An Absent Presence: Quaker Narratives of Journeys to America and Barbados, 1671-81

Through case studies of writings by George Fox, Alice Curwen and Joan Vokins, this article identifies a marked discrepancy in style and focus between early Quaker accounts of journeys to the American mainland and to Barbados. Accounts of the mainland journeys are detailed and often dramatic narratives which, like most early Quaker writing, read the spiritual in and from the places and people encountered, whilst those concerned with Barbados are brief, bland and apparently unconcerned with the immanence of God in the material and social world. An explanation for this discrepancy is sought in the particular cultural and social circumstances of Barbados, and in particular in the pressures on the Quaker habit of elision between the social and the spiritual brought to bear by the institution and practice of slavery

The Journal of George Fox: A Technology of Presence

Critics have debated at length whether George Fox\u27s Journal is primarily to be understood within the tradition of seventeenth-century autobiographical writing, or as an historical account of the early Quaker movement. This article suggests that this is a false dichotomy, and argues instead that the Journal might be reconceived as a \u27technology of presence\u27: that is, in its attention both to the figure of Fox and to the detailed chronicling of time and place, its principal narrative impetus was to record, demonstrate and reproduce the presence of the returned and indwelling Christ. The Journal thus constitutes, in its form and narrative procedure, an enactment of core Quaker belief

Going nowhere:the stranger and pilgrim in the Journal of George Fox

This article examines the rhetoric and poetics of movement and stillness in early Quaker culture. George Fox urged Friends to ‘stand still’, and stillness was valued as the godly heart of the meeting for worship. Nonetheless, the lives of Fox and other early Public Friends were insistently peripatetic, and Fox’s Journal is largely structured around accounts of his travels. How, then, might we understand the place of the journey and the rhetoric of movement in early Quaker practice and culture? By means of a close analysis of the figure of the stranger in Fox’s Journal and a comparative reading of this text in relation to seventeenth-century pilgrimage literature, the article argues that the early Quakerism’s conception of the inward light as a unifying force reframed the meanings of travel in a way that informed both the practice and the writings of early Friends

\u27The Journeys of George Fox, 1652-1653\u27: Interim Report on a Research Project and Website

The research project on \u27Early Quakers in the North West\u27 recently issued a test version of the opening sections of the website in which it will publish its findings. Here the project member responsible for the website\u27s construction describes its structure and ethos, and explains why web presentation is particularly well suited to this topic, as a research tool as well as a means of publication. At present the account by George Fox of his travels through \u27the 1652 country\u27 provides the organising narrative thread. A new electronic edition of the three versions of Fox\u27s Journal for 1652-53 showcases how the medium facilitates an editorial presentation and comparison of texts which is much more user-friendly than a printed book. High-resolution scans have highlighted Fox\u27s methods of oral composition. The supporting materials, contemporary and later, on places and routes show the extent of topographical change that has taken place. Biographies and associated contemporary texts are already shifting the focus from Fox\u27s programme to those of the other \u27Publishers of Truth\u27

Detailed empirical studies of student information storing in the context of distributed design team-based project work

This paper presents the findings of six empirical case studies investigating the information stored by engineering design students in distributed team-based Global Design Projects. The aim is to understand better how students store distributed design information in order to prepare them for work in today‟s international and global context. This paper outlines the descriptive element of the work, the qualitative and quantitative research methods used and the results. It discusses the issues around the emergent themes of information storing; information storing systems; information storing patterns; and information strategy, making recommendations; establishing that there is a need for more prescriptive measures to supporting distributed design information management. This work will be of great value to industry also

Shared genetic aetiology of puberty timing between sexes and with health-related outcomes.

Understanding of the genetic regulation of puberty timing has come largely from studies of rare disorders and population-based studies in women. Here, we report the largest genomic analysis for puberty timing in 55,871 men, based on recalled age at voice breaking. Analysis across all genomic variants reveals strong genetic correlation (0.74, P=2.7 × 10(-70)) between male and female puberty timing. However, some loci show sex-divergent effects, including directionally opposite effects between sexes at the SIM1/MCHR2 locus (Pheterogeneity=1.6 × 10(-12)). We find five novel loci for puberty timing (P<5 × 10(-8)), in addition to nine signals in men that were previously reported in women. Newly implicated genes include two retinoic acid-related receptors, RORB and RXRA, and two genes reportedly disrupted in rare disorders of puberty, LEPR and KAL1. Finally, we identify genetic correlations that indicate shared aetiologies in both sexes between puberty timing and body mass index, fasting insulin levels, lipid levels, type 2 diabetes and cardiovascular disease.This work was supported by the Medical Research Council [U106179472; MC_U106179472; U106179471; MC_U106179471] and the National Human Genome Research Institute of the National Institutes of Health (grant number R44HG006981 to 23andMe)This is the final version of the article. It was first available from NPG via http://dx.doi.org/10.1038/ncomms984

An investigation of the effects of lipid-lowering medications: genome-wide linkage analysis of lipids in the HyperGEN study

