ライフサイエンスコーパス: EET

1 EET analogs (10 mg/kg/d) attenuated cisplatin-induced ne

2 EET decreased expression of IL6 (P < 0.05), C/EBPbeta (P

3 EET levels were measured in tissue homogenates of rat li

4 EET of Geobacter sulfurreducens has been extensively stu

5 EET substrate preference for both COX-1 and COX-2 were e

6 EETs are decorated with the granule protein major basic

7 EETs are in the third (Cytochrome P450) pathway of arach

8 EETs are produced predominantly in the endothelium.

9 EETs formation was reversed by DNase treatment.

10 EETs may have clinical application in marrow or cord blo

11 11,12-EET and 19,20-EDP also inhibited leukocyte adherence to

12 In adult HSPCs, 11,12-EET induced transcriptional programs, including AP-1 act

13 Exogenous addition of 11,12-EET or 19,20-EDP when combined with 12-(3-adamantane-1-y

14 the developing zebrafish embryo, where 11,12-EET promoted HSPC specification by activating a unique a

15 entration-dependent manner by 8,9-EET, 11,12-EET, and 14,15-EET (IC(50) values of 444, 11.7, and 8.28

16 were estimated as 8,9-EET > 5,6-EET > 11,12-EET, whereas 14,15-EET was inactive.

17 dent manner by 8,9-EET, 11,12-EET, and 14,15-EET (IC(50) values of 444, 11.7, and 8.28 nM, respective

18 6-fold more potent, respectively, than 14,15-EET as vasorelaxants; on the other hand, their ability t

19 ncer cell growth in part through (+/-)-14,15-EET biosynthesis.

20 20-I-14,15-EE8ZE-APSA and 14,15-EET displaced 20-(125)I-14,15-epoxyeicosa-5(Z)-enoic aci

21 In polarized M1 cells, 14,15-EET inhibited amiloride-sensitive apical to basolateral

22 of 15-epi LXA4 by rapidly hydrolyzing 14,15-EET into its cognate diol, eliminating a proresolving si

23 Because 14,15-EET is chemically and metabolically labile, structurally

24 to the nucleus, suggesting that (+/-)-14,15-EET may be involved in an autocrine/paracrine pathway dr

25 dium transport effects of EGF, and its 14,15-EET metabolite rescued the knockdown phenotype.

26 cromolar concentrations of 7 inhibited 14,15-EET production in T47D breast cancer cells transfected w

27 The (+/-)-14,15-EET regioisomer selectively rescues breast cancer cells

28 educes nuclear Tyr(P)-705-Stat3, (+/-)-14,15-EET restores this signaling process and promotes Tyr(P)-

29 8,9-EET > 5,6-EET > 11,12-EET, whereas 14,15-EET was inactive.

30 4,15-epoxyeicosa-5,8,11-trienoic acid (14,15-EET) is a powerful endogenous autacoid that has been asc

31 erates 14,15-epoxyeicosatrienoic acid (14,15-EET), a metabolite known to influence cellular prolifera

32 sanoid 14,15-epoxyeicosatrienoic acid (14,15-EET).

33 ndent mechanism for ENaC inhibition by 14,15-EET, (b) point to ENaC as a proximal target for EET-acti

34 ere observed with the omega-6 epoxide, 14,15-EET, and nonoxidized DHA.

35 s, 5,6-epoxyeicosatrienoic acid (EET), 14,15-EET, and the corresponding dihydroxyeicosatrienoic acids

36 ogically inactive thiirane analogue of 14,15-EET, the opioid antagonist naloxone, the thromboxane mim

37 cancer cell growth and abrogates (+/-)-14,15-EET-induced proliferation, indicating a Stat3 requiremen

38 dicating a Stat3 requirement for (+/-)-14,15-EET-mediated cell growth.

39 s with an ED(50) comparable to that of 14,15-EET.

40 acid-derived lipid mediators, such as 5',6'-EET, that activate TRPV4.

