Thesis (Ph. D.)--Illinois State University, 1983. / Title from title page screen, viewed May 10, 2005. Dissertation Committee: Arlan Richardson, Joshua Fierer (co-chairs), H. Tak Cheung, Harry Huizinga, Mathew Nadakavukaren. Includes bibliographical references (leaves 130-144) and abstract. Also available in print.

This thesis presents a new description and theoretical analysis of the nominal system of Katcha (Nilo-Saharan, Kadu), spoken in the Nuba Mountains of Sudan. The description and analysis are based on a synthesis of data from several sources, including unpublished archive material and original fieldwork. The study is placed in context with a discussion of the demographic, cultural and political background affecting the Katcha linguistic community, a review of the current state of linguistic research on Katcha and a discussion of the ongoing controversy over the place of the Kadu languages within the language phyla of Africa. The morphosyntactic descriptions first focus on the role of nominals as heads, considering phenomena such as classification, agreement and modification. It is shown that Katcha has a unusual system of gender agreement with three agreement classes based on the concepts of Masculine, Feminine and Plural and that the gender of a noun may change between its singular and plural forms. Surprisingly, these phenomena are both most commonly found in Afro-Asiatic, which is not a phylum to which Kadu has previously been ascribed. The gender changes are shown to be predictable, determined by number-marking affixes. The study then gives a unified analysis of various types of nominal modifiers; relative clauses, possessives, demonstratives and adjectives all display similar morphological properties and this is accounted for by analysing all modfiers as appositional, headed by a demonstrative pronoun. This analysis of modifiers shows them to be related to, though not the same as, the notions of relative markers and construct state found widely in African languages. The role of nominals within sentential argument structure is then considered, with discussion of phenomena such as prepositional phrases, case and verbal valency. From the interaction of prepositions and pronouns, it is tentatively concluded that Katcha has three cases: Nominative, Accusative and Oblique. From the interaction of verbs and nouns, it is demonstrated that the verbal suffixes known as ‘verb extensions’ primarily serve to license the absence of otherwise mandatory core arguments. The second part of the thesis provides a theoretical analysis of the nominal system within the framework of Dynamic Syntax (DS). Two key features of the DS formalism come into play. Firstly, DS construes semantic individuals as terms of the epsilon calculus. Verb extensions are analysed as projecting context-dependent epsilon terms, providing a value for the ‘missing’ argument. Secondly, DS allows information sharing between propositions by means of a ‘LINK’ relation. Prepositional phrases are analysed as projecting a subordinate proposition which shares an argument with the matrix tree. These two formal tools come together in the analysis of nominal modifiers, which are construed as projecting an arbitrarily complex epsilon term LINKed to some term in the matrix tree, directly reflecting their descriptive analysis as appositional nominals. In presenting new data for a little studied language, this thesis adds to our knowledge and understanding of Nuba Mountain languages. In describing and analysing some of the typologically unsual features of Katcha’s nominal system, it challenges some standard assumptions about these constructions and about the genetic affiliation of the Kadu family. And in the theoretical analysis it demonstrates the suitability of Dynamic Syntax to model some of the key insights of the descriptive analysis.

