ライフサイエンスコーパス: ARB

1 ARB inhibited EBOV Zaire Kikwit infection when added bef

2 ARB inhibited HHV-8 replication to a similar degree as c

3 ARB is currently used clinically in several countries bu

4 ARBs significantly reduced the risk of the composite out

5 ARBs surviving UV treatment were negatively correlated w

6 34% used statins, 30% ACE inhibitors, and 4% ARBs.

7 er than MRSA, and ASB in 7 ARB-endemic and 7 ARB-nonendemic hospitals between 1998 and 2007.

8 us (MRSA), ARB other than MRSA, and ASB in 7 ARB-endemic and 7 ARB-nonendemic hospitals between 1998

9 he full-field ERG results were abnormal in 8 ARB patients, whereas 2 patients demonstrated normal con

10 associated with lower IOP and systemic ACEI, ARB, statin, and sulfonylurea use was associated with hi

11 ta-analysis showed that treatment with ACEI, ARB, BB, MRA, and ARNI and their combinations were bette

12 ACEI/ARB administration was associated with a significantly l

13 ACEI/ARB therapy had a significant negative effect on the DST

14 SE]: 2.7%), statin in 33.1% (SE: 2.4%), ACEI/ARB in 28.4% (SE: 2.0%), and cilostazol in 4.7% (SE: 1.0

15 statins (OR: 2.6; 95% CI: 1.8 to 3.9), ACEI/ARB (OR: 2.6; 95% CI: 1.8 to 3.9), and smoking cessation

16 n (7.1% vs. 4.8%, p < 0.0001) or for an ACEI/ARB (29.1% vs. 22.4%, p < 0.0001), but similar proportio

17 rted therapy with a statin, 11% with an ACEI/ARB, and 5% with both.

18 The association between ACEI/ARB treatment and outcomes (mortality, myocardial infarc

19 ondialysis-dependent patients with CKD, ACEI/ARB administration was associated with greater survival.

20 te outcome of AKI and mortality favored ACEI/ARB treatment.

21 We examined the association of ACEI/ARB administration with all-cause mortality in patients

22 In particular, the low likelihood of ACEI/ARB after coronary artery bypass grafting surgery or in

23 was used to calculate the propensity of ACEI/ARB initiation in 141,413 U.S. veterans with nondialysis

24 The association of ACEI/ARB treatment with lower risk of mortality was present i

25 he 3-year mortality was 19.8% (17.4% of ACEI/ARB users and 25.4% of nonusers).

26 charge and continuous follow-up data on ACEI/ARB use among AMI survivors (2006 to 2009) included in a

27 ind consistent evidence that statins or ACEI/ARB have an effect on global neurocognitive function.

28 stimated the causal effect of statin or ACEI/ARB initiation on neurocognitive function; initial const

29 e seen in single domains with statin or ACEI/ARB therapy, we did not find consistent evidence that st

30 participants not receiving a statin or ACEI/ARB within 30 days of first neurologic assessment (basel

31 lants analyzed, 15,250 (38.9%) received ACEI/ARB and 24,001 (61.1%) received other antihypertensive t

32 lants analyzed, 15,250 (38.9%) received ACEI/ARB and 24,001 (61.1%) received other antihypertensive t

33 th was similar in patients who received ACEI/ARB therapy or other antihypertensive treatment overall

34 th was similar in patients who received ACEI/ARB therapy or other antihypertensive treatment overall

35 idney disease), 49,682 (81.7%) received ACEI/ARB with an increase in the rate of treatment over the s

36 kidney transplant recipients receiving ACEI/ARB or other antihypertensive medications is virtually i

37 kidney transplant recipients receiving ACEI/ARB or other antihypertensive medications is virtually i

38 sociation class I guideline-recommended ACEI/ARB therapy, and the use varies by patient factors.

39 is CKD who were previously unexposed to ACEI/ARB treatment.

40 raft were analyzed according to whether ACEI/ARB or other antihypertensive therapy (excluding diureti

41 raft were analyzed according to whether ACEI/ARB or other antihypertensive therapy (excluding diureti

42 his study sought to investigate whether ACEI/ARB treatment after AMI is associated with better outcom

43 Yet the extent to which ACEI/ARB therapy is applied in patients with acute coronary s

44 was observed for patients treated with ACEI/ARB (3-year hazard ratio: 0.80; 95% confidence interval:

45 Treatment with ACEI/ARB after AMI was associated with improved long-term sur

46 Overall, those treated with ACEI/ARB also had lower 3-year risk for myocardial infarction

47 analysis confirmed that treatment with ACEI/ARB did not confer a beneficial effect beyond that confe

48 analysis confirmed that treatment with ACEI/ARB did not confer a beneficial effect beyond that confe

49 ories but was significantly higher with ACEI/ARB treatment.

50 45,697 patients (71%) were treated with ACEI/ARB.

51 usted OR: 8.22 (95% CI: 6.20 to 10.90); ACEI/ARBs, adjusted OR: 5.80 (95% CI: 2.56 to 13.16); p < 0.0

52 al doses of beta-blockers, statins, and ACEI/ARBs were achieved in only 12%, 26%, and 32% of eligible

53 ratios than patients receiving PCI for ACEI/ARBs (69.4% vs. 77.8%, p < 0.0001), beta-blockers (76.1%

54 s only, 0.98 (95% CI: 0.91 to 1.07) for ACEI/ARBs and statins only, 1.17 (95% CI: 1.10 to 1.25) beta-

55 uded in the processes of any HHRA addressing ARB.

56 itor HR = 1.2, 95% CI, 0.97 to 1.4; adjusted ARBs HR = 1.1, 95% CI, 0.85 to 1.3).

57 d the foulant layer synergistically affected ARB removal, but the foulant layer was the main factor t

58 odds ratio 0.62, 95% CI 0.43-0.90) and after ARB monotherapy (0.77, 0.65-0.92).

59 I type 1 receptors (AT1R, encoded by AGTR1) (ARBs or sartans) are strongly neuroprotective, neurorest

60 All ARB patients were hyperopic, and some had shallow anteri

61 All ARBs were found to be potent inhibitors of G protein act

62 lisinopril) and placebo or lisinopril and an ARB (telmisartan), with the doses adjusted to achieve a

63 , the combination of an ACE inhibitor and an ARB failed to provide significant benefits on major outc

64 0 mmHg with a combination of diuretic and an ARB or ACEI.

65 ination therapy with an ACE inhibitor and an ARB was associated with an increased risk of adverse eve

66 The addition of an ARB did not alter the decline in the estimated GFR.

67 or an increased risk of cancer with ACEi and ARB combination (OR 1.14, 95% CI 1.04-1.24; p=0.004) and

68 However, for the ACEi and ARB combination, the cumulative Z curve crossed the tria

69 clase (AC) by testing the effect of ACEI and ARB in mice with juxtaglomerular cell-specific deficienc

70 t the cellular level, implying that ACEI and ARB may work by reducing intracellular calcium.

71 d with lower doses, higher doses of ACEI and ARB significantly though modestly improved the composite

72 e density difference between ARB-endemic and ARB-nonendemic hospitals from 2.9 to 11.0.

73 ithout ARB (F0), with ARB 5 g/100 g (F5) and ARB 10 g/100 g (F10) presented 4.23%, 2.83% and 0.11% fa

74 ACE inhibitor and ARB exposures were defined in aggregate.

75 injury, although combined ACE inhibitor and ARB treatment had the lowest rank among all intervention

76 Any benefits of combined ACE inhibitor and ARB treatment need to be balanced against potential harm

77 y, with the exception of ARB monotherapy and ARB plus ACEI.

78 of all nosocomial BSIs in ARB-nonendemic and ARB-endemic hospitals, respectively (P < .001), the over

79 k of cancer with the combination of ACEi and ARBs cannot be ruled out.

80 o investigate the effect of dose of ACEI and ARBs on outcomes and drug discontinuation in patients wi

81 sary to determine whether ACE inhibitors and ARBs also differ with respect to their effects on cardio

82 expenditure variation for ACE inhibitors and ARBs and 56.3% for statins but only 36.1% for SSRIs and

83 To test whether ACE inhibitors and ARBs differentially affect markers of oxidative stress,

84 showed similar effects of ACE inhibitors and ARBs on major cardiovascular and renal outcomes.

85 ences were showed between ACE inhibitors and ARBs with respect to all-cause mortality, cardiovascular

86 and from 0.24 to 0.55 for ACE inhibitors and ARBs, 0.29 to 0.60 for statins, and 0.15 to 0.51 for SSR

87 ACE inhibitors and ARBs, alone or in combination, were the most effective s

88 s, and to a lesser extent ACE inhibitors and ARBs, are associated with improved pneumonia-related out

89 ients at high CV risk without HF, ACE-Is and ARBs reduced the risk of the composite outcome of CV dea

90 Arbidol (ARB) is a synthetic antiviral originally developed to co

91 The antiviral drug arbidol (ARB), already in clinical use in several countries as an

92 from more than 250 tests and 34 vehicles at ARB's Haagen-Smit Laboratory (HSL).

