A Static Time Analysis of 1-bit to 32-page SCA architecture for Logic Test

This research proposes the Static Time Analysis  of  32  page  Single  cycle  access  (SCA)  architecture  for Logic test. The timing analysis of each and very path of Logic test are observed that is setup and hold timings are calculated.  It also eliminates the peak power consumption problem of conventional shift-based scan chains and reduces the activity during shift and capture cycles using Clock-Gating technique. This leads to more realistic circuit behavior during at-speed tests. It enables the complete test to run at much higher frequencies equal or close to the one in functional mode. It will be shown, that a lesser number of test cycles can be achieved compared to other published solutions. The test cycle per net based on a simple test pattern generator algorithm without test pattern compression is below 1 for larger designs and is independent of the design size. The structure allows an additional on-chip debugging signal visibility for each register. The method is backward compatible to full scan designs and existing test pattern generators and simulators can be used with a minor enhancement. It is shown how to combine the proposed solution with built-in self-test  (BIST)  and  massive parallel   scan   chains.   The   results   are   observed   on   Xilinx XC3s1600e-5fgg48

ADHD desynchronizes brain activity during watching a distracted multi-talker conversation

Individuals with attention-deficit/hyperactivity disorder (ADHD) have difficulties navigating dynamic everyday situations that contain multiple sensory inputs that need to either be attended to or ignored. As conventional experimental tasks lack this type of everyday complexity, we administered a film-based multi-talker condition with auditory distractors in the background. ADHD-related aberrant brain responses to this naturalistic stimulus were identified using intersubject correlations (ISCs) in functional magnetic resonance imaging (fMRI) data collected from 51 adults with ADHD and 29 healthy controls. A novel permutation-based approach introducing studentized statistics and subject-wise voxel-level null-distributions revealed that several areas in cerebral attention networks and sensory cortices were desynchronized in participants with ADHD (n = 20) relative to healthy controls (n = 20). Specifically, desynchronization of the posterior parietal cortex occurred when irrelevant speech or music was presented in the background, but not when irrelevant white noise was presented, or when there were no distractors. We also show regionally distinct ISC signatures for inattention and impulsivity. Finally, post-scan recall of the film contents was associated with stronger ISCs in the default-mode network for the ADHD and in the dorsal attention network for healthy controls. The present study shows that ISCs can further our understanding of how a complex environment influences brain states in ADHD.Peer reviewe

UBQLN4 Represses Homologous Recombination and Is Overexpressed in Aggressive Tumors

Genomic instability can be a hallmark of both human genetic disease and cancer. We identify a deleterious UBQLN4 mutation in families with an autosomal recessive syndrome reminiscent of genome instability disorders. UBQLN4 deficiency leads to increased sensitivity to genotoxic stress and delayed DNA double-strand break (DSB) repair. The proteasomal shuttle factor UBQLN4 is phosphorylated by ATM and interacts with ubiquitylated MRE11 to mediate early steps of homologous recombination-mediated DSB repair (HRR). Loss of UBQLN4 leads to chromatin retention of MRE11, promoting non-physiological HRR activity in vitro and in vivo. Conversely, UBQLN4 overexpression represses HRR and favors non-homologous end joining. Moreover, we find UBQLN4 overexpressed in aggressive tumors. In line with an HRR defect in these tumors, UBQLN4 overexpression is associated with PARP1 inhibitor sensitivity. UBQLN4 therefore curtails HRR activity through removal of MRE11 from damaged chromatin and thus offers a therapeutic window for PARP1 inhibitor treatment in UBQLN4-overexpressing tumors