652 research outputs found

    A simple all-microwave entangling gate for fixed-frequency superconducting qubits

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    We demonstrate an all-microwave two-qubit gate on superconducting qubits which are fixed in frequency at optimal bias points. The gate requires no additional subcircuitry and is tunable via the amplitude of microwave irradiation on one qubit at the transition frequency of the other. We use the gate to generate entangled states with a maximal extracted concurrence of 0.88 and quantum process tomography reveals a gate fidelity of 81%

    Efficient measurement of quantum gate error by interleaved randomized benchmarking

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    We describe a scalable experimental protocol for obtaining estimates of the error rate of individual quantum computational gates. This protocol, in which random Clifford gates are interleaved between a gate of interest, provides a bounded estimate of the average error of the gate under test so long as the average variation of the noise affecting the full set of Clifford gates is small. This technique takes into account both state preparation and measurement errors and is scalable in the number of qubits. We apply this protocol to a superconducting qubit system and find gate errors that compare favorably with the gate errors extracted via quantum process tomography.Comment: 5 pages, 2 figures, published versio

    Lower extremity fatigue increases complexity of postural control during a single-legged stance

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    <p>Abstract</p> <p>Background</p> <p>Non-linear approaches to assessment of postural control can provide insight that compliment linear approaches. Control entropy (CE) is a recently developed statistical tool from non-linear dynamical systems used to assess the complexity of non-stationary signals. We have previously used CE of high resolution accelerometry in running to show decreased complexity with exhaustive exercise. The purpose of this study was to determine if complexity of postural control decreases following fatiguing exercise using CE.</p> <p>Methods</p> <p>Ten subjects (5 M/5 F; 25 ± 3 yr; 169.4 ± 11.7 cm; 79.0 ± 16.9 kg) consented to participation approved by Western Oregon University IRB and completed two trials separated by 2-7 days. Trials consisted of two single-legged balance tests separated by two Wingate anaerobic tests (WAnT; PreFat/PostFat), or rest period (PreRest/PostRest). Balance tests consisted of a series of five single-legged stances, separated by 30 s rest, performed while standing on the dominant leg for 15-s with the participant crossing the arms over the chest and flexing the non-dominant knee to 90 degrees. High resolution accelerometers (HRA) were fixed superficial to L3/L4 at the approximate center of mass (COM). Triaxial signals from the HRA were streamed in real time at 625 Hz. COM accelerations were recorded in g's for vertical (VT), medial/lateral (ML), and anterior/posterior (AP) axes. A newly developed statistic (R-test) was applied to group response shapes generated by Karhunen Loeve (KL) transform modes resulting from Control Entropy (CE) analysis.</p> <p>Results</p> <p>R-tests showed a significant mean vector difference (<it>p </it>< .05) within conditions, between axes in all cases, except PostFat, indicating the shape of the complexity response was different in these cases. R-test between conditions, within axis, differences were only present in PostFat for AP vs. PreFat (<it>p </it>< .05). T-tests showed a significantly higher overall CE PostFat in VT and ML compared to PreFat and PostRest (<it>p </it>< .0001). PostFat CE was also higher than PostRest in AP (<it>p </it>< .0001).</p> <p>Conclusions</p> <p>These data indicate that fatiguing exercise eliminates the differential complexity response between axes, but increases complexity in all axes compared to the non-fatigued condition. This has implications with regard to the effects of fatigue on strategies of the control system to maintain postural control.</p

    Цитокіновий профіль у вагітних з хламідійно-вірусною інфекцією

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    Урогенитальный хламидиоз и вирусная инфекция – это актуальная медико-социальная проблема, поэтому углубленные исследования клинических, иммунологических и эндокринологических аспектов этой проблемы у беременных, разработка и внедрение лечебно-профилактических программ является одним из перспективных резервов снижения репродуктивных потерь, материнской и перинатальной заболеваемости. Вместе с этим, такие исследования составляют значительный научный интерес и большую практическую ценность. При изучении механизмов осложнений беременности большой интерес вызывают исследования функционального состояния клеток ММС (путем определения уровня провоспалительных цитокинов ИЛ - 1β, ФНО -α), а также Т-лимфоцитов (путем определения провоспалительных цитокинов ИЛ -2, ИФН-γ и провоспалительных цитокинов ИЛ -4, ИЛ -10).Urogenital chlamydia and viral infection are actual medical and social problems. That is why the most promising reserves to reduce reproductive losses, maternal and perinatal morbidity are deep study of clinical, immunological, microbiological and endocrinological aspects of this problem among pregnant women, as well as developing and implementing of health care programs. Moreover, such studies have significant scientific interest and great practical value. While studying the mechanisms of pregnancy complications, the most interesting are the study of the functional state of MMS cells (by determining the level of proinflammatory cytokines IL-1β TNF-α), and T-lymphocytes (by determining the level of proinflammatory cytokines IL-2, IFN-γ and anti-inflammatory cytokines IL-4, IL-10)

    Standing Variation and the Capacity for Change: Are Endocrine Phenotypes More Variable That Other Traits?

