“No Place Is So Dear to My Childhood”: Evangelicalism, Nostalgia, and the History of an American Hymn

This article tracks the surprising history of a love ballad about a lost sweetheart that went on to become a celebrated gospel hymn about the rural roots of America\u27s greatness. Titled “The Little Brown Church,” but sometimes called “The Church in the Wildwood,” the song\u27s evolution speaks to the ways in which nostalgia became central to the social and religious imagination of those American Protestants call themselves “evangelicals.” Though it first appeared in college songbooks after its publication in 1865, “The Little Brown Church” eventually became a favorite of evangelists, revivalists, and other gospel singers at the dawn of the twentieth century. For these new singers, “The Little Brown Church” spoke to more than just the simple faith they wished to restore. It also illustrated the centrality of white Protestants to the American experience at a moment when the hold these believers had on the nation was beginning to slip. And they would alter both the lyrics and the church\u27s history to bring the two in line. The process not only reveals how nostalgia for a bygone era became vital to those who think of themselves as evangelicals in the twentieth century, but also how evangelicalism itself is something of a historical construction

Corrigendum: the unknown and the unexplored: insights into the Pacific deep-sea following NOAA CAPSTONE expeditions

Published versio

The unknown and the unexplored: insights Into the Pacific deep-sea following NOAA CAPSTONE expeditions

Over a 3-year period, the National Oceanic and Atmospheric Administration (NOAA) organized and implemented a Pacific-wide field campaign entitled CAPSTONE: Campaign to Address Pacific monument Science, Technology, and Ocean NEeds. Under the auspices of CAPSTONE, NOAA mapped 597,230 km2 of the Pacific seafloor (with ∼61% of mapped area located within US waters), including 323 seamounts, conducted 187 ROV dives totaling 891.5 h of ROV benthic imaging time, and documented >347,000 individual organisms. This comprehensive effort yielded dramatic insight into differences in biodiversity across depths, regions, and features, at multiple taxonomic scales. For all deep sea taxonomic groups large enough to be visualized with the ROV, we found that fewer than 20% of the species were able to be identified. The most abundant and highest diversity taxa across the dataset were from three phyla (Cnidaria, Porifera, and Echinodermata). We further examined these phyla for taxonomic assemblage patterns by depth, geographic region, and geologic feature. Within each taxa, there were multiple genera with specific distribution and abundance by depth, region, and feature. Additionally, we observed multiple genera with broad abundance and distribution, which may focus future ecological research efforts. Novel taxa, records, and behaviors were observed, suggestive of many new types of species interactions, drivers of community composition, and overall diversity patterns. To date, only 13.8% of the Pacific has been mapped using modern methods. Despite the incredible amount of new known and unknown information about the Pacific deep-sea, CAPSTONE is far from the culminating experience the name suggests. Rather, it marks the beginning of a new era for exploration that will offer extensive opportunities via mapping, technology, analysis, and insights.Published versio

Differential Affinity and Catalytic Activity of CheZ in E. coli Chemotaxis

Push–pull networks, in which two antagonistic enzymes control the activity of a messenger protein, are ubiquitous in signal transduction pathways. A classical example is the chemotaxis system of the bacterium Escherichia coli, in which the kinase CheA and the phosphatase CheZ regulate the phosphorylation level of the messenger protein CheY. Recent experiments suggest that both the kinase and the phosphatase are localized at the receptor cluster, and Vaknin and Berg recently demonstrated that the spatial distribution of the phosphatase can markedly affect the dose–response curves. We argue, using mathematical modeling, that the canonical model of the chemotaxis network cannot explain the experimental observations of Vaknin and Berg. We present a new model, in which a small fraction of the phosphatase is localized at the receptor cluster, while the remainder freely diffuses in the cytoplasm; moreover, the phosphatase at the cluster has a higher binding affinity for the messenger protein and a higher catalytic activity than the phosphatase in the cytoplasm. This model is consistent with a large body of experimental data and can explain many of the experimental observations of Vaknin and Berg. More generally, the combination of differential affinity and catalytic activity provides a generic mechanism for amplifying signals that could be exploited in other two-component signaling systems. If this model is correct, then a number of recent modeling studies, which aim to explain the chemotactic gain in terms of the activity of the receptor cluster, should be reconsidered

