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1 ocyclic lactones consisting of units of this prostaglandin.
2 nociceptive signaling molecule families, the prostaglandins.
3 ich is dependent on guanylyl cyclase but not prostaglandins.
4 ds to increased levels of the cyclopentenone prostaglandin 15-deoxy-Delta(12,14)-prostaglandin-J(2) t
9 differ between patients receiving a topical prostaglandin analog (latanoprost) or placebo eye drops
10 rwent a procedure initially (13.5%); topical prostaglandin analogs (n = 2887/5120 [56.4%]) and laser
12 of the efficacy and tolerability of generic prostaglandin analogues (PGAs) compared with their origi
17 olism of arachidonic acid to proinflammatory prostaglandins and leukotrienes by targeting cyclooxygen
20 pid mediators (for example, leukotrienes and prostaglandins) and specialized pro-resolving lipid medi
21 is changing our understanding of eicosanoid, prostaglandin, and PL biology in health and disease.
22 regulated processes by which eicosanoids or prostaglandins are attached to phospholipids (PLs) in im
23 mbogenic nature of heparinized biomaterials, prostaglandin biomaterials, and block copolymer systems.
25 rleukin(IL)-1beta treatment markedly induced prostaglandin biosynthesis in diseased compared to healt
26 OX-1 and -2), catalyze the committed step in prostaglandin biosynthesis-the conversion of arachidonic
27 Aspirin not only blocks the biosynthesis of prostaglandins, but also stimulates the endogenous produ
28 s cyclopentenone metabolites [cyclopentenone prostaglandins (CyPGs)], Delta(12)prostaglandin J(2) and
29 e report that depletion of endogenous L-type prostaglandin D synthase (L-PGDS) in HeLa cells inhibite
30 cyclooxygenase)-2 and L-PGDS (lipocalin-type prostaglandin D synthase) expression, which appeared to
32 ich inhibit cyclooxygenases or hematopoietic prostaglandin D synthase, respectively, or use of Crth2
34 DS) in HeLa cells inhibited recycling of the prostaglandin D(2) (PGD(2)) DP1 receptor (DP1) to the ce
41 activation of Crth2 by 13,14-dihydro-15-keto-prostaglandin D(2) increased Ca(2+) influx through store
43 or increases in urinary leukotriene E(4) and prostaglandin D(2) metabolite levels during aspirin-indu
44 duced increases in urinary leukotriene E(4), prostaglandin D(2) metabolite, or thromboxane B(2) level
45 igh-fat diet; conversely, direct addition of prostaglandin D(2) rescued myogenic tone in high-fat die
46 ot, confocal microscopy, cell degranulation, prostaglandin D(2) secretion, and proteases gene transcr
47 /2 inhibitor flurbiprofen, the hematopoietic prostaglandin D(2) synthase (HPGDS) inhibitor KMN698, an
49 allergy (such as cysteinyl leukotrienes and prostaglandin D(2)) and the neurotransmitter acetylcholi
50 ells stimulated the synthesis and release of prostaglandin D(2), to our knowledge a previously unrepo
51 at Ptgds encodes the enzyme that synthesizes prostaglandin D2 (PGD(2)), we further explored its role
55 ls, along with increased production of IL-5, prostaglandin D2, and eosinophil and T-helper type 2 cel
57 his effect was mediated by an increase in 15-prostaglandin dehydrogenase (15-Pgdh) activity, which ox
58 sed tendon cells, we also found increased 15-Prostaglandin Dehydrogenase (15-PGDH) expression as well
62 aspirin decreased nasal symptoms and urinary prostaglandin E metabolite (P < 0.05) and increased urin
63 oup was accompanied by a decrease in urinary prostaglandin E metabolite levels (-27% +/- 7%; p = 0.01
65 ersus a combination of inflammation (PTGER2 [prostaglandin E receptor 2] and IL-6) plus growth/repair
66 trated that cyclooxygenase-2 (COX-2) and the prostaglandin E receptor, prostanoid E receptor subtype
69 ether PPI treatment affects NOX5, microsomal prostaglandin E synthase (mPGES)-1 and inducible nitric
70 in-endoperoxide synthase 2 (Ptgs2/Cox-2) and prostaglandin E synthase (Ptges/mPGES-1) was compromised
74 m of COX-1 that synthesizes PgE2 (microsomal prostaglandin E synthase-1) depends critically for its v
78 -catenin signaling, cyclooxygenase-2 (COX-2)/prostaglandin E(2) (PGE(2) ) signaling, and the apeliner
79 adult human lung fibroblasts, but found that prostaglandin E(2) (PGE(2)) and fibroblast growth factor
84 ndin dehydrogenase (HPGD), which catabolizes prostaglandin E(2) (PGE(2)) into the metabolite 15-keto
86 5a) during MCC fate choice, where modulating prostaglandin E(2) (PGE(2)) levels rescued MCC number.