BACKGROUND: Use of anti-hyperlipidemic medications compromises genetic analysis because of altered lipid profiles. We propose an empirical method to adjust lipid levels for medication effects so that the adjusted lipid values substitute the unmedicated lipid values in the genetic analysis. RESULTS: Published clinical trials were reviewed for HMG-CoA reductase inhibitors and fibric acid derivatives as mono-drug therapy. HMG-CoA reductase inhibitors showed similar effects in African Americans (AA) and non-African Americans (non-AA) for lowering total cholesterol (TC, -50.7 mg/dl), LDL cholesterol (LDL-C, -48.1 mg/dl), and triglycerides (TG, -19.7 mg/dl). Their effect on increasing HDL cholesterol (HDL-C) in AA (+0.4 mg/dl) was lower than in Non-AA (+2.3 mg/dl). The effects of fibric acid derivatives were estimated as -46.1 mg/dl for TC, -40.1 mg/dl for LDL-C, and +5.9 mg/dl for HDL-C in non-AA. The corresponding effects in AA were less extreme (-20.1 mg/dl, -11.4 mg/dl, and +3.1 mg/dl). Similar effect for TG (59.0 mg/dl) was shown in AA and non-AA. The above estimated effects were applied to a multipoint variance components linkage analysis on the lipid levels in 2,403 Whites and 2,214 AA in the HyperGEN study. The familial effects did vary depending on whether the lipids were adjusted for medication use. For example, the heritabilities increased after medication adjustment for TC and LDL-C, but did not change significantly for HDL-C and TG. CONCLUSION: Ethnicity-specific medication adjustments using our empirical method can be employed in epidemiological and genetic analysis of lipids.National Heart, Lung, and Blood Institute (HL554471, HL54472, HL54473, HL54495, HL54496, HL54497, HL54509, HL54515

Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use

Tobacco and alcohol use are leading causes of mortality that influence risk for many complex diseases and disorders 1 . They are heritable 2,3 and etiologically related 4,5 behaviors that have been resistant to gene discovery efforts 6–11 . In sample sizes up to 1.2 million individuals, we discovered 566 genetic variants in 406 loci associated with multiple stages of tobacco use (initiation, cessation, and heaviness) as well as alcohol use, with 150 loci evidencing pleiotropic association. Smoking phenotypes were positively genetically correlated with many health conditions, whereas alcohol use was negatively correlated with these conditions, such that increased genetic risk for alcohol use is associated with lower disease risk. We report evidence for the involvement of many systems in tobacco and alcohol use, including genes involved in nicotinic, dopaminergic, and glutamatergic neurotransmission. The results provide a solid starting point to evaluate the effects of these loci in model organisms and more precise substance use measures

Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk

The timing of puberty is a highly polygenic childhood trait that is epidemiologically associated with various adult diseases. Using 1000 Genomes Project-imputed genotype data in up to similar to 370,000 women, we identify 389 independent signals (P <5 x 10(-8)) for age at menarche, a milestone in female pubertal development. In Icelandic data, these signals explain similar to 7.4% of the population variance in age at menarche, corresponding to similar to 25% of the estimated heritability. We implicate similar to 250 genes via coding variation or associated expression, demonstrating significant enrichment in neural tissues. Rare variants near the imprinted genes MKRN3 and DLK1 were identified, exhibiting large effects when paternally inherited. Mendelian randomization analyses suggest causal inverse associations, independent of body mass index (BMI), between puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men. In aggregate, our findings highlight the complexity of the genetic regulation of puberty timing and support causal links with cancer susceptibility

Association of whole-genome and NETRIN1 signaling pathway-derived polygenic risk scores for Major Depressive Disorder and white matter microstructure in UK Biobank

Background: Major depressive disorder is a clinically heterogeneous psychiatric disorder with a polygenic architecture. Genome-wide association studies have identified a number of risk-associated variants across the genome and have reported growing evidence of NETRIN1 pathway involvement. Stratifying disease risk by genetic variation within the NETRIN1 pathway may provide important routes for identification of disease mechanisms by focusing on a specific process, excluding heterogeneous risk-associated variation in other pathways. Here, we sought to investigate whether major depressive disorder polygenic risk scores derived from the NETRIN1 signaling pathway (NETRIN1-PRSs) and the whole genome, excluding NETRIN1 pathway genes (genomic-PRSs), were associated with white matter microstructure. Methods: We used two diffusion tensor imaging measures, fractional anisotropy (FA) and mean diffusivity (MD), in the most up-to-date UK Biobank neuroimaging data release (FA: n = 6401; MD: n = 6390). Results: We found significantly lower FA in the superior longitudinal fasciculus (β = −.035, p =.029) and significantly higher MD in a global measure of thalamic radiations (β =.029, p =.021), as well as higher MD in the superior (β =.034, p =.039) and inferior (β =.029, p =.043) longitudinal fasciculus and in the anterior (β =.025, p =.046) and superior (β =.027, p =.043) thalamic radiation associated with NETRIN1-PRS. Genomic-PRS was also associated with lower FA and higher MD in several tracts. Conclusions: Our findings indicate that variation in the NETRIN1 signaling pathway may confer risk for major depressive disorder through effects on a number of white matter tracts