Magnusson, P. K. E., additional, Pedersen, N. L., additional, Dahl Aslan, A. K., additional, Baker, L. A., additional, Tuvblad, C., additional, Bjerregaard-Andersen, M., additional, Beck-Nielsen, H., additional, Sodemann, M., additional, Ullemar, V., additional, Almqvist, C., additional, Tan, Q., additional, Zhang, D., additional, Swan, G. E., additional, Krasnow, R., additional, Jang, K. L., additional, Knafo-Noam, A., additional, Mankuta, D., additional, Abramson, L., additional, Lichtenstein, P., additional, Krueger, R. F., additional, McGue, M., additional, Pahlen, S., additional, Tynelius, P., additional, Rasmussen, F., additional, Duncan, G. E., additional, Buchwald, D., additional, Corley, R. P., additional, Huibregtse, B. M., additional, Nelson, T. L., additional, Whitfield, K. E., additional, Franz, C. E., additional, Kremen, W. S., additional, Lyons, M. J., additional, Ooki, S., additional, Brandt, I., additional, Nilsen, T. S., additional, Harris, J. R., additional, Sung, J., additional, Park, H. A., additional, Lee, J., additional, Lee, S. J., additional, Willemsen, G., additional, Bartels, M., additional, van Beijsterveldt, C. E. M., additional, Llewellyn, C. H., additional, Fisher, A., additional, Rebato, E., additional, Busjahn, A., additional, Tomizawa, R., additional, Inui, F., additional, Watanabe, M., additional, Honda, C., additional, Sakai, N., additional, Hur, Y.-M., additional, Sørensen, T. I. A., additional, Boomsma, D. I., additional, and Kaprio, J., additional

Published
2019
Full Text
View/download PDF

6. The CODATwins Project: The Current Status and Recent Findings of COllaborative Project of Development of Anthropometrical Measures in Twins

Author

Silventoinen, K., Jelenkovic, A., Yokoyama, Y., Sund, R., Sugawara, M., Tanaka, M., Matsumoto, S., Bogl, L. H., Freitas, D. L., Maia, J. A., Hjelmborg, J. v. B., Aaltonen, S., Piirtola, M., Latvala, A., Calais-Ferreira, L., Oliveira, V. C., Ferreira, P. H., Ji, F., Ning, F., Pang, Z., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Burt, S. A., Klump, K. L., Martin, N. G., Medland, S. E., Montgomery, G. W., Kandler, C., McAdams, T. A., Eley, T. C., Gregory, A. M., Saudino, K. J., Dubois, L., Boivin, M., Brendgen, M., Dionne, G., Vitaro, F., Tarnoki, A. D., Tarnoki, D. L., Haworth, C. M. A., Plomin, R., Oncel, S. Y., Aliev, F., Medda, E., Nistico, L., Toccaceli, V., Craig, J. M., Saffery, R., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Jeong, H. -U., Spector, T., Mangino, M., Lachance, G., Gatz, M., Butler, D. A., Gao, W., Yu, C., Li, L., Bayasgalan, G., Narandalai, D., Harden, K. P., Tucker-Drob, E. M., Christensen, K., Skytthe, A., Kyvik, K. O., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Cozen, W., Hwang, A. E., Mack, T. M., He, M., Ding, X., Silberg, J. L., Maes, H. H., Cutler, T. L., Hopper, J. L., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, A. K., Baker, L. A., Tuvblad, C., Bjerregaard-Andersen, M., Beck-Nielsen, H., Sodemann, M., Ullemar, V., Almqvist, C., Tan, Q., Zhang, D., Swan, G. E., Krasnow, R., Jang, K. L., Knafo-Noam, A., Mankuta, D., Abramson, L., Lichtenstein, P., Krueger, R. F., McGue, M., Pahlen, S., Tynelius, P., Rasmussen, F., Duncan, G. E., Buchwald, D., Corley, R. P., Huibregtse, B. M., Nelson, T. L., Whitfield, K. E., Franz, C. E., Kremen, W. S., Lyons, M. J., Ooki, S., Brandt, I., Nilsen, T. S., Harris, J. R., Sung, J., Park, H. A., Lee, J., Lee, S. J., Willemsen, G., Bartels, M., Van Beijsterveldt, C. E. M., Llewellyn, C. H., Fisher, A., Rebato, E., Busjahn, A., Tomizawa, R., Inui, F., Watanabe, M., Honda, C., Sakai, N., Hur, Y. -M., Sørensen, T. I. A., Boomsma, D. I., Kaprio, J., Silventoinen, K., Jelenkovic, A., Yokoyama, Y., Sund, R., Sugawara, M., Tanaka, M., Matsumoto, S., Bogl, L. H., Freitas, D. L., Maia, J. A., Hjelmborg, J. v. B., Aaltonen, S., Piirtola, M., Latvala, A., Calais-Ferreira, L., Oliveira, V. C., Ferreira, P. H., Ji, F., Ning, F., Pang, Z., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Burt, S. A., Klump, K. L., Martin, N. G., Medland, S. E., Montgomery, G. W., Kandler, C., McAdams, T. A., Eley, T. C., Gregory, A. M., Saudino, K. J., Dubois, L., Boivin, M., Brendgen, M., Dionne, G., Vitaro, F., Tarnoki, A. D., Tarnoki, D. L., Haworth, C. M. A., Plomin, R., Oncel, S. Y., Aliev, F., Medda, E., Nistico, L., Toccaceli, V., Craig, J. M., Saffery, R., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Jeong, H. -U., Spector, T., Mangino, M., Lachance, G., Gatz, M., Butler, D. A., Gao, W., Yu, C., Li, L., Bayasgalan, G., Narandalai, D., Harden, K. P., Tucker-Drob, E. M., Christensen, K., Skytthe, A., Kyvik, K. O., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Cozen, W., Hwang, A. E., Mack, T. M., He, M., Ding, X., Silberg, J. L., Maes, H. H., Cutler, T. L., Hopper, J. L., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, A. K., Baker, L. A., Tuvblad, C., Bjerregaard-Andersen, M., Beck-Nielsen, H., Sodemann, M., Ullemar, V., Almqvist, C., Tan, Q., Zhang, D., Swan, G. E., Krasnow, R., Jang, K. L., Knafo-Noam, A., Mankuta, D., Abramson, L., Lichtenstein, P., Krueger, R. F., McGue, M., Pahlen, S., Tynelius, P., Rasmussen, F., Duncan, G. E., Buchwald, D., Corley, R. P., Huibregtse, B. M., Nelson, T. L., Whitfield, K. E., Franz, C. E., Kremen, W. S., Lyons, M. J., Ooki, S., Brandt, I., Nilsen, T. S., Harris, J. R., Sung, J., Park, H. A., Lee, J., Lee, S. J., Willemsen, G., Bartels, M., Van Beijsterveldt, C. E. M., Llewellyn, C. H., Fisher, A., Rebato, E., Busjahn, A., Tomizawa, R., Inui, F., Watanabe, M., Honda, C., Sakai, N., Hur, Y. -M., Sørensen, T. I. A., Boomsma, D. I., and Kaprio, J.

