bluuebunny/crossref_metadata_2025_split huggingface dataset:
‘So the Meaning Escapes’: On Literature and the Representation of Linguistic Realities
Authors: Widdowson H. 
Published: June 2010

A formalist model of language is said to be inappropriate for applied linguistics in that it deals with idealized abstractions and does not come to terms with the real language as actually experienced by its users. Two current areas of linguistic enquiry, corpus linguistics and critical discourse analysis, claim to redress this deficiency by revealing how language is actually put to use. One area of linguistic experience, however, continues to be neglected, namely the imaginative and individual exploration of meaning potential that is characteristic of literature, and particularly of poetry. Corpus analysis does use prose fiction as data, but very selectively. Drama and poetry are excluded altogether, presumably because they tend to be nonconformist and not reliably representative of normal usage. Since corpus descriptions are designed to reveal commonalities and regularities across individual uses of language, it is not surprising that they should avoid what is abnormal and eccentric. But then such descriptions inevitably reduce language to some kind of ideal representation of what is commonly attested as ‘standard’ or ‘normal’: a social construct of the conventional in which individual expression has no place. Critical discourse analysis has also used the data of literary texts but again its purpose is to show how texts are ideologically informed and so exemplify a more general social significance. The individual is again reduced to a common factor. In both corpus and critical linguistics, where literature is taken account of at all, it is used expediently as data to exemplify social aspects of language and sustain convenient generalities. But the essence of creative writing is that it is indeed creative, and so subverts such generalities and in exploiting the unrealized potential of language is expressive of alternative realities not recognised by social convention. To ignore this is to misrepresent the reality of the individual's experience of language which applied linguistics needs to take account of.
Comparing Phonological and Orthographic Vocabulary Size: Do Vocabulary Tests Underestimate the Knowledge of Some Learners?
Authors: Milton James , Hopkins Nicola 
Published: June 2010

Abstract: Any description of what it means to know a word in a foreign language is likely to include recognition of form, both how a word sounds when heard and what it looks like when written. However, tests of vocabulary knowledge focus almost exclusively on the written form of the word. We have little idea of learners' phonological vocabulary knowledge or how it might interact with orthographic knowledge. It is suspected that written vocabulary tests may underestimate the vocabulary knowledge of native Arabic speakers, who often handle English orthography poorly. This paper reports a comparison of the phonological and orthographic vocabulary sizes of Greek and Arabic native speakers. Results suggest that written tests do not underestimate Arabic speakers' vocabulary size. The two aspects of vocabulary knowledge develop differently with language level. Very proficient learners of EFL are characterized by an orthographic word recognition much greater than their phonological word recognition.
Breaking up is not so Hard to do: Individual Differences in L2 Memorization
Authors: Fitzpatrick Tess , Wray Alison 
Published: June 2010

Abstract:Six intermediate/advanced learners of English, studying in the United Kingdom, identified messages that they wanted to convey in specific future conversations and memorized native-like versions of them. Their ability to use them in practice and in the real conversation was analyzed. Propensity to attempt using memorized material correlated with aural-repetition aptitude, but neither propensity nor accuracy of reproduction correlated with proficiency. It is hypothesized that increased proficiency invites increased risk-taking during memorization. Individual differences in motivation and attitude, and the relationship with the interlocutor, are all discussed as salient variables.
From Faible to Strong: How Does Their Vocabulary Grow?
Authors: Horst Marlise , Collins Laura 
Published: June 2010

Abstract: The study drew on an 80,000-word corpus consisting of narrative texts produced in response to picture prompts by 210 beginner-level francophone learners of English (11-12-year-olds). The unique feature of the corpus is its longitudinal character: The samples were collected at four 100-hour intervals of intensive language instruction, during which time students made considerable progress in listening and speaking. However, analysis of these staged sub-corpora using Laufer and Nation's 1995 Lexical Frequency Profile did not identify the expected increase in use of less frequent words. Further analyses using three measures available at (a Greco-Latin cognate index, a count of word families, and a types-per-family ratio) showed that although the learners continued to use large proportions of frequent words, their productive vocabulary featured fewer French cognates, a greater variety of frequent words, and more morphologically developed forms. Implications for frequency-based vocabulary acquisition research and vocabulary teaching are discussed.
Breadth and Depth Specialized Vocabulary Learning in Theology among Native and Non-native English Speakers
Authors: Lessard-Clouston Michael 
Published: June 2010

