The Second Joint NASA/FAA/DOD Conference on Aging Aircraft

The purpose of the Conference was to bring together world leaders in aviation safety research, aircraft design and manufacturing, fleet operation and aviation maintenance to disseminate information on current practices and advanced technologies that will assure the continued airworthiness of the aging aircraft in the military and commercial fleets. The Conference included reviews of current industry practices, assessments of future technology requirements, and status of aviation safety research. The Conference provided an opportunity for interactions among the key personnel in the research and technology development community, the original equipment manufacturers, commercial airline operators, military fleet operators, aviation maintenance, and aircraft certification and regulatory authorities. Conference participation was unrestricted and open to the international aviation community

Développement d'architectures HW/SW tolérantes aux fautes et auto-calibrantes pour les technologies Intégrées 3D

Malgré les avantages de l'intégration 3D, le test, le rendement et la fiabilité des Through-Silicon-Vias (TSVs) restent parmi les plus grands défis pour les systèmes 3D à base de Réseaux-sur-Puce (Network-on-Chip - NoC). Dans cette thèse, une stratégie de test hors-ligne a été proposé pour les interconnections TSV des liens inter-die des NoCs 3D. Pour le TSV Interconnect Built-In Self-Test (TSV-IBIST) on propose une nouvelle stratégie pour générer des vecteurs de test qui permet la détection des fautes structuraux (open et short) et paramétriques (fautes de délaye). Des stratégies de correction des fautes transitoires et permanents sur les TSV sont aussi proposées aux plusieurs niveaux d'abstraction: data link et network. Au niveau data link, des techniques qui utilisent des codes de correction (ECC) et retransmission sont utilisées pour protégé les liens verticales. Des codes de correction sont aussi utilisés pour la protection au niveau network. Les défauts de fabrication ou vieillissement des TSVs sont réparé au niveau data link avec des stratégies à base de redondance et sérialisation. Dans le réseau, les liens inter-die défaillante ne sont pas utilisables et un algorithme de routage tolérant aux fautes est proposé. On peut implémenter des techniques de tolérance aux fautes sur plusieurs niveaux. Les résultats ont montré qu'une stratégie multi-level atteint des très hauts niveaux de fiabilité avec un cout plus bas. Malheureusement, il n'y as pas une solution unique et chaque stratégie a ses avantages et limitations. C'est très difficile d'évaluer tôt dans le design flow les couts et l'impact sur la performance. Donc, une méthodologie d'exploration de la résilience aux fautes est proposée pour les NoC 3D mesh.3D technology promises energy-efficient heterogeneous integrated systems, which may open the way to thousands cores chips. Silicon dies containing processing elements are stacked and connected by vertical wires called Through-Silicon-Vias. In 3D chips, interconnecting an increasing number of processing elements requires a scalable high-performance interconnect solution: the 3D Network-on-Chip. Despite the advantages of 3D integration, testing, reliability and yield remain the major challenges for 3D NoC-based systems. In this thesis, the TSV interconnect test issue is addressed by an off-line Interconnect Built-In Self-Test (IBIST) strategy that detects both structural (i.e. opens, shorts) and parametric faults (i.e. delays and delay due to crosstalk). The IBIST circuitry implements a novel algorithm based on the aggressor-victim scenario and alleviates limitations of existing strategies. The proposed Kth-aggressor fault (KAF) model assumes that the aggressors of a victim TSV are neighboring wires within a distance given by the aggressor order K. Using this model, TSV interconnect tests of inter-die 3D NoC links may be performed for different aggressor order, reducing test times and circuitry complexity. In 3D NoCs, TSV permanent and transient faults can be mitigated at different abstraction levels. In this thesis, several error resilience schemes are proposed at data link and network levels. For transient faults, 3D NoC links can be protected using error correction codes (ECC) and retransmission schemes using error detection (Automatic Retransmission Query) and correction codes (i.e. Hybrid error correction and retransmission).For transients along a source-destination path, ECC codes can be implemented at network level (i.e. Network-level Forward Error Correction). Data link solutions also include TSV repair schemes for faults due to fabrication processes (i.e. TSV-Spare-and-Replace and Configurable Serial Links) and aging (i.e. Interconnect Built-In Self-Repair and Adaptive Serialization) defects. At network-level, the faulty inter-die links of 3D mesh NoCs are repaired by implementing a TSV fault-tolerant routing algorithm. Although single-level solutions can achieve the desired yield / reliability targets, error mitigation can be realized by a combination of approaches at several abstraction levels. To this end, multi-level error resilience strategies have been proposed. Experimental results show that there are cases where this multi-layer strategy pays-off both in terms of cost and performance. Unfortunately, one-fits-all solution does not exist, as each strategy has its advantages and limitations. For system designers, it is very difficult to assess early in the design stages the costs and the impact on performance of error resilience. Therefore, an error resilience exploration (ERX) methodology is proposed for 3D NoCs.SAVOIE-SCD - Bib.électronique (730659901) / SudocGRENOBLE1/INP-Bib.électronique (384210012) / SudocGRENOBLE2/3-Bib.électronique (384219901) / SudocSudocFranceF

