No abstract

Librarians and archivists are intimately involved in scholarly communication systems, both as information providers and instructors. However, very little is known regarding their activities as scholars. This study seeks to examine the scholarly communication practices of librarians and archivists, the role that tenure plays in scholarly communication practices, and the degree to which institutional support is provided in librarians' efforts to consume and disseminate research and reports of best practices. A questionnaire was sent to professional librarians and archivists at 91 ARL institutions. The responses demonstrate that ARL librarians and archivists are avid consumers and creators of scholarship, and they use emerging technologies to stay up-to-date on the profession's latest research.he duties of academic librarians and archivists are inherently tied to the world of scholarly research. By organizing, disseminating, and providing access to information, librarians and archivists act as gatekeepers of knowledge for countless students, researchers, and professors. The role of librarians and archivists in scholarly communication has expanded in recent years. In addition to their traditional job duties, librarians now perform liaison functions, wherein information professionals act as educators for both students and faculty. Modern librarians also advocate for "sustainable models" of scholarly communication, help faculty members to develop tools that facilitate scholarly communication, and work in the field of digital preservation.

Wirtz, M. (2004). Uber das Problem fehlender Werte: Wie der Einfluss fehlender Informationen auf Analyseergebnisse entdeckt und reduziert werden kann [On the problem of missing data: How to identify and reduce the impact of missing data on findings from data analysis].

In scientific and academic circles, the value of Google Scholar as an information resource has received much scrutiny. Numerous articles have examined its search ability, but few have asked whether it has the accuracy, authority and currency to be trustworthy enough for scholars. This article takes a look at reliability factors that go into Google Scholar citation counts, selection of resources, and its commercial partnerships. Research data culled from correspondence with Google Scholar, analysis of citation metrics, metadata and search processes, and an appraisal of its strengths and weaknesses compared to other science-specific indexes led to the conclusion that Google Scholar may be useful for initial and supplemental information gathering, but lacks a deeper reliability than other existing services currently provide scholars. Advice is offered to science librarians about how to regard Google Scholar as a research tool. [ABSTRACT FROM AUTHOR]

Epidermal keratinocytes are enriched with at least nine connexins that are key regulators of epidermal homeostasis. The role of Cx30.3 in keratinocytes and epidermal health became evident when fourteen autosomal dominant mutations in the Cx30.3-encoding GJB4 gene were linked to a rare and incurable skin disorder called erythrokeratodermia variabilis et progressiva (EKVP). While these variants are linked to EKVP, they remain largely uncharacterized hindering therapeutic options. In this study, we characterize the expression and functional status of three EKVP-linked Cx30.3 mutants (G12D, T85P, and F189Y) in tissue-relevant and differentiation-competent rat epidermal keratinocytes. We found that GFP-tagged Cx30.3 mutants were non-functional likely due to their impaired trafficking and primary entrapment within the endoplasmic reticulum (ER). However, all mutants failed to increase BiP/GRP78 levels suggesting they were not inducing an unfolded protein response. FLAG-tagged Cx30.3 mutants were also trafficking impaired yet occasionally exhibited some capacity to assemble into gap junctions. The pathological impact of these mutants may extend beyond their trafficking deficiencies as keratinocytes expressing FLAG-tagged Cx30.3 mutants exhibited increased propidium iodide uptake in the absence of divalent cations. Attempts to rescue the delivery of trafficking impaired GFP-tagged Cx30.3 mutants into gap junctions by chemical chaperone treatment were ineffective. However, co-expression of wild type Cx30.3 greatly enhanced the assembly of Cx30.3 mutants into gap junctions, although endogenous levels of Cx30.3 do not appear to prevent the skin pathology found in patients harboring these autosomal dominant mutations. In addition, a spectrum of connexin isoforms (Cx26, Cx30, and Cx43) exhibited the differential ability to trans-dominantly rescue the assembly of GFP-tagged Cx30.3 mutants into gap junctions suggesting a broad range of connexins found in keratinocytes may favourably interact with Cx30.3 mutants. We conclude that selective upregulation of compatible wild type connexins in keratinocytes may have potential therapeutic value in rescuing epidermal defects invoked by Cx30.3 EKVP-linked mutants.