41 -1 and COX-2 were estimated as 8,9-EET > 5,6-EET > 11,12-EET, whereas 14,15-EET was inactive.

42 Levels of 5,6-EET and 15-HETE were increased in colons of mice with, b

43 inally, in vivo intrathecal injection of 5,6-EET caused mechanical allodynia in wild-type but not TRP

44 Furthermore, 5,6-EET could be metabolized to a thromboxane analog.

45 In spinal cord slices, 5,6-EET dose dependently enhanced the frequency, but not the

46 In a bioassay, 5,6-EET increased the beating rate of neonatal cardiomyocyte

47 a (DRGs) and the dorsal spinal cord, and 5,6-EET is released from activated sensory neurons in vitro.

48 We conclude that 5,6-EET is synthesized on the acute activation of nociceptor

49 t, during capsaicin-induced nociception, 5,6-EET levels increased in dorsal root ganglia (DRGs) and t

50 5,6-EET potently induced a calcium flux (100 nm) in cultured

51 shed in TRPA1-null mice, suggesting that 5,6-EET presynaptically facilitated spinal cord synaptic tra

52 nvestigated the specific contribution of 5,6-EET to transient receptor potential (TRP) channel activa

53 supernatants from IBS biopsies produced 5,6-EET via a mechanism that involved the proteinase-activat

54 Levels of the TRPV4 agonist 5,6-EET, but not levels of TRPV1 or TRPA1 agonists, were inc

55 Furthermore, 5,6-EET-induced enhancement of sEPSC frequency was abolished

56 r both COX-1 and COX-2 were estimated as 8,9-EET > 5,6-EET > 11,12-EET, whereas 14,15-EET was inactiv

57 ucture of two major products formed from 8,9-EET in this COX pathway were confirmed by chemical synth

58 (5,6-epoxyeicosatrienoic acid [EET] and 8,9-EET), and TRPA1 (PGA1, 8-iso-prostaglandin A2, and 15-de

59 d in a concentration-dependent manner by 8,9-EET, 11,12-EET, and 14,15-EET (IC(50) values of 444, 11.

60 8R-HETE and 8R,9S-eicosatrienoic acid (8R,9S-EET), plus other chiral monoepoxides and bis-allylic 10S

61 -, and (+/-)-14,15-epoxyeicosatrienoic acid (EET) (total turnover of approximately 2 pmol/pmol CYP3A4

62 ovel orally active epoxyeicosatrienoic acid (EET) analogs and investigated their prophylactic effect

63 n cirrhosis, 11,12-epoxyeicosatrienoic acid (EET) induces mesenteric arterial vasodilation, which con

64 genase and for its epoxyeicosatrienoic acid (EET) metabolites in the in vivo control of ENaC activity

65 is of the enzymes' epoxyeicosatrienoic acid (EET) substrates, so they accumulate inducing vasodilatio

66 2 metabolites, 5,6-epoxyeicosatrienoic acid (EET), 14,15-EET, and the corresponding dihydroxyeicosatr

67 ne B4), TRPV4 (5,6-epoxyeicosatrienoic acid [EET] and 8,9-EET), and TRPA1 (PGA1, 8-iso-prostaglandin

68 Epoxyeicosatrienoic acids (EET) and related epoxy fatty acids (EpFA) are endogenous

69 of proangiogenic epoxyeicosatrienoic acids (EET) by the cytochrome P450 arachidonic acid epoxygenase

70 e increased media epoxyeicosatrienoic acids (EETs) and reduced cell membrane levels of EETs.

71 Epoxyeicosatrienoic acids (EETs) are anti-inflammatory molecules synthesized by var

72 Epoxyeicosatrienoic acids (EETs) are cytochrome P450-epoxygenase-derived metabolite

73 ogenous levels of epoxyeicosatrienoic acids (EETs) are known for their analgesic, antihypertensive, a

74 Epoxyeicosatrienoic acids (EETs) are small molecules produced by cytochrome P450 ep

75 een, and identify epoxyeicosatrienoic acids (EETs) as a family of lipids that enhance HSPC engraftmen

76 d CYP2J2 generate epoxyeicosatrienoic acids (EETs) from arachidonic acid.

