A Pattern Language for High-Performance Computing Resilience

High-performance computing systems (HPC) provide powerful capabilities for modeling, simulation, and data analytics for a broad class of computational problems. They enable extreme performance of the order of quadrillion floating-point arithmetic calculations per second by aggregating the power of millions of compute, memory, networking and storage components. With the rapidly growing scale and complexity of HPC systems for achieving even greater performance, ensuring their reliable operation in the face of system degradations and failures is a critical challenge. System fault events often lead the scientific applications to produce incorrect results, or may even cause their untimely termination. The sheer number of components in modern extreme-scale HPC systems and the complex interactions and dependencies among the hardware and software components, the applications, and the physical environment makes the design of practical solutions that support fault resilience a complex undertaking. To manage this complexity, we developed a methodology for designing HPC resilience solutions using design patterns. We codified the well-known techniques for handling faults, errors and failures that have been devised, applied and improved upon over the past three decades in the form of design patterns. In this paper, we present a pattern language to enable a structured approach to the development of HPC resilience solutions. The pattern language reveals the relations among the resilience patterns and provides the means to explore alternative techniques for handling a specific fault model that may have different efficiency and complexity characteristics. Using the pattern language enables the design and implementation of comprehensive resilience solutions as a set of interconnected resilience patterns that can be instantiated across layers of the system stack.Comment: Proceedings of the 22nd European Conference on Pattern Languages of Program

Calibration and Evaluation of Building Energy Models to Assess and Mitigate Canadian Building Overheating Risks in Current and Future Climates

Climate change continues to impact weather conditions globally, requiring cities to adapt to new environments. In Canada, indoor summer overheating in buildings is problematic due to their primary design for cold winters, making them susceptible to extreme heatwave events. This research focuses on calibrating building models and employing model calibration methodologies to evaluate and address overheating risks in various building types across Canada using current and future weather data. The study's objectives are to accurately assess summertime overheating risks in selected buildings in Montreal, Quebec, and evaluate effective mitigation strategies. Bayesian calibration and multi-objective genetic algorithms are used as calibration methods, with the latter showing superiority in producing highly accurate calibrated models based on five performance criteria. By incorporating field measurements and novel methodologies, the research ensures precise assessment and mitigation of summertime overheating risks. After calibrating several buildings, including schools, a hospital, and a residential building, which demonstrates the reliability and repeatability of the calibration process, the assessment of overheating is conducted on calibrated models to determine the number of overheating hours during the summer. In conclusion, this thesis demonstrates the repeatability of the calibration methods on a variety of existing Canadian buildings and the effective use of passive cooling techniques, such as external shading, night cooling, and high albedo surfaces, that are implemented in the building models, to mitigate overheating based on current and future weather data

A molecularly detailed Na V 1.5 model reveals a new Class I antiarrhythmic target

Antiarrhythmic treatment strategies remain suboptimal due to our inability to predict how drug interactions with ion channels will affect the ability of the tissues to initiate and sustain an arrhythmia. We built a multiscale molecular model of the N

Mep72, a metzincin protease that is preferentially secreted by biofilms of Pseudomonas aeruginosa.

In this work, we compared the profile of proteins secreted by planktonic and biofilm cultures of Pseudomonas aeruginosa using two-dimensional difference gel electrophoresis (2D-DiGE). This revealed that a novel metzincin protease, Mep72, was secreted during biofilm growth. Subsequent Western blotting and reverse transcription-PCR (RT-PCR) analyses demonstrated that Mep72 was expressed only during biofilm growth. Mep72 has a tridomain structure comprised of a metzincin protease-like domain and two tandem carbohydrate-binding domains. Unlike the only other metzincin (alkaline protease; AprA) in P. aeruginosa, Mep72 is secreted through the type II pathway and undergoes processing during export. During this processing, the metzincin domain is liberated from the carbohydrate-binding domains. This processing may be self-catalyzed, since purified Mep72 autodegraded in vitro. This autodegradation was retarded in the presence of alginate (an extracellular matrix component of many P. aeruginosa biofilms). The expression of full-length mep72 in Escherichia coli was toxic. However, this toxicity could be alleviated by coexpression of mep72 with the adjacent gene, bamI. Mep72 and BamI were found to form a protein-protein complex in vitro. 2D-DiGE revealed that the electrophoretic mobility of several discrete protein spots was altered in the biofilm secretome of an mep72 mutant, including type III secretion proteins (PopD, PcrV, and ExoS) and a flagellum-associated protein (FliD). Mep72 was found to bind directly to ExoS and PcrV and to affect the processing of these proteins in the biofilm secretome. We conclude that Mep72 is a secreted biofilm-specific regulator that affects the processing of a very specific subset of virulence factors.This study was funded by the BBSRC, the Isaac Newton Trust (Cambridge), and a grant from the Japanese Society for Acute Infection to K.N.The paper was originally published by the American Society for Microbiology in the Journal of Bacteriology with a CC-BY licence (IJ Passmore, K Nishikawa, KS Lilley, SD Bowden, JCS Chung, M Welch, Journal of Bacteriology 2015, 197, 762–773

Striking Deals : Concertation in the Reform of Continental European Welfare States

