De la "tierra para los pobres" a espacios de conservación y disputa: la Selva Lacandona y la Sierra Madre de Chiapas desde la perspectiva de la justicia ambiental

This article considers an agrarian problem faced by a number of settlements in protected areas in two regions of Chiapas, the Lacandon Forest and the Sierra Madre, both important for their biological and cultural diversity. Through case studies, we show the varied legal situations and difficulties that exist in legalizing these settlements, located at an intersection of interests. Using an environmental justice approach, we conclude that land users in these settlements pay many of the costs of conservation and have been historically segregated in the two regions considered.En este artículo se aborda el problema agrario que enfrentan varios asentamientos en áreas naturales protegidas federales de dos regiones importantes en Chiapas por su riqueza biológica y cultural, la Selva Lacandona y la Sierra Madre. A partir de estudios de caso, se muestran las múltiples situaciones jurídicas existentes y las dificultades para regularizar estos asentamientos, en una intersección de intereses. Empleando el enfoque de justicia ambiental, se concluye que estos posesionarios cargan con costos de conservación desmedidos y son objeto de una segregación histórica en las dos regiones

Manejo de recursos forestales no maderables y las políticas de simplificación: El caso de la palma xate en la Selva Lacandona, México

Resumen El uso de Recursos Forestales No Maderables (RFNM) puede crear oportunidades de desarrollo para poblaciones locales; pero ello requiere de determinadas condiciones. En México, el uso de RFNM considerados oficialmente como “amenazados” es regulado por Unidades de Manejo para la Conservación de la Vida Silvestre (UMA), un instrumento que busca conciliar la conservación biológica con desarrollo local. Sus resultados varían en función de las características del contexto en que se aplica. La mayoría de las UMA del sur del país, especialmente de RFNM, muestran resultados poco alentadores, pues no consideran en su diseño e implementación, la complejidad y diversidad de condiciones presentes en los espacios rurales de esta región. Aquí analizamos la implementación de una UMA de palma camedor en dos comunidades rurales de la Selva Lacandona, Chiapas, México, a través de registro etnográfico, entrevistas a profundidad y cuestionarios socioeconómicos. Argumentamos que las UMA de palma parten de una concepción simplificada de la realidad compleja de las comunidades en donde se implementan y trastocan su equilibrio de poder; su diseño burocrático y sobre-regulatorio fomenta discrecionalidad, simulación y corrupción, lo que acentúa la exclusión y favorece a las élites locales. Abstract The use of non-timber forest products (NTFPs) can create development opportunities for local populations, but this requires certain conditions. In Mexico, the use of NTFP considered by the government to be “at risk” is regulated by “wildlife conservation management units” (UMAs), a policy instrument that seeks to reconcile biological conservation with local development. Its effectiveness varies according to the context in which the instrument is applied. The majority of UMAs in the south of the Mexico, particularly for NTFPs, have shown less than encouraging results, partly because their design and implementation do not take into account the complexity and diversity of the conditions present in rural areas in this part of the country. Based on ethnographic observation, in-depth interviews, and socioeconomic surveys, this article analyzes the implementation of a palm (palma camedor) UMA in two rural villages in the Lacandon rain forest in Chiapas, Mexico. We argue that these palm UMAs assume a simplified conception of the complex reality of these communities, in which the implementation of the management instrument alters the local balance of power. Its bureaucratic design and overregulating character generates discretionality, simulation, and corruption, which in turn accentuates exclusions and favors local elites

Territories and sustainable tourism: a reading from the political culture in Chiapas (México)

En el marco de investigaciones que indagan sobre el papel del turismo sustentable como política pública y estrategia de conservación o desarrollo en zonas rurales campesinas e indígenas de Chiapas, se estudia a la cultura política como referencia integradora de las dimensiones simbólica y política del territorio. El artículo analiza la articulación entre las esferas gubernamental y social en torno a la implementación del turismo como alternativa a las actividades primarias. A partir de diversas fuentes (relatos de actores locales, gubernamentalesy otros; instrumentos y discursos oficiales) se describen los mecanismos y comportamientos políticos que guían los procesos y las decisiones territoriales. Se destaca que con la introducción del turismo sustentable se siguen admitiendo formas de “participación toleradas”, opuestas a las propuestas teóricas pero características del gobierno centralizado, y asociadas a una aparente inclusión social, promoviéndose la configuración de territorios dominados.In the context of research on the role of sustainable tourism as public policy and a strategy for conservation and rural development in indigenous and peasant regions of Chiapas, we look at the political culture as a fundamental reference point for understanding the symbolic and political dimensions of the territories. This article analyzes the articulation between government and local spheres in the implementation of tourism as an alternative to primary sector activities. Using diverse sources (interviews with local actors, government representatives and others; policy instruments and official discourses) we describe the political mechanisms and behaviors that guide territorial and decision-making processes. What stands out is that with the introduction of sustainable tourism ‘tolerated’ forms of participation are permitted, which contradict the theory behind sustainable tourism but reflect a centralized government and are associated with apparent social inclusion that actually configures increasingly dominated territories

