Afrikaanse Spreekwoorde en Uitdrukkings: In makrostrukturele beskouing

n Beperkte sinchroniese woordeboek soos die Afrikaanse Spreekwoorde en Uitdrukkings het 'n belangrike rol te vervul in die moderne leksikografie waar gebruikersvriendelike naslaanbronne kommunikasie vergemaklik. Heelwat teoretiese riglyne bestaan vir die keuse van taalvorme wat in die woordeboek ingesluit moet word, en hierdie resensieartikel probeer om 'n paar rigtingwysers te verskaf. Die ondersoek betrek ook sosiolinguistiese implikasies wat volg uit die sames telling van die makrostruktuur van 'n betrokke woordeboek. Die fokuspunte is eerstens die taboes waaraan leksikograwe van Afrikaanse woordeboeke onderwerp word, en tweed ens die bepaling van watter uitdrukkings binne die grens van idiomatiese taalgebruik val. Veral die hantering van idioomagtige kollokasies blyk problema ties te wees. 'n Ander kwessie wat kortliks aandag sal geniet, is die morfologiese aanbieding van trefwoorde.Sleutelwoorde: spreekwoorde, vaste uitdrukkings, idiome, kollokasies, trefwoorde, teikengebrulkers, bevolkingsgroepe, ander sosiale groepe, rassistiese taal, kwetsende taal, nuutskeppings, leksikografiese etikette, morfologiese aanbiedingAfrikaanse Spreekwoorde en Uitdrukkings: A Macrostructural Study. A restricted synchronic dictionary such as Afrikaanse Spreekwoorde en Uitdrukkings has an important role to play in modern lexicography where user-friendly reference sources facilitate communication. A considerable number of theoretical guidelines exist for the choice of lexicon items to be included in a dictionary, and this review article attempts to provide some pointers. The research also includes sociolinguistic implications which result from the compilation of the macrostructure of a particular dictionary. The focal points are firstly taboos to which lexicographers of Afrikaans dictionaries are subjected, and secondly establishing which expressions fall within the limits of idiomatic language usage. The treatment of idiom-like collocations particularly appears to be problematic. Another issue which will be considered briefly, is the morphological presentation of lemmas

TNF-induced NF-κB Signal Transduction in the Liver

Gut-derived bacteria enter the liver via the portal vein where they induce an innate immune response leading to inflammation. Lipopolysaccharide, a part the bacterial cell wall component endotoxin, functions as stimulus for toll-like receptors in non-parenchymal liver cells leading to secretion of di- verse cytokines. Among these cytokines tumor necrosis factor (TNF) is one of the first to be produced. It binds to the TNF receptors of hepatocytes and activates NF-κB signalling. The transcription factor NF-κB enhances gene expressions of acute phase proteins. Its signalling primes hepatocytes for cell proliferation. In this work, I have studied NF-κB signalling in hepatocytes in various ways, using computational models trained and validated with experimental data from primary murine cells. First, I extended an ODE model of canonical NF- κB signalling to include the experimentally validated influence of p38 MAPK signalling on this signalling pathway. Additionally, by including the receptor level to the model, I ensured an accurate description of dose response mea- surements for the main pathway components. This was especially important for the second part of this work, where I used the ODE intra-hepatocellular model to investigate the influence of different non-parenchymal cells on hepatocytes in the liver. By combining information on cell abundance and cell size, and experimental TNF secretion profiles in response to LPS with this ODE model, I was able to establish for the first time a computational model combing all liver cell types relevant to LPS-induced TNF secretion and intra-hepatocellular NF-κB signalling. I could show that liver resident macrophages and liver sinusoidal endothelial cells produce the most TNF in response to LPS. Furthermore, my simulations showed that not the final lev- els of TNF regulate the in vivo response, rather the initial cytokine increase defines how strongly NF-κB signalling is activated in hepatocytes. As a third part I converted the ODE model into a PDE model, which describes possible temporal and spatial aspects of single cell microscopy measurements. I was able to show that the relevant reaction parameters of the ODE model could be used for PDE simulations to describe experimental data on the localisa- tion of fluorescently labeled NF-κB molecules after TNF stimulation. Further- more, I could show that the dynamics observed on a population-based level were comparable to those observable on a single cell level. These new insights into NF-κB signalling in the liver may change experi- mental procedures with respect to cytokine administration when analysing inflammation. Furthermore, the new multi-cellular model can serve as a basis for simulating the influence of non-parenchymal cells on hepatocytes under various experimental conditions