93 ncluded any of the seven currently available ARBs.

94 olonized with antibiotic-resistant bacteria (ARB) are prone to systemic infections that are difficult

95 Is) caused by antibiotic-resistant bacteria (ARB) replace antibiotic-susceptible bacteria (ASB), leav

96 emoving three antibiotic-resistant bacteria (ARB), namely, blaNDM-1-positive Escherichia coli PI-7, b

97 evelopment of antibiotic-resistant bacteria (ARB); b) identifying and describing rates of horizontal

98 f highly efficient anode-respiring bacteria (ARB) able to produce high current densities (>1.5 A/m(2)

99 rs, acetogens, and anode-respiring bacteria (ARB).

100 the spread of antibiotic-resistant bacteria (ARBs) and antibiotic resistance genes (ARGs).

101 r a gram positive anode respiring bacterium (ARB).

102 iver discharge in the Athabasca River Basin (ARB) with (i) a generalized least-squares (GLS) regressi

103 n (GWA) study on anxiety-related behaviours (ARBs) in childhood.

104 ing the incidence density difference between ARB-endemic and ARB-nonendemic hospitals from 2.9 to 11.

105 ckdown of AT1 and inhibited by AT1 blockade (ARB).

106 effects of angiotensin II receptor blockade (ARB) in patients with structural heart disease is well e

107 atment with an angiotensin-receptor blocker (ARB) and an angiotensin-converting-enzyme (ACE) inhibito

108 ACE inhibitor/angiotensin receptor blocker (ARB) in LV dysfunction (64.1% vs. 56.3%; aPR: 1.11; 95%

109 The selective AT1 receptor blocker (ARB) losartan abrogated aneurysm progression in the mice

110 iuretic and an angiotensin receptor blocker (ARB) or angiotensin-converting enzyme inhibitor (ACEI) h

111 gh-dose angiotensin type 1 receptor blocker (ARB) or angiotensin-converting enzyme inhibitor can indu

112 tor (ACEI) and angiotensin receptor blocker (ARB) should be used for secondary prevention in all or i

113 ith a focus on angiotensin receptor blocker (ARB) therapy, as recent published data surrounding their

114 hibitor (ACEI)/angiotensin receptor blocker (ARB) use and mortality in patients with chronic kidney d

115 ibitor, and angiotensin II receptor blocker (ARB) use with pneumonia-related outcomes.

116 ) inhibitor or angiotensin receptor blocker (ARB) use, ESA use, dialysis access type, dialysis access

117 nhibitor or angiotensin II-receptor blocker (ARB).

118 tan [an angiotensin type 1 receptor blocker (ARB)] ameliorated colitis in wild-type mice, confirming

119 ors (ACEI) or angiotensin receptor blockers (ARB) are generally well tolerated, the impact of these t

120 rs (ACEI) and angiotensin receptor blockers (ARB) doses on outcomes in patients with heart failure (H

121 ors (ACEI) or angiotensin receptor blockers (ARB) initiated after myocardial infarction (MI) reduce m

122 (ACEI) or angiotensin II receptor blockers (ARB) presumably stimulate renin secretion by interruptin

123 itors (ACEI), angiotensin receptor blockers (ARB), beta-blockers (BB), mineralocorticoid receptor ant

124 inhibitors/angiotensin II receptor blockers (ARB), beta-blockers and statins are recommended after ac

125 ors (ACEI) or angiotensin receptor blockers (ARB).

126 AT1R blockers (ARBs) have been widely used in clinical settings as anti

127 rugs have been developed as AT(1)R blockers (ARBs), the structural basis for AT(1)R ligand-binding an

128 This explains why AT1 receptor blockers (ARBs) and inhibitors of Ang II synthesis, such as ACE in

129 Angiotensin-receptor blockers (ARBs) are a widely used drug class approved for treatmen

130 suggest that angiotensin receptor blockers (ARBs) are ideal drugs to explore for Alzheimer's disease

131 Ang II receptor blockers (ARBs) are neuroprotective in models of stroke but little

132 rs (ACEIs) or angiotensin receptor blockers (ARBs) are widely prescribed after kidney transplantation

133 rs (ACEIs) or angiotensin receptor blockers (ARBs) are widely prescribed after kidney transplantation

134 ors (ACEI)/angiotensin II receptor blockers (ARBs) at discharge and 12 months after AMI among 6,748 p

135 The use of angiotensin receptor blockers (ARBs) correlates with reduced onset and progression of A

136 nhibitors and angiotensin-receptor blockers (ARBs) decreases proteinuria; however, its safety and eff

137 atients using angiotensin receptor blockers (ARBs) did not show a decline in pCBF, whereas patients u

138 introduction, angiotensin receptor blockers (ARBs) have been widely promulgated as an acceptable alte

139 benefit of angiotensin II-receptor blockers (ARBs) in heart failure is thought to be a class effect,

140 inhibitors or angiotensin receptor blockers (ARBs) in patients with type 2 diabetes and chronic kidne

141 s (ACEis) and angiotensin receptor blockers (ARBs) may increase the risk of hyperkalemia (serum potas

142 (ACE-Is) and angiotensin receptor blockers (ARBs) on the composite of cardiovascular (CV) death, myo

143 nhibitors and angiotensin-receptor blockers (ARBs) reduce cardiovascular mortality in the general pop

144 inhibitors or angiotensin-receptor blockers (ARBs) who filled brand-name drug prescriptions and perce

145 nhibitors and angiotensin-receptor blockers (ARBs), 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) r

146 ) inhibitors, angiotensin receptor blockers (ARBs), and direct renin (DR) inhibitors.

147 ) inhibitors, angiotensin receptor blockers (ARBs), beta blockers, and mineralocorticoid receptor ant

148 anaphylaxis, angiotensin-receptor blockers (ARBs), beta-adrenergic blockers, epinephrine, and Kounis

149 itors (ACEI), angiotensin receptor blockers (ARBs), beta-blockers, and statins.

150 stem, such as angiotensin receptor blockers (ARBs), have been associated with lower incidence and pro

151 bitors and angiotensin II receptor blockers (ARBs), more effectively than non-RAS inhibitor therapy r

152 inhibitors or angiotensin receptor blockers (ARBs).

153 sed risk with angiotensin-receptor blockers (ARBs).

154 tors [ACEIs], angiotensin receptor blockers [ARBs], and beta-blockers adjusted for blood pressure, st

155 rs [ACEIs] or angiotensin receptor blockers [ARBs], and cilostazol) and lifestyle counseling (exercis

156 gonist drugs (angiotensin receptor blockers, ARBs, or sartans) at preventing activation of these two

157 The California Air Resources Board (ARB) adopted the low emission vehicle (LEV) III particul

158 The California Air Resources Board (ARB) and the City of Sacramento undertook this study to

159 The California Air Resources Board (ARB) undertook this study to characterize the in-use emi

160 g from mouse thoracic aorta was abolished by ARB or genetic deletion of AT1.

161 pand the list of viruses that are blocked by ARB in a laboratory setting to include Ebola virus, Taca

162 33 130 nosocomial BSIs (14% caused by ARB) yielded 36 679 microorganisms.

163 rats with regression of sclerosis induced by ARB, glomerular enlargement was due to a significantly i

164 nd the list of viruses that are inhibited by ARB and demonstrate that ARB suppresses in vitro infecti

165 otein showed that infection was inhibited by ARB at early stages, most likely at the level of viral e

166 clerosis and is mediated at least in part by ARB-induced increased complexity and branching of capill

167 ssion of hepatitis B virus and poliovirus by ARB.

168 gene, and in 1 patient with a characteristic ARB phenotype, only 1 mutation could be identified.

169 Twenty-six randomized trials comparing ARBs or ACE-Is versus placebo in 108,212 patients withou

170 rticipants, 15/20 (75%) experienced complete ARB decolonization.

171 The primary endpoint was complete ARB decolonization at 1 month after FMT.

172 gs being equal, it is reasonable to consider ARBs in those with cognitive risks.

173 ation, compare the capabilities of different ARB consortia, and find ARB with useful metabolic capaci

174 ific interactions between AT1R and different ARBs, including olmesartan derivatives with inverse agon

175 oborating a common binding mode of different ARBs.

176 splantation (FMT) could be used to eradicate ARB in humans.

177 d the best, followed by ANN, SMM and finally ARB.

