A Proposed SEU Tolerant Dynamic Random Access Memory (DRAM) Cell

A novel DRAM cell technology consisting of an n-channel access transistor and a bootstrapped storage capacitor with an integrated breakdown diode is proposed. This design offers considerable resistance to single event cell errors. The informational charge packet is shielded from the single event by placing the vulnerable node in a selfcompensating state while the cell is in standby mode. The proposed cell is comparable in size to a conventional DRAM cell, and computer simulations show an improvement in critical charge of two orders of magnitude over conventional 1-T DRAM cells. I. INTRODUCTION The merger of commercial and space/military integrated circuit technologies is an increasingly important goal. Important factors leading toward this merger are the high speed, integration density, processing power, and reduced power consumption of the state-of-the-art commercial technologies. The expense of traditional radiation-hardened and military-qualified integrated circuits (IC's) is also..

Single Event Mirroring and DRAM Sense Amplifier Designs for Improved Single-Event-Upset Performance

This paper proposes and investigates schemes for hardening the conventional CMOS cross-coupled DRAM sense amplifier to single event upset (SEU). These schemes, adapted from existing SRAM hardening techniques, are intended to harden the dynamic random access memory to bitline-mode errors during the sensing period. Simulation results indicate that a 9kW L-resistor hardening scheme provides greater than 24-fold improvement in critical charge over a significant part of the sensing period. Also proposed is a novel single event (SE) mirroring concept for SEU hardening of DRAMs. This concept has been implemented for hardening the bitlines to hits on diffusion regions connected to the lines during the highly susceptible highimpedance state of the bitlines. It is shown to result in over 26-fold improvement in the level of critical charge using a 2pF dynamic capacitive coupling

The SARS-CoV-2 UTR’s Intrudes Host RBP’s and Modulates Cellular Splicing

SARS-CoV-2 is a novel coronavirus that causes a potentially fatal respiratory disease known as coronavirus disease (COVID-19) and is responsible for the ongoing pandemic with increasing mortality. Understanding the host-virus interaction involved in SARS-CoV-2 pathophysiology will enhance our understanding of the mechanistic basis of COVID-19 infection. The characterization of post-transcriptional gene regulatory networks, particularly pre-mRNA splicing, and the identification and characterization of host proteins interacting with the 5′ and 3′UTRs of SARS-CoV-2 will improve our understanding of post-transcriptional gene regulation during SARS-CoV-2 pathogenesis. Here, we demonstrate that either SARS-CoV-2 infection or exogenous overexpression of the 5′ and 3’UTRs of the viral genomic RNAs, results in reduced mRNA levels possibly due to modulation of host cell pre-mRNA splicing. Further, we have investigated the potential RNA-binding proteins interacting with the 5′ and 3′UTRs, using in-silico approaches. Our results suggest that 5′ and 3′UTRs indeed interact with many RNA-binding proteins. Our results provide a primer for further investigations into the UTR-mediated regulation of splicing and related molecular mechanisms in host cells

The SARS-CoV-2 UTR’s Intrudes Host RBP’s and Modulates Cellular Splicing

SARS-CoV-2 is a novel coronavirus that causes a potentially fatal respiratory disease known as coronavirus disease (COVID-19) and is responsible for the ongoing pandemic with increasing mortality. Understanding the host-virus interaction involved in SARS-CoV-2 pathophysiology will enhance our understanding of the mechanistic basis of COVID-19 infection. The characterization of post-transcriptional gene regulatory networks, particularly pre-mRNA splicing, and the identification and characterization of host proteins interacting with the 5\u27 and 3\u27UTRs of SARS-CoV-2 will improve our understanding of posttranscriptional gene regulation during SARS-CoV-2 pathogenesis. Here, we demonstrate that either SARS-CoV-2 infection or exogenous overexpression of the 5\u27 and 3’UTRs of the viral genomic RNAs, results in reduced mRNA levels possibly due to modulation of host cell pre-mRNA splicing. Further, we have investigated the potential RNA-binding proteins interacting with the 5\u27 and 3\u27UTRs, using in-silico approaches. Our results suggest that 5\u27 and 3\u27UTRs indeed interact with many RNA-binding proteins. Our results provide a primer for further investigations into the UTR-mediated regulation of splicing and related molecular mechanisms in host cells

Long-Term Outcomes in Patients With Diabetes Mellitus Related to Prolonging Clopidogrel More Than 12 Months After Coronary Stenting

AbstractBackgroundRecent large clinical trials show lower rates of late cardiovascular events by extending clopidogrel >12 months after percutaneous coronary revascularization (PCI). However, concerns of increased bleeding have elicited support for limiting prolonged treatment to high-risk patients.ObjectivesThe aim of this analysis was to determine the effect of prolonging clopidogrel therapy >12 months versus ≤12 months after PCI on very late outcomes in patients with diabetes mellitus (DM).MethodsUsing the Veterans Health Administration, 28,849 patients undergoing PCI between 2002 and 2006 were categorized into 3 groups: 1) 16,332 without DM; 2) 9,905 with DM treated with oral medications or diet; and 3) 2,612 with DM treated with insulin. Clinical outcomes, stratified by stent type, ≤4 years after PCI were determined from the Veterans Health Administration and Medicare databases and risk was assessed by multivariable and propensity score analyses using a landmark analysis starting 1 year after the index PCI. The primary endpoint of the study was the risk of all-cause death or myocardial infarction (MI).ResultsIn patients with DM treated with insulin who received drug-eluting stents (DES), prolonged clopidogrel treatment was associated with a decreased risk of death (hazard ratio [HR]: 0.59; 95% confidence interval [CI]: 0.42 to 0.82) and death or MI (HR: 0.67; 95% CI: 0.49 to 0.92). Similarly, in patients with noninsulin-treated DM receiving DES, prolonged clopidogrel treatment was associated with less death (HR: 0.61; 95% CI: 0.48 to 0.77) and death or MI (HR: 0.61; 95% CI: 0.5 to 0.75). Prolonged clopidogrel treatment was not associated with a lower risk in patients without DM or in any group receiving bare-metal stents.ConclusionsExtending the duration of clopidogrel treatment >12 months may decrease very late death or MI only in patients with DM receiving first-generation DES. Future studies should address this question in patients receiving second-generation DES