Robert O\u27Neil Bristow Papers - Accession 3

Robert O’Neil Bristow (1926-2018) was an accomplished writer, author, and professor of journalism at Winthrop College from 1962-1987. The Robert O. Bristow Papers consist of drafts, revisions, galley proofs, notices of publication, book reviews, promotional literature and photographs, mainly related to the sale, publication, promotion and review of four Bristow novels: Time for Glory was published in 1968, Night Season in 1970, A Faraway Drummer in 1972 and Laughter in Darkness was originally called Rebel in Darkness. The papers cover the period from 1961-1974 with all of the material pertaining to the four published novels extending from 1967 to 1974.https://digitalcommons.winthrop.edu/manuscriptcollection_findingaids/2616/thumbnail.jp

A Risk-Adjusted Model for Ovarian Cancer Care and Disparities in Access to High-Performing Hospitals.

ObjectiveTo validate the observed/expected ratio for adherence to ovarian cancer treatment guidelines as a risk-adjusted measure of hospital quality care, and to identify patient characteristics associated with disparities in access to high-performing hospitals.MethodsThis was a retrospective population-based study of stage I-IV invasive epithelial ovarian cancer reported to the California Cancer Registry between 1996 and 2014. A fit logistic regression model, which was risk-adjusted for patient and disease characteristics, was used to calculate the observed/expected ratio for each hospital, stratified by hospital annual case volume. A Cox proportional hazards model was used for survival analyses, and a multivariable logistic regression model was used to identify independent predictors of access to high-performing hospitals.ResultsThe study population included 30,051 patients who were treated at 426 hospitals: low observed/expected ratio (n=304) 23.5% of cases; intermediate observed/expected ratio (n=92) 57.8% of cases; and high observed/expected ratio (n=30) 18.7% of cases. Hospitals with high observed/expected ratios were significantly more likely to deliver guideline-adherent care (53.3%), compared with hospitals with intermediate (37.8%) and low (27.5%) observed/expected ratios (P<.001). Median disease-specific survival time ranged from 73.0 months for hospitals with high observed/expected ratios to 48.1 months for hospitals with low observed/expected ratios (P<.001). Treatment at a hospital with a high observed/expected ratio was an independent predictor of superior survival compared with hospitals with intermediate (hazard ratio [HR] 1.06, 95% CI 1.01-1.11, P<.05) and low (HR 1.10, 95% CI 1.04-1.16, P<.001) observed/expected ratios. Being of Hispanic ethnicity (odds ratio [OR] 0.85, 95% CI 0.78-0.93, P<.001, compared with white), having Medicare insurance (OR 0.74, 95% CI 0.68-0.81 P<.001, compared with managed care), having a Charlson Comorbidity Index score of 2 or greater (OR 0.91, 95% CI 0.83-0.99, P<.05), and being of lower socioeconomic status (lowest quintile OR 0.41, 95% CI 0.36-0.46, P<.001, compared with highest quintile) were independent negative predictors of access to a hospital with a high observed/expected ratio.ConclusionOvarian cancer care at a hospital with a high observed/expected ratio is an independent predictor of improved survival. Barriers to high-performing hospitals disproportionately affect patients according to sociodemographic characteristics. Triage of patients with suspected ovarian cancer according to a performance-based observed/expected ratio hospital classification is a potential mechanism for expanded access to expert care

Divergent mutational processes distinguish hypoxic and normoxic tumours.

