Band gap renormalization in photoexcited semiconductor quantum wire structures in the GW approximation

We investigate the dynamical self-energy corrections of the electron-hole plasma due to electron-electron and electron-phonon interactions at the band edges of a quasi-one dimensional (1D) photoexcited electron-hole plasma. The leading-order $GW$ dynamical screening approximation is used in the calculation by treating electron-electron Coulomb interaction and electron-optical phonon Fr\"{o}hlich interaction on an equal footing. We calculate the exchange-correlation induced band gap renormalization (BGR) as a function of the electron-hole plasma density and the quantum wire width. The calculated BGR shows good agreement with existing experimental results, and the BGR normalized by the effective quasi-1D excitonic Rydberg exhibits an approximate one-parameter universality.Comment: 11 pages, 3 figure

The radical cation of bacteriochlorophyll b. A liquid-phase endor and triple resonance study

The previous termradical cationnext term of bacterioehlorophyll b (BChl b) is investigated by ENDOR and TRIPLE resonance in liquid solution. The experimental hyperfine coupling constants, ten proton and three nitrogen couplings, are compared with the predictions from advanced molecular-orbital calculations (RHF INDO/SP). The detailed picture obtained of the spin density distribution is a prerequisite for the investigation of the primary electron donor previous termradical cationnext term in BChl b containing photosynthetic bacteria

Experimental therapy of malignant gliomas using the inhibitor of histone deacetylase MS-275

Inhibitors of histone deacetylases are promising compounds for the treatment of cancer but have not been systematically explored in malignant brain tumors. Here, we characterize the benzamide MS-275, a class I histone deacetylase inhibitor, as potent drug for experimental therapy of glioblastomas. Treatment of four glioma cell lines (U87MG, C6, F98, and SMA-560) with MS-275 significantly reduced cell growth in a concentration-dependent manner (IC90, 3.75 μmol/L). Its antiproliferative effect was corroborated using a bromodeoxyuridine proliferation assay and was mediated by G0-G1 cell cycle arrest (i.e., up-regulation of p21/WAF) and apoptotic cell death. Implantation of enhanced green fluorescent protein–transfected F98 glioma cells into slice cultures of rat brain confirmed the cytostatic effect of MS-275 without neurotoxic damage to the organotypic neuronal environment in a dose escalation up to 20 μmol/L. A single intratumoral injection of MS-275 7 days after orthotopic implantation of glioma cells in syngeneic rats confirmed the chemotherapeutic efficacy of MS-275 in vivo. Furthermore, its propensity to pass the blood-brain barrier and to increase the protein level of acetylated histone H3 in brain tissue identifies MS-275 as a promising candidate drug in the treatment of malignant gliomas