6 results
Communal breeding by women is associated with lower investment from husbands – ERRATUM
- Qiao-Qiao He, Jun-Wen Rui, Li Zhang, Yi Tao, Jia-Jia Wu, Ruth Mace, Ting Ji
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- Journal:
- Evolutionary Human Sciences / Volume 4 / 2022
- Published online by Cambridge University Press:
- 13 December 2022, e55
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Communal breeding by women is associated with lower investment from husbands
- Qiao-Qiao He, Jun-Wen Rui, Li Zhang, Yi Tao, Jia-Jia Wu, Ruth Mace, Ting Ji
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- Journal:
- Evolutionary Human Sciences / Volume 4 / 2022
- Published online by Cambridge University Press:
- 20 October 2022, e50
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According to Hamilton's rule, matrilineal-biased investment restrains men in matrilineal societies from maximising their inclusive fitness (the ‘matrilineal puzzle'). A recent hypothesis argues that when women breed communally and share household resources, a man should help his sisters' household, rather than his wife's household, as investment to the later but not the former would be diluted by other unrelated members (Wu et al., 2013). According to this hypothesis, a man is less likely to help on his wife's farm when there are more women reproducing in the wife's household, because on average he would be less related to his wife's household. We used a farm-work observational dataset, that we collected in the matrilineal Mosuo in southwest China, to test this hypothesis. As predicted, high levels of communal breeding by women in his wife's households do predict less effort spent by men on their wife's farm, and communal breeding in men's natal households do not affect whether men help on their natal farms. Thus, communal breeding by women dilutes the inclusive fitness benefits men receive from investment to their wife and children, and may drive the evolution of matrilineal-biased investment by men. These results can help solve the ‘matrilineal puzzle'.
Zygosity Differences in Height and Body Mass Index of Twins From Infancy to Old Age: A Study of the CODATwins Project
- Aline Jelenkovic, Yoshie Yokoyama, Reijo Sund, Chika Honda, Leonie H Bogl, Sari Aaltonen, Fuling Ji, Feng Ning, Zengchang Pang, Juan R. Ordoñana, Juan F. Sánchez-Romera, Lucia Colodro-Conde, S. Alexandra Burt, Kelly L. Klump, Sarah E. Medland, Grant W. Montgomery, Christian Kandler, Tom A. McAdams, Thalia C. Eley, Alice M. Gregory, Kimberly J. Saudino, Lise Dubois, Michel Boivin, Adam D. Tarnoki, David L. Tarnoki, Claire M. A. Haworth, Robert Plomin, Sevgi Y. Öncel, Fazil Aliev, Maria A. Stazi, Corrado Fagnani, Cristina D’Ippolito, Jeffrey M. Craig, Richard Saffery, Sisira H. Siribaddana, Matthew Hotopf, Athula Sumathipala, Fruhling Rijsdijk, Timothy Spector, Massimo Mangino, Genevieve Lachance, Margaret Gatz, David A. Butler, Gombojav Bayasgalan, Danshiitsoodol Narandalai, Duarte L Freitas, José Antonio Maia, K. Paige Harden, Elliot M. Tucker-Drob, Bia Kim, Youngsook Chong, Changhee Hong, Hyun Jung Shin, Kaare Christensen, Axel Skytthe, Kirsten O. Kyvik, Catherine A. Derom, Robert F. Vlietinck, Ruth J. F. Loos, Wendy Cozen, Amie E. Hwang, Thomas M. Mack, Mingguang He, Xiaohu Ding, Billy Chang, Judy L. Silberg, Lindon J. Eaves, Hermine H. Maes, Tessa L. Cutler, John L. Hopper, Kelly Aujard, Patrik K. E. Magnusson, Nancy L. Pedersen, Anna K. Dahl Aslan, Yun-Mi Song, Sarah Yang, Kayoung Lee, Laura A. Baker, Catherine Tuvblad, Morten Bjerregaard-Andersen, Henning Beck-Nielsen, Morten Sodemann, Kauko Heikkilä, Qihua Tan, Dongfeng Zhang, Gary E. Swan, Ruth Krasnow, Kerry L. Jang, Ariel Knafo-Noam, David Mankuta, Lior Abramson, Paul Lichtenstein, Robert F. Krueger, Matt McGue, Shandell Pahlen, Per Tynelius, Glen E. Duncan, Dedra Buchwald, Robin P. Corley, Brooke M. Huibregtse, Tracy L. Nelson, Keith E. Whitfield, Carol E. Franz, William S. Kremen, Michael J. Lyons, Syuichi Ooki, Ingunn Brandt, Thomas Sevenius Nilsen, Fujio Inui, Mikio Watanabe, Meike Bartels, Toos C. E. M. van Beijsterveldt, Jane Wardle, Clare H. Llewellyn, Abigail Fisher, Esther Rebato, Nicholas G. Martin, Yoshinori Iwatani, Kazuo Hayakawa, Joohon Sung, Jennifer R. Harris, Gonneke Willemsen, Andreas Busjahn, Jack H. Goldberg, Finn Rasmussen, Yoon-Mi Hur, Dorret I. Boomsma, Thorkild I. A. Sørensen, Jaakko Kaprio, Karri Silventoinen
