Living the Library of the Future: A Reminiscence

How do we create the library of the future? Throughout my library career I\u27ve attempted to make the library of the future a reality. Starting with Holorith cards to Dialog and BRS AfterDark, to COMCats and Online catalogs, to CD-ROM database networks, to Gopher, InfoTrac 2000, and the Web; from paper to media to bits; from preservation to digital curation; from owning and storing to licensing and accessing to creating and collaborating, I learned that we\u27re always creating the library of the future, that it\u27s always just beyond our reach. While everything is new, much remains and some returns

The Library of the Future and the Idea of Change

Presentation at the University of Nevada - Reno, 2 May 1996

Reference Services in Minnesota: Alive or Dead?

This document was written to guide my comments at the MINITEX conference: Reference Services in Minnesota: Dead or Alive, held on Thursday, November 9, 1995, at the Earle Brown Center at the University of Minnesota, St. Paul Campus. The conference was organized to discuss the themes set forward in Is Traditional Reference Service Obsolete, the lead article for the Symposium on Reference Service in Journal of Academic Librarianship, volume 21, number 1, January 1995

Designing and Implementing Instruction on the World Wide Web: A Case Study

This case study describes some tips and lessons learned from a project at St. Cloud State University designed to teach information literacy over the World Wide Web. The information literacy project has two primary components: Under the auspices of LEO: Literacy Education Online (a project to disseminate resources to improve composition and writing skills), to develop content resources providing guidance in library and internet use and application in research; Under the Center for Information Media, to disseminate self-paced instructional modules on library and internet use and application in research that could be used in credit-generating courses. As the two components exhibited considerable overlap, it was decided to develop inter-related resources within a single project environment

Effects of Monobutyl and Di(n-butyl) Phthalate in Vitro on Steroidogenesis and Leydig Cell Aggregation in Fetal Testis Explants from the Rat: Comparison with Effects in Vivo in the Fetal Rat and Neonatal Marmoset and in Vitro in the Human

BACKGROUND: Certain phthalates can impair Leydig cell distribution and steroidogenesis in the fetal rat in utero, but it is unknown whether similar effects might occur in the human. OBJECTIVES: Our aim in this study was to investigate the effects of di(n-butyl) phthalate (DBP), or its metabolite monobutyl phthalate (MBP), on testosterone production and Leydig cell aggregation (LCA) in fetal testis explants from the rat and human, and to compare the results with in vivo findings for DBP-exposed rats. We also wanted to determine if DBP/MBP affects testosterone production in vivo in the neonatal male marmoset. METHODS: Fetal testis explants obtained from the rat [gestation day (GD)19.5] and from the human (15–19 weeks of gestation) were cultured for 24–48 hr with or without human chorionic gonadotropin (hCG) or 22R-hydroxycholesterol (22R-OH), and with or without DBP/MBP. Pregnant rats and neonatal male marmosets were dosed with 500 mg/kg/day DBP or MBP. RESULTS: Exposure of rats in utero to DBP (500 mg/kg/day) for 48 hr before GD21.5 induced major suppression of intratesticular testosterone levels and cytochrome P450 side chain cleavage enzyme (P450scc) expression; this short-term treatment induced LCA, but was less marked than longer term (GD13.5–20.5) DBP treatment. In vitro, MBP (10(−3) M) did not affect basal or 22R-OH-stimulated testosterone production by fetal rat testis explants but slightly attenuated hCG-stimulated steroidogenesis; MBP induced minor LCA in vitro. None of these parameters were affected in human fetal testis explants cultured with 10(−3) M MBP for up to 48 hr. Because the in vivo effects of DBP/MBP were not reproduced in vitro in the rat, the absence of MBP effects in vitro on fetal human testes is inconclusive. In newborn (Day 2–7) marmosets, administration of a single dose of 500 mg/kg MBP significantly (p = 0.019) suppressed blood testosterone levels 5 hr later. Similar treatment of newborn co-twin male marmosets for 14 days resulted in increased Leydig cell volume per testis (p = 0.011), compared with co-twin controls; this is consistent with MBP-induced inhibition of steroidogenesis followed by compensatory Leydig cell hyperplasia/hypertrophy. CONCLUSIONS: These findings suggest that MBP/DBP suppresses steroidogenesis by fetal-type Leydig cells in primates as in rodents, but this cannot be studied in vitro

Protocol for a randomised controlled trial of an outreach support program for family carers of older people discharged from hospital

