Ingress of threshold voltage-triggered hardware trojan in the modern FPGA fabric–detection methodology and mitigation

The ageing phenomenon of negative bias temperature instability (NBTI) continues to challenge the dynamic thermal management of modern FPGAs. Increased transistor density leads to thermal accumulation and propagates higher and non-uniform temperature variations across the FPGA. This aggravates the impact of NBTI on key PMOS transistor parameters such as threshold voltage and drain current. Where it ages the transistors, with a successive reduction in FPGA lifetime and reliability, it also challenges its security. The ingress of threshold voltage-triggered hardware Trojan, a stealthy and malicious electronic circuit, in the modern FPGA, is one such potential threat that could exploit NBTI and severely affect its performance. The development of an effective and efficient countermeasure against it is, therefore, highly critical. Accordingly, we present a comprehensive FPGA security scheme, comprising novel elements of hardware Trojan infection, detection, and mitigation, to protect FPGA applications against the hardware Trojan. Built around the threat model of a naval warship’s integrated self-protection system (ISPS), we propose a threshold voltage-triggered hardware Trojan that operates in a threshold voltage region of 0.45V to 0.998V, consuming ultra-low power (10.5nW), and remaining stealthy with an area overhead as low as 1.5% for a 28 nm technology node. The hardware Trojan detection sub-scheme provides a unique lightweight threshold voltage-aware sensor with a detection sensitivity of 0.251mV/nA. With fixed and dynamic ring oscillator-based sensor segments, the precise measurement of frequency and delay variations in response to shifts in the threshold voltage of a PMOS transistor is also proposed. Finally, the FPGA security scheme is reinforced with an online transistor dynamic scaling (OTDS) to mitigate the impact of hardware Trojan through run-time tolerant circuitry capable of identifying critical gates with worst-case drain current degradation

Towards Control-Centric Representations in Reinforcement Learning from Images

Image-based Reinforcement Learning is a practical yet challenging task. A major hurdle lies in extracting control-centric representations while disregarding irrelevant information. While approaches that follow the bisimulation principle exhibit the potential in learning state representations to address this issue, they still grapple with the limited expressive capacity of latent dynamics and the inadaptability to sparse reward environments. To address these limitations, we introduce ReBis, which aims to capture control-centric information by integrating reward-free control information alongside reward-specific knowledge. ReBis utilizes a transformer architecture to implicitly model the dynamics and incorporates block-wise masking to eliminate spatiotemporal redundancy. Moreover, ReBis combines bisimulation-based loss with asymmetric reconstruction loss to prevent feature collapse in environments with sparse rewards. Empirical studies on two large benchmarks, including Atari games and DeepMind Control Suit, demonstrate that ReBis has superior performance compared to existing methods, proving its effectiveness

A Cross-Tissue Investigation of Molecular Targets and Physiological Functions of Nsun6 Using Knockout Mice

The 5-methylcytosine (m5C) modification on an mRNA molecule is deposited by Nsun2 and its paralog Nsun6. While the physiological functions of Nsun2 have been carefully studied using gene knockout (KO) mice, the physiological functions of Nsun6 remain elusive. In this study, we generated an Nsun6-KO mouse strain, which exhibited no apparent phenotype in both the development and adult stages as compared to wild-type mice. Taking advantage of this mouse strain, we identified 80 high-confident Nsun6-dependent m5C sites by mRNA bisulfite sequencing in five different tissues and systematically analyzed the transcriptomic phenotypes of Nsun6-KO tissues by mRNA sequencing. Our data indicated that Nsun6 is not required for the homeostasis of these organs under laboratory housing conditions, but its loss may affect immune response in the spleen and oxidoreductive reaction in the liver under certain conditions. Additionally, we further investigated T-cell-dependent B cell activation in KO mice and found that Nsun6 is not essential for the germinal center B cell formation but is associated with the formation of antibody-secreting plasma cells. Finally, we found that Nsun6-mediated m5C modification does not have any evident influence on the stability of Nsun6 target mRNAs, suggesting that Nsun6-KO-induced phenotypes may be associated with other functions of the m5C modification or Nsun6 protein