Dipole excited states in 11^{11}Li with complex scaling

The 1$^-$ excitations of the three--body halo nucleus $^{11}$Li are investigated. We use adiabatic hyperspherical expansion and solve the Faddeev equations in coordinate space. The method of complex scaling is used to compute the resonance states. The Pauli forbidden states occupied by core neutrons are excluded by constructing corresponding complex scaled phase equivalent two-body potentials. We use a recently derived neutron--core interaction consistent with known structure and reaction properties of $^{10}$Li and $^{11}$Li. The computed dipole excited states with $J^\pi=1/2^+$, $J^\pi=3/2^+$, and $J^\pi=5/2^+$ have energies ranging from 0.6 MeV to 1.0 MeV and widths between 0.15 MeV and 0.65 MeV. We investigate the dependence of the complex energies of these states on the $^{10}$Li spectrum. The finite spin 3/2 of the core and the resulting core-neutron spin-spin interaction are important. The connection with Coulomb dissociation experiments is discussed and a need for better measurements is pointed out.Comment: 28 pages, 6 figures, Nuclear Physics A, in pres

Unbound exotic nuclei studied by projectile fragmentation

We call "projectile fragmentation" of neutron halo nuclei the elastic breakup (diffraction) reaction, when the observable studied is the neutron-core relative energy spectrum. This observable has been measured in relation to the Coulomb breakup on heavy target and recently also on light targets. Such data enlighten the effect of the neutron final state interaction with the core of origin. Projectile fragmentation is studied here by a time dependent model for the excitation of a nucleon from a bound state to a continuum resonant state in a neutron-core complex potential which acts as a final state interaction. The final state is described by an optical model S-matrix so that both resonant and non resonant states of any continuum energy can be studied as well as deeply bound initial states. It turns out that due to the coupling between the initial and final states, the neutron-core free particle phase shifts are modified, in the exit channel, by an additional phase. Some typical numerical calculations for the relevant observables are presented and compared to experimental data. It is suggest that the excitation energy spectra of an unbound nucleus might reflect the structure of the parent nucleus from whose fragmentation they are obtained.Comment: Proceedings of the 11th Conference on Problems in Theoretican Nuclear Physics, Cortona, Italy, 2006. World Scientifi

Structure of unstable light nuclei

The structure of light nuclei out to the drip lines and beyond up to Z = 8 is interpreted in terms of the shell model. Special emphasis is given to the underlying supermultiplet symmetry of the p-shell nuclei which form cores for neutrons and protons added in sd-shell orbits. Detailed results are given on the wave functions, widths, and Coulomb energy shifts for a wide range of non-normal parity states in the p-shell.Comment: 21 pages, to appear in Nuclear Physics

Controlled density-downramp injection in a beam-driven plasma wakefield accelerator

This paper describes the utilization of beam-driven plasma wakefield acceleration to implement a high-quality plasma cathode via density-downramp injection in a short injector stage at the FLASHForward facility at DESY. Electron beams with charge of up to 105 pC and energy spread of a few percent were accelerated by a tunable effective accelerating field of up to 2.7 GV/m. The plasma cathode was operated drift-free with very high injection efficiency. Sources of jitter, the emittance and divergence of the resulting beam were investigated and modeled, as were strategies for performance improvements that would further increase the wide-ranging applications for a plasma cathode with the demonstrated operational stabilityComment: 11 pages, 9 figure

Capsaicin-Induced Changes in LTP in the Lateral Amygdala Are Mediated by TRPV1

The transient receptor potential vanilloid type 1 (TRPV1) channel is a well recognized polymodal signal detector that is activated by painful stimuli such as capsaicin. Here, we show that TRPV1 is expressed in the lateral nucleus of the amygdala (LA). Despite the fact that the central amygdala displays the highest neuronal density, the highest density of TRPV1 labeled neurons was found within the nuclei of the basolateral complex of the amygdala. Capsaicin specifically changed the magnitude of long-term potentiation (LTP) in the LA in brain slices of mice depending on the anesthetic (ether, isoflurane) used before euthanasia. After ether anesthesia, capsaicin had a suppressive effect on LA-LTP both in patch clamp and in extracellular recordings. The capsaicin-induced reduction of LTP was completely blocked by the nitric oxide synthase (NOS) inhibitor L-NAME and was absent in neuronal NOS as well as in TRPV1 deficient mice. The specific antagonist of cannabinoid receptor type 1 (CB1), AM 251, was also able to reduce the inhibitory effect of capsaicin on LA-LTP, suggesting that stimulation of TRPV1 provokes the generation of anandamide in the brain which seems to inhibit NO synthesis. After isoflurane anesthesia before euthanasia capsaicin caused a TRPV1-mediated increase in the magnitude of LA-LTP. Therefore, our results also indicate that the appropriate choice of the anesthetics used is an important consideration when brain plasticity and the action of endovanilloids will be evaluated. In summary, our results demonstrate that TRPV1 may be involved in the amygdala control of learning mechanisms

Merging Mouse Transcriptome Analyses with Parkinson's Disease Linkage Studies

The hallmark of Parkinson's disease (PD OMIM #168600) is the degeneration of the nigral dopaminergic system affecting approximately 1% of the human population older than 65. In pursuit of genetic factors contributing to PD, linkage and association studies identified several susceptibility genes. The majority of these genes are expressed by the dopamine-producing neurons in the substantia nigra. We, therefore, propose expression by these neurons as a selection criterion, to narrow down, in a rational manner, the number of candidate genes in orphan PD loci, where no mutation has been associated thus far. We determined the corresponding human chromosome locations of 1435 murine cDNA fragments obtained from murine expression analyses of nigral dopaminergic neurons and combined these data with human linkage studies. These fragments represent 19 genes within orphan OMIM PD loci. We used the same approach for independent association studies and determined the genes in neighborhood to the peaks with the highest LOD score value. Our approach did not make any assumptions about disease mechanisms, but it, nevertheless, revealed α-synuclein, NR4A2 (Nurr1), and the tau genes, which had previously been associated to PD. Furthermore, our transcriptome analysis identified several classes of candidate genes for PD mutations and may also provide insight into the molecular pathways active in nigral dopaminergic neurons

Intellectual enrichment and genetic modifiers of cognition and brain volume in Huntington's disease

An important step towards the development of treatments for cognitive impairment in ageing and neurodegenerative diseases is to identify genetic and environmental modifiers of cognitive function and understand the mechanism by which they exert an effect. In Huntington’s disease, the most common autosomal dominant dementia, a small number of studies have identified intellectual enrichment, i.e. a cognitively stimulating lifestyle and genetic polymorphisms as potential modifiers of cognitive function. The aim of our study was to further investigate the relationship and interaction between genetic factors and intellectual enrichment on cognitive function and brain atrophy in Huntington’s disease. For this purpose, we analysed data from Track-HD, a multi-centre longitudinal study in Huntington’s disease gene carriers and focused on the role of intellectual enrichment (estimated at baseline) and the genes FAN1, MSH3, BDNF, COMT and MAPT in predicting cognitive decline and brain atrophy. We found that carrying the 3a allele in the MSH3 gene had a positive effect on global cognitive function and brain atrophy in multiple cortical regions, such that 3a allele carriers had a slower rate of cognitive decline and atrophy compared with non-carriers, in agreement with its role in somatic instability. No other genetic predictor had a significant effect on cognitive function and the effect of MSH3 was independent of intellectual enrichment. Intellectual enrichment also had a positive effect on cognitive function; participants with higher intellectual enrichment, i.e. those who were better educated, had higher verbal intelligence and performed an occupation that was intellectually engaging, had better cognitive function overall, in agreement with previous studies in Huntington’s disease and other dementias. We also found that intellectual enrichment interacted with the BDNF gene, such that the positive effect of intellectual enrichment was greater in Met66 allele carriers than non-carriers. A similar relationship was also identified for changes in whole brain and caudate volume; the positive effect of intellectual enrichment was greater for Met66 allele carriers, rather than for non-carriers. In summary, our study provides additional evidence for the beneficial role of intellectual enrichment and carrying the 3a allele in MSH3 in cognitive function in Huntington’s disease and their effect on brain structure

Inherited Human ITK Deficiency Impairs IFN-γ Immunity and Underlies Tuberculosis

Inborn errors of IFN-γ immunity can underlie tuberculosis (TB). We report three patients from two kindreds without EBV viremia or disease but with severe TB and inherited complete ITK deficiency, a condition associated with severe EBV disease that renders immunological studies challenging. They have CD4+ αβ T lymphocytopenia with a concomitant expansion of CD4-CD8- double-negative (DN) αβ and Vδ2- γδ T lymphocytes, both displaying a unique CD38+CD45RA+T-bet+EOMES- phenotype. Itk-deficient mice recapitulated an expansion of the γδ T and DN αβ T lymphocyte populations in the thymus and spleen, respectively. Moreover, the patients\u27 T lymphocytes secrete small amounts of IFN-γ in response to TCR crosslinking, mitogens, or forced synapse formation with autologous B lymphocytes. Finally, the patients\u27 total lymphocytes secrete small amounts of IFN-γ, and CD4+, CD8+, DN αβ T, Vδ2+ γδ T, and MAIT cells display impaired IFN-γ production in response to BCG. Inherited ITK deficiency undermines the development and function of various IFN-γ-producing T cell subsets, thereby underlying TB