2,306 research outputs found
Simulating Majorana zero modes on a noisy quantum processor
The simulation of systems of interacting fermions is one of the most
anticipated applications of quantum computers. The most interesting simulations
will require a fault-tolerant quantum computer, and building such a device
remains a long-term goal. However, the capabilities of existing noisy quantum
processors have steadily improved, sparking an interest in running simulations
that, while not necessarily classically intractable, may serve as device
benchmarks and help elucidate the challenges to achieving practical
applications on near-term devices. Systems of non-interacting fermions are
ideally suited to serve these purposes. While they display rich physics and
generate highly entangled states when simulated on a quantum processor, their
classical tractability enables experimental results to be verified even at
large system sizes that would typically defy classical simulation. In this
work, we use a noisy superconducting quantum processor to prepare Majorana zero
modes as eigenstates of the Kitaev chain Hamiltonian, a model of
non-interacting fermions. Our work builds on previous experiments with
non-interacting fermionic systems. Previous work demonstrated error mitigation
techniques applicable to the special case of Slater determinants. Here, we show
how to extend these techniques to the case of general fermionic Gaussian
states, and demonstrate them by preparing Majorana zero modes on systems of up
to 7 qubits.Comment: 12 pages, 6 figure
Dual disassembly and biological evaluation of enzyme/oxidation-responsive polyester-based nanoparticulates for tumor-targeting delivery
Polyester-based nanoparticulates (NPs) are ideal nanocarriers for intracellular delivery of anticancer drugs because of their biocompatibility. However, an on-going challenge is the controlled and enhanced release of encapsulated therapeutics in response to unique changes that occur within cancer cells. Herein, we report the versatility of dual responses to enzymatic and oxidative reactions found in cancer cells toward the development of polyester-NPs as effective tumor-targeting intracellular nanocarriers. A facile nanoprecipitation method allows for the preparation of hydrophobic cores composed of novel polyester designed with esterase-responsive ester groups and oxidation-responsive sulfide linkages on their backbones, physically stabilized with poly(ethylene glycol)-based polymeric shells. The formed core/shell-type NPs with a diameter of 120 nm exhibit excellent colloidal stability in physiological conditions and in the presence of serum proteins. When exposed to esterase and hydrogen peroxide, NP integrity is disrupted, leading to the enhanced release of encapsulated doxorubicin, confirmed by dynamic light scattering and spectroscopic analysis. Combined results from epifluorescence microscopy, confocal laser scanning microscopy, flow cytometry, and cell viability demonstrate that doxorubicin-loaded NPs reveal rapid penetration and enhanced intracellular release of doxorubicin, thus inhibiting tumor progression. Importantly, the cellular uptake of doxorubicin-loaded core/shell NPs primarily via caveolae-dependent mechanism promotes their use in targeting a broad spectrum of cancers
Basal reactive oxygen species determine the susceptibility to apoptosis in cirrhotic hepatocytes
Hepatocytes from cirrhotic murine livers exhibit increased basal ROS activity and resistance to TGFβ-induced apoptosis, yet when ROS levels are decreased by antioxidant pretreatment, these cells recover susceptibility to apoptotic stimuli. To further study these redox events, hepatocytes from cirrhotic murine livers were pretreated with various antioxidants prior to TGFβ treatment and the ROS activity, apoptotic response, and mitochondrial ROS generation were assessed. In addition, normal hepatocytes were treated with low-dose H2O2 and ROS and apoptotic responses determined. Treatment of cirrhotic hepatocytes with various antioxidants decreased basal ROS and rendered them susceptible to apoptosis. Examination of normal hepatocytes by confocal microscopy demonstrated co-localization of ROS activity and respiring mitochondria. Basal assessment of cirrhotic hepatocytes showed non-focal ROS activity that was abolished by antioxidants. After pretreatment with an adenovirus expressing MnSOD, basal cirrhotic hepatocyte ROS was decreased and TGFβ-induced co-localization of ROS and mitochondrial respiration was present. Treatment of normal hepatocytes with H2O2 resulted in a sustained increase in ROS and resistance to TGFβ apoptosis that was reversed when these cells were pretreated with an antioxidant. In conclusion, cirrhotic hepatocytes have a non-focal distribution of ROS. However, normal and cirrhotic hepatocytes exhibit mitochondrial localization of ROS that is necessary for apoptosis
OpenFermion: The Electronic Structure Package for Quantum Computers
Quantum simulation of chemistry and materials is predicted to be an important
application for both near-term and fault-tolerant quantum devices. However, at
present, developing and studying algorithms for these problems can be difficult
due to the prohibitive amount of domain knowledge required in both the area of
chemistry and quantum algorithms. To help bridge this gap and open the field to
more researchers, we have developed the OpenFermion software package
(www.openfermion.org). OpenFermion is an open-source software library written
largely in Python under an Apache 2.0 license, aimed at enabling the simulation
of fermionic models and quantum chemistry problems on quantum hardware.