Published
2019

7. The CODATwins Project: The Current Status and Recent Findings of COllaborative Project of Development of Anthropometrical Measures in Twins

Author

Silventoinen, K, Jelenkovic, A, Yokoyama, Y, Sund, R, Sugawara, M, Tanaka, M, Matsumoto, S, Bogl, L H, Freitas, D L, Maia, J A, Hjelmborg, J V B, Aaltonen, S, Piirtola, M, Latvala, A, Calais-Ferreira, L, Oliveira, V C, Ferreira, P H, Ji, F, Ning, F, Pang, Z, Ordoñana, J R, Sánchez-Romera, J F, Colodro-Conde, L, Burt, S A, Klump, K L, Martin, N G, Medland, S E, Montgomery, G W, Kandler, C, McAdams, T A, Eley, T C, Gregory, A M, Saudino, K J, Dubois, L, Boivin, M, Brendgen, M, Dionne, G, Vitaro, F, Tarnoki, A D, Tarnoki, D L, Haworth, C M A, Plomin, R, Öncel, S Y, Aliev, F, Medda, E, Nisticò, L, Toccaceli, V, Craig, J M, Saffery, R, Siribaddana, S H, Hotopf, M, Sumathipala, A, Rijsdijk, F, Jeong, H-U, Spector, T, Mangino, M, Lachance, G, Gatz, M, Butler, D A, Gao, W, Yu, C, Li, L, Bayasgalan, G, Narandalai, D, Harden, K P, Tucker-Drob, E M, Christensen, K, Skytthe, A, Kyvik, K O, Derom, C A, Vlietinck, R F, Loos, R J F, Cozen, W, Hwang, A E, Mack, T M, He, M, Ding, X, Silberg, J L, Maes, H H, Cutler, T L, Hopper, J L, Magnusson, P K E, Pedersen, N L, Dahl Aslan, A K, Baker, L A, Tuvblad, C, Bjerregaard-Andersen, M, Beck-Nielsen, H, Sodemann, M, Ullemar, V, Almqvist, C, Tan, Q, Zhang, D, Swan, G E, Krasnow, R, Jang, K L, Knafo-Noam, A, Mankuta, D, Abramson, L, Lichtenstein, P, Krueger, R F, McGue, M, Pahlen, S, Tynelius, P, Rasmussen, F, Duncan, G E, Buchwald, D, Corley, R P, Huibregtse, B M, Nelson, T L, Whitfield, K E, Franz, C E, Kremen, W S, Lyons, M J, Ooki, S, Brandt, I, Nilsen, T S, Harris, J R, Sung, J, Park, H A, Lee, J, Lee, S J, Willemsen, Gonneke, Bartels, Meike, van Beijsterveldt, C.E.M., Llewellyn, C H, Fisher, A, Rebato, E, Busjahn, A, Tomizawa, R, Inui, F, Watanabe, M, Honda, C, Sakai, N, Hur, Y-M, Sørensen, T I A, Boomsma, D.I., Kaprio, J, Silventoinen, K, Jelenkovic, A, Yokoyama, Y, Sund, R, Sugawara, M, Tanaka, M, Matsumoto, S, Bogl, L H, Freitas, D L, Maia, J A, Hjelmborg, J V B, Aaltonen, S, Piirtola, M, Latvala, A, Calais-Ferreira, L, Oliveira, V C, Ferreira, P H, Ji, F, Ning, F, Pang, Z, Ordoñana, J R, Sánchez-Romera, J F, Colodro-Conde, L, Burt, S A, Klump, K L, Martin, N G, Medland, S E, Montgomery, G W, Kandler, C, McAdams, T A, Eley, T C, Gregory, A M, Saudino, K J, Dubois, L, Boivin, M, Brendgen, M, Dionne, G, Vitaro, F, Tarnoki, A D, Tarnoki, D L, Haworth, C M A, Plomin, R, Öncel, S Y, Aliev, F, Medda, E, Nisticò, L, Toccaceli, V, Craig, J M, Saffery, R, Siribaddana, S H, Hotopf, M, Sumathipala, A, Rijsdijk, F, Jeong, H-U, Spector, T, Mangino, M, Lachance, G, Gatz, M, Butler, D A, Gao, W, Yu, C, Li, L, Bayasgalan, G, Narandalai, D, Harden, K P, Tucker-Drob, E M, Christensen, K, Skytthe, A, Kyvik, K O, Derom, C A, Vlietinck, R F, Loos, R J F, Cozen, W, Hwang, A E, Mack, T M, He, M, Ding, X, Silberg, J L, Maes, H H, Cutler, T L, Hopper, J L, Magnusson, P K E, Pedersen, N L, Dahl Aslan, A K, Baker, L A, Tuvblad, C, Bjerregaard-Andersen, M, Beck-Nielsen, H, Sodemann, M, Ullemar, V, Almqvist, C, Tan, Q, Zhang, D, Swan, G E, Krasnow, R, Jang, K L, Knafo-Noam, A, Mankuta, D, Abramson, L, Lichtenstein, P, Krueger, R F, McGue, M, Pahlen, S, Tynelius, P, Rasmussen, F, Duncan, G E, Buchwald, D, Corley, R P, Huibregtse, B M, Nelson, T L, Whitfield, K E, Franz, C E, Kremen, W S, Lyons, M J, Ooki, S, Brandt, I, Nilsen, T S, Harris, J R, Sung, J, Park, H A, Lee, J, Lee, S J, Willemsen, Gonneke, Bartels, Meike, van Beijsterveldt, C.E.M., Llewellyn, C H, Fisher, A, Rebato, E, Busjahn, A, Tomizawa, R, Inui, F, Watanabe, M, Honda, C, Sakai, N, Hur, Y-M, Sørensen, T I A, Boomsma, D.I., and Kaprio, J

Abstract

The COllaborative project of Development of Anthropometrical measures in Twins (CODATwins) project is a large international collaborative effort to analyze individual-level phenotype data from twins in multiple cohorts from different environments. The main objective is to study factors that modify genetic and environmental variation of height, body mass index (BMI, kg/m2) and size at birth, and additionally to address other research questions such as long-term consequences of birth size. The project started in 2013 and is open to all twin projects in the world having height and weight measures on twins with information on zygosity. Thus far, 54 twin projects from 24 countries have provided individual-level data. The CODATwins database includes 489,981 twin individuals (228,635 complete twin pairs). Since many twin cohorts have collected longitudinal data, there is a total of 1,049,785 height and weight observations. For many cohorts, we also have information on birth weight and length, own smoking behavior and own or parental education. We found that the heritability estimates of height and BMI systematically changed from infancy to old age. Remarkably, only minor differences in the heritability estimates were found across cultural-geographic regions, measurement time and birth cohort for height and BMI. In addition to genetic epidemiological studies, we looked at associations of height and BMI with education, birth weight and smoking status. Within-family analyses examined differences within same-sex and opposite-sex dizygotic twins in birth size and later development. The CODATwins project demonstrates the feasibility and value of international collaboration to address gene-by-exposure interactions that require large sample sizes and address the effects of different exposures across time, geographical regions and socioeconomic status.

Published
2019
Full Text
View/download PDF

8. Differences in genetic and environmental variation in adult BMI by sex, age, time period, and region : An individual-based pooled analysis of 40 twin cohorts

Author

Silventoinen, K., Jelenkovic, A., Sund, R., Yokoyama, Y., Hur, Y. -M, Cozen, W., Hwang, A. E., Mack, T. M., Honda, C., Inui, F., Iwatani, Y., Watanabe, M., Tomizawa, R., Pietilainen, K. H., Rissanen, A., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Tan, Q., Zhang, D., Pang, Z., Piirtola, M., Aaltonen, S., Oncel, S. Y., Aliev, F., Rebato, E., Hjelmborg, J. B., Christensen, K., Skytthe, A., Kyvik, K. O., Silberg, J. L., Eaves, L. J., Cutler, T. L., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Song, Y. -M, Yang, S., Lee, K., Franz, C. E., Kremen, W. S., Lyons, M. J., Busjahn, A., Nelson, T. L., Whitfield, K. E., Kandler, C., Jang, K. L., Gatz, M., Butler, D. A., Stazi, M. A., Fagnani, C., D'Ippolito, C., Duncan, G. E., Buchwald, D., Martin, N. G., Medland, S. E., Montgomery, G. W., Jeong, H. -U, Swan, G. E., Krasnow, R., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, Anna K., McAdams, T. A., Eley, T. C., Gregory, A. M., Tynelius, P., Baker, L. A., Tuvblad, C., Bayasgalan, G., Narandalai, D., Spector, T. D., Mangino, M., Lachance, G., Burt, S. A., Klump, K. L., Harris, J. R., Brandt, I., Nilsen, T. S., Krueger, R. F., McGue, M., Pahlen, S., Corley, R. P., Huibregtse, B. M., Bartels, M., Van Beijsterveldt, C. E. M., Willemsen, G., Goldberg, J. H., Rasmussen, F., Tarnoki, A. D., Tarnoki, D. L., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Hopper, J. L., Sung, J., Maes, H. H., Turkheimer, E., Boomsma, D. I., Sørensen, T. I. A., Kaprio, J., Silventoinen, K., Jelenkovic, A., Sund, R., Yokoyama, Y., Hur, Y. -M, Cozen, W., Hwang, A. E., Mack, T. M., Honda, C., Inui, F., Iwatani, Y., Watanabe, M., Tomizawa, R., Pietilainen, K. H., Rissanen, A., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Tan, Q., Zhang, D., Pang, Z., Piirtola, M., Aaltonen, S., Oncel, S. Y., Aliev, F., Rebato, E., Hjelmborg, J. B., Christensen, K., Skytthe, A., Kyvik, K. O., Silberg, J. L., Eaves, L. J., Cutler, T. L., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Song, Y. -M, Yang, S., Lee, K., Franz, C. E., Kremen, W. S., Lyons, M. J., Busjahn, A., Nelson, T. L., Whitfield, K. E., Kandler, C., Jang, K. L., Gatz, M., Butler, D. A., Stazi, M. A., Fagnani, C., D'Ippolito, C., Duncan, G. E., Buchwald, D., Martin, N. G., Medland, S. E., Montgomery, G. W., Jeong, H. -U, Swan, G. E., Krasnow, R., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, Anna K., McAdams, T. A., Eley, T. C., Gregory, A. M., Tynelius, P., Baker, L. A., Tuvblad, C., Bayasgalan, G., Narandalai, D., Spector, T. D., Mangino, M., Lachance, G., Burt, S. A., Klump, K. L., Harris, J. R., Brandt, I., Nilsen, T. S., Krueger, R. F., McGue, M., Pahlen, S., Corley, R. P., Huibregtse, B. M., Bartels, M., Van Beijsterveldt, C. E. M., Willemsen, G., Goldberg, J. H., Rasmussen, F., Tarnoki, A. D., Tarnoki, D. L., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Hopper, J. L., Sung, J., Maes, H. H., Turkheimer, E., Boomsma, D. I., Sørensen, T. I. A., and Kaprio, J.

Abstract

Background: Genes and the environment contribute to variation in adult body mass index [BMI (in kg/m2)], but factors modifying these variance components are poorly understood. Objective: We analyzed genetic and environmental variation in BMI between men and women from young adulthood to old age from the 1940s to the 2000s and between cultural-geographic regions representing high (North America and Australia), moderate (Europe), and low (East Asia) prevalence of obesity. Design: We used genetic structural equation modeling to analyze BMI in twins ≥20 y of age from 40 cohorts representing 20 countries (140,379 complete twin pairs). Results: The heritability of BMI decreased from 0.77 (95% CI: 0.77, 0.78) and 0.75 (95% CI: 0.74, 0.75) in men and women 20-29 y of age to 0.57 (95% CI: 0.54, 0.60) and 0.59 (95% CI: 0.53, 0.65) in men 70-79 y of age and women 80 y of age, respectively. The relative influence of unique environmental factors correspondingly increased. Differences in the sets of genes affecting BMI in men and women increased from 20-29 to 60-69 y of age. Mean BMI and variances in BMI increased from the 1940s to the 2000s and were greatest in North America and Australia, followed by Europe and East Asia. However, heritability estimates were largely similar over measurement years and between regions. There was no evidence of environmental factors shared by co-twins affecting BMI. Conclusions: The heritability of BMI decreased and differences in the sets of genes affecting BMI in men and women increased from young adulthood to old age. The heritability of BMI was largely similar between cultural-geographic regions and measurement years, despite large differences in mean BMI and variances in BMI. Our results show a strong influence of genetic factors on BMI, especially in early adulthood, regardless of the obesity level in the population.

Published
2017
Full Text
View/download PDF

9. Genetic and environmental influences on adult human height across birth cohorts from 1886 to 1994

Author

Jelenkovic, A., Hur, Y. -M, Sund, R., Yokoyama, Y., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Tan, Q., Zhang, D., Pang, Z., Aaltonen, S., Heikkilä, K., Öncel, S.Y., Aliev, F., Rebato, E., Tarnoki, A. D., Tarnoki, D. L., Christensen, K., Skytthe, A., Kyvik, K. O., Silberg, J. L., Eaves, L. J., Maes, H. H., Cutler, T. L., Hopper, J. L., Ordoñana, J. R., Sánchez-Romera, J. F., Colodro-Conde, L., Cozen, W., Hwang, A. E., Mack, T. M., Sung, J., Song, Y. -M, Yang, S., Lee, K., Franz, C. E., Kremen, W. S., Lyons, M. J., Busjahn, A., Nelson, T. L., Whitfield, K. E., Kandler, C., Jang, K. L., Gatz, M., Butler, D. A., Stazi, M. A., Fagnani, C., D’Ippolito, C., Duncan, G. E., Buchwald, D., Derom, C. A., Vlietinck, R. F., Loos, R. J., Martin, N. G., Medland, S. E., Montgomery, G. W., Jeong, H. -U, Swan, G. E., Krasnow, R., Magnusson, P. K., Pedersen, N. L., Dahl-Aslan, Anna K., McAdams, T. A., Eley, T. C., Gregory, A. M., Tynelius, P., Baker, L. A., Tuvblad, C., Bayasgalan, G., Narandalai, D., Lichtenstein, P., Spector, T. D., Mangino, M., Lachance, G., Bartels, M., Van Beijsterveldt, T. C., Willemsen, G., Alexandra Burt, S., Klump, K. L., Harris, J. R., Brandt, I., Nilsen, T. S., Krueger, R. F., McGue, M., Pahlen, S., Corley, R. P., Hjelmborg, J. V. B., Goldberg, J. H., Iwatani, Y., Watanabe, M., Honda, C., Inui, F., Rasmussen, F., Huibregtse, B. M., Boomsma, D. I., Sørensen, T. I. A., Kaprio, J., Silventoinen, K., Jelenkovic, A., Hur, Y. -M, Sund, R., Yokoyama, Y., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Tan, Q., Zhang, D., Pang, Z., Aaltonen, S., Heikkilä, K., Öncel, S.Y., Aliev, F., Rebato, E., Tarnoki, A. D., Tarnoki, D. L., Christensen, K., Skytthe, A., Kyvik, K. O., Silberg, J. L., Eaves, L. J., Maes, H. H., Cutler, T. L., Hopper, J. L., Ordoñana, J. R., Sánchez-Romera, J. F., Colodro-Conde, L., Cozen, W., Hwang, A. E., Mack, T. M., Sung, J., Song, Y. -M, Yang, S., Lee, K., Franz, C. E., Kremen, W. S., Lyons, M. J., Busjahn, A., Nelson, T. L., Whitfield, K. E., Kandler, C., Jang, K. L., Gatz, M., Butler, D. A., Stazi, M. A., Fagnani, C., D’Ippolito, C., Duncan, G. E., Buchwald, D., Derom, C. A., Vlietinck, R. F., Loos, R. J., Martin, N. G., Medland, S. E., Montgomery, G. W., Jeong, H. -U, Swan, G. E., Krasnow, R., Magnusson, P. K., Pedersen, N. L., Dahl-Aslan, Anna K., McAdams, T. A., Eley, T. C., Gregory, A. M., Tynelius, P., Baker, L. A., Tuvblad, C., Bayasgalan, G., Narandalai, D., Lichtenstein, P., Spector, T. D., Mangino, M., Lachance, G., Bartels, M., Van Beijsterveldt, T. C., Willemsen, G., Alexandra Burt, S., Klump, K. L., Harris, J. R., Brandt, I., Nilsen, T. S., Krueger, R. F., McGue, M., Pahlen, S., Corley, R. P., Hjelmborg, J. V. B., Goldberg, J. H., Iwatani, Y., Watanabe, M., Honda, C., Inui, F., Rasmussen, F., Huibregtse, B. M., Boomsma, D. I., Sørensen, T. I. A., Kaprio, J., and Silventoinen, K.

