Integrating fMRI and SNP data for biomarker identification for schizophrenia with a sparse representation based variable selection method

BACKGROUND: In recent years, both single-nucleotide polymorphism (SNP) array and functional magnetic resonance imaging (fMRI) have been widely used for the study of schizophrenia (SCZ). In addition, a few studies have been reported integrating both SNPs data and fMRI data for comprehensive analysis. METHODS: In this study, a novel sparse representation based variable selection (SRVS) method has been proposed and tested on a simulation data set to demonstrate its multi-resolution properties. Then the SRVS method was applied to an integrative analysis of two different SCZ data sets, a Single-nucleotide polymorphism (SNP) data set and a functional resonance imaging (fMRI) data set, including 92 cases and 116 controls. Biomarkers for the disease were identified and validated with a multivariate classification approach followed by a leave one out (LOO) cross-validation. Then we compared the results with that of a previously reported sparse representation based feature selection method. RESULTS: Results showed that biomarkers from our proposed SRVS method gave significantly higher classification accuracy in discriminating SCZ patients from healthy controls than that of the previous reported sparse representation method. Furthermore, using biomarkers from both data sets led to better classification accuracy than using single type of biomarkers, which suggests the advantage of integrative analysis of different types of data. CONCLUSIONS: The proposed SRVS algorithm is effective in identifying significant biomarkers for complicated disease as SCZ. Integrating different types of data (e.g. SNP and fMRI data) may identify complementary biomarkers benefitting the diagnosis accuracy of the disease

Efficient purification and assembly of ribonucleoprotein complex for interaction analysis by MST assay coupled with GaMD simulations

Here, we describe a generic protocol for monitoring protein-RNA interaction using a cleavable GFP fusion of a recombinant RNA-binding protein. We detail each expression and purification step, including high salt and heparin column for contaminant RNA removal. After the assembly of RNA into the ribonucleoprotein complex, the MicroScale Thermophoresis assay enables the binding affinity to be obtained quickly with a small amount of sample. Further Gaussian accelerated molecular dynamics simulations allow us to analyze protein:RNA interactions in detail

Secure transmission via joint precoding optimization for downlink MISO NOMA

Non-orthogonal multiple access (NOMA) is a prospective technology for radio resource constrained future mobile networks. However, NOMA users far from base station (BS) tend to be more susceptible to eavesdropping because they are allocated more transmit power. In this paper, we aim to jointly optimize the precoding vectors at BS to ensure the legitimate security in a downlink multiple-input single-output (MISO) NOMA network. When the eavesdropping channel state information (CSI) is available at BS, we can maximize the sum secrecy rate by joint precoding optimization. Owing to its non-convexity, the problem is converted into a convex one, which is solved by a second-order cone programming based iterative algorithm. When the CSI of the eavesdropping channel is not available, we first consider the case that the secure user is not the farthest from BS, and the transmit power of the farther users is maximized via joint precoding optimization to guarantee its security. Then, we consider the case when the farthest user from BS requires secure transmission, and the modified successive interference cancellation order and joint precoding optimization can be adopted to ensure its security. Similar method can be exploited to solve the two non-convex problems when the CSI is unknown. Simulation results demonstrate that the proposed schemes can improve the security performance for MISO NOMA systems effectively, with and without eavesdropping CSI

The Synergistic Effect of Valsartan and LAF237 [(S)-1-[(3-Hydroxy-1-Adamantyl)Ammo]acetyl-2-Cyanopyrrolidine] on Vascular Oxidative Stress and Inflammation in Type 2 Diabetic Mice