178 ilities of different ARB consortia, and find ARB with useful metabolic capacities for future applicat

179 ere detected in cancer-related mortality for ARBs (death rate 1.33%; odds ratio 1.00, 95% CI 0.87-1.1

180 genus Geobacter, a known and commonly found ARB, dominate only two of the biofilm communities produc

181 Hospitals with high ARB infection rates in 2005 had an excess burden of BSI

182 extracellular form and present within a host ARBs: methicillin-resistant Staphylococcus aureus (MRSA)

183 The mechanism depicting how ARBs such as losartan restore cerebrovascular and cognit

184 on and CAD were less likely to receive ACE-I/ARB therapy (unadjusted RR: 0.88; 95% CI: 0.84 to 0.93),

185 e were 9% less likely to be prescribed ACE-I/ARB therapy.

186 bitor/angiotensin II receptor blocker (ACE-I/ARB), and lipid-lowering therapy, respectively, than pri

187 d from 3.1 to 11.7 (annual increase, 10%) in ARB-endemic hospitals (P = .2), increasing the incidence

188 d from 1.5 to 17.4 (annual increase, 22%) in ARB-endemic hospitals (P < .001), changing the incidence

189 ed from 0.2 to 0.7 (annual increase, 22%) in ARB-nonendemic hospitals, and from 3.1 to 11.7 (annual i

190 sed from 2.8 to 4.1 (annual increase, 5%) in ARB-nonendemic hospitals, and from 1.5 to 17.4 (annual i

191 s of 3.8% and 5.4% of all nosocomial BSIs in ARB-nonendemic and ARB-endemic hospitals, respectively (

192 -frequency variability must be considered in ARB water allocation, which has not been the case.

193 therapeutic options should be considered in ARB, a disease that seems to be a suitable candidate for

194 to estimate the total amount of variance in ARBs that can be accounted for by SNPs on the array.

195 d randomized trials have compared individual ARBs.

196 LV assessment and ACE inhibitor/ARB use were associated with reductions in 1-year post-d

197 o 1.21) for being adherent to ACE inhibitors/ARBs and beta-blockers only, 0.98 (95% CI: 0.91 to 1.07)

198 Patients adherent to ACE inhibitors/ARBs and statins only had similar mortality rates as tho

199 Nonadherence to ACE inhibitors/ARBs and/or statins was associated with higher mortality

200 19 (95% CI: 1.07 to 1.32) for ACE inhibitors/ARBs only, 1.32 (95% CI: 1.21 to 1.44) for beta-blockers

201 of tradeoffs in adherence to ACE inhibitors/ARBs, beta-blockers, and statins on survival among older

202 age who had prescriptions for ACE inhibitors/ARBs, beta-blockers, and statins, and survived >/=180 da

203 were adherent to statins and ACE inhibitors/ARBs.

204 or (OR, 0.73; 95% CI, .58-.92) and inpatient ARB use (OR, 0.47; 95% CI, .30-.72) was only associated

205 polymer from Agrobacterium radiobacter k84 (ARB) were characterised during 60days of frozen storage.

206 The non-MRSA ARB incidence density increased from 2.8 to 4.1 (annual

207 llin-resistant Staphylococcus aureus (MRSA), ARB other than MRSA, and ASB in 7 ARB-endemic and 7 ARB-

208 o UV disinfection than the two Gram-negative ARBs (E. coli and P. aeruginosa).

209 Nine ARB patients carried biallelic mutations in the BEST1 ge

210 ities contained different known and/or novel ARB.

211 ic mutations that confirmed the diagnosis of ARB.

212 dose-response approaches to address doses of ARB for various health outcomes and pathways.

213 ing action of angiotensin II, the effects of ARB therapy on reduction in cardiovascular and renal out

214 roaden the spectrum of antiviral efficacy of ARB to include globally prevalent viruses that cause sig

215 isorders is safe and promotes eradication of ARB from the gastrointestinal tract.

216 g all-cause mortality, with the exception of ARB monotherapy and ARB plus ACEI.

217 d chicken flavour decreased with increase of ARB; no difference was found for tenderness among the fo

218 ogressed to subcritical fouling, the LRVs of ARB decreased at increasing operating transmembrane pres

219 thymine dimers is not the sole mechanism of ARB inactivation.

220 The presence of ARB in geographically diverse locations indicates that A

221 zed by a median of 2 (range, 1-4) strains of ARB.

222 layer could remove more than 5 log units of ARB.

223 One year of ARB therapy per se does not reduce the number of AF epis

224 rmacological insights into the drug class of ARBs and medicinal chemistry insights for future drug de

225 k patients without HF whereas the effects of ARBs are less certain.

226 The clinical efficacy of ARBs to prevent atrial fibrillation (AF) so far only has

227 RECENT FINDINGS: The role of ARBs in the prevention of