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1 with reduced cellular toxicity compared with cyclosporine.
2 ith high-dose prednisolone, methotrexate and cyclosporine.
3 including cyclophosphamide, vincristine, and cyclosporine.
4 centiles, and history of using prednisone or cyclosporine.
5 ot genotype 1b, had increased sensitivity to cyclosporine.
6 compatible groups and were not suppressed by cyclosporine.
7 ns of cytotoxic T-lymphocyte antigen 4-Ig or cyclosporine.
8 often treated with steroids, rituximab, and cyclosporine.
9 r standard-dose cyclosporine or reduced-dose cyclosporine.
10 dard of care 40 years after the discovery of cyclosporine.
11 release, and 152 at-risk patients receiving cyclosporine.
12 JW47, using a quinolinium cation tethered to cyclosporine.
13 Interventions: Short course (3-7 days) of cyclosporine.
14 en and the less-intensive regimen) than with cyclosporine.
15 NS2 modulates sensitivity of HCV to cyclosporines.
18 al dexamethasone 40 mg for days 1 to 4, oral cyclosporine 2.5 to 3 mg/kg daily for day 1 to 28, and i
20 s received an intravenous bolus injection of cyclosporine, 2.5 mg/kg, at the onset of advanced cardio
24 ts were randomized to receive an IV bolus of cyclosporine A (10 mg/kg) or normal saline (placebo, con
26 monly prescribed topical treatments included cyclosporine A (CSA) 0.05 % (71/104, 68 %), fluoromethol
27 antly, a pharmacological inhibition of CN by cyclosporine A (CsA) ameliorated the alpha-syn-induced l
28 ated in DHHC5-deficient hearts, inhibited by cyclosporine A (CsA) and adenosine, promoted by staurosp
29 whereas inhibitors of immunophilins, such as cyclosporine A (CsA) and FK506, inhibited CrkII, but not
31 on of rituximab to corticosteroids (CSs) and cyclosporine A (CsA) as first-line therapy for newly dia
32 s are administered the calcineurin inhibitor cyclosporine A (CsA) chronically and demonstrate an incr
40 mic or pharmacological postconditioning with cyclosporine A (CsA) might protect the kidney from letha
41 Patients with acute GvHD are treated with cyclosporine A (CsA) or tacrolimus (FK506), which not on
42 s of 3-8 or 6-12 ng/mL plus reduced-exposure cyclosporine A (CsA) or to mycophenolic acid (MPA) 1.44
43 after renal transplantation) conversion from cyclosporine A (CsA) to everolimus versus continued CsA
44 warm ischemia), and rats subjected to acute cyclosporine A (CSA) toxicity (50 mg/kg for 2 d intraper
45 the RNA-induced silencing complex (RISC) of cyclosporine A (CsA) treated and control human proximal
47 ive strategies combining tacrolimus (TAC) or cyclosporine A (CsA) with mycophenolate mofetil (MMF) an
50 terestingly, the calcineurin inhibitor (CNI) cyclosporine A (CsA), an immunosuppressant used to preve
51 treated with immunosuppressant drugs such as cyclosporine A (CsA), an inhibitor of calcineurin phosph
52 more than that of M6G (80.31 +/- 21.75 muM); Cyclosporine A (CsA), an inhibitor of OATP2B1, can inhib
53 splant recipients treated with prednisolone, cyclosporine A (CsA), and mycophenolate sodium (MPS) for
55 ugs, such as mycophenolate mofetil (MMF) and cyclosporine A (CsA), are often used together after HSCT
56 y side effect of the immunosuppressive drug, cyclosporine A (CsA), can be a major issue in transplant
57 of AM19 and AM1c9, secondary metabolites of cyclosporine A (CsA), have been associated with nephroto
58 in mice treated with a potent SC activator, cyclosporine A (CSA), which inhibits the phosphatase cal
60 s of fibrosis-related IL-6-type cytokines in cyclosporine A (CsA)-induced gingival overgrowth (GO).
61 Recipients were immunosuppressed either with cyclosporine A (CsA, 1.5 mg/kg/day subcutaneously) or wi
62 nd during infusion (6, 12, or 24 mg/kg/h) of cyclosporine A (CsA, a P-glycoprotein [P-gp] inhibitor).
