Thesis (doctoral)--Universität, Mainz, 2002.

Utgångspunkten vid konkurs och utmätning i svensk rätt är att alla borgenärer ska behandlas lika och drabbas av gäldenärens betalningsoförmåga proportionellt i relation till storleken på sin fordran. Olika omständigheter, som exempelvis förmånsrättsordningen och borgenärernas inbördes olika förutsättningar att riskbedöma sina krediter gör dock att det i realiteten föreligger stora skillnader mellan olika borgenärsgruppers möjligheter att få betalt för sina fordringar när gäldenären hamnat på obestånd. Leverantörer av varor har flera gånger lyfts fram som en av de borgenärsgrupper som har sämst utsikter att få utdelning för sina fordringar i en obeståndssituation. I början av 2015 kom SOU 2015:18, i vilken Lösöreköpskommittén föreslår en övergång från traditionsprincipen till avtalsprincipen för borgenärsskydd vid köp av lösöre, samt ett införande av en möjlighet att registrera panträtt i sådant lösöre som ska finnas kvar hos gäldenären under pantsättningstiden. I denna uppsats analyseras leverantörers ställning vid konkurs före och efter ett eventuellt införande av Lösöreköpskommitténs förslag och föreslås åtgärder för att förbättra för leverantörerna. Inledningsvis analyseras leverantörernas position utifrån dagens rättsläge, där det konstateras att leverantörer i jämförelse med andra borgenärsgrupper har svårt att säkerställa sina anspråk, och i regel får begränsad utdelning vid konkurs. Det visas också att en dålig ställning för leverantörer vid konkurs har negativa effekter på samhällsekonomin. Detta följs av en analys av Lösöreköpskommitténs förslag och de effekter detta skulle få för leverantörerna om det genomförs. Därefter diskuteras möjliga åtgärder som skulle kunna förbättra leverantörernas ställning, nämligen en förändring av återtagandeförbehållen, ett avskaffande av företagshypoteket, och ett införande av en allmän förmånsrätt för leverantörsfordringar. I den avslutande diskussionen konstateras att leverantörernas dåliga ställning vid konkurs får sådana konsekvenser att något måste göras för att stärka denna redan i det rättsläge som råder idag. Införs Lösöreköpskommitténs förslag blir behovet än mer trängande. Det konstateras att det bästa medlet för att stärka leverantörernas position vore att begränsa befintliga separations- och förmånsrätter, och därigenom öka viljan hos borgenärskollektivet att bidra till rekonstruktioner utom konkurs. Utöver detta efterfrågas också en översyn av återtagandeförbehållen – inte bara för att förbättra för leverantörerna, utan också för att anpassa svensk rätt till rådande internationella trender och därigenom stärka svenska företags konkurrenskraft.

<p>Liver cancer is a devastating disease that is the 5th most common cancer in men, 7th most common cancer in women, and the 3rd leading cause of cancer-related mortality. This disease arises from multiple etiological factors, including hepatitis viruses, environmental toxins, alcohol abuse, and metabolic syndrome, which induce a state of chronic inflammation. This diseased liver tissue background is a drastically different microenvironment from the healthy liver, especially with regards to immune cell prevalence and presence of mediators of immune function. It has been well-established that this altered tissue background contributes significantly to the tumorigenic process, yet its effects on the progression of the disease are more poorly understood. </p><p>To better understand the consequences of liver disease on tumor growth and the interplay with its microenvironment, we first utilized two standard methods of fibrosis induction and orthotopic implantation of tumors into the inflamed and fibrotic liver to mimic the liver condition in human HCC patients, and examined the immune infiltrate. Compared to non-diseased controls, tumor growth is significantly enhanced under fibrotic conditions. The immune cells that infiltrated the tumors are also drastically different, with decreased proportions of natural killer cells but greatly increased numbers of immune-suppressive CD11b+ Gr1hi myeloid cells in both models of fibrosis. In addition, there are model-specific differences: increased proportions of CD11b+ myeloid cells and CD4+ CD25+ T-cells are found in tumors in the bile duct ligation model but not in the carbon tetrachloride model. Importantly, the skewed immune infiltration into the tumor, while having some commonalities with the non-tumor tissue, had several distinct, tumor-specific populations. Induction of fibrosis also alters the cytokine production of implanted tumor cells, which could have far-reaching consequences on the immune infiltrate and its functionality. Taken together, this work demonstrates that the combination of fibrosis induction with orthotopic tumor implantation results in a markedly different tumor microenvironment and tumor growth kinetics. </p><p>Appreciating that the altered immune microenvironment dramatically shifts tumor progression, we sought to further explore the effects of individual inflammatory mediators on the development of the disease. Interleukin 18 (IL-18) is an inflammatory cytokine that is markedly increased in the circulation of patients with HCC correlated with poor prognosis. However, the precise role for IL-18 in HCC remains unclear, with reports presenting both pro- and anti-tumorigenic activities. To answer this question definitively, we interrogated in more detail the expression profiles of IL-18 in tissue specimens from HCC patients and conducted experimentation using multiple clinically relevant mouse models to explore the functional role of this cytokine in the context of HCC. Our results indicate that IL-18 exerts a tumor-suppressive effect mediated in large part by alterations in survival and functionality of T-lymphocytes which infiltrated the tumor microenvironment. This tumor-suppressive effect is however dependent upon the inflammatory milieu: In the absence of an inflammatory environment, whether from a chemical carcinogenesis model or a fibrosis induction model, loss of IL-18 signaling does not affect tumor growth. This effect is also stage-dependent. Taken together, our findings establish a tumor-suppressive role for IL-18 in established HCC and provide a mechanistic explanation for the complex relationship between its expression pattern and HCC prognosis. </p><p>In summary, this work demonstrates a dramatic shift in the microenvironment of developing HCC tumors in the presence of chronic inflammatory stimuli. This microenvironment, which more accurately models the situation in which tumors develop and progress in patients, alters the presence and functionality of many immune mediators. In particular, IL-18 signaling is a powerful mediator of tumor progression, however observation of its functionality is dependent on an inflammatory context. This work provides new insight into the complex processes underlying HCC tumor progression, and emphasizes the necessity for more accurate modeling of HCC progression in mice which takes into account the drastic changes in the tissue caused by chronic liver disease.</p> / Dissertation

"Was war die Nase im 18. Jahrhundert? Wie sah die "Nasologie" des Zeitalters aus, die der Hannoveraner Arzt Johann Georg Zimmermann (1728-1795) als neue Wissenschaft konzipieren wollte?

Σκοπός της παρούσας μελέτης είναι η χαρτογράφηση των καλλιεργειών του Νομού Αιτωλοακαρνανίας. Στη συνέχεια αφού γίνεται απολογισμός της χαρτογράφησης καθώς και περιγραφή των καλλιεργούμενων εκτάσεων για το έτος 2012 ακολουθεί ο ρόλος του μάρκετινγκ στα αγροτικά προϊόντα. Έπειτα γίνονται προτάσεις για τους παραγωγού που θέλουν να εισχωρήσουν με το παραγόμενο προϊόν τους σε μια αγορά. / The purpose of this study is to map crop Aitoloakarnania. Then after taking stock of the mapping and description of cultivated land in the year 2012 followed by the role of marketing in agricultural products. Following are recommendations for producers who want to penetrate with the product in a market.

The Caenorhabditis elegans Eph RTK, VAB-1, has known roles in neuronal and epidermal morphogenesis as well as oocyte maturation through interaction with its ephrin ligands. In humans, Eph receptors are involved in nervous and vascular system development and have been implicated in cancer formation and progression. DAF-18, a C. elegans ortholog of the human tumour suppressor gene, PTEN, has been identified as an interacting partner with the Eph RTK, VAB-1. Mutations in human PTEN have been associated with numerous cancers and in the worm, DAF-18 is a well studied member of the DAF-2/Insulin receptor-like signaling pathway which has roles in dauer formation, thermotolerance and adult longevity. Our lab has previously shown that VAB-1/EphR binds DAF-18. To further investigate the significance of this interaction as well as offer additional function to the proteins involved, I have shown that VAB-1/EphR is a negative regulator of DAF-18/PTEN at the protein level. Western blotting reveals that endogenous expression of DAF-18/PTEN is low in wild-type animals and expression is increased in a vab-1/ephR mutant. Additionally, VAB-1/EphR and DAF-18/PTEN are expressed in head neurons, oocytes and the germline precursor cells, Z2/Z3. vab-1/ephR mutants show increases longevity and sensitivity to dauer conditions which is consistent with increased DAF-18/PTEN activity. Lastly, daf-18(ok480) is able to suppress the oocyte maturation phenotype and increased MAPK expression displayed by vab-1(dx31) animals, providing genetic evidence of an interaction. By identifying the tissues where these proteins are co-expressed and substantiating the interaction with multiple analyses, novel roles may be proposed for each: VAB-1/EphR in DAF-2/Insulin signaling and DAF-18/PTEN in oocyte maturation downstream of VAB-1/EphR signaling. This work provides further understanding of how an organism coordinates complex developmental processes and reiterates the notion that cellular signaling is a complex network of interacting players. As many signaling pathways are evolutionarily conserved, my research in C. elegans may provide a mechanism on how Eph RTKs and PTEN are regulated in more complex organisms, including humans. / Thesis (Master, Biology) -- Queen's University, 2009-02-27 17:09:10.582

La prolifération, la différenciation ainsi que les fonctions des cellules du système immunitaire sont contrôlées en partie par les cytokines. Lors de l’infection par le VIH-1, les défauts observés dans les fonctions, la maintenance, ainsi que la consistance des cellules du système immunitaire sont en large partie attribués à une production altérée des cytokines et à un manque d’efficacité au niveau de leurs effets biologiques. Durant ces études, nous nous sommes intéréssés à la régulation et aux fonctions de deux cytokines qui sont l’IL-18 et l’IL-21. Nous avons observé une corrélation inversée significative entre les concentrations sériques d’IL-18 et le nombre des cellules NK chez les patients infectés par le VIH-1. Nos expériences in vitro ont démontré que cette cytokine induit l’apoptose des cellules NK primaires et que cette mort peut être inhibée par des anticorps neutralisants spécifiques pour FasL et TNF-α. Cette mort cellulaire est due à l’expression de FasL sur les cellules NK et à la production de TNF-α par ces cellules. L’IL-18 augmente aussi la susceptibilité à la mort des cellules NK par un stimulus pro-apoptotique, en diminuant l’expression de la protéine anti-apoptotique Bcl-XL. Nous démontrons aussi que, contrairement à l’IL-18, les niveaux d’IL-18BP sont plus faibles dans les sérum de patients infectés. Ceci résulte sur une production non coordonnée de ces deux facteurs, aboutissant à des niveaux élevés d’IL-18 libre et biologiquement active chez les patients infectés. L’infection de macrophages in vitro induit la production d’IL-18 et réduit celle d’IL-18BP. De plus, l’IL-10 et le TGF-β, dont les concentrations sont élevées chez les patients infectés, réduisent la production d’IL-18BP par les macrophages in