A Defect-tolerant Cluster in a Mesh SRAM-based FPGA

International audienceIn this paper, we propose the implementation of multiple defect-tolerant techniques on an SRAM-based FPGA. These techniques include redundancy at both the logic block and intra-cluster interconnect. In the logic block, redundancy is implemented at the multiplexer level. Its efficiency is analyzed by injecting a single defect at the output of a multiplexer, considering all possible locations and input combinations. While at the interconnect level, fine grain redundancy is introduced which not only bypasses defects but also increases routability. Taking advantage of the sparse intra-cluster interconnect structures, routability is further improved by efficient distribution of feedback paths allowing more flexibility in the connections among logic blocks. Emulation results show a significant improvement of about 15% and 34% in the robustness of logic block and intra-cluster interconnect respectively. Furthermore, the impact of these hardening schemes on the testability of the FPGA cluster for manufacturing defects is also investigated in terms of maximum achievable fault coverage and the respective cost

Synthèse d'architectures de circuits FPGA tolérants aux défauts

The increasing integration density according to Moore’s law is being slowed due to economic and physical limits. However, this technological evolution involves an higher number of physical defects after manufacturing circuit. As yield goes down, one of the future challenges is to find a way to use a maximum of fabricated circuits while tolerating physical defects spread all over the chip. Fiel Programmable Gate Array (FPGA) are integrated circuits that contain logic blocks and reconfigurable interconnect. Their ability to integrate more complex applications, their flexibility and good performance make FPGAs the perfect target architecture. The aim of this thesis is to propose an FPGA architecture containing mechanisms to tolerate more than 20% of defective resources after manufacture. The first part of the manuscript studies the different FPGA architectures (mesh and tree) and different defects bypass techniques. In the second part of this thesis, we present the target architecture called Mesh of Clusters (MoC). This architecture combines the advantages of mesh architectures (genericity) and tree (reduction of the interconnect). The third contribution of this thesis is the development of a method to identify the most critical blocks in the FPGA and the impact of all bypass techniques on the architecture and on the criticality. Finally, we define the performance of all bypass techniques in terms of defect tolerance, timing and area overhead. Finally, thanks to these local redundancy techniques, we are able to tolerate more than 20% of defect on the FPGA architecture. In addition, the designer can fix his own metric in terms of area, timing and defect tolerance.L'essor considérable de la technologie CMOS a permis l'accroissement de la densité d'intégration selon la loi de Moore. Cependant, la poursuite de cette évolution est en voie de ralentissement dû aux contraintes physiques et économiques. Le défi devient alors de pouvoir utiliser un maximum de circuits tout en tolérant des défauts physiques présents en leur sein. Les circuits reconfigurables de type FPGA (Field Programmable Gate Array) connaissent un succès croissant car leurs performances et leurs capacités d'intégrer des applications très complexes ont directement bénéficié de l'évolution technologique. Le but de cette thèse est de proposer une architecture de FPGA contenant des mécanismes permettant de tolérer plus de 20% d'éléments défectueux après fabrication. La première partie du manuscrit étudie les différentes architectures de FPGA (matricielles et arborescentes) ainsi que les différentes techniques de contournement des défauts. Dans la seconde partie de cette thèse, nous présentons l'architecture cible matricielle (matrice de grappes ou groupes). Cette architecture combine les avantages des architectures matricielles (sa généricité) et arborescentes (réduction du taux d'utilisation de l'interconnexion. La troisième partie de cette thèse présente le développement d'une méthode d'identification des blocs les plus critiques contenus dans le FPGA ainsi que l'impact des différentes techniques de contournement retenues et proposées sur l'architecture et sur la criticité des blocs de base du FPGA. Pour finir, nous définissons les performances des différentes techniques de contournements en termes de tolérance aux défauts, de performances temporelles et de surface

Risk of lung cancer mortality in nuclear workers from internal exposure to alpha particle-emitting radionuclides