Meiotic recombination, known as crossover, is a vital mechanism for generating genetic diversity in sexually reproducing populations. Recombination events are non-uniform across the genome, due to a variety of influences including chromatin structure, DNA-sequence, epigenetic marks and interference from other recombination events. These known factors do not fully explain the distribution of recombination events, and additionally do not account for all the variability in recombination frequency observed both between and within species. Furthermore, of the mechanisms that have been identified, many are not yet fully understood. In Arabidopsis thaliana, considerable variation is observed in recombination frequency and distribution between natural accessions. By investigating recombination events in A.thaliana, this project aimed to identify trans-acting modifiers of recombination frequency that varied between natural accessions. Identification of meiotic recombination modifiers was performed through Quantitative Trait Loci (QTL) mapping in A.thaliana natural-accession cross populations. Populations were generated from crosses between two accessions which differed significantly for recombination frequency as measured across a defined region of the genome flanked by a fluorescent-reporter system. F1 plants were then self-fertilised to produce segregating mosaic F2 populations for mapping. Recombination frequency for specific genomic intervals was determined for each individual in the population through measurement of the segregation of flanking fluorescence-genes expressed in the products of meiosis - seeds or pollen. Individuals were also genotyped using accession-specific markers across the genome, at a marker density of one marker per 2-5Mb, depending on the chromosome. Association of variation in recombination frequency with specific sections of the genome differing between the parental accessions through QTL mapping revealed significant modifiers of meiotic recombination segregating within the populations. This resulted in the identification of three significant large-effect modifiers that differed between Col-0 and Cvi-0 accessions, on chromosomes 1 ,2 and 5, affecting recombination in an interval in the sub-telomere region of chromosome 3. An additional modifier on chromosome 4 affecting the same sub-telomeric interval was identified that differed between the Col-0 and Can-0 accessions. Further fine-mapping of modifiers to improve location resolution was performed by repeated backcrosses into the Col-0 genetic background to remove the influence of other large-effect QTL and possible unknown small-effect modifiers. Improving the resolution provided a number of potential candidates for genes underlying the recombination phenotype for each QTL. Candidate testing was then performed, either through transformation of different accession alleles into the fluorescent-reporter system, or through analysis of T-DNA insertion lines that interrupted candidate genes. Preliminary results from T-DNA insertion mutants crossed to the fluorescent-reporter system suggest a potential role for the AT2G31510 gene in modification of meiotic recombination frequency, though the mode of action remains unknown. These results demonstrate the presence of large-effect modifiers of meiotic recombination frequency that vary between the natural A.thaliana accessions Col-0, Cvi-0 and Can-0. Confirmation of underlying genes or sequence elements and characterisation of their mechanism of action are opportunities for exploration in future experiments.

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Immunotherapy offers a promising approach to cancer treatment by harnessing a patient’s own immune system to fight malignant cells. However, the clinical application of immunotherapy has been hindered by the immunosuppressive tumor microenvironment generated by cancer cells as a mechanism to impede immune function and evade immune detection. Clinically used immunotherapies, such as immune checkpoint inhibitors and adoptive cell therapy, aim to overcome the immunosuppressive tumor microenvironment by blocking key regulatory pathways and exogenously activating immune cells. While effective against some cancers, these therapies are still limited by systemic toxicity, poor delivery kinetics, and continuous tumor adaptation that leads to immune escape. Herein, we propose the synthesis of nanoscale branching DNA architectures, known as dendrons, to (1) encode and deliver a DNA sequence, termed G3YSD, capable of activating the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway; and (2) deliver epigenetic modifiers to reprogram immunosuppressive cues in tumor cells. This solution exploits the modularity, programmability, and ease of control over DNA synthesis to generate architectures that exhibit improved delivery kinetics and favorable presentation of cargo to enhance immunomodulatory effects. Our proposed solution directly targets immunosuppressive mechanisms in tumor cells to sensitize them to immune attack and make them more easily recognized by the immune system. Delivery of G3YSD-encoding dendrons to murine B16 melanoma significantly increased the expression of major histocompatibility complex I (MHC I) and programmed cell death-ligand 1 (PD-L1) surface-bound receptors, which are critical for immune signaling pathways. The chemical conjugation of romidepsin, a histone deacetylase inhibitor, to G3YSD-encoding dendrons resulted in more than a 2-fold increase in MHC I expression compared to unconjugated G3YSD sequences and free romidepsin, indicating that the spatial arrangement and presentation of romidepsin has a synergistic impact on cGAS-STING signaling. In addition, pretreatment of B16 melanoma cells with zebularine, a DNA methyltransferase inhibitor, followed by G3YSD-encoding dendrons significantly increased levels of cytotoxic T lymphocyte-mediated lysis in a physiologically relevant co-culture. Developing novel architectures capable of interacting with tumor cells to remodel and overcome immunosuppressive cues will lead to significant advances in the field of immunotherapeutic design and cancer treatment. / 2026-05-23T00:00:00Z

Thesis (PhD)--Stellenbosch University, 2003. / ENGLISH ABSTRACT: Alkali-soluble rheology modifiers are commercially synthesised via conventional freeradical polymerisation processes. This results in the end product having certain limitations; there is poor control over the molar mass, molar mass distribution and chain architecture of the polymer chains. These limitations can be overcome by using a controlled/living free radical polymerisation process, for example the RAFT process. This alternate method of synthesis was used here to prepare model alkali-soluble rheology modifiers. The structure/property relationships of model alkali-soluble rheology modifiers synthesised via the RAFT process were studied. Model alkali-soluble rheology modifiers of different molar masses and chain architectures (block, co- and ter-polymers) were successfully synthesised by the RAFT polymerisation of methyl methacrylate, methacrylic acid and various hydrophobic macromonomers. The different types of alkali-soluble rheology modifiers were synthesised in solution and in miniemulsion. Each of the two systems had certain advantages and disadvantages. The conversion limit of reactions in solution was about 60 % and reaction times were much slower than those of the miniemulsion reactions. Higher final conversions were recorded for miniemulsion reactions, reactions were faster and no solvent removal was required. Unfortunately it was not possible to synthesise all the different types of associative rheology modifiers investigated here in a miniemulsion system. The latex solutions thickened with conventional rheology modifiers (co-polymers) show very contrasting behaviour (rheology profile and dynamic properties) to that of the latex solutions thickened with the associative rheology modifiers (ter-polymers). The AB block copolymers gave the latex solutions rheology results between those obtained with conventional rheology modifiers and those with the associative rheology modifiers. Varying the number of ethylene oxide spacer units in the hydrophobic macromonomers of the associative rheology modifiers had a significant influence on the rheology properties of the latex and alkali solutions. As the number of ethylene oxide spacer units was increased from 20 to 100 there was a significant increase in the zero-shear viscosity of the latex solutions thickened with the associative rheology modifiers. Contrasting results were obtained for the polymer solutions (no latex present), where the use of the associative rheology modifiers containing the highest number (EO = 100) of ethylene oxide spacer units resulted in solutions with the lowest viscosity, but the rheology modifiers containing the 50 ethylene oxide spacer units gave the highest steady shear viscosity. / AFRIKAANSE OPSOMMING: Alkali-oplosbare reologie-modifiseerders word kommersieël gesintetiseer d.m.v. konvensionele vrye-radikaal polimerisasieprosesse. Hierdie prosesse lewer gewoonlik 'n eindproduk met sekere tekortkominge, a.g.v. swak beheer oor molekulêre massa, molekulêre massa-verspreiding, en polimeerkettingstruktuur (Eng. chain architecture). Hierdie tekortkominge kan oorbrug word deur gebruik te maak van 'n beheerde/lewende vrye-radikaal polimerisasieproses, soos byvoorbeeld die RAFT-proses (Eng. RAFT: reversible addition-fragmentation chain transfer polymerisation). Hierdie alternatiewe metode is in die studie gebruik om model alkali-oplosbare reologiemodifiseerders te sintetiseer. Die struktuur-eienskapverhoudings van die model alkali-oplosbare reologie modifiseerders wat d.m.v. die RAFT-proses gesintetiseer is, is bestudeer. Model alkali-oplosbare reologiemodifiseerders van verskillende molekulêre massas en kettingstrukture (blok, ko- en ter-polimere) is suksesvol gesintetiseer d.m.v. RAFT-polimerisasie van metielakrilaat, metakrielsuur en hidrofobiese makromonomere. Die verskillende alkali-oplosbare reologiemodifiseerders is in organiese oplosmiddel sowel as in mini-emulsie gesintetiseer. Elkeen van die sisteme het sekere voordele en nadele getoon. In die reaksies wat in organiese oplosmiddels gedoen is, is slegs 60 % van die monomere ingebou in die polimeerkettings en die tydsduur van hierdie reaksie was heelwat langer as by die wat uitgevoer is in mini-emulsie. Meer as 60 % van die monomere is omgeskakel na polimeer tydens die reaksies wat in mini-emulsie uitgevoer is, die reaksietempo was vinniger en dit was nie nodig om die organiese oplosmiddel te verwyder nie. Ongelukkig was dit nie moontlik om al die verskillende tipes assosiatiewe-reologiemodifiseerders (Eng: associative rheology modifiers) in miniemulsie te sintetiseer nie. Die lateks wat met konvensionele reologiemodifiseerders (ko-polimere) verdik is, het kontrasterende eienskappe (reologie-profiel en dinamiese eienskappe) getoon teenoor die van die lateks-oplossings wat met assosiatiewe-reologiemodifiseerders (ter-polimere) verdik is. Die AB-tipe blok ko-polimere gee reologieresultate vir die lateks-oplossings wat lê tussen die wat bepaal is vir konvensionele reologieodifiseerders en assosiatiewe reologiemodifiseerders. Variasie in die aantal etileenoksiedeenhede in die hidrofobiese makromonomere van die assosiatiewe reologiemodifiseerders het 'n betekenisvolle invloed op die reologie-eienskappe van die lateks, sowel as die alkali-oplossings gehad. Namate die aantal etileenoksiedeenhede van 20 tot 100 vermeerder is, het 'n betekenisvolle verhoging in die "zero-shear " viskositeit van die lateks oplossings wat met die assosiatiewe reologiemodifiseerders verdik is voorgekom. Teenstrydige resultate is verkry vir die polimeeroplossings met geen lateks teenwoordig nie: die assosiatiewe reologiemodifiseerders met die hoogste aantal etieleenoksiedeenhede (EO = 100) het die laagste viskositeitsresultate opgelewer en die reologiemodifiseerders met slegs 50 etieleenoksiedeenhede het die hoogste viskositeitsresultate gelewer.

