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Dissertations / Theses on the topic 'Cyclosporin'

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Published: 4 June 2021

Last updated: 21 February 2023

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1

Husi, Holger. "Cyclosporins and cyclosporin binding proteins : an insight into the mechanism of immunosuppression /." [S.l.] : [s.n.], 1994. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10937.

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2

James, Jacqueline A. "Cyclosporin A and gingival overgrowth." Thesis, Queen's University Belfast, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282191.

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3

French, Martin Thomas. "Fluorescence immunoassay for cyclosporin A." Thesis, Loughborough University, 1991. https://dspace.lboro.ac.uk/2134/33279.

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Monodansylcadavarine (MDC) was used to synthesise a fluorescent derivative of cyclosporin A and the product of the reaction was isolated by preparative thin layer chromatography (TLC) and purified by high performance liquid chromatography (HPLC). The fluorescent derivative was shown to bind with a polyclonal antibody to cyclosporin A by submitting the derivative for analysis by cyclosporin radioimmunoassay (RIA). However this derivative did not bind with a monoclonal antibody used in a RIA specific for the parent compound. To achieve this fluorescent derivatives were synthesised using cyclosporin-C-hemisuccinate as the staring material with MDC, 4-bromomethyl-7-methoxycoumarin (BMMC), 4-bromomethyl-6,7-dimethoxycoumarin (BMDC) and tetramethyl rhodaminecadavarine (TRC) as the labels. All derivatives were isolated and purified by TLC and HPLC and shown to have antibody binding in the parent compound specific RIA. The fluorescent properties of the derivatives were investigated and the most promising, BMMC and TRC used in the immunoassay development.

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4

Gerber, Andreas. "Totalsynthese von Cyclosporin A an der Festphase /." [S.l.] : [s.n.], 2009. http://edoc.unibas.ch/diss/DissB_8755.

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5

Mereish, Kulthoum A. "Alteration of cyclosporin : a bioavailability through complexation /." Ann Arbor : University Microfilms International, 1985. http://www.gbv.de/dms/bs/toc/01641747x.pdf.

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6

David, Oliver Jean Claude. "New approaches to improve cyclosporin A monitoring." Thesis, Queen Mary, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395488.

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7

Hutchison, Stephen Michael William. "Studies in cyclosporin nephrotoxicity in the rat." Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335321.

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8

Powles, A. V. "Cyclosporin for psoriasis : clinical and immunopathological studies." Thesis, University of Aberdeen, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253658.

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Ten patients with severe intractable psoriasis were treated with cyclosporin (CyA) at an average dose of 3 mg/kg/day for a period of 12 weeks. At the end of the study, 5 patients had a greater than 90% reduction in their PASI (psoriasis area severity index) score, 3 an 80%, one a 69% and one a 52% reduction. In a long term study, 13 patients with severe psoriasis were treated with CyA for an average duration of 2.5 years. The average dose of CyA was 3 mg/kg/day, with a range of 1 - 5 mg/kg/day. The average reduction in mean PASI score throughout the study was 70 - 80%. Seven of the 13 patients developed a rise in blood pressure, 3 of whom required antihypertensive therapy. Studies on possible nephrotoxicity showed that 4 of the 13 had a greater than 30% rise in their serum creatinine compared to their baseline value. 6 of the 13 patients had a low glomerular filtration rate (GFR) at the end of the study, but this rose in all 6 when CyA was discontinued, and to normal levels in 5 patients. In the sixth, a renal biopsy was performed which showed no structural damage due to CyA. In a further 11 patients, the mean GFR was shown to fall significantly after 9 weeks of CyA. Thus, CyA causes impairment of renal function with a dose of 3 mg/kg/day, but this impairment appears to be reversible when CyA is stopped. Six patients with plaque psoriasis were treated with topical CyA, and a further 10 with intralesional CyA. Topical CyA was ineffective, but intralesional CyA was effective in clearing psoriasis, implying that failure of topical preparations is probably due to lack of penetration. T cell and dendritic cell subsets in psoriasis were studied during oral CyA, and at the end of intralesional CyA treatment. After oral CyA, total CD4 and CD8, and DR+CD8 cells were decreased in the epidermis and dermis. However, DR+CD4 cells were decreased in the dermis but not the epidermis. After intralesional CyA, total and DR+CD4 and CD8 cells were decreased in both dermis and epidermis. The most significant effect of both intralesional and oral CyA on the dendritic cells was the decrease of the DR+CD1-subset.

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9

Spitzfaden, Claus. "Strukturbestimmung des Cyclophilin/Cyclosporin-Komplexes mittels NMR-Spektroskopie /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10406.

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10

Gillam, Elizabeth Maree Jeffery. "The interaction of cyclosporin A with cytochromes P450." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280968.

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11

Wastling, Jonathan Mark. "The action of cyclosporin A on helminth parasites." Thesis, University of Aberdeen, 1990. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU031936.

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The influence of the immunomodulatory/antiparasitic drug cyclosporin A (CsA) on parasitic infections is discussed and its effects on three helminths examined. The biology of the tapeworm Hymenolepis microstoma is reviewed and the action of CsA on this parasite investigated. Therapeutic CsA treatment was antagonistic to both juvenile and adult H.microstoma, reducing worm weight, delaying migration into the bile duct, suppressing egg production and lowering parasite survival. CsA also showed significant chemoprophylactic properties against H.microstoma CsA treatment in vivo caused gross and ultrastructural changes to the work surface and appeared to alter the permeability of the worm tegument to 14[C]-glucose in vitro. The protein composition of whole-worm and tegumentary fractions was analysed by one- and two-dimensional SDS-PAGE but was largely unaffected by drug treatment. A speculative scheme for the mode of action of CsA against H.microstoma is proposed which postulates that the work surface may be the site of action of the drug but the exact molecular target of CsA remains elusive. In marked contrast to its effect on H.microstoma, CsA delayed the normal host-mediated expulsion of H.diminuta from CBA, MF1 and BALB/C mice, enabling the parasite to reach patency. Worm recovery and weight both increased with CsA treatment. These paradoxical drug effects reflect the putative antagonism between immunosuppression and anthelmintic activity of CsA. The ability of CsA to suppress the host-mediated expulsion of H.diminuta from mice may implicate the importance of T-cells in protective immunity to this parasite. The influence of CsA treatment on the protein profiles of Schistomsoma mansoni was examined by SDS-PAGE. CsA significantly altered the concentration of a 31 kD protein sub-unit in female schistosomes and this is considered to corroborate the hypothesis that CsA targets haemoglobinase in female adult S.mansoni.

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12

Khan, Lillian Nasreen. "Effect of cyclosporin A on the immunopathology of asthma." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409081.

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13

Aldridge, R. D. "Modulation of delayed-type hypersensitivity reactions by cyclosporin A." Thesis, University of Aberdeen, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234482.

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The investigations have given rise to the following findings: 1. CsA is an effective immunosuppressant of both the induction and elicitation phases of tuberculin-like and contact delayed-type hypersensitivity (DTH) and of the induction phase of Jones-Mote hypersensitivity. 2. The effective suppression of tuberculin-like DTH responses in the guinea pig is not dependent upon cyclophosphamide-sensitive suppressor cells. 3. Topically applied CsA inhibits the elicitation of contact dermatitis in experimental animals. 4. The kinetics of percutaneous CsA absorption have been determined, as has the extent to which this mode of drug delivery obviates systemic toxicity. 5. The investigation of CsA-induced DTH enhancement indicates that the phenomenon is restricted to cellular as opposed to humoral responses, develops some days after drug withdrawal and can be reversed by the administration of putative suppressor cells from immunised but untreated animals. 6. CsA is able to effectively inhibit T cell dependent hyper-eosinophilia. It would appear that the effects of CsA on DTH responses and on T dependent eosinophilia occur primarily by the inhibition of T helper cell function. Enhancement phenomena seem to arise from drug impaired development of antigen-specific suppressor cells which, following drug withdrawal, fail to develop, in contrast to the maturation of T effector cells. Although the phenomenon of enhancement may limit the potential of CsA in the control of diseases in which DTH responses are a component, topical application is effective and may well be suitable for use over a prolonged period without systemic toxicity.

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14

Gudgeon, M. C. "Studies on the mechanism of action of cyclosporin A." Thesis, University of Sussex, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378279.

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15

Diehl, Rita. "Verträglichkeit und Effektivität Cyclosporin A-vermittelter Immunsuppression beim Schaf für die xenogene, intrazerebrale Transplantation." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-214365.

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Einleitung Der Einsatz von Stammzellen als Grundlage neuer therapeutischer Strategien wird bereits seit über 25 Jahren intensiv erforscht. Stammzellen sind in der Lage, in verschiedene funktionale Zelltypen auszudifferenzieren und verfügen über ein enormes Proliferationspotential (NAM et al. 2015). Ausgehend von den Fähigkeiten von Stammzellen sehen Forscher und Kliniker erstmals eine realistische Möglichkeit, kurative Therapieoptionen für Erkrankungen zu entwickeln, die bisher als schwer behandelbar oder sogar unheilbar angesehen wurden. Davon könnten insbesondere Patienten chronisch-degenerativer neurologischer und zerebrovaskulärer Erkrankungen, einschließlich der großen Anzahl an Schlaganfallopfern, profitieren. Schlaganfälle repräsentieren eine der häufigsten Todesursachen in der westlichen Welt (LOPEZ et al. 2006). Ein Drittel der betroffenen Patienten verstirbt innerhalb eines Jahres, während etwa 40% von dauerhaften Behinderungen betroffen sind (MOZAFFARIAN et al. 2015). Trotz intensiver Forschung existieren neben der systemischen Thrombolyse, die auf einen engen Zeitraum von maximal 4,5 Stunden nach dem Akutereignis beschränkt ist, keine zugelassenen Therapieoptionen (HACKE et al. 2008, SAVER et al. 2009). Zelltherapeutische Strategien zur Behandlung des Schlaganfalls werden daher als besonders vielversprechend angesehen (ANDRES et al. 2011). Neben den bereits gesicherten Erkenntnissen zur stammzelltherapeutischen Sicherheit und Wirksamkeit aus Studien unter Einsatz gängiger Nagermodellen (BLISS et al. 2006, JOO et al. 2013) wird insbesondere die Überprüfung der Wirksamkeit an geeigneten Großtiermodellen gefordert, die die Situation des menschlichen Schlaganfallpatienten möglichst realistisch wiedergeben sollen (SAVITZ et al. 2011). Eine Voraussetzung für die erfolgreiche Testung eines zelltherapeutischen Ansatzes in einem Großtiermodell mit fokaler zerebraler Ischämie besteht darin, ein langfristiges Überleben xenogener Zelltransplantate durch ein geeignetes Immunsuppressionsprotokoll zu erreichen. Die Notwendigkeit einer Immunsuppression besteht darin, dass sowohl allo- als auch xenogene Transplantate eine Immunantwort beim Empfänger auslösen und somit zu einer Abstoßungsreaktion führen können (JANEWAY 2002). Die Anwendung von immunsuppressiven Medikamenten geht dabei aber häufig mit Nebenwirkungen einher. Insbesondere beim Schaf existiert jedoch nur eine limitierte Datenlage zu immunsuppressiven Protokollen und deren Nebenwirkungen. Ziele der Untersuchung Das Ziel der vorliegenden Studie bestand darin, eine xenogene Transplantation von fetalen humanen neuralen Progenitorzellen (fhNPZ) in einem gesunden Schafsmodell durchzuführen, um die Wirksamkeit in Hinblick auf das Transplantatüberleben und die Nebenwirkungen einer Immunsuppression mittels Cyclosporin A (CsA) zu untersuchen. Materialien und Methoden Hierfür wurden je 5 Schafe in zwei Gruppen über einen Zeitraum von 64 Tagen immunsupprimiert (iCsA: 3 mg CsA/kg 2x tägl. bis einschließlich Tag 36, danach 3 mg CsA/kg 1x tägl. jeden 3. Tag; kCsA: kontinuierlich 3 mg CsA/kg 2x tägl.), während eine Kontrollgruppe (Kon) von ebenfalls 5 Tieren keine Immunsuppression erhielt. Am Versuchstag 22 wurde den Schafen eisenmarkierte fhNPZ (Eisenkonzentration: 3,0 mM, ca. 200.000 Zellen pro Transplantationsposition) stereotaktisch in das gesunde Gehirn transplantiert. Aufgrund der Eisenmarkierung der Stammzellen konnten diese an den Versuchstagen 23, 36 und 64 mittels 3,0 MRT-Aufnahmen in vivo überwacht und anschließend ex vivo das Überleben der fhNPZ im Schafhirn 42 Tage nach Transplantation histologisch untersucht werden. Für die Untersuchungen zu Wirkspiegeln und Nebenwirkungen von CsA im Schaf wurden den Versuchstieren innerhalb des Versuchszeitraums regelmäßig Blutproben entnommen und am Versuchsende eine pathologische und histologische Untersuchung von Leber und Nieren durchgeführt. Ergebnisse Bei den durchgeführten Untersuchungen konnte festgestellt werden, dass die CsA-Wirkspiegel im Blut bei der kCsA (424,0 ± 135,0 ng/ml) signifikant höher waren im Vergleich zur iCsA (198,5 ± 155,9 ng/ml). Diese Unterschiede besaßen jedoch keinen Einfluss auf das Langzeitüberleben der transplantierten fhNPZ. In keiner der drei Versuchsgruppen konnten vitale Zellen 42 Tage nach der Transplantation aufgefunden werden. Die Untersuchung der Nebenwirkungen von CsA ergab, dass die Langzeitgabe von CsA Anzeichen für einen hämatologischen Einfluss zeigt. Ebenso konnte sowohl eine hepatotoxische, als auch eine nephrotoxische Wirkung von CsA beim Schaf nachgewiesen werden. Schlussfolgerungen Schlussfolgernd kann zusammengefasst werden, dass die Gabe von 3 mg CsA/kg 2x tägl. nicht suffizient einer Abstoßungsreaktion xenogener ins Schafhirn transplantierter fhNPZ entgegenwirkt. Für das Ziel einer suffizienten zelltherapeutischen Anwendung im Schaf nach einem Schlaganfall sind somit weitere Untersuchungen zu einer wirksamen Immunsuppression beim Schaf und zu einem verbesserten Transplantatüberleben notwendig. Desweiteren konnten klinische und pathologische Nebenwirkungen beim Schaf durch die Langzeitgabe des Immunsuppressivums CsA festgestellt werden.

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16

Riether, Carsten. "Peripheral mediatory mechanisms of behaviorally conditioned immunosuppression by cyclosporin A /." [S.l.] : [s.n.], 2008. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=18085.

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17

Zhang, Yixin. "Rational design of cyclosporin A derivatives for selective enzyme inhibition." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=964279401.

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18

Ormrod, Douglas James. "Modulation of non-specific cellular defence mechanisms by cyclosporin A." Thesis, University of Auckland, 1990. http://hdl.handle.net/2292/3195.

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The immune response modifier Cyclosporin A (CsA) is widely used in the management of organ graft rejection and in the treatment of inflammatory disorders. CsA is a potent suppressor of T-lymphocyte function and it’s biological effects have been defined almost exclusively in these terms. However, recent studies in which the agent was shown to exacerbate a T-lymphocyte independent, experimentally induced bacterial infection of the kidney (pyelonephritis), indicated that CsA had effects on host defence mechanisms other than T-lymphocytes. The present study, using animal models, was undertaken to identify the host defence component modified by CsA. Neutrophils are a key component in the early response to infection and the administration of CsA resulted in an increase in the number of these cells in the circulation. When the effect of CsA on the in vitro metabolic activity of neutrophils and their ability to kill microorganisms was investigated, no changes were observed, but the in vivo ability of neutrophils to emigrate from the vasculature to a sterile inflammatory foci was markedly impaired. A model of localised subcutaneous infection was used to determine the effect of this CsA-associated suppression of neutrophil emigration on the ability of the host to mount a response to an infectious challenge. In CsA treated animals, neutrophil accumulation in E. coli infected, subcutaneously implanted sponges was initially suppressed, allowing bacterial numbers to increase rapidly. By 48 hours this powerful bacterial stimulus overrode the suppressive effects of CsA and led to a substantial increase in the size of the neutrophilic infiltrate. This finding of an initially reduced inflammatory response, followed by an increase in the influx of inflammatory cells, provided a possible explanation for the earlier observation that CsA promoted infection and tissue damage in experimental pyelonephritis. The relationship between the effect of CsA on neutrophil emigration and the pathogenesis of experimental pyelonephritis was therefore investigated. When CsA was administered to animals prior to inducing pyelonephritis, the neutrophilic infiltrate was markedly suppressed in the early stages. As predicted, this led to a logarithmic increase in bacterial numbers, the infiltration of large numbers of neutrophils and, ultimately, an exacerbation of tissue damage. Further studies, examining the effects of CsA on neutrophil-mediated inflammatory mechanisms, identified impaired neutrophil-to-endothelial cell adhesion as the most likely explanation for the observed defect in host defences. The integrated nature of cellular defence mechanisms in infectious disease is highlighted by these investigations. when microorganisms invade tissue, even though the number and function of circulating leucocytes may be normal their effective participation in the host response to infection depends on the ability to emigrate from the blood vessels to the site of infection. In summary, the discovery of additional properties of CsA provide an explanation for the patterns of infectious disease in patients treated with CsA, in whom infection with extracellular pathogens is common. It also seems likely that the ability of CsA to suppress neutrophil emigration may contribute to the effectiveness of the agent in the management of inflammatory diseases, such as rheumatoid arthritis, uveitis and psoriasis.

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19

Wang, Su. "Transdermal delivery of cyclosporin A by electrically enhanced permeation techniques." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq23183.pdf.

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20

Misseghers, Byron S. "The histologic characterization of perianal fistulas during treatment with cyclosporin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0016/NQ47400.pdf.

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21

KONDO, TATSUHEI, HIROSHI TAKAGI, and TAKESHI MORIMOTO. "Canine Pancreatic Allotransplantation with Duodenum (Pancreaticoduodenal Transplantation) Using Cyclosporin A." Nagoya University School of Medicine, 1985. http://hdl.handle.net/2237/17478.

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22

Baumgart, Alessandra. "Cyclosporin A und dessen möglicher Einsatz bei der Tigerschecken-Uveitis." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-168992.

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23

McNally, P. G. "The influence of calcium channel blockers on cyclosporin A nephrotoxicity." Thesis, University of Leicester, 1990. http://hdl.handle.net/2381/34162.

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Intrarenal vasoconstriction is a characteristic feature of cyclosporin A nephrotoxicity. This thesis investigates the effect of nifedipine, a dihydropyridine calcium channel blocker and potent renal vasodilator, on various aspects of experimental and clinical cyclosporin A nephrotoxicity. In the surgically intact spontaneously hypertensive rat (two-kidney model), short-term administration of cyclosporin A (14 days) induced a marked reduction in glomerular filtration rate and effective renal plasma flow, and an increase in renal vascular resistance. These changes were both reversible on stopping treatment and without histological evidence of renal cell injury. Concomitant nifedipine from day 1 prevented these adverse alterations in renal haemodynamics. However, administering nifedipine after cyclosporin A (from day 7) failed to improve renal function. By contrast, neither renal denervation nor nifedipine prevented cyclosporin A-induced renal dysfunction in uninephrectomized rats. The mechanism mediating these alterations in renal vascular tone is unclear, however, studies in isolated blood vessels demonstrate that it is independent of phosphoinositide hydrolysis. In man, short-term administration of nifedipine (28 days) to stable cyclosporin A-treated renal allograft recipients led to a significant, albeit small, increase in glomerular filtration rate, without a parallel increase in effective renal plasma flow or reduction in renal vascular resistance. Using cell culture techniques, this beneficial effect was not secondary to a reduction in the uptake of cyclosporin A into proximal tubular cells. Thus, these results suggest that nifedipine can under certain experimental and clinical conditions ameliorate cyclosporin A-induced renal dysfunction. The protective mechanism afforded appears to involve both vascular and non-vascular mechanisms. Adaptive changes in renal haemodynamics occurring after uninephrectomy may account for the poor response in this model. Finally, the failure of renal denervation to preserve renal function infers that the sympathetic nervous system is not mediating cyclosporin A-induced alterations in renal vascular tone.

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24

Wang, Su. "Transdermal delivery of cyclosporin B by electrically enhanced permeation techniques /." St. John's, NF : [s.n.], 1997.

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25

Richter, Sebastian. "Rapamycin vs. Cyclosporin A : Auswirkungen auf Transplantatabstossung und Tumorwachstum im Tiermodell." kostenfrei, 2009. http://www.opus-bayern.de/uni-regensburg/volltexte/2009/1352/.

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26

Bäuerle, Alexander Lutz [Verfasser]. "Die Therapie der membranösen Glomerulonephritis mit Cyclosporin A / Alexander Lutz Bäuerle." Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1028033567/34.

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27

McLauchlan, P. E. "Host-parasite interactions : cellular immune responses and modulation by cyclosporin A." Thesis, University of Aberdeen, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.593084.

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The role of cyclosporin A (CsA) as an immunomodulatory and antiparasitic drug was examined. The immune responses in various host:parasite relationships were examined giving an insight into the complicated nature of this relationship. In addition, analogues of CsA were screened to investigate the antiparasitic mode of action of cyclosporins. Expulsion of intestinal parasites has been proposed to involve the cellular immune response but its precise role is unknown. In CBA/ca mice infected with Hymenolepsis diminuta, peak intestinal mucosal mast cell (IMMC) numbers and release of mast cell protease (mMCP-I) correlated with parasite expulsion. Immunosuppression by cyclosporin A (CsA) treatment abrogated the response and allowed H. diminuta to survive to maturity. In contrast, H. microstroma survived long-term in MF1 mice, despite a significant and sustained IMMC response and mMCP-I release. It is proposed that the protease has different roles in these hymenolepid infections. Goblet cell proliferation did not occur in either infection. Adult Schistosoma mansoni are less susceptible to CsA than juveniles and reduced drug efficacy correlates with the onset of egg deposition and pathology in the liver of the host. This may alter metabolism of CsA and prevent the production of an active metabolite. CsA and metabolites were identified in mice tissues using reverse phase HPLC but problems with background peaks and low drug recovery prevented examination of the metabolite profile. CsA is antiparasitic against a range of protozoa and helminths but its mode of action is unknown. One possibility is that it involves the binding protein, cyclphilin (CyP). Three analogues of CsA, B-5-49, CsH and CsA-acetate (CsA-A) were screened against H. microstroma in vitro, which is susceptible to CsA. All analogues induced drug damage comparable to CsA. However, only B-5-49 bound to H. microstroma cytosolic CyP, suggesting that CyP is not necessary for the antiparasitic action of cyclosporins. Schistosomes suppress the activity of the internal defence system in their host in order to ensure their survival.

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28

Myrillas, Theofilos T. "Cellular mechanisms underlying the pathogenesis of cyclosporin A-induced gingival overgrowth." Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284391.

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29

Chan, Weng C. "A study of the medicinal chemistry related to the C9-ene amino acid of cyclosporin." Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381104.

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30

Gennai, Stéphane. "Effets de la cyclosporine A sur des poumons porcins reperfusés ex vivo." Thesis, Grenoble, 2013. http://www.theses.fr/2013GRENS012/document.

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Objectif De nombreux travaux ont souligné le rôle de la Cyclosporine A (CsA) dans la prévention des lésions d'ischémie-reperfusion (I/R) mais aucun n'a été effectué sur poumons isolés de grands mammifères. Notre objectif était de mesurer pour la première fois les effets de la CsA sur les lésions d'I/R dans un modèle de poumons porcins reperfusés ex vivo, en évaluant plusieurs doses de CsA pour différents temps d'ischémie. Méthodes L'expérimentation A a été conduite sur 4 groupes de 8 paires de poumons chacune : un groupe contrôle et 3 groupes recevant différentes concentrations de CsA (1, 10 ou 30 μM) au moment de l'ischémie et au début de la reperfusion, après 2 heures d'ischémie. L'expérimentation B a été conduite sur 3 groupes de 5 paires de poumons chacune. Les poumons de chaque paire étaient séparés juste après le début de l'ischémie. Les premiers poumons étaient évalués après une ischémie de 2 heures (jour 0), sans CsA. Les seconds poumons étaient évalués après une ischémie de 24 heures (jour 1), soit sans soit avec CsA (1 ou 5 μM), administrée le cas échéant au début de la reperfusion. Résultats La CsA augmentait le rapport PO2/FiO2 avec un effet dose mais augmentait également la pression artérielle pulmonaire, la pression capillaire et les résistances vasculaires pulmonaires, à 10 et 30 μM mais pas à 1 ni 5 μM. Les poumons qui recevaient 30 μM de CsA affichaient des concentrations élevées en cytokines pro-inflammatoires. La concentration en RAGE (receptor for advanced glycation endproducts) dans le lavage broncho-alvéolaire diminuait avec la CsA à J1 en comparaison à J0. Conclusions Lors de l'I/R pulmonaire, les bénéfices cellulaires des doses élevées de CsA sont contrebalancés par ses effets hémodynamiques sur la microvascularisation. A faibles doses, la CsA semble améliorer la fonction pulmonaire
Objective Several works highlighted the role of Cyclosporine A (CsA) in the prevention of ischemia reperfusion (I/R) injuries but none on isolated lungs of big mammals. Our objective was to measure for the first time the effects of CsA in I/R injuries in an ex vivo reperfused pig lungs model, by evaluating several doses of CsA for different times of ischemia. Methods Experimentation A was performed on 4 groups of 8 pairs of lungs each: a control group and 3 groups receiving different concentrations of CsA (1, 10 or 30 μM) at the time of ischemia and at the beginning of the reperfusion, after a 2 hours ischemia. Experimentation B was performed on 3 groups of 5 pairs of lungs each. Lungs from each pair were separated just after the beginning of ischemia. The first lungs were evaluated after a 2 hours ischemia (day 0), without CsA. The second lungs were evaluated after a 24 hours ischemia (day 1), either without or with CsA (1 or 5 μM), administered when appropriate at the beginning of the reperfusion. Results CsA improved the PO2/FiO2 ratio with a dose dependent effect but increased pulmonary arterial pressure, capillary pressure, and pulmonary vascular resistances, at 10 and 30 μM but neither at 1 or 5 μM. Lungs receiving 30 μM of CsA displayed elevated concentrations in pro-inflammatory cytokines. Concentrations in RAGE (receptor for advanced glycation endproducts) in broncho-alveolar lavage decreased with CsA at day 1 compared to day 0. Conclusions During pulmonary I/R, the cellular benefits of high doses of CsA are counterbalanced by its hemodynamic effects on microvascularisation. At low doses, CsA seems to improve lung function

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31

Saunders, R. N. "The effect of rapamycin after cyclosporin dose reduction on chronic allograft nephropathy." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/29442.

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Chronic allograft nephropathy (CAN) is the commonest cause of late decline in renal allograft function and subsequent failure. Histopathologically it is underpinned by the accumulation of extracellular matrix. The first chapter provides a thorough review of the current opinions regarding the aetiology, pathophysiology and management of this complex condition. Overexposure to Cyclosporin is a major risk factor for chronic allograft nephropathy and thus Cyclosporin dose reduction has been advocated in some reports. Rapamycin is a relatively new immunosuppressant, recently introduced in renal transplantation. The second chapter reviews this new agent and discusses experimental evidence supporting its use in patients with chronic allograft nephropathy. The aim of this work was to determine the impact of the addition of Rapamycin after Cyclosporin dose reduction in renal allograft recipients with chronic allograft nephropathy and thus to ascertain whether such a regimen was beneficial. In order to achieve this 31 renal transplant recipients with biopsy confirmed CAN were prospectively randomised to receive either a 40% dose reduction in Cyclosporin (control), or a 40% dose reduction in Cyclosporin with the addition of Rapamycin 2mg/day (Rapa). Renal function and side effect parameters were assessed at 1,2,4,6,8 weeks, 3 and 6 months. The third chapter presents the clinical results. Proteinuria, serum creatinine and calculated GFR were similar in both groups. However the rate of decline of the calculated GFR was reduced over the study in control but not Rapa patients. Furthermore radio-isotope GFR fell in those in the Rapa group but not controls. The use of Rapamycin was safe with only relatively minor side effects and some temporary haematological and hyperlipidaemic changes. The patients above had a renal allograft biopsy on recruitment and again at 6 months. Glomeruli were plucked from the surface of each biopsy core and these as well as a small sample of interstitium underwent total mRNA extraction. Complementary DNA was synthesized by reverse transcription and polymerase chain reactions used to amplify specific genes involved in the turnover of extracellular matrix in CAN. These were quantified using an ELISA technique. The fourth chapter details the changes in expression of some of these genes in. In glomeruli, TGF|3-1 remained constant in Rapa patients but fell in controls. Collagen III and TIMP-2 increased in those taking Rapamycin but not in controls. TIMP-1 and MMP-2 expression increased in a similar fashion in both groups. Glomerular TGFp-1, TIMP-1 and -2 expression appeared to be related to calculated GFR. There were fewer molecular changes within the interstitium but collagen III expression increased in Rapa patients. The fifth chapter discusses the use of Sirius red staining and computerised histomorphometry in order to obtain an accurate assessment of the impact of this regimen on the amount of collagen present in the biopsies taken above. The interstitial volume fraction of biopsy cores stained with Sirius Red fell over the study in controls but a similar effect did not occur in Rapa patients. The final chapter concludes that the addition of Rapamycin (2 mg/day) after Cyclosporin dose reduction in patients with CAN did not improve functional outcome or molecular and histological markers of CAN. Possible explanations are discussed and the need for a larger multicentre trial emphasised in order to substantiate these findings. Studies utilising complete Cyclosporin elimination with the addition of Rapamycin may have better prospects for the future.

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32

Horrocks, C. "Immunological studies into the mechanisms of action of cyclosporin A in psoriasis." Thesis, University of Aberdeen, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.592590.

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Seven chronic plaque psoriasis patients were treated with cyclosporin A (CsA, 2.5-5.0 mg/kg/day). A marked resolution of psoriasis was observed within 4 weeks of treatment. Immunophenotypic analysis of patients' peripheral blood mononuclear cells (PBML) before and during CsA therapy revealed no difference in comparison to normal nor any change following CsA therapy. Immunocytochemical analysis of lesional skin, however, revealed marked reductions in infiltrating CD3+ (pan T), CD4+ (T helper), CD25+ (interleukin 2 receptor) and to a lesser extent CD8+ (T cytotoxic/suppressor) cells within 4 weeks of CsA therapy. These data may indicate a preferential depletion of activated lesional T cells by CsA. Lesional epidermal CD1+ (Langerhans cells) numbers were reduced in comparison to normal skin whilst dermal CD1+ cells were increased. CsA treatment normalised both the distribution and frequency of CD1+ cells in the lesions. In normal epidermis CD29 was the only adhesion molecule detected and was confined to basal keratinocytes (KC). In addition to CD29, lesional KC also expressed LFA-3 and CD11c which were unaffected by CsA therapy. The dermal infiltrate and blood vessels were strongly positive for ICAM-1 and HLA-DR (both reduced by CsA) whilst no staining was observed on KC. In addition to EGFR (epidermal growth factor receptor) and CK10+ 11 (cytokeratin), which are expressed in normal epidermis, lesional epidermal keratinocytes were also found to express the hyperproliferation marker C13+ 16. Neither EGFR nor CK expression was altered during CsA therapy. Normal human keratinocyte proliferation in vitro was inhibited by both CsA (6-10 μg/ml) and IFNγ (25-200 U/ml) which was accompanied by decreased EGFR expression, measured by flow cytometry, and a paradoxical increase in KC TGFα production. IFNγ, but not CsA, was also able to induce KC ICAM-1 expression. The inhibitory effects of CsA on cultured KC occurred at concentrations greater than those reported in the lesions of CsA treated psoriatics and therefore the anti-psoriatic effect of CsA is probably mediated via inhibition of lesional T cell function.

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Heys, Stephen D. "The potentiation and alleviation of cyclosporin A nephrotoxicity in the Lewis rat." Thesis, University of Aberdeen, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254668.

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Cyclosporin A immunosuppression following organ transplantation is associated with a reversible nephrotoxicity as manifested by elevations in serum urea and creatinine concentrations and urinary N-acetyl-B-D-glucosaminidase activities. The metabolism of Cyclosporin A is primarily via the hepatic cytochrome P-450 mono-oxygenase system with previous studies having demonstrated that the short term co-administration of phenobarbitone, an inducer of this enzyme system, ameliorates this nephrotoxicity in the non-renal allografted rat. Initial studies demonstrated that the induction of Cyclosporin A nephrotoxicity in the Lewis rat followed by the co-administration of phenobarbitone in the long term abolished nephrotoxicity in the female whilst alleviating it in the male animal. In addition Cyclosporin A hepatotoxicity was also abolished in female rats co-treated with phenobarbitone. A rat renal transplantation model was successfully developed to allow the study of Cyclosporin A nephrotoxicity in the renal allografted animal. Initial studies demonstrated a protective effect of phenobarbitone against Cyclosporin A nephrotoxicity within the first 14 days of treatment in female, but not male allografted animals. These studies also demonstrated a greater susceptibility of the male renal allografted and surgically intact rat to Cyclosporin A induced nephrotoxicity. The effect of ischaemia and sympathetic nervous system denervation were investigated using a series of Lewis syngeneic renal transplanted animals. Histological examination revealed Cyclosporin A induced renal damage to be more marked in non-transplanted than transplanted kidneys. The results are discussed in relation to cold and warm ischaemia and also to the role of the sympathetic nervous and renin-angiotensin-aldosterone systems in the potentiation of Cyclosporin A induced nephrotoxicity. The effect of long term phenobarbitone treatment on Cyclosporin A induced deteriorations in renal and hepatic function was determined using the Lewis syngeneic transplant model. The effect of intraoperative liver ischaemia and diethyl ether anaesthesia on hepatic function and their potentiation of Cyclosporin A hepatotoxicity is also considered. Finally the role of surgical stress and reduction of renal mass by unilateral nephrectomy, on Cyclosporin A nephrotoxicity was studied revealing a protective effect of unilateral nephrectomy against nephrotoxicity in the female animal. Previous studies have demonstrated that reduction in renal mass results in glomerulosclerosis with a progressive impairment of renal function. The protective effect of unilateral nephrectomy reported here is discussed in relation to a Cyclosporin A induced reduction in glomerular filtration rate and subsequent protection against glomerulosclerosis.

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Takayama, Akira. "Transport of cyclosporin A in kidney epithelial cell line (LLC-PK[1])." Kyoto University, 1995. http://hdl.handle.net/2433/160728.

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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものである
Kyoto University (京都大学)
0048
新制・論文博士
博士(医学)
乙第8919号
論医博第1514号
新制||医||613(附属図書館)
UT51-95-P410
(主査)教授藤田潤, 教授吉田修, 教授乾賢一
学位規則第4条第2項該当

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35

Cunningham, Charles. "Aspects of the relationship between the metabolism and toxicity of cyclosporin A." Thesis, University of Aberdeen, 1985. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU356459.

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The fungal metabolite cyclosporin A (CsA) is the first of a new order of immunosuppressant drugs. Unlike conventional immunosuppressive therapy, which produces "blanket suppression", CsA has a selective inhibitory effect on T cell activation. Although CsA does not cause the serious side-effects, such as myelotoxicity, normally associated with cytotoxic agents, the drug is not without its problems, the most clinically important of which are nephro- and hepatotoxicity. The primary aim of the work presented in this thesis was to study mechanisms of CsA- induced toxicity in the rat. In an initial study a toxic oral dose of CsA was administered daily along with the diuretic frusemide (Fr) for a period of 14 days. Although CsA had no effect on Fr-induced diuresis, Fr did enhance the nephrotoxicity associated with the immunosuppressant. The nature of this interaction was unclear but it was postulated that Fr might inhibit the metabolism of CsA by the hepatic cytochrome P-450 (cyt P-450) dependent mono-oxygenase enzyme system, thus producing toxic circulating levels of CsA. To further investigate this important role of the cyt P-450 system, the effect of inhibition, suppression or induction of hepatic drug metabolism on the toxicity of CsA was investigated. The co-administration of either an inhibitor (SKF-525A) or a suppressor (CoCl2) of hepatic mono-oxygenase activity with a toxic dose of CsA produced inconclusive results. When, however, CsA was given along with known inducers of both cyt P-450 and the conjugating enzyme glucuronyl transferase (GT), namely either Aroclor 1254 or low doses of phenobarbitone (PB: 40 or 60 mg/kg/ 24 hr), the trough serum CsA levels were reduced and the nephrotoxicity associated with CsA either ameliorated (when assessed by serum and urinary biochemical criteria) or abolished (when assessed histologically). The co-administration of 3-methylcholanthrene (3-MC), a compound which induces cyt P-450 and GT isozymes distinct from those induced by PB, with CsA had no effect on either the trough serum levels or toxicity of the immunosuppressant. Since Aroclor 1254 combines the inducing properties of PB and 3-MC, it was concluded that the amelioration of the nephrotoxicity associated with CsA by Aroclor 1254 was due to its PB-type induction of either cyt P-450 or GT. None of the inducers had any effect on the CsA-evoked changes in hepatic biochemical function, although the co-administration of CsA and Aroclor 1254 resulted in a quite severe fatty change in the liver. This was in contrast to the relatively mild fatty changes seen when CsA was co-administered with either PB or 3-MC. No inducer had any effect on either the immunosuppressive property of CsA or on CsA- induced changes in lymphoid and bone marrow tissue morphology. As a result of these studies, an experiment was designed to determine whether the spontaneous remission in CsA-induced renal damage noted previously in this laboratory could be related to changes in the activity of the hepatic mono-oxygenase enzyme system and in the possible hepatic metabolism of CsA. A toxic dose of CsA was administered to rats for a seven-week period, during which time groups of 4 rats were killed at various times. Nephrotoxicity appeared within 4 days of starting treatment and continued until day 28. There was then a one-week period of remission followed by the return of renal damage. Hepatic mono-oxygenase activity, as indicated by aminopyrine N-demethylation (AD) and NADPH-cytochrome c (P-450) reductase activity in vitro, fell during the first 28 days but as the rats entered the remission period AD activity rose to above pretreatment levels, while NADPH-cyt c reductase activity returned to a level similar to its pretreatment value. During the same remission period the serum CsA level fell to its lowest concentration. With subsequent relapse, hepatic enzyme activity and serum CsA levels both returned to their pre-remission values. These results were consistent with cyclical changes in CsA induced nephrotoxicity being caused by corresponding variations in circulating drug levels. The changes in serum levels of CsA were, it was suggested, best explained by cyclical changes in the drugs metabolic detoxification by the hepatic mono-oxygenase enzyme system, due to the production of a hepatic CsA metabolite which "suicide inactivated" the hepatic mono-oxygenase system. The results presented in this thesis indicate that, in the rat, either the parent CsA, molecule or a, non-PB inducible metabolite recognised, in the CsA radioimmunoassay is responsible for the CsA-induced nephrotoxicity. In addition, these results, taken together with recent published case reports, suggest that the co-administration of CsA, with drugs which either induce or inhibit cyt P-450 should, whenever possible, be avoided.

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Sieber, Matthias. "Modulatoren des Calcineurin-NFATc-Signalweges in humanen TH-Zellen." Phd thesis, Universität Potsdam, 2010. http://opus.kobv.de/ubp/volltexte/2010/4467/.

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Die Ca2+/Calmodulin-aktivierte Serin/Threonin-Phosphatase Calcineurin ist ein Schlüsselmolekül des T-Zell-Rezeptorabhängigen Signalnetzwerkes. Calcineurin aktiviert die Transkriptionsfaktoren der NFATc-Familie durch Dephosphorylierung und reguliert darüber die Expression wichtiger Zytokine und Oberflächenproteine. Die Aktivität von Calcineurin wird durch zahlreiche endogene Proteine moduliert und ist Angriffspunkt der immunsuppressiven Substanzen Cyclosporin A und FK506. In dieser Arbeit wurde der alternative niedermolekulare Calcineurin-NFATc-Inhibitor NCI3 hinsichtlich seiner Effekte auf T-Zell-Rezeptor-abhängige Signalwege charakterisiert. Die Ergebnisse zeigen, daß das Pyrazolopyrimidinderivat NCI3 nichttoxisch und zellmembranpermeabel ist. In T-Zell-Rezeptor-stimulierten primären humanen TH-Zellen unterdrückt NCI3 die Proliferation und IL-2-Produktion (IC50-Wert ~4 µM), da die Dephosphorylierung von NFATc und die anschließende nukleäre Translokation gehemmt wird. NCI3 inhibiert die calcineurinabhängige NFAT- und NF-κB-, aber nicht die AP-1-kontrollierte Reprtergenexpression, in mikromolaren Konzentrationen (IC50-Werte 2 bzw. 7 µM). Im Gegensatz zu Cyclosporin A stört NCI3 nicht die Phosphataseaktivität von Calcineurin, sondern interferiert mit der Calcineurin-NFATc-Bindung. Ein wichtiges endogenes Modulatorprotein für die Calcineurinaktivität ist RCAN1, das vermutlich den Calcineurin-NFATc-Signalweg über einen negativen Rückkopplungsmechanismus reguliert. Hier wurde gezeigt, daß RCAN1 in humanen TH-Zellen exprimiert wird. Die Spleißvariante RCAN1-1 ist in ruhenden T-Zellen basal exprimiert und wird nicht durch T-Zell-Rezeptor-Stimulierung in seiner Expression verändert. RCAN1-4 dagegen ist in ruhenden Zellen kaum zu detektieren und wird stimulierungsabhängig induziert. Durch die Verwendung Calcineurin-NFATc-spezifischer Inhibitoren wie NCI3 wurde gezeigt, daß die RCAN1-4-Induktion durch diesen Signalweg limitiert ist. Die in dieser Arbeit gewonnenen Daten und Erkenntnisse tragen dazu bei, das Verständnis der Funktion und Regulation von Calcineurin in T-Zellen zu vertiefen.
The Ca2+/calmodulin dependent serine/threonine phosphatase calcineurin is a key molecule in the T cell receptor dependent signalling network. Calcineurin dephosphorylates and thereby activates the transcription factors of the NFATc family that, among others, control the expression of important cytokines and cell surface molecules. The activity of Calcineurin is modulated by several endogenous proteins and is inhibited by the immunosuppressants cyclosporine A and FK506. Here, the novel low molecular weight inhibitor NCI3 was characterized in respect to its effects on T cell receptor dependent signalling. The results of this work show, that the pyrazolopyrimidine derivate NCI3 is nontoxic and permeates the cell membrane. Upon TCR stimulation NCI3 suppresses T cell proliferation and IL-2 production of primary human TH cells with IC50 values of ~4 µM by blocking the dephosphorylation and subsequent nuclear translocation of NFATc. NCI3 conse-quently inhibits calcineurin dependent NFAT- and NF-κB-, but not AP-1-controlled reporter gene expression, in micromolar concentrations (IC50 values 2 and 7 µM, respectively). In opposite to cyclosporine A and FK506, NCI3 does not interfere with the phosphatase activity of calcineurin but rather disturbs the calcineurin-NFATc interaction. A major endogenous modulator of calcineurin is the protein RCAN1, which is supposed to regulate calcineurin-NFATc signalling in a negative feedback loop. The presented data show that RCAN1 is expressed in human TH cells. The splice variant RCAN1-1 is basally expressed in resting T cells, and its expression levels are not changed by T cell receptor stimulation. Expression of RCAN1-4, on the other hand, is nearly undetectable in resting TH cells and is induced upon cell stimulation. By using calcineurin-NFATc specific inhibitors such as NCI3 it could be shown that RCAN1-4 induction is limited by this pathway. This work provides a comprehensive characterization of the novel inhibitor NCI3 and insights into the regulation of calcineurin by RCAN1 in human TH cells.

