ライフサイエンスコーパス: CsA

1 CsA causes specific changes in miRNAs and mRNAs associat

2 CsA CE was well tolerated.

3 CsA concentration at C4 correlated better with AUC than

4 CsA continued to maintain a favorable safety profile.

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

6 CsA enhanced the generation of intracellular ROS at conc

7 CsA inhibited the expressions of gelatinase MMPs and EMM

8 CsA supplementation during cold storage or the first 15-

9 CsA use significantly alters GCF and plasma levels of TG

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

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

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

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

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

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

16 % (Astagraf XL), 33.6% (Prograf), and 21.3% (CsA).

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

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

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

20 (65.9% Astagraf XL, 69.8% Prograf, and 65.6% CsA).

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

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

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

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

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

26 Cyclosporin A (CsA) and tacrolimus (FK506) are valuable immunosuppressa

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

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

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

32 hat of an Rgg in complex with cyclosporin A (CsA), an inhibitor of SHP-induced Rgg activity, reveals

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

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

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

36 escued by the mPTP inhibitor, Cyclosporin A (CsA).

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

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

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

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

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

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

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

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

45 onal therapy for severe VKC, cyclosporine A (CsA) cationic emulsion (CE), an oil-in-water emulsion wi

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

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

48 ted their ability to deliver cyclosporine A (CsA) for immunomodulatory applications.

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 l-prolyl isomerase inhibitor Cyclosporine A (CsA) selectively kills EGFR+ or HER2+ breast cancer cell

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

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

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

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

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

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

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

67 ation of cardiac exposure to cyclosporine A (CsA), another putative mitochondrial protectant, on card

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

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

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

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

72 1) infection caused cSCCs in cyclosporine A (CsA)-treated mice, even in the absence of UV light.

73 with ABCB1 inhibition using cyclosporine A (CsA).

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

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

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

77 keratitis, symptoms, and QoL achieved after CsA CE treatment for 4 months remained stable over the 8

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

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

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

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

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

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

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

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

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

87 ER2/EGFR protein folding, including DDAs and CsA, have the potential to kill cancers that overexpress

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

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

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

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

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

93 h concurrent binding of SPP with keratin and CsA.

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

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

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

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

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

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

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

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

102 Both CsA-loaded DIANAs inhibited the proliferation and activa

103 f N57A by G94D in HIV-1(LAI) is abrogated by CsA treatment in some cell types, demonstrating that thi

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

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

106 grees C in either Celsior alone or Celsior + CsA (0.2 uM), then reperfused for 45 minutes in Krebs so

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

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

109 in liver transplant recipients with chronic CsA nephrotoxicity.

110 In addition, in this study cohort, CsA CE was well tolerated.

111 for the nMIC and nFIB) without compromising CsA's pharmacological activity.

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

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

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

115 ncreased bioavailability versus conventional CsA formulations.

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

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

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

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

120 Tacrolimus (Tac) and Cyclosporine (CsA) levels obtained during the first 15 days post-LT we

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

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

123 rus strains in the presence of cyclosporine (CsA), indicating that N57A infectivity is dependent upon

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

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

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

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

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

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

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

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

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

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

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

135 The efficacy of high-dose CsA CE in improving keratitis, symptoms, and QoL for tho

136 with significant improvements for high-dose CsA CE versus vehicle.

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 mg/ml) eye drops 4 times daily (high dose), CsA CE twice daily (low dose) plus vehicle twice daily,

140 During CsA infusion, whole-brain gray matter V (T) and K (1) we

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

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

143 s regulated by miRNAs specifically following CsA treatment.

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

145 Further, CsA synergizes with the DDA tcyDTDO to kill HER2/EGFR ov

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

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

148 nMIC and nFIB displayed good CsA encapsulation efficiency (up to 4.5 and 2 mg/mL, res

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

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

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

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

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

156 01; and H group: P <0.001) and was higher in CsA GO- than in H (P = 0.048).

