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We theoretically investigate the nonadiabatic subcycle electron dynamics in orthogonally polarized two-color laser fields with comparable intensities. The photoelectron dynamics is simulated by exact solution to the 3D time-dependent Schrödinger equation, and also by two other semiclassical methods, i.e., the quantum trajectory Monte Carlo simulation and the Coulomb-corrected strong field approximation. Through these methods, we identify the underlying mechanisms of the subcycle electron dynamics and find that both the nonadiabatic effects and the Coulomb potential play very important roles. The contribution of the nonadiabatic effects manifest in two aspects, i.e., the nonadiabatic ionization rate and the nonzero initial velocities at the tunneling exit. The Coulomb potential has a different impact on the electrons' trajectories for different relative phases between the two pulses.
RESUMO
Most previous studies have focused on high-order harmonic generation beyond the ionization threshold; mechanisms of below-threshold harmonics are less understood. We schematically study the harmonic emission process in this region by numerically solving the time-dependent Schrödinger equation of an atom in laser fields. We show that, besides the quantum path interference mechanism recently identified, the effects induced by the Coulomb potential also have a critical impact on these harmonics. These mechanisms can be distinguished in the structure of harmonic spectra by changing the laser wavelength and peak intensity. We find that the long quantum orbits can influence lower-order harmonics at a higher laser intensity. In addition, we show that the intensity-dependent steps of harmonic yield can disappear for certain harmonic orders, due to the trapping in the Rydberg states before recombination, which can explain recent experimental observations.
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We measure high resolution photoelectron angular distributions (PADs) for above-threshold ionization of xenon atoms in infrared laser fields. Based on the Ammosov-Delone-Krainov theory, we develop an intuitive quantum-trajectory Monte Carlo model encoded with Feynman's path-integral approach, in which the Coulomb effect on electron trajectories and interference patterns are fully considered. We achieve a good agreement with the measured PADs of atoms for above-threshold ionization. The quantum-trajectory Monte Carlo theory sheds light on the role of ionic potential on PADs along the longitudinal and transverse direction with respect to the laser polarization, allowing us to unravel the classical coordinates (i.e., tunneling phase and initial momentum) at the tunnel exit for all of the photoelectrons of the PADs. We study the classical-quantum correspondence and build a bridge between the above-threshold ionization and the tunneling theory.
RESUMO
OBJECTIVE: To investigate the relationship between methylation of the CDH1 gene promoter on the expression of E-cadherin and ß-catenin, and to evaluate the correlation with clinicopathological characteristics of the colonic carcinoma. METHODS: Methylation specific PCR (MSP) was used to detect CDH1 gene promoter methylation in the cancer tissue, adjacent tissues and normal tissues in 68 patients. The expression of E-cadherin and ß-catenin was determined by immunohistochemistry staining. RESULTS: The positive rate of CDH1 gene promoter methylation was 32.4% in adjacent tissues and 57.4% in cancer tissue, while no detectable methylation was found in all the normal tissues. The difference was statistically significant. The positive rate of E-cadherin was 92.6% in the normal tissues, 66.2% in the adjacent tissues and 44.1% in the cancer tissues. In all normal tissues, ß-catenin was expressed only at the cellular membrane but not in the cytosol or nucleus, while the expression of ß-catenin was present in the cytosol or nucleus in 29.4% of the adjacent tissues and 50.0% of the cancer tissues. The positive rate of CDH1 gene promoter methylation was negatively correlated with E-cadherin expression(r=-0.312, P=0.01) and positively correlated with ß-catenin cytosolic/nucleus expression(r=0.309, P=0.018). The differentiation and metastasis of colonic carcinoma were associated with the aberrant expression of E-cadherin, ß-catenin, and methylation of CDH1 promoter (P<0.05). CONCLUSION: CDH1 gene promoter methylation may lead to aberrant expression of E-cadherin and ß-catenin in colonic carcinoma, and may play an important role in promoting the invasion of tumor.