ライフサイエンスコーパス: ESA

1 ESA and PSV were significantly lower in the renal artery

2 ESA decay kinetics were oxidation-state dependent and co

3 ESA decreased significantly from the CCA to the ICA (P <

4 ESA fluorescence was monitored in animals for more than

5 ESA hyporesponsiveness may be useful in identifying pote

6 ESA hyporesponsiveness was primarily defined as a monthl

7 ESA induced greater chemotaxis of endothelial progenitor

8 ESA release was sustained for 4 weeks in vitro, remained

9 ESA requirements are independent of age when dose is sca

10 ESA sensitivity was positively associated with residual

11 ESA treatment continues to be recommended for patients w

12 ESA treatment of anemia to obtain higher hemoglobin targ

13 ESA treats RNA structures as 3D curves with sequence inf

14 ESA treats RNA structures as three dimensional curves wi

15 ESA use decreased from 25.6% at 1 month to 8.23% at 24 m

16 ESA was encapsulated in hyaluronic acid hydrogels during

17 ESAs did not affect SVR or discontinuation rates among p

18 ESAs have also been reported to promote angiogenesis.

19 ESAs have effects beyond erythropoiesis.

20 ESAs should be avoided in patients with cancer not recei

21 ESAs should be discontinued after 6 to 8 weeks in nonres

22 ESAs should be used cautiously with chemotherapy, or in

23 ESAs should be used cautiously with chemotherapy, or in

24 ESAs show great promise in preventing and treating brain

25 ESAs were permitted for anemic patients (hemoglobin [Hb]

26 (ESA) of the ligand-centered S(1) state; (2) ESA of a receiver ligand-to-metal or metal-to-ligand cha

27 nsfer triplet state (tau(1) </= 300 fs); (3) ESA of the vibrationally excited, ligand-centered T(1) s

28 tered T(1) state (tau(3) = 7-10 ps); and (4) ESA of the relaxed T(1) state.

29 e in Arabidopsis produced approximately 7.5% ESA in seed lipids.

30 Excited-state absorption (ESA) by 9-methyladenine is 50% stronger than by 7-methyl

31 re assigned to (1) excited state absorption (ESA) of the ligand-centered S(1) state; (2) ESA of a rec

32 (2) broad visible excited-state absorption (ESA), and (3) stimulated emission (SE) at 670 nm.

33 ur knowledge, this is the first time an ACFC-ESA system has been used to capture, recover, and liquef

34 ts of a gas recovery system (GRS) using ACFC-ESA for three adsorbates with relative pressures between

35 ated polyenoic FAs (alpha-eleostearic acids [ESAs]) using Arabidopsis (Arabidopsis thaliana) as a mod

36 the habitat needs of Endangered Species Act (ESA)-listed salmonids relative to climate change in the

37 the influence of: (1) each-step activation (ESA) of NADH supply (including glycolysis) and oxidative

38 quence that is essential for Sirt1 activity (ESA).

39 Encoding success activity (ESA) was identified by comparing study-phase activity fo

40 In addition, ESA was detected in the rat heart >3 weeks when delivere

41 averaged) hemoglobin values and administered ESA dose in a 2-yr (July 2001 to June 2003) cohort of 58

42 udinal changes in hemoglobin or administered ESA have meaningful associations with survival after adj

43 followed by electrothermal swing adsorption (ESA) and postdesorption pressure and temperature control

44 Electrothermal swing adsorption (ESA) of organic compounds from gas streams with activate

45 Here, we analyzed outcome after ESA failure and the effect of second-line treatments.

46 and investigational drugs, may be used after ESA failure in some countries, but their effect on disea

47 The Committee also cautions against ESA use for patients with cancer who are not receiving c

48 The Committee cautions against ESA use under other circumstances.

49 n Agency (JAXA F/NF), European Space Agency (ESA F/NF), Boston University (MCD12Q1 F/NF), Food and Ag

50 European Space Agency (ESA) studies demonstrated that bull sperm swim with high

51 Erythropoiesis stimulating agent (ESA) administration may reduce mortality in severe traum

52 ne; use of erythropoiesis-stimulating agent (ESA) and iron; and immunosuppressive regimen data were o

53 mes in the erythropoiesis-stimulating agent (ESA) arm.

54 tiating an erythropoiesis-stimulating agent (ESA) as hemoglobin (Hb) approaches, or falls below, 10 g

55 ime to the erythropoiesis stimulating agent (ESA) products, which facilitated novel, in-depth charact

56 tide-based erythropoiesis-stimulating agent (ESA) that may have therapeutic potential for anemia in p

57 tide-based erythropoiesis-stimulating agent (ESA), is a potential therapy for anemia in patients with

58 sponse to erythropoiesis-stimulating agents (ESA) is associated with morbidity and mortality among di

59 isease by erythropoiesis-stimulating agents (ESA) may improve survival, most studies have examined as

60 analogs [erythropoiesis-stimulating agents (ESA)] are clinically used to treat anemia in patients wi

61 al use of erythropoiesis-stimulating agents (ESAs) and intravenous iron in hemodialysis patients with

62 he use of erythropoiesis stimulating agents (ESAs) and iron.

63 Erythropoiesis-stimulating agents (ESAs) are commonly used to treat anemia in patients with

64 djunct to erythropoiesis-stimulating agents (ESAs) compared with ESA alone in the treatment of chemot

65 trials of erythropoiesis-stimulating agents (ESAs) comparing lower and higher hemoglobin targets in p

66 doses of erythropoiesis-stimulating agents (ESAs) during dialysis to manage anemia, but the influenc

67 The erythropoiesis-stimulating agents (ESAs) erythropoietin and darbepoetin are licensed to tre

68 ficacy of erythropoietin-stimulating agents (ESAs) for improving health-related quality of life (HRQO

69 Erythropoiesis stimulating agents (ESAs) have been reported to activate erythropoietin rece

70 lines for erythropoiesis-stimulating agents (ESAs) in 2011 appear to have influenced use of injectabl

71 effect of erythropoiesis-stimulating agents (ESAs) in critically ill trauma patients.

72 sponse to erythropoiesis-stimulating agents (ESAs) in iron-replete patients with chemotherapy-associa

73 or use of erythropoiesis-stimulating agents (ESAs) in patients with cancer.

74 ment with erythropoiesis-stimulating agents (ESAs) may result in undesired patterns of hemoglobin var

75 ssued for erythropoietin-stimulating agents (ESAs) regarding serious adverse events, such as venous t

76 he use of erythropoiesis-stimulating agents (ESAs) such as erythropoietin and darbepoetin in preterm

77 Erythropoietin-stimulating agents (ESAs) were originally designed to replace endogenous ery

78 Erythropoiesis-stimulating agents (ESAs) were prescribed to 92% of patients, and neither th

79 required; erythropoiesis-stimulating agents (ESAs) were used at the investigator's discretion.

80 ated with erythropoiesis-stimulating agents (ESAs), with a response rate of approximately 50%.

81 tivity of erythropoiesis stimulating agents (ESAs).

82 of use of erythropoiesis-stimulating agents (ESAs).

83 on and/or erythropoiesis-stimulating agents (ESAs).

84 rom using erythropoiesis-stimulating agents (ESAs).

85 iron and erythropoiesis-stimulating agents (ESAs).

86 The binding modes to equine serum albumin (ESA) of two nonsteroidal anti-inflammatory drugs (NSAIDs

87 le is a summary of a lecture presented at an ESA/NASA Workshop on Cell and Molecular Biology Research

88 We discovered an ESA mutant peptide that can bind to the deacetylase core

89 7 critically ill patients after trauma to an ESA or placebo (or no ESA).

90 , a novel engineered SDF polypeptide analog (ESA) more efficiently induces EPC migration and improves

91 gineered stromal cell-derived factor analog [ESA]) induces continuous homing of endothelial progenito

92 F polypeptide analog (engineered SDF analog [ESA]) that splices the N-terminus (activation and bindin

93 new method based on elastic shape analysis (ESA) that compares RNA molecules by combining both seque

94 ment method based on elastic shape analysis (ESA).

95 In a multivariable analysis, ESA misuse was associated with MD degree, female sex of

96 (beta=-0.28, P=0.003, CI:-0.47 to -0.09) and ESA use (beta=-0.73, P<0.001, CI:-0.93 to -0.52), and pr

97 sessed based on decreases in Hb, anemia, and ESA use.

