The Advancement of Science: Science Without Legend, Objectivity Without Illusions Philip Kitcher, 1993 Oxford University Press pp. ix + 421, £30.00, ISBN 019 504628 5 Mind, Brain, Behavior. The Mind‐Body Problem and the Philosophy of Psychology Martin Carrier & JÜrgen Mittelstrass, 1991 Berlin, Walter de Gruyter pp. 314, £51.82, ISBN 3 11012876 4 Rewriting the History of Madness: Studies in Foucault's Histoire de la Folie Arthur Still & Irving Velody (Eds), 1992 Routledge pp. x + 225, £45, ISBN 0 415 06654 9 Economics and the Philosophy of Science Deborah Redman, 1993 Oxford, Oxford University Press pp. xiv + 252, £10.95 (paperback), ISBN 019 508274 5 The Disorder of Things John Dupré, 1993 Cambridge, MA/London, UK, Harvard University Press pp. viii+ 308, £27.95, ISBN 0 674 21260 6 The Philosophy of Vacuum Simon Saunders & Harvey R. Brown (Eds), 1991 Oxford, Oxford University Press pp. 291, £37.50, ISBN 0 19 824449 5 The Laboratory of the Mind James R. Brown, 1991 London, Routledge pp. xi+ 175, £11.99 (paperback), ISBN 0 415 095794 The Revision Theory of Truth A. Gupta & N. D. Belnap, 1993 Cambridge, MA, MIT Press pp. xii + 299, £31.50, ISBN 0 262 07144 4
Enterovirus 74 (EV74) is a rarely detected viral infection of children. In 2010, EV74 was identified in New Zealand in a 2 year old child with acute flaccid paralysis (AFP) through routine polio AFP surveillance. A further three cases of EV74 were identified in children within six months. These cases are the first report of EV74 in New Zealand. In this study we describe the near complete genome sequence of four EV74 isolates from New Zealand, which shows only limited sequence identity in the non-structural proteins when compared to the other two known EV74 sequences. As is typical of enteroviruses multiple recombination events were evident, particularly in the P2 region and P3 regions. This is the first complete EV74 genome sequenced from a patient with acute flaccid paralysis.
Approximately 99% of all viruses are still to be described, and in our changing world, any one of these unknown viruses could potentially expand their host range and cause epidemic disease in wildlife, agricultural animals, or humans. Avian avulavirus 1 causes outbreaks in wild birds and poultry and is thus well described. However, for many avulavirus species, only a single specimen has been described, and their viral ecology and epidemiology are unknown. Through the detection of avian avulaviruses in penguins from Antarctica, we have been able to expand upon our understanding of three avian avulavirus species (avian avulaviruses 17 to 19) and report a potentially novel avulavirus species. Importantly, we show that penguins appear to play a key role in the epidemiology of avian avulaviruses, and we encourage additional sampling of this avian group.
Competition structures ecological communities and alters host-pathogen interactions. In environmentally transmitted pathogens, an infection-resistant competitor may influence infection dynamics in a susceptible species through the negative impacts of competition (e.g., by reducing host density or causing nutritional stress that increases susceptibility to infection) and/or the positive impacts of reducing transmission efficiency (e.g., by removing environmental pathogen stages). Thus, a non-susceptible competitor may enhance, reduce, or have no net effect on susceptible host density and infection prevalence. Here, we couple an epidemiological model with experimental epidemics to test how resource competition with a non-susceptible competitor (Daphnia pulicaria) influences fungal microparasite (Metschnikowia bicuspidata) infection dynamics in a susceptible host species (D. dentifera). Our model and experiments suggest that competitor density can mediate the direction and magnitude of the effect of competition on infection dynamics, with a peak in infection prevalence occurring at intermediate competitor densities. At low densities, the non-susceptible competitor D. pulicaria may reduce infection prevalence in the susceptible host by removing fungal spores from the environment through feeding. However, when competitor density is increased and resources become limiting, D. pulicaria negatively impacts the susceptible host by increasing susceptible host feeding rates, and therefore fungal spore intake, and further by reducing susceptible host population size as it is driven toward competitive exclusion. In conclusion, these results show that a tradeoff between the competitor as a consumer of pathogen, which serves to reduce epidemic size, and as a modifier of susceptible host foraging ecology, which influences infection rates, may alternately enhance or dampen the magnitude of local epidemics.
The red deer (Cervus elaphus) is an iconic species in Scotland and, due to its value as a game species, an important element of the Scottish rural economy. The native status of this species is sometimes questioned because of many recorded introductions of nonnative deer in the past that were an attempt to improve trophy size. In this study, we assessed the impact of past introductions on the genetic makeup of Scottish red deer by genotyping at 15 microsatellite loci a large number of samples (n = 1152), including mainland and island Scottish red deer and individuals from several putative external source populations used in introductions to improve trophy size. Population structure and introgression assessment analyses revealed that the impact of introductions was weak in Highland red deer populations but more prominent on the islands, especially on those where current red deer populations are mostly or entirely derived from introductions (Harris & Lewis, Arran, and Rum). Frequent imports of Central-Eastern European red deer into English deer parks were reflected in the higher genetic introgression values found in some of the individuals collected in parks.
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