Breakdown of Burton-Prim-Slichter approach and lateral solute segregation in radially converging flows

A theoretical study is presented of the effect of a radially converging melt flow, which is directed away from the solidification front, on the radial solute segregation in simple solidification models. We show that the classical Burton-Prim-Slichter (BPS) solution describing the effect of a diverging flow on the solute incorporation into the solidifying material breaks down for the flows converging along the solidification front. The breakdown is caused by a divergence of the integral defining the effective boundary layer thickness which is the basic concept of the BPS theory. Although such a divergence can formally be avoided by restricting the axial extension of the melt to a layer of finite height, radially uniform solute distributions are possible only for weak melt flows with an axial velocity away from the solidification front comparable to the growth rate. There is a critical melt velocity for each growth rate at which the solution passes through a singularity and becomes physically inconsistent for stronger melt flows. To resolve these inconsistencies we consider a solidification front presented by a disk of finite radius $R_0$ subject to a strong converging melt flow and obtain an analytic solution showing that the radial solute concentration depends on the radius $r$ as $\sim\ln^{1/3}(R_0/r)$ and $\sim\ln(R_0/r)$ close to the rim and at large distances from it. The logarithmic increase of concentration is limited in the vicinity of the symmetry axis by the diffusion becoming effective at a distance comparable to the characteristic thickness of the solute boundary layer. The converging flow causes a solute pile-up forming a logarithmic concentration peak at the symmetry axis which might be an undesirable feature for crystal growth processes.Comment: 15 pages, 5 figure

Constraint of the Nuclear Dissipation Coefficient in Fission of Hypernuclei

Experimental studies of nuclear fission induced by fusion, transfer, spallation, fragmentation, and electromagnetic reactions in combination with state-of-the-art calculations are successful to investigate the nuclear dissipation mechanism in normal nuclear matter, containing only nucleons. The dissipation mechanism has been widely studied by the use of many different fission observables and nowadays the dissipation coefficients involved in transport theories are well constrained. However, the existence of hypernuclei and the possible presence of hyperons in neutron stars make it necessary to extend the investigation of the nuclear dissipation coefficient to the strangeness sector. In this Letter, we use fission reactions of hypernuclei to constrain for the first time the dissipation coefficient in hypernuclear matter, observing that this coefficient increases a factor of 6 in presence of a single $\Lambda$-hyperon with respect to normal nuclear matter.Comment: 6 pages, 2 figure

Cerebrospinal fluid phospho-tau T217 outperforms T181 as a biomarker for the differential diagnosis of Alzheimer\u27s disease and PET amyloid-positive patient identification

BACKGROUND: Cerebrospinal fluid biomarker profiles characterized by decreased amyloid-beta peptide levels and increased total and phosphorylated tau levels at threonine 181 (pT181) are currently used to discriminate between Alzheimer\u27s disease and other neurodegenerative diseases. However, these changes are not entirely specific to Alzheimer\u27s disease, and it is noteworthy that other phosphorylated isoforms of tau, possibly more specific for the disease process, have been described in the brain parenchyma of patients. The precise detection of these isoforms in biological fluids remains however a challenge. METHODS: In the present study, we used the latest quantitative mass spectrometry approach, which achieves a sensitive detection in cerebrospinal fluid biomarker of two phosphorylated tau isoforms, pT181 and pT217, and first analyzed a cohort of probable Alzheimer\u27s disease patients and patients with other neurological disorders, including tauopathies, and a set of cognitively normal controls. We then checked the validity of our results on a second cohort comprising cognitively normal individuals and patients with mild cognitive impairments and AD stratified in terms of their amyloid status based on PiB-PET imaging methods. RESULTS: In the first cohort, pT217 but not pT181 differentiated between Alzheimer\u27s disease patients and those with other neurodegenerative diseases and control subjects much more specificity and sensitivity than pT181. T217 phosphorylation was increased by 6.0-fold in patients with Alzheimer\u27s disease whereas T181 phosphorylation was only increased by 1.3-fold, when compared with control subjects. These results were confirmed in the case of a second cohort, in which the pT217 cerebrospinal fluid levels marked out amyloid-positive patients with a sensitivity and a specificity of more than 90% (AUC 0.961; CI 0.874 to 0.995). The pT217 concentrations were also highly correlated with the PiB-PET values (correlation coefficient 0.72; P \u3c 0.001). CONCLUSIONS: Increased cerebrospinal fluid pT217 levels, more than those of pT181, are highly specific biomarkers for detecting both the preclinical and advanced forms of Alzheimer\u27s disease. This finding should greatly improve the diagnosis of Alzheimer\u27s disease, along with the correlations found to exist between pT217 levels and PiB-PET data. It also suggests that pT217 is a promising potential target for therapeutic applications and that a link exists between amyloid and tau pathology