The U.S. public’s support for being tough on crime has been a main determinant of changes to the incarceration rate

The U.S. is famous for being the country with the highest incarceration rate in the world – but what has driven the massive expansion of imprisonment in the last forty years? In new research that tracks public attitudes, Peter K. Enns finds that the public’s punitiveness is closely related to changes in the incarceration rate. He suggests that this stems not only from voters enacting laws such as ‘Three Strikes’, but also through the influence on criminal justice policy of state and federal legislators, who rely on public support for reelection

Using Election Forecasts to Understand the Potential Influence of Campaigns, Media, and the Law in U.S. Presidential Elections

How do campaigns, media, and voting laws influence the outcome of U.S. Presidential elections? Political scientists often argue that these factors influence outcomes much less than commonly thought. To illustrate this argument, we show that we can predict the presidential vote in each state with a high degree of accuracy. Specifically, between 2004 and 2016, we correctly predict 94% of all state presidential vote outcomes. Our predictions are based on a forecasting model of the Electoral College, based primarily on each state’s approval rating of the incumbent president (using almost 90,000 survey responses from June and July of election years), current economic conditions in each state, and state votes in the previous election. We use these forecasts to help establish the upper bounds of campaign and media effects. We argue that identifying the limits of these effects is a critical step when trying to estimate their impact. We also show how our forecasts can be used to test the aggregate effects of election-related laws, such as Florida’s Amendment 4—which enfranchised hundreds of thousands of Floridians who previously could not vote due to felony convictions—and voter ID laws, whose effects are notoriously difficult to study. We have made our data publicly available to facilitate further research on these topics

Variations in Adipokine Genes AdipoQ, Lep, and LepR are Associated with Risk for Obesity-Related Metabolic Disease: The Modulatory Role of Gene-Nutrient Interactions

Obesity rates are rapidly increasing worldwide and facilitate the development of many related disease states, such as cardiovascular disease, the metabolic syndrome, type 2 diabetes mellitus, and various types of cancer. Variation in metabolically important genes can have a great impact on a population's susceptibility to becoming obese and/or developing related complications. The adipokines adiponectin and leptin, as well as the leptin receptor, are major players in the regulation of body energy homeostasis and fat storage. This paper summarizes the findings of single nucleotide polymorphisms in these three genes and their effect on obesity and metabolic disease risk. Additionally, studies of gene-nutrient interactions involving adiponectin, leptin, and the leptin receptor are highlighted to emphasize the critical role of diet in susceptible populations

The uniform nature of mass opinion

This dissertation consists of three distinct chapters, which develop and test a theory of Proportional Message Reception. Chapter 1 outlines the theory of Proportional Message Reception and the resulting hypothesis of uniform opinion change. I test the hypothesis using individual-level and sub-aggregate data on Vietnam attitudes and defense spending preferences. Chapter 2 examines the implications of Proportional Message reception and uniform opinion change for welfare attitudes and inequality in the United States. Chapter 3 questions previous conceptions of opinion aggregation by showing that all segments of the public update their Policy Mood in response to changing economic conditions. The three chapters show that it is the proportion of countervailing messages an individual receives, not the number of messages, that matters for opinion change. Furthermore, the analyses demonstrate - in a substantial departure from previous literature - that the most and least politically aware segments of the public update their opinions at the same time, in the same direction, and in response to the same pattern of messages

Conditional Status Quo Bias and Top Income Shares: How U.S. Political Institutions Have Benefited the Rich

This article develops and tests a model of conditional status quo bias and American inequality. We find that institutional features that bias policy outcomes toward the status quo have played a central role in the path of inequality. Using time-series analysis of top income shares during the post-Depression period, we identify the Senate as a key actor in the politics of income inequality. Our findings suggest that the supermajoritarian nature of the Senate and policy stagnation, when coupled with economic and social factors that produce rising inequality, create a situation in which inequality becomes difficult to reverse

Moving forward with time series analysis

In a recent Research and Politics article, we showed that for many types of time series data, concerns about spurious relationships can be overcome by following standard procedures associated with cointegration tests and the general error correction model (GECM). Matthew Lebo and Patrick Kraft (LK) incorrectly argue that our recommended approach will lead researchers to identify false (i.e., spurious) relationships. In this article, we show how LK\u27s response is incorrect or misleading in multiple ways. Most importantly, when we correct their simulations, their results reinforce our previous findings, highlighting the utility of the GECM when estimated and interpreted correctly

Congressional gridlock helps to make income inequality worse

Last December, President Obama warned of ‘dangerous and growing inequality’ in America, reflecting growing concerns that inequality is increasing, especially in relation to other countries. Peter K. Enns, Nathan J. Kelly, Jana Morgan, Thomas Volscho and Christopher Witko investigate the role of what they argue is a major contributing factor to rising inequality: the tendency for the current political and economic conditions to maintain the policy status quo. They argue that the increasing political polarization that makes it harder for Congress to pass laws in turn contributes to rising inequality, especially when inequality is already growing rapidly

The Molecular Mechanism for Receptor-Stimulated Iron Release from the Plasma Iron Transport Protein Transferrin

Human transferrin receptor 1 (TfR) binds iron-loaded transferrin (Fe-Tf) and transports it to acidic endosomes where iron is released in a TfR-facilitated process. Consistent with our hypothesis that TfR binding stimulates iron release from Fe-Tf at acidic pH by stabilizing the apo-Tf conformation, a TfR mutant (W641A/F760A-TfR) that binds Fe-Tf, but not apo-Tf, cannot stimulate iron release from Fe-Tf, and less iron is released from Fe-Tf inside cells expressing W641A/F760A-TfR than cells expressing wild-type TfR (wtTfR). Electron paramagnetic resonance spectroscopy shows that binding at acidic pH to wtTfR, but not W641A/F760A-TfR, changes the Tf iron binding site ≥30 Å from the TfR W641/F760 patch. Mutation of Tf histidine residues predicted to interact with the W641/F760 patch eliminates TfR-dependent acceleration of iron release. Identification of TfR and Tf residues critical for TfR-facilitated iron release, yet distant from a Tf iron binding site, demonstrates that TfR transmits long-range conformational changes and stabilizes the conformation of apo-Tf to accelerate iron release from Fe-Tf

Ferristatin II Promotes Degradation of Transferrin Receptor-1 In Vitro and In Vivo

Previous studies have shown that the small molecule iron transport inhibitor ferristatin (NSC30611) acts by down-regulating transferrin receptor-1 (TfR1) via receptor degradation. In this investigation, we show that another small molecule, ferristatin II (NSC8679), acts in a similar manner to degrade the receptor through a nystatin-sensitive lipid raft pathway. Structural domains of the receptor necessary for interactions with the clathrin pathway do not appear to be necessary for ferristatin II induced degradation of TfR1. While TfR1 constitutively traffics through clathrin-mediated endocytosis, with or without ligand, the presence of Tf blocked ferristatin II induced degradation of TfR1. This effect of Tf was lost in a ligand binding receptor mutant G647A TfR1, suggesting that Tf binding to its receptor interferes with the drug’s activity. Rats treated with ferristatin II have lower TfR1 in liver. These effects are associated with reduced intestinal 59Fe uptake, lower serum iron and transferrin saturation, but no change in liver non-heme iron stores. The observed hypoferremia promoted by degradation of TfR1 by ferristatin II appears to be due to induced hepcidin gene expression