98 hen dose is scaled to body surface area, and ESA resistance is associated with inflammation, fluid re

99 abeling, does not seem to be beneficial, and ESA therapy should be discontinued.

100 d label, does not seem to be beneficial, and ESA therapy should be discontinued.

101 ntified that surface markers CD49f, CD61 and ESA were aberrantly overexpressed in Her2-overexpressing

102 ed that posttransplant anemia is common, and ESA/iron use remains suboptimal, and Hb is independently

103 ly varying administered intravenous iron and ESA doses, iron markers, and nutritional status, hemoglo

104 arent after 12 weeks and reduces iv iron and ESA use while maintaining hemoglobin over 52 weeks, with

105 RI and ESA decrease as a result of increasing downstream cross-

106 rial bed cross-sectional area and the RI and ESA.

107 ctrometry in the + (parent compounds) and - (ESA and OA degradates) ion modes by monitoring appropria

108 cy of peginesatide, as compared with another ESA, darbepoetin, in 983 such patients who were not unde

109 CD44, CD24, and epithelial-specific antigen (ESA).

110 2 [also known as epidermal surface antigens (ESAs)] are two families of mammalian caveolae-associated

111 gest that the environmentally suitable area (ESA) for An. dirus and An. minimus would increase by an

112 tic Scoring System score, and progression at ESA failure, there was no significant OS difference amon

113 geting of a lower hemoglobin range may avoid ESA-associated risks.

114 More intensive use of both ESAs and iron was associated with increased mortality ri

115 ls injected with as few as 100 CD44(+)CD24(+)ESA(+) cells forming tumors that were histologically ind

116 The CD44(+)CD24(+)ESA(+) pancreatic cancer cells showed the stem cell prop

117 The enhanced ability of CD44(+)CD24(+)ESA(+) pancreatic cancer cells to form tumors was confir

118 ncreatic cancer cells with the CD44(+)CD24(+)ESA(+) phenotype (0.2-0.8% of pancreatic cancer cells) h

119 -like cells (CSC) defined by CD44(+)/CD24(-)/ESA(+) phenotype, where it plays a critical role in the

120 ne using cell surface markers (CS24(-)CD44(+)ESA(+)) and found that this cell population has signific

121 report, we found that CSCs (CD24(-)/CD44(+)/ESA(+)) isolated from metastatic breast cell lines are s

122 In BCSCs sorted with CD44(+)/ESA(+)/CD24(-) markers, Gb3 activates c-Src/beta-catenin

123 with peginesatide relative to the comparator ESA in the four pooled studies (2591 patients) and 0.95

124 satide was similar to that of the comparator ESA in the pooled cohort.

125 with peginesatide relative to the comparator ESA of more than 1.3.

126 , for randomized controlled trials comparing ESAs to placebo (or no ESA).

127 The two structures of the ternary complex ESA/Dic/Nps, obtained by competitive cocrystallization (

128 Continuing ESAs beyond 6 to 8 weeks in the absence of response, ass

129 Continuing ESAs beyond 6 to 8 weeks in the absence of response, ass

130 Cumulative ESA over 52 weeks was lower with FC than AC (median [int

131 nd the structure of the previously described ESA/Nps complex (2.42 A), it was found that both NSAIDs

132 Our previously designed ESA peptide was synthesized by the addition of a fluorop

133 contextual information along the disynaptic "ESA" (entorhinal cortex-ventral subiculum-nucleus accumb

134 , 1.12 to 1.42) predicted prolonged-duration ESA use, whereas female oncologists (OR, 0.79; 95% CI, 0

135 The four parent components and their eight ESA and OA degradates are isolated using 80/20 methanol/

136 ntify patients likely to benefit from either ESAs or anti-hepcidin agents.

137 Chemotactic properties of the eluted ESA were assessed at multiple time points using rat endo

138 Compared with placebo (or no ESA), ESA therapy was associated with a substantial reduction

139 enamid, and their respective ethanesulfonic (ESA) and oxanillic (OA) acid degradates in ground and su

140 Experiments were performed examining ESA function on these cells.

141 Of 1,147 patients experiencing ESA failure, 653 experienced primary failure and 494 exp

142 First, ESA-RSA differences were found within the medial tempora

143 ported the neuroprotective effects following ESA administration, and improved neurodevelopmental outc

144 ies to sustain critical instream habitat for ESA-listed salmonids.

