First-principles LDA+U and GGA+U study of neptunium dioxide

We have performed a systematic first-principles investigation to calculate the electronic structures, mechanical properties, and phonon dispersion curves of NpO$_{2}$. The local density approximation$+U$ and the generalized gradient approximation$+U$ formalisms have been used to account for the strong on-site Coulomb repulsion among the localized Np $5f$ electrons. By choosing the Hubbard \emph{U} parameter around 4 eV, the orbital occupancy characters of Np 5\emph{f} and O 2\emph{p} are in good agreement with recent experiments [J. Nucl. Mater. \textbf{389}, 470 (2009)]. Comparing with our previous study of ThO$_{2}$, we note that stronger covalency exists in NpO$_{2}$ due to the more localization behavior of 5\emph{f} electrons of Np in line with the localization-delocalization trend exhibited by the actinides series.Comment: 7 pages, 6 figure

General Tasks and Extension-Based Proofs

The concept of extension-based proofs models the idea of a valency argument which is widely used in distributed computing. Extension-based proofs are limited in power: it has been shown that there is no extension-based proof of the impossibility of a wait-free protocol for $(n,k)$-set agreement among $n > k \geq 2$ processes. A discussion of a restricted type of reduction has shown that there are no extension-based proofs of the impossibility of wait-free protocols for some other distributed computing problems. We extend the previous result to general reductions that allow multiple instances of tasks. The techniques used in the previous work are designed for certain tasks, such as the $(n,k)$-set agreement task. We give a necessary and sufficient condition for general colorless tasks to have no extension-based proofs of the impossibility of wait-free protocols, and show that different types of extension-based proof are equivalent in power for colorless tasks. Using this necessary and sufficient condition, the result about reductions can be understood from a topological perspective

Identification of androgen response elements in the insulin-like growth factor I upstream promoter

Journal ArticleTestosterone stimulates the expression of IGF-I in cells and tissues that include prostate, muscle and muscle satellite cells, and the uterus. Here, the molecular mechanisms of this effect of testosterone were explored. Testosterone increased IGF-I mRNA levels in HepG2 and LNCaP cells and stimulated the activity of reporter genes controlled by 1.6 kb of the upstream promoter of the human IGF-I gene. An androgen-responsive region that was located between -1320 and -1420 bases upstream of the first codon was identified by truncation studies. The androgen-responsive region was found to contain two sequences resembling known androgen receptor (AR)-binding sites from the Pem1 gene. Reporter genes incorporating these sequences were strongly stimulated by androgens. Each of the androgen-responsive elements (AREs) bound recombinant AR-DNA-binding domain in gel-shift experiments; binding was greatly enhanced by sequences flanking the apparent AR-binding half-sites. Testosterone induced recruitment of AR to sequences of genomic DNA containing these AREs. The two AREs were activated 5-fold more by AR than glucocorticoid receptor. Collectively, these findings indicate the presence of two AREs within the IGF-I upstream promoter that act in cis to activate IGF-I expression. These AREs seem likely to contribute to the up-regulation of the IGF-I gene in prostate tissues, HepG2 cells, and potentially other tissues