Abstract

Human height variation is determined by genetic and environmental factors, but it remains unclear whether their influences differ across birth-year cohorts. We conducted an individual-based pooled analysis of 40 twin cohorts including 143,390 complete twin pairs born 1886-1994. Although genetic variance showed a generally increasing trend across the birth-year cohorts, heritability estimates (0.69-0.84 in men and 0.53-0.78 in women) did not present any clear pattern of secular changes. Comparing geographic-cultural regions (Europe, North America and Australia, and East Asia), total height variance was greatest in North America and Australia and lowest in East Asia, but no clear pattern in the heritability estimates across the birth-year cohorts emerged. Our findings do not support the hypothesis that heritability of height is lower in populations with low living standards than in affluent populations, nor that heritability of height will increase within a population as living standards improve.

Published
2016
Full Text
View/download PDF

10. Genetic and environmental influences on adult human height across birth cohorts from 1886 to 1994

Author

University of Helsinki, Department of Social Research, University of Helsinki, Department of Public Health, University of Helsinki, Clinicum, Jelenkovic, Aline, Hur, Yoon-Mi, Sund, Reijo, Yokoyama, Y., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Tan, Q., Zhang, D., Pang, Z., Aaltonen, Sari, Heikkilä, Kauko, Oncel, S. Y., Aliev, F., Rebato, E., Tarnoki, A. D., Tarnoki, D. L., Christensen, K., Skytthe, A., Kyvik, K. O., Silberg, J. L., Eaves, L. J., Maes, H. H., Cutler, T. L., Hopper, J. L., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Cozen, W., Hwang, A. E., Mack, T. M., Sung, J., Song, Y. M., Yang, S., Lee, K., Franz, C. E., Kremen, W. S., Lyons, M. J., Busjahn, A., Nelson, T. L., Whitfield, K. E., Kandler, C., Jang, K. L., Gatz, M., Butler, D. A., Stazi, M. A., Fagnani, C., D'Ippolito, C., Duncan, G. E., Buchwald, D., Derom, C. A., Vlietinck, R. F., Loos, R. J., Martin, N. G., Medland, S. E., Montgomery, G. W., Jeong, H. U., Swan, G. E., Krasnow, R., Magnusson, P. K., Pedersen, N. L., Dahl-Aslan, A. K., McAdams, T. A., Eley, T. C., Gregory, A. M., Tynelius, P., Baker, L. A., Tuvblad, C., Bayasgalan, G., Narandalai, D., Lichtenstein, P., Spector, T. D., Mangino, M., Lachance, G., Bartels, M., van Beijsterveldt, T. C., Willemsen, G., Burt, S. A., Klump, K. L., Harris, J. R., Brandt, I., Nilsen, T. S., Krueger, R. F., McGue, M., Pahlen, S., Corley, R. P., Hjelmborg, J. V., Goldberg, J. H., Iwatani, Y., Watanabe, M., Honda, C., Inui, F., Rasmussen, F., Huibregtse, B. M., Boomsma, D. I., Sorensen, T. I., Kaprio, Jaakko, Silventoinen, Karri, University of Helsinki, Department of Social Research, University of Helsinki, Department of Public Health, University of Helsinki, Clinicum, Jelenkovic, Aline, Hur, Yoon-Mi, Sund, Reijo, Yokoyama, Y., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Tan, Q., Zhang, D., Pang, Z., Aaltonen, Sari, Heikkilä, Kauko, Oncel, S. Y., Aliev, F., Rebato, E., Tarnoki, A. D., Tarnoki, D. L., Christensen, K., Skytthe, A., Kyvik, K. O., Silberg, J. L., Eaves, L. J., Maes, H. H., Cutler, T. L., Hopper, J. L., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Cozen, W., Hwang, A. E., Mack, T. M., Sung, J., Song, Y. M., Yang, S., Lee, K., Franz, C. E., Kremen, W. S., Lyons, M. J., Busjahn, A., Nelson, T. L., Whitfield, K. E., Kandler, C., Jang, K. L., Gatz, M., Butler, D. A., Stazi, M. A., Fagnani, C., D'Ippolito, C., Duncan, G. E., Buchwald, D., Derom, C. A., Vlietinck, R. F., Loos, R. J., Martin, N. G., Medland, S. E., Montgomery, G. W., Jeong, H. U., Swan, G. E., Krasnow, R., Magnusson, P. K., Pedersen, N. L., Dahl-Aslan, A. K., McAdams, T. A., Eley, T. C., Gregory, A. M., Tynelius, P., Baker, L. A., Tuvblad, C., Bayasgalan, G., Narandalai, D., Lichtenstein, P., Spector, T. D., Mangino, M., Lachance, G., Bartels, M., van Beijsterveldt, T. C., Willemsen, G., Burt, S. A., Klump, K. L., Harris, J. R., Brandt, I., Nilsen, T. S., Krueger, R. F., McGue, M., Pahlen, S., Corley, R. P., Hjelmborg, J. V., Goldberg, J. H., Iwatani, Y., Watanabe, M., Honda, C., Inui, F., Rasmussen, F., Huibregtse, B. M., Boomsma, D. I., Sorensen, T. I., Kaprio, Jaakko, and Silventoinen, Karri

Abstract

Human height variation is determined by genetic and environmental factors, but it remains unclear whether their influences differ across birth-year cohorts. We conducted an individual-based pooled analysis of 40 twin cohorts including 143,390 complete twin pairs born 1886-1994. Although genetic variance showed a generally increasing trend across the birth-year cohorts, heritability estimates (0.69-0.84 in men and 0.53-0.78 in women) did not present any clear pattern of secular changes. Comparing geographic-cultural regions (Europe, North America and Australia, and East Asia), total height variance was greatest in North America and Australia and lowest in East Asia, but no clear pattern in the heritability estimates across the birth-year cohorts emerged. Our findings do not support the hypothesis that heritability of height is lower in populations with low living standards than in affluent populations, nor that heritability of height will increase within a population as living standards improve.

