An \u3ci\u3eab initio\u3c/i\u3e Potential Energy Surface for the Ne-CO

A new ab initio two-dimensional potential energy surface for the Ne-CO interaction is described. The surface was obtained by the supermolecule method at the CCSD(T) level of theory. It is compared with several experimental data sets and with the symmetry-adapted perturbation theory (SAPT) surface of Moszynski et al. [J. Phys. Chem. A 101, 4690 (1997)]. The new surface gives modestly better predictions of experimental results that depend on close approach of Ne to CO, but does not describe the ground state geometry as well as the SAPT surface

Effects of global O-GlcNAcylation on galectin gene-expression profiles in human cancer cell lines

Background/Aim: The effects of O-linked β-N-acetyl-D-glucosamine (O-GlcNAc) transferase (OGT) and O-GlcNAcase (OGA) inhibitors on galectin gene expression profiles were examined in MCF7, HT-29, and HL-60 cancer cell lines. Materials and Methods: Cell cultures were treated for 24 h with OGA inhibitor thiamet G or OGT inhibitor 2-acetamido-1,3,4,6-tetra-O-acetyl-2-deoxy-5-thio-α-D-glucopyranose, and global O-GlcNAc levels and expression of galectin genes were determined using an immunodot blot assay and real-time quantitative polymerase chain reaction. Results: Two galectin genes, LGALS3 in MCF7 cells and LGALS12 in HL-60 cells, were up-regulated by O-GlcNAc, whereas other cell-specific galectins were unresponsive to changes in O-GlcNAc level. Of interest, basal levels of O-GlcNAc in resting HL-60 and HT-29 cells were significantly higher than those in cells differentiated into neutrophilic or enterocytic lineages, respectively. Conclusion: O-GlcNAc-mediated signaling pathways may be involved in regulating the expression of only a limited number of galectin genes. Additional O-GlcNAc-dependent mechanisms may work at the protein level (galectin secretion and intracellular localization) and warrant further investigation

A case of carotid body paraganglioma and haemangioblastoma of the spinal cord in a patient with the N131K missense mutation in the VHL gene

The article describes paraganglioma case in woman with von Hippel–Lindau disease. She was found to be a carrier of a rare germline mutation in the VHL gene (393C>A; N131K). The patient developed large, untypical for von Hippel–Lindau disease, carotid body paraganglioma at the common carotid artery bifurcation. The carotid body paraganglioma coexisted with the haemangioblastoma situated intramedullary in region C5/C6. The haemangioblastoma reached the right-sided dorsal part of the spinal cord in section C5/C6. It produced radicular symptoms within C5/C6, followed by the later paresis of the right limbs. The haemangioblastoma was resected completely. Twelve months after the operation, the spinal symptoms receded and the carotid body paraganglioma still was asymptomatic. The current case of carotid body paraganglioma in patient with the 393C>A (N131K) missense mutation in the VHL gene, supports association of this specific mutation and VHL disease type 2, and suggests its correlation with susceptibility to paragangliomas

On the Clustering of Sub-millimeter Galaxies

We measure the angular two-point correlation function of sub-millimeter galaxies (SMGs) from 1.1-millimeter imaging of the COSMOS field with the AzTEC camera and ASTE 10-meter telescope. These data yields one of the largest contiguous samples of SMGs to date, covering an area of 0.72 degrees^2 down to a 1.26 mJy/beam (1-sigma) limit, including 189 (328) sources with S/N greater than 3.5 (3). We can only set upper limits to the correlation length r_0, modeling the correlation function as a power-law with pre-assigned slope. Assuming existing redshift distributions, we derive 68.3% confidence level upper limits of r_0 < 6-8 h^-1 Mpc at 3.7 mJy, and r_0 < 11-12 h^-1 Mpc at 4.2 mJy. Although consistent with most previous estimates, these upper limits imply that the real r_0 is likely smaller. This casts doubts on the robustness of claims that SMGs are characterized by significantly stronger spatial clustering, (and thus larger mass), than differently selected galaxies at high-redshift. Using Monte Carlo simulations we show that even strongly clustered distributions of galaxies can appear unclustered when sampled with limited sensitivity and coarse angular resolution common to current sub-millimeter surveys. The simulations, however, also show that unclustered distributions can appear strongly clustered under these circumstances. From the simulations, we predict that at our survey depth, a mapped area of two degrees^2 is needed to reconstruct the correlation function, assuming smaller beam sizes of future surveys (e.g. the Large Millimeter Telescope's 6" beam size). At present, robust measures of the clustering strength of bright SMGs appear to be below the reach of most observations.Comment: 23 pages, 8 figures, accepted for publication in The Astrophysical Journa

Entropic Uncertainty Relations in Quantum Physics

Uncertainty relations have become the trademark of quantum theory since they were formulated by Bohr and Heisenberg. This review covers various generalizations and extensions of the uncertainty relations in quantum theory that involve the R\'enyi and the Shannon entropies. The advantages of these entropic uncertainty relations are pointed out and their more direct connection to the observed phenomena is emphasized. Several remaining open problems are mentionedComment: 35 pages, review pape

Rare germline variants in DNA repair genes and the angiogenesis pathway predispose prostate cancer patients to develop metastatic disease

Background Prostate cancer (PrCa) demonstrates a heterogeneous clinical presentation ranging from largely indolent to lethal. We sought to identify a signature of rare inherited variants that distinguishes between these two extreme phenotypes. Methods We sequenced germline whole exomes from 139 aggressive (metastatic, age of diagnosis < 60) and 141 non-aggressive (low clinical grade, age of diagnosis ≥60) PrCa cases. We conducted rare variant association analyses at gene and gene set levels using SKAT and Bayesian risk index techniques. GO term enrichment analysis was performed for genes with the highest differential burden of rare disruptive variants. Results Protein truncating variants (PTVs) in specific DNA repair genes were significantly overrepresented among patients with the aggressive phenotype, with BRCA2, ATM and NBN the most frequently mutated genes. Differential burden of rare variants was identified between metastatic and non-aggressive cases for several genes implicated in angiogenesis, conferring both deleterious and protective effects. Conclusions Inherited PTVs in several DNA repair genes distinguish aggressive from non-aggressive PrCa cases. Furthermore, inherited variants in genes with roles in angiogenesis may be potential predictors for risk of metastases. If validated in a larger dataset, these findings have potential for future clinical application