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1 ric oxide synthase or prostanoid production (indomethacin).
2 nase (LO; baicalein) but not cyclooxygenase (indomethacin).
3 alpha antibody, IL-1-receptor antagonist, or indomethacin.
4 mediate- (10 mg/kg), and low- (5 mg/kg) dose indomethacin.
5 of the mitochondrial pathway of apoptosis by indomethacin.
6 -V241G) in humans that confers resistance to indomethacin.
7 r combined with the cyclooxygenase inhibitor indomethacin.
8 vely inhibiting cyclooxygenase isoforms with indomethacin.
9 wnstream of cyclooxygenase 2 and a target of indomethacin.
10 ation of N-nitro-l-arginine methyl ester and indomethacin.
11 cosa both with and without administration of indomethacin.
12 gregation by SQ29548 (TXA(2) antagonist) and indomethacin.
13 ug ( 26) was about 1.6-fold less potent than indomethacin.
14 attenuated after blocking COX activity with indomethacin.
15 in gastric lesion score compared to that of indomethacin.
16 lon proteins from elimination by sulindac or indomethacin.
17 c symptoms, and is exquisitely responsive to indomethacin.
18 that is deactivated by the administration of indomethacin.
19 observed with the dual COX-1/COX-2 inhibitor indomethacin.
20 ted with the classic anti-inflammatory agent indomethacin.
21 ge and increased susceptibility to injury by indomethacin.
22 inhibitors, aspirin, naproxen, ibuprofen, or indomethacin.
23 ntractions include tocolytic agents, such as indomethacin.
24 or, was evaluated as a control together with indomethacin.
25 ne, but not by the cyclooxygenase inhibitor, indomethacin.
26 bese mice was not affected by treatment with indomethacin.
27 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)
28 kg x 7 days; N = 16), general COX inhibitor (indomethacin; 1 mg/kg x 7 days; N = 16), or no inhibitor
30 dent manner by intraperitoneal injections of indomethacin (10 mg/kg), a nonselective COX-1/COX-2 inhi
33 ments with one time daily 75 mg slow-release indomethacin, 150 mg eplerenone, or 20 mg amiloride adde
34 ly dosed with dexamethasone (0.1 mg/kg/day), indomethacin (2 mg/kg/day), or the specific angiogenesis
37 ned in three states: (1) acute PH attack-off indomethacin; (2) pain-free-off indomethacin; and (3) pa
39 nine, 250 microm; l-NNA) and cyclooxygenase (indomethacin, 5 microm; INDO) had no effect on the ampli
41 the resveratrol response was not affected by indomethacin (a cyclooxygenase inhibitor) and sulfaphena
45 asoconstriction that was sensitive to either indomethacin, a cyclooxygenase inhibitor, or SQ29548, a
46 , and treatment of infected macrophages with indomethacin, a cyclooxygenase-1/cyclooxygenase-2 inhibi
47 nistration of the anti-inflammatory compound indomethacin, a general cyclooxygenase inhibitor, affect
51 died interactions between the microbiota and indomethacin, a nonsteroidal anti-inflammatory drug (NSA
55 , and inhibition of COX-2 with ibuprofen and indomethacin abrogated STIM1-mediated CRC cell motility.
56 onstrate that sulindac, sulindac sulfone and indomethacin activate the NF-kappaB pathway in colorecta
57 estradiol-17-glucuronide and the xenobiotic indomethacin-acyl-glucuronide are found to exhibit marke
62 lished anti-inflammatories dexamethasone and indomethacin, AFC's action was restricted to the site of
64 ar leakage with a cyclo-oxygenase inhibitor (indomethacin), agents that interfere with histamine (pyr
66 y two cyclooxygenase inhibitors (aspirin and indomethacin) also suggests that prostaglandins may be i
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
75 n-steroidal anti-inflammatory drugs, such as indomethacin and ibuprofen, and minocycline, a tetracycl
76 d proliferation response were inhibited with indomethacin and in dominant negative stable transfectio
80 The addition of PG synthesis inhibitors (indomethacin and NS-398) substantially abrogated LR-MSC-
81 Furthermore, FeTM-4-PyP(5+) synergized with indomethacin and NS397 (1-10 mg/kg) to block both hypera
82 ngs have important clinical implications, as indomethacin and other anti-inflammatory agents are admi
84 ctions in mean pain score were observed with indomethacin and prednisolone in the ED (approximately 1
85 cumulation in caudate putamen 3-5 times, and indomethacin and probenecid increased accumulation in ep
86 nfection overrode the protection provided by indomethacin and restored the increased mortality and mi
88 drugs (NSAIDs) such as the COX-1/2 inhibitor indomethacin and the COX-2-specific inhibitors NS-398 an
89 urred with a latency of only 1-2 s, and both indomethacin and the cyclooxygenase-1 inhibitor SC-560 b
90 inal autonomic cephalalgias, such as oxygen, indomethacin and triptans, and some part of their therap
93 e that a subset of NSAIDs such as ibuprofen, indomethacin, and flurbiprofen may have direct Abeta-low
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
97 H attack-off indomethacin; (2) pain-free-off indomethacin; and (3) pain-free after administration of
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
104 s such as dicoumarol, N-acetylserotonin, and indomethacin blocked sepiapterin reduction, with no effe
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 antibody partially, but in combination with indomethacin, completely abrogated the protective effect
110 data indicate that Jurkat T cells exposed to indomethacin continue to accumulate fluorescent calcein
112 nding affinity between a set of drugs (i.e., indomethacin, coumarin, sulfadymethoxine, warfarin, and
113 elective (ketorolac tromethamine, ibuprofen, indomethacin), COX-1-selective (SC-560), or COX-2-select
115 cting SIVH as well as shown that exposure to indomethacin decreases the incidence of SIVH overall.
117 0.59% of these patients who received rectal indomethacin developed moderate-to-severe PEP vs 4.32% w
118 2.31% of these patients who received rectal indomethacin developed PEP vs 7.53% who did not receive
120 consecutive patients undergoing ERCP, rectal indomethacin did not prevent post-ERCP pancreatitis.
125 ction and inhibition of COX-2 by NS-398, and indomethacin drastically reduced the levels of PGE(2) an
130 e nonselective COX inhibitors salicylate and indomethacin enhanced the expression of iNOS in the rat
131 ment of BHK cells with therapeutic levels of indomethacin enhances cholesterol-dependent nanoclusteri
132 complexes with an enantiomeric pair of these indomethacin ethanolamides were determined at resolution
135 The nonsteroidal anti-inflammatory drug indomethacin exhibits diverse biological effects, many o
137 ex vivo administration of either aspirin or indomethacin failed to prevent platelet activation acros
138 atory drugs (such as aspirin, ibuprofen, and indomethacin) failed to influence endotoxin-induced HMGB
139 ly recognized beneficial side effects of the indomethacin family of nonsteroidal antiinflammatory dru
141 nes recently recommended prophylactic rectal indomethacin for all patients undergoing ERCP, including
144 titis developed in 13 patients (4.4%) in the indomethacin group and in 27 patients (8.8%) in the plac
145 eveloped in 27 of 295 patients (9.2%) in the indomethacin group and in 52 of 307 patients (16.9%) in
156 ate the efficacy of rectal administration of indomethacin in reducing the incidence of post-ERCP panc
162 acrophages with the cyclooxygenase inhibitor indomethacin increases TNFalpha production to the level
164 t of the nonsteroidal anti-inflammatory drug indomethacin (IND) on MDSCs, depending on whether they w
165 armacologically reduced by administration of indomethacin (INDO; 1.2 mg kg(-1)) or unaltered (placebo
166 Neither blockade of cyclooxygenase with indomethacin (Indo; 5 microm) nor blockade of endothelia
171 with H. pylori also stimulated formation of indomethacin-induced gastric lesions and mucosal cell de
172 ent mice are sensitive to the development of indomethacin-induced gastric lesions and mucosal cell de
174 seline morphology or morphometry but reduced indomethacin-induced injury in overexpressing hPSTI regi
176 ed MOS, as is evident from the inhibition of indomethacin-induced mitochondrial protein carbonyl form
177 GI2 receptor (IP) signaling was critical for indomethacin-induced, STAT6-independent proallergic effe
178 applications in EOC and found that (i) NSAID Indomethacin induces robust cell death in primary patien
179 tically examined whether amphiphiles such as indomethacin influence Ras protein nanoclustering in int
181 , but activation of GPR40 in the presence of indomethacin inhibited glucose-dependent insulin secreti
182 In this mouse model, both dexamethasone and indomethacin inhibited TPA-induced edema and MPO activit
184 n of the TLS found in ultrastable glasses of indomethacin is argued to be due to their particular ani
185 tial G1/S arrest, the G1/S arrest induced by indomethacin is, at least in part, caused by the inhibit
188 potencies of aspirin, celecoxib, diclofenac, indomethacin, lumiracoxib, meloxicam, naproxen, rofecoxi
189 and salicylate, but not aspirin, celecoxib, indomethacin, lumiracoxib, meloxicam, or SC560, against
190 anti-inflammatory drugs, tolfenamic acid and indomethacin, markedly reduce direct cell-to-cell spread
194 y COX product(s) responsible for restraining indomethacin-mediated STAT6-independent allergic inflamm
196 given either a single 100-mg dose of rectal indomethacin (n = 223) or a placebo suppository (n = 226
197 One HS diet group subset received 100 mg of indomethacin (non-selective COX-1 and COX-2 inhibitor),
199 ry in rat gastric mucosa; (2) the effects of indomethacin, NS-398, SC-560, and SC-560 plus NS-398 on
202 intolerance was monitored, and the effect of indomethacin on glucose-stimulated insulin secretion (GS
204 the effects of early postnatal ibuprofen and indomethacin on ocular and systemic VEGF, IGF-I, and GH
205 heets similarly showed a selective effect of indomethacin on promoting cholesterol-dependent, but not
206 iciency diminished the stimulatory effect of indomethacin on STAT6-independent IL-5 and IL-13 respons
207 re further used to follow crystallization of indomethacin on tablet surfaces under two storage condit
210 is were assigned to receive 100 mg of rectal indomethacin or a 2.6 g suppository of glycerin immediat
