Glucagon-like peptide-1 (GLP-1) is an intestinal-secreted incretin that increases cellular glucose up-take to decrease blood sugar. Recent studies, however, suggest that the function of GLP-1 is not only to decrease blood sugar, but also acts as a neurotrophic factor that plays a role in neuronal survival, neurite outgrowth, and protects synaptic plasticity and memory formation from effects of β-amyloid. Oxidative DNA damage occurs during normal neuron-activity and in many neurological diseases. Our study describes how GLP-1 affected the ability of neurons to ameliorate oxidative DNA damage. We show that activation of GLP-1 receptor (GLP-1R) protect cortical neurons from menadione induced oxidative DNA damage via a signaling pathway involving enhanced DNA repair. GLP-1 stimulates DNA repair by activating the cyclic AMP response element binding protein (CREB) which, consequently, induces the expression of apurinic/apyrimidinic endonuclease 1 (APE1), a key enzyme in the base excision DNA repair (BER) pathway. In this study, APE1 expression was down-regulated as a consequence phosphatidylinositol-3 kinase (PI3K) suppression by the inhibitor LY294002, but not by the suppression of MEK activity. Ischemic stroke is typically caused by overwhelming oxidative-stress in brain cells. Administration of exentin-4, an analogue of GLP-1, efficiently enhanced DNA repair in brain cells of ischemic stroke rats. Our study suggests that a new function of GLP-1 is to elevate DNA repair by inducing the expression of the DNA repair protein APE1.

A CPW‐fed bow‐tie slot antenna is presented. Experimental results show that the widest bandwidth can be adjusted by the slot width when the extended angle is zero, while the far field is in the broadside direction and the cross polarization is kept at a low level. The bow‐tie slot antenna can obtain at least 36% bandwidth (VSWR<2) with a 20° extended angle. A smaller slot width needs a larger extended angle to reach the widest bandwidth; meanwhile, the far field has a wider 3 dB beamwidth in the H‐plane than that using a larger slot width. © 1998 John Wiley & Sons, Inc. Microwave Opt Technol Lett 19: 358–360, 1998.

A new quinone derivative, flexibilisquinone (1), was isolated from the cultured soft coral Sinularia flexibilis, originally distributed in the waters of Taiwan. The structure of quinone 1 was established by extensive spectroscopic methods, particularly 1D and 2D NMR experiments. In the in vitro anti-inflammatory effects test, quinone 1 was found to significantly inhibit the accumulation of the pro-inflammatory iNOS and COX-2 proteins of the LPS-stimulated RAW264.7 macrophage cells.

Developing full-wave simulators for high-frequency circuit simulation is a topic many researchers have investigated. Generally speaking, methods invoking analytic pre-processing of the device's V-I relations (admittance or impedance) are computationally more efficient than methods employing numerical procedure to iteratively process the device at each time step. For circuits providing complex functionality, two-port or possibly multi-port devices whether passive or active, are sure to appear in the circuits. Therefore, extensions to currently available full-wave methods for handling one-port devices to process multi-port devices would be useful for hybrid microwave circuit designs. In this dissertation, an efficient scheme for processing arbitrary multi-port devices in the finite-difference time-domain (FDTD) method is proposed. The device's admittance is analytically pre-processed and fitted into one grid cell. With an improved time-stepping expression, the computation efficiency is further increased.Multi-port devices in the circuit can be systematically incorporated and analyzed in a full-wave manner. The accuracy of the proposed method is verified by comparison with results from the equivalent current-source method and is numerically stable.iii