Thesis (PhD)--Stellenbosch University, 2014. / ENGLISH ABSTRACT: Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity and mortality, and is a feature of common diseases, such as hypertension and diabetes. It is therefore vital to understand the underlying mechanisms influencing its development. However, investigating the mechanisms underlying LVH in such complex disorders can be challenging. For this reason, many researchers have focused their attention on the autosomal dominant cardiac muscle disorder, hypertrophic cardiomyopathy (HCM), since it is considered a model disease in which to study the causal molecular factors underlying isolated cardiac hypertrophy. HCM is a heterogeneous disease that manifests with various phenotypes and clinical symptoms, even in families with the same genetic defects, suggesting that additional factors contribute to the disease phenotype. Despite the identification of several HCM-causing genes, the genetic factors that modify the extent of hypertrophy in HCM patients remain relatively unknown. The gene encoding the sarcomeric protein, cardiac myosin binding protein C, cMyBPC (MyBPC3) is one of the most frequently implicated genes in HCM. Identification of proteins that interact with cMyBPC has led to improved insights into the function of this protein and its role in cardiac hypertrophy. However, very little is known about another member of the myosin binding protein family, myosin binding protein H (MyBPH). Given the sequence homology and similarity in structure between cMyBPC and MyBPH, we propose that MyBPH, like cMyBPC, may play a critical role in the structure and functionality of the cardiac sarcomere and could therefore be involved in HCM pathogenesis. The present study aimed to identify MyBPH-interacting proteins by using yeast two-hybrid (Y2H) analysis and to verify these interactions using three-dimensional (3D) co-localisation and co-immunoprecipitation (Co-IP) analyses. We further hypothesized that both MyBPH and cMyBPC may be involved in autophagy. To test this hypothesis, both MyBPH and cMyBPC were analysed for co-localisation with a marker for autophagy, LC3b-II. The role of MyBPH and cMyBPC in cardiac cell contractility were analysed by measuring the planar cell surface area of differentiated H9c2 rat cardiomyocytes in response to β-adrenergic stress after individual and concurrent siRNA-mediated knockdown of MyBPH and cMyBPC. In the present study we employed a family-based genetic association analysis approach to investigate the contribution of genes encoding the novel MyBPH-interacting proteins in modifying the hypertrophy phenotype. This study investigated the hypertrophy modifying effects of 38 SNPs and haplotypes in four candidate HCM modifier genes, in 388 individuals from 27 HCM families, in which three unique South African HCM-causing founder mutations segregate. Yeast two-hybrid analysis identified three putative MyBPH-interacting proteins namely, cardiac β-myosin heavy chain (MYH7), cardiac α-actin (ACTC1) and the SUMO-conjugating enzyme UBC9 (UBC9). These interactions were verified using both 3D co-localisation and Co-IP analyses. Furthermore, MyBPH and cMyBPC were implicated in autophagy, since both these proteins were being recruited to the membrane of autophagosomes. In addition, a cardiac contractility assay demonstrated that the concurrent siRNA-mediated knockdown of MyBPH and cMyBPC resulted in a significant reduction in cardiomyocyte contractility, compared to individual protein and control knockdowns under conditions of β-adrenergic stress. These results indicated that MyBPH could compensate for cMyBPC, and vice versa, further confirming that both these proteins are required for efficient sarcomere contraction. Results from genetic association analyses found a number of SNPs and haplotypes that had a significant effect on HCM hypertrophy. Single SNP and haplotype analyses identified SNPs and haplotypes within genes encoding MyBPH, MYH7, ACTC1 and UBC9, which contribute to the extent of hypertrophy in HCM. In addition, we found that several variants and haplotypes had markedly different statistical significant effects