Abstract:This article describes a case study on native and non-native English-speaker (NES and NNES) students' knowledge and learning of specialized vocabulary over one academic term in a graduate school of theology. After outlining the collection of baseline data on theological vocabulary and the development of a Test of Theological Language (TTL), the article discusses the five NNES and seven NES participants' scores on the TTL. Results on the initial TTL revealed that both groups brought some breadth and depth knowledge of specialized theological vocabulary to their studies, but that the NNES group's scores on both measures tended to be lower than those of NESs. At the end of the term the TTL results indicated an overall increase in scores, but while the gap between the NNES and NES groups in breadth vocabulary knowledge was essentially bridged, for depth knowledge it actually widened. These and other findings are discussed.
L1 Use in the L2 Classroom: One Teacher's Self-Evaluation
Authors: Edstrom Anne 
Published: June 2010

Abstract: Predominant, if not exclusive, use of the target language has long been considered an important principle of second language (L2) instruction. Previous research has attempted to quantify the amount of the first language (L1) used in the classroom and has explored the purposes or functions of teachers' ‘lapses’ into their students' L1. The present study is a detailed analysis of one teacher's language use during one semester of a university-level Spanish course. The goal is fivefold: to determine the amount of L1 used; to analyze the functions of L1 use; to compare the teacher's perceptions with her actual L1 use; to compare students' perceptions with the teacher's actual L1 use; and to identify motivations or reasons underlying her L1 use. The findings have implications for classroom practice and emphasize the value of self-recording in teacher development.
Journals as Innovators and the Innovation of Journals: The Council of Editors of Learned Journals Keynote Addresses MLA Convention 2004
Authors: Regier Willis , English James , Hanson David 
Published: June 2010

At the 2004 conference of the Modern Language Association in Philadelphia, the theme for the keynote session of the Council of Editors of Learned Journals (CELJ) was ‘Journals as Innovators and the Innovation of Journals’ — an idea suggested to us by Hayden Ward, retiring editor of Victorian Poetry (VP). VP itself has been as instrumental in prodding innovation in Victorian studies as in responding to change; likewise, all journals in the humanities aspire to help lead their respective fields, as well as to register how their fields are leading them. A related theme is how journal editors, precisely in thinking about ways to innovate, must periodically remake their journals; and how scholars who may be altogether new to editing, but who wish to speak to emerging fields, must invent new journals to spread the word.To address the latter theme, CELJ invited Willis Regier, who directs the University of Illinois Press, to offer recommendations about the new and ongoing lives and liveliness — and, occasionally, deaths — of university press journals. To address the former, CELJ asked James English, professor of English and comparative literature and chair of the English Department at the University of Pennsylvania, to discuss ways in which even the most forward-looking of journals in the humanities, Postmodern Culture, which he co-edited with Lisa Brawley for five years, could profit by re-examining its claims to being innovative. Both keynotes, edited for publication in JSP, provide a valuable distillation of their authors' scholarly and practical wisdom.
Replies to Alcoff, Goldberg, and Hookway on Epistemic Injustice
Authors: Fricker Miranda 
Published: June 2010

ABSTRACTIn this paper I respond to three commentaries on Epistemic Injustice: Power and the Ethics of Knowing. In response to Alcoff, I primarily defend my conception of how an individual hearer might develop virtues of epistemic justice. I do this partly by drawing on empirical social psychological evidence supporting the possibility of reflective self-regulation for prejudice in our judgements. I also emphasize the fact that individual virtue is only part of the solution – structural mechanisms also have an essential role in combating epistemic injustice. My response to Goldberg principally concerns my perceptual account of the epistemology of testimony, which I defend as being both well-motivated and best categorized as a species of non-inferentialism. I also explain its relation to the reductionism/non-reductionism contrast, and defend my resistance to casting it as any kind of default view. In response to Hookway, I contrast discriminatory with distributive forms of epistemic injustice, and defend the basic taxonomy I present in the book, which casts testimonial and hermeneutical injustice as the two fundamental discriminatory forms of epistemic injustice.
An IL-2 Paradox: Blocking CD25 on T Cells Induces IL-2–Driven Activation of CD56bright NK Cells
Authors: Martin Jayne F. , Perry Justin S. A. , Jakhete Neha R. , Wang Xiang , Bielekova Bibiana 
Published: June 2010

Abstract
Daclizumab (Dac), an Ab against the IL-2R α-chain, inhibits brain inflammation in patients with multiple sclerosis, while expanding CD56bright immunoregulatory NK cells in vivo. We hypothesized that this unexpected expansion is paradoxically IL-2 driven; caused by the increased availability of T cell-derived IL-2 for NK cell signaling. To this end, we performed ex vivo functional analyses of CD56bright NK cells and T cells from patients in clinical trials with Dac. We developed in vitro models to investigate mechanisms for ex vivo observations. We observed that Dac treatment caused decreased numbers and proliferation of FoxP3+ T regulatory cells (Tregs), a model T cell population known to be dependent on IL-2 for proliferation and survival. As anticipated, Dac therapy inhibited IL-2 signaling in all T cells; however, we also observed functional adaptation of T cells to low IL-2 signal in vivo, characterized by the concomitant enhancement of IL-7 signaling on all T cells and parallel increase of CD127 expression by Tregs. In contrast, IL-2 signaling on CD56bright NK cells was not inhibited by Dac and their in vivo proliferation and cytotoxicity actually increased. Mechanistic studies indicated that the activation of CD56bright NK cells was likely IL-2 driven, as low doses of IL-2, but not IL-15, mimicked this activation in vitro. Our study provides insight into the role that IL-2 and CD25 play in functional regulation of two important immunoregulatory cell populations in humans: FoxP3+ Tregs and CD56bright NK cells.
Francisella tularensis Suppresses the Proinflammatory Response of Endothelial Cells via the Endothelial Protein C Receptor
Authors: Bublitz DeAnna C. , Noah Courtney E. , Benach Jorge L. , Furie Martha B. 
Published: June 2010

Abstract
Various bacterial pathogens activate the endothelium to secrete proinflammatory cytokines and recruit circulating leukocytes. In contrast, there is a distinct lack of activation of these cells by Francisella tularensis, the causative agent of tularemia. Given the importance of endothelial cells in facilitating innate immunity, we investigated the ability of the attenuated live vaccine strain and virulent Schu S4 strain of F. tularensis to inhibit the proinflammatory response of HUVECs. Living F. tularensis live vaccine strain and Schu S4 did not stimulate secretion of the chemokine CCL2 by HUVECs, whereas material released from heat-killed bacteria did. Furthermore, the living bacteria suppressed secretion in response to heat-killed F. tularensis. This phenomenon was dose and contact dependent, and it occurred rapidly upon infection. The living bacteria did not inhibit the activation of HUVECs by Escherichia coli LPS, highlighting the specificity of this suppression. The endothelial protein C receptor (EPCR) confers anti-inflammatory properties when bound by activated protein C. When the EPCR was blocked, F. tularensis lost the ability to suppress activation of HUVECs. To our knowledge, this is the first report that a bacterial pathogen inhibits the host immune response via the EPCR. Endothelial cells are a critical component of the innate immune response to infection, and suppression of their activation by F. tularensis is likely a mechanism that aids in bacterial dissemination and evasion of host defenses.
The Adaptor Molecule Act1 Regulates BAFF Responsiveness and Self-Reactive B Cell Selection during Transitional B Cell Maturation
Authors: Giltiay Natalia V. , Lu Yi , Allman David , Jørgensen Trine N. , Li Xiaoxia 
Published: June 2010