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition

Messiness of forest governance:How technical approaches suppress politics in REDD+ and conservation projects

Reduction of Emissions from Deforestation and Forest Degradation (REDD+) was originally conceived to address the global problem of climate change by reducing deforestation and forest degradation at national and subnational levels in developing countries. Since its inception, REDD+ proponents have increasingly had to adapt global ideas to local demands, as the rollout process was met with on-the-ground realities, including suspicion and protest. As is typical in aid or ‘development’ projects conceived in the global North, most of the solutions advanced to improve REDD+ tend to focus on addressing issues of justice (or ‘fairness’) in distributive terms, rather than addressing more inherently political objections to REDD+ such as those based on rights or social justice. Using data collected from over 700 interviews in five countries with both REDD+ and non-REDD+ cases, we argue that the failure to incorporate political notions of justice into conservation projects such as REDD+ results in ‘messiness’ within governance systems, which is a symptom of injustice and illegitimacy. We find that, first, conservation, payment for ecosystem services, and REDD+ project proponents viewed problems through a technical rather than political lens, leading to solutions that focused on procedures, such as ‘benefit distribution.’ Second, focusing on the technical aspects of interventions came at the expense of political solutions such as the representation of local people's concerns and recognition of their rights. Third, the lack of attention to representation and recognition justices resulted in illegitimacy. This led to messiness in the governance systems, which was often addressed in technical terms, thereby perpetuating the problem. If messiness is not appreciated and addressed from appropriate notions of justice, projects such as REDD+ are destined to fail

Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio

Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk

The timing of puberty is a highly polygenic childhood trait that is epidemiologically associated with various adult diseases. Using 1000 Genomes Project-imputed genotype data in up to similar to 370,000 women, we identify 389 independent signals (P <5 x 10(-8)) for age at menarche, a milestone in female pubertal development. In Icelandic data, these signals explain similar to 7.4% of the population variance in age at menarche, corresponding to similar to 25% of the estimated heritability. We implicate similar to 250 genes via coding variation or associated expression, demonstrating significant enrichment in neural tissues. Rare variants near the imprinted genes MKRN3 and DLK1 were identified, exhibiting large effects when paternally inherited. Mendelian randomization analyses suggest causal inverse associations, independent of body mass index (BMI), between puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men. In aggregate, our findings highlight the complexity of the genetic regulation of puberty timing and support causal links with cancer susceptibility

Evidence for SMAD3 as a modifier of breast cancer risk in BRCA2 mutation carriers

Abstract Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P &lt; 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r 2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, P trend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, P trend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations

Common Genetic Variants and Modification of Penetrance of BRCA2-Associated Breast Cancer

Peer reviewe

Common breast cancer susceptibility alleles are associated with tumor subtypes in BRCA1 and BRCA2 mutation carriers : results from the Consortium of Investigators of Modifiers of BRCA1/2.

Abstract Introduction Previous studies have demonstrated that common breast cancer susceptibility alleles are differentially associated with breast cancer risk for BRCA1 and/or BRCA2 mutation carriers. It is currently unknown how these alleles are associated with different breast cancer subtypes in BRCA1 and BRCA2 mutation carriers defined by estrogen (ER) or progesterone receptor (PR) status of the tumour. Methods We used genotype data on up to 11,421 BRCA1 and 7,080 BRCA2 carriers, of whom 4,310 had been affected with breast cancer and had information on either ER or PR status of the tumour, to assess the associations of 12 loci with breast cancer tumour characteristics. Associations were evaluated using a retrospective cohort approach. Results The results suggested stronger associations with ER-positive breast cancer than ER-negative for 11 loci in both BRCA1 and BRCA2 carriers. Among BRCA1 carriers, single nucleotide polymorphism (SNP) rs2981582 (FGFR2) exhibited the biggest difference based on ER status (per-allele hazard ratio (HR) for ER-positive = 1.35, 95% CI: 1.17 to 1.56 vs HR = 0.91, 95% CI: 0.85 to 0.98 for ER-negative, P-heterogeneity = 6.5 &#215; 10-6). In contrast, SNP rs2046210 at 6q25.1 near ESR1 was primarily associated with ER-negative breast cancer risk for both BRCA1 and BRCA2 carriers. In BRCA2 carriers, SNPs in FGFR2, TOX3, LSP1, SLC4A7/NEK10, 5p12, 2q35, and 1p11.2 were significantly associated with ER-positive but not ER-negative disease. Similar results were observed when differentiating breast cancer cases by PR status. Conclusions The associations of the 12 SNPs with risk for BRCA1 and BRCA2 carriers differ by ER-positive or ER-negative breast cancer status. The apparent differences in SNP associations between BRCA1 and BRCA2 carriers, and non-carriers, may be explicable by differences in the prevalence of tumour subtypes. As more risk modifying variants are identified, incorporating these associations into breast cancer subtype-specific risk models may improve clinical management for mutation carriers