Photoelectron spectroscopy of NpPd3 and PuPd3

We present the results of x-ray and ultraviolet photoelectron spectroscopy of NpPd3 and PuPd3. The spectra indicate that for both compounds, the 5f electrons are well localized on the actinide sites. Comparison with bulk measurements indicates that for NpPd3 the electrons have a valence of Np3+ and thus a ground state 5f4 with a Hund's rules 5I4 configuration. Similarly for PuPd3, we find a Pu3+ valence, 5f5 ground state and a Hund's rules 6H5/2 configuration

Process control plan for 242-A Evaporator Campaign 95-1

The wastes from tanks 106-AP, 107-AP, and 106-AW have been selected to be candidate feed wastes for Evaporator Campaign 95-1. The wastes in tank 106-AP and 107-AP are primarily from B-Plant strontium processing and PUREX neutralized cladding removal, respectively. The waste in tank 106-AW originated primarily from the partially concentrated product from 242-A Evaporator Campaign 94-2. Approximately 8.67 million liters of waste from these tanks will be transferred to tank 102-AW during the campaign. Tank 102-AW is the dedicated waste feed tank for the evaporator and currently contains 647,000 liters of processable waste. The purpose of the 242-A Evaporator Campaign 95-1 Process Control Plan (hereafter referred to as PCP) is to certify that the wastes in tanks 106-AP, 107-AP, 102-AW, and 106-AW are acceptable for processing through evaporator and provide a general description of process strategies and activities which will take place during Campaign 95-1. The PCP also summarizes and presents a comprehensive characterization of the wastes in these tanks

Hereditary pancreatitis in children: surgical implications with special regard to genetic background.

PURPOSE: Hereditary pancreatitis (HP) is the primary etiology of chronic pancreatitis during childhood, progressing through recurrent episodes of acute pancreatitis and finally leading to pancreatic insufficiencies. Hereditary pancreatitis is because of mutations of the cationic trypsinogen (PRSS1) gene. Some other genes, such as SPINK1 or CFTR, have been associated with familial idiopathic chronic pancreatitis. The aim of our study was to clearly define diagnostic and therapeutic strategies for HP patients, through an analysis of our study group and a review of the literature. METHODS: All children admitted from 1995 to 2007 with a final diagnosis of hereditary pancreatitis were restrospectively included in the study. We analyzed all medical records with special attention given to cases involving genetic screening (PRSS1, SPINK1, and CFTR genes). RESULTS: Ten children were included. Eight had HP with PRSS1 mutation, 2 of them without a familial history of chronic pancreatitis. The 2 others patients had SPINK1 mutations. Three HP patients were operated on for acute complications of pancreatitis and are well with a mean follow-up of 5.5 years. No patient had pancreatic insufficiencies or weight loss. CONCLUSIONS: Hereditary pancreatitis is associated with severe pancreatitis, with a greater risk of developing pancreatic cancer. It must therefore be diagnosed correctly and treated to prevent its considerable complications

Cytogenetic and molecular analysis of the acute monocytic leukemia cell line THP-1 with an MLL-AF9 translocation

Cell lines derived from patients with leukemia are used in many molecular biology studies. Here we report the cytogenetic analysis of the THP-1 cell line using G-banding, fluorescence in situ hybridization (FISH), and spectral karyotyping (SKY), and the molecular characterization of the MLL-AF9 rearrangement by RT-PCR. The THP-1 cell line was established from the peripheral blood of a 1-year-old boy with acute monocytic leukemia (AML-M5). THP-1 is near-diploid and consists of two related subclones with a number of aberrations, including the t(9;11), associated with AML M5. The use of FISH allowed us to identify and characterize otherwise hidden cytogenetic rearrangements, which include duplication of the 3' portion of MLL in the derivative 9 chromosome and a deletion of the 5' portion of the AF9 gene involved in the translocation. In addition to confirming the FISH results, SKY allowed for a more precise characterization of the karyotype of THP-1 and allowed us to identify other abnormalities in this cell line, including der(1)t(1;12), der(20)t(1;20), deletions 6p, 12p, and 17p, trisomy 8, and monosomy 10. Sequencing of the RT-PCR product showed a direct in-frame fusion product on the derivative chromosome 11 between exon 6 (exon 9) of MLL and exon 5 of AF9, which is most commonly involved in MLL-AF9 translocations. This study demonstrates that combining different techniques to achieve a more precise characterization of the THP-1 cell line provides important information that will be valuable for understanding the critical events required for leukemogenesis

