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Remodeling of extracellular matrix (ECM) is an important physiologic feature of normal growth and development. In addition to this critical function in physiology many diseases have been associated with an imbalance of ECM synthesis and degradation. In the kidney, dysregulation of ECM turnover can lead to interstitial fibrosis, and glomerulosclerosis. The major physiologic regulators of ECM degradation in the glomerulus are the large family of zinc-dependent proteases, collectively refered to matrix metalloproteinases (MMPs). The tight regulation of most of these proteases is accomplished by different mechanisms, including the regulation of MMP gene expression, the processing and conversion of the inactive zymogen by other proteases such as serine proteases and finally the inhibition of active MMPs by endogenous inhibitors of MMPs, denoted as tissue inhibitors of metalloproteinases (TIMPs). Namely, the MMP-9 has been shown to be critically involved in the dysregulation of ECM turnover associated with severe pathologic conditions such as rheumatoid arthritis or fibrosis of lung, skin and kidney. In the present work I searched for a possible modulation of MMP-9 expression and/or activity in glomerular mesangial cells which are thought as key players of many inflammatory and non-inflammatory glomerular diseases. I found that various structurally different PPARalpha agonists such as WY-14,643, LY-171883 and fibrates potently suppress the cytokine-induced MMP-9 expression in renal MC. Furthermore, I demonstrate that the inhibition of MMP-9 expression by PPARalpha agonists was paralleled by a strong increase of cytokine-induced iNOS expression and subsequent NO formation, suggesting that PPARalpha-dependent effects on MMP-9 expression level primarily result from alterations in NO production which in turn reduces the MMP-9 mRNA half-life. Searching for the detailed mechanism of NO-dependent effects on MMP-9 mRNA stability, I found that NO either given from exogenous sources or endogenously produced increases the MMP-9 mRNA degradation by decreasing the expression of the mRNA stabilizing factor HuR. Furthermore, I demonstrate a reduction in the RNA-binding capacity of HuR containing complexes to MMP-9 ARE motifs in cells treated with NO. Since the reduction of HuR expression can be mimicked by the cGMP analog 8-Bromo-cGMP, I suggest that NO reduces in a cGMP-dependent manner the expression of HuR. Finally, I elucidated the modulatory effect of extracellular nucleotides, mainly ATP, on cytokine-triggered MMP-9 expression. Interestingly, I found that in contrast to NO, gamma-S-ATP the stable analog of ATP potently amplifies the IL-beta mediated MMP-9 expression. The increase in mRNA stability was paralleled by an increase in the nuclear-cytosolic shuttling of the mRNA stabilizing factor HuR. Furthermore, I demonstrate an increase in the RNA-binding capacity of HuR containing complexes to the 3'-UTR of MMP-9 by ATP. In summary, the data presented here may help to find new targets (posttranscriptional regulation) that could be used to manipulate or modulate the expression of not only MMP-9 but also other genes regulated on the level of mRNA stability.
Hepatitis E virus (HEV) is a positive-stranded RNA virus with a 7.2 kb genome that is capped and polyadenylated. The virus is currently unclassified : the organisation of the genome resembles that of the Caliciviridae but sequence analyses suggest that it is more closely related to the Togaviridae. HEV is an enterically transmitted virus that causes both epidemics and sporadic cases of acute hepatitis in many countries of Asia and Africa but only rarely causes disease in more industrialised countries. Initially the virus was believed to have a limited geographical distribution. However, serological studies suggest that that HEV may be endemic also in the United states and Europe even though it infrequently causes overt disease in these countries. Many different animal species worldwide recently have been shown to have antibodies to HEV suggesting that hepatitis E may be zoonotic. Although two related strains have been experimentally transmitted between species, direct transmission from animal to a human has not been documented. Our main objective in this study is to evaluate the suitability of current available HEV antibody assays for use in low-endemicity areas such as in Germany. Methods: We selected sera on the basis of at least borderline reactivity in the routinely used Abbot EIA. Most were tested as part of routine screening of long-term expatriates in endemic countries. The following assays (recombinant antigens : ORF2 and ORF3) were used: Abbot EIA, Genelabs ELISA, Mikrogen recomBlot and a 'Prototype' DSL-ELISA. We observed a wide range of sensitivity ( average of 56.8%) and specificity ( an average of 61.4%) in these used assays. These results implies that , these assays might be unreliable for detection of HEV infection in areas where hepatitis E is not endemic. However, most anti- HEV assays have not been correlated with the HEV RNA determined by reverse transcription. Many of these unexpected results and discrepancies can be alluded to the following reasons: I. The choice and the size of the HEV antigen. II. Duration of the antibody persistence III. A cross reactivity with different agent IV. Due to geographic species V. A low sensitivity of the available assays. VI. And infection with non-pathogenic HEV strain. (zoonotic strain?). We therefore suggest that, further studies will be required to improve the sensitivity and specificity of the available commercial assays on the market.
