Preserve Local and Institution-Specific Data During Migration to a Network Cataloging Environment

During the fall of 2015, the Augusta University Libraries began the process of implementing Ex Libris’ nextgeneration library management solution, Alma. This process is occurring in various phases, with the initial steps being data clean-up and migration. As part of the migration process, cataloging records that are currently created and maintained by both university libraries will be migrated into a collaborative Alma network zone comprised of 29 institutions in the University System of Georgia (USG) consortium. The network zone will allow for collaborative cataloging among multiple libraries. One of the main challenges for Augusta University, however, was finding a way to preserve the libraries’ local data which included medical subject headings (MeSH) used by the health sciences library. This paper addresses the challenges faced and strategies employed by Augusta University Libraries to ensure local information was migrated from the existing Ex Libris’ Voyager traditional integrated library system (ILS) into Alma

Increasing Colorectal Cancer Screening Among Hispanic Primary Care Patients: RE-AIM Analysis.

Context: Hispanic adults experience disparities in rates of colorectal cancer (CRC) screening. This RE-AIM analysis encompassed a multilevel decision support and navigation intervention (DSNI) for CRC screening. Interim findings were previously presented; we now aim to share the final analysis, particularly for effectiveness and implementation. Objective: Apply RE-AIM framework to a completed randomized controlled trial of a CRC screening intervention for Hispanic adults Setting: Five primary care practices Patients or Other Participants: Potential participants included a sampling frame of 2,720 screening-eligible patients, ages 50-75, Hispanic ethnicity, without history of CRC and polyps. 400 participants were enrolled. Intervention/Instrument: Decision support and navigation by a bilingual Patient Assistant (PA) as compared to a standard mailed intervention (SI) Main and Secondary Outcome Measures: 1) Reach- Study participants as compared to sampling frame 2) Effectiveness- Screening adherence 3) Adoption- Number of practice participants to complete intervention, engagement of patient and stakeholder advisory committee (PASAC) 4) Implementation- Quantitative data pertaining to patient contacts and communication of screening plan to primary care practices, Qualitative data on PA and Telephone Interviewer (TI) experiences 5) Maintenance- Health system dissemination (Pending). Results: 1) Reach- Study participants differed from the sampling frame in that ages 50-59 were overrepresented. There were no differences in race, gender, or language. 2) Effectiveness- Screening adherence was significantly increased in the DSNI group (73%) as compared to the SI group (44%) (OR=3.48, CI: 2.29-4.29,

Common and low Frequency variants in MERTK are independently associated with multiple sclerosis susceptibility with discordant association dependent upon HLA-DRB1*15:01 status

Multiple Sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. The risk of developing MS is strongly influenced by genetic predisposition, and over 100 loci have been established as associated with susceptibility. However, the biologically relevant variants underlying disease risk have not been defined for the vast majority of these loci, limiting the power of these genetic studies to define new avenues of research for the development of MS therapeutics. It is therefore crucial that candidate MS susceptibility loci are carefully investigated to identify the biological mechanism linking genetic polymorphism at a given gene to the increased chance of developing MS. MERTK has been established as an MS susceptibility gene and is part of a family of receptor tyrosine kinases known to be involved in the pathogenesis of demyelinating disease. In this study we have refined the association of MERTK with MS risk to independent signals from both common and low frequency variants. One of the associated variants was also found to be linked with increased expression of MERTK in monocytes and higher expression of MERTK was associated with either increased or decreased risk of developing MS, dependent upon HLA-DRB1*15:01 status. This discordant association potentially extended beyond MS susceptibility to alterations in disease course in established MS. This study provides clear evidence that distinct polymorphisms within MERTK are associated with MS susceptibility, one of which has the potential to alter MERTK transcription, which in turn can alter both susceptibility and disease course in MS patients

Fine-mapping of the HNF1B multicancer locus identifies candidate variants that mediate endometrial cancer risk.

Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 × 10(-14), odds ratio = 0.86, 95% confidence interval = 0.82-0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression