Molecular-orbital theory for the stopping power of atoms in the low velocity regime:the case of helium in alkali metals

A free-parameter linear-combination-of-atomic-orbitals approach is presented for analyzing the stopping power of slow ions moving in a metal. The method is applied to the case of He moving in alkali metals. Mean stopping powers for He present a good agreement with local-density-approximation calculations. Our results show important variations in the stopping power of channeled atoms with respect to their mean values.Comment: LATEX, 3 PostScript Figures attached. Total size 0.54

Three-body non-additive forces between spin-polarized alkali atoms

Three-body non-additive forces in systems of three spin-polarized alkali atoms (Li, Na, K, Rb and Cs) are investigated using high-level ab initio calculations. The non-additive forces are found to be large, especially near the equilateral equilibrium geometries. For Li, they increase the three-atom potential well depth by a factor of 4 and reduce the equilibrium interatomic distance by 0.9 A. The non-additive forces originate principally from chemical bonding arising from sp mixing effects.Comment: 4 pages, 3 figures (in 5 files

Scattering of Stark-decelerated OH radicals with rare-gas atoms

We present a combined experimental and theoretical study on the rotationally inelastic scattering of OH (X\,^2\Pi_{3/2}, J=3/2, f) radicals with the collision partners He, Ne, Ar, Kr, Xe, and D$_2$ as a function of the collision energy between $\sim 70$ cm$^{-1}$ and 400~cm$^{-1}$. The OH radicals are state selected and velocity tuned prior to the collision using a Stark decelerator, and field-free parity-resolved state-to-state inelastic relative scattering cross sections are measured in a crossed molecular beam configuration. For all OH-rare gas atom systems excellent agreement is obtained with the cross sections predicted by close-coupling scattering calculations based on accurate \emph{ab initio} potential energy surfaces. This series of experiments complements recent studies on the scattering of OH radicals with Xe [Gilijamse \emph{et al.}, Science {\bf 313}, 1617 (2006)], Ar [Scharfenberg \emph{et al.}, Phys. Chem. Chem. Phys. {\bf 12}, 10660 (2010)], He, and D$_2$ [Kirste \emph{et al.}, Phys. Rev. A {\bf 82}, 042717 (2010)]. A comparison of the relative scattering cross sections for this set of collision partners reveals interesting trends in the scattering behavior.Comment: 10 pages, 5 figure

Four-nucleon scattering with a correlated Gaussian basis method

Elastic-scattering phase shifts for four-nucleon systems are studied in an $ab$-$initio$ type cluster model in order to clarify the role of the tensor force and to investigate cluster distortions in low energy $d+d$ and $t+p$ scattering. In the present method, the description of the cluster wave function is extended from a simple (0$s$) harmonic-oscillator shell model to a few-body model with a realistic interaction, in which the wave function of the subsystems are determined with the Stochastic Variational Method. In order to calculate the matrix elements of the four-body system, we have developed a Triple Global Vector Representation method for the correlated Gaussian basis functions. To compare effects of the cluster distortion with realistic and effective interactions, we employ the AV8$^{\prime}$ potential as a realistic interaction and the Minnesota potential as an effective interaction. Especially for $^1S_0$, the calculated phase shifts show that the $t+p$ and $h+n$ channels are strongly coupled to the $d+d$ channel for the case of the realistic interaction. On the contrary, the coupling of these channels plays a relatively minor role for the case of the effective interaction. This difference between both potentials originates from the tensor term in the realistic interaction. Furthermore, the tensor interaction makes the energy splitting of the negative parity states of $^4$He consistent with experiments. No such splitting is however reproduced with the effective interaction

Evidence for a dual-pathway, 2-hit genetic model for focal cortical dysplasia and epilepsy

Background and Objectives: The 2-hit model of genetic disease is well established in cancer, yet has only recently been reported to cause brain malformations associated with epilepsy. Pathogenic germline and somatic variants in genes in the mechanistic target of rapamycin (mTOR) pathway have been implicated in several malformations of cortical development. We investigated the 2-hit model by performing genetic analysis and searching for germline and somatic variants in genes in the mTOR and related pathways. Methods: We searched for germline and somatic pathogenic variants in 2 brothers with drug-resistant focal epilepsy and surgically resected focal cortical dysplasia (FCD) type IIA. Exome sequencing was performed on blood- and brain-derived DNA to identify pathogenic variants, which were validated by droplet digital PCR. In vitro functional assays of a somatic variant were performed. Results: Exome analysis revealed a novel, maternally inherited, germline pathogenic truncation variant (c.48delG; p.Ser17Alafs*70) in NPRL3 in both brothers. NPRL3 is a known FCD gene that encodes a negative regulator of the mTOR pathway. Somatic variant calling in brain-derived DNA from both brothers revealed a low allele fraction somatic variant (c.338C>T; p.Ala113Val) in the WNT2 gene in 1 brother, confirmed by droplet digital PCR. In vitro functional studies suggested a loss of WNT2 function as a consequence of this variant. A second somatic variant has not yet been found in the other brother. Discussion: We identify a pathogenic germline mTOR pathway variant (NPRL3) and a somatic variant (WNT2) in the intersecting WNT signaling pathway, potentially implicating the WNT2 gene in FCD and supporting a dual-pathway 2-hit model. If confirmed in other cases, this would extend the 2-hit model to pathogenic variants in different genes in critical, intersecting pathways in a malformation of cortical development. Detection of low allele fraction somatic second hits is challenging but promises to unravel the molecular architecture of FCDs.Mark F. Bennett, Michael S. Hildebrand, Sayaka Kayumi, Mark A. Corbett, Sachin Gupta, Zimeng Ye, Michael Krivanek, Rosemary Burgess, Olivia J. Henry, John A. Damiano, Amber Boys, Jozef Gécz, Melanie Bahlo, Ingrid E. Scheffer, and Samuel F. Berkovi