Beginning with an interface to common electronic structure packages, it
simplifies the translation between a molecular specification and a quantum
circuit for solving or studying the electronic structure problem on a quantum
computer, minimizing the amount of domain expertise required to enter the
field. The package is designed to be extensible and robust, maintaining high
software standards in documentation and testing. This release paper outlines
the key motivations behind design choices in OpenFermion and discusses some
basic OpenFermion functionality which we believe will aid the community in the
development of better quantum algorithms and tools for this exciting area of
research.Comment: 22 page
Charge order induced Dirac pockets in the nonsymmorphic crystal TaTe
The interplay between charge order (CO) and nontrivial band topology has
spurred tremendous interest in understanding topological excitations beyond the
single-particle description. In a quasi-one-dimensional nonsymmorphic crystal
TaTe, the (2a2b3c) charge ordered ground state drives the
system into a space group where the symmetry indicator features the emergence
of Dirac fermions and unconventional double Dirac fermions. Using
angle-resolved photoemission spectroscopy and first-principles calculations, we
provide evidence of the CO induced Dirac fermion-related bands near the Fermi
level. Furthermore, the band folding at the Fermi level is compatible with the
new periodicity dictated by the CO, indicating that the electrons near the
Fermi level follow the crystalline symmetries needed to host double Dirac
fermions in this system.Comment: 9 pages, 4 figures. Second version of the manuscript following the
first submission in April 202
Transforming growth factor beta mediates hepatocyte apoptosis through Smad3 generation of reactive oxygen species
TGFβ induces hepatocyte apoptosis via reactive oxygen species (ROS) generation, the mitochondrial permeability transition (MPT), and caspase activation. The role of the Smad pathway in these events is unknown. In this study primary hepatocytes were isolated from Smad3 wild-type (+/+) and knockout (−/−) mice, and were treated with TGFβ (5 ng/ml) and/or trolox (2 mM). ROS generation, MPT, TGFβ-dependent transcription, and apoptosis were assessed in the presence or absence of Smad3 wild-type (WT) and dominant-negative (DN) plasmids. With TGFβ treatment, Smad3 (−/−) hepatocytes did not generate ROS activity, exhibit MPT, activate caspases, or undergo apoptosis when compared to Smad 3 (+/+) hepatocytes. Similarly, transfection of Smad3 (+/+) hepatocytes with DN-Smad3 inhibited TGFβ-mediated transcription, ROS generation, MPT, and apoptosis. However, Smad3 (−/−) cells transfected with WT-Smad3 and treated with TGFβ demonstrated increased transcriptional activity, the MPT, and TGFβ-induced apoptosis. TGFβ-mediated ROS generation occurred through an NADPH–like oxidase pathway since diphenyleneiodonium chloride inhibited ROS induction. In conclusion, TGFβ-induced hepatocyte apoptosis occurs through Smad3 dependent activation of ROS with subsequent activation of the MPT and caspases
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