Solving the spectral gap problem with a four-mirror bow-tie cavity in waveguide free-electron laser oscillators.

The generation of intense coherent radiation pulses in the far-infrared and terahertz regimes is of considerable interest to the free-electron laser (FEL) radiation user community. At long wavelengths, the diffraction effect can be quite severe, therefore, an optical waveguide is required to confine the radiation field. However, it will also bring about some new phenomena, and the most noteworthy one is the spectral gap phenomenon: at some particular wavelengths, regardless of electron beam adjustments, the coupling efficiency and output power of waveguide FEL oscillators drop significantly. Such spectral gap has an adverse effect on experimental results since numerous experiments require continuous spectral scanning. In this paper, we propose to utilize a bow-tie cavity instead of conventional cavities to the waveguide FEL to solve the spectral gap problem. The simulation was carried out based on the parameters of FELiChEM, a newly built user facility in China. Numerical simulation code OPC combining with modified GENESIS is used to enable the modelling, for the first time, of a bow-tie cavity based FEL in the far-infrared wavelength regime. The simulation results indicate that this novel structure can effectively eliminate the spectral gaps and substantially enhance long-wavelength laser performance.

GROalpha/KC, a chemokine receptor CXCR2 ligand, can be a potent trigger for neuronal ERK1/2 and PI-3 kinase pathways and for tau hyperphosphorylation-a role in Alzheimer's disease?

Inflammation has been implicated in the pathogenesis of Alzheimer's disease (AD) and other neurodegenerative diseases. We have examined the potential role of some chemokine/chemokine receptors in this process. It is known that CXCR2 is a strongly expressed chemokine receptor on neurons and is strongly upregulated in AD in a subpopulation of neuritic plaques. Here, we show that one of the CXCR2 ligand GROalpha/KC can be a potent trigger for the ERK1/2 and PI-3 kinase pathways, as well as tau hyperphosphorylation in the mouse primary cortical neurons. GROalpha immunoreactivity can be detected in a subpopulation of neurons in normal and AD. Therefore, the CXCR2-ligand pair may have a potent pathophysiological role in neurodegenerative diseases.