The Role of Anti-Money Laundering Law in Mobile Money Systems in Developing Countries

This Article explains that the application of anti-money laundering (AML) regulation, supervision, and enforcement is relevant to financial inclusion, but is not, in itself, necessarily determinative of the success or failure of financial inclusion initiatives or their impact on economic growth. Successful payments system innovation, particularly payment tools targeting underserved markets, requires effective entrepreneurship operating in an environment of good governance and rational economic policies. AML safeguards help to deter corruption and other forms of financial crime, which helps to establish and maintain economic stability and preserve the rule of law, creating a supportive environment for innovation and financial inclusion. This Article explains that the revised Financial Action Task Force (FATF) Recommendations, the international standard for AML practices, promote a risk-based approach to implementation, allowing countries flexibility in order to encourage the widest possible participation in the regulated and supervised financial system

Empty Silos: Eliminating the ICBM From the U.S. Nuclear Force Structure

As of December 2011, the Department of Defense faces significant budgetary cuts. One way of meeting such cuts would be to eliminate one leg of the current nuclear triad -“ land-based intercontinental ballistic missiles (ICBMs). Such a cut would preserve billions of dollars in spending, but would also require a reassessment of U.S. nuclear strategy and policy goals. This paper argues that elimination of ICBMs is a feasible action that would preserve the nuclear force's flexibility with submarine- and bomber-based platforms. Additionally, such a move could refocus international efforts on nuclear disarmament and nonproliferation. However, the elimination of our perceived strongest technological capability could have a significant normative impact on the perception of U.S. military strength and capabilities. Domestic audiences, such as conservative elements or elder generations, would question the administration's ability to secure the U.S. against threats, and more aggressive nations may respond with shows of their own military missile capabilities. ICBMs serve more as a symbol of power and technology than as a practical weapon capable of being integrated into a feasible U.S. security strategy

Children's biobehavioral reactivity to challenge predicts DNA methylation in adolescence and emerging adulthood.

A growing body of research has documented associations between adverse childhood environments and DNA methylation, highlighting epigenetic processes as potential mechanisms through which early external contexts influence health across the life course. The present study tested a complementary hypothesis: indicators of children's early internal, biological, and behavioral responses to stressful challenges may also be linked to stable patterns of DNA methylation later in life. Children's autonomic nervous system reactivity, temperament, and mental health symptoms were prospectively assessed from infancy through early childhood, and principal components analysis (PCA) was applied to derive composites of biological and behavioral reactivity. Buccal epithelial cells were collected from participants at 15 and 18 years of age. Findings revealed an association between early life biobehavioral inhibition/disinhibition and DNA methylation across many genes. Notably, reactive, inhibited children were found to have decreased DNA methylation of the DLX5 and IGF2 genes at both time points, as compared to non-reactive, disinhibited children. Results of the present study are provisional but suggest that the gene's profile of DNA methylation may constitute a biomarker of normative or potentially pathological differences in reactivity. Overall, findings provide a foundation for future research to explore relations among epigenetic processes and differences in both individual-level biobehavioral risk and qualities of the early, external childhood environment

Use of novel DNA methylation signatures to distinguish between human airway structural cell types

INTRODUCTION: Chronic inflammatory and fibrotic lung diseases like asthma, COPD and pulmonary fibrosis are characterised by modified phenotype of the airway structural cells. Airway walls are comprised of a robust epithelial layer that lines the lumen followed by the basement membrane, submucosa predominantly composed of fibroblasts and finally enveloped by a bulk of smooth muscle cells that determine the relaxation and constriction of the airways. The phenotype of airway structural cells is determined by epigenetic alterations such as DNA methylation, which alters the activation status of a range of important inflammatory and remodelling genes. Here we determined if airway structural cells (Epithelial cells, fibroblasts and smooth muscle cells) have different DNA methylome signatures that can be used to distinguish between them. This will offer a reference standard for identifying cell type specific DNA methylation changes induced by various inflammatory stimuli. EXPERIMENTAL METHODS: Illumina Human Methylation 450K Beadchip (HM450K) was used to perform genome-wide methylome screening on 17 bronchial fibroblast (BrF), 23 lung parenchymal fibroblast (LgF), 17 airway epithelial cell (Ep) and 6 airway smooth muscle cell (ASM) samples isolated from healthy individuals. The data was normalised using funtoonorm, a specialised algorithm in R developed for multiple tissue types. R packages minfi, limma and DMRcate was used for CpG site exclusion and identification of significant differentially methylated regions (DMR) specific to each of the four cell types. RESULTS AND DISCUSSION: Epithelial cells distinctly separated from other lung cells (791 DMR). LgF, BrF and ASM had 13, 10 and 1 signature DMR respectively. Despite close anatomical proximity, ASM and BrF displayed 2 DMR when compared to each other. Interestingly, fibroblasts obtained from airway showed 6 DMR in comparison to those obtained from lung parenchyma, suggesting that the same cell type obtained from different parts of the lung can have significantly different methylation patterns that might lead to phenotypic differences. CONCLUSION: We have identified cell and tissue specific methylation signatures which can be used to differentiate between different types of airway structural cells. The airway epithelial cells showed the greatest separation from other airway structural cells. The Bronchial fibroblasts varied minimally from airway smooth muscle cells despite its significant separation from airway epithelial cells and parenchymal fibroblasts

The biological embedding of early-life socioeconomic status and family adversity in children's genome-wide DNA methylation.

AimTo examine variation in child DNA methylation to assess its potential as a pathway for effects of childhood social adversity on health across the life course.Materials & methodsIn a diverse, prospective community sample of 178 kindergarten children, associations between three types of social experience and DNA methylation within buccal epithelial cells later in childhood were examined.ResultsFamily income, parental education and family psychosocial adversity each associated with increased or decreased DNA methylation (488, 354 and 102 sites, respectively) within a unique set of genomic CpG sites. Gene ontology analyses pointed to genes serving immune and developmental regulation functions.ConclusionFindings provided support for DNA methylation as a biomarker linking early-life social experiences with later life health in humans

Optimized CRISPR-mediated gene knockin reveals FOXP3-independent maintenance of human Treg identity

Regulatory T cell (Treg) therapy is a promising curative approach for a variety of immune-mediated conditions. CRISPR-based genome editing allows precise insertion of transgenes through homology-directed repair, but its use in human Tregs has been limited. We report an optimized protocol for CRISPR-mediated gene knockin in human Tregs with high-yield expansion. To establish a benchmark of human Treg dysfunction, we target the master transcription factor FOXP3 in naive and memory Tregs. Although FOXP3-ablated Tregs upregulate cytokine expression, effects on suppressive capacity in vitro manifest slowly and primarily in memory Tregs. Moreover, FOXP3-ablated Tregs retain their characteristic protein, transcriptional, and DNA methylation profile. Instead, FOXP3 maintains DNA methylation at regions enriched for AP-1 binding sites. Thus, although FOXP3 is important for human Treg development, it has a limited role in maintaining mature Treg identity. Optimized gene knockin with human Tregs will enable mechanistic studies and the development of tailored, next-generation Treg cell therapies