Power, Social Conflict, Institutional Formation, and Credible Commitment

This chapter develops a social conflict theory of institutions. The third hypothesis posits that unequal distributions of power shape the creation, evolution, and demise of economic and political institutions. A background discussion defines power—a slightly slippery concept—and addresses key sources and manifestations of power. Unequal distributions of power then generate a series of CAPs associated with asymmetric influence on institutional construction and evolution. A flowchart model illustrates. To complicate matters, the fourth hypothesis posits that powerful parties cannot, left to themselves, credibly promise to refrain from using their power for their own future gain—often at the expense of others. Specifically, without institutional and motivational constraint, powerful parties may seize the gains from others’ investments in potentially fruitful economic and political activities. Functional development thus requires resolving multiple, largely second-order, CAPs related to credibly restraining powerful actors—when such actors, simultaneously, exert disproportionate influence over institution building.

Smoking induces coordinated DNA methylation and gene expression changes in adipose tissue with consequences for metabolic health

Tobacco smoking is a risk factor for multiple diseases, including cardiovascular disease and diabetes. Many smoking-associated signals have been detected in the blood methylome, but the extent to which these changes are widespread to metabolically relevant tissues, and impact gene expression or cardio-metabolic health, remains unclear.We investigated smoking-associated DNA methylation and gene expression variation in adipose tissue from 542 healthy female twins with available well-characterized cardio-metabolic phenotype profiles. We identified 42 smoking-methylation and 42 smoking-expression signals, where five genes (AHRR, CYP1A1, CYP1B1, CYTL1, F2RL3) were both hypo-methylated and up-regulated in smokers. We replicated and validated a proportion of the signals in blood, adipose, skin, and lung tissue datasets, identifying tissue-shared effects. Smoking leaves systemic imprints on DNA methylation after smoking cessation, with stronger but shorter-lived effects on gene expression. We tested for associations between the observed smoking signals and several adiposity phenotypes that constitute cardio-metabolic disease risk. Visceral fat and android/gynoid ratio were associated with methylation at smoking-markers with functional impacts on expression, such as CYP1A1, and in signals shared across tissues, such as NOTCH1. At smoking-signals BHLHE40 and AHRR DNA methylation and gene expression levels in current smokers were predictive of future gain in visceral fat upon smoking cessation.Our results provide the first comprehensive characterization of coordinated DNA methylation and gene expression markers of smoking in adipose tissue, a subset of which link to human cardio-metabolic health and may give insights into the wide ranging risk effects of smoking across the body.Author SummaryTobacco smoking is the strongest environmental risk factor for human disease. Here, we investigate how smoking systemically changes methylome and transcriptome signatures in multiple tissues in the human body. We observe strong and coordinated epigenetic and gene expression changes in adipose tissue, some of which are mirrored in blood, skin, and lung tissue. Smoking leaves a strong short-lived impact on gene expression levels, while methylation changes are long-lasting after smoking cessation. We investigated if these changes observed in a metabolically-relevant (adipose) tissue had impacts on human disease, and observed strong associations with cardio-metabolic disease traits. Some of the smoking signals could predict future gain in obesity and cardio-metabolic disease risk in current smokers who subsequently go on to quit smoking. Our results provide novel insights into understanding the widespread health consequence of smoking outside the lung.

A Review of Control Options and Externalities for Verticillium Wilts

Plant pathogens migrate to new regions through human activities such as trade, where they may establish themselves and cause disease on agriculturally important crops. Verticillium wilt of lettuce, caused by Verticillium dahliae, is a soilborne fungus that was introduced to coastal California via infested spinach seeds. It has caused significant losses for lettuce growers. Once introduced, Verticillium wilt could be managed by fumigating with methyl bromide and chloropicrin, but this option is no longer available. Growers can also manage the disease by planting broccoli or not planting spinach. These control options require long-term investments for future gain. Verticillium wilt can also be prevented or controlled by testing and providing spinach seeds with little or no V. dahliae infestation. However, seed companies have been reluctant to test or clean spinach seeds, as spinach crops are not affected by Verticillium wilt. Thus, available control options are affected by externalities. Renters and other producers with short time horizons will not undertake long-term investments and seed companies do not take into account the effect of their decision not to test on lettuce producers. We review the literature on the economics of managing crop disease; discuss the economics of managing Verticillium wilt; and review the recent research on the externalities that arise with short-term growers, and between seed companies and growers due to Verticillium wilt. An externality arises whenever the actions of one individual or firm affects the payoffs to another individual or firm not involved in a specific transaction. These externalities have important implications for the management of Verticillium wilt and, more broadly, for the management of migratory pathogens and the diseases they cause in agriculture in general. This review is of interest to policy-makers, the producers, marketers, seed companies, and researchers.

Overlapping defaults. The case of intertemporal choices

People make different choices depending on which decision is the default option. In intertemporal choices, the default option is typically imposed externally. For example, people expect more for delaying the gain (default in the present) than are willing to pay for accelerating the future gain over the same period (default in the future). We claim that apart from the external default, people’s choices are also influenced by the internal (natural) default such as the time perspective resulting in the reference point in the present. By manipulating the congruency between the internal and external defaults, we show that incongruence between defaults decreases the strength of discounting of gains, but not of losses.

Scenes of Reenactment/Logics of Derivation in Dance

The spatial, temporal, and kinesthetic features of reenactment in dance also apply to what is perhaps the most creative and destructive figure of the present day, the derivative. Quite literally, derivatives restage past performance as a prospect of future gain, they seek profits from sudden shifts in equilibrium, mining volatility for inventive returns. As avatars of the ways in which value is realized in movement, derivatives invite consideration of what dance knows so well. Dance, of course, relies upon risk, but also engenders other ways of valuing the creation of the unexpected. Whereas finance insists upon obligatory movement, it lacks a language of motion that dance discloses. In short, if reenactment today assumes the body of a derivative, one should turn to movement practices to grasp the social kinesthetic.

The logic of skipped spawning in fish

That sexually mature fish skip reproduction, especially in response to poor condition, has been documented in many species. We present results from an energy-allocation life history model that shed light on the underlying logic of skipped spawning, based on the Northeast Arctic stock of Atlantic cod (Gadus morhua). The model predicts that skipped spawning is a regular phenomenon, with up to 30% of the sexually mature biomass skipping spawning. Spawning should be skipped if the expected future gain in reproductive output, discounted by survival, more than balances the expected reproductive success the current year. Skipped spawning was most common (i) among potential second-time spawners and (ii) early in life, (iii) when fishing mortality at the spawning grounds was high, (iv) when fishing mortality at the feeding grounds was low, (v) when natural mortality was low, and (vi) when the energetic and mortality costs associated with migration and spawning were high. Cod skipped spawning more often when food availability was both increased (opportunities for better growth) and decreased (too little energy for gonad development), and this pattern interacted with mortality rate. We conclude that skipped spawning may be more widespread than appreciated and highlight potential consequences for the understanding of stock–recruitment relationships.