@phdthesis{Riedel2013,
  author    = {Riedel, Simone Stefanie},
  title     = {Characterization of the fluorescence protein FP635 for in vivo imaging and establishment of a murine multiple myeloma model for non-invasive imaging of disease progression and response to therapy},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77894},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {Optical in vivo imaging methods have advanced the fields of stem cell transplantation, graft-versus-host disease and graft-versus-tumor responses. Two well known optical methods, based on the transmission of light through the test animal are bioluminescence imaging (BLI) and fluorescence imaging (FLI). Both methods allow whole body in vivo imaging of the same animal over an extended time span where the cell distribution and proliferation can be visualized. BLI has the advantages of producing almost no unspecific background signals and no necessity for external excitation light. Hence, BLI is a highly sensitive and reliable detection method. Yet, the BLI reporter luciferase is not applicable with common microscopy techniques, therefore abolishing this method for cellular resolution imaging. FLI in turn, presents the appealing possibility to use one fluorescent reporter for whole body imaging as well as cellular resolution applying microscopy techniques. The absorption of light occurs mainly due to melanin and hemoglobin in wavelengths up to 650 nm. Therefore, the wavelength range beyond 650 nm may allow sensitive optical imaging even in deep tissues. For this reason, significant efforts are undertaken to isolate or develop genetically enhanced fluorescent proteins (FP) in this spectral range. "Katushka" also called FP635 has an emission close to this favorable spectrum and is reported as one of the brightest far-red FPs. Our experiments also clearly showed the superiority of BLI for whole body imaging over FLI. Based on these results we applied the superior BLI technique for the establishment of a pre-clinical multiple myeloma (MM) mouse model. MM is a B-cell disease, where malignant plasma cells clonally expand in the bone marrow (BM) of older people, causing significant morbidity and mortality. Chromosomal abnormalities, considered a hallmark of MM, are present in nearly all patients and may accumulate or change during disease progression. The diagnosis of MM is based on clinical symptoms, including the CRAB criteria: increased serum calcium levels, renal insufficiency, anemia, and bone lesions (osteolytic lesions or osteoporosis with compression fractures). Other clinical symptoms include hyperviscosity, amyloidosis, and recurrent bacterial infections. Additionally, patients commonly exhibit more than 30\% clonal BM plasma cells and the presence of monoclonal protein is detected in serum and/or urine. With current standard therapies, MM remains incurable and patients diagnosed with MM between 2001 and 2007 had a 5-year relative survival rate of only 41\%. Therefore, the development of new drugs or immune cell-based therapies is desirable and necessary. To this end we developed the MOPC-315 cell line based syngeneic MM mouse model. MOPC-315 cells were labeled with luciferase for in vivo detection by BLI. We validated the non-invasively obtained BLI data with histopathology, measurement of idiotype IgA serum levels and flow cytometry. All methods affirmed the reliability of the in vivo BLI data for this model. We found that this orthotopic MM model reflects several key features of the human disease. MOPC-315 cells homed efficiently to the BM compartment including subsequent proliferation. Additionally, cells disseminated to distant skeletal parts, leading to the typical multifocal MM growth. Osteolytic lesions and bone remodeling was also detected. We found evidence that the cell line had retained plasticity seen by dynamic receptor expression regulation in different compartments such as the BM and the spleen.},
  subject      = {Fluoreszenzproteine},
  language  = {en}
}
@article{RiedelMofoloAvotaetal.2013,
  author    = {Riedel, Alice and Mofolo, Boitumelo and Avota, Elita and Schneider-Schaulies, Sibylle and Meintjes, Ayton and Mulder, Nicola and Kneitz, Susanne},
  title     = {Accumulation of Splice Variants and Transcripts in Response to PI3K Inhibition in T Cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77917},
  year      = {2013},
