Identification of AFLP markers linked to Fusarium wilt disease in pigeonpea [Cajanus cajan (L.) Millsp.]

An experiment was conducted to identify markers linked to Fusarium wilt disease resistance, Parents namely TTB 7 and ICP 8863 were screened using 151 SSRs markers and 16 AFLP primer combinations. Parental screening revealed five SSR primers and 12 AFLP primer combinations polymorphic between parents. Bulk segregant analysis identified five AFLP primer combinations generating seven markers polymorphic between resistant and susceptible bulks while, none of the SSR markers were polymorphic. This indicates that, these markers are putatively linked to wilt disease. Screening of F2 segregating population of cross TTB 7 x ICP 8863 with these putatively linked markers revealed four markers (E-AAT/M-CTG850, ETCG/M-CTT650, E-TCG/M-CTA730 and E-TCG/M-CTT230) which segregated in 3:1 mendelian pattern. Simple linear regression performed on these four markers had identified two markers namely E-TCG/M-CTT650 and E-TCG/M-CTA730 linked to disease

GPR56/ADGRG1 Inhibits Mesenchymal Differentiation and Radioresistance in Glioblastoma

A mesenchymal transition occurs both during the natural evolution of glioblastoma (GBM) and in response to therapy. Here, we report that the adhesion G-protein-coupled receptor, GPR56/ADGRG1, inhibits GBM mesenchymal differentiation and radioresistance. GPR56 is enriched in proneural and classical GBMs and is lost during their transition toward a mesenchymal subtype. GPR56 loss of function promotes mesenchymal differentiation and radioresistance of glioma initiating cells both in vitro and in vivo. Accordingly, a low GPR56-associated signature is prognostic of a poor outcome in GBM patients even within non-G-CIMP GBMs. Mechanistically, we reveal GPR56 as an inhibitor of the nuclear factor kappa B (NF-κB) signaling pathway, thereby providing the rationale by which this receptor prevents mesenchymal differentiation and radioresistance. A pan-cancer analysis suggests that GPR56 might be an inhibitor of the mesenchymal transition across multiple tumor types beyond GBM

GPR56/ADGRG1 inhibits mesenchymal differentiation and radioresistance in glioblastoma

A mesenchymal transition occurs both during the natural evolution of glioblastoma (GBM) and in response to therapy. Here, we report that the adhesion G-protein-coupled receptor, GPR56/ADGRG1, inhibits GBM mesenchymal differentiation and radioresistance. GPR56 is enriched in proneural and classical GBMs and is lost during their transition toward a mesenchymal subtype. GPR56 loss of function promotes mesenchymal differentiation and radioresistance of glioma initiating cells both in vitro and in vivo. Accordingly, a low GPR56-associated signature is prognostic of a poor outcome in GBM patients even within non-G-CIMP GBMs. Mechanistically, we reveal GPR56 as an inhibitor of the nuclear factor kappa B (NF-κB) signaling pathway, thereby providing the rationale by which this receptor prevents mesenchymal differentiation and radioresistance. A pan-cancer analysis suggests that GPR56 might be an inhibitor of the mesenchymal transition across multiple tumor types beyond GBM

Nickel Nanoparticles Decorated Porous Carbons for Highly Active Catalytic Reduction of Organic Dyes and Sensitive Detection of Hg(II) Ions

[[sponsorship]]原子與分子科學研究所[[note]]已出版;[SCI];有審查制度;具代表性[[note]]http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Drexel&SrcApp=hagerty_opac&KeyRecord=1944-8244&DestApp=JCR&RQ=IF_CAT_BOXPLO

Direction sensitive wavelet packet for despeckling of ultrasound images

The study attempts to despeckle ultrasound images by the application of a direction sensitive wavelet packet transform. In the proposed method, wavelet packet decomposition is performed on the image and best subbands are selected using singular value decomposition. The low frequency subband is preserved, as it has the maximum information content. Iterated directional filter bank (IDFB) is applied on all other selected subbands. The vertical cells of the IDFB in the horizontal subbands and horizontal cells of IDFB in vertical subbands are eliminated because of their minimum edge information and maximum noise. Shrinkages are also applied on the remaining cells to be evaluated. The performance of the proposed algorithm is evaluated in terms of mean square error (MSE), peak signal to noise ratio, mean structural SIMilarity index, speckle suppression index, signal to MSE and speckle signal to noise ratio. It is found after the evaluation that the obtained experimental results are better than the existing state of the art despeckling techniques

Modeling and Optimal Tuning of Hybrid ESS Supporting Fast Active Power Regulation of Fully Decoupled Wind Power Generators

The frequency stability of the power system is challenged by the high penetration of power electronic interfaced renewable energy sources (RES). This paper investigates the improvements of the frequency response of fully decoupled wind power generators (FDWG) by proposing a novel generic model implementation of ultracapacitors (UC) within a hybrid scheme in real-time simulations of wind power plants. UCs are selected as ideal power sources in fast active power-frequency control due to their high power density and fast-reacting speed. Batteries and UCs combined hybrid energy storage systems (HESS) are formed to complement their characteristics. Droop-based and frequency derivative-based control and virtual synchronous power (VSP) are the selected control strategies to support power system frequency stability. The best trade-off between frequency performance and HESS cost is found by solving a proposed optimization problem formulation. The proposed optimization problem is used to define the HESS size and the controller parameters. The optimization results show how the fast active power-frequency response is enhanced by the fast UC power injection. It also shown that VSP leads to faster frequency support than the droop-based control and the frequency derivative control.Intelligent Electrical Power Grid