Insensitivity of the elastic proton-nucleus reaction to the neutron radius of 208Pb

The sensitivity--or rather insensitivity--of the elastic proton-nucleus reaction to the neutron radius of 208Pb is investigated using a non-relativistic impulse-approximation approach. The energy region (Tlab=500 MeV and Tlab=800 MeV) is selected so that the impulse approximation may be safely assumed. Therefore, only free nucleon-nucleon scattering data are used as input for the optical potential. Further, the optical potential includes proton and neutron ground-state densities that are generated from accurately-calibrated models. Even so, these models yield a wide range of values (from 0.13 fm to 0.28 fm) for the poorly known neutron skin thickness in 208Pb. An excellent description of the experimental cross section is obtained with all neutron densities. We have invoked analytic insights developed within the eikonal approximation to understand the insensitivity of the differential cross section to the various neutron densities. As the diffractive oscillations of the cross sections are controlled by the matter radius of the nucleus, the large spread in the neutron skin among the various models gets diluted into a mere 1.5% difference in the matter radius. This renders ineffective the elastic reaction as a precision tool for the measurement of neutron radii.Comment: 17 pages with 5 figure

Modelling nucleon-nucleon scattering above 1 GeV

Motivated by the recent measurement of proton-proton spin-correlation parameters up to 2.5 GeV laboratory energy, we investigate models for nucleon-nucleon (NN) scattering above 1 GeV. Signatures for a gradual failure of the traditional meson model with increasing energy can be clearly identified. Since spin effects are large up to tens of GeV, perturbative QCD cannot be invoked to fix the problems. We discuss various theoretical scenarios and come to the conclusion that we do not have a clear phenomenological understanding of the spin-dependence of the NN interaction above 1 GeV.Comment: 36 pages, 8 figure

Diagnosis and management of glutaric aciduria type I – revised recommendations

Glutaric aciduria type I (synonym, glutaric acidemia type I) is a rare organic aciduria. Untreated patients characteristically develop dystonia during infancy resulting in a high morbidity and mortality. The neuropathological correlate is striatal injury which results from encephalopathic crises precipitated by infectious diseases, immunizations and surgery during a finite period of brain development, or develops insidiously without clinically apparent crises. Glutaric aciduria type I is caused by inherited deficiency of glutaryl-CoA dehydrogenase which is involved in the catabolic pathways of L-lysine, L-hydroxylysine and L-tryptophan. This defect gives rise to elevated glutaric acid, 3-hydroxyglutaric acid, glutaconic acid, and glutarylcarnitine which can be detected by gas chromatography/mass spectrometry (organic acids) or tandem mass spectrometry (acylcarnitines). Glutaric aciduria type I is included in the panel of diseases that are identified by expanded newborn screening in some countries. It has been shown that in the majority of neonatally diagnosed patients striatal injury can be prevented by combined metabolic treatment. Metabolic treatment that includes a low lysine diet, carnitine supplementation and intensified emergency treatment during acute episodes of intercurrent illness should be introduced and monitored by an experienced interdisciplinary team. However, initiation of treatment after the onset of symptoms is generally not effective in preventing permanent damage. Secondary dystonia is often difficult to treat, and the efficacy of available drugs cannot be predicted precisely in individual patients. The major aim of this revision is to re-evaluate the previous diagnostic and therapeutic recommendations for patients with this disease and incorporate new research findings into the guideline

Probabilistic (Bayesian) Modeling of Gene Expression in Transplant Glomerulopathy

Transplant glomerulopathy (TG) is associated with rapid decline in glomerular filtration rate and poor outcome. We used low-density arrays with a novel probabilistic analysis to characterize relationships between gene transcripts and the development of TG in allograft recipients. Retrospective review identified TG in 10.8% of 963 core biopsies from 166 patients; patients with stable function were studied for comparison. The biopsies were analyzed for expression of 87 genes related to immune function and fibrosis by using real-time PCR, and a Bayesian model was generated and validated to predict histopathology based on gene expression. A total of 57 individual genes were increased in TG compared with stable function biopsies (P < 0.05). The Bayesian analysis identified critical relationships between ICAM-1, IL-10, CCL3, CD86, VCAM-1, MMP-9, MMP-7, and LAMC2 and allograft pathology. Moreover, Bayesian models predicted TG when derived from either immune function (area under the curve [95% confidence interval] of 0.875 [0.675 to 0.999], P = 0.004) or fibrosis (area under the curve [95% confidence interval] of 0.859 [0.754 to 0.963], P < 0.001) gene networks. Critical pathways in the Bayesian models were also analyzed by using the Fisher exact test and had P values <0.005. This study demonstrates that evaluating quantitative gene expression profiles with Bayesian modeling can identify significant transcriptional associations that have the potential to support the diagnostic capability of allograft histology. This integrated approach has broad implications in the field of transplant diagnostics