Evaluated version of the 2015 model

This book describes the business model of Language Science Press as devised in 2015. It gives some theoretical background and the text of the actual model itself. Each section of the model is then evaluated based on the knowledge of 2018, and possible alternatives which could have been adopted are discussed. An appendix with projected figures and actual figures for costs and revenue completes the book

Cookbook for Open Access books

This book describes the experiences of setting up a community-based publisher, Language Science Press. It discusses the main principles of community-based publishing and gives a very granular breakdown of the different tasks. The discussion of the different tasks is complemented by readings, time lines, and a list of time sinks. This book is complemented by the business model, open business data, and a spreadsheet for drafting and calculating own business models

Nomen/Verb-Distinktion im Guarani

Außerhalb der indoeuropäischen Sprachen [erfreut sich] [d]ie Kategorie „Adjektiv“ […] einer geringeren Verbreitung als man als Laie vermuten würde, und es zeigen sich in nicht-indoeuropäischen Sprachen von den europäischen Sprachen stark verschiedene Aufteilungen der Welt in Nomina und Verba. Eine bisher nicht beschriebene Verteilung von Konzepten auf Wortarten in der Sprache Guarani, welche hauptsächlich in Paraguay gesprochen wird, ist das Thema dieser Arbeit

Towards a Grammar of the Recreative Industries

The “transfer of the responsibility of paying for publication to the individual author (or the author’s funding agency or institution)” that is brought about by gold author-pays open access is, as Gary Hall notes in Pirate Philosophy, a “typical neoliberal move.” By placing researchers in a position where they have to compete for the inevitably limited amounts of funding that are available to enable them to publish on an article- or book-processing-charge (APC/BPC) basis, gold author-pays open access serves as a means of introducing yet further competition into the public system of higher education. It also establishes a commercial market for A/BPCs, and with it another way of “inflicting debt” onto the university, to set alongside that achieved by the “imposition of a system of tuition fees in England” (Hall 2016: 193, n60). It is not surprising then that calls are increasingly being made within the open access movement for non-profit presses, projects and institutions to cooperate horizontally in order to counter the hegemony of both free market economics and commercial publishing. When it comes to actually building non-profit alternatives, however, questions of funding soon come into play. A number of interesting innovations have emerged, not least in the form of library consortium subsidy models that redirect money otherwise used to purchase subscriptions to exorbitantly priced journals. Still, the long-term financial sustainability of numerous open access initiatives currently depends on already overstretched institutional budgets. As a result, even though many non-profit projects wish to work together cooperatively, they find themselves in a situation where they are forced to compete against one other (and against for-profits) for funding from libraries, foundations, research councils and other sources

Phosphorylation of TRIM28 Enhances the Expression of IFN-β and Proinflammatory Cytokines During HPAIV Infection of Human Lung Epithelial Cells

Human infection with highly pathogenic avian influenza viruses (HPAIV) is often associated with severe tissue damage due to hyperinduction of interferons and proinflammatory cytokines. The reasons for this excessive cytokine expression are still incompletely understood, which has hampered the development of efficient immunomodulatory treatment options. The host protein TRIM28 associates to the promoter regions of over 13,000 genes and is recognized as a genomic corepressor and negative immune regulator. TRIM28 corepressor activity is regulated by post-translational modifications, specifically phosphorylation of S473, which modulates binding of TRIM28 to the heterochromatin-binding protein HP1. Here, we identified TRIM28 as a key immune regulator leading to increased IFN-β and proinflammatory cytokine levels during infection with HPAIV. Using influenza A virus strains of the subtype H1N1 as well as HPAIV of subtypes H7N7, H7N9, and H5N1, we could demonstrate that strain-specific phosphorylation of TRIM28 S473 is induced by a signaling cascade constituted of PKR, p38 MAPK, and MSK1 in response to RIG-I independent sensing of viral RNA. Furthermore, using chemical inhibitors as well as knockout cell lines, our results suggest that phosphorylation of S473 facilitates a functional switch leading to increased levels of IFN-β, IL-6, and IL-8. In summary, we have identified TRIM28 as a critical factor controlling excessive expression of type I IFNs as well as proinflammatory cytokines during infection with H5N1, H7N7, and H7N9 HPAIV. In addition, our data indicate a novel mechanism of PKR-mediated IFN-β expression, which could lay the ground for novel treatment options aiming at rebalancing dysregulated immune responses during severe HPAIV infection

Phosphorylation of TRIM28 Enhances the Expression of IFN-β and Proinflammatory Cytokines During HPAIV Infection of Human Lung Epithelial Cells

Human infection with highly pathogenic avian influenza viruses (HPAIV) is often associated with severe tissue damage due to hyperinduction of interferons and proinflammatory cytokines. The reasons for this excessive cytokine expression are still incompletely understood, which has hampered the development of efficient immunomodulatory treatment options. The host protein TRIM28 associates to the promoter regions of over 13,000 genes and is recognized as a genomic corepressor and negative immune regulator. TRIM28 corepressor activity is regulated by post-translational modifications, specifically phosphorylation of S473, which modulates binding of TRIM28 to the heterochromatin-binding protein HP1. Here, we identified TRIM28 as a key immune regulator leading to increased IFN-β and proinflammatory cytokine levels during infection with HPAIV. Using influenza A virus strains of the subtype H1N1 as well as HPAIV of subtypes H7N7, H7N9, and H5N1, we could demonstrate that strain-specific phosphorylation of TRIM28 S473 is induced by a signaling cascade constituted of PKR, p38 MAPK, and MSK1 in response to RIG-I independent sensing of viral RNA. Furthermore, using chemical inhibitors as well as knockout cell lines, our results suggest that phosphorylation of S473 facilitates a functional switch leading to increased levels of IFN-β, IL-6, and IL-8. In summary, we have identified TRIM28 as a critical factor controlling excessive expression of type I IFNs as well as proinflammatory cytokines during infection with H5N1, H7N7, and H7N9 HPAIV. In addition, our data indicate a novel mechanism of PKR-mediated IFN-β expression, which could lay the ground for novel treatment options aiming at rebalancing dysregulated immune responses during severe HPAIV infection

Public access to research data in language documentation: Challenges and possible strategies

The Open Access Movement promotes free and unfettered access to research publications and, increasingly, to the primary data which underly those publications. As the field of documentary linguistics seeks to record and preserve culturally and linguistically relevant materials, the question of how openly accessible these materials should be becomes increasingly important. This paper aims to guide researchers and other stakeholders in finding an appropriate balance between accessibility and confidentiality of data, addressing community questions and legal, institutional, and intellectual issues that pose challenges to accessible dat

Acknowledgments

National Foreign Language Resource Cente

Contents

National Foreign Language Resource Cente