We introduce a Force-directed List Scheduling (FDLS) algorithm for resource-constrained assay compilation targeting Digital Microfluidic Biochips (DMFBs). This algorithm has been used in the past for high-level synthesis of digital signal processing systems, and is now applied to DMFB synthesis. The results show improvements compared to List Scheduling (LS) and Path Scheduling (PS), the most efficient heuristics that have been proposed, to date, for DMFBs. FDLS was also competitive with longer-running iterative improvement DMFB scheduling algorithms based on genetic algorithms. © 2012 IEEE.

Synthesis of digital microfluidic biochips (DMFBs) is a crucial to the advancement and realization of miniaturized, automated, programmable biochemistry solutions; synthesis is performed in three steps: scheduling, placement and routing. In principle, algorithms for specific steps should be interchangeable with one another; however, different research groups typically develop algorithms for each step in isolation from one another. Thus, it is difficult to compare algorithms against one another, or to determine which algorithms for different steps share synergies. We introduce an open source DMFB synthesis framework to encourage collaboration between researchers working in the area. We introduce a common interface and describe the internal data structures that must be updated to ensure that the interfaces are adhered to. We also present and describe a number of high-quality 2D and 3D debugging tools that provide graphical output for each stage of synthesis. © 2012 IEEE.

HIV +Elite and Viremic controllers (EC/VCs) are able to control virus infection, perhaps because of host genetic determinants. We identified 16% (21 of 131) EC/VCs with CD4 +T cells with resistance specific to R5-tropic HIV, reversed after introduction of ccr5. R5 resistance was not observed in macrophages and depended upon the method of T cell activation. CD4 +T cells of these EC/VCs had lower ccr2 and ccr5 RNA levels, reduced CCR2 and CCR5 cell-surface expression, and decreased levels of secreted chemokines. T cells had no changes in chemokine receptor mRNA half-life but instead had lower levels of active transcription of ccr2 and ccr5, despite having more accessible chromatin by ATAC-seq. Other nearby genes were also down-regulated, over a region of ~500 kb on chromosome 3p21. This same R5 resistance phenotype was observed in family members of an index VC, also associated with ccr2/ccr5 down-regulation, suggesting that the phenotype is heritable.