ライフサイエンスコーパス: MTX

1 MTX (0.75 mg/kg per day) was administered for 5 days, an

2 MTX AUC0-48h was a significant predictor of overall toxi

3 MTX concentrations in a patient's serum undergoing chemo

4 MTX decreases cortical Bdnf expression, which is restore

5 MTX induces death in rapidly replicating cells and is us

6 MTX inhibits 5-aminoimidazole-4-carboxamide ribonucleoti

7 MTX inhibits thymidine synthesis by targeting dihydrofol

8 MTX use was associated with a 70% reduction in mortality

9 MTX use was associated with reduced risk of death (adjus

10 MTX-ARG rats demonstrated greater jejunal and ileal bowe

11 MTX-inducible changes in DHFR(FS) and TYMS(SS) expressio

12 MTX-related clinical neurotoxicity is transient, and mos

13 co-2 vs. co-culture cell model: Caco-2:HT-29-MTX (90:10%) and colonic fermentation were determined fo

14 etter to mucus-producing cells such as HT-29-MTX than to the parental HT-29 cells.

15 olon cancer cell line and was effective in a MTX-transport resistant leukemic cell line.

16 single-agent methotrexate and folinic acid (MTX-FA; SIR, 0.7; 95% CI, 0.5 to 1.1) and also for patie

17 replications via interaction with Cdt1 after MTX treatment, and DHFR amplification proceeded in v-K-r

18 nths with folinic acid rescue 24 hours after MTX administration.

19 h myelination and cognitive impairment after MTX chemotherapy.

20 lative risk of early menopause was low after MTX-FA but was substantial after EMA-CO, reaching 13% by

21 o overall increased risk of malignancy after MTX-FA or EMA-CO.

22 This rescue after MTX depends on intact TrkB expression in OPCs.

23 NR could deliver the chemotherapeutic agent, MTX to tumor cells and induce effective cell killing.

24 Inclusion of low-dose prednisone in an MTX-based treatment strategy for tight control in early

25 ssed transgenes is similarly decreased in an MTX-inducible manner.

26 rthermore, enforced expression of Cks1 in an MTX-resistant breast cancer cell line was found to resto

27 This has led to the development of an MTX-resistant DHFR, DHFR L22F, F31S (DHFR(FS)), to rescu

28 Patients were randomly assigned to an MTX-based, tight control strategy starting with either M

29 , FPGS mRNA expression (P = 2.1 x 10-3), and MTX systemic clearance (P = 4.4 x 10-2) explained 42% of

30 Cotherapy with AICAR and MTX could represent a novel strategy to treat metabolic

31 ith the adenosine binding domain of DHFR and MTX interacting with the loop domain.

32 ated with a single dose of methotrexate, and MTX-ARG rats were treated with oral ARG following inject

33 onditions, a decrease in the IC50 of MTX and MTX-loaded MSNR was observed when compared to normoxic c

34 ions allowed the locations of the NADPH and MTX ligands to be mapped, with NADPH associated with the

35 ibitor methotrexate (MTX), or both NADPH and MTX were characterized by 193 nm ultraviolet photodissoc

36 of MTX plus etanercept, triple therapy, and MTX monotherapy among patients with early RA with active

37 the MTX plus etanercept, triple therapy, and MTX monotherapy arms.

38 vity significantly decreased during UDCA and MTX-treatment and also after OLT.

39 (parSlo) is inherently insensitive to MTX as MTX shifted the activation of heterologously expressed p

40 for AMPK as a direct molecular link between MTX and energy metabolism in skeletal muscle.

41 failure were nonrandomly assigned to ABFM C-MTX plus nelarabine.

42 augmented Berlin-Frankfurt-Muenster (ABFM) C-MTX regimen.

43 ents treated with the best-performing arm, C-MTX plus nelarabine, had a 5-year DFS of 91% (n = 147).

44 otrexate (HD-MTX) or Capizzi methotrexate (C-MTX) during interim maintenance (IM) or prednisone or de

45 h Capizzi-based methotrexate/pegaspargase (C-MTX) in patients with newly diagnosed pediatric T-cell l

46 vs 58% +/- 4% for MRD-negative vs positive C-MTX subjects; 88% +/- 2% vs 68% +/- 4% for HD-MTX subjec

47 Although HD-MTX was superior to C-MTX, MRD retained prognostic significance in both groups

48 The COG ABFM regimen with C-MTX provided excellent EFS and OS without cranial radiat

49 loading, in vitro MTX release, and cellular MTX delivery under hypoxic conditions.

50 PB compared with BM: 34% versus 38% with CNI-MTX and 27% versus 20% with CNI-MMF GVHD prophylaxis.

51 Compared with a normal control, MTX increased the density of osteoclasts within the meta

52 e testing during MTX therapy, the cumulative MTX dose corresponded to a statistically significant ass

53 Fourteen patients (3.8%) developed MTX-related clinical neurotoxicity.

54 UVPD of the binary DHFR.NADPH and DHFR.MTX complexes led to an unprecedented number of fragment

55 TX with leucovorin rescue or escalating dose MTX with PEG asparaginase without leucovorin rescue.

56 tudy that included five courses of high-dose MTX and 13 to 25 doses of triple intrathecal therapy.

57 data on safety of intrathecal and high-dose MTX rechallenge in patients with neurotoxicity.

58 uence the kinetics and response to high-dose MTX therapy in childhood ALL.

59 were randomly assigned to receive high-dose MTX with leucovorin rescue or escalating dose MTX with P

60 challenged with intrathecal and/or high-dose MTX, 12 did not experience recurrence of neurotoxicity.

61 = .009), a frequent side effect of high-dose MTX.

62 ictor of overall toxic adverse events during MTX courses (R(2) = 0.043; P < .001), whereas the thymid

63 onitor for risk of worsening fibrosis during MTX therapy.

64 worsening of hepatic fibrosis scores during MTX therapy.

65 ars) underwent NASH FibroSure testing during MTX therapy and were eligible for correlation analysis.

66 who underwent NASH FibroSure testing during MTX therapy, the cumulative MTX dose corresponded to a s

67 tight control strategy starting with either MTX and prednisone or MTX and placebo.

68 All major treatments except MTX-FA increased the risk of early menopause.

69 ompared with no GC use, after adjustment for MTX and TNF inhibitor use (HR(adj) 3.1 [95% CI 2.0, 4.7]

70 he binding constant (K) value calculated for MTX was 3.821x10(5)M(-1).

71 The sensor was calibrated for MTX in phosphate buffer at different dynamic range by va

72 Our results demonstrate mechanisms for MTX-induced osteoclastogenesis and show that MTX induces

73 We found MTX markedly reduced the threshold for AICAR-induced AMP

74 al methotrexate (MTX) based treatments (free MTX, MTX loaded Lecithin-PVA nanoparticles, MTX loaded L

75 ne plus hydroxychloroquine), or step-up from MTX monotherapy to one of the combination therapies (MTX

76 ediate combination treatment or step-up from MTX monotherapy.

77 Furthermore, MTX activated AMPK in wild-type HEK-293 cells.

78 ative affinities: raltitrexed > pemetrexed > MTX) at low pH.

79 HD-MTX was given at 3.5 g/m(2) every 2 weeks for a total of

80 med 5 days after HD-MTX infusion or after HD-MTX clearance.

81 HD-MTX infusion and resumed 5 days after HD-MTX infusion or after HD-MTX clearance.

82 Although HD-MTX was superior to C-MTX, MRD retained prognostic signi

83 TX subjects; 88% +/- 2% vs 68% +/- 4% for HD-MTX subjects).

84 The combination of ibrutinib, HD-MTX, and rituximab was tolerated with an acceptable safe

85 fter completing 4 cycles of the ibrutinib/HD-MTX/rituximab combination.

86 aily dosing) with high-dose methotrexate (HD-MTX) and rituximab in patients with CNS lymphoma (CNSL).

87 to receive either high-dose methotrexate (HD-MTX) or Capizzi methotrexate (C-MTX) during interim main

88 Ibrutinib was held on days of HD-MTX infusion and resumed 5 days after HD-MTX infusion or

89 HT29-MTX cells contained >1000-fold higher levels of UGT1A8 m

90 f Caco-2 monoculture and 90% Caco-2/10% HT29-MTX co-cultures on L-pNIPAM hydrogels were increased, an

91 s using mucus-producing (90% Caco-2:10% HT29-MTX-E12 co-cultures) vs. non-mucus-producing intestinal

92 In the intestinal Caco-2/HT29-MTX co-culture model, overall relative glucuronidation r

93 es, Caco-2 (colorectal adenocarcinoma), HT29-MTX-E12 (colorectal adenocarcinoma) and HepG2 (hepatocel

94 -term 3D co-culture model of Caco-2 and HT29-MTX cells under conditions analogous to inflammation, to

95 rse effects were observed on Caco-2 and HT29-MTX cells.

96 ls and an inducer of IL-8 production by HT29-MTX cells.

97 of living cultured human colonic cells (HT29-MTX) and human colonic tissue explants.

98 lateral parts of the plasma membrane of HT29-MTX cells.

99 l geometries of the MTX(Glu)5 and hydrolyzed MTX(Glu)1 in the mutant complexes differ significantly f

100 tant complexes with MTX(Glu)5 and hydrolyzed MTX(Glu)1, revealing the complete set of key residues in

101 (TYMS(SS)) is resistant to MTX and improves MTX resistance of DHFR(FS) in primary T cells.

102 The interindividual variability in MTX kinetics had a substantial genetic component between

103 EGylated MSNR (PMSNR) demonstrated increased MTX release compared to non-PEGylated particles.

104 amine outcomes of a blinded trial of initial MTX monotherapy with the option to step-up to combinatio

105 demonstrate in a blinded trial that initial MTX monotherapy with the option to step-up to combinatio

106 he 370 evaluable participants in the initial MTX group, 28% achieved low levels of disease activity a

107 Participants assigned to initial MTX who required step-up to combination therapy at 24 we

108 re and 72 hours following vehicle injection, MTX rats were treated with a single dose of methotrexate

109 actory to high-dose systemic and intrathecal MTX plus IV rituximab.

110 Interventions: Intravenous MTX (4 mg/kg) monthly for 5 months with folinic acid res

111 ) compared with intrathecal methotrexate (IT MTX), when given on a modified augmented Berlin-Frankfur

112 andomly assigned to receive postinduction IT MTX or ITT.

113 cognitive outcomes for patients receiving IT MTX compared with ITT.

114 oxicities observed for patients receiving IT MTX compared with ITT.

115 -ALL and no overt CNS involvement remains IT MTX.

116 (+/- SE) of children randomly assigned to IT MTX versus ITT were 93.2% +/- 2.1% v 90.6% +/- 2.3% (P =

117 ITT could not be shown to be superior to IT MTX.

118 ificantly from those of the previously known MTX(Glu)1, providing polymorphic information.

119 [CI, 1.07 to 1.23]) AEs were elevated for LD-MTX versus placebo.

120 Low-dose methotrexate (LD-MTX) is the most commonly used drug for systemic rheumat

121 Use of LD-MTX was associated with small to moderate elevations in

122 Renal AEs were reduced in the LD-MTX group (HR, 0.85 [CI, 0.78 to 0.93]).

123 Random allocation to LD-MTX (<=20 mg/wk) or placebo.

124 Of 2391 participants assigned to LD-MTX, 2080 (87.0%) had an AE of interest, compared with 1

125 s without rheumatic disease who tolerated LD-MTX during an active run-in period.

126 the tumor, subsequently increasing the local MTX and hROS levels, and safely eliminating the biocompa

127 tent activator of BK channels is mallotoxin (MTX), which produces a very large hyperpolarizing shift

128 Methotrexate (MTX) and pemetrexed (PTX) are two examples of antifolate

129 Methotrexate (MTX) can cause significant clinical neurotoxicity and as

130 Methotrexate (MTX) is a widely used anticancer and antirheumatic drug

131 Methotrexate (MTX) is an anti-folate that inhibits de novo purine and

132 Methotrexate (MTX) taken as monotherapy is recommended as the initial

133 Methotrexate (MTX), a tight binding inhibitor of DHFR, is one of the m

134 h as 5-Fluorouracil (5-FU) and methotrexate (MTX) leading to enhanced sensitivity in vitro and in viv

135 lates and antifolates, such as methotrexate (MTX), a widely used anticancer drug.

136 nistered along with background methotrexate (MTX), for the treatment of RA.

137 ological inhibition of DHFR by methotrexate (MTX) causes severe defects in oligodendrocyte survival a

138 amined the impact of different methotrexate (MTX) and corticosteroid treatment strategies on neurocog

139 alysis of an anti-cancer drug, methotrexate (MTX) as a potential analytical tool used in clinical che

140 in inhibitor (CNI) with either methotrexate (MTX) or mycophenolate mofetil (MMF).

141 ration and apoptosis following methotrexate (MTX)-induced intestinal damage in a rat.

142 therapy regimens that included methotrexate (MTX), cisplatin (CDP), and doxorubicin (ADM) with or wit

143 of these compounds, including methotrexate (MTX), promoted P23H rhodopsin degradation that also clea

144 ning cofactor NADPH, inhibitor methotrexate (MTX), or both NADPH and MTX were characterized by 193 nm

145 globulins (IVIG), mepolizumab, methotrexate (MTX), omalizumab, upadacitinib and ustekinumab.

146 tically relevant drug molecule methotrexate (MTX) and its metabolites 7-hydroxy methotrexate (7-OH MT

147 The pharmacogenetics of methotrexate (MTX) was investigated in a large cohort of pediatric pat

148 ed to study the interaction of methotrexate (MTX) with DNA immobilized on the bare surface of glassy

149 effects of v-K-ras and p53 on Methotrexate (MTX)-mediated DHFR amplification.

150 gh-dose intravenous (IV) pulse methotrexate (MTX) as a treatment for EF.

151 a decrease in immune response, methotrexate (MTX) was used only to compare the PnV effects on innate

152 nine moiety of affibody sealed methotrexate (MTX)-loaded MUA-Au NCs through charge effect, as well as

153 Several methotrexate (MTX) based treatments (free MTX, MTX loaded Lecithin-PVA

154 we recently demonstrated that methotrexate (MTX) chemotherapy induces complex glial dysfunction for

155 etrexed influx [in contrast to methotrexate (MTX), folic acid, and reduced folates] could be detected

156 eight received during a trial methotrexate (MTX).

157 -NPY conjugates containing two methotrexate (MTX) molecules are presented.

158 Treatment with methotrexate (MTX) and tumor necrosis factor (TNF) inhibitors was cate

159 ministered in combination with methotrexate (MTX) during the second treatment each week.

160 Cancer chemotherapy with methotrexate (MTX) is known to cause bone loss.

161 , 36 of whom were treated with methotrexate (MTX).

162 otherapy (rituximab, high-dose methotrexate [MTX], vincristine, procarbazine) followed by a novel con

163 4 mug subcutaneously 3 times weekly or 20 mg MTX subcutaneously once weekly.

164 ian (range) monthly dose of 288 (230-336) mg MTX.

165 emolysis, colloidal stability, mitoxantrone (MTX) loading, in vitro MTX release, and cellular MTX del

166 In a multiple regression model, MTX area under the concentration time curve (AUC)0-48h i

167 thotrexate (MTX) based treatments (free MTX, MTX loaded Lecithin-PVA nanoparticles, MTX loaded Lecith

168 At 300 muM MTX, influx was one-third that of pemetrexed; influx of

169 e conformational changes upon binding NADPH, MTX, or both ligands.

170 observed upon UVPD of the ternary DHFR.NADPH.MTX complex.

171 MTX, MTX loaded Lecithin-PVA nanoparticles, MTX loaded Lecithin-Tween 80 nanoparticles) as well as t

172 As the shell of MUA-Au NCs-MTX-Affibody (MAMA), polyarginine chains of affibody cou

173 ry protein strongly inhibited the ability of MTX to activate BK channels, we found that it had only a

174 act with immobilized hDHFR in the absence of MTX and this interaction was inhibited in the presence o

175 26 channels were resistant to the actions of MTX.

176 ic shifts in the maximum absorption bands of MTX after interaction with DNA.

177 TNF-alpha antagonists can be used in case of MTX failure.

178 Treatment with the combination of MTX plus etanercept resulted in a statistically signific

179 ter) 2000 trial who received 1996 courses of MTX at 5 g/m(2) were genotyped for 8 single nucleotide p

180 MTX) therapy, monitor for the development of MTX-induced hepatotoxic effects, and monitor for worseni

181 tigated whether selective discontinuation of MTX immediately prior to death altered the risk of morta

182 d we examined the association of duration of MTX use with survival.

183 p53, amplification of DHFR and formation of MTX-resistant colonies occurred.

184 ics bands of C=O, N-H, C-H and O-H groups of MTX endow evidence for the interaction of MTX with DNA s

185 ypoxic conditions, a decrease in the IC50 of MTX and MTX-loaded MSNR was observed when compared to no

186 Here, the identification of MTX, 7-OH MTX and DAMPA are based on their unique SERS s

187 ease in enterocyte apoptosis in the ileum of MTX-ARG rats (vs MTX) was accompanied by decreased bax m

188 eased comparably shortly after initiation of MTX plus etanercept, triple therapy, and MTX monotherapy

189 treated with oral ARG following injection of MTX.

190 of MTX endow evidence for the interaction of MTX with DNA supporting the intercalative binding betwee

191 FT-IR investigations of MTX-DNA interaction revealed significant changes in the

192 TNF inhibitor use (irrespective of MTX) resulted in a similar rate of infection as use of M

193 r plasma MTX to leucovorin ratio (measure of MTX exposure) was associated with increased risk of leuk

194 The binding mechanism of MTX with DNA was elucidated by using constant current po

195 Here we find that a known mechanism of MTX-induced increase in DHFR expression persists with DH

196 Results The method of MTX delivery and corticosteroid assignment were unrelate

197 interaction was inhibited in the presence of MTX.

198 absence of cranial radiation, regardless of MTX delivery or corticosteroid type.

199 hain of Phe20 and the 6-methylpterin ring of MTX(Glu)5 invoke pi-pi interactions to promote distinct

200 Here we show crystal structures of MTX and PTX bound to plant SHMT isozymes from cytosol an

201 Initial use of MTX monotherapy with the addition of sulfasalazine plus

202 The use of MTX to treat cancer also causes bone marrow suppression

203 ted in a similar rate of infection as use of MTX without a TNF inhibitor (HR(adj) 1.2 [95% CI 0.8, 1.

204 Here, the identification of MTX, 7-OH MTX and DAMPA are based on their unique SERS spectra, pr

205 its metabolites 7-hydroxy methotrexate (7-OH MTX) and 2,4-diamino-N(10)-methylpteroic acid (DAMPA) in

206 njugates revealed higher potency than MTX on MTX-resistant cells.

207 A negative effect of PEGylation on MTX loading was observed but PEGylated MSNR (PMSNR) demo

208 y to determine the effects of vitamin B12 or MTX on fitness and the epigenome.

209 ombination therapies (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroquine) at week

210 combination therapy (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroquine).

211 y starting with either MTX and prednisone or MTX and placebo.

212 nation approaches, whether triple therapy or MTX plus etanercept, were similar.

213 e trial support superiority of IFN beta over MTX in the treatment of macular edema in the setting of

214 Patients' MTX pharmacokinetics, MTX toxicities, and outcomes were

215 Patients' MTX pharmacokinetics, MTX toxicities, and outcomes were correlated with the ge

216 A high 42-hour plasma MTX to leucovorin ratio (measure of MTX exposure) was as

217 one intravitreal injection (IVI) of 25 pmol MTX increased electroretinogram (ERG) response and rhodo

218 ty and effects of monthly high-dose IV pulse MTX in EF.

219 onclusions and Relevance: High-dose IV pulse MTX is a safe and effective treatment option in EF.

220 poor-prognosis RA were randomized to receive MTX monotherapy or combination therapy (MTX plus etanerc

221 Participants randomized to receive MTX monotherapy stepped-up to combination therapy at 24

222 8-102 between subjects randomized to receive MTX plus etanercept and those randomized to triple thera

223 iple therapy and those randomized to receive MTX plus etanercept.

224 Participants who received MTX monotherapy had less radiographic progression at wee

225 nisone (n = 117) than in the group receiving MTX and placebo (n = 119).

226 was limited and less in the group receiving MTX and prednisone (n = 117) than in the group receiving

227 ts from baseline between the group receiving MTX plus etanercept and the group receiving oral triple

228 s score in patients with psoriasis receiving MTX.

229 d be digested by trypsin, helping to release MTX from MAMA.

230 The released MTX accelerated destroying MUA-Au NCs through inducing t

231 Here, we demonstrate that remote MTX exposure blocks activity-regulated myelination.

232 cates a therapeutic potential of repurposing MTX for the treatment of rhodopsin-associated RP.

233 e of CNS NHL with intraventricular rituximab/MTX, including 1 with CNS lymphoma refractory to high-do

234 We showed MTX increased P23H rhodopsin degradation via the lysosom

235 rmining eligibility for methotrexate sodium (MTX) therapy, monitor for the development of MTX-induced

236 ent NASH FibroSure testing prior to starting MTX; 19 of those patients (27.5%) had elevated fibrosis

237 nt, and most patients can receive subsequent MTX without recurrence of acute or subacute symptoms.

238 DAS28-ESR in participants continuing to take MTX monotherapy at week 102 was 2.7 +/- 1.2, which is si

239 e of infection as those not currently taking MTX (HR(adj) 1.2 [95% CI 0.9, 1.7]).

240 , JIA patients who were not currently taking MTX or TNF inhibitors had an increased rate of infection

241 For those taking MTX without TNF inhibitor use, the SIR was 3.9 (95% CI 0

242 patients with psoriasis receiving long-term MTX therapy.

243 antagonists seemed to be more effective than MTX.

244 est that, on average, MMF may be faster than MTX in achieving corticosteroid-sparing success in ocula

245 ss was shorter (more favorable) for MMF than MTX (hazard ratio = 0.68, 95% confidence interval: 0.46-

246 s higher at every point in time for MMF than MTX from 2 to 8 months, then converges at 9 months.

247 ore, conjugates revealed higher potency than MTX on MTX-resistant cells.

248 However, we found that MTX shifted the steady-state activation of BK channels i

249 MTX-induced osteoclastogenesis and show that MTX induces osteoclast differentiation by generating a p

250 The MTX and prednisone strategy was also more effective in r

251 CC4) transporter ratio (P = 3.6 x 10-4), the MTX infusion time (P = 1.5 x 10-3), FPGS mRNA expression

252 (P = .01), with no interactions between the MTX and nelarabine randomizations (P = .41).

253 n both groups, but some occurred less in the MTX and prednisone group.

254 n (range, 0.12 to -0.38, 4.7 letters) in the MTX arm (P = .0435, Mann-Whitney U test).

255 sed by 47 mum (range, 108 to -28 mum) in the MTX group (P < .0001).

256 Attrition at 24 weeks was similar in the MTX monotherapy and combination groups.

257 increases in mean cholesterol levels in the MTX plus etanercept, triple therapy, and MTX monotherapy

258 Gene silencing of the MTX target ATIC activated AMPK and stimulated lipid oxid

259 The structural geometries of the MTX(Glu)5 and hydrolyzed MTX(Glu)1 in the mutant complex

260 de polymorphisms in 5 candidate genes of the MTX/folate pathway.

261 The MoAb1 antibody, recognizing the MTX-Man cap epitope, is a novel analyte for active TB de

262 Then, MTX was introduced at positions four and 22 of [F(7),P(3

263 therapy to one of the combination therapies (MTX plus etanercept or MTX plus sulfasalazine plus hydro

264 and did not step-up to combination therapy (MTX monotherapy group).

265 eive MTX monotherapy or combination therapy (MTX plus etanercept or MTX plus sulfasalazine plus hydro

266 s etanercept, immediate oral triple therapy (MTX plus sulfasalazine plus hydroxychloroquine), or step

267 atients not receiving TNF inhibitor therapy, MTX users had a similar rate of infection as those not c

268 okinetic, and genetic risk factors for these MTX-related toxicities during childhood acute lymphoblas

269 This MTX assay was subsequently adapted to a fully integrated

270 Even though MTX had a minimal effect on steady-state activation of p

271 ileum and crypt depth in ileum, compared to MTX animals.

272 soform (parSlo) is inherently insensitive to MTX as MTX shifted the activation of heterologously expr

273 Conversely, exposing D. magna to MTX negatively influenced the fitness of the animals and

274 Ten were randomized to MTX, and 9 were randomized to IFN beta.

275 t TYMS T51S, G52S (TYMS(SS)) is resistant to MTX and improves MTX resistance of DHFR(FS) in primary T

276 gic agents and had an inadequate response to MTX were randomly assigned to receive 125 mg SC abatacep

277 postoperatively when pathologic response to MTX-CDP-ADM was poor (arm A) or given in the primary pha

278 ogenesis may contribute to susceptibility to MTX-related neurotoxicity.

279 th 13,003 person-years of followup; 36% took MTX and 16% took TNF inhibitors.

280 bility, mitoxantrone (MTX) loading, in vitro MTX release, and cellular MTX delivery under hypoxic con

281 simulated a clinical trial comparing MMF vs MTX for noninfectious inflammatory eye disorders.

282 Outcomes of treatment (MMF vs MTX) were similar across all anatomic sites of inflammat

283 e apoptosis in the ileum of MTX-ARG rats (vs MTX) was accompanied by decreased bax mRNA and protein e

284 We explored whether MTX promotes AMPK activation in cultured myotubes and is

285 56 variant was significantly associated with MTX kinetics.

286 en in the primary phase of chemotherapy with MTX-CDP-ADM (arm B).

287 traventricular rituximab in combination with MTX is feasible and highly active in the treatment of dr

288 mab biweekly, both given in combination with MTX, in a 2-year study.

289 nanoparticles (FA-AuNP) in competition with MTX for the bioreceptor, human dihydrofolate reductase (

290 from zebrafish and the mutant complexes with MTX(Glu)5 and hydrolyzed MTX(Glu)1, revealing the comple

291 e taking single-agent immunosuppression with MTX or MMF at 4 tertiary uveitis clinics.

292 the rate of infection was not increased with MTX or TNF inhibitor use, but was significantly increase

293 ortance, combination treatment of NADPS with MTX displayed significant synergy in a metastatic colon

294 is RA validate the strategy of starting with MTX monotherapy.

295 hort of patients with psoriasis treated with MTX who underwent NASH FibroSure testing between January

296 of that observed in the animals treated with MTX.

297 f 4 treatment arms: immediate treatment with MTX plus etanercept, immediate oral triple therapy (MTX

298 nts with psoriasis undergoing treatment with MTX, 69 (53.5%) underwent NASH FibroSure testing prior t

299 nts with psoriasis undergoing treatment with MTX, while 107 patients (57 women and 50 men; mean [SD]

300 recognizing the 5-methylthio-D-xylofuranose(MTX)-mannose(Man) cap epitope, performed the best, was l