Converged HPC-Cloud computing is an emerging computing paradigm that aims to support increasingly complex and multi-tenant scientific workflows. These systems require reconciliation of the isolation requirements of native cloud workloads and the performance demands of HPC applications. In this context, networking hardware is a critical boundary component: it is the conduit for high-throughput, low-latency communication and enables isolation across tenants. HPE Slingshot is a high-speed network interconnect that provides up to 200 Gbps of throughput per port and targets high-performance computing (HPC) systems. The Slingshot host software, including hardware drivers and network middleware libraries, is designed to meet HPC deployments, which predominantly use singletenant access modes. Hence, the Slingshot stack is not suited for secure use in multi-tenant deployments, such as converged HPCCloud deployments. In this paper, we design and implement an extension to the Slingshot stack targeting converged deployments on the basis of Kubernetes. Our integration provides secure, container-granular, and multi-tenant access to Slingshot RDMA networking capabilities at minimal overhead.

HPC systems use monitoring and operational data analytics to ensure efficiency, performance, and orderly operations. Application-specific insights are crucial for analyzing the increasing complexity and diversity of HPC workloads, particularly through the identification of unknown software and recognition of repeated executions, which facilitate system optimization and security improvements. However, traditional identification methods using job or file names are unreliable for arbitrary user-provided names. Fuzzy hashing the content of executables detects similarities despite different code versions or compilation approaches while preserving privacy and file integrity, overcoming these limitations. We introduce SIREN, a process-level data collection framework for software identification and recognition. SIREN improves observability in HPC job execution by enabling analysis of process metadata, environment information, and executable fuzzy hashes. Findings from an opt-in deployment campaign on LUMI show SIREN’s ability to provide insights into software usage, recognition of repeated executions of known applications, and similarity-based identification of unknown applications.

Whilst Field-Programmable Gate Arrays (FPGAs) have been popular in accelerating high-frequency financial workload for many years, their application in quantitative finance, the utilisation of mathematical models to analyse financial markets and securities, is less mature. Nevertheless, recent work has demonstrated the benefits that FPGAs can deliver to quantitative workloads, and in this paper, we study whether the Versal ACAP and its AI Engines (AIEs) can also deliver improved performance. We focus specifically on the industry standard Strategic Technology Analysis Center's (STAC) derivatives risk analysis benchmark STAC-A2. Porting a purely FPGA-based accelerator STAC-A2 inspired market risk (SIMR) benchmark to the Versal ACAP device by combining Programmable Logic (PL) and AIEs, we explore the development approach and techniques, before comparing performance across PL and AIEs. Ultimately, we found that our AIE approach is slower than a highly optimised existing PL-only version due to limits on both the AIE and PL that we explore and describe.

In recent years the use of FPGAs to accelerate scientific applications has grown, with numerous applications demonstrating the benefit of FPGAs for high performance workloads. However, whilst High Level Synthesis (HLS) has significantly lowered the barrier to entry in programming FPGAs by enabling programmers to use C++, a major challenge is that most often these codes are not originally written in C++. Instead, Fortran is the lingua franca of scientific computing and-so it requires a complex and time consuming initial step to convert into C++ even before considering the FPGA. In this paper we describe work enabling Fortran for AMD Xilinx FPGAs by connecting the LLVM Flang front end to AMD Xilinx's LLVM back end. This enables programmers to use Fortran as a first-class language for programming FPGAs, and as we demonstrate enjoy all the tuning and optimisation opportunities that HLS C++ provides. Furthermore, we demonstrate that certain language features of Fortran make it especially beneficial for programming FPGAs compared to C++. The result of this work is a lowering of the barrier to entry in using FPGAs for scientific computing, enabling programmers to leverage their existing codebase and language of choice on the FPGA directly.

MOTIVATION: Elementary modes (EMs) and minimal cut sets (MCSs) provide important techniques for metabolic network modeling. Whereas EMs describe minimal subnetworks that can function in steady state, MCSs are sets of reactions whose removal will disable certain network functions. Effective algorithms were developed for EM computation while calculation of MCSs is typically addressed by indirect methods requiring the computation of EMs as initial step. RESULTS: In this contribution, we provide a method that determines MCSs directly without calculating the EMs. We introduce a duality framework for metabolic networks where the enumeration of MCSs in the original network is reduced to identifying the EMs in a dual network. As a further extension, we propose a generalization of MCSs in metabolic networks by allowing the combination of inhomogeneous constraints on reaction rates. This framework provides a promising tool to open the concept of EMs and MCSs to a wider class of applications. CONTACT: [email protected]; [email protected] SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

T cells orchestrate the adaptive immune response, making them targets for immunotherapy. Although immunosuppressive therapies prevent disease progression, they also leave patients susceptible to opportunistic infections. To identify novel drug targets, we established a logical model describing T-cell receptor (TCR) signaling. However, to have a model that is able to predict new therapeutic approaches, the current drug targets must be included. Therefore, as a next step we generated the interleukin-2 receptor (IL-2R) signaling network and developed a tool to merge logical models. For IL-2R signaling, we show that STAT activation is independent of both Src- and PI3-kinases, while ERK activation depends upon both kinases and additionally requires novel PKCs. In addition, our merged model correctly predicted TCR-induced STAT activation. The combined network also allows information transfer from one receptor to add detail to another, thereby predicting that LAT mediates JNK activation in IL-2R signaling. In summary, the merged model not only enables us to unravel potential cross-talk, but it also suggests new experimental designs and provides a critical step towards designing strategies to reprogram T cells.

3,41Max Planck Institute for Dynamics of Complex Technical Systems, Magdeburg, Germany, 2Institute for Mathematical Optimization, Faculty of Mathematics, Otto-von-Guericke University Magdeburg, Magdeburg, Germany, 3Institute for Bioinformatics and Systems Biology, Helmholtz Zentrum Mu¨nchen—German Research Center forEnvironmental Health, Neuherberg, Germany, 4Max Planck Institute for Dynamics and Self-Organization, Go¨ttingen, Germany

Cellular decisions are determined by complex molecular interaction networks. Large-scale signaling networks are currently being reconstructed, but the kinetic parameters and quantitative data that would allow for dynamic modeling are still scarce. Therefore, computational studies based upon the structure of these networks are of great interest. Here, a methodology relying on a logical formalism is applied to the functional analysis of the complex signaling network governing the activation of T cells via the T cell receptor, the CD4/CD8 co-receptors, and the accessory signaling receptor CD28. Our large-scale Boolean model, which comprises 94 nodes and 123 interactions and is based upon well-established qualitative knowledge from primary T cells, reveals important structural features (e.g., feedback loops and network-wide dependencies) and recapitulates the global behavior of this network for an array of published data on T cell activation in wild-type and knock-out conditions. More importantly, the model predicted unexpected signaling events after antibody-mediated perturbation of CD28 and after genetic knockout of the kinase Fyn that were subsequently experimentally validated. Finally, we show that the logical model reveals key elements and potential failure modes in network functioning and provides candidates for missing links. In summary, our large-scale logical model for T cell activation proved to be a promising in silico tool, and it inspires immunologists to ask new questions. We think that it holds valuable potential in foreseeing the effects of drugs and network modifications.