Trasslig terminologi: En undersökning om översättning av sömnads- och textiltermer

Denna uppsats undersöker översättningen av engelska sömnads- och textiltermer till svenska. Undersökningen utgår ifrån sömnadsboken "Sewing Basics: All You Need to Know About Machine and Hand Sewing" av Sandra Bardwell och dess svenska översättning "Sy dina egna kläder: En komplett handbok med tekniker, material och inspiration", som är översatt av Ulrika Junker Miranda. Syftet med undersökningen är att se hur väl källtexttermernas betydelseomfång motsvarar måltexttermernas betydelseomfång samt vilken ekvivalensgrad och vilken diskrepans det finns mellan termerna i de olika språken och hur detta yttrar sig i översättningen. Syftet är också att se om det är en viss sorts termer som ställer till problem i översättningen, eller om det finns en viss sort som sällan ställer till problem. Det visade sig att det framför allt är termer som rör material, sömnad och mönsterkonstruktion som är svåröversatta. Det går dock inte på grund av undersökningens begränsningar att dra någon definitiv slutsats för att säga att detta gäller för sömnads- och textilområdet generellt. Några av dessa svåröversatta termer (baste, tack, weft, woof, filler thread, warp, grain, straight grain, cross grain, opposite grain, muslin och toile) analyseras i detalj i uppsatsen och den inledande hypotesen att de engelska termerna skulle vara mer intensionella än de svenska har bara delvis fått stöd. Terminologiområdet som behandlar sömnad och textil är inte särskilt undersökt och denna uppsats tar bara upp en bråkdel av de termer och problemområden som hör till ämnet. Mycket mer kan och behöver göras inom området för att underlätta det framtida arbetet för översättare, språkvetare och skräddare med flera

MIR137 is an androgen regulated repressor of an extended network of transcriptional coregulators

Androgens and the androgen receptor (AR) play crucial roles in male development and the pathogenesis and progression of prostate cancer (PCa). The AR functions as a ligand dependent transcription factor which recruits multiple enzymatically distinct epigenetic coregulators to facilitate transcriptional regulation in response to androgens. Over-expression of AR coregulators is implicated in cancer. We have shown that over-expression of KDM1A, an AR coregulator, contributes to PCa recurrence by promoting VEGFA expression. However the mechanism(s) whereby AR coregulators are increased in PCa remain poorly understood. In this study we show that the microRNA hsa-miR-137 (miR137) tumor suppressor regulates expression of an extended network of transcriptional coregulators including KDM1A/LSD1/AOF1, KDM2A/JHDM1A/FBXL11, KDM4A/JMJD2A, KDM5B JARID1B/PLU1, KDM7A/JHDM1D/PHF8, MED1/TRAP220/DRIP205 and NCoA2/SRC2/TIF2. We show that expression of miR137 is increased by androgen in LnCaP androgen PCa responsive cells and that the miR137 locus is epigenetically silenced in androgen LnCaP:C4-2 and PC3 independent PCa cells. In addition, we found that restoration of miR137 expression down-regulates expression of VEGFA, an AR target gene, which suggests a role of miR137 loss also in cancer angiogenesis. Finally we show functional inhibition of mIR137 function enhanced androgen induction of PSA/KLK3 expression. Our data indicate that miR137 functions as an androgen regulated suppressor of androgen signaling by modulating expression of an extended network of transcriptional coregulators. Therefore, we propose that epigenetic silencing of miR137 is an important event in promoting androgen signaling during prostate carcinogenesis and progression

Differential Roles of Fibroblast Growth Factor Receptors (FGFR) 1, 2 and 3 in the Regulation of S115 Breast Cancer Cell Growth

