ライフサイエンスコーパス: CsA

1 CsA and its six main metabolites in whole blood and urin

2 CsA causes specific changes in miRNAs and mRNAs associat

3 CsA concentration at C4 correlated better with AUC than

4 CsA could induce Type 2 EMT in gingiva by changing the m

5 CsA enhanced the generation of intracellular ROS at conc

6 CsA further promoted T-cell apoptosis, DeltaPsim loss, a

7 CsA inhibited the expressions of gelatinase MMPs and EMM

8 CsA promoted T-cell apoptosis via upregulating Fas/FasL

9 CsA protected IOBA-NHC from cell death by blocking both

10 CsA use significantly alters GCF and plasma levels of TG

11 CsA's effects on AD skin pathology were evaluated by usi

12 CsA-enhanced gingival beta-catenin stability may be invo

13 The CsA group received 10 mg Kg(-1) d(-1) CsA for 8 days.

14 mly divided into four groups: 1) control; 2) CsA; 3) ligature (Lig); and 4) ligature plus CsA (Lig +

15 medicated patients with GO (CsA GO+); and 20 CsA-medicated patients without GO (CsA GO-).

16 viduals; 20 patients with gingivitis (G); 20 CsA-medicated patients with GO (CsA GO+); and 20 CsA-med

17 % (Astagraf XL), 33.6% (Prograf), and 21.3% (CsA).

18 nalyzed as intention-to-treat (TAC-MMF n=30; CsA-MMF n=30).

19 ntrols, p = 0.17) or cardiogenic shock (2.4% CsA vs. 1.5% controls, p = 0.33).

20 Eighty non-smokers were included (40 CsA-medicated renal transplant patients with GO [GO+; n

21 (65.9% Astagraf XL, 69.8% Prograf, and 65.6% CsA).

22 am group (n = 4), an ischemic group (n = 6), CsA-postconditioned group (postcond-CsA, injection of 3

23 nificant excesses of 6-month mortality (5.7% CsA vs. 3.2% controls, p = 0.17) or cardiogenic shock (2

24 nation, 129 Astagraf XL, 113 Prograf, and 79 CsA patients had continued follow-up.

25 uire a systemic therapy, and ciclosporine A (CsA) is the only medicinal product approved for this ind

26 ll death that were blocked by cyclosporin A (CsA) and EGTA.

27 Cyclosporin A (CsA) and tacrolimus (FK506) has been reported to reduce

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

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

30 in activity by treatment with cyclosporin A (CsA) or FK506 is a cornerstone of immunosuppressive ther

31 liver transplant patients on cyclosporin A (CsA) or tacrolimus (Tac).

32 f long-term corticosteroid or cyclosporin A (CsA) therapy complicate the treatment of children with f

33 amorphous particles (UAPs) of cyclosporin A (CsA) were prepared with synthesized ACQ dyes physically

34 such as tacrolimus (TaC) and cyclosporin A (CsA), is important in the outpatient follow-up of kidney

35 ted T cells (NFAT) inhibitor, cyclosporin A (CsA), suggesting that NFAT controls BCATc expression.

36 tive stress markers (OSMs) in cyclosporin A (CsA)-induced gingival overgrowth (GO).

37 piperonyl butoxide (PBO) and cyclosporin A (CsA).

38 hibition of calcineurin using cyclosporin A (CsA).

39 mine the inhibitory effect of cyclosporin-A (CsA) on periodontal breakdown and to further explore the

40 emic preconditioning (IPC) or cyclosporin-A (CsA) treatment.

41 ceiving tacrolimus (n=34) or cyclosporine A (CsA) (n=24) or an mTORi (n=26).

42 ological inhibition of CN by cyclosporine A (CsA) ameliorated the alpha-syn-induced loss of mDA neuro

43 ficient hearts, inhibited by cyclosporine A (CsA) and adenosine, promoted by staurosporine (STS), red

44 rs of immunophilins, such as cyclosporine A (CsA) and FK506, inhibited CrkII, but not CrkI associatio

45 or Everolimus combined with cyclosporine A (CsA) and steroids.

46 to corticosteroids (CSs) and cyclosporine A (CsA) as first-line therapy for newly diagnosed cGVHD aft

47 ed the calcineurin inhibitor cyclosporine A (CsA) chronically and demonstrate an increased incidence

48 Here we show that AS and cyclosporine A (CsA) exerted synergistic inhibitory effect on cell growt

49 Whether cyclosporine A (CsA) has beneficial effects in reperfused myocardial inf

50 Cyclosporine A (CsA) increases beta-catenin messenger RNA (mRNA) and pro

51 It has been suggested that cyclosporine A (CsA) induces gingival enlargement by promoting an increa

52 Cyclosporine A (CsA) is a well-known immunosuppressive agent that gained

53 Cyclosporine A (CsA) is an immunosuppressive drug which has been widely

54 Cyclosporine A (CsA) is used for the treatment of psoriasis; however sys

55 ogical postconditioning with cyclosporine A (CsA) might protect the kidney from lethal reperfusion in

56 acute GvHD are treated with cyclosporine A (CsA) or tacrolimus (FK506), which not only often causes

57 ng/mL plus reduced-exposure cyclosporine A (CsA) or to mycophenolic acid (MPA) 1.44 g per day plus s

58 splantation) conversion from cyclosporine A (CsA) to everolimus versus continued CsA during 1-year fo

59 silencing complex (RISC) of cyclosporine A (CsA) treated and control human proximal tubule cells and

60 2:1) to sirolimus (n=314) or cyclosporine A (CsA) treatment (n=161).

61 s: (a) SRL (CNI-free) versus cyclosporine A (CsA) treatment de novo, (b) CsA+SRL versus CsA (SRL-free

62 ombining tacrolimus (TAC) or cyclosporine A (CsA) with mycophenolate mofetil (MMF) and steroids after

63 Cyclosporine A (CsA), a mitochondrial permeability transition inhibitor,

64 The PLGA-GA NS loaded with cyclosporine A (CsA), a model peptide, upon peroral dosing to rodents le

65 calcineurin inhibitor (CNI) cyclosporine A (CsA), an immunosuppressant used to prevent allograft rej

66 unosuppressant drugs such as cyclosporine A (CsA), an inhibitor of calcineurin phosphatase, frequentl

67 f M6G (80.31 +/- 21.75 muM); Cyclosporine A (CsA), an inhibitor of OATP2B1, can inhibit their intrace

68 s treated with prednisolone, cyclosporine A (CsA), and mycophenolate sodium (MPS) for the first 6 mon

69 mycophenolate mofetil (MMF), cyclosporine A (CsA), and prednisone (pred).

70 ophenolate mofetil (MMF) and cyclosporine A (CsA), are often used together after HSCT to prevent graf

71 the immunosuppressive drug, cyclosporine A (CsA), can be a major issue in transplantation medicine.

72 c9, secondary metabolites of cyclosporine A (CsA), have been associated with nephrotoxicity in organ

73 ) plays an important role in cyclosporine A (CsA)-induced chronic hypoxia.

74 lated IL-6-type cytokines in cyclosporine A (CsA)-induced gingival overgrowth (GO).

75 immunosuppressed either with cyclosporine A (CsA, 1.5 mg/kg/day subcutaneously) or with CsA and erlot

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

77 at of the standard inhibitor cyclosporine-A (CsA).

78 l hydrophobic macromolecule (Cyclosporine A, CsA), herein we provide a mechanistic understanding of S

79 human gingival epithelial (hGE) cells after CsA treatment and to investigate the role of transformin

80 -smooth muscle actin) in the hGE cells after CsA treatment with and without TGF-beta1 inhibitor were

81 The gingival morphology after CsA treatment was evaluated by histology, and the genes

82 on of DMF has a protective potential against CsA nephrotoxicity.

83 essive regimen based on the same main agent (CsA=23, Tcr=31, and Sir=35), were reexamined after 44 mo

84 as Klotho downregulation and could alleviate CsA-induced renal histological changes and function.

85 The DMF cotreatment ameliorated CsA-induced renal dysfunction as evidenced by significan

86 s treated with a combination of IL-1beta and CsA showed a decrease in the MMP-1/TIMP-1 ratio.