211 if exposure of pregnant rats to analgesics (indomethacin or acetaminophen) affected GC development a
212 by EPCs were inhibited by the COX inhibitor indomethacin or by genetic inactivation of COX-1 or PGI(
213 ndin E2-dependent phase, which is blocked by indomethacin or by null mutation of the EP3 prostanoid r
214 itivity was not altered by pretreatment with indomethacin or capsazepine, a selective antagonist of t
216 d by inhibition of cyclooxygenase-2 (COX-2) (indomethacin or celecoxib) or of TXA2/prostaglandin H2 r
221 combined inhibition of COX-1 and COX-2 with indomethacin or selective inhibition of COX-2 with Merck
223 and treated the mice with the COX inhibitor indomethacin or vehicle for analyses of the primary and
227 oped PEP vs 7.53% who did not receive rectal indomethacin (P < .001) and 0.59% of these patients who
230 ice treated subcutaneously with slow-release indomethacin pellets, suggesting a role for prostanoids,
231 l microbiome by antibiotic treatment altered indomethacin pharmacokinetics and pharmacodynamics, whic
233 re potent AI agent than aspirin, whereas the indomethacin prodrug ( 26) was about 1.6-fold less poten
234 d that the aspirin prodrug 23 (UI = 0.7) and indomethacin prodrug 26 (UI = 0) were substantially less
235 patients with malignant obstruction, rectal indomethacin provided the greatest benefit to patients w
240 ibition of prostaglandin (PG) synthesis with indomethacin reduced the magnitude of the changes in 20:
242 patients with malignant obstruction, rectal indomethacin reduced the risk of PEP by 64% (OR, 0.36; 9
243 MK886 but not the cyclooxygenase inhibitor, indomethacin, reduced growth, increased apoptosis, and u
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
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
252 inistration of a nonselective COX inhibitor (indomethacin), selective COX-1 (valeryl salicylate), or
253 l cycle analysis of HT-29 cells exposed with indomethacin showed a partial G1/S arrest and slow DNA s
256 high risk for post-ERCP pancreatitis, rectal indomethacin significantly reduced the incidence of the
257 At the CP, verapamil and probenecid (but not indomethacin) significantly increased 125I-T4 accumulati
259 y because of gastrointestinal intolerance to indomethacin (six patients) and hypotension with epleren
261 ation was inhibited by acetaminophen but not indomethacin, suggesting catalysis occurred by the perox
262 plication of the model to patients receiving indomethacin suggests a benefit at the highest risk leve
263 rs) derivatized with clinically used NSAIDs (indomethacin, sulindac, ketoprofen, ibuprofen, diclofena
264 ing nitric oxide (l-NAME) and prostaglandin (indomethacin) synthesis increased CGRP EC50 in both age
265 -heat measurements of ultrastable glasses of indomethacin that clearly show the disappearance of the
266 s and during interictal pain-free states off indomethacin that is deactivated by the administration o
267 ntiinflammatory drugs (NSAIDs) ibuprofen and indomethacin, the drugs widely used as pain relievers in
269 fteen patients became normokalemic: six with indomethacin, three with eplerenone, and six with amilor
270 s in their microbiota and their responses to indomethacin - thus, the drug-microbe interactions descr
271 -type, and c-fos-null mice were treated with indomethacin to assess the response to acute inflammatio
272 xposed CD-1 mice were topically treated with indomethacin to block endogenous PGE(2) production, and
273 Our results showed that administration of indomethacin to PiZ mice resulted in increased hepatic i
277 olymerized alpha(1)-ATZ protein in livers of indomethacin-treated PiZ mice compared to vehicle-treate
278 was observed only in selenium-deficient and indomethacin-treated selenium-supplemented mice but not
279 fection compared to monomicrobial infection; indomethacin treatment also decreased elevated PGE2 leve
285 ophen, and other NSAID (ibuprofen, naproxen, indomethacin) use were based on a self-administered ques
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
292 n, acetaminophen (paracetamol), sulindac and indomethacin, was also achieved in supramolecular gel me
294 further evaluate the biophysical effects of indomethacin, we measured fluorescence polarization of t
296 nd after the ex vivo addition of aspirin and indomethacin) were analyzed in 700 consecutive aspirin-t
298 ant (a neurokinin 1 receptor antagonist), or indomethacin with pyrilamine significantly reduced vascu
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
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