Analyzing procedural equity in government-led community-based forest management

Participatory approaches to forest management have been promoted as a means of returning rights historically removed, and as a way of managing natural resources sustainably, fairly, and to improve livelihoods in communities. Top-down models of community-based forest management take the perspective that if people feel ownership over, have a voice in decisions about, and can benefit from surrounding ecosystems, then they will be motivated to maintain and protect them. However, even participatory approaches, such as community-based forest management, may not always result in clear positive outcomes for involvement in decision making and forest conservation. We examine whether an Indonesian government initiative for community-based forest management was positively associated with community members' participation in local decision making and support for conservation and sustainable management of forest resources, in the context of state-owned lands. We used household questionnaire data to compare villages with and without a community forest, and community forests over time in a case study region of West Kalimantan. Analyzing forest visitations, conservation support, and indicators of procedural equity, we found no consistent association between having a community forest and higher levels of participation in decision making or household support for forest conservation. However, well-being indicators were positively associated with more active participation. The level of support for forest conservation was also positively related to households' leadership in village institutions and higher levels of well-being, particularly subjective well-being, land tenure, and material wealth. These social-demographic factors are important considerations when designing and implementing community-based forest management, which strives for fair and just decision-making processes along with forest conservation. The findings highlight how existing socioeconomic contexts factor into local institutions, and that accounting for these in program design and implementation may help address existing social inequalities that influence achieving joint social and ecological objectives

A Follow-Up of the Multicenter Collaborative Study on HIV-1 Drug Resistance and Tropism Testing Using 454 Ultra Deep Pyrosequencing

Background: Ultra deep sequencing is of increasing use not only in research but also in diagnostics. For implementation of ultra deep sequencing assays in clinical laboratories for routine diagnostics, intra- and inter-laboratory testing are of the utmost importance. Methods: A multicenter study was conducted to validate an updated assay design for 454 Life Sciences’ GS FLX Titanium system targeting protease/reverse transcriptase (RTP) and env (V3) regions to identify HIV-1 drug-resistance mutations and determine co-receptor use with high sensitivity. The study included 30 HIV-1 subtype B and 6 subtype non-B samples with viral titers (VT) of 3,940–447,400 copies/mL, two dilution series (52,129–1,340 and 25,130–734 copies/mL), and triplicate samples. Amplicons spanning PR codons 10–99, RT codons 1–251 and the entire V3 region were generated using barcoded primers. Analysis was performed using the GS Amplicon Variant Analyzer and geno2pheno for tropism. For comparison, population sequencing was performed using the ViroSeq HIV-1 genotyping system. Results: The median sequencing depth across the 11 sites was 1,829 reads per position for RTP (IQR 592–3,488) and 2,410 for V3 (IQR 786–3,695). 10 preselected drug resistant variants were measured across sites and showed high inter-laboratory correlation across all sites with data (P20% were missed, variants 2–10% were detected at most sites (even at low VT), and variants 1–2% were detected by some sites. All mutations detected by population sequencing were also detected by UDS. Conclusions: This assay design results in an accurate and reproducible approach to analyze HIV-1 mutant spectra, even at variant frequencies well below those routinely detectable by population sequencing

Heterogeneous impacts of community forestry on forest conservation and poverty alleviation: evidence from Indonesia

1. Community forestry is a participatory approach aiming to achieve sustainable forest management while also reducing poverty among rural communities. Yet, evidence of the impacts of community forestry programmes on both forest conservation and poverty alleviation is scarce, and there is limited understanding of impacts across different social and biophysical contexts. 2. We applied a matching method to assess the extent to which deforestation has decreased and village well‐being has improved as a result of Indonesia's community forestry scheme, Hutan Desa (Village Forest). We assessed five dimensions of well‐being: basic (living conditions), physical (access to health and education), financial (income support), social (security and equity) and environmental (natural hazard prevention). 3. We found that Hutan Desa was associated with reduced deforestation and poverty. ‘Win‐win’ outcomes were found in 51% of cases, comprising (a) positive outcomes for both forests and poverty, (b) a positive outcome for one aspect and a negligible outcome for the other, or (c) a positive outcome for poverty in areas where natural forest had already been lacking prior to Hutan Desa tenure. Benefits to forests and people systematically differed depending on land‐use zones, reflecting subtle interactions between anthropogenic pressures and community livelihood characteristics. 4. In Watershed Protection Zones, which are dominated by subsistence‐based forest livelihoods, community forestry provided mild conservation benefits, but resulted in the greatest improvements in well‐being through improved land tenure. In Limited Production Zones, community forestry provided modest benefits for both conservation and well‐being because restrictions on timber harvest due to Hutan Desa designation reduced the financial well‐being of logging communities. The greatest conservation benefits were experienced in Permanent or Convertible Production Zones, but well‐being improvements were minimal. Here, living conditions and environmental well‐being were reduced due to pressure to intensify agricultural production under increased land scarcity in these predominantly cash crop‐oriented communities. 5. Our results highlight the spatial and contextual variation in impacts of community forestry policies on poverty alleviation and forest conservation outcomes. Crucially, our study provides vital objective information for future policy development in Indonesia and other tropical countries implementing community forestry schemes