BACKGROUND: Carcinogenic risks of internal exposures to alpha-emitters (except radon) are poorly understood. Since exposure to alpha particles-particularly through inhalation-occurs in a range of settings, understanding consequent risks is a public health priority. We aimed to quantify dose-response relationships between lung dose from alpha-emitters and lung cancer in nuclear workers. METHODS: We conducted a case-control study, nested within Belgian, French, and UK cohorts of uranium and plutonium workers. Cases were workers who died from lung cancer; one to three controls were matched to each. Lung doses from alpha-emitters were assessed using bioassay data. We estimated excess odds ratio (OR) of lung cancer per gray (Gy) of lung dose. RESULTS: The study comprised 553 cases and 1,333 controls. Median positive total alpha lung dose was 2.42 mGy (mean: 8.13 mGy; maximum: 316 mGy); for plutonium the median was 1.27 mGy and for uranium 2.17 mGy. Excess OR/Gy (90% confidence interval)-adjusted for external radiation, socioeconomic status, and smoking-was 11 (2.6, 24) for total alpha dose, 50 (17, 106) for plutonium, and 5.3 (-1.9, 18) for uranium. CONCLUSIONS: We found strong evidence for associations between low doses from alpha-emitters and lung cancer risk. The excess OR/Gy was greater for plutonium than uranium, though confidence intervals overlap. Risk estimates were similar to those estimated previously in plutonium workers, and in uranium miners exposed to radon and its progeny. Expressed as risk/equivalent dose in sieverts (Sv), our estimates are somewhat larger than but consistent with those for atomic bomb survivors.See video abstract at, http://links.lww.com/EDE/B232

Absorbed dose evaluation at different organs after 131I oral contamination of two Wistar rat models

Iodine-131 (131I) is one of the most frequently used radionuclides for diagnosis and therapy of thyroid diseases. It is administered orally in the treatment of cancer to eliminate the residual postoperative microscopic tumor foci, and the residual normal thyroid tissue for early detection of recurrence [1]. The comparative behavior of 131I concentration into two animalmodels with total and partial thyroid has been investigated in our previous work [2]. The accumulated activities have been measured in fourteen organs. In this study, the mean absorbed doses resulting from 131I accumulated in all organs have been evaluated using RODES software [3, 4]. With this software, mean absorbed doses were calculatedfor selected organs (thyroid, lungs, heart, liver, kidneys, stomach, spleen, large and small intestine, testes, urinary bladder wall) by combining the specific absorbed fractions (SAF) of energy with radiation emission spectra and biokinetic data determined from our previous experimental study [2]. Calculations were based on the 131I photon and electron emissions reported by [5] and SAFs previously calculated by Monte Carlo simulation in the voxel phantom of an adult male rate [3, 4]. The obtained results show high absorbed dosesdeliveredto stomach and lungs for both models compared to other organs. The dose received by the testes and salivary glands is found to be higher in the case of the rat model without thyroid. Conversely, the spleen and bladder wall received lower doses in this latter model compared to those received by the rat model with thyroid. One can also note that the difference in mean absorbed dose received by liver, lungs, heart, and walls of the stomach is not significant between the two rat models

Lmo Mutants Reveal a Novel Role for Circadian Pacemaker Neurons in Cocaine-Induced Behaviors

Drosophila has been developed recently as a model system to investigate the molecular and neural mechanisms underlying responses to drugs of abuse. Genetic screens for mutants with altered drug-induced behaviors thus provide an unbiased approach to define novel molecules involved in the process. We identified mutations in the Drosophila LIM-only (LMO) gene, encoding a regulator of LIM-homeodomain proteins, in a genetic screen for mutants with altered cocaine sensitivity. Reduced Lmo function increases behavioral responses to cocaine, while Lmo overexpression causes the opposite effect, reduced cocaine responsiveness. Expression of Lmo in the principal Drosophila circadian pacemaker cells, the PDF-expressing ventral lateral neurons (LN(v)s), is sufficient to confer normal cocaine sensitivity. Consistent with a role for Lmo in LN(v) function, Lmo mutants also show defects in circadian rhythms of behavior. However, the role for LN(v)s in modulating cocaine responses is separable from their role as pacemaker neurons: ablation or functional silencing of the LN(v)s reduces cocaine sensitivity, while loss of the principal circadian neurotransmitter PDF has no effect. Together, these results reveal a novel role for Lmo in modulating acute cocaine sensitivity and circadian locomotor rhythmicity, and add to growing evidence that these behaviors are regulated by shared molecular mechanisms. The finding that the degree of cocaine responsiveness is controlled by the Drosophila pacemaker neurons provides a neuroanatomical basis for this overlap. We propose that Lmo controls the responsiveness of LN(v)s to cocaine, which in turn regulate the flies' behavioral sensitivity to the drug