Abstract
The transitional stage is a key check-point for elimination of autoreactive B cells in the periphery. This selection process requires fine regulation of signals received through BCR and B cell activating factor (BAFF) receptor. We previously identified the adaptor molecule Act1 as a negative regulator of BAFF-mediated signaling. Deficiency of Act1 in mice results in peripheral B cell hyperplasia and development of autoimmunity. In this study, we demonstrate that Act1 plays a critical role in the regulation of transitional B cell survival and maturation. We found that the ratio of late-transitional (T2) to early-transitional (T1) cells was increased in spleens from Act1-deficient mice. Moreover, BAFF stimulation induced better T1 cell survival and promoted more efficient maturation of T1 cells into T2 cells ex vivo in the absence of Act1. BAFF stimulation induced higher levels of the anti-apoptotic Bcl-2 member Mc1-l in Act1-deficient T1 cells than in wild-type control cells, suggesting that Mcl-1 might be one of the key effector molecules for BAFF-mediated survival of the Act1-deficient transitional B cells. Importantly, costimulation with BAFF was able to rescue Act1-deficient T1 cells from BCR-induced apoptosis more effectively than Act1-sufficient T1 B cells. Finally, by using hen egg lysozyme double transgenic mice, we demonstrated that Act1 deficiency can promote the maturation of Ag-specific autoreactive B cells. Taken together, our results suggest that the transitional stage is a critical point of action of Act1 in the elimination of autoreactive B cells and in the regulation of peripheral B cell homeostasis.
Allergen-Induced Airway Remodeling Is Impaired in Galectin-3–Deficient Mice
Authors: Ge Xiao Na , Bahaie Nooshin S. , Kang Bit Na , Hosseinkhani M. Reza , Ha Sung Gil , Frenzel Elizabeth M. , Liu Fu-Tong , Rao Savita P. , Sriramarao P. 
Published: June 2010

Abstract
The role played by the β-galactoside–binding lectin galectin-3 (Gal-3) in airway remodeling, a characteristic feature of asthma that leads to airway dysfunction and poor clinical outcome in humans, was investigated in a murine model of chronic allergic airway inflammation. Wild-type (WT) and Gal-3 knockout (KO) mice were subjected to repetitive allergen challenge with OVA up to 12 wk, and bronchoalveolar lavage fluid (BALF) and lung tissue collected after the last challenge were evaluated for cellular features associated with airway remodeling. Compared to WT mice, chronic OVA challenge in Gal-3 KO mice resulted in diminished remodeling of the airways with significantly reduced mucus secretion, subepithelial fibrosis, smooth muscle thickness, and peribronchial angiogenesis. The higher degree of airway remodeling in WT mice was associated with higher Gal-3 expression in the BALF as well as lung tissue. Cell counts in BALF and lung immunohistology demonstrated that eosinophil infiltration in OVA-challenged Gal-3 KO mice was significantly reduced compared with that WT mice. Evaluation of cellular mediators associated with eosinophil recruitment and airway remodeling revealed that levels of eotaxin-1, IL-5, IL-13, found in inflammatory zone 1, and TGF-β were substantially lower in Gal-3 KO mice. Finally, leukocytes from Gal-3 KO mice demonstrated decreased trafficking (rolling) on vascular endothelial adhesion molecules compared with that of WT cells. Overall, these studies demonstrate that Gal-3 is an important lectin that promotes airway remodeling via airway recruitment of inflammatory cells, specifically eosinophils, and the development of a Th2 phenotype as well as increased expression of eosinophil-specific chemokines and profibrogenic and angiogenic mediators.
IL-13 Induces Esophageal Remodeling and Gene Expression by an Eosinophil-Independent, IL-13Rα2–Inhibited Pathway
Authors: Zuo Li , Fulkerson Patricia C. , Finkelman Fred D. , Mingler Melissa , Fischetti Christine A. , Blanchard Carine , Rothenberg Marc E. 
Published: June 2010

