67 research outputs found
Learning Symbolic Models of Stochastic Domains
In this article, we work towards the goal of developing agents that can learn
to act in complex worlds. We develop a probabilistic, relational planning rule
representation that compactly models noisy, nondeterministic action effects,
and show how such rules can be effectively learned. Through experiments in
simple planning domains and a 3D simulated blocks world with realistic physics,
we demonstrate that this learning algorithm allows agents to effectively model
world dynamics
Inferring gene-to-phenotype and gene-to-disease relationships at Mouse Genome Informatics: challenges and solutions
Mitogen-activated protein kinases and NFκB are involved in SP-A-enhanced responses of macrophages to mycobacteria
Surfactant protein a promotes attachment of Mycobacterium tuberculosis to alveolar macrophages during infection with human immunodeficiency virus.
Massively parallel reporter assay confirms regulatory potential of hQTLs and reveals important variants in lupus and other autoimmune diseases
Summary: We designed a massively parallel reporter assay (MPRA) in an Epstein-Barr virus transformed B cell line to directly characterize the potential for histone post-translational modifications, i.e., histone quantitative trait loci (hQTLs), expression QTLs (eQTLs), and variants on systemic lupus erythematosus (SLE) and autoimmune (AI) disease risk haplotypes to modulate regulatory activity in an allele-dependent manner. Our study demonstrates that hQTLs, as a group, are more likely to modulate regulatory activity in an MPRA compared with other variant classes tested, including a set of eQTLs previously shown to interact with hQTLs and tested AI risk variants. In addition, we nominate 17 variants (including 11 previously unreported) as putative causal variants for SLE and another 14 for various other AI diseases, prioritizing these variants for future functional studies in primary and immortalized B cells. Thus, we uncover important insights into the mechanistic relationships among genotype, epigenetics, and gene expression in SLE and AI disease phenotypes
- …