ライフサイエンスコーパス: ACE

1 ACE C-domain overexpression in macrophages drove them to

2 ACE inhibitor/ARB dose was abstracted from medical recor

3 ACE inhibitor/ARB exposure status was landmarked at 30 d

4 ACE inhibitor/ARB therapy is associated with a protectiv

5 ACE is composed of two independent catalytic domains.

6 ACE mice exhibited the enhanced anxiety-like behaviors i

7 ACE modeling was also completed.

8 ACE overexpression does not change cell or mitochondrial

9 ACE prefers to cleave substrates with Phe or Leu at the

10 ACE uses an evolutionary algorithm approach to perform l

11 ACE-2-correlated gene signatures were used to interrogat

12 ACEs were more prevalent in low-income adults compared w

13 ACEs were statistically associated with higher rates of

14 Angiotensin-converting enzyme 2 (ACE-2), neprilysin (NEP), and plasma kallikrein (KLKB1)

15 iscovery of angiotensin converting enzyme-2 (ACE-2) as the receptor for SARS- CoV-2 (Severe Acute Res

16 d, double-blind, placebo-controlled, phase 3 ACE trial at 22 specialist cancer centres in China.

17 raction <40% (OR, 0.97 [95% CI, 0.69-1.35]), ACE (angiotensin-converting enzyme) inhibitor or angiote

18 for low educational attainment comparing 4+ ACEs with no ACEs was 2.0 (1.7-2.4, p < 0.001).

19 and health outcomes range from 5%-15% for 4+ ACEs and 1%-19% for low maternal education.

20 For example, odds ratios (ORs) for 4+ ACEs compared with no ACEs after adjustment for confound

21 For example, ORs for 4+ ACEs compared with no ACEs after adjustment for confound

22 cant linkage was observed with RVs in ABCA7, ACE, EPHA1, and SORL1, genes that were previously report

23 system-angiotensin-converting enzymes (ACEs) ACE and ACE2, angiotensin II (Ang II), Ang-(1-7), and re

24 ement was distinct for antioxidant activity, ACE-, alpha-glucosidase-, and Kunitz trypsin-inhibitory

25 0, ADAMTS1, and WWOX), two of which (ADAM10, ACE) were identified in a recent genome-wide association

26 In addition, ACE overexpression in myeloid cells increases their immu

27 Confirmatory studies of whether adjunctive ACE inhibitor or statin treatment truly can enhance scle

28 Routine laboratory monitoring after ACE inhibitor or angiotensin II receptor blocker initiat

29 Cognitive impairment at 3 years affected all ACE-R subdomains and was associated with ACE-R 1 year (b

30 ang (GV29) and Baihui (GV20) also alleviated ACE-induced anxiety-like behaviors, and rescued ACE-impa

31 c blocking PV interneurons in PrL alleviated ACE-enhanced anxiety-like behaviors in mice.

32 vities of tempe peptides obtained were as an ACE inhibitor, antioxidant, and antithrombotic.

33 ain catalytic activity; it is reversed by an ACE inhibitor but not by an angiotensin II AT1 receptor

34 t a 30-day course of high-dose captopril, an ACE inhibitor, initiated 1-4 h after total body irradiat

35 of the renin- angiotensin system, either an ACE (angiotensin-converting enzyme) inhibitor or an ARB

36 Patients who received an ACE inhibitor/ARB within 30 days post-operatively had a

37 Of 7085 participants with CKD, 34.9% used an ACE/ARB.

38 on reverted to that of the WT enzyme with an ACE inhibitor but not with an angiotensin II type 1 (AT1

39 worsening chronic HF) and treatment with an ACE inhibitor or ARB (i.e., ACE inhibitor or ARB-yes vs.

40 421 (48%) patients had been treated with an ACE inhibitor or ARB, while 458 (52%) had not been treat

41 while 458 (52%) had not been treated with an ACE inhibitor or ARB.