in the presence of each of the three HCM founder mutations. The results of this study ascribe novel functions to MyBPH. Cardiac MyBPC and MyBPH play a critical role in sarcomere contraction and have been implicated in autophagy. This has further implications for understanding the patho-etiology of HCM-causing mutations in the gene encoding MyBPH and its interacting proteins. This is to our knowledge the first genetic association analysis to investigate the modifying effect of interactors of MyBPH, as indication of the risk for developing LVH in the context of HCM. Our findings suggest that the hypertrophic phenotype of HCM is modulated by the compound effect of a number of variants and haplotypes in MyBPH, and genes encoding protein interactors of MyBPH. These results provide a basis for future studies to investigate the risk profile of hypertrophy development in the context of HCM, which could consequently lead to improved risk stratification and patient management. / AFRIKAANSE OPSOMMING: Linker ventrikulêre hipertrofie (LVH) is 'n primêre risikofaktor vir kardiovaskulêre morbiditeit en mortaliteit asook 'n kenmerk van algemene siektes soos hipertensie en diabetes. Daarom is dit van kardinale belang om te verstaan wat die onderliggende meganismes is wat die ontwikkeling van LVH beïnvloed. Die ondersoek na die onderliggende meganismes wat lei tot LVH in sulke komplekse siektes is ‟n uitdaging. Om hierdie rede fokus baie navorsers hul aandag op die autosomaal dominante hartspier siekte, hipertrofiese kardiomiopatie (HKM), wat beskou word as 'n model siekte om die molekulêre oorsake onderliggend tot geïsoleerde kardiovaskulêre hipertrofie te ondersoek. HKM is 'n heterogene siekte wat manifesteer met verskeie fenotipes en kliniese simptome, selfs in families met dieselfde genetiese defekte, wat impliseer dat addisionele faktore bydra tot die modifisering van die siekte fenotipe. Ten spyte van die identifisering van verskeie HKM-versoorsakende gene, bly die genetiese faktore wat die mate van hipertrofie in HKM pasiente modifiseer relatief onbekend. Die geen wat kodeer vir die sarkomeriese proteïen, kardiale miosien-bindingsproteïen C (kMyBPC) is die algemeenste betrokke in HKM. Die identifisering van proteïene wat bind met kMyBPC het gelei tot verbeterde insigte tot die funksie van hierdie proteïen en die rol wat hierdie proteïen in hipertrofie speel. Ten spyte hiervan, is daar baie min inligting beskikbaar oor 'n ander lid van die miosien-bindingsproteïen families, miosien-bindingsproteïen H (MyBPH). Gegewe die ooreenstemming tussen die DNA basispaar-volgorde en struktuur tussen hierdie twee proteïene, stel ons voor dat MyBPH, net soos kMyBPC, 'n kritiese rol in die struktuur en funksie van die kardiale sarkomeer speel en kan daarom betrokke wees in die patogenese van HKM. Die huidige studie het beoog om proteïene wat met MyBPH bind te identifiseer deur die gebruik van gis-twee-hibried (G2H) kardiale biblioteek sifting en om hierdie interaksies te verifieer met behulp van drie-dimensionele (3D) ko-lokalisering en ko-immunopresipitasie eksperimente. Ons het verder gehipotiseer dat beide MyBPH and kMyBPC betrokke kan wees in outofagie. Om hierdie hipotese te toets is beide MyBPH en kMyBPC geanaliseer vir ko-lokalisering met 'n merker vir outofagie, LC3b-II. Verder het ons beplan om die rol van MyBPH en kMyBPC in kardiale spiersel-sametrekking te ondersoek deur die oppervlak van gedifferensieerde H9c2 rot kardiomiosiete in reaksie op β-adrenergiese stres te meet, na individuele en gesamentlike siRNA-bemiddelde uitklopping van MyBPH en kMyBPC. In hierdie studie het ons 'n familie-gebaseerde genetiese assosiasie analise benadering gevolg om vas te stel of MyBPH en gene wat kodeer vir die geverifieerde bindingsgenote van MyBPH bydra tot die modifisering van die hipertrofiese fenotipe. Die doel van hierdie studie was om die hipertrofiese effek van 38 enkel nukleotied polimorfismes (SNPs) en haplotipes in vier kandidaat HKM modifiserende gene in 388 individue van 27 HCM families te toets, waarin drie unieke Suid-Afrikaanse HKM-stigters mutasies segregeer. G2H analise het drie verneemde MyBPH bindingsgenote geidentifiseer, naamlik miosien (MYH7), alfa kardiale aktien (ACTC1) en die SUMO-konjugerende ensiem UBC9 (UBC9). Hierdie interaksies is geverifieer deur middel van 3D ko-lokalisering en ko-immunopresipitasie analises. Verder is bewys dat MyBPH en kMyBPC betrokke is in outofagie, siende dat beide proteïene gewerf is tot die membraan van die outofagosoom. 