87 trate that MDV infection activates the COX-2/prostaglandin E(2) (PGE(2)) pathway, as evident by incre
89 g monocytes and macrophages, which can cause prostaglandin E(2) (PGE(2)) release and consequently und
90 ulation-specific changes in sensitization by prostaglandin E(2) (PGE(2)) were observed, when compared
91 Receptors for leukotriene B(4) (LTB(4)), prostaglandin E(2) (PGE(2)), and SPMs are expressed on l
92 xpression of inflammatory mediators, such as prostaglandin E(2) (PGE(2)), bradykinin (BK), and nerve
93 sphoprotein (p-VASP) by isoproterenol (ISO), prostaglandin E(2) (PGE(2)), or forskolin (FSK) as well
94 tumorigenicity of GSCs through production of prostaglandin E(2) (PGE(2)), which stimulates beta-caten
95 xyprostaglandin dehydrogenase (15-PGDH), the prostaglandin E(2) (PGE(2))-degrading enzyme, as a hallm
96 oid 2-arachidonoylglycerol (2-AG) to produce prostaglandin E(2) (PGE(2))-glycerol (PGE(2)-G); PGE(2)-
98 so called COX2) to increase the synthesis of prostaglandin E(2) (PGE2) by mast cells, which activates
99 , we hypothesized that inhibiting microsomal prostaglandin E(2) (PGE2) synthase-1 (mPGES-1), the enzy
100 iators, like tumor necrosis factor-alpha and prostaglandin E(2) , increased by LPS-induced EP, were d
101 ts confirmed that silencing of MGL decreases prostaglandin E(2) accumulation in the intestine and up-
103 e outcome of drug-induced ICD and pose COX-2/prostaglandin E(2) blockade as a strategy to harness ICD
104 R4 AS-ODN) prevented OIH and prolongation of prostaglandin E(2) hyperalgesia (priming) induced by LDM
106 cell carcinoma, ASA reduced plasma and skin prostaglandin E(2) levels and indices of UVB-induced DNA
107 nts in MCs triggered to migration by IL-8 or prostaglandin E(2) or to FcepsilonRI-stimulated secretio
108 ion, which is caused by reduced hypothalamic prostaglandin E(2) production and increased heat loss in
110 glandin F receptor activated with U46619 and prostaglandin E(2) receptor subtype 3 activated with ilo
111 activation of prostaglandin F receptors and prostaglandin E(2) receptors as well as thromboxane rece
112 ies reveal gemcitabine concurrently triggers prostaglandin E(2) release as an inhibitory DAMP to coun
114 plication of MGO together with bradykinin or prostaglandin E(2) resulted in an overadditive effect on
115 ase 4D (PDE4D) activity to amplify autocrine prostaglandin E(2) signaling in airway smooth muscle cel
116 and an aberrant dependency on COX-1-derived prostaglandin E(2) to maintain a tenuous homeostasis.
117 eries of small-molecule full agonists of the prostaglandin E(2) type 4 (EP(4)) receptor have been gen
118 ule sensing, a competitive FP immunoassay of Prostaglandin E(2) was demonstrated using the developed
119 CRs agonists, including thrombin, histamine, prostaglandin E(2), and ADP, stimulated robust p38 autop
124 h and bone density (P <0.01), enhanced 7-day prostaglandin E2 (P <0.01), and reduced 28-day inflammat
125 regnancy, including the initiation of labor, prostaglandin E2 (PGE(2)) and prostaglandin F2alpha (PGF
129 glandins, including the pro-algesic mediator prostaglandin E2 (PGE(2)), was decreased in myeloid cell
132 cell activation via producing high level of prostaglandin E2 (PGE2) due to their thousands-fold high
134 sing activities, we found that tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation of
137 n strongly linked to adhesion formation, and Prostaglandin E2 (PGE2) is associated with both adhesion
141 We tested the hypothesis that astrocytic prostaglandin E2 (PgE2) plays a key role for cerebrovasc
142 endothelial cells, we demonstrate that local prostaglandin E2 (PGE2) production in deep brain areas,
143 expression, whereas increased production of prostaglandin E2 (PGE2) promotes the differentiation of
145 ge (0.57-fold Nrf-2 and 0.34-fold HO-1), and prostaglandin E2 (PGE2) release was increased in samples
147 pithelial cell culture system, we found that prostaglandin E2 (PGE2) signaling through one of its rec
149 TLR4 ligand, induces macrophages to generate prostaglandin E2 (PGE2) through inducible COX-2 and micr
151 nthesis and receptor pathways for eicosanoid prostaglandin E2 (PGE2) were more highly induced in IL-1
152 looxygenases (COXs) and their final product, prostaglandin E2 (PGE2), are known to play important rol
154 at the key products of NOS2 and COX2, NO and prostaglandin E2 (PGE2), respectively, promote feed-forw
155 Human amnion fibroblasts produce abundant prostaglandin E2 (PGE2), which plays a crucial role in p
157 ted macrophages and expressed high levels of prostaglandin E2 (PGE2)-forming enzymes microsomal PGE2
161 a result of autonomic responses triggered by prostaglandin E2 action on EP3 receptors expressed by ne
162 n were performed and included measurement of prostaglandin E2 and cytosolic phospholipase A2 activity
163 isruption of the protein's ability to induce prostaglandin E2 and cytosolic phospholipase A2 synthesi
164 tion initiating mediators leukotriene B4 and prostaglandin E2 and pro-resolving mediators resolvin D1
167 ia-synapse cross talk requires production of prostaglandin E2 by microglia, leading to the activation
168 , increased free water reabsorption, urinary prostaglandin E2 excretion, and reduced excretion of ser
171 DON-induced cyclooxygenase-2 expression and prostaglandin E2 production and pro-inflammatory cytokin
173 els of acquired AI resistance indicated that prostaglandin E2 receptor 4 (PTGER4) is upregulated afte
174 resistance protein 4, and G-protein-coupled prostaglandin E2 receptors 1 and 2), abolished P-glycopr
175 Increased cyclooxygenase-2 expression and prostaglandin E2 release could be abrogated in metastati
176 g components in the cyclooxygenase-2 (COX-2)/prostaglandin E2 signaling cascade (phospholipase A2, CO
179 also been linked to asthma, where deficient prostaglandin E2 synthesis has been associated with airw
180 sion induced by inflammatory pain depends on prostaglandin E2 that is synthesized by cyclooxygenase 2
181 erinatal lethal with reduced brain levels of prostaglandin E2 The non-functional phospholipase A2-act
182 reversed hyperalgesia induced by intrathecal prostaglandin E2 To distinguish between a peripheral/spi
184 the patients with low urinary metabolite of prostaglandin E2 who received celecoxib (HR = 1.57; 95%
186 induced by diverse pronociceptive mediators, prostaglandin E2, epinephrine, TNFalpha, and interleukin
187 Elevation of baseline urinary metabolite of prostaglandin E2, indicating activation of the COX-2 pat
189 s activators of PKA, including adenosine and prostaglandin E2, results in a profound delay of neutrop
190 DUSP2 led to overproduction of COX-2-derived prostaglandin E2, which promoted cancer stemness via the
191 ide lipase (ATGL) activity in neutrophils in prostaglandin E2-dependent and -independent manners.
193 genesis and involves FGF receptor-3 (FGFR3), prostaglandin-E2 and interaction between estrogen recept
196 thesis-the conversion of arachidonic acid to prostaglandin endoperoxide H(2) Both COX isoforms are se
197 nase, ephrin-A receptor 2 (EPHA2), regulates prostaglandin endoperoxide synthase 2 (PTGS2) (encodes C
198 pithelium and included IL-1 receptor like 1, prostaglandin-endoperoxide synthase 1, CCL26, and perios
199 cyclooxygenase 2 (COX-2) gene, also known as prostaglandin-endoperoxide synthase 2 ( PTGS2), occurs i
200 s, such as histamine and proteases, activate prostaglandin-endoperoxide synthase 2 (also called COX2)
201 rowth/differentiation factor 15 (GDF15), and Prostaglandin-endoperoxide synthase 2 (PTGS2) genes, pre
206 ls were inhibited by activating G(s)-coupled prostaglandin-EP2 and G(q)-coupled bradykinin B2 (BK2) r
209 and proven anabolic selective agonist of the prostaglandin EP4 receptor, compound 5, and alendronic a
210 ction of structurally diverse molecules, the prostaglandins exhibit a wide range of biological proper
212 ivity was not limited to TP receptor because prostaglandin F receptor activated with U46619 and prost
213 We found that agonist-mediated activation of prostaglandin F receptors and prostaglandin E(2) recepto
216 signaling and also reduces expression of the prostaglandin F2a receptor negative regulator (PTGFRN),
217 tion of labor, prostaglandin E2 (PGE(2)) and prostaglandin F2alpha (PGF(2alpha)), are enzymatically d
218 inflammation-initiating mediators including prostaglandin F2alpha and leukotriene B4 and pro-resolvi
220 inflammation-initiating mediators (including prostaglandin F2alpha) and select proresolving pathways
221 t aggregate inhibitor and two members of the prostaglandin family of compounds by catalytic cross-met
223 th a mechanism downstream of proinflammatory prostaglandin formation, acetaminophen also reversed hyp
224 clooxygenase-2 catalyses the biosynthesis of prostaglandins from arachidonic acid but also the biosyn
225 hate, L-carnitine, L-aspartate, glutathione, prostaglandin G2, alpha-linolenic acid and linoleic acid
226 rachidonic acid but also the biosynthesis of prostaglandin glycerol esters (PG-Gs) from 2-arachidonoy
228 n the presence of U46619, a stable analog of prostaglandin H(2) Half-maximal effective potential (V(0
229 so observed enhanced autocrine production of prostaglandin I2 (PGI2, also called prostacyclin) in Cav
230 arry out the first step in the production of prostaglandins, important mediators of inflammation, pai
235 opentenone prostaglandins (CyPGs)], Delta(12)prostaglandin J(2) and 15-deoxy-Delta(12,14)-prostagland
236 prostaglandin J(2) and 15-deoxy-Delta(12,14)-prostaglandin J(2), act through 2 GPCRs, d-type prostano
237 landin J(2) (Delta(12)-PGJ(2)) and Delta(12)-prostaglandin J(3) (Delta(12)-PGJ(3)), whose unusual str
238 entenone prostaglandin 15-deoxy-Delta(12,14)-prostaglandin-J(2) that can activate the NLPR3 inflammas
239 oduct of inflammation, 15-deoxy-Delta(12,14)-prostaglandin J2 (15-d-PGJ2), triggers eIF2alpha phospho
244 8:1 fatty acids; increases in lipoxin A4 and prostaglandin J2; and a decrease in 20-hydroxyeicosatetr
247 We evaluated changes in leukotriene and prostaglandin metabolites for NIUA patients, using patie
248 anti-progesterone drug mifepristone and the prostaglandin misoprostol can be used to treat missed mi
251 utic effect superior to global inhibition of prostaglandin (PG) biosynthesis by aspirin-like drugs.
252 old), cysteinyl leukotrienes (4.5-fold), and prostaglandin (PG) D(2) (5.4-fold), as well as PGE(2) (6
256 is known to mediate the protective effect of prostaglandin (PG) E(2) in the gastrointestinal tract; h
257 in temperature (Tsk) analysis, assessment of prostaglandin (PG) E(2) levels (the proximal mediator of
258 isoproterenol, epinephrine, norepinephrine, prostaglandin (PG) E(2), PGD(2), and adenosine strongly
260 otypes were distinguished by thromboxane B2, prostaglandin (PG) E2, and PGD2 production, in addition
261 in vitro: for example, formation of TxA(2) , prostaglandin (PG) F(2alpha) , 11-hydroxyeicosatraenoic
262 C3) catalyzes the synthesis of 9alpha,11beta-prostaglandin (PG) F(2alpha) and PGF(2alpha) prostanoids
263 re comparable in tumors from both genotypes, prostaglandin (PG) levels were higher in the PyMT(Delta2
265 idespread reduction (between 50% and 90%) in prostaglandin (PG) profiles in fish tissues and plasma w
266 Aspirin (acetylsalicylic acid) inhibits prostaglandin (PG) synthesis by transfer of its acetyl g
269 -derived eicosanoids (leukotriene [LT] C(4), prostaglandin [PG] D(2), and thromboxane A(2)), which me
271 icosanoid profile of reduced proinflammatory prostaglandins (PGE(2) and TXB(2)) and an increased abun
278 he effects of nicotinic acid indicating that prostaglandins play a key role in mediating the sleep an
281 ry rate-based statistics identified a higher prostaglandin reductase 2 expression at early reperfusio
282 ), an enzyme involved in production of these prostaglandins, results in delayed parturition in mice.
283 negative regulator (PTGFRN), an inhibitor of prostaglandin signaling and follicle-stimulating hormone
284 ny in the zebrafish embryo kidney, and found prostaglandin signaling is essential both for renal MCC
289 ENT By using mice with selective deletion of prostaglandin synthesis in brain endothelial cells, we d
290 long-term objective of specific targeting of prostaglandin synthesis in prevention of preterm birth.
292 and significant upregulation (p < 0.0001) of prostaglandin-synthesising enzymes on brain tissue.
294 hough proinflammatory eicosanoids, including prostaglandins, thromboxanes, and leukotrienes, are crit
296 t through its downstream derivatives such as prostaglandins, to activate Akt and inhibit cisplatin-in
298 Therefore, we predicted that inhibiting the prostaglandin transporter SLCO2A1 may selectively kill c