34 research outputs found
Spatz: A Compact Vector Processing Unit for High-Performance and Energy-Efficient Shared-L1 Clusters
While parallel architectures based on clusters of Processing Elements (PEs)
sharing L1 memory are widespread, there is no consensus on how lean their PE
should be. Architecting PEs as vector processors holds the promise to greatly
reduce their instruction fetch bandwidth, mitigating the Von Neumann Bottleneck
(VNB). However, due to their historical association with supercomputers,
classical vector machines include micro-architectural tricks to improve the
Instruction Level Parallelism (ILP), which increases their instruction fetch
and decode energy overhead. In this paper, we explore for the first time vector
processing as an option to build small and efficient PEs for large-scale
shared-L1 clusters. We propose Spatz, a compact, modular 32-bit vector
processing unit based on the integer embedded subset of the RISC-V Vector
Extension version 1.0. A Spatz-based cluster with four Multiply-Accumulate
Units (MACUs) needs only 7.9 pJ per 32-bit integer multiply-accumulate
operation, 40% less energy than an equivalent cluster built with four Snitch
scalar cores. We analyzed Spatz' performance by integrating it within MemPool,
a large-scale many-core shared-L1 cluster. The Spatz-based MemPool system
achieves up to 285 GOPS when running a 256x256 32-bit integer matrix
multiplication, 70% more than the equivalent Snitch-based MemPool system. In
terms of energy efficiency, the Spatz-based MemPool system achieves up to 266
GOPS/W when running the same kernel, more than twice the energy efficiency of
the Snitch-based MemPool system, which reaches 128 GOPS/W. Those results show
the viability of lean vector processors as high-performance and
energy-efficient PEs for large-scale clusters with tightly-coupled L1 memory.Comment: 9 pages. Accepted for publication in the 2022 International
Conference on Computer-Aided Design (ICCAD 2022
IgD attenuates the IgM-induced anergy response in transitional and mature B cells
Self-tolerance by clonal anergy of B cells is marked by an increase in IgD and decrease in IgM antigen receptor surface expression, yet the function of IgD on anergic cells is obscure. Here we define the RNA landscape of the in vivo anergy response, comprising 220 induced sequences including a core set of 97. Failure to co-express IgD with IgM decreases overall
expression of receptors for self-antigen, but paradoxically increases the core anergy response,
exemplified by increased Sdc1 encoding the cell surface marker syndecan-1. IgD expressed on
its own is nevertheless competent to induce calcium signalling and the core anergy mRNA response. Syndecan-1 induction correlates with reduction of surface IgM and is exaggerated
without surface IgD in many transitional and mature B cells. These results show that IgD attenuates the response to self-antigen in anergic cells and promotes their accumulation. In this way, IgD minimizes tolerance-induced holes in the pre-immune antibody repertoire.This work was supported by NIH grant U19 AI100627 and NHMRC grants 585490,
1016953 and 1081858 to C.C.G., NHMRC CJ Martin Fellowship 595989 to J.H.R., an
Endeavour Award from the Australian Government to Z.S. and the National Collaborative
Research Infrastructure Scheme Australian Phenomics Facilit
IgD attenuates the IgM-induced anergy response in transitional and mature B cells
Self-tolerance by clonal anergy of B cells is marked by an increase in IgD and decrease in IgM antigen receptor surface expression, yet the function of IgD on anergic cells is obscure. Here we define the RNA landscape of the in vivo anergy response, comprising 220 induced sequences including a core set of 97. Failure to co-express IgD with IgM decreases overall expression of receptors for self-antigen, but paradoxically increases the core anergy response, exemplified by increased Sdc1 encoding the cell surface marker syndecan-1. IgD expressed on its own is nevertheless competent to induce calcium signalling and the core anergy mRNA response. Syndecan-1 induction correlates with reduction of surface IgM and is exaggerated without surface IgD in many transitional and mature B cells. These results show that IgD attenuates the response to self-antigen in anergic cells and promotes their accumulation. In this way, IgD minimizes tolerance-induced holes in the pre-immune antibody repertoire
Infected pancreatic necrosis: outcomes and clinical predictors of mortality. A post hoc analysis of the MANCTRA-1 international study
: The identification of high-risk patients in the early stages of infected pancreatic necrosis (IPN) is critical, because it could help the clinicians to adopt more effective management strategies. We conducted a post hoc analysis of the MANCTRA-1 international study to assess the association between clinical risk factors and mortality among adult patients with IPN. Univariable and multivariable logistic regression models were used to identify prognostic factors of mortality. We identified 247 consecutive patients with IPN hospitalised between January 2019 and December 2020. History of uncontrolled arterial hypertension (p = 0.032; 95% CI 1.135-15.882; aOR 4.245), qSOFA (p = 0.005; 95% CI 1.359-5.879; aOR 2.828), renal failure (p = 0.022; 95% CI 1.138-5.442; aOR 2.489), and haemodynamic failure (p = 0.018; 95% CI 1.184-5.978; aOR 2.661), were identified as independent predictors of mortality in IPN patients. Cholangitis (p = 0.003; 95% CI 1.598-9.930; aOR 3.983), abdominal compartment syndrome (p = 0.032; 95% CI 1.090-6.967; aOR 2.735), and gastrointestinal/intra-abdominal bleeding (p = 0.009; 95% CI 1.286-5.712; aOR 2.710) were independently associated with the risk of mortality. Upfront open surgical necrosectomy was strongly associated with the risk of mortality (p < 0.001; 95% CI 1.912-7.442; aOR 3.772), whereas endoscopic drainage of pancreatic necrosis (p = 0.018; 95% CI 0.138-0.834; aOR 0.339) and enteral nutrition (p = 0.003; 95% CI 0.143-0.716; aOR 0.320) were found as protective factors. Organ failure, acute cholangitis, and upfront open surgical necrosectomy were the most significant predictors of mortality. Our study confirmed that, even in a subgroup of particularly ill patients such as those with IPN, upfront open surgery should be avoided as much as possible. Study protocol registered in ClinicalTrials.Gov (I.D. Number NCT04747990)
25th annual computational neuroscience meeting: CNS-2016
The same neuron may play different functional roles in the neural circuits to which it belongs. For example, neurons in the Tritonia pedal ganglia may participate in variable phases of the swim motor rhythms [1]. While such neuronal functional variability is likely to play a major role the delivery of the functionality of neural systems, it is difficult to study it in most nervous systems. We work on the pyloric rhythm network of the crustacean stomatogastric ganglion (STG) [2]. Typically network models of the STG treat neurons of the same functional type as a single model neuron (e.g. PD neurons), assuming the same conductance parameters for these neurons and implying their synchronous firing [3, 4]. However, simultaneous recording of PD neurons shows differences between the timings of spikes of these neurons. This may indicate functional variability of these neurons. Here we modelled separately the two PD neurons of the STG in a multi-neuron model of the pyloric network. Our neuron models comply with known correlations between conductance parameters of ionic currents. Our results reproduce the experimental finding of increasing spike time distance between spikes originating from the two model PD neurons during their synchronised burst phase. The PD neuron with the larger calcium conductance generates its spikes before the other PD neuron. Larger potassium conductance values in the follower neuron imply longer delays between spikes, see Fig. 17.Neuromodulators change the conductance parameters of neurons and maintain the ratios of these parameters [5]. Our results show that such changes may shift the individual contribution of two PD neurons to the PD-phase of the pyloric rhythm altering their functionality within this rhythm. Our work paves the way towards an accessible experimental and computational framework for the analysis of the mechanisms and impact of functional variability of neurons within the neural circuits to which they belong