Signature of two-electron interference in angular resolved double photoionization of Mg

The double photoionization of Mg has been studied experimentally and theoretically in a kinematic where the two photoelectrons equally share the excess energy. The observation of a symmetrized gerade amplitude, which strongly deviates from the Gaussian ansatz, is explained by a two-electron interference predicted theoretically, but never before observed experimentally. Similar to the Cooper minima in the single photoionization cross section, the effect finds its origin in the radial extent and oscillation of the target wave function

Signature of two-electron interference in angular resolved double photoionization of Mg

The double photoionization of Mg has been studied experimentally and theoretically in a kinematic where the two photoelectrons equally share the excess energy. The observation of a symmetrized gerade amplitude, which strongly deviates from the Gaussian ansatz, is explained by a two-electron interference predicted theoretically, but never before observed experimentally. Similar to the Cooper minima in the single photoionization cross section, the effect finds its origin in the radial extent and oscillation of the target wave function

Two electron interference in angular resolved double photoionization of Mg

The signature of the target wavefunction has been observed in the symmetrized amplitude of the resonant double photoionization of Mg. This observation is based on our experimental study of angle-resolved double photoionization of Mg at the photon energy of 55.49 eV (2p → 3d resonance) under equal energy sharing conditions

Loss of Heterozygosity at the CYP2D6 Locus in Breast Cancer: Implications for Germline Pharmacogenetic Studies

Controversy exists regarding the impact of CYP2D6 genotype on tamoxifen responsiveness. We examined loss of heterozygosity (LOH) at the CYP2D6 locus and determined its impact on genotyping error when tumor tissue is used as a DNA source

Photo-double-ionization of Mg studied by electron-electron-coincidence experiments

The photo-double-ionization (PDI) of Mg to the Mg2+(3s−2) state has been studied by photoelectron-photoelectron-coincidence experiments at a photon energy corresponding to the excitation of the 2p→3d resonance. The equal energy sharing (E1 = E2 = 16.4 eV) as well as the complementary unequal energy (E1↔E2 = 10.4↔22.4 eV) sharing kinematics have been investigated. From the experimental results without any approximation the symmetrized gerade and ungerade amplitudes have been obtained. The experimental angular correlation patterns as well as the amplitudes are compared to CCC calculations in which the resonant process has been incorporated. The results confirm that the amplitudes of the photo-double-ionization carry the signature of the target radial wave function. The investigation of the triple differential cross sections has been then extended by simulations to a kinematics with the fixed detector at 90°, which can not be studied experimentally by the present setup. These simulations shed light on results of previous measurements on alkaline-earth-metal atoms in this kinematics, which were not consistent with the common understanding of photo-double-ionization derived from He experiments

Cancer-specific CTCF binding facilitates oncogenic transcriptional dysregulation

Background: The three-dimensional genome organization is critical for gene regulation and can malfunction in diseases like cancer. As a key regulator of genome organization, CCCTC-binding factor (CTCF) has been characterized as a DNA-binding protein with important functions in maintaining the topological structure of chromatin and inducing DNA looping. Among the prolific binding sites in the genome, several events with altered CTCF occupancy have been reported as associated with effects in physiology or disease. However, hitherto there is no comprehensive survey of genome-wide CTCF binding patterns across different human cancers. Results: To dissect functions of CTCF binding, we systematically analyze over 700 CTCF ChIP-seq profiles across human tissues and cancers and identify cancer-specific CTCF binding patterns in six cancer types. We show that cancer-specific lost and gained CTCF binding events are associated with altered chromatin interactions, partially with DNA methylation changes, and rarely with sequence mutations. While lost bindings primarily occur near gene promoters, most gained CTCF binding events exhibit enhancer activities and are induced by oncogenic transcription factors. We validate these findings in T cell acute lymphoblastic leukemia cell lines and patient samples and show that oncogenic NOTCH1 induces specific CTCF binding and they cooperatively activate expression of target genes, indicating transcriptional condensation phenomena. Conclusions: Specific CTCF binding events occur in human cancers. Cancer-specific CTCF binding can be induced by other transcription factors to regulate oncogenic gene expression. Our results substantiate CTCF binding alteration as a functional epigenomic signature of cancer