Why US Senators obstruct some executive agency nominations over others

The average delay between an executive nomination and confirmation by the US Senate is 120 days, but some nominees can experience delays of more than 400 or 500 days. In new research which examines over 8,000 bureaucratic nominations over 25 years, Ian Ostrander finds that nominations are targeted for delay based on their policy value, public importance, and the perceived ideology of the agency in question. For example, important agencies with low public importance, such as the Federal Election Commission, are often targeted by Senators for nomination delays

Winning the Waiting Game: Senatorial Delay in Executive Nominations

Presidents have a strong incentive to control executive agencies through the nomination of like-minded and responsive individuals to leadership posts. The Senate, however, must provide its advice and consent for appointments to these key positions. While most nominees are successfully confirmed, this success rate tends to mask wide variation in the length of time it takes the Senate to make a decision. Delay of critical nominees can influence the character of an agency while hampering the policy ambitions of a president. In this way the power to delay can be as important as the power to reject a nominee. Building on prior literature, I suggest a conditional theory of delay based upon the ideological predispositions of agencies relative to a president. Using a novel data set of several thousand executive nominations from 1987 to 2010, this project tests hypotheses related to delay, failure, and ultimately considers the merits of potential reforms. My findings suggest that agency predispositions along with position level, independence, and political contexts are all important predictors of obstruction. These results help to explain the context and history of conflict over executive nominations as well as why some nominees are delayed or fail while other, seemingly similar, nominees are not

Anxiety, Depression, Immunity, Quality of Life, and Cannabis in Appalachia

As decriminalization of cannabis in the United States increases, understanding how cannabis use may alter physical and mental health is important. The Appalachian Mountain region is an area with poor support systems, stigma against mental health, and historic drug use problems, resulting in residents being more vulnerable to societal change. The theoretical framework for this research is psychoneuroimmunology (PNI), which is the study of the interconnections between psychology, neurology, and immunology as a holistic approach to health. Via SurveyMonkey, 160 participants completed the study, and data were based on self-reporting of cannabis use patterns in relation to anxiety, depression, immunity, and quality of life. This quantitative research study involved using multiple regression analysis to determine if relationships exist between longevity and frequency of cannabis use and anxiety, depression, immune function, and quality of life. Findings found that longer histories of cannabis use reduced anxiety and depression levels, while frequency of use had a non-linear relationship with anxiety where low and high frequency of use reduced scores compared to intermittent use. Cannabis was found to worsen immune function scores. Quality of life was unaffected by cannabis use frequency or longevity, but perceived quality of life improved. The data set was created to capture a baseline for future research involving the Appalachian Mountain region to improve the livelihood and quality of life of residents and protect them from further exploitation

Global Patterns of Prostate Cancer Incidence, Aggressiveness, and Mortality in Men of African Descent

Prostate cancer (CaP) is the leading cancer among men of African descent in the USA, Caribbean, and Sub-Saharan Africa (SSA). The estimated number of CaP deaths in SSA during 2008 was more than five times that among African Americans and is expected to double in Africa by 2030. We summarize publicly available CaP data and collected data from the men of African descent and Carcinoma of the Prostate (MADCaP) Consortium and the African Caribbean Cancer Consortium (AC3) to evaluate CaP incidence and mortality in men of African descent worldwide. CaP incidence and mortality are highest in men of African descent in the USA and the Caribbean. Tumor stage and grade were highest in SSA. We report a higher proportion of T1 stage prostate tumors in countries with greater percent gross domestic product spent on health care and physicians per 100,000 persons. We also observed that regions with a higher proportion of advanced tumors reported lower mortality rates. This finding suggests that CaP is underdiagnosed and/or underreported in SSA men. Nonetheless, CaP incidence and mortality represent a significant public health problem in men of African descent around the world

Fast and efficient QTL mapper for thousands of molecular phenotypes

In order to discover quantitative trait loci, multi-dimensional genomic datasets combining DNA-seq and ChiP-/RNA-seq require methods that rapidly correlate tens of thousands of molecular phenotypes with millions of genetic variants while appropriately controlling for multiple testing

Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10−15), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification

Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction.

Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction

Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe

Replication Data for: The Logic of Collective Inaction: Senatorial Delay in Executive Nominations

While most executive nominees are successfully confirmed, this success masks wide variation in how long it takes the Senate to decide. Delay of critical nominees influences the character and effectiveness of agencies while hampering the policy ambitions of presidents. The exact logic of which nominees are targeted for delay and why, however, remains difficult to uncover. Building on prior literature, this project suggests that delay can be used to protect allied agencies from presidential politicization. Using a data set of several thousand executive nominations from 1987 to 2012, the ideological predisposition of an agency relative to the President is demonstrated to influence senatorial delay. Ultimately, these findings help explain why some nominees are delayed while other, seemingly similar, nominees are not