The spin structure of the Lambda hyperon in quenched lattice QCD

It has been suggested to use the production of Lambda hyperons for investigating the nucleon spin structure. The viability of this idea depends crucially on the spin structure of the Lambda. Using nonperturbatively O(a) improved Wilson fermions in the quenched approximation we have studied matrix elements of two-quark operators in the Lambda. We present results for the axial vector current, which give us the contributions of the u, d, and s quarks to the Lambda spin.Comment: Lattice2001(matrixelement), 3 pages, 2 figure

Depopulation of dense α-synuclein aggregates is associated with rescue of dopamine neuron dysfunction and death in a new Parkinson's disease model.

Parkinson's disease (PD) is characterized by the presence of α-synuclein aggregates known as Lewy bodies and Lewy neurites, whose formation is linked to disease development. The causal relation between α-synuclein aggregates and PD is not well understood. We generated a new transgenic mouse line (MI2) expressing human, aggregation-prone truncated 1-120 α-synuclein under the control of the tyrosine hydroxylase promoter. MI2 mice exhibit progressive aggregation of α-synuclein in dopaminergic neurons of the substantia nigra pars compacta and their striatal terminals. This is associated with a progressive reduction of striatal dopamine release, reduced striatal innervation and significant nigral dopaminergic nerve cell death starting from 6 and 12 months of age, respectively. In the MI2 mice, alterations in gait impairment can be detected by the DigiGait test from 9 months of age, while gross motor deficit was detected by rotarod test at 20 months of age when 50% of dopaminergic neurons in the substantia nigra pars compacta are lost. These changes were associated with an increase in the number and density of 20-500 nm α-synuclein species as shown by dSTORM. Treatment with the oligomer modulator anle138b, from 9 to 12 months of age, restored striatal dopamine release, prevented dopaminergic cell death and gait impairment. These effects were associated with a reduction of the inner density of large α-synuclein aggregates and an increase in dispersed small α-synuclein species as revealed by dSTORM. The MI2 mouse model recapitulates the progressive dopaminergic deficit observed in PD, showing that early synaptic dysfunction is associated to fine behavioral motor alterations, precedes dopaminergic axonal loss and neuronal death that become associated with a more consistent motor deficit upon reaching a certain threshold. Our data also provide new mechanistic insight for the effect of anle138b's function in vivo supporting that targeting α-synuclein aggregation is a promising therapeutic approach for PD

Color coherent phenomena on nuclei and the QCD evolution equation

We review the phenomenon of color coherence in quantum chromodynamics (QCD), its implications for hard and soft processes with nuclei, and its experimental manifestations. The relation of factorization theorems in QCD with color coherence phenomena in deep inelastic scattering (DIS) and color coherence phenomena in hard exclusive processes is emphasized. Analyzing numerically the QCD evolution equation for conventional and skewed parton densities in nuclei, we study the onset of generalized color transparency and nuclear shadowing of the sea quark and gluon distributions in nuclei as well as related phenomena. Such novel results as the dependence of the effective coherence length on $Q^2$ and general trends of the QCD evolution are discussed. The limits of the applicability of the QCD evolution equation at small Bjorken $x$ are estimated by comparing the inelastic quark-antiquark- and two gluon-nucleon (nucleus) cross sections, calculated within the DGLAP approximation, with the dynamical boundaries, which follow from the unitarity of the $S$ matrix for purely QCD interactions. We also demonstrate that principles of color coherence play an important role in the processes of soft diffraction off nuclei.Comment: 58 pages, 19 figures, Revtex. Minor editor's changes, final version published in J.Phys. G27 (2001) R23-6

Tensor interaction constraints from beta decay recoil spin asymmetry of trapped atoms

We have measured the angular distribution of recoiling daughter nuclei emitted from the Gamow-Teller $\beta$ decay of spin-polarized $^{80}$Rb. The asymmetry of this distribution vanishes to lowest order in the Standard Model (SM) in pure Gamow-Teller decays, producing an observable very sensitive to new interactions. We measure the non-SM contribution to the asymmetry to be $A_{T}$= 0.015 $\pm$ 0.029 (stat) $\pm$ 0.019 (syst), consistent with the SM prediction. We constrain higher-order SM corrections using the measured momentum dependence of the asymmetry, and their remaining uncertainty dominates the systematic error. Future progress in determining the weak magnetism term theoretically or experimentally would reduce the final errors. We describe the resulting constraints on fundamental 4-Fermi tensor interactions.Comment: 11 pages, 13 figures; v2 published in Phys. Rev. C, with referee clarifications and figures improved for black-and-whit