Using the High Productivity Language Chapel to Target GPGPU Architectures

It has been widely shown that GPGPU architectures offer large performance gains compared to their traditional CPU counterparts for many applications. The downside to these architectures is that the current programming models present numerous challenges to the programmer: lower-level languages, explicit data movement, loss of portability, and challenges in performance optimization. In this paper, we present novel methods and compiler transformations that increase productivity by enabling users to easily program GPGPU architectures using the high productivity programming language Chapel. Rather than resorting to different parallel libraries or annotations for a given parallel platform, we leverage a language that has been designed from first principles to address the challenge of programming for parallelism and locality. This also has the advantage of being portable across distinct classes of parallel architectures, including desktop multicores, distributed memory clusters, large-scale shared memory, and now CPU-GPU hybrids. We present experimental results from the Parboil benchmark suite which demonstrate that codes written in Chapel achieve performance comparable to the original versions implemented in CUDA.NSF CCF 0702260Cray Inc. Cray-SRA-2010-016962010-2011 Nvidia Research Fellowshipunpublishednot peer reviewe

Implementing scalable matrix-vector products for the exact diagonalization methods in quantum many-body physics

Exact diagonalization is a well-established method for simulating small quantum systems. Its applicability is limited by the exponential growth of the so-called Hamiltonian matrix that needs to be diagonalized. Physical symmetries are usually utilized to reduce the matrix dimension, and distributed-memory parallelism is employed to explore larger systems. This paper focuses on the implementation the core distributed algorithms, with a special emphasis on the matrix-vector product operation. Instead of the conventional MPI+X paradigm, Chapel is chosen as the language for these distributed algorithms. We provide a comprehensive description of the algorithms and present performance and scalability tests. Our implementation outperforms the state-of-the-art MPI-based solution by a factor of 7--8 on 32 compute nodes or 4096 cores and exhibits very good scaling on up to 256 nodes or 32768 cores. The implementation has 3 times fewer software lines of code than the current state of the art while remaining fully generic.Comment: 11 pages, 9 figure

A Region-based Approach for Sparse Parallel Computing

This paper introduces a technique for parallel sparse computation by extending the array-language concept of regions---regular programmer-specified index sets used for specifying array computations. We introduce the notion of sparse regions which can represent an arbitrary set of indices. Sparse regions inherit the benefits of regular regions, including conciseness, a direct encapsulation of parallelism, and support for language performance models that highlight parallel overheads. We show that region-based array languages can benefit from the use of sparse regions, both in terms of the semantic richness available to the programmer and the execution times of the resulting program. We also demonstrate that regions result in efficient implementations as compared to array-based approachs, due to their role in amortizing sparse overheads and enabling optimizations

teaMPI---replication-based resiliency without the (performance) pain.

In an era where we can not afford to checkpoint frequently, replication is a generic way forward to construct numerical simulations that can continue to run even if hardware parts fail. Yet, replication often is not employed on larger scales, as naïvely mirroring a computation once effectively halves the machine size, and as keeping replicated simulations consistent with each other is not trivial. We demonstrate for the ExaHyPE engine—a task-based solver for hyperbolic equation systems—that it is possible to realise resiliency without major code changes on the user side, while we introduce a novel algorithmic idea where replication reduces the time-to-solution. The redundant CPU cycles are not burned “for nothing”. Our work employs a weakly consistent data model where replicas run independently yet inform each other through heartbeat messages whether they are still up and running. Our key performance idea is to let the tasks of the replicated simulations share some of their outcomes, while we shuffle the actual task execution order per replica. This way, replicated ranks can skip some local computations and automatically start to synchronise with each other. Our experiments with a production-level seismic wave-equation solver provide evidence that this novel concept has the potential to make replication affordable for large-scale simulations in high-performance computing

Design and implementation of a parallel array operator for the arbitrary remapping of data.

The data redistribution or remapping functions, gather and scatter, are of long-standing in high-performance computing, having been included in Cray Fortran for decades. In this paper, we present a highly-general array operator with powerful ga.ther and scatter capa.bilities unmatched in other array languages. We discuss an efficient parallel implementation, introducing several new optimizations-run length encoding, dead army reuse, and direct conimunica.tion-that lessen the costs associa.ted with the operator's wide applicability. In our implementation of this operator in ZPL, we demonstrade comparable performance to the highly-tuned, hand-coded Fortran plus MPI versions of the NAS FT and NAS CG benchmarks

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 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

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 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