This paper describes an authentication protocol using a Hardware-Embedded Delay PUF called HELP. HELP derives randomness from within-die path delay variations that occur along the paths within a hardware implementation of a cryptographic primitive, such as AES or SHA-3. The digitized timing values which represent the path delays are stored in a database on a secure server (verifier) as an alternative to storing PUF response bitstrings. This enables the development of an efficient authentication protocol that provides both privacy and mutual authentication. The security properties of the protocol are analyzed using data collected from a set of Xilinx Zynq FPGAs.

The gut microbiome is intricately coupled with immune regulation and metabolism, but its role in Coronavirus Disease 2019 (COVID-19) is not fully understood. Severe and fatal COVID-19 is characterized by poor anti-viral immunity and hypercoagulation, particularly in males. Here, we define multiple pathways by which the gut microbiome protects mammalian hosts from SARS-CoV-2 intranasal infection, both locally and systemically, via production of short-chain fatty acids (SCFAs). SCFAs reduced viral burdens in the airways and intestines by downregulating the SARS-CoV-2 entry receptor, angiotensin-converting enzyme 2 (ACE2), and enhancing adaptive immunity via GPR41 and 43 in male animals. We further identify a novel role for the gut microbiome in regulating systemic coagulation response by limiting megakaryocyte proliferation and platelet turnover via the Sh2b3-Mpl axis. Taken together, our findings have unraveled novel functions of SCFAs and fiber-fermenting gut bacteria to dampen viral entry and hypercoagulation and promote adaptive antiviral immunity.

Abstract:The magnitude of the information content associated with a particular implementation of a Physical Unclonable Function (PUF) is critically important for security and trust in emerging Internet of Things (IoT) applications. Authentication, in particular, requires the PUF to produce a very large number of challenge-response-pairs (CRPs) and, of even greater importance, requires the PUF to be resistant to adversarial attacks that attempt to model and clone the PUF (model-building attacks). Entropy is critically important to the model-building resistance of the PUF. A variety of metrics have been proposed for reporting Entropy, each measuring the randomness of information embedded within PUF-generated bitstrings. In this paper, we report the Entropy, MinEntropy, conditional MinEntropy, Interchip hamming distance and National Institute of Standards and Technology (NIST) statistical test results using bitstrings generated by a Hardware-Embedded Delay PUF called HELP. The bitstrings are generated from data collected in hardware experiments on 500 copies of HELP implemented on a set of Xilinx Zynq 7020 SoC Field Programmable Gate Arrays (FPGAs) subjected to industrial-level temperature and voltage conditions. Special test cases are constructed which purposely create worst case correlations for bitstring generation. Our results show that the processes proposed within HELP to generate bitstrings add significantly to their Entropy, and show that classical re-use of PUF components, e.g., path delays, does not result in large Entropy losses commonly reported for other PUF architectures.

IRE1α-XBP1 signaling is emerging as a central orchestrator of malignant progression and immunosuppression in various cancer types. Employing a computational XBP1s detection method applied to TCGA datasets, we demonstrate that expression of the XBP1s mRNA isoform predicts poor survival in non-small cell lung cancer (NSCLC) patients. Ablation of IRE1α in malignant cells delays tumor progression and extends survival in mouse models of NSCLC. This protective effect is accompanied by alterations in intratumoral immune cell subsets eliciting durable adaptive anti-cancer immunity. Mechanistically, cancer cell-intrinsic IRE1α activation sustains mPGES-1 expression, enabling production of the immunosuppressive lipid mediator prostaglandin E2. Accordingly, restoring mPGES-1 expression in IRE1αKO cancer cells rescues normal tumor progression. We have developed an IRE1α gene signature that predicts immune cell infiltration and overall survival in human NSCLC. Our study unveils an immunoregulatory role for cancer cell-intrinsic IRE1α activation and suggests that targeting this pathway may help enhance anti-tumor immunity in NSCLC.