Amplitude dependent frequency, desynchronization, and stabilization in noisy metapopulation dynamics

The enigmatic stability of population oscillations within ecological systems is analyzed. The underlying mechanism is presented in the framework of two interacting species free to migrate between two spatial patches. It is shown that that the combined effects of migration and noise cannot account for the stabilization. The missing ingredient is the dependence of the oscillations' frequency upon their amplitude; with that, noise-induced differences between patches are amplified due to the frequency gradient. Migration among desynchronized regions then stabilizes a "soft" limit cycle in the vicinity of the homogenous manifold. A simple model of diffusively coupled oscillators allows the derivation of quantitative results, like the functional dependence of the desynchronization upon diffusion strength and frequency differences. The oscillations' amplitude is shown to be (almost) noise independent. The results are compared with a numerical integration of the marginally stable Lotka-Volterra equations. An unstable system is extinction-prone for small noise, but stabilizes at larger noise intensity

Transition Phenomena Induced by Internal Noise and Quasi-absorbing State

We study a simple chemical reaction system and effects of the internal noise. The chemical reaction system causes the same transition phenomenon discussed by Togashi and Kaneko [Phys. Rev. Lett. 86 (2001) 2459; J. Phys. Soc. Jpn. 72 (2003) 62]. By using the simpler model than Togashi-Kaneko's one, we discuss the transition phenomenon by means of a random walk model and an effective model. The discussion makes it clear that quasi-absorbing states, which are produced by the change of the strength of the internal noise, play an important role in the transition phenomenon. Stabilizing the quasi-absorbing states causes bifurcation of the peaks in the stationary probability distribution discontinuously.Comment: 6 pages, 5 figure

Optimizing Metapopulation Sustainability through a Checkerboard Strategy

The persistence of a spatially structured population is determined by the rate of dispersal among habitat patches. If the local dynamic at the subpopulation level is extinction-prone, the system viability is maximal at intermediate connectivity where recolonization is allowed, but full synchronization that enables correlated extinction is forbidden. Here we developed and used an algorithm for agent-based simulations in order to study the persistence of a stochastic metapopulation. The effect of noise is shown to be dramatic, and the dynamics of the spatial population differs substantially from the predictions of deterministic models. This has been validated for the stochastic versions of the logistic map, the Ricker map and the Nicholson-Bailey host-parasitoid system. To analyze the possibility of extinction, previous studies were focused on the attractiveness (Lyapunov exponent) of stable solutions and the structure of their basin of attraction (dependence on initial population size). Our results suggest that these features are of secondary importance in the presence of stochasticity. Instead, optimal sustainability is achieved when decoherence is maximal. Individual-based simulations of metapopulations of different sizes, dimensions and noise types, show that the system's lifetime peaks when it displays checkerboard spatial patterns. This conclusion is supported by the results of a recently published Drosophila experiment. The checkerboard strategy provides a technique for the manipulation of migration rates (e.g., by constructing corridors) in order to affect the persistence of a metapopulation. It may be used in order to minimize the risk of extinction of an endangered species, or to maximize the efficiency of an eradication campaign

E2F5 status significantly improves malignancy diagnosis of epithelial ovarian cancer

<p>Abstract</p> <p>Background</p> <p>Ovarian epithelial cancer (OEC) usually presents in the later stages of the disease. Factors, especially those associated with cell-cycle genes, affecting the genesis and tumour progression for ovarian cancer are largely unknown. We hypothesized that over-expressed transcription factors (TFs), as well as those that are driving the expression of the OEC over-expressed genes, could be the key for OEC genesis and potentially useful tissue and serum markers for malignancy associated with OEC.</p> <p>Methods</p> <p>Using a combination of computational (selection of candidate TF markers and malignancy prediction) and experimental approaches (tissue microarray and western blotting on patient samples) we identified and evaluated E2F5 transcription factor involved in cell proliferation, as a promising candidate regulatory target in early stage disease. Our hypothesis was supported by our tissue array experiments that showed E2F5 expression only in OEC samples but not in normal and benign tissues, and by significantly positively biased expression in serum samples done using western blotting studies.</p> <p>Results</p> <p>Analysis of clinical cases shows that of the E2F5 status is characteristic for a different population group than one covered by CA125, a conventional OEC biomarker. E2F5 used in different combinations with CA125 for distinguishing malignant cyst from benign cyst shows that the presence of CA125 or E2F5 increases sensitivity of OEC detection to 97.9% (an increase from 87.5% if only CA125 is used) and, more importantly, the presence of both CA125 and E2F5 increases specificity of OEC to 72.5% (an increase from 55% if only CA125 is used). This significantly improved accuracy suggests possibility of an improved diagnostics of OEC. Furthermore, detection of malignancy status in 86 cases (38 benign, 48 early and late OEC) shows that the use of E2F5 status in combination with other clinical characteristics allows for an improved detection of malignant cases with sensitivity, specificity, F-measure and accuracy of 97.92%, 97.37%, 97.92% and 97.67%, respectively.</p> <p>Conclusions</p> <p>Overall, our findings, in addition to opening a realistic possibility for improved OEC diagnosis, provide an indirect evidence that a cell-cycle regulatory protein E2F5 might play a significant role in OEC pathogenesis.</p