• Journal of the Korean Society for information Management
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• v.22 no.3 s.57
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• pp.307-326
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• 2005

Open access movement supports the principle that the published output of scientific research should be available to everyone without charge. The term open access is used in the broad context of the wider movement. To achieve the objectives of open access to scholarly journal literature, BOAI(Budapest Open Access Initiative) recommends using two complementary strategies: 'self-archiving' in institutional/disciplinary repositories and 'open access journals.' This study introduces the strategies of open access movements and analyzes the ways to help the cause of open access by academic stakeholders(i.e., researchers, librarians, universities, publishers, foundations, learned societies, and government) from the perspective of two BOAI strategies.

• Journal of the Korean Society for information Management
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• v.31 no.3
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• pp.111-131
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• 2014

The purpose of this study was to propose a guide for the acceptance and processes of open access in Korean Societies. Firstly, this study developed journal publishers' open access model focused on the relationship between types and strategies of open access. Secondly, this study investigated current status of journal publishers' open access strategies and the adoption degrees through SHERPA/RoMEO, DOAJ and PMC databases. Finally, on the basis of the result, this study proposed a guide to help Korean societies make journals more open or less open according to their situations as real. Korean societies can make informed decisions about how to derive open access.

• Journal of the Korean Society for information Management
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• v.19 no.4
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• pp.384-399
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• 2002

The ownership of scholarly communication, i.e. copyright is very important to solve the problem of access to many academic journals in network environment. The purpose of this article is to give a conceptual model for the open access based scholarly communication. The main point of this model is for the authors of research paper to retain copyright on their works and to license the work whenever it is reproduced or redistributed for non-profit use with academic purpose. And library have to construct full text journal databases under this open access license.

• Journal of Information Management
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• v.34 no.2
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• pp.1-23
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• 2003

The serials pricing and licensing crises have caused the problem of limited access to scholarly information and the problem of its preservation. To cope with these crises, various types of scholarly communication models are under study now. Open Access is one of the possible solutions among these new trials. This study has investigated the history of Open Access, articulated the first considerations for the spread of Open Access, and proposed the role of librarians during the progress.

• Biomolecules & Therapeutics
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• v.22 no.6
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• pp.532-539
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• 2014

Peripheral neuropathy induced by human immunodeficiency virus (HIV) infection and antiretroviral therapy is not only difficult to distinguish in clinical practice, but also difficult to relieve the pain symptoms by analgesics because of the severity of the disease at the later stage. Hence, to explore the mechanisms of HIV-related neuropathy and find new therapeutic options are particularly important for relieving neuropathic pain symptoms of the patients. In the present study, primary cultured embryonic rat dorsal root ganglion (DRG) neurons were used to determine the neurotoxic effects of HIV-gp120 protein and/or antiretroviral drug dideoxycytidine (ddC) and the therapeutic actions of insulin-like growth factor-1 (IGF-1) on gp120- or ddC-induced neurotoxicity. DRG neurons were exposed to gp120 (500 pmol/L), ddC ($50{\mu}mol/L$), gp120 (500 pmol/L) plus ddC ($50{\mu}mol/L$), gp120 (500 pmol/L) plus IGF-1 (20 nmol/L), ddC ($50{\mu}mol/L$) plus IGF-1 (20 nmol/L), gp120 (500 pmol/L) plus ddC ($50{\mu}mol/L$) plus IGF-1 (20 nmol/L), respectively, for 72 hours. The results showed that gp120 and/or ddC caused neurotoxicity of primary cultured DRG neurons. Interestingly, the severity of neurotoxicity induced by gp120 and ddC was different in different subpopulation of DRG neurons. gp120 mainly affected large diameter DRG neurons (> $25{\mu}m$), whereas ddC mainly affected small diameter DRG neurons (${\leq}25{\mu}m$). IGF-1 could reverse the neurotoxicity induced by gp120 and/or ddC on small, but not large, DRG neurons. These data provide new insights in elucidating the pathogenesis of HIV infection- or antiretroviral therapy-related peripheral neuropathy and facilitating the development of novel treatment strategies.