ライフサイエンスコーパス: indomethacin

1 nase (LO; baicalein) but not cyclooxygenase (indomethacin).

2 ric oxide synthase or prostanoid production (indomethacin).

3 ne, but not by the cyclooxygenase inhibitor, indomethacin.

4 bese mice was not affected by treatment with indomethacin.

5 alpha antibody, IL-1-receptor antagonist, or indomethacin.

6 of the mitochondrial pathway of apoptosis by indomethacin.

7 -V241G) in humans that confers resistance to indomethacin.

8 r combined with the cyclooxygenase inhibitor indomethacin.

9 vely inhibiting cyclooxygenase isoforms with indomethacin.

10 wnstream of cyclooxygenase 2 and a target of indomethacin.

11 ation of N-nitro-l-arginine methyl ester and indomethacin.

12 cosa both with and without administration of indomethacin.

13 gregation by SQ29548 (TXA(2) antagonist) and indomethacin.

14 ug ( 26) was about 1.6-fold less potent than indomethacin.

15 attenuated after blocking COX activity with indomethacin.

16 in gastric lesion score compared to that of indomethacin.

17 lon proteins from elimination by sulindac or indomethacin.

18 c symptoms, and is exquisitely responsive to indomethacin.

19 that is deactivated by the administration of indomethacin.

20 observed with the dual COX-1/COX-2 inhibitor indomethacin.

21 nd cysteinyl leukotrienes in the presence of indomethacin.

22 mediate- (10 mg/kg), and low- (5 mg/kg) dose indomethacin.

23 ntractions include tocolytic agents, such as indomethacin.

24 or, was evaluated as a control together with indomethacin.

25 terval [95% CI], 0.23 to 0.53; P<0.001) with indomethacin, 0.15 mmol/L (95% CI, 0.02 to 0.29; P=0.03)

26 e hypothesis that acutely-reduced CBF (using indomethacin [1.2 mg kg(-1) oral dose]) would impair cog

27 l-NAME 10(-4) m) or cyclooxygenase blockade (indomethacin 10(-5) m).

28 dent manner by intraperitoneal injections of indomethacin (10 mg/kg), a nonselective COX-1/COX-2 inhi

29 Nifedipine (10-6 M) and indomethacin (10-5 M) were included in all solutions to

30 n-free after administration of intramuscular indomethacin 100 mg.

31 ments with one time daily 75 mg slow-release indomethacin, 150 mg eplerenone, or 20 mg amiloride adde

32 ly dosed with dexamethasone (0.1 mg/kg/day), indomethacin (2 mg/kg/day), or the specific angiogenesis

33 vivo with clopidogrel (10 mg/kg per day) or indomethacin (2.4 mg/kg per day).

34 Pretreatment with U-73122, indomethacin, 2-aminoethoxydiphenylborane, or verapamil

35 ned in three states: (1) acute PH attack-off indomethacin; (2) pain-free-off indomethacin; and (3) pa

36 utamide drug resistance can be surmounted by indomethacin a potent inhibitor of AKR1C3.

37 the resveratrol response was not affected by indomethacin (a cyclooxygenase inhibitor) and sulfaphena

38 Indomethacin, a cyclooxygenase inhibitor, countered the

39 asoconstriction that was sensitive to either indomethacin, a cyclooxygenase inhibitor, or SQ29548, a

40 , and treatment of infected macrophages with indomethacin, a cyclooxygenase-1/cyclooxygenase-2 inhibi

41 nistration of the anti-inflammatory compound indomethacin, a general cyclooxygenase inhibitor, affect

42 e sensitivity of HSA-modified NAA-RFs toward indomethacin, a model drug.

43 Indomethacin, a nonselective cyclooxygenase (COX) inhibi

44 died interactions between the microbiota and indomethacin, a nonsteroidal anti-inflammatory drug (NSA

45 We found that indomethacin, a nonsteroidal anti-inflammatory drug, ind

46 Rectal indomethacin, a nonsteroidal anti-inflammatory drug, is

47 bility to small intestinal injury induced by indomethacin, a nonsteroidal anti-inflammatory drug.

