Ethnopharmacological relevance The documentation and protection of traditional knowledge face new challenges in the era of open science. Focusing on medicinal and food uses, we discuss two innovative initiatives in Spain to document, protect and return to the society traditional knowledge. Materials and methods The Spanish Inventory of Traditional Knowledge related to Biodiversity has compiled and published information on the traditional use and management of flora, fauna, fungi, geodiversity, and ecosystems. CONECT-e (www.conecte.es) is an online platform where citizens can document knowledge and uses of wild and domesticated species. We describe the extent of these initiatives in terms of participation and accomplishment, and discuss their complementarities and challenges. Results The initiatives described have fostered the establishment of a common standard for organizing traditional knowledge in databases that facilitate knowledge documentation: 131,066 uses and 152,246 local names have been documented so far. Using open data and copyleft licenses, these initiatives also contribute to the maintenance of traditional knowledge in the commons domain, guaranteeing the free exchange and reproduction of knowledge. However, the extensive focus of these initiatives on data sharing does not necessarily guarantee knowledge holders¿ data sovereignty. Conclusion To protect TEK in a context of open science more efforts should be done to operationalize traditional knowledge holders' rights to data sovereignty. ; Research leading to this paper has received funding from 1) the Spanish government through the Ministry of Economy and Competitiveness (CSO 2014-59704-P), the Ministry of Agriculture, Fisheries and Food (202005000018) and the ministries responsible for the Environment and Agriculture (TEC0003351, TEC0003909, and TEC0004583); 2) the Catalan government (project 2016SGR1116); 3) the Fundación Biodiversidad; and 4) the Institut d'Estudis Catalans (IEC-PRO2017-2021-S02-VALLES). ; Abstract Keywords 1. Introduction 2. Spanish inventory of traditional knowledge related to biodiversity 3. Conect-e online platform 4. Protecting TEK in the era of open science 5. Conclusion Author's contributions Acknowledgments References
AbstractAging is a multifactorial process influenced by both biological and sociocultural factors. The objective of this study was to identify current and past factors with an impact on the quality of aging in a sample of people 65 years of age or older born in the postwar period after the Spanish civil war. Socioeconomic, health, anthropometric, and food consumption data were collected in public Leisure Centers for the elderly in Madrid. The sample consists of 587 people (64.6% women), with a mean age of 71.8 ±5.3 years. Following the World Health Organization (WHO) guidelines regarding what is considered Healthy Aging, an index called the Index of Quality of Aging was calculated from four variables: the Mini Mental State Examination score, perception of health, satisfaction with life and the number of diseases that affect daily life. Another index called the Diet Inflammation Index was created based on the inflammatory or anti-inflammatory potential of different foods. The Index of Quality of Ageing was used as a dependent variable in linear regression models for men and women. Differences by gender were observed in the factors that influence the quality of aging. Education had a positive influence on men quality of ageing while it does not on women. In these, a relationship between the quality of the current diet and the quality of aging was observed.
Ethnic-racial classification criteria are widely recognized to vary according to historical, cultural and political contexts. In Brazil, the strong influence of individual socio-economic factors on race/colour self-classification is well known. With the expansion of genomic technologies, the use of genomic ancestry has been suggested as a substitute for classification procedures such as self-declaring race, as if they represented the same concept. We investigated the association between genomic ancestry, the racial composition of census tracts and individual socioeconomic factors and self-declared race/colour in a cohort of 15,105 Brazilians. Results show that the probability of self-declaring as black or brown increases according to the proportion of African ancestry and varies widely among cities. In Porto Alegre, where most of the population is white, with every 10% increase in the proportion of African ancestry, the odds of self-declaring as black increased 14 times (95%CI 6.08–32.81). In Salvador, where most of the population is black or brown, that increase was of 3.98 times (95%CI 2.96–5.35). The racial composition of the area of residence was also associated with the probability of selfdeclaring as black or brown. Every 10% increase in the proportion of black and brown inhabitants in the residential census tract increased the odds of self-declaring as black by 1.33 times (95%CI 1.24–1.42). Ancestry alone does not explain self-declared race/colour. An emphasis on multiple situational contexts (both individual and collective) provides a more comprehensive framework for the study of the predictors of self-declared race/colour, a highly relevant construct in many different scenarios, such as public policy, sociology and medicine.
