On abandoning life when it is least difficult

Abstract

Suicide data from Sweden (1911–1993) and New Zealand (1975–1995) were used to test a hypothesis derived as an extension of the Seasonal Affective Disorder concept. Contrary to the hypothesis, but similar to what Durkheim had reported regarding Central Europe in the nineteenth century, suicides peaked in late spring (May in Sweden, November in New Zealand). Durkheim's hypothesis that there would be more monthly variation in suicides in rural areas was strongly supported. Our hypothesis is that people abandon life when it is least difficult because of a disjuncture between experience and expectation.     

Female choice for male immunocompetence: when is it worth it?

Disease resistance is not determined by any single immune component.Nevertheless, female choice for individual immune componentscould produce more disease-resistant offspring. Using a mathematicalmodel, we tested whether female choice for male immune responsivenesswas maintained or lost in simulated populations. We dividedimmunity into three different components: two different typesof immune responsiveness and the ability to recognize pathogens.Immune responsiveness was divided into constitutive immunity(CI) and inducible immunity (IN) to simulate the fact that mountingan effective immune response requires independently regulatedcomponents. By using an immunologically relevant division, empiricaldata were available to constrain the model parameters. Whenthe pathogen prevalence fluctuated from generation to generation,female choice for IN or CI was usually lost. Female choice forCI was often lost even when choosiness carried no fitness penalty.Choosing for CI or IN produced a fitness advantage over nonchoosersduring some generations, but not for others, depending on theidentity of the most prevalent pathogens. Choosing for IN orCI led to high mortality when pathogens sensitive to the nonchosencomponent became prevalent in the population, giving nonchoosersthe advantage. Given that most animals experience fluctuatingpathogen pressure, our model suggests that there may be littleselection for female choice for male CI and/or IN in some species.We discuss the implications of our results for the study offemale choice for male disease resistance.     

On the assignment of fitness to parents and offspring: whose fitness is it and when does it matter?

There has been a long‐standing conceptual debate over the legitimacy of assigning components of offspring fitness to parents for purposes of evolutionary analysis. The benefits and risks inherent in assigning fitness of offspring to parents have been given primarily as verbal arguments and no explicit theoretical analyses have examined quantitatively how the assignment of fitness can affect evolutionary inferences. Using a simple quantitative genetic model, we contrast the conclusions drawn about how selection acts on a maternal character when components of offspring fitness (such as early survival) are assigned to parents vs. when they are assigned directly to the individual offspring. We find that there are potential shortcomings of both possible assignments of fitness. In general, whenever there is a genetic correlation between the parental and direct effects on offspring fitness, assigning components of offspring fitness to parents yields incorrect dynamical equations and may even lead to incorrect conclusions about the direction of evolution. Assignment of offspring fitness to parents may also produce incorrect estimates of selection whenever environmental variation contributes to variance of the maternal trait. Whereas assignment of offspring fitness to the offspring avoids these potential problems, it introduces the possible problem of missing components of kin selection provided by the mother, which may not be detected in selection analyses. There are also certain conditions where either model can be appropriate because assignment of offspring fitness to parents may yield the same dynamical equations as assigning offspring fitness directly to offspring. We discuss these implications of the alternative assignments of fitness for modelling, selection analysis and experimentation in evolutionary biology.     

Why it is difficult to determine resource requirements for family planning.

This paper describes the efforts of Family Health International to develop a simple, standard and replicable methodology to estimate expenditures on family planning in developing countries. The study found that it is not possible, at least at this time, to develop such a methodology. Numerous problems were encountered in making expenditure estimates. First and most important, expenditure accounts are not always readily available. Even when these accounts are available, they may require some adjustments. In some instances, for example, the salaries of health workers who also provide family planning are in the health accounts, whereas in other cases the workers covered in the family planning accounts spend some of their time providing health services. Allocation variables then must be developed to separate spending on family planning from that on health. In some instances allocation variables were developed and used to separate family planning from health expenditures, but in this case allocation variables were not available and a cost analysis was performed. It is concluded that it takes considerable time and effort to estimate expenditures, and that the approach that was followed varied by country, reflecting the data available to make estimates.     

Biofilm dispersal: deciding when it is better to travel

Bacteria live predominantly in biofilms, and the internal signal cyclic diguanylate (c‐di‐GMP) is a universal signal that governs the formation and the dispersal of these communities. Pseudomonas aeruginosa is one of the most important reference systems for studying bacterial biofilms and contains numerous diguanylate cyclases (DGCs) for synthesizing c‐di‐GMP and phosphodiesterases (PDEs) for degrading c‐di‐GMP. However, few studies have discerned how cells in biofilms respond to their environment to regulate c‐di‐GMP concentrations through this sophisticated network of enzymes. Basu Roy and Sauer (2014) provide insights on how cells disperse in response to an increase in nutrient levels. Their results show that the inner membrane protein NicD is a DGC that controls dispersal by sensing nutrient levels: when glutamate concentrations are increased, NicD is dephosphorylated, which increases c‐di‐GMP levels and leads to phosphorylation and processing of dispersal regulator BdlA. Processing of BdlA leads to activation of PDE DipA, which results in a net reduction of c‐di‐GMP and biofilm dispersal. These results suggest biofilm dispersal relies on surprisingly dynamic c‐di‐GMP concentrations as a result of a sophisticated interaction between DGCs and PDEs.     

Dismantling the autophagic arsenal when it is time to die

Under stress conditions cells activate different response pathways which result in cell survival or apoptosis depending on: (1) the nature of the insults, (2) the type, if acute or chronic stress, and (3) how long the stress persists. Generally, autophagy is induced early to sustain cell survival and inhibit cell death. However, adverse conditions are able to overcome autophagy to promote cell death. Increasing evidence suggests that the inhibition of autophagy by the apoptotic machinery has been proposed as one of the crucial events responsible for the irreversible switch from survival to death. The mechanism seems to be related to the selective apoptotic protease-mediated degradation of key autophagic proteins. We recently found that AMBRA1, an important regulator of the autophagic process mediating the initial steps of autophagosome formation, is also irreversibly degraded by the combined activity of caspases and calpains. This phenomenon is not merely a consequence of apoptosis execution but represents a key step required to efficiently promote the autophagic vs apoptosis switch.     

Removing Cancer when it is Correlated with other Causes of Death

This paper presents an identifiability theorem in the theory of dependent competing risks and it applies the result by examining the effect of removing cancer from the United States population when cancer is correlated with the other causes of death. The paper shows how dependence can be modeled with copula functions and it shows that calculating the survival probabilities after cancer is removed is equivalent to solving a system of nonlinear differential equations.     

Adaptive developmental plasticity: what is it,how can we recognize it and when can it evolve?

Developmental plasticity describes situations where a specific input during an individual''s development produces a lasting alteration in phenotype. Some instances of developmental plasticity may be adaptive, meaning that the tendency to produce the phenotype conditional on having experienced the developmental input has been under positive selection. We discuss the necessary assumptions and predictions of hypotheses concerning adaptive developmental plasticity (ADP) and develop guidelines for how to test empirically whether a particular example is adaptive. Central to our analysis is the distinction between two kinds of ADP: informational, where the developmental input provides information about the future environment, and somatic state-based, where the developmental input enduringly alters some aspect of the individual''s somatic state. Both types are likely to exist in nature, but evolve under different conditions. In all cases of ADP, the expected fitness of individuals who experience the input and develop the phenotype should be higher than that of those who experience the input and do not develop the phenotype, while the expected fitness of those who do not experience the input and do not develop the phenotype should be higher than those who do not experience the input and do develop the phenotype. We describe ancillary predictions that are specific to just one of the two types of ADP and thus distinguish between them.     

When cytoprotective autophagy isn’t… and even when it is

Multiple papers have been published that have identified and/or characterized the cytoprotective function of autophagy, primarily in tumor cells exposed to chemotherapy or radiation. These studies have relied on pharmacological and/or genetic interference with autophagy to establish its protective function, often primarily by demonstrating that cells in which autophagy has been suppressed undergo increased apoptosis. The purpose of this Editor’s Corner is to emphasize that these approaches, while absolutely necessary, are of themselves insufficient to support the conclusion that autophagy is cytoprotective in a given experimental tumor line exposed to a particular agent; complementary studies are required that demonstrate that autophagy inhibition sensitizes the tumor cell to the autophagy-inducing treatment. Otherwise, autophagy may be responsible for the growth arrest and/or cell death that is observed with the drug or radiation treatment alone, and autophagy inhibition may simply be converting one form of growth inhibition/cell death to an alternative pathway that achieves the same end result in terms of sensitivity to the treatment.     

Relaxed selection when you least expect it: why declining bird populations might fail to respond to phenological mismatches

Ongoing climate change threatens to cause mismatches between the phenology of many organisms and their resources. Populations of migratory birds may need to undergo ‘evolutionary rescue’ if resource availability moves to earlier dates in the year, as shifted arrival dates at the breeding grounds may be required for persistence under new environmental schedules. Here we show a counterintuitive process that can reduce the strength of selection for early arrival when the resource peaks earlier. This happens when two processes combine to determine selection for early arrival: breeding success is higher if a bird does not miss the resource peak, but this occurs together with a ‘zero‐sum game’ where birds acquire good territories ahead of their competitors if they arrive early. The latter process can relax if the population has experienced a recent decline. Therefore, climate change can have two opposing effects: its direct effect on breeding success strengthens selection for early arrival, but this combines with an indirect effect of relaxed selection due to population declines, if territoriality is a significant determinant of population dynamics and fitness. We show that the latter process can predominate, and this can cause a failure for a population to adapt to a new schedule under changing environmental conditions.