Ab Initio Study of Phase Stability in Doped TiO2

Ab-initio density functional theory (DFT) calculations of the relative stability of anatase and rutile polymorphs of TiO2 were carried using all-electron atomic orbitals methods with local density approximation (LDA). The rutile phase exhibited a moderate margin of stability of ~ 3 meV relative to the anatase phase in pristine material. From computational analysis of the formation energies of Si, Al, Fe and F dopants of various charge states across different Fermi level energies in anatase and in rutile, it was found that the cationic dopants are most stable in Ti substitutional lattice positions while formation energy is minimised for F- doping in interstitial positions. All dopants were found to considerably stabilise anatase relative to the rutile phase, suggesting the anatase to rutile phase transformation is inhibited in such systems with the dopants ranked F>Si>Fe>Al in order of anatase stabilisation strength. Al and Fe dopants were found to act as shallow acceptors with charge compensation achieved through the formation of mobile carriers rather than the formation of anion vacancies

Extracting CP violation and strong phase in D decays by using quantum correlations in psi(3770)-> D0\bar{D}0 -> (V1V2)(V3V4) and psi(3770)->D0\bar{D}0 -> (V1V2)(K pi)

The charm quark offers interesting opportunities to cross-check the mechanism of CP violation precisely tested in the strange and beauty sectors. In this paper, we exploit the angular and quantum correlations in the D\bar{D} pairs produced through the decay of the psi(3770) resonance in a charm factory to investigate CP-violation in two different ways. We build CP-violating observables in psi(3770) -> D\bar{D} -> (V_1V_2)(V_3 V_4) to isolate specific New Physics effects in the charm sector. We also consider the case of psi(3770) -> D\bar{D} -> (V_1V_2)(K\pi) decays, which provide a new way to measure the strong phase difference delta between Cabibbo-favored and doubly-Cabibbo suppressed D decays required in the determination of the CKM angle gamma. Neglecting the systematics, we give a first rough estimate of the sensitivities of these measurements at BES-III with an integrated luminosity of 20 fb^-1 at psi(3770) peak and at a future Super tau-charm factory with a luminosity of 10^35 cm^-2.s^-1.Comment: 13 pages

Measurement of sin2beta in tree-dominated B0-decays and ambiguity removal

The most recent results from the B-factories on the time-dependent CP asymmetries measured in B0-decays mediated by b --> c c(bar) s quark-transitions are reviewed. The Standard Model interpretation of the results in terms of the parameter sin2beta leads to a four-fold ambiguity on the unitarity triangle beta which can be reduced to a two-fold ambiguity by measuring the sign of the parameter cos2beta. The results on cos2beta obtained so far are reviewed.Comment: 6 pages, 3 postscript figues, contributed to the Proceedings of Beauty200

What can we learn from B→a1(1260)(b1(1235))π(K)B\to a_1(1260)(b_1(1235))\pi(K) decays?

We investigate the $B\to a_1(1260)(b_1(1235))\pi(K)$ decays under the factorization scheme and find many discrepancies between theoretical predictions and the experimental data. In the tree dominated processes, large contributions from color-suppressed tree diagrams are required in order to accommodate with the large decay rates of $B^-\to a_1^0\pi^-$ and $B^-\to a_1^-\pi^0$. For $\bar B^0\to (a_1^+, b_1^+)K^-$ decays which are both induced by $b\to s$ transition, theoretical predictions on their decay rates are larger than the data by a factor of 2.8 and 5.5, respectively. Large electro-weak penguins or some new mechanism are expected to explain the branching ratios of $B^-\to b_1^0K^-$ and $B^-\to a_1^-\bar K^0$. The soft-collinear-effective-theory has the potential to explain large decay rates of $B^-\to a_1^0\pi^-$ and $B^-\to a_1^-\pi^0$ via a large hard-scattering form factor $\zeta_J^{B\to a_1}$. We will also show that, with proper charming penguins, predictions on the branching ratios of $\bar B^0\to (a_1^+, b_1^+)K^-$ can also be consistent with the data.Comment: 16 pages, no figur

Dynamic Business Share Allocation in a Supply Chain with Competing Suppliers

This paper studies a repeated game between a manufacturer and two competing suppliers with imperfect monitoring. We present a principal-agent model for managing long-term supplier relationships using a unique form of measurement and incentive scheme. We measure a supplier's overall performance with a rating equivalent to its continuation utility (the expected total discounted utility of its future payoffs), and incentivize supplier effort with larger allocations of future business. We obtain the vector of the two suppliers' ratings as the state of a Markov decision process, and we solve an infinite horizon contracting problem in which the manufacturer allocates business volume between the two suppliers and updates their ratings dynamically based on their current ratings and the current performance outcome. Our contributions are both theoretical and managerial: we propose a repeated principal-agent model with a novel incentive scheme to tackle a common, but challenging, incentive problem in a multiperiod supply chain setting. Assuming binary effort choices and performance outcomes by the suppliers, we characterize the structure of the optimal contract through a novel fixed-point analysis. Our results provide a theoretical foundation for the emergence of “business-as-usual” (low effort) trapping states and tournament competition (high effort) recurrent states as the long-run incentive drivers for motivating critical suppliers

Mutations in hepatitis C virus E2 located outside the CD81 binding sites lead to escape from broadly neutralizing antibodies but compromise virus infectivity.

