Homomorphic Multiple Precision Multiplication for CKKS and Reduced Modulus Consumption

Homomorphic Encryption (HE) schemes such as BGV, BFV, and CKKS consume some ciphertext modulus for each multiplication. Bootstrapping (BTS) restores the modulus and allows homomorphic computation to continue, but it is time-consuming and requires a significant amount of modulus. For these reasons, decreasing modulus consumption is crucial topic for BGV, BFV and CKKS, on which numerous studies have been conducted. We propose a novel method, called $\mathsf{mult}^2$, to perform ciphertext multiplication in the CKKS scheme with lower modulus consumption. $\mathsf{mult}^2$ relies an a new decomposition of a ciphertext into a pair of ciphertexts that homomorphically performs a weak form of Euclidean division. It multiplies two ciphertexts in decomposed formats with homomorphic double precision multiplication, and its result approximately decrypts to the same value as does the ordinary CKKS multiplication. $\mathsf{mult}^2$ can perform homomorphic multiplication by consuming almost half of the modulus. We extend it to $\mathsf{mult}^t$ for any $t\geq 2$, which relies on the decomposition of a ciphertext into $t$ components. All other CKKS operations can be equally performed on pair/tuple formats, leading to the double-CKKS (resp. tuple-CKKS) scheme enabling homomorphic double (resp. multiple) precision arithmetic. As a result, when the ciphertext modulus and dimension are fixed, the proposed algorithms enable the evaluation of deeper circuits without bootstrapping, or allow to reduce the number of bootstrappings required for the evaluation of the same circuits. Furthermore, they can be used to increase the precision without increasing the parameters. For example, $\mathsf{mult}^2$ enables 8 sequential multiplications with 100 bit scaling factor with a ciphertext modulus of only 680 bits, which is impossible with the ordinary CKKS multiplication algorithm

Fault-Tolerant Multicasting in Multistage Interconnection Networks

Abstract In this paper, we study fault-toleran

META-BTS: Bootstrapping Precision Beyond the Limit

Bootstrapping, which enables the full homomorphic encryption scheme that can perform an infinite number of operations by restoring the modulus of the ciphertext with a small modulus, is an essential step in homomorphic encryption. However, bootstrapping is the most time and memory consuming of all homomorphic operations. As we increase the precision of bootstrapping, a large amount of computational resources is required. Specifically, for any of the previous bootstrap designs, the precision of bootstrapping is limited by rescaling precision. In this paper, we propose a new bootstrapping algorithm of the Cheon-Kim-Kim-Song (CKKS) scheme to use a known bootstrapping algorithm repeatedly, so called { Meta-BTS}. By repeating the original bootstrapping operation twice, one can obtain another bootstrapping with its precision essentially doubled; it can be generalized to be $k$-fold bootstrapping operations for some $k>1$ while the ciphertext size is large enough. Our algorithm overcomes the precision limitation given by the rescale operation

Mechanical transistors for logic-with-memory computing

As a potential revolutionary topic in future information processing, mechanical computing has gained tremendous attention for replacing or supplementing conventional electronics vulnerable to power outages, security attacks, and harsh environments. Despite its potential for constructing intelligent matter towards nonclassical computing systems beyond the von Neumann architecture, most works on mechanical computing demonstrated that the ad hoc design of simple logic gates cannot fully realize a universal mechanical processing framework involving interconnected arithmetic logic components and memory. However, such a logic-with-memory computing architecture is critical for complex and persistent state-dependent computations such as sequential logic. Here we propose a mechanical transistor (M-Transistor), abstracting omnipresent temperatures as the input-output mechanical bits, which consists of a metamaterial thermal channel as the gate terminal driving a nonlinear bistable soft actuator to selectively connect the output terminal to two other variable thermal sources. This M-Transistor is an elementary unit to modularly form various combinational and sequential circuits, such as complex logic gates, registers (volatile memory), and long-term memories (non-volatile memory) with much fewer units than the electronic counterparts. Moreover, they can establish a universal processing core comprising an arithmetic circuit and a register in a compact, reprogrammable network involving periodic read, write, memory, and logic operations of the mechanical bits. Our work contributes to realizing a non-electric universal mechanical computing architecture that combines multidisciplinary engineering with structural mechanics, materials science, thermal engineering, physical intelligence, and computational science.Comment: 25 pages, 4 figures, Articl

