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Scale-out datacenter network fabrics enable network operators to translate improved link and switch speeds directly into end-host throughput. Unfortunately, limits in the underlying CMOS packet switch chip manufacturing roadmap mean that NICs, links, and switches are not getting faster fast enough to meet demand. As a result, operators have introduced alternative, parallel fabric designs in the core of the network that deliver N-times the bandwidth by simply forwarding traffic over any of N parallel network fabrics. In this work, we consider extending this parallel network idea all the way to the end host. Our initial impressions found that direct application of existing path selection and forwarding techniques resulted in poor performance. Instead, we show that appropriate path selection and forwarding protocols can not only improve the performance of existing, homogeneous parallel fabrics, but enable the development of heterogeneous parallel network fabrics that can deliver even higher bandwidth, lower latency, and improved resiliency than traditional designs constructed from the same constituent components. 

Burst-parallel serverless applications invoke thousands of short-lived distributed functions to complete complex jobs such as data analytics, video encoding, or compilation. While these tasks execute in seconds, starting and configuring the virtual network they rely on is a major bottleneck that can consume up to 84% of total startup time. In this paper we characterize the magnitude of this network cold start problem in three popular overlay networks, Docker Swarm, Weave, and Linux Overlay. We focus on end-to-end startup time that encompasses both the time to boot a group of containers as well as interconnecting them. Our primary observation is that existing overlay approaches for serverless networking scale poorly in short-lived serverless environments. Based on our findings we develop Particle, a network stack tailored for multi-node serverless overlay networks that optimizes network creation without sacrificing multi-tenancy, generality, or throughput. When integrated into a serverless burst-parallel video processing pipeline, Particle improves application runtime by 2.4--3X over existing overlays. 

The Lightwave Energy-Efficient Datacenter (LEED) project within the ARPA-e ENLITENED program is developing novel energy-efficient multichannel lightwave networks. These networks are enabled by a new optical “rotor” switch that can reconfigure the network topology in less than 20 µs and a field-programmable-gate-array-based network interface controller called Corundum that can provide precise network-wide synchronization of packets admitted into the lightwave network. Here we review the optical networking research within LEED and discuss future directions.

 

Sprocket is a highly configurable, stage-based, scalable, serverless video processing framework that exploits intra-video parallelism to achieve low latency. Sprocket enables developers to program a series of operations over video content in a modular, extensible manner. Programmers implement custom operations, ranging from simple video transformations to more complex computer vision tasks, in a simple pipeline specification language to construct custom video processing pipelines. Sprocket then handles the underlying access, encoding and decoding, and processing of video and image content across operations in a highly parallel manner. In this paper we describe the design and implementation of the Sprocket system on the AWS Lambda serverless cloud infrastructure, and evaluate Sprocket under a variety of conditions to show that it delivers its performance goals of high parallelism, low latency, and low cost (10s of seconds to process a 3,600 second video 1000-way parallel for less than $3). 

Rationale: NAA15 (N-alpha-acetyltransferase 15) is a component of the NatA (N-terminal acetyltransferase complex). The mechanism by which NAA15 haploinsufficiency causes congenital heart disease remains unknown. To better understand molecular processes by which NAA15 haploinsufficiency perturbs cardiac development, we introduced NAA15 variants into human induced pluripotent stem cells (iPSCs) and assessed the consequences of these mutations on RNA and protein expression. Objective: We aim to understand the role of NAA15 haploinsufficiency in cardiac development by investigating proteomic effects on NatA complex activity and identifying proteins dependent upon a full amount of NAA15. Methods and Results: We introduced heterozygous loss of function, compound heterozygous, and missense residues (R276W) in iPSCs using CRISPR/Cas9. Haploinsufficient NAA15 iPSCs differentiate into cardiomyocytes, unlike NAA15 -null iPSCs, presumably due to altered composition of NatA. Mass spectrometry analyses reveal ≈80% of identified iPSC NatA targeted proteins displayed partial or complete N-terminal acetylation. Between null and haploinsufficient NAA15 cells, N-terminal acetylation levels of 32 and 9 NatA-specific targeted proteins were reduced, respectively. Similar acetylation loss in few proteins occurred in NAA15 R276W induced pluripotent stem cells. In addition, steady-state protein levels of 562 proteins were altered in both null and haploinsufficient NAA15 cells; 18 were ribosomal-associated proteins. At least 4 proteins were encoded by genes known to cause autosomal dominant congenital heart disease. Conclusions: These studies define a set of human proteins that requires a full NAA15 complement for normal synthesis and development. A 50% reduction in the amount of NAA15 alters levels of at least 562 proteins and N-terminal acetylation of only 9 proteins. One or more modulated proteins are likely responsible for NAA15-haploinsufficiency mediated congenital heart disease. Additionally, genetically engineered induced pluripotent stem cells provide a platform for evaluating the consequences of amino acid sequence variants of unknown significance on NAA15 function. 

Damaging GATA6 variants cause cardiac outflow tract defects, sometimes with pancreatic and diaphragmic malformations. To define molecular mechanisms for these diverse developmental defects, we studied transcriptional and epigenetic responses to GATA6 loss of function (LoF) and missense variants during cardiomyocyte differentiation of isogenic human induced pluripotent stem cells. We show that GATA6 is a pioneer factor in cardiac development, regulating SMYD1 that activates HAND2, and KDR that with HAND2 orchestrates outflow tract formation. LoF variants perturbed cardiac genes and also endoderm lineage genes that direct PDX1 expression and pancreatic development. Remarkably, an exon 4 GATA6 missense variant, highly associated with extra-cardiac malformations, caused ectopic pioneer activities, profoundly diminishing GATA4 , FOXA1/2, and PDX1 expression and increasing normal retinoic acid signaling that promotes diaphragm development. These aberrant epigenetic and transcriptional signatures illuminate the molecular mechanisms for cardiovascular malformations, pancreas and diaphragm dysgenesis that arise in patients with distinct GATA6 variants.