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

6 activation pathways may not be sensitive to cyclosporin.

7 PP2B utilized by the immunosuppressive drug cyclosporin.

8 ges on the effective preorganization of seco-cyclosporins.

9 NS2 modulates sensitivity of HCV to cyclosporines.

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

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

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

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

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

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

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

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

18 ysteine (NAC) and Trolox (TX), as well as by cyclosporin A (CsA) and bongkrekic acid (BKA).

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

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

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

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

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

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

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

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

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

28 The widely used immunosuppressive drug cyclosporin A (CsA) inhibited DAF induction by VEGF in a

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

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

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

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

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

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

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

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

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

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

39 d) value) were determined for the binding of cyclosporin A (CsA) to a cyclophilin A (CypA) sample in

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

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

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

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

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

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

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

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

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

49 Although cyclosporin A (CsA), an inhibitory ligand of cyclophilin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 ir sensitivity to the immunosuppressive drug cyclosporin A (CsA).

69 1(R91W), and inhibition of calcineurin using cyclosporin A (CsA).

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

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

72 , 1% methylprednisolone (P < .01), and 0.05% cyclosporin A (P < .03).

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

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

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

76 Cyclosporin A also improved maturation of ABCB4-I541F in

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

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

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

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

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

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

83 Cyclosporin A and FK506, which target calcineurin and th

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

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

86 he half-life of cyclin D1 in the presence of cyclosporin A and found no difference from control cells

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

88 Cyclosporin A and IkBalpha inhibitor blocked TLR2-mediat

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

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

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

92 Furthermore, both cyclosporin A and NAD(+) blocked translocation of the ap

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 Indeed, cyclosporin A injection and stereotaxic delivery of the

126 Cyclosporin A is recommended as first-line treatment for

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

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

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

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

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

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

133 H(o) 7.4, as long as phosphatase inhibitors (cyclosporin A or endothal) were present.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 Treatment with cyclosporin A significantly reduced surface expression o

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

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

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

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

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

154 Cyclosporin A treatment inhibited VA opening, implying t

155 Upon cyclosporin A treatment, Nupr1-deficient mice exhibited

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

157 1% methylprednisolone, and were absent after cyclosporin A treatment.

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

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

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

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

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

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

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

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

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

167 neration synthetic approach to cyclosporine (cyclosporin A).

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

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

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

171 Cyclosporin A, a competitive substrate for ABCB1, restor

172 Nonetheless, cyclosporin A, a direct mitochondrial permeability trans

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

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

175 Cyclosporin A, an inhibitor of calcineurin, increased AS

176 However, cyclosporin A, an inhibitor of calcineurin-mediated NFAT

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 or the immunosuppressants mycophenolic acid, cyclosporin A, and FK-506 provide a potential explanatio

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

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

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

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

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

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

190 eptors for immunosuppressive drugs including cyclosporin A, FK506, and rapamycin.

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

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

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

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

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

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 uction of the change in DeltaPsim and PCD by cyclosporin A, which inhibits mitochondrial permeability

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

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

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

207 of mutant SOD1 protects these cells against cyclosporin A-induced cell death.

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

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

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

211 e cyclin D1 mRNA was induced normally in the cyclosporin A-treated cells, we analyzed the half-life o

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

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

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

215 ochondrial permeability transition pore with cyclosporin A.

216 ochondrial permeability transition inhibitor cyclosporin A.

217 were inhibited by the calcineurin inhibitor cyclosporin A.

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

219 n the presence of nontoxic concentrations of cyclosporin A.

220 or for the important immunosuppressant drug, cyclosporin A.

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

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

223 ect was blocked by the calcineurin inhibitor cyclosporin A.

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

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

226 tes were mutated or following treatment with cyclosporin A.

227 cause systemic toxicity as was observed for cyclosporin A.

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

229 differ in sensitivity to the immunomodulator cyclosporin A.

230 , slightly overcoming those of verapamil and cyclosporin A.

231 of cyclophilin A with the immunosuppressant cyclosporin A.

232 gnaling antagonist, the cyclic undecapeptide cyclosporin A.

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

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

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

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

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

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

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

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

241 Cyclosporin-A improved plasma membrane localization of b

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

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

244 Cyclosporin-A-induced endothelial dysfunction is related

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

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

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

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

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

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

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

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

253 Cyclosporin and tacrolimus lead to a severe osteopenic s

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

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

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

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

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

259 e achieved with immunosuppressive drugs like cyclosporin, arrests the disease, but the cost in side e

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

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

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

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

264 p could be responsible for increased hepatic cyclosporin clearance.

265 8 HIV-positive patients of whom 31 initiated cyclosporin (CsA) and 47 tacrolimus (Tac) based immunosu

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

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

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

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

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

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

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

273 irmed ezetimibe had no significant effect on cyclosporin levels.

274 Cyclosporin, microcystins, and nodularins are all notabl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

292 Cyclosporin taken at the currently recommended low dosag

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

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

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

296 arding the safety of this during concomitant cyclosporin treatment.

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

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

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

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