An adaptive method to tolerate soft errors in SRAM-based FPGAs

AbstractIn this paper, we present an adaptive method that is a combination of SEU-avoidance in CAD flow and adaptive redundancy to tolerate soft error effects in SRAM-based FPGAs. This method is based on the modification of T-VPack and VPR tools. Three different steps of these tools are modified for SEU-awareness: (1) clustering, (2) placement and (3) routing. Then we use the unused resources as redundancy. We have investigated the effect of this method on several MCNC benchmarks. This investigation has been performed using three experiments: (1) SEU-awareness in clustering with redundancy, (2) SEU-awareness in clustering and placement with redundancy and (3) SEU-awareness in clustering, placement and routing with redundancy. With a confidence level of 95%, the results show that, using each of these three experiments, the system failure rate of ten MCNC circuits has been decreased between 4.52% and 10.42%, between 10.25% and 21.63%, and between 10.48% and 24.39%, respectively

The Hippo Tumor Suppressor Pathway (YAP/TAZ/TEAD/MST/LATS) and EGFR-RAS-RAF-MEK in cancer metastasis

Hippo Tumor Suppressor Pathway is the main pathway for cell growth that regulates tissue enlargement and organ size by limiting cell growth. This pathway is activated in response to cell cycle arrest signals (cell polarity, transduction, and DNA damage) and limited by growth factors or mitogens associated with EGF and LPA. The major pathway consists of the central kinase of Ste20 MAPK (Saccharomyces cerevisiae), Hpo (Drosophila melanogaster) or MST kinases (mammalian) that activates the mammalian AGC kinase dmWts or LATS effector (MST and LATS). YAP in the nucleus work as a cofactor for a wide range of transcription factors involved in proliferation (TEA domain family, TEAD1-4), stem cells (Oct4 mononuclear factor and SMAD-related TGFβ effector), differentiation (RUNX1), and Cell cycle/apoptosis control (p53, p63, and p73 family members). This is due to the diverse roles of YAP and may limit tumor progression and establishment. TEAD also coordinates various signal transduction pathways such as Hippo, WNT, TGFβ and EGFR, and effects on lack of regulation of TEAD cancerous genes, such as KRAS, BRAF, LKB1, NF2 and MYC, which play essential roles in tumor progression, metastasis, cancer metabolism, immunity, and drug resistance. However, RAS signaling is a pivotal factor in the inactivation of Hippo, which controls EGFR-RAS-RAF-MEK-ERK-mediated interaction of Hippo signaling. Thus, the loss of the Hippo pathway may have significant consequences on the targets of RAS-RAF mutations in cancersem informaçãosem informaçã