64 from four AD patients who had received oral cyclosporine A (CyA) treatment for up to 17 months regar
66 clobetasol, or in combination with systemic cyclosporine A and anti-alphabeta-T-cell receptor antibo
70 A-matched related donor and prophylaxis with cyclosporine A and methotrexate were associated with low
74 bunit ring and unhooks it from cyclophilin D/cyclosporine A binding sites in the ATP synthase F1, pro
76 ucted from June 22, 2010, to March 13, 2013 (Cyclosporine A in Out-of-Hospital Cardiac Arrest Resusci
78 or PLCgamma2 or inhibiting calcineurin with cyclosporine A leads to increased expression of PD-1 lig
80 aling pathway in lymphoma cells, either with cyclosporine A or anti-CD1d blocking antibody, prolonged
81 hat short term (4-6 h) treatment with 15 muM cyclosporine A or FK506 rescues the pre-formed immature
82 indicated that inhibition of calcineurin by cyclosporine A or knockdown of NFATc4 using small interf
83 with chaperone Hsp70, and the treatment with cyclosporine A reduces the association of mutant P-gp, t
84 ion with costimulation blockade and low-dose cyclosporine A resulted in a complete deletion of periph
88 keratin 16 (K16) mRNA] at baseline and after cyclosporine A treatment in 25 moderate to severe AD pat
94 -principle, the known binding interaction of Cyclosporine A with cyclophilin A protein in a yeast cel
95 -dependent migration (including SP600125 and cyclosporine A) and differentiation (cyclosporine A only
98 ubating cells with the cyclophilin inhibitor cyclosporine A, a treatment that triggered efficient ER
100 rapies using calcineurin inhibitors, such as cyclosporine A, are associated with a higher incidence o
103 tide) and a model hydrophobic macromolecule (Cyclosporine A, CsA), herein we provide a mechanistic un
104 three specific calcineurin inhibitors FK506, cyclosporine A, or calcineurin inhibitory peptide preven
105 Ca(2+) signaling or calcineurin with BAPTA, cyclosporine A, or FK506 prevented activation of NF-kapp
106 tochondrial Ca(2+) influx, by mPTP inhibitor cyclosporine A, sanglifehrin, and in cyclophilin D knock
108 kidneys long-term after 12 days of high-dose cyclosporine A, uniformly accepted donor-major histocomp
110 rtrophy group (n = 5), and aortic-banded and cyclosporine A- treated cardiomyopathy group (n = 5).
120 pulses of cyclophosphamide, vincristine, or cyclosporine A; or salvage splenectomy are considered.
121 tion were observed both in mice treated with cyclosporine, a known stimulator of the HCM response, an
125 had been prescribed psoralen, methotrexate, cyclosporine, acitretin, adalimumab, etanercept, inflixi
126 onary artery to receive a bolus injection of cyclosporine (administered intravenously at a dose of 2.
129 cyclosporine and daily UV exposures, dietary cyclosporine after a period of UV exposures, and bolus d
132 received cyclophosphamide at 120 mg/kg plus cyclosporine and antibacterial, antiviral, and antifunga
133 come at discharge was comparable between the cyclosporine and control groups: 7 (1.8%) vs 5 (1.3%) pa
134 rless SKH-1 mice by three protocols: dietary cyclosporine and daily UV exposures, dietary cyclosporin
137 HCV replicons, containing or lacking NS2, to cyclosporine and other direct-acting antiviral agents.
139 d for effects on conidiation, hyphal growth, cyclosporine and stress resistance, and insect virulence
141 We confirm that the immunosuppressive drugs cyclosporine and tacrolimus also inhibit BCR-mediated ly
146 iple comorbidities, concomitant therapy with cyclosporine, and a high Psoriasis Area and Severity Ind
148 raacetate-AM acetoxymethyl ester (BAPTA-AM), cyclosporine, and inhibitor of nuclear factor of activat
149 rferon (IFN-alpha), telaprevir, daclatasvir, cyclosporine, and ribavirin, despite no prior exposure t
150 inary metabolic patterns varied over time in cyclosporine- and tacrolimus-treated patients and were s
152 Mixed-chirality peptide macrocycles such as cyclosporine are among the most potent therapeutics iden
153 orticosteroids; other medications, including cyclosporine, are used in patients who fail to respond.
156 that the postresuscitation administration of cyclosporine attenuates myocardial and cardiac mitochond
158 AIDs were replaced by oral prednisolone with cyclosporine, azathioprine, or mycophenolate as steroid-
160 has been demonstrated to be as efficient as cyclosporine-based immunosuppression and is associated w
161 pt-based immunosuppression, as compared with cyclosporine-based immunosuppression, was associated wit
166 fferent drugs, such as PF74, CAP-1, IXN-053, cyclosporine, Bi2 (also known as BI-2), and the peptide
169 pt) by 106 (27.2%), acitretin by 57 (14.6%), cyclosporine by 30 (7.7%), fumaric acid esters by 19 (4.
171 with dietary cyclosporine, bolus dosages of cyclosporine by gavage, resulting in strongly varying bl
175 uced blocks in THP-1 cells by treatment with cyclosporine (Cs) or its nonimmunosuppressive analogue S
176 kidney-pancreas transplant recipients during cyclosporine (CSA) and TAC eras, analyzed by intention-t
179 HIV, tacrolimus (TAC) trough levels (C0) or cyclosporine (CsA) drawn at C0 or 2 hours after dosing (
183 ing as defined in parallel drug addition and cyclosporine (CsA) washout assays to detect the kinetics
184 locked by the nonimmunosuppressive analog of cyclosporine (CsA), sarcosine-3(4-methylbenzoate)-CsA (S
185 ts under immunosuppressive regimens based on cyclosporine (CsA), tacrolimus (Tcr), and sirolimus (Sir
186 Groups included: no treatment, full dose cyclosporine (CsA, 10 mg/kg per day), ixazomib (0.25 mg/
188 d been referred for primary PCI, intravenous cyclosporine did not result in better clinical outcomes
189 with nonshockable cardiac rhythm after OHCA, cyclosporine does not prevent early multiple organ failu
190 d their efficacy in combination with reduced cyclosporine dosing in de novo heart transplant recipien
191 itraconazole, voriconazole, or posaconazole; cyclosporine; erythromycin or clarithromycin; dronedaron
192 ate analyses, the use of Olopatadine 0.1% or cyclosporine eye drops before DALK (OR = 14.51, 95% CI =
195 of cyclophilins, including the approved drug cyclosporine, greatly reduced the viability of glioblast
197 rate of the primary outcome was 59.0% in the cyclosporine group and 58.1% in the control group (odds
198 R]) ages were 63.0 (54.0-71.8) years for the cyclosporine group and 66.0 (57.0-74.0) years for the co
199 set of advanced cardiovascular life support (cyclosporine group) or no additional intervention (contr
201 , respectively (belatacept more-intensive vs cyclosporine: hazard ratio [HR] = 0.95; 95% confidence i
202 13.9%, respectively (belatacept 4-weekly vs cyclosporine: HR = 1.06, 95% CI 0.35-3.17, P = .92; bela
203 -1.92; P = .89; belatacept less-intensive vs cyclosporine: HR = 1.61; 95% CI 0.85-3.05; P = .15).
204 I 0.35-3.17, P = .92; belatacept 8-weekly vs cyclosporine: HR = 2.00, 95% CI 0.75-5.35, P = .17).
205 s, approximately 35x10(6)) versus vehicle in cyclosporine-immunosuppressed swine with a chronic left
208 nous steroid therapy in 35 patients (26.5%), cyclosporine in 98 patients (74.2%), and azathioprine in
216 e, we show that endothelial cells exposed to cyclosporine in vitro and in vivo release microparticles
217 ho-NKCC2, and treatment of isolated TAL with cyclosporine increased the chloride affinity and transpo
218 esulting in strongly varying blood levels of cyclosporine, increased tumor development in chronically
219 infection was enhanced 4-fold by addition of cyclosporine, indicating that the requirement for TNPO3
222 tates exploration into the role of miRNAs in cyclosporine-induced nephrotoxicity (CIN) and the gene p
224 for concurrent use of verapamil; diltiazem; cyclosporine; ketoconazole, itraconazole, voriconazole,
226 egib administration and weekly monitoring of cyclosporine levels ensured that therapeutic immunosuppr
227 %) in DSS was seen in all sites treated with cyclosporine lipogel, (P < .001; 95% CI, 77.48-88.22).
