Theoretical Analysis and Evaluation of NoCs with Weighted Round-Robin Arbitration

Fast and accurate performance analysis techniques are essential in early design space exploration and pre-silicon evaluations, including software eco-system development. In particular, on-chip communication continues to play an increasingly important role as the many-core processors scale up. This paper presents the first performance analysis technique that targets networks-on-chip (NoCs) that employ weighted round-robin (WRR) arbitration. Besides fairness, WRR arbitration provides flexibility in allocating bandwidth proportionally to the importance of the traffic classes, unlike basic round-robin and priority-based arbitration. The proposed approach first estimates the effective service time of the packets in the queue due to WRR arbitration. Then, it uses the effective service time to compute the average waiting time of the packets. Next, we incorporate a decomposition technique to extend the analytical model to handle NoC of any size. The proposed approach achieves less than 5% error while executing real applications and 10% error under challenging synthetic traffic with different burstiness levels.Comment: This paper is accepted in International Conference on Computer Aided Design (ICCAD), 202

End-to-End Benchmarking of Chiplet-Based In-Memory Computing

In-memory computing (IMC)-based hardware reduces latency and energy consumption for compute-intensive machine learning (ML) applications. Several SRAM/RRAM-based IMC hardware architectures to accelerate ML applications have been proposed in the literature. However, crossbar-based IMC hardware poses several design challenges. We first discuss the different ML algorithms recently adopted in the literature. We then discuss the hardware implications of ML algorithms. Next, we elucidate the need for IMC architecture and the different components within a conventional IMC architecture. After that, we introduce the need for 2.5D or chiplet-based architectures. We then discuss the different benchmarking simulators proposed for monolithic IMC architectures. Finally, we describe an end-to-end chiplet-based IMC benchmarking simulator, SIAM

Black Hole Formation and Space-Time Fluctuations in Two Dimensional Dilaton Gravity and Complementarity

We study black hole formation in a model of two dimensional dilaton gravity and 24 massless scalar fields with a boundary. We find the most general boundary condition consistent with perfect reflection of matter and the constraints. We show that in the semiclassical approximation and for the generic value of the parameter which characterizes the boundary conditions, the boundary starts receeding to infinity at the speed of light whenever the total energy of the incoming matter flux exceeds a certain critical value. This is also the critical energy which marks the onset of black hole formation. We then compute the quantum fluctuations of the boundary and of the rescaled scalar curvature and show that as soon as the incoming energy exceeds this critical value, an asymptotic observer using normal time resolutions will always measure large fluctuations of space-time near the horizon, even though the freely falling observer does not. This is an aspect of black hole complementarity relating directly the quantum gravity effects.Comment: (Some typographical errors corrected and some equations added to clarify the nature of the singularity in the in the semiclassical solution), 30 pagers, TIFR/TH/94-01, IC/94/1

Molecular association of glucose-6- phosphate isomerase and pyruvate kinase M2 with glyceraldehyde-3-phosphate dehydrogenase in cancer cells

Background: For a long time cancer cells are known for increased uptake of glucose and its metabolization through glycolysis. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a key regulatory enzyme of this pathway and can produce ATP through oxidative level of phosphorylation. Previously, we reported that GAPDH purified from a variety of malignant tissues, but not from normal tissues, was strongly inactivated by a normal metabolite, methylglyoxal (MG).Molecular mechanism behind MG mediated GAPDH inhibition in cancer cells is not well understood. Methods: GAPDH was purified from Ehrlich ascites carcinoma (EAC) cells based on its enzymatic activity. GAPDH associated proteins in EAC cells and 3-methylcholanthrene (3MC) induced mouse tumor tissue were detected by mass spectrometry analysis and immunoprecipitation (IP) experiment, respectively. Interacting domains of GAPDH and its associated proteins were assessed by in silico molecular docking analysis. Mechanism of MG mediated GAPDH inactivation in cancer cells was evaluated by measuring enzyme activity, Circular dichroism (CD) spectroscopy, IP and mass spectrometry analyses. Result: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue. Molecular docking analyses suggest C-terminal domain preference for the interaction between GAPDH and GPI. However, both C and N termini of PKM2 might be interacting with the C terminal domain of GAPDH. Expression of both PKM2 and GPI is increased in 3MC induced tumor compared with the normal tissue. In presence of 1 mM MG,association of GAPDH with PKM2 or GPI is not perturbed, but the enzymatic activity of GAPDH is reduced to 26.8 ± 5 % in 3MC induced tumor and 57.8 ± 2.3 % in EAC cells. Treatment of MG to purified GAPDH complex leads to glycation at R399 residue of PKM2 only, and changes the secondary structure of the protein complex. Conclusion: PKM2 may regulate the enzymatic activity of GAPDH. Increased enzymatic activity of GAPDH in tumor cells may be attributed to its association with PKM2 and GPI. Association of GAPDH with PKM2 and GPI could be a signature for cancer cells. Glycation at R399 of PKM2 and changes in the secondary structure of GAPDH complex could be one of the mechanisms by which GAPDH activity is inhibited in tumor cells by MG