48 lated glyoxalase 1 (GLO1) as a new target of indomethacin, a widely used antiinflammatory drug.

49 , and inhibition of COX-2 with ibuprofen and indomethacin abrogated STIM1-mediated CRC cell motility.

50 onstrate that sulindac, sulindac sulfone and indomethacin activate the NF-kappaB pathway in colorecta

51 injury model, here we report that the NSAID indomethacin activates the protein kinase Czeta (PKCzeta

52 estradiol-17-glucuronide and the xenobiotic indomethacin-acyl-glucuronide are found to exhibit marke

53 In addition, indomethacin administered into the L5-DRG prevented the

54 These results indicate that indomethacin administration reduces rate of onset of aor

55 ical and flow cytometry analyses showed that indomethacin administration resulted in inhibition of mo

56 Indomethacin administration to obese mice did not reduce

57 ups, and IL-6 was quantified with or without indomethacin administration.

58 lished anti-inflammatories dexamethasone and indomethacin, AFC's action was restricted to the site of

59 12, with a few exceptions, patients received indomethacin after their procedure.

60 ar leakage with a cyclo-oxygenase inhibitor (indomethacin), agents that interfere with histamine (pyr

61 In contrast, indomethacin alone enhanced the bronchoconstriction (E(m

62 Indomethacin also abrogated efficient GTP-dependent late

63 Indomethacin also increased ILC2 proliferation, the perc

64 y two cyclooxygenase inhibitors (aspirin and indomethacin) also suggests that prostaglandins may be i

65 Many indomethacin amides and esters are cyclooxygenase-2 (COX

66 A number of indomethacin-amides were found to bind to TCCYP51, inhib

67 f cyclooxygenase-2-selective inhibitors, the indomethacin-amides.

68 Intracerebroventricular infusion of indomethacin, an anti-inflammatory drug, mitigates the e

69 Tse et al. now report on the use of indomethacin, an anti-inflammatory drug, to sensitize th

70 trategies were used to generate libraries of indomethacin analogues, which exhibit reduced cyclooxyge

71 n pSTAT6 inhibition by all concentrations of indomethacin and aspirin: between aspirin-sensitive and

72 Nanoliposomes encapsulating indomethacin and decorated with clinically used oxytocin

73 Furthermore, the combination of indomethacin and enzalutamide resulted in significant in

74 Both indomethacin and flurbiprofen augmented the release of I

75 We found that indomethacin and flurbiprofen significantly increased th

76 y inhibited by the cyclooxygenase inhibitors indomethacin and flurbiprofen.

77 n-steroidal anti-inflammatory drugs, such as indomethacin and ibuprofen, and minocycline, a tetracycl

78 Combined indomethacin and inhibition of endothelial nitric oxide

79 ed in a dose-dependent manner by aspirin and indomethacin and minimally by sodium salicylate.

80 Both indomethacin and morphine were able to block or reverse

81 The addition of PG synthesis inhibitors (indomethacin and NS-398) substantially abrogated LR-MSC-

82 Furthermore, FeTM-4-PyP(5+) synergized with indomethacin and NS397 (1-10 mg/kg) to block both hypera

83 ngs have important clinical implications, as indomethacin and other anti-inflammatory agents are admi

84 dds ratios (ORs) for the association between indomethacin and PEP.

85 ctions in mean pain score were observed with indomethacin and prednisolone in the ED (approximately 1

86 cumulation in caudate putamen 3-5 times, and indomethacin and probenecid increased accumulation in ep

87 nfection overrode the protection provided by indomethacin and restored the increased mortality and mi

88 Indomethacin and SC-236, a selective cyclooxygenase-2 (C

89 drugs (NSAIDs) such as the COX-1/2 inhibitor indomethacin and the COX-2-specific inhibitors NS-398 an

90 urred with a latency of only 1-2 s, and both indomethacin and the cyclooxygenase-1 inhibitor SC-560 b

91 inal autonomic cephalalgias, such as oxygen, indomethacin and triptans, and some part of their therap

92 Indomethacin and verapamil also inhibit the luminal Ca(2

93 Treatment with the COX-inhibitor indomethacin and/or the clinical monoclonal antibody aga

94 , time-dependent COX inhibitors (diclofenac, indomethacin, and flurbiprofen) were unaffected by those

95 al anti-inflammatory drugs (NSAIDs), such as indomethacin, and infection with Helicobacter pylori are

96 mice after co-administration of propranolol, indomethacin, and L-NAME.

97 H attack-off indomethacin; (2) pain-free-off indomethacin; and (3) pain-free after administration of

98 Ibuprofen and indomethacin are nonselective prostaglandin synthetase i

99 ted the ranked order of drug sensitivity for indomethacin, aspirin, MRS-2179 (a P2Y(1) inhibitor), an

100 ctions of low and high doses of ibuprofen or indomethacin at birth (postnatal day [P]1) and on P2 and

101 rted that cyclooxygenase (COX) inhibition by indomethacin augmented allergic airway inflammation in a

102 ntiation in vitro, whereas its inhibition by indomethacin augmented alpha-SMA expression.

103 gh the postnatal period by giving the mother indomethacin before birth.

104 s such as dicoumarol, N-acetylserotonin, and indomethacin blocked sepiapterin reduction, with no effe

105 itching task was slightly (7%) reduced after indomethacin, but not significantly associated with redu

106 lective nonsteroidal anti-inflammatory drug, indomethacin, by amidation presents a promising strategy

107 sical assays of model membranes suggest that indomethacin can enhance phase separation and stabilize

108 tios measured through the skin distinguished indomethacin-challenged from same day control rats.

109 The cyclooxygenase inhibitor indomethacin completely abolished the effects of nicotin

110 antibody partially, but in combination with indomethacin, completely abrogated the protective effect

111 data indicate that Jurkat T cells exposed to indomethacin continue to accumulate fluorescent calcein

112 Amphipathic indomethacin could therefore potentially modulate cell s

113 tigated whether the anti-inflammatory agent, indomethacin, could inhibit monocyte/macrophage accumula

114 nding affinity between a set of drugs (i.e., indomethacin, coumarin, sulfadymethoxine, warfarin, and

115 elective (ketorolac tromethamine, ibuprofen, indomethacin), COX-1-selective (SC-560), or COX-2-select

116 The AKR1C3.NADP(+).2'-des-methyl-indomethacin crystal structure was determined, and it re

117 s on the crystal complexes of COX-2 with two indomethacin-dansyl conjugates (compounds 1 and 2) at 2.

118 ar and rank-based mixed models revealed that indomethacin decreased MCAv(mean) by 31% (95% confidence

119 cting SIVH as well as shown that exposure to indomethacin decreases the incidence of SIVH overall.

120 le the best 5-LOX inhibition was attained by indomethacin derivative 17 (IC(5)(0) = 0.9 muM).

121 0.59% of these patients who received rectal indomethacin developed moderate-to-severe PEP vs 4.32% w

122 2.31% of these patients who received rectal indomethacin developed PEP vs 7.53% who did not receive

123 We demonstrate that indomethacin did not inhibit GSIS per se, but activation

124 consecutive patients undergoing ERCP, rectal indomethacin did not prevent post-ERCP pancreatitis.

125 related peptide along with the COX inhibitor indomethacin did not result in phosphorylation of ERK1/2

126 In the presence of L-NAME and indomethacin, dilation to 10(-4) M ATP was significantly

127 Indomethacin diminished the accumulation of microglia/ma

128 re and sugar ratios reflect gut injury in an indomethacin dose dependent manner.

129 ction and inhibition of COX-2 by NS-398, and indomethacin drastically reduced the levels of PGE(2) an

130 Restoration of of PORH by indomethacin during a HS diet suggests an important role

131 Dexamethasone and indomethacin each reduced pain behavior, synovial inflam

132 Therapeutic levels of indomethacin enhanced phase separation in DPPC/DOPC/Chol

133 Indomethacin enhanced the clustering of H-Ras.GDP and N-

134 e nonselective COX inhibitors salicylate and indomethacin enhanced the expression of iNOS in the rat

135 ment of BHK cells with therapeutic levels of indomethacin enhances cholesterol-dependent nanoclusteri

136 complexes with an enantiomeric pair of these indomethacin ethanolamides were determined at resolution

137 A series of alpha-substituted indomethacin ethanolamides, which exist as R/S-enantiome

138 vity observed with the (S)-alpha-substituted indomethacin ethanolamides.

139 The nonsteroidal anti-inflammatory drug indomethacin exhibits diverse biological effects, many o

140 Deep sequencing analysis showed that indomethacin exposure was associated with alterations in

141 ex vivo administration of either aspirin or indomethacin failed to prevent platelet activation acros

142 atory drugs (such as aspirin, ibuprofen, and indomethacin) failed to influence endotoxin-induced HMGB

143 ly recognized beneficial side effects of the indomethacin family of nonsteroidal antiinflammatory dru

144 hous and recrystallized samples of the drugs indomethacin, felodipine, and acetaminophen.

145 Mice were treated with the COX inhibitors indomethacin, flurbiprofen, or vehicle and challenged in

146 nes recently recommended prophylactic rectal indomethacin for all patients undergoing ERCP, including

147 Sixteen patients in the indomethacin group (7.2%) and 11 in the placebo group (4

148 titis developed in 13 patients (4.4%) in the indomethacin group and in 27 patients (8.8%) in the plac

149 eveloped in 27 of 295 patients (9.2%) in the indomethacin group and in 52 of 307 patients (16.9%) in

150 During the ED phase, patients in the indomethacin group had more minor adverse events than th

151 ammatory pain) of the formalin test, whereas indomethacin had activity only in phase 2.

152 WT mice treated with indomethacin had greater numbers of total cells, eosinop

153 Indomethacin had no effect on adipose tissue mass, gluco

154 Dexamethasone reduced, but indomethacin had no significant effect on, the total joi

155 Oral prednisolone and indomethacin had similar analgesic effectiveness among p

156 Stable glasses of indomethacin (IMC) were prepared by using physical vapor

157 For indomethacin (IMC), an organic glass able to grow surfac

158 Indomethacin impaired mitochondrial dynamics by promotin

159 een the alpha and gamma solid-state forms of indomethacin in biorelevant media.

160 topical serosal acetic acid or subcutaneous indomethacin in C57BL/6J mice.

161 beta-catenin is partially driving effects of Indomethacin in cisplatin-resistant cells.

162 ate the efficacy of rectal administration of indomethacin in reducing the incidence of post-ERCP panc

163 as potent inhibitors such as diclofenac and indomethacin in the same experimental conditions).

164 Inhibition of PGE2 synthesis by indomethacin in vitro, targeted deletion of EP2 in prima

165 by coinjection of the anti-inflammatory drug indomethacin in wild-type but not TKO brains.

166 By contrast, indomethacin increased proliferation in the SGZ and late

167 acrophages with the cyclooxygenase inhibitor indomethacin increases TNFalpha production to the level

168 Administration of indomethacin (IND) leads to the formation of lipid rafts

169 t of the nonsteroidal anti-inflammatory drug indomethacin (IND) on MDSCs, depending on whether they w

170 armacologically reduced by administration of indomethacin (INDO; 1.2 mg kg(-1)) or unaltered (placebo

171 Neither blockade of cyclooxygenase with indomethacin (Indo; 5 microm) nor blockade of endothelia

172 t or a regular diet supplemented or not with indomethacin (+/-INDO) for 7 weeks.

173 rvivin confer protection against ethanol and indomethacin induced injury.