'n Kardiale sametrekkings eksperiment het gevind dat die gesamentlike siRNA-bemiddelde uitklopping van MyBPH en kMyBPC 'n merkwaardige vermindering in die kardiomiosiet sametrekking veroorsaak het in reaksie op β-adrenergiese stres kondisies, in vergelyking met die individuele proteïen en kontrole uitkloppings eksperimente. Hierdie resultate bevestig dat MyBPH vir kMyBPC kan instaan en ook andersom, wat verder bevestig dat beide proteïene benodig word vir effektiewe sarkomeer sametrekking. Resultate van die genetiese assosiasie studie het gevind dat 'n aantal SNPs en haplotipes 'n beduidende effek of HKM hipertrofie het. Enkel SNP en haplotipe analises in gene wat kodeer vir MyBPH, MYH7, ACTC1 en UBC9 het SNPs en haplotipes geidentifiseer wat bydra tot die omvang van hipertrofie in HKM. Verder het ons gevind dat sekere SNPs en haplotipes kenmerkend verskillende statisties beduidende effekte in die teenwoordigheid van elk van die drie HKM-stigter mutasies gehad het. Die resultate van hierdie studie skryf twee nuwe funksies aan MyBPH toe. Kardiale MyBPC en MyBPH speel 'n kritiese rol in sarkomeer sametrekking en is betrokke in outofagie. Hierdie resultate het verdere implikasies vir die verstaan van die pato-etiologie van die HKM-veroorsakende mutasies in die MyBPH, MYH7, ACTC1 en UBC9 gene. So vêr dit ons kennis strek is dit die eerste genetiese assosiasie studie wat die modifiserende effek van bindingsgenote van MyBPH ondersoek as risiko aanduiding vir die ontwikkeling van LVH in die konteks van HKM. Ons bevindinge bewys dat die hipertrofiese fenotipe van HKM gemoduleer word deur die komplekse effekte van SNPs en haplotipes in die MyBPH geen en gene wat MyBPH proteïen-bindingsgenote enkodeer. Hierdie resultate verskaf dus 'n basis vir toekomstige studies om die risiko profiel van hipertrofie ontwikkeling met betrekking tot HKM te ondersoek, wat gevolglik kan bydra tot die verbeterde risiko stratifikasie en pasiënte bestuur.

<p>The following essay is an analysis of a translation from English into Swedish of two articles concerning tourism, travelling and the environment. The language of the articles is expressive and rich in metaphors, which evokes images in the mind of the reader. The translation was performed with the aim to transfer this effect into the translated texts and the aspects to be examined in the analysis were chosen with this in mind.One of the three aspects to be examined is the use of metaphors and how they are translated into Swedish. Many of the metaphors bear reference to travelling and the environment which gives them a function of enforcing the message and engaging the reader in the text. In order to obtain the same effect in the Swedish translations several translation strategies had to be used.The second aspect to be examined is the terminology used within tourism and the environment.  The environmental concern is a growing trend which inevitably influences the language and requires a new set of useful and understandable terms. This becomes clear when reading and translating the articles at hand. The environmental terms are fairly new and sometimes hard to distinguish. In this study focus is set on the translation strategies and the procedures used in order to find the Swedish equivalents of the terms in this context.The third aspect is the translation of hyphenated pre-modifiers. This aspect is particularly interesting, since the phenomenon is more or less unknown in Swedish. Of the fifteen hyphenated pre-modifiers in the source texts none were translated into hyphenated pre-modifiers in Swedish although five of them were translated into regular pre-modifiers. The analysis is based on the translation strategies applied and the comparison of syntactic structures of the expressions in English and Swedish.</p>