Error-rate-agnostic decoding of topological stabilizer codes

Efficient high-performance decoding of topological stabilizer codes has the potential to crucially improve the balance between logical failure rates and the number and individual error rates of the constituent qubits. High-threshold maximum-likelihood decoders require an explicit error model for Pauli errors to decode a specific syndrome, whereas lower-threshold heuristic approaches such as minimum weight matching are "error agnostic". Here we consider an intermediate approach, formulating a decoder that depends on the bias, i.e., the relative probability of phase-flip to bit-flip errors, but is agnostic to error rate. Our decoder is based on counting the number and effective weight of the most likely error chains in each equivalence class of a given syndrome. We use Metropolis-based Monte Carlo sampling to explore the space of error chains and find unique chains, that are efficiently identified using a hash table. Using the error-rate invariance the decoder can sample chains effectively at an error rate which is higher than the physical error rate and without the need for "thermalization" between chains in different equivalence classes. Applied to the surface code and the XZZX code, the decoder matches maximum-likelihood decoders for moderate code sizes or low error rates. We anticipate that, because of the compressed information content per syndrome, it can be taken full advantage of in combination with machine-learning methods to extrapolate Monte Carlo-generated data.Comment: 15 pages, 9 figures; V2 Added analysis of low error-rate performanc

Capacitive crosstalk in gate-based dispersive sensing of spin qubits

In gate-based dispersive sensing, the response of a resonator attached to a quantum dot gate is detected by a reflected radio-frequency signal. This enables fast readout of spin qubits and tune up of arrays of quantum dots, but comes at the expense of increased susceptibility to crosstalk, as the resonator can amplify spurious signals and induce fluctuations in the quantum dot potential. We attach tank circuits with superconducting NbN inductors and internal quality factors $Q_{\mathrm{i}}$>1000 to the interdot barrier gate of silicon double quantum dot devices. Measuring the interdot transition in transport, we quantify radio-frequency crosstalk that results in a ring-up of the resonator when neighbouring plunger gates are driven with frequency components matching the resonator frequency. This effect complicates qubit operation and scales with the loaded quality factor of the resonator, the mutual capacitance between device gate electrodes, and with the inverse of the parasitic capacitance to ground. Setting qubit frequencies below the resonator frequency is expected to substantially suppress this type of crosstalk.Comment: 7 pages, 4 figures, supplementary informatio

Multibound solitons generation with a controllable number of bound states in a passive mode-locked all-fiber erbium-doped ring laser

We have studied generation of stable and low-noise de-chirped ultrashort solitons in bound states and we have experimentally demonstrated the formation multi-bound solitons with the controllable number of bound states 7 < N < 17 by pump power variation. A numerical simulation of the influence of various types of fluctuations on the generation mode was also carried out

Role of Phagocytosis in the Pro-Inflammatory Response in LDL-Induced Foam Cell Formation; a Transcriptome Analysis