vitro. Finalement, nous démontrons que l’IL-18 augmente la réplication du VIH-1 dans les lymphocytes T CD4+ infectés. Les niveaux élevés d’IL-18 libres et biologiquement actives chez les patients infectés contribuent donc à l’immuno-pathogénèse induite par le VIH-1 en perturbant l’homéostasie des cellules NK ainsi qu’en augmentant la réplication du virus chez les patients. Ces études suggèrent donc la neutralisation des effets néfastes de l’IL-18 en utilisant son inhibiteur naturel soit de l’IL-18BP exogène. Ceci permettrait de moduler l’activité de l’IL-18 in vivo à des niveaux souhaitables. L’IL-21 joue un rôle clef dans le contrôle des infections virales chroniques. Lors de ces études, nous avons déterminé la dynamique de la production d’IL-21 lors de l’infection par le VIH-1 et sa conséquence sur la survie des cellules T CD4+ et la fréquence des cellules T CD8+ spécifiques au VIH-1. Nous avons démontré que sa production est compromise tôt au cours de l’infection et que les concentrations d’IL-21 corrèlent avec le compte de cellules T CD4+ chez les personnes infectées. Nos études ont démontré que le traitement antirétroviral restaure partiellement la production d’IL-21. De plus, l’infection par le VIH-1 de cellules T CD4+ humaines inhibe sa production en réduisant l’expression du facteur de transcription c-Maf. Nous avons aussi démontré que la fréquence des cellules T CD4+ spécifiques au VIH-1 qui produisent de l’IL-21 est réduite chez les patients virémiques. Selon nos résultats, l’IL-21 empêche l’apoptose spontanée des cellules T CD4+ de patients infectés et l’absence d’IL-21 réduit la fréquence des cellules T CD8+ spécifiques au VIH-1 chez ces patients. Nos résultats démontrent que l'IL-21R est exprimé de façon égale sur tous les sous-types de cellules NK chez les donneurs sains et chez les patients infectés. L’IL-21 active les protéines STAT-3, MAPK et Akt afin d'augmenter les fonctions effectrices des cellules NK. L'activation de STAT-3 joue un rôle clef dans ces fonctions avec ou sans un traitement avec de l'IL-21. L'IL-21 augmente l'expression des protéines anti-apoptotiques Bcl-2 et Bcl-XL, augmente la viabilité des cellules NK, mais ne possède aucun effet sur leur prolifération. Nous démontrons de plus que l'IL-21 augmente l'ADCC, les fonctions sécrétrices et cytotoxiques ainsi que la viabilité des cellules NK provenant de patients chroniquement infectés par le VIH-1. De plus, cette cytokine semble présenter ces effets sans augmenter en contrepartie la réplication du VIH-1. Elle permet donc d'inhiber la réplication virale lors de co-cultures autologues de cellules NK avec des cellules T CD4+ infectées d'une manière dépendante à l'expression de perforine et à l'utilisation de la protéine LFA-1. Les niveaux d’IL-21 pourraient donc servir de marqueurs biologiques pour accompagner les informations sur le taux de cellules T CD4+ circulantes en nous donnant des informations sur l’état de fonctionnalité de ce compartiment cellulaire. De plus, ces résultats suggèrent l’utilisation de cette cytokine en tant qu’agent immunothérapeutique pour restaurer les niveaux normaux d’IL-21 et augmenter la réponse antivirale chez les patients infectés par le VIH-1. / The proliferation, differentiation, function and maintenance of immune cells is controlled in large part by cytokines. HIV-induced dysfunctions of the antiviral immunity is in part related to defects in the cytokine network, as manifested by altered cytokine secretion and responsiveness to these cytokines. In these studies, we investigated the regulation and the functions of two cytokines, IL-18 and IL-21, during HIV-1 infection. In our studies, we observed an inverse correlation between IL-18 concentrations and absolute numbers of various subsets of NK cells in infected persons. IL-18 caused increased death of a human NK cell line, as well as of primary human NK cells in vitro. The IL-18-mediated cell death was dependent upon Fas-FasL interactions and TNF- secretion. IL-18 induced the expression of TNF-, induced the expression of FasL on NK cells, increased