87 e periodontal breakdown than the control and CsA groups but less periodontal breakdown than the Lig g

88 addition of rituximab to corticosteroid and CsA appeared to be safe and effective for first-line tre

89 ociation between assessed IL-6 cytokines and CsA-induced GO might indicate distinct effects of these

90 rol analog 1-oleoyl-2-acetyl-sn-glycerol and CsA blocked cell death and arachidonic acid release not

91 Both CsA GO+ and CsA GO- groups had lower GCF TOS levels than H (P <0.001

92 Plasma FRAP level was higher in H and CsA GO- than in CsA GO+ (P = 0.008 and P = 0.02).

93 As expected, both IPC and CsA reduced MI size.

94 Our results suggest that IPC and CsA, administered immediately before reperfusion, protec

95 h concurrent binding of SPP with keratin and CsA.

96 e Lig + CsA group received silk ligature and CsA treatment.

97 tween the sirolimus (69.1+/-18.7 mL/min) and CsA (66.0+/-15.2 mL/min) treatment groups.

98 cteristics, it was hypothesized that MMF and CsA might have different effects on CB and PB T cells.

99 e of a physical mixture of SPACE-peptide and CsA in an aqueous ethanol solution to enhance the dermal

100 nt survival in the Astagraf XL, Prograf, and CsA groups were 93.2, 91.2, and 91.7%, respectively, whi

101 ilable for validation of creatinine, TaC and CsA, respectively.

102 In Tcr and CsA groups, although not significant, occurrence of GO d

103 50) delivered about 30% of topically applied CsA into the porcine skin in vitro and led to an approxi

104 g per day of olive oil as vehicle), group B (CsA, 30 mg/kg per day), group C (CsA + Val, 30 + 30 mg/k

105 cyclosporine A (CsA) treatment de novo, (b) CsA+SRL versus CsA (SRL-free) treatment de novo, (c) SRL

106 Both CsA GO+ and CsA GO- groups had lower GCF TOS levels than

107 and arachidonic acid release were blocked by CsA and 1-oleoyl-2-acetyl-sn-glycerol but not by pyrroph

108 for the metabolic complications elicited by CsA in transplant patients.

109 In addition, TGM-2 induced by CsA is downregulated by PD98059, LY294002, NAC, curcumin

110 TGM-2 protein induced by CsA was found in HGFs in a dose- and time-dependent mann

111 ), group B (CsA, 30 mg/kg per day), group C (CsA + Val, 30 + 30 mg/kg per day), and group D (Val, 30

112 The molecular signature of chronic CsA nephrotoxicity using transcriptomic analyses demonst

113 rom liver transplant recipients with chronic CsA nephrotoxicity showed significantly greater Nox2, al

114 in liver transplant recipients with chronic CsA nephrotoxicity.

115 In conclusion, CsA and FK506 inhibit proteinuria by protecting against

116 orine A (CsA) to everolimus versus continued CsA during 1-year follow-up.

117 In contrast, CsA treatment mainly resulted in downregulation of Major

118 by significant decrease in serum creatinine (CsA 0.79 +/- 0.02 mg/dL vs CsA + DMF 0.62 +/- 0.04 mg/dL

119 e patients of whom 31 initiated cyclosporin (CsA) and 47 tacrolimus (Tac) based immunosuppression.

120 Cyclosporine (CsA) is an immunosuppressant that is highly effective fo

121 tability were assessed using a cyclosporine (CsA) washout assay.

122 in parallel drug addition and cyclosporine (CsA) washout assays to detect the kinetics of drug susce

123 luded: no treatment, full dose cyclosporine (CsA, 10 mg/kg per day), ixazomib (0.25 mg/kg on days -5,

124 nonimmunosuppressive analog of cyclosporine (CsA), sarcosine-3(4-methylbenzoate)-CsA (SmBz-CsA), we f

125 osuppressive regimens based on cyclosporine (CsA), tacrolimus (Tcr), and sirolimus (Sir).

126 , tacrolimus (Prograf) bid, or cyclosporine (CsA) bid.

127 us (TAC) trough levels (C0) or cyclosporine (CsA) drawn at C0 or 2 hours after dosing (C2) correlate

128 We recently utilized the cyclosporine (CsA) washout assay, in which TRIM-CypA-mediated restrict

129 of P2Ns was demonstrated using cyclosporine (CsA) as a model peptide.

