Mathematical modelling of host-parasitoid systems: effects of chemically mediated parasitoid foraging strategies on within- and between-generation spatio-temporal dynamics.

In this paper we develop a novel discrete, individual-based mathematical model to investigate the effect of parasitoid foraging strategies on the spatial and temporal dynamics of host-parasitoid systems. The model is used to compare na?ve or random search strategies with search strategies that depend on experience and sensitivity to semiochemicals in the environment. It focuses on simple mechanistic interactions between individual hosts, parasitoids, and an underlying field of a volatile semiochemical (emitted by the hosts during feeding) which acts as a chemoattractant for the parasitoids. The model addresses movement at different spatial scales, where scale of movement also depends on the internal state of an individual. Individual interactions between hosts and parasitoids are modelled at a discrete (micro-scale) level using probabilistic rules. The resulting within-generation dynamics produced by these interactions are then used to generate the population levels for successive generations. The model simulations examine the effect of various key parameters of the model on (i) the spatio-temporal patterns of hosts and parasitoids within generations; (ii) the population levels of the hosts and parasitoids between generations. Key results of the model simulations show that the following model parameters have an important effect on either the development of patchiness within generations or the stability/instability of the population levels between generations: (i) the rate of diffusion of the kairomones; (ii) the specific search strategy adopted by the parasitoids; (iii) the rate of host increase between successive generations. Finally, evolutionary aspects concerning competition between several parasitoid subpopulations adopting different search strategies are also examined.     

Shading and texture: separate information channels with a common adaptation mechanism?

We outline a scheme for the way in which early vision may handle information about shading (luminance modulation, LM) and texture (contrast modulation, CM). Previous work on the detection of gratings has found no sub-threshold summation, and no cross-adaptation, between LM and CM patterns. This strongly implied separate channels for the detection of LM and CM structure. However, we now report experiments in which adapting to LM (or CM) gratings creates tilt aftereffects of similar magnitude on both LM and CM test gratings, and reduces the perceived strength (modulation depth) of LM and CM gratings to a similar extent. This transfer of aftereffects between LM and CM might suggest a second stage of processing at which LM and CM information is integrated. The nature of this integration, however, is unclear and several simple predictions are not fulfilled. Firstly, one might expect the integration stage to lose identity information about whether the pattern was LM or CM. We show instead that the identity of barely detectable LM and CM patterns is not lost. Secondly, when LM and CM gratings are combined in-phase or out-of-phase we find no evidence for cancellation, nor for 'phase-blindness'. These results suggest that information about LM and CM is not pooled or merged--shading is not confused with texture variation. We suggest that LM and CM signals are carried by separate channels, but they share a common adaptation mechanism that accounts for the almost complete transfer of perceptual aftereffects.     

Active site mutations of recombinant deacetoxycephalosporin C synthase

Site-directed mutagenesis of active site residues of deacetoxycephalosporin C synthase active site residues was carried out to investigate their role in catalysis. The following mutations were made and their effects on the conversion of 2-oxoglutarate and the oxidation of penicillin N or G were assessed: M180F, G299N, G300N, Y302S, Y302F/G300A, Y302E, Y302H, and N304A. The Y302S, Y302E, and Y302H mutations reduced 2-oxoglutarate conversions and abolished (<2%) penicillin G oxidation. The Y302F/G300A mutation caused partial uncoupling of penicillin G oxidation from 2-oxoglutarate conversion, but did not uncouple penicillin N oxidation from 2-oxoglutarate conversion. Met-180 is involved in binding 2-oxoglutarate, and the M180F mutation caused uncoupling of 2-oxoglutarate from penicillin oxidation. The N304A mutation apparently enhanced in vitro conversion of penicillin N but had little effect on the oxidation of penicillin G, under standard assay conditions.     

Osmoregulation in the parasitic protozoan Tritrichomonas foetus

Tritrichomonas foetus was shown to undergo a regulatory volume increase (RVI) when it was subjected to hyperosmotic challenge, but there was no regulatory volume decrease after hypoosmotic challenge, as determined by using both light-scattering methods and measurement of intracellular water space to monitor cell volume. An investigation of T. foetus intracellular amino acids revealed a pool size (65 mM) that was similar to that of Trichomonas vaginalis but was considerably smaller than those of Giardia intestinalis and Crithidia luciliae. Changes in amino acid concentrations in response to hyperosmotic challenge were found to account for only 18% of the T. foetus RVI. The T. foetus intracellular sodium and potassium concentrations were determined to be 35 and 119 mM, respectively. The intracellular K(+) concentration was found to increase considerably during exposure to hyperosmotic stress, and, assuming that there was a monovalent accompanying anion, this increase was estimated to account for 87% of the RVI. By using light scattering it was determined that the T. foetus RVI was enhanced by elevated external K(+) concentrations and was inhibited when K(+) and/or Cl(-) was absent from the medium. The results suggested that the well-documented Na(+)-K(+)-2Cl(-) cotransport system was responsible for the K(+) influx activated during the RVI. However, inhibitors of Na(+)-K(+)-2Cl(-) cotransport in other systems, such as quinine, ouabain, furosemide, and bumetanide, had no effect on the RVI or K(+) influx in T. foetus.     

Unusual presentation of choriocarcinoma

Background  

Choriocarcinoma is an aggressive neoplasm arising in the body of the uterus. The disease normally spreads to lung and brain.     

Isolation of COV1, a gene involved in the regulation of vascular patterning in the stem of Arabidopsis

The molecular mechanisms that control the ordered patterning of vascular tissue development in plants are not well understood. Several models propose a two-component system for vascular differentiation. These components include an inducer of vascular tissue development and an inhibitor that prevents the formation of vascular bundles near pre-existing bundles. We have identified two recessive allelic mutants in Arabidopsis, designated continuous vascular ring (cov1), that display a dramatic increase in vascular tissue development in the stem in place of the interfascicular region that normally separates the vascular bundles. The mutant plants exhibited relatively normal vascular patterning in leaves and cotyledons. Analysis of the interaction of cov1 with a known auxin signalling mutant and direct analysis of auxin concentrations suggests that cov1 affects vascular pattering by some mechanism that is independent of auxin. The COV1 protein is predicted to be an integral membrane protein of unknown function, highly conserved between plants and bacteria. In plants, COV1 is likely to be involved in a mechanism that negatively regulates the differentiation of vascular tissue in the stem.     

Yeast resolving enzyme CCE1 makes sequential cleavages in DNA junctions within the lifetime of the complex

CCE1 is a DNA junction-resolving enzyme of Saccharomyces cerevisiae. Such enzymes are required to make two symmetrically paired cleavages in order to resolve the four-way junction productively. Using a cruciform assay, we show here that CCE1 introduces two unilateral cleavages in a sequential manner. This requires that the protein remains bound to the junction, preventing branch migration of the point of strand exchange. From a detailed kinetic analysis, we find that the CCE1 cleavage at a given site is accelerated by a factor of 5-10 when it occurs subsequently to the initial cleavage. These properties ensure a productive resolution of the four-way junction and may be general for junction-resolving enzymes.