Utilization of High Throughput Screening to Identify Therapeutic Targets for Defective MCPH1/BRIT1 Function- Induced Premature Chromosome Condensation in Breast and Ovarian Cancer.

Mutations in the N-terminal region of MCPH1/BRIT1 cause premature chromosome condensation (PCC), whereby cells enter mitosis before completing DNA replication. 792 chemical compounds (CC) were selected based on the crystal structure of the N-terminus of MCPH1/BRIT1 and assayed using high throughput- high content imaging to identify CC that induced PCC. Hit validation revealed 4 potential CC, 2 of which induced high PCC at low concentrations. A screen using a human protein kinase (hPK) siRNA sub-library was performed to identify genes that induced PCC. Four hits were selected for validation, however PCC induction was not confirmed. A complementary hPK siRNA screen combined with MCPH1/BRIT1 siRNA knockdown was performed. The cell number outputs from both hPK siRNA screens were analysed to identify synthetic lethal (SL) genes in MCPH1/BRIT1-deficient cells. CDK1/CDC2, STK39, VRK1 and TTK/MPS1 were subsequently validated as potential MCPH1/BRIT1 SL genes. The expression of MCPH1/BRIT1 was examined by immunostaining in breast cancer (BC) tissue pre and post neoadjuvant chemotherapy (NACT) to determine its effect on response and survival. MCPH1/BRIT1 expression increased in response to NACT with high expression in 51.4% (36/70) of cases pre-NACT compared to 81.4% (57/70) post-NACT (p = 0.0002). Reduced MCPH1/BRIT1 expression correlated with longer overall survival (OS) pre- but not post-NACT (p = 0.017). Change in MCPH1/BRIT1 expression (from low-high) post-NACT was significantly correlated with better OS (p = 0.010). MCPH1/BRIT1 has previously been found to regulate p53 stability in BC cell lines. Notably, in this study a significant increase in MCPH1/BRIT1 staining was accompanied by a decrease in p53 staining in post-NACT samples (p < 0.0001). In conclusion, these data support the idea that CC inhibitors targeting MCPH1/BRIT1 may sensitize BC cells to chemotherapy. Additionally, genes whose inhibition could promote cell death in MCPH1/BRIT1–deficient cells have been identified as potential therapeutic targets in tumours where MCPH1/BRIT1 expression or function has been compromised

Craniofacial anomalies in children: diagnosis, management, outcomes

The causes of facial anomalies in children may be congenital, traumatic, oncologic (or in some cases) remain unknown. Many of these craniofacial conditions warrant further elucidation of the clinical features, to allow accurate diagnosis and targeted management. Long term outcome studies of children with craniofacial anomalies, are essential to evaluate treatment protocols and to aid those who treat affected children to improve and advance their standards of care. These objectives require clinicians, along with their scientific colleagues to strive to increase their recognition of morphological anomalies and understanding of the underlying disease processes, so as to develop specific management strategies. The aim is to find new answers to improve the quality of life of affected children throughout the world. This collection of papers has been prompted by a desire to contribute towards that goal