174 Indomethacin-induced acute ileitis led to repression of

175 d mice exhibited increased susceptibility to indomethacin-induced damage in the small intestine; this

176 n or SB203580-induced p38 inhibition reduced indomethacin-induced damage to AGSs.

177 l permeability and prevented exacerbation of indomethacin-induced damage.

178 SEGA (3a) inhibits indomethacin-induced down-regulation of bcl-2 and up-reg

179 on-preventing mito-protective drug, reversed indomethacin-induced DRP1 phosphorylation on Ser-616, mi

180 with H. pylori also stimulated formation of indomethacin-induced gastric lesions and mucosal cell de

181 ent mice are sensitive to the development of indomethacin-induced gastric lesions and mucosal cell de

182 Indomethacin-induced ileal injury was greater in the c-f

183 seline morphology or morphometry but reduced indomethacin-induced injury in overexpressing hPSTI regi

184 Mdivi-1 also prevented indomethacin-induced mitochondrial macromolecular damage

185 ed MOS, as is evident from the inhibition of indomethacin-induced mitochondrial protein carbonyl form

186 ) values were strongly associated with their indomethacin-induced reductions (r = 0.70 to 0.89, P < 0

187 GI2 receptor (IP) signaling was critical for indomethacin-induced, STAT6-independent proallergic effe

188 applications in EOC and found that (i) NSAID Indomethacin induces robust cell death in primary patien

189 tically examined whether amphiphiles such as indomethacin influence Ras protein nanoclustering in int

190 , but activation of GPR40 in the presence of indomethacin inhibited glucose-dependent insulin secreti

191 In this mouse model, both dexamethasone and indomethacin inhibited TPA-induced edema and MPO activit

192 Finally, we infused indomethacin intracerebroventricularly during the week o

193 n of the TLS found in ultrastable glasses of indomethacin is argued to be due to their particular ani

194 The slow, tight-binding inhibitor, indomethacin, is a potent inhibitor of 2-AG and AA oxyge

195 nonsteroidal anti-inflammatory drug (NSAID), indomethacin, is reported.

196 anti-inflammatory drugs, tolfenamic acid and indomethacin, markedly reduce direct cell-to-cell spread

197 Prophylactic indomethacin may decrease Severe Intraventricular Hemorr

198 SEGA (3a) corrects indomethacin-mediated mitochondrial dysfunction in vivo

199 SEGA (3a) in vivo blocks indomethacin-mediated MOS, as is evident from the inhibi

200 y COX product(s) responsible for restraining indomethacin-mediated STAT6-independent allergic inflamm

201 tion of l-NAME with cyclooxygenase inhibitor indomethacin mimicked the effect of denudation.

202 given either a single 100-mg dose of rectal indomethacin (n = 223) or a placebo suppository (n = 226

203 One HS diet group subset received 100 mg of indomethacin (non-selective COX-1 and COX-2 inhibitor),

204 SEGA (3a) prevents indomethacin (NSAID)-induced mitochondrial oxidative str

205 intolerance was monitored, and the effect of indomethacin on glucose-stimulated insulin secretion (GS

206 Here we examined the effect of indomethacin on membrane lateral heterogeneity.

207 the effects of early postnatal ibuprofen and indomethacin on ocular and systemic VEGF, IGF-I, and GH

208 heets similarly showed a selective effect of indomethacin on promoting cholesterol-dependent, but not

209 iciency diminished the stimulatory effect of indomethacin on STAT6-independent IL-5 and IL-13 respons

210 re further used to follow crystallization of indomethacin on tablet surfaces under two storage condit

211 Inhibition of cyclooxygenase by indomethacin only slightly reduced the vasodilatory resp

212 For glasses prepared from indomethacin or 1,3-bis-(1-naphthyl)-5-(2-naphthyl)benze

213 is were assigned to receive 100 mg of rectal indomethacin or a 2.6 g suppository of glycerin immediat

214 if exposure of pregnant rats to analgesics (indomethacin or acetaminophen) affected GC development a

215 by EPCs were inhibited by the COX inhibitor indomethacin or by genetic inactivation of COX-1 or PGI(

216 Systemic administration of indomethacin or celecoxib (cyclo-oxygenase inhibitors),

217 d by inhibition of cyclooxygenase-2 (COX-2) (indomethacin or celecoxib) or of TXA2/prostaglandin H2 r

218 ndogenous biosynthetic pathway of CyPGs with indomethacin or HQL79, which inhibit cyclooxygenases or

219 creatitis to receive a single dose of rectal indomethacin or placebo immediately after ERCP.