Toward improved impact evaluation of community forest management in Indonesia

Many tropical countries continue to devolve forest management to forest‐dwelling communities. The assumption is that local knowledge of forests and community engagement in forest management will attain multiple social and environmental co‐benefits, such as poverty alleviation and reduced deforestation and fires. Evidence for this, however, is scant, commonly hampered by data availability and a lack of technical capacity for implementing statistically robust impact evaluations. Based on a practice‐based review of policy implementation, impact evaluation of case studies and examples of counterfactual analyses from Indonesia, we demonstrate that it is increasingly feasible to determine the conditions under which community forest management will most likely achieve its social and environmental objectives. Adapting community forest management implementation based on feedback from accurate impact evaluation could lead to positive outcomes for people and environment in Indonesia, and across the tropical realm

Social Anxiety Modulates Subliminal Affective Priming

BACKGROUND: It is well established that there is anxiety-related variation between observers in the very earliest, pre-attentive stage of visual processing of images such as emotionally expressive faces, often leading to enhanced attention to threat in a variety of disorders and traits. Whether there is also variation in early-stage affective (i.e. valenced) responses resulting from such images, however, is not yet known. The present study used the subliminal affective priming paradigm to investigate whether people varying in trait social anxiety also differ in their affective responses to very briefly presented, emotionally expressive face images. METHODOLOGY/PRINCIPAL FINDINGS: Participants (n = 67) completed a subliminal affective priming task, in which briefly presented and smiling, neutral and angry faces were shown for 10 ms durations (below objective and subjective thresholds for visual discrimination), and immediately followed by a randomly selected Chinese character mask (2000 ms). Ratings of participants' liking for each Chinese character indicated the degree of valenced affective response made to the unseen emotive images. Participants' ratings of their liking for the Chinese characters were significantly influenced by the type of face image preceding them, with smiling faces generating more positive ratings than neutral and angry ones (F(2,128) = 3.107, p<0.05). Self-reported social anxiety was positively correlated with ratings of smiling relative to neutral-face primed characters (Pearson's r = .323, p<0.01). Individual variation in self-reported mood awareness was not associated with ratings. CONCLUSIONS: Trait social anxiety is associated with individual variation in affective responding, even in response to the earliest, pre-attentive stage of visual image processing. However, the fact that these priming effects are limited to smiling and not angry (i.e. threatening) images leads us to propose that the pre-attentive processes involved in generating the subliminal affective priming effect may be different from those that generate attentional biases in anxious individuals

Color afterimages in autistic adults

It has been suggested that attenuated adaptation to visual stimuli in autism is the result of atypical perceptual priors (e.g., Pellicano and Burr in Trends Cogn Sci 16(10):504–510, 2012. doi:10.​1016/​j.​tics.​2012.​08.​009). This study investigated adaptation to color in autistic adults, measuring both strength of afterimage and the influence of top-down knowledge. We found no difference in color afterimage strength between autistic and typical adults. Effects of top-down knowledge on afterimage intensity shown by Lupyan (Acta Psychol 161:117–130, 2015. doi:10.​1016/​j.​actpsy.​2015.​08.​006) were not replicated for either group. This study finds intact color adaptation in autistic adults. This is in contrast to findings of attenuated adaptation to faces and numerosity in autistic children. Future research should investigate the possibility of developmental differences in adaptation and further examine top-down effects on adaptation

Localization of type 1 diabetes susceptibility to the MHC class I genes HLA-B and HLA-A

The major histocompatibility complex (MHC) on chromosome 6 is associated with susceptibility to more common diseases than any other region of the human genome, including almost all disorders classified as autoimmune. In type 1 diabetes the major genetic susceptibility determinants have been mapped to the MHC class II genes HLA-DQB1 and HLA-DRB1 (refs 1-3), but these genes cannot completely explain the association between type 1 diabetes and the MHC region. Owing to the region's extreme gene density, the multiplicity of disease-associated alleles, strong associations between alleles, limited genotyping capability, and inadequate statistical approaches and sample sizes, which, and how many, loci within the MHC determine susceptibility remains unclear. Here, in several large type 1 diabetes data sets, we analyse a combined total of 1,729 polymorphisms, and apply statistical methods - recursive partitioning and regression - to pinpoint disease susceptibility to the MHC class I genes HLA-B and HLA-A (risk ratios >1.5; Pcombined = 2.01 × 10-19 and 2.35 × 10-13, respectively) in addition to the established associations of the MHC class II genes. Other loci with smaller and/or rarer effects might also be involved, but to find these, future searches must take into account both the HLA class II and class I genes and use even larger samples. Taken together with previous studies, we conclude that MHC-class-I-mediated events, principally involving HLA-B*39, contribute to the aetiology of type 1 diabetes. ©2007 Nature Publishing Group

