P-EdgeCoolingMode: An Agent Based Performance Aware Thermal Management Unit for DVFS Enabled Heterogeneous MPSoCs

Thermal cycling as well as spatial and thermal gradient affects the lifetime reliability and performance of heterogeneous multiprocessor systems-on-chips (MPSoCs). Conventional temperature management techniques are not intelligent enough to cater for performance, energy efficiency as well as operating temperature of the system. In this paper we propose a light-weight novel thermal management mechanism (P-EdgeCoolingMode) in the form of intelligent software agent, which monitors and regulates the operating temperature of the CPU cores to improve reliability of the system while catering for performance requirements. P-EdgeCoolingMode is capable of pro-actively monitoring performance and based on the user’s demand the agent takes necessary action, making the proposed methodology highly suitable for implementation on existing as well as conceptual Edge devices utilizing heterogeneous MPSoCs with dynamic voltage and frequency scaling (DVFS) capabilities. We validated our methodology on the Odroid-XU4 MPSoC and Huawei P20 Lite (HiSilicon Kirin 659 MPSoC). P-EdgeCoolingMode has been successful to reduce the operating temperature while improving performance and reducing power consumption for chosen test cases than the state-of-the-art. For applications with demanding performance requirement P-EdgeCoolingMode has been found to improve the power consumption by 30.62% at the most in comparison to existing state-of-the-art power management methodologies

Towards Deeply Scaled 3D MPSoCs with Integrated Flow Cell Array Technology

Deeply-scaled three-dimensional (3D) Multi-Processor Systemson-Chip (MPSoCs) enable high performance and massive communication bandwidth for next-generation computing. However as process nodes shrink, temperature-dependent leakage dramatically increases, and thermal and power management becomes problematic. In this context, Integrated Flow Cell Array (FCA) technology, which consists of inter-tier microfluidic channels, combines onchip electrochemical power generation and liquid cooling of 3D MPSoCs. When connected to power delivery networks (PDN) of dies, FCAs provide an additional current compensating the voltage drop (IR-drop). In this paper, we evaluate for the first time how the IR-drop reduction and cooling capabilities of FCAs scale with advanced CMOS processes. We develop a framework to quantify the system-level impact of FCAs at technology nodes from 22 to 3. Our results show that, across all considered nodes, FCAs reduce the peak temperature of a multi-core processor (MCP) and a Machine Learning (ML) accelerator by over 22°C and 35°C, respectively, compared to off-chip direct liquid cooling. Moreover, the low operation voltages and high temperatures at advanced nodes improve up to 2× FCA power generation. Hence, FCAs allow to keep the IR-drop below 5% for both the MCP and ML accelerator, saving over 10% TSV-reserved area, as opposed to using a HighPerformance Computing (HPC) MPSoC liquid cooling solution

Loss of SMEK, a Novel, Conserved Protein, Suppresses mek1 Null Cell Polarity, Chemotaxis, and Gene Expression Defects

MEK/extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase signaling is imperative for proper chemotaxis. Dictyostelium mek1(−) (MEK1 null) and erk1(−) cells exhibit severe defects in cell polarization and directional movement, but the molecules responsible for the mek1(−) and erk1(−) chemotaxis defects are unknown. Here, we describe a novel, evolutionarily conserved gene and protein (smkA and SMEK, respectively), whose loss partially suppresses the mek1(−) chemotaxis phenotypes. SMEK also has MEK1-independent functions: SMEK, but not MEK1, is required for proper cytokinesis during vegetative growth, timely exit from the mound stage during development, and myosin II assembly. SMEK localizes to the cell cortex through an EVH1 domain at its N terminus during vegetative growth. At the onset of development, SMEK translocates to the nucleus via a nuclear localization signal (NLS) at its C terminus. The importance of SMEK's nuclear localization is demonstrated by our findings that a mutant lacking the EVH1 domain complements SMEK deficiency, whereas a mutant lacking the NLS does not. Microarray analysis reveals that some genes are precociously expressed in mek1(−) and erk1(−) cells. The misexpression of some of these genes is suppressed in the smkA deletion. These data suggest that loss of MEK1/ERK1 signaling compromises gene expression and chemotaxis in a SMEK-dependent manner