42 he distribution of virus particles within an ACE-II, a M/M , and a Neu.IMPORTANCE Generally, it is di

43 D Symptom Scale (M-PSS) was administered and ACE-I/ARB status was determined by self-report.

44 ion, total phenolic content, antioxidant and ACE inhibitory activities were evaluated at storage time

45 es showed an increase in the antioxidant and ACE inhibitory activities.

46 ce for the combined dose of beta blocker and ACE-I or ARB: +6% [+2%, +10%]).

47 tive compounds (total phenolic compounds and ACE-inhibitory activity), changes in fatty acid composit

48 els, but with higher carotenoids content and ACE inhibitory activity.

49 reater alpha-amylase, alpha-glucosidase, and ACE inhibitory activity than the pasteurized product, si

50 It is plausible that the ACE inhibitors and ACE receptor blockers may have the potential to prevent

51 ion and LTL for the combined PANTHER-IPF and ACE-IPF clinical trials (P(interaction) = 0.048), and th

52 the subjects enrolled in the PANTHER-IPF and ACE-IPF, 62% (49/79) and 56% (28/50) had an LTL less tha

53 elective vasopeptidase inhibitors of NEP and ACE for effective treatment in hypertension and heart fa

54 ile the effect on the fatty acid profile and ACE inhibitory activity is dependent on the process para

55 s are accompanied by inhibition of renin and ACE.

56 trategy is here reported, which took SAC and ACE as leads and produced a series of 2H-benzo[e][1,2,4]

57 ACEs than previous prevalence estimates and ACEs were associated with higher rates of multiple cardi

58 significantly correlated with BSA-MGO, anti-ACE, anti-AChE and PCLACW parameters.

59 0 MPa/5 min) significantly enhanced the anti-ACE (14.09 mg/mL) and anti-AChE (16.95 mg/mL) potentials

60 The interaction and imbalance between ACE and ACE2 result in an unopposed angiotensin II.

61 This study demonstrates associations between ACEs and lower educational attainment and higher risks o

62 We detected a strong relationship between ACEs and a self-reported history of a hypertension diagn

63 pulation and assess the relationship between ACEs and cardiovascular disease risk factors.

64 drenergic receptor blockers (beta-blockers), ACE (angiotensin-converting enzyme) inhibitors and ANG (

65 Because angiotensin II receptor blockers, ACE inhibitors, and mineralocorticoid receptor antagonis

66 Both ACE inhibitors and antidepressants showed statistically

67 try, similar patterns were observed for both ACE inhibitors or ARBs and beta blockers, with women hav

68 ar stress and aging, is associated with both ACE exposure and psychopathology, providing the basis fo

69 The low PAFs for both ACEs and socioeconomic factors imply that interventions

70 otension and vasodilation and is degraded by ACE and enhanced by the angiotensin(1-9) produced by ACE

71 , and the potential bioactivity evaluated by ACE inhibition activity.

72 (ACE) from angiotensin I and metabolized by ACE 2 (ACE2), plays a pivotal role in the pathogenesis o

73 the spasmogenic C3f, which was processed by ACE ex vivo and in vitro.

74 driven more by ARBs (e.g., Losartan) than by ACE-Is.

75 significantly heritable under the classical ACE twin model (h(2) = 0.28-0.59), which included cerami

76 e compounds (DPPD, Total Phenolic Compounds, ACE-inhibitory activity values), fatty acid composition,

77 In conclusion, ACE can produce results for very large searches in a sho

78 Es), the activity of angiotensin-converting (ACE) and acetylcholinesterase (AChE) enzymes.

79 rSADS-CoV did not use human coronavirus ACE-2, DPP4, or CD13 receptors for docking and entry.

80 ed to share a common receptor with SARS-CoV (ACE-2).

81 lity rank, implantable cardiac defibrillator+ACE inhibitor or ARB+BB+mineralocorticoid receptor antag

82 ntagonist, implantable cardiac defibrillator+ACE inhibitor or ARB+BB, and angiotensin receptor-nepril

83 DAs generate a signal upon ligand-dependent ACE-aptamer dehybridization.

84 reatment with an ACE inhibitor or ARB (i.e., ACE inhibitor or ARB-yes vs. ACE inhibitor or ARB-no) at

85 , and (ii) an aptamer-complementary element (ACE), such as a short DNA oligonucleotide, which is desi

86 Combined elevated ACE and lymphopenia were strongly suggestive of systemic

87 ect with a positive skin biopsy had elevated ACE, lymphopenia, and bihilar lymphadenopathy on CXR.

88 All subjects with elevated ACE and lymphopenia had evidence of systemic sarcoidosis

89 tion with the angiotensin converting enzyme (ACE) 2 protein at the surface of many cells.

90 ng and kidney angiotensin-converting enzyme (ACE) activity, established in F1 offspring from 3 weeks

91 inhibition of angiotensin converting enzyme (ACE) activity.

92 Angiotensin-converting enzyme (ACE) affects blood pressure.

93 btained had angiotensin-I-converting enzyme (ACE) and dipeptidyl peptidase IV (DPP-IV) inhibitory act

94 e activity of angiotenisn-converting enzyme (ACE) and the enzyme acetylcholinesterase (AChE).

95 sin (NEP) and angiotensin-converting enzyme (ACE) are two key zinc-dependent metallopeptidases in the

96 Angiotensin-converting enzyme (ACE) can hydrolyze many peptides and plays a central rol

97 Angiotensin-converting enzyme (ACE) converts angiotensin I into the potent vasoconstric

98 converted by angiotensin-converting enzyme (ACE) from angiotensin I and metabolized by ACE 2 (ACE2),

99 tion of the angiotensin I-converting enzyme (ACE) from its default biochemical conversion of Ang I to

100 tment with an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) aff

101 Angiotensin Converting Enzyme (ACE) Inhibitor treatment (aHR=1.69, 95% CI: 1.18-2.35) w

102 ications were angiotensin-converting enzyme (ACE) inhibitors (17.9%), antidepressants (17.8%), and li

103 ugs, mostly angiotensin I converting enzyme (ACE) inhibitors and angiotensin receptor type I (AT(1)R)

104 rmine whether angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB) w

105 consisting of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)

106 lysis (DH), angiotensin-I converting enzyme (ACE) inhibitory activity of hydrolysates showed signific

107 Three angiotensin converting enzyme (ACE) inhibitory peptides, IPP (0.42-0.49 mg/kg), LPP (0.

108 idative and angiotensin-1 converting enzyme (ACE) inhibitory potential compared to cow milk upon simu

109 expression of angiotensin-converting enzyme (ACE), an amyloid-beta protein degrading enzyme, to brain

110 of renin and angiotensin-converting enzyme (ACE), and found both were sharply increased in CKD heart

111 ful effect of angiotensin-converting-enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs)

112 rs (ARBs) and angiotensin-converting-enzyme (ACE) inhibitors and the risk of coronavirus disease 2019

113 nded doses of angiotensin-converting-enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs),

114 pounds, DPPH, angiotensin-converting-enzyme (ACE) inhibitory activity, fatty acids profile, and volat

115 about use of angiotensin-converting enzyme (ACEs) inhibitors or angiotensin II receptor blockers (AR

116 imbalance of angiotensin converting enzymes (ACE)1 and ACE2 (ACE2 being the severe acute respiratory

117 ensin system-angiotensin-converting enzymes (ACEs) ACE and ACE2, angiotensin II (Ang II), Ang-(1-7),

118 n daily post-operative lisinopril-equivalent ACE inhibitor/ARB dose was >5 mg, the risk of major GIB

119 o have experienced adverse childhood events (ACEs) around puberty are at the greatest risk for neurop

120 We examined ACE/ARB trends from 1999 to 2014 among 38,885 adult Nati

121 tions between adverse childhood experiences (ACEs) and ill health throughout the life course.

122 Adverse childhood experiences (ACEs) are associated with mental and physical health ris

123 cing multiple adverse childhood experiences (ACEs) is a risk factor for many adverse outcomes.

124 Atlas Correlation Explorer (ACE) is a user-friendly workbench for seeking associatio

125 ntly found that adolescent cocaine exposure (ACE) resulted in an enhancement of the gamma-aminobutyri

126 ptome ribosome profiling of cells expressing ACE-tRNA at levels which repair PTC indicate that there

127 for ARBs and 0.96 [95% CI, 0.87 to 1.07] for ACE inhibitors) or among patients who had a severe or fa

128 for ARBs and 0.91 [95% CI, 0.69 to 1.21] for ACE inhibitors), and no association between these variab

129 ned below guideline recommendations (42% for ACE-Is or ARBs, 29% for beta blockers in 2014) and was l

130 bular tissue, EP promoted mRNA increases for ACE, AT1 receptor, and inflammatory mediators as well as

131 ncrease soluble ACE-2 in plasma in order for ACE-2 to capture and thereby inactivate SARS-CoV-2.

132 A fourth ACE inhibitory peptide, KP (0.93-1.5 mg/kg), was enhance

133 In contrast, macrophages from ACE knockout (null) mice averaged only 28% of the ATP le

134 ACE substrates in mice with distinct genetic ACE backgrounds.

135 Furthermore, the beverages showed a good ACE inhibitory activity.

136 e with the ACE genotype associated with high ACE level.

137 Higher ACE-R scores were associated with faster TUG (beta=-0.27

138 se and Black Prince tomatoes had the highest ACE (0.50-0.44mg/mL) and AChE (7.93-5.83mg/mL) inhibitor

139 tial inhibitors of ACE, WPH with the highest ACE inhibitory activity was analysed using Sephadex G-75

140 However, ACE activity is also essential for other physiological f

141 In total, we identify ACE-tRNA with a high degree of suppression activity targ

142 llic acid), QT (quercetin), LT (luteolin) in ACE (acetone) and RT (rutin) in EtOH (ethanol) solvent a

143 arked changes of intermediate metabolites in ACE-overexpressing macrophages and neutrophils, with inc

144 Our findings suggest that a 10% reduction in ACE prevalence could equate to annual savings of 3 milli

145 Replication cohorts included ACE-IPF (Anticoagulant Effectiveness in Idiopathic Pulmo

146 a wide range of relevant factors, including ACEs, socioeconomic deprivation, parental substance use,

147 wth of B16-F10 melanoma because of increased ACE expression in macrophages, whereas Tg-CKO mice resis

148 n and phagocytosis associated with increased ACE expression.

149 onic urticaria (mast cell mediator-induced), ACE-inhibitor intake and hereditary angioedema (both bra

150 as angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs), may be

151 nd angiotensin-converting-enzyme inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) both inc

152 tassium testing within 30 days of initiating ACE (angiotensin-converting enzyme) inhibitor or angiote

153 e identified 75 251 matched pairs initiating ACE inhibitor or angiotensin II receptor blocker therapy

154 nd identify five new genome-wide loci (IQCK, ACE, ADAM10, ADAMTS1, and WWOX), two of which (ADAM10, A

155 Independent variables were the 10-item ACEs questions covering neglect, abuse, and household dy

156 sweeteners saccharin (SAC) and acesulfame K (ACE) recently entered the topic of anticancer human carb

157 e attrition from 4 to 18 months and maternal ACEs was examined as a predictor of infant scores on the

158 sed to test the association between maternal ACEs and infant internalizing and externalizing behavior

159 Higher maternal ACEs were associated with shorter infant TL across infan

160 fects modeling was used to test how maternal ACEs influenced infant TL trajectory.

161 The authors tested the effect of maternal ACEs on both the trajectory of infant TL and infant soci

162 from 4 to 18 months interacted with maternal ACEs to predict externalizing behaviors.

163 66/151 (44%) had cognitive impairment, mean ACE-R 88 (SD 9, range 54-100/100), 61/156 (39%) had depr

164 ability in general population, in which mean ACE level in DD carriers is approximately twice that in

165 elatively low-cost heart failure medication (ACE [angiotensin-converting enzyme] inhibitor or angiote

166 -, sex-, and race/ethnicity-adjusted models, ACE/ARB use was significantly associated with era (adjus

167 ted at least one ACE, 24% reported 4 or more ACEs, and 54.5% received 5 or more General Certificates

168 costs arose in individuals with two or more ACEs.

169 Moreover, ACE overexpression in monocytes and macrophages increase

170 Natural ACE C-domain-specific substrates are not well-described,

171 Analyses with N-domain-inactive (NKO) ACE allowed clarification of domain selectivity toward s

172 ds ratios (ORs) for 4+ ACEs compared with no ACEs after adjustment for confounders were depression, 2

173 or example, ORs for 4+ ACEs compared with no ACEs after adjustment for confounders were harmful alcoh

174 ational attainment comparing 4+ ACEs with no ACEs was 2.0 (1.7-2.4, p < 0.001).

175 Several of the novel ACE substrates are known to have biological activities,

176 finding was replicated in the placebo arm of ACE-IPF for those exposed to immunosuppression (hazard r

177 regarding a potential harmful association of ACE inhibitors or ARBs with in-hospital death in this cl

178 Characterization of ACE-083 in vitro revealed its high affinity for heparin

179 nterneurons within PrL in the development of ACE-induced anxiety-like behavior, and to assess whether

180 ht be sex differences in the optimal dose of ACE inhibitors or ARBs and beta blockers in patients wit

181 eached guideline-recommended target doses of ACE inhibitors or ARBs (99 [25%] vs 304 [23%], p=0.61) a

182 t women with HFrEF might need lower doses of ACE inhibitors or ARBs and beta blockers than men, and b

183 The effect of ACE overexpression reverted to that of the WT enzyme wit

184 e robustly replicated the overall effects of ACE-I/ARB medication associated with lower rate of PTSD

185 sease, here we tested whether the effects of ACE-I/ARB status on PTSD differ by sex.

186 fect are needed to elucidate the efficacy of ACE inhibitors, ARBs, beta blockers, and aldosterone ant

187 n RAS represented by decreased expression of ACE in combination with increases in ACE2, renin, angiot

188 This study highlights the vast extent of ACE promiscuity and provides a valuable platform for fur

189 V) inhibitory activities, with inhibition of ACE being stronger than that of DPP-IV.

190 peptides that may be potential inhibitors of ACE, WPH with the highest ACE inhibitory activity was an

191 uable platform for further investigations of ACE functionality.

192 ungs, probably because of the high number of ACE-2 receptors in this organ.

193 E-treated and untreated plasma peptidomes of ACE-knockout (KO) mice, validation with select synthetic

194 present study, we evaluated the potential of ACE-083 - a locally acting, follistatin-based fusion pro

195 Our results demonstrate the potential of ACE-083 as a therapeutic agent for patients with CMT, mu

196 ify novel natural substrates and products of ACE through a series of mass-spectrometric experiments.

197 x vivo as possible substrates or products of ACE, demonstrating high promiscuity of the enzyme.

198 sure Ang II and Ang (1-7) synthesis rates of ACE, chymase and NEP, ACE2, PEP (prolyl-endopeptidase),

199 Rates of ACE/ARB use increased in the early 2000s among United St

200 ructures and the corresponding structures of ACE with these inhibitors has provided the molecular bas

201 eptides, and a quantitative in vivo study of ACE substrates in mice with distinct genetic ACE backgro

202 The binary solvent system of ACE: EtOH (1:1) at 60 degrees C was optimized as extract

203 Results Combination therapy of ACE (angiotensin-converting enzyme) inhibitors or ARBs (

204 ilure in whom initiation and up-titration of ACE inhibitors or ARBs and beta blockers was encouraged

205 are attributable to one or multiple types of ACE and the associated financial costs.

206 h was found to be associated with the use of ACE inhibitors (2.1% vs. 6.1%; odds ratio, 0.33; 95% CI,

207 The use of ACE inhibitors and ARBs was more common among case patie

208 is large, population-based study, the use of ACE inhibitors and ARBs was more frequent among patients

209 land in 1991-1992, we assess associations of ACEs between birth and 16 years (sexual, physical, or em

210 We explore associations of ACEs with educational attainment and adolescent health a

211 conomic factors modified the associations of ACEs with educational or health outcomes.