130 mens from 19 patients treated with 5 mg/kg/d CsA for 12 weeks.

131 not significant, occurrence of GO decreased (CsA [BE=56.5% and FE=34.8%; P=0.063] and Tcr [BE=19.4% a

132 , and among the most effective at delivering CsA into the skin.

133 f CsA nephrotoxicity by probably diminishing CsA-induced renal Klotho downregulation and oxidative st

134 omib alone or in combination with (1/2) dose CsA reduced donor-specific antibody, intragraft transcri

135 Compared to full dose CsA, the CNI minimization strategy with ixazomib inhibit

136 on days -5, -2 and +2) alone, and half dose CsA (5 mg/kg per day) + ixazomib.

137 A (group A, low-dose CsA; group B, high-dose CsA) or placebo (carrier only) implants at the time of h

138 es of subconjunctival CsA (group A, low-dose CsA; group B, high-dose CsA) or placebo (carrier only) i

139 relapses occurred in 85% of patients during CsA therapy and in 64% of patients during MMF therapy (P

140 olyarginine and TD-1) significantly enhanced CsA penetration into the skin.

141 SPPs enhanced CsA skin penetration, via a transcellular pathway, enhan

142 l function versus MPA plus standard-exposure CsA over the 2-year period.

143 (MPA) 1.44 g per day plus standard-exposure CsA.

144 s regulated by miRNAs specifically following CsA treatment.

145 for TAC-MMF and 90.0%, 83.3%, and 80.0% for CsA-MMF (P=ns).

146 Early conversion from CsA-based to everolimus-based immunosuppressive treatmen

147 itis (G); 20 CsA-medicated patients with GO (CsA GO+); and 20 CsA-medicated patients without GO (CsA

148 ); and 20 CsA-medicated patients without GO (CsA GO-).

149 vated in CsA GO+ compared with other groups (CsA GO- group: P = 0.003; G group: P <0.001; and H group

150 se of calcium channel blockers (P=0.029); in CsA and Tcr groups, GO was associated with papillary ble

151 years was in TAC-MMF 64.0% and 45.8%, and in CsA-MMF 36.0% (log-rank 3.0, P=0.085) and 8.0% (log-rank

152 GCF TGM-2 level was elevated in CsA GO+ compared with G (P = 0.048) and H (P = 0.001) gr

153 Plasma TGM-2 level was elevated in CsA GO+ compared with G (P = 0.048) and H (P = 0.002).

154 GCF TBARS level was elevated in CsA GO+ compared with other groups (CsA GO- group: P = 0

155 TGM-2 may contribute to CsA-induced GO in CsA-treated patients by changing GCF and plasma levels o

156 GCF TAC was higher in CsA GO+ than in H (P = 0.02).

157 01; and H group: P <0.001) and was higher in CsA GO- than in H (P = 0.048).

158 al growth factor expression was increased in CsA-treated allografts which developed intense chronic c

159 was 2,160 (Q1 to Q3: 1,087 to 3,274) ng/l in CsA and 2,068 (1,117 to 3,690) ng/l in controls (p = 0.8

160 GCF FRAP level was lower in CsA GO- than in H (P = 0.04).

161 , along with a greater than 60% reduction in CsA exposure, was associated with comparable efficacy an

162 he severity of GO decreased significantly in CsA group (mean score BE=10.29 +/- 7.70 and mean score F

163 AP level was higher in H and CsA GO- than in CsA GO+ (P = 0.008 and P = 0.02).

164 Infarct site did not influence CsA efficacy.

165 temic CsA metabolite exposure and intrarenal CsA accumulation.

166 is suggestive of CYP3A5-dependent intrarenal CsA metabolism.

167 onary intervention, to 2.5 mg/kg intravenous CsA (n = 207) or control (n = 203) groups.

168 dial Infarction) trial, a single intravenous CsA bolus just before primary percutaneous coronary inte

169 in the experimental group were fed 30 mg/kg CsA daily for 4 weeks, whereas the control rats were fed

170 ature (Lig); and 4) ligature plus CsA (Lig + CsA).

171 mong the groups demonstrating that the Lig + CsA group had significantly less gingival protein expres

172 By micro-CT and histology, the Lig + CsA group had significantly more periodontal breakdown t

173 The Lig + CsA group received silk ligature and CsA treatment.

174 This suggests that local CsA has negligible antiangiogenic effects in the human c

175 The mean CsA oral clearance was similar between CYP3A5 expressors

176 PP and keratin best correlated with measured CsA skin transport.

177 sporine (CsA), sarcosine-3(4-methylbenzoate)-CsA (SmBz-CsA), we found a significant reduction in CD10

178 (hydroethanolic solution) containing 5mg/mL CsA and 50mg/mL of free SPACE-peptide (SP50) delivered a

179 A, and quantitative PCR, the effects of MMF, CsA, and the combination of both drugs were studied on r

180 d a rejection episode: MMF/pred (27.0%), MMF/CsA (6.8%) and MMF/CsA/pred (1.4%) (P<0.001).

181 de: MMF/pred (27.0%), MMF/CsA (6.8%) and MMF/CsA/pred (1.4%) (P<0.001).

182 nts were randomized for MMF/pred, 76 for MMF/CsA, and 73 for MMF/CsA/pred.

183 for MMF/pred, 76 for MMF/CsA, and 73 for MMF/CsA/pred.

184 Therefore, for neither TaC nor CsA, a conversion formula is required.

185 However, IPC, but not CsA, also reduced myocardial edema leading to an underes

186 ificantly associated with lower Tac, but not CsA, dose-normalized trough levels.

187 Notably, CsA inhibited integrin-LFA-1-dependent and NFAT-independ

188 ment resolution >/=70% was found in 52.0% of CsA patients and 49.0% of controls (p = 0.55).

189 .5) and skin/liver ratio (1059.5+/-110.8) of CsA compared to all other groups (p<0.01).

190 PMA/alphaCD3, in the presence or absence of CsA.

191 l toxicity may depend on the accumulation of CsA and its metabolites in the renal tissue.

192 At steady state, intrarenal accumulation of CsA and its secondary metabolites should depend on the C

193 into 4 groups based on the administration of CsA and/or Val: group A (control, 1 mL/kg per day of oli

194 soriasis; however systemic administration of CsA is potentially life threatening and there are long-t

195 udies suggest that chronic administration of CsA to organ transplant patients could have significant

196 evaluating the Val effect in alleviation of CsA nephrotoxicity by probable increase in renal Klotho

197 tration of Val might lead to amelioration of CsA nephrotoxicity by probably diminishing CsA-induced r

198 Topical application of CsA has the potential to overcome this hurdle; however,

199 rovements to realize the maximum benefits of CsA.

200 dents led to maximum plasma concentration of CsA at 6 h as opposed to 24 h with PLGA-NS with at least

201 Concentrations of CsA >500 ng/mL demonstrated cytotoxicity to HGFs (P < 0.

202 n and to further explore the correlations of CsA-induced attenuation of periodontal bone loss with th

203 d the efficacy of SP50 in dermal delivery of CsA and also demonstrated its advantages over other rout

204 romising approach for the dermal delivery of CsA.

205 (CypD) enzymatic activity, nor displaced of CsA from CypD protein, suggesting a mechanism independen

206 An oral dose of CsA was administered to 24 healthy volunteers who were s

207 ings suggest that the differential effect of CsA on T cells versus ocular surface resident epithelial

208 in signaling further confirmed the effect of CsA: beta-catenin and Dvl-1 expression increased, but AP

209 the neuro- and cardio-protective effects of CsA (CiCloMulsion(R); NeuroSTAT(R)) are being tested in

210 The effects of CsA and inflammation (as assessed using interleukin [IL]

211 this study is to investigate the effects of CsA and inflammation on the production of ECM homeostati

212 blot were used to investigate the effects of CsA in human gingival fibroblasts (HGFs).

213 The effects of CsA on ligature-induced expressions of gelatinases and E

214 The inhibitory effects of CsA on the ligature-induced periodontal breakdown was ex

215 The effects of CsA, with and without TGF-beta1 inhibitor, on the morpho

216 /37) and ubiquitinylation in the gingivae of CsA-treated rats.