  abstract  = {Background: Measles virus (MV) causes T cell suppression by interference with phosphatidylinositol-3-kinase (PI3K) activation. We previously found that this interference affected the activity of splice regulatory proteins and a T cell inhibitory protein isoform was produced from an alternatively spliced pre-mRNA. Hypothesis: Differentially regulated and alternatively splice variant transcripts accumulating in response to PI3K abrogation in T cells potentially encode proteins involved in T cell silencing. Methods: To test this hypothesis at the cellular level, we performed a Human Exon 1.0 ST Array on RNAs isolated from T cells stimulated only or stimulated after PI3K inhibition. We developed a simple algorithm based on a splicing index to detect genes that undergo alternative splicing (AS) or are differentially regulated (RG) upon T cell suppression. Results: Applying our algorithm to the data, 9\% of the genes were assigned as AS, while only 3\% were attributed to RG. Though there are overlaps, AS and RG genes differed with regard to functional regulation, and were found to be enriched in different functional groups. AS genes targeted extracellular matrix (ECM)-receptor interaction and focal adhesion pathways, while RG genes were mainly enriched in cytokine-receptor interaction and Jak-STAT. When combined, AS/RG dependent alterations targeted pathways essential for T cell receptor signaling, cytoskeletal dynamics and cell cycle entry. Conclusions: PI3K abrogation interferes with key T cell activation processes through both differential expression and alternative splicing, which together actively contribute to T cell suppression.},
  subject      = {Biologie},
  language  = {en}
}
@phdthesis{JosephNedumparambil2013,
  author    = {Joseph Nedumparambil, George},
  title     = {A Search of the Roots of Syro-Malabar Church in Kerala},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77747},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {A Search of the Roots of Syro-Malabar Church in Kerala},
  subject      = {Syro-Malabarische Kirche},
  language  = {en}
}
@phdthesis{Meyer2013,
  author    = {Meyer, Sebastian},
  title     = {Model System for Correlation Phenomena in Reduced Dimensions - Gold-induced Atomic Chains on Germanium},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77723},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {Atomic chains, often called nanowires, form in a self-organized process after the adsorption of metal atoms. These wires are spatially well confined representing a close approach of a true one-dimensional structure. The low-dimensional architecture thereby often leads to anisotropic electronic states with vanishing interchain interaction. In the presence of weak coupling to the substrate a one-dimensional metal can experience a phase transition according to Peierls into an insulating ground state upon temperature, which is accompanied by a periodic lattice distortion. Without any coupling a strict onedimensional regime is reached, where the common Fermi liquid description breaks down with the quasi-particles being replaced by collective excitations of spin and charge. This state is referred to as a Tomonaga-Luttinger liquid (TLL), which has been observed so far only in anisotropic bulk materials. An experimental fingerprint for both phenomena can be obtained from the electronic states close to the chemical potential, i.e. the Fermi energy. Using a semiconducting substrate provides the best observation conditions since any bulk projection onto the interesting bands is avoided. In case of Au/Ge(001) the growth of gold-induced chains is guided by the dimerized bare Ge (2×1) reconstruction yielding two different domains of wires rotated by 90° going from one terrace to the next by a single height step. The superior wetting capabilities of gold on germanium enables a complete coverage of the Ge(001) surface with longrange ordered wires. Their length scale and defect density is limited by the underlying substrate, for which a cleaning procedure is introduced based on wet-chemical etching followed by thermal dry oxidation. The band structure of Au/Ge(001) is investigated by angle-resolved photoelectron spectroscopy as a function of temperature. Two states are observed: a two-dimensional metallic state with hole-like dispersion and a one-dimensional electron pocket, whose band-integrated spectral function does not show the typical Fermi distribution at the chemical potential. Instead, a decrease of spectral weight applies following a power-law. This behavior can be well explained within the Tomonaga-Luttinger liquid theory which replaces the Fermi-Landau formalism in strictly one-dimensional systems. To enable theoretical modeling, a structural analysis was performed on the basis of surface x-ray diffraction (SXRD). From the in-plane scattering data a Patterson-map could be extracted leading to in-plane distances between gold atoms in the unit cell. This provides the first step towards a complete structural model and therefore towards a band structure calculation. First successful attempts have been made to manipulate the system by controlled adsorption of potassium. Here, an n-type doping effect is observed for submonolayer coverage whereas slightly increased coverages in combination with thermal energy lead to a new surface reconstruction.},
  subject      = {Nanodraht},
  language  = {en}
}
@phdthesis{KannenCardoso2013,
  author    = {Kannen Cardoso, Vinicius},
  title     = {The role of Fluoxetine against preneoplastic lesions and tumors in colon tissue},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77589},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {Introduction: Colon cancer is one of the major human malignancies worldwide, and much effort has been applied to understand the process of colon carcinogenesis, as well as the role of potential treatments and co-therapeutical agents against it. A growing body of evidence suggests that the use of fluoxetine (FLX), an antidepressant belonging to the selective serotonin reuptake inhibitors (SSRIs), may be associated with a reduced colon cancer risk. However, controversial opinions have been published and an identification of the mechanisms of the activity of FLX on colon cells would help in the clarification of this controversy. Objectives: Using several in vitro and in vivo-based methods and analyses, we aimed to verify whether FLX has antioxidant, pro-oxidant or DNA-damaging potential in standard toxicological assays; to check whether and how FLX could prevent and reduce colon preneoplastic lesions; to ascertain whether FLX has any oncostatic potential against colon tumors; and, to investigate whether FLX activity could be comparable with a known and current applied chemotherapeutic agent against colon cancer. Results: FLX did not have any antioxidant potential in our experiments. Although it did not induce reactive oxygen species (ROS) generation or DNA-damage in fibroblast and colon tumor cell lines, FLX reduced dysplasia and proliferation in two different carcinogen models. Further, a significant decrease in colon stromal reactivity and angiogenesis was found in both carcinogen-induced preneoplasia models. In a xenograft model of colon cancer, FLX shrank tumors, reduced tumor proliferation, arrested cancer cells at the G0/G1 cell-cycle phase, and took ROS generation under control. Such effects were detected together with an intracellular acidification and loss of mitochondrial membrane potential in FLX-treated cells. Modulating mitochondrial respiratory chain, HIF-1 expression and Akt/mTOR signaling pathway, FLX was found to reduce colon tumors similar to the widely used chemotherapeutic agent 5-Fluoracil activity. Conclusion: Our collective data suggest that FLX is a remarkable chemopreventive and oncostatic agent against colon preneoplastic lesions and tumors, acting without DNA-damage or ROS generation.},
  subject      = {Fluoxetin},
  language  = {en}
}
@phdthesis{ThangarajSelvaraj2013,
  author    = {Thangaraj Selvaraj, Bhuvaneish},
  title     = {Role of CNTF-STAT3 signaling for microtubule dynamics inaxon growth and maintenance: Implications in motoneuron diseases},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76889},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {Neurotrophic factor signaling modulates differentiation, axon growth and maintenance, synaptic plasticity and regeneration of neurons after injury. Ciliary neurotrophic factor (CNTF), a Schwann cell derived neurotrophic factor, has an exclusive role in axon maintenance, sprouting and synaptic preservation. CNTF, but not GDNF, has been shown to alleviate motoneuron degeneration in pmn mutant mice carrying a missense mutation in Tbce gene, a model for Amyotrophic Lateral Sclerosis (ALS). This current study elucidates the distinct signaling mechanism by which CNTF rescues the axonal degeneration in pmn mutant mice. ...},
  subject      = {Ciliary neurotrophic factor},
  language  = {en}
}
@phdthesis{Niederlechner2013,
  author    = {Niederlechner, Stefanie},
  title     = {Assessment of the basic molecular mechanisms underlying L-glutamine's cytoprotective effects after intestinal injury},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77399},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {Critical illness like sepsis, shock, and intestinal bowel disease are one of the leading causes of morbidity and mortality in the US and around the world. At present, studies to define new therapeutic interventions that can protect tissues and cells against injury and attenuate inflammation are fields of intense investigation. While research over the past decade has clearly identified GLN as a vital stress substrate facilitating cellular survival following injury, the initiation steps in GLN's cytoprotective molecular mechanism still remain elusive. Previously published work suggested that stabilization of ECM proteins and activation of ECM receptor osmosignaling may play a central role in the orchestration of many cellular pathways following stress. Thus, I hypothesized that preservation of ECM protein and EGFR levels as well as ECM receptor signaling play key roles in the molecular mechanisms underlying GLN's protection against thermal injury in the intestine. I was able to confirm via Western blotting and by using silencing RNA against FN, Ntn-1, EGFR, and their negative controls, that GLN-mediated preservation of FN, Ntn-1, and EGFR levels is critical in GLN's protection against hyperthermia in IEC-6 cells. By using a selective FN-Integrin interaction inhibitor GRGDSP, its negative control peptide GRGESP, and Src-kinase inhibitor PP2, I showed that FN-Integrin signaling and Src-kinase activation are essential in GLN-mediated protection in the intestine. This applied to EGFR signaling as demonstrated using the EGFR tyrosine kinase inhibitor AG1478. In addition to GRGDSP and AG1478, ERK1/2 inhibitors PD98059 and UO126 as well as the p38MAPK inhibitor SB203580 revealed that GLN is protective by activating ERK1/2 and dephosphorylating p38MAPK via FN-Integrin and EGFR signaling. However, GLN-mediated PI3-K/Akt/Hsp70 activation seems to occur independently of FN-Integrin and EGFR signaling as indicated by Western blots as well as experiments using the PI3-K inhibitor LY294002, GRGDSP, and AG1478. The results showed that GLN activates cell survival signaling pathways via integrins as well as EGFRs after hyperthermia. Moreover, I found that GLN-mediated preservation of FN expression after HS is regulated via PI3-K signaling. Whether GLN-mediated PI3-K signaling happens simultaneously to FN-Integrin and EGFR signaling or whether PI3-K signaling coordinates FN-Integrin and EGFR signaling needs to be investigated in future studies. Further, experiments with PD98059 and GRGDSP revealed that ERK1/2 assists in mediating transactivation of HSF-1 following HS. This leads to increases in Hsp70 expression via FN-Integrin signaling, which is known to attenuate apoptosis after thermal injury. Fluorescence microscopy results indicated that HS and GLN regulate cell are size changes and the morphology of F-actin via FN-Integrin signaling. Experiments using GRGDSP and GRGESP showed that GLN enhances cellular survival via FN-Integrin signaling in a manner that does not require increased intracellular GLN concentrations (as quantified using LC-MS/MS). In summary, my thesis work gives new and potentially clinically relevant mechanistic insights into GLN-mediated molecular cell survival pathways. These results warrant clinical translation to assess if clinical outcome of critically ill patients suffering from gastrointestinal diseases can be improved by GLN treatment and/or by targeting the molecular pathways found in my studies.},
  subject      = {Glutamin},
  language  = {en}
}
@article{Hoegger2013,
  author    = {H{\"o}gger, Petra},
  title     = {Nutrition-derived bioactive metabolites produced by gut microbiota and their potential impact on human health},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-77349},
  year      = {2013},
  abstract  = {The functional role of human gut microbiota has attracted substantial interest and recent research has uncovered various aspects of the interplay between the complex communities of microorganisms colonizing the intestine and their hosts' health. The present review focuses on nutrition-derived bioactive metabolites produced by gut microbiota with potential beneficial effects upon human health. Thereby, the emphasis is on newly generated bacterial metabolites that are not concomitantly present at higher amounts in dietary sources and that have been previously detected in human blood samples. Since a multitude of different substances is generated by gut microbes primarily those metabolites which exert a more pronounced activity than their immediate precursor compound are discussed here. Specifically, the in vitro and in vivo nutridynamics as well as the nutrikinetics of equol, enterolactone / enterodiol, urolithins, 8-prenylnaringenin, 3,4-dihydroxyphenylacetic acid and 5-(3',4'-dihydroxyphenyl)-g-valerolactone, the short-chain fatty acids butyrate, propionate and acetate, and indole-3-propionic acid are reviewed. Though the metabolites' mechanism of action and the influence of health conditions on metabolite production are not always fully understood yet, there are many reasons to direct the attention to "gut health". It could offer new options for preventing or treating a variety of disease states and nutrition-derived microbial products might inspire future drug development.},
  subject      = {Kohlenhydrate},
  language  = {en}
}
@phdthesis{Reuss2013,
  author    = {Reuß, Heiko},
  title     = {The interplay of unconscious processing and cognitive control},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76950},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {The aim of this study was both to investigate the influence of cognitive control on unconscious processing, and to investigate the influence of unconscious processing on cognitive control. At first, different mechanisms and accounts to explain unconscious priming are presented. Here, perceptual and motor processes, as well as stimulus-response learning, semantic categorization, and the action trigger account as theories to explain motor priming are discussed. Then, the issue of the potential limits of unconscious processing is presented. Findings that indicate that active current intentions and expertise modulate unconscious processing are illustrated. Subsequently, results that imply an influence of unconsciously presented stimuli that goes beyond motor processes are discussed, with a special focus on inhibition processes, orienting of attention, task set activation, and conflict adaptation. Then I present the results of my own empirical work. Experiment 1 shows that the effective processing of unconsciously presented stimuli depends on expertise, even when potentially confounding difference between the expert and novice groups are controlled. The results of Experiments 2 and 3 indicate that the intention to use particular stimuli is a crucial factor for the effectiveness of these stimuli when they are presented unconsciously. Additionally, these findings show that shifts of attention can be triggered by centrally presented masked arrow cues. Experiments 4 and 5 broaden these results to cue stimuli that are not inherently associated with a spatial meaning. The finding corroborate that typically endogenously controlled shifts of attention can also be induced by unconscious stimuli. Experiments 6 and 7 demonstrate that even a central cognitive control process like task set activation is not contingent on conscious awareness, but can in contrast be triggered through unconscious stimulation. Finally, these results are integrated and I discuss how the concept of cognitive control and the limits of unconscious processing may have to be reconsidered. Furthermore, potential future research possibilities in this field are presented.},
  subject      = {Bewusstsein},
  language  = {en}
}
@phdthesis{Shiban2013,
  author    = {Shiban, Youssef},
  title     = {Attenuating Renewal following Exposure Therapy : Mechanisms of Exposure in Multiple Contexts and its Influence on the Renewal of Fear: Studies in Virtual Reality},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76673},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {„Renewal" bezeichnet das Wiederauftreten von Angst nach erfolgreicher Expositionstherapie in Folge einer erneuten Konfrontation mit dem phobischen Stimulus in einem neuen, sich vom Expositionskontext unterscheidenden Kontext. Bouton (1994) zufolge deutet diese Angstr{\"u}ckkehr durch einen Kontextwechsel darauf hin, dass die Angst nicht gel{\"o}scht wurde. Stattdessen wurde w{\"a}hrend der Expositionssitzung eine neue Assoziation gelernt, die das gef{\"u}rchtete Objekt mit „keiner Angst", also den konditionierten Reiz (conditioned stimulus, CS) mit „keinem unkonditionierten Reiz" (no unconditioned stimulus, no US), verbindet. Bouton argumentiert weiter, dass diese Assoziation kontextabh{\"a}ngig ist, wodurch Effekte wie Angst-Renewal erkl{\"a}rt werden k{\"o}nnen. Da in einem neuen Kontext die CS-no US-Assoziation nicht aktiviert wird, wird die Angst auch nicht gehemmt. Die Kontextabh{\"a}ngigkeit der CS-no US-Assoziation wurde in mehreren Studien belegt (Balooch \& Neumann, 2011; Siavash Bandarian Balooch, Neumann, \& Boschen, 2012; Culver, Stoyanova, \& Craske, 2011; Kim \& Richardson, 2009; Neumann \& Kitlertsirivatana, 2010). Aktuell konzentriert sich die Forschung zur Therapie von Angstst{\"o}rungen auf die Frage, wie Angst reduziert und gleichzeitig ein R{\"u}ckfall verhindert werden kann. Hierzu werden verschiedene Expositionsprotokolle untersucht, wie zum Beispiel (1) Exposition in mehreren Kontexten (multiple contexts exposure, MCE), um Renewal zu reduzieren (z.B. Balooch \& Neumann, 2011); (2) verl{\"a}ngerte Exposition (prolonged exposure, PE), um die hemmende Assoziation w{\"a}hrend des Extinktionslernes zu st{\"a}rken (z.B. Thomas, Vurbic, \& Novak, 2009) und (3) Rekonsolidierungs-Updates (reconsolidation update, RU), die den Rekonsolidierungsprozess durch eine kurze Exposition des CS+ vor der eigentlichen Exposition aktualisieren sollen (Schiller et al., 2010). Bisher liegen jedoch nur sehr wenige Studien vor, die diese neuen Expositionsprotokolle an klinischen Stichproben untersucht haben, und - soweit bekannt - keine Studie, welche die Wirkmechanismen dieser Protokolle an einer klinischen Stichprobe erforscht. Die vorliegende Dissertation hat drei Ziele. Das erste Ziel besteht darin zu pr{\"u}fen, ob Expositionstherapie in multiplen Kontexten die Wahrscheinlichkeit von Renewal reduziert. Das zweite Ziel ist die Untersuchung der Mechanismen, die dem Effekt der Exposition in multiplen Kontexten zugrunde liegen und das dritte ist den Kontext im Zusammenhang mit Konditionierung und Extinktion zu konzeptualisieren. Insgesamt wurden drei Studien durchgef{\"u}hrt. Die erste Studie untersuchte den Effekt von Exposition in multiplen Kontexten auf Renewal, die zweite und dritte Studie die Wirkmechanismen von MCE. In der ersten Studie wurden spinnenphobische Probanden (N = 30) viermal mit einer virtuellen Spinne konfrontiert. Die Expositionstrials wurden entweder in einem gleichbleibenden Kontext oder in vier verschiedenen Kontexten durchgef{\"u}hrt. Am Ende der Sitzung absolvierten alle Teilnehmer einen virtuellen Renewaltest, bei dem die virtuelle Spinne in einem neuen Kontext gezeigt wurde, und einen in vivo Verhaltensvermeidungstest (behavioral avoidance test, BAT) mit einer echten Spinne. Die Ergebnisse zeigten, dass Probanden, welche die vier Expositionstrials in unterschiedlichen Kontexten erfuhren, weniger Angst, sowohl im virtuellen Renewaltest als auch im BAT, erlebten. In dieser Studie konnte die Wirksamkeit von MCE f{\"u}r die Reduktion von Renewal erfolgreich nachgewiesen werden. Studie 2 (N = 35) untersuchte die Wirkmechanismen von MCE in einem differentiellen Konditionierungsparadigma. Die Extinktion wurde in multiplen Kontexten durchgef{\"u}hrt. Hierbei war das Ziel, eine {\"a}hnliche Verminderung von Renewal wie in Studie 1 nachzuweisen. Der Extinktion folgten zwei Tests, mit dem Ziel m{\"o}gliche hemmende Effekte des Kontexts, die w{\"a}hrend der Extinktionsphase erworben wurden, aufzudecken. Bez{\"u}glich des Effektes von MCE wurden drei Hypothesen aufgestellt: (1) Der Extinktionskontext wird mit der Exposition assoziiert, fungiert folglich w{\"a}hrend der Extinktion als Sicherheitssignal und konkurriert daher mit dem Sicherheitslernen des CS. Dies f{\"u}hrt zu einem verminderten Extinktionseffekt auf den CS, wenn die Extinktion nur in einem Kontext durchgef{\"u}hrt wird. (2) Die Elemente im Extinktionskontext (z.B. Raumfarbe, M{\"o}bel) stehen im Zusammenhang mit der CS-no US-Assoziation und erinnern daher an die Extinktion, was zu einer gr{\"o}ßeren Angsthemmung f{\"u}hrt, wenn sie w{\"a}hrend eines Tests gezeigt werden. (3) Nach der emotionalen Prozesstheorie (emotional process theory; Bouton, 1994; Foa et al., 1996) bestimmen die Therapieprozessfaktoren die St{\"a}rke des Renewals. Beispielsweise korrelieren initiale Angstaktivierung, Aktivierung in und zwischen den Sitzungen mit der St{\"a}rke des Renewals. Jedoch waren in dieser Studie keine Unterschiede zwischen den Gruppen im Renewaltest zu beobachten, weswegen die Ergebnisse der zwei Nachtests nicht zu interpretieren sind. Das Ziel von Studie 3 (N = 61) war es, das Konzept des Kontexts im Rahmen von Konditionierung und Exposition zu definieren. In Studie 3 wurde das Auftreten der Generalisierungsabnahme (generalization decrement) genutzt, bei der eine konditionierte Reaktion infolge eines Kontextwechsels nur reduziert auftritt. Auf diesem Weg kann Kontext{\"a}hnlichkeit quantifiziert werden. Nach einer Akquisitonsphase in einem Kontext wurden die Teilnehmer in einem von drei verschiedenen Kontexten getestet. Zwei dieser Kontexte unterschieden sich nur in einer Dimension (Anordnung der Objekte vs. Objekteigenschaften). Die dritte Gruppe wurde im Akquisitonskontext getestet und diente als Kontrollgruppe. Es fanden sich jedoch keine Unteschiede zwischen den Gruppen in den Testphasen. Eine m{\"o}gliche Erkl{\"a}rung ist die Neuartigkeit des Testkontextes. Teilnehmer, die nach der Extinktion einem neuen Kontext ausgesetzt waren, erwarteten in einem anderen Kontext eine zweite Extinktionsphase und zeigten daher mehr statt weniger Angst als erwartet.},
  subject      = {Angst},
  language  = {en}
}