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1 ory actions to effects on oxidation state of cyclo-oxygenase.
2 ng terminals, but resistant to inhibition of cyclo-oxygenases.
3 man vessels and endothelial cells containing cyclo-oxygenase-1 (COX-1) without any detectable COX-2,
4 hacin or diclofenac, which also inhibit both cyclo-oxygenase-1 and cyclo-oxygenase-2, were unaffected
5 hrombogenicity, whereas markers sensitive to cyclo-oxygenase-1 blockade are increased in the absence
6                         Markers sensitive to cyclo-oxygenase-1 blockade, including platelet reactivit
7 2 selective inhibitor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase-2 inhibitors ibuprofen
8 ts the inducible isoform of cyclo-oxygenase, cyclo-oxygenase 2 (COX-2).
9                                              Cyclo-oxygenase 2 (COX2), an inducible isoform of prosta
10          Methylation status of the p14, p16, cyclo-oxygenase 2 (COX2), O(6)-methyl-guanine methyltran
11                                              Cyclo-oxygenase 2 (COX2)-selective inhibitors should red
12                            The potential for cyclo-oxygenase 2 (COX2)-selective inhibitors to increas
13 OCS-3]) and mediators of energy expenditure (cyclo-oxygenase 2 [COX-2]), we studied the effect of CNT
14 appaBalpha and proinflammatory genes such as cyclo-oxygenase 2 and interleukin 8.
15                  Non-selective and selective cyclo-oxygenase 2 inhibitors have preliminary data from
16 a-2 agonists, beta-blockers,corticosteroids, cyclo-oxygenase 2 inhibitors, and regional anesthetic bl
17 A search for chemoprevention agents, such as cyclo-oxygenase 2 inhibitors, as well as for putative en
18                          Current exposure to cyclo-oxygenase 2 selective and non-selective NSAIDs was
19  including overexpression of IL-6, IL-1beta, cyclo-oxygenase 2, M-CSF, and IDO.
20 nducible NO synthase, arginase-1, TNF-alpha, cyclo-oxygenase 2, vascular endothelial growth factor [V
21 ripts of a limited number of genes including cyclo-oxygenase-2 (COX-2) and major histocompatibility c
22       Prostanoids produced via the action of cyclo-oxygenase-2 (COX-2) appear central to many inflamm
23 ates parathyroid-related peptide (PTHrP) and cyclo-oxygenase-2 (COX-2) as possible factors underlying
24 ophosphatidic acid (LPA) lead to synergistic cyclo-oxygenase-2 (COX-2) expression, an enzyme strongly
25 e, mutagenesis, apoptosis, angiogenesis, and cyclo-oxygenase-2 (COX-2) expression.
26 inhibits nitric-oxide synthase-2 (NOS-2) and cyclo-oxygenase-2 (COX-2) expressions in RAW 264.7 stimu
27 -2), matrix metalloproteinase-9 (MMP-9), and cyclo-oxygenase-2 (COX-2) in the mammary gland.
28 dies suggest that treatment with a selective cyclo-oxygenase-2 (COX-2) inhibitor may augment the anti
29                                              Cyclo-oxygenase-2 (COX-2) selective inhibitors have been
30 of interleukin-8 (IL-8), IL-6, IL-1beta, and cyclo-oxygenase-2 (COX-2) were greatest in differentiate
31                                              Cyclo-oxygenase-2 (COX-2), a rate-limiting enzyme for pr
32                                              Cyclo-oxygenase-2 (COX-2), an inducible enzyme important
33 SAIDs), particularly selective inhibitors of cyclo-oxygenase-2 (COX-2), is associated with an increas
34  expression of the pro-inflammatory mediator cyclo-oxygenase-2 (COX-2), providing a mechanism whereby
35 s, such as inflammatory responses, including cyclo-oxygenase-2 (Cox-2).
36         We have demonstrated previously that cyclo-oxygenase-2 (COX2), the rate-limiting enzyme in th
37      Here, we have used an in vitro model of cyclo-oxygenase-2 activity (A549 cells stimulated with I
38 uated by inhibiting the prostanoid mediators cyclo-oxygenase-2 and 5-lipoxygenase and CC chemokine re
39 tivity, and (iii) protein expression of ODC, cyclo-oxygenase-2 and nitric oxide synthase.
40 t of titres of lentiviral vectors expressing Cyclo-oxygenase-2 by 600-fold, and adenoviral vectors ex
41       Here we have generated mouse models of cyclo-oxygenase-2 deficiency from relevant cell types to
42                                  Deletion of cyclo-oxygenase-2 from fibroblasts reduced total renal e
43                      Selective inhibition of cyclo-oxygenase-2 has been associated with an increased
44  evidence for a role of fibroblast and renal cyclo-oxygenase-2 in anti-thrombotic protection and demo
45 e is increasing evidence for a role of renal cyclo-oxygenase-2 in NSAID-induced cardiovascular side e
46 over nonsteroidal anti-inflammatory drug and cyclo-oxygenase-2 inhibitor safety continues.
47 ked current also was blocked by the specific cyclo-oxygenase-2 inhibitor SC-236.
48 following treatment with NS-398, a selective cyclo-oxygenase-2 inhibitor was evaluated.
49 sessed the effect of 3-year treatment with a cyclo-oxygenase-2 inhibitor, rofecoxib (25 mg), on recur
50 tor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase-2 inhibitors ibuprofen and naproxen were
51 ear has led to a reassessment of the role of cyclo-oxygenase-2 inhibitors in osteoarthritis therapy a
52 c pain is typically treated with opioids and cyclo-oxygenase-2 inhibitors with well known side effect
53  of nonsteroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors.
54                                   Fibroblast cyclo-oxygenase-2 knockout increased thrombosis after ar
55 on, pro-thrombotic phenotypes in endothelial cyclo-oxygenase-2 knockout mice, which occur via a vascu
56  resulted in specific induction of Bcl-2 and cyclo-oxygenase-2 proteins, both of which are thought to
57      Similarly the inhibitory effects of the cyclo-oxygenase-2 selective inhibitor rofecoxib or the m
58  some NSAIDs, including the newly introduced cyclo-oxygenase-2 selective inhibitor rofecoxib, owe par
59                                              Cyclo-oxygenase-2 selective inhibitors and non-selective
60 s of nonsteroidal anti-inflammatory drug and cyclo-oxygenase-2 therapy for individuals is covered.
61                                              Cyclo-oxygenase-2(-/-) mice had increased plasma levels
62 okeratin, high-molecular-weight cytokeratin, cyclo-oxygenase-2, EMA, HER2, matrix metalloproteinases
63 ory drugs (NSAIDs), which work by inhibiting cyclo-oxygenase-2, is associated with an increased risk
64  such as inducible nitric oxide synthase and cyclo-oxygenase-2, reduce ischemic damage with an extend
65 hich also inhibit both cyclo-oxygenase-1 and cyclo-oxygenase-2, were unaffected by t-butylOOH.
66 ious impact that select therapies (including cyclo-oxygenase-2-specific inhibitors) may have in terms
67    These observations dispel the notion that cyclo-oxygenase-3 is involved in the actions of acetamin
68 inhibits a distinct form of cyclo-oxygenase, cyclo-oxygenase-3.
69 sm that is, at least in part, independent of cyclo-oxygenase activation.
70 , alternatively, the restoration of PTHrP or cyclo-oxygenase activity by the administration of PTH an
71 t acetaminophen is an effective inhibitor of cyclo-oxygenase activity in intact cells.
72 ise mechanism of action for acetaminophen on cyclo-oxygenase activity is debated.
73  +/- 54.9 % of control following blockade of cyclo-oxygenase activity with naproxen (10 microM).
74 g of free radicals, or by inhibition of both cyclo-oxygenase and lipoxygenase in combination.
75 se of arachidonic acid, which is acted on by cyclo-oxygenase and lipoxygenase resulting in the format
76 e to ANG II depends largely on activation of cyclo-oxygenase and production of prostaglandins.
77               Aspirin, a nonselective COX-1 (cyclo-oxygenase) and COX-2 inhibitor may result in gastr
78 ytokines, and suppresses phospholipase A(2), cyclo-oxygenase, and nitric oxide synthase.
79 e caused by the previous suggested effect on cyclo-oxygenase, as inhibition also was observed in the
80 ophen has no affinity for the active site of cyclo-oxygenase but instead blocks activity by reducing
81 xide synthase, soluble guanylate cyclase and cyclo-oxygenase but was blocked by 25 mm potassium.
82  (200 microg/5 microl aCSF), an inhibitor of cyclo-oxygenase, but not with losartan (25 microg/5 micr
83 athways were downregulated, as were S100 and cyclo-oxygenase components.
84                             Should selective cyclo-oxygenase (COX) 2 inhibitors be used?
85 and whether its effects are mediated through cyclo-oxygenase (COX) and prostaglandins (PG).
86  inhibition of prostaglandin synthesis via a cyclo-oxygenase (COX) enzyme was central to both the the
87            The role of different isoforms of cyclo-oxygenase (COX) in mediating the acute (0-6 h) and
88 g(-1)) and SB-222200 (5 mg kg(-1)) or by the cyclo-oxygenase (COX) inhibitor indomethacin (20 mg kg(-
89 the stomach, production of prostaglandins by cyclo-oxygenase (COX) is believed to be important in muc
90        Metabolism of arachidonic acid by the cyclo-oxygenase (COX) pathway generates a family of pros
91 ed vasodilatation with nitric oxide (NO) and cyclo-oxygenase (COX) signalling pathways, microdialysis
92                                              Cyclo-oxygenase (COX), the enzyme responsible for conver
93  of NSAIDs is their inhibition of the enzyme cyclo-oxygenase (COX), which catalyses the synthesis of
94 dal anti-inflammatory drugs (NSAIDs) inhibit cyclo-oxygenase (COX), which leads to suppression of COX
95 ighly-sensitive assay, and on serum platelet-cyclo-oxygenase (COX)-1-derived thromboxane (Tx) B2 conc
96  prostacyclin (PGI2) derived from adenoviral cyclo-oxygenase (COX)-1/prostacyclin synthase (PGIS) (Ad
97                                              Cyclo-oxygenase (COX)-2 selective inhibitors decrease up
98             Upper gastrointestinal safety of cyclo-oxygenase (COX)-2 selective inhibitors versus trad
99 (NSAID) can be associated with inhibition of cyclo-oxygenase (COX)-2 whereas their harmful side effec
100 ed rapid expression of interleukin-15, CD83, cyclo-oxygenase (COX)-2, and CD25 by CD3- cells (p=0.005
101 ction of aspirin is inhibition of the enzyme cyclo-oxygenase (COX).
102  inhibition of nitric oxide (NO) synthase or cyclo-oxygenase (COX).
103                      Increased generation of cyclo-oxygenase (COX-1 and COX-2)-derived vasoconstricto
104  interaction between PPARgamma and inducible cyclo-oxygenase (COX-2) in rat aortic vascular smooth mu
105 of nitric oxide synthase (NOS; with l-NAME), cyclo-oxygenase (COX; with indomethacin) and endothelium
106  a 1-week high-salt (HS) diet on the role of cyclo-oxygenases (COX-1 and COX-2) and the vasoconstrict
107 selectively targets the inducible isoform of cyclo-oxygenase, cyclo-oxygenase 2 (COX-2).
108 phen selectively inhibits a distinct form of cyclo-oxygenase, cyclo-oxygenase-3.
109                In addition, nitric oxide and cyclo-oxygenase-derived byproducts are required for full
110 extent of I(CRAC), whereas inhibition of the cyclo-oxygenase enzymes was without effect.
111 ic responses, such as inducible NO synthase, cyclo-oxygenase II, and collagenase.
112 l effective in the presence of inhibitors of cyclo-oxygenase (indomethacin, 10 microM), lipoxygenase
113 shes bombesin-induced gastroprotection while cyclo-oxygenase inhibition partially reverses this effec
114 .v.) and NPC-17731 (40 micrograms kg-1 i.v., cyclo-oxygenase inhibition with indomethacin (5 mg kg-1
115 d reduced ET-induced vascular leakage with a cyclo-oxygenase inhibitor (indomethacin), agents that in
116 t influenced by pretreatment with either the cyclo-oxygenase inhibitor indomethacin or the leukotrien
117 gene expression in T cells, whereas the weak cyclo-oxygenase inhibitor salicylic acid was at least as
118 yet, undeveloped therapeutic window for the "cyclo-oxygenase inhibitor".
119 ed in the presence of high concentrations of cyclo-oxygenase inhibitor, aspirin.
120                 The development of selective cyclo-oxygenase inhibitors (COX-II) and confirmation of
121 administration of indomethacin or celecoxib (cyclo-oxygenase inhibitors), pyrilamine, aprepitant (a n
122 omethacin, suggesting that the activation of cyclo-oxygenase is not involved.
123  tested are physiological substrates for the cyclo-oxygenase, lipoxygenase and epoxygenase pathways,
124 esting that AA did not exert its effects via cyclo-oxygenase, lipoxygenase or cytochrome P-450 (cP-45
125 ibition of Kv4 channels was not prevented by cyclo-oxygenase, lipoxygenase, or cytochrome P-450 inhib
126 do), an inhibitor of the metabolism of AA by cyclo-oxygenase, nor nordihydroguaiaretic acid (NDGA), a
127 ls, and is independent of the release of NO, cyclo-oxygenase or cytochrome P450 products.
128 ce for metabolism of arachidonic acid by the cyclo-oxygenase pathway.
129 e afferents appears to be independent of the cyclo-oxygenase pathway.
130 and substrate supply, and not the isoform of cyclo-oxygenase present, dictate the effects of NSAIDs o
131  Increased production of bradykinin (BK) and cyclo-oxygenase products (i.e. prostaglandins (PGs)) occ
132              Acetaminophen works by lowering cyclo-oxygenase products preferentially in the central n
133  of endothelin and possibly vasoconstrictive cyclo-oxygenase products.
134  micro g/5 micro l, i.c.v.), an inhibitor of cyclo-oxygenase, showing that they are mediated by prost
135  (200 microg/5 microl; icv), an inhibitor of cyclo-oxygenase, significantly attenuated the ANG II-ind
136 , unco-ordinated-5H3 (unc5H3), doublecortin, cyclo-oxygenase, sonic hedgehog and Disrupted in schizop
137 vity by reducing the active oxidized form of cyclo-oxygenase to an inactive form.
138                                Inhibition of cyclo-oxygenase with naproxen (10 microM) prevented sens

 
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