Realising Potential: Disability Confidence Builds Better Business

[Excerpt] ‘Realising potential’ sets out the latest thinking on how disabled people contribute to business success and how business, in the UK and globally, benefits from disability confidence. It provides the information senior business decision makers need to manage and profit from the disability dimension to key business trends: including an aging population, increasingly individualised customer relations, changing working patterns and enabling technology. Business must address the disability component of these trends and develop disability confidence if it is to compete in an increasingly complex environment and create value from difference. ‘Realising potential’ highlights the strategic, commercial, legal, societal, ethical, and professional benefits of getting it right on disability – the six building blocks of any business case for disability confidence

Use of non-adiabatic geometric phase for quantum computing by nuclear magnetic resonance

Geometric phases have stimulated researchers for its potential applications in many areas of science. One of them is fault-tolerant quantum computation. A preliminary requisite of quantum computation is the implementation of controlled logic gates by controlled dynamics of qubits. In controlled dynamics, one qubit undergoes coherent evolution and acquires appropriate phase, depending on the state of other qubits. If the evolution is geometric, then the phase acquired depend only on the geometry of the path executed, and is robust against certain types of errors. This phenomenon leads to an inherently fault-tolerant quantum computation. Here we suggest a technique of using non-adiabatic geometric phase for quantum computation, using selective excitation. In a two-qubit system, we selectively evolve a suitable subsystem where the control qubit is in state |1>, through a closed circuit. By this evolution, the target qubit gains a phase controlled by the state of the control qubit. Using these geometric phase gates we demonstrate implementation of Deutsch-Jozsa algorithm and Grover's search algorithm in a two-qubit system

Sex identification from distinctive gene expression patterns in Antarctic krill (Euphausia superba)

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Proposal for measurment of harmonic oscillator Berry phase in ion traps

We propose a scheme for measuring the Berry phase in the vibrational degree of freedom of a trapped ion. Starting from the ion in a vibrational coherent state we show how to reverse the sign of the coherent state amplitude by using a purely geometric phase. This can then be detected through the internal degrees of freedom of the ion. Our method can be applied to preparation of Schr\"odinger cat states.Comment: Replaced with revised versio

Berry's Phase in the Presence of a Stochastically Evolving Environment: A Geometric Mechanism for Energy-Level Broadening

The generic Berry phase scenario in which a two-level system is coupled to a second system whose dynamical coordinate is slowly-varying is generalized to allow for stochastic evolution of the slow system. The stochastic behavior is produced by coupling the slow system to a heat resevoir which is modeled by a bath of harmonic oscillators initially in equilibrium at temperature T, and whose spectral density has a bandwidth which is small compared to the energy-level spacing of the fast system. The well-known energy-level shifts produced by Berry's phase in the fast system, in conjunction with the stochastic motion of the slow system, leads to a broadening of the fast system energy-levels. In the limit of strong damping and sufficiently low temperature, we determine the degree of level-broadening analytically, and show that the slow system dynamics satisfies a Langevin equation in which Lorentz-like and electric-like forces appear as a consequence of geometrical effects. We also determine the average energy-level shift produced in the fast system by this mechanism.Comment: 29 pages, RevTex, submitted to Phys. Rev.

E119D Neuraminidase Mutation Conferring Pan-Resistance to Neuraminidase Inhibitors in an A(H1N1)pdm09 Isolate From a Stem-Cell Transplant Recipient

Background. An influenza A(H1N1)pdm09 infection was diagnosed in a hematopoietic stem cell transplant recipient during conditioning regimen. He was treated with oral oseltamivir, later combined with intravenous zanamivir. The H275Y neuraminidase (NA) mutation was first detected, and an E119D NA mutation was identified during zanamivir therapy. Methods. Recombinant wild-type (WT) E119D and E119D/H275Y A(H1N1)pdm09 NA variants were generated by reverse genetics. Susceptibility to NA inhibitors (NAIs) was evaluated with a fluorometric assay using the 2′-(4-methylumbelliferyl)-α-d-N-acetylneuraminic acid (MUNANA) substrate. Susceptibility to favipiravir (T-705) was assessed using plaque reduction assays. The NA affinity and velocity values were determined with NA enzymatic studies. Results. We identified an influenza A(H1N1)pdm09 E119D mutant that exhibited a marked increase in the 50% inhibitory concentrations against all tested NAIs (827-, 25-, 286-, and 702-fold for zanamivir, oseltamivir, peramivir, and laninamivir, respectively). The double E119D/H275Y mutation further increased oseltamivir and peramivir 50% inhibitory concentrations by 790- and >5000-fold, respectively, compared with the WT. The mutant viruses remained susceptible to favipiravir. The NA affinity and velocity values of the E119D variant decreased by 8.1-fold and 4.5-fold, respectively, compared with the WT. Conclusions. The actual emergence of a single NA mutation conferring pan-NAI resistance in the clinical setting reinforces the pressing need to develop new anti-influenza strategie

A revised scheme for the reactivity of iron (oxyhydr)oxide minerals towards dissolved sulfide

The reaction between dissolved sulfide and synthetic iron (oxyhydr)oxide minerals was studied in artificial seawater and 0.1 M NaCl at pH 7.5 and 25°C. Electron transfer between surface-complexed sulfide and solid phase Fe(III) results in the oxidation of dissolved sulfide to elemental sulfur, and the subsequent dissolution of the surface-reduced Fe. Sulfide oxidation and Fe(II) dissolution kinetics were evaluated for freshly precipitated hydrous ferric oxide (HFO), lepidocrocite, goethite, magnetite, hematite, and Al-substituted lepidocrocite. Reaction kinetics were expressed in terms of an empirical rate equation of the form: R-i = k(i)(H2S)(t=0)(0.5)A where Ri is the rate of Fe(II) dissolution (RFe) or the rate of sulfide oxidation (RS), ki is the appropriate rate constant (kFe or kS), (H2S)t=0 is the initial dissolved sulfide concentration, and A is the initial mineral surface area. The rate constants derived from the above equation suggest that the reactivity of Fe (oxyhydr)oxide minerals varies over two orders of magnitude, with increasing reactivity in the order, goethite < hematite < magnetite << lepidocrocite ≈ HFO. Competitive adsorption of major seawater solutes has little effect on reaction kinetics for the most reactive minerals, but results in rates which are reduced by 65-80% for goethite, magnetite, and hematite. This decrease in reaction rates likely arises from the blocking of surface sites for sulfide complexation by the adsorption of seawater solutes during the later, slower stages of adsorption (possibly attributable to diffusion into micropores or aggregates). The derivation of half lives for the sulfide-promoted reductive dissolution of Fe (oxyhydr)oxides in seawater, suggests that mineral reactivity can broadly be considered in terms of two mineral groups. Minerals with a lower degree of crystal order (hydrous ferric oxides and lepidocrocite) are reactive on a time-scale of minutes to hours. The more ordered minerals (goethite, magnetite, and hematite) are reactive on a time-scale of tens of days. Substitution of impurities within the mineral structure (as is likely in nature) has an effect on mineral reactivity. However, these effects are unlikely to have a significant impact on the relative reactivities of the two mineral groups

Impact of periconceptional and preimplantation undernutrition on factors regulating myogenesis and protein synthesis in muscle of singleton and twin fetal sheep.

In this study, we determined the effect of maternal undernutrition in the periconceptional (PCUN: ~80 days before to 6 days after conception) and preimplantation (PIUN: 0-6 days after conception) periods on the mRNA and protein abundance of key factors regulating myogenesis and protein synthesis, and on the relationship between the abundance of these factors and specific microRNA expression in the quadriceps muscle of singleton and twin fetal sheep at 135-138 days of gestation. PCUN and PIUN resulted in a decrease in the protein abundance of MYF5, a factor which determines the myogenic lineage, in singletons and twins. Interestingly, there was a concomitant increase in insulin-like growth factor-1 mRNA expression, a decrease in the protein abundance of the myogenic inhibitor, myostatin (MSTN), and an increase in the mRNA and protein abundance of the MSTN inhibitor, follistatin (FST), in the PCUN and PIUN groups in both singletons and twins. These promyogenic changes may compensate for the decrease in MYF5 protein abundance evoked by early embryonic undernutrition. PCUN and PIUN also increased the protein abundance of phosphorylated eukaryotic translation initiation factor binding protein 1 (EIF4EBP1; T70 and S65) in fetal muscle in singletons and twins. There was a significant inverse relationship between the expression of miR-30a-5p, miR-30d-5p, miR-27b-3p, miR106b-5p, and miR-376b and the protein abundance of mechanistic target of rapamycin (MTOR), FST, or MYF5 in singletons or twins. In particular, the expression of miR-30a-5p was increased and MYF5 protein abundance was decreased, in PCUN and PIUN twins supporting the conclusion that the impact of PCUN and PIUN is predominantly on the embryo

AMP Is a True Physiological Regulator of AMP-Activated Protein Kinase by Both Allosteric Activation and Enhancing Net Phosphorylation

SummaryWhile allosteric activation of AMPK is triggered only by AMP, binding of both ADP and AMP has been reported to promote phosphorylation and inhibit dephosphorylation at Thr172. Because cellular concentrations of ADP and ATP are higher than AMP, it has been proposed that ADP is the physiological signal that promotes phosphorylation and that allosteric activation is not significant in vivo. However, we report that: AMP is 10-fold more potent than ADP in inhibiting Thr172 dephosphorylation; only AMP enhances LKB1-induced Thr172 phosphorylation; and AMP can cause >10-fold allosteric activation even at concentrations 1–2 orders of magnitude lower than ATP. We also provide evidence that allosteric activation by AMP can cause increased phosphorylation of acetyl-CoA carboxylase in intact cells under conditions in which there is no change in Thr172 phosphorylation. Thus, AMP is a true physiological regulator of AMPK, and allosteric regulation is an important component of the overall activation mechanism