77 (COX) pathway and epoxyeicosatrienoic acids (EETs) from the cytochrome P450/soluble epoxide hydrolase

78 Epoxyeicosatrienoic acids (EETs) generated from arachidonic acid by cytochrome P450

79 450 (CYP)-derived epoxyeicosatrienoic acids (EETs) possess potent anti-inflammatory effects in vitro.

80 Specifically, epoxyeicosatrienoic acids (EETs) produced from the P450 pathway are angiogenic, ind

81 dothelium-derived epoxyeicosatrienoic acids (EETs) relax vascular smooth muscle by activating potassi

82 , total levels of epoxyeicosatrienoic acids (EETs), but not epoxydocosapentaenoic acids (EDPs), were

83 , and whether the epoxyeicosatrienoic acids (EETs), derived via cytochrome P450, were the predominant

84 es, including the epoxyeicosatrienoic acids (EETs), epoxidized lipids produced from arachidonic acid

85 metabolites, the epoxyeicosatrienoic acids (EETs), in ENaC activity have been identified; however, t

86 Epoxyeicosatrienoic acids (EETs), lipid mediators produced by cytochrome P450 epoxy

87 ves to inactivate epoxyeicosatrienoic acids (EETs), which are generated in the brain to couple neuron

88 n the presence of epoxyeicosatrienoic acids (EETs).

89 sis of protective epoxyeicosatrienoic acids (EETs).

90 0.01), vasoactive epoxyeicosatrienoic acids (EETs; -60%, p < 0.001) synthesis, large-conductance, cal

91 metabolites (cis-epoxyeicosatrienoic acids [EETs]) in the lung.

92 esults strongly suggest that Acsl4 activates EETs to form EET-CoAs that are incorporated into glycero

93 U937 cell membranes contain a high-affinity EET binding protein that may represent an EET receptor.

94 for close endoscopic surveillance even after EET.

95 henylsulfonamide (20-I-14,15-EE8ZE-APSA), an EET analogue with a photoactive azido group.

96 2/13 cells, and in Acsl4 knockdown cells, an EET receptor antagonist partially rescued GSIS.

97 Since S. oneidensis is a member of an EET-encoding clade, the genetic circuitry of taxis to in

98 ty EET binding protein that may represent an EET receptor.

99 By considering the inter-ring distance and EET rate, we demonstrate that this group can achieve min

100 sed cortical activity and that K+ fluxes and EET signaling mediate a large part of the hemodynamic re

101 mentary and terrestrial environments, an AOM-EET niche would have implications for minimizing the net

102 cell, and isotopic experiments supported AOM-EET to the anode.

103 ificant gene expression responses to applied EET stimuli occur in only two microbial groups, Desulfob

104 ncreasing electrode potential and associated EET current leads to more negative membrane potential.

105 There was a significant correlation between EET formation and TSLP expression (P = 0.02) as well as

106 icant negative correlation was found between EET formation and LEKTI expression (P = 0.016).

107 m was to investigate a possible link between EET formation and the presence of Staphylococcus aureus,

108 s study identifies a functional link between EETs and COX and identifies ct-8,9-E-11-HET as an angiog

109 sue regeneration via production of bioactive EETs.

110 f Zea and active LHCX1 is essential for both EET and CT quenching in N. oceanica.

111 obtained evidence for the operation of both EET and CT quenching by observing spectral features asso

112 a diminished role of cytochromes in cathodic EET.

113 dynamic community-wide response to changing EET rates.

114 othelial Cyp2c44 expression, and circulating EET levels.

115 high as 270 A/m(2) if only Ohmic-conduction EET was limiting.

