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1.
Nat Commun ; 10(1): 3715, 2019 Sep 16.
Article in English | MEDLINE | ID: mdl-31527608

ABSTRACT

Accurate characterization of the noise influencing a quantum system of interest has far-reaching implications across quantum science, ranging from microscopic modeling of decoherence dynamics to noise-optimized quantum control. While the assumption that noise obeys Gaussian statistics is commonly employed, noise is generically non-Gaussian in nature. In particular, the Gaussian approximation breaks down whenever a qubit is strongly coupled to discrete noise sources or has a non-linear response to the environmental degrees of freedom. Thus, in order to both scrutinize the applicability of the Gaussian assumption and capture distinctive non-Gaussian signatures, a tool for characterizing non-Gaussian noise is essential. Here, we experimentally validate a quantum control protocol which, in addition to the spectrum, reconstructs the leading higher-order spectrum of engineered non-Gaussian dephasing noise using a superconducting qubit as a sensor. This first experimental demonstration of non-Gaussian noise spectroscopy represents a major step toward demonstrating a complete spectral estimation toolbox for quantum devices.

2.
Nanotechnology ; 27(46): 464003, 2016 Nov 18.
Article in English | MEDLINE | ID: mdl-27749276

ABSTRACT

Microwave-frequency superconducting resonators are ideally suited to perform dispersive qubit readout, to mediate two-qubit gates, and to shuttle states between distant quantum systems. A prerequisite for these applications is a strong qubit-resonator coupling. Strong coupling between an electron-spin qubit and a microwave resonator can be achieved by correlating spin- and orbital degrees of freedom. This correlation can be achieved through the Zeeman coupling of a single electron in a double quantum dot to a spatially inhomogeneous magnetic field generated by a nearby nanomagnet. In this paper, we consider such a device and estimate spin-resonator couplings of order ∼1 MHz with realistic parameters. Further, through realistic simulations, we show that precise placement of the double-dot relative to the nanomagnet allows to select between a purely longitudinal coupling (commuting with the bare spin Hamiltonian) and a purely transverse (spin non-conserving) coupling. Additionally, we suggest methods to mitigate dephasing and relaxation channels that are introduced in this coupling scheme. This analysis gives a clear route toward the realization of coherent state transfer between a microwave resonator and a single electron spin in a GaAs double quantum dot with a fidelity above 90%. Improved dynamical decoupling sequences, low-noise environments, and longer-lived microwave cavity modes may lead to substantially higher fidelities in the near future.

3.
J Clin Invest ; 124(11): 4807-22, 2014 Nov.
Article in English | MEDLINE | ID: mdl-25271625

ABSTRACT

Immunological activity in the CNS is largely dependent on an innate immune response and is heightened in diseases, such as diabetic retinopathy, multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. The molecular dynamics governing immune cell recruitment to sites of injury and disease in the CNS during sterile inflammation remain poorly defined. Here, we identified a subset of mononuclear phagocytes (MPs) that responds to local chemotactic cues that are conserved among central neurons, vessels, and immune cells. Patients suffering from late-stage proliferative diabetic retinopathy (PDR) had elevated vitreous semaphorin 3A (SEMA3A). Using a murine model, we found that SEMA3A acts as a potent attractant for neuropilin-1-positive (NRP-1-positive) MPs. These proangiogenic MPs were selectively recruited to sites of pathological neovascularization in response to locally produced SEMA3A as well as VEGF. NRP-1-positive MPs were essential for disease progression, as NRP-1-deficient MPs failed to enter the retina in a murine model of oxygen-induced retinopathy (OIR), a proxy for PDR. OIR mice with NRP-1-deficient MPs exhibited decreased vascular degeneration and diminished pathological preretinal neovascularization. Intravitreal administration of a NRP-1-derived trap effectively mimicked the therapeutic benefits observed in mice lacking NRP-1-expressing MPs. Our findings indicate that NRP-1 is an obligate receptor for MP chemotaxis, bridging neural ischemia to an innate immune response in neovascular retinal disease.


Subject(s)
Chemotaxis , Myeloid Cells/physiology , Neuropilin-1/physiology , Adult , Aged , Aged, 80 and over , Animals , Cell Proliferation , Cells, Cultured , Choroid/immunology , Diabetic Retinopathy/immunology , Diabetic Retinopathy/metabolism , Humans , Immunity, Innate , Mice, Inbred C57BL , Middle Aged , Mononuclear Phagocyte System/immunology , Neovascularization, Physiologic , Neuroimmunomodulation , Semaphorin-3A/metabolism , Tissue Culture Techniques
4.
Cell Metab ; 18(4): 505-18, 2013 Oct 01.
Article in English | MEDLINE | ID: mdl-24093675

ABSTRACT

The deterioration of the inner blood-retinal barrier and consequent macular edema is a cardinal manifestation of diabetic retinopathy (DR) and the clinical feature most closely associated with loss of sight. We provide evidence from both human and animal studies for the critical role of the classical neuronal guidance cue, semaphorin 3A, in instigating pathological vascular permeability in diabetic retinas via its cognate receptor neuropilin-1. We reveal that semaphorin 3A is induced in early hyperglycemic phases of diabetes within the neuronal retina and precipitates initial breakdown of endothelial barrier function. We demonstrate, by a series of orthogonal approaches, that neutralization of semaphorin 3A efficiently prevents diabetes-induced retinal vascular leakage in a stage of the disease when vascular endothelial growth factor neutralization is inefficient. These observations were corroborated in Tg(Cre-Esr1)/Nrp1(flox/flox) conditional knockout mice. Our findings identify a therapeutic target for macular edema and provide further evidence for neurovascular crosstalk in the pathogenesis of DR.


Subject(s)
Diabetic Retinopathy/metabolism , Neurons/metabolism , Semaphorin-3A/metabolism , Aged , Aged, 80 and over , Animals , Cells, Cultured , Diabetes Mellitus, Experimental/chemically induced , Diabetes Mellitus, Experimental/metabolism , Diabetes Mellitus, Experimental/pathology , Diabetic Retinopathy/pathology , Endothelial Cells/cytology , Endothelial Cells/drug effects , Humans , Mice , Mice, Inbred C57BL , Mice, Knockout , Mice, Obese , Middle Aged , Neuropilin-1/deficiency , Neuropilin-1/genetics , Neuropilin-1/metabolism , Permeability/drug effects , RNA, Messenger/metabolism , Retina/metabolism , Retina/physiopathology , Semaphorin-3A/genetics , Semaphorin-3A/pharmacology , Vascular Endothelial Growth Factor A/pharmacology
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