Aim. To investigate the combination effects and mechanisms of valsartan (angiotensin II type 1 receptor blocker) and LAF237 (DPP-IV inhibitor) on prevention against oxidative stress and inflammation injury in db/db mice aorta. Methods. Db/db mice (n = 40) were randomized to receive valsartan, LAF237, valsartan plus LAF237, or saline. Oxidative stress and inflammatory reaction in diabetic mice aorta were examined. Results. Valsartan or LAF237 pretreatment significantly increased plasma GLP-1 expression, reduced apoptosis of endothelial cells isolated from diabetic mice aorta. The expression of NAD(P)H oxidase subunits also significantly decreased resulting in decreased superoxide production and ICAM-1 (fold change: valsartan : 7.5 ± 0.7, P < 0.05; LAF237: 10.2 ± 1.7, P < 0.05), VCAM-1 (fold change: valsartan : 5.2 ± 1.2, P < 0.05; LAF237: 4.8 ± 0.6, P < 0.05), and MCP-1 (fold change: valsartan: 3.2 ± 0.6, LAF237: 4.7 ± 0.8; P < 0.05) expression. Moreover, the combination treatment with valsartan and LAF237 resulted in a more significant increase of GLP-1 expression. The decrease of the vascular oxidative stress and inflammation reaction was also higher than monotherapy with valsartan or LAF237. Conclusion. These data indicated that combination treatment with LAF237 and valsartan acts in a synergistic manner on vascular oxidative stress and inflammation in type 2 diabetic mice

Topological Atomic Spinwave Lattices by Dissipative Couplings

Recent experimental advance in creating dissipative couplings provides a new route for engineering exotic lattice systems and exploring topological dissipation. Using the spatial lattice of atomic spinwaves in a vacuum vapor cell, where purely dissipative couplings arise from diffusion of atoms, we experimentally realize a dissipative version of the Su-Schrieffer-Heeger (SSH) model. We construct the dissipation spectra of the topological or trivial lattices via electromagnetically-induced-transparency (EIT) spectroscopy. The topological dissipation spectrum is found to exhibit edge modes at dissipation rates within a dissipative gap, decoupled from the bulk. We also validate chiral symmetry of the dissipative SSH couplings. This work paves the way for realizing topology-enabled quantum correlations and non-Hermitian topological quantum optics via dissipative couplings.Comment: 5 pages, 4 figure

Cardioprotective effects of tanshinone IIA pretreatment via kinin B2 receptor-Akt-GSK-3β dependent pathway in experimental diabetic cardiomyopathy

<p>Abstract</p> <p>Aims</p> <p>Diabetic cardiomyopathy, characterized by myocardial structural and functional changes, is a specific cardiomyopathy develops in patients with diabetes mellitus. The present study was to investigate the role of kinin B2 receptor-Akt-glycogen synthase kinase (GSK)-3β signalling pathway in mediating the protective effects of tanshinone IIA (TSN) on diabetic cardiomyopathy.</p> <p>Methods and results</p> <p>Streptozocin (STZ) induced diabetic rats (n = 60) were randomized to receive TSN, TSN plus HOE140 (a kinin B2 receptor antagonist), or saline. Healthy Sprague-Dawley (SD) rats (n = 20) were used as control. Left ventricular function, myocardial apoptosis, myocardial ultrastructure, Akt, GSK-3β and NF-κB phosphorylation, the expression of TNF-α, IL-6 and myeloperoxidase (MPO) were examined. Cardiac function was well preserved as evidenced by increased left ventricular ejection fraction (LVEF) and ± dp/dt (maximum speed of contraction/relaxation), along with decreased myocardial apoptotic death after TSN administration. TSN pretreatment alleviated mitochondria ultrastructure changes. TSN also enhanced Akt and GSK-3β phosphorylation and inhibited NF-κB phosphorylation, resulting in decreased TNF-α, IL-6 and MPO activities. Moreover, pretreatment with HOE140 abolished the beneficial effects of TSN: a decrease in LVEF and ± dp/dt, an inhibition of cardiomyocyte apoptosis, a destruction of cardiomyocyte mitochondria cristae, a reduction of Akt and GSK-3β phosphorylation, an enhancement of NF-κB phosphorylation and an increase of TNF-α, IL-6 and MPO production.</p> <p>Conclusion</p> <p>These data indicated that TSN is cardioprotective in the context of diabetic cardiomyopathy through kinin B2 receptor-Akt-GSK-3β dependent pathway.</p