The 4^4He(e,e′p)(e,e'p) Cross Section at Large Missing Energy

The $(e,e'p)$ reaction on $^{4}{He}$ nuclei was studied in kinematics designed to emphasize effects of nuclear short-range correlations. The measured cross sections display a peak in the kinematical regions where two-nucleon processes are expected to dominate. Theoretical models incorporating short-range correlation effects agree reasonably with the data.Comment: 4 pages LaTeX, using espcrc1.sty and wrapfig.sty (included), two figures. Talk presented by J. Templon at the 15th Int. Conf. on Few-Body Problems in Physics, Groningen, The Netherlands, 22-26 July, 199

Electron-induced neutron knockout from 4^{4}He

The differential cross section for electron-induced neutron knockout in the reaction 4He(e,e′n)3He has been measured for the first time with a statistical accuracy of 11%. The experiment was performed in quasielastic kinematics at a momentum transfer of 300  MeV/c and in the missing-momentum range of 25–70  MeV/c. The comparison of the data with theoretical calculations shows an impressive increase of the cross section resulting from final state interaction effects. Specifically , the p−n charge-exchange process dominates the cross section in this kinematical regime. (APS

Signatures for short-range correlations in {16}O, observed in the reaction {16}O(e,e'pp){14}C.

The reaction O-16(e,e'pp)C-14 has been studied at a transferred four-momentum (omega,\q\) = (210 MeV, 300 MeV/c). The differential cross sections for the transitions to the ground state and the lowest excited states in C-14 were determined as a function of the momentum of the recoiling C-14 nucleus and the angle between the momentum of the proton emitted in the forward direction and the momentum transfer q. A comparison of the data to the results of calculations, performed with a microscopic model, shows clear signatures for short-range correlations in the O-16 ground state

Untargeted metabolic analysis in dried blood spots reveals metabolic signature in 22q11.2 deletion syndrome

Contains fulltext : 252344.pdf (Publisher’s version ) (Open Access)The 22q11.2 deletion syndrome (22q11.2DS) is characterized by a well-defined microdeletion and is associated with increased risk of neurodevelopmental phenotypes including autism spectrum disorders (ASD) and intellectual impairment. The typically deleted region in 22q11.2DS contains multiple genes with the potential of altering metabolism. Deficits in metabolic processes during early brain development may help explain the increased prevalence of neurodevelopmental phenotypes seen in 22q11.2DS. However, relatively little is known about the metabolic impact of the 22q11.2 deletion, while such insight may lead to increased understanding of the etiology. We performed untargeted metabolic analysis in a large sample of dried blood spots derived from 49 22q11.2DS patients and 87 controls, to identify a metabolic signature for 22q11.2DS. We also examined trait-specific metabolomic patterns within 22q11.2DS patients, focusing on intelligence (intelligence quotient, IQ) and ASD. We used the Boruta algorithm to select metabolites distinguishing patients from controls, patients with ASD from patients without, and patients with an IQ score in the lowest range from patients with an IQ score in the highest range. The relevance of the selected metabolites was visualized with principal component score plots, after which random forest analysis and logistic regression were used to measure predictive performance of the selected metabolites. Analysis yielded a distinct metabolic signature for 22q11.2DS as compared to controls, and trait-specific (IQ and ASD) metabolomic patterns within 22q11.2DS patients. The metabolic characteristics of 22q11.2DS provide insights in biological mechanisms underlying the neurodevelopmental phenotype and may ultimately aid in identifying novel therapeutic targets for patients with developmental disorders