116 the maximum energy loss for Ohmic-conduction EET was negligible, 0.085 mV.

117 Here, we demonstrate EET-dependent AOM in a biofilm anode dominated by Geobac

118 To determine whether endothelial-derived EETs affect physiologic tissue growth in vivo, we used g

119 le of cardiomyocyte- vs. endothelial-derived EETs or compared the effects of different CYP epoxygenas

120 We show that endothelial-derived EETs play a critical role in accelerating tissue growth

121 r growth but depended on endothelium-derived EETs at the site of metastasis.

122 re of the phycobilisome supports directional EET to reaction centers with minimal losses due to therm

123 ow the involvement of the nuclear DoF during EET through the participation of higher-lying vibronic c

124 king density, achieving robust and efficient EET.

125 e, we show that phenazines mediate efficient EET through interactions with extracellular DNA (eDNA) i

126 nic angiotensin II rat, we observed elevated EET, dihydroxyeicosatrienoic acid, and preeclamptic feat

127 pidermidis, the latter were unable to elicit EET formation and eosinophils required additional TSLP s

128 drolase inhibitors, which elevate endogenous EET levels, promote liver and lung regeneration.

129 e that metabolizes EETs, elevated endogenous EET levels and promoted primary tumor growth and metasta

130 armacological tools to manipulate endogenous EET levels.

131 d pharmacological manipulation of endogenous EET levels, we demonstrate that EETs are critical for pr

132 as sEH inhibitors, which increase endogenous EETs, stimulate primary tumor growth and metastasis.

133 d transgenic mice with increased endothelial EET biosynthesis (Tie2-CYP2C8 Tr and Tie2-CYP2J2 Tr) or

134 provide evidence for a Cyp2c44 epoxygenase, EET-mediated mechanism of ENaC regulation involving an E

135 cellular ET, (2) non-Ohmic extracellular ET (EET) from an outer membrane protein to an extracellular

136 published, only a few reports have examined EET from marine strains of Shewanella.

137 ometrical arrangement that ensures excellent EET.

138 8% of the infiltrating eosinophils exhibited EETs in patients' nasal polyp tissues.

139 Further, exogenous EETs reduced GSIS in INS 832/13 cells, and in Acsl4 knoc

140 Finally, EET may be the physical mechanism underlying many cases

141 Following EET, the change in M2 macrophages was positively associa

142 a (r = -0.58) and MuRF (r = -0.46) following EET.

143 ges (CD206+/CD163+) also increased following EET (P < 0.001), and were associated with fiber hypertro

144 igration to insoluble electron acceptors for EET has been shown to be nonrandom and tactic, seemingly

145 de the multiheme cytochromes responsible for EET, rather than pilin-based structures as previously th

146 , (b) point to ENaC as a proximal target for EET-activated ERK1/2 mitogenic kinases, (c) characterize

147 d Cyp2J2, the principal Cyps responsible for EETs synthesis, as well as soluble epoxide hydrolase (sE

148 and in vitro studies demonstrate a role for EETs in limiting cisplatin-induced renal apoptosis.

149 our observations indicate a central role for EETs in organ and tissue regeneration and their contribu

150 Thus, our data indicate a central role for EETs in tumorigenesis, offering a mechanistic link betwe

151 ly suggest that Acsl4 activates EETs to form EET-CoAs that are incorporated into glycerophospholipids

152 s and possibly other microorganisms and form EETs at sites of airway epithelial damage to protect the

153 ted with eosinophil granule proteins forming EETs and the expression of filaggrin, the protease inhib

154 p could be identified, they may benefit from EET, whereas, the majority may be managed conservatively

155 gate whether eosinophils generate functional EETs as a direct response to TSLP, and further to study

156 Furthermore, EET/dihydroxy-epoxyeicosatrienoic acid isomer ratios wer

157 are promising in the context of implementing EET-dependent anammox process for energy-efficient treat

158 sulation of the conjugated backbone improves EET, increasing the fraction of CPs possessing epsilon =

159 ion of NO(2)(-) and NO(3)(-) was achieved in EET-dependent anammox.

160 atment with MS-PPOH reversed the increase in EET levels.

161 ble to reveal the subpopulation variation in EET or link the observed electrochemical currents to ene

162 These data suggest that an increase in EETs due to sEH-gene knockout leads to an increase in th

163 Two stimuli were employed: to increase EET and to stop EET.

164 ion of sEH is used as a strategy to increase EET levels leading to lower inflammation.

165 and mask the beneficial effects of increased EET production following I/R.

166 ng soluble epoxide hydrolase (sEH) increased EET concentration and mildly promoted tumor growth.

167 trong transcriptional responses to increased EET rates, with one responding positively and the other

168 strogen loss decreased the anti-inflammatory EETs in the cardiovascular system.

169 Inhibitors of these anti-inflammatory EETs reversed TGA inhibition.

170 oss would reduce levels of anti-inflammatory EETs.

171 metabolically channels arachidonic acid into EETs, whereas in failing hearts, increased iPLA2gamma ac

172 cal techniques have been used to investigate EET in a wide range of microbes, with emphasis on dissim

173 OS production and degranulation and involves EET formation.

174 sible existence of a nonheme, iron-involving EET process in cathodic mode.

175 While extensive studies involving EET from a fresh water Shewanella microbe (S. oneidensis

176 ecapitulated these results, whereas lowering EET levels, either genetically or pharmacologically, del

177 hydrolase (sEH), the enzyme that metabolizes EETs, elevated endogenous EET levels and promoted primar

178 de hydrolase (sEH, EPHX2), which metabolizes EETs to their less active diols.

179 ex vivo human mucosal disease tissue model, EET formation was induced (4.2 +/- 0.9-fold) on exposure

180 ty led to a complete inhibition (P < .05) of EET formation by S aureus.

181 ted in vitro that the protective activity of EET analogs does not compromise the anticancer effects o

182 t study demonstrating a direct comparison of EET and EDP on vascular inflammatory endpoints, and we h

183 d to study the single-cell-level dynamics of EET not only on electrode surfaces, but also during resp

184 mportance of considering possible effects of EET-modulating drugs on cancer.

185 cell can reduce or remove the frustration of EET rates across the photosynthetic network.

186 A new generation of EET mimics incorporating modifications to the carboxylat

187 ane potential as a bioenergetic indicator of EET by S. oneidensis MR-1 cells.

188 , P < 0.05) was reversed after inhibition of EET production (-6.388 +/- 0.263, P < 0.05).

189 hemodynamic effects of in vivo inhibition of EET production in experimental cirrhosis.

190 n rats with cirrhosis, in vivo inhibition of EET production normalizes the response of mesenteric art

191 rent evidence for the two proposed models of EET taxis, "electrokinesis" and flavin-mediated taxis, a

192 and after one bout of RE, after 12 weeks of EET (cycling), and after a final bout of RE.

193 The availability of EETs is limited primarily by the soluble epoxide hydrola

194 growth, suggesting that the contribution of EETs to angiogenesis and subsequent tumor growth may be

195 investigate the presence and distribution of EETs in esophageal tissues from EoE patients and their a

196 The pro-haematopoietic effects of EETs were conserved in the developing zebrafish embryo,

197 This study explores the fate of EETs with COX, the angiogenic activity of the primary me

198 ophil survival, but induced the formation of EETs consisting of mitochondrial DNA in association with

199 The formation of EETs could serve as a firewall against the invasion of p

200 Formation of EETs was associated with increased IL-5 (P < .05) and pe

201 s spectrometry was used to measure levels of EETs and their metabolites, dihydroxyeicosatrienoic acid

202 easured in plasma or aortic tissue levels of EETs.

203 s (EETs) and reduced cell membrane levels of EETs.

204 a physiological role for COX metabolites of EETs.

