Self-trapped electrons and holes in PbBr2_2 crystals

We have directly observed self-trapped electrons and holes in PbBr$_{2}$ crystals with electron-spin-resonance (ESR) technique. The self-trapped states are induced below 8 K by two-photon interband excitation with pulsed 120-fs-width laser light at 3.10 eV. Spin-Hamiltonian analyses of the ESR signals have revealed that the self-trapping electron centers are the dimer molecules of Pb$_2$$^{3+}$ along the crystallographic a axis and the self-trapping hole centers are those of Br$_2$$^-$ with two possible configurations in the unit cell of the crystal. Thermal stability of the self-trapped electrons and holes suggests that both of them are related to the blue-green luminescence band at 2.55 eV coming from recombination of spatially separated electron-hole pairs.Comment: 8 pages (7 figures, 2 tables), ReVTEX; revised the text and figures 1, 4, and

Self-trapped states and the related luminescence in PbCl2_2 crystals

We have comprehensively investigated localized states of photoinduced electron-hole pairs with electron-spin-resonance technique and photoluminescence (PL) in a wide temperature range of 5-200 K. At low temperatures below 70 K, holes localize on Pb$^{2+}$ ions and form self-trapping hole centers of Pb$^{3+}$. The holes transfer to other trapping centers above 70 K. On the other hand, electrons localize on two Pb$^{2+}$ ions at higher than 50 K and form self-trapping electron centers of Pb$_2$$^{3+}$. From the thermal stability of the localized states and PL, we clarify that blue-green PL band at 2.50 eV is closely related to the self-trapped holes.Comment: 8 pages (10 figures), ReVTEX; removal of one figure, Fig. 3 in the version

Lipoprotein lipase is frequently overexpressed or translocated in cervical squamous cell carcinoma and promotes invasiveness through the non-catalytic C terminus.

BACKGROUND: We studied the biological significance of genes involved in a novel t(8;12)(p21.3;p13.31) reciprocal translocation identified in cervical squamous cell carcinoma (SCC) cells. METHODS: The rearranged genes were identified by breakpoint mapping, long-range PCR and sequencing. We investigated gene expression in vivo using reverse-transcription PCR and tissue microarrays, and studied the phenotypic consequences of forced gene overexpression. RESULTS: The rearrangement involved lipoprotein lipase (LPL) and peroxisome biogenesis factor-5 (PEX5). Whereas LPL-PEX5 was expressed at low levels and contained a premature stop codon, PEX5-LPL was highly expressed and encoded a full-length chimeric protein (including the majority of the LPL coding region). Consistent with these findings, PEX5 was constitutively expressed in normal cervical squamous cells, whereas LPL expression was negligible. The LPL gene was rearranged in 1 out of 151 cervical SCCs, whereas wild-type LPL overexpression was common, being detected in 10 out of 28 tissue samples and 4 out of 10 cell lines. Forced overexpression of wild-type LPL and PEX5-LPL fusion transcripts resulted in increased invasiveness in cervical SCC cells, attributable to the C-terminal non-catalytic domain of LPL, which was retained in the fusion transcripts. CONCLUSION: This is the first demonstration of an expressed fusion gene in cervical SCC. Overexpressed wild-type or translocated LPL is a candidate for targeted therapy