Torsion points and the Lattes family

We give a dynamical proof of a result of Masser and Zannier [MZ2, MZ3] about torsion points on the Legendre family of elliptic curves. Our methods also treat points of small height. A key ingredient is the arithmetic equidistribution theorem on $\mathbb{P}^1$ of Baker-Rumely, Chambert-Loir, and Favre-Rivera-Letelier. Torsion points on the elliptic curve coincide with preperiodic points for the degree-4 Lattes family of rational functions. Our main new results concern properties of the bifurcation measures for this Lattes family associated to marked points.Comment: Theorem 1.3 now states the strongest form of the main theorem, the result of combining our methods with the conclusions of Masser-Zannier, for rational points with complex coefficients. To appear, American Journal of Mat

Greatwall and Polo-like Kinase 1 Coordinate to Promote Checkpoint Recovery

Checkpoint recovery upon completion of DNA repair allows the cell to return to normal cell cycle progression and is thus a crucial process that determines cell fate after DNA damage. We previously studied this process in Xenopus egg extracts and established Greatwall (Gwl) as an important regulator. Here we show that preactivated Gwl kinase can promote checkpoint recovery independently of cyclin-dependent kinase 1 (Cdk1) or Plx1 (Xenopus polo-like kinase 1), whereas depletion of Gwl from extracts exhibits no synergy with that of Plx1 in delaying checkpoint recovery, suggesting a distinct but related relationship between Gwl and Plx1. In further revealing their functional relationship, we found mutual dependence for activation of Gwl and Plx1 during checkpoint recovery, as well as their direct association. We characterized the protein association in detail and recapitulated it in vitro with purified proteins, which suggests direct interaction. Interestingly, Gwl interaction with Plx1 and its phosphorylation by Plx1 both increase at the stage of checkpoint recovery. More importantly, Plx1-mediated phosphorylation renders Gwl more efficient in promoting checkpoint recovery, suggesting a functional involvement of such regulation in the recovery process. Finally, we report an indirect regulatory mechanism involving Aurora A that may account for Gwl-dependent regulation of Plx1 during checkpoint recovery. Our results thus reveal novel mechanisms underlying the involvement of Gwl in checkpoint recovery, in particular, its functional relationship with Plx1, a well characterized regulator of checkpoint recovery. Coordinated interplays between Plx1 and Gwl are required for reactivation of these kinases from the G2/M DNA damage checkpoint and efficient checkpoint recovery

Phenomenology of quintessino dark matter -- Production of NLSP particles

In the model of quintessino as dark matter particle, the dark matter and dark energy are unified in one superfield, where the dynamics of the Quintessence drives the Universe acceleration and its superpartner, quintessino, makes up the dark matter of the Universe. This scenario predicts the existence of long lived $\tilde{\tau}$ as the next lightest supersymmetric particle. In this paper we study the possibility of detecting $\tilde{\tau}$ produced by the high energy cosmic neutrinos interacting with the earth matter. By a detailed calculation we find that the event rate is one to several hundred per year at a detector with effective area of $1 km^2$. The study in this paper can be also applied for models of gravitino or axino dark matter particles.Comment: 16 pages, 5 figures, a new section about NLSP stau is added, references adde

Detection and Interpretation Of Long-Lived X-Ray Quasi-Periodic Pulsations in the X-Class Solar Flare On 2013 May 14

Quasi-periodic pulsations (QPP) seen in the time derivative of the GOES soft X-ray light curves are analyzed for the near-limb X3.2 event on 14 May 2013. The pulsations are apparent for a total of at least two hours from the impulsive phase to well into the decay phase, with a total of 163 distinct pulses evident to the naked eye. A wavelet analysis shows that the characteristic time scale of these pulsations increases systematically from $\sim$25 s at 01:10 UT, the time of the GOES peak, to $\sim$100 s at 02:00 UT. A second ridge in the wavelet power spectrum, most likely associated with flaring emission from a different active region, shows an increase from $\sim$40 s at 01:40 UT to $\sim$100 s at 03:10 UT. We assume that the QPP that produced the first ridge result from vertical kink-mode oscillations of the newly formed loops following magnetic reconnection in the coronal current sheet. This allows us to estimate the magnetic field strength as a function of altitude given the density, loop length, and QPP time scale as functions of time determined from the GOES light curves and RHESSI images. The calculated magnetic field strength of the newly formed loops ranges from about $\sim$500 G at an altitude of 24 Mm to a low value of $\sim$10 G at 60 Mm, in general agreement with the expected values at these altitudes. Fast sausage mode oscillations are also discussed and cannot be ruled out as an alternate mechanism for producing the QPP

An unreleased mm-wave resonant body transistor

In this work, we present the first fully unreleased Micro-Electro-Mechanical (MEM) resonator. The 1st harmonic longitudinal resonance of a silicon FinFET fully clad in SiO[subscript 2] is demonstrated. The device exhibits two resonances at 39 and 41 GHz, corresponding well with simulation results. The quality factor (Q) of 129 at 39 GHz is ~4× lower than that of its released counterpart. Methods to improve Q and reduce spurious modes are introduced. This first demonstration of unreleased resonators in a hybrid MEMS-CMOS technology can provide RF and microwave CMOS circuit designers with active high-Q devices monolithically integrated in Front-End-of-Line (FEOL) processing without the need for post-processing or special packaging.Microelectronics Advanced Research Corporation (MARCO)United States. Defense Advanced Research Projects Agenc

Tumor-reactive immune cells protect against metastatic tumor and induce immunoediting of indolent but not quiescent tumor cells

Two major barriers to cancer immunotherapy include tumor-induced immune suppression mediated by myeloid-derived suppressor cells and poor immunogenicity of the tumor-expressing self-antigens. To overcome these barriers, we reprogrammed tumor-immune cell cross-talk by combined use of decitabine and adoptive immunotherapy, containing tumor-sensitized T cells and CD25+ NKT cells. Decitabine functioned to induce the expression of highly immunogenic cancer testis antigens in the tumor, while also reducing the frequency of myeloid-derived suppressor cells and the presence of CD25+ NKT cells rendered T cells, resistant to remaining myeloid-derived suppressor cells. This combinatorial therapy significantly prolonged survival of animals bearing metastatic tumor cells. Adoptive immunotherapy also induced tumor immunoediting, resulting in tumor escape and associated disease-related mortality. To identify a tumor target that is incapable of escape from the immune response, we used dormant tumor cells. We used Adriamycin chemotherapy or radiation therapy, which simultaneously induce tumor cell death and tumor dormancy. Resultant dormant cells became refractory to additional doses of Adriamycin or radiation therapy, but they remained sensitive to tumor-reactive immune cells. Importantly, we discovered that dormant tumor cells contained indolent cells that expressed low levels of Ki67 and quiescent cells that were Ki67 negative. Whereas the former were prone to tumor immunoediting and escape, the latter did not demonstrate immunoediting. Our results suggest that immunotherapy could be highly effective against quiescent dormant tumor cells. The challenge is to develop combinatorial therapies that could establish a quiescent type of tumor dormancy, which would be the best target for immunotherapy

Regulation of p53 Stability and Apoptosis by a ROR Agonist

Activation of p53 function leading to cell-cycle arrest and/or apoptosis is a promising strategy for development of anticancer therapeutic agents. Here, we describe a novel mechanism for stabilization of p53 protein expression via activation of the orphan nuclear receptor, RORa. We demonstrate that treatment of cancer cells with a newly described synthetic ROR agonist, SR1078, leads to p53 stabilization and induction of apoptosis. These data suggest that synthetic ROR agonists may hold utility in the treatment of cancer