205 g in vivo that pharmacological modulation of EETs can affect cancer growth.

206 nstrating that pharmacological modulation of EETs can affect normal organ and tissue growth.

207 slides were investigated for the presence of EETs and S aureus by using immunofluorescent staining an

208 Active EoE exhibits the presence of EETs.

209 immunoblotting and linked to the presence of EETs.

210 To address the role of EETs in regulating glucose homeostasis and insulin signa

211 Consequently, targeting of EETs diminished thrombus formation in vivo, which identi

212 hesis (Tie2-CYP2C8 Tr and Tie2-CYP2J2 Tr) or EET hydrolysis (Tie2-sEH Tr).

213 n directly stimulates eosinophils to produce EETs.

214 As a result, drugs that raise EET levels are in clinical trials for the treatment of h

215 bacterial nanowires that mediate long-range EET by the previously proposed multistep redox hopping m

216 ctronic-vibrational mixing facilitates rapid EET over moderately size energy gaps.

217 support an efficient redox cycle with rapid EET that is faster than the rate of PYO loss from the bi

218 lyngbya ohadii strain identified (i) reduced EET between phycobilisome components, (ii) shorter fluor

219 The resulting EET path will exhibit increased coupling to the environm

220 o glycerophospholipids, thereby sequestering EETs.

221 Here we identify specific EET-active microbes and genes in a diverse biofilm using

222 gn observed oscillatory features to specific EET pathways, demonstrating a significant step in mappin

223 i were employed: to increase EET and to stop EET.

224 These data also suggest EETs contribute to about half of the EDHF response.

225 rofiling revealed that MCF7 cells synthesize EETs in a CYP3A4-dependent manner.

226 Administration of synthetic EETs recapitulated these results, whereas lowering EET l

227 Administration of synthetic EETs recapitulated these results, while EET antagonists

228 lphaMHC-CYP2J2 Tr) or treated with synthetic EETs have increased functional recovery after ischemia/r

229 employed a novel endogenous epitope tagging (EET) approach, which revealed that endogenous PTEN inter

230 It is demonstrated that EET between tryptophan or tyrosine and a disulfide bond

231 Collectively, our data provide evidence that EET analogs attenuate cisplatin-induced nephrotoxicity b

232 It is noted that EET could occur in many systems, making measured entropi

233 Here we experimentally show that EET in single antennas can be characterized by 2D polari

234 f endogenous EET levels, we demonstrate that EETs are critical for primary tumor growth and metastasi

235 Remarkably, we found that EETs stimulated extensive multiorgan metastasis and esca

236 In this study, we tested the hypothesis that EETs are involved in glucose regulation and in retarding

237 Recent evidence suggests that EETs act via a membrane binding site or receptor.

238 The EET analogue relaxed preconstricted bovine coronary arte

239 The EET effects were associated with increased threonine pho

240 secreted by C. marina were facilitating the EET process.

241 However, the EET pathway of cathodic conversion of fumarate to succin

242 e moieties resulting in the cessation of the EET (electronic energy transfer) process from borane to

243 e lattice for the global optimization of the EET network.

244 Quantification of the EET processes operating in this planktonic system assist

245 ts into the expression and regulation of the EET receptor.

246 In this study, the EET activity of the photosynthetic marine raphidophyte,

247 ave been made to develop drugs targeting the EET pathway.

248 Furthermore, we demonstrate that the EET effects on enhancing HSPC homing and engraftment are

249 While the EET conduits of S. oneidensis have been studied extensiv

250 Through its metabolism of the EETs and other lipid mediators, sEH contributes to the r

251 on various endoscopic eradication therapies (EET) specifically in this patient population are limited

252 This EET photoaffinity labeling method with a high signal-to-

253 This EET-induced membrane hyperpolarization is spatially limi

254 Three EET regioisomers were found to be substrates for COX, ba

255 Less attention has been given to EET by planktonic organisms in oxic environments where e

256 tanding of the synergetic effects leading to EET optimization of light-harvesting antenna systems whi

257 of functional microbes and genes related to EET activity in a diverse community, representing the ne

258 crease with RE, but increased in response to EET (P < 0.01).

259 ophages contribute to the muscle response to EET, potentially including modulation of TWEAK-FN14 sign

260 k and the associated short-term responses to EET stimuli that induce changes to metabolic flow and co

261 unknown genes that are highly responsive to EET stimuli and associated with our identified draft gen

262 ermined whether endurance exercise training (EET) alters macrophage content and characteristics in re

263 that we term entropy-enthalpy transduction (EET), in which the thermodynamic character of a local pe

264 Extracellular electron transfer (EET) allows microorganisms to gain energy by linking int

265 Shewanella extracellular electron transfer (EET) are highly conserved.

266 cteria have extracellular electron transfer (EET) capability with transfer of electrons to insoluble

267 interest in extracellular electron transfer (EET) from organisms to receptors, particularly in anaero

268 Extracellular electron transfer (EET) in microorganisms is prevalent in nature and has be

269 iration via extracellular electron transfer (EET) is a ubiquitous reaction that occurs throughout ano

270 Microbial extracellular electron transfer (EET) stimulates a plethora of intellectual concepts lead

271 ior support extracellular electron transfer (EET) through a solid conductive matrix - the first such

272 current via extracellular electron transfer (EET) to a solid electrode surface.

273 oupled with extracellular electron transfer (EET) to conductive solids is relatively insufficient.

274 es catalyze extracellular electron transfer (EET) within biofilms without being lost to the environme

275 d model for extracellular electron transfer (EET), a respiratory mechanism in which electrons are tra

276 zeaxanthin (Zea) excitation energy transfer (EET) and charge transfer (CT) as possible NPQ mechanisms

277 (DoF) during the excitation energy transfer (EET) dynamics of light-harvesting complex II (LHCII) wit

278 is rapid singlet excitation energy transfer (EET) from the macrocycle to the hexayne (tau = 3.0 ps),

279 and compare the excitation energy transfer (EET) properties of various natural and artificial antenn

280 fficiency of the excitation energy transfer (EET) reached 95 % at a donor/acceptor ratio of 100:1 and

281 try that enables excitation energy transfer (EET) to be accurately measured via action spectroscopy o

282 he efficiency of excitation energy transfer (EET) to fit light energy supply to biochemical demands.

283 a intramolecular excitation energy transfer (EET).

284 otion of maximum excitation energy transfer (EET).

285 P-to-chromophore excitation energy transfer (EET).

286 ms of electronic excitation energy transfer (EET).

287 s offer an extracellular electron transport (EET) pathway for linking the respiratory chain of bacter

288 < 0.0001) or eosinophil extracellular trap (EET) formation (P = 0.048).

289 so-called extracellular eosinophilic traps (EETs) under similar pathologic conditions.

290 ils generate eosinophil extracellular traps (EETs) able to kill bacteria.

291 would induce eosinophil extracellular traps (EETs) in bronchoalveolar lavage fluid and lung tissue.

292 By releasing eosinophil extracellular traps (EETs), eosinophils achieve an efficient extracellular ba

293 formation of eosinophil extracellular traps (EETs), which are present in human thrombi and constitute

294 eas in the rhenium-rotaxane there is triplet EET, from the macrocycle complex (3)MLCT state to the he

295 SIS by regulating the levels of unesterified EETs and that arachidonate controls the expression of it

296 The structurally unrelated EET ligands miconazole, MS-PPOH, and ketoconazole also i

297 etic EETs recapitulated these results, while EET antagonists suppressed tumor growth and metastasis,

298 membrane potential strongly correlates with EET.

299 Lastly, MCs incubated with EET and challenged through FcepsilonRI had a significant

300 its taxis pathways and their interplay with EET are not yet understood, making investigation into ta