Building a Quantum Engineering Undergraduate Program

Contribution: A roadmap is provided for building a quantum engineering education program to satisfy U.S. national and international workforce needs. Background: The rapidly growing quantum information science and engineering (QISE) industry will require both quantum-aware and quantum-proficient engineers at the bachelor\u27s level. Research Question: What is the best way to provide a flexible framework that can be tailored for the full academic ecosystem? Methodology: A workshop of 480 QISE researchers from across academia, government, industry, and national laboratories was convened to draw on best practices; representative authors developed this roadmap. Findings: 1) For quantum-aware engineers, design of a first quantum engineering course, accessible to all STEM students, is described; 2) for the education and training of quantum-proficient engineers, both a quantum engineering minor accessible to all STEM majors, and a quantum track directly integrated into individual engineering majors are detailed, requiring only three to four newly developed courses complementing existing STEM classes; 3) a conceptual QISE course for implementation at any postsecondary institution, including community colleges and military schools, is delineated; 4) QISE presents extraordinary opportunities to work toward rectifying issues of inclusivity and equity that continue to be pervasive within engineering. A plan to do so is presented, as well as how quantum engineering education offers an excellent set of education research opportunities; and 5) a hands-on training plan on quantum hardware is outlined, a key component of any quantum engineering program, with a variety of technologies, including optics, atoms and ions, cryogenic and solid-state technologies, nanofabrication, and control and readout electronics

Building a Quantum Engineering Undergraduate Program

The rapidly growing quantum information science and engineering (QISE) industry will require both quantum-aware and quantum-proficient engineers at the bachelor's level. We provide a roadmap for building a quantum engineering education program to satisfy this need. For quantum-aware engineers, we describe how to design a first quantum engineering course accessible to all STEM students. For the education and training of quantum-proficient engineers, we detail both a quantum engineering minor accessible to all STEM majors, and a quantum track directly integrated into individual engineering majors. We propose that such programs typically require only three or four newly developed courses that complement existing engineering and science classes available on most larger campuses. We describe a conceptual quantum information science course for implementation at any post-secondary institution, including community colleges and military schools. QISE presents extraordinary opportunities to work towards rectifying issues of inclusivity and equity that continue to be pervasive within engineering. We present a plan to do so and describe how quantum engineering education presents an excellent set of education research opportunities. Finally, we outline a hands-on training plan on quantum hardware, a key component of any quantum engineering program, with a variety of technologies including optics, atoms and ions, cryogenic and solid-state technologies, nanofabrication, and control and readout electronics. Our recommendations provide a flexible framework that can be tailored for academic institutions ranging from teaching and undergraduate-focused two- and four-year colleges to research-intensive universities.Comment: 25 pages, 2 figure

Common genetic variants in the CLDN2 and PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis

Pancreatitis is a complex, progressively destructive inflammatory disorder. Alcohol was long thought to be the primary causative agent, but genetic contributions have been of interest since the discovery that rare PRSS1, CFTR, and SPINK1 variants were associated with pancreatitis risk. We now report two significant genome-wide associations identified and replicated at PRSS1-PRSS2 (1×10-12) and x-linked CLDN2 (p < 1×10-21) through a two-stage genome-wide study (Stage 1, 676 cases and 4507 controls; Stage 2, 910 cases and 4170 controls). The PRSS1 variant affects susceptibility by altering expression of the primary trypsinogen gene. The CLDN2 risk allele is associated with atypical localization of claudin-2 in pancreatic acinar cells. The homozygous (or hemizygous male) CLDN2 genotype confers the greatest risk, and its alleles interact with alcohol consumption to amplify risk. These results could partially explain the high frequency of alcohol-related pancreatitis in men – male hemizygous frequency is 0.26, female homozygote is 0.07

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele