ライフサイエンスコーパス: ACE

1 ACE ('Assessing Changes to Exons') converts phased genot

2 ACE avoids overfitting by constructing a sparse network

3 ACE can be readily applied to diverse species including

4 ACE inhibition relies on the formation of hydrogen bonds

5 ACE inhibition restores the HP (13)C DHA reduction to Vi

6 ACE inhibitor-based therapy was associated with poorer c

7 ACE inhibitors (captopril, fosinopril and fosinoprilat)

8 ACE is written in open-source C ++ and Perl and is avail

9 ACE, ANI and BEN showed mild toxicity at effective antio

10 ACE-I therapy might therefore have a role in the context

11 ACEs were associated with higher AL for both men and wom

12 ment interaction was significant (p = 0.04); ACE use in blacks was associated with poorer cardiovascu

13 .02; 95% credible interval [CrI] 0.90-1.18), ACE inhibitor plus ARB (0.97; 95% CrI 0.79-1.19), DR inh

14 therapies: ARB (OR 1.10; 95% CrI 0.90-1.40), ACE inhibitor plus ARB (0.97; 95% CrI 0.72-1.29), DR inh

15 Pro had the highest ACE inhibitory activity (ACE IC50=5.21+/-0.94muM).

16 An ACE inhibitory peptide sorted from the library was custo

17 rs), during which 30 patients experienced an ACE.

18 The use of an ACE inhibitor and a statin did not change the albumin-to

19 assigned in a placebo-controlled trial of an ACE inhibitor and a statin with the use of a 2-by-2 fact

20 ed with monotherapies, the combination of an ACE inhibitor and an ARB failed to provide significant b

21 The use of an ACE inhibitor was associated with a lower incidence of m

22 omized to either 10 weeks of therapy with an ACE inhibitor (10 mg enalapril) or placebo.

23 er outcomes than whites when treated with an ACE inhibitor-based regimen.

24 M-HF (Prospective Comparison of ARNI With an ACE-Inhibitor to Determine Impact on Global Mortality an

25 In multivariate analysis, ACE inhibitor therapy was an independent indicator of de

26 Serum levels of sIL-2R and ACE and chest radiographic findings were assessed.

27 Measurements of sIL-2R and ACE in serum samples and data extraction from patient fi

28 with uveitis who had their serum sIL-2R and ACE levels determined and underwent chest radiography.

29 e optimal cutoff points for serum sIL-2R and ACE levels to define sarcoidosis in patients with uveiti

30 Serum sIL-2R and ACE levels were significantly correlated (Pearson correl

31 o], 0.070, P = .27) nor uveitis activity and ACE (rho, -0.071; P = .27).

32 es with significant in vitro antioxidant and ACE inhibitor activities.

33 ctions exhibited the highest antioxidant and ACE inhibitor activities.

34 hydrolysates with potential antioxidant and ACE inhibitory activities, which can be used to obtain n

35 A significant increase in antioxidant and ACE inhibitory capacities was observed.

36 The antioxidant and ACE-inhibitory activities of the extracted proteins were

37 epithelial transport of an antioxidative and ACE inhibitory peptide, VLPVPQK (named peptide C) derive

38 beta-Blockers and ACE inhibitors synergistically aggravate anaphylaxis at

39 prevention of ACEs, resilience building, and ACE-informed service provision.

40 a reverse correlation between chronicity and ACE level (P-value <0.05).

41 Effect of Strict Blood Pressure Control and ACE Inhibition on Progression of CKD in Pediatric Patien

42 e SP hydrolysate exhibited the lowest DH and ACE inhibition.

43 s (phenolic compounds, anthocyanin, DPPH and ACE activity) and the volatile compounds were performed.

44 draft cookstoves (FDCS; Philips HD4012LS and ACE-1), and three institutional cookstoves.

45 Variants in KLKB1 and ACE were associated with a fragment of complement compon

46 kinin-kallikrein genes KNG1, F12, KLKB1, and ACE were associated with several different peptides.

47 itor therapy and elevated blood lysozyme and ACE levels in sarcoidosis patients.

48 an (SD) serum sIL-2R (6047 [2533] pg/mL) and ACE (61 [38] U/L) levels, elevated serum sIL-2R levels w

49 013-1.432mumol Trolox eq./mumol peptide) and ACE inhibitory activities (IC50=44-120muM).

50 p was observed between isoelectric point and ACE inhibition.

51 irect relationship between SCCD pressure and ACE inhibitory activity was observed, with 34.63, 38.75,

52 est bioactivities (ORAC, DPPH scavenging and ACE-inhibitory activities) generated from alkali extract

53 e accessed through ORAC, DPPH scavenging and ACE-inhibitory activities.

54 in patients who were adherent to statins and ACE inhibitors/ARBs.

55 and taking stable antidiabetic treatment and ACE inhibitors or ARBs, for at least 8 weeks before stud

56 68523 and rs2478544 at AGT and rs11658531 at ACE) and 1 SNP in women (rs12451328 at ACE).

57 31 at ACE) and 1 SNP in women (rs12451328 at ACE).

58 Three SNPs (rs8075924 and rs4277404 at ACE and rs12721297 at AGTR1) were individually associate

59 eractivated renin angiotensin system because ACE inhibition reverses the hypertension induced by peri

60 HVH-N-FIV (3-1kDa) fractions showed the best ACE-inhibitory activities with IC50 values of 53.31 and

61 ignificant differences were detected between ACE inhibitor and each of the remaining therapies: ARB (

62 othesized that an interactive effect between ACE and TD would be observed when women were hypogonadal

63 significant differences were showed between ACE inhibitors and ARBs with respect to all-cause mortal

64 AVVPPSDKM, TTMYPGIA, and VKPLPQSG could bind ACE active site with low interaction scores.

65 rs), in patients treated with beta-blockers, ACE inhibitors or monoamine oxidase inhibitors, in child

66 Blood ACE concentrations are determined by proteolytic cleavag

67 domain of somatic ACE) that increases blood ACE activity 7-fold and interrogated the mechanism by wh

68 this mutation significantly increases blood ACE levels.

69 s thiols, to yield an acetone-linked bridge (ACE).

70 All the extracts inhibited ACE, but ACE inhibition was thought to be improved by the increas

71 The primary outcome was not affected by ACE inhibitor therapy, statin therapy, or the combinatio

72 rentiation which is processed exclusively by ACE.

73 elioration of DDT-associated hypertension by ACE inhibition.

74 Models inferred by ACE more accurately describe the statistics of the data,

75 Novel transcripts predicted by ACE are commonly supported by spliced RNA-seq reads, and

76 the absence of exogenous estradiol, a TD by ACE interaction was observed on BOLD signal in the right

77 effectiveness of ablative chemoembolization (ACE) in the treatment of hepatocellular carcinoma (HCC)

78 Most clinical ACE inhibitor(s) (ACEi) have been shown to inhibit both

79 ved and MF was present as determined on CMR, ACE inhibitor therapy was associated with significantly

80 ia or acute kidney injury, although combined ACE inhibitor and ARB treatment had the lowest rank amon

81 Any benefits of combined ACE inhibitor and ARB treatment need to be balanced agai

82 Conclusion ACE is a feasible, safe, and well-tolerated treatment fo

83 y V. halodenitrificans proteinases contained ACE inhibitory peptides that are potentially bioavailabl

84 ted protein co-precipitates showed decreased ACE inhibitory activity and increased antioxidant activi

85 g-(1-7)/Mas that counteracts the deleterious ACE/AngII/AT1R axis has been established.

86 and GFPTLKIF were most potent, demonstrating ACE-I IC50 values of 28.2 muM and 41.2 muM respectively.

87 dilated cardiomyopathy were elevated despite ACE inhibition with elevated chymase activity, and Ang I

88 In this study, we analyzed different ACE levels in 148 patients diagnosed with sarcoidosis.

89 may stabilize ACE conformation and diminish ACE shedding.

90 gh resolution crystal structures of N-domain ACE in complex with the dipeptide products of Ac-SDKP cl

91 ing of lips, tongue, pharynx, or face during ACE inhibitor use and no swelling in the absence of ACE

92 Early ACEs in children aged 3 to 7 years; volume of a subregio

93 An increase from 0 to 3 early ACEs was associated with 15% and 25% increases in depres

94 trajectory of the association between early ACEs and adolescent general and emotional health outcome

95 ed to investigate associations between early ACEs and brain structure, emotion development, and healt

96 anism by which the association between early ACEs and later poor mental and physical health outcomes

97 ially mediated the association between early ACEs and poor general health (model parameter estimate =

98 iation in the association between high early ACEs and emotional and physical health outcomes were fou

99 y and the Australian Childhood Encephalitis (ACE) study between 2013 and 2015.

100 y and the Australian Childhood Encephalitis (ACE) study between 2013 and 2015.

101 as porcine angiotensin-I-converting enzyme (ACE I) and aminopeptidase N (AP-N).

102 e most potent angiotensin converting enzyme (ACE) and dipeptidyl peptidase IV (DPP-IV) inhibitory and

103 Angiotensin I-converting enzyme (ACE) hydrolyzes numerous peptides and is a critical part

104 fect of early angiotensin-converting enzyme (ACE) inhibitor therapy in patients with normal left vent

105 eated with an angiotensin converting enzyme (ACE) inhibitor, captopril, to evaluate sensitivity to am

106 resolution of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema in 1 study of Europ

107 allergies to angiotensin-converting enzyme (ACE) inhibitors and HMG CoA reductase inhibitors (statin

108 an adjunct to angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)

109 ent including angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs).

110 interest were angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), a

111 tion, such as angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), b

112 dentical to angiotensin I-converting enzyme (ACE) inhibitors, antioxidant, antimicrobial, immunomodul

113 Angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARB),

114 oxidant and angiotensin I converting enzyme (ACE) inhibitory activities released from lentil proteins

115 a-amylase and angiotensin converting enzyme (ACE) inhibitory activities were successfully identified

116 The angiotensin I-converting enzyme (ACE) inhibitory activity and structural properties of ov

117 The angiotensin I-converting enzyme (ACE) inhibitory activity of protein hydrolysates from ti

118 e increased angiotensin I-converting enzyme (ACE) inhibitory activity, and in vitro gastrointestinal

119 sitions and angiotensin I-converting enzyme (ACE) inhibitory potentials.

120 Angiotensin-I converting enzyme (ACE) is a zinc metalloprotease consisting of two catalyt

121 inogen (AGT), angiotensin-converting enzyme (ACE), angiotensin II type 1 receptor (AGTR1), and aldost

122 to mammalian angiotensin-converting enzyme (ACE), are insecticidal to larvae of the mosquitoes, Aede

123 Angiotensin-converting enzyme (ACE)-2 is the primary enzyme of the vasoprotective axis

124 bitors of the angiotensin-converting enzyme (ACE).

125 Angiotensin-I-converting enzyme (ACE-I) plays a key role in control of hypertension, and

126 reatment with angiotensin-converting-enzyme (ACE) inhibitors accounts for one third of angioedema cas

127 benefit from angiotensin-converting-enzyme (ACE) inhibitors and statins, drugs that have not been fu

128 eart failure, angiotensin-converting-enzyme (ACE) inhibitors reduce mortality and hospitalization, bu

129 tioxidant and angiotensin-converting-enzyme (ACE) inhibitory activities were measured.

130 e inhibition, angiotensin-converting-enzyme (ACE)-inhibition, antioxidant and proteolytic activity) o

131 e tolerant to angiotensin-converting-enzyme (ACE)-inhibitors were randomly assigned after a run-in pe

132 lysozyme and angiotensin-converting enzyme [ACE]) are lacking in high sensitivity and specificity.

133 y classified most patients who had equivocal ACE-R scores.

134 The Acarbose Cardiovascular Evaluation (ACE) trial was a randomised, double-blind, placebo-contr

135 n heart dose (MHD) and acute coronary event (ACE) rate was reported in a study of patients with breas

136 revised Addenbrooke's Cognitive Examination (ACE-R), had a neurological examination, clinical diagnos

137 Ser-Val and Ile-Phe were shown to exhibit ACE inhibitory activity with IC50 values of 60.68+/-1.06

138 we describe the adaptive cluster expansion (ACE) method to quickly and accurately infer Ising or Pot

139 tion (TD) and adverse childhood experiences (ACE) on brain activation during a working memory task in

140 mined whether adverse childhood experiences (ACEs) are associated with elevated AL in midlife.

141 Adverse childhood experiences (ACEs) are one of the greatest predictors of affective di

142 Adverse childhood experiences (ACEs) have been associated with poor mental and physical

143 effects that adverse childhood experiences (ACEs; occurring during childhood or adolescence; eg, chi

144 udies identify a novel mouse model of female ACEs that can be used to examine how additional life adv

145 tatins only, 1.19 (95% CI: 1.07 to 1.32) for ACE inhibitors/ARBs only, 1.32 (95% CI: 1.21 to 1.44) fo

146 arded as a promoting or hindering factor for ACE-I peptide release during cheese digestion.

147 tients without an established indication for ACE-I, reduced the peak work rate response to exercise t

148 >/=65 years of age who had prescriptions for ACE inhibitors/ARBs, beta-blockers, and statins, and sur

149 ent conversions to hepatectomy was seven for ACE and three for cTACE.

150 lu411, Lys511, His513, Tyr520 and Tyr523 for ACE had corresponded to the catalytic and substrate bind

151 The IC50 values for ACE inhibition by OD-FPH and FD-FPH samples were found t

152 ty was 10.03-23.33mM, whereas the values for ACE inhibitory activity were of 1.52-31.88muM.

153 icant dose-effect relationship was found for ACEs within 9 years after RT.

154 al tissue complication probability model for ACEs consisted of LV-V5, age, and weighted ACE risk scor

155 n, LV-V5 seemed to be a better predictor for ACEs than MHD.

156 ibution parameters are better predictors for ACEs than MHD.

157 estimates for individuals with at least four ACEs compared with those with none for outcomes with suf

158 Individuals with at least four ACEs were at increased risk of all health outcomes compa

159 The frequent ACE insertion/deletion polymorphism (I/D) is, albeit inc

160 gonist would shorten time-to-resolution from ACE inhibitor-associated angioedema.

161 Homology models of the larval An. gambiae ACE proteins (AnoACE2 and AnoACE3) reveal structural dif

162 newer vista for food derived peptides having ACE inhibitory potential for nutraceutical or therapeuti

163 FC such that TD increased activation in high ACE subjects but decreased activation in low ACE subject

164 Critically, in our human studies, the high ACE women showed a significant blunting of the HPA respo

165 According to their high ACE-inhibitory potential, FIV and FV were fractionated b

166 slationally, pregnant women with low or high ACEs were examined for their maternal stress responsiven

167 Higher ACE-inhibitory activity was generated in the trypsin and

168 sin and pepsin hydrolysates exhibited higher ACE-inhibitory activity than HT (P<0.05).

169 Highest ACE-inhibitory activity of hydrolyzed protein fractions

170 iltrate (1 mg/ml), that demonstrated highest ACE-I inhibitory activity of 70.37%, was characterised i

171 f solar dried Jameed also led to the highest ACE inhibitory activities whereas antioxidant activity w

172 Tyr-Pro had the highest ACE inhibitory activity (ACE IC50=5.21+/-0.94muM).

173 egree of hydrolysis (DH)) showed the highest ACE inhibitory activity, with an IC50 value of 0.54mg/ml

174 The highest ACE-inhibition of the WSE from camel milk fermented by L

175 HG demonstrated the highest ACE-inhibitory activity, DPPH, ABTS radical scavenging a

176 ich yielded the hydrolysate with the highest ACE-inhibitory capacity.

177 However, ACEs frequently co-occur and no synthesis of findings fr

178 eal structural differences compared to human ACE, suggesting that structure-based drug design offers

179 ent being obtained from the 3 h hydrolysate (ACE IC50=2.9+/-0.3 mug/ml).

180 DPP-IV) and angiotensin converting enzyme I (ACE) inhibition, glucose uptake stimulation and antioxid

181 ated protein co-precipitates showed improved ACE inhibitory activity and diminished antioxidant poten

182 cy of a bradykinin B2 receptor antagonist in ACE inhibitor-associated angioedema.

183 iven in addition to standard care, including ACE inhibitors or ARBs.

184 have quantified such effects for individual ACEs.

185 -2,3,4,9-tetrahydro-1H-pyrido[3,4-b]indole), ACE (6-methoxy-1-methyl-2,3,4,9-tetrahydro-1H-pyrido[3,4

186 ulate ACE conformation and thereby influence ACE shedding.

187 , IQKVAGTW) synthesized was found to inhibit ACE with an IC50 of 300+/-2microM.

188 All the extracts inhibited ACE, but ACE inhibition was thought to be improved by th

189 Pork kidney extract, isolated ACE I, and AP-N were able to activate patient basophils

190 had comparable scores on other PANSS items, ACE-III, and GAF at baseline, with no difference in outc

191 , BPP-12b) were all inhibitors of the larval ACE activity of both mosquitoes.

192 sozyme and also a Low Molecular Weight (LMW) ACE effector, bilirubin, which act in concert to regulat

193 ACE subjects but decreased activation in low ACE subjects.

194 ermeates of FlavH and CorH resulted in lower ACE IC50 values than their respective hydrolysates.

195 Luspatercept (ACE-536) is a novel fusion protein that blocks transform

196 Afterward the mean ACE level of each group was calculated and compared.

197 s index, use of antihypertensive medication (ACE inhibitors, non-ophthalmic beta blockers, calcium ch

198 tal mediated effect was 59% (for two or more ACEs) via health behaviors, education level, and wealth.

199 elopment of selective inhibitors of mosquito ACE enzymes as novel larvicides.

200 rom studies measuring the effect of multiple ACE types has been done.

201 INTERPRETATION: To have multiple ACEs is a major risk factor for many health conditions.

202 comes most strongly associated with multiple ACEs represent ACE risks for the next generation (eg, vi

203 tus and conditions, associated with multiple ACEs.

204 h outcomes compared with individuals with no ACEs.

205 In this study, we identified a novel ACE gene mutation (Arg532Trp substitution in the N domai

206 The novel ACE inhibitory peptide with the highest inhibition was f

207 emales and white patients except for NSAIDs, ACE inhibitors, and thiazide diuretics, which were more

208 ibitor use and no swelling in the absence of ACE inhibitor use) were enrolled at Vanderbilt Universit

209 ns are determined by proteolytic cleavage of ACE from the endothelial cell surface, a process that re

210 ed bradycardia, clinically relevant doses of ACE inhibitors, beta-blockade and the funny channel bloc

211 ent with estradiol attenuated the effects of ACE and TD such that no between or within group differen

212 erent RAS blockers showed similar effects of ACE inhibitors and ARBs on major cardiovascular and rena

213 In this work, the hyphenation of ACE with mass spectrometry (MS) is presented as a novel,

214 The cumulative incidence of ACE increased by 16.5% per Gy (95% CI, 0.6 to 35.0; P =

215 such as blood pressure, lipids, and lack of ACE inhibitor use, but not with sex.

216 tic insight into the elevated blood level of ACE observed in patients on ACE inhibitor therapy and el

217 databases as tools for predicting release of ACE-I inhibitory peptides from barley proteins.

218 and guidelines now recommend substitution of ACE inhibitors or ARBs with ARNIs in appropriate patient

219 ecently observed an enhanced upregulation of ACE by elevated fat intake in GG-carriers of the I/D-sur

220 Our analysis included 59,316 new users of ACE inhibitors, 47% of whom were black.

221 No main effect of ACEs on average BP levels was found.

222 rimary end point was cumulative incidence of ACEs within 9 years of follow-up.

223 es a shift in focus to include prevention of ACEs, resilience building, and ACE-informed service prov

224 e heart to radiation to avoid excess risk of ACEs after radiotherapy for BC.

225 d blood level of ACE observed in patients on ACE inhibitor therapy and elevated blood lysozyme and AC

226 Optimum ACE-inhibitory and antioxidant activities of proteins se

227 axis after monotherapy with beta-blockers or ACE inhibitors, which was more pronounced when both drug

228 erl and is available from geneprediction.org/ACE.

229 ociated with poorer cardiovascular outcomes (ACE vs. NoACE: 8.69% vs. 7.74%; p = 0.05) but not in whi

230 d standardised symptom rating scales (PANSS, ACE-III, GAF) at baseline, and tested serum samples for

231 (0.97; 95% CrI 0.72-1.29), DR inhibitor plus ACE inhibitor (0.99; 95% CrI 0.65-1.57), and DR inhibito

232 (0.97; 95% CrI 0.79-1.19), DR inhibitor plus ACE inhibitor (1.32; 95% CrI 0.96-1.81), and DR inhibito

233 ial sources of bioactive peptides possessing ACE inhibitory and antioxidant activities.

234 chemical synthesis based on their predicted ACE-I inhibitory properties.

235 e randomized (1:1) to receive or not receive ACE inhibitor therapy.

236 andomization (1:1) to receive or not receive ACE inhibitor therapy.

237 domized (21 patients in each arm) to receive ACE inhibitors demonstrated slower MF progression compar

238 In chronic HF patients receiving ACE inhibition, plasma Ang II was suppressed and plasma

239 nt Goals provide a global platform to reduce ACEs and their life-course effect on health.

240 bilirubin, which act in concert to regulate ACE conformation and thereby influence ACE shedding.

241 ngly associated with multiple ACEs represent ACE risks for the next generation (eg, violence, mental

242 The mean (SD) ACE score was 5.44 (3.46).

243 Compared to SelenoPrecise and Se-ACE tablets, a yoghurt-based supplement exhibited a much

244 ynthesized and tested for N-domain selective ACE inhibition.

245 fidence interval [CI], -22 to -11) and serum ACE activity (Delta, -18 IU/L; 95% CI, -23 to -12) versu

246 Combined chest radiography and serum ACE levels at the standard cutoff of 68 U/L resulted in

247 2Trp substitution in the N domain of somatic ACE) that increases blood ACE activity 7-fold and interr

248 Sotatercept (ACE-011, and its murine ortholog RAP-011) acts as an act

249 ite for blood components which may stabilize ACE conformation and diminish ACE shedding.

250 ntain 3-4 amino acid residues showing strong ACE inhibition.

251 172 patients (33%) were taking ACE-I.

252 The effects of TD, ACE, and TD x ACE were evaluated using a voxel-wise, mix

253 nd has slightly better diagnostic value than ACE.