145 ron stores and supplementing iron intake for ESA-treated patients.

146 s for initiating treatment or as targets for ESA therapy.

147 nt, and long-term regeneration technique for ESA systems.

148 Exploratory analyses for ESAs showed no association with DFS events (HR, 1.02; P

149 Greater ESA and iron use were associated with decreased mortalit

150 least in part, prior observations of greater ESA doses administered to African-American dialysis pati

151 Anemia and high ESA dose requirements independently predict mortality.

152 One phenotype, termed CD44(high)ESA(high), was proliferative and retained epithelial cha

153 hereas the other phenotype, termed CD44(high)ESA(low), was migratory and had mesenchymal traits chara

154 Given historically higher ESA and vitamin D use among black patients, we assessed

155 Falling hemoglobin and requiring higher ESA doses were associated with decreased survival.

156 coadministration of parenteral iron improves ESA efficacy in patients with CAA.

157 Endothelial progenitor cells (EPCs) in ESA gradient, assayed by Boyden chamber, showed signific

158 sis of mRNA expression and protein levels in ESA-treated animals revealed reduced matrix metalloprote

159 an increase of 36% and 11%, respectively, in ESA of An. lesteri and An. sinensis, was estimated under

160 ed adverse events and/or reduced survival in ESA-treated patients, concerns have been raised about th

161 The trends in ESA use remained similar between the intervention and co

162 The two binary dependent variables included ESA use and hospitalized VTE.

163 mbined with suppression of AtDGAT1 increased ESA accumulation to 14% to 15%.

164 Coexpression of VfDGAT2 increased ESA levels to approximately 11%.

165 These results suggest that individualized ESA dosing decreases total hemoglobin variability compar

166 necessitating earlier treatment, initiating ESAs at Hb levels greater than 10 g/dL either spares mor

167 In patients with traumatic brain injury, ESA therapy did not increase the number of patients surv

168 s in iron/hematologic parameters and iv iron/ESA use at time points throughout the active control per

169 t http://stat.fsu.edu/ approximately jinfeng/ESA.html.

170 However, centers that used larger ESA doses in patients with hematocrit between 33% and 35

171 fferences, dialysis centers that used larger ESA doses in patients with hematocrit less than 30% had

172 The mean ESA in the branching network was inversely proportional

173 The median ESA dosage per patient was 2000 IU/wk in both groups.

174 aline, hydrogel alone, or hydrogel+25 microg ESA was injected into the borderzone.

175 istance was increased in the in vitro model, ESA was more rapid, systole was shortened, EDV was decre

176 nsiveness was primarily defined as a monthly ESA dose of 75,000 units or higher and hematocrit 33% or

177 obinopathy traits associated with 13.2% more ESA per treatment (P=0.001).

178 Within the left MTL, ESA was greater in the anterior hippocampus, and RSA was

179 Compared with placebo (or no ESA), ESA therapy was associated with a substantial redu

180 nts after trauma to an ESA or placebo (or no ESA).

181 lled trials comparing ESAs to placebo (or no ESA).

182 8 to -1.27] for heart failure), although non-ESA-related changes in practice and Medicare payment pen

183 been established that the administration of ESA in critically ill trauma victims has been associated

184 recovery kinetics, and the time constant of ESA decay was slower following severe (180 s) than moder

185 In addition, slow decay of ESA was required to fit phosphocreatine recovery kinetic

186 Administration of any dose of ESA was associated with better survival, whereas among t

187 to the time from admission to first dose of ESA.

188 pathy traits received higher median doses of ESA than patients with normal hemoglobin (4737.4 versus

189 the hypothesis that individualized dosing of ESA improves hemoglobin variability over a standard popu

190 both NSAIDs bind within drug site 2 (DS2) of ESA and both occupy secondary binding sites in separate

191 ntly shown a potential detrimental effect of ESA administration on tumor progression and survival in

192 methods were used to estimate the effect of ESA hyporesponsiveness on allograft failure and all-caus

193 natural experiment to examine the effects of ESA boxed warnings on utilization and risk of VTE.

194 nical data showed neuroprotective effects of ESA, however, the literature regarding impact on outcome

195 human Epo (rHuEpo), none showed evidence of ESA-induced EpoR activation.