Published
2016

11. The CODATwins Project: the cohort description of collaborative project of development of anthropometrical measures in twins to study macro-environmental variation in genetic and environmental effects on anthropometric traits

Author

Silventoinen, K., Jelenkovic, A., Sund, R., Honda, C., Aaltonen, S., Yokoyama, Y., Tarnoki, AD, Tarnoki, D. L., Ning, F., Ji, F., Pang, Z., Ordoñana, J. R., Sánchez-Romera, J. F., Colodro-Conde, L., Burt, S. A., Klump, K. L., Medland, S. E., Montgomery, G. W., Kandler, C., McAdams, T. A., Eley, T. C., Gregory, A. M., Saudino, K. J., Dubois, L., Boivin, M., Haworth, C. M. A., Plomin, R., Öncel, S. Y., Aliev, F., Stazi, M. A., Fagnani, C., D'Ippolito, C., Craig, J., Saffery, R., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Spector, T., Mangino, M., Lachance, G., Gatz, M., Butler, D. A., Bayasgalan, G., Narandalai, D., Freitas, D. L., Maia, J. A., Harden, K. P., Tucker-Drob, E. M., Christensen, K., Skytthe, A., Kyvik, K. O., Hong, C., Chong, Y., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Cozen, W., Hwang, A. E., Mack, T. M., He, M., Ding, X., Chang, B., Silberg, J. L., Eaves, L. J., Maes, H. H., Cutler, T. L., Hopper, J. L., Aujard, K., Magnusson, P. K. E., Pedersen, N. L., Aslan, A. K. D., Song, Y.- M., Yang, S., Lee, K., Baker, L. A., Tuvblad, C., Bjerregaard-Andersen, M., Beck-Nielsen, H., Sodemann, M., Heikkilä, K., Tan, Q., Zhang, D., Swan, G. E., Krasnow, R., Jang, K. L., Knafo-Noam, A., Mankuta, D., Abramson, L., Lichtenstein, P., Krueger, R. F., McGue, M., Pahlen, S., Tynelius, P., Duncan, G. E., Buchwald, D., Corley, R. P., Huibregtse, B. M., Nelson, T. L., Whitfield, K. E., Franz, C. E., Kremen, W. S., Lyons, M. J., Ooki, S., Brandt, I., Nilsen, T. S., Inui, F., Watanabe, M., Bartels, M., van Beijsterveldt, T. C. E. M., Wardle, J., Llewellyn, C. H., Fisher, A., Rebato, E., Martin, N. G., Iwatani, Y., Hayakawa, K., Rasmussen, F., Sung, J., Harris, J. R., Willemsen, G., Busjahn, A., Goldberg, J. H., Boomsma, D. I., Hur, Y. - M., Sørensen, T. I. A., Kaprio, J., Silventoinen, K., Jelenkovic, A., Sund, R., Honda, C., Aaltonen, S., Yokoyama, Y., Tarnoki, AD, Tarnoki, D. L., Ning, F., Ji, F., Pang, Z., Ordoñana, J. R., Sánchez-Romera, J. F., Colodro-Conde, L., Burt, S. A., Klump, K. L., Medland, S. E., Montgomery, G. W., Kandler, C., McAdams, T. A., Eley, T. C., Gregory, A. M., Saudino, K. J., Dubois, L., Boivin, M., Haworth, C. M. A., Plomin, R., Öncel, S. Y., Aliev, F., Stazi, M. A., Fagnani, C., D'Ippolito, C., Craig, J., Saffery, R., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Spector, T., Mangino, M., Lachance, G., Gatz, M., Butler, D. A., Bayasgalan, G., Narandalai, D., Freitas, D. L., Maia, J. A., Harden, K. P., Tucker-Drob, E. M., Christensen, K., Skytthe, A., Kyvik, K. O., Hong, C., Chong, Y., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Cozen, W., Hwang, A. E., Mack, T. M., He, M., Ding, X., Chang, B., Silberg, J. L., Eaves, L. J., Maes, H. H., Cutler, T. L., Hopper, J. L., Aujard, K., Magnusson, P. K. E., Pedersen, N. L., Aslan, A. K. D., Song, Y.- M., Yang, S., Lee, K., Baker, L. A., Tuvblad, C., Bjerregaard-Andersen, M., Beck-Nielsen, H., Sodemann, M., Heikkilä, K., Tan, Q., Zhang, D., Swan, G. E., Krasnow, R., Jang, K. L., Knafo-Noam, A., Mankuta, D., Abramson, L., Lichtenstein, P., Krueger, R. F., McGue, M., Pahlen, S., Tynelius, P., Duncan, G. E., Buchwald, D., Corley, R. P., Huibregtse, B. M., Nelson, T. L., Whitfield, K. E., Franz, C. E., Kremen, W. S., Lyons, M. J., Ooki, S., Brandt, I., Nilsen, T. S., Inui, F., Watanabe, M., Bartels, M., van Beijsterveldt, T. C. E. M., Wardle, J., Llewellyn, C. H., Fisher, A., Rebato, E., Martin, N. G., Iwatani, Y., Hayakawa, K., Rasmussen, F., Sung, J., Harris, J. R., Willemsen, G., Busjahn, A., Goldberg, J. H., Boomsma, D. I., Hur, Y. - M., Sørensen, T. I. A., and Kaprio, J.

Published
2015

12. Up-regulation of -catenin by a viral oncogene correlates with inhibition of the seven in absentia homolog 1 in B lymphoma cells

Author

Shackelford, J., Seo, S. Y., Jang, K. L., and Pagano, J. S.

Abstract

The protein levels of β-catenin are tightly regulated by the ubiquitin/proteasome system. We provide evidence that two distinct ubiquitin-dependent degradation pathways for β-catenin are active in the same Burkitt's lymphoma cells: Along with the classical glycogen-synthase kinase 3β-dependent destruction machinery, degradation of β-catenin through seven in absentia homolog 1 (Siah-1) ubiquitin ligase is functional in these cells. We show that inhibition of endogenous Siah-1 stabilizes and activates β-catenin in B cells. The principal Epstein–Barr virus oncoprotein, latent membrane protein 1, is involved in β-catenin up-regulation, and expression of latent membrane protein 1 in B lymphoma cells is associated with decreased Siah-1 RNA and protein levels. Thus, we demonstrate the significance of the endogenous Siah-1-dependent ubiquitin/proteasome pathway for β-catenin degradation in malignant human cells and its regulation by a viral oncogene.

Published
2005
Full Text
View/download PDF

23. Sources of structure: genetic, environmental, and artifactual influences on the covariation of personality traits.

Author

McCrae, Robert R., Jang, Kerry L., Livesley, W. John, Riemann, Rainer, Angleitner, Alois, McCrae, R R, Jang, K L, Livesley, W J, Riemann, R, and Angleitner, A

Subjects
PERSONALITY, PHENOTYPES, PSYCHOLOGY, BEHAVIOR genetics, GENETICS, ANALYSIS of covariance, BEHAVIOR
Abstract

The phenotypic structure of personality traits has been well described, but it has not yet been explained causally. Behavior genetic covariance analyses can identify the underlying causes of phenotypic structure; previous behavior genetic research has suggested that the effects from both genetic and nonshared environmental influences mirror the phenotype. However, nonshared environmental effects are usually estimated as a residualterm that may also include systematic bias, such as that introduced by implicit personality theory. To reduce that bias, we supplemented data from Canadian and German twin studies with cross-observer correlations on the Revised NEO Personality Inventory. The hypothesized five-factor structure was found in both the phenotypic and genetic/familial covariances. When the residual covariance was decomposed into true nonshared environmental influences and method bias, only the latter showed the five-factor structure. True nonshared environmental influences are not structured as genetic influences are, although there was some suggestion that they do affect two personality dimensions, Conscientiousness and Love. These data reaffirm the value of behavior genetic analyses for research on the underlying causes of personality traits. [ABSTRACT FROM AUTHOR]

Published
2001
Full Text
View/download PDF

24. Behavioural-genetic perspectives on personality function.

Author

Jang, Kerry L, Vernon, Philip A, Livesley, W John, Jang, K L, Vernon, P A, and Livesley, W J

