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Artykuły w czasopismach na temat „Cyclosporin”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 21 lutego 2023

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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 n

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2

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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3

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 me

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4

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 eit

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5

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, lumin

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6

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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7

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

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8

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 NAD

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9

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 met

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10

&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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11

&NA;. "Cyclosporin see Azathioprine/cyclosporin." Reactions Weekly &NA;, no. 331 (December 1990): 6. http://dx.doi.org/10.2165/00128415-199003310-00029.

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12

&NA;. "Cyclosporin see Aminoglycosides + cyclosporin." Reactions Weekly &NA;, no. 365 (August 1991): 6. http://dx.doi.org/10.2165/00128415-199103650-00021.

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13

Feliciani, Claudio, Anna Zampetti, Pietro Forleo, Luca Cerritelli, Paolo Amerio, Gianluca Proietto, Antonio Tulli, and Pierluigi Amerio. "Nail Psoriasis: Combined Therapy with Systemic Cyclosporin and Topical Calcipotriol." Journal of Cutaneous Medicine and Surgery 8, no. 2 (March 2004): 122–25. http://dx.doi.org/10.1177/120347540400800208.

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Background: Nail psoriasis is a common problem in psoriatic patients and often it is difficult to cure. Several treatments have been proposed in the last decade using new molecules like vitamin-D analog and/or immunosuppressive drugs both systemically and locally. Objective: Our goal was to evaluate a combination of cyclosporin and topical calcipotriol cream versus cyclosporin alone in a matched group of patients treated with cyclosporin alone. Method: Fifty-four patients affected by severe psoriasis and nail involvement were selected and matched for severity of nail involvement, sex, age, and

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14

Feliciani, C., and A. Tulli. "Topical Cyclosporin in the Treatment of Dermatologic Diseases." International Journal of Immunopathology and Pharmacology 15, no. 2 (May 2002): 89–93. http://dx.doi.org/10.1177/039463200201500203.

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In spite of the drug's toxicity, cyclosporine A (CsA) is largely used in several diseases, including dermatological pathologies, with beneficial results. In dermatology cyclosporin-A reduces the severity of psoriasis symptoms, Bechet's disease, pyoderma gangrenosum, blistering disorders, aftous stomatitis, lichen planus, atopic dermatitis, alopecia and allergic contact dermatitis.

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15

Gelfand, E. W., R. K. Cheung, and G. B. Mills. "The cyclosporins inhibit lymphocyte activation at more than one site." Journal of Immunology 138, no. 4 (February 15, 1987): 1115–20. http://dx.doi.org/10.4049/jimmunol.138.4.1115.

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Abstract Cyclosporin A (CsA), a potent immunosuppressive agent, acts primarily by inhibiting T cell function. Although several potential sites of action have been identified, the mechanisms whereby CsA mediates its immunosuppressive properties have not been fully delineated. We have examined the effects of the immunosuppressive cyclosporins, CsA, dihydrocyclosporin D, and cyclosporin G, and a nonimmunosuppressive analog, cyclosporin H, on early events associated with activation of human T cells. Interleukin 2 (IL 2) receptor expression, as measured by immunofluorescence, was unaffected by CsA.

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16

Kobchikova, Polina P., Sergey V. Efimov, and Vladimir V. Klochkov. "Binding of Different Cyclosporin Variants to Micelles Evidenced by NMR and MD Simulations." Membranes 13, no. 2 (February 5, 2023): 196. http://dx.doi.org/10.3390/membranes13020196.

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Peptides play a critical role in the life of organisms, performing completely different functions. The biological activity of some peptides, such as cyclosporins, can be determined by the degree of membrane permeability. Thus, it becomes important to study how the molecule interacts with lipid bilayers. Cyclosporins C, E, H and L were characterised molecular dynamics simulation; NMR spectroscopy studies were also carried out for cyclosporins C and E. The comparison of one- and two-dimensional spectra revealed certain similarities between spatial structures of the studied cyclosporin variants.

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17

Riks, Inna A. "Cyclosporine use in “dry eye” syndrome." Ophthalmology journal 12, no. 3 (December 16, 2019): 75–82. http://dx.doi.org/10.17816/ov15853.

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This literature review focuses on the need for anti-inflammatory therapy for dry eye disease (DED). Causes of development and mechanisms of pathogenesis of DED are presented. Principles of action of various groups of anti-inflammatory medications, as well as recommendations for cyclosporine use of are described. The results of studies on cyclosporine efficacy are highlighted, principles of cyclosporin prescription in DED are listed.

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18

Frickhofen, Norbert, Hermann Heimpel, Joachim P. Kaltwasser, and Hubert Schrezenmeier. "Antithymocyte globulin with or without cyclosporin A: 11-year follow-up of a randomized trial comparing treatments of aplastic anemia." Blood 101, no. 4 (February 15, 2003): 1236–42. http://dx.doi.org/10.1182/blood-2002-04-1134.

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Immunosuppression with antithymocyte globulin, (methyl)prednisolone, and cyclosporin A is considered the treatment of choice for the patient with aplastic anemia without a donor for standard-risk stem cell transplantation. This consensus is supported by the results of several series, including a randomized German trial. Here we report 11-year results of the latter trial. With stringent response criteria and 4 months as the time to evaluate responses, this analysis confirms the superiority of the cyclosporine regimen regarding the response rate in all patients treated (70% vs 41%, with or witho

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19

Anık, İhsan, M. Konuralp İlbay, Gül İlbay, Murat Yılmaz, Bedrettin Özsoy, Cengiz Erçin, and Savaş Ceylan. "Effects of Topical Cyclosporin A Application on Preventing Epineural Scar Formation in Rats: Experimental Study." Sinir Sistemi Cerrahisi Dergisi 8, no. 3 (December 21, 2022): 104–13. http://dx.doi.org/10.54306/sscd.2022.217.

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The aim of this study is to evaluate macroscopic, histopathologic and immunohistochemical effects of topical cyclosporin administration on prevention of epineural scar formation in rats.This experimental study was performed in two groups, each consisting of ten rats. Sciatic nerve was opened bilaterally. Tibial and peroneal components were set apart with blunt dissection. Abrasion injury was achieved by repetitive rubbing over biceps femoris muscle. In the control group saline sucked cotton peds were administered over opened sciatic nerve region bilaterally, whereas cyclosporin sucked peds wer

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20

&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 694 (March 1998): 8. http://dx.doi.org/10.2165/00128415-199806940-00023.

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21

&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 709 (July 1998): 5–6. http://dx.doi.org/10.2165/00128415-199807090-00016.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 711 (July 1998): 7. http://dx.doi.org/10.2165/00128415-199807110-00022.

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23

&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 714 (August 1998): 7. http://dx.doi.org/10.2165/00128415-199807140-00022.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 714 (August 1998): 8. http://dx.doi.org/10.2165/00128415-199807140-00028.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 715 (August 1998): 7. http://dx.doi.org/10.2165/00128415-199807150-00019.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 727 (November 1998): 7–8. http://dx.doi.org/10.2165/00128415-199807270-00018.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 732 (December 1998): 8. http://dx.doi.org/10.2165/00128415-199807320-00025.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 734 (January 1999): 7. http://dx.doi.org/10.2165/00128415-199907340-00016.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 735 (January 1999): 7. http://dx.doi.org/10.2165/00128415-199907350-00016.

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30

&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 742 (March 1999): 6–7. http://dx.doi.org/10.2165/00128415-199907420-00015.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 751 (May 1999): 7. http://dx.doi.org/10.2165/00128415-199907510-00022.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 752 (May 1999): 8. http://dx.doi.org/10.2165/00128415-199907520-00026.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 753 (May 1999): 8. http://dx.doi.org/10.2165/00128415-199907530-00027.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 757 (June 1999): 8. http://dx.doi.org/10.2165/00128415-199907570-00025.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 760 (July 1999): 7. http://dx.doi.org/10.2165/00128415-199907600-00018.

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&NA;. "Cyclosporin." Inpharma Weekly &NA;, no. 1174 (February 1999): 20. http://dx.doi.org/10.2165/00128413-199911740-00038.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 535 (January 1995): 6. http://dx.doi.org/10.2165/00128415-199505350-00020.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 538 (February 1995): 7. http://dx.doi.org/10.2165/00128415-199505380-00025.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 539 (February 1995): 7. http://dx.doi.org/10.2165/00128415-199505390-00019.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 546 (April 1995): 6. http://dx.doi.org/10.2165/00128415-199505460-00017.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 547 (April 1995): 5. http://dx.doi.org/10.2165/00128415-199505470-00011.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 548 (April 1995): 7. http://dx.doi.org/10.2165/00128415-199505480-00023.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 551 (May 1995): 6. http://dx.doi.org/10.2165/00128415-199505510-00023.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 554 (June 1995): 6. http://dx.doi.org/10.2165/00128415-199505540-00021.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 556 (June 1995): 7. http://dx.doi.org/10.2165/00128415-199505560-00025.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 557 (July 1995): 5. http://dx.doi.org/10.2165/00128415-199505570-00015.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 563 (August 1995): 6. http://dx.doi.org/10.2165/00128415-199505630-00017.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 564 (August 1995): 6. http://dx.doi.org/10.2165/00128415-199505640-00015.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 567 (September 1995): 5. http://dx.doi.org/10.2165/00128415-199505670-00012.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 569 (September 1995): 7. http://dx.doi.org/10.2165/00128415-199505690-00017.

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