Phase Coupling of a Circadian Neuropeptide With Rest/Activity Rhythms Detected Using a Membrane-Tethered Spider Toxin

Drosophila clock neurons are self-sustaining cellular oscillators that rely on negative transcriptional feedback to keep circadian time. Proper regulation of organismal rhythms of physiology and behavior requires coordination of the oscillations of individual clock neurons within the circadian control network. Over the last decade, it has become clear that a key mechanism for intercellular communication in the circadian network is signaling between a subset of clock neurons that secrete the neuropeptide pigment dispersing factor (PDF) and clock neurons that possess its G protein-coupled receptor (PDFR). Furthermore, the specific hypothesis has been proposed that PDF-secreting clock neurons entrain the phase of organismal rhythms, and the cellular oscillations of other clock neurons, via the temporal patterning of secreted PDF signals. In order to test this hypothesis, we have devised a novel technique for altering the phase relationship between circadian transcriptional feedback oscillation and PDF secretion by using an ion channel–directed spider toxin to modify voltage-gated Na+ channel inactivation in vivo. This technique relies on the previously reported “tethered-toxin” technology for cell-autonomous modulation of ionic conductances via heterologous expression of subtype-specific peptide ion channel toxins as chimeric fusion proteins tethered to the plasma membrane with a glycosylphosphatidylinositol (GPI) anchor. We demonstrate for the first time, to our knowledge, the utility of the tethered-toxin technology in a transgenic animal, validating four different tethered spider toxin ion channel modifiers for use in Drosophila. Focusing on one of these toxins, we show that GPI-tethered Australian funnel-web spider toxin δ-ACTX-Hv1a inhibits Drosophila para voltage-gated Na+ channel inactivation when coexpressed in Xenopus oocytes. Transgenic expression of membrane-tethered δ-ACTX-Hv1a in vivo in the PDF-secreting subset of clock neurons induces rhythmic action potential bursts and depolarized plateau potentials. These in vitro and in vivo electrophysiological effects of membrane-tethered δ-ACTX-Hv1a are consistent with the effects of soluble δ-ACTX-Hv1a purified from venom on Na+ channel physiological and biophysical properties in cockroach neurons. Membrane-tethered δ-ACTX-Hv1a expression in the PDF-secreting subset of clock neurons induces an approximately 4-h phase advance of the rhythm of PDF accumulation in their terminals relative to both the phase of the day:night cycle and the phase of the circadian transcriptional feedback loops. As a consequence, the morning anticipatory peak of locomotor activity preceding dawn, which has been shown to be driven by the clocks of the PDF-secreting subset of clock neurons, phase advances coordinately with the phase of the PDF rhythm of the PDF-secreting clock neurons, rather than maintaining its phase relationship with the day:night cycle and circadian transcriptional feedback loops. These results (1) validate the tethered-toxin technology for cell-autonomous modulation of ion channel biophysical properties in vivo in transgenic Drosophila, (2) demonstrate that the kinetics of para Na+ channel inactivation is a key parameter for determining the phase relationship between circadian transcriptional feedback oscillation and PDF secretion, and (3) provide experimental support for the hypothesis that PDF-secreting clock neurons entrain the phase of organismal rhythms via the temporal patterning of secreted PDF signals