Abstract
Eosinophilic esophagitis (EE) is an emerging disease associated with both food and respiratory allergy characterized by extensive esophageal tissue remodeling and abnormal esophageal gene expression, including increased IL-13. We investigated the ability of increased airway IL-13 to induce EE-like changes. Mice with pulmonary (but not esophageal) overexpression of IL-13 evidenced esophageal IL-13 accumulation and developed prominent esophageal remodeling with epithelial hyperplasia, angiogenesis, collagen deposition, and increased circumference. IL-13 induced notable changes in esophageal transcripts that overlapped with the human EE esophageal transcriptome. IL-13–induced esophageal eosinophilia was dependent on eotaxin-1 (but not eotaxin-2). However, remodeling occurred independent of eosinophils as demonstrated by eosinophil lineage-deficient, IL-13 transgenic mice. IL-13–induced remodeling was significantly enhanced by IL-13Rα2 deletion, indicating an inhibitory effect of IL-13Rα2. In the murine system, there was partial overlap between IL-13–induced genes in the lung and esophagus, yet the transcriptomes were divergent at the tissue level. In human esophagus, IL-13 levels correlated with the magnitude of the EE transcriptome. In conclusion, inducible airway expression of IL-13 results in a pattern of esophageal gene expression and extensive tissue remodeling that resembles human EE. Notably, we identified a pathway that induces EE-like changes and is IL-13–driven, eosinophil-independent, and suppressed by IL-13Rα2.
IL-33 Reduces Macrophage Foam Cell Formation
Authors: McLaren James E. , Michael Daryn R. , Salter Rebecca C. , Ashlin Tim G. , Calder Claudia J. , Miller Ashley M. , Liew Foo Y. , Ramji Dipak P. 
Published: June 2010

Abstract
The development of atherosclerosis, a chronic inflammatory disease characterized by the formation of arterial fibrotic plaques, has been shown to be reduced by IL-33 in vivo. However, whether IL-33 can directly affect macrophage foam cell formation, a key feature of atherosclerotic plaques, has not been determined. In this study, we investigated whether IL-33 reduces macrophage foam cell accumulation in vivo and if IL-33 reduces their formation in vitro using THP-1 and primary human monocyte-derived macrophages. In Apolipoprotein E−/− mice fed on a high fat diet, IL-33 treatment significantly reduced the accumulation of macrophage-derived foam cells in atherosclerotic plaques. IL-33 also reduced macrophage foam cell formation in vitro by decreasing acetylated and oxidized low-density lipoprotein uptake, reducing intracellular total and esterified cholesterol content and enhancing cholesterol efflux. These changes were associated with IL-33–mediated reduction in the expression of genes involved in modified low-density lipoprotein uptake, such as CD36, and simultaneous increase in genes involved in cholesterol efflux, including Apolipoprotein E, thereby providing a mechanism for such an action for this cytokine. IL-33 also decreased the expression of key genes implicated in cholesterol esterification and triglyceride storage, including Acyl-CoA:cholesterol acyltransferase 1 and Adipocyte differentiation-related protein. Furthermore, using bone marrow-derived macrophages from ST2−/− mice, we demonstrate that the IL-33 receptor, ST2, is integral to the action of IL-33 on macrophage foam cell formation. In conclusion, IL-33 has a protective role in atherosclerosis by reducing macrophage foam cell formation suggesting that IL-33 maybe a potential therapeutic agent against atherosclerosis.
Serine Protease Inhibitor 6 Protects iNKT Cells from Self-Inflicted Damage
Authors: Ansari A. Wahid , Temblay Jeff N. , Alyahya Syarifah H. , Ashton-Rickardt Philip G. 
Published: June 2010

Abstract
The role played by apoptosis in the homeostasis of effector cells of the innate immune system is unclear. Serine protease inhibitor 6 (Spi6) is an inhibitor of granzyme B (GrB) that protects cytotoxic T lymphocytes of the adaptive immune system from apoptosis. To determine whether Spi6 also protects cells of the innate immune system from self-inflicted damage we have examined invariant NKT (iNKT) cells. Spi6-deficient iNKT cells harbored increased levels of GrB after TCR stimulation with the PBS-57 glycolipid Ag and were susceptible to apoptosis. The increased apoptosis of Spi6 knock-out (KO) iNKT cells lead to a complete loss in the production of IL-4 and IFN-γ by Spi6 KO iNKT cells after PBS-57 challenge. The increased activation-induced apoptosis resulted in impaired survival and a decreased clonal burst size of Spi6 KO iNKT cells, which could be corrected by GrB deficiency. However, the clonal burst of Spi6 KO iNKT cells after TCR-independent activation with lymphocytic choriomeningitis virus was not affected. Our findings demonstrate that Spi6 protects cytotoxic cells of the innate immune system from GrB-mediated self-inflicted triggered by the recognition of Ag.