Broadly neutralizing antibodies are commonly present in the sera of patients with chronic hepatitis C virus (HCV) infection. To elucidate possible mechanisms of virus escape from these antibodies, retrovirus particles pseudotyped with HCV glycoproteins (HCVpp) isolated from sequential samples collected over a 26-year period from a chronically infected patient, H, were used to characterize the neutralization potential and binding affinity of a panel of anti-HCV E2 human monoclonal antibodies (HMAbs). Moreover, AP33, a neutralizing murine monoclonal antibody (MAb) to a linear epitope in E2, was also tested against selected variants. The HMAbs used were previously shown to broadly neutralize HCV and to recognize a cluster of highly immunogenic overlapping epitopes, designated domain B, containing residues that are also critical for binding of viral E2 glycoprotein to CD81, a receptor essential for virus entry. Escape variants were observed at different time points with some of the HMAbs. Other HMAbs neutralized all variants except for the isolate 02.E10, obtained in 2002, which was also resistant to MAb AP33. The 02.E10 HCVpp that have reduced binding affinities for all antibodies and for CD81 also showed reduced infectivity. Comparison of the 02.E10 nucleotide sequence with that of the strain H-derived consensus variant, H77c, revealed the former to have two mutations in E2, S501N and V506A, located outside the known CD81 binding sites. Substitution A506V in 02.E10 HCVpp restored binding to CD81, but its antibody neutralization sensitivity was only partially restored. Double substitutions comprising N501S and A506V synergistically restored 02.E10 HCVpp infectivity. Other mutations that are not part of the antibody binding epitope in the context of N501S and A506V were able to completely restore neutralization sensitivity. These findings showed that some nonlinear overlapping epitopes are more essential than others for viral fitness and consequently are more invariant during earlier years of chronic infection. Further, the ability of the 02.E10 consensus variant to escape neutralization by the tested antibodies could be a new mechanism of virus escape from immune containment. Mutations that are outside receptor binding sites resulted in structural changes leading to complete escape from domain B neutralizing antibodies, while simultaneously compromising viral fitness by reducing binding to CD81

Activation of Extracellular-signal Regulated Kinase (ERK1/2) by Fluid Shear is Ca\u3csup\u3e2+\u3c/sup\u3e- and ATP-dependent in MC3T3-E1 Osteoblasts

To determine the role of Ca2+ signaling in activation of the Mitogen-Activated Protein Kinase (MAPK) pathway, we subjected MC3T3-E1 pre-osteoblastic cells to inhibitors of Ca2+ signaling during application of fluid shear stress (FSS). FSS only activated ERK1/2, rapidly inducing phosphorylation within 5 min of the onset of shear. Phosphorylation of ERK1/2 (pERK1/2) was significantly reduced when Cai2+ was chelated with BAPTA or when Ca2+ was removed from the flow media. Inhibition of both the L-type voltage-sensitive Ca2+ channel and the mechanosensitive cation-selective channel blocked FSS-induced pERK1/2. Inhibition of phospholipase C with U73122 significantly reduced pERK1/2. This inhibition did not result from blockage of intracellular Ca2+ release, but a loss of PKC activation. Recent data suggests a role of ATP release and purinergic receptor activation in mechanotransduction. Apyrase-mediated hydrolysis of extracellular ATP completely blocked FSS-induced phosphorylation of ERK1/2, while the addition of exogenous ATP to static cells mimicked the effects of FSS on pERK1/2. Two P2 receptors, P2Y2 and P2X7, have been associated with the anabolic responses of bone to mechanical loading. Using both iRNA techniques and primary osteoblasts isolated from P2X7 knockout mice, we found that the P2X7, but not the P2Y2, purinergic receptor was involved in ERK1/2 activation under FSS. These data suggest that FSS-induced ERK1/2 phosphorylation requires Ca2+-dependent ATP release, however both increased Cai2+ and PKC activation are needed for complete activation. Further, this ATP-dependent ERK1/2 phosphorylation is mediated through P2X7, but not P2Y2, purinergic receptors

Effects of Voluntary Breathing on Force Responses to Electrical Stimulation (ES) of Finger Extensors : A Pilot Study

Voluntary breathing can influence motor functions of non-respiratory skeletal muscles, e.g., finger muscles. The influence was proposed to be mediated by the ventilation-associated enhancement on corticospinal excitability of the finger muscles, possibly including spinal mechanisms. Force responses to electrical stimulation include spinal mechanisms. The purpose was to investigate the potential spinal mechanism mediating the voluntary breathing effects on responses of finger extension forces to electrical stimulation. A single-pulse electrical stimulation of the same intensity was delivered to the extensor digitorum communis (EDC) during voluntary breathing (forced inspiration, IN and force expiration, OUT) and normal breathing (Norm) across various submaximal levels (10 ~30%) of isometric finger extension. Among the tested 3 subjects, differences of background finger extension forces were 2~3% at each force level. The evoked force increment was greater during IN and OUT than during Norm consistently at all tested force levels. However, the increment seemed not to be different between IN and OUT. Latency of the ES-evoked response was in the range from 52ms to 68ms. These pilot results demonstrated that voluntary breathing modulated finger extension force responses to electrical stimulation, most likely mediated by spinal mechanisms