43 research outputs found

    The Joe and Rika Mansueto Library at the University of Chicago

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    Collecting and Acquiring in Earnest (The 14th Annual Health Sciences Lively Lunch)

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    In this year\u27s sponsored but no holds barred lunch, host Wendy Bahnsen (substituting for colleague Nicole Gallo) offered a brief greeting, and Ramune Kubilius provided the traditional “year in review” synopsis of developments since the last Charleston Conference. Panelists then shared insights and led discussion on earnest attempts to meet users’ information needs and satisfy administrations’ budget and other expectations. No matter how information has become repackaged, two formats remain important in health sciences communication: books and journals (articles). Speakers focused on library experiments with these formats. Is PDA a solution? Bahnsen contributed highlights and findings from a survey by Rittenhouse on health sciences customers’ experience with the R2 PDA program. Yumin Jiang shared some impressions on the experience of her institution with a few e‐book PDA/DDA (patron‐driven or demand‐driven acquisition) packages. Suggestions were made about best practices in e‐book collection building with PDA programs. What conclusions can be reached from experimentation with and implementation of on‐demand article acquisitions? Emma O\u27Hagan shared insights and experience with journal article “on demand” and “pay per view” services at two institutions. Andrea Twiss‐Brooks fielded questions and moderated discussion with session participants about the services and programs described by panelists, ranging from discussion about specific programs and models to broader collection and service implications

    A Guided Tour of Issues and Trends: The Thirteenth Annual Health Sciences Lively Lunch

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    In this year\u27s sponsored but no holds barred lunch, the conference theme, Too much is not enough , resonates. Lunch host, Wendy Bahnsen from Rittenhouse offers a brief greeting, and Ramune Kubilius provides the traditional “year in review” synopsis. Moderator Andrea Twiss-Brooks sets the scene and provides a brief introduction to issues of current interest in the health sciences information arena. Topics of this session include: methods of measurement of health sciences journal use (Deborah Blecic); shared collection development and policies (Elizabeth Ketterman); scholarly communication activities in health sciences libraries (Robin Champieux); current challenges, trials, pitfalls and successes of e-books in the health sciences (Anneliese Taylor); provision of information resources for basic scientists (Marysue Schaffer)

    Storing the wisdom: chemical concepts and chemoinformatics

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    The purpose of the paper is to examine the nature of chemical concepts, and the ways in which they are applied in chemoinformatics systems. An account of concepts in philosophy and in the information sciences leads to an analysis of chemical concepts, and their representation. The way in which concepts are applied in systems for information retrieval and for structure–property correlation are reviewed, and some issues noted. Attention is focused on the basic concepts or substance, reaction and property, on the organising concepts of chemical structure, structural similarity, periodicity, and on more specific concepts, including two- and three-dimensional structural patterns, reaction types, and property concepts. It is concluded that chemical concepts, despite (or perhaps because of) their vague and mutable nature, have considerable and continuing value in chemoinformatics, and that an increased formal treatment of concepts may have value in the future

    Fragment C of Tetanus Toxin : New Insights into Its Neuronal Signaling Pathway

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    When Clostridium tetani was discovered and identified as a Gram-positive anaerobic bacterium of the genus Clostridium, the possibility of turning its toxin into a valuable biological carrier to ameliorate neurodegenerative processes was inconceivable. However, the non-toxic carboxy-terminal fragment of the tetanus toxin heavy chain (fragment C) can be retrogradely transported to the central nervous system; therefore, fragment C has been used as a valuable biological carrier of neurotrophic factors to ameliorate neurodegenerative processes. More recently, the neuroprotective properties of fragment C have also been described in vitro and in vivo, involving the activation of Akt kinase and extracellular signal-regulated kinase (ERK) signaling cascades through neurotrophin tyrosine kinase (Trk) receptors. Although the precise mechanism of the molecular internalization of fragment C in neuronal cells remains unknown, fragment C could be internalized and translocated into the neuronal cytosol through a clathrin-mediated pathway dependent on proteins, such as dynamin and AP-2. In this review, the origins, molecular properties and possible signaling pathways of fragment C are reviewed to understand the biochemical characteristics of its intracellular and synaptic transport

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Best Practices for Presentation of E‐Journals

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    A Day in the Life Mapping Handout

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    <p>Applied ethnographic method applied to information seeking behavior of third year medical students in clinical settings.</p
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