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

158 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

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

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

161 ors were observed in 70% of MmuPV1-infected, CsA-treated mice on back as well as on tail skin.

162 Infarct site did not influence CsA efficacy.

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

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

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

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

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

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

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

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

171 The mean CsA oral clearance was similar between CYP3A5 expressors

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

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

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

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

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

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

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

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

180 ility, and comfort profile supports this new CsA formulation as having a positive benefit-to-risk rat

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

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

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

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

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

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

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

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

189 These actions of CsA likely contribute to the adverse effects associated

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

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

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

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

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

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

196 Rgg activity, reveals the molecular basis of CsA function.

197 rovements to realize the maximum benefits of CsA.

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

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

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

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

202 romising approach for the dermal delivery of CsA.

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

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

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

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

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

208 Effects of CsA addition to the perfusate during reperfusion were ti

209 These effects of CsA involve at least two of the stress-activated protein

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

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

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

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

214 The impact of CsA on outcome parameters was significant and similar ac

215 Inclusion of CsA during cold storage is cardioprotective.

216 Subcutaneous injections of CsA-loaded DIANAs in mice provided CsA sustained release

217 iable bioavailability and toxicity issues of CsA.

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

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

220 ctional recovery and potential mechanisms of CsA action in an isolated working rat heart model of don

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

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

225 The toxic effect with the presence of CsA for the full 45-minute reperfusion is associated wit

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

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

228 ounts and provided more sustained release of CsA in vitro, nFIB enhanced cellular uptake and promoted

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

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

231 However, use of CsA is associated with more serious side effects and wor

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

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

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

235 en (CsA CE 4 times daily [QID, high-dose] or CsA CE twice daily [BID, low-dose] + vehicle BID) and ve

236 = 8, 20 mg/kg per day intraperitoneally) or CsA + DMF (n = 7, 50 mg/kg per day orally) for 28 days.

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

238 IS regimen was based on either Tac or CsA in 243 (56.3%) and 189 (43.8%), respectively.

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

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

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

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

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

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

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

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

247 ctions of CsA-loaded DIANAs in mice provided CsA sustained release, decreasing alloantigen-induced im

248 enal function compared to patients receiving CsA.

249 patients remained on their original regimen (CsA CE 4 times daily [QID, high-dose] or CsA CE twice da

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

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

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

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

254 Immunosuppression by systemic CsA, but not UV-B irradiation, was a prerequisite, as im

255 sion (IS) was considered as a median of Tac, CsA blood trough levels 12 hours after drug administrati

256 Optimal IS was defined as a median of Tac, CsA blood trough levels 12 hours after drug administrati

257 These results demonstrate that CsA significantly upregulates intracellular ROS generati

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

259 Here we show that CsA, but not FK506, causes activation of the integrated

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

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

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

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

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

265 reported in 15 (20.8%) and 11 (15.7%) of the CsA CE high-dose and low-dose patients, respectively, mo

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

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

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

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

270 Hearts exposed to CsA for 45 minutes at reperfusion recovered poorly with

271 ndred sixty-nine patients were randomized to CsA CE 0.1% (1 mg/ml) eye drops 4 times daily (high dose

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

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

274 r-alone stored hearts were exposed to 0.2 uM CsA for the initial 15 minutes (nonworking period) or th

275 d administration frequency than unformulated CsA.

276 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,

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

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

279 = 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

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

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

282 original cobblestone monolayer pattern when CsA was added.

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

284 ed the 8-month follow-up period during which CsA CE patients remained on their original regimen (CsA

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

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

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

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

289 ut poor predictability will occur at C0 with CsA.

290 creased significantly with MMF compared with CsA.

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

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

293 ssessed by QUICK questionnaire observed with CsA CE compared with vehicle during the 4-month evaluati

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

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

296 o observed in mice treated systemically with CsA.

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

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