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    Circulating steroid hormone levels exhibit high variation both within and between individuals, leading some to hypothesize that these phenotypes are more variable than other morphological, physiological, and behavioral traits. This should have profound implications for the evolution of steroid signaling systems, but few studies have examined how endocrine variation compares to that of other traits or differs among populations. Here we provide such an analysis by first exploring how variation in three measures of corticosterone (CORT)—baseline, stress-induced, and post-dexamethasone injection—compares to variation in key traits characterizing morphology (wing length, mass), physiology (reactive oxygen metabolite concentration [d-ROMs] and antioxidant capacity), and behavior (provisioning rate) in two populations of tree swallow (Tachycineta bicolor). After controlling for measurement precision and within-individual variation, we found that only post-dex CORT was more variable than all other traits. Both baseline and stress-induced CORT exhibit higher variation than antioxidant capacity and provisioning rate, but not oxidative metabolite levels or wing length. Variation in post-dex CORT and d-ROMs was also elevated in the higher-latitude population in that inhabits a less predictable environment. We next studied how these patterns might play out on a macroevolutionary scale, assessing patterns of variation in baseline testosterone (T) and multiple non-endocrine traits (body length, mass, social display rate, and locomotion rate) across 17 species of Anolis lizards. At the macroevolutionary level, we found that circulating T levels and the rate of social display output are higher than other behavioral and morphological traits. Altogether, our results support the idea that within-population variability in steroid levels is substantial, but not exceptionally higher than many other traits that define animal phenotypes. As such, circulating steroid levels in free-living animals should be considered traits that exhibit similar levels of variability from individual to individual in a population

    Use of Risk Models to Predict Death in the Next Year Among Individual Ambulatory Patients With Heart Failure

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    Importance: The clinical practice guidelines for heart failure recommend the use of validated risk models to estimate prognosis. Understanding how well models identify individuals who will die in the next year informs decision making for advanced treatments and hospice. Objective: To quantify how risk models calculated in routine practice estimate more than 50% 1-year mortality among ambulatory patients with heart failure who die in the subsequent year. Design, Setting, and Participants: Ambulatory adults with heart failure from 3 integrated health systems were enrolled between 2005 and 2008. The probability of death was estimated using the Seattle Heart Failure Model (SHFM) and the Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) risk calculator. Baseline covariates were collected from electronic health records. Missing covariates were imputed. Estimated mortality was compared with actual mortality at both population and individual levels. Main Outcomes and Measures: One-year mortality. Results: Among 10930 patients with heart failure, the median age was 77 years, and 48.0% of these patients were female. In the year after study enrollment, 1661 patients died (15.9% by life-table analysis). At the population level, 1-year predicted mortality among the cohort was 9.7% for the SHFM (C statistic of 0.66) and 17.5% for the MAGGIC risk calculator (C statistic of 0.69). At the individual level, the SHFM predicted a more than 50% probability of dying in the next year for 8 of the 1661 patients who died (sensitivity for 1-year death was 0.5%) and for 5 patients who lived at least a year (positive predictive value, 61.5%). The MAGGIC risk calculator predicted a more than 50% probability of dying in the next year for 52 of the 1661 patients who died (sensitivity, 3.1%) and for 63 patients who lived at least a year (positive predictive value, 45.2%). Conversely, the SHFM estimated that 8496 patients (77.8%) had a less than 15% probability of dying at 1 year, yet this lower-risk end of the score range captured nearly two-thirds of deaths (n = 997); similarly, the MAGGIC risk calculator estimated a probability of dying of less than 25% for the majority of patients who died at 1 year (n = 914). Conclusions and Relevance: Although heart failure risk models perform reasonably well at the population level, they do not reliably predict which individual patients will die in the next year

    Gene expression signature of atypical breast hyperplasia and regulation by SFRP1

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    BACKGROUND: Atypical breast hyperplasias (AH) have a 10-year risk of progression to invasive cancer estimated at 4-7%, with the overall risk of developing breast cancer increased by ~ 4-fold. AH lesions are estrogen receptor alpha positive (ERalpha+) and represent risk indicators and/or precursor lesions to low grade ERalpha+ tumors. Therefore, molecular profiles of AH lesions offer insights into the earliest changes in the breast epithelium, rendering it susceptible to oncogenic transformation. METHODS: In this study, women were selected who were diagnosed with ductal or lobular AH, but no breast cancer prior to or within the 2-year follow-up. Paired AH and histologically normal benign (HNB) tissues from patients were microdissected. RNA was isolated, amplified linearly, labeled, and hybridized to whole transcriptome microarrays to determine gene expression profiles. Genes that were differentially expressed between AH and HNB were identified using a paired analysis. Gene expression signatures distinguishing AH and HNB were defined using AGNES and PAM methods. Regulation of gene networks was investigated using breast epithelial cell lines, explant cultures of normal breast tissue and mouse tissues. RESULTS: A 99-gene signature discriminated the histologically normal and AH tissues in 81% of the cases. Network analysis identified coordinated alterations in signaling through ERalpha, epidermal growth factor receptors, and androgen receptor which were associated with the development of both lobular and ductal AH. Decreased expression of SFRP1 was also consistently lower in AH. Knockdown of SFRP1 in 76N-Tert cells resulted altered expression of 13 genes similarly to that observed in AH. An SFRP1-regulated network was also observed in tissues from mice lacking Sfrp1. Re-expression of SFRP1 in MCF7 cells provided further support for the SFRP1-regulated network. Treatment of breast explant cultures with rSFRP1 dampened estrogen-induced progesterone receptor levels. CONCLUSIONS: The alterations in gene expression were observed in both ductal and lobular AH suggesting shared underlying mechanisms predisposing to AH. Loss of SFRP1 expression is a significant regulator of AH transcriptional profiles driving previously unidentified changes affecting responses to estrogen and possibly other pathways. The gene signature and pathways provide insights into alterations contributing to AH breast lesions
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