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- Journal:
- Twin Research and Human Genetics / Volume 18 / Issue 5 / October 2015
- Published online by Cambridge University Press:
- 04 September 2015, pp. 557-570
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A trend toward greater body size in dizygotic (DZ) than in monozygotic (MZ) twins has been suggested by some but not all studies, and this difference may also vary by age. We analyzed zygosity differences in mean values and variances of height and body mass index (BMI) among male and female twins from infancy to old age. Data were derived from an international database of 54 twin cohorts participating in the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins), and included 842,951 height and BMI measurements from twins aged 1 to 102 years. The results showed that DZ twins were consistently taller than MZ twins, with differences of up to 2.0 cm in childhood and adolescence and up to 0.9 cm in adulthood. Similarly, a greater mean BMI of up to 0.3 kg/m2 in childhood and adolescence and up to 0.2 kg/m2 in adulthood was observed in DZ twins, although the pattern was less consistent. DZ twins presented up to 1.7% greater height and 1.9% greater BMI than MZ twins; these percentage differences were largest in middle and late childhood and decreased with age in both sexes. The variance of height was similar in MZ and DZ twins at most ages. In contrast, the variance of BMI was significantly higher in DZ than in MZ twins, particularly in childhood. In conclusion, DZ twins were generally taller and had greater BMI than MZ twins, but the differences decreased with age in both sexes.
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
- Karri Silventoinen, Aline Jelenkovic, Reijo Sund, Chika Honda, Sari Aaltonen, Yoshie Yokoyama, Adam D. Tarnoki, David L. Tarnoki, Feng Ning, Fuling Ji, Zengchang Pang, Juan R. Ordoñana, Juan F. Sánchez-Romera, Lucia Colodro-Conde, S. Alexandra Burt, Kelly L. Klump, Sarah E. Medland, Grant W. Montgomery, Christian Kandler, Tom A. McAdams, Thalia C. Eley, Alice M. Gregory, Kimberly J. Saudino, Lise Dubois, Michel Boivin, Claire M. A. Haworth, Robert Plomin, Sevgi Y. Öncel, Fazil Aliev, Maria A. Stazi, Corrado Fagnani, Cristina D’Ippolito, Jeffrey M. Craig, Richard Saffery, Sisira H. Siribaddana, Matthew Hotopf, Athula Sumathipala, Timothy Spector, Massimo Mangino, Genevieve Lachance, Margaret Gatz, David A. Butler, Gombojav Bayasgalan, Danshiitsoodol Narandalai, Duarte L. Freitas, José Antonio Maia, K. Paige Harden, Elliot M. Tucker-Drob, Kaare Christensen, Axel Skytthe, Kirsten O. Kyvik, Changhee Hong, Youngsook Chong, Catherine A. Derom, Robert F. Vlietinck, Ruth J. F. Loos, Wendy Cozen, Amie E. Hwang, Thomas M. Mack, Mingguang He, Xiaohu Ding, Billy Chang, Judy L. Silberg, Lindon J. Eaves, Hermine H. Maes, Tessa L. Cutler, John L. Hopper, Kelly Aujard, Patrik K. E. Magnusson, Nancy L. Pedersen, Anna K. Dahl Aslan, Yun-Mi Song, Sarah Yang, Kayoung Lee, Laura A. Baker, Catherine Tuvblad, Morten Bjerregaard-Andersen, Henning Beck-Nielsen, Morten Sodemann, Kauko Heikkilä, Qihua Tan, Dongfeng Zhang, Gary E. Swan, Ruth Krasnow, Kerry L. Jang, Ariel Knafo-Noam, David Mankuta, Lior Abramson, Paul Lichtenstein, Robert F. Krueger, Matt McGue, Shandell Pahlen, Per Tynelius, Glen E. Duncan, Dedra Buchwald, Robin P. Corley, Brooke M. Huibregtse, Tracy L. Nelson, Keith E. Whitfield, Carol E. Franz, William S. Kremen, Michael J. Lyons, Syuichi Ooki, Ingunn Brandt, Thomas Sevenius Nilsen, Fujio Inui, Mikio Watanabe, Meike Bartels, Toos C. E. M. van Beijsterveldt, Jane Wardle, Clare H. Llewellyn, Abigail Fisher, Esther Rebato, Nicholas G. Martin, Yoshinori Iwatani, Kazuo Hayakawa, Finn Rasmussen, Joohon Sung, Jennifer R. Harris, Gonneke Willemsen, Andreas Busjahn, Jack H. Goldberg, Dorret I. Boomsma, Yoon-Mi Hur, Thorkild I. A. Sørensen, Jaakko Kaprio
