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1 esults against gastric damage induced by non-steroidal anti-inflammatory drugs.
2 es, antidiabetic thiazolidinediones, and non-steroidal anti-inflammatory drugs.
3 s and is one of the principle targets of non-steroidal anti-inflammatory drugs.
4 s the principal target for the action of non-steroidal anti-inflammatory drugs.
5 a target for the development of specific non-steroidal anti-inflammatory drugs.
6 ioselective oxidation of several anionic non-steroidal anti-inflammatory drugs.
7 m for chemoprevention of colon cancer by non-steroidal anti-inflammatory drugs.
8 available therapies, such as opioids or non-steroidal anti-inflammatory drugs.
10 lumiracoxib (59 events [0.65%]) and the non-steroidal anti-inflammatory drugs (50 events [0.55%]; ha
11 ations was 1.09% (95% CI 0.82-1.36) with non-steroidal anti-inflammatory drugs (64 events) versus 0.2
12 antial evidence that binding of heme and non-steroidal anti-inflammatory drugs alters the conformatio
13 nesthetics, ketamine, acetaminophen, and non-steroidal anti-inflammatory drugs) analgesic drugs can m
14 population, 0.55% (50/9127) of those on non-steroidal anti-inflammatory drugs and 0.65% (59/9117) of
17 genase site, which is the target for the non-steroidal anti-inflammatory drugs, and a spatially disti
19 Although Helicobacter pylori and use of non-steroidal anti-inflammatory drugs are common causes, dem
25 omplications compared with non-selective non-steroidal anti-inflammatory drugs, but evidence is limit
26 and analgesic properties to traditional non-steroidal anti-inflammatory drugs, but with significantl
27 that the carboxylate group of an acidic non-steroidal anti-inflammatory drug can bind to a COX enzym
28 ow that fatty acids, prostaglandins, and non-steroidal anti-inflammatory drugs, compounds that are su
29 cancer, and is a key molecular target of non-steroidal anti-inflammatory drugs, compounds that reduce
30 Other agents, such as aspirin, other non-steroidal anti-inflammatory drugs, COX-2 inhibitors, ret
31 tments have been suggested, ranging from non-steroidal anti-inflammatory drugs, drugs for neuropathic
34 eatment, we examined the efficacy of the non-steroidal anti-inflammatory drug, flurbiprofen, to suppr
36 t individuals taking aspirin and related non-steroidal anti-inflammatory drugs have reduced risk of l
39 systemic antibiotic (doxycycline) and a non-steroidal anti-inflammatory drug (ibuprofen), administer
40 y observed lack of efficacy of classical non-steroidal anti-inflammatory drugs in the treatment of hy
41 e blockade, and further investigation of non-steroidal anti-inflammatory drugs, in the chemopreventio
43 diuretics, antivirals, methotrexate, and non-steroidal anti-inflammatory drugs) is organic anion tran
44 ecretase modulators (GSMs), such as some non-steroidal anti-inflammatory drugs, is a promising therap
45 lation of serine 121 in cells exposed to non-steroidal anti-inflammatory drugs leads to HSP90 dissoci
46 ve consistently demonstrated that common non-steroidal anti-inflammatory drugs may protect against th
48 n pharmacotherapies, which have included non-steroidal anti-inflammatory drugs, must take into accoun
49 was designed to determine if non-aspirin non-steroidal anti-inflammatory drugs (NANSAIDs) are associa
51 inhibitor lumiracoxib compared with two non-steroidal anti-inflammatory drugs, naproxen and ibuprofe
52 Define the effectiveness of a topical non-steroidal anti-inflammatory drug (NSAID) added to topica
55 se (GERD), Barrett's esophagus (BE), and non-steroidal anti-inflammatory drug (NSAID) bleeding prophy
56 The unprecedented polymorphism of the non-steroidal anti-inflammatory drug (NSAID) flufenamic acid
58 s about the cardiovascular safety of the non-steroidal anti-inflammatory drug (NSAID) rofecoxib, espe
60 ow that inhibition of endogenous PGE2 by non-steroidal anti-inflammatory drug (NSAID) treatment in mi
62 h or standard doses compared with remote non-steroidal anti-inflammatory drug (NSAID) use or celecoxi
63 urgery and to evaluate the effect of the non-steroidal anti-inflammatory drug (NSAID), ibuprofen, on
64 mine-gallic acid hybrid molecule against non-steroidal anti-inflammatory drug (NSAID)-induced gastrop
65 eports in the literature have shown that non-steroidal anti-inflammatory drugs (NSAID) may affect oss
67 ose and regularity of aspirin use, other non-steroidal anti-inflammatory drugs (NSAID), and the effec
69 (i.e., TGF-beta 1, PDGF, and IGF-1), and non-steroidal anti-inflammatory drugs (NSAIDs) (indomethacin
70 that underlie the antitumour activity of non-steroidal anti-inflammatory drugs (NSAIDs) against color
73 2 selective inhibitors and non-selective non-steroidal anti-inflammatory drugs (NSAIDs) are associate
78 As an additional pharmacologic approach, non-steroidal anti-inflammatory drugs (NSAIDs) can reduce gi
81 terviewed about use of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) during the 7
83 selective inhibitors versus traditional non-steroidal anti-inflammatory drugs (NSAIDs) has not been
85 for reducing gastrointestinal effects of non-steroidal anti-inflammatory drugs (NSAIDs) have been sub
88 sis (FASS) for the determination of five non-steroidal anti-inflammatory drugs (NSAIDs) in bovine mil
89 rticoid therapy, hydroxychloroquine, and non-steroidal anti-inflammatory drugs (NSAIDs) in the treatm
95 elicobacter pylori in patients receiving non-steroidal anti-inflammatory drugs (NSAIDs) is unclear.
96 trials demonstrate that long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) markedly redu
97 opreventive effect for aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) on colorectal
98 inically important errors: non-selective non-steroidal anti-inflammatory drugs (NSAIDs) prescribed to
99 al evidence suggests that chronic use of non-steroidal anti-inflammatory drugs (NSAIDs) reduces the r
101 Furthermore, topical application of non-steroidal anti-inflammatory drugs (NSAIDs) significantly
104 respectively), while anti-infectives and non-steroidal anti-inflammatory drugs (NSAIDs) were frequent
106 statin drugs, low-dose aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs), and even fis
108 al trials have suggested that the use of non-steroidal anti-inflammatory drugs (NSAIDs), including as
111 reasing prevalence of individuals taking non-steroidal anti-inflammatory drugs (NSAIDs), there is con
115 gs in four therapeutic areas: analgesia (non-steroidal anti-inflammatory drugs [NSAIDs]), diabetes (m
116 ects of tetracyclines, and the effect of non-steroidal anti-inflammatory drugs on decreasing alveolar
117 vity by the administration of PTH and/or non-steroidal anti-inflammatory drugs or COX-2 selective inh
118 e of such therapies precluded the use of non-steroidal anti-inflammatory drugs or other enzyme inhibi
119 tack therapies (eg, simple analgesics or non-steroidal anti-inflammatory drugs) or specific agents wi
120 d PUD was associated with current use of non-steroidal anti-inflammatory drugs, oral steroids or acid
122 nsteroidal anti-inflammatory drugs (NSAIDs), steroidal anti-inflammatory drugs (SAIDs), immunosuppres
123 ics, antimotility agents, narcotics, and non-steroidal anti-inflammatory drugs should not be given to
124 studies have shown that long-term use of non-steroidal anti-inflammatory drugs, statins, histamine H2
125 In this study we evaluate the effect of non-steroidal anti-inflammatory drugs, such as indomethacin
126 d placebo-controlled trials, traditional non-steroidal anti-inflammatory drugs, such as naproxen, dic
130 statin, antihypertensive medications and non-steroidal anti-inflammatory drugs therapy) as well as 4
133 f the drugs was sulindac, a prototypical non-steroidal anti-inflammatory drug with established chemop
135 ion in ulcer complications compared with non-steroidal anti-inflammatory drugs without an increase in
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