196 There was no evidence of ESA-induced intracellular signaling in endothelial cells

197 nd peri-infarct intramyocardial injection of ESA, SDF-1alpha, or saline.

198 5) were less likely to use 1 week or less of ESA treatment.

199 ession to correlate center-level patterns of ESA and iron use with 1-year mortality risk in 269,717 i

200 isozyme competition influenced production of ESA.

201 Although early studies showed promise of ESA administration in reducing the need for transfusions

202 ce showing increased survival as a result of ESA treatment.

203 d cancers, raise concern about the safety of ESA administration to patients with cancer.

204 On the basis of the crystal structure of ESA/Dic determined to a resolution of 1.92 A and the str

205 to 92% of patients, and neither the type of ESA nor the dosing interval appeared to affect efficacy.

206 re likely to prescribe more than 24 weeks of ESA treatment.

207 s exploring direct, "pleiotropic" actions of ESAs.

208 The administration of ESAs to critically ill trauma patients is associated wit

209 The effect of ESAs varied by time to anemia; patients with early-onset

210 ay be related to nonhematopoietic effects of ESAs.

211 red the potential neuroprotective effects of ESAs.

212 Primary failure of ESAs was associated with a higher risk of acute myeloid

213 Early failure of ESAs was associated with a higher risk of AML progressio

214 t reduction ( P < .001) in the likelihood of ESAs being used to treat cancers targeted by the warning

215 confirmed the neuroprotective properties of ESAs, including promotion of oligodendrocyte development

216 nd physician-related factors with receipt of ESAs were analyzed.

217 Receipt of ESAs while not actively receiving chemotherapy (off labe

218 hese preliminary studies, the future role of ESAs and iron replacement will be determined by ongoing

219 tive trials are needed to assess the role of ESAs in HCV treatment.

220 have been raised about the potential role of ESAs in promoting tumor progression, possibly through tu

221 dies have called into question the safety of ESAs as supportive therapy in patients being treated for

222 and benefits (eg, decreased transfusions) of ESAs and compare these with potential harms (eg, serious

223 and benefits (eg, decreased transfusions) of ESAs and compare these with potential harms (eg, serious

224 lity risk was associated with greater use of ESAs and iron in these patients.

225 strated widespread variability in the use of ESAs.

226 d and Drug Administration's boxed warning of ESAs used to treat chemotherapy-induced anemia because e

227 Based on ESA, a rigorous mathematical framework can be built for

228 pathy traits and quantify their influence on ESA dosing.

229 acteristics exerted substantial influence on ESA use.

230 diagnosed between 1995 and 2005 who had one ESA and chemotherapy claim.

231 to borderzone injection of saline (n=18) or ESA (n=18).

232 isolated with CD44(+)CD24(-/lo)SSEA-3(+) or ESA(hi)PROCR(hi)SSEA-3(+) markers had higher tumorigenic

233 resulting from implementation of the PPS or ESA label change.

234 The novel, biomolecularly designed peptide ESA induces chemotaxis of endothelial progenitor stem ce

235 eral (i.e., for both semantic and perceptual ESA and RSA): the left hippocampus.

236 Within the left PFC, ESA was greater in ventrolateral PFC, and RSA was greate

237 nships are real, as the slopes of the plots (ESA vs cross-sectional area, P = .001; RI vs cross-secti

238 43-1.81), respectively, supporting that poor ESA response during hemodialysis is associated with adve

239 nclear whether the risk associated with poor ESA response during dialysis extends beyond kidney trans

240 We examined pretransplantation ESA response and its effect on allograft failure and mor

241 .93) were less likely to prescribe prolonged ESA treatment.

242 Patients were randomly assigned to receive ESA doses guided by the Smart Anemia Manager algorithm (

243 r survival, whereas among those who received ESA, requiring higher doses were surrogates of higher de

244 91 patients analyzed, 5,099 (24.2%) received ESAs for 1 week or less (misuse), and 1,601 (7.6%) recei

245 or less (misuse), and 1,601 (7.6%) received ESAs for more than 14 weeks (prolonged use).

246 eviated Injury Scale (AIS), >or=3] receiving ESA while in the surgical intensive care unit from Janua

247 trait and 2.4% hemoglobin C trait) receiving ESAs, demographic and clinical variables were similar ac

248 d that the warning was effective in reducing ESA utilization.

