Prediction of predator–prey populations modelled by perturbed ODEs

In this paper we explore a stochastic model in continuous time for predator-prey interactions, which accounts for the periodical behaviour observed in many animal populations. More precisely, we consider a solution to the classical Lotka-Volterra system of equations, but we view the actual population sizes as random perturbations of the solutions to this ODE system. Namely, we assume that the perturbations follow correlated Ornstein-Uhlenbeck processes; this approach generalizes the one of Froda and Colavita [Aust N Z J Stat 2:235-254, 2005] who considered only i.i.d. errors. This type of perturbed deterministic model allows to perform parameter estimation and to predict population sizes at future times. On the other hand, the present model refines the previous one since it takes into account the variability due to external factors and the time dependence in the random component. Moreover, this more flexible model improves the predictions of population sizes at future times. In order to illustrate this last point, we analyse two data sets.     

RGC-32 increases p34CDC2 kinase activity and entry of aortic smooth muscle cells into S-phase.

Proliferation of aortic smooth muscle cells contributes to atherogenesis and neointima formation. Sublytic activation of complement, particularly C5b-9, induces cell cycle progression in aortic smooth muscle cells. RGC-32 is a novel protein that may promote cell cycle progression in response to complement activation. We cloned human RGC-32 cDNA from a human fetal brain cDNA library. The human RGC-32 cDNA encodes a 117-amino acid protein with 92% similarity to the rat and mouse protein. Human RGC-32 maps to chromosome 13 and is expressed in most tissues. Sublytic complement activation enhanced RGC-32 mRNA expression in human aortic smooth muscle cells and induced nuclear translocation of the protein. RGC-32 was physically associated with cyclin-dependent kinase p34CDC2 and increased the kinase activity in vivo and in vitro. In addition, RGC-32 was phosphorylated by p34CDC2-cyclin B1 in vitro. Mutation of RGC-32 protein at Thr-91 prevented the p34CDC2-mediated phosphorylation and resulted in loss of p34CDC2 kinase enhancing activity. Overexpression of RGC-32 induced quiescent aortic smooth muscle cells to enter S-phase. These data indicate that cell cycle activation by C5b-9 may involve p34CDC2 activity through RGC-32. RGC-32 appears to be a cell cycle regulatory factor that mediates cell proliferation, both as an activator and substrate of p34CDC2.     

Dual Regulatory Functions of SUFU and Targetome of GLI2 in SHH Subgroup Medulloblastoma

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TRPV1 gene required for thermosensory transduction and anticipatory secretion from vasopressin neurons during hyperthermia

Increases in core body temperature promote thermoregulatory cooling by stimulating sweat production and preemptive renal water reabsorption through the release of vasopressin (VP, antidiuretic hormone). The mechanism by which the hypothalamus orchestrates this anticipatory VP release during hyperthermia is unknown but has been linked to a central thermosensory mechanism. Here, we report that thermal stimuli spanning core body temperatures activate a calcium-permeable, ruthenium red- and SB366791-sensitive nonselective cation conductance in hypothalamic VP neurons. This response is associated with a depolarizing receptor potential and an increase in action potential firing rate, indicating that these neurons are intrinsically thermosensitive. The thermosensitivity of VP neurons isolated from trpv1 knockout (Trpv1(-/-)) mice was significantly lower than that of wild-type counterparts. Moreover, Trpv1(-/-) mice showed an impaired VP response to hyperthermia in vivo. Channels encoded by the trpv1 gene thus confer thermosensitivity in central VP neurons and contribute to the thermal control of VP release in vivo.     

Prolonged Ketamine Effects in Sp4 Hypomorphic Mice: Mimicking Phenotypes of Schizophrenia

It has been well established that schizophrenia patients display impaired NMDA receptor (NMDAR) functions as well as exacerbation of symptoms in response to NMDAR antagonists. Abnormal NMDAR signaling presumably contributes to cognitive deficits which substantially contribute to functional disability in schizophrenia. Establishing a mouse genetic model will help investigate molecular mechanisms of hypoglutmatergic neurotransmission in schizophrenia. Here, we examined the responses of Sp4 hypomorphic mice to NMDAR antagonists in electroencephalography and various behavioral paradigms. Sp4 hypomorphic mice, previously reported to have reduced NMDAR1 expression and LTP deficit in hippocampal CA1, displayed increased sensitivity and prolonged responses to NMDAR antagonists. Molecular studies demonstrated reduced expression of glutamic acid decarboxylase 67 (GAD67) in both cortex and hippocampus, consistent with abnormal gamma oscillations in Sp4 hypomorphic mice. On the other hand, human SP4 gene was reported to be deleted in schizophrenia. Several human genetic studies suggested the association of SP4 gene with schizophrenia and other psychiatric disorders. Therefore, elucidation of the Sp4 molecular pathway in Sp4 hypomorphic mice may provide novel insights to our understanding of abnormal NMDAR signaling in schizophrenia.     

Simple testing procedures for the Holling type II model

In this paper, we consider predator–prey data that can be viewed as solutions to a planar system of ordinary differential equations (ODE) observed with random error. The ODE system admits a limit cycle, while the random error is supposed to act additively in the log-scale. One of the oldest such systems is Holling’s type II model. In spite of its simplicity, it is still very popular in data analyses, although more sophisticated models have been introduced in the literature. We propose a simple way of deciding whether a set of predator–prey pairs is indicative or not of a departure from this basic model by exploiting the geometric properties of the solution in the phase plane. To illustrate our method, we use simulated and real data.     

Eco-coenotic conditions and structure of Trollius europaeus L. populations in an extrazonal habitat complex (Transylvanian Carpathian foothills)

To estimate the importance of community structure and environmental factors for maintenance and in situ conservation of populations of European Globeflower (Trollius europaeus subsp. europaeus) in four sites (one within a natural reserve) in a low elevation but cool valley of the Transylvanian Carpathian foothills, an inventory of all globeflower individuals was performed and floristic relevés were recorded in different community types (meadow, fen and scrub). As a surrogate for habitat conditions, we used plant species indicator values for light, moisture and nitrogen. Globeflower density is highest in mesic habitats, the ecological optimum estimated (about 6 on Ellenberg's scale) being slightly lower than that indicated for Central Europe (7). The juvenile:fertile plants ratio (J:F) declines with increasing soil moisture. Larger flower production in hygrophilous communities does not result in a higher proportion of juveniles or J:F ratio. Despite the presumed strong competition determined by high species richness in some host communities, the most dynamic population (large proportion of juveniles) was found in mesophilous, mown meadows. A clumped distribution of fertile plants under the open scrub canopy seems to be responsible for the significantly larger number of flowers per individual observed, as compared with the relative amount of flowers produced in the adjacent sward. Irrespective of host community, the juveniles display an aggregated distribution with respect to fertile plants, which is probably related to short-distance dispersal of seeds. Our results reveal the importance of host community species richness and soil moisture for the target population stage structure and reproductive investment.