Fibroblast growth factors (FGFs) regulate the growth and progression of breast cancer. FGF signaling is transduced through FGF receptors 1-4, which have oncogenic or anti-oncogenic roles depending on the ligand and the cellular context. Our aim was to clarify the roles of FGFR1-3 in breast cancer cell growth in vitro and in vivo. Pools of S115 mouse breast cancer cells expressing shRNA against FGFR1, 2 and 3 were created by lentiviral gene transfer, resulting in cells with downregulated expression of FGFR1, FGFR2 or FGFR3 (shR1, shR2 and shR3 cells, respectively) and shLacZ controls. FGFR1-silenced shR1 cells formed small, poorly vascularized tumors in nude mice. Silencing of FGFR2 in shR2 cells was associated with strong upregulation of FGFR1 expression and the formation of large, highly vascularized tumors compared to the control tumors. Silencing FGFR3 did not affect cell survival or tumor growth. Overexpressing FGFR2 in control cells did not affect FGFR1 expression, suggesting that high FGFR1 expression in shR2 cells and tumors was associated with FGFR2 silencing by indirect mechanisms. The expression of FGFR1 was, however, increased by the addition of FGF-8 to starved shLacZ or MCF-7 cells and decreased by the FGFR inhibitor PD173074 in shR2 cells with an elevated FGFR1 level. In conclusion, our results demonstrate that FGFR1 is crucial for S115 breast cancer cell proliferation and tumor growth and angiogenesis, whereas FGFR2 and FGFR3 are less critical for the growth of these cells. The results also suggest that the expression of FGFR1 itself is regulated by FGF-8 and FGF signaling, which may be of importance in breast tumors expressing FGFs at a high level

Molecular characterization of adipose tissue in the African elephant (Loxodonta africana)

Adipose tissue (AT) is a dynamic and flexible organ with regulatory roles in physiological functions including metabolism, reproduction and inflammation; secreted adipokines, including leptin, and fatty acids facilitate many of these roles. The African elephant (Loxodonta africana) is experiencing serious challenges to optimal reproduction in captivity. The physiological and molecular basis of this impaired fertility remains unknown. AT production of leptin is a crucial molecular link between nutritional status, adiposity and fertility in many species. We propose that leptin has a similar function in the African elephant. African elephant visceral and subcutaneous adipose tissue (AT) was obtained from both sexes and a range of ages including females with known pregnancy status. RNA was extracted and histological sections created and analyzed by microarray, PCR and immunohistochemistry respectively. Gas-chromatography was used to determine the fatty acid composition of AT. Microarray expression profiling was used to compare gene expression profiles of AT from pre-pubertal versus reproductively competent adult African elephants. This study demonstrates, for the first time, leptin mRNA and protein expression in African elephant AT. The derived protein sequence of the elephant leptin protein was exploited to determine its relationship within the class I helical cytokine superfamily, which indicates that elephant leptin is most closely related to the leptin orthologs of Oryctolagus cuniculus (European rabbit), Lepus oiostolus (woolly hare), and members of the Ochotonidae (Pika). Immunohistological analysis identified considerable leptin staining within the cytoplasm of adipocytes. Significant differences in fatty acid profiles between pregnant and non-pregnant animals were revealed, most notably a reduction in both linoleic and α linoleic acid in pregnant animals. This report forms the basis for future studies to address the effect of nutrient composition and body condition on reproduction in captive and wild elephants

Complement C4 Copy Number Variation is Linked to SSA/Ro and SSB/La Autoantibodies in Systemic Inflammatory Autoimmune Diseases

Objective Copy number variation of the C4 complement components, C4A and C4B, has been associated with systemic inflammatory autoimmune diseases. This study was undertaken to investigate whether C4 copy number variation is connected to the autoimmune repertoire in systemic lupus erythematosus (SLE), primary Sjögren's syndrome (SS), or myositis. Methods Using targeted DNA sequencing, we determined the copy number and genetic variants of C4 in 2,290 well-characterized Scandinavian patients with SLE, primary SS, or myositis and 1,251 healthy controls. Results A prominent relationship was observed between C4A copy number and the presence of SSA/SSB autoantibodies, which was shared between the 3 diseases. The strongest association was detected in patients with autoantibodies against both SSA and SSB and 0 C4A copies when compared to healthy controls (odds ratio [OR] 18.0 [95% confidence interval (95% CI) 10.2–33.3]), whereas a weaker association was seen in patients without SSA/SSB autoantibodies (OR 3.1 [95% CI 1.7–5.5]). The copy number of C4 correlated positively with C4 plasma levels. Further, a common loss-of-function variant in C4A leading to reduced plasma C4 was more prevalent in SLE patients with a low copy number of C4A. Functionally, we showed that absence of C4A reduced the individuals’ capacity to deposit C4b on immune complexes. Conclusion We show that a low C4A copy number is more strongly associated with the autoantibody repertoire than with the clinically defined disease entities. These findings may have implications for understanding the etiopathogenetic mechanisms of systemic inflammatory autoimmune diseases and for patient stratification when taking the genetic profile into account.publishedVersio

The KDM5B and KDM1A lysine demethylases cooperate in regulating androgen receptor expression and signalling in prostate cancer

Histone H3 lysine 4 (H3K4) methylation is key epigenetic mark associated with active transcription and is a substrate for the KDM1A/LSD1 and KDM5B/JARID1B lysine demethylases. Increased expression of KDM1A and KDM5B is implicated in many cancer types, including prostate cancer (PCa). Both KDM1A and KDM5B interact with AR and promote androgen regulated gene expression. For this reason, there is great interested in the development of new therapies targeting KDM1A and KDM5B, particularly in the context of castrate resistant PCa (CRPC), where conventional androgen deprivation therapies and androgen receptor signalling inhibitors are no longer effective. As there is no curative therapy for CRPC, new approaches are urgently required to suppress androgen signalling that prevent, delay or reverse progression to the castrate resistant state. While the contribution of KDM1A to PCa is well established, the exact contribution of KDM5B to PCa is less well understood. However, there is evidence that KDM5B is implicated in numerous pro-oncogenic mechanisms in many different types of cancer, including the hypoxic response, immune evasion and PI3/AKT signalling. Here we elucidate the individual and cooperative functions of KDM1A and KDM5B in PCa. We show that KDM5B mRNA and protein expression is elevated in localised and advanced PCa. We show that the KDM5 inhibitor, CPI-455, impairs androgen regulated transcription and alternative splicing. Consistent with the established role of KDM1A and KDM5B as AR coregulators, we found that individual pharmacologic inhibition of KDM1A and KDM5 by namoline and CPI-455 respectively, impairs androgen regulated transcription. Notably, combined inhibition of KDM1A and KDM5 downregulates AR expression in CRPC cells. Furthermore, combined KDM1A and KDM5 inhibition impairs PCa cell proliferation and invasion more than individual inhibition of KDM1A and KDM5B. Collectively our study has identified individual and cooperative mechanisms involving KDM1A and KDM5 in androgen signalling in PCa. Our findings support the further development of KDM1A and KDM5B inhibitors to treat advanced PCa. Further work is now required to confirm the therapeutic feasibility of combined inhibition of KDM1A and KDM5B as a novel therapeutic strategy for targeting AR positive CRPC

Fibroblast growth factor-8 regulation of breast cancer cell growth

Expression of fibroblast growth factor-8 (FGF-8) is increased in a large number of breast cancers. In in vitro and in vivo breast cancer models FGF-8 promotes growth, invasion and angiogenesis. In the present work we have studied the mechanisms by which FGF-8b and its receptors (FGFR1-3) promote breast cancer cell growth using S115 murine and human MCF-7 breast cancer cell lines in in vitro and in vivo models. We have also examined FGF-8 protein level together with FGFR2, and the androgen receptor by means of immunohistochemical staining of tumour tissues from 144 women diagnosed with invasive breast cancer. We found that FGF-8b induces cell cycle progression and proliferation by upregulating cyclin D1 via the MAPK/ERK, PI3K/Akt and p38/MAPK pathways in breast cancer cells. Moreover, we found that FGF-8b promotes growth and survival of breast cancer cells by protecting against cell death. FGF-8b-regulated breast cancer cell growth was further characterised by gene expression profiling of breast cancer cells treated with FGF-8b, from 1 to 24 hours. The most up- or downregulated genes in response to FGF-8b treatment mainly belonged to the functional categories and pathways related to mitosis, cell cycle regulation, cancer, and cell death. A number of key regulatory genes of cell cycle and mitosis including Btg2, Plk1 and aurora A were identified as novel targets for FGF-8b. The role of FGF receptors 1-3 in breast cancer cell growth was studied in three different cell lines silenced for expression of FGFR1, 2 and 3, respectively. Studies on growth and signalling of the FGFR1-3 silenced cell lines in vitro as well as in nude mouse tumours revealed differential roles of FGFR1 and FGFR2 in this breast cancer cell model. While FGFR1 strongly promoted growth, FGFR2 seemed to have tumour suppressing functions. In human breast cancer specimens FGF-8 and FGFR2 protein expression was shown to correlate negatively with each other. We also found downregulation of FGFR2 protein expression by FGF-8b in vitro in breast cancer cells. In accordance with these results, FGFR2 expression correlated negatively with tumour size. These results further suggest a tumour suppressor function for FGFR2. In conclusion, FGF-8 and its receptors primarily regulate breast cancer cell proliferation and survival. The novel targets and mechanisms identified may be of importance in developing therapies against breast cancer

Att överföra intertextualitet. Om svårigheterna kring att översätta en text full av citat och anspelningar

Detta magisterarbete grundar sig på min analys och översättning av boken The Body: An Essay av Jenny Boully, utgiven år 2007. Uppsatsen inleds med en källtextanalys som till stor del bygger på Lennart Hellspong och Per Ledins Vägar genom texten (1997) och Rune Ingos Konsten att översätta (2007). Denna analys åtföljs sedan av en genomgång av ett antal problem som jag stötte på under översättningsarbetets gång. Resonemangen kring översättningen tar stöd mot Lita Lundquists Oversættelse (2010 [2007]). Uppsatsens fokus ligger på hur man överför källtextens intertextualitet och stil till målspråkskontexten, eftersom min källtext innehåller många citat och hänvisningar ur och till andra verk. Målet med översättningen har varit att skapa en god och idiomatisk svensk översättning som är lika stilistiskt varierande som källtexten

Den norska pensionsreformen 2005. En studie av en välfärdsreforms tillkomst ur tre maktperspektiv.

The aim of this thesis is to spread some light over the coming into being of the 2005 Pension Reform in Norway. The point of departure lies within an interest in Welfare State politics and the development in this field. Pensions constitute a cornerstone in the Welfare State. Making use of J. Kingdon´s Theory of the Agenda Setting Process, Discourse Theory and Institutional Theory the thesis seek to visualize the implications of structures, central actors and discourses on the reform processes. It also evaluates the use of Kingdon´s theory applied to Scandinavian politics and concludes that it points out some important features but tend to miss others e.g. the importance of interest groups in Norwegian politics. The political debate about pensions is about basic material matters and we should focus on the classical institutions and organisations as labour unions and parties. It also concludes that both discourses and structures have a strong impact on the process. Norms, values and symbols are built into the process and by appealing to these, to us well known values, discourses can gain hegemony in the field

Humana svenskar och främlingsfientliga danskar? - en studie i svensk medierepresentation av dansk migrationspolitik

The aim of this thesis is to study how Denmark and the Danish people has been represented in the Swedish press and which images of them that appears. For this purpose I make use of discourse analysis and discourse theory. By analysing three cases were the debate about the Danish migration policy has been scrutinized in Swedish newspapers I seek to discover different ways of looking at the world. The study concentrates on the descriptions made by journalists and others who contribute to the debate in the media. The results show an image of the Danes as a people reluctant to foreigners and restrictive in their politics. Discourse theory stipulates that in describing others we automatically describe ourselves. The attributes we allot the Danish people confirm our own normality and difference towards others. This leaves us with the picture of ourselves (the Swedes) as a tolerant, open minded and generous people which, I argue, contains a danger in putting ourselves above others and legitimating our migration policies as prominent. In doing this we run the risk of forgetting to be self-critical and aware of the problems that may exist