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  1. Quantum Random Access Memory (QRAM) has the potential to revolutionize the area of quantum computing. QRAM uses quantum computing principles to store and modify quantum or classical data efficiently, greatly accelerating a wide range of computer processes. Despite its importance, there is a lack of comprehensive surveys that cover the entire spectrum of QRAM architectures. We fill this gap by providing a comprehensive review of QRAM, emphasizing its significance and viability in existing noisy quantum computers. By drawing comparisons with conventional RAM for ease of understanding, this survey clarifies the fundamental ideas and actions of QRAM. QRAM provides an exponential time advantage compared to its classical counterpart by reading and writing all data at once, which is achieved owing to storage of data in a superposition of states. Overall, we compare six different QRAM technologies in terms of their structure and workings, circuit width and depth, unique qualities, practical implementation, and drawbacks. In general, with the exception of trainable machine learning-based QRAMs, we observe that QRAM has exponential depth/width requirements in terms of the number of qubits/qudits and that most QRAM implementations are practical for superconducting and trapped-ion qubit systems. 
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    Free, publicly-accessible full text available September 1, 2024
  2. Free, publicly-accessible full text available July 1, 2024
  3. Spiking neural networks (SNNs) are quickly gaining traction as a viable alternative to deep neural networks (DNNs). Compared to DNNs, SNNs are computationally more powerful and energy efficient. The design metrics (synaptic weights, membrane threshold, etc.) chosen for such SNN architectures are often proprietary and constitute confidential intellectual property (IP). Our study indicates that SNN architectures implemented using conventional analog neurons are susceptible to side channel attack (SCA). Unlike the conventional SCAs that are aimed to leak private keys from cryptographic implementations, SCANN (SCA̲ of spiking n̲eural n̲etworks) can reveal the sensitive IP implemented within the SNN through the power side channel. We demonstrate eight unique SCANN attacks by taking a common analog neuron (axon hillock neuron) as the test case. We chose this particular model since it is biologically plausible and is hence a good fit for SNNs. Simulation results indicate that different synaptic weights, neurons/layer, neuron membrane thresholds, and neuron capacitor sizes (which are the building blocks of SNN) yield distinct power and spike timing signatures, making them vulnerable to SCA. We show that an adversary can use templates (using foundry-calibrated simulations or fabricating known design parameters in test chips) and analysis to identify the specifications of the implemented SNN. 
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    Free, publicly-accessible full text available June 1, 2024
  4. The stress response protein regulated in development and DNA damage response 1 (REDD1) has been implicated in visual deficits in patients with diabetes. The aim here was to investigate the mechanism responsible for the increase in retinal REDD1 protein content that is observed with diabetes. We found that REDD1 protein expression was increased in the retina of streptozotocin-induced diabetic mice in the absence of a change in REDD1 mRNA abundance or ribosome association. Oral antioxidant supplementation reduced retinal oxidative stress and suppressed REDD1 protein expression in the retina of diabetic mice. In human retinal Müller cell cultures, hyperglycemic conditions increased oxidative stress, enhanced REDD1 expression, and inhibited REDD1 degradation independently of the proteasome. Hyperglycemic conditions promoted a redox-sensitive cross-strand disulfide bond in REDD1 at C150/C157 that was required for reduced REDD1 degradation. Discrete molecular dynamics simulations of REDD1 structure revealed allosteric regulation of a degron upon formation of the disulfide bond that disrupted lysosomal proteolysis of REDD1. REDD1 acetylation at K129 was required for REDD1 recognition by the cytosolic chaperone HSC70 and degradation by chaperone-mediated autophagy. Disruption of REDD1 allostery upon C150/C157 disulfide bond formation prevented the suppressive effect of hyperglycemic conditions on REDD1 degradation and reduced oxidative stress in cells exposed to hyperglycemic conditions. The results reveal redox regulation of REDD1 and demonstrate the role of a REDD1 disulfide switch in development of oxidative stress. 
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