Background: Presentations to hospital of older people receiving family care at home incur substantial costs for patients, families, and the health care system, yet there can be positive carer outcomes when systematically assessing/addressing their support needs, and reductions in older people's returns to hospital attributed to appropriate discharge planning. This study will trial the Further Enabling Care at Home program, a 2-week telephone outreach initiative for family carers of older people returning home from hospital. Hypotheses are that the program will (a) better prepare families to sustain their caregiving role and (b) reduce patients' re-presentations/readmissions to hospital, and/or their length of stay; also that reduced health system costs attributable to the program will outweigh costs of its implementation. Methods/Design: In this randomised controlled trial, family carers of older patients aged 70+ discharged from a Medical Assessment Unit in a Western Australian tertiary hospital, plus the patients themselves, will be recruited at discharge (N = 180 dyads). Carers will be randomly assigned (block allocation, assessors blinded) to receive usual care (control) or the new program (intervention). The primary outcome is the carer's self-reported preparedness for caregiving (Preparedness for Caregiving Scale administered within 4 days of discharge, 2-3 weeks post-discharge, 6 weeks post-discharge). To detect a clinically meaningful change of two points with 80 % power, 126 carers need to complete the study. Patients' returns to hospital and subsequent length of stay will be ascertained for a minimum of 3 months after the index admission. Regression analyses will be used to determine differences in carer and patient outcomes over time associated with the group (intervention or control). Data will be analysed using an Intention to Treat approach. A qualitative exploration will examine patients' and their family carers' experiences of the new program (interviews) and explore the hospital staff's perceptions (focus groups). Process evaluation will identify barriers to, and facilitators of, program implementation. A comprehensive economic evaluation will determine cost consequences. Discussion: This study investigates a novel approach to identifying and addressing family carers' needs following discharge from hospital of the older person receiving care. If successful, the program has potential to be incorporated into routine post-discharge support. Trial registration: Australian and New Zealand Clinical Trial Registry: ACTRN12614001174673

Paradoxical patterns of sinusoidal obstruction syndrome-like liver injury in aged female CD-1 mice triggered by cannabidiol-rich cannabis extract and acetaminophen co-administration

© 2019 The Authors. Environmental Toxicology published by Wiley Periodicals, Inc. Exposure to environmental contaminants and consumption of a high, saturated fatty diet has been demonstrated to promote precursors for metabolic syndrome (hyperglycemia, hyperinsulinemia, and hypertriglyceridemia). The purpose of this study was to determine if exposure to the most prevalent environmental persistent organic pollutants (POPs) would act as causative agents to promote metabolic syndrome independent of dietary intake. We hypothesized that POPs will activate the advanced glycated end-product (AGE)-and receptor for AGE (RAGE) signaling cascade to promote downstream signaling modulators of cardiovascular remodeling and oxidative stress in the heart. At 5-weeks of age nondiabetic (WT) and diabetic (ob/ob) mice were exposed POPs mixtures by oral gavage twice a week for 6-weeks. At the end of 6-weeks, animals were sacrificed and the hearts were taken for biochemical analysis. Increased activation of the AGE-RAGE signaling cascade via POPs exposure resulted in elevated levels of fibroblast differentiation (α-smooth muscle actin) and RAGE expression indicated maladaptive cardiac remodeling. Conversely, the observed decreased superoxide dismutase-1 and -2 (SOD-1 and SOD-2) expression may exacerbate the adverse changes occurring as a result of POPs treatment to reduce innate cardioprotective mechanisms. In comparison, ventricular collagen levels were decreased in mice exposed to POPs. In conclusion, exposure to organic environmental pollutants may intensify oxidative and inflammatory stressors to overwhelm protective mechanisms allowing for adverse cardiac remodeling

Genomic organization and evolution of the Atlantic salmon hemoglobin repertoire

<p>Abstract</p> <p>Background</p> <p>The genomes of salmonids are considered pseudo-tetraploid undergoing reversion to a stable diploid state. Given the genome duplication and extensive biological data available for salmonids, they are excellent model organisms for studying comparative genomics, evolutionary processes, fates of duplicated genes and the genetic and physiological processes associated with complex behavioral phenotypes. The evolution of the tetrapod hemoglobin genes is well studied; however, little is known about the genomic organization and evolution of teleost hemoglobin genes, particularly those of salmonids. The Atlantic salmon serves as a representative salmonid species for genomics studies. Given the well documented role of hemoglobin in adaptation to varied environmental conditions as well as its use as a model protein for evolutionary analyses, an understanding of the genomic structure and organization of the Atlantic salmon α and β hemoglobin genes is of great interest.</p> <p>Results</p> <p>We identified four bacterial artificial chromosomes (BACs) comprising two hemoglobin gene clusters spanning the entire α and β hemoglobin gene repertoire of the Atlantic salmon genome. Their chromosomal locations were established using fluorescence <it>in situ </it>hybridization (FISH) analysis and linkage mapping, demonstrating that the two clusters are located on separate chromosomes. The BACs were sequenced and assembled into scaffolds, which were annotated for putatively functional and pseudogenized hemoglobin-like genes. This revealed that the tail-to-tail organization and alternating pattern of the α and β hemoglobin genes are well conserved in both clusters, as well as that the Atlantic salmon genome houses substantially more hemoglobin genes, including non-Bohr β globin genes, than the genomes of other teleosts that have been sequenced.</p> <p>Conclusions</p> <p>We suggest that the most parsimonious evolutionary path leading to the present organization of the Atlantic salmon hemoglobin genes involves the loss of a single hemoglobin gene cluster after the whole genome duplication (WGD) at the base of the teleost radiation but prior to the salmonid-specific WGD, which then produced the duplicated copies seen today. We also propose that the relatively high number of hemoglobin genes as well as the presence of non-Bohr β hemoglobin genes may be due to the dynamic life history of salmon and the diverse environmental conditions that the species encounters.</p> <p>Data deposition: BACs S0155C07 and S0079J05 (fps135): GenBank <ext-link ext-link-id="GQ898924" ext-link-type="gen">GQ898924</ext-link>; BACs S0055H05 and S0014B03 (fps1046): GenBank <ext-link ext-link-id="GQ898925" ext-link-type="gen">GQ898925</ext-link></p

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy