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Thematische Bibliographien / FK-506 (Drug) / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „FK-506 (Drug)“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 19. Februar 2022

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1

Shaw, L. M., and K. L. Brayman. "FK-506 therapeutic drug monitoring." Clinical Chemistry 40, no. 12 (December 1, 1994): 2207–8. http://dx.doi.org/10.1093/clinchem/40.12.2207.

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2

Winkler, M., B. Ringe, J. Baumann, M. Loss, K. Wonigeit, and R. Pichlmayr. "Plasma vs whole blood for therapeutic drug monitoring of patients receiving FK 506 for immunosuppression." Clinical Chemistry 40, no. 12 (December 1, 1994): 2247–53. http://dx.doi.org/10.1093/clinchem/40.12.2247.

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Abstract By retrospective analysis of 13,000 blood samples obtained from 248 patients receiving FK 506 therapy, we compared the suitability of plasma with that of whole blood as the matrix for therapeutic drug monitoring of FK 506. The plasma concentrations did not correlate with the concentrations in whole blood (r = 0.56). In contrast to plasma samples (analyzed by enzyme immunoassay), FK 506 was detectable in all whole-blood samples (analyzed by enzyme immunoassay/microparticle enzyme immunoassay). The inter- and intraindividual variations of FK 506 measurements were greater in plasma than

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3

Dumont, F. J., M. J. Staruch, S. L. Koprak, J. J. Siekierka, C. S. Lin, R. Harrison, T. Sewell, V. M. Kindt, T. R. Beattie, and M. Wyvratt. "The immunosuppressive and toxic effects of FK-506 are mechanistically related: pharmacology of a novel antagonist of FK-506 and rapamycin." Journal of Experimental Medicine 176, no. 3 (September 1, 1992): 751–60. http://dx.doi.org/10.1084/jem.176.3.751.

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FK-506 inhibits Ca(2+)-dependent transcription of lymphokine genes in T cells, and thereby acts as a powerful immunosuppressant. However, its potential therapeutic applications may be seriously limited by several side effects, including nephrotoxicity and neurotoxicity. At present, it is unclear whether these immunosuppressive and toxic effects result from interference with related biochemical processes. FK-506 is known to interact with FK-binding protein-12 (FKBP-12), an abundant cytosolic protein with cis-trans peptidyl-prolyl isomerase activity (PPIase) activity. Because rapamycin (RAP) sim

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4

Rokaw, M. D., M. E. West, P. M. Palevsky, and J. P. Johnson. "FK-506 and rapamycin but not cyclosporin inhibit aldosterone-stimulated sodium transport in A6 cells." American Journal of Physiology-Cell Physiology 271, no. 1 (July 1, 1996): C194—C202. http://dx.doi.org/10.1152/ajpcell.1996.271.1.c194.

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The immunosuppressants cyclosporin A (CyA), FK-506, and rapamycin (RAP) have multiple actions on target cells that appear to be mediated by interaction of drug-binding protein complexes. Both FK-506 and CyA, but not RAP, inhibit the Ca2(+)-dependent phosphatase, calcineurin, and in so doing have been found to inhibit Na(+)-K(+)-ATPase activity in various nephron segments. Of interest, FK-506 and RAP, but not CyA, are bound by the steroid receptor-associated FK-506-binding heat shock protein of 56 kDa, HSP56. To determine the physiological effect of this interaction on a steroid-mediated phenom

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5

Di Padova, F. E. "Pharmacology of CsA and FK-506." Perspectives in Drug Discovery and Design 2, no. 1 (August 1994): 49–56. http://dx.doi.org/10.1007/bf02171736.

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6

Goulet, Mark T., Kathleen M. Rupprecht, Peter J. Sinclair, Matthew J. Wyvratt, and William H. Parsons. "The medicinal chemistry of FK-506." Perspectives in Drug Discovery and Design 2, no. 1 (August 1994): 145–62. http://dx.doi.org/10.1007/bf02171741.

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7

Petros, Andrew M., Gerd Gemmecker, Placido Neri, Edward T. Olejniczak, David Nettesheim, Robert X. Xu, Earl G. Gubbins, Harriet Smith, and Stephen W. Fesik. "NMR studies of an FK-506 analog, [U-carbon-13]ascomycin, bound to FK-506-binding protein." Journal of Medicinal Chemistry 35, no. 13 (June 1992): 2467–73. http://dx.doi.org/10.1021/jm00091a015.

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8

Kay, John E., Senam E. A. Doe, and C. Robin Benzie. "The mechanism of action of the immunosuppressive drug FK-506." Cellular Immunology 124, no. 1 (November 1989): 175–81. http://dx.doi.org/10.1016/0008-8749(89)90121-4.

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9

O'connor, Stephen P., Robert L. Ellsworth, Mary Nallin Omstead, Rosalind G. Jenkins, and Louis Kaplan. "The preparation of 14C-labeled FK-506." Journal of Labelled Compounds and Radiopharmaceuticals 31, no. 2 (February 1992): 103–8. http://dx.doi.org/10.1002/jlcr.2580310205.

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10

Jusko, William J. "Analysis of Tacrolimus (FK 506) in Relation to Therapeutic Drug Monitoring." Therapeutic Drug Monitoring 17, no. 6 (December 1995): 596–601. http://dx.doi.org/10.1097/00007691-199512000-00009.

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11

Clardy, Jon. "Structural studies on FK-506, cyclosporin A and their immunophilin complexes." Perspectives in Drug Discovery and Design 2, no. 1 (August 1994): 127–44. http://dx.doi.org/10.1007/bf02171740.

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12

DOE, SENAM E. A., C. ROBIN BENZIE, and JOHN E. KAY. "Early effects of the immunosuppressive drug FK-506 on signal transduction in lymphocytes." Biochemical Society Transactions 18, no. 3 (June 1, 1990): 451–52. http://dx.doi.org/10.1042/bst0180451.

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13

Takabayashi, Katsuhiko, Takao Koike, Kazuhiro Kurasawa, Ryutaro Matsumura, Toshiko Sato, Hisao Tomioka, Isao Ito, Takashi Yoshiki, and Sho Yoshida. "Effect of FK-506, a novel immunosuppressive drug on murine systemic lupus erythematosus." Clinical Immunology and Immunopathology 51, no. 1 (April 1989): 110–17. http://dx.doi.org/10.1016/0090-1229(89)90211-0.

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14

Patel, S. S., M. S. Patel, S. Salampure, B. Vishwanath, and N. M. Patel. "Development and Evaluation of Liposomes for Topical Delivery of Tacrolimus (Fk-506)." Journal of Scientific Research 2, no. 3 (August 24, 2010): 585. http://dx.doi.org/10.3329/jsr.v2i3.3258.

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In the present work Tacrolimus loaded liposomal systems were developed and evaluated for their topical delivery. Neutral multilamellar liposomes (MLVs) were prepared by thin film hydration method. The amount of drug loaded into vesicles ranged from 4.4 mg per 115mg to 8.2mg per 140mg of total lipid. Entrapment efficiency of tacrolimus in liposomes was studied by altering the amount of cholesterol ratio to lipid ratio. After performing stability study at different temperatures (4, 25, and 37°C) was affirms that drug leakage increased at higher temperature. The in-vitro permeation study shows si

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Shitrit, David, Jacob E. Ollech, Ayelet Ollech, Ilana Bakal, Milton Saute, Gideon Sahar, and Mordechai R. Kramer. "Itraconazole Prophylaxis in Lung Transplant Recipients Receiving Tacrolimus (FK 506): Efficacy and Drug Interaction." Journal of Heart and Lung Transplantation 24, no. 12 (December 2005): 2148–52. http://dx.doi.org/10.1016/j.healun.2005.05.003.

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Acemoglu, Murat, Hendrik Andres, and Thomas Moenius. "Regio- and stereoselective preparation of ascomycin-d1 and FK 506-d1." Journal of Labelled Compounds and Radiopharmaceuticals 45, no. 5 (2002): 361–70. http://dx.doi.org/10.1002/jlcr.558.

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17

Kramer, Mordechai R., Anat Amital, Leonardo Fuks, and David Shitrit. "Voriconazole and itraconazole in lung transplant recipients receiving tacrolimus (FK 506): efficacy and drug interaction." Clinical Transplantation 25, no. 2 (December 16, 2010): E163—E167. http://dx.doi.org/10.1111/j.1399-0012.2010.01373.x.

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18

O'Keefe, Stephen J., and Edward A. O'Neill. "Cyclosporin A and FK-506: Immunosuppression, inhibition of transcription and the role of calcineurin." Perspectives in Drug Discovery and Design 2, no. 1 (August 1994): 85–102. http://dx.doi.org/10.1007/bf02171738.

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19

White, James D., Jörg Deerberg, Steven G. Toske, and Takayuki Yakura. "Application of stereocontrolled aldol coupling to synthesis of segments of immunosuppressants FK-506 and rapamycin." Tetrahedron 65, no. 33 (August 2009): 6635–41. http://dx.doi.org/10.1016/j.tet.2009.06.030.

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20

Oyouni, AtifAbdulwahab A., Shalini Saggu, Ehab Tousson, Anand Mohan, and Abdullah Farasani. "Mitochondrial nephrotoxicity induced by tacrolimus (FK-506) and modulatory effects of Bacopa monnieri (Farafakh) of Tabuk Region." Pharmacognosy Research 11, no. 1 (2019): 20. http://dx.doi.org/10.4103/pr.pr_100_18.

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21

Schnider, Jonas T., Matthias Weinstock, Jan A. Plock, Mario G. Solari, Raman Venkataramanan, Xin Xiao Zheng, and Vijay S. Gorantla. "Site-Specific Immunosuppression in Vascularized Composite Allotransplantation: Prospects and Potential." Clinical and Developmental Immunology 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/495212.

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Skin is the most immunogenic component of a vascularized composite allograft (VCA) and is the primary trigger and target of rejection. The skin is directly accessible for visual monitoring of acute rejection (AR) and for directed biopsy, timely therapeutic intervention, and management of AR. Logically, antirejection drugs, biologics, or other agents delivered locally to the VCA may reduce the need for systemic immunosuppression with its adverse effects. Topical FK 506 (tacrolimus) and steroids have been used in clinical VCA as an adjunct to systemic therapy with unclear beneficial effects. How

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Kay, John E., and C. Robin Benzie. "T lymphocyte activation through the C28 pathway is insensitive to inhibition by the immunosuppressive drug FK-506." Immunology Letters 23, no. 2 (December 1989): 155–59. http://dx.doi.org/10.1016/0165-2478(89)90129-6.

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23

Shevchenko, V. P., I. Yu Nagaev, N. F. Myasoedov, H. Andres, T. Moenius, and A. Susan. "Synthesis of tritiated Cyclosporin A and FK-506 by metal-catalyzed hydrogen isotope exchange." Journal of Labelled Compounds and Radiopharmaceuticals 47, no. 7 (June 2004): 407–14. http://dx.doi.org/10.1002/jlcr.827.

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24

Chung, Shu-Ying, Fu-Chou Cheng, Ming-Shih Lee, Jing-Ying Lin, Ming-Cheng Lin, and Ming-Fu Wang. "Ginkgo biloba Leaf Extract (EGb761) Combined with Neuroprotective Agents Reduces the Infarct Volumes of Gerbil Ischemic Brain." American Journal of Chinese Medicine 34, no. 05 (January 2006): 803–17. http://dx.doi.org/10.1142/s0192415x06004302.

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Ginkgo biloba exerts many pharmacological actions. It possesses antioxidant properties, the ability of neurotransmitter/receptor modulation and antiplatelet activation factor. This research is designed to investigate the neuroprotective effects of long-term treatment with EGb761 (a standard form of the extract of Ginkgo biloba leaf) in combination with MgSO 4, FK506, or MK-801 on the infarct volume of male gerbils' brain induced by unilateral middle cerebral artery occlusion (MCAO). Thirty-five gerbils fed a standard diet were intragastrically given water or EGb761 (100 mg/kg/day) for one week

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Wong, S. H. Y., B. Ghodgaonkar, P. Fong, B. Campbell, J. F. Burdick, and F. Boctor. "Supercritical Fluid Chromatography for Therapeutic Drug Monitoring of Immunosuppressants: Selectivity for Cyclosporine A, Fk 506 (Tacrolimus), and Rapamycin." Journal of Liquid Chromatography 17, no. 10 (June 1994): 2093–109. http://dx.doi.org/10.1080/10826079408013534.

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26

Lhoest, G., N. Maton, A. Laurent, and R. K. Verbeeck. "Isolation and identification of a FK-506 C36–C37 dihydrodiol from erythromycin-induced rabbit liver microsomes." Journal of Pharmaceutical and Biomedical Analysis 12, no. 2 (February 1994): 235–41. http://dx.doi.org/10.1016/0731-7085(94)90034-5.

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27

Yu, JS, S. Lee, HJ Eom, HR Kang, SR Lee, TK Lee, J. Baek, et al. "Protective effect of Korean red ginseng against FK-506-induced damage in LLC-PK1 cells." Planta Medica 81, S 01 (December 14, 2016): S1—S381. http://dx.doi.org/10.1055/s-0036-1596887.

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28

Cryan, John, Shirley H. Y. Hung, Gregory Wiederrecht, Nolan H. Sigal, and John J. Siekierka. "FKBP, the binding protein for the immunosuppressive drug, FK-506, is not an inhibitor of protein kinase C activity." Biochemical and Biophysical Research Communications 180, no. 2 (October 1991): 846–52. http://dx.doi.org/10.1016/s0006-291x(05)81142-8.

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29

Petros, A. M., R. T. Gampe, G. Gemmecker, P. Neri, T. F. Holzman, R. Edalji, J. Hochlowski, M. Jackson, and J. McAlpine. "NMR studies of an FK-506 analog [U-13C]ascomycin, bound to FKBP: conformation and regions of ascomycin involved in binding." Journal of Medicinal Chemistry 34, no. 9 (September 1991): 2925–28. http://dx.doi.org/10.1021/jm00113a037.

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Banholzer, R., A. P. Nair, H. H. Hirsch, X. F. Ming, and C. Moroni. "Rapamycin destabilizes interleukin-3 mRNA in autocrine tumor cells by a mechanism requiring an intact 3' untranslated region." Molecular and Cellular Biology 17, no. 6 (June 1997): 3254–60. http://dx.doi.org/10.1128/mcb.17.6.3254.

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We analyzed the effect of rapamycin on autocrine mast cell tumor lines with abnormally stable interleukin-3 (IL-3) transcripts due to a defect in mRNA degradation. Rapamycin inhibited IL-3 mRNA expression specifically, while transcripts of IL-4 and IL-6 were not affected. As indicated by the use of the transcriptional inhibitor actinomycin D or by reporter constructs, inhibition was posttranscriptional and resulted from destabilization of the mRNA. Transcripts from transgenes lacking the AU-rich 3' untranslated region were refractory to drug-induced degradation, suggesting that these 3' sequen

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Bansal, Puneet, and Anil Kumar. "P1-194: Novel drug strategies and molecular mechanisms of lycopene, FK-506 and venlafaxine against 3-NP induced Huntington's-like symptoms in rats." Alzheimer's & Dementia 8, no. 4S_Part_5 (July 2012): P174—P175. http://dx.doi.org/10.1016/j.jalz.2012.05.472.

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Tran, Quang Hieu Dé, Elizabeth Guay, Suzanne Chartier, and Jacqueline Tousignant. "Tacrolimus in Dermatology." Journal of Cutaneous Medicine and Surgery 5, no. 4 (July 2001): 329–35. http://dx.doi.org/10.1177/120347540100500409.

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Background: Tacrolimus (FK 506), a metabolite of the fungus Streptomyces tsukubaensis, is an anti-T-cell drug. It acts by inhibiting the production of IL-2, IL-3, IL-4, TNFα, and GM-CSF. More potent and with slightly less secondary effects than cyclosporine, it has been the object of considerable interest, especially in conditions that could benefit from the latter. Objective: In psoriasis, a placebo-controlled double-blind study has shown oral tacrolimus at 0.1 mg/kg/day to be effective in controlling recalcitrant lesions. In human, small studies have reported tacrolimus ointment to be effect

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Furue, Masutaka, Atsushi Osada, and Kunihiko Tamaki. "Inhibition of contact hypersensitivity by an anti-allergic drug, azelastine, is likely to be mediated by its novel immunosuppressive effects distinct from FK-506." Journal of Dermatological Science 6, no. 1 (August 1993): 75. http://dx.doi.org/10.1016/0923-1811(93)91148-n.

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WOO, J., C. S. K. ROSS, J. I. MILTON, and A. W. THOMSON. "Immunosuppressive activity of FK-506 in rats: flow cytometric analysis of lymphocyte populations in blood, spleen and thymus during treatment and following drug withdrawal." Clinical & Experimental Immunology 79, no. 1 (June 28, 2008): 109–14. http://dx.doi.org/10.1111/j.1365-2249.1990.tb05136.x.

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35

Vannucchi, AM, A. Grossi, A. Bosi, D. Rafanelli, M. Statello, S. Guidi, R. Saccardi, and P. Rossi-Ferrini. "Effects of cyclosporin A on erythropoietin production by the human Hep3B hepatoma cell line." Blood 82, no. 3 (August 1, 1993): 978–84. http://dx.doi.org/10.1182/blood.v82.3.978.978.

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Abstract There is evidence that the inadequate erythropoietin (Epo) production observed in patients undergoing allogeneic bone marrow transplantation (BMT) might be ascribed to an inhibitory effect caused by the immunosuppressive drug cyclosporin A (CsA). In this in vitro study, we have evaluated the effects of CsA on the release of Epo in the culture medium by the human Hep3B hepatoma cell line. In cultures incubated with both CsA and the nonimmunosuppressive CsA analog MeAla-6, but not with the CsA-unrelated immunosuppressive agent FK-506, the levels of Epo in the medium were significantly r

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Vannucchi, AM, A. Grossi, A. Bosi, D. Rafanelli, M. Statello, S. Guidi, R. Saccardi, and P. Rossi-Ferrini. "Effects of cyclosporin A on erythropoietin production by the human Hep3B hepatoma cell line." Blood 82, no. 3 (August 1, 1993): 978–84. http://dx.doi.org/10.1182/blood.v82.3.978.bloodjournal823978.

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There is evidence that the inadequate erythropoietin (Epo) production observed in patients undergoing allogeneic bone marrow transplantation (BMT) might be ascribed to an inhibitory effect caused by the immunosuppressive drug cyclosporin A (CsA). In this in vitro study, we have evaluated the effects of CsA on the release of Epo in the culture medium by the human Hep3B hepatoma cell line. In cultures incubated with both CsA and the nonimmunosuppressive CsA analog MeAla-6, but not with the CsA-unrelated immunosuppressive agent FK-506, the levels of Epo in the medium were significantly reduced in

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KASS, LEONARD, DORETTE Z. ELLIS, JANICE PELLETIER, NATHAN E. TABLEMAN, and SAMUEL C. EDWARDS. "Inhibition of the calcineurin-like protein phosphatase activity in Limulus ventral eye photoreceptor cells alters the characteristics of the spontaneous quantal bumps and the light-mediated inward currents, and enhances arrestin phosphorylation." Visual Neuroscience 15, no. 6 (November 1998): 1039–49. http://dx.doi.org/10.1017/s0952523898156031.

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Changes in intracellular calcium are involved in phototransduction processes in both vertebrate and invertebrate photoreceptors. During this phototransduction process in the Limulus ventral eye, there is a biochemical change in the protein phosphatase, calcineurin, such that it becomes capable of activation by calcium and calmodulin. Here we show that the calcium/calmodulin-dependent calcineurin-like activity in light-adapted ventral eye was completely inhibited by the CaN autoinhibitory peptide, CaN A457–482 and the Merck analog of the membrane-permeable, immunosuppressant drug, FK 506, L-683

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Lopatynska-Mazurek, Malgorzata, Lukasz Komsta, Ewa Gibula-Tarlowska, and Jolanta H. Kotlinska. "Aversive Learning Deficits and Depressive-Like Behaviors Are Accompanied by an Increase in Oxidative Stress in a Rat Model of Fetal Alcohol Spectrum Disorders: The Protective Effect of Rapamycin." International Journal of Molecular Sciences 22, no. 13 (June 30, 2021): 7083. http://dx.doi.org/10.3390/ijms22137083.

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Fetal alcohol spectrum disorders (FASDs) are one of the most common consequences of ethanol exposure during pregnancy. In adulthood, these disorders can be manifested by learning and memory deficits and depressive-like behavior. Ethanol-induced oxidative stress may be one of the factors that induces FASD development. The mammalian target of the Rapamycin (mTOR) signaling pathway that acts via two distinct multiprotein complexes, mTORC1 and mTORC2, can affect oxidative stress. We investigated whether mTOR-dependent or mTOR-independent mechanisms are engaged in this phenomenon. Thus, Rapamycin—a

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Lemster, B., L. L. Huang, W. Irish, J. Woo, P. B. Carroll, K. Abu-Elmagd, H. R. Rilo, et al. "Influence of FK 506 (Tacrolimus) On Circulating CD4+T Cells Expressing Cd25 and Cd45ra Antigens in 19 Patients with Chronic Progressive Multiple Sclerosis Participating in an Open Label Drug Safety Trial." Autoimmunity 19, no. 2 (January 1994): 89–98. http://dx.doi.org/10.3109/08916939409009536.

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Chow, Kai Uwe, Daniel Nowak, Soo-Zin Kim, Bernd Schneider, Martina Komor, Simone Boehrer, Paris S. Mitrou, Dieter Hoelzer, Eckhart Weidmann, and Wolf-Karsten Hofmann. "In Vivo Drug-Response in Patients with Leukemic Non-Hodgkin’s Lymphomas Is Predicted by In Vitro Chemosensitivity Testing and Gene Expression Profiling." Blood 104, no. 11 (November 16, 2004): 2273. http://dx.doi.org/10.1182/blood.v104.11.2273.2273.

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Abstract Only a few approaches are available to address the mechanisms of cell death in vivo which are induced by anticancer treatment in patients with malignancies. In this study in vitro chemosensitivity testing of primary peripheral blood leukemic cells of five patients suffering from different leukemic Non-Hodgkin’s lymphomas (atypical CLL, typical CLL, Immunocytoma, Mantle Cell Lymphoma, Prolymphocytic Leukemia (PLL)) was combined with the analysis of the in vivo rate of apoptosis by flow-cytometry (Annexin V and depolarisation of mitochondrial membrane potential (MMP) by JC-1). Furthermo

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Yue, Gang, Robert S. Edinger, Hui-Fang Bao, John P. Johnson, and Douglas C. Eaton. "The effect of rapamycin on single ENaC channel activity and phosphorylation in A6 cells." American Journal of Physiology-Cell Physiology 279, no. 1 (July 1, 2000): C81—C88. http://dx.doi.org/10.1152/ajpcell.2000.279.1.c81.

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Rapamycin and FK-506 are immunosuppressive drugs that bind a ubiquitous immunophilin, FKBP12, but immunosuppressive mechanisms and side effects appear to be different. Rapamycin binds renal FKBP12 to change renal transport. We used cell-attached patch clamp to examine rapamycin's effect on Na+ channels in A6 cells. Channel NP o was 0.5 ± 0.08 ( n = 6) during the first 5 min but fell close to zero after 20 min. Application of 1 μM rapamycin reactivated Na+ channels ( NP o = 0.47 ± 0.1; n=6), but 1 μM FK-506 did not. Also, GF-109203X, a protein kinase C (PKC) inhibitor, mimicked the rapamycin-in

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Edinger, Robert S., Simon C. Watkins, David Pearce, and John P. Johnson. "Effect of immunosuppressive agents on glucocorticoid receptor function in A6 cells." American Journal of Physiology-Renal Physiology 283, no. 2 (August 1, 2002): F254—F261. http://dx.doi.org/10.1152/ajprenal.00337.2001.

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Immunosuppressive agents such as FK-506 and rapamycin inhibit aldosterone- stimulated Na+ transport in A6 cells. Concentration dependence is consistent with the known affinities of these agents for immunophilins. The inhibition was also dependent on time, requiring preincubation with FK-506 or rapamycin before inhibition was seen. The present studies were designed to determine whether this inhibition was pretranscriptional and whether it was due to an effect on either receptor translocation or nuclear accumulation. Because transport effects of steroids in A6 cells are mediated by glucocorticoi

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Tumlin, J. A., J. T. Someren, C. E. Swanson, and J. P. Lea. "Expression of calcineurin activity and alpha-subunit isoforms in specific segments of the rat nephron." American Journal of Physiology-Renal Physiology 269, no. 4 (October 1, 1995): F558—F563. http://dx.doi.org/10.1152/ajprenal.1995.269.4.f558.

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Calcineurin activity and alpha-subunit expression were studied in microdissected proximal tubules (S2), medullary thick ascending limbs (MTAL), cortical collecting ducts (CCD), connecting tubules (CNT), and outer medullary collecting ducts (OMCD). We have shown that cyclosporin A (CsA) and FK-506 inhibit sodium-potassium-adenosinetriphosphatase (Na-K-ATPase) activity in CCD, OMCD, and MTAL but did not uncover the mechanism for resistance of proximal tubule segments to these drugs. Because cells expressing high calcineurin activity are relatively resistant to the biological effects of CsA and F

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Dušková, M., L. Dušek, M. Čìž, A. Lojek, and H. Slavíková. "The Influence of Some Immunosuppressive Drugs on the Metabolic Activity of Human Phagocytes and Lymphocytes in vitro." International Journal of Immunopathology and Pharmacology 11, no. 3 (September 1998): 155–62. http://dx.doi.org/10.1177/039463209801100305.

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The effect of azathioprine, cyclosporine A and FK 506 on the production of reactive oxygen species by polymorphonuclear leukocytes (Iuminol-dependent chemiluminescence) and on the blast transformation of lymphocytes ([3H]thymidine incorporation) was studied in dose-response experiments under in vitro conditions. Although there were no significant effects of immunosuppressives on non-stimulated blast transformation, FK 506 and cyclosporine A significantly inhibited the blast transformation stimulated by concanavaline A and protein A and the effects made it possible to build 2nd-order polynomial

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Hodge, Shekema, Juliette de Rosayro, Amanda Glenn, Ifeoma C. Ojukwu, Stephen Dewhurst, Harold M. McClure, Norbert Bischofberger, Daniel C. Anderson, Sherry A. Klumpp, and Francis J. Novembre. "Postinoculation PMPA Treatment, but Not Preinoculation Immunomodulatory Therapy, Protects against Development of Acute Disease Induced by the Unique Simian Immunodeficiency Virus SIVsmmPBj." Journal of Virology 73, no. 10 (October 1, 1999): 8630–39. http://dx.doi.org/10.1128/jvi.73.10.8630-8639.1999.

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ABSTRACT The fatal disease induced by SIVsmmPBj4 clinically resembles endotoxic shock, with the development of severe gastrointestinal disease. While the exact mechanism of disease induction has not been fully elucidated, aspects of virus biology suggest that immune activation contributes to pathogenesis. These biological characteristics include induction of peripheral blood mononuclear cell (PBMC) proliferation, upregulation of activation markers and Fas ligand expression, and increased levels of apoptosis. To investigate the role of immune activation and viral replication on disease inductio

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Siekierka, John J. "Probing T-cell signal transduction pathways with the immunosuppressive drugs, FK-506 and rapamycin." Immunologic Research 13, no. 2-3 (June 1994): 110–16. http://dx.doi.org/10.1007/bf02918272.

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Poolos, Nicholas P. "Hypoxia Results in GABAergic Channelopathy." Epilepsy Currents 5, no. 6 (November 2005): 234–35. http://dx.doi.org/10.1111/j.1535-7511.2005.00073.x.

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AMPA/Kainate Receptor–mediated Downregulation of GABAergic Synaptic Transmission by Calcineurin after Seizures in the Developing Rat Brain Sanchez RM, Dai W, Levada RE, Lippman JJ, Jensen FE J Neurosci 2005;25:3442–3451 Hypoxia is the most common cause of perinatal seizures and can be refractory to conventional anticonvulsant drugs, suggesting an age-specific form of epileptogenesis. A model of hypoxia-induced seizures in immature rats reveals that seizures result in immediate activation of the phosphatase calcineurin (CaN) in area CA1 of hippocampus. After seizures, CA1 pyramidal neurons exhi

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Esteves, Iracema, Juliana F. Fernandes, Andreza Feitosa Ribeiro, Fabio P. S. Santos, Ricardo Helman, Claudio Castro Junior, Vinicius R. P. Mattos, et al. "The Clinical and Therapeutic Drug Monitoring of Oral and Intravenous Busulfan in Patients with Acute Leukemia That Underwent to Stem Cell Transplantation with a Test Dose of Busulfan." Blood 124, no. 21 (December 6, 2014): 5841. http://dx.doi.org/10.1182/blood.v124.21.5841.5841.

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Abstract Introduction: Busulfan (Bu) is used in the conditioning regimen for hematopoietic stem cell transplantation (HSCT). Therapeutic drug monitoring (TDM) of Bu with subsequents adjustments doses based on a “target” therapeutic concentration may reduce toxicity after HSCT. Objectives: To evaluatethe impact of TDM of Bu and clinical outcomes in patients with acute leukemia that underwent to allogeneic matched related donor (MRD) and allogeneic matched unrelated donor (MUD) HSCT. Patients and methods: From January 2009 to January 2014, we prospectively analyzed 42 patients with diagnosis of

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Li, Dailin, Sam Xian Jun Cheng, Gilberto Fisone, Michael J. Caplan, Yoshiyuki Ohtomo, and Anita Aperia. "Effects of okadaic acid, calyculin A, and PDBu on state of phosphorylation of rat renal Na+-K+-ATPase." American Journal of Physiology-Renal Physiology 275, no. 6 (December 1, 1998): F863—F869. http://dx.doi.org/10.1152/ajprenal.1998.275.6.f863.

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Several indirect lines of evidence suggest that protein kinases and phosphatases modulate the activity of renal Na+-K+-ATPase. The aim of this study was to examine whether such regulation may occur via modulation of the state of phosphorylation of Na+-K+-ATPase. Slices from rat renal cortex were prelabeled with [32P]orthophosphate and incubated with the inhibitors of protein phosphatase (PP)-1 and PP-2A, okadaic acid (OA) and calyculin A (CL-A), respectively, the protein kinase C (PKC) activator, phorbol 12,13-dibutyrate (PDBu), or the PP-2B inhibitor, FK-506. Phosphorylation of Na+-K+-ATPase

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Karpas, A., M. Lowdell, S. K. Jacobson, and F. Hill. "Inhibition of human immunodeficiency virus and growth of infected T cells by the immunosuppressive drugs cyclosporin A and FK 506." Proceedings of the National Academy of Sciences 89, no. 17 (September 1, 1992): 8351–55. http://dx.doi.org/10.1073/pnas.89.17.8351.

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