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1 d be decreased by treatment with a selective cyclooxygenase-2 inhibitor.
2 and this induction could be antagonized by a cyclooxygenase-2 inhibitor.
3 ncreased cardiovascular risk associated with cyclooxygenase-2 inhibitors.
4 astrointestinal safety outcomes of selective cyclooxygenase-2 inhibitors.
5  retinoids, statins, and tyrosine kinase and cyclooxygenase-2 inhibitors.
6           These effects were suppressed by a cyclooxygenase-2 inhibitor, a drug type known to reduce
7 ntake; administration of NS-398, a selective cyclooxygenase-2 inhibitor, abolished the arterial press
8 emity edema, and hypertension indicates that cyclooxygenase-2 inhibitors affect the kidney in a manne
9    Wild-type mice or human volunteers taking cyclooxygenase-2 inhibitors also showed increased plasma
10 onstatin cholesterol-lowering medications or cyclooxygenase 2 inhibitors and the development of TAO.
11 ogy; however, simultaneous administration of cyclooxygenase-2 inhibitors and dietary hen egg-white ly
12 uding newer N-methyl-D-asparate antagonists, cyclooxygenase-2 inhibitors and membrane stabilizing ana
13 ing other agents with NSAID-like mechanisms (cyclooxygenase-2 inhibitors and salicylates).
14     Newly developed drugs, such as selective cyclooxygenase-2 inhibitors and soluble tumor necrosis f
15  provided evidence that aspirin, celecoxib, (cyclooxygenase-2 inhibitor), and statins (3-hydroxy-3-me
16 atins, nonsteroidal anti-inflammatory drugs, cyclooxygenase-2 inhibitors, and aspirin on colorectal c
17                       Mast cell stabilizers, cyclooxygenase-2 inhibitors, and PGE2 receptor antagonis
18 ased risk associated with the use of certain cyclooxygenase-2 inhibitors, and randomized trial data s
19   The anticancer effects of bisphosphonates, cyclooxygenase-2 inhibitors, and statins may expand thei
20 f the anticancer effects of bisphosphonates, cyclooxygenase-2 inhibitors, and statins, may lead to th
21 r events has been demonstrated with multiple cyclooxygenase-2 inhibitors, and this increased risk has
22                                    Selective cyclooxygenase-2 inhibitors are as effective as nonselec
23 The European Medicines Agency concluded that cyclooxygenase-2 inhibitors are contraindicated in patie
24 oidal anti-inflammatory drugs) and selective cyclooxygenase-2 inhibitors are generating interest beca
25                 However, these new selective cyclooxygenase-2 inhibitors are not risk free, and care
26                                              Cyclooxygenase-2 inhibitors are potent anti-inflammatory
27 L-4 since treating UV-irradiated mice with a cyclooxygenase-2 inhibitor blocked its production.
28                                   A specific cyclooxygenase-2 inhibitor blocked the formation of thre
29 phages with indomethacin, a cyclooxygenase-1/cyclooxygenase-2 inhibitor, blocked PGE(2) production.
30                       For example, selective cyclooxygenase-2 inhibitors can provide the same symptom
31     A recent study showing that celecoxib, a cyclooxygenase-2 inhibitor, can alter the natural histor
32 reliminary data suggested that the selective cyclooxygenase -2 inhibitor celecoxib (CBX) might enhanc
33 e antidepressant properties of the selective cyclooxygenase 2 inhibitor celecoxib (SMD, -0.29; 95% CI
34                             Treatment with a cyclooxygenase 2 inhibitor celecoxib significantly impro
35               Systemic administration of the cyclooxygenase 2 inhibitor celecoxib suppressed both PGE
36 tion with arachidonic acid and the selective cyclooxygenase-2 inhibitor celecoxib.
37 1 (MUC1)-based vaccine in combination with a cyclooxygenase-2 inhibitor (celecoxib), and low-dose che
38                   Treatment with a selective cyclooxygenase-2 inhibitor, celecoxib, markedly inhibite
39 linical cancer prevention studies by using a cyclooxygenase-2 inhibitor, celecoxib.
40 d gliosis were assessed in pups treated with cyclooxygenase-2 inhibitor compared to controls at Day 1
41  increased risk associated with a variety of cyclooxygenase-2 inhibitors compared with either a tradi
42 roidal anti-inflammatory drugs and selective cyclooxygenase-2 inhibitors consistently reduce postoper
43 iovascular risks of treatment with selective cyclooxygenase 2 inhibitors (coxibs) and nonselective no
44 ular risks associated with anti-inflammatory cyclooxygenase 2 inhibitors (coxibs) by targeting the pr
45                                              Cyclooxygenase-2 inhibitors (coxibs) are characterized b
46          Over the past five years, selective cyclooxygenase-2 inhibitors (coxibs) have accounted for
47                                     Although cyclooxygenase-2 inhibitors (coxibs) were developed to c
48 ted to an 'imbalance theory' suggesting that cyclooxygenase-2 inhibitors create an 'imbalance' betwee
49                   Lumiracoxib is a selective cyclooxygenase-2 inhibitor developed for the symptomatic
50  Cardiovascular side effects associated with cyclooxygenase-2 inhibitor drugs dominate clinical conce
51 /2 randomized clinical trial (TBCOX2) of the cyclooxygenase-2 inhibitor etoricoxib.
52 tudies indicated that celecoxib, a selective cyclooxygenase-2 inhibitor, exhibits potent antitumor ac
53 may be an important alternative to selective cyclooxygenase-2 inhibitors for patients who need aspiri
54 ophen, nonsteroidal anti-inflammatory drugs, cyclooxygenase-2 inhibitors, gabapentinoids, and ketamin
55 ophen, nonsteroidal anti-inflammatory drugs, cyclooxygenase-2 inhibitors, gabapentinoids, ketamine, p
56 epidermal growth factor receptor inhibitors, cyclooxygenase-2 inhibitors, green tea extract, and pero
57 t concentrations (1-2 microM) of a selective cyclooxygenase-2 inhibitor had no detectable, direct eff
58 ds, non-steriodal antiinflammatory drugs and cyclooxygenase-2 inhibitors have been shown not to impac
59 ors for a nonselective NSAID and a selective cyclooxygenase 2 inhibitor in a double-blind outcomes tr
60 d clarify the true benefits of perioperative cyclooxygenase-2 inhibitors in acute pain management str
61 y justification for using the more expensive cyclooxygenase-2 inhibitors in preference to nonsteroida
62 tion of epidermal growth factor receptor and cyclooxygenase-2 inhibitors in SCCHN is warranted.
63  controversy surrounding the proper place of cyclooxygenase-2 inhibitors in the hierarchy of treatmen
64 udies have demonstrated an important role of cyclooxygenase-2 inhibitors in the management of acute p
65 increased myocardial infarction with certain cyclooxygenase-2 inhibitors, in particular rofecoxib.
66 studies, one may conclude that perioperative cyclooxygenase-2 inhibitors, in standard doses, decrease
67                       The data comparing the cyclooxygenase-2 inhibitors is difficult to interpret be
68 -daily treatment with 400 mg of celecoxib, a cyclooxygenase-2 inhibitor, leads to a significant reduc
69 tamin D, other 5-alpha-reductase inhibitors, cyclooxygenase-2 inhibitors, lycopene, and green tea.
70 demiologic and molecular evidence also makes cyclooxygenase-2 inhibitors, lycopene, soy, and green te
71                                              Cyclooxygenase-2 inhibitors may also reduce colorectal p
72               Concerns have been raised that cyclooxygenase-2 inhibitors may increase thrombotic card
73               Rofecoxib, but perhaps not all cyclooxygenase-2 inhibitors, may be associated with incr
74  that target enzymes in the cascade, such as cyclooxygenase 2 inhibitors, might be candidate treatmen
75      This IPDT agent integrates a celecoxib (cyclooxygenase-2 inhibitor) moiety with a near-infrared
76 ith dysplastic Barrett's esophagus by use of cyclooxygenase 2 inhibitors, nonsteroidal anti-inflammat
77                        In previous work, the cyclooxygenase-2 inhibitor NS-398 inhibited interleukin
78 pression and activity and was blocked by the cyclooxygenase-2 inhibitors NS-398 and Resveratrol.
79 t of cAMP were inhibited only by a selective cyclooxygenase-2 inhibitor, NS-398.
80                                          The cyclooxygenase-2 inhibitor NS398 blocked PPARgamma-induc
81 or 30 mg/kg (high dose) of a known selective cyclooxygenase-2 inhibitor (NS398).
82 y simultaneous adolescent treatment with the cyclooxygenase-2 inhibitor, NS398.
83 studied the effect of celecoxib, a selective cyclooxygenase-2 inhibitor, on colorectal polyps in pati
84  prescription NSAIDs, particularly selective cyclooxygenase 2 inhibitors (OR = 0.38, 95% CI: 0.25, 0.
85 e treated with either rofecoxib (a selective cyclooxygenase-2 inhibitor) or indomethacin (a non-selec
86                                              Cyclooxygenase-2 inhibitors, or coxibs, designed to prov
87 (1 mg/kg intraperitoneally) or the selective cyclooxygenase-2 inhibitor parecoxib (20 mg/kg intraperi
88                             In contrast, the cyclooxygenase-2 inhibitor parecoxib did not affect the
89           The potential thrombogenic risk of cyclooxygenase-2 inhibitors remains controversial, and c
90  reverse order; aspirin two hours before the cyclooxygenase-2 inhibitor rofecoxib (25 mg every mornin
91 is antiapoptotic effect was inhibited by the cyclooxygenase-2 inhibitor rofecoxib and was restored by
92  a protective strategy such as the selective cyclooxygenase 2 inhibitor, rofecoxib, to avert a clinic
93 of 4T1-tumor-bearing wild-type mice with the cyclooxygenase 2 inhibitor, SC58236, delays primary tumo
94  exposure and chemoprevention, possibly with cyclooxygenase 2 inhibitors, should reduce the incidence
95 us to demonstrate that pain was blocked by a cyclooxygenase-2 inhibitor, suggesting an indirect effec
96 roidal anti-inflammatory drugs and selective cyclooxygenase-2 inhibitors that block prostanoid synthe
97 ho initiated nonselective NSAID or selective cyclooxygenase 2 inhibitor therapy between January 1, 19
98 -year nonvertebral fracture risk, a study of cyclooxygenase 2 inhibitors versus nonselective nonstero
99 e of nonsteroidal anti-inflammatory drug and cyclooxygenase-2 inhibitor was associated with a reduced
100                             Prolonged use of cyclooxygenase-2 inhibitors was minimal, but for those r
101                     A novel class of NSAIDs, cyclooxygenase-2 inhibitors, was introduced in 1999.
102                                    Selective cyclooxygenase-2 inhibitors were developed to reduce the
103   This is exemplified by the clinical use of cyclooxygenase 2 inhibitors, which interfere with PGE2 s
104 emotherapeutic agents suggest that combining cyclooxygenase-2 inhibitors with other agents may have s
105 al studies combining antiangiogenic drugs or cyclooxygenase-2 inhibitors with PDT show improved treat
106 multimodal techniques, for example combining cyclooxygenase-2 inhibitors with regional blocks, may he
107 findings led to the development of selective cyclooxygenase-2 inhibitors, with comparable anti-inflam

 
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