Simulating Male Selfish Strategy in Reproduction Dispute

We introduce into the Penna Model for biological ageing one of the possible male mechanisms used to maximize the ability of their sperm to compete with sperm from other males. Such a selfish mechanism increases the male reproduction success but may decrease the survival probability of the whole female population, depending on how it acts. We also find a dynamic phase transition induced by the existence of an absorbing state where no selfish males survive.Comment: 7 pages, latex including 2 eps figure

The new biology of ageing

Human life expectancy in developed countries has increased steadily for over 150 years, through improvements in public health and lifestyle. More people are hence living long enough to suffer age-related loss of function and disease, and there is a need to improve the health of older people. Ageing is a complex process of damage accumulation, and has been viewed as experimentally and medically intractable. This view has been reinforced by the realization that ageing is a disadvantageous trait that evolves as a side effect of mutation accumulation or a benefit to the young, because of the decline in the force of natural selection at later ages. However, important recent discoveries are that mutations in single genes can extend lifespan of laboratory model organisms and that the mechanisms involved are conserved across large evolutionary distances, including to mammals. These mutations keep the animals functional and pathology-free to later ages, and they can protect against specific ageing-related diseases, including neurodegenerative disease and cancer. Preliminary indications suggest that these new findings from the laboratory may well also apply to humans. Translating these discoveries into medical treatments poses new challenges, including changing clinical thinking towards broad-spectrum, preventative medicine and finding novel routes to drug development

Individual variation in age‐dependent reproduction: Fast explorers live fast but senesce young?

Adaptive integration of life history and behaviour is expected to result in variation in the pace‐of‐life. Previous work focused on whether ‘risky’ phenotypes live fast but die young, but reported conflicting support. We posit that individuals exhibiting risky phenotypes may alternatively invest heavily in early‐life reproduction but consequently suffer greater reproductive senescence. We used a 7‐year longitudinal dataset with >1,200 breeding records of >800 female great tits assayed annually for exploratory behaviour to test whether within‐individual age dependency of reproduction varied with exploratory behaviour. We controlled for biasing effects of selective (dis)appearance and within‐individual behavioural plasticity. Slower and faster explorers produced moderate‐sized clutches when young; faster explorers subsequently showed an increase in clutch size that diminished with age (with moderate support for declines when old), whereas slower explorers produced moderate‐sized clutches throughout their lives. There was some evidence that the same pattern characterized annual fledgling success, if so, unpredictable environmental effects diluted personality‐related differences in this downstream reproductive trait. Support for age‐related selective appearance was apparent, but only when failing to appreciate within‐individual plasticity in reproduction and behaviour. Our study identifies within‐individual age‐dependent reproduction, and reproductive senescence, as key components of life‐history strategies that vary between individuals differing in risky behaviour. Future research should thus incorporate age‐dependent reproduction in pace‐of‐life studies

Exact Solution of an Evolutionary Model without Ageing

We introduce an age-structured asexual population model containing all the relevant features of evolutionary ageing theories. Beneficial as well as deleterious mutations, heredity and arbitrary fecundity are present and managed by natural selection. An exact solution without ageing is found. We show that fertility is associated with generalized forms of the Fibonacci sequence, while mutations and natural selection are merged into an integral equation which is solved by Fourier series. Average survival probabilities and Malthusian growth exponents are calculated indicating that the system may exhibit mutational meltdown. The relevance of the model in the context of fissile reproduction groups as many protozoa and coelenterates is discussed.Comment: LaTeX file, 15 pages, 2 ps figures, to appear in Phys. Rev.

Integrating evolution into ecological modelling: accommodating phenotypic changes in agent based models.

PMCID: PMC3733718This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Evolutionary change is a characteristic of living organisms and forms one of the ways in which species adapt to changed conditions. However, most ecological models do not incorporate this ubiquitous phenomenon. We have developed a model that takes a 'phenotypic gambit' approach and focuses on changes in the frequency of phenotypes (which differ in timing of breeding and fecundity) within a population, using, as an example, seasonal breeding. Fitness per phenotype calculated as the individual's contribution to population growth on an annual basis coincide with the population dynamics per phenotype. Simplified model variants were explored to examine whether the complexity included in the model is justified. Outputs from the spatially implicit model underestimated the number of individuals across all phenotypes. When no phenotype transitions are included (i.e. offspring always inherit their parent's phenotype) numbers of all individuals are always underestimated. We conclude that by using a phenotypic gambit approach evolutionary dynamics can be incorporated into individual based models, and that all that is required is an understanding of the probability of offspring inheriting the parental phenotype

Why leveraging sex differences in immune trade‐offs may illuminate the evolution of senescence

The immune system affects senescence (declines in probabilities of survival or reproduction with age), by shaping late age vulnerability to chronic inflammatory diseases and infections. It is also a dynamic interactive system that must balance competing demands across the life course. Thus, immune system function remains an important frontier in understanding the evolution of senescence. Here, we review our expanding mechanistic understanding of immune function over the life course, in the context of theoretical predictions from life-history evolution. We are especially interested in stage- and sex-dependent costs and benefits of investment in the immune system, given differential life-history priorities of the life stages and sexes. We introduce the costs likely to govern immune allocation across the life course. We then discuss theoretical expectations for differences between the sexes and their likely consequences in terms of how the immune system is both modulated by and may modulate senescence, building on information from life-history theory, experimental immunology and demography. We argue that sex differences in immune function provide a potentially powerful probe of selection pressures on the immune system across the life course. In particular, differences in 'competing' and 'caring' between the sexes have evolved across the tree of life, providing repeated instances of divergent selection pressures on immune function occurring within the same overall bauplan. We conclude by detailing an agenda for future research, including development of theoretical predictions of the differences between the sexes under an array of existing models for sex differences in immunity, and empirical tests of such predictions across the tree of life. A free Plain Language Summary can be found within the Supporting Information of this article

Change and Aging Senescence as an adaptation

Understanding why we age is a long-lived open problem in evolutionary biology. Aging is prejudicial to the individual and evolutionary forces should prevent it, but many species show signs of senescence as individuals age. Here, I will propose a model for aging based on assumptions that are compatible with evolutionary theory: i) competition is between individuals; ii) there is some degree of locality, so quite often competition will between parents and their progeny; iii) optimal conditions are not stationary, mutation helps each species to keep competitive. When conditions change, a senescent species can drive immortal competitors to extinction. This counter-intuitive result arises from the pruning caused by the death of elder individuals. When there is change and mutation, each generation is slightly better adapted to the new conditions, but some older individuals survive by random chance. Senescence can eliminate those from the genetic pool. Even though individual selection forces always win over group selection ones, it is not exactly the individual that is selected, but its lineage. While senescence damages the individuals and has an evolutionary cost, it has a benefit of its own. It allows each lineage to adapt faster to changing conditions. We age because the world changes.Comment: 19 pages, 4 figure

Effect of preoperative thoracic duct drainage on canine kidney transplantation

Chronic drainage of the thoracic duct to the esophagus was developed in dogs, and its efficacy in immunomodulation was tested using kidney transplantation. Compared to 9.7 days in the control, the mean animal survival was prolonged to 9.9 days, 17.8 days, and 18.5 days when TDD was applied preoperatively for 3 weeks, 6 weeks, and 9 weeks, respectively. Prolongation was significant after 6 weeks. Patency of the fistula was 93.5, 80.4, and 76.1% at respective weeks. Number of peripheral T-lymphocytes determined by a new monoclonal antibody diminished after 3 weeks. All animals were in normal health, requiring no special care for fluid, electrolyte, or protein replacement