ライフサイエンスコーパス: cyclosporine A

1 20-30% by calcineurin inhibitors (FK506 and cyclosporine A).

2 trast to the HBV inhibitors, telbivudine and cyclosporine A.

3 unosuppression with mycophenolate mofetil or cyclosporine A.

4 and therapy with the immunosuppressive agent cyclosporine A.

5 n infection was conducted in the presence of cyclosporine A.

6 ynthesis of the important cyclic polypeptide cyclosporine A.

7 me inhibitor Velcade or an immunosuppressant cyclosporine A.

8 disparity, followed by 12 days of high-dose cyclosporine A.

9 All animals were maintained on oral cyclosporine A.

10 iature swine treated with a 12-day course of cyclosporine A.

11 adation induced by the calcineurin inhibitor cyclosporine A.

12 as receptors for the immunosuppressive drug, cyclosporine A.

13 vitro at a concentration 10 times lower than cyclosporine A.

14 imilar concentration as pharmaceutical grade cyclosporine A.

15 s a target of the natural products FK506 and Cyclosporine A.

16 e cellular receptor of the immunosuppressant cyclosporine A.

17 e trough level (C0) and used higher doses of cyclosporine A.

18 decreased sensitivity to the Rgg2 antagonist cyclosporine A.

19 transplantation (HCT) and a 45-day course of cyclosporine A.

20 e trough level (C0) and used higher doses of cyclosporine A.

21 nd is inhibited by the cyclophilin inhibitor cyclosporine A.

22 tion of the Itpr2 promoter was attenuated by cyclosporine-A.

23 40 mg/kg per day (n = 10), positive control (cyclosporine A 10 mg/kg per day by oral gavage, n = 10),

24 ts were randomized to receive an IV bolus of cyclosporine A (10 mg/kg) or normal saline (placebo, con

25 xic T-lymphocyte antigen-4 immunoglobulin or cyclosporine A (15 mg/kg), graft survival was significan

26 randomized to receive intravenous boluses of cyclosporine A (2.5, 10, or 25 mg/kg) or normal saline (

27 haride (3.0 mg/kg, intravenously; n = 8), or cyclosporine A (6.0 mg/kg, intravenously; n = 6) or tacr

28 and reperfused for 4 or 8 hours or 90 days (cyclosporine A 7.5 mg/kg on postoperative day [POD] 0-9)

29 FK506 (50 ng/mL) and cyclosporine A (800 ng/mL) had comparable effects.

30 Moreover, cyclosporine A, a blocker of mPTP opening, attenuates is

31 f inflammation in peripheral tissues, and by cyclosporine A, a CyPA inhibitor.

32 neuronal co-cultures through the addition of cyclosporine A, a potent immune-modulator.

33 loyed to determine whether pretreatment with cyclosporine A, a potent inhibitor of the mitochondrial

34 ubating cells with the cyclophilin inhibitor cyclosporine A, a treatment that triggered efficient ER

35 l other grafts were accepted with 12 days of cyclosporine A across both MHC-matched and MHC class I b

36 We show that cyclosporine A added to a sample containing NS5B(Delta21

37 orine A (TCD arm; n=201) or methotrexate and cyclosporine A after transplantation of T-replete marrow

38 Cell death was partially blocked by cyclosporine A [an inhibitor of the mitochondrial permea

39 Cyclosporine A, an inhibitor of mitochondria permeabilit

40 Cyclosporine A, an inhibitor of mitochondrial permeabili

41 ing justification for a clinical trial using cyclosporine A, an inhibitor of PTP opening.

42 ) or cyclophilin (using nonimmunosuppressive cyclosporine A analog) reduced tissue neutrophilia by up

43 eceptor antagonists, calpain inhibitors, and cyclosporine A analogues.

44 clobetasol, or in combination with systemic cyclosporine A and anti-alphabeta-T-cell receptor antibo

45 ium opens the channel, which is inhibited by cyclosporine A and ATP/ADP.

46 on of immune tolerance--via oral delivery of cyclosporine A and azathioprine for two months at the ti

47 Experiments using cyclosporine A and cardiac-specific CaMKIIdelta knockout

48 In addition to rescue by cyclosporine A and collagen VI, this cellular phenotype

49 ath and ROS production were also reversed by cyclosporine A and diazoxide, chemicals that regulate th

50 Calcineurin inhibitors such as cyclosporine A and FK506 are effective immunosuppressant

51 ibitors of calcineurin/NFAT binding, such as cyclosporine A and FK506, are broadly used in organ tran

52 ited by both calcineurin-specific inhibitors cyclosporine A and FK506.

53 Restasis is 0.05% cyclosporine A and is the first immunomodulatory agent a

54 A-matched related donor and prophylaxis with cyclosporine A and methotrexate were associated with low

55 noclonal antibodies, total body irradiation, cyclosporine A and mycophenolate mofetil (12 doses), and

56 Cyclosporine A and nonimmunosuppressive cyclophilin (Cyp

57 overy of powerful immunotherapeutics such as cyclosporine A and rapamycin that has allowed for the wi

58 Alisporivir (Debio-025) is an analogue of cyclosporine A and represents the prototype of a new cla

59 The immunosuppressive natural products cyclosporine A and sanglifehrin A inhibit the enzymatic

60 f the most commonly used immunosuppressants, cyclosporine A and tacrolimus (FK506), inhibit the activ

61 Cyclosporine A and tacrolimus significantly reduced IFNg

62 n was strongly potentiated by combination of cyclosporine A and UVA treatment.

63 -dependent migration (including SP600125 and cyclosporine A) and differentiation (cyclosporine A only

64 Calcineurin inhibitors (FK506 and cyclosporine A) and the cathepsin L inhibitor E64 all in

65 Cyclophilin inhibitors, cyclosporine A, and alisporivir and NS5A inhibitor BMS-7

66 ross a class I MHC disparity with 12 days of cyclosporine A, and two across a class I MHC disparity w

67 ochondria and that such an effect of CypD is cyclosporine A- and Bcl2-dependent.

68 rapies using calcineurin inhibitors, such as cyclosporine A, are associated with a higher incidence o

69 e agents, azathioprine, 6-mercaptopurine and cyclosporine A, are compatible with pregnancy.

70 wis XX to DA XY allografts were treated with cyclosporine A at 10 mg/kg/day.

71 iliximab (n=5), calcineurin inhibitor (CNI) (cyclosporine A)/basiliximab (n=4) or CNI (tacrolimus)-ba

72 vulnerability to mPT and in higher levels of cyclosporine A being required to inhibit mPTP opening.

73 re proline-containing peptide substrates and cyclosporine A bind and that are vital for the enzymatic

74 bunit ring and unhooks it from cyclophilin D/cyclosporine A binding sites in the ATP synthase F1, pro

75 N-acetyl-L-cysteine and cyclosporine A, blocked ethanol and acetaldehyde-induced

76 patency (*P<0.01 vs. vehicle and P=0.14 vs. cyclosporine A) but not epithelialization (P>0.2 vs. veh

77 was rescued upon MG132 treatment as well as cyclosporine A, but not by FK506 or bile acids, suggesti

78 leukin-8, and inhibited by dexamethasone and cyclosporine A, consistent with a role as a proinflammat

79 omplex systems, including the cyclic peptide cyclosporine A, constrained peptide systems, and heteroc

80 for 10 or 100 days or immunosuppressed with cyclosporine A continuously for 50 days and then withdra

81 f virions depleted of CyPA by treatment with cyclosporine A could be restored by NERT treatment, whil

82 In contrast, we found that cyclosporine A could inhibit the AA-induced loss of Delt

83 L without a calcineurin inhibitor (33%), SRL+cyclosporine A (CsA) (33%), and SRL+tacrolimus (TAC) (34

84 ipients (RTX) receiving tacrolimus (n=34) or cyclosporine A (CsA) (n=24) or an mTORi (n=26).

85 Group C received cyclosporine A (CsA) (Neoral, Novartis, Basel, Switzerla

86 monly prescribed topical treatments included cyclosporine A (CSA) 0.05 % (71/104, 68 %), fluoromethol

87 antly, a pharmacological inhibition of CN by cyclosporine A (CsA) ameliorated the alpha-syn-induced l

88 ses for CypA independence using Debio-025, a cyclosporine A (CsA) analog that disrupts CypA-capsid in

89 C3 and that received immunosuppression with cyclosporine A (CsA) and a predegenerated PNG (termed I-

90 ated in DHHC5-deficient hearts, inhibited by cyclosporine A (CsA) and adenosine, promoted by staurosp

91 We found that both cyclosporine A (CsA) and ascomycin inhibited removal of

92 whereas inhibitors of immunophilins, such as cyclosporine A (CsA) and FK506, inhibited CrkII, but not

93 ions, the inhibitory effects of TPR ligands, cyclosporine A (CsA) and FK506, on AR activity were not

94 The immunosuppressive drug cyclosporine A (CsA) and its nonimmunosuppressive analog

95 til (MMF) are considered more efficient than cyclosporine A (CsA) and MMF, but recent studies have ch

96 f two commonly used immunosuppressive drugs, cyclosporine A (CsA) and sirolimus (SRL), on the develop

97 te mofetil (MMF) or Everolimus combined with cyclosporine A (CsA) and steroids.

98 microperfusion due to the administration of cyclosporine A (CsA) and tacrolimus (Tac) can be evidenc

99 Cyclosporine A (CsA) and tacrolimus (Tac) provide effect

100 Cyclosporine A (CsA) and tacrolimus (TAC) were associate

101 of reduced nephron mass on nephrotoxicity by cyclosporine A (CsA) and/or sirolimus (SRL).

102 on of rituximab to corticosteroids (CSs) and cyclosporine A (CsA) as first-line therapy for newly dia

103 rapamil as the prototypic P-gp substrate and cyclosporine A (CsA) as the prototypic inhibitor.

104 etreatment with the NFAT signaling inhibitor cyclosporine A (CsA) blocked NaBT-mediated PTEN inductio

105 s are administered the calcineurin inhibitor cyclosporine A (CsA) chronically and demonstrate an incr

106 in an era of lower prednisone doses, whether cyclosporine A (CsA) contributes, whether hypothalamic-p

107 ts who received the combination of sirolimus-cyclosporine A (CsA) demonstrated AVN, compared with 1.4

108 Data indicate that tacrolimus and cyclosporine A (CsA) differentially affect the risk of a

109 Here we show that AS and cyclosporine A (CsA) exerted synergistic inhibitory effe

110 In addition to steroids, cyclosporine A (CsA) has been implicated in contributing

111 Whether cyclosporine A (CsA) has beneficial effects in reperfuse

112 To evaluate the treatment with topical 0.05% cyclosporine A (CsA) in patients with subepithelial corn

113 cardiovascular/metabolic risk profile versus cyclosporine A (CsA) in the Belatacept Evaluation of Nep

114 Cyclosporine A (CsA) increases beta-catenin messenger RN

115 It has been suggested that cyclosporine A (CsA) induces gingival enlargement by pro

116 dro-N6-propyl-2,6-benzothiazole-diamine) and cyclosporine A (CSA) inhibited increases in ion conducta

117 Cyclosporine A (CsA) inhibits HCV replication and CsA de

118 , disruption of the CypA-CA interaction with cyclosporine A (CsA) inhibits HIV-1 infectivity only if

119 Cyclosporine A (CsA) is a well-known immunosuppressive a

120 Cyclosporine A (CsA) is an immunosuppressive drug which

121 Cyclosporine A (CSA) is considered a "gold standard" the

122 Cyclosporine A (CsA) is used for the treatment of psoria

123 The narrow therapeutic window of cyclosporine A (CsA) means its use is controlled by phar

124 ds of patients initiated on monotherapy with cyclosporine A (CsA) microemulsion require addition of s

125 mic or pharmacological postconditioning with cyclosporine A (CsA) might protect the kidney from letha

126 in the progression of fibrosis in a chronic cyclosporine A (CsA) nephrotoxicity animal model.

127 correlates with the variation in response to cyclosporine A (CsA) noted in some clinical trials.

128 tudy evaluated whether sirolimus (SRL), with cyclosporine A (CsA) or alone, affects TA, and examined

129 Patients with acute GvHD are treated with cyclosporine A (CsA) or tacrolimus (FK506), which not on

130 n is inhibited by the immunosuppressant drug cyclosporine A (CsA) or tacrolimus (FK506).

131 s of 3-8 or 6-12 ng/mL plus reduced-exposure cyclosporine A (CsA) or to mycophenolic acid (MPA) 1.44

132 rapy combined with the calcineurin inhibitor cyclosporine A (CsA) prolonged median primary graft surv

133 ng a 7-day alphabeta- T-cell receptor (TCR)/ cyclosporine A (CsA) protocol.

134 pressive action of the calcineurin inhibitor cyclosporine A (CsA) stems from the inhibition of nuclea

135 alcineurin inhibitors tacrolimus (FK506) and cyclosporine A (CSA) to enhance the activity of PHMB, am

136 after renal transplantation) conversion from cyclosporine A (CsA) to everolimus versus continued CsA

137 ty of rapamycin or the calcineurin inhibitor cyclosporine A (CSA) to promote chimerism in a murine ha

138 warm ischemia), and rats subjected to acute cyclosporine A (CSA) toxicity (50 mg/kg for 2 d intraper

139 the RNA-induced silencing complex (RISC) of cyclosporine A (CsA) treated and control human proximal

140 nts randomized (2:1) to sirolimus (n=314) or cyclosporine A (CsA) treatment (n=161).

141 veral time points: (a) SRL (CNI-free) versus cyclosporine A (CsA) treatment de novo, (b) CsA+SRL vers

142 Calcineurin inhibitors such as cyclosporine A (CsA) were shown to be effective in the t

143 ive strategies combining tacrolimus (TAC) or cyclosporine A (CsA) with mycophenolate mofetil (MMF) an

144 After the introduction of cyclosporine A (CsA), 2-year graft survival of transplan

145 Cyclosporine A (CsA), a mitochondrial permeability trans

146 The PLGA-GA NS loaded with cyclosporine A (CsA), a model peptide, upon peroral dosi

147 Intraperitoneal injection of cyclosporine A (CsA), a pharmacological inhibitor of the

148 ression with mycophenolate mofetil (MMF) and cyclosporine A (CsA), achieved stable engraftment of dog

149 terestingly, the calcineurin inhibitor (CNI) cyclosporine A (CsA), an immunosuppressant used to preve

150 treated with immunosuppressant drugs such as cyclosporine A (CsA), an inhibitor of calcineurin phosph

151 more than that of M6G (80.31 +/- 21.75 muM); Cyclosporine A (CsA), an inhibitor of OATP2B1, can inhib

152 were allocated to EVL plus reduced-exposure cyclosporine A (CsA), and 20 to standard dose CsA.

153 kin-2 receptor antagonists, tacrolimus (FK), cyclosporine A (CSA), and mycophenolate mofetil/sodium (

154 splant recipients treated with prednisolone, cyclosporine A (CsA), and mycophenolate sodium (MPS) for

155 ly treated with mycophenolate mofetil (MMF), cyclosporine A (CsA), and prednisone (pred).

156 free protocol was compared with a sirolimus, cyclosporine A (CsA), and prednisone-based immunosuppres

157 re swine can be induced by a short course of cyclosporine A (CsA), and that this stable tolerance is

158 ugs, such as mycophenolate mofetil (MMF) and cyclosporine A (CsA), are often used together after HSCT

159 Combining Treg cells with cyclosporine A (CSA), but not rapamycin (RAPA) or mycoph

160 y side effect of the immunosuppressive drug, cyclosporine A (CsA), can be a major issue in transplant

161 tion of drug transport by the Pgp modulator, cyclosporine A (CSA), can increase GO sensitivity in Pgp

162 on, we tested an anti-inflammatory compound, cyclosporine A (CsA), for its ability to block JCV infec

163 of AM19 and AM1c9, secondary metabolites of cyclosporine A (CsA), have been associated with nephroto

164 , following treatment with the PPI inhibitor cyclosporine A (CsA), or overexpression of a dominant-ne

165 ith immunosuppressive reagents that included cyclosporine A (CSA), rapamycin (RAP), mycophenylate mof

166 atients taking immunosuppressive drugs, like cyclosporine A (CsA), that inhibit calcineurin are highl

167 in mice treated with a potent SC activator, cyclosporine A (CSA), which inhibits the phosphatase cal

168 oxidase 2 (Nox2) plays an important role in cyclosporine A (CsA)-induced chronic hypoxia.

169 s of fibrosis-related IL-6-type cytokines in cyclosporine A (CsA)-induced gingival overgrowth (GO).

170 In this study, we examined the effects of cyclosporine A (CsA)-induced immune suppression during e

171 This study determined whether cyclosporine A (CsA)-treated renal allograft recipients

172 orally with STN alone or in combination with cyclosporine A (CsA).

173 nd are targets of the immunosuppressive drug cyclosporine A (CsA).

174 s, thymoglobulin, mycophenolate mofetil, and cyclosporine A (CsA).

175 ith a 21-day course of the immunosuppressant cyclosporine A (CsA).

176 s well as incubation with the CypA inhibitor cyclosporine A (CsA).

177 st as well or better than the Pgp modulator, cyclosporine A (CSA).

178 and September 2002; group II (168) was given cyclosporine A (CsA)/MMF/P between January 1999 and July

179 )/mycophenolate sodium+tacrolimus (TAC), MMF+cyclosporine A (CsA); mammalian target of rapamycin inhi

180 Recipients were immunosuppressed either with cyclosporine A (CsA, 1.5 mg/kg/day subcutaneously) or wi

181 nd during infusion (6, 12, or 24 mg/kg/h) of cyclosporine A (CsA, a P-glycoprotein [P-gp] inhibitor).

182 neuroprotective effects of immunosuppressant cyclosporine-A (CsA) and the anti-inflammatory methylpre

183 e absence and presence of the P-gp inhibitor cyclosporine-A (CsA).

184 y higher than that of the standard inhibitor cyclosporine-A (CsA).

185 pening during the preconditioning phase with cyclosporine-A (CsA, 0.2 micromol/L) or sanglifehrin-A (

186 tide) and a model hydrophobic macromolecule (Cyclosporine A, CsA), herein we provide a mechanistic un

187 Tacrolimus (Tac) and Cyclosporine A (CyA) calcineurin inhibitors (CNIs) are 2

188 reviously shown that a 12-day treatment with cyclosporine A (CyA) facilitates induction of tolerance

189 from four AD patients who had received oral cyclosporine A (CyA) treatment for up to 17 months regar

190 to cyclosporine A monotherapy, CMPD 167 with cyclosporine A delayed alloantibody production, suppress

191 oprotein-specific transport of a fluorescent cyclosporine A derivative into capillary lumens.

192 tion in the fundus vessels (P < 0.01), while cyclosporine A did not.

193 A cyclophilin D inhibitor, cyclosporine A, disrupts the CypD-Bcl2 interaction.

194 The average total daily cyclosporine A dose at month 3 was 208+/-62 mg per day a

195 rkat cells or treatment of Jurkat cells with cyclosporine A eliminated the Vif-sensitive inhibition a

196 (also called niacinamide), minocycline, and cyclosporine A exhibited a uniform protective effect.

197 degrees C) or by treatment with substrates (cyclosporine A, FK506), modulators (tariquidar), or smal

198 tory agents, including prednisolone acetate, cyclosporine A, FK506, autologous serum, and retinoic ac

199 findings may explain why patients receiving cyclosporine A for immunosuppressive therapy display exc

200 Combined administration of BJ486K and cyclosporine A had a synergistic effect in inhibition of

201 For example, use of the Cn inhibitor cyclosporine A has been shown to delay muscle regenerati

202 ochondrial permeability transition inhibitor cyclosporine A, has a requirement for mitochondrial Ca(2

203 regeneration and recruitment are impeded by cyclosporine A immunosuppression, and (4) donor GFP-posi

204 e alloimmune response, which was reversed by cyclosporine A in a dose-dependent fashion.

205 Partial blocking of AIF release by cyclosporine A in OmpU-treated cells further suggests th

206 ucted from June 22, 2010, to March 13, 2013 (Cyclosporine A in Out-of-Hospital Cardiac Arrest Resusci

207 In the CYCLE (CYCLosporinE A in Reperfused Acute Myocardial Infarction

208 Immunosuppression for 12 weeks using cyclosporine A in such woodchucks resulted in transient

209 s also enhanced viral resistance to the drug cyclosporine A, indicating a reduced dependence of the c

210 Nifedipine- and cyclosporine A-induced gingival overgrowth tissues simil

211 Cyclosporine A-induced nephrotoxicity is multifactorial

212 he immunosuppressants tacrolimus (FK506) and cyclosporine A inhibit calcineurin and have potent antif

213 phosphorylation through a calcium-dependent, cyclosporine A-inhibitable pathway.

214 28.5 microM), and lipophilic agents such as cyclosporine A (K(i(app)), 14.4 microM).

215 tion were observed both in mice treated with cyclosporine, a known stimulator of the HCM response, an

216 or PLCgamma2 or inhibiting calcineurin with cyclosporine A leads to increased expression of PD-1 lig

217 Calcineurin blockade by cyclosporine A led to a failure of CD8 but not CD4 toler

218 The mean doses of cyclosporine A (mg/kg/day) were recorded.

219 ) and ACI donors (group 5) were treated with cyclosporine A monotherapy (16 mg/kg/day, tapered to 2 m

220 Cyclosporine A monotherapy prevented acute rejection of

221 raft transplants across an MHC barrier under cyclosporine A monotherapy protocol.

222 In contrast, relative to cyclosporine A monotherapy, CMPD 167 with cyclosporine A

223 Allografts in group 3 (n=6) received tapered cyclosporine A monotherapy.

224 maintenance immunosuppression consisting of cyclosporine A, mycophenolate mofetil, and steroids.

225 ependent of immunosuppressive therapy (using cyclosporine A, mycophenolate mofetil, or azathioprine a

226 =27), were compared to no treatment (n=4) or cyclosporine A (n=6).

227 immunosuppression with cyclosporine A (with cyclosporine A, n=6; no cyclosporine A, n=7).

228 cyclosporine A (with cyclosporine A, n=6; no cyclosporine A, n=7).

229 Combined treatment with cyclosporine A, OA further prolonged the islet allograft

230 Medication with phenytoin, nifedipine, and cyclosporine-A often causes gingival overgrowth.

231 125 and cyclosporine A) and differentiation (cyclosporine A only) of osteoclast precursors.

232 ell treatment with the calcineurin inhibitor cyclosporine A or a NFAT-specific inhibitor led to a sha

233 aling pathway in lymphoma cells, either with cyclosporine A or anti-CD1d blocking antibody, prolonged

234 ous mutations in NPHS2 who were treated with cyclosporine A or cyclophosphamide demonstrated complete

235 hat short term (4-6 h) treatment with 15 muM cyclosporine A or FK506 rescues the pre-formed immature

236 eliorated in T4C3 cells by pretreatment with cyclosporine A or FK506, implicating the calcium-depende

237 ation in its catalytic site, antagonism with cyclosporine A or FK506, or intracellular perfusion with

238 264)K variant was rescued by the addition of cyclosporine A or infection of a cyclophilin A-deficient

239 indicated that inhibition of calcineurin by cyclosporine A or knockdown of NFATc4 using small interf

240 si(m), and were protected from cell death by cyclosporine A or ppif ablation, implicating the mitocho

241 In addition, dasatinib combined with cyclosporine A or rapamycin led to a much more potent in

242 three specific calcineurin inhibitors FK506, cyclosporine A, or calcineurin inhibitory peptide preven

243 Ca(2+) signaling or calcineurin with BAPTA, cyclosporine A, or FK506 prevented activation of NF-kapp

244 c acid, the calcineurin inhibitors FK506 and cyclosporine A, or use of acinar cells from calcineurin

245 acheal grafts and were treated with PX3.102, cyclosporine A, or vehicle.

246 pulses of cyclophosphamide, vincristine, or cyclosporine A; or salvage splenectomy are considered.

247 p treatment with dexamethasone (P < 0.01) or cyclosporine A (P < 0.01) significantly lowered MS adhes

248 ecedented strategy for preparing polylactide-cyclosporine A (PLA-CsA) NPs (termed CsA-NPs) through Cs

249 tch1+/- mice with immunosuppressive doses of cyclosporine A plus prednisolone for 4-1/2 mo increased

250 nts spanned four immunosuppressive eras: pre-cyclosporine A (pre-CsA) era (16%), CsA era (23%), tacro

251 Cyclosporine A pretreatment attenuated lipopolysaccharid

252 In contrast, reduction of p53 levels or cyclosporine A pretreatment of mice prevents this comple

253 ading to cell death, which was attenuated by cyclosporine A pretreatment.