the transcription from the human FasL promoter, reduced the expression of Bcl-XL in NK cells, and increased their sensitivity to FasL-mediated cell death. In contrast to IL-18 levels, IL-18BP levels decreased in the serum of HIV-infected patients. This decrease resulted in enhanced levels of free IL-18 in the serum of such patients. The infection increased production of IL-18 but decreased that of IL-18BP in monocyte-derived macrophages (MDM). Furthermore, IL-10 and TGF-β, two cytokines for which concentrations are increased in HIV-infected persons, also decreased production of IL-18BP by human MDM. Finally, recombinant human IL-18 enhanced HIV-1 replication in human CD4+ T cells. The uncoordinated production of these two cytokines represents an imbalance between these two soluble factors in HIV-infected patients. Our study shows that enhanced IL-18 bioactivity in HIV-infected patients may contribute to the pathogenesis of AIDS by disrupting NK cell homoeostasis and increasing viral replication. This uncoordinated production of IL-18 and IL-18BP contribute to IL-18-induced immunopathology and pathogenesis in HIV-infected AIDS patients. Therefore, these studies suggest that the neutralization of IL-18 may represent an appropriate and useful immunotherapeutic strategy in these patients. It may delay AIDS progression and improve the immune status of infected persons. The best way to achieve this goal may be using exogenous interleukin-18 binding protein. IL-21 is a relatively newly discovered immune enhancing cytokine, which plays an essential role in controlling chronic viral infections. Therefore, we sought to determine the dynamics of the cytokine production and its potential consequences on the viability of CD4+ T cells in HIV-infected persons. We show here that the cytokine production is compromised early in the course of the infection. The serum cytokine concentrations correlated with CD4+ T cell counts in the infected persons. Among different groups of HIV-infected persons, only Elite Controllers maintain normal production of the cytokine. The HAART partially restores production of this cytokine. Interestingly, HIV-1 infection of human PBMC as well as of purified CD4+ T cells inhibits the production of the cytokine by decreasing the expression of c-Maf, a transcription factor involved in the activation of the cytokine gene, in the virus-infected cells but not in uninfected bystander cells. We also show that the frequencies of IL-21 producing HIV-specific antigen experienced CD4+ T cells are decreased in HIV-infected viremic patients. Furthermore, we show that recombinant human IL-21 acts as pro-survival factor and prevents enhanced spontaneous apoptosis of ex vivo cultured CD4+ T cells from HIV-infected patients and that increased serum levels of the cytokine are associated with higher frequencies as well as with better functions of HIV-specific CTL in HIV-infected individuals. We show that the cytokine receptors are expressed equally on all NK cell subsets. We demonstrate that the cytokine activates STAT-3, MAPK and Akt to enhance NK cell functions. IL-21 increases expression of anti-apoptotic proteins Bcl-2 and Bcl-XL, and enhances viability of NK cells, but has no effect on their proliferation. We further show that the cytokine enhances HIV-specific ADCC, secretory and cytotoxic functions as well as viability of NK cells from HIV-infected persons. Furthermore, it exerts its biological effects on NK cells with minimal enhancement of HIV-1 replication, and the cytokine-activated NK cells inhibit viral replication in co-cultured HIV-infected autologous CD4+ T cells in a perforin- and LFA-1-dependent manner. These studies suggest that serum IL-21 concentrations may serve as useful biomarker to accompany CD4+ T cell counts for monitoring HIV-1 disease progression and the fitness of the antiviral immunity. Furthermore, the cytokine may be considered for immunotherapy in HIV-infected patients in order to restore the physiological levels of the cytokine and promote their antiviral immunity.