Determination of glucose exchange rates and permeability of erythrocyte membrane in preeclampsia and subsequent oxidative stress-related protein damage using dynamic-19F-NMR

The cause of the pregnancy condition preeclampsia (PE) is thought to be endothelial dysfunction caused by oxidative stress. As abnormal glucose tolerance has also been associated with PE, we use a fluorinated-mimic of this metabolite to establish whether any oxidative damage to lipids and proteins in the erythrocyte membrane has increased cell membrane permeability. Data were acquired using 19F Dynamic-NMR (DNMR) to measure exchange of 3-fluoro-3-deoxyglucose (3-FDG) across the membrane of erythrocytes from 10 pregnant women (5 healthy control women, and 5 from women suffering from PE). Magnetisation transfer was measured using the 1D selective inversion and 2D EXSY pulse sequences, over a range of time delays. Integrated intensities from these experiments were used in matrix diagonalisation to estimate the values of the rate constants of exchange and membrane permeability. No significant differences were observed for the rate of exchange of 3-FDG and membrane permeability between healthy pregnant women and those suffering from PE, leading us to conclude that no oxidative damage had occurred at this carrier-protein site in the membrane

Mapping genetic variations to three- dimensional protein structures to enhance variant interpretation: a proposed framework

The translation of personal genomics to precision medicine depends on the accurate interpretation of the multitude of genetic variants observed for each individual. However, even when genetic variants are predicted to modify a protein, their functional implications may be unclear. Many diseases are caused by genetic variants affecting important protein features, such as enzyme active sites or interaction interfaces. The scientific community has catalogued millions of genetic variants in genomic databases and thousands of protein structures in the Protein Data Bank. Mapping mutations onto three-dimensional (3D) structures enables atomic-level analyses of protein positions that may be important for the stability or formation of interactions; these may explain the effect of mutations and in some cases even open a path for targeted drug development. To accelerate progress in the integration of these data types, we held a two-day Gene Variation to 3D (GVto3D) workshop to report on the latest advances and to discuss unmet needs. The overarching goal of the workshop was to address the question: what can be done together as a community to advance the integration of genetic variants and 3D protein structures that could not be done by a single investigator or laboratory? Here we describe the workshop outcomes, review the state of the field, and propose the development of a framework with which to promote progress in this arena. The framework will include a set of standard formats, common ontologies, a common application programming interface to enable interoperation of the resources, and a Tool Registry to make it easy to find and apply the tools to specific analysis problems. Interoperability will enable integration of diverse data sources and tools and collaborative development of variant effect prediction methods

Frontotemporal dementia and its subtypes: a genome-wide association study

SummaryBackground Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. Mutations in three genes—MAPT, GRN, and C9orf72—have been associated with FTD. We sought to identify novel genetic risk loci associated with the disorder. Methods We did a two-stage genome-wide association study on clinical FTD, analysing samples from 3526 patients with {FTD} and 9402 healthy controls. To reduce genetic heterogeneity, all participants were of European ancestry. In the discovery phase (samples from 2154 patients with {FTD} and 4308 controls), we did separate association analyses for each {FTD} subtype (behavioural variant FTD, semantic dementia, progressive non-fluent aphasia, and {FTD} overlapping with motor neuron disease FTD-MND), followed by a meta-analysis of the entire dataset. We carried forward replication of the novel suggestive loci in an independent sample series (samples from 1372 patients and 5094 controls) and then did joint phase and brain expression and methylation quantitative trait loci analyses for the associated (p&lt;5 × 10−8) single-nucleotide polymorphisms. Findings We identified novel associations exceeding the genome-wide significance threshold (p&lt;5 × 10−8). Combined (joint) analyses of discovery and replication phases showed genome-wide significant association at 6p21.3, \{HLA\} locus (immune system), for rs9268877 (p=1·05 × 10−8; odds ratio=1·204 95% \{CI\} 1·11–1·30), rs9268856 (p=5·51 × 10−9; 0·809 0·76–0·86) and rs1980493 (p value=1·57 × 10−8, 0·775 0·69–0·86) in the entire cohort. We also identified a potential novel locus at 11q14, encompassing RAB38/CTSC (the transcripts of which are related to lysosomal biology), for the behavioural \{FTD\} subtype for which joint analyses showed suggestive association for rs302668 (p=2·44 × 10−7; 0·814 0·71–0·92). Analysis of expression and methylation quantitative trait loci data suggested that these loci might affect expression and methylation in cis. Interpretation Our findings suggest that immune system processes (link to 6p21.3) and possibly lysosomal and autophagy pathways (link to 11q14) are potentially involved in FTD. Our findings need to be replicated to better define the association of the newly identified loci with disease and to shed light on the pathomechanisms contributing to FTD. Funding The National Institute of Neurological Disorders and Stroke and National Institute on Aging, the Wellcome/MRC Centre on Parkinson's disease, Alzheimer's Research UK, and Texas Tech University Health Sciences Center