A convenient band-gap interpolation technique and an improved band line-up model for InGaAlAs on InP

The band-gap energy and the band line-up of InGaAlAs quaternary compound material on InP are essential information for the theoretical study of physical properties and the design of optoelectronics devices operating in the long-wavelength communication window. The band-gap interpolation of In1-x-y Ga (x) Al (y) As on InP is known to be a challenging task due to the observed discrepancy of experimental results arising from the bowing effect. Besides, the band line-up results of In1-x-y Ga (x) Al (y) As on InP based on previously reported models have limited success by far. In this work, we propose an interpolation solution using the single-variable surface bowing estimation interpolation method for the fitting of experimentally measured In1-x-y Ga (x) Al (y) As band-gap data with various degree of bowing using the same set of input parameters. The suggested solution provides an easier and more physically interpretable way to determine not only lattice matched, but also strained band-gap energy of In1-x-y Ga (x) Al (y) As on InP based on the experimental results. Interpolated results from this convenient method show a more favourable match to multiple independent experiment data sets measured under different temperature conditions as compared to those obtained from the commonly used weighted-sum approach. On top of that, extended framework of the model-solid theory for the band line-up of In1-x-y Ga (x) Al (y) As/InP heterostructure is proposed. Our model-solid theory band line-up result using the proposed extended framework has shown an improved accuracy over those without the extension. In contrast to some previously reported works, it is worth noting that the band line-up result based on our proposed extended model-solid theory has also shown to be more accurate than those given by Harrison's mode

The Theta+ (1540) as a heptaquark with the overlap of a pion, a kaon and a nucleon

We study the very recently discovered Theta+ (1540) at SPring-8, at ITEP and at CLAS-Thomas Jefferson Lab. We apply the same RGM techniques that already explained with success the repulsive hard core of nucleon-nucleon, kaon-nucleon exotic scattering, and the attractive hard core present in pion-nucleon and pion-pion non-exotic scattering. We find that the K-N repulsion excludes the Theta+ as a K-N s-wave pentaquark. We explore the Theta+ as a heptaquark, equivalent to a N+pi+K borromean bound-state, with positive parity and total isospin I=0. We find that the kaon-nucleon repulsion is cancelled by the attraction existing both in the pion-nucleon and pion-kaon channels. Although we are not yet able to bind the total three body system, we find that the Theta^+ may still be a heptaquark state. We conclude with predictions that can be tested experimentally.Comment: 5 pages, 5 figures, 2 tables, submitted to Phys. Rev. D, rapid communicatio

Frequency and Prognostic Impact of ALK Amplifications and Mutations in the European Neuroblastoma Study Group (SIOPEN) High-Risk Neuroblastoma Trial (HR-NBL1).

In neuroblastoma (NB), the ALK receptor tyrosine kinase can be constitutively activated through activating point mutations or genomic amplification. We studied ALK genetic alterations in high-risk (HR) patients on the HR-NBL1/SIOPEN trial to determine their frequency, correlation with clinical parameters, and prognostic impact. Diagnostic tumor samples were available from 1,092 HR-NBL1/SIOPEN patients to determine ALK amplification status (n = 330), ALK mutational profile (n = 191), or both (n = 571). Genomic ALK amplification (ALKa) was detected in 4.5% of cases (41 out of 901), all except one with MYCN amplification (MNA). ALKa was associated with a significantly poorer overall survival (OS) (5-year OS: ALKa [n = 41] 28% [95% CI, 15 to 42]; no-ALKa [n = 860] 51% [95% CI, 47 to 54], [P < .001]), particularly in cases with metastatic disease. ALK mutations (ALKm) were detected at a clonal level (> 20% mutated allele fraction) in 10% of cases (76 out of 762) and at a subclonal level (mutated allele fraction 0.1%-20%) in 3.9% of patients (30 out of 762), with a strong correlation between the presence of ALKm and MNA (P < .001). Among 571 cases with known ALKa and ALKm status, a statistically significant difference in OS was observed between cases with ALKa or clonal ALKm versus subclonal ALKm or no ALK alterations (5-year OS: ALKa [n = 19], 26% [95% CI, 10 to 47], clonal ALKm [n = 65] 33% [95% CI, 21 to 44], subclonal ALKm (n = 22) 48% [95% CI, 26 to 67], and no alteration [n = 465], 51% [95% CI, 46 to 55], respectively; P = .001). Importantly, in a multivariate model, involvement of more than one metastatic compartment (hazard ratio [HR], 2.87; P < .001), ALKa (HR, 2.38; P = .004), and clonal ALKm (HR, 1.77; P = .001) were independent predictors of poor outcome. Genetic alterations of ALK (clonal mutations and amplifications) in HR-NB are independent predictors of poorer survival. These data provide a rationale for integration of ALK inhibitors in upfront treatment of HR-NB with ALK alterations