ライフサイエンスコーパス: cyclosporin

1 9, Timothy syndrome) or domain IV (Ser-1517, cyclosporin).

2 dark agouti rats on subtherapeutic doses of cyclosporin.

3 able in cardiac transplant recipients taking cyclosporin.

4 e in cardiac transplant recipients receiving cyclosporin.

5 ers also distinguish these isomeric forms of cyclosporin.

6 ctor of activated T-cells (NF-AT) inhibitor, cyclosporin.

7 activation pathways may not be sensitive to cyclosporin.

8 PP2B utilized by the immunosuppressive drug cyclosporin.

9 lecular hydrogen bonding between each of the cyclosporins.

10 ges on the effective preorganization of seco-cyclosporins.

11 NS2 modulates sensitivity of HCV to cyclosporines.

12 y) in vivo, but not in rats pre-treated with cyclosporin A (20 mg/kg/day subcutaneously) for 3 days (

13 prevented by the calcineurin/NFAT inhibitor, cyclosporin A (25 mg/kg/day s.c.).

14 verolimus (3.5 versus 4.5 ug/L, P<0.001) and cyclosporin A (47.4 versus 64.1 ug/L, P<0.001).

15 ochondrial permeability transition pore with cyclosporin A (5 microM) had no significant effect on th

16 uced permeability increase was suppressed by cyclosporin A (60%) and 1,3-dicyclohexylcarbodiimide (90

17 latonin (a non-specific antioxidant), and by cyclosporin A (a permeability transition pore blocker).

18 utylated hydroxyanisol and the MMP inhibitor cyclosporin A (Cs A) blocked apoptosis induced by MX3350

19 Treatment with AR-C117977 or cyclosporin A (CsA) administered at a dose of 30 mg/kg s

20 olyl cis-trans isomerase (PPIase) inhibitors cyclosporin A (CsA) and a derivative of cyclosporin A wi

21 Calcineurin inhibitor cyclosporin A (CsA) and calcineurin-siRNA increase beta4

22 and necrotic cell death that were blocked by cyclosporin A (CsA) and EGTA.

23 Cyclosporin A (CsA) and tacrolimus (FK506) are valuable

24 Cyclosporin A (CsA) and tacrolimus (FK506) has been repo

25 ors of activated T cell (NFAT) activation by cyclosporin A (CsA) and VIVIT suppressed PDGF-BB-induced

26 Calcineurin inhibitors such as cyclosporin A (CsA) are the mainstay of immunosuppressiv

27 the presence of ligand is demonstrated using cyclosporin A (CsA) as a test ligand.

28 Cyclosporin A (CsA) has been used widely to prevent reje

29 pectrometry (MS/MS) for the determination of cyclosporin A (CsA) in biological fluids in support of i

30 Although the clinical efficacy of cyclosporin A (CSA) in retinoblastoma (RB) has been attr

31 Cyclosporin A (CSA) is commonly used to prevent graft-ve

32 Cyclosporin A (CsA) is known to preserve cardiac contrac

33 The therapeutic use of cyclosporin A (CsA) is limited by nephrotoxicity that is

34 It has been proposed that cyclosporin A (CsA) may induce epithelial-to-mesenchymal

35 Hence, the authors hypothesize that cyclosporin A (CsA) may regulate TGM-2 via ROS, and this

36 myocardium, hearts were perfused with either cyclosporin A (CsA) or 4-chlorodiazepam (4-Cl-DZP) to in

37 on of calcineurin activity by treatment with cyclosporin A (CsA) or FK506 is a cornerstone of immunos

38 Current immunosuppressive strategies use cyclosporin A (CsA) or FK506 to inhibit calcineurin, whi

39 function in 170 liver transplant patients on cyclosporin A (CsA) or tacrolimus (Tac).

40 side effects of long-term corticosteroid or cyclosporin A (CsA) therapy complicate the treatment of

41 Although NC1153 acted synergistically with cyclosporin A (CsA) to prolong allograft survival, it wa

42 It has been observed that cyclosporin A (CsA) treatment, particularly in transplan

43 effects of the prototypic immunosuppressant cyclosporin A (CsA) were investigated.