Introduction We measured the excitation functions of natZn (p,x) reactions up to 17.6 MeV using the stacked-foils activation technique. High-purity natural zinc (and copper) foils were irradiated with proton beams from an 18MeV medical cyclotron, the predominant purpose of which is to provide a routine regional service for clinical PET radiopharmaceuticals. Thick-target integral yields were also deduced from the measured excitation functions of the produced radioisotopes. These results were compared with the literature and were found to be in good agreement with most but not all published reports. Material and Methods The excitation functions of the natZn(p,x) reactions were measured by the well-known stacked foil technique (1). High purity zinc foils (99.99%; Goodfellow Metals Ltd., UK) each thickness 0.025 ± 0.003 mm with isotopic composition 64Zn (48.6 %), 66Zn (27.9 %), 67Zn (4.1 %), 68Zn (18.8 %) and 70Zn (0.6 %) were loaded into a solid targetry system on a 300-mm external beam line utilising helium-gas and chilled water to cool the target body (2). A typical foils stack consisted of repeated units of four Zn foils interleaved with a high purity copper foil (0.025 ± 0.004 mm); the latter for monitoring beam flux using the well documented 63,65Cu(p,n)63,65Zn reactions. Foil stacks were irradiated with a primary beam of energy 17.6 MeV, accounting for beam degradation by an obligatory 0.0250 ± 0.0005 mm-thick Havar® foil beam-line vacuum window. Irradiation was for 3 min at a beam current of 5 µA. Activated foils were measured using cryo high-purity Ge γ-spectroscopy to quantify the product radionuclides 61Cu, 66Ga, 67Ga and 65Zn. Radioactivity of each isotope was corrected to end of bombardment (EOB). Results and Conclusion New cross-sectional data for natZn(p,x) reactions up to 17.6 MeV yielding 61Cu, 66Ga, 67Ga and 65Zn isotopes were measured in independent replicated (N = 3) experiments. Results were generally in good agreement with published data. These isotopes can potentially be used in clinical or preclinical studies, following appropriate chemical separations of the zinc, gallium and copper (3). The FIG. 1 shows thick-target integral yields calculated from excitation functions measured in this study. It can be calculated (for example) that useful activities of 61Cu can be produced using a 100 µm thick natZn target in a beam provided by a standard medium-energy medical cyclotron. For example, an irradiation at 40 µA for 2 hr at 17.6 MeV would produce approximately 1.7 GBq of 61Cu at EOB. Such currents are readily achievable using solid targetry in our laboratory (2).

Im Februar 1777 lobte die Ökonomische Gesellschaft zu Bern einen Preis von 100 Louis d’Or aus für den besten Vorschlag eines umfassenden Kriminalgesetzes. Das Preisgeld kam aus dem Kreis der französischen Aufklärer. Eine Hälfte stammte vermutlich von dem Pariser Parlamentsadvokaten Elie de Beaumont, der sich in den Justizaffären um Jean Calas und Pierre Paul Sirven einen Namen gemacht hatte. Die andere Hälfte hatte Voltaire beigesteuert, der das Geld von Friedrich II. von Preussen erhalten hatte. Das Preisausschreiben war ein großer Erfolg. Neben zahlreichen unbekannten Juristen beteiligten sich eine Reihe bekannter Persönlichkeiten, von denen hier nur die späteren Revolutionäre Marat, Brissot de Warville sowie die deutschen Strafrechtsprofessoren Quistorp und Gmelin genannt seien. Die historische Bedeutung des Berner Preisausschreibens liegt darin, dass es die bis dato vorwiegend programmatische Debatte um die Strafrechtsreform in eine praktische Phase überleitete. Es trat eine Welle praktischer Reformschriften los, in denen die Forderungen von Thomasius, Montesquieu und Beccaria umgesetzt wurden. Entscheidend dafür war, dass es mittels des Preisausschreibens gelang, eine große Zahl juristischer Experten zu aktivieren, die neben dem Reformwillen auch über das Fachwissen verfügten, das für die Entwicklung eines neuen Strafrechts erforderlich war. Von den 46 eingesendeten Preisschriften sind neun im Druck überliefert. Sechsundzwanzig befinden sich in Manuskriptform im Archiv der Ökonomischen Gesellschaft zu Bern. Der vorliegende Band versammelt die Transkriptionen von sieben manuskriptförmig überlieferten Preisschriften. Vier sind in französischer und drei in deutscher Sprache verfasst. Eine Preisschrift stammt von dem Genfer Jakobiner Julien Dentand, eine andere von dem deutschen Publizisten Johann Wolfgang Brenk. Die Autoren der übrigen fünf Manuskripte sind unbekannt. Die transkribierten Preisschriften sind Teil der quellenmäßigen Basis einer Untersuchung des strafrechtlichen Denkens im späten 18. Jahrhundert. Diese erscheint demnächst in den Studien zur Europäischen Rechtsgeschichte (Christoph Luther: Aufgeklärt strafen. Menschengerechtigkeit im 18. Jahrhundert). / In february 1777 the Economic Society of Bern hosted a promotional contest. 