220 domly assigned (1:1 ratio) to receive either indomethacin or prednisolone.

221 Inhibition of 15-PGDH using either indomethacin or SW033291 significantly reduced the furth

222 and treated the mice with the COX inhibitor indomethacin or vehicle for analyses of the primary and

223 The COX inhibitor indomethacin or vehicle was administered in drinking wat

224 (GLP-1) was functionalized with diflunisal, indomethacin, or both.

225 Blocking PGE2 synthesis with indomethacin overcame the phagocytic and killing defects

226 oped PEP vs 7.53% who did not receive rectal indomethacin (P < .001) and 0.59% of these patients who

227 vere PEP vs 4.32% who did not receive rectal indomethacin (P = .001).

228 rformance was impaired 7% (IQR = 0-19) after indomethacin (P = 0.04), but not significantly associate

229 s of compound 2 were similar to those of the indomethacin parent compound against WT COX-2, and the R

230 Indomethacin partially blocked and did not reverse paw e

231 ice treated subcutaneously with slow-release indomethacin pellets, suggesting a role for prostanoids,

232 l microbiome by antibiotic treatment altered indomethacin pharmacokinetics and pharmacodynamics, whic

233 Indomethacin prevented death from abdominal aortic disse

234 We found that supplementation with indomethacin prevented HF/HS-induced obesity and diet-in

235 re potent AI agent than aspirin, whereas the indomethacin prodrug ( 26) was about 1.6-fold less poten

236 d that the aspirin prodrug 23 (UI = 0.7) and indomethacin prodrug 26 (UI = 0) were substantially less

237 patients with malignant obstruction, rectal indomethacin provided the greatest benefit to patients w

238 In conclusion, indomethacin reduced MCAv(mean) and impaired cognition s

239 Indomethacin reduced PKA and Akt activation by approxima

240 Rectal indomethacin reduced the incidence of post-ERCP pancreat

241 ibition of prostaglandin (PG) synthesis with indomethacin reduced the magnitude of the changes in 20:

242 Rectal indomethacin reduced the odds of PEP by 65% (OR, 0.35; 9

243 patients with malignant obstruction, rectal indomethacin reduced the risk of PEP by 64% (OR, 0.36; 9

244 Treatment with the cyclooxygenase inhibitor indomethacin reduces beta-catenin levels and leads to a

245 mice with the cyclooxygenase (COX) inhibitor indomethacin reduces the infectious burden, proinflammat

246 Rectal indomethacin reduces the risk of pancreatitis after endo

247 r inhibition of AKR1C3 enzymatic activity by indomethacin resensitized enzalutamide-resistant prostat

248 ayed larger clots and another presented with indomethacin resistance (revealing a novel heterozygote

249 egrin and Cox-2 activation by echistatin and indomethacin, respectively, each blocked the fluid shear

250 Indomethacin restored microcirculatory blood flow and re

251 Inhibition of the COX pathway with indomethacin resulted in delayed worm expulsion in selen

252 inistration of a nonselective COX inhibitor (indomethacin), selective COX-1 (valeryl salicylate), or

253 Contrary to our expectations, indomethacin significantly decreased both the initial re

254 Indomethacin significantly reduced eGFR and plasma renin

255 high risk for post-ERCP pancreatitis, rectal indomethacin significantly reduced the incidence of the

256 At the CP, verapamil and probenecid (but not indomethacin) significantly increased 125I-T4 accumulati

257 y because of gastrointestinal intolerance to indomethacin (six patients) and hypotension with epleren