44 udy, ultrafine amorphous particles (UAPs) of cyclosporin A (CsA) were prepared with synthesized ACQ d

45 n eliminated the HIV-1 stimulatory effect of cyclosporin A (CsA), a competitive inhibitor of the CypA

46 pretreatment with the calcineurin inhibitor cyclosporin A (CsA), an antagonist of NFAT signaling, de

47 Treatment of kidney rudiments with Cyclosporin A (CSA), an inhibitor of Calcium/NFAT signal

48 Here, we show that cyclosporin A (CsA), an inhibitor of MPT, protects the m

49 ructures with that of an Rgg in complex with cyclosporin A (CsA), an inhibitor of SHP-induced Rgg act

50 s was caspase dependent, and a blockade with cyclosporin A (CsA), an inhibitor of the mitochondrial p

51 lect immunophilin ligands [FK506, rapamycin, cyclosporin A (CsA), and cyclosporin H (CsH)], which are

52 ected cells with the immunosuppressive agent cyclosporin A (CsA), HIV-1 infection also is inhibited.

53 concentrations, such as tacrolimus (TaC) and cyclosporin A (CsA), is important in the outpatient foll

54 Cyclosporin A (CSA), methylprednisolone (MP), methotrexa

55 common side-effect of the administration of cyclosporin A (CSA), phenytoin, and calcium blockers.

56 actor of activated T cells (NFAT) inhibitor, cyclosporin A (CsA), suggesting that NFAT controls BCATc

57 Cyclosporin A (CsA), tacrolimus (Tac), rapamycin (Rap),

58 Pretreatment with topical cyclosporin A (CsA), verapamil, or XR9576, modulators of

59 Mouse embryos exposed to cyclosporin A (CsA), which inhibits calcineurin phosphat

60 TGM-2 and oxidative stress markers (OSMs) in cyclosporin A (CsA)-induced gingival overgrowth (GO).

61 dothelial growth factor (VEGF) expression in cyclosporin A (CsA)-induced rat overgrown gingival tissu

62 an antigen-independent, NF-kappaB-dependent, cyclosporin A (CsA)-resistant manner.

63 1(R91W), and inhibition of calcineurin using cyclosporin A (CsA).

64 the target of immunosuppressants, FK506 and cyclosporin A (CSA).

65 the cyclophilin family of proteins that bind cyclosporin A (CsA).

66 otein targets of the immunosuppressive drug, cyclosporin A (CsA).

67 d by treatment with the proton pump modifier cyclosporin A (CsA).

68 significantly rescued by the mPTP inhibitor, Cyclosporin A (CsA).

69 ligands in a competition binding assay with cyclosporin A (CsA).

70 d the effects of the immunosuppressive agent cyclosporin A (CsA).

71 maleate (DEM), piperonyl butoxide (PBO) and cyclosporin A (CsA).

72 This study compares cyclosporin A (CyA) with the pan-HDACi suberoylanilide h

73 , 1% methylprednisolone (P < .01), and 0.05% cyclosporin A (P < .03).

74 ) prophylaxis, while the ATG groups received cyclosporin A + prednisone.

75 (2) cells transfected with ABCB4-I541F cDNA, cyclosporin A allowed a significant amount of the mutant

76 The calcineurin inhibitor cyclosporin A also blocks the dephosphorylation of TRPC6

77 Cyclosporin A also improved maturation of ABCB4-I541F in

78 n competition and uses a fluorescein-labeled cyclosporin A analog and purified human CypA to quantita

79 , we predicted that the nonimmunosuppressive cyclosporin A analog valspodar would inhibit Rgg activat

80 (alisporivir, DEB025, a nonimmunosuppressive cyclosporin A analog).

81 partially blocked by haemoglobin, melatonin, cyclosporin A and DPQ, but was not affected by uric acid

82 Both groups received immunosuppression with cyclosporin A and everolimus in the same target range of

83 g as current calcineurin inhibitors, such as cyclosporin A and FK-506, rely upon binding sites on bot

84 were sensitive to the calcineurin inhibitors cyclosporin A and FK-506, to scavengers of ROS, and to i

85 Cyclosporin A and FK506, which target calcineurin and th

86 duced IL-21 gene expression was inhibited by cyclosporin A and FK506.

87 e to the calcineurin-NFAT pathway inhibitors cyclosporin A and FK506.

88 Finally, cyclosporin A and IkappaBalpha and PI3K inhibitors but n

89 Cyclosporin A and IkBalpha inhibitor blocked TLR2-mediat

90 s-linking, and its activity was inhibited by cyclosporin A and MAPK inhibitors.

91 PTP), which was blocked by the PTP inhibitor cyclosporin A and MnTBAP, and reversed by L-arginine sup

92 in clinical studies and understanding of how cyclosporin A and model cyclic hexapeptides cross cell m

93 Both viruses were efficiently inhibited by cyclosporin A and NIM811, a nonimmunosuppressive analog

94 Calcineurin inhibitors, such as cyclosporin A and tacrolimus (FK506), have played a pivo

95 mice treated with the calcineurin inhibitor cyclosporin A and transgenic mice expressing a targeted

96 changes are inhibited by immunosuppressants cyclosporin A and triptolide.

97 e recoupling agent 6-ketocholestanol but not cyclosporin A and were nonexistent in mitochondrial DNA-

98 They identify cyclosporin A as a potential novel therapeutic tool for

99 -ATG group received mycophenolate mofetile + cyclosporin A as graft-versus-host disease (GVHD) prophy

100 Cyclosporin A blockade of the mitochondrial permeability

101 Sub-micromolar concentrations of cyclosporin A blocked MPT and cell death, suggesting tha

102 Cyclosporin A blocked the inhibitory effect of JNK on mi

103 otein phosphatase 2B (calcineurin) inhibitor cyclosporin A blocked the nicotine-induced reversal.

104 osuppressor in human transplantation such as cyclosporin A blocks tissue rejection in marine sponges

105 The PTP blockers bongkrekic acid and cyclosporin A both reduced inhibition of transient K(Ca)

106 Cyclosporin A coadministered for 2 weeks with ART provid

107 The complexes included the CypA-cyclosporin A complex and the BCAII-4-carboxybenzenesulf

108 Guided by the Rgg-cyclosporin A complex structure, we predicted that the n

109 tenuate NFATc1 activity further, we injected cyclosporin A daily.

110 Furthermore, cyclosporin A decreased protein synthesis and abolished

111 racts, and inhibitors of calcineurin such as cyclosporin A delay the destruction of cyclins, the glob

112 thermore, sensitivity to the drugs FK506 and cyclosporin A demonstrates that the RAM pathway acts in

113 Fourteen trials consistently indicate that cyclosporin A efficaciously improves clinical signs of A

114 immunosuppressant and antifungal antibiotic cyclosporin A enhances subsequent binding of cardiolipin

115 Treatment of human platelets with cyclosporin A gave a similar phenotype.

116 In intact mitochondria, cyclosporin A had no effect, indicating that ATP consump

117 over, anti-IL-13 therapy in combination with cyclosporin A had profound effects on reducing murine BO

118 ients treated with xenon in combination with cyclosporin A had prolonged renal allograft survival.

119 , insulin exposure was still as effective as cyclosporin A in delaying mitochondrial permeability tra

120 of calcineurin (Cn) by low concentrations of cyclosporin A increases osteoblast differentiation in vi

121 treated with calcineurin inhibitors such as cyclosporin A indicates that calcineurin/nuclear factor

122 d upregulated expression of renal NUPR1, and cyclosporin A induced Nupr1 expression in cultured human

123 scriptional signature in vivo, we found that cyclosporin A induces pathways dependent on the transcri

124 mone-binding site and the mechanism by which cyclosporin A inhibits activation of the peptide pheromo

125 Cyclosporin A inhibits pore opening by binding to cyclop

126 Indeed, cyclosporin A injection and stereotaxic delivery of the

127 Cyclosporin A is recommended as first-line treatment for

128 Moreover, the administration of cyclosporin A markedly inhibited (99m)Tc-mebrofenin excr

129 Pore opening can be inhibited by cyclosporin A mediated via cyclophilin D.

130 or-dependent IL-4 secretion was blocked with cyclosporin A or 11R-VIVIT peptide.

131 ion was prevented by the calcineurin blocker cyclosporin A or A-285222.

132 eincubation with the calcineurin inhibitors, cyclosporin A or ascomycin, significantly reduced the ab

133 liculi, was obtained by cell treatments with cyclosporin A or C and, to a lesser extent, B, D, or H.

134 neurin is inhibited either by the inhibitors cyclosporin A or FK506 or by small interfering RNA-targe

135 types, long-term calcineurin inhibition with cyclosporin A or FK506, both clinically approved drugs,

136 ully abrogated by the calcineurin inhibitors cyclosporin A or FK506, confirming that SrRan activates

137 udies have shown that the immunosuppressants cyclosporin A or FK506, which interact with the peptidyl

138 s blocked by specific calcineurin inhibitors cyclosporin A or FK520.

139 chondria, or if neurons were pretreated with cyclosporin A or N-methyl-4-isoleucine-cyclosporin (NIM8

140 When endocytosis was promoted by cyclosporin A pretreatment, the dye uptake was significa

141 Neither Btk deficiency nor cyclosporin A prevented FOXO1 protein phosphorylation, i

142 The MPTP inhibitor cyclosporin A protects mouse bone marrow and human cord

143 Treatment with cyclosporin A provided only a marginal and transient enh

144 ore opening with the cyclophilin D inhibitor cyclosporin A restored Deltapsi(m) and rescued cell viab

145 protection, but addition of the MPTP closer cyclosporin A restored protection.

146 ons with the calcineurin inhibitors FK506 or cyclosporin A resulted in nuclear accumulation of phosph

147 Furthermore, administration of cyclosporin A reversed the LPS-induced increase in podoc

148 ndria by the uniporter inhibitor RU360 or by cyclosporin A significantly prevented the OSW-1-induced

149 Treatment with cyclosporin A significantly reduced surface expression o

150 Furthermore, xenon works additively with cyclosporin A to preserve post-transplant renal function

151 hibition of calcineurin with either FK506 or cyclosporin A totally abolished both depolarization- and

152 nsplant when ischemia-reperfusion injury and cyclosporin A toxicity may coexist.

153 n microdissected tubules from a rat model of cyclosporin A toxicity to describe the related epithelia

154 A randomized, controlled trial of cyclosporin A treatment for 2 weeks was performed in per

155 Cyclosporin A treatment inhibited VA opening, implying t

156 Upon cyclosporin A treatment, Nupr1-deficient mice exhibited

157 romotion of IL-2 production was resistant to cyclosporin A treatment, suggesting that CD44 costimulat

158 1% methylprednisolone, and were absent after cyclosporin A treatment.

159 Taxol and cyclosporin A treatments also did not enhance Tx-67 perm

160 Initial and 3- to 6-month cyclosporin A trough level targets were 250 to 300 and 2

161 '-chlorodiazepam, an IMAC inhibitor, whereas cyclosporin A was ineffective.

162 transplanted from PVG.R8 donors and low-dose cyclosporin A was initiated.

163 inst high Ca2+ in the presence of ATP, where cyclosporin A was reported to be ineffective.

164 0)) of MDR modulators LY335979, PSC 833, and cyclosporin A were 69 nmol/L, 1 micromol/L, and 3 microm

165 tors cyclosporin A (CsA) and a derivative of cyclosporin A with modifications in the d-Ser side chain

166 nt ligands (e.g., drugs such as tamoxifen or cyclosporin A) in complex protein mixtures such as cell

167 s (valproate, doxycycline, tetracycline, and cyclosporin A) in cultured hepatic cells and the livers

168 neration synthetic approach to cyclosporine (cyclosporin A).

169 artan, 1 micromol/l), calcineurin inhibitor (cyclosporin A, 0.5 micromol/l), calcium chelator (1,2-Bi

170 Thus, like cyclosporin A, 1,25-dihydroxyvitamin D3 inhibits TCR-dri

171 lear factor of activated T cells (NFAT), and cyclosporin A, a calcineurin inhibitor that reduces NFAT

172 Cyclosporin A, a competitive substrate for ABCB1, restor

173 Nonetheless, cyclosporin A, a direct mitochondrial permeability trans

174 e ability to restrict FIV in the presence of cyclosporin A, a drug that normally abolishes the intera

175 In wild-type mice, the co-administration of cyclosporin A, a known P-gp inhibitor, resulted in a 6-f

176 Cyclosporin A, an inhibitor of calcineurin, increased AS

177 Cyclosporin A, an inhibitor of cell death dependent on t

178 Accordingly, cyclosporin A, an inhibitor of T cell stimulation via th

179 However, cyclosporin A, an inhibitor of the Ca(2+)-dependent phos

180 ndrial-targeted CaMKII inhibitory protein or cyclosporin A, an mPTP antagonist with clinical efficacy

181 Calcineurin inhibitors (FK506, cyclosporin A, and a peptide calcineurin inhibitor [CAIN

182 ning 5% IL-1Ra, 1% methylprednisolone, 0.05% cyclosporin A, and a vehicle control containing carboxym

183 However, alisporivir, cyclosporin A, and most other cyclosporins are potent in

184 ne-N,N,N',N'-tetraacetic acid, deltamethrin, cyclosporin A, and okadaic acid each alone significantly

185 dy for induction, and mycophenolate mofetil, cyclosporin A, and prednisone for maintenance.

186 ansition pore inhibitors bongkrekic acid and cyclosporin A, as well as by the sulfhydryl-reducing age

187 were completely blocked by pretreatment with cyclosporin A, consistent with induction of the MPT.

188 ally approved immunosuppressive drugs (e.g., cyclosporin A, FK506) possess dose-dependent biphasic ef

189 in humans, including dexamethasone, digoxin, cyclosporin A, ondansetron, domperidone, and loperamide.

190 ating the lymphocytes with N-acetylcysteine, cyclosporin A, or bongkrekic acid, emphasizing the essen

191 In primary cultures treated with cyclosporin A, renal tubular cells isolated from Nupr1-d

192 erolimus and nonsignificantly lower doses of cyclosporin A, resulting in significantly lower trough l

193 ules known to interact with OATPs, including cyclosporin A, rifampicin, and glibenclamide, each demon

194 Cyclosporin A, sanglifehrin A, and Mg2+, inhibitors of t

195 While the most popular drug in this group is cyclosporin A, several other analogues are available, in

196 ation-induced Foxp3 binding was abrogated by cyclosporin A, suggesting a role for the phosphatase cal

197 147 is sensitive to cyclophilin-binding drug cyclosporin A, suggesting involvement of a cyclophilin i

198 The loss of pFAK is inhibited by cyclosporin A, suggesting that these Ca2+ transients exe

199 The permeability transition pore blocker cyclosporin A, the caspase-3 inhibitor Z-DEVD-fmk (40 mi

200 e, intracellular dialysis of deltamethrin or cyclosporin A, the specific calcineurin (protein phospha

201 Indeed, we found that, like cyclosporin A, valspodar inhibits peptide pheromone acti

202 Cyclosporin A, which inhibits calcineurin upstream of NF

203 Administration of cyclosporin A, which stabilizes synaptopodin, reduced LP

204 Calcineurin inhibitors, such as the cyclosporin A-cyclophilin A and FK506-FKBP12 complexes,

205 iration, induced a time- and dose-dependent, cyclosporin A-independent permeability transition (PT) o

206 hat form "unregulated," constitutively open, cyclosporin A-insensitive permeability transition (PT) p

207 nscription of the Il2 gene and several other cyclosporin A-sensitive cytokine genes important for the

208 e IL-3 gene, and included a highly inducible cyclosporin A-sensitive enhancer at -37 kb that increase

209 riggered transient, spontaneously reversible cyclosporin A-sensitive swelling closely resembling remo

210 Cyclosporin A-treated Nfatc1(+/-) mice demonstrated rapi

211 ion by PEITC treatment was not influenced by cyclosporin A.

