Konventionelle CD8 T-Zellen im intestinalen Epithel unterscheiden sich von T-Zellen gleicher Spezifität in anderen Organen. In dieser Arbeit sollten Mechanismen identifiziert werden, welche die Migration dieser T-Zellen in intestinale Gewebe bestimmen und/oder welche die funktionelle Adaption der T-Zellen an die mukosale Umgebung beeinflussen. Hierfür wurden Mäuse mit einem rekombinanten Listeria monocytogenes Stamm (LmOVA) infiziert, OVA-spezifische CD8 T-Zellen aus der Milz und dem intestinalem Epithel isoliert, und die mRNA-Expressionsprofile dieser Zellen mittels einer Mikroarray-Analyse verglichen. Eine Gruppe von NK-Rezeptoren zeigte auf OVA-spezifischen CD8 T-Zellen aus der intestinalen Mukosa eine geringere Expression. Dieser Unterschied war nach einer oralen Infektion wesentlich stärker ausgeprägt, als nach einer intravenösen Infektion. Die Präsenz der natürlichen Darmflora hatte nur einen sehr geringen Einfluss auf diese organspezifisch unterschiedliche NK-Rezeptor-Expression. Untersuchungen in transgenen CD4dnTGFbetaRII Mäusen wiesen auf TGFbeta als ein entscheidendes Element für die niedrigere NK-Rezeptor-Expression auf T-Zellen in der Darmmukosa hin. Die zweite Fragestellung war die, ob nach einer Lm-Infektion die primäre Aktivierung naiver CD8 T-Zellen und die Re-Aktivierung von Gedächtnis-T-Zellen auch außerhalb sekundärer lymphoider Organe stattfinden kann. Hierfür wurden Mäuse mit der immunmodulatorischen Substanz FTY720 behandelt und splenektomiert. Eine FTY720-Behandlung beeinträchtigte nach iv und nach ig Infektion weder die Ausbreitung der Lm, noch die Fähigkeit der Mäuse zu einer Elimination der Bakterien. Orale Infektionen sowie höher dosierte iv Infektionen führten auch in FTY720-behandelten und zusätzlich splenektomierten Mäusen zu einer T-Zell-Akkumulation und Proliferation in nicht-lymphoiden Organen. Nach einer niedrig dosierten iv Lm-Infektion wurden dagegen in FTY720-behandelten und splenektomierten Mäusen keine OVA-spezifischen T-Zell-Antworten ausgelöst. Insbesondere die Milz schien hier für die T-Zell Aktivierung und Proliferation erforderlich zu sein. Auch für eine Sekundärantwort nach einer iv Infektion mit LmOVA waren lymphoide Gewebe für die Ausbildung einer effektiven T-Zell-Antwort essentiell. / Conventional CD8 T cells in the intestinal epithelium differ from T cells with identical antigen specificity in other organs. One aim of this study was, to identify mechanisms, which determine gut-tropism of these T cells or which influence the functional adaptation of these cells to the mucosal environment. For this purpose, mice were infected with a recombinant Listeria monocytogenes strain (LmOVA). OVA-specific CD8 T cells were isolated from spleen and intestinal epithelium and the mRNA-expression profiles of these cells were compared in a microarray-analysis. One group of NK-receptors were substantially less expressed on Lm-specific CD8 T cells from the intestinal mucosa than on corresponding cells from the spleen. This difference was much more pronounced following oral infection than following iv infection. The presence of the natural gut-flora only slightly influenced the organ-specific NK-receptor expression in CD8 T cells. Experiments with transgenic CD4dnTGFbetaRII mice point to TGFbeta as a decisive factor for the low NK-receptor expression on T cells from the gut mucosa. In the second part of this study it was investigated, whether, following Lm infection, priming of naive CD8 T cells and re-activation of memory T cells could occur outside of secondary lymphoid organs. Mice were treated with the immunomodulatory drug FTY720 and splenectomized. Treatment with FTY720 did neither diminish bacterial dissemination into spleen, liver and MLN, nor impaired the ability of the mice to control the bacteria and to eradicate them from these organs. Oral infection and high dose iv infection led to T cell accumulation and proliferation in nonlymphoid organs of FTY720-treated and additionally splenectomized mice. Following low dose iv infection with LmOVA, no OVA-specific T cell responses were induced in FTY720-treated and additionally splenectomized mice. Especially the spleen seemed to be important for T cell activation and proliferation under these conditions. Also following a secondary iv infection with LmOVA, lymphoid tissues were essential for the generation of an effective T cell response.

Eine Vielzahl strikt anaerober Organismen verwendet den reduktiven Acetyl-CoA-Weg zum autotrophen Wachstum mit Kohlenmonoxid als einziger Kohlenstoffquelle. Die Kohlenmonoxid-Dehydrogenase (CODH) ist das Schlüsselenzym dieses Stoffwechselweges und katalysiert die Oxidation von CO mit Raten von bis zu 31,000 s–1 und die Reduktion von CO2 mit bis zu 12 s–1 an einem [Ni4Fe4S-OHx]-Cluster (C-Cluster). Das Genom des thermophilen und hydrogenogenen Bakteriums Carboxydothermus hydrogenoformans enthält insgesamt fünf Gene, die für CODHs kodieren. Anhand der Genumgebung wurden dabei unterschiedliche Rollen für die einzelnen CODHs vorgeschlagen. Für ein besseres Verständnis der molekularen Prozesse in der Katalyse, wurden CODH-IICh und -VCh heterolog in Escherichia coli produziert und biochemisch und strukturell charakterisiert. / A variety of strict anaerobic organisms employ the reductive acetyl-CoA path for autotrophic growth, using carbon monoxide as sole carbon source. Carbon monoxide dehydrogenase (CODH) is the key enzyme of the path and catalyzes CO oxidation with rates of 31,000 s–1 and CO2 reduction with rates of 12 s–1 at a [Ni4Fe4S-OHx] cluster (cluster C). The genome of the thermophilic and hydrogenogenic bacterium Carboxydothermus hydrogenoformans contains five copies of genes coding for the catalytic subunit of a CODH. According to the gene environment, different physiological roles for the individual CODHs were proposed. To compare their respective structure and catalytic function, CODH-IICh and -VCh were heterologously produced in Escherichia coli and biochemically and structurally investigated.

Glukokortikoide (GK) zählen zu den effizientesten Medikamenten bei der Behandlung akuter und chronischer Entzündungskrankheiten. Ihr Einsatz ist häufig durch das Auftreten zahlreicher und teilweise irreversibler Nebenwirkungen beeinträchtigt. Aus diesem Grund wurden neue Glukokortikoid-Rezeptor-Liganden, wie die nicht-steroidalen selektiven Glukokortikoid-Rezeptor-Agonisten (SEGRAs), die eine potente anti-entzündliche Wirkung bei gleichzeitig vermindertem Nebenwirkungspotential aufweisen sollen, entwickelt. Im Rahmen der vorliegenden Arbeit wurde die SEGRA-Substanz BAY1155975 hinsichtlich ihrer hemmenden Wirkung auf die CD28-kostimulierte Aktivierung primärer humaner T-Zellpopulationen mit der von klassischen GK, wie z.B. Prednisolon, verglichen. In humanen Gedächtnis/Effektor- CD4+ T-Zellen wies die höchste Konzentration von BAY1155975 im Vergleich zu Prednisolon eine statistisch signifikant größere Hemmung der CD28-kostimulierten Sekretion von Effektorzytokinen (IFN-gamma, TNF-alpha, IL17 und IL22) auf. Proliferation, Apoptose und die Expression verschiedener Aktivierungsmarker wurden dagegen durch BAY1155975 und Prednisolon gleichermaßen reguliert. Es wird eine stärkere Hemmung des Kalzium-Kalzineurin-NFAT Signalweges durch BAY1155975 in diesen Zellen vermutet. In vivo zeigten BAY1155975 und Prednisolon eine ähnlich starke Hemmung der T-Zell-vermittelten Hautentzündung im DNFB-induzierten Kontaktallergiemodell in Mäusen, wenn die Behandlung der Mäuse mit den Substanzen vor dem Challenge erfolgte. Bei einer Substanzbehandlung der Mäuse während der Sensibilisierung wurde die Hautentzündung dagegen deutlich stärker durch BAY1155975 als durch Prednisolon gehemmt. Zusammenfassend geben die Ergebnisse dieser Arbeit einen Hinweis auf eine stärkere Hemmung der T-Zellsensibilisierung und der Effektorzytokinsekretion durch die SEGRA Substanz BAY1155975 im Vergleich zum klassischen GK Prednisolon. / Glucocorticoids (GCs) are the most effective therapeutic agents for the treatment of acute and chronic inflammatory diseases. Their use is often accompanied with numerous and sometimes irreversible side-effects. Therefore, new glucocorticoid receptor (GR) ligands with should have potent anti inflammatory efficacy but a reduced side-effect profile have been developed. Non steroidal selective glucocorticoid receptor agonists (SEGRAs) represent a new class of GR ligands with an improved therapeutic index. In this study, we compared the SEGRA, BAY1155975, and the classical GC, prednisolone, regarding their suppressive effect on CD28-costimulated activation of human primary T cell subpopulations. In human memory/effector CD4+ T cells, BAY1155975 at the highest concentration exhibited a significantly stronger inhibition of CD28-costimulated effector cytokine secretion (IFN-gamma, TNF-alpha, IL17 and IL22) in comparison to prednisolone. Interestingly, proliferation, apoptosis and expression of activation markers were similarly regulated by BAY1155975 and prednisolone. Further studies on different signal transduction pathways suggested that BAY1155975 stronger inhibited the calcium-calcineurin-NFAT pathway than prednisolone in these cells. In vivo BAY1155975 and prednisolone showed comparable efficacy in inhibition of T cell dependent skin inflammation in DNFB-induced contact hypersensitivity models in mice, when mice were treated before hapten challenge. In contrast, when mice were treated around hapten sensitization markedly stronger inhibition of skin inflammation was observed for BAY1155975 than prednisolone. In summary, the data of this study give evidence for a stronger inhibition of T cell sensitization and effector cytokine secretion by the SEGRA, BAY1155975, in comparison to the classical GC, prednisolone.

In dieser Diplomarbeit wurde das astrophysikalisch interessante Resonanztriplett der Reaktion 40Ca(α,γ)44Ti bei 4,5MeV untersucht. Am 3-MV-Tandetron des Helmholtz-Zentrums Dresden-Rossendorf wurden dafür die Energien von Protonen- und -Strahlen kalibriert, Anregungsfunktionen im Energiebereich der drei Resonanzen aufgenommen, vier CaOTargets aktiviert und deren Struktur mittels der Reaktion 40Ca(p,γ)41Sc überprüft. Im Felsenkeller-Niederniveaumesslabor wurde anschließend die Aktivität der Proben gemessen. Schließlich konnte die Summe der Resonanzstärken bei 4497 und 4510 keV -Energie im Laborsystem zu (12;8 2;3) eV und die Summe der Resonanzstärken des gesamten Tripletts, d.h. zusätzlich bei 4523 keV, zu (12;0 2;0) eV bestimmt werden. Bei der ersten Resonanzstärke konnte die Unsicherheit im Vergleich zur Literatur von 19% auf 18% verbessert werden. Außerdem bieten die Daten der vorliegenden Arbeit die Grundlage, zukünftig die Unsicherheiten noch erheblich weiter zu reduzieren. / In this thesis the astrophysically interesting resonance triplet of the 40Ca(α ,γ)44Ti reaction at 4.5MeV has been studied. For this purpose energies of proton and beams provided by 3MVTandetron at Helmholtz-Zentrum Dresden-Rossendorf have been calibrated. Excitation functions of energy regions near the resonances and in-beam spectra of four different targets have been measured. The 40Ca(p,γ)41Sc reaction has been used to scan the structure of the activated targets. Afterwards their activity has been measured in the underground laboratory Felsenkeller Dresden. Hence the sum of resonance strengths at laboratory energies of 4497 and 4510 keV of (12:8 2:3) eV has been determined as well as the sum of the total triplet strength, including 4523 keV, of (12:0 2:0) eV. In the case of the first resonance, the uncertainty was decreased from 19% to 18 %. Furthermore the results of this work establish a basis for reaching much lower uncertainties in the future.

The assessment of teratogenic effects of chemicals is generally performed using in vivo teratogenicity assays e.g., in rats or rabbits. Following the 3R principles, the development of alternative methods is encouraged to reduce the number of animal tests. From this perspective, we have developed an in vitro assay (mDarT) using the zebrafish Danio rerio embryo teratogenicity assay (DarT) combined with an exogenous mammalian metabolic activation system (MAS), able to biotransform proteratogenic compounds. Cyclophosphamide, ethanol, benzo[a]pyrene and thalidomide were used as test materials to assess the efficiency of this assay. Briefly, the zebrafish embryos were co-cultured at 2 hpf (hours post fertilization) with the test material at varying concentrations, mammalian liver microsomes from different species and NADPH for 60 min at 32°C under moderate agitation in Tris buffer. The negative control (test material alone) and the MAS control (MAS alone) were incubated in parallel. For each test group, 20 eggs were used for statistical robustness. Afterwards fish embryos were transferred individually into 24-well plates filled with fish medium for 48 hours at 26°C with a 12 hour-light cycle. Teratogenicity was scored after 24 and 48 hpf using morphological endpoints. The test was considered to be valid if a minimum of 90% of fish eggs developed normally for the two controls (test material alone and MAS alone). For each test material, the experiment was repeated three times with the controls satisfying the validation criteria (≤ 10% impaired embryos). Indeed, no significant teratogenic effects were observed compared to controls in fish embryos exposed to the proteratogens alone (i.e., without metabolic activation) or the MAS alone. In contrast, the four test materials induced significant abnormalities in fish embryos when co-incubated with animal liver microsomes. For cyclophosphamide, ethanol and thalidomide a concentration-response relationship was shown and the qualitative nature of the malformations was similar between fish embryos and humans. Benzo[a]pyrene was demonstrated to be significantly teratogenic in fish embryos in spite of no concentration-response and unspecific teratogenic fingerprints. We conclude that the application of animal liver microsomes will improve and refine the DarT as a predictive and valuable alternative method to screen teratogenic substances.

Aufgrund ihrer herausragenden Eigenschaften haben ultrafeinkörnige Werkstoffe, die aus konventionellen normalkörnigen Halbzeugen über eine extrem große Kaltverformung hergestellt wurden, in den letzten zwei Jahrzehnten zunehmend an Bedeutung erlangt. In der vorliegenden Arbeit wird das Fließspannungsverhalten eines Reinaluminiumwerkstoffes (EN AW-1070 – Al99,7) und einer ausscheidungshärtbaren Aluminiumlegierung (EN AW-6060 – AlMgSi) mit Korngrößen von bis zu 660 nm und 310 nm in einem weiten Bereich von Dehnungen und Dehnraten analysiert und mit den zzt. existierenden Modellvorstellungen zu den mikrostrukturellen Abläufen in Verbindung gebracht. Um die Voraussetzung zur Herstellung von ultrafeinkörnigen Werkstoffen zu schaffen, wurden mehrere Werkzeugprototypen für die ECAP-Umformung im Labormaßstab entwickelt und erprobt. Die Untersuchungen zum Fließspannungsverhalten erfolgten anhand von Zug- und Druckversuchen über insgesamt sieben Dekaden der Dehnrate bis in den Bereich der hochdynamischen Belastung von 10^3 s^-1. Die Tests zeigen, dass das Fließspannungsverhalten ultrafeinkörniger Aluminiumwerkstoffe vollständig mithilfe der thermisch aktivierbaren Mechanismen erklärbar ist, wobei Ausscheidungen eine wichtige Rolle spielen. / Because of their exceptional properties ultrafine-grained materials, processed from conventional polycrystalline materials by severe plastic deformation, have gained increasing scientific and industrial interest during the last two decades. Based on the concept of work-hardening for f.c.c. metals the commercially pure aluminium AA1070 (Al99,7 – soft annealed) and the aluminium alloy AA6060 (AlMgSi – peak aged) were investigated. ECAP was used to introduce very high strains and an ultrafine-grained microstructure with grain sizes down to 660 nm and 310 nm. Subsequently compression and tensile tests were performed in a wide range of strain rates over seven decades up to the range of impact loading of 10^3 s^-1. The results indicate that strain path and the corresponding dislocation structure is important for the post-ECAP yielding and the following hardening response. Furthermore the precipitates of the AA6060 clearly constrain the interactions of dislocations in work-hardening stage III – causing lower strain rate sensitivity. If compared to the AA1070 they avoid hardening in stage V where an additional rate and temperature depending effect contributes – caused by the interaction of deformation induced vacancies and dislocations. The results indicate that the strain-hardening behavior can be described by thermal activated mechanisms.

No description available.

Fluoreszenzfarbstoffe wurden über neuartige Palladium-katalysierte Domino-Reaktionen synthetisiert, die aus einer Sonogshira-Reaktion, zwei Carbopalladierungen und einer C-H-Aktivierung bestanden.

No description available.

In the first part of this work, a convenient and high yielding synthetic strategy was developed to approach highly electrophilic fluorophosphonium cations as triflate salts. Through in situ electrophilic fluorination of phosphanes with commercially available bench-stable N-fluorobenzenesulfonimide (NFSI), followed by subsequent methylation of the [N(PhSO2)2]- anion with MeOTf, a library of mono-, di- and tri- cationic fluorophosphonium triflates were obtained in excellent yields. The Lewis acidities of all synthesized fluorophosphonium triflates salts were evaluated by both theoretical and experimental methods. These fluorophosphonium triflates have been develop as catalysts for the conversation of formamides into N-sulfonyl formamidines. CHAPTER II of this work focus on developing electrophilic fluorophosphonium cation as Lewis acid pedant in both inter- and intra- molecular FLP systems, as well as exploring their application in small molecular activation and functionalization, such as reversible CO2 sequestration and binding of carbonyls, nitriles and acetylenes. CHAPTER III of this thesis reports on the reaction of electrophilic fluorophosphonium triflates with trimethylsilyl nucleophiles (Me3SiX, X = CN, N3), which selectively yields either pseudohalo-substituted flurophosphoranes or pseudohalo-substituted phosphonium cations.:1. Introduction 1 1.1. Frustrated Lewis Pair chemistry 2 1.2. Phosphorus derivatives as strong Lewis acids 6 2. Objective 11 3. CHAPTER I: Synthesis of fluorophosphonium triflate salts and application as catalyst 15 3.1. Electrophilic fluorination of phosphanes: a convenient approach to electrophilic fluorophosphonium cations 15 3.2. Fluorophilicities and Lewis acidities of the obtained fluorophosphonium derivatives 23 3.2.1. Evaluation of fluorophilicities and Lewis acidities of the obtained fluorophosphonium cations 24 3.2.2. Reactions of fluorophosphonium salts with selected formamides. 27 3.2.3. Reactions of fluorophosphonium salts with selected urea derivatives 31 3.3. Transformation of formamides to N-sulfonyl formamidines using fluorophosphonium triflates as active catalysts 34 4. CHAPTER II: Bifunctional electrophilic fluorophosphonium triflates as intramolecular Frustrated Lewis Pairs 45 5. CHAPTER III: Reaction of fluorophosphonium triflate salts with trimethylsilyl nucleophiles 63 6. Summary 73 7. Perspective 77 8. Experimental section 80 8.1. Materials and methods 80 8.2. Experimental details for CHAPTER I 82 8.2.1. Preparation of imidazoliumyl-substituted phosphanes. 82 8.2.1.1. Preparation of [Ph2LcMeP][OTf] 82 8.2.1.2. Preparation of [Ph2LciPrP][OTf] 83 8.2.1.3. Preparation of [(C6F5)2LcMeP][OTf] 83 8.2.1.4. Preparation of [(C6F5)2LciPrP][OTf] 84 8.2.1.5. Preparation of [PhLcMe2P][OTf]2 85 8.2.1.6. Preparation of [PhLciPr2P][OTf]2 85 8.2.2. Preparation of fluorophosphonium bis(phenylsulfonyl)amide salts 86 8.2.2.1. Preparation of [36(NSI)]. 86 8.2.2.2. Preparation of 58a[NSI] 87 8.2.2.3. Preparation of 58b[N(SO2Ph)2] 88 8.2.3. Preparation of fluorophosphonium triflate salts 88 8.2.3.1. Preparation of 36[OTf] 89 8.2.3.2. Preparation of 36[H(OTf)2] 89 8.2.3.3. Preparation of 58a[OTf] 90 8.2.3.4. Preparation of 58b[OTf] 91 8.2.3.5. Preparation of 58c[OTf] 91 8.2.3.6. Preparation of 59a[OTf] 92 8.2.3.7. Preparation of 59b[OTf] 93 8.2.3.8. Preparation of 60Mea[OTf]2 94 8.2.3.9. Preparation of 60iPra[OTf]2 94 8.2.2.10. Preparation of 60Meb[OTf]2 95 8.2.3.11. Preparation of 60iPrb[OTf]2 96 8.2.3.12. Preparation of 61Me[OTf]3 97 8.2.3.13. Preparation of 61iPr[OTf]3 97 8.2.4. Reaction of fluorophosphonium triflate salts with nucleophiles 98 8.2.4.1. Preparation of 62a[OTf] 98 8.2.4.2. Preparation of 62b[OTf] 99 8.2.4.3. Preparation of 62c[OTf] 100 8.2.4.4. Preparation of 63 100 8.2.4.5. Preparation of 65 101 8.2.4.6. Preparation of 69a[OTf] 102 8.2.4.7. Preparation of 69b[OTf] 103 8.2.5. Synthesis of H[N(SO2R)(SO2Ph)] and corresponding sodium salt 103 8.2.5.1. General procedure for the formation of N-sulfonyl-sulfonamides 103 8.2.5.2. General procedure for the formation of sodium bis(sulfonyl)amides 104 8.2.5.3. Preparation of HN(SO2Ph)2, Na[N(SO2Ph)2] and [nBu4N][N(SO2Ph)2] 104 8.2.5.4. Preparation of 81a and 82a 105 8.2.5.5. Preparation of 81b and 82b 106 8.2.5.6. Preparation of 81c and 82c 106 8.2.5.7. Preparation of 81d and 82d 107 8.2.5.8. Preparation of 81e and 82e 108 8.2.5.9. Preparation of 81f and 82f 108 8.2.5.10. Preparation of 81g and 82g 109 8.2.5.11. Preparation of 81h and 82h 109 8.2.6. Synthesis of N-sulfonyl amidines 110 8.2.6.1. General procedure for the catalytic formation of N-sulfonyl amidines 110 8.2.6.2. Preparation of 64 110 8.2.6.3. Preparation of 72 111 8.2.6.4. Preparation of 73 112 8.2.6.5. Preparation of 74 112 8.2.6.6. Preparation of 75 113 8.2.6.7. Preparation of 76 114 8.2.6.8. Preparation of 77 114 8.2.6.9. Preparation of 78 115 8.2.6.10. Preparation of 79 116 8.2.6.11. Preparation of 80a,b 116 8.2.6.12. Preparation of 83b 117 8.2.6.13. Preparation of 83c 118 8.2.6.14. Preparation of 83d 119 8.2.6.15. Preparation of 83e 119 8.2.6.16. Preparation of 83f 120 8.2.6.17. Preparation of 83g 121 8.2.6.18. Preparation of 83h 122 8.3. Experimental details for CHAPTER II 123 8.3.1. Preparation of N-containing phosphanes 123 8.3.1.1. Preparation of 2-(bis(perfluorophenyl)phosphaneyl)pyridine 123 8.3.1.2. Preparation of 2-(bis(perfluorophenyl)phosphaneyl)-1-methylimidazole 124 8.3.1.3. Preparation of 2-(bis(perfluorophenyl)phosphaneyl)-N,N-dimethylaniline 124 8.3.2. Preparation of N/P Frustrated Lewis Pairs 125 8.3.2.1. General procedure for the synthesis of N/P-Frustrated Lewis pairs 125 8.3.2.2. Preparation of 85[OTf] 126 8.3.2.3. Preparation of 86[OTf] 126 8.3.2.4. Preparation of 87[OTf] 127 8.3.2.5. Preparation of 88[OTf] 128 8.3.2.6. Preparation of 89[OTf] 129 8.3.3. Synthesis of compound 84[OTf] 130 8.3.4. Reaction of N/P FLP with carbonyls, nitriles or acetylenes 131 8.3.4.1. General reaction conditions for the reaction of N/P FLP with carbonyls and nitriles 131 8.3.4.2. Preparation of 90[OTf] 131 8.3.4.3. Preparation of 91[OTf] 132 8.3.4.4. Preparation of 92[OTf] 133 8.3.4.5. Preparation of 93a[OTf] 134 8.3.4.6. Preparation of 93b[OTf] 134 8.3.4.7. Preparation of 94[OTf] 135 8.3.4.8. Preparation of 95[OTf] 136 8.3.4.9. Preparation of 96[OTf] 137 8.3.4.10. Preparation of 97a[OTf] 138 8.3.4.11. Preparation of 97b[OTf] 139 8.3.4.12. Preparation of 99a[OTf]2 140 8.3.4.13 Preparation of 100b[OTf] 141 8.3.5. Reaction of N/P FLPs with CO2 142 8.3.5.1 Reaction of 85[OTf] with CO2 142 8.3.5.2 Reaction of 86[OTf] with CO2 142 8.4. Experimental details for CHAPTER III 144 8.4.1 Synthesis of 105a,b[OTf] and 106c 144 8.4.1.1. General procedure for the reaction of fluorophosphonium triflate with Me3SiCN 144 8.4.1.2. Preparation of 105a[OTf] 144 8.4.1.3. Preparation of 105b[OTf] 145 8.4.1.4. Preparation of 106c 145 8.4.2. Reaction of fluorophosphonium triflate salt with Me3SiN3 146 8.4.2.1. General procedure for preparation of azidofluorophosphorane 146 8.4.2.2. General procedure for preparation of azidofluorophosphonium triflate salts 146 8.4.2.3. Preparation of 107a[OTf] 146 8.4.2.4. Preparation of 107b[OTf] 147 8.4.2.5. Preparation of 107c[OTf] 147 8.4.2.6. Preparation of 108c 148 8.4.2.7. Preparation of 109[OTf] 149 8.4.2.8. Preparation of 110[OTf]2 149 8.4.2.9. Preparation of 113[OTf]3 150 8.4.2.10. Preparation of 114[OTf] 151 8.4.2.11. Preparation of 115[OTf] 151 8.4.2.12. Preparation of 116[OTf] 152 8.4.3 Transformation of azido-fluorophosphorane under heating conditions 153 8.4.3.1 Preparation of 118 153 8.4.3.2 Preparation of 120a,b[OTf] 154 9. Crystallographic details 156 9.1. X-ray Diffraction refinements 156 9.2. Crystallographic details for CHAPTER I 157 9.3. Crystallographic details for CHAPTER II 169 9.4. Crystallographic details for CHAPTER III 176 10. Computational methods 179 11. Abbreviations 181 12. Nomenclature of compounds according to IUPAC recommendations 183 13. References 187 14. Acknowledgment 205 15. Publications and conference contributions 207 15.1. Peer-reviewed publication 207 15.2. Poster presentations 207 Versicherung 209 Erklärung 209