Subjects
PERSONALITY disorders, BEHAVIOR genetics, MOLECULAR genetics, GENETICS, COMPARATIVE studies, ECOLOGY, EPIDEMIOLOGICAL research, GENOMES, RESEARCH methodology, MEDICAL cooperation, PERSONALITY, MATHEMATICAL models of psychology, RESEARCH, PHENOTYPES, EVALUATION research
Abstract

In the wake of the recent announcements that the human genome has been mapped, efforts to identify the genetic loci underlying personality function will grow and intensify. Much research has already been done in this area, but it has for the most part been limited to classical biometrical approaches designed to determine if personality has a heritable basis. These so-called "heritability" studies estimate how much of the individual differences in personality are attributable to genetic differences among people. Molecular-genetic approaches, on the other hand, are designed to identify specific putative loci, but have yielded mixed results. The inconsistency in research findings can be attributed in part to the lack of sufficient numbers of genetic markers in the chromosomal regions of interest--a problem that the creation of a map of the human genome will help to rectify. This map and its inevitable refinements, however, can only advance the search for the genes for personality to a limited degree. Serious unresolved problems in the conceptualization and definition of personality and its dysfunction remain, which will hamper the search for personality genes. [ABSTRACT FROM AUTHOR]

Published
2001
Full Text
View/download PDF

36. Assignment<FOOTREF>[sup 1] </FOOTREF> of the human RhoHP1 gene (ARHD) to chromosome 11q14.3 by radiation hybrid mapping.

Author

H. -S. Kim, N. C., Choi, J. -Y., Jung, A. -R., Jang, K. -L., Lee, W. -H., Choi, W. -C., T. J. Crow, W. -C., and B. H. Hyun, W. -C.

Subjects
HUMAN genetics, HUMAN gene mapping, HUMAN chromosomes, GENE expression, PROTEIN kinases, GUANOSINE triphosphatase, SOMATIC hybrids
Abstract

This article studies the assignment of the human RhoHP1 gene (ARHD) to chromosome by radiation hybrid mapping. The Rho family proteins play a critical role in muscle differentiation by regulating the expression of the myogenin and MEF2 genes. The Rho proteins directly interact with protein kinases, which may serve as downstream effector targets of the activated GTPase. PCR analysis of the monochromosomal somatic cell hybrid DNA panel localized ARHD to human chromosome 11. The results indicate that ARHD is on chromosome 11 with a lod score of >3.0.

Published
2000
Full Text
View/download PDF

39. Bringing up bashful baby. Developmental pathways to social phobia.

Author

Stein MB, Chavira DA, and Jang KL

Subjects
Adolescent, Autistic Disorder psychology, Child, Genetic Predisposition to Disease, Humans, Mutism etiology, Parent-Child Relations, Phenotype, Phobic Disorders genetics, Phobic Disorders psychology, Risk Factors, Autistic Disorder genetics, Child Rearing psychology, Phobic Disorders etiology, Shyness
Abstract

Shyness is a risk factor for, or an early manifestation of, more enduring problems with social anxiety. But the majority of shy children do not develop social phobia, and factors that further increase risk are poorly understood, underscoring the complexity of this relationship. Studies uniformly show that social phobia (particularly the generalized subtype) runs in families, and twin studies suggest that a moderate component of this familial tendency is genetic in origin. Understanding the genetic etiology of other neuropsychiatric disorders characterized by abnormal social interest, social communication (e.g., autism), or both may prove informative for social phobia. The contribution of unique experiences to the development of social phobia is clear from genetic studies, but studies to date have failed to elucidate what kinds of experiences might be involved. Given patient reports that socially traumatic conditioning experiences have often occurred, detailed evaluation of these kinds of experiences in monozygotic twins discordant for social phobia would be a particularly informative research strategy. Nongenetic familial factors probably have more limited effects on the development of social phobia, although the impact of parental modeling of, and acquiescence to, childhood social fears deserves to be further investigated. These factors may be particularly salient for the expression of social phobia in children whose genes render them susceptible. If so, it should be possible to design early interventions to prevent the progression from phobia proneness (e.g., designated on the basis of family history) to phobic disorder.

Published
2001
Full Text
View/download PDF

40. Intra- and extra-familial influences on alcohol and drug misuse: a twin study of gene-environment correlation.

Author

Jang KL, Vernon PA, Livesley WJ, Stein MB, and Wolf H

Subjects
Adolescent, Adult, Aged, Alcoholism genetics, Alcoholism psychology, British Columbia, Family Relations, Female, Humans, Male, Middle Aged, Pedigree, Risk Factors, Social Environment, Substance-Related Disorders psychology, Surveys and Questionnaires, Twins, Dizygotic, Twins, Monozygotic, Substance-Related Disorders genetics
Abstract

Aims: Genotype-environment correlation refers to the extent to which individuals are exposed to environments as a function of their genetic propensities. These correlations are important in the study of psychopathology because they identify environments that may maintain the expression of underlying genetic liabilities for a disorder. The present study examined the correlation between genetic liabilities for alcohol and drug misuse with perceptions of the social environments of the family of origin and the classroom., Design: Postal survey data were collected from monozygotic and dizygotic twin pairs., Setting: Twin pairs were recruited from Vancouver, British Columbia, Canada using newspaper advertisements and media stories., Participants: Eighty-five monozygotic and 77 dizygotic twin pairs were recruited from the general population., Measurements: Twin pairs completed self-report measures of alcohol and drug misuse contained in the Dimensional Assessment of Personality Pathology, the Family Environment Scale, the Classroom Environment Scale, and the Traumatic Events Questionnaire., Findings: Genetically indexed alcohol and drug misuse scores were regressed on the environmentally indexed FES and CES scales. Genetic liabilities for alcohol and drug misuse were associated with decreased perceived family moral-religious emphases, family cohesion and classroom task orientation and increased perceptions of classroom order and organization (strictness)., Conclusions: Genotype-environment correlations, in particular, moral-religious emphases in the home, appear to be important in the development of substance misuse.

Published
2001
Full Text
View/download PDF

41. Covariance structure of neuroticism and agreeableness: a twin and molecular genetic analysis of the role of the serotonin transporter gene.

Author

Jang KL, Hu S, Livesley WJ, Angleitner A, Riemann R, Ando J, Ono Y, Vernon PA, and Hamer DH

Subjects
Adult, Analysis of Variance, Canada, Carrier Proteins genetics, Female, Genetics, Behavioral methods, Germany, Humans, Japan, Male, Membrane Glycoproteins genetics, Nuclear Family psychology, Personality physiology, Principal Component Analysis, Serotonin genetics, Serotonin physiology, Serotonin Plasma Membrane Transport Proteins, Twins, Dizygotic genetics, Twins, Dizygotic psychology, Twins, Monozygotic genetics, Twins, Monozygotic psychology, United States, Carrier Proteins physiology, Emotions physiology, Membrane Glycoproteins physiology, Membrane Transport Proteins, Nerve Tissue Proteins, Personality genetics, Personality Inventory statistics & numerical data, Twins genetics, Twins psychology
Abstract

The Revised NEO Personality Inventory domains of Neuroticism and Agreeableness are considered factorially distinct despite several intercorrelations between these domains. The genetic correlation, an index of the degree to which these intercorrelations are caused by genetic influences, was estimated using data from 913 monozygotic and 562 dizygotic volunteer twin pairs from Canada, Germany, and Japan. The serotonin transporter gene, 5-HTTLPR, was assayed in a sample of 388 nontwin sibling pairs from the United States to determine the contribution of the serotonin transporter locus to the covariation between the Neuroticism and Agreeableness scales. In all four samples, genetic influences contributed to the covariance of Neuroticism and Agreeableness, with the serotonin transporter gene accounting for 10% of the relationship between these domains.