212 ith the anti-psoriasis systemic therapeutic, cyclosporin A.

213 ochondrial permeability transition pore with cyclosporin A.

214 ochondrial permeability transition inhibitor cyclosporin A.

215 were inhibited by the calcineurin inhibitor cyclosporin A.

216 t, which was attenuated by pretreatment with cyclosporin A.

217 n the presence of nontoxic concentrations of cyclosporin A.

218 or for the important immunosuppressant drug, cyclosporin A.

219 mycin and was blocked by the NFAT antagonist cyclosporin A.

220 ctivation, and this response is inhibited by cyclosporin A.

221 ect was blocked by the calcineurin inhibitor cyclosporin A.

222 ation was seen when CXCR2(-/-) mice received cyclosporin A.

223 (SIV) Nef become resistant to treatment with cyclosporin A.

224 tes were mutated or following treatment with cyclosporin A.

225 cause systemic toxicity as was observed for cyclosporin A.

226 raft-versus-host disease (GVHD) consisted of cyclosporin A.

227 , slightly overcoming those of verapamil and cyclosporin A.

228 of cyclophilin A with the immunosuppressant cyclosporin A.

229 gnaling antagonist, the cyclic undecapeptide cyclosporin A.

230 are only possible for the short-term use of cyclosporin A.

231 g(63) in the catalytic motif or inhibited by cyclosporin A.

232 nterference had an effect similar to that of cyclosporin A: reduction of cell surface expression of C

233 in this effort, allowing access to epimeric cyclosporins A and H from a single precursor by variatio

234 g activated rCD4s with the immunosuppressant cyclosporin, a calcineurin inhibitor, robustly inhibited

235 er serum levels of IS needed higher doses of cyclosporin, a P-gp substrate, to obtain the cyclosporin

236 udy aims to examine the inhibitory effect of cyclosporin-A (CsA) on periodontal breakdown and to furt

237 following ischemic preconditioning (IPC) or cyclosporin-A (CsA) treatment.

238 Cyclosporin-A improved plasma membrane localization of b

239 Cyclosporin-A increased expression of ABCB4(S320F) and A

240 M-244769), or two inhibitors of calcineurin (cyclosporin-A, FK506).

241 Cyclosporin-A-induced endothelial dysfunction is related

242 Both 125I-T4 and 3H-cyclosporin accumulation increased by 80%, suggesting th

243 we demonstrate that immune suppression with cyclosporin after SCT limits T-helper cell (Th) 1 differ

244 second course of antithymocyte globulin plus cyclosporin, although response in the refractory setting

245 monstrate the separation and analysis of six cyclosporin analogues using liquid chromatography (LC) a

246 th the highest prevalence among those taking cyclosporin and CCBs (76%) and the lowest among tacrolim

247 hypersensitive to the calcineurin inhibitors cyclosporin and FK506 and to ER and osmotic stresses.

248 T. gondii growth was inhibited by cyclosporin and FK506 in a moderately synergistic manner

249 herapy (IST) with antithymocyte globulin and cyclosporin and is manifested as persistence of severe c

250 Nor is it clear whether cyclosporin and tacrolimus differ in their skeletal acti

251 Cyclosporin and tacrolimus lead to a severe osteopenic s

252 transplant recipients (RTRs) in relation to cyclosporin and tacrolimus while controlling for the eff

253 CCBs should be avoided among patients taking cyclosporin and those with poor oral hygiene.

254 ty relationships of the nonimmunosuppressive cyclosporins and sanglifehrins in clinical and preclinic

255 Cyclosporins are an invaluable class of drug used to pre

256 , alisporivir, cyclosporin A, and most other cyclosporins are potent inhibitors of OATP1B1, MRP2, MDR

257 CypA antagonists, such as cyclosporines, are potent inhibitors of HCV replication.

258 al products, including FK506, rapamycin, and cyclosporin, bind PPIases with nanomolar or better affin

259 hat belong to one of two large families, the cyclosporin-binding cyclophilins (CyPs) and the FK506-bi

260 r which we propose the name FCBP (FK506- and cyclosporin-binding protein).

261 ofetil or EC-MPS in combination with Tac and cyclosporin, but this was not seen with isolated SRL.

262 p could be responsible for increased hepatic cyclosporin clearance.

263 8 HIV-positive patients of whom 31 initiated cyclosporin (CsA) and 47 tacrolimus (Tac) based immunosu

264 by drugs such as phenytoin, nifedipine, and cyclosporin develops due to an increase in the connectiv

265 [FK506, rapamycin, cyclosporin A (CsA), and cyclosporin H (CsH)], which are commonly thought to incr

266 separation of three isomers: CycA and CycH (cyclosporin H), which are enantiomers, and isocyclospori

267 pecific FPR Ab and a defined FPR antagonist, cyclosporin H, abolished the chemotactic response of pha

268 aking tacrolimus, compared with those taking cyclosporin, had less acute rejection (11% versus 22%, P

269 ing over time with the calcineurin inhibitor cyclosporin in neural tube explants or in whole embryos,

270 eneration immunosuppressant as successful as cyclosporin in suppressing organ transplant rejection.

271 Although cyclosporin is known to cause gingival enlargement (GE),

272 irmed ezetimibe had no significant effect on cyclosporin levels.

273 Cyclosporin, microcystins, and nodularins are all notabl

274 ed high FRET efficiency states, whereas with cyclosporin, more molecules showed low FRET efficiency.

275 Histological features common with cyclosporin nephrotoxicity including matrix expansion, a

276 king the alpha or beta isoform to a model of cyclosporin nephrotoxicity.

277 Here we report that two human conditions, cyclosporin neurotoxicity and Timothy syndrome, increase

278 line, tetracycline, or N-methyl-4-isoleucine cyclosporin (NIM811) of explants and recipients.

279 with cyclosporin A or N-methyl-4-isoleucine-cyclosporin (NIM811) to inhibit the mitochondrial permea

280 dren and young adults who were randomized to cyclosporin or mycophenolate mofetil plus pulse oral dex

281 e did not influence proteinuria responses to cyclosporin or mycophenolate mofetil/dexamethasone.

282 n = 242), who was administered standard-dose cyclosporin or tacrolimus and an antimetabolite, mostly

283 cial tears, nutritional supplements, topical cyclosporins, punctal plugs and autologus serum as well

284 Recipients treated with a cyclosporin regimen had a 2.7-fold higher incidence of d

285 We investigated why cyclosporines require NS2 to increase their inhibitory e

286 irst generation P-gp inhibitors verapamil or cyclosporin, respectively.

287 r inhibitor relative to previously described cyclosporins, retains anti-HCV activity in cell culture,

288 , and we find that the calcineurin inhibitor cyclosporin reverses fluconazole resistance of cka2 muta

289 capacity to oxidize bulky substrates such as cyclosporin, statins, taxanes, and macrolide antibiotics

290 The patient's ability to absorb cyclosporin, tacrolimus (Tac), enteric-coated mycophenol

291 Cyclosporin taken at the currently recommended low dosag

292 cyclosporin, a P-gp substrate, to obtain the cyclosporin target blood concentration.

293 of AUG kidney grafts after a short course of cyclosporin to inhibit the early direct pathway response

294 iated with Timothy syndrome and with chronic cyclosporin treatment of transplant patients.

295 arding the safety of this during concomitant cyclosporin treatment.

296 Cyclosporin was found to be associated with GE in a univ

297 The absorption of Tac and cyclosporin was greater than expected.

298 cohort (n = 59), who also received low-dose cyclosporin, was compared with a control cohort (n = 242

299 For several of the cyclosporins, we can separate different conformers for e

300 gic features and matrix expansion similar to cyclosporin, whereas loss of the beta does not.