Pengaruh Indeks Harga Saham Syariah Internasional dan Variabel Makro Ekonomi terhadap Jakarta Islamic Index

The Impact of International Islamic Stock Market and Macroeconomic Variables Towards Jakarta Islamic Index (JII) This research atempts to examine the impact of International Islamic stock market and macroeconomic variables towards Jakarta Islamic Index (JII). By using Vector Error Correction Model (VECM) as the method, this research utilizes time series monthly data from January 2007 to October 2012. The finding shows that JII is positively significantly affected by DJIEU, DJIMY and IPI, and it is negatively significantly affected by DJIJP, IMUS, M2 and SBIS.JII reaches its stability condition fastest when dealing with money supply shock. This study recommends: strengthening coordination between monetary authority and financial services authority, strengthening real sector of the economy, minimizing the influence of interest Rate towards Islamic financial market, and developing early warning system to anticipate financial crises. DOI:10.15408/aiq.v6i2.122

Genetic and Epigenetic Fine-Mapping of Causal Autoimmune Disease Variants

Summary Genome-wide association studies have identified loci underlying human diseases, but the causal nucleotide changes and mechanisms remain largely unknown. Here we developed a fine-mapping algorithm to identify candidate causal variants for 21 autoimmune diseases from genotyping data. We integrated these predictions with transcription and cis-regulatory element annotations, derived by mapping RNA and chromatin in primary immune cells, including resting and stimulated CD4+ T-cell subsets, regulatory T-cells, CD8+ T-cells, B-cells, and monocytes. We find that ~90% of causal variants are noncoding, with ~60% mapping to immune-cell enhancers, many of which gain histone acetylation and transcribe enhancer-associated RNA upon immune stimulation. Causal variants tend to occur near binding sites for master regulators of immune differentiation and stimulus-dependent gene activation, but only 10–20% directly alter recognizable transcription factor binding motifs. Rather, most noncoding risk variants, including those that alter gene expression, affect non-canonical sequence determinants not well-explained by current gene regulatory models