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Even mass neutron-rich niobium isotopes are among the principal contributors to the reactor antineutrino energy spectrum. They are also among the most challenging to measure due to the refractory nature of niobium, and because they exhibit isomeric states lying very close in energy. The β-intensity distributions of ^{100gs,100m}Nb and ^{102gs,102m}Nb β decays have been determined using the total absorption γ-ray spectroscopy technique. The measurements were performed at the upgraded Ion Guide Isotope Separator On-Line facility at the University of Jyväskylä. Here, the double Penning trap system JYFLTRAP was employed to disentangle the β decay of the isomeric states. The new data obtained in this challenging measurement have a large impact in antineutrino summation calculations. For the first time the discrepancy between the summation model and the reactor antineutrino measurements in the region of the shape distortion has been reduced.

The structure of deformed neutron-rich nuclei in the rare-earth region is of significant interest for both the astrophysics and nuclear structure fields. At present, a complete explanation for the observed peak in the elemental abundances at A∼160 eludes astrophysicists, and models depend on accurate quantities, such as masses, lifetimes, and branching ratios of deformed neutron-rich nuclei in this region. Unusual nuclear structure effects are also observed, such as the unexpectedly low energies of the first 2^{+} levels in some even-even nuclei at N=98. In order to address these issues, mass and β-decay spectroscopy measurements of the ^{160}Eu_{97} and ^{162}Eu_{99} nuclei were performed at the Californium Rare Isotope Breeder Upgrade radioactive beam facility at Argonne National Laboratory. Evidence for a gap in the single-particle neutron energies at N=98 and for large deformation (β_{2}∼0.3) is discussed in relation to the unusual phenomena observed at this neutron number.

The study was aimed to determine the role of ki- 67 and vimentin markers in choosing the tactics of surgical treatment of patients with metastatic kidney cancer. The analysis of the results of treatment of 71 patients with metastatic renal cell carcinoma was performed. The first group included 16 (22.5%) patients, who underwent complete removal of distant metastases after nephrectomy. The second group consisted of 55 (77.5 %) patients who underwent cytoreductive nephrectomy only. Immunohistochemical analyses of tissues removed were performed in all patients for the evaluation of ki-67 and vimentin expression levels. When comparing the outcomes of patients after complete removal of metastases depending on the vimentin and ki-67 expression levels (< 10% and > 10%), a significant increase in the cumulative survival in the case of absence of vimentin and ki-67 expression of <10 % (log - rank test, P = 0.0001) was revealed. The same pattern was noted in the group of patients who underwent nephrectomy only. In the absence of expression of vimentin and ki-67 < 10%, survival rate in patients who underwent metastasectomy after nephrectomy was significantly higher compared with patients who underwent nephrectomy only (P = 0.001). In the case of positive expression of vimentin and ki-67 > 10%, differences in survival rate in these groups were not observed (P > 0.082). Thus, an association between the vimentin and ki-67 expression levels and the degree of spread of metastatic renal cell carcinoma was identified: the high level of expression of these markers precludes the increase of life expectancy of patients after removal of all metastases.

Pure samples of (131m)Xe, (133m)Xe, (133)Xe and (135)Xe facilitate the calibration and testing of noble gas sampler stations and related laboratory instrumentation. We have earlier reported a Penning trap-based production method for pure (133m)Xe and (133)Xe samples. Here we complete the work by reporting the successful production of pure (131m)Xe and (135)Xe samples using the same technique. In addition, we present data on xenon release from graphite., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Atomic masses of the neutron-rich isotopes (121-128)Cd, (129,131)In, (130-135)Sn, (131-136)Sb, and (132-140)Te have been measured with high precision (10 ppb) using the Penning-trap mass spectrometer JYFLTRAP. Among these, the masses of four r-process nuclei (135)Sn, (136)Sb, and (139,140)Te were measured for the first time. An empirical neutron pairing gap expressed as the odd-even staggering of isotopic masses shows a strong quenching across N = 82 for Sn, with a Z dependence that is unexplainable by the current theoretical models.

WT2 is defined by maternal-specific loss of heterozygosity (LOH) on chromosome 11p15.5 in Wilms' tumors (WTs). The imprinted H19 gene, in this region, is silenced and hypermethylated in most WTs, and this is linked to pathological biallelic expression of IGF2. However, H19 and IGF2 lie within a larger imprinted domain, and the gene specificity of H19 epimutation has been a persistent question. To address this, we assessed LOH, gene expression and DNA methylation at multiple sites in and around the imprinted domain. LOH mapping showed that the entire domain, including IGF2/H19, is within the minimal WT2 region. Genes within the domain, including IPL/TSSC3/BWR1C, IMPT1/ORCTL2/BWR1A/TSSC5, KvLQT1/KCNA9 and TAPA1/CD81, as well as the zinc finger gene ZNF195/ZNFP104 near the centromeric border, were expressed persistently in many WTs. DNA hypermethylation was not detected with 5" upstream probes for IPL, IMPT1, KvLQT1 and ZNF195 in WTs or WT-associated kidneys. Fully developed WTs showed variable hypomethylation at an imprinted CpG island in a KvLQT1 intron, but this was only complete in the cases with LOH and was not observed in pre-neoplastic WT-associated kidneys with H19 epimutation. Analysis of the corresponding region of mouse chromosome 7 using methyltransferase-hypomorphic mice showed that the H19 imprint was fully erased, but that the allelic bias at Ipl, Impt1, p57 Kip2 and, to a lesser extent, Kvlqt1, persisted. Pre-existing massive allelic asymmetry for DNA methylation and hyper-dependence of transcription on methylation status may underlie the mechanism of gene-specific silencing of H19 in Wilms' tumorigenesis.