From Gestuno Interpreting to International Sign Interpreting: Improved Accessibility?

In order to shape the future of our profession, I believe it is necessary for us to also take a critical look at both past and present practices. With that goal in mind, this commentary presents a case study of the sign language interpreting services provided at the World Federation of the Deaf (WFD) Congresses held between 1983 and 2019. During the 1980s and 1990s we witnessed both the professionalization of signed language interpreting at international conferences, and improved accessibility for official delegates of various National Associations of the Deaf (NADs) as well as for other participants. Increasing numbers of interpreters worked at the congresses. Additionally, measures were gradually taken to provide all working interpreters with adequate preparation materials, quiet rooms to prepare in, meetings with presenters, easy and quick access to food in breaks, etc. Gradually, however, we have seen a decline in the numbers of NAD-interpreters working into/from their national signed languages at WFD congresses. The so called Gestuno-interpreting has been replaced with International Sign-interpreting (IS-interpreting). This has gradually also lead to increased focus on providing specialized IS-interpreters, and also on providing services for them. Ii is now time for us to step back and take a look at the changes we have seen. Are we convinced that the development we have seen is for the best? Will the increasing use of IS-interpreting at a number of international conferences and meetings ensure deaf people around the globe equal accessibility in a broader sense? Will this focus on interpreting into/from something other than national signed language ensure that the linguistic rights of deaf people are being preserved? Is this what is best for the interpreting profession in the long run

Working with Active Interpreters: A Commentary about Interpreting Terminology and Concepts

This commentary is a critical discussion of some terms that are frequently used when we talk about interpreting. Several of the popular terms may actually downplay the work done by both the interpreters and the other participants in interpreted interaction. In order to accentuate the work done by the interpreter as well as the active contribution by all participants in an interpreted dialogue, the commentary suggests some other terms. We would rather have us talk about working with interpreters than to ‘use’ interpreters, that interpreters interpret from a signed language to a spoken language rather than ‘voice for’, and that we refer to processing time instead of ‘lag time’ or ‘delay’. Interpreter educators, trainers, and researchers in the field of interpreting are in a position where it is both possible and desirable to strive towards using terms that more accurately represent interpreting and the interpreting process than some of the terms currently in use

The pirate and the navy: Challenger brands and their utilization of counter-hegemonic ideology in identity communication

Challenger branding is a phenomenon that is gaining significant exposure in academia. However, most research on this branding approach relates to a practical or technical knowledge interest, ignoring the counter-hegemonic critique that exemplifies challenger branding. The critique that these brands base their identity on often shifts after they have been acquired into a hegemonic context, by joining a large corporation or becoming hegemonic brands themselves. This thesis aims to extend critical knowledge by connecting theories of ideology, hegemony, and brand communication to the identity construction of two challenger brands, The Body Shop and Innocent Drinks, and further explores the identity shift of the brands after their acquisition by L’Oréal and Coca-Cola. Counter-hegemony was found to be a pervasive tool activated through a number of signs for challenger identity construction. Further, challenger brand identity differed substantially before and after the challenger brands joined L’Oréal and Coca-Cola

Temporal Variation of Ljungan Virus Antibody Levels in Relation to Islet Autoantibodies and Possible Correlation to Childhood Type 1 Diabetes

Viral infection may trigger islet autoimmunity, type 1diabetes (T1D), or both. Fluctuating population density of bank voles as a putative reservoir of Ljungan virus has been claimed to be associated with variations in T1D incidence rate (IR). We tested the hypothesis that Ljungan virus antibodies reflecting prior exposure(s) to the virus may be associated with islet autoimmunity, childhood diabetes or both. Incident, 0-18y, T1D patients (n = 63) were studied along with age and sample time matched controls (n = 126). The younger children (< 9 years) tended to have a higher incidence rate during winter (IR = 67.6, 95%CI 41.9-103.5) compared to summer (IR = 33.6, 95%CI 15.3-63.9) months. The proportion of children with high level antibodies against Ljungan virus (LVAb) were both younger compared to the rest of the children (p < 0.002) and correlated with half yearly T1D IR (r = 0.78, p = 0.005). High level LVAb fluctuating with season and correlating with T1D IR indicates that past exposure to Ljungan virus may be associated with T1D

Adrenocorticotrophic hormone lowers serum Lp(a) and LDL cholesterol concentrations in hemodialysis patients

Adrenocorticotrophic hormone lowers serum Lp(a) and LDL cholesterol concentrations in hemodialysis patients. Previously, we have shown that short-term administration of adrenocorticotrophic hormone (ACTH) results in reduced concentrations of apolipoprotein B-containing lipoproteins, including lipoprotein(a), and reduced activities of hepatic lipase. These effects were observed in steroid-treated patients suffering from iatrogenic ACTH deficiency and in healthy individuals. The direct nature of the influence of ACTH on hepatic lipoprotein metabolism was confirmed by in vitro experiments. The aim of the present investigation was to study the effects of ACTH treatment on uremic patients, who exhibit disturbed lipoprotein pattern due to the slow removal of triglyceride-rich lipoproteins and who probably are ACTH resistant. Eight patients on chronic hemodialysis were studied. After one intramuscular injection of Synacthen Depot (a synthetic ACTH1–24 preparation from Ciba Geigy AG, Basel, Switzerland) 1 mg, the only change noted was a significant reduction of 26% in median lipoprotein(a) concentration. After five injections, a further decrease (65%) was found in the lipoprotein(a) concentration. Also, reductions in median concentrations of total cholesterol, low density lipoprotein cholesterol and apolipoprotein B were observed. The magnitude of these changes was 15 to 30%. In contrast to previously studied groups, no changes were observed regarding triglyceride metabolism. Significantly increased median concentration of apolipoprotein CIII was found. However, the excess apolipoprotein CIII was confined to the fraction that was not associated with apolipoprotein B. Thus, administration of ACTH to uremic patients improved their atherogenic lipoprotein profile, a fact that may have future therapeutic implications. In comparison to previously studied groups, the uremic patients responded rather slowly and not at all regarding triglyceride metabolism

Temporal expression and cellular origin of CC chemokine receptors CCR1, CCR2 and CCR5 in the central nervous system: insight into mechanisms of MOG-induced EAE

<p>Abstract</p> <p>Background</p> <p>The CC chemokine receptors CCR1, CCR2 and CCR5 are critical for the recruitment of mononuclear phagocytes to the central nervous system (CNS) in multiple sclerosis (MS) and other neuroinflammatory diseases. Mononuclear phagocytes are effector cells capable of phagocytosing myelin and damaging axons. In this study, we characterize the regional, temporal and cellular expression of CCR1, CCR2 and CCR5 mRNA in the spinal cord of rats with myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (MOG-EAE). While resembling human MS, this animal model allows unique access to CNS-tissue from various time-points of relapsing neuroinflammation and from various lesional stages: early active, late active, and inactive completely demyelinated lesions.</p> <p>Methods</p> <p>The expression of CCR1, CCR2 and CCR5 mRNA was studied with <it>in situ </it>hybridization using radio labelled cRNA probes in combination with immunohistochemical staining for phenotypic cell markers. Spinal cord sections from healthy rats and rats with MOG-EAE (acute phase, remission phase, relapse phase) were analysed. In defined lesion stages, the number of cells expressing CCR1, CCR2 and CCR5 mRNA was determined. Data were statistically analysed by the nonparametric Mann-Whitney U test.</p> <p>Results</p> <p>In MOG-EAE rats, extensive up-regulation of CCR1 and CCR5 mRNA, and moderate up-regulation of CCR2 mRNA, was found in the spinal cord during episodes of active inflammation and demyelination. Double staining with phenotypic cell markers identified the chemokine receptor mRNA-expressing cells as macrophages/microglia. Expression of all three receptors was substantially reduced during clinical remission, coinciding with diminished inflammation and demyelination in the spinal cord. Healthy control rats did not show any detectable expression of CCR1, CCR2 or CCR5 mRNA in the spinal cord.</p> <p>Conclusion</p> <p>Our results demonstrate that the acute and chronic-relapsing phases of MOG-EAE are associated with distinct expression of CCR1, CCR2, and CCR5 mRNA by cells of the macrophage/microglia lineage within the CNS lesions. These data support the notion that CCR1, CCR2 and CCR5 mediate recruitment of both infiltrating macrophages and resident microglia to sites of CNS inflammation. Detailed knowledge of expression patterns is crucial for the understanding of therapeutic modulation and the validation of CCR1, CCR2 and CCR5 as feasible targets for therapeutic intervention in MS.</p

CX(3)CL1 (fractalkine) and CX(3)CR1 expression in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis: kinetics and cellular origin

BACKGROUND: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). It is associated with local activation of microglia and astroglia, infiltration of activated macrophages and T cells, active degradation of myelin and damage to axons and neurons. The proposed role for CX(3)CL1 (fractalkine) in the control of microglia activation and leukocyte infiltration places this chemokine and its receptor CX(3)CR1 in a potentially strategic position to control key aspects in the pathological events that are associated with development of brain lesions in MS. In this study, we examine this hypothesis by analyzing the distribution, kinetics, regulation and cellular origin of CX(3)CL1 and CX(3)CR1 mRNA expression in the CNS of rats with an experimentally induced MS-like disease, myelin oligodendrocyte glycoprotein (MOG)-induced autoimmune encephalomyelitis (EAE). METHODS: The expression of CX(3)CL1 and its receptor CX(3)CR1 was studied with in situ hybridization histochemical detection of their mRNA with radio labeled cRNA probes in combination with immunohistochemical staining of phenotypic cell markers. Both healthy rat brains and brains from rats with MOG EAE were analyzed. In defined lesional stages of MOG EAE, the number of CX(3)CR1 mRNA-expressing cells and the intensity of the in situ hybridization signal were determined by image analysis. Data were statistically evaluated by ANOVA, followed by Tukey\primes multiple comparison test. RESULTS: Expression of CX(3)CL1 mRNA was present within neuronal-like cells located throughout the neuraxis of the healthy rat. Expression of CX(3)CL1 remained unaltered in the CNS of rats with MOG-induced EAE, with the exception of an induced expression in astrocytes within inflammatory lesions. Notably, the brain vasculature of healthy and encephalitic animals did not exhibit signs of CX(3)CL1 mRNA expression. The receptor, CX(3)CR1, was expressed by microglial cells in all regions of the healthy brain. Induction of MOG-induced EAE was associated with a distinct accumulation of CX(3)CR1 mRNA expressing cells within the inflammatory brain lesions, the great majority of which stained positive for markers of the microglia-macrophage lineage. Analysis in time-staged brain lesions revealed elevated levels of CX(3)CR1 mRNA in microglia in the periplaque zone, as well as a dramatically enhanced accumulation of CX(3)CR1 expressing cells within the early-active, late-active and inactive, demyelinated lesions. CONCLUSION: Our data demonstrate constitutive and regulated expression of the chemokine CX(3)CL1 and its receptor CX(3)CR1 by neurons/astrocytes and microglia, respectively, within the normal and inflamed rat brain. Our findings propose a mechanism by which neurons and reactive astrocytes may control migration and function of the surrounding microglia. In addition, the accumulation of CX(3)CR1 expressing cells other than microglia within the inflammatory brain lesions indicate a possible role for CX(3)CL1 in controlling invasion of peripheral leucocytes to the brain