217 In vitro incubations of CsA, AM1, AM9, and AM1c with recombinant CYP3A4 and CYP3

218 iable bioavailability and toxicity issues of CsA.

219 group (postcond-CsA, injection of 3 mg/kg of CsA 5 minutes before the end of ischemia, (n = 6), and a

220 significantly increased the localization of CsA in the target skin (113.1+/-13.6(mug/g)/mg) compared

221 e, investigated the protective mechanisms of CsA and FK506 on proteinuria in a rat model of MCD induc

222 studies suggest that Nox2 is a modulator of CsA-induced hypoxia upstream of HIF-1alpha and define th

223 Nonetheless, the variable occurrence of CsA-induced gingival enlargement in patients receiving t

224 t inflammation may alter the pathogenesis of CsA-induced gingival enlargement by promoting a synergis

225 ation may have a role in the pathogenesis of CsA-induced gingival overgrowth.

226 nd perfusion, and the molecular phenotype of CsA nephrotoxicity.

227 The potency of CsA to inhibit P-gp was tissue-independent (maternal BBB

228 rats and mice resulted in the prevention of CsA-induced hypoxia independent of regional perfusion (b

229 However, due to the safety profile of CsA and its approval conditions, this treatment can only

230 IL-6 and OSM increases in GCF as a result of CsA usage or an immunosuppressed state irrespective of t

231 e to interpatient variability in the risk of CsA-induced nephrotoxicity.

232 ociated with the development and severity of CsA-induced gingival enlargement.

233 itors turned out to be additive with that of CsA, suggesting for these inhibitors a molecular target

234 ective effects of dimethyl fumarate (DMF) on CsA-induced nephrotoxicity by enhancing the antioxidant

235 at 1 year was 58% and 21% among patients on CsA and Tac, respectively (P =0.003).

236 esponsible for the higher rejection rates on CsA that has been reported in these subjects.

237 = 8, 20 mg/kg per day intraperitoneally) or CsA + DMF (n = 7, 50 mg/kg per day orally) for 28 days.

238 mals, and were not affected by either IPC or CsA.

239 c acid trough level of 1.5-2.5 microg/ml) or CsA (target trough level of 80-100 ng/ml) in 60 pediatri

240 inhibitor (P/EVL; n=10), prednisolone/CsA (P/CsA; n=7), or prednisolone/MPS (P/MPS; n=9).

241 therapy with P/EVL but not after switch to P/CsA or P/MPS.

242 CsA; 3) ligature (Lig); and 4) ligature plus CsA (Lig + CsA).

243 (n = 6), CsA-postconditioned group (postcond-CsA, injection of 3 mg/kg of CsA 5 minutes before the en

244 sion, serum creatinine decreased in postcond-CsA and IPC compared to ischemic group.

245 n was improved significantly in the postcond-CsA and IPC group.

246 as also significantly improved with postcond-CsA and IPC.

247 n mTOR inhibitor (P/EVL; n=10), prednisolone/CsA (P/CsA; n=7), or prednisolone/MPS (P/MPS; n=9).

248 Valsartan prevented CsA-induced oxidative stress as well as Klotho downregul

249 enal function compared to patients receiving CsA.

250 sA), sarcosine-3(4-methylbenzoate)-CsA (SmBz-CsA), we found a significant reduction in CD107a/MIP-1be

251 otility was significantly impaired by STIM1, CsA, and NFAT2 knockdown using RNAi.

252 High-dose subconjunctival CsA implants do not significantly affect corneal neovasc

253 eceived either of 2 doses of subconjunctival CsA (group A, low-dose CsA; group B, high-dose CsA) or p

254 inferred enzyme expression, affects systemic CsA metabolite exposure and intrarenal CsA accumulation.