The focus of this study were Celtic gold coins excavated from the Martberg, a Celtic oppidium and sanctuary, occupied in the first century B.C. by a Celtic tribe known as the Treveri. These coins and a number of associated coinages, were characterised in terms of their alloy compositions and their geochemical and isotopic signatures so as to answer archaeological and numismatic questions of coinage development and metal sources. This required the development of analytical methods involving; Electron Microprobe (EPMA), Laser Ablation-ICP-MS, solution Multicollector-ICPMS and LA-MC-ICP-MS. The alloy compositions (Au-Ag-Cu-Sn) were determined by EPMA on a small polished area on the edge of the coins. A large beam size, 50µm (diameter), was used to overcome the extreme heterogeneity of these alloys. These analyses were shown to be representative of the bulk composition of the coins. The metallurgical development of the coinages was defined and showed that the earlier coinages followed a debasement trend, which was superceded by a trend of increasing copper at the expense of sliver while gold compositions remained stable. This change occurred with the appearance of the inscribed "POTTINA" coinage, Scheers 30/V. Two typologically different coinages, Scheers 16 and 18 ("Armorican Types") were found to have markedly different compositions which do not fit into the trends described above. A Flan for a gold coin, which may indicate the presence of a mint at the Martberg, was found to have an identicle weight and composition as the Scheers 30/I coins, which preceeded the majority of the coins found at the Martberg in the coin development chronology. The trace element anaylses were made by Laser Ablation-ICPMS using an AridusTM desolvating nebuliser to introduce matrix matched solution standards to calibrate the measurements, which were then normalised to 100%. Quantitative results were obtained for the following elements: Sc, Ti, Cr, Mn, Co, Ni, Cu, Zn, Se, Ru, Rh, Pd, Ag, Sb, Te, W, Ir, Pt, Pb, Bi. The remaining elements remain problematic as they produced incorrect standardisations mainly due to chemical effects in solution such as adsorption onto the beaker walls or oxidation : V, Fe, Ga, Ge, As, Mo, Sn, Re, Os, Hg. Changes in the sources of Au, Ag and Cu were observed during the development of the coinages through the variation of trace elements, which correlate positively with the major components of the coin alloys. Changes in the Pt/Au ratios show that the Scheers 23 coins contain distinctly different gold from the later coinages and that the Scheers 18 gold source was also different. Te/Ag was used to show that the Sch.23 coins also contained different silver and some subgroups were observed in the Sch. 30/V coins. A major change in copper source is indicated by the sudden increase of Sb and Ni with the introduction of the Sch. 30/V coins (POTTINA), which can be linked to a similar change in copper observed in the contemporary silver coinage, Sch. 55 (with a ring). Lead isotopic analyses were made by solution- and Laser Ablation - MC-ICP-MS, The laser technique proved to be in good agreement with the solution analyses with precisions between 1 and 0.1%o (per mil). The development of the laser method opens the way for easy and virtually non-destructive Pb isotopic determinations of ancient gold coins. The results showed that Sch. 23 is very different from the following coinages, Sch. 16 and 18 are also different, forming their own group, and all the later "Eye" staters (Sch. 30/I-VI) lie on a mixing line controlled by the addition of copper from a Mediterranean source, probably Sardinia or Spain. An indication of gold and silver sources should be possible with further analyses of the Sch. 23 and Rainbow Cup gold coins and the Sch. 54 and 55 silver coinages. Copper Isotopic analyses were made by solution- and Laser Ablation - MC-ICP-MS. Both techniques require further development to produce more reproducible results. The results show that there appears to be a trend to more positive d Cu65 values for the later coinages and that the link between the copper used in the Sch. 30/V (POTTINA) coins and the silver Sch. 55 (with a ring) coins is also shown by similarly postive d Cu65 values. The full suite of analyses were also made on samples of gold from the region. They were mostly composed of "placer gold", alluvial gold found in rivers. It was found that when a study is restricted to a limited number of deposits or areas then it is possible to distinguish between deposits based on the concentration of those elements which are least affected by transport related alteration processes. These elements include; the PGE's, due to their refractory nature, and those elements which are usually present in high enough concentrations to remain relatively unaffected, eg: Cu, Pb and Sb. Due to the nature of the coin alloy it is not possible to link the gold used in the coins studied here with gold deposits, as the large amounts of Ag and Cu, added to the coin alloys, have masked the Au signature. However, further Pb isotopic analyses of gold deposits should prove useful in determining from which regions Celtic gold was derived.
In this thesis the anti-proton to proton ratio in 197Au + 197Au collisions, measured at mid-rapidity, at a center of mass energy of psNN = 200GeV is reported. The value was measured to be ¹p/p = 0.81+-0.002stat +- 0.05syst: in the 5% most central collisions. The ratio shows no dependence on rapidity in the range jyj < 0:5. Furthermore, a dependence on transverse momentum within 0:4< p? < 1:0 GeV/c is not observed. At higher p?, a slight drop in the ratio is observed. In the present analysis, the highest momentum considered is p? = 4:5 GeV/c yielding ¹p=p = 0:645§0:005stat: §0:10syst:. However, the systematic error is higher in this momentum range. A slight centrality dependence was observed, where a decrease from ¹p=p = 0:83§0:002stat:§0:05syst: for most peripheral collisions (less than 80% central) to ¹p=p = 0:78§0:002stat:§0:05syst: for the 5% most central collisions was measured. An estimate of the feed-down contributions fromthe decay of heavier strange baryons results in ¹p=p = 0:77 § 0:05syst:. The measured ratio indicates a » 12:5 times higher value compared to the highest SPS energy of psNN = 17:3 and an \almost net-baryon free" region, at mid- rapidity. The asymmetry of protons and anti-protons may be explained by the contribution ofvalence quarks in a nucleus break-up picture. In such a scenario, the absolute value of the ratio and the fact that the ratio does not depend on rapidity (at mid-rapidity) is well reproduced. Fragmentation of quarks and anti- quarks into protons and anti-protons is assumed. An estimate of the ratio, when feed-down correction is taken into consideration, agrees well with the prediction of a statistical model analysis at a temperature of T = 177 § 7 MeV and a baryon chemical potential of ¹B = 29 § 8 MeV. The temperature achieved is only slightly higher when compared to the top SPS energy, while the baryochemical potential is factor »10 lower. As in the case of the SPS results, these parameters are close to the phase boundary of Figure 1.6. The measurement of the ratio at high transverse momentum was of special in- terest in this analysis, since at RHIC energies, the cross section for hadrons at high transverse momentum is increased with respect to SPS energies. The weak dependence of the ratio on the transverse momentum is well described by the non- perturbative quenched and baryon junction scenario (i.e. Soft+Quench model), where baryon creation is enhanced by baryon junctions. In comparison the ratio does not decrease within the considered momentum range as predicted by pQCD.
In contrast to the class A heat stress transcription factors (Hsfs) of plants, a considerable number of Hsfs assigned to classes B and C have no evident function as transcription activators on their own. In the course of my PhD work I showed that tomato HsfB1, a heat stress induced member of class B Hsf family, is a novel type of transcriptional coactivator in plants. Together with class A Hsfs, e.g. tomato HsfA1, it plays an important role in efficient transcrition initiation during heat stress by forming a type of enhanceosome on fragments of Hsp promoter. Characterization of promoter architecture of hsp promoters led to the identification of novel, complex heat stress element (HSE) clusters, which are required for optimal synergistic interactions of HsfA1 and HsfB1. In addition, HsfB1 showed synergistic activation of the expression of a subset of viral and house keeping promoters. CaMV35S promoter, the most widely expressed constitutive promoter turned out to be the the most interesting candidate to study this effect in detail. Because, for most house-keeping promoters tested during this study, the activators responsible for constitutive expression are not known, but in case of CaMV35S promoter they are quite well known (the bZip proteins, TGA1/2). These proteins belong to the acidic activators, similar to class A Hsfs. Actually, on heat stress inducible promoters HsfA1 or other class A Hsfs are the synergistic partners of HsfB1, whereas on house-keeping or viral promoters, HsfB1 shows synergistic transcriptional activation in cooperation with the promoter specific acidic activators, e.g. with TGA proteins on 35S promoter. In agreement with this the binding sites for HsfB1 were identified in both house-keeping and 35S promoter. It has been suggested during this study that HsfB1 acts in the maintenance of transcription of a sub-set of house-keeping and viral genes during heat stress. The coactivator function of HsfB1 depends on a single lysine residue in the GRGK motif in its CTD. Since, this motif is highly conserved among histones as the acetylation motif, especially in histones H2A and H4,. It was suggested that the GRGK motif acts as a recruitment motif, and together with the other acidic activator is responsible for corecruitment of a histone acetyl transferase (HAT). So, the effect of mammalian CBP (a well known HAT) and its plant orthologs (HAC1) was tested on the stimulation of synergistic reporter gene activation obtained with HsfA1 and HsfB1. Both in plant and mammalian cells, CBP/HAC1 further stimulated the HsfA1/B1 synergistic effect. Corecruitment of HAC1 was proven by in vitro pull down assays, where the NTD of HAC1 interacted specifically both with HsfA1 and HsfB1. Formation of a ternary complex between HsfA1, HsfB1 and CBP/HAC1 was shown via coimmunoprecipitation and electrophoretic mobility shift assays (EMSA). In conclusion, the work presented in my thesis presents a new model for transcriptional regulation during an ongoing heat stress.
In an attempt to search for potential candidate molecules involved in the pathogenesis of endometriosis, a novel 2910 bp cDNA encoding a putative 411 amino acid protein, shrew-1 was discovered. By computational analysis it was predicted to be an integral membrane protein with an outside-in transmembrane domain but no homology with any known protein or domain could be identified. Antibodies raised against the putative open-reading frame peptide of shrew-1 labelled a protein of ca. 48 kDa in extracts of shrew-1 mRNA positive tissues and also detected ectopically expressed shrew-1. In the course of my PhD work, I confirmed the prediction that shrew-1 is indeed a transmembrane protein, by expressing epitope-tagged shrew-1 in epithelial cells and analysing the transfected cells by surface biotinylation and immunoblots. Additionally, I could show that shrew-1 is able to target to E-cadherin-mediated adherens junctions and interacts with the E-cadherin-catenin complex in polarised MCF7 and MDCK cells, but not with the N-cadherin-catenin complex in non-polarised epithelial cells. A direct interaction of shrew-1 with beta-catenin could be shown in an in vitro pull-down assay. From this data, it could be assumed that shrew-1 might play a role in the function and/or regulation of the dynamics of E-cadherin-mediated junctional complexes. In the next part of my thesis, I showed that stable overexpression of shrew-1 in normal MDCK cells. causes changes in morphology of the cells and turns them invasive. Furthermore, transcription by ²-catenin was activated in these MDCK cells stably overexpressing shrew-1. It was probably the imbalance of shrew-1 protein at the adherens junctions that led to the misregulation of adherens junctions associated proteins, i.e. E-cadherin and beta-catenin. Caveolin-1 is another integral membrane protein that forms complexes with Ecadherin- beta-catenin complexes and also plays a role in the endocytosis of E-cadherin during junctional disruption. By immunofluorescence and biochemical studies, caveolin-1 was identified as another interacting partner of shrew-1. However, the functional relevance of this interaction is still not clear. In conclusion, it can be said that shrew-1 interacts with the key players of invasion and metastasis, E-cadherin and caveolin-1, suggesting its possible role in these processes and making it an interesting candidate to unravel other unknown mechanisms involved in the complex process of invasion.
We consider the long-time behaviour of spatially extended random populations with locally dependent branching. We treat two classes of models: 1) Systems of continuous-time random walks on the d-dimensional grid with state dependent branching rate. While there are k particles at a given site, a branching event occurs there at rate s(k), and one of the particles is replaced by a random number of offspring (according to a fixed distribution with mean 1 and finite variance). 2) Discrete-time systems of branching random walks in random environment. Given a space-time i.i.d. field of random offspring distributions, all particles act independently, the offspring law of a given particle depending on its position and generation. The mean number of children per individual, averaged over the random environment, equals one The long-time behaviour is determined by the interplay of the motion and the branching mechanism: In the case of recurrent symmetrised individual motion, systems of the second type become locally extinct. We prove a comparison theorem for convex functionals of systems of type one which implies that these systems also become locally extinct in this case, provided that the branching rate function grows at least linearly. Furthermore, the analysis of a caricature model leads to the conjecture that local extinction prevails generically in this case. In the case of transient symmetrised individual motion the picture is more complex: Branching random walks with state dependent branching rate converge towards a non-trivial equilibrium, which preserves the initial intensity, whenever the branching rate function grows subquadratically. Systems of type 1) and systems of type 2) with quadratic branching rate function show very similar behaviour. They converge towards a non-trivial equilibrium if a conditional exponential moment of the collision time of two random walks of an order that reflects the variability in the branching mechanism is finite almost surely. The equilibrium population has finite variance of the local particle number if the corresponding unconditional exponential moment is finite. These results are proved by means of genealogical representations of the locally size-biased population. Furthermore, we compute the threshold values for existence of conditional exponential moments of the collision time of two random walks in terms of the entropy of the transition functions, using tools from large deviations theory. Our results prove in particular that - in contrast to the classical case of independent branching - there is a regime of equilibria with variance of the local number of particles.
One of the known apoptotic pathways in mammalian cells involves release of mitochondrial Cytochrome c into the cytosol. Cyt c then together with ATP or dATP induces a conformational change in the adaptator protein Apaf-1 (a homologue of the C. elegans CED4 protein) (Zou, Henzel et al. 1997), leading to its oligomerization and the recruitment of several pro-Casp-9 molecules. This protein complex assembly called "apoptosome" leads to the activation of Casp-9 which then initiates or amplifies the caspase cascade. The cell death program can be stalled at several points and we were interested in identifying new proteins inhibiting cell death downstream of Cyt c release. This thesis describes how I have screened a cDNA library derived from a pool of human breast carcinomas in a yeast-based survival screen, using the S. pombe yeast strain HC4 containing an inducible CED4 construct(James, Gschmeissner et al. 1997). The screen resulted in the identification of six proteins displaying cell death-inhibiting activity in S. pombe as well as anti-apoptotic potential in mammalian cells. Those six molecules were RoRet (Ruddy, Kronmal et al. 1997), Aven (Chau, Cheng et al. 2000), Fte-1/S3a (Kho, Wang et al. 1996), PGC2 (Padilla, Kaur et al. 2000; Goetze, Eilers et al. 2002), SAA1-2ß (Moriguchi, Terai et al. 2001) and FBP (Brockstedt, Rickers et al. 1998) of which I selected RoRet, Aven and Fte-1/S3a for further analysis. RoRet is a new anti-apoptotic molecule that can inhibit the mitochondrial pathway via its PRY-SPRY domain. RoRet does not seem to bind to Apaf-1, and does not co-localize with the activated Apaf-1/Caspase-9 complex. Aven was published to act as an anti-apoptotic protein and suggested to function via the recruitment of Bcl-XL to Apaf-1. This work shows that its C-terminal domain can bind to Apaf-1 and has a strong anti-apoptotic activity by itself. Moreover, Aven co-localizes with the activated Apaf-1/Caspase-9 complex suggesting that it is a component of the apoptosome. Furthermore, the expression of Aven is regulated in mammary glands during the pregnancy cycle. Fte-1/S3a has been already implicated in increased transformation capacity of v-Fos in fibroblasts (Kho and Zarbl 1992; Kho, Wang et al. 1996). This work shows that it has anti-apoptotic activity and can protect against Bak- and Apaf-1-induced apoptosis. It can bind directly to activated Apaf-1 at the linker domain between the WD40 repeats and the CED4-like domain, suggesting that it may protect by sequestering the activated Apaf-1 to some organelles whose nature remains to be determined. Moreover, expression studies on mRNA and protein level showed upregulation of Fte-1/S3a in colon, lung and kidney carcinoma. Hmgb1 (Flohr, Rogalla et al. 2001; Pasheva, Ugrinova et al. 2002; Stros, Ozaki et al. 2002) was identified during a survival screen performed with a NIH 3T3 mouse fibroblast cDNA library in a Bak-expressing yeast S. pombe strain. HMGB1 can protect against Bak-, UV-, FasL- and TRAIL-induced apoptosis. Significant overexpression of HMGB1 was found in breast and colon carcinoma, and elevated mRNA amounts were detected in uterus, colon and stomach carcinoma, suggesting that it may be a tumour marker (Brezniceanu et al., 2003).