Excessive accumulation of lipid inclusions in the arterial wall cells (foam cell formation) caused by modified low-density lipoprotein (LDL) is the earliest and most noticeable manifestation of atherosclerosis. The mechanisms of foam cell formation are not fully understood and can involve altered lipid uptake, impaired lipid metabolism, or both. Recently, we have identified the top 10 master regulators that were involved in the accumulation of cholesterol in cultured macrophages induced by the incubation with modified LDL. It was found that most of the identified master regulators were related to the regulation of the inflammatory immune response, but not to lipid metabolism. A possible explanation for this unexpected result is a stimulation of the phagocytic activity of macrophages by modified LDL particle associates that have a relatively large size. In the current study, we investigated gene regulation in macrophages using transcriptome analysis to test the hypothesis that the primary event occurring upon the interaction of modified LDL and macrophages is the stimulation of phagocytosis, which subsequently triggers the pro-inflammatory immune response. We identified genes that were up- or downregulated following the exposure of cultured cells to modified LDL or latex beads (inert phagocytosis stimulators). Most of the identified master regulators were involved in the innate immune response, and some of them were encoding major pro-inflammatory proteins. The obtained results indicated that pro-inflammatory response to phagocytosis stimulation precedes the accumulation of intracellular lipids and possibly contributes to the formation of foam cells. In this way, the currently recognized hypothesis that the accumulation of lipids triggers the pro-inflammatory response was not confirmed. Comparative analysis of master regulators revealed similarities in the genetic regulation of the interaction of macrophages with naturally occurring LDL and desialylated LDL. Oxidized and desialylated LDL affected a different spectrum of genes than naturally occurring LDL. These observations suggest that desialylation is the most important modification of LDL occurring in vivo. Thus, modified LDL caused the gene regulation characteristic of the stimulation of phagocytosis. Additionally, the knock-down effect of five master regulators, such as IL15, EIF2AK3, F2RL1, TSPYL2, and ANXA1, on intracellular lipid accumulation was tested. We knocked down these genes in primary macrophages derived from human monocytes. The addition of atherogenic naturally occurring LDL caused a significant accumulation of cholesterol in the control cells. The knock-down of the EIF2AK3 and IL15 genes completely prevented cholesterol accumulation in cultured macrophages. The knock-down of the ANXA1 gene caused a further decrease in cholesterol content in cultured macrophages. At the same time, knock-down of F2RL1 and TSPYL2 did not cause an effect. The results obtained allowed us to explain in which way the inflammatory response and the accumulation of cholesterol are related confirming our hypothesis of atherogenesis development based on the following viewpoints: LDL particles undergo atherogenic modifications that, in turn, accompanied by the formation of self-associates; large LDL associates stimulate phagocytosis; as a result of phagocytosis stimulation, pro-inflammatory molecules are secreted; these molecules cause or at least contribute to the accumulation of intracellular cholesterol. Therefore, it became obvious that the primary event in this sequence is not the accumulation of cholesterol but an inflammatory response

Macrophages in Health and Non-Infectious Disease

In this Special Issue of Biomedicines, we have many insightful reviews and research papers on the subject “Macrophages in Health and Non-infectious Disease”, but first; we should discuss briefly the current situation in the field [...

Macrophages in Health and Non-Infectious Disease 2.0

This Special Issue (SI) has collected the most recent publications on the mechanisms that macrophages use to regulate homeostasis and their involvement in the pathogenesis of various non-infectious diseases [...

Macrophages in Immunopathology of Atherosclerosis: A Target for Diagnostics and Therapy

Immunopathology plays important roles in the development of different life-threatening diseases, such as atherosclerosis and its consequences (acute myocardial infarction and stroke), cancer, chronic inflammatory diseases. Effective modulation of the immune system may significantly increase the efficacy of prevention and therapy efforts. Currently there are no marketed drugs capable of normalizing immune system function in an intrinsic and comprehensive way. Here, we describe a test system designed for complex analysis of monocyte activity in individuals to diagnose immunopathology and monitor treatment efficacy. This cell-based test system may also be useful for screening compounds with an immune-correcting effects. Both diagnostic and screening systems are based on primary culture of human monocytes and/or monocyte-derived macrophages. This is the first step in creating a method for assessment of macrophage activity, which is required for further development of immune-correcting drugs. The existing preliminary data provide the basis for realization of this idea

Macrophages in immunopathology of atherosclerosis a target for diagnostics and therapy

Immunopathology plays important roles in the development of different life-threatening diseases, such as atherosclerosis and its consequences (acute myocardial infarction and stroke), cancer, chronic inflammatory diseases. Effective modulation of the immune system may significantly increase the efficacy of prevention and therapy efforts. Currently there are no marketed drugs capable of normalizing immune system function in an intrinsic and comprehensive way. Here, we describe a test system designed for complex analysis of monocyte activity in individuals to diagnose immunopathology and monitor treatment efficacy. This cell-based test system may also be useful for screening compounds with an immune-correcting effects. Both diagnostic and screening systems are based on primary culture of human monocytes and/or monocyte-derived macrophages. This is the first step in creating a method for assessment of macrophage activity, which is required for further development of immune-correcting drugs. The existing preliminary data provide the basis for realization of this idea