Sums of hermitian squares and the BMV conjecture

Recently Lieb and Seiringer showed that the Bessis-Moussa-Villani conjecture from quantum physics can be restated in the following purely algebraic way: The sum of all words in two positive semidefinite matrices where the number of each of the two letters is fixed is always a matrix with nonnegative trace. We show that this statement holds if the words are of length at most 13. This has previously been known only up to length 7. In our proof, we establish a connection to sums of hermitian squares of polynomials in noncommuting variables and to semidefinite programming. As a by-product we obtain an example of a real polynomial in two noncommuting variables having nonnegative trace on all symmetric matrices of the same size, yet not being a sum of hermitian squares and commutators.Comment: 21 pages; minor changes; a companion Mathematica notebook is now available in the source fil

Recovery of 150-250 MeV/nuc Cosmic Ray Helium Nuclei Intensities Between 2004-2010 Near the Earth, at Voyager 2 and Voyager 1 in the Heliosheath - A Two Zone Helioshpere

The recovery of cosmic ray He nuclei of energy ~150-250 MeV/nuc in solar cycle #23 from 2004 to 2010 has been followed at the Earth using IMP and ACE data and at V2 between 74-92 AU and also at V1 beyond the heliospheric termination shock (91-113 AU). The correlation coefficient between the intensities at the Earth and at V1 during this time period is remarkable (0.921), after allowing for a ~0.9 year delay due to the solar wind propagation time from the Earth to the outer heliosphere. To describe the intensity changes and to predict the absolute intensities measured at all three locations we have used a simple spherically symmetric (no drift) two-zone heliospheric transport model with specific values for the diffusion coefficient in both the inner and outer zones. The diffusion coefficient in the outer zone, assumed to be the heliosheath from about 90 to 120 (130) AU, is determined to be ~5 times smaller than that in the inner zone out to 90 AU. This means the Heliosheath acts much like a diffusing barrier in this model. The absolute magnitude of the intensities and the intensity changes at V1 and the Earth are described to within a few percent by a diffusion coefficient that varies with time by a factor ~4 in the inner zone and only a factor of ~1.5 in the outer zone over the time period from 2004-2010. For V2 the observed intensities follow a curve that is as much as 25% higher than the calculated intensities at the V2 radius and at times the observed V2 intensities are equal to those at V1. At least one-half of the difference between the calculated and observed intensities between V1 and V2 can be explained if the heliosphere is squashed by ~10% in distance (non-spherical) so that the HTS location is closer to the Sun in the direction of V2 compared to V1.Comment: 13 Pages, 8 Figure

A t(11;15) fuses MLL to two different genes, AF15q14 and a novel gene MPFYVE on chromosome 15

The mixed lineage leukemia gene (MLL, also known as HRX, ALL-1 and Htrx) located at 11q23 is involved in translocations with over 40 different chromosomal bands in a variety of leukemia subtypes. Here we report our analysis of a rare but recurring translocation, t(11;15)(q23;q14). This translocation has been described in a small subset of cases with both acute myeloblastic leukemia and ALL. Recent studies have shown that MLL is fused to AF15q14 in the t(11;15). Here we analyse a sample from another patient with this translocation and confirm the presence of an MLL-AF15q14 fusion. However, we have also identified and cloned another fusion transcript from the same patient sample. In this fusion transcript, MLL is fused to a novel gene, MLL partner containing FYVE domain (MPFYVE). Both MLL-AF15q14 and MLL-MPFYVE are in-frame fusion transcripts with the potential to code for novel fusion proteins. MPFYVE is also located on chromosome 15, approximately 170 kb telomeric to AF15q14. MPFYVE contains a highly conserved motif, the FYVE domain which, in other proteins, has been shown to bind to phosphotidyl-inositol-3 phosphate (PtdIns(3)P). The MLL-MPFYVE fusion may be functionally important in the leukemia process in at least some patients containing this translocation