Structure of the Isovector Dipole Resonance in Neutron-Rich 60Ca^{60}Ca Nucleus and Direct Decay from Pygmy Resonance

The structure of the isovector dipole resonance in neutron-rich calcium isotope, $^{60}Ca$, has been investigated by implementing a careful treatment of the differences of neutron and proton radii in the continuum random phase approximation ($RPA$). The calculations have taken into account the current estimates of the neutron skin. The estimates of the escape widths for direct neutron decay from the pygmy dipole resonance ($PDR$) were shown rather wide, implicating a strong coupling to the continuum. The width of the giant dipole resonance ($GDR$) was evaluated, bringing on a detailed discussion about its microscopic structure.Comment: 13 pages, 2 figures, RevTex

miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis

MicroRNAs (miRNAs) are increasingly implicated in regulating the malignant progression of cancer. Here we show that miR-9, which is upregulated in breast cancer cells, directly targets CDH1, the E-cadherin-encoding messenger RNA, leading to increased cell motility and invasiveness. miR-9-mediated E-cadherin downregulation results in the activation of β-catenin signalling, which contributes to upregulated expression of the gene encoding vascular endothelial growth factor (VEGF); this leads, in turn, to increased tumour angiogenesis. Overexpression of miR-9 in otherwise non-metastatic breast tumour cells enables these cells to form pulmonary micrometastases in mice. Conversely, inhibiting miR-9 by using a 'miRNA sponge' in highly malignant cells inhibits metastasis formation. Expression of miR-9 is activated by MYC and MYCN, both of which directly bind to the mir-9-3 locus. Significantly, in human cancers, miR-9 levels correlate with MYCN amplification, tumour grade and metastatic status. These findings uncover a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasis-suppressing protein E-cadherin.Life Sciences Research Foundation FellowshipMargaret and Herman Sokol AwardNational Institutes of Health (U.S.) (Pathway to Independence Award (K99/R00))Howard Hughes Medical Institute (Undergraduate Fellowship)Breast Cancer Research Program (U.S.) (Predoctoral Fellowship)National Institutes of Health (U.S.) (Grant)Ludwig Center for Molecular Oncology at MI

Examples of inclusions of unital C\sp*-algebras of index-finite type with the Rokhlin property

In this note, we provide several examples of inclusions of unital C\sp*-algebras of index finite-type with the Rokhlin property lacking in literature and more importantly we construct the example which does not belong to the fixed point algebra model which means that for the inclusion $P \subset A$ there is neither finite group action $G \curvearrowright A$ such that $P=A^{G}$ nor finite dimensional C\sp*- Hopf algebra action $H \curvearrowright A$ such that $P=A^{H}$.Comment: 12pages, 1 figur

On intermediate subfactors of Goodman-de la Harpe-Jones subfactors

In this paper we present a conjecture on intermediate subfactors which is a generalization of Wall's conjecture from the theory of finite groups. Motivated by this conjecture, we determine all intermediate subfactors of Goodman-Harpe-Jones subfactors, and as a result we verify that Goodman-Harpe-Jones subfactors verify our conjecture. Our result also gives a negative answer to a question motivated by a conjecture of Aschbacher-Guralnick.Comment: To appear in Comm. Math. Phy

Marine Cyanobacteria Compounds with Anticancer Properties: Implication of Apoptosis

Marine cyanobacteria have been proved to be an important source of potential anticancer drugs. Although several compounds were found to be cytotoxic to cancer cells in culture, the pathways by which cells are affected are still poorly elucidated. For some compounds, cancer cell death was attributed to an implication of apoptosis through morphological apoptotic features, implication of caspases and proteins of the Bcl-2 family, and other mechanisms such as interference with microtubules dynamics, cell cycle arrest and inhibition of proteases other than caspases