228 ird arm comprised 7 patients randomized with cyclosporine lipogel, 2.0% or standard clobetasol propio
229 was observed after 2 weeks of treatment with cyclosporine lipogel, 2.0% w/w (P < .001; 95% CI, 13.77-
230 4 patients were randomized to receive either cyclosporine lipogel, 2.0% weight by weight (w/w), or pl
231 d arm, 7 patients were randomized to receive cyclosporine lipogel, 2.0%, or conventional cyclosporine
232 (41%) psoriasis lesional sites treated with cyclosporine lipogel, 85.7% of sites treated with clobet
233 rimental and clinical evidence suggests that cyclosporine may attenuate reperfusion injury and reduce
234 nts suggests that the mode of administrating cyclosporine may be crucial for the increased skin cance
235 was not significantly different between the cyclosporine (median, 10.0; IQR, 7.0-13.0) and the contr
236 between 1989 and 2015, prescribed any ISDs (cyclosporine, methotrexate, azathioprine, anti-TNF drugs
237 3 years posttransplant, she is maintained on cyclosporine, MMF and prednisone with no PRES recurrence
238 nance immunosuppressive regime consisting of cyclosporine, mycophenolate mofetil, and prednisolone we
240 ore (mPTP) opener, and N-methyl-4-isoleucine cyclosporine (NIM811), an mPTP inhibitor, were administe
243 attributable mostly to a single medication, cyclosporine ophthalmic emulsion (Restasis, Allergan, Ir
244 r samples from patients treated with topical cyclosporine or corticosteroids showed a dramatic reduct
246 astatin, whereas combining atorvastatin with cyclosporine or mycophenolate in place of rapamycin was
250 orticosteroids, intravenous immunoglobulins, cyclosporine, plasmapheresis, thalidomide, cyclophospham
252 ive belatacept regimens as compared with the cyclosporine regimen (hazard ratio with the more-intensi
253 regimen, and 131 of the 215 treated with the cyclosporine regimen were followed for the full 84-month
259 re-intensive, belatacept less-intensive, and cyclosporine, respectively (belatacept more-intensive vs
262 rsensitivity reaction that were treated with cyclosporine, resulting in rapid and significant clinica
263 ate (RR, 0.98 [95% CI, 0.78-1.23]; P = .83), cyclosporine (RR, 1.16 [95% CI, 0.48-2.80]; P = .49), an
266 on-attenuated NS3-5B JFH1 RNAs, showing that cyclosporine sensitivity is linked to reduced replicatio
268 rred, new observational studies suggest that cyclosporine, tacrolimus, and rituximab may be effective
269 is approach was validated for phylloquinone, cyclosporine, testosterone undecanoate, cabazitaxel and
273 as significantly higher with tacrolimus than cyclosporine; there was no difference between the two ta
275 ns included topical corticosteroids, topical cyclosporine, topical vitamin A, oral doxycycline, punct
277 o experience less side effects compared with cyclosporine-treated patients, except for dry skin.
283 , higher serum level of uric acid, and blood cyclosporine trough level (C0) and used higher doses of
284 , higher serum level of uric acid, and blood cyclosporine trough level (C0) and used higher doses of
285 nine, BUN, folate and vitamin B12, and blood cyclosporine trough level (C0) are independently associa
286 tinine (P=0.03), and BUN (P=0.05), and blood cyclosporine trough level (C0, P=0.005) were independent
288 gnificantly different between the 98 (24.5%) cyclosporine vs 101 (25.6%) control patients at hospital
291 Conclusions and Relevance: A short course of cyclosporine was of therapeutic benefit in the treatment
294 elatacept 4-weekly, belatacept 8-weekly, and cyclosporine were 11.1%, 21.9%, and 13.9%, respectively
295 elatacept 4-weekly, belatacept 8-weekly, and cyclosporine were 67.0, 68.7, and 42.7 mL/min per 1.73 m
296 l, had limitations, glucocorticosteroids and cyclosporine were the most promising systemic immunomodu
297 acy of systemic drugs are scarce, except for cyclosporine, which has been approved for the therapy of
298 t transplant, immunosuppressed with low-dose cyclosporine, who presented to a specialty dermatology t
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