Unfolding Quantum Computer Readout Noise

In the current era of noisy intermediate-scale quantum (NISQ) computers, noisy qubits can result in biased results for early quantum algorithm applications. This is a significant challenge for interpreting results from quantum computer simulations for quantum chemistry, nuclear physics, high energy physics, and other emerging scientific applications. An important class of qubit errors are readout errors. The most basic method to correct readout errors is matrix inversion, using a response matrix built from simple operations to probe the rate of transitions from known initial quantum states to readout outcomes. One challenge with inverting matrices with large off-diagonal components is that the results are sensitive to statistical fluctuations. This challenge is familiar to high energy physics, where prior-independent regularized matrix inversion techniques (`unfolding') have been developed for years to correct for acceptance and detector effects when performing differential cross section measurements. We study various unfolding methods in the context of universal gate-based quantum computers with the goal of connecting the fields of quantum information science and high energy physics and providing a reference for future work. The method known as iterative Bayesian unfolding is shown to avoid pathologies from commonly used matrix inversion and least squares methods.Comment: 13 pages, 16 figures; v2 has a typo fixed in Eq. 3 and a series of minor modification

Expression of Ifnlr1 on intestinal epithelial cells is critical to the antiviral effects of IFN-lambda against norovirus and reovirus

Lambda interferon (IFN-λ) has potent antiviral effects against multiple enteric viral pathogens, including norovirus and rotavirus, in both preventing and curing infection. Because the intestine includes a diverse array of cell types, however, the cell(s) upon which IFN-λ acts to exert its antiviral effects is unclear. Here, we sought to identify IFN-λ-responsive cells by generation of mice with lineage-specific deletion of the receptor for IFN-λ, Ifnlr1. We found that expression of IFNLR1 on intestinal epithelial cells (IECs) in the small intestine and colon is required for enteric IFN-λ antiviral activity. IEC Ifnlr1 expression also determines the efficacy of IFN-λ in resolving persistent murine norovirus (MNoV) infection and regulates fecal shedding and viral titers in tissue. Thus, the expression of Ifnlr1 by IECs is necessary for the response to both endogenous and exogenous IFN-λ. We further demonstrate that IEC Ifnlr1 expression is required for the sterilizing innate immune effects of IFN-λ by extending these findings in Rag1-deficient mice. Finally, we assessed whether our findings pertained to multiple viral pathogens by infecting mice specifically lacking IEC Ifnlr1 expression with reovirus. These mice phenocopied Ifnlr1-null animals, exhibiting increased intestinal tissue titers and enhanced reovirus fecal shedding. Thus, IECs are the critical cell type responding to IFN-λ to control multiple enteric viruses. This is the first genetic evidence that supports an essential role for IECs in IFN-λ-mediated control of enteric viral infection, and these findings provide insight into the mechanism of IFN-λ-mediated antiviral activity. IMPORTANCE Human noroviruses (HNoVs) are the leading cause of epidemic gastroenteritis worldwide. Type III interferons (IFN-λ) control enteric viral infections in the gut and have been shown to cure mouse norovirus, a small-animal model for HNoVs. Using a genetic approach with conditional knockout mice, we identified IECs as the dominant IFN-λ-responsive cells in control of enteric virus infection in vivo. Upon murine norovirus or reovirus infection, Ifnlr1 depletion in IECs largely recapitulated the phenotype seen in Ifnlr1(−/−) mice of higher intestinal tissue viral titers and increased viral shedding in the stool. Moreover, IFN-λ-mediated sterilizing immunity against murine norovirus requires the capacity of IECs to respond to IFN-λ. These findings clarify the mechanism of action of this cytokine and emphasize the therapeutic potential of IFN-λ for treating mucosal viral infections

Geophysics

Contains reports on three research projects

Quantity Evaluation of the Release of Heavy Metal Ions; Voltamperometric Study

In recent years there has been an decrease in the use of non-precious casting alloys in dentistry. These materials offer many physical, chemical and financial advantages. In order to achieve the necessary mechanical and physical properties, the alloys often contain metals which are known to be biologically active. We have continued and expanded our research into the release of these heavy metal ions by concentrating on the processes that occur when two different alloys are together in the same environment. The aim of this study was to evaluate and compare the influence of one, two or three different non-precious alloys on the degree of release of the selected ions, which are their components. An analysis of the alloys Remanium G-Weich, Remanium CS and Remanium GM 380 was made both individually or in combinations of two samples, which were prepared from these alloys. One of the metal samples was prepared in the laboratory in the shape of a cylinder from Cr-Ni, Cr-Co, Ag-Pd. The size of the samples, their shape, length and weight were matched. These elements were placed in an incubator of a definite time of permeability and 25 ml of the artificial saliva at a temperature of 37° C was poured. They were then transferred to an incubator at the same temperature and left for 1, 2 ,4, 6, 7 and 30 days, after which the released ions Cr, Co, Ni were evaluated by means of inversion voltamperometry.The amount of nickel released into the artificial saliva from chrom-nickel alloys in combination with silver-palladium alloy was increased. The release of chromium and cobalt was detected and depended on the proportion of these ions in the alloy compositions. Exact results are given in tables and diagrams

Amino acid substitution equivalent to human chorea-acanthocytosis I2771R in yeast Vps13 protein affects its binding to phosphatidylinositol 3-phosphate

