653 research outputs found

    Learning many-body Hamiltonians with Heisenberg-limited scaling

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    Learning a many-body Hamiltonian from its dynamics is a fundamental problem in physics. In this work, we propose the first algorithm to achieve the Heisenberg limit for learning an interacting NN-qubit local Hamiltonian. After a total evolution time of O(Ļµāˆ’1)\mathcal{O}(\epsilon^{-1}), the proposed algorithm can efficiently estimate any parameter in the NN-qubit Hamiltonian to Ļµ\epsilon-error with high probability. The proposed algorithm is robust against state preparation and measurement error, does not require eigenstates or thermal states, and only uses polylog(Ļµāˆ’1)\mathrm{polylog}(\epsilon^{-1}) experiments. In contrast, the best previous algorithms, such as recent works using gradient-based optimization or polynomial interpolation, require a total evolution time of O(Ļµāˆ’2)\mathcal{O}(\epsilon^{-2}) and O(Ļµāˆ’2)\mathcal{O}(\epsilon^{-2}) experiments. Our algorithm uses ideas from quantum simulation to decouple the unknown NN-qubit Hamiltonian HH into noninteracting patches, and learns HH using a quantum-enhanced divide-and-conquer approach. We prove a matching lower bound to establish the asymptotic optimality of our algorithm.Comment: 11 pages, 1 figure + 27-page appendi

    Interval Estimation for the Difference in Paired Areas under the ROC Curves in the Absence of a Gold Standard Test

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    Receiver operating characteristic (ROC) curves can be used to assess the accuracy of tests measured on ordinal or continuous scales. The most commonly used measure for the overall diagnostic accuracy of diagnostic tests is the area under the ROC curve (AUC). A gold standard test on the true disease status is required to estimate the AUC. However, a gold standard test may sometimes be too expensive or infeasible. Therefore, in many medical research studies, the true disease status of the subjects may remain unknown. Under the normality assumption on test results from each disease group of subjects, using the expectation-maximization (EM) algorithm in conjunction with a bootstrap method, we propose a maximum likelihood based procedure for construction of confidence intervals for the difference in paired areas under ROC curves in the absence of a gold standard test. Simulation results show that the proposed interval estimation procedure yields satisfactory coverage probabilities and interval lengths. The proposed method is illustrated with two examples

    The Differential Role of Human Cationic Trypsinogen (PRSS1) p.R122H Mutation in Hereditary and Nonhereditary Chronic Pancreatitis: A Systematic Review and Meta-Analysis.

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    Background:Environmental factors and genetic mutations have been increasingly recognized as risk factors for chronic pancreatitis (CP). The PRSS1 p.R122H mutation was the first discovered to affect hereditary CP, with 80% penetrance. We performed here a systematic review and meta-analysis to evaluate the associations of PRSS1 p.R122H mutation with CP of diverse etiology. Methods:The PubMed, EMBASE, and MEDLINE database were reviewed. The pooled odds ratio (OR) with 95% confidence intervals was used to evaluate the association of p.R122H mutation with CP. Initial analysis was conducted with all etiologies of CP, followed by a subgroup analysis for hereditary and nonhereditary CP, including alcoholic or idiopathic CP. Results:A total of eight case-control studies (1733 cases and 2415 controls) were identified and included. Overall, PRSS1 p.R122H mutation was significantly associated with an increased risk of CP (ORā€‰=ā€‰4.78[1.13-20.20]). Further analysis showed p.R122H mutation strongly associated with the increased risk of hereditary CP (ORā€‰=ā€‰65.52[9.09-472.48]) but not with nonhereditary CP, both alcoholic and idiopathic CP. Conclusions:Our study showing the differential role of p.R122H mutation in various etiologies of CP indicates that this complex disorder is likely influenced by multiple genetic factors as well as environmental factors

    Ganoderma Lucidum Stimulates Autophagy-Dependent Longevity Pathways in Caenorhabditis Elegans and Human Cells

