Static rate-optimal scheduling of multirate DSP algorithms via retiming and unfolding.

This paper presents an exact method and a heuristic method for static rate-optimal multiprocessor scheduling of real-time multi rate DSP algorithms represented by synchronous data flow graphs (SDFGs). Through exploring the state-space generated by a self-timed execution (STE) of an SDFG, a static rate-optimal schedule via explicit retiming and implicit unfolding can be found by our exact method. By constraining the number of concurrent firings of actors of an STE, the number of processors used in a schedule can be limited. Using this, we present a heuristic method for processor-constrained rate-optimal scheduling of SDFGs. Both methods do not explicitly convert an SDFG to its equivalent homogenous SDFG. Our experimental results show that the exact method gives a significant improvement compared to the existing methods, our heuristic method further reduces the number of processors used

Memory-constrained static rate-optimal scheduling of synchronous dataflow graphs via retiming

Synchronous dataflow graphs (SDFGs) are widely used to model digital signal processing (DSP) and streaming media applications. In this paper, we use retiming to optimize SDFGs to achieve a high throughput with low storage requirement. Using a memory constraint as an additional enabling condition, we define a memory constrained self-timed execution of an SDFG. Exploring the state-space generated by the execution, we can check whether a retiming exists that leads to a rate-optimal schedule under the memory constraint. Combining this with a binary search strategy, we present a heuristic method to find a proper retiming and a static scheduling which schedules the retimed SDFG with optimal rate (i.e., maximal throughput) and with as little storage space as possible. Our experiments are carried out on hundreds of synthetic SDFGs and several models of real applications. Differential synthetic graph results and real application results show that, in 79% of the tested models, our method leads to a retimed SDFG whose rate-optimal schedule requires less storage space than the proven minimal storage requirement of the original graph, and in 20% of the cases, the returned storage requirements equal the minimal ones. The average improvement is about 7.3%. The results also show that our method is computationally efficient

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease