The role of regulatory mechanisms for control of plant diseases and food security — case studies from potato production in Britain

Being aware of the potentially devastating impacts of plant diseases on food security, governments have designed and employ plant health legislation to prevent or inhibit the worst impacts. The development of such policies in Britain, and latterly in Europe, can be closely linked to disease events that have occurred in the potato sector. We analyse early and current examples of policies governing potato diseases in Britain to identify the decision processes leading to the implementation of such phytosanitary policies and how they have evolved over time and in response to different disease threats. Reasons for developing and implementing phytosanitary policies include the desire to prevent pathogens being introduced (entering and establishing in a new area), the protection of export markets, and the lack of effective control measures. Circumstances in which regulatory policies would not be appropriate could include situations where a disease is already widely distributed, unacceptable costs, lack of exclusion measures, or difficulties of disease diagnosis. We conclude that in general, government policies have worked well in protecting British potato growing over the last one hundred years, despite of the failures of some of the policies discussed here. They have also contributed much to the development of plant health policies for other crops. Voluntary grower initiatives are a new mechanism complementing existing formal policies with an additional level of security that allows individual growers to take on additional responsibility rather than relying entirely on government legislation

Activation Energy for Grain Growth in Bismuth Coatings

The knowledge of both activation energy and diffusion coefficient is needed for a predictive processing of grain size in coatings. However, for metals as Bismuth there is insufficient information available in the literature for these parameters. To determine these values, a method is adopted wherein an examination of the grain size is conducted for coatings deposited isothermally. The exponent for grain growth with time is determined, thereby enabling quantification of the activation energy and diffusion coefficient. Bismuth coatings that range from 10 {micro}m to 1 mm thick are deposited using electron-beam evaporation onto temperature-controlled substrate surfaces of glass and lithium fluoride. The grain size of each coating is measured upon examination of the microstructure in cross-section using the intercept method. Ideal grain growth is observed over the experimental range of deposition temperatures examined from 317 to 491 K. The activation energy (Q) for grain growth in bismuth is fit as 0.47 eV {center_dot} atom{sup -1} with a diffusion coefficient (D{sub 0}) of 3.3 x 10{sup -4} cm{sup 2} {center_dot} sec{sup -1}

A Compensatory Mutation Provides Resistance to Disparate HIV Fusion Inhibitor Peptides and Enhances Membrane Fusion

Fusion inhibitors are a class of antiretroviral drugs used to prevent entry of HIV into host cells. Many of the fusion inhibitors being developed, including the drug enfuvirtide, are peptides designed to competitively inhibit the viral fusion protein gp41. With the emergence of drug resistance, there is an increased need for effective and unique alternatives within this class of antivirals. One such alternative is a class of cyclic, cationic, antimicrobial peptides known as θ-defensins, which are produced by many non-human primates and exhibit broad-spectrum antiviral and antibacterial activity. Currently, the θ-defensin analog RC-101 is being developed as a microbicide due to its specific antiviral activity, lack of toxicity to cells and tissues, and safety in animals. Understanding potential RC-101 resistance, and how resistance to other fusion inhibitors affects RC-101 susceptibility, is critical for future development. In previous studies, we identified a mutant, R5-tropic virus that had evolved partial resistance to RC-101 during in vitro selection. Here, we report that a secondary mutation in gp41 was found to restore replicative fitness, membrane fusion, and the rate of viral entry, which were compromised by an initial mutation providing partial RC-101 resistance. Interestingly, we show that RC-101 is effective against two enfuvirtide-resistant mutants, demonstrating the clinical importance of RC-101 as a unique fusion inhibitor. These findings both expand our understanding of HIV drug-resistance to diverse peptide fusion inhibitors and emphasize the significance of compensatory gp41 mutations. © 2013 Wood et al

Instantons and unitarity in quantum cosmology with fixed four-volume

We find a number of complex solutions of the Einstein equations in the so-called unimodular version of general relativity, and we interpret them as saddle points yielding estimates of a gravitational path integral over a space of almost everywhere Lorentzian metrics on a spacetime manifold with topology of the "no-boundary" type. In this setting, the compatibility of the no-boundary initial condition with the definability of the quantum measure reduces reduces to the normalizability and unitary evolution of the no-boundary wave function \psi. We consider the spacetime topologies R^4 and RP^4 # R^4 within a Taub minisuperspace model with spatial topology S^3, and the spacetime topology R^2 x T^2 within a Bianchi type I minisuperspace model with spatial topology T^3. In each case there exists exactly one complex saddle point (or combination of saddle points) that yields a wave function compatible with normalizability and unitary evolution. The existence of such saddle points tends to bear out the suggestion that the unimodular theory is less divergent than traditional Einstein gravity. In the Bianchi type I case, the distinguished complex solution is approximately real and Lorentzian at late times, and appears to describe an explosive expansion from zero size at T=0. (In the Taub cases, in contrast, the only complex solution with nearly Lorentzian late-time behavior yields a wave function that is normalizable but evolves nonunitarily, with the total probability increasing exponentially in the unimodular "time" in a manner that suggests a continuous creation of new universes at zero volume.) The issue of the stability of these results upon the inclusion of more degrees of freedom is raised.Comment: 32 pages, REVTeX v3.1 with amsfonts. (v2: minor typos etc corrected.

Wind-Powered Wheel Locomotion, Initiated by Leaping Somersaults, in Larvae of the Southeastern Beach Tiger Beetle (Cicindela dorsalis media)

Rapid movement is challenging for elongate, soft-bodied animals with short or no legs. Leaping is known for only a few animals with this “worm-like” morphology. Wheel locomotion, in which the animal's entire body rolls forward along a central axis, has been reported for only a handful of animals worldwide. Here we present the first documented case of wind-powered wheel locomotion, in larvae of the coastal tiger beetle Cicindela dorsalis media. When removed from their shallow burrows, larvae easily can be induced to enter a behavioral sequence that starts with leaping; while airborne, larvae loop their body into a rotating wheel and usually either “hit the ground rolling” or leap again. The direction larvae wheel is closely related to the direction in which winds are blowing; thus, all our larvae wheeled up-slope, as winds at our study site consistently blew from sea to land. Stronger winds increased both the proportion of larvae wheeling, and the distance traveled, exceeding 60 m in some cases. In addition, the proportion of larvae that wheel and the distance traveled by wheeling larvae are significantly greater on smooth sandy beaches than on beach surfaces made rough and irregular by pedestrian, equestrian, and vehicular traffic. Like other coastal species of tiger beetles, C. dorsalis media has suffered major declines in recent years that are clearly correlated with increased human impacts. The present study suggests that the negative effects of beach traffic may be indirect, preventing larvae from escaping from predators using wheel locomotion by disrupting the flat, hard surface necessary for efficient wheeling

Regularity Properties and Pathologies of Position-Space Renormalization-Group Transformations

We reconsider the conceptual foundations of the renormalization-group (RG) formalism, and prove some rigorous theorems on the regularity properties and possible pathologies of the RG map. Regarding regularity, we show that the RG map, defined on a suitable space of interactions (= formal Hamiltonians), is always single-valued and Lipschitz continuous on its domain of definition. This rules out a recently proposed scenario for the RG description of first-order phase transitions. On the pathological side, we make rigorous some arguments of Griffiths, Pearce and Israel, and prove in several cases that the renormalized measure is not a Gibbs measure for any reasonable interaction. This means that the RG map is ill-defined, and that the conventional RG description of first-order phase transitions is not universally valid. For decimation or Kadanoff transformations applied to the Ising model in dimension $d \ge 3$, these pathologies occur in a full neighborhood $\{ \beta > \beta_0 ,\, |h| < \epsilon(\beta) \}$ of the low-temperature part of the first-order phase-transition surface. For block-averaging transformations applied to the Ising model in dimension $d \ge 2$, the pathologies occur at low temperatures for arbitrary magnetic-field strength. Pathologies may also occur in the critical region for Ising models in dimension $d \ge 4$. We discuss in detail the distinction between Gibbsian and non-Gibbsian measures, and give a rather complete catalogue of the known examples. Finally, we discuss the heuristic and numerical evidence on RG pathologies in the light of our rigorous theorems.Comment: 273 pages including 14 figures, Postscript, See also ftp.scri.fsu.edu:hep-lat/papers/9210/9210032.ps.

The combined effect of two mutations that alter serially homologous color pattern elements on the fore and hindwings of a butterfly

<p>Abstract</p> <p>Background</p> <p>The ability for serially homologous structures to acquire a separate identity has been primarily investigated for structures dependent on Hox gene input but is still incompletely understood in other systems. The fore and hindwings of butterflies are serially homologous structures as are the serially homologous eyespots that can decorate each of these wings. Eyespots can vary in number between fore and hindwings of the same individual and mutations of large effect can control the total number of eyespots that each of the wings displays. Here we investigate the genetics of a new spontaneous color pattern mutation, <it>Missing</it>, that alters eyespot number in the nymphalid butterfly, <it>Bicyclus anynana</it>. We further test the interaction of <it>Missing </it>with a previously described mutation, <it>Spotty</it>, describe the developmental stage affected by <it>Missing</it>, and test whether <it>Missing </it>is a mutant variant of the gene <it>Distal-less </it>via a linkage association study.</p> <p>Results</p> <p><it>Missing </it>removes or greatly reduces the size of two of the hindwing eyespots from the row of seven eyespots, with no detectable effect on the rest of the wing pattern. Offspring carrying a single <it>Missing </it>allele display intermediate sized eyespots at these positions. <it>Spotty </it>has the opposite effect of <it>Missing</it>, i.e., it introduces two extra eyespots in homologous wing positions to those affected by <it>Missing</it>, but on the forewing. When <it>Missing </it>is combined with <it>Spotty </it>the size of the two forewing eyespots decreases but the size of the hindwing spots stays the same, suggesting that these two mutations have a combined effect on the forewing such that <it>Missing </it>reduces eyespot size when in the presence of a <it>Spotty </it>mutant allele, but that <it>Spotty </it>has no effect on the hindwing. <it>Missing </it>prevents the complete differentiation of two of the eyespot foci on the hindwing. We found no evidence for any linkage between the <it>Distal-less </it>and <it>Missing </it>genes.</p> <p>Conclusion</p> <p>The spontaneous mutation <it>Missing </it>controls the differentiation of the signaling centers of a subset of the serial homologous eyespots present on both the fore and the hindwing in a dose-dependent fashion. The effect of <it>Missing </it>on the forewing, however, is only observed when the mutation <it>Spotty </it>introduces additional eyespots on this wing. <it>Spotty</it>, on the other hand, controls the differentiation of eyespot centers only on the forewing. <it>Spotty</it>, unlike <it>Missing</it>, may be under Ubx gene regulation, since it affects a subset of eyespots on only one of the serially homologous wings.</p

Rescue of a H3N2 Influenza Virus Containing a Deficient Neuraminidase Protein by a Hemagglutinin with a Low Receptor-Binding Affinity

Influenza viruses possess at their surface two glycoproteins, the hemagglutinin and the neuraminidase, of which the antagonistic functions have to be well balanced for the virus to grow efficiently. Ferraris et al. isolated in 2003–2004 viruses lacking both a NA gene and protein (H3NA- viruses) (Ferraris O., 2006, Vaccine, 24(44–46):6656-9). In this study we showed that the hemagglutinins of two of the H3NA- viruses have reduced affinity for SAα2.6Gal receptors, between 49 and 128 times lower than that of the A/Moscow/10/99 (H3N2) virus and no detectable affinity for SAα2.3Gal receptors. We also showed that the low hemagglutinin affinity of the H3NA- viruses compensates for the lack of NA activity and allows the restoration of the growth of an A/Moscow/10/99 virus deficient in neuraminidase. These observations increase our understanding of H3NA- viruses in relation to the balance between the functional activities of the neuraminidase and hemagglutinin

Assessment of corrosive attack of Fe9Cr1Mo alloys in pressurised CO2 for prediction of breakaway oxidation

To provide clarity on the poorly-understood mechanism of breakaway oxidation, corrosion of Fe9Cr1Mo steel in pressurised CO is quantified and modelled. The temperature range 400–640 , relevant to nuclear power plants, is emphasised. Attack is in the form of combined oxide scale growth and internal carburisation of the metal. Carbon activity in the metal at its surface exhibits a strong time dependence consistent with the kinetically-limited transport of carbon due to the slow Boudouard reaction. Breakaway is associated with the approach to saturation of the steel with respect to carbon. Diffusion modelling agrees well with steel carbide precipitation observations