Quantum Electrodynamics at Large Distances III: Verification of Pole Factorization and the Correspondence Principle

In two companion papers it was shown how to separate out from a scattering function in quantum electrodynamics a distinguished part that meets the correspondence-principle and pole-factorization requirements. The integrals that define the terms of the remainder are here shown to have singularities on the pertinent Landau singularity surface that are weaker than those of the distinguished part. These remainder terms therefore vanish, relative to the distinguished term, in the appropriate macroscopic limits. This shows, in each order of the perturbative expansion, that quantum electrodynamics does indeed satisfy the pole-factorization and correspondence-principle requirements in the case treated here. It also demonstrates the efficacy of the computational techniques developed here to calculate the consequences of the principles of quantum electrodynamics in the macroscopic and mesoscopic regimes.Comment: latex, 39 pages, 2 Figures included as uuencoded, tarred, gzipped, encapsulated postscript files, uses math_macros.te

WKB analysis of higher order Painlevé equations with a large parameter—Local reduction of 0-parameter solutions for Painlevé hierarchies (PJ)(J=I,II-1 or II-2)

AbstractWe generalize the reduction theorem for 0-parameter solutions of a traditional (i.e., second order) Painlevé equation with a large parameter to those of some higher order Painlevé equation, that is, each member of the Painlevé hierarchies (PJ)(J=I,II-1 or II-2). Thus the scope of applicability of the reduction theorem in [KT1] has been substantially enlarged; only six equations were covered by our previous result, while Theorem 3.2.1 of this paper applies to infinitely many equations

Reinterpretation of the Starobinsky model

The Starobinsky model of inflation, consistent with Planck 2015, has a peculiar form of the action, which contains the leading Einstein term $R$, the $R^2$ term with a huge coefficient, and negligible higher-order terms. We propose an explanation of this form based on compactification of extra dimensions. Once tuning of order $10^{-4}$ is accepted to suppress the linear term $R$, we no longer have to suppress higher-oder terms, which give nontrivial corrections to the Starobinsky model. We show our predictions of the spectral index, its runnings, and the tensor-to-scalar ratio. Finally, we discuss a possibility that quantum gravity may appear at the scale $\Lambda \gtrsim 5 \times 10^{15}$ GeV.Comment: 13 pages, 2 figures; published version, references and discussion on the uncertainties of the predictions adde

Alkylator-Induced DNA Excision Repair in Human Leukemia CCRF-CEM Cells In Vitro, Measured Using the Single-Cell Gel Electrophoresis (Comet) Assay

The capacity to repair DNA damage is an important factor that affects the therapeutic outcome in cancer treatment. To clarify the cellular repair response, we investigated the kinetics of DNA excision repair initiated by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in human leukemia CCRF-CEM cells at an exponential growth phase in vitro. Using the alkaline single-cell gel electrophoresis (comet) assay, we quantitated the repair kinetics as the amount of DNA single-strand breaks that were generated from the incision and were diminished by the rejoining in the repair process. CEM cells could initiate DNA excision repair in response to BCNU by starting an incision reaction. However, the incision capacity came to a plateau at a concentration of 80 to 1003M or after an incubation time of 90 to 120 minutes. When the cells were pulsed with 403M BCNU, the maximal incision occurred at the end of the incubation period, and the repair process was completed within 4 hours.When cells were treated with 1003M BCNU, the incised DNA was not rejoined at 4 hours, suggesting that the repair was not completed. Higher concentrations might surpass the cellular capacity for repair and would be associated with increased cell death. Evaluation of the repair process may provide a clue for therapeutic strategies to improve clinical efficacy if accelerated DNA repair is responsible for the drug resistance