254 We show that ACE accurately reproduces the true parameters of the und

255 ublicly available RNA-seq data, we show that ACE predictions confirm earlier results regarding the qu

256 The ACE inhibitor-treated group demonstrated a significant r

257 The ACE rs4343 variant is a novel nutrient-sensitive type 2

258 The ACE-inhibitory activity of HG showed the highest stabili

259 The ACE-inhibitory activity of OD-FPH was more stable (durin

260 e test, the TYM-MCI performed as well as the ACE-R in the distinction of patients with aMCI/AD from p

261 We compared the ACE inhibitor enalapril with the renin inhibitor aliskir

262 We identified the ACE-binding protein in the blood as lysozyme and also a

263 adhesion to Caco-2 cells while improved the ACE-inhibitory and antioxidant activity.

264 When convergence of the ACE algorithm is slow, we combine it with a Boltzmann Ma

265 idues of lentil peptides and residues of the ACE catalytic site.

266 Use of the ACE inhibitor enalapril, together with a program of PR,

267 A significant increase of the ACE-inhibiting effect was observed following butanol ext

268 The suitability of the ACE-MS methodology for the affinity profiling of heterog

269 ompleted the trial (34 on placebo, 31 on the ACE inhibitor).

270 vitro gastrointestinal digestion reduced the ACE inhibitory activity of the M hydrolysate but enhance

271 The study suggested that the ACE inhibitory activity of protein hydrolysate was not a

272 st exclusively be attributed to Ile-Trp, the ACE inhibition by plant protein hydrolysates is caused b

273 We have used the ACE-CRIS instrument to collect 3.55 x 10(5) iron nuclei,

274 Using the ACE model (proportion of variance in a trait heritable s

275 Used in combination with the ACE-R, it provided additional value and identified almos

276 xpression levels correlate strongly with the ACE/ACE2 ratio, suggesting a conserved mechanism.

277 We hypothesized that this ACE mutation disrupts the binding site for blood compone

278 Elevated tissue ACE levels are associated with increased risk for cardio

279 ated the effect of tradeoffs in adherence to ACE inhibitors/ARBs, beta-blockers, and statins on survi

280 (95% CI: 1.04 to 1.21) for being adherent to ACE inhibitors/ARBs and beta-blockers only, 0.98 (95% CI

281 Patients adherent to ACE inhibitors/ARBs and statins only had similar mortali

282 n 300 mg per day or placebo as an adjunct to ACE inhibitors or ARBs.

283 An increase in reported allergies to ACE inhibitors and statins is noteworthy.

284 NSCEND, 5810 patients who were intolerant to ACE-inhibitors were randomly assigned to oral telmisarta

285 ncreased plasma Ang-(1-7) level is linked to ACE inhibitor use, whereas acute HF reduced Ang-(1-7) le

286 Nonadherence to ACE inhibitors/ARBs and/or statins was associated with h

287 to examine the relation between exposure to ACEs and BP development.

288 e-containing dipeptides, 50-80% of the total ACE-inhibiting potential of butanol extracts from plant

289 und in two of eight specimens that underwent ACE and three of three that underwent cTACE.

290 brary was custom synthesized and an in vitro ACE assay was performed.

291 O filtrates were assessed for their in vitro ACE-I inhibitory activities.

292 up (placebo Delta, +9 W; 95% CI, 5 to 13 vs. ACE-I Delta, +1 W; 95% CI, -2 to 4; between-group differ

293 r ACEs consisted of LV-V5, age, and weighted ACE risk score per patient (c-statistic, 0.83; 95% CI, 0

294 soluble interleukin 2 receptor (sIL-2R) with ACE as diagnostic biomarkers of sarcoidosis in patients

295 When compared with ACE inhibitor, no other RAS blocker used in monotherapy

296 er Waals and electrostatic interactions with ACE catalytic pockets.

297 ntly different from the values obtained with ACE-UV and were in agreement with an earlier reported va

298 Patients with ACE inhibitor-associated angioedema (defined as swelling

299 Results Treatment with ACE was successfully completed in all patients without a

300 The effects of TD, ACE, and TD x ACE were evaluated using a voxel-wise, mixed-effects, 2