255 l of depression-like behavior, both systemic CsA treatment and shRNA-mediated calcineurin blockade in

256 These results demonstrate that CsA significantly upregulates intracellular ROS generati

257 Further studies revealed that CsA and FK506 inhibited PAN-induced p38 and JNK signalin

258 Our results showed that CsA and FK506 treatment decreased proteinuria via a mech

259 ot CrkI activity in T cells and suggest that CsA and FK506 inhibit selected effector T cell functions

260 The CsA group received 10 mg Kg(-1) d(-1) CsA for 8 days.

261 The CsA-induced attenuation of periodontal bone loss was str

262 The CsA-induced gingival EMT is dependent or at least partia

263 eatment of TGF-beta1 inhibitor on top of the CsA treatment.

264 ming growth factor beta1 (TGF-beta1) on this CsA-induced EMT.

265 for both tacrolimus formulations compared to CsA; 41.1% (Astagraf XL), 33.6% (Prograf), and 21.3% (Cs

266 TGM-2 may contribute to CsA-induced GO in CsA-treated patients by changing GCF a

267 ese results indicate that MMF is inferior to CsA in preventing relapses in pediatric patients with FR

268 Conversely, 3D cultures responded to CsA treatment with a reduction in MMP-10 secretion.

269 Fibroblast monolayers responded to CsA with no changes in the secretion of ECM mediators.

270 Activated CB T cells were more sensitive to CsA than activated PB T cells, which might be explained

271 vation is found in CnAbeta(-/-) mice or upon CsA treatment to inhibit calcineurin.

272 MF 0.62 +/- 0.04 mg/dL, P = 0.001) and urea (CsA 66.9 +/- 0.4 mg/dL vs CsA + DMF 53.3 +/- 2.6 mg/dl,

273 The mean apparent urinary CsA clearance based on a 48-hr collection was 20.4% lowe

274 ) was significantly higher in TAC-MMF versus CsA-MMF (65.5% vs. 21.7%, log-rank 8.3, P=0.004).

275 (CsA) treatment de novo, (b) CsA+SRL versus CsA (SRL-free) treatment de novo, (c) SRL+tacrolimus eli

276 serum creatinine (CsA 0.79 +/- 0.02 mg/dL vs CsA + DMF 0.62 +/- 0.04 mg/dL, P = 0.001) and urea (CsA

277 = 0.001) and urea (CsA 66.9 +/- 0.4 mg/dL vs CsA + DMF 53.3 +/- 2.6 mg/dl, P < 0.0001) levels, as wel

278 associated with AR (hazard ratio for Tac vs CsA 0.25 [95% confidence interval, 0.11-0.57], P = 0.001

279 When CsA was given, the protein and mRNA expressions of E-cad

280 original cobblestone monolayer pattern when CsA was added.

281 This study investigated whether CsA improved ST-segment resolution in a randomized, mult

282 While CsA has been widely used to prevent graft rejection in p

283 emic inhibition of calcineurin activity with CsA or local downregulation of calcineurin levels in the

284 olved in biologic mechanisms associated with CsA-induced GO.

285 The low correlation of C0 with CsA AUC could be responsible for the higher rejection ra

286 ut poor predictability will occur at C0 with CsA.

287 opsy-confirmed acute rejection compared with CsA-based immunosuppression and is not recommended.

288 creased significantly with MMF compared with CsA.

289 treated mouse podocytes, pre-incubation with CsA and FK506 restored the distribution of the actin cyt

290 ithout relapse was significantly longer with CsA than with MMF during the first year (P<0.05), but no

291 deaths reported with sirolimus and one with CsA; higher rates of biopsy-confirmed acute rejection (2

292 (CsA, 1.5 mg/kg/day subcutaneously) or with CsA and erlotinib (10 mg/kg/day orally).

293 The reversal of the molecular phenotype with CsA and the associated biomarkers can serve as a referen

294 o observed in mice treated systemically with CsA.

295 patient per year occurred with MMF than with CsA during the first year (P=0.03), but not during the s

296 Male Sprague-Dawley rats were treated with CsA (n = 8, 20 mg/kg per day intraperitoneally) or CsA +

297 monolayers and 3D cultures were treated with CsA alone or in combination with IL-1beta for up to 72 h

298 In rats treated with CsA, overgrowth of gingivae was observed, and altered ex

299 Treatment with CsA and FK506 also inhibited PAN-induced podocytes apopt

300 increased in response to cell treatment with CsA and FK506, reflecting increased trans-to-cis convers