212 Associations of ACEs with harmful alcohol use and obesity were weak.

213 There were associations of ACEs with lower educational attainment and higher risk o

214 picture of the cohort members' experience of ACEs; however, a limitation of our study is that this re

215 of this study was to estimate the extent of ACEs in a low-income, nonclinical, uninsured adult popul

216 rope and north America live with a legacy of ACEs.

217 were associated with cumulative measures of ACEs (ie, number of ACEs).

218 h cumulative measures of ACEs (ie, number of ACEs).

219 Low-income adults have high rates of ACEs than previous prevalence estimates and ACEs were as

220 populations that did not have a high risk of ACEs, that had sample sizes of at least 1000 people, and

221 hile previous studies were focused mainly on ACE inhibitory (ACEi) peptides, this work also studied p

222 w, we introduce a framework for DAs based on ACEs, and use this framework to distinguish DAs from oth

223 mply that interventions that focus solely on ACEs or solely on socioeconomic deprivation, whilst bene

224 cational outcomes, 84% reported at least one ACE, 24% reported 4 or more ACEs, and 54.5% received 5 o

225 tion between prior HF history (p = 0.350) or ACE inhibitor or ARB treatment (p = 0.880) and the effec

226 ng potential effects of beta-blockers and/or ACE inhibitors in coexisting venom allergy are inconclus

227 Use of ARBs or ACE inhibitors did not show any association with Covid-1

228 april irrespective of previous HF history or ACE inhibitor or ARB treatment.

229 overexpressed either WT ACE (Tg-ACE mice) or ACE lacking N- or C-domain catalytic activity (Tg-NKO an

230 th were highest for mental illness outcomes: ACEs were attributed to about 30% of cases of anxiety an

231 Myeloid cells overexpressing ACE indicate the existence of a novel pathway in which m

232 Macrophages overexpressing ACE have increased mitochondrial membrane potential (24%

233 are increased in macrophages overexpressing ACE.

234 he regulation of the SBP by acting on plasma ACE, plasma renin and the vascular system.

235 Programmes to prevent ACEs and moderate their effects are available.

236 s of at least 1000 people, and that provided ACE prevalence data.

237 pregnancy, modeling the effects of pubertal ACEs we also reported in women.

238 (48%) returned a follow-up survey reporting ACEs in 2012.

239 -induced anxiety-like behaviors, and rescued ACE-impaired GABAergic neurotransmitter system and PV in

240 identify anticodon engineered transfer RNAs (ACE-tRNA) which can effectively suppress in-frame PTCs a

241 Serum ACE was elevated in 43 subjects, of whom 29 (67.4%) had

242 Sensitivity of serum ACE was 38.2% and specificity 97.8%, with an area under

243 To showcase ACE, we assessed which RNA sequencing transcripts were a

244 eutic considerations how to increase soluble ACE-2 in plasma in order for ACE-2 to capture and thereb

245 chieved by administering recombinant soluble ACE-2.

246 otassium tests in the 30 days after starting ACE inhibitor or angiotensin II receptor blocker therapy

247 the peptide(s) responsible for the striking ACE-mediated enhancement of myeloid function are substra

248 Tg-ACE and Tg-NKO mice exhibited strongly suppressed growth

249 sistance, we overexpressed either WT ACE (Tg-ACE mice) or ACE lacking N- or C-domain catalytic activi

250 sonance and cell-based assays confirmed that ACE-083 binds and potently neutralizes myostatin, activi

251 However, there was no evidence that ACE inhibitors or ARBs affected the risk of COVID-19.

252 in P1 are typical residues in peptides that ACE does not cleave.

253 alysis of COVID-19 cohorts has revealed that ACE inhibitors (ACEIs) or angiotensin receptor blockers

254 The ACE competes with ligand binding, such that DAs generate

255 nsin(1-7)-angiotensin AT(2) receptor and the ACE-2-angiotensin(1-7)-Mas receptor pathways have been s

256 tivity against these enzymes by blocking the ACE-dependent conversion of angiotensin I to the potent

257 This included comparing the ACE-treated and untreated plasma peptidomes of ACE-knock

258 t and adjunct culture addition increased the ACE inhibitory activity.

