Chaos and flights in the atom-photon interaction in cavity QED

We study dynamics of the atom-photon interaction in cavity quantum electrodynamics (QED), considering a cold two-level atom in a single-mode high-finesse standing-wave cavity as a nonlinear Hamiltonian system with three coupled degrees of freedom: translational, internal atomic, and the field. The system proves to have different types of motion including L\'{e}vy flights and chaotic walkings of an atom in a cavity. It is shown that the translational motion, related to the atom recoils, is governed by an equation of a parametric nonlinear pendulum with a frequency modulated by the Rabi oscillations. This type of dynamics is chaotic with some width of the stochastic layer that is estimated analytically. The width is fairly small for realistic values of the control parameters, the normalized detuning $\delta$ and atomic recoil frequency $\alpha$. It is demonstrated how the atom-photon dynamics with a given value of $\alpha$ depends on the values of $\delta$ and initial conditions. Two types of L\'{e}vy flights, one corresponding to the ballistic motion of the atom and another one corresponding to small oscillations in a potential well, are found. These flights influence statistical properties of the atom-photon interaction such as distribution of Poincar\'{e} recurrences and moments of the atom position $x$. The simulation shows different regimes of motion, from slightly abnormal diffusion with $\sim\tau^{1.13}$ at $\delta =1.2$ to a superdiffusion with $\sim \tau^{2.2}$ at $\delta=1.92$ that corresponds to a superballistic motion of the atom with an acceleration. The obtained results can be used to find new ways to manipulate atoms, to cool and trap them by adjusting the detuning $\delta$.Comment: 16 pages, 7 figures. To be published in Phys. Rev.

Inhibition of Casein kinase-2 induces p53-dependent cell cycle arrest and sensitizes glioblastoma cells to tumor necrosis factor (TNFα)-induced apoptosis through SIRT1 inhibition

Glioblastoma multiforme (GBM) are resistant to TNFα-induced apoptosis and blockade of TNFα-induced NF-κB activation sensitizes glioma cells to apoptosis. As Casein kinase-2 (CK2) induces aberrant NF-κB activation and as we observed elevated CK2 levels in GBM tumors, we investigated the potential of CK2 inhibitors (CK2-Is) - DRB and Apigenin in sensitizing glioma cells to TNFα-induced apoptosis. CK2-Is and CK2 small interfering RNA (siRNA) reduced glioma cell viability, inhibited TNFα-mediated NF-κB activation, and sensitized cell to TNFα-induced apoptosis. Importantly, CK2-Is activated p53 function in wild-type but not in p53 mutant cells. Activation of p53 function involved its increased transcriptional activation, DNA-binding ability, increased expression of p53 target genes associated with cell cycle progression and apoptosis. Moreover, CK2-Is decreased telomerase activity and increased senescence in a p53-dependent manner. Apoptotic gene profiling indicated that CK2-Is differentially affect p53 and TNFα targets in p53 wild-type and mutant glioma cells. CK2-I decreased MDM2-p53 association and p53 ubiquitination to enhance p53 levels. Interestingly, CK2-Is downregulated SIRT1 activity and over-expression of SIRT1 decreased p53 transcriptional activity and rescued cells from CK2-I-induced apoptosis. This ability of CK2-Is to sensitize glioma to TNFα-induced death via multiple mechanisms involving abrogation of NF-κB activation, reactivation of wild-type p53 function and SIRT1 inhibition warrants investigation

Imaginal Discs – A New Source of Chromosomes for Genome Mapping of the Yellow Fever Mosquito Aedes aegypti

Dengue fever is an emerging health threat to as much as half of the human population around the world. No vaccines or drug treatments are currently available. Thus, disease prevention is largely based on efforts to control its major mosquito vector Ae. aegypti. Novel vector control strategies, such as population replacement with pathogen-incompetent transgenic mosquitoes, rely on detailed knowledge of the genome organization for the mosquito. However, the current genome assembly of Ae. aegypti is highly fragmented and requires additional physical mapping onto chromosomes. The absence of readable polytene chromosomes makes genome mapping for this mosquito extremely challenging. In this study, we discovered and investigated a new source of chromosomes useful for the cytogenetic analysis in Ae. aegypti – mitotic chromosomes from imaginal discs of 4th instar larvae. Using natural banding patterns of these chromosomes, we developed a new band-based approach for physical mapping of DNA probes to the precise chromosomal positions. Further application of this approach for genome mapping will greatly enhance the utility of the existing draft genome sequence assembly for Ae. aegypti and thereby facilitate application of advanced genome technologies for investigating and developing novel genetic control strategies for dengue transmission