Correlations in Quasi-Periodic Oscillation and Noise Frequencies Among Neutron-Star and Black-Hole X-ray Binaries

We study systematically the ~0.1-1200 Hz quasi-periodic oscillations (QPOs) and broad noise components observed in the power spectra of non-pulsing neutron-star and black-hole low-mass X-ray binaries. We show that among these components we can identify two, occurring over a wide range of source types and luminosities, whose frequencies follow a tight correlation. The variability components involved in this correlation include neutron-star kilohertz QPOs and horizontal-branch oscillations, as well as black-hole QPOs and noise components. Our results suggest that the same types of variability may occur in both neutron-star and black-hole systems over three orders of magnitude in frequency and with coherences that vary widely but systematically. Confirmation of this hypothesis will strongly constrain theoretical models of these phenomena and provide additional clues to understanding their nature.Comment: 15 pages, 2 figures (one color figure), to appear in the Astrophysical Journa

Long-term exposure of human renal carcinoma cells to PD98059 induces epithelial-mesenchymal transition-like phenotype and enhanced motility.

Extracellular signal-regulated kinases (ERK) have fundamental roles in tumor progression. However, human clinical trials have shown little or no effect of inhibitors of their upstream signaling molecule, mitogen-activated protein kinase/ERK kinase (MEK), in advanced cancers. To determine the molecular mechanism underlying the limited antitumor effect, we cultured two human renal carcinoma cell lines, ACHN cells and VMRC-RCW cells in the presence of a MEK inhibitor PD98059 for more than 4 weeks (PD98059-exposed cells). PD98059-exposed ACHN cells showed elongated cell shape with scattering morphology, increase in vimentin expression, loss of beta-catenin junctional localization, stress fiber formation, and increased motility. In contrast, VMRC-RCW cells showed scattered phenotype without PD98059-treatment, and this treatment failed to increase the expression of vimentin. Rho A activity was increased in PD98059-exposed ACHN cells. In these cells, enhanced stress fiber formation and motility were observed, both of which were inhibited by treatment with small interfering RNA for Rho A or an Rho kinase inhibitor Y27632. Our results suggest that long-term exposure of human renal carcinoma cells to PD98059 increases cell motility by upregulating Rho A-Rho kinase signaling

Loss of PTEN function may account for reduced proliferation pathway sensitivity to LY294002 in human prostate and bladder cancer cells.

PURPOSE: Inhibition of phosphoinositide 3 (PI3)-kinase pathway is attractive for cancer treatment. To examine the role of the phosphatase and tensin homolog (PTEN) in the development of resistance to the treatment. METHODS: We cultured human prostate cancer cells (DU145 and PC-3 cells) and bladder cancer cells (EJ-1 and UM-UC-3 cells) with a PI3-kinase inhibitor, LY294002 for more than 6 weeks and cell proliferation was studied. Activation of Akt1 and ERK was examined by immunoblotting. We introduced the wild type PTEN in UM-UC-3 cells and their proliferation along with the signaling pathways was also examined. RESULTS: After 6 weeks, proliferation pathway sensitivity to LY294002 was reduced in cells expressing PTEN, but not in PTEN-null cells. PD98059, a MAPK/ERK kinase inhibitor, significantly inhibited proliferation of PTEN-expressing cells, but not PTEN-null cells. Stable PTEN expression in PTEN-null UM-UC-3 cells increased serum-induced ERK activation and sensitivity to PD98059-treatment, and reduced sensitivity to LY294002 after 6 weeks of exposure. CONCLUSIONS: Loss of PTEN function may protect against resistance to PI3-kinase inhibitors through an addiction to the PI3-kinase/Akt pathway