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1 genes (endothelial nitric oxide synthase and cyclooxygenase-1).
2 The activation of PKA is downstream of COX1 (cyclooxygenase-1).
3 eroidal anti-inflammatory drugs that inhibit cyclooxygenase 1.
4  prostaglandins and thromboxane, produced by cyclooxygenase-1.
5 tion of proangiogenic 15(S)-HETE by platelet cyclooxygenase-1.
6 d an intolerance of medications that inhibit cyclooxygenase-1.
7 here was no coexpression between mPGES-1 and cyclooxygenase-1.
8 activity of the molecular target of aspirin, cyclooxygenase-1.
9 ts newly discovered inhibition of the enzyme cyclooxygenase-1.
10  Similar to MSCs, ICC-SCs strongly expressed cyclooxygenase 1/2 and basally secreted prostaglandin E2
11  blockade of each of the downstream enzymes, cyclooxygenase-1/2 and 5-lipooxygenase.
12 activities of lipoxygenase (720 kIU/g d.w.), cyclooxygenase-1 (97 kIU/g d.w.), and xanthine oxidase (
13                            Mice deficient in cyclooxygenase-1, a critical enzyme in prostaglandin bio
14                      Aspirin, which inhibits cyclooxygenase-1 activity and thromboxane generation in
15                      Measurement of platelet cyclooxygenase-1 activity following immunoprecipitation
16   Serum thromboxane B(2) levels (an index of cyclooxygenase-1 activity in platelets) and platelet agg
17      The highest inhibition of activities of cyclooxygenase 1 and -2, as well as amylase and glucosid
18                                        Renal cyclooxygenase 1 and 2 activity produces five primary pr
19 nstrictor and platelet agonist, whereas both cyclooxygenase 1 and 2 contribute to production of endot
20  which is converted primarily to PGs via the cyclooxygenase 1 and 2 pathways and to leukotrienes via
21 ding enzymes involved in lipid biosynthesis (cyclooxygenase 1 and thromboxane A synthase 1) and a thr
22 otal prostaglandin concentration and to show cyclooxygenase-1 and -2 (COX-1 and -2) immunoreactivitie
23                                              Cyclooxygenase-1 and -2 (COX1 and COX2) derived endogeno
24  prostaglandin (PG) synthesis is mediated by cyclooxygenase-1 and -2 (COX1 and COX2).
25 nflammatory drugs (NSAIDs) are inhibitors of cyclooxygenase-1 and -2 and are useful for prevention an
26 oth compounds were shown to inhibit purified cyclooxygenase-1 and -2 by a reversible mechanism.
27                                              Cyclooxygenase-1 and -2 did not oxidize alkynyl linoleic
28 141.6 and 138.8 muM, respectively) inhibited cyclooxygenase-1 and -2 enzymes by 50%.
29 eries of uni-x sheep, accompanied by reduced cyclooxygenase-1 and -2 gene expression (P<0.05).
30 ize the current understanding of the role of cyclooxygenase-1 and -2 in different physiological situa
31 release of isoprostanes was inhibited by the cyclooxygenase-1 and -2 inhibitor indomethacin as well b
32 rine signaling molecules synthesized via the cyclooxygenase-1 and -2 pathways.
33 ty on angiotensin-1 converting enzyme (ACE), cyclooxygenase-1 and -2, and 15-lipoxygenase (LOX), and
34 . canina hips showed some anti-inflammatory (cyclooxygenase-1 and 12-lipooxygense inhibition potency)
35  production of some monitored eicosanoids in cyclooxygenase-1 and 12-lipoxygenase pathways.
36                                  The enzymes cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2)
37 rsor RNA, H19, correlated with expression of cyclooxygenase-1 and cyclooxygenase-2 and shorter surviv
38 nd nitric oxide production, increased aortic cyclooxygenase-1 and cyclooxygenase-2 expression, and in
39 tric mucosal integrity, the precise roles of cyclooxygenase-1 and cyclooxygenase-2 in these processes
40  (2) in the remaining patients, occurs via a cyclooxygenase-1 and cyclooxygenase-2 independent pathwa
41             The two cyclooxygenase isoforms, cyclooxygenase-1 and cyclooxygenase-2, both metabolize a
42 ost mouse with indomethacin, an inhibitor of cyclooxygenase-1 and cyclooxygenase-2, or with NS-398, a
43 l NSAIDs and aspirin inhibit active sites of cyclooxygenase-1 and cyclooxygenase-2.
44 e-2, and >100-fold selectivity against ovine cyclooxygenase-1 and human cyclooxygnease-2.
45 ilization [Ca(t)]i controls granule release, cyclooxygenase-1 and integrin activation, and phosphatid
46  occurrence of events despite treatment with cyclooxygenase-1 and P2Y12 inhibitors.
47                                     However, cyclooxygenase-1 and prostanoid receptor 2-4 levels were
48 ytic cytochrome P450 epoxygenase, astrocytic cyclooxygenase-1 and smooth muscle cytochrome P450 omega
49 sident peritoneal macrophages contained only cyclooxygenase-1 and synthesized (from either endogenous
50 reatment of inflammatory diseases and target cyclooxygenases 1 and 2 (Cox-1, Cox-2) that are responsi
51 -Prostaglandin (PG) F2alpha may be formed by cyclooxygenases 1 and 2 or by a free radical catalyzed p
52 werful inhibitor of prostaglandin synthases (cyclooxygenases 1 and 2), did not inhibit the formation
53 broblasts, mediated by the induction of both cyclooxygenases 1 and 2.
54 roxide H synthases-1 and -2, commonly called cyclooxygenases-1 and -2 (COX-1 and -2), catalyze the co
55                                              Cyclooxygenases-1 and -2 (Cox-1 and Cox-2) are two disti
56                   Prostaglandin synthesis by cyclooxygenases-1 and -2 (COX-1 and COX-2) involves an i
57 of alpha-glucosidase, alpha-amylase, lipase, cyclooxygenases-1 and -2 (COX-1/COX-2), and lipoxygenase
58 H synthases-1 and 2 (PGHS-1 and PGHS-2; also cyclooxygenases-1 and 2, COX-1 and COX-2) catalyze the c
59  In contrast, the expression of fibronectin, cyclooxygenase 1, and GAPDH was not affected.
60                            Fasted wild-type, cyclooxygenase-1, and cyclooxygenase-2 knockout mice wer
61  platelet 12-hLO, epithelial 15-hLO-2, ovine cyclooxygenase-1, and human cyclooxygenase-2.
62 e aspirin through faster renewal of platelet cyclooxygenase-1, and impaired platelet inhibition can b
63 ignaling migration, constitutively expressed cyclooxygenase-1 appears to contribute approximately 25%
64 d Bruton's tyrosine kinase (ibrutinib); GPCR-cyclooxygenase 1 (aspirin); and P2Y12 (clopidogrel).
65 W-480 colorectal cancer cells, which express cyclooxygenase-1 but little cyclooxygenase-2.
66 s diminished in HCT-116 cells overexpressing cyclooxygenase-1 compared with normal HCT-116 cells sugg
67 ons to generate three-dimensional models for cyclooxygenase-1 complexes with a series of indomethacin
68 stigate the role of the two cyclooxygenases, cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2), i
69                           Sex differences in cyclooxygenase 1 (COX-1) direct and indirect platelet ac
70 step in the cyclooxygenase reaction cycle of cyclooxygenase 1 (COX-1) is abstraction of the pro-S hyd
71 loproteinase 1, MCP-1, IL-1beta, IL-6, IL-8, cyclooxygenase 1 (COX-1), COX-2, leukemia inhibitory fac
72              Here we show that inhibitors of cyclooxygenase 1 (COX-1), including aspirin, enhance imm
73 l-specific, alternatively spliced isoform of cyclooxygenase 1 (COX-1).
74  by aspirin in vitro or in vivo, implicating cyclooxygenase-1 (COX).
75                We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolat
76                                              Cyclooxygenase-1 (Cox-1) and Cox-2 convert arachidonic a
77 dal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase-1 (COX-1) and COX-2 enzymes.
78 ndins (PGs), generated through the action of cyclooxygenase-1 (COX-1) and COX-2 protect the intestina
79 ucible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing
80           PGE2 biosynthesis is controlled by cyclooxygenase-1 (COX-1) and COX-2, whose induction invo
81 ioactive lipids derived from the activity of cyclooxygenase-1 (COX-1) and COX-2.
82                                              Cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) ar
83                                         Both cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) co
84                   NSAIDs inhibit the enzymes cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), w
85                   NSAIDs inhibit the enzymes cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), w
86     NSAIDs inhibit the enzymatic activity of cyclooxygenase-1 (COX-1) and inducible COX-2, which cata
87 esult from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin.
88 to discover structurally novel inhibitors of cyclooxygenase-1 (COX-1) by screening a selected number
89 r studied in monoamine oxidase B (MAO-B) and cyclooxygenase-1 (COX-1) enzyme through molecular dockin
90                         Estrogen upregulates cyclooxygenase-1 (COX-1) expression in endothelial cells
91                                              Cyclooxygenase-1 (COX-1) has been implicated in the path
92 d G-protein coupled receptor X2 (MRGPRX2) or Cyclooxygenase-1 (COX-1) inhibition and their associated
93 d evaluated for cyclooxygenase-2 (COX-2) and cyclooxygenase-1 (COX-1) inhibition in human whole blood
94 he most common type is bred by pharmacologic cyclooxygenase-1 (COX-1) inhibition, after chemically un
95 neration may reduce the duration of platelet cyclooxygenase-1 (COX-1) inhibition.
96 yl-4-phenylisoxazole (P6), a known selective cyclooxygenase-1 (COX-1) inhibitor, was used to design a
97           The ingestion of aspirin and other cyclooxygenase-1 (COX-1) inhibitors induces exacerbation
98                                              Cyclooxygenase-1 (COX-1) is the rate-limiting component
99                                     Vascular cyclooxygenase-1 (COX-1) is the rate-limiting step in pr
100 mboxane A(2) formed by platelets from AA via cyclooxygenase-1 (COX-1) mediates thrombosis.
101 -hydroxyeicosatrienoic acid [12-HETrE]) over cyclooxygenase-1 (COX-1) or 12-lipoxygenase (12-LOX) met
102                     Prostaglandins formed by cyclooxygenase-1 (COX-1) or COX-2 produce hyperalgesia i
103 achidonate by either of two cyclooxygenases, cyclooxygenase-1 (Cox-1) or cyclooxygenase-2 (Cox-2), wh
104 ibed a new bioactive eicosanoid generated by cyclooxygenase-1 (COX-1) turnover during platelet activa
105            From this analysis, we found that cyclooxygenase-1 (COX-1), 5-lipoxygenase (5-LOX), and FL
106                                              Cyclooxygenase-1 (COX-1), a biomarker for neuroinflammat
107                       The mechanism by which cyclooxygenase-1 (COX-1), a heme- and tyrosyl radical-co
108                                  Deletion of cyclooxygenase-1 (Cox-1), an enzyme involved in producti
109 ess the prostaglandin (PG) synthesis enzyme, cyclooxygenase-1 (COX-1), as well as both components of
110 directed ligand that simultaneously inhibits cyclooxygenase-1 (COX-1), COX-2, and fatty acid amide hy
111 cytes by examining its respective effects on cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and
112 ed and used to characterize their binding to cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), seve
113 nti-inflammatory drugs (NSAIDs) inhibit both cyclooxygenase-1 (COX-1), whose inhibition is associated
114 is and in tail bleeding assays, including in cyclooxygenase-1 (COX-1)-deficient animals.
115 -nociceptors; for example, inhibition of the cyclooxygenase-1 (COX-1)-prostaglandin system within the
116 anced expression of the rate-limiting enzyme cyclooxygenase-1 (COX-1).
117  of endothelial cell NO synthase (ecNOS) and cyclooxygenase-1 (COX-1).
118  as a PET radioligand to selectively measure cyclooxygenase-1 (COX-1).
119 e-2 (COX-2) expression, but has no effect on cyclooxygenase-1 (COX-1).
120 upplementation and genetic variations in the cyclooxygenase-1 (COX1) pathway.
121                                              Cyclooxygenase-1 (COX1), an enzyme with known vasodilato
122 ction was also diminished in vessels lacking cyclooxygenase-1 [COX1 knockout (KO)] or the thromboxane
123 vels of proinflammatory effectors, including cyclooxygenase-1, cyclooxygenase-2, inducible nitric oxi
124 of infected macrophages with indomethacin, a cyclooxygenase-1/cyclooxygenase-2 inhibitor, blocked PGE
125      The antagonism of the thromboxane A(2), cyclooxygenase-1/cyclooxygenase-2, or phospholipase C pa
126 nontransformed cells derived from wild-type, cyclooxygenase 1-deficient (COX-1(-/-)) or cyclooxygenas
127  PGES3 and an arrestin-dependent increase in cyclooxygenase 1-dependent prostaglandin E(2) synthesis.
128 lso shown to be a high-affinity receptor for cyclooxygenase-1 derived 12(S)-hydroxyheptadeca-5Z, 8E,
129 ne loop in macrophages involving cPLA2alpha, cyclooxygenase 1-derived prostaglandins and increased cA
130 2, a unique receptor for 5-lipoxygenase- and cyclooxygenase-1-derived lipid mediators, represents a n
131 ition reflect an idiosyncratic dependency on cyclooxygenase-1-derived products, likely prostaglandin
132                                  Endothelial cyclooxygenase-1-derived prostanoids, including prostacy
133  capacitative calcium influx, and inhibiting cyclooxygenase-1, endothelial NO limits platelet activat
134  polyps (CRSwNP), asthma, and intolerance to cyclooxygenase-1 enzyme inhibitors.
135 panied by a compensatory increase in ovarian cyclooxygenase 1 expression and prostaglandin E(2) synth
136        Here the ability of recombinant human cyclooxygenase-1 (hCOX-1) and cyclooxygenase-2 (hCOX-2)
137 eport the long-sought structure of the human cyclooxygenase-1 (hCOX-1) that we refined to an R/R(free
138                 The constitutively expressed cyclooxygenase-1, however, was not affected by the sugar
139 thrombin, the thrombospondin-1/CD36 axis and cyclooxygenase 1 in subsequent platelet activation and s
140 spirin are consistent with the inhibition of cyclooxygenase-1 in platelets, we used liquid chromatogr
141         The detection of 12-lipoxygenase and cyclooxygenase-1 in single bovine coronary artery endoth
142  activity and endothelial NO production in a cyclooxygenase-1-independent fashion.
143 ailable vascular NO in an eNOS-dependent and cyclooxygenase-1-independent manner.
144  cysteinyl leukotriene generation induced by cyclooxygenase-1 inhibition reflect an idiosyncratic dep
145 y supplied by PGE2, are removed secondary to cyclooxygenase-1 inhibition.
146  effect of aspirin is attributed to platelet cyclooxygenase-1 inhibition.
147 of only 1-2 s, and both indomethacin and the cyclooxygenase-1 inhibitor SC-560 blocked the photolysis
148 asal polyposis, and respiratory reactions to cyclooxygenase-1 inhibitors (nonsteroidal anti-inflammat
149 c respiratory reactions to aspirin and other cyclooxygenase-1 inhibitors is accompanied by high level
150 onic rhinosinusitis, and hypersensitivity to cyclooxygenase-1 inhibitors.
151 espiratory hypersensitivity reactions to the cyclooxygenase 1-inhibitory effects of nonsteroidal anti
152 e studies provide insight into the nature of cyclooxygenase-1 interactions with a series of novel inh
153 que ability to irreversibly inhibit platelet cyclooxygenase-1 is a key mechanism by which aspirin exe
154 The gastric injury induced by aspirin/HCl in cyclooxygenase-1 knockout mice could be prevented if the
155 ed increase in gastric prostaglandin E(2) in cyclooxygenase-1 knockout mice seemed to correspond to a
156 ofound decrease in surface hydrophobicity in cyclooxygenase-1 knockout mice than in wild-type mice, w
157 re, we have used unique endothelial-specific cyclooxygenase-1 knockout mice to show that endothelial
158                        The gastric mucosa of cyclooxygenase-1 knockout mice was more severely injured
159  mucosal prostaglandin E(2) concentration in cyclooxygenase-1 knockout mice, possibly by the inductio
160 osal prostaglandin E(2) concentration in the cyclooxygenase-1 knockout mice, whereas it decreased pro
161         However, prostaglandins generated by cyclooxygenase-1 may play an important permissive role i
162                  Interleukin-6 signaling and cyclooxygenase-1 mediated prostaglandin synthesis in the
163                                              Cyclooxygenase-1 mediates production of platelet thrombo
164 okines, inducible nitric oxide synthase, and cyclooxygenase-1 mRNA expression (P< or =0.013 for each)
165 imulus, this reaction is catalyzed by either cyclooxygenase-1 or cyclooxygenase-2 (COX-1 or COX-2).
166               E-7869 does not inhibit either cyclooxygenase-1 or cyclooxygenase-2.
167 tion of a pathological role for the vascular cyclooxygenase-1 pathway, highlighting its potential as
168 ay exert antiplatelet properties through non-cyclooxygenase-1 pathways and deserves further investiga
169 OS-1 cells that overexpress iPLA(2)gamma and cyclooxygenase-1, PGE(2) production was induced by co-ex
170 aces (h2=0.266 to 0.762; P<0.01), but direct cyclooxygenase-1 phenotypes were not.
171 itric oxide (NO)-releasing derivative of the cyclooxygenase-1-preferring nonsteroidal anti-inflammato
172 ase-1 knockout mice to show that endothelial cyclooxygenase-1 produces both protective and pathologic
173 esults reveal 15(S)-HETE as a major platelet cyclooxygenase-1 product with strong proangiogenic effec
174 s have been available that separate vascular cyclooxygenase-1 products from those generated elsewhere
175 teins including the monotopic lumenal enzyme cyclooxygenase 1 (prostaglandin H synthase 1) that share
176 in the spinal cord of diabetic rats, whereas cyclooxygenase-1 protein was reduced.
177  aggregation, indicative of aspirin-mediated cyclooxygenase-1 suppression, occurred in 95% and >99% o
178  transcripts of 5000 were induced >2.5-fold: cyclooxygenase-1, tenascin-C, and plasminogen activator
179  pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA.
180 stanoids with diverse effects as mediated by cyclooxygenase-1 to the preferential synthesis of two pr
181 activation in pathways indirectly related to cyclooxygenase-1 was less pronounced and more variable (
182  shift in product profile was accentuated if cyclooxygenase-1 was permanently inactivated with aspiri
183                                  Conversely, cyclooxygenase-1 was significantly up-regulated.
184             Phenotypes indirectly related to cyclooxygenase-1 were strongly and consistently heritabl
185 t effects through irreversible inhibition of cyclooxygenase-1, whereas its anticancer effects may be
186  cyclooxygenase have been characterized: (i) cyclooxygenase-1, which is found in many tissues and is

 
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