Relevant bibliographies by topics / Cyclosporin

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cyclosporin'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Cyclosporin"

1

Charuk, J. H., P. Y. Wong, and R. A. Reithmeier. "Differential interaction of human renal P-glycoprotein with various metabolites and analogues of cyclosporin A." American Journal of Physiology-Renal Physiology 269, no. 1 (July 1, 1995): F31—F39. http://dx.doi.org/10.1152/ajprenal.1995.269.1.f31.

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Interactions of P-glycoprotein with several analogues and metabolites of cyclosporin A were studied to gain a better understanding of this immunosuppressant's mechanism of excretion and nephrotoxicity. Incorporation of [3H]azidopine into human renal P-glycoprotein in the presence of various concentrations of different cyclosporins was quantitated. Competitive [3H]azidopine photolabeling and 3H drug transport assays of CHRC5 multidrug-resistant cells were also conducted to evaluate effects of cyclosporins on P-glycoprotein function. Cyclosporins A [half-maximal inhibition constant (K0.5) = 20 nM] and G (K0.5 = 40 nM) blocked [3H]azidopine photolabeling of renal P-glycoprotein at very low concentrations, whereas higher concentrations of cyclosporin C (K0.5 = 500 nM) and metabolites 1, 17, and 21 (K0.5 = 200 nM) were required to inhibit photolabeling. Metabolites H and 8 were ineffective in inhibition of [3H]azidopine photolabeling of human renal P-glycoprotein. Similarly, cyclosporins A, C, and G were the best inhibitors of [3H]azidopine photolabeling of P-glycoprotein in multidrug-resistant C5 cells; the various metabolites were less effective. Cyclosporins A, C, and G also enhanced cellular accumulation of [3H]cyclosporin A and several other 3H-labeled compounds known to be transported by P-glycoprotein in multidrug-resistant C5 cells. Differential affinities of cyclosporin A metabolites for P-glycoprotein suggest considerable drug-binding site specificity. Our current hypothesis is that cyclosporin A may be more nephrotoxic than its metabolites by virtue of its superior ability to bind to and competitively inhibit urinary excretion of an endogenous P-glycoprotein substrate. Our findings provide the basis for future design and testing of new cyclosporin derivatives that have immunosuppressive activity yet may be less nephrotoxic because of their poor interaction with renal P-glycoprotein.
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Hušák, Michal, Bohumil Kratochvíl, Martin Buchta, Ladislav Cvak, and Alexandr Jegorov. "Crystal Structure of Cyclosporin E." Collection of Czechoslovak Chemical Communications 63, no. 1 (1998): 115–20. http://dx.doi.org/10.1135/cccc19980115.

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The structure of cyclosporin E was determined by X-ray diffraction methods and compared with the structure of related cyclosporins. In contrast to cyclosporin A, which crystallizes from acetone as tetragonal dihydrate, cyclosporin E acetone solvate monohydrate (C61H109N11O12·C3H6O·H2O) crystallizes under the same conditions in the monoclinic space group P21 with a = 15.698(2) Å, b = 21.333(3) Å, c = 13.224(2) Å, β = 103.74(1)°, Z = 2, and V = 4 302(1) Å3.
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Traber, R., H. Kobel, H. R. Loosli, H. Senn, B. Rosenwirth, and A. Lawen. "[Melle4]Cyclosporin, a Novel Natural Cyclosporin with anti-HIV Activity: Structural Elucidation, Biosynthesis and Biological Properties." Antiviral Chemistry and Chemotherapy 5, no. 5 (October 1994): 331–39. http://dx.doi.org/10.1177/095632029400500507.

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From fermentations of Tolypocladium niveum supplemented with D-threonine, a novel natural cyclosporin, [Melle4]cyclosporin, was isolated. Its structural elucidation is based on amino acid analysis and spectroscopic data; the amino acid sequence was deduced from two-dimensional NMR investigations applied to the iso-derivative of [Melle4]cyclosporin which, in contrast to the natural product, is present as one homogenous conformation in solution. We show that one of the four N-methyl-L-leucine units of cyclosporin A, namely that in position 4, is replaced by N-methyl-L-isoleucine. The putative mechanism by which D-threonine induces in vivo biosynthesis of [Melle4]cyclosporin is discussed. In vitro biosynthesis of [Melle4]cyclosporin was achieved using the previously described enzymatic system [Lawen and Traber (1993) J Biol Chem268: 20452–20465], thereby demonstrating the high affinity of cyclosporin synthetase for isoleucine in position 4. In a long series of cyclosporins obtained by in vitro and in vivo biosynthesis, [Melle4]cyclosporin represents the first example that is devoid of immunosuppressive efficacy while retaining strong binding to cyclophilin. It exerts potent in vitro anti-HIV-1 activity.
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Lawen, A., R. Traber, R. Reuille, and M. Ponelle. "In vitro biosynthesis of ring-extended cyclosporins." Biochemical Journal 300, no. 2 (June 1, 1994): 395–99. http://dx.doi.org/10.1042/bj3000395.

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Cyclosporin synthetase, a multifunctional polypeptide, catalyses the biosynthesis of the set of natural cyclosporins. We report that this enzyme is also capable of introducing a beta-alanine into position 7 or 8 of the ring instead of the alpha-alanines present at these positions in cyclosporin A. This leads to 34-membered rings in contrast to the 33-membered ring of the cyclo-undecapeptide cyclosporin A. Both [beta Ala7]CyA and [beta Ala8]CyA show immunosuppressive activity. The cyclosporin synthetase-related enzyme peptolide SDZ 214-103 synthetase, on the other hand, does not incorporate either beta-alanine into position 7 or beta-hydroxy acids into position 8, confirming the previously described higher substrate specificity of this enzyme compared with cyclosporin synthetase [Lawen and Traber (1993) J. Biol. Chem. 268, 20452-20465].
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Schramm, U., G. Fricker, R. Wenger, and D. S. Miller. "P-glycoprotein-mediated secretion of a fluorescent cyclosporin analogue by teleost renal proximal tubules." American Journal of Physiology-Renal Physiology 268, no. 1 (January 1, 1995): F46—F52. http://dx.doi.org/10.1152/ajprenal.1995.268.1.f46.

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The transport of a fluorescent cyclosporin analogue was measured in killifish (Fundulus heteroclitus) proximal tubules by means of epifluorescence microscopy and digital image analysis. Renal cells rapidly accumulated the cyclosporin analogue from the medium and attained steady state within 60 min; luminal fluorescence increased over the first 60-90 min. At steady state, luminal fluorescence intensity was two to three times higher than cellular. Cellular fluorescence intensity was a linear function of medium substrate concentration and was not affected by any treatment used. In contrast, luminal fluorescence exhibited a saturable component as the medium concentration of the cyclosporin was increased. Secretion into the lumen was blocked by metabolic inhibitors, vanadate, other cyclosporins, such as cyclosporin A and cyclosporin G, and substrates for P-glycoprotein (verapamil, vinblastine, and quinine) but not by substrates for the renal organic anion or organic cation transport systems, such as p-aminohippurate or tetraethylammonium. The data are consistent with the fluorescent cyclosporin analogue entering proximal tubule cells by simple diffusion and then being pumped into the tubular lumen by P-glycoprotein.
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Langman, L., D. LeGatt, and R. Yatscoff. "Cross-reactivities of cyclosporin G (NVa2 cyclosporin) and metabolites in cyclosporine A immunoassays." Clinical Biochemistry 26, no. 2 (April 1993): 122. http://dx.doi.org/10.1016/0009-9120(93)90040-d.

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Kratochvíl, Bohumil, Alexandr Jegorov, Svetlana Pakhomova, Michal Hušák, Petr Bulej, Ladislav Cvak, Petr Sedmera, and Vladimír Havlíček. "Crystal Structures of Cyclosporin Derivatives: O-Acetyl-(4R)-4-(E-2-butyl)-4,N-dimethyl-L-threonyl-cyclosporin A and O-Acetyl-(4R)-4-[E-2-(4-bromobutyl)]-4,N-dimethyl-L-threonyl-cyclosporin A." Collection of Czechoslovak Chemical Communications 64, no. 1 (1999): 89–98. http://dx.doi.org/10.1135/cccc19990089.

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The structures of O-acetyl-(4R)-4-(E-2-butyl)-4,N-dimethyl-L-threonyl-cyclosporin A (1) and O-acetyl-(4R)-4-[E-2-(4-bromobutyl)]-4,N-dimethyl-L-threonyl-cyclosporin A (2) were determined by X-ray diffraction methods and compared with the structure of related cyclosporins. In contrast to expectation, neither the acetylation nor the subsequent bromination of 1 affects the conformation and packing of cyclosporins in the solid state. Both compounds are isomorphous and crystallize in the orthorhombic space group P212121 with a = 12.936(2) Å, b = 15.590(2) Å, c = 36.280(3) Å, and a = 12.916(3) Å, b = 15.675(4) Å, c = 36.715(7) Å, for 1 and 2, respectively.
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Elbakidze, G. M., A. G. Medentsev, and A. G. Elbakidze. "INFLUENCE OF PRODIGIOZAN-DEPENDENT COMUTON ON THE RESISTANCE OF LIVER MITOCHONDRIA AGAINST DAMAGE BY PROTONOFOR." Annals of the Russian academy of medical sciences 69, no. 1-2 (August 20, 2015): 75–79. http://dx.doi.org/10.15690/vramn.v69.i1-2.946.

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An effector of tissue stress of hepatocytes, prodigiozan-dependent comuton (PDC), provokes deenergiezation of liver mitochondria, preloaded by Ca2+ ions. In this case a decrease of membrane potential (MP) and Ca2+ efflux by cyclosporine A sensitive mechanism of megapore is observed. If megapore is blocked by cyclosporin A, protonofor FCCP provoked decrease of MP and Ca2+ efflux by cyclosporin A-insensitive mechanism. It is shown that PDC increases resistance of mitochondria to mentioned protonofor action by inhibition of both these effects. An inhibitory action of PDC is realized by K+ and NADH-dependent mechanism. The effector of hepatocyte tissue stress, prodigiozan-dependent comuton (PDC), evokes deenergizing liver mitochondria preloaded with Ca2+, both membrane potential (MP) decrease and Ca2+ release in according to cyclosporine A- sensitive mechanism of megapore being observed. If megapore is blocked by cyclosporin A, protonophore FCCP reduces of MP and Ca2+ release in according to cyclosporin A-insensitive mechanism. PDC is shown to increase the resistance of mitochondria against protonophore action mentioned above by means of inhibition of both these effects. Inhibitory action of PDC is realized due to both K+ and NADH-dependent mechanism. protective effect takes place only in intact mitochondria of these cells providig (on condition that) its megapore mechanism is not activated. Moreover, the results obttained are evidence of PDC can function as protector due to intensification of energy generation in damaged.
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Kim, J. Y., S. H. Park, K. S. Cho, H. J. Kim, C. K. Lee, K. K. Park, S. H. Choi, and W. Y. Chung. "Mechanism of Azithromycin Treatment on Gingival Overgrowth." Journal of Dental Research 87, no. 11 (November 2008): 1075–79. http://dx.doi.org/10.1177/154405910808701110.

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Azithromycin is effective for the remission of cyclosporine A-induced gingival overgrowth (CIGO) in persons who have undergone renal transplant. To explain its mechanism in alleviating the clinical symptoms of these indivduals, we examined the effect of azithromycin on cell proliferation and collagen turnover modified by cyclosporin A in human gingival fibroblasts from healthy persons and from persons who had undergone renal transplant. Cyclosporin A-induced proliferation of renal transplant fibroblasts and normal fibroblasts was inhibited by azithromycin. Azithromycin elevated the reduced metalloproteinase (MMP)-1 and MMP-2 activities in cyclosporine A-treated renal transplant fibroblasts and normal fibroblasts. In cyclosporine A-treated renal transplant fibroblasts, azithromycin blocked the accumulation of total collagen in culture media and the increase in type I collagen mRNA level, but recovered the reduced MMP-2 mRNA level to the control. These results suggest that azithromycin may improve CIGO by blocking cyclosporine A-induced cell proliferation and collagen synthesis, and by activating MMP-2 in gingival fibroblasts of persons with cyclosporine A-induced gingival overgrowth.
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&NA;. "Cyclosporin see Minoxidil/cyclosporin." Reactions Weekly &NA;, no. 312 (August 1990): 6. http://dx.doi.org/10.2165/00128415-199003120-00024.