Many primary tumours have low levels of molecular oxygen (hypoxia), and hypoxic tumours respond poorly to therapy. Pan-cancer molecular hallmarks of tumour hypoxia remain poorly understood, with limited comprehension of its associations with specific mutational processes, non-coding driver genes and evolutionary features. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we quantify hypoxia in 1188 tumours spanning 27 cancer types. Elevated hypoxia associates with increased mutational load across cancer types, irrespective of underlying mutational class. The proportion of mutations attributed to several mutational signatures of unknown aetiology directly associates with the level of hypoxia, suggesting underlying mutational processes for these signatures. At the gene level, driver mutations in TP53, MYC and PTEN are enriched in hypoxic tumours, and mutations in PTEN interact with hypoxia to direct tumour evolutionary trajectories. Overall, hypoxia plays a critical role in shaping the genomic and evolutionary landscapes of cancer

Updating State Comprehensive Outdoor Recreation Plans, an Application of Geographic Information Systems and Census Data

Abstract Modeling supply and demand data is useful for regional outdoor recreation planning. At the statewide level, State Comprehensive Outdoor Recreation Plans (SCORPs) are prepared to satisfy the requirements of the Land and Water Conservation Fund (LWCF). In Massachusetts, the most recent SCORP was prepared in 2006. Two of the primary tasks were updating the recreation resource inventory statewide and developing an extensive GIS data base. For the demand side, the Commonwealth of Massachusetts utilized data collected in 1995 that focused on recreation site usage patterns, assessed satisfaction with outdoor recreation areas, and evaluated unmet needs. This paper presents an example of updating SCORPs using current demographic data (US Census) and geographic supply data (MassGIS)

Metabolic inflammatory response to major upper gastrointestinal surgery

Imperial Users onl

CheMin-V: A Definitive Mineralogy Instrument for Landed Science on Venus

An X-ray diffraction instrument is described that will provide quantitative mineralogical analyses of up to 4 individual samples of Venus regolith in ~1 hour

Spatial Transformation of a Layer-To-Layer Control Model for Selective Laser Melting

Selective Laser Melting (SLM) is an Additive Manufacturing (AM) technique with challenges in its complexity of process parameters and lack of control schemes. Traditionally, people tried time-domain or frequency-domain control methods, but the complexity of the process goes beyond these methods. In this paper, a novel spatial transformation of SLM models is proposed, which transforms the time-domain process into a spatial domain model and, thus, allows for state-space layer-to-layer control methods. In a space domain, this also provides the convenience of modelling laser path changes. Finally, a layer-to-layer Iterative Learning Control (ILC) method is designed and demonstrates the methodology of spatial control for SLM. A simulation demonstrates its application and performance

Inhibition of α4-integrin stimulates epicardial–mesenchymal transformation and alters migration and cell fate of epicardially derived mesenchyme

AbstractEpithelial–mesenchymal transformation of the embryonic epicardium produces the subepicardial mesenchyme that is essential for normal coronary vascular development. Gene targeting experiments in mice have demonstrated an essential role for α4-integrin in normal epicardial development, but the precise cellular consequences of α4-integrin loss remain uncertain. To better understand the function of α4-integrin in epicardial development, we constructed a replication-incompetent adenovirus (AdlacZα4AS) that expresses antisense chicken α4-integrin as the 3′ untranslated region of a lacZ reporter gene. This construct effectively labeled cells while greatly reducing levels of α4-integrin mRNA and protein. In quail chick chimeras, transplanted epicardial cells infected with AdlacZα4AS adhered to the heart and were incorporated into the epicardium, but 4 days after grafting, were largely absent from the epicardial epithelium, recapitulating the defect in α4-null mice. This did not result from epicardial cell apoptosis or anomalous migration of epicardial cells to extracardiac sites. Rather, AdlacZα4AS-infected epicardial cells were particularly invasive, being three to four times more likely to migrate to the interstitium of the myocardium than AdlacZ-infected epicardial cells. Accelerated epicardial–mesenchymal transformation and migration of α4-negative epicardium was observed in an organ culture system that does not require prior culture of epicardial cells. Remarkably, AdlacZα4AS infection also prevented targeting of epicardially derived mesenchyme to the media of developing coronary vasculature in the myocardial interstitium. This study provides evidence that epicardial α4-integrin normally restrains epicardial–mesenchymal transformation, invasion, and migration and is essential for correct targeting of epicardially derived mesenchyme to the developing coronary vasculature