Disturbance and stress - different meanings in ecological dynamics?

There is an increasing frequency of papers addressing disturbance and stress in ecology without clear delimitation of their meaning. Some authors use the terms disturbance and stress exclusively as impacts, while others use them for the entire process, including both causes and effects. In some studies, the disturbance is considered as a result of a temporary impact, which is positive for the ecosystem, while stress is a negative, debilitating impact. By developing and testing simple theoretical models, the authors propose to differentiate disturbance and stress by frequency. If the frequency of the event enables the variable to reach a dynamic equilibrium which might be exhibited without this event, then the event (plus its responses) is a disturbance for the system. If frequency prevents the variable’s return to similar pre-event dynamics and drives or shifts it to a new trajectory, then we are facing stress. The authors propose that changes triggered by the given stimuli can be evaluated on an absolute scale, therefore, direction of change of the variable must not be used to choose one term or the other, i.e. to choose between stress and disturbance

Impact of measurement error on testing genetic association with quantitative traits

10.1371/journal.pone.0087044PLoS ONE91-POLN

The Circadian Clock Protein Timeless Regulates Phagocytosis of Bacteria in Drosophila

Survival of bacterial infection is the result of complex host-pathogen interactions. An often-overlooked aspect of these interactions is the circadian state of the host. Previously, we demonstrated that Drosophila mutants lacking the circadian regulatory proteins Timeless (Tim) and Period (Per) are sensitive to infection by S. pneumoniae. Sensitivity to infection can be mediated either by changes in resistance (control of microbial load) or tolerance (endurance of the pathogenic effects of infection). Here we show that Tim regulates resistance against both S. pneumoniae and S. marcescens. We set out to characterize and identify the underlying mechanism of resistance that is circadian-regulated. Using S. pneumoniae, we found that resistance oscillates daily in adult wild-type flies and that these oscillations are absent in Tim mutants. Drosophila have at least three main resistance mechanisms to kill high levels of bacteria in their hemolymph: melanization, antimicrobial peptides, and phagocytosis. We found that melanization is not circadian-regulated. We further found that basal levels of AMP gene expression exhibit time-of-day oscillations but that these are Tim-independent; moreover, infection-induced AMP gene expression is not circadian-regulated. We then show that phagocytosis is circadian-regulated. Wild-type flies exhibit up-regulated phagocytic activity at night; Tim mutants have normal phagocytic activity during the day but lack this night-time peak. Tim appears to regulate an upstream event in phagocytosis, such as bacterial recognition or activation of phagocytic hemocytes. Interestingly, inhibition of phagocytosis in wild type flies results in survival kinetics similar to Tim mutants after infection with S. pneumoniae. Taken together, these results suggest that loss of circadian oscillation of a specific immune function (phagocytosis) can have significant effects on long-term survival of infection

Spectroscopic Observations and Analysis of the Peculiar SN 1999aa

We present an extensive new time-series of spectroscopic data of the peculiar SN 1999aa in NGC 2595. Our data set includes 25 optical spectra between -11 and +58 days with respect to B-band maximum light, providing an unusually complete time history. The early spectra resemble those of a SN 1991T-like object but with a relatively strong Ca H&K absorption feature. The first clear sign of Si II 6355, characteristic of Type Ia supernovae, is found at day -7 and its velocity remains constant up to at least the first month after B-band maximum light. The transition to normal-looking spectra is found to occur earlier than in SN 1991T suggesting SN 1999aa as a possible link between SN 1991T-like and Branch-normal supernovae. Comparing the observations with synthetic spectra, doubly ionized Fe, Si and Ni are identified at early epochs. These are characteristic of SN 1991T-like objects. Furthermore, in the day -11 spectrum, evidence is found for an absorption feature which could be identified as high velocity C II 6580 or H-alpha. At the same epoch C III 4648.8 at photospheric velocity is probably responsible for the absorption feature at 4500 A. High velocity Ca is found around maximum light together with Si II and Fe II confined in a narrow velocity window. Implied constraints on supernovae progenitor systems and explosion hydrodynamical models are briefly discussed.Comment: 46 pages including 23 figures. Accepted for publication by AJ. For full-resolution figures see http://www.physto.se/~gabri/sn99aa

A Genetic Signature of Spina Bifida Risk from Pathway-Informed Comprehensive Gene-Variant Analysis

Despite compelling epidemiological evidence that folic acid supplements reduce the frequency of neural tube defects (NTDs) in newborns, common variant association studies with folate metabolism genes have failed to explain the majority of NTD risk. The contribution of rare alleles as well as genetic interactions within the folate pathway have not been extensively studied in the context of NTDs. Thus, we sequenced the exons in 31 folate-related genes in a 480-member NTD case-control population to identify the full spectrum of allelic variation and determine whether rare alleles or obvious genetic interactions within this pathway affect NTD risk. We constructed a pathway model, predetermined independent of the data, which grouped genes into coherent sets reflecting the distinct metabolic compartments in the folate/one-carbon pathway (purine synthesis, pyrimidine synthesis, and homocysteine recycling to methionine). By integrating multiple variants based on these groupings, we uncovered two provocative, complex genetic risk signatures. Interestingly, these signatures differed by race/ethnicity: a Hispanic risk profile pointed to alterations in purine biosynthesis, whereas that in non-Hispanic whites implicated homocysteine metabolism. In contrast, parallel analyses that focused on individual alleles, or individual genes, as the units by which to assign risk revealed no compelling associations. These results suggest that the ability to layer pathway relationships onto clinical variant data can be uniquely informative for identifying genetic risk as well as for generating mechanistic hypotheses. Furthermore, the identification of ethnic-specific risk signatures for spina bifida resonated with epidemiological data suggesting that the underlying pathogenesis may differ between Hispanic and non-Hispanic groups

Antagonism between DNA and H3K27 Methylation at the Imprinted Rasgrf1 Locus

At the imprinted Rasgrf1 locus in mouse, a cis-acting sequence controls DNA methylation at a differentially methylated domain (DMD). While characterizing epigenetic marks over the DMD, we observed that DNA and H3K27 trimethylation are mutually exclusive, with DNA and H3K27 methylation limited to the paternal and maternal sequences, respectively. The mutual exclusion arises because one mark prevents placement of the other. We demonstrated this in five ways: using 5-azacytidine treatments and mutations at the endogenous locus that disrupt DNA methylation; using a transgenic model in which the maternal DMD inappropriately acquired DNA methylation; and by analyzing materials from cells and embryos lacking SUZ12 and YY1. SUZ12 is part of the PRC2 complex, which is needed for placing H3K27me3, and YY1 recruits PRC2 to sites of action. Results from each experimental system consistently demonstrated antagonism between H3K27me3 and DNA methylation. When DNA methylation was lost, H3K27me3 encroached into sites where it had not been before; inappropriate acquisition of DNA methylation excluded normal placement of H3K27me3, and loss of factors needed for H3K27 methylation enabled DNA methylation to appear where it had been excluded. These data reveal the previously unknown antagonism between H3K27 and DNA methylation and identify a means by which epigenetic states may change during disease and development

NICE : A Computational solution to close the gap from colour perception to colour categorization

The segmentation of visible electromagnetic radiation into chromatic categories by the human visual system has been extensively studied from a perceptual point of view, resulting in several colour appearance models. However, there is currently a void when it comes to relate these results to the physiological mechanisms that are known to shape the pre-cortical and cortical visual pathway. This work intends to begin to fill this void by proposing a new physiologically plausible model of colour categorization based on Neural Isoresponsive Colour Ellipsoids (NICE) in the cone-contrast space defined by the main directions of the visual signals entering the visual cortex. The model was adjusted to fit psychophysical measures that concentrate on the categorical boundaries and are consistent with the ellipsoidal isoresponse surfaces of visual cortical neurons. By revealing the shape of such categorical colour regions, our measures allow for a more precise and parsimonious description, connecting well-known early visual processing mechanisms to the less understood phenomenon of colour categorization. To test the feasibility of our method we applied it to exemplary images and a popular ground-truth chart obtaining labelling results that are better than those of current state-of-the-art algorithms