Published
2001
Full Text
View/download PDF

42. The heritability of attitudes: a study of twins.

Author

Olson JM, Vernon PA, Harris JA, and Jang KL

Subjects
Achievement, Adult, Female, Humans, Individuality, Male, Personality genetics, Social Environment, Social Values, Twins, Dizygotic genetics, Twins, Monozygotic genetics, Attitude, Twins, Dizygotic psychology, Twins, Monozygotic psychology
Abstract

The genetic basis of individual differences in attitudes was examined in a survey of 195 pairs of monozygotic twins and 141 pairs of same-sex dizygotic twins. A principal components analysis of the 30 attitude items in the survey identified 9 attitude factors, of which 6 yielded significant heritability coefficients. Nonshared environmental factors accounted for the most variance in the attitude factors. Possible mediators of attitude heritability were also assessed, including personality traits, physical characteristics, and academic achievement. Analyses showed that several of these possible mediators correlated at a genetic level with the heritable attitude factors, suggesting that the heritability of the mediator variables might account for part of the heritable components of some attitudes. There was also some evidence that highly heritable attitudes were psychologically "stronger" than less heritable attitudes.

Published
2001

43. Causal modeling of relations among learning history, anxiety sensitivity, and panic attacks.

Author

Stewart SH, Taylor S, Jang KL, Cox BJ, Watt MC, Fedoroff IC, and Borger SC

Subjects
Adult, Factor Analysis, Statistical, Female, Humans, Male, Models, Structural, Panic Disorder physiopathology, Psychiatric Status Rating Scales, Retrospective Studies, Anxiety physiopathology, Arousal, Learning, Panic Disorder etiology
Abstract

We used structural equation modeling (SEM) to test the hypothesis that childhood instrumental and vicarious learning experiences influence frequency of panic attacks in young adulthood both directly, and indirectly through their effects on anxiety sensitivity (AS). A total of 478 university students participated in a retrospective assessment of their childhood learning experiences for arousal-reactive sensations (e.g., nausea, racing heart, shortness of breath, dizziness) and arousal-non-reactive sensations (i.e., colds, aches and pains, and rashes). SEM revealed that learning history for arousal-reactive somatic symptoms directly influenced both AS levels and panic frequency; AS directly influenced panic frequency; and learning history for arousal-non-reactive symptoms directly influenced AS but did not directly influence panic frequency. These results are consistent with the findings of previous retrospective studies on the learning history origins of AS and panic attacks, and provide the first empirical evidence of a partial mediation effect of AS in explaining the relation between childhood learning experiences and panic attacks in young adulthood. Implications for understanding the etiology of panic disorder are discussed.

Published
2001
Full Text
View/download PDF

44. Heritability of personality disorders in childhood: a preliminary investigation.

Author

Coolidge FL, Thede LL, and Jang KL

Subjects
Adolescent, Child, Child, Preschool, Female, Humans, Male, Personality Disorders diagnosis, Psychiatric Status Rating Scales, Surveys and Questionnaires, Temperament physiology, Twins genetics, Personality Disorders genetics
Abstract

The heritability of personality disorder features was investigated in 112 child (ages 4-15 years) twin pairs (70 monozygotic and 42 dizygotic pairs). Parents assessed personality disorder features using the Coolidge Personality and Neuropsychological Inventory for Children (CPNI; Coolidge, 1998) that measures 12 personality disorders according to the criteria in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (American Psychiatric Association, 1994). Structural equation model-fitting methods indicated that the median heritability coefficient for the 12 scales was .75 (ranging from .81 for the Dependent and Schizotypal Personality Disorder scales to .50 for the Paranoid and Passive-Aggressive Personality Disorder scales). These results suggest that childhood personality disorders have a substantial genetic component and that they are similar to heritability estimates of personality disorder traits in adults and counter hypotheses that only temperaments and higher-order personality disorder traits have significant genetic components (Paris, 1997).

Published
2001
Full Text
View/download PDF

45. Familial aggregation of anxiety-related quantitative traits in generalized social phobia: clues to understanding "disorder" heritability?

Author

Stein MB, Chartier MJ, Lizak MV, and Jang KL

Subjects
Adult, Family, Female, Humans, Male, Middle Aged, Phenotype, Regression Analysis, Statistics as Topic, Anxiety genetics, Phobic Disorders genetics, Quantitative Trait, Heritable
Abstract

Social phobia, particularly the generalized form, is strongly familial. Given the probable continuity from extremes of normative personality (e.g., shyness) to social phobia to personality disorder (e.g., avoidant personality disorder), it is unlikely that social phobia itself, at the level of an Axis I disorder, is transmitted. Rather, it seems more parsimonious, and in keeping with current notions about the structure and heritability of mental disorders, that one or more temperamental risk factors for social phobia is transmitted. The goal of this study was to explore this possibility by examining relevant quantitative traits in a family study of generalized social phobia (GSP). First-degree (n = 103) relatives of patients with DSM-IV GSP and 65 first-degree relatives of not socially phobic comparison subjects (NC) completed a panel of self-report questionnaires that included measures of trait anxiety, social anxiety, and personality. Regression analysis was used to examine associations between group membership (i.e., whether that family member was a first-degree relative of a GSP proband) and these measures. First-degree relatives of GSP probands scored significantly higher than first-degree relatives of not socially phobic probands on measures of trait anxiety and social anxiety and on the Harm Avoidance subscale of the TPQ. One large factor, accounting for 84% of the variance, was strongly associated with being a first-degree relative of a GSP proband. Quantitative traits elevated in probands with generalized social phobia are also elevated in their first-degree relatives. Future family and genetic studies of social phobia should consider the possibility that one or more traits (or some aggregation thereof) may better approximate the phenotype of interest. More extensive efforts at phenotype refinement should be undertaken before such studies proceed.

Published
2001

46. Personality disorder traits, family environment, and alcohol misuse: a multivariate behavioural genetic analysis.

Author

Jang KL, Vernon PA, and Livesley WJ

Subjects
Adolescent, Adult, Age Distribution, Aged, Aged, 80 and over, Alcoholism psychology, Antisocial Personality Disorder diagnosis, Antisocial Personality Disorder psychology, Family Relations, Female, Humans, Male, Middle Aged, Multivariate Analysis, Pedigree, Risk Factors, Sex Distribution, Twins, Dizygotic, Twins, Monozygotic, Alcoholism genetics, Antisocial Personality Disorder genetics
Abstract

Aims: This study seeks to estimate the extent to which a common genetic and environmental basis is shared between (i) traits delineating specific aspects of antisocial personality and alcohol misuse, and (ii) childhood family environments, traits delineating broad domains of personality pathology and alcohol misuse., Design: Postal survey data were collected from monozygotic and dizygotic twin pairs., Setting: Twin pairs were recruited from Vancouver, British Columbia and London, Ontario, Canada using newspaper advertisements, media stories and twin clubs., Participants: Data obtained from 324 monozygotic and 335 dizygotic twin pairs were used to estimate the extent to which traits delineating specific antisocial personality traits and alcohol misuse shared a common genetic and environmental aetiology. Data from 81 monozygotic and 74 dizygotic twin pairs were used to estimate the degree to which traits delineating personality pathology, childhood family environment and alcohol misuse shared a common aetiology., Measurements: Current alcohol misuse and personality pathology were measured using scales contained in the self-report Dimensional Assessment of Personality Pathology. Perceptions of childhood family environment were measured using the self-report Family Environment Scale., Findings: Multivariate genetic analyses showed that a subset of traits delineating components of antisocial personality (i.e. grandiosity, attention-seeking, failure to adopt social norms, interpersonal violence and juvenile antisocial behaviours) are influenced by genetic factors in common to alcohol misuse. Genetically based perceptions of childhood family environment had little relationship with alcohol misuse., Conclusions: Heritable personality factors that influence the perception of childhood family environment play only a small role in the liability to alcohol misuse. Instead, liability to alcohol misuse is related to genetic factors common a specific subset of antisocial personality traits describing conduct problems, narcissistic and stimulus-seeking behaviour.

