Controllable coupling between a nanomechanical resonator and a coplanar-waveguide resonator via a superconducting flux qubit

We study a tripartite quantum system consisting of a coplanar-waveguide (CPW) resonator and a nanomechanical resonator (NAMR) connected by a flux qubit, where the flux qubit has a large detuning from both resonators. By a unitray transformation and a second-order approximation, we obtain a strong and controllable (i.e., magnetic-field-dependent) effective coupling between the NAMR and the CPW resonator. Due to the strong coupling, vacuum Rabi splitting can be observed from the voltage-fluctuation spectrum of the CPW resonator. We further study the properties of single photon transport as inferred from the reflectance or equivalently the transmittance. We show that the reflectance and the corresponding phase shift spectra both exhibit doublet of narrow spectral features due to vacuum Rabi splitting. By tuning the external magnetic field, the reflectance and the phase shift can be varied from 0 to 1 and $-\pi$ to $\pi$, respectively. The results indicate that this hybrid quantum system can act as a quantum router.Comment: 8 pages, 6 figure

Detecting Photon-Photon Interactions in a Superconducting Circuit

A local interaction between photons can be engineered by coupling a nonlinear system to a transmission line. The required high impedance transmission line can be conveniently formed from a chain of Josephson junctions. The nonlinearity is generated by side-coupling this chain to a Cooper pair box. We propose to probe the resulting photon-photon interactions via their effect on the current-voltage characteristic of a voltage-biased Josephson junction connected to the transmission line. Considering the Cooper pair box to be in the weakly anharmonic regime, we find that the dc current through the probe junction yields features around the voltages $2eV=n\hbar\omega_s$, where $\omega_s$ is the plasma frequency of the superconducting circuit. The features at $n\ge 2$ are a direct signature of the photon-photon interaction in the system.Comment: 10 pages, 7 figure

Magneto-optical transmission in magnetic nanoparticle suspensions for different optical applications: a review

Recently, the magneto-optical properties of magnetic nanofluids have received increasing attention due to their wide range of applications in solar energy conversions and also as smart fluids in tunable photonic devices, optical switch, optical fiber sensor, etc. This review discusses up-to-date developments in magneto-optical transmission in ferrofluids. The magnetic nanoparticle would undergo various structural transitions under external magnetic field, including chainlike formation and lateral coalescence which, in turn, leads to various interesting light transmission phenomena. It is thus possible to alter the properties of the transmitted light by adjusting the orientation of the magnetic field with respect to that of the incident light. The polarization direction of light has a negligible effect on the magneto-optical transmission while light passing along the magnetic field. However, it makes a significant difference for light normal to the field direction. These characteristics are comprehensively reviewed, and their potential applications are presented. It is supposed to provide a general view on the research trends, existing problems and future work for the investigation of magneto-optical transmission in magnetic nanofluids

General Quantum Key Distribution in Higher Dimension

We study a general quantum key distribution protocol in higher dimension. In this protocol, quantum states in arbitrary $g+1$ ($1\le g\le d$) out of all $d+1$ mutually unbiased bases in a d-dimensional system can be used for the key encoding. This provides a natural generalization of the quantum key distribution in higher dimension and recovers the previously known results for $g=1$ and $d$. In our investigation, we study Eve's attack by two slightly different approaches. One is considering the optimal cloner for Eve, and the other, defined as the optimal attack, is maximizing Eve's information. We derive results for both approaches and show the deviation of the optimal cloner from the optimal attack. With our systematic investigation of the quantum key distribution protocols in higher dimension, one may balance the security gain and the implementation cost by changing the number of bases in the key encoding. As a side product, we also prove the equivalency between the optimal phase covariant quantum cloning machine and the optimal cloner for the $g=d-1$ quantum key distribution

ALS Mutations of FUS Suppress Protein Translation and Disrupt the Regulation of Nonsense-Mediated Decay

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease characterized by preferential motor neuron death. Approximately 15% of ALS cases are familial, and mutations in the fused in sarcoma (FUS) gene contribute to a subset of familial ALS cases. FUS is a multifunctional protein participating in many RNA metabolism pathways. ALS-linked mutations cause a liquid–liquid phase separation of FUS protein in vitro, inducing the formation of cytoplasmic granules and inclusions. However, it remains elusive what other proteins are sequestered into the inclusions and how such a process leads to neuronal dysfunction and degeneration. In this study, we developed a protocol to isolate the dynamic mutant FUS-positive cytoplasmic granules. Proteomic identification of the protein composition and subsequent pathway analysis led us to hypothesize that mutant FUS can interfere with protein translation. We demonstrated that the ALS mutations in FUS indeed suppressed protein translation in N2a cells expressing mutant FUS and fibroblast cells derived from FUS ALS cases. In addition, the nonsense-mediated decay (NMD) pathway, which is closely related to protein translation, was altered by mutant FUS. Specifically, NMD-promoting factors UPF1 and UPF3b increased, whereas a negative NMD regulator, UPF3a, decreased, leading to the disruption of NMD autoregulation and the hyperactivation of NMD. Alterations in NMD factors and elevated activity were also observed in the fibroblast cells of FUS ALS cases. We conclude that mutant FUS suppresses protein biosynthesis and disrupts NMD regulation, both of which likely contribute to motor neuron death

