Higher Level Open String States from Vacuum String Field Theory

We construct massive open string states around a classical solution in the oscillator formulation of Vacuum String Field Theory. In order for the correct mass spectrum to be reproduced, the projection operators onto the modes of the left- and right-half of the string must have an anomalous eigenvalue 1/2, and the massive states are constructed using the corresponding eigenvector. We analyze numerically the projection operators by regularizing them to finite size matrices and confirm that they indeed have eigenvalue 1/2. Beside the desired massive states, we have spurious massive as well as massless states, which are infinitely degenerate. We show that these unwanted states can be gauged away.Comment: 16 pages, no figures, LaTeX, v2:minor correction

Acquired resistance of leukemic cells to AraC is associated with the upregulation of aldehyde dehydrogenase 1 family member A2.

The elucidation of drug resistance mechanisms is important in the development of clinical therapies for the treatment of leukemia. To study the drug resistance mechanisms, protein expression profiles of 1-β-D-arabinofuranosylcytosine (AraC)-sensitive K562 (K562S) cells and AraC-resistant K562 (K562AC) cells were compared using two-dimensional fluorescence difference gel electrophoresis. In a comparison of protein expression profiles, 2073 protein spots were found to be altered, and 15 proteins of them were remarkably altered. These proteins were identified by mass spectrometry. The most differently expressed proteins were aldehyde dehydrogenase 1 family member A2 (ALDH1A2) and vimentin. Both proteins were verified using reverse transcriptase polymerase chain reaction and Western blot analysis. ALDH1A2 protein was found to be effective in AraC resistance. ALDH1A2 knock-down induced sensitivity to AraC treatment in K562AC cells, and ALDH1A2 overexpressed K562S cells acquired the AraC resistance. Furthermore, the findings also suggest that ALDH1A2 expression is increased after the appearance of AraC resistance in clinical cases. These results will be helpful in understanding the mechanism of AraC resistance

Dinuclear Mn complexes as functional models of Mn catalase

Abstract : p-Phenoxo-bis(p-carboxy1ato)dimanganese complexes with a core structure of Cs symmetry show a high catalytic activity to disproportionate H202 (2H202 + 2 H 2 0 + 02), whereas complexes with a core structure of C2 symmetry and mononuclear Mn complexes show only a low activity. For the Cs symmetric complexes, a dinuclear cis-{ MnIV(=O)]2 intermediate has been detected in the H202 disproportionation reaction and a mechanistic scheme to catalyze the H202 disproportionation through the interconversion cis-{ MnIV(=O)]~cis-{ MnIII(OH)]2 is proposed. It is shown that the equivalence of two Mn ions in electronic nature is essential to show a CAT-like activity