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- Journal:
- Twin Research and Human Genetics / Volume 18 / Issue 4 / August 2015
- Published online by Cambridge University Press:
- 27 May 2015, pp. 348-360
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For over 100 years, the genetics of human anthropometric traits has attracted scientific interest. In particular, height and body mass index (BMI, calculated as kg/m2) have been under intensive genetic research. However, it is still largely unknown whether and how heritability estimates vary between human populations. Opportunities to address this question have increased recently because of the establishment of many new twin cohorts and the increasing accumulation of data in established twin cohorts. We started a new research project to analyze systematically (1) the variation of heritability estimates of height, BMI and their trajectories over the life course between birth cohorts, ethnicities and countries, and (2) to study the effects of birth-related factors, education and smoking on these anthropometric traits and whether these effects vary between twin cohorts. We identified 67 twin projects, including both monozygotic (MZ) and dizygotic (DZ) twins, using various sources. We asked for individual level data on height and weight including repeated measurements, birth related traits, background variables, education and smoking. By the end of 2014, 48 projects participated. Together, we have 893,458 height and weight measures (52% females) from 434,723 twin individuals, including 201,192 complete twin pairs (40% monozygotic, 40% same-sex dizygotic and 20% opposite-sex dizygotic) representing 22 countries. This project demonstrates that large-scale international twin studies are feasible and can promote the use of existing data for novel research purposes.
12 - TGF-β signaling in stem cells and tumorigenesis
- from Part 2.1 - Molecular pathways underlying carcinogenesis: signal transduction
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- By Ying Li, The University of Texas, M.D. Anderson Cancer Center, Houston, TX, USA, Ruth He, Lombardi Comprehensive Cancer Center, Georgetown University, Washington DC, USA, Lopa Mishra, The University of Texas, M.D. Anderson Cancer Center, Houston, TX, USA
- Edited by Edward P. Gelmann, Columbia University, New York, Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, Frank J. Rauscher, III
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- Molecular Oncology
- Published online:
- 05 February 2015
- Print publication:
- 19 December 2013, pp 119-134
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Summary
The transformation growth factor-β (TGF-β) signaling pathway is involved in many cellular processes in both the adult organism and the developing embryo, including cell growth, cell differentiation, apoptosis, cellular homeostasis, and other cellular functions, and deregulation of the pathway can result in tumor development. TGF-β signaling maintains tissue homeostasis and prevents tumorigenesis by regulating cellular proliferation, differentiation, survival, and micro-environment. Malignant cells can overcome the tumor-suppressive effects of TGF-β, usually through two different mechanisms. First, inactivation of core components of the pathway, demonstrated as frequent mutations of core proteins, results in loss of function in TGF-β signaling in many cancers. Second, downstream alterations that disable just the tumor-suppressor arm of the pathways, allow cancer cells to utilize the remainder of the TGF-β pathway for invasion and metastasis. Insight into the powerful TGF-β pathway in the context of type and stage of cancer, micro-environment, and alteration of other signaling transduction pathways within the cancer cells is crucial to decipher the role of TGF-β as tumor suppressor or promoter, followed by the development of anti-cancer therapeutics targeting TGF-β signaling.