The rare human disorder chorea-acanthocytosis (ChAc) is caused by mutations in hVPS13A gene. The hVps13A protein interacts with actin and regulates the level of phosphatidylinositol 4-phosphate (PI4P) in the membranes of neuronal cells. Yeast Vps13 is involved in vacuolar protein transport and, like hVps13A, participates in PI4P metabolism. Vps13 proteins are conserved in eukaryotes, but their molecular function remains unknown. One of the mutations found in ChAc patients causes amino acids substitution I2771R which affects the localization of hVps13A in skeletal muscles. To dissect the mechanism of pathogenesis of I2771R, we created and analyzed a yeast strain carrying the equivalent mutation. Here we show that in yeast, substitution I2749R causes dysfunction of Vps13 protein in endocytosis and vacuolar transport, although the level of the protein is not affected, suggesting loss of function. We also show that Vps13, like hVps13A, influences actin cytoskeleton organization and binds actin in immunoprecipitation experiments. Vps13-I2749R binds actin, but does not function in the actin cytoskeleton organization. Moreover, we show that Vps13 binds phospholipids, especially phosphatidylinositol 3-phosphate (PI3P), via its SHR_BD and APT1 domains. Substitution I2749R attenuates this ability. Finally, the localization of Vps13-GFP is altered when cellular levels of PI3P are decreased indicating its trafficking within the endosomal membrane system. These results suggest that PI3P regulates the functioning of Vps13, both in protein trafficking and actin cytoskeleton organization. Attenuation of PI3P-binding ability in the mutant hVps13A protein may be one of the reasons for its mislocalization and disrupted function in cells of patients suffering from ChAc

Stride variability measures derived from wrist- and hip-worn accelerometers

Many epidemiological and clinical studies use accelerometry to objectively measure physical activity using the activity counts, vector magnitude, or number of steps. These measures use just a fraction of the information in the raw accelerometry data as they are typically summarized at the minute level. To address this problem we define and estimate two gait measures of temporal stride-to-stride variability based on raw accelerometry data: Amplitude Deviation (AD) and Phase Deviation (PD). We explore the sensitivity of our approach to on-body placement of the accelerometer by comparing hip, left and right wrist placements. We illustrate the approach by estimating AD and PD in 46 elderly participants in the Developmental Epidemiologic Cohort Study (DECOS) who worn accelerometers during a 400 meter walk test. We also show that AD and PD have a statistically significant association with the gait speed and sit-to-stand test performanc

Geophysics

Contains research objectives and reports on three research projects

Ocena właściwości mechanicznych tętnic ludzkich poddanych procesowi wyjałowienia oraz kontrolowanego zamrażania przy wykorzystaniu krioprotektora

Background: Assessment of the mechanical properties of human arteries after cryopreservation processing protocol including antibiotic sterilisation and controlled freezing with the use of cryoprotector (10% DMSO). Material and methods: 12 aortic and 9 femoral artery segments were investigated; the donor age ranged from 18 to 42 years, the time of the storage in the liquid nitrogen vapours was from 1 to 36 months. The stretching tests of vessel specimens (using INSTRON tensile testing machine) and manometric investigations were performed. The mechanical resistance (breaking stress) and elastic moduli were evaluated (at maximal stress value and at the stress of 300 kPa). The results were compared with fresh homograft specimens. Results: The mechanical resistance (breaking stress) of the investigated cryopreserved aortic segments ranged from 1.5 MPa (± 0.34) (if stretched perpendicular to the vessel long axis) to 1.05 MPa (± 0.3) (if stretching was performed in parallel). For the femoral artery specimens the respective values were 2.4 MPa (± 0.93) and 1.35 MPa (± 0.5). Elastic moduli at the stress of 300 kPa in aortic specimens achieved 1.38 (± 0.4) and 1.8 (± 0.85). For the attained femoral arteries respective values were 2.83 (± 1.34) and 1.47 (± 0.9). There were no significant differences concerning mechanical properties between fresh and cryopreserved aortic wall segments. Conclusions: 1. Cryopreserved allogenic arteries (aorta, femoral arteries) maintain high mechanical resistance against breaking stress and intra-arterial pressure. 2. Despite vessel preparation (including sterilisation and control freezing protocols), cryopreserved arteries maintain elastic properties, justifying an implementation of this material in human circulatory system. 3. The use of arterial segments with low number of collaterals and their correct suture or ligation can influence the allograft mechanical stress resistance

Phosphatidylinositol-3-phosphate regulates response of cells to proteotoxic stress

Human Nedd4 ubiquitin ligase, or its variants, inhibit yeast cell growth by disturbing the actin cytoskeleton organization and dynamics, and lead to an increase in levels of ubiquitinated proteins. In a screen for multicopy suppressors which rescue growth of yeast cells producing Nedd4 ligase with an inactive WW4 domain (Nedd4w4), we identified a fragment of ATG2 gene encoding part of the Atg2 core autophagy protein. Expression of the Atg2-C1 fragment (aa 1074-1447) improved growth, actin cytoskeleton organization, but did not significantly change the levels of ubiquitinated proteins in these cells. The GFP-Atg2-C1 protein in Nedd4w4-producing cells primarily localized to a single defined structure adjacent to the vacuole, surrounded by an actin filament ring, containing Hsp42 and Hsp104 chaperones. This localization was not affected in several atg deletion mutants, suggesting that it might be distinct from the phagophore assembly site (PAS). However, deletion of ATG18 encoding a phosphatidylinositol-3-phosphate (PI3P)-binding protein affected the morphology of the GFP-Atg2-C1 structure while deletion of ATG14 encoding a subunit of PI3 kinase suppressed toxicity of Nedd4w4 independently of GFP-Atg2-C1. Further analysis of the Atg2-C1 revealed that it contains an APT1 domain of previously uncharacterized function. Most importantly, we showed that this domain is able to bind phosphatidylinositol phosphates, especially PI3P, which is abundant in the PAS and endosomes. Together our results suggest that human Nedd4 ubiquitinates proteins in yeast and causes proteotoxic stress and, with some Atg proteins, leads to formation of a perivacuolar structure, which may be involved in sequestration, aggregation or degradation of proteins