No abstract

A sensitive surface-enhanced Raman scattering (SERS) signal dependent double detection of mycotoxins is achieved for the first time, without the aid of nucleic acid amplification strategies. SERS labels embedded Ag@Au core-shell (CS) nanoparticles (NPs) as novel SERS tags are successfully prepared through a galvanic replacement-free deposition. SERS tags produce stable and quantitative SERS signal, emerging from the plasmonic coupling at the junction of Ag core and Au shell. SERS tags engineered Raman aptasensors are developed for the double detection of ochratoxin A (OTA) and aflatoxin B1 (AFB1) in maize meal. The limits of detection (LODs) are as low as 0.006 ng/mL for OTA and 0.03 ng/mL for AFB1. The developed protocol can be extended to a large set of different SERS tags for the sensitive detection of multiple targets that possess different lengths of aptamers.

The molecular basis for induction of apoptosis in melanoma cells by vincristine remains unknown. Here we tested the potential involvement of AMP-activated protein kinase (AMPK) in this process. We found for the first time that vincristine induces AMPK activation (AMPKα, Thr 172) and Acetyl-CoA carboxylase (ACC, Ser 79) (a downstream molecular target of AMPK) phosphorylation in cultured melanoma cells in vitro. Reactive oxygen species (ROS) dependent LKB1 activation serves as the upstream signal for AMPK activation. AMPK inhibitor (compound C) or AMPKα siRNA knockdown inhibits vincristine induced B16 melanoma cell apoptosis, while AMPK activator 5-aminoimidazole-4-carboxamide-1-β-riboside (AICAR) enhances it. AMPK activation is involved in vincristine induced p53 phosphorylation and stabilization, the latter is known to mediate melanoma cell apoptosis. Further, activation of AMPK by vincristine inhibits mTOR Complex 1 (mTORC1) in B16 melanoma cells, which serves as another important mechanism to induce melanoma cell apoptosis. Our study provides new insights into understanding the cellular and molecular mechanisms of vincristine induced cancer cell death/apoptosis. We suggest that combining AMPK activator AICAR with vincristine may have potential to be used as a new therapeutic intervention against melanoma.

ABSTRACT:The resistance distance r ij between vertices i and j of a connected (molecular) graph G is computed as the effective resistance between nodes i and j in the corresponding network constructed from G by replacing each edge of G with a unit resistor. The Kirchhoff index Kf (G) is the sum of resistance distances between all pairs of vertices. In this work, according to the decomposition theorem of Laplacian polynomial, we obtain that the Laplacian spectrum of linear hexagonal chain L n consists of the Laplacian spectrum of path P 2n+1 and eigenvalues of a symmetric tridiagonal matrix of order 2n + 1. By applying the relationship between roots and coefficients of the characteristic polynomial of the above matrix, explicit closed-form formula for Kirchhoff index of L n is derived in terms of Laplacian spectrum. To our surprise, the Krichhoff index of L n is approximately to one half of its Wiener index. Finally, we show thatholds for all graphs G in a class of graphs including L n .

ABSTRACT:The resistance distance r ij between vertices i and j of a connected (molecular) graph G is computed as the effective resistance between nodes i and j in the corresponding network constructed from G by replacing each edge of G with a unit resistor. The Kirchhoff index Kf (G) is the sum of resistance distances between all pairs of vertices. In this work, closed-form formulae for Kirchhoff index and resistance distances of circulant graphs are derived in terms of Laplacian spectrum and eigenvectors. Special formulae are also given for four classes of circulant graphs complete graphs, complete graphs minus a perfect matching, cycles, Möbius ladders M p . In particular, the asymptotic behavior of Kf