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Dissertations / Theses on the topic "Cyclosporin"

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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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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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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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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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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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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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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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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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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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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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Books on the topic "Cyclosporin"

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Thomson, Angus W., ed. Cyclosporin. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8.

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Carton, Angela Shirleen. The ultrastructural effects of Cyclosporin A. on Trichinella Spriralis. Manchester: University of Manchester, 1994.

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Lian, Jeromy. In vitro induction of P-glycoprotein by cyclosporin A. Ottawa: National Library of Canada, 2003.

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Kappos, Ludwig. Immunsuppressive Therapie der multiplen Sklerose mit Cyclosporin A und Azathioprin. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74876-9.

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Green, Colin. Recent progress in organ transplantation. Oxford: Medicine Group for the Medicine Publishing Foundation, 1988.

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Edwards, Brian David. Mechanisms and reduction of cyclosporin toxicity in the normal human kidney. Manchester: University of Manchester, 1994.

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Midha, Rajiv. Comparison of regeneration across rat nerve allografts with temporary or continuous cyclosporin A immunosuppression. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Warner, Ellen. Phase I - II study of vinblastine and oral cyclosporin a in metastatic renal cell carcinoma. Ottawa: National Library of Canada, 1996.

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Wilkie, Martin Erskine. Clinical and laboratory based studies into the effects of calcium antagonists on cyclosporin A nephrotoxicity. Manchester: University of Manchester, 1994.

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Jutta Wehrens. Einfluß der Immunsuppressiva Cyclosporin A und Tacrolimus auf den Gefäßtonus von Nierenarterien der Ratte und des Menschen. Freiburg im Breisgau: Selbstverlag, 2000.

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Book chapters on the topic "Cyclosporin"

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Kay, John E. "Inhibitory effects of cyclosporin A on lymphocyte activation." In Cyclosporin, 1–23. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_1.

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Powles, Anne V., Barbara S. Baker, and Lionel Fry. "Cyclosporin A and skin disease." In Cyclosporin, 191–212. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_10.

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von Graffenried, Beat, David Friend, Nicholas Shand, Wilfried Scheiss, and Pentti Timonen. "Cyclosporin A (Sandimmun®) in autoimmune disorders." In Cyclosporin, 213–51. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_11.

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Grevel, Joachim, and Barry D. Kahan. "Pharmacokinetics of cyclosporin A." In Cyclosporin, 252–66. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_12.

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Burke, M. Danny, Fiona Macintyre, D. Cameron, and Paul H. Whiting. "Cyclosporin A Metabolism and Drug Interactions." In Cyclosporin, 267–302. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_13.

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Whiting, Paul H., and Angus W. Thompson. "Pathological effects of cyclosporin A in experimental models." In Cyclosporin, 303–23. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_14.

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Thiru, Sathia. "Pathological effects of cyclosporin A in clinical practice." In Cyclosporin, 324–64. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_15.

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Hess, Allan D. "Effect of cyclosporin A on the immune response: pivotal role of the interleukin-2/ interleukin-2 receptor autocrine pathway." In Cyclosporin, 24–33. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_2.

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Motta, Iris, and Paolo Truffa-Bachi. "Influence of CsA on humoral immunity and on B lymphocyte activation." In Cyclosporin, 34–49. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_3.

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Thomson, Angus W., and Janet I. Duncan. "The influence of cyclosporin A on T cell activation, cytokine gene expression and cell-mediated immunity." In Cyclosporin, 50–81. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0859-8_4.

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Conference papers on the topic "Cyclosporin"

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Zoja, C., L. Furci, F. Ghilardi, P. Zilio, A. Benigni, and G. Remuzzi. "CYCLOSPORIN A (CyA) INDUCED ENDOTHELIAL CELL INJURY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644123.

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The chronic administration of CyA to animals and humans to prevent graft rejection may induce renal arteriolar damage resembling hemolytic uremic syndrome (HUS). This is a syndrome of vascular damage with thrombotic occlusions of the microcirculation. Endothelial damage is considered the first event in the pathogenetic cascade leading to HUS. We have used bovine aortic endothelial cells in culture to address the issue of CyA-induced arteriolar damage. CyA-induced a time (1-24 hours) and dose (1-50 μM) dependent cell damage. CyA-induced injury was characterized by an early cell detachment followed by lysis as documented by the increase in LDH and Cr release. 1 μM CyA did not induce cell detachment and lysis was evident only after prolonged incubations. 10 and 50 μM CyA both induced marked cell detachment and lysis: lysis started 3 hours after incubation of endothelial cells with CyA and was maximal at the end of 24 hour incubation (LDH release, percent specific increase over control values: 10 μM CyA, 47%; 50 μM CyA, 70%; 51 Cr release, percent specific increase over control values: 10 μM CyA, 28%; 50 μM CyA, 34%). CyA-induced injury was associated with dose- and time-depedent increase in prostacyclin (PGI2) and thromboxane A2 (TxA2) release by endothelial cells exposed to 10 and 50 μM CyA. CyA-induced generation of PGI2 and TxA2 was inhibited when the incubations were carried-on in the presence of acetyl salicilic acid (500 μM). These studies indicate that CyA exerts a direct toxic effect on endothelial cells and might help to understand the pathogenesis of CyA-induced vascular damage.
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Gerards, AH, RB Landewé, AP Prins, GA Bruijn, HS Goei The, and BA Dijkmans. "FRI0031 Cyclosporin-a plus methotrexate combination therapy is as safe as cyclosporin-a alone in patients with early rheumatoid arthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1160.

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Koreeda, Y., K. Kubota, T. Matsuda, T. Taira, S. Noma, and T. Kawabata. "Factors Influencing Cyclosporin Blood Concentration in Interstitial Pneumonia Patients." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4048.

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Han, Weinong, Mei Ming, Tong-Chuan He, and Yu-Ying He. "Abstract 341: Effects of immunosuppressive cyclosporin A on epidermal keratinocytes." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-341.

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Shaw, R. A., Henry H. Mantsch, and Babur Z. Chowdhry. "Solvent and metal ion effects on the conformation of cyclosporin." In Fourier Transform Spectroscopy: Ninth International Conference, edited by John E. Bertie and Hal Wieser. SPIE, 1994. http://dx.doi.org/10.1117/12.166699.

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Schuh, L., and R. Mischke. "Anwendung von Cyclosporin A bei Hunden mit primärer immunvermittelter hämolytischer Anämie." In 27. Jahrestagung der FG „Innere Medizin und klinische Labordiagnostik“ der DVG (InnLab), 2./3. Februar 2019 in München – Teil 2. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679117.

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Boda, Z., J. Hársfalvi, K. Pecze, and K. Rak. "ACQUIRED HAEMOPHILIA DUE TO FACTOR VIII INHIBITOR WITH SEVERE HAEMORRHAGES IN A 46-YEAR-OLD WOMAN SUCCESSFULLY TREATED WITH CYCLOSPORIN A." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644845.