100 Louis d’Or were offered for the best draft of a penal law codification. The prize money was donated by two proponents of the French Enlightenment. One half presumably came from the Parisian advocat Elie de Beaumont, who had made himself a name in the legal scandals involving Jean Calas and Pierre Paul Sirven. The other half of the prize money originated from Voltaire, to whom it had been given by Frederick II. of Prussia. The contest was a great success. Amongst a big number of unknown jurists several of well-known individuals took part, of which the future revolutionaries Marat and Brissot de Warville as well as the German law-professors Quistorp and Gmelin shall be mentioned here. The historical significance of the prize contest resides in the fact that it inaugurated the practical stage of the formerly programmatic debate on the reform of the penal law. It unleashed a wave of proposals for the implementation of the changes Thomasius, Montesquieu and Beccaria had sought. A condition for the practical turn of the debate was the mobilization of experts who among the good will disposed of the technical knowledge necessary to create a new penal law. In establishing this condition the Bern promotional contest played a decisive role. 46 reform proposals were handed in. Nine were published, 26 remain as manuscripts in the archive of the Economic Society of Bern. The present book gathers the transcriptions of four French and three German manuscripts. One was written by the further Genevan Jacobin Julien Dentand, another by the German publicist Johann Wolfgang Brenk. The other five authors remain anonymous. The transcribed manuscripts are part of the sources of a study on the thinking of penal law in the late 18th century, that will appear soon in the series Studien zur Europäischen Rechtsgeschichte (Christoph Luther: Aufgeklärt strafen. Menschengerechtigkeit im 18. Jahrhundert).

NBG–18 graphite is developed by SGL Carbon for the Pebble Bed Modular Reactor Company (PBMR), and is used as the preferred material for the internal graphite core structures of a high–temperature gas–cooled nuclear reactor (HTR). The NBG–18 graphite is manufactured using pitch coke, and is vibrationally molded. To assess the structural behaviour of graphite many destructive techniques have been performed in the past. Though the destructive techniques are easy and in some cases relative inexpensive to perform, these methods lead to waste material and require cumbersome time consuming sample preparations. To overcome this problem numerous non–destructive testing techniques are available such as sonic resonance, resonant inspection, ultrasonic testing, low and multifrequency Eddy current analysis, acoustic emission and impulse excitation techniques. The Hammer Impulse Excitation technique was used as a method in predicting the fatigue life of NBG–18 graphite by focussing on the application of modal frequency analysis of determined natural frequencies. Moreover, the typical fatigue characteristics of NBG–18 graphite were determined across a comprehensive set of load ranges. In order to be able to correlate modal frequency parameters with fatigue life, suitable uniaxial fatigue test specimen geometry needed to be obtained. The uniaxial fatigue test specimens were manufactured from two NBG–18 graphite sample blocks. The relationship between natural frequencies of uniaxial test specimens, fatigue life, sample positioning and sample orientation was investigated for different principle stress ratios. Load ratios R = –oo and R = +2 tested proved to show the highest r–values for the Pearson correlation coefficients investigated. However, there was no significant trend found between the natural frequency and the fatigue life. / Thesis (M.Ing. (Nuclear Engineering))--North-West University, Potchefstroom Campus, 2011.