Molecular mechanism of TGF-β signaling: ligands, receptors, and signaling molecules, the Smads
TGF-β represents a large family of pleiotrophic growth and differentiation factors that include activin/inhibins and bone morphogenetic proteins (BMPs) (1–3). These proteins mobilize a complex signaling network to control cell fate by regulating differentiation, proliferation, motility, adhesion, and apoptosis. TGF-β is represented by three isoforms, TGF-β1, -β2, and -β3, TGF-β is secreted as an inactive latent homodimeric polypeptide that is bound to other extra-cellular proteins (4–6). The mature, bioactive ligand is produced upon proteolytic cleavage of the latent complex. Binding of the active TGF-β dimer to the type I and II receptors results in the activation of type II (TβRII), which phosphorylates and activates type I (TβRI), then propagates the signals by phosphorylating Smad transcription factors (Figure 12.1). Smad proteins together comprise a unique signaling pathway with key roles in signal transduction by TGF-β. Currently, at least eight vertebrate Smads have been identified (1,7,8). They are characterized by homologous regions at their N- and C-termini known as Mad homology, MH-1 and MH-2 domains, respectively.
The case for strategic international alliances to harness nutritional genomics for public and personal health†
- Jim Kaput, Jose M. Ordovas, Lynnette Ferguson, Ben van Ommen, Raymond L. Rodriguez, Lindsay Allen, Bruce N. Ames, Kevin Dawson, Bruce German, Ronald Krauss, Wasyl Malyj, Michael C. Archer, Stephen Barnes, Amelia Bartholomew, Ruth Birk, Peter van Bladeren, Kent J. Bradford, Kenneth H. Brown, Rosane Caetano, David Castle, Ruth Chadwick, Stephen Clarke, Karine Clément, Craig A. Cooney, Dolores Corella, Ivana Beatrice Manica da Cruz, Hannelore Daniel, Troy Duster, Sven O. E. Ebbesson, Ruan Elliott, Susan Fairweather-Tait, Jim Felton, Michael Fenech, John W. Finley, Nancy Fogg-Johnson, Rosalynn Gill-Garrison, Michael J. Gibney, Peter J. Gillies, Jan-Ake Gustafsson, John L. Hartman IV, Lin He, Jae-Kwan Hwang, Jean-Philippe Jais, Yangsoo Jang, Hans Joost, Claudine Junien, Mitchell Kanter, Warren A. Kibbe, Berthold Koletzko, Bruce R. Korf, Kenneth Kornman, David W. Krempin, Dominique Langin, Denis R. Lauren, Jong Ho Lee, Gilbert A. Leveille, Su-Ju Lin, John Mathers, Michael Mayne, Warren McNabb, John A. Milner, Peter Morgan, Michael Muller, Yuri Nikolsky, Frans van der Ouderaa, Taesun Park, Norma Pensel, Francisco Perez-Jimenez, Kaisa Poutanen, Matthew Roberts, Wim H.M. Saris, Gertrud Schuster, Andrew N. Shelling, Artemis P. Simopoulos, Sue Southon, E. Shyong Tai, Bradford Towne, Paul Trayhurn, Ricardo Uauy, Willard J. Visek, Craig Warden, Rick Weiss, John Wiencke, Jack Winkler, George L. Wolff, Xi Zhao-Wilson, Jean-Daniel Zucker
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- Journal:
- British Journal of Nutrition / Volume 94 / Issue 5 / November 2005
- Published online by Cambridge University Press:
- 08 March 2007, pp. 623-632
- Print publication:
- November 2005
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Nutrigenomics is the study of how constituents of the diet interact with genes, and their products, to alter phenotype and, conversely, how genes and their products metabolise these constituents into nutrients, antinutrients, and bioactive compounds. Results from molecular and genetic epidemiological studies indicate that dietary unbalance can alter gene–nutrient interactions in ways that increase the risk of developing chronic disease. The interplay of human genetic variation and environmental factors will make identifying causative genes and nutrients a formidable, but not intractable, challenge. We provide specific recommendations for how to best meet this challenge and discuss the need for new methodologies and the use of comprehensive analyses of nutrient–genotype interactions involving large and diverse populations. The objective of the present paper is to stimulate discourse and collaboration among nutrigenomic researchers and stakeholders, a process that will lead to an increase in global health and wellness by reducing health disparities in developed and developing countries.