Negative entanglement measure for bipartite separable mixed states

We define a negative entanglement measure for separable states which shows that how much entanglement one should compensate the unentangled state at least for changing it into an entangled state. For two-qubit systems and some special classes of states in higher-dimensional systems, the explicit formula and the lower bounds for the negative entanglement measure have been presented, and it always vanishes for bipartite separable pure states. The negative entanglement measure can be used as a useful quantity to describe the entanglement dynamics and the quantum phase transition. In the transverse Ising model, the first derivatives of negative entanglement measure diverge on approaching the critical value of the quantum phase transition, although these two-site reduced density matrices have no entanglement at all. In the 1D Bose-Hubbard model, the NEM as a function of $t/U$ changes from zero to negative on approaching the critical point of quantum phase transition.Comment: 6 pages, 3 figure

catena-Poly[[bis­(3,5-dicarboxy­benzo­ato)cobalt(II)]-μ-4,4′-bipyridine]

In the title compound, [Co(C9H5O6)2(C10H8N2)]n, the asymmetric unit consists of one Co2+ ion with site symmetry 2, one mono-deprotonated 1,3,5-benzene­tricarboxylic acid anion and one-half of a 4,4′-bipyridine (4,4′-bipy) mol­ecule, in which two N and two C atoms have site symmetry 2. In the crystal structure, the Co2+ centre is coordinated by four O atoms from two bidentate carboxyl­ate groups of two anions and two N atoms of two 4,4′-bipy mol­ecules, resulting in infinite chains propagating in [010]. The cobalt coordination is distorted trans-CoO4N2 octa­hedral and inter­chain O—H⋯O hydrogen bonds complete the structure

The Metastasectomy and Timing of Pulmonary Metastases on the Outcome of Osteosarcoma Patients

Background The author intended to clarify the therapeutic effect and prognostic factors of metastasectomy and timing of pulmonary metastases in osteosarcoma patents. Methods Data was obtained retrospectively on all consecutive osteosarcoma patients from 1985 to 2005 in author's institute. Fifty-two patients with pulmonary nodules were identified, including 24 patients undergoing pulmonary metastasectomy treatment. These patients were categorized into four groups: group 1, patients with lung metastases at the initial presentation; group 2, lung metastases identified during the period of pre-operative chemotherapy; group 3, lung metastases identified during period of the post-operative chemotherapy; group 4, lung metastases identified after therapy for the primary osteosarcoma completed. Results In our study, the 2-, 3-, and 5-year overall survival rates for 52 patients were 49%, 39% and 20%. The 2-year overall survival rates were 18% for group 1, 32% for group 3, and 70% for group 4 (p < 0.001). The 5-year overall survival rate was 34% for group 4. Patients who underwent metastesectomy showed a better survival outcome as compared with the patients not undergoing metastasectomy (p = 0.003). The 2-year and 5-year overall survival rates of only one lung metastatic nodule were 62% and 50%, and for initially multiple lung metastatic nodules, 45% and 5%, respectively. In addition, the patients presented with lung metastases had a worse prognosis as compared with those without initial lung metastases (p = 0.0001). Conclusions The patients having single metastatic nodule showed a better prognosis than those with multiple lung nodules. Furthermore, those patients who underwent metastasectomy survived longer than those not undergoing metastasectomy. Patients who had late metastases after complete chemotherapy had a better prognosis; whereas those who had metastases identified at the initial presentation predicted a poor prognosis

Infectomic Analysis of Gene Expression Profiles of Human Brain Microvascular Endothelial Cells Infected with Cryptococcus neoformans

In order to dissect the pathogenesis of Cryptococcus neoformans meningoencephalitis, a genomic survey of the changes in gene expression of human brain microvascular endothelial cells infected by C. neoformans was carried out in a time-course study. Principal component analysis (PCA) revealed significant fluctuations in the expression levels of different groups of genes during the pathogen-host interaction. Self-organizing map (SOM) analysis revealed that most genes were up- or downregulated 2 folds or more at least at one time point during the pathogen-host engagement. The microarray data were validated by Western blot analysis of a group of genes, including β-actin, Bcl-x, CD47, Bax, Bad, and Bcl-2. Hierarchical cluster profile showed that 61 out of 66 listed interferon genes were changed at least at one time point. Similarly, the active responses in expression of MHC genes were detected at all stages of the interaction. Taken together, our infectomic approaches suggest that the host cells significantly change the gene profiles and also actively participate in immunoregulations of the central nervous system (CNS) during C. neoformans infection

Phosphorylation at Ser473 regulates heterochromatin protein 1 binding and corepressor function of TIF1beta/KAP1

<p>Abstract</p> <p>Background</p> <p>As an epigenetic regulator, the transcriptional intermediary factor 1β (TIF1β)/KAP1/TRIM28) has been linked to gene expression and chromatin remodeling at specific loci by association with members of the heterochromatin protein 1 (HP1) family and various other chromatin factors. The interaction between TIF1β and HP1 is crucial for heterochromatin formation and maintenance. The HP1-box, PXVXL, of TIF1β is responsible for its interaction with HP1. However, the underlying mechanism of how the interaction is regulated remains poorly understood.</p> <p>Results</p> <p>This work demonstrates that TIF1β is phosphorylated on Ser473, the alteration of which is dynamically associated with cell cycle progression and functionally linked to transcriptional regulation. Phosphorylation of TIF1β/Ser473 coincides with the induction of cell cycle gene <it>cyclin A2 </it>at the S-phase. Interestingly, chromatin immunoprecipitation demonstrated that the promoter of <it>cyclin A2 </it>gene is occupied by TIF1β and that such occupancy is inversely correlated with Ser473 phosphorylation. Additionally, when HP1β was co-expressed with TIF1β/S473A, but not TIF1β/S473E, the colocalization of TIF1β/S473A and HP1β to the promoters of <it>Cdc2 </it>and <it>Cdc25A </it>was enhanced. Non-phosphorylated TIF1β/Ser473 allowed greater TIF1β association with the regulatory regions and the consequent repression of these genes. Consistent with possible inhibition of TIF1β's corepressor function, the phosphorylation of the Ser473 residue, which is located near the HP1-interacting PXVXL motif, compromised the formation of TIF1β-HP1 complex. Finally, we found that the phosphorylation of TIF1β/Ser473 is mediated by the PKCδ pathway and is closely linked to cell proliferation.</p> <p>Conclusion</p> <p>The modulation of HP1β-TIF1β interaction through the phosphorylation/de-phosphorylation of TIF1β/Ser473 may constitute a molecular switch that regulates the expression of particular genes. Higher levels of phosphorylated TIF1β/Ser473 may be associated with the expression of key regulatory genes for cell cycle progression and the proliferation of cells.</p