Published
2000
Full Text
View/download PDF

47. Toward an empirically based classification of personality disorder.

Author

Livesley WJ and Jang KL

Subjects
Genetic Predisposition to Disease, Humans, Individuality, Personality Disorders diagnosis, Personality Disorders genetics, Self Concept, Social Adjustment, Empiricism, Personality Disorders classification, Psychiatric Status Rating Scales
Abstract

A framework for an empirically based classification of personality disorder is proposed that has two components: (a) a definition of personality disorder, and (b) a scheme for describing individual differences in personality disorder traits. It is suggested that the diagnosis process should begin by establishing the presence of personality disorder and then proceed to a description of the personality on a set of trait dimensions. It is argued that a definition of personality disorder should reflect an understanding of the nature of the "harmful dysfunction" implied by a diagnosis of personality disorder. With this approach, personality disorder is defined as the failure to solve life tasks involving the development of integrated representations of self and others, and the capacity for adaptive kinship and societal relationships. The second component of a classification is a system to describe individual differences. It is suggested that these should be based on taxonomies of normal and disordered traits, and that the classification incorporates both higher-order patterns and more specific basic traits. Given that personality appears to be inherited as a large number of genetic dimensions, it is suggested that the primary level for describing individual differences is that of the basic or lower-level traits rather than broader or higher-level traits used in descriptions of normal personality.

Published
2000
Full Text
View/download PDF

48. Nucleotide sequence and phylogenetic analysis of long terminal repeats of human endogenous retrovirus K family (HERV-K) on human chromosomes.

Author

Kim HS, Choi JY, Lee WH, Jang KL, and Hyun BH

Subjects
DNA, Viral analysis, Genetic Variation, Humans, Hybrid Cells, Phylogeny, Sequence Analysis, RNA, Sequence Homology, Nucleic Acid, Terminal Repeat Sequences, Chromosomes, Human, Endogenous Retroviruses genetics
Abstract

It has been suggested that human endogenous retroviruses K family (HERV-K) has a role in disease, and solitary long terminal repeats (LTRs) of HERV-K have been potentially capable of affecting the expression of closely located genes. Using the human monochromosomes 8, 9, 17, and 18, with specific PCR primers, we identified thirty-four sequences of new HERV-K LTRs. Those LTR elements were analyzed phylogenetically with the human-specific HERV-K LTRs using neighbor-joining and maximum parsimony methods. Clones HKL8-5, HKL9-5, and HKL9-8 are related by more than 99% homology with the human-specific HERV-K LTRs. The HKL9-5 clone on chromosome 9 was 100% identical with the sequences of human-specific LTR, AC002400, on chromosome 16. The findings suggest that there has been recent proliferation, transposition, or chromosomal translocation of HERV-K LTR elements on human chromosomes.

Published
2000
Full Text
View/download PDF

49. Transcriptional regulation of herpes simplex virus type 1 ICP0 promoter by virion protein 16.

Author

Kwun HJ and Jang KL

Subjects
Animals, Binding Sites, Cell Line, Chloramphenicol O-Acetyltransferase metabolism, Cricetinae, DNA Mutational Analysis, Gene Deletion, Herpes Simplex Virus Protein Vmw65 metabolism, Immediate-Early Proteins metabolism, Oligonucleotides metabolism, Plasmids metabolism, Point Mutation, Ubiquitin-Protein Ligases, Gene Expression Regulation, Viral, Herpes Simplex Virus Protein Vmw65 genetics, Herpesvirus 1, Human genetics, Immediate-Early Proteins genetics, Promoter Regions, Genetic, Transcription, Genetic
Abstract

HSV regulatory proteins ICP0 and VP16 independently regulate transcription of the ICP0 gene during virus infection. In this study, we tried to determine the possible regulatory mechanism of ICP0 expression during virus infection. Among eight putative VP16 binding sites present in the ICP0 regulatory sequence, the most upstream one alone was sufficiently responsive to VP16-mediated activation. When the G/C-rich sequence present in front of the last TAATGARAT sequence of the ICP0 promoter was either deleted or point mutated, the activational effect of VP16 on the promoter was completely abolished. Furthermore, according to the gel mobility shift assay using a labeled double-stranded oligonucleotide derived from the G/C-rich sequence in the ICP0 promoter, specific protein binding to the probe was clearly demonstrated and was approximately fivefold upregulated by HSV-1 infection. Therefore, the G/C-rich sequence might play a critical role in VP16-mediated activation of the ICP0 promoter and the effect may be a result of the enhanced binding of a protein to the G/C-rich sequence during virus infection., (Copyright 2000 Academic Press.)

Published
2000
Full Text
View/download PDF

50. A novel function of IL-12p40 as a chemotactic molecule for macrophages.

Author

Ha SJ, Lee CH, Lee SB, Kim CM, Jang KL, Shin HS, and Sung YC

Subjects
Animals, COS Cells, Carcinoma, Hepatocellular, Cell Movement immunology, Chemotactic Factors administration & dosage, Chemotactic Factors biosynthesis, Chemotactic Factors genetics, Doxycycline pharmacology, Female, Genetic Vectors administration & dosage, Interleukin-12 administration & dosage, Interleukin-12 biosynthesis, Interleukin-12 genetics, Interleukin-12 metabolism, Liver Neoplasms etiology, Liver Neoplasms pathology, Liver Neoplasms therapy, Macrophages, Peritoneal pathology, Mice, Mice, Inbred BALB C, Neoplasm Transplantation, Peptide Fragments immunology, Peptide Fragments metabolism, Peptide Fragments physiology, Protein Binding immunology, Rats, Rats, Inbred BUF, Receptors, Interleukin metabolism, Receptors, Interleukin-12, Remission, Spontaneous, Transfection, Tumor Cells, Cultured, Chemotactic Factors physiology, Interleukin-12 physiology, Macrophages, Peritoneal immunology
Abstract

IL-12p70 plays a pivotal role in regulating the Th1/Th2 balance in the initial stage of immune responses. In contrast, IL-12p40, which is produced excess over IL-12p70, has been known to down-regulate IL-12p70-mediated responses by acting as an antagonist. To investigate in vivo function of IL-12p40, RH7777 rat hepatoma cells were engineered to inducibly express mouse IL-12p40 under the tight control of doxycycline (dox). In the absence of dox, s.c. injection of these cells into syngeneic rat was shown to generate tumors. However, the induction of IL-12p40 by dox was sufficient for inhibiting tumor formation, as well as for tumor regression. Immunohistochemical analysis showed that macrophages, but not CD4+ T, CD8+ T, and NK cells, were predominantly recruited into tumor sites as early as 3 days after IL-12p40 induction. These results were further supported by the observation that IL-12p40, but not C-terminal deletion mutants by more than 5 amino acids, was able to chemoattract peritoneal macrophages in vitro, suggesting that IL-12p40, when produced in a large excess over IL-12p70 in vivo, can initially amplify the immune responses against tumors by directly recruiting macrophages. Our findings indicate that IL-12p40 may function as an effector molecule as well as an antagonist of IL-12p70.

Published
1999

Catalog

Books, media, physical & digital resources
See catalog results