Publisher's version (útgefin grein) ; Rationale: Idiopathic pulmonary fibrosis (IPF) is a complex lung disease characterized by scarring of the lung that is believed to result from an atypical response to injury of the epithelium. Genome-wide association studies have reported signals of association implicating multiple pathways including host defense, telomere maintenance, signaling, and cell-cell adhesion. Objectives: To improve our understanding of factors that increase IPF susceptibility by identifying previously unreported genetic associations. Methods: We conducted genome-wide analyses across three independent studies and meta-analyzed these results to generate the largest genome-wide association study of IPF to date (2,668 IPF cases and 8,591 controls). We performed replication in two independent studies (1,456 IPF cases and 11,874 controls) and functional analyses (including statistical fine-mapping, investigations into gene expression, and testing for enrichment of IPF susceptibility signals in regulatory regions) to determine putatively causal genes. Polygenic risk scores were used to assess the collective effect of variants not reported as associated with IPF. Measurements and Main Results: We identified and replicated threenewgenome-wide significant (P<5×10-8) signals of association with IPF susceptibility (associated with altered gene expression of KIF15, MAD1L1, and DEPTOR) and confirmed associations at 11 previously reported loci. Polygenic risk score analyses showed that the combined effect of many thousands of as yet unreported IPF susceptibility variants contribute to IPF susceptibility. Conclusions: The observation that decreased DEPTOR expression associates with increased susceptibility to IPF supports recent studies demonstrating the importance of mTOR signaling in lung fibrosis. New signals of association implicating KIF15 and MAD1L1 suggest a possible role of mitotic spindle-assembly genes in IPF susceptibility. ; R.J.A. is an Action for Pulmonary Fibrosis Research Fellow. L.V.W. holds a GSK/British Lung Foundation Chair in Respiratory Research. R.G.J. is supported by a National Institute for Health Research (NIHR) Research Professorship (NIHR reference RP-2017-08-ST2-014). I.N. is supported by the NHLBI (R01HL130796). B.G.-G. is funded by Agencia Canaria de Investigación, Innovación y Sociedad de la Información (TESIS2015010057) cofunded by European Social Fund. J.M.O. is supported by the NHLBI (K23HL138190). C.F. is supported by the Spanish Ministry of Science, Innovation and Universities (grant RTC-2017-6471-1; Ministerio de Ciencia e Innovacion/Agencia Estatal de Investigación/Fondo Europeo de Desarrollo Regional, Unión Europea) cofinanced by the European Regional Development Funds "A way of making Europe" from the European Union and by agreement OA17/008 with Instituto Tecnológico y de Energías Renovables to strengthen scientific and technological education, training, research, development and innovation in Genomics, Personalized Medicine and Biotechnology. The Spain Biobank array genotyping service was performed at CEGEN-PRB3-ISCIII, which is supported by PT17/0019, of the PE I+D+i 2013–2016, funded by Instituto de Salud Carlos III, and cofinanced by the European Regional Development Funds. P.L.M. is an Action for Pulmonary Fibrosis Research Fellow. M.O. is a fellow of the Parker B. Francis Foundation and a Scholar of the Michael Smith Foundation for Health Research. B.D.H. is supported by NIH K08 HL136928, Parker B. Francis Research Opportunity Award. M.H.C. and G.M.H. are supported by NHLBI grants R01HL113264 (M.H.C.), R01HL137927 (M.H.C.), R01HL135142 (M.H.C. and G.M.H.), R01111024 (G.M.H.), and R01130974 (G.M.H.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. The funding body has no role in the design of the study and collection, analysis, and interpretation of data and in writing the manuscript. T.M.M. is supported by an NIHR Clinician Scientist Fellowship (NIHR Ref: CS-2013-13-017) and a British Lung Foundation Chair in Respiratory Research (C17-3). M.D.T. is supported by a Wellcome Trust Investigator Award (WT202849/Z/16/Z). The research was partially supported by the NIHR Leicester Biomedical Research Centre; the views expressed are those of the author(s) and not necessarily those of the National Health Service (NHS), the NIHR, or the Department of Health. I.P.H. was partially supported by the NIHR Nottingham Biomedical Research Centre; the views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, or the Department of Health. I.S. is supported by Medical Research Council (G1000861) and Asthma UK (AUK-PG-2013-188). D.F. was supported by an Intermediate Fellowship from the Wellcome Trust (097152/Z/11/Z). This work was partially supported by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre. V.N. is funded by an NIHR Clinical Lectureship. G.G. is supported by project grant 141513-051 from the Icelandic Research Fund and Landspitali Scientific Fund A-2016-023, A-2017-029, and A-2018-025. D.J.L. and A.M. are supported by Multi-Ethnic Study of Atherosclerosis (MESA) and the MESA SNP Health Association Resource (SHARe) project are conducted and supported by the NHLBI in collaboration with MESA investigators. Support for MESA is provided by contracts HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, UL1-TR-000040, UL1-TR-001079, UL1-TR-001420, UL1-TR-001881, and DK063491. Funding for SHARe genotyping was provided by NHLBI Contract N02-HL-64278. Genotyping was performed at Affymetrix (Santa Clara, California) and the Broad Institute of Harvard and Massachusetts Institute of Technology (Boston, Massachusetts) using the Affymetrix Genome-Wide Human SNP Array 6.0. This work was supported by NIH grants R01 HL131565 (A.M.), R01 HL103676 (D.J.L.), and R01 HL137234 (D.J.L.). ; Peer Reviewed