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A formerly healthy 46-year-old woman suffering from acquired haemophilia caused by factor VIII antibodies was admitted in an unconscious state following subarachnoid haemorrhage. Treatment with prothrombin complex concentrates (taken as a whole 100 000 U of PCC, home made and 10 OOOUofFEIBA, Immuno) , steroid (Prednison 50 mg/day) and cyclophosphamide (100 mg/day) was only partially successful: neurological state improved but the haemorrhagic tendency remained. Significant haematuria, and skin and mucosal bleeding characterized her clinical picture. In the meantime, signs of non-A non-B hepatitis were observed. After recovery treatment with Cyclosporin A (Sandimmun, Sandoz) was started (250 mg/day per os) together with small dose of Prednison (15 mg/day). No PCC was applied since that time and the partial thromboplastin times (PTT) became gradually shorter. Level of factor VIII inhibitor was 160 Bethesda unit prior and 9 unit after treatment, the duration of that was 60 days till now. Factor VIII coagulant activity (VIIIC) increased from value of less than 1 percent to 13.7 percent.Treatment of acquired haemophilia caused by factor VIII antibodies, particularly in cases with central nervous system bleeding, may be very difficult. History of our patient may indicate that patients resistent to substitution therapy, steroid and cytostatics may response well to Cyclosporin A. Therefore, its use is recommended.
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Krajnc, I., K. Lukanoviè, and I. Holc. "SAT0101 Analysis of the efficacy of cyclosporin a in 56 psoriatic patients." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.484.

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Cohen, H., I. J. Mackie, R. Patel, G. Neild, and S. J. Machin. "PERSISTENT DECREASED FIBRINOLYTIC ACTIVITY IN CYCLOSPORIN A (CyA) TREATED RENAL ALLOGRAFT RECIPIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644659.

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CyA administration isssociated with histological evidenceof vascular injury. Since vascularendothelial cell components are known to modify fibrinolytic activity, we have examined fibrinolytic changes in renal allograft recipients onCyA and, in addition, markers of vascular endothelial cell damage: plasma vWFRiCof activity and AT-III activity.Parameters of fibrinolytic activity have been assessed serially in 21 renal allograft recipients for 1 year post-transplantation by study of the following: euglobulin clot lysis time (ELT), plasminogen activator activity (PAA) by fibrin plate assay, tissue plasminogen activator (t-PA) by ELISA and fast-acting t-PA inhibitor (t-PAI) by chromogenic assay.From 1 month onwards, fibrinolytic activity (ELTs and fibrin plates) is significantly decreased, p<0.002 and p<0.002 respectively, compared to normal controls, and this decrease persists at oneyear post-transplantation. Mean ELTs (mins) and ranges at 1 and 6 months and 1 year are 363 (120-1740), 598 (135-1610) and 538(80-870) respectively. Mean PAA (% of pooled normal plasma) and ranges at these times are 104 (70-154), 79 (48-118) and 83 (65-108) respectively.In contrast, serial t-PA levels (%of pooled normal plasma) are significantly increased (p<0.02), 428 (86-3686), 297 (81-1130) and 198 ( 44-637 ) at 1 and 6 months and 1 year respectively.These results suggest that the decreased fibrinolytic activity is due to increased levels of t-PA inhibitor, too high to be surpassed by the amount of t-PA released. vWFRiCof activity and AT III activity aresimilarly increased.In conclusion, CyA-treated renal allograft recipients show evidence of chronic vascular endothelial damage and a prothromboticstate.
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Forstner, M., S. Lin, X. Yang, S. Kinting, I. Rothenaigner, K. Schorpp, Y. Li, K. Hadian, and M. Griese. "High-content screen identifies cyclosporin A as a novel ABCA3-specific molecular corrector." In 43. Jahrestagung der Gesellschaft für Pädiatrische Pneumologie. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1754515.

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Reports on the topic "Cyclosporin"

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Drayna, Paul M., Matthew Caldwell, Vasudha Panday, and Charles Reilly. Evaluation of Topical Cyclosporine in Preventing the Development of Corneal Haze after Photorefractive Keratectomy. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada602027.

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Hofmann, Nina, Robert Ambühl, Suzana Jordan, and Oliver Distler. A systematic literature review- Calcineurin inhibitors treatment in systemic sclerosis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0095.

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Review question / Objective: To systematically review treatment effectiveness and adverse events of calcineurin inhibitors (CNIs) such as cyclosporine A (CsA) and tacrolimus in patients with systemic sclerosis (SSc). Condition being studied: Systemic sclerosis. Eligibility criteria: • Publications with SSc patients treated with CNIs and available information on the outcome of CNI therapy on SSc disease manifestation will be analysed.• Article types: case reports, clinical study, clinical trial, controlled clinical trial, historical article, randomized controlled trial.
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