Solution of the Schr\"odinger Equation for Quantum Dot Lattices with Coulomb Interaction between the Dots

The Schr\"odinger equation for quantum dot lattices with non-cubic, non-Bravais lattices built up from elliptical dots is investigated. The Coulomb interaction between the dots is considered in dipole approximation. Then only the center of mass (c.m.) coordinates of different dots couple with each other. This c.m. subsystem can be solved exactly and provides magneto- phonon like collective excitations. The inter-dot interaction is involved only through a single interaction parameter. The relative coordinates of individual dots form decoupled subsystems giving rise to intra-dot excitations. As an example, the latter are calculated exactly for two-electron dots. Emphasis is layed on qualitative effects like: i) Influence of the magnetic field on the lattice instability due to inter-dot interaction, ii) Closing of the gap between the lower and the upper c.m. mode at B=0 for elliptical dots due to dot interaction, and iii) Kinks in the single dot excitation energies (versus magnetic field) due to change of ground state angular momentum. It is shown that for obtaining striking qualitative effects one should go beyond simple cubic lattices with spherical dots. We also prove a more general version of the Kohn Theorem for quantum dot lattices. It is shown that for observing effects of electron- electron interaction between the dots in FIR spectra (breaking Kohn's Theorem) one has to consider dot lattices with at least two dot species with different confinement tensors.Comment: 11 figures included as ps-file

The basic helix-loop-helix transcription factor TCF4 impacts brain architecture as well as neuronal morphology and differentiation

Germline mutations in the basic helix-loop-helix transcription factor 4 (TCF4) cause the Pitt–Hopkins syndrome (PTHS), a developmental disorder with severe intellectual disability. Here, we report findings from a new mouse model with a central nervous system-specific truncation of Tcf4 leading to severe phenotypic abnormalities. Furthermore, it allows the study of a complete TCF4 knockout in adult mice, circumventing early postnatal lethality of previously published mouse models. Our data suggest that a TCF4 truncation results in an impaired hippocampal architecture affecting both the dentate gyrus as well as the cornu ammonis. In the cerebral cortex, loss of TCF4 generates a severe differentiation delay of neural precursors. Furthermore, neuronal morphology was critically affected with shortened apical dendrites and significantly increased branching of dendrites. Our data provide novel information about the role of Tcf4 in brain development and may help to understand the mechanisms leading to intellectual deficits observed in patients suffering from PTHS

Hydrocephalus caused by conditional ablation of the Pten or beta-catenin gene

To investigate the roles of Pten and β-Catenin in the midbrain, either the Pten gene or the β-catenin gene was conditionally ablated, using Dmbx1 (diencephalon/mesencephalon-expressed brain homeobox gene 1)-Cre mice. Homozygous disruption of the Pten or β-catenin gene in Dmbx1-expressing cells caused severe hydrocephalus and mortality during the postnatal period. Conditional deletion of Pten resulted in enlargement of midbrain structures. β-catenin conditional mutant mice showed malformation of the superior and inferior colliculi and stenosis of the midbrain aqueduct. These results demonstrate that both Pten and β-Catenin are essential for proper midbrain development, and provide the direct evidence that mutations of both Pten and β-catenin lead to hydrocephalus

"What's (the) Matter?", A Show on Elementary Particle Physics with 28 Demonstration Experiments

We present the screenplay of a physics show on particle physics, by the Physikshow of Bonn University. The show is addressed at non-physicists aged 14+ and communicates basic concepts of elementary particle physics including the discovery of the Higgs boson in an entertaining fashion. It is also demonstrates a successful outreach activity heavily relying on the university physics students. This paper is addressed at anybody interested in particle physics and/or show physics. This paper is also addressed at fellow physicists working in outreach, maybe the experiments and our choice of simple explanations will be helpful. Furthermore, we are very interested in related activities elsewhere, in particular also demonstration experiments relevant to particle physics, as often little of this work is published. Our show involves 28 live demonstration experiments. These are presented in an extensive appendix, including photos and technical details. The show is set up as a quest, where 2 students from Bonn with the aid of a caretaker travel back in time to understand the fundamental nature of matter. They visit Rutherford and Geiger in Manchester around 1911, who recount their famous experiment on the nucleus and show how particle detectors work. They travel forward in time to meet Lawrence at Berkeley around 1950, teaching them about the how and why of accelerators. Next, they visit Wu at DESY, Hamburg, around 1980, who explains the strong force. They end up in the LHC tunnel at CERN, Geneva, Switzerland in 2012. Two experimentalists tell them about colliders and our heroes watch live as the Higgs boson is produced and decays. The show was presented in English at Oxford University and University College London, as well as Padua University and ICTP Trieste. It was 1st performed in German at the Deutsche Museum, Bonn (5/'14). The show has eleven speaking parts and involves in total 20 people.Comment: 113 pages, 88 figures. An up to date version of the paper with high resolution pictures can be found at http://www.th.physik.uni-bonn.de/People/dreiner/Downloads/. In v2 the acknowledgements and a citation are correcte

MEDB-41. Identifying a subgroup of patients with early childhood sonic hedgehog-activated medulloblastoma with unfavorable prognosis after treatment with radiation-sparing regimens including intraventricular methotrexate [Abstract]

PURPOSE/METHODS: Clinical and molecular risk factors in 142 patients 3 years] 47% vs 85% [<1 year] vs 84% [1-3 years], p<0.001). No TP53 mutations were detected (n=47). DNA methylation classification identified three subgroups: SHH-1(v12.3) (n=39), SHH-2(v12.3) (n=19), and SHH-3(v12.3) (n=19), with distinct cytogenetic profiles (chromosome 2 gains in SHH-1(v12.3), very few alterations in SHH-2(v12.3), and chromosome 9q losses in SHH-3(v12.3)), age profiles (median age [years] SHH-1(v12.3): 1.7, SHH-2(v12.3): 0.9, SHH-3(v12.3): 3.0, p<0.001), and histological distribution (SHH-2(v12.3): 74% MBEN, SHH-1(v12.3)/SHH-3(v12.3): 77%/79% DMB, p<0.001). PFS was more unfavorable in patients with SHH-3(v12.3)-medulloblastoma (5-year PFS 53% vs 86% [SHH-1(v12.3)] vs 95% [SHH-2(v12.3)], p=0.002), which remained the only risk factor on multivariable Cox regression for PFS. OS was comparable (5-year OS 94% [SHH-3(v12.3)] vs 97% [SHH-1(v12.3)] vs 100% [SHH-2(v12.3)], p=0.6). 8/9 patients with SHH-3(v12.3)-medulloblastoma received radiotherapy at relapse (6 craniospinal, 2 local [1 Gorlin syndrome, 1 BRCA2 germline mutation], 1 no radiotherapy [Gorlin syndrome]). CONCLUSION: We identify patients with an increased risk of relapse when treated with radiation-sparing approaches among children with early childhood SHH-medulloblastoma. If these tumors differ from SHH-3-medulloblastoma typically described in older children remains to be verified. Treatment recommendations need to consider cancer predisposition syndromes