A low overhead error confinement method based on application statistical characteristics

Reliability has emerged as a critical design constraint especially in memories. Designers are going to great lengths to guarantee fault free operation of the underlying silicon by adopting redundancy-based techniques, which essentially try to detect and correct every single error. However, such techniques come at a cost of large area, power and performance overheads which making many researchers to doubt their efficiency especially for error resilient systems where 100% accuracy is not always required. In this paper, we present an alternative method focusing on the confinement of the resulting output error induced by any reliability issues. By focusing on memory faults, rather than correcting every single error the proposed method exploits the statistical characteristics of any target application and replaces any erroneous data with the best available estimate of that data. To realize the proposed method a RISC processor is augmented with custom instructions and special-purpose functional units. We apply the method on the proposed enhanced processor by studying the statistical characteristics of the various algorithms involved in a popular multimedia application. Our experimental results show that in contrast to state-of-the-art fault tolerance approaches, we are able to reduce runtime and area overhead by 71.3% and 83.3% respectively.

A Rare Loss-of-Function Variant in Scavenger Receptor Class B Type I (SCARB1) Raises HDL Cholesterol and Increases Risk of Coronary Disease

Scavenger receptor BI (SR-BI) is the major receptor for high-density lipoprotein (HDL)
cholesterol (HDL-C). In humans, high amounts of HDL-C in plasma are associated with a
lower risk of coronary heart disease (CHD). Mice that have depleted Scarb1 (SR-BI
knockout mice) have markedly elevated HDL-C levels but, paradoxically, increased
atherosclerosis. The impact of SR-BI on HDL metabolism and CHD risk in humans remains
unclear. Through targeted sequencing of coding regions of lipid-modifying genes in 328
individuals with extremely high plasma HDL-C levels, we identified a homozygote for a lossof-function
variant, in which leucine replaces proline 376 (P376L), in SCARB1, the gene
encoding SR-BI. The P376L variant impairs posttranslational processing of SR-BI and
abrogates selective HDL cholesterol uptake in transfected cells, in hepatocyte-like cells
derived from induced pluripotent stem cells from the homozygous subject, and in mice.
Large population-based studies revealed that subjects who are heterozygous carriers of
the P376L variant have significantly increased levels of plasma HDL-C. P376L carriers have
a profound HDL-related phenotype and an increased risk of CHD (odds ratio = 1.79, which is
statistically significant).