Single Event Transients in Linear Integrated Circuits

On November 5, 2001, a processor reset occurred on board the Microwave Anisotropy Probe (MAP), a NASA mission to measure the anisotropy of the microwave radiation left over from the Big Bang. The reset caused the spacecraft to enter a safehold mode from which it took several days to recover. Were that to happen regularly, the entire mission would be compromised, so it was important to find the cause of the reset and, if possible, to mitigate it. NASA assembled a team of engineers that included experts in radiation effects to tackle the problem. The first clue was the observation that the processor reset occurred during a solar event characterized by large increases in the proton and heavy ion fluxes emitted by the sun. To the radiation effects engineers on the team, this strongly suggested that particle radiation might be the culprit, particularly when it was discovered that the reset circuit contained three voltage comparators (LM139). Previous testing revealed that large voltage transients, or glitches appeared at the output of the LM139 when it was exposed to a beam of heavy ions [NI96]. The function of the reset circuit was to monitor the supply voltage and to issue a reset command to the processor should the voltage fall below a reference of 2.5 V [PO02]. Eventually, the team of engineers concluded that ionizing particle radiation from the solar event produced a negative voltage transient on the output of one of the LM139s sufficiently large to reset the processor on MAP. Fortunately, as of the end of 2004, only two such resets have occurred. The reset on MAP was not the first malfunction on a spacecraft attributed to a transient. That occurred shortly after the launch of NASA s TOPEX/Poseidon satellite in 1992. It was suspected, and later confirmed, that an anomaly in the Earth Sensor was caused by a transient in an operational amplifier (OP-15) [KO93]. Over the next few years, problems on TDRS, CASSINI, [PR02] SOHO [HA99,HA01] and TERRA were also attributed to transients. In some cases, such events produced resets by falsely triggering circuits designed to protect against over- voltage or over-current. On at least three occasions, transients caused satellites to switch into "safe mode" in which most of the systems on board the satellites were powered down for an extended period. By the time the satellites were reconfigured and returned to full operational state, much scientific data had been lost. Fortunately, no permanent damage occurred in any of the systems and they were all successfully re-activated

Total Dose Effects on Error Rates in Linear Bipolar Systems

The shapes of single event transients in linear bipolar circuits are distorted by exposure to total ionizing dose radiation. Some transients become broader and others become narrower. Such distortions may affect SET system error rates in a radiation environment. If the transients are broadened by TID, the error rate could increase during the course of a mission, a possibility that has implications for hardness assurance

Total Dose Effects on Single Event Transients in Linear Bipolar Systems

Single Event Transients (SETs) originating in linear bipolar integrated circuits are known to undermine the reliability of electronic systems operating in the radiation environment of space. Ionizing particle radiation produces a variety of SETs in linear bipolar circuits. The extent to which these SETs threaten system reliability depends on both their shapes (amplitude and width) and their threshold energies. In general, SETs with large amplitudes and widths are the most likely to propagate from a bipolar circuit's output through a subsystem. The danger these SET pose is that, if they become latched in a follow-on circuit, they could cause an erroneous system response. Long-term exposure of linear bipolar circuits to particle radiation produces total ionizing dose (TID) and/or displacement damage dose (DDD) effects that are characterized by a gradual degradation in some of the circuit's electrical parameters. For example, an operational amplifier's gain-bandwidth product is reduced by exposure to ionizing radiation, and it is this reduction that contributes to the distortion of the SET shapes. In this paper, we compare SETs produced in a pristine LM124 operational amplifier with those produced in one exposed to ionizing radiation for three different operating configurations - voltage follower (VF), inverter with gain (IWG), and non-inverter with gain (NIWG). Each configuration produces a unique set of transient shapes that change following exposure to ionizing radiation. An important finding is that the changes depend on operating configuration; some SETs decrease in amplitude, some remain relatively unchanged, some become narrower and some become broader

Future Challenges Facing SEE Pulsed Laser Technique

This viewgraph presentation reviews the challenges for the pulsed laser in the following categories: 1. Metal 2. Package 3. Scaling 4. Exotic materials 5. Novel devices 6. Equipmen

The Effects of Low Dose-Rate Ionizing Radiation on the Shapes of Transients in the LM124 Operational Amplifier

Shapes of single event transients (SETs) in a linear bipolar circuit (LM124) change with exposure to total ionizing dose (TID) radiation. SETs shape changes are a direct consequence of TID-induced degradation of bipolar transistor gain. A reduction in transistor gain causes a reduction in the drive current of the current sources in the circuit, and it is the lower drive current that most affects the shapes of large amplitude SETs

Investigation of Current Spike Phenomena During Heavy Ion Irradiation of NAND Flash Memories

A series of heavy ion and laser irradiations were performed to investigate previously reported current spikes in flash memories. High current events were observed, however, none matches the previously reported spikes. Plausible mechanisms are discussed

Heavy Ion Microbeam and Broadbeam Transients in SiGe HBTs

SiGe HBT heavy ion current transients are measured using microbeam and both high- and low-energy broadbeam sources. These new data provide detailed insight into the effects of ion range, LET, and strike location

Heavy Ion Current Transients in SiGe HBTs

Time-resolved ion beam induced charge reveals heavy ion response of IBM 5AM SiGe HBT: a) Position correlation[ b) Unique response for different bias schemes; c) Similarities to TPA pulsed-laser data. Heavy ion broad-beam transients provide more realistic device response: a) Feedback using microbeam data; b) Overcome issues of LET and ion range with microbeam. Both micro- and broad-beam data sets yield valuable input for TCAD simulations. Uncover detailed mechanisms for SiGe HBTs and other devices fabricated on lightly-doped substrates

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease