Beyond the project cycle: an evaluation of agroforestry adoption and diffusion over the medium term in a south Indian village

Few studies explicitly assess the temporal and spatial dynamics of agroforestry adoption occurring beyond the project cycle. Where ex-post evaluations are published, abandonment of introduced agroforestry after project cessation is often reported. This paper presents an analysis of agroforestry adoption in a poor, peri-urban village in semi-arid south India, where 97 % of initial adopters had retained their plots six to eight years after implementation. The intervention was facilitated by BAIF, an Indian non-governmental organisation specialising in natural resource management. The complex technological package promoted was known as �wadi� and comprised fruit trees planted in crop fields, with a boundary of multi-purpose trees and integrated soil and water conservation measures. Sixty four agroforestry plots belonging to 43 households were surveyed in 2010/11 and interviews were held with both adopting and non-adopting farmers. Beyond retention, a quarter of adopters had expanded the practice on to additional areas of land and some diffusion to initially non-adopting farmers had also occurred. Adopters were found to have modified the practice to suit their own objectives, capabilities and constraints, highlighting that adoption is more than a simple binary choice. The study demonstrates the importance of external support for adoption of agroforestry. The intervention was not, however, especially pro-poor with adoption occurring disproportionately among relatively wealthier households with larger landholdings. Where poorer households adopted, this tended to occur later. Participation was entirely voluntary and, by 2011, conversion of suitable farmland to agroforestry had reached 18 %; while beneficial to individual adopters, this patchy coverage arguably limits the potential for enhanced ecosystem service provision at landscape-scale

Biocompatible silk fibroin scaffold prepared by reactive inkjet printing

It has recently been shown that regenerated silk fibroin (RSF) aqueous solution can be printed using an inkjet printer. In this communication, we demonstrate an alternative reactive inkjet printing method that provides control over RSF crystallinity through β-sheet concentration. A biocompatible film has successfully been produced through the alternate printing of RSF aqueous solution and methanol using reactive inkjet printing. Control over the formation of the β-sheet structure was achieved by printing different ratios of RSF to methanol and was confirmed using Fourier Transform Infra Red spectroscopy. The biocompatibility of the printed silk scaffold was demonstrated by the growth of fibroblast cells upon its surface

3D printed tissue engineered model for bone invasion of oral cancer

Recent advances in three-dimensional printing technology have led to a rapid expansion of its applications in tissue engineering. The present study was designed to develop and characterize an in vitro multi-layered human alveolar bone, based on a 3D printed scaffold, combined with tissue engineered oral mucosal model. The objective was to incorporate oral squamous cell carcinoma (OSCC) cell line spheroids to the 3D model at different anatomical levels to represent different stages of oral cancer. Histological evaluation of the 3D tissue model revealed a tri-layered structure consisting of distinct epithelial, connective tissue, and bone layers; replicating normal oral tissue architecture. The mucosal part showed a well-differentiated stratified oral squamous epithelium similar to that of the native tissue counterpart, as demonstrated by immunohistochemistry for cytokeratin 13 and 14. Histological assessment of the cancerous models demonstrated OSCC spheroids at three depths including supra-epithelial level, sub-epithelial level, and deep in the connective tissue-bone interface. The 3D tissue engineered composite model closely simulated the native oral hard and soft tissues and has the potential to be used as a valuable in vitro model for the investigation of bone invasion of oral cancer and for the evaluation of novel diagnostic or therapeutic approaches to manage OSCC in the future

Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe