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Bienertova-Vasku, J.

Publications and source records attributed to Bienertova-Vasku, J..

4 recordsLinked to original sources

Biological Factors and Self-Perception of Stress Predict Human Freeze-Like Responses in the Context of Self-Defence Training and Personal Experience with Violence

Many animals react to threatening stimuli such as a predator attacks by freezing. However, little experimental research investigated freeze response in humans. Here, we have employed practices commonly used in self-defence training to create two unique scenarios simulating armed physical attacks. Sixty healthy men volunteers divided into three groups of twenty (untrained, trained but unexperienced, trained and experienced) underwent these scenarios accompanied by measurement of biochemical, physiological, and psychological markers of stress. All participants also underwent an fMRI session during which they observed neutral and negative images from the International Affective Picture System (IAPS). Our results show that scenarios simulating physical attacks can induce a freeze-like response in men. In addition, we demonstrate that while electrodermal activity (EDA), subjective stress perception, and brain activity in fMRI predict freeze-like response in men, their effect on freeze-like response is entirely dependent on the level of training and experience of a given individual.

neuroscience↗

Learning Mitigates Genetic Drift

Genetic drift is a basic evolutionary principle describing random changes in allelic frequencies, with far-reaching consequences in various topics ranging from species conservation efforts to speciation. The conventional approach assumes that genetic drift has the same effect on all populations undergoing the same change in size, regardless of different behaviors and history of the populations. However, here we reason that processes leading to a systematic increase of individuals chances of survival, such as learning or immunological memory, can mitigate the effects of genetic drift even if the overall mortality rate in the population does not change. We further test this notion in an agent-based model monitoring allele frequencies in a population of prey, either able or not able to learn. Importantly, both these populations start with the same effective size and have the same and constant overall mortality rates. Our results demonstrate that even under these conditions, learning can mitigate drift if generations overlap. Furthermore, this effect holds regardless if the population is haploid or diploid or whether it reproduces sexually or asexually. Therefore, our findings demonstrate that learning is an overlooked factor affecting the effective population size. These findings may be of importance not only for basic evolutionary theory but also for other fields using the concept of genetic drift.

evolutionary biology↗

Predation Has Small, Short-Term, and in Certain Conditions Random Effect on the Evolution of Aging

The pace of aging varies considerably in nature. Historically, scientists focused mostly on why and how has aging evolved, while only a few studies explored mechanisms driving evolution of specific rates of aging. Here we develop an agent-based model simulating evolution of aging in prey subject to predation. Our results suggest that predation affects the pace of aging in prey only if young, vivid animals are not much more likely to escape predators than the old ones. However, even this effect slowly vanishes when the predator diet composition evolves, too. Furthermore, evolution of a specific aging rate, in our model, is driven mainly by a single parameter, the strength of a trade-off between aging and fecundity. Indeed, in absence of this trade-off the evolutionary impacts of predation on the prey aging rate appear random. Our model produces several testable predictions which may be useful for other areas of aging research.

evolutionary biology↗

Evolution favors aging in populations with assortative mating and strong pathogen pressure

Since at first sight aging seems to be omnipresent, many authors to this very day regard it as an inevitable consequence of the laws of physics. However, studies published in the past two decades have conclusively shown that a number of organisms do not age, or at least do not age on a scale comparable with other aging organisms. This disparity leads us to question why aging evolved in some organisms and not in others. We thus present a mathematical model which simulates evolution in a sexually reproducing population composed of aging and non-aging individuals. We have observed that aging individuals may outcompete non-aging individuals if they have a higher starting fertility or if the main mating pattern in the population is assortative mating. Furthermore, stronger pathogen pressure was found to help the aging phenotype when compared to the non-aging phenotype. Last but not least, the aging phenotype was found to more easily outcompete the non-aging one or to resist the dominance of the latter for a longer period of time in populations composed of dimorphic sexually reproducing individuals compared to populations of hermaphrodites. Our findings are consistent with both classical evolutionary theories of aging and with evolutionary theories of aging which assume the existence of an aging program. They can thus potentially work as a bridge between these two opposing views, suggesting that the truth in fact lies somewhere in between.\n\nSignificance StatementThis study presents the first mathematical model which simulates the evolution of aging in a population of sexually reproducing organisms. Our model shows that aging individuals may outcompete non-aging individuals in several scenarios known to occur in nature. Our work thus provides important insight into the question why aging has evolved in most, but not all, organisms.

evolutionary biology↗