Market-Based Aid and Economic Reform

This study examines the empirical links between market-based aid and economic reform in sub-Sahara Africa. My research question: Is market-based aid necessary for economic reform across sub-Sahara Africa? To answer that question, I applied both quantitative and qualitative approaches. Specifically, regression analyses were conducted to determine whether or not causality could be established between my dependent and independent variables. 22 sub-Saharan states were used. In addition, two case studies (Ghana and Senegal) were conducted to help explain some of the cultural nuances that may be missing from the statistical analysis. As a result of the Washington Consensus, International Financial Institutions (IFIs) and advanced economies have advocated for economic reforms -- namely macro-level neoliberal structural adjustments - to help facilitate sustainable economic growth and development across emerging economies. This approach has been critiqued in the past since it uses a \u27one-size-fits-all\u27 approach and assumes that since similar reform efforts were successful in the west, then they should work in the sub-Sahara region absent of accounting for internal nuances such as cultural and traditional values, customs, structures and conditions. I argue that more market-based aid could be the best way forward, especially if economic reform efforts are tailored toward four key conduits that are essential for driving subsequent economic growth and development: government capacity, economic freedom, private sector investments, and domestic savings. I hypothesized the aforementioned are positively linked with market-based aid

Genomic mapping of the MHC transactivator CIITA using an integrated ChIP-seq and genetical genomics approach

BACKGROUND: The master transactivator CIITA is essential to the regulation of Major Histocompatibility Complex (MHC) class II genes and an effective immune response. CIITA is known to modulate a small number of non-MHC genes involved in antigen presentation such as CD74 and B2M but its broader genome-wide function and relationship with underlying genetic diversity has not been resolved. RESULTS: We report the first genome-wide ChIP-seq map for CIITA and complement this by mapping inter-individual variation in CIITA expression as a quantitative trait. We analyse CIITA recruitment for pathophysiologically relevant primary human B cells and monocytes, resting and treated with interferon-gamma, in the context of the epigenomic regulatory landscape and DNA-binding proteins associated with the CIITA enhanceosome including RFX, CREB1/ATF1 and NFY. We confirm recruitment to proximal promoter sequences in MHC class II genes and more distally involving the canonical CIITA enhanceosome. Overall, we map 843 CIITA binding intervals involving 442 genes and find 95% of intervals are located outside the MHC and 60% not associated with RFX5 binding. Binding intervals are enriched for genes involved in immune function and infectious disease with novel loci including major histone gene clusters. We resolve differentially expressed genes associated in trans with a CIITA intronic sequence variant, integrate with CIITA recruitment and show how this is mediated by allele-specific recruitment of NF-kB. CONCLUSIONS: Our results indicate a broader role for CIITA beyond the MHC involving immune-related genes. We provide new insights into allele-specific regulation of CIITA informative for understanding gene function and disease. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13059-014-0494-z) contains supplementary material, which is available to authorized users