Towards maximized volumetric capacity via pore-coordinated design for large-volume-change lithium-ion battery anodes

To achieve the urgent requirement for high volumetric energy density in lithium-ion batteries, alloy-based anodes have been spotlighted as next-generation alternatives. Nonetheless, for the veritable accomplishment with regards to high-energy demand, alloy-based anodes must be evaluated considering several crucial factors that determine volumetric capacity. In particular, the electrode swelling upon cycling must be contemplated if these anodes are to replace conventional graphite anodes in terms of volumetric capacity. Herein, we propose macropore-coordinated graphite-silicon composite by incorporating simulation and mathematical calculation of numerical values from experimental data. This unique structure exhibits minimized electrode swelling comparable to conventional graphite under industrial electrode fabrication conditions. Consequently, this hybrid anode, even with high specific capacity (527 mAh g(-1)) and initial coulombic efficiency (93%) in half-cell, achieves higher volumetric capacity (493.9 mAh cm(-3)) and energy density (1825.7 Wh L-1) than conventional graphite (361.4 mAh cm(-3) and 1376.3 Wh L-1) after 100 cycles in the full-cell configuration

Repurposing pyridoxamine for therapeutic intervention of intravascular cell-cell interactions in mouse models of sickle cell disease

Adherent neutrophils on vascular endothelium positively contribute to cell-cell aggregation and vaso-occlusion in sickle cell disease. In the present study, we demonstrated that pyridoxamine, a derivative of vitamin B6, might be a therapeutic agent to alleviate intravascular cell-cell aggregation in sickle cell disease. Using real-time intravital microscopy, we found that one oral administration of pyridoxamine dose-dependently increased the rolling influx of neutrophils and reduced neutrophil adhesion to endothelial cells in cremaster microvessels of sickle cell disease mice challenged with hypoxia-reoxygenation. Short-term treatment also mitigated neutrophil-endothelial cell and neutrophil-platelet interactions in the microvessels and improved the survival of sickle cell disease mice challenged with tumor necrosis factor-α. The inhibitory effects of pyridoxamine on intravascular cell-cell interactions were potentiated by co-treatment with hydroxyurea. We observed that long-term (5.5 months) oral treatment with pyridoxamine significantly diminished the adhesive function of neutrophils and platelets and down-regulated the expression of E-selectin and intercellular adhesion molecule-1 on the vascular endothelium in tumor necrosis factor-α-challenged sickle cell disease mice. Ex vivo studies revealed that the surface amount of αMβ2 integrin was significantly decreased in stimulated neutrophils isolated from sickle cell disease mice treated with pyridoxamine-containing water. Studies using platelets and neutrophils from sickle cell disease mice and patients suggested that treatment with pyridoxamine reduced the activation state of platelets and neutrophils. These results suggest that pyridoxamine may be a novel therapeutic and a supplement to hydroxyurea to prevent and treat vaco-occlusion events in sickle cell disease

Redox Regulation of Mitochondrial Fission Protein Drp1 by Protein Disulfide Isomerase Limits Endothelial Senescence.