258 ation was inhibited by acetaminophen but not indomethacin, suggesting catalysis occurred by the perox

259 plication of the model to patients receiving indomethacin suggests a benefit at the highest risk leve

260 rs) derivatized with clinically used NSAIDs (indomethacin, sulindac, ketoprofen, ibuprofen, diclofena

261 ing nitric oxide (l-NAME) and prostaglandin (indomethacin) synthesis increased CGRP EC50 in both age

262 -heat measurements of ultrastable glasses of indomethacin that clearly show the disappearance of the

263 s and during interictal pain-free states off indomethacin that is deactivated by the administration o

264 al and common subcellular event triggered by indomethacin that promotes apoptosis in both gastric can

265 ntiinflammatory drugs (NSAIDs) ibuprofen and indomethacin, the drugs widely used as pain relievers in

266 Three different solid-state forms of indomethacin-the crystalline gamma and alpha forms, as w

267 fteen patients became normokalemic: six with indomethacin, three with eplerenone, and six with amilor

268 s in their microbiota and their responses to indomethacin - thus, the drug-microbe interactions descr

269 -type, and c-fos-null mice were treated with indomethacin to assess the response to acute inflammatio

270 xposed CD-1 mice were topically treated with indomethacin to block endogenous PGE(2) production, and

271 We investigated the potential of rectal indomethacin to prevent post-ERCP pancreatitis (PEP) in

272 We used oral indomethacin to reduce the cerebrovascular reactivity to

273 oth crystal structures, the linker tethering indomethacin to the dansyl moiety passes through the con

274 omide, vitamin A cogeners, or retinoids; and indomethacin tocolysis.

275 was observed only in selenium-deficient and indomethacin-treated selenium-supplemented mice but not

276 fection compared to monomicrobial infection; indomethacin treatment also decreased elevated PGE2 leve

277 d pregnancies are not maintained to term and indomethacin treatment increases maternal mortality.

278 Indomethacin treatment partially restored T cell prolife

279 Inhibition of PGE(2) production with indomethacin treatment resulted in increased numbers of

280 Neither indomethacin treatment to block PG synthesis nor anti-CD

281 regnancy loss can be temporarily deferred by indomethacin treatment, but treated pregnancies are not

282 than the parent drugs aspirin (UI = 51) and indomethacin (UI = 64).

283 Indomethacin ultimately induced mitochondrial metabolic

284 ophen, and other NSAID (ibuprofen, naproxen, indomethacin) use were based on a self-administered ques

285 Indomethacin, used to inhibit cyclooxygenase, also inhib

286 Indomethacin was administered (from 3 days prior with da

287 s with malignant biliary obstruction, rectal indomethacin was associated with a significant decrease

288 the anti-inflammatory (AI) drugs aspirin and indomethacin was covalently linked to the 1-(2-carboxypy

289 Indomethacin was tested in both acute and chronic exposu

290 Indomethacin was the most effective but can cause gastro

291 Indomethacin was used as a model active pharmaceutical i

292 n, acetaminophen (paracetamol), sulindac and indomethacin, was also achieved in supramolecular gel me

293 AYPGKF in the presence of the COX inhibitor indomethacin, we found that PTPN7 KO mouse platelets agg

294 By blocking PGE2 production with indomethacin, we made a striking finding that endogenous

295 further evaluate the biophysical effects of indomethacin, we measured fluorescence polarization of t

296 Electrolyte supplements and indomethacin were used frequently to induce catch-up gro

297 ant (a neurokinin 1 receptor antagonist), or indomethacin with pyrilamine significantly reduced vascu

298 ly-reduced CBF (using a pharmacological aid; indomethacin) would impair cognition in young and older

299 2 and COX2 using amino-guanidine and aspirin/indomethacin yielded an additive reduction in the growth

300 difications on the 3-acetic acid part of the indomethacin yielding an amide-nitrate derivative 32 and