254 tructive jaundice, prostaglandin inhibitors, cyclosporine A, radiocontrast dyes and volatile anesthet

255 After brain injury, cyclosporine A reduces damage but is ineffective followi

256 with chaperone Hsp70, and the treatment with cyclosporine A reduces the association of mutant P-gp, t

257 Immunosuppression with high doses of Cyclosporine A, required for MSC survival, was provided

258 rt that immunomodulation using topical 0.05% cyclosporine A (Restasis) may also have a positive effec

259 ion with costimulation blockade and low-dose cyclosporine A resulted in a complete deletion of periph

260 ith phosphatase inhibitors (okadaic acid and cyclosporine A) resulted in a modest inhibition of the T

261 toxicity equivalents of model P-gp inhibitor cyclosporine A) revealed high inhibitory potential of po

262 tochondrial Ca(2+) influx, by mPTP inhibitor cyclosporine A, sanglifehrin, and in cyclophilin D knock

263 Cyclosporine A selectively ameliorated the Anesthesia/Su

264 ha treated mice underwent calcium-dependent, cyclosporine A-sensitive swelling, which was prevented b

265 ells markedly induced COX-2 expression via a cyclosporine A-sensitive, calcineurin/NFAT-dependent pat

266 gamma-inducing effect of NcAg was blocked by cyclosporine, a specific ligand for CyP, in a dose-depen

267 Cyclosporine A stabilizes Ets-2 mRNA and protein when th

268 eta-turns of the orally bioavailable peptide cyclosporine A, suggests that the introduction of bioact

269 otrexate along with a calcineurin inhibitor (cyclosporine A, tacrolimus) for GVHD prophylaxis.

270 currently available immunosuppressive agents cyclosporine A, tacrolimus, and rapamycin have potent an

271 ation with either T-cell depleted marrow and cyclosporine A (TCD arm; n=201) or methotrexate and cycl

272 ptotic effects of the calcineurin inhibitor, cyclosporine A, the chimeric anti-interleukin-2 receptor

273 Upon introducing the nephrotoxin, Cyclosporine A, the epithelial barrier is disrupted in a

274 enal transplantation with a 12-day course of cyclosporine A to induce long-term tolerance.

275 It synergizes with cyclosporine A to inhibit HCV infection.

276 wever, we demonstrate that a brief course of cyclosporine A to rat renal allograft recipients promote

277 Administration of cyclosporine-A to enhance graft survival demonstrated th

278 rtrophy group (n = 5), and aortic-banded and cyclosporine A- treated cardiomyopathy group (n = 5).

279 ed liver allografts, but not in syngeneic or cyclosporine A-treated allografts.

280 Cyclosporine A-treated animals that were given antibioti

281 Cyclosporine A-treated mice showed no signs of chronic r

282 We previously demonstrated that cyclosporine A treatment during resuscitation can signif

283 keratin 16 (K16) mRNA] at baseline and after cyclosporine A treatment in 25 moderate to severe AD pat

284 Cyclosporine A treatment reduced renal expression and se

285 We hypothesized that cyclosporine A treatment would attenuate myocardial and

286 idized to total glutathione ratio induced by cyclosporine A treatment.

287 late of diabetes development; tacrolimus and cyclosporine A treatments were associated with increased

288 kidneys long-term after 12 days of high-dose cyclosporine A, uniformly accepted donor-major histocomp

289 er patients, in women, in patients receiving cyclosporine A versus tacrolimus, and in patients with b

290 Cyclosporine A was used to enhance levels of the PET rad

291 The mitochondrial membrane stabilizer, cyclosporine A, was also able to protect these cells fro

292 yl-Val-Ala-Asp-(OMe) fluoromethyl ketone and cyclosporine A, we also showed that AD198-induced PLS3 p

293 HLA mismatches and cyclosporine A were independently associated with increa

294 The calcineurin phosphatase inhibitor cyclosporine A, which blocks KC terminal differentiation

295 This was mitigated by cyclosporine A, which inhibits opening of the mitochondr

296 T-cell IFN-gamma production were ablated by cyclosporine A, which inhibits signaling through the T-c

297 Higher concentrations of cyclosporine A, which interacts with cyclophilin D to de

298 -principle, the known binding interaction of Cyclosporine A with cyclophilin A protein in a yeast cel

299 ation with or without immunosuppression with cyclosporine A (with cyclosporine A, n=6; no cyclosporin

300 Cyclosporine A, with or without concurrent corticosteroi