The reform of the welfare state entails changes in interdependent policy fields stretching from social policies to employment and wage policies. These linked policy fields are often governed by varying sets of corporate actors and involve different decision making procedures. Adaptation in one policy field is often uncoordinated with other policies, and can work at cross-purposes, produce negative externalities, or fail due to missing supporting conditions. The paper has two objectives. It first argues that renewed emergence of tripartite concertation is due to the need to co-ordinate policies across policy fields. Second, it evaluates the institutional factors which have facilitated concertation in some cases, but not in others. Using a similar country design, the paper compares four continental European countries with similar reform pressures but different reform trajectories: France, Germany, Italy, and the Netherlands.Die Reform des Wohlfahrtsstaates erfordert Veränderungen in interdependenten Politikfeldern, von der Sozialpolitik bis hin zur Beschäftigungs- und Lohnpolitik. Diese interdependenten Politikfelder werden von unterschiedlichen Konstellationen korporativer und politischer Akteure kontrolliert und sind unterschiedlichen Verfahren der Entscheidungsfindung unterworfen. Adaptionen in einem Sektor sind häufig nicht mit anderen politischen Entscheidungen koordiniert und können somit negative Auswirkungen haben oder aufgrund der ungünstigen Grundbedingungen fehlschlagen. In dem vorliegenden Discussion Paper wird zunächst argumentiert, daß die Notwendigkeit, politische Entscheidungen über die Grenzen der politischen Sektoren hinaus zu koordinieren, zu einer Renaissance dreiseitiger Konzertierung zwischen Tarifparteien und Regierungen geführt hat. Weiterhin werden die institutionellen Faktoren herausgearbeitet, die eine Konzertierung in einigen Fällen ermöglicht haben, in anderen jedoch nicht. Es werden vier Länder verglichen, die ähnliche Strukturen und Reformzwänge aufweisen, aber unterschiedliche Lösungswege gewählt haben: Frankreich, Deutschland, Italien und die Niederlande

A Riemann solver at a junction compatible with a homogenization limit

We consider a junction regulated by a traffic lights, with n incoming roads and only one outgoing road. On each road the Phase Transition traffic model, proposed in [6], describes the evolution of car traffic. Such model is an extension of the classic Lighthill-Whitham-Richards one, obtained by assuming that different drivers may have different maximal speed. By sending to infinity the number of cycles of the traffic lights, we obtain a justification of the Riemann solver introduced in [9] and in particular of the rule for determining the maximal speed in the outgoing road.Comment: 19 page

Tracking Cyber Adversaries with Adaptive Indicators of Compromise

A forensics investigation after a breach often uncovers network and host indicators of compromise (IOCs) that can be deployed to sensors to allow early detection of the adversary in the future. Over time, the adversary will change tactics, techniques, and procedures (TTPs), which will also change the data generated. If the IOCs are not kept up-to-date with the adversary's new TTPs, the adversary will no longer be detected once all of the IOCs become invalid. Tracking the Known (TTK) is the problem of keeping IOCs, in this case regular expressions (regexes), up-to-date with a dynamic adversary. Our framework solves the TTK problem in an automated, cyclic fashion to bracket a previously discovered adversary. This tracking is accomplished through a data-driven approach of self-adapting a given model based on its own detection capabilities. In our initial experiments, we found that the true positive rate (TPR) of the adaptive solution degrades much less significantly over time than the naive solution, suggesting that self-updating the model allows the continued detection of positives (i.e., adversaries). The cost for this performance is in the false positive rate (FPR), which increases over time for the adaptive solution, but remains constant for the naive solution. However, the difference in overall detection performance, as measured by the area under the curve (AUC), between the two methods is negligible. This result suggests that self-updating the model over time should be done in practice to continue to detect known, evolving adversaries.Comment: This was presented at the 4th Annual Conf. on Computational Science & Computational Intelligence (CSCI'17) held Dec 14-16, 2017 in Las Vegas, Nevada, US

Kinetochore genes are coordinately up-regulated in human tumors as part of a FoxM1-related cell division program

The key player in directing proper chromosome segregation is the macromolecular kinetochore complex, which mediates DNA–microtubule interactions. Previous studies testing individual kinetochore genes documented examples of their overexpression in tumors relative to normal tissue, leading to proposals that up-regulation of specific kinetochore genes may promote tumor progression. However, kinetochore components do not function in isolation, and previous studies did not comprehensively compare the expression behavior of kinetochore components. Here we analyze the expression behavior of the full range of human kinetochore components in diverse published expression compendia, including normal tissues and tumor samples. Our results demonstrate that kinetochore genes are rarely overexpressed individually. Instead, we find that core kinetochore genes are coordinately regulated with other cell division genes under virtually all conditions. This expression pattern is strongly correlated with the expression of the forkhead transcription factor FoxM1, which binds to the majority of cell division promoters. These observations suggest that kinetochore gene up-regulation in cancer reflects a general activation of the cell division program and that altered expression of individual kinetochore genes is unlikely to play a causal role in tumorigenesis.Leukemia & Lymphoma Society of America (Scholar Award)National Institute of General Medical Sciences (U.S.) (Grant GM088313)American Cancer Society (Research Scholar Grant 121776)National Science Foundation (U.S.). Graduate Research Fellowshi