Mitochondrial dynamics are tightly controlled by fusion and fission, and their dysregulation and excess reactive oxygen species (ROS) contribute to endothelial cell (EC) dysfunction. How redox signals regulate coupling between mitochondrial dynamics and endothelial (dys)function remains unknown. Here, we identify protein disulfide isomerase A1 (PDIA1) as a thiol reductase for the mitochondrial fission protein Drp1. A biotin-labeled Cys-OH trapping probe and rescue experiments reveal that PDIA1 depletion in ECs induces sulfenylation of Drp1 at Cys644, promoting mitochondrial fragmentation and ROS elevation without inducing ER stress, which drives EC senescence. Mechanistically, PDIA1 associates with Drp1 to reduce its redox status and activity. Defective wound healing and angiogenesis in diabetic or PDIA1+/- mice are restored by EC-targeted PDIA1 or the Cys oxidation-defective mutant Drp1. Thus, this study uncovers a molecular link between PDIA1 and Drp1 oxidoreduction, which maintains normal mitochondrial dynamics and limits endothelial senescence with potential translational implications for vascular diseases associated with diabetes or aging.This research was supported by NIH R01HL135584 (to M.U.-F.), NIH R21HL112293 (to M.U.-F.), NIH R01HL133613 (to T.F. and M.U.-F.), NIH R01HL116976 (to T.F. and M.U.-F.), NIH R01HL070187 (to T.F.), NIH R01HL112626 (to J.K.), Department of Veterans Affairs Merit Review Grant 2I01BX001232 (to T.F.), AHA 16GRNT31390032 (to M.U.-F.), AHA 15SDG25700406 (to S.V.), AHA 16POST27790038 (to A.D.), and NIH T32HL07829 (to R.C.). We thank Mr. Kyle Taylor at Keyence Corporation for assisting with taking images using the Keyence microscope; Dr. John O’Bryan at UIC for assisting with the BiFC assays; Dr. Leslie Poole at Wake Forest University for providing DCP-Bio1, as well as Dr. Jody Martin and the Center for Cardiovascular Research-supported Vector Core Facility at UIC for amplifying adenoviruses.S

Scalable Generation of Universal Platelets from Human Induced Pluripotent Stem Cells

Summary Human induced pluripotent stem cells (iPSCs) provide a potentially replenishable source for the production of transfusable platelets. Here, we describe a method to generate megakaryocytes (MKs) and functional platelets from iPSCs in a scalable manner under serum/feeder-free conditions. The method also permits the cryopreservation of MK progenitors, enabling a rapid “surge” capacity when large numbers of platelets are needed. Ultrastructural/morphological analyses show no major differences between iPSC platelets and human blood platelets. iPSC platelets form aggregates, lamellipodia, and filopodia after activation and circulate in macrophage-depleted animals and incorporate into developing mouse thrombi in a manner identical to human platelets. By knocking out the β2-microglobulin gene, we have generated platelets that are negative for the major histocompatibility antigens. The scalable generation of HLA-ABC-negative platelets from a renewable cell source represents an important step toward generating universal platelets for transfusion as well as a potential strategy for the management of platelet refractoriness

Platelets generated from human embryonic stem cells are functional in vitro and in the microcirculation of living mice

Platelets play an essential role in hemostasis and atherothrombosis. Owing to their short storage time, there is constant demand for this life-saving blood component. In this study, we report that it is feasible to generate functional megakaryocytes and platelets from human embryonic stem cells (hESCs) on a large scale. Differential-interference contrast and electron microscopy analyses showed that ultrastructural and morphological features of hESC-derived platelets were indistinguishable from those of normal blood platelets. In functional assays, hESC-derived platelets responded to thrombin stimulation, formed microaggregates, and facilitated clot formation/retraction in vitro. Live cell microscopy demonstrated that hESC-platelets formed lamellipodia and filopodia in response to thrombin activation, and tethered to each other as observed in normal blood. Using real-time intravital imaging with high-speed video microscopy, we have also shown that hESC-derived platelets contribute to developing thrombi at sites of laser-induced vascular injury in mice, providing the first evidence for in vivo functionality of hESC-derived platelets. These results represent an important step toward generating an unlimited supply of platelets for transfusion. Since platelets contain no genetic material, they are ideal candidates for early clinical translation involving human pluripotent stem cells