259 -acupuncture (EA) therapeutically manage the ACE-induced abnormal behaviors in adulthood.

260 In healthy young mice, neither the ACE inhibitor ramipril nor the AT1 receptor blocker telm

261 loid function are substrates/products of the ACE C-domain.

262 hysiology of ARDS, whereas activation of the ACE-2-angiotensin(1-7)-angiotensin AT(2) receptor and th

263 seem to perform it beneficial effects on the ACE-induced abnormal emotional behaviors by "calming dow

264 in-I converting enzyme 2 (ACE2) promotes the ACE/angiotensin-II (Ang-II)/angiotensin type 1 receptor

265 It is plausible that the ACE inhibitors and ACE receptor blockers may have the po

266 Considering that the ACE insertion (I)/deletion (D) gene polymorphism contrib

267 fic drug classes, results indicated that the ACE-I/ARB effect on PTSD may be driven more by ARBs (e.g

268 ion (D) gene polymorphism contributes to the ACE level variability in general population, in which me

269 V-2 infection, especially for those with the ACE genotype associated with high ACE level.

270 GLT2 inhibitor) versus conventional therapy (ACE inhibitor or ARB and beta blocker) in patients with

271 These ACE-tRNAs display high suppression potency in mammalian

272 Increased ATP is due to ACE C-domain catalytic activity; it is reversed by an AC

273 with potential hypertensive activity due to ACE inhibition were identified.

274 ble fractions (PAFs) of risk attributable to ACEs and the disability-adjusted life-years (DALYs) and

275 cational and health outcomes attributable to ACEs or family or socioeconomic measures.

276 ts of cardiovascular disease attributable to ACEs were substantially higher than for most other cause

277 the control group of the EMPHASIS-HF trial (ACE inhibitor or ARB and beta blocker).

278 eurons in PrL may be key etiology underlying ACE-induced anxiety-like behaviors.

279 f SARS-CoV-2 to invade endothelial cells via ACE-2 (angiotensin-converting enzyme 2), which is expres

280 Virtual ACE also gave them skills to manage complex older patien

281 Virtual ACE was developed to deliver evidence-based geriatric ca

282 f the Virtual Acute Care for Elders (Virtual ACE) program, a novel intervention that improves outcome

283 rovement, our stakeholders felt that Virtual ACE empowered them and provided effective tools to impro

284 Nurse managers felt that Virtual ACE helped them allocate limited resources and plan thei

285 Previous work demonstrated that Virtual ACE increased mobility and decreased delirium rates for

286 Our stakeholders indicated that Virtual ACE was extremely empowering for bedside nurses.

287 The main criticism was that the Virtual ACE Tracker that displayed patient status was difficult

288 r or ARB (i.e., ACE inhibitor or ARB-yes vs. ACE inhibitor or ARB-no) at admission.

289 Among the identified peptides were ACE-inhibitory peptides (LDAQSAPLR, LKGYGGVSLPEW, and LK

290 DH had no correlations (p > 0.05) with ACE inhibitory activity for all three legumes.

291 all ACE-R subdomains and was associated with ACE-R 1 year (beta=1.054, p<0.001) and NART (beta=1.023,

292 Among individuals treated with ACE-Is/ARBs in the initial sample, women had significant

293 RVs, and at least 3 months of treatment with ACE inhibitor, ARB, beta blocker, or aldosterone antagon

294 the relation between previous treatment with ACE inhibitors, angiotensin-receptor blockers, beta-bloc

295 rug use had the highest PAFs associated with ACEs of all the risk factors assessed in both regions (3

296 se, anxiety, and depression) associated with ACEs.

297 (DALYs) and financial costs associated with ACEs.

298 udies in which risk data in individuals with ACEs were compared with these data in those without ACEs

299 re compared with these data in those without ACEs.

300 tumor resistance, we overexpressed either WT ACE (Tg-ACE mice) or ACE lacking N- or C-domain catalyti