CMOS Based Scalable Cryogenic Control Electronics for Qubits

The feasibility of using commercial CMOS processes for implementing scalable cryogenic control electronics for universal quantum computers is investigated. Using a systems engineering approach, we break the system down into sub-systems and model the individual components down to transistor level. First results for area demand and power consumption indicate that even with a standard CMOS process, it should be possible to operate hundreds of qubits. Using dedicated low power processes with reduced supply voltage, this number could be further increased in the long term by four or more orders of magnitude, allowing the control of millions of qubits

Bias Voltage DAC Operating at Cryogenic Temperatures for Solid-State Qubit Applications

A scalable eight channel DAC designed in a TSMC 65-nm CMOS technology for generation of solid-state quantum bit (qubit) bias voltages is presented. Measurement results of the DAC and some additional auxiliary components like an on-chip amplifier and sigma-delta modulator at 6 K are discussed. With a low-power consumption of 2.7 μW per channel, the DAC fulfills the requirements to be placed next to qubits inside a mixing chamber of a dilution refrigerator, showing a promising way for scaling qubit numbers toward a quantum computer

Systems Engineering of Cryogenic CMOS Electronics for Scalable Quantum Computers

We report on our systems engineering activities concerning cryogenic CMOS electronics as building blocks for scalable quantum computers. Following the V-model of engineering, the topic is approached both in top-down and in bottom-up fashion. We show the main results from the top-down study using system modeling and simulations. In a bottom-up fashion, a prototype chip was designed and implemented in a commercial 65nm CMOS process. The chip contains a DC digital-to-analog-converter (DC-DAC) and a Pulse-DAC as building blocks for an integrated quantum bit control. The DC-DAC is able to tune a qubit into its operating point. The Pulse-DAC generates pulse patterns with 250MHz sampling frequency to perform gate operations on a qubit

Towards the Development of Cryogenic Integrated Power Management Units

Integrated Circuits (ICs) operating at cryogenic temperatures are expected to allow the development of scalable quantum computing systems consisting of thousands of physical quantum bits (qubits). However, since these ICs require undistorted power supply lines for optimal performance, the development of Power Management Units (PMUs) capable of cryogenic operation is also needed for the quantum computing systems scalability. To develop such PMUs, it is necessary to understand the cryogenic electrical behavior of its components. Therefore, this brief present the measurement results obtained from an exploratory cryogenic DC characterization of some of the passive and active components belonging to a commercial 22nm FDSOI IC technology

Integrated genetic and physical map of the 1q31-->q31.1 region, encompassing the RP12 locus, the F13B and HF1 genes, and the EEF1AL11 and RPL30 pseudogenes

The gene for autosomal recessive retinitis pigmentosa (RP12) with preserved para-arteriolar retinal pigment epithelium was previously mapped close to the F13B gene in region 1q31-->q32.1. A 4-Mb yeast artificial chromosome contig spanning this interval was constructed to facilitate cloning of the RP12 gene. The contig comprises 25 sequence-tagged sites, polymorphic markers, and single-copy probes, including five newly obtained probes. The contig orders the F13B and HF1 genes, as well as five expressed sequence tags, with respect to the integrated genetic map of this region. Homozygosity mapping resulted in refinement of the candidate gene locus for RP12 to a 1. 3-cM region. Currently, approximately 1 Mb of the contig is represented in P1-derived artificial chromosome (PAC) clones. Direct screening of a cDNA library derived from neural retina with PACs resulted in identification of the human elongation factor 1alpha pseudogene (EEF1AL11) and a human ribosomal protein L30 pseudogene (RPL30). A physical and genetic map covering the entire RP12 candidate gene region was constructe

Mild intermittent hypoxia exposure induces metabolic and molecular adaptations in men with obesity

OBJECTIVE: Recent studies suggest that hypoxia exposure may improve glucose homeostasis, but well-controlled human studies are lacking. We hypothesized that mild intermittent hypoxia (MIH) exposure decreases tissue oxygen partial pressure (pO(2)) and induces metabolic improvements in people who are overweight/obese. METHODS: In a randomized, controlled, single-blind crossover study, 12 men who were overweight/obese were exposed to MIH (15 % O(2), 3 × 2 h/day) or normoxia (21 % O(2)) for 7 consecutive days. Adipose tissue (AT) and skeletal muscle (SM) pO(2), fasting/postprandial substrate metabolism, tissue-specific insulin sensitivity, SM oxidative capacity, and AT and SM gene/protein expression were determined. Furthermore, primary human myotubes and adipocytes were exposed to oxygen levels mimicking the hypoxic and normoxic AT and SM microenvironments. RESULTS: MIH decreased systemic oxygen saturation (92.0 ± 0.5 % vs 97.1 ± 0.3, p < 0.001, respectively), AT pO(2) (21.0 ± 2.3 vs 36.5 ± 1.5 mmHg, p < 0.001, respectively), and SM pO(2) (9.5 ± 2.2 vs 15.4 ± 2.4 mmHg, p = 0.002, respectively) compared to normoxia. In addition, MIH increased glycolytic metabolism compared to normoxia, reflected by enhanced fasting and postprandial carbohydrate oxidation (p(AUC) = 0.002) and elevated plasma lactate concentrations (p(AUC) = 0.005). Mechanistically, hypoxia exposure increased insulin-independent glucose uptake compared to standard laboratory conditions (~50 %, p < 0.001) and physiological normoxia (~25 %, p = 0.019) through AMP-activated protein kinase in primary human myotubes but not in primary human adipocytes. MIH upregulated inflammatory/metabolic pathways and downregulated extracellular matrix-related pathways in AT but did not alter systemic inflammatory markers and SM oxidative capacity. MIH exposure did not induce significant alterations in AT (p = 0.120), hepatic (p = 0.132) and SM (p = 0.722) insulin sensitivity. CONCLUSIONS: Our findings demonstrate for the first time that 7-day MIH reduces AT and SM pO(2), evokes a shift toward glycolytic metabolism, and induces adaptations in AT and SM but does not induce alterations in tissue-specific insulin sensitivity in men who are overweight/obese. Future studies are needed to investigate further whether oxygen signaling is a promising target to mitigate metabolic complications in obesity. CLINICAL TRIAL REGISTRATION: This study is registered at the Netherlands Trial Register (NL7120/NTR7325)