Exact Variance Component Tests for Longitudinal Microbiome Studies

In metagenomic studies, testing the association of microbiome composition and clinical outcomes translates to testing the nullity of variance components. Motivated by a lung HIV (human immunodeficiency virus) microbiome project, we study longitudinal microbiome data by variance component models with more than two variance components. Current testing strategies only apply to the models with exactly two variance components and when sample sizes are large. Therefore, they are not applicable to longitudinal microbiome studies. In this paper, we propose exact tests (score test, likelihood ratio test, and restricted likelihood ratio test) to (1) test the association of the overall microbiome composition in a longitudinal design and (2) detect the association of one specific microbiome cluster while adjusting for the effects from related clusters. Our approach combines the exact tests for null hypothesis with a single variance component with a strategy of reducing multiple variance components to a single one. Simulation studies demonstrate that our method has correct type I error rate and superior power compared to existing methods at small sample sizes and weak signals. Finally, we apply our method to a longitudinal pulmonary microbiome study of human immunodeficiency virus (HIV) infected patients and reveal two interesting genera Prevotella and Veillonella associated with forced vital capacity. Our findings shed lights on the impact of lung microbiome to HIV complexities. The method is implemented in the open source, high-performance computing language Julia and is freely available at https://github.com/JingZhai63/VCmicrobiome

Toll-like receptor 4-dependent upregulation of cytokines in a transgenic mouse model of Alzheimer's disease

<p>Abstract</p> <p>Background</p> <p>Aβ deposits in the brains of patients with Alzheimer's disease (AD) are closely associated with innate immune responses such as activated microglia and increased cytokines. Accumulating evidence supports the hypothesis that innate immune/inflammatory responses play a pivotal role in the pathogenesis of AD: either beneficial or harmful effects on the AD progression. The molecular mechanisms by which the innate immune system modulates the AD progression are not well understood. Toll-like receptors (TLRs) are first-line molecules for initiating the innate immune responses. When activated through TLR signaling, microglia respond to pathogens and damaged host cells by secreting chemokines and cytokines and express the co-stimulatory molecules needed for protective immune responses to pathogens and efficient clearance of damaged tissues. We previously demonstrated that an AD mouse model homozygous for a destructive mutation of TLR4 has increases in diffuse and fibrillar Aβ deposits as well as buffer-soluble and insoluble Aβ in the brain as compared with a TLR4 wild-type AD mouse model. Here, we investigated the roles of TLR4 in Aβ-induced upregulation of cytokines and chemokines, Aβ-induced activation of microglia and astrocytes and Aβ-induced immigration of leukocytes.</p> <p>Methods</p> <p>Using the same model, levels of cytokines and chemokines in the brain were determined by multiplex cytokine/chemokine array. Activation of microglia and astrocytes and immigration of leukocytes were determined by immunoblotting and immunohistochemistry followed by densitometry and morphometry, respectively.</p> <p>Results</p> <p>Levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-10 and IL-17 in the brains of TLR4 wild-type AD mice were significantly higher than those in TLR4 wild-type non-transgenic littermates. Such increases in cytokines were not found in TLR4 mutant AD mice as compared with TLR4 mutant non-transgenic littermates. Although expression levels of CD11b (a microglia marker) and GFAP (a reactive astrocyte marker) in the brains of TLR4 mutant AD mice were higher than those in TLR4 wild type AD mice, no difference was found in levels of CD45 (common leukocyte antigen).</p> <p>Conclusion</p> <p>This is the first demonstration of TLR4-dependent upregulation of cytokines in an AD mouse model. Our results suggest that TLR4 signaling is involved in AD progression and that TLR4 signaling can be a new therapeutic target for AD.</p

Morphine modulation of pain processing in medial and lateral pain pathways

<p>Abstract</p> <p>Background</p> <p>Despite the wide-spread use of morphine and related opioid agonists in clinic and their powerful analgesic effects, our understanding of the neural mechanisms underlying opioid analgesia at supraspinal levels is quite limited. The present study was designed to investigate the modulative effect of morphine on nociceptive processing in the medial and lateral pain pathways using a multiple single-unit recording technique. Pain evoked neuronal activities were simultaneously recorded from the primary somatosensory cortex (SI), ventral posterolateral thalamus (VPL), anterior cingulate cortex (ACC), and medial dorsal thalamus (MD) with eight-wire microelectrode arrays in awake rats.</p> <p>Results</p> <p>The results showed that the noxious heat evoked responses of single neurons in all of the four areas were depressed after systemic injection of 5 mg/kg morphine. The depressive effects of morphine included (i) decreasing the neuronal response magnitude; (ii) reducing the fraction of responding neurons, and (iii) shortening the response duration. In addition, the capability of cortical and thalamic neural ensembles to discriminate noxious from innocuous stimuli was decreased by morphine within both pain pathways. Meanwhile, morphine suppressed the pain-evoked changes in the information flow from medial to lateral pathway and from cortex to thalamus. These effects were completely blocked by pre-treatment with the opiate receptor antagonist naloxone.</p> <p>Conclusion</p> <p>These results suggest that morphine exerts analgesic effects through suppressing both sensory and affective dimensions of pain.</p