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37

Sedighiani, Fazilat. "Tacrolimus vs. Cyclosporin als primäre immunsuppressive Therapie bei akuten rezidivierenden Abstoßungsreaktionen nach Herztransplantation." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-60184.

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38

Marlowe, Sharon Nalini Singh. "Azathioprine and cyclosporin A as second line treatments for severe leprosy type reactions." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424945.

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39

Cheah, Su-Yin. "Methotrexate, cyclosporin and sulfasalazine in the treatment of rheumatoid arthritis : a systematic review." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285683.

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40

Gerlach, Thomas [Verfasser], Markus [Akademischer Betreuer] Neurath, and Benno [Akademischer Betreuer] Weigmann. "Molekulare Analyse des Immunsuppressivums Cyclosporin A / Thomas Gerlach. Gutachter: Markus Neurath ; Benno Weigmann." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2015. http://d-nb.info/1075840473/34.

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41

Fischer, Ricardo Guimaräes. "The ferret in periodontal research clinical features, histology, microbiology and immunosuppression (Cyclosporin-A) /." Malmö : Dept. of Periodontology, Center for Oral Health Sciences, Lund University, 1993. http://catalog.hathitrust.org/api/volumes/oclc/28161627.html.

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42

MITSUYAMA, Hirohito, Fukushi KAMBE, Ryuichiro MURAKAMI, Naoki ISHIGURO, and Hisao SEO. "Analysis of Interieukin-8 Gene Promoter function in Human Osteoblast-like Cells : Regulation by Ca^<2+>-signaling and Cyclosporin A." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2782.

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43

Östraat, Öyvind. "Experimental modulation and suppression of anti-allograft immune response." Malmö : Dept. of Surgery, Lund University, Malmö University Hospital, 1997. http://catalog.hathitrust.org/api/volumes/oclc/38950482.html.

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44

Mangels, Corinna. "Unerwünschte Arzneimittelwirkungen bei der Anwendung von Cyclosporin A (Atopica®) bei Hund und Katze." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-147364.

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45

Hodgkinson, Brent C. "The effect of cyclosporin A (CsA) on antioxidant status in the male Wistar rat." Thesis, University of Ottawa (Canada), 2000. http://hdl.handle.net/10393/9042.

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Antioxidant utilization potentially is an excellent index of oxidative stress. These studies assessed the effects of two doses of CsA (10 mg/kg/day and 20 mg/kg/day for 14 days) on antioxidant status in numerous tissues, and on the function and structure of testis and kidney in male Wistar rats. Animals were placed on either vitamin E sufficient or deficient diets and injected subcutaneously with either CsA or vehicle. Vitamin E levels in various tissues were measured using the very sensitive technique of gas chomatography and mass spectrometry (GC-MS) to determine the effect of CsA on vitamin E status and the protective extent of vitamin E on CsA toxicity. Oxidative damage was also assessed by measuring levels of GSH and protein sulfliydryl (PSH) content using colorimetric methods. In addition, frozen sections of kidney and testes were subjected to standard Hematoxylin and Eosin staining to examine these tissues for structural alterations following CsA treatment. (Abstract shortened by UMI.)

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46

Echtler, Silvia. "Einfluss einer auf Cyclosporin A basierenden immunsuppressiven Therapie auf den Knochenmineralstoffwechsel nach orthotoper Herztransplantation." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-172602.

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Cusack, Rodney Michael. "An investigation of the interaction of metal ions with cyclic octapeptides and cyclosporin A /." [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16238.pdf.

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Passoth, Peter René. "Das Auftreten einer neurodermitisähnlichen Dermatitis bei Kindern nach Herztransplantation im ersten Lebensjahr unter Cyclosporin A." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=965520749.

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Malinowski, Michael. "Systemisches Mycophenolatmofetil versus Cyclosporin A nach perforierender Hochrisiko-Keratoplastik Ergebnisse einer randomisierten, prospektiven klinischen Studie /." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=967644240.

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KAMBE, Fukushi, Hisao SEO, and Xia CAO. "Cyclosporin A (CsA)-sensitive Pathway for the Induction of ZAKI-4 Expression by Thyroid Hormone." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2778.

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