E-QED: Electrical Bug Localization During Post-Silicon Validation Enabled by Quick Error Detection and Formal Methods

During post-silicon validation, manufactured integrated circuits are extensively tested in actual system environments to detect design bugs. Bug localization involves identification of a bug trace (a sequence of inputs that activates and detects the bug) and a hardware design block where the bug is located. Existing bug localization practices during post-silicon validation are mostly manual and ad hoc, and, hence, extremely expensive and time consuming. This is particularly true for subtle electrical bugs caused by unexpected interactions between a design and its electrical state. We present E-QED, a new approach that automatically localizes electrical bugs during post-silicon validation. Our results on the OpenSPARC T2, an open-source 500-million-transistor multicore chip design, demonstrate the effectiveness and practicality of E-QED: starting with a failed post-silicon test, in a few hours (9 hours on average) we can automatically narrow the location of the bug to (the fan-in logic cone of) a handful of candidate flip-flops (18 flip-flops on average for a design with ~ 1 Million flip-flops) and also obtain the corresponding bug trace. The area impact of E-QED is ~2.5%. In contrast, deter-mining this same information might take weeks (or even months) of mostly manual work using traditional approaches

A Upf3b-mutant mouse model with behavioral and neurogenesis defects.

Nonsense-mediated RNA decay (NMD) is a highly conserved and selective RNA degradation pathway that acts on RNAs terminating their reading frames in specific contexts. NMD is regulated in a tissue-specific and developmentally controlled manner, raising the possibility that it influences developmental events. Indeed, loss or depletion of NMD factors have been shown to disrupt developmental events in organisms spanning the phylogenetic scale. In humans, mutations in the NMD factor gene, UPF3B, cause intellectual disability (ID) and are strongly associated with autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD) and schizophrenia (SCZ). Here, we report the generation and characterization of mice harboring a null Upf3b allele. These Upf3b-null mice exhibit deficits in fear-conditioned learning, but not spatial learning. Upf3b-null mice also have a profound defect in prepulse inhibition (PPI), a measure of sensorimotor gating commonly deficient in individuals with SCZ and other brain disorders. Consistent with both their PPI and learning defects, cortical pyramidal neurons from Upf3b-null mice display deficient dendritic spine maturation in vivo. In addition, neural stem cells from Upf3b-null mice have impaired ability to undergo differentiation and require prolonged culture to give rise to functional neurons with electrical activity. RNA sequencing (RNAseq) analysis of the frontal cortex identified UPF3B-regulated RNAs, including direct NMD target transcripts encoding proteins with known functions in neural differentiation, maturation and disease. We suggest Upf3b-null mice serve as a novel model system to decipher cellular and molecular defects underlying ID and neurodevelopmental disorders