Mitogen activated protein kinases (MAPKs) are found in all eukaryotic cells and represent crucial elements in the signal transduction from the plasma membrane to the nucleus. Although a broad variety of extracellular stimuli activate MAPKs, they evoke very distinct cellular responses. The amplitude and duration of MAPK activation determine signal identity and ultimately cell fate. A tight and finely tuned regulation is therefore critical for a specific cellular response. The role and the regulation of extracellular signal-regulated kinase 5 (ERK5), a MAPK with a large and unique C-terminal tail, were studied in different cellular systems. The study highlights two aspects of ERK5 regulation: control of the phosphorylation state and regulated protein stability. In analogy to other MAPKs ERK5 is activated by dual phosphorylation of threonine and tyrosine residues in its activation motif. A first part of the study concentrates on whether and how the protein tyrosine phosphatase PTP-SL is involved in the downregulation of the ERK5 signal. The direct interaction of both proteins is shown to result in mutual modulation of their enzymatic activities. PTP-SL is a substrate of ERK5 and, independent of its phosphorylation, binding to the kinase enhances its catalytic phosphatase activity. On the other hand, interaction with PTP-SL does not only downregulate enzymatic ERK5 activity but also effectively impedes its translocation to the nucleus. The second part of this study focuses on the interaction of ERK5 with c-Abl and its oncogenic variants Bcr/Abl and v-Abl. In this study these tyrosine kinases are demonstrated to regulate ERK5 by two mechanisms: first, by induction of kinase activity and secondly, by stabilisation of the ERK5 protein. Stabilisation involves the direct interaction of unique ERK5 domains with Abl kinases and is independent of MAPK cascade activation. The level of ERK5 and its intrinsic basal activity – rather than its activation – are essential for v-Abl-induced transformation as well as for survival of Bcr/Abl-positive leukaemia cells. Stabilisation of ERK5 thus contributes to cell survival and should therefore be considered as an additional aspect in therapy of chronic myeloid leukaemia. Taken together, the results obtained in this study demonstrate that diverse pathways regulate ERK5 signalling by affecting kinase activity, localisation and protein stability. While the phosphatase PTP-SL is involved in negative regulation of ERK5, Abl kinases potently activate ERK5 and increase its half-life. Protein stabilisation thus is presented as a novel mechanism in the regulation of MAPKs.
Die Entwicklung der Renormierungsgruppen-Technik, die in ihrer feldtheoretischen Version auf Ideen von Stückelberg und Petermann und in der Festkörperphysik auf K.G. Wilson zurückgeht, hat wesentliche Einsichten in die Natur physikalischer Systeme geliefert. Insbesondere das Konzept der so genannten Universalitätsklassen erhellt, warum Systeme, die durch scheinbar sehr verschiedene Hamilton-Operatoren beschrieben werden, doch im Wesentlichen die selbe (Niederenergie-)Physik zeigen. Ein weiterer Grund für den Erfolg dieser Methode liegt darin begründet, dass sie in systematischer Weise unendlich viele Feynman-Diagramme aufsummiert und somit über konventionelle Störungstheorie hinaus geht. Dies spielt in der Festkörperphysik vor allem dann eine wichtige Rolle, wenn das vorliegende physikalische System stark korreliert ist. Entsprechend der Vielzahl von Anwendungsmöglichkeiten hat sich in den vergangenen Jahrzehnten eine große Bandbreite verschiedener Formulierungen der Renormierungsgruppen-Technik ergeben. Eine davon ist die sogenannte funktionale Renormierungsgruppe, die auf Wegner und Houghton zurück geht und die auch in der vorliegenden Arbeit benutzt und weiter entwickelt wurde. Wir haben hier insbesondere auf die Einbeziehung der wichtigen Reskalierungsschritte wertgelegt. Als erstes Anwendungsgebiet des neu entwickelten Formalismus wurden stark korrelierte Elektronen in einer Raumdimension ausgewählt und hier insbesondere ein Modell, das als Tomonaga-Luttinger-Modell (TLM) bezeichnet wird. Im TLM wechselwirken Elektronen mit einer strikt linearen Energiedispersion ausschließlich über so genannte Vorwärtsstreu-Prozesse. Aufgrund der Linearisierung der Energiedispersion nahe der Fermipunkte ergibt sich ein Modell, das z.B. mit Hilfe der so genannten Bosonisierungs-Technik exakt gelöst werden kann. Hauptziel der vorliegenden Arbeit ist es, die bekannte Spektralfunktion dieses Modells unter Verwendung des Renormierungsgruppen-Formalismus zu reproduzieren. Gegenüber der bisherigen Implementierung der Renormierungsgruppe, bei der lediglich der Fluss einer endlichen Anzahl von Kopplungskonstanten betrachtet wird, stellt die Berechnung des Flusses ganzer Korrelationsfunktionen eine enorme Erweiterung dar. Der Erfolg dieser Herangehensweise im TLM bestärkt die Hoffnung, dass es in Zukunft auch möglich sein wird, die Spektralfunktionen anderer Modelle mit dieser Methode zu berechnen, bei denen herkömmliche Techniken versagen.