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    The medicinal fungus Ganoderma lucidum is used as a dietary supplement and health tonic, but whether it affects longevity remains unclear. We show here that a water extract of G. lucidum mycelium extends lifespan of the nematode Caenorhabditis elegans. The G. lucidum extract reduces the level of fibrillarin (FIB-1), a nucleolar protein that correlates inversely with longevity in various organisms. Furthermore, G. lucidum treatment increases expression of the autophagosomal protein marker LGG-1, and lifespan extension is abrogated in mutant C. elegans strains that lack atg-18, daf-16, or sir-2.1, indicating that autophagy and stress resistance pathways are required to extend lifespan. In cultured human cells, G. lucidum increases concentrations of the LGG-1 ortholog LC3 and reduces levels of phosphorylated mTOR, a known inhibitor of autophagy. Notably, low molecular weight compounds (\u3c10 kDa) isolated from the G. lucidum water extract prolong lifespan of C. elegans and the same compounds induce autophagy in human cells. These results suggest that G. lucidum can increase longevity by inducing autophagy and stress resistance

    Ethanol Induced Disordering of Pancreatic Acinar Cell Endoplasmic Reticulum: An ER Stress/Defective Unfolded Protein Response Model.

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    Background & aimsHeavy alcohol drinking is associated with pancreatitis, whereas moderate intake lowers the risk.Ā Mice fed ethanol long term show no pancreas damage unlessĀ adaptive/protective responses mediating proteostasis are disrupted. Pancreatic acini synthesize digestive enzymes (largely serine hydrolases) in the endoplasmic reticulum (ER), where perturbations (eg, alcohol consumption) activate adaptive unfolded protein responses orchestrated by spliced X-box binding protein 1 (XBP1). Here, we examined ethanol-induced early structural changes in pancreatic ERĀ proteins.MethodsWild-type and Xbp1+/- mice were fed control andĀ ethanol diets, then tissues were homogenized and fractionated. ER proteins were labeled with a cysteine-reactive probe, isotope-coded affinity tag to obtain a novel pancreatic redox ER proteome. Specific labeling of active serine hydrolases in ER with fluorophosphonate desthiobiotin also was characterized proteomically. Protein structural perturbation by redox changes was evaluated further in molecular dynamic simulations.ResultsEthanol feeding and Xbp1 genetic inhibition altered ER redox balance and destabilized key proteins. Proteomic data and molecular dynamic simulations of Carboxyl ester lipase (Cel), a unique serine hydrolase active within ER, showed an uncoupled disulfide bond involving Cel Cys266, Cel dimerization, ER retention, and complex formation in ethanol-fed, XBP1-deficient mice.ConclusionsResults documented in ethanol-fed mice lacking sufficient spliced XBP1 illustrate consequences of ER stress extended by preventing unfolded protein response from fully restoring pancreatic acinar cell proteostasis during ethanol-induced redox challenge. In this model, orderly protein folding and transport to the secretory pathway were disrupted, and abundant molecules including Cel with perturbed structures were retained in ER, promoting ER stress-relatedĀ pancreas pathology

    Increasing Ceftriaxone Resistance in Salmonellae, Taiwan

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    In Taiwan, despite a substantial decline of Salmonella enterica serotype Choleraesuis infections, strains resistant to ciprofloxacin and ceftriaxone persist. A self-transferable blaCMY-2-harboring IncI1 plasmid was identified in S. enterica serotypes Choleraesuis, Typhimurium, Agona, and Enteritidis and contributed to the overall increase of ceftriaxone resistance in salmonellae

    Ultraquantum magnetoresistance in Kramers Weyl semimetal candidate Ī²\beta-Ag2Se

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    The topological semimetal Ī²\beta-Ag2Se features a Kramers Weyl node at the origin in momentum space and a quadruplet of spinless Weyl nodes, which are annihilated by spin-orbit coupling. We show that single crystalline Ī²\beta-Ag2Se manifests giant Shubnikov-de Haas oscillations in the longitudinal magnetoresistance which stem from a small electron pocket that can be driven beyond the quantum limit by a field less than 9 T. This small electron pocket is a remainder of the spin-orbit annihilatedWeyl nodes and thus encloses a Berry-phase structure. Moreover, we observed a negative longitudinal magnetoresistance when the magnetic field is beyond the quantum limit. Our experimental findings are complemented by thorough theoretical band structure analyses of this Kramers Weyl semimetal candidate, including first-principle calculations and an effective k*p model.Comment: A new version based on arXiv:1502.0232
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