249 nk-shaping exponential spectral analysis (RS-ESA) (both plasma and reference input) and the simplifie

250 ization of exponential spectral analysis (RS-ESA).

251 Voxelwise RS-ESA yielded similar V(T)s and coefficients of variation.

252 = 0.811, P < 10(-5)) when calculated with RS-ESA and less so (r = 0.507, P < 0.005) when SRTM was use

253 Similarly, ESAs did not reproducibly provide cytoprotection to neur

254 nsfer-appropriate processing principle, some ESA regions were reactivated during RSA in a content-spe

255 g regimens employed in the included studies, ESA therapy did not increase the risk of lower limb prox

256 llel activation of ATP usage and ATP supply (ESA), and a strong inhibition of ATP supply by anaerobic

257 Assuming that ESA by the corresponding tautomers of adenine is unchang

258 A potential explanation was that ESA-activated erythropoietin (Epo) receptors (EpoRs) pro

259 Although the ESA+ patients experienced protracted hospital length of

260 verestimates the size of the infarct and the ESA-based area at risk.

261 ss-sectional area, but not as greatly as the ESA did; the mean RI in the bed with eight times the ups

262 ion in microG and at 1 G was examined in the ESA Biorack on two space shuttle missions.

263 ased capillary and arteriolar density in the ESA group (P<0.01).

264 Animals in the ESA treatment group also had significant reductions in i

265 increase in angiopoietin-1 expression in the ESA- and SDF-treated hearts.

266 etylase core, competes with and inhibits the ESA region from interacting with the deacetylase core.

267 The administration of the ESA epoetin alfa to critically ill trauma patients has b

268 Regressions showed that the ESA boxed warning was associated with a 20.2-percentage-

269 ted as supportive of the hypothesis that the ESA pathway mediates contextual modulation of CRs during

270 Our results indicate that the ESA region interacts with and functions as an "on switch

271 Therefore, the ESA region is a potential target for development of ther

272 with the area at risk as determined with the ESA method and is localized in the perfusion territory o

273 cid hydrogels during gel formation, and then ESA release, along with gel degradation, was monitored f

274 n and LacNAc extension patterns of the three ESAs were similar, with a maximum of four N-acetyl-neura

275 P < .0001) and the area at risk according to ESA (17% +/- 13, P < .0001).

276 FDG uptake and the area at risk according to ESA was observed (r = .70, P = .001).

277 dely used pharmaceutical drugs in binding to ESA.

278 Bottom Line: Addition of iron to ESAs improves hematopoietic response, reduces the need f

279 Results Erythroid response to ESAs was 61.5%, and median response duration was 17 mont

280 rly-onset anemia (</= 8 weeks of treatment), ESAs were associated with higher SVR rate (45.0% vs 25.9

281 r or angiotensin receptor blocker (ARB) use, ESA use, dialysis access type, dialysis access change, a

282 patients (28.6%); 449 of these (51.9%) used ESAs.

283 If used, ESAs should be administered at the lowest dose possible

284 ls that provide evidence in support of using ESA to improve the neurodevelopmental outcomes in term a

285 n encouraging signals of the safety of using ESAs in heart failure and potential benefit that may be

286 Caution should be exercised when using ESAs with chemotherapeutic agents in diseases associated

287 The weekly ESA dose inversely correlated with age when scaled to we

288 um albumin and was inversely associated with ESA dose.

289 tion taken to mitigate risks associated with ESA use and changes in payment policy did not result in

290 trials have identified risks associated with ESA use.

291 esis-stimulating agents (ESAs) compared with ESA alone in the treatment of chemotherapy-induced anemi

292 enting 16 tumor types were low compared with ESA-responsive positive controls.

293 ion and the area at risk, as determined with ESA, were assessed and compared with the area of reduced

294 ly-onset anemia had higher rates of SVR with ESA use, whereas no effect was observed in those with la

295 fractional area change in mice treated with ESA compared with controls.

296 f phosphorylated AKT, and cells treated with ESA yielded significantly greater phosphorylated AKT lev

297 lobin between 12 and 13 g/dl, treatment with ESA, and rising hemoglobin.

298 s, none have identified mortality risks with ESAs.

299 with non-del(5q) lower-risk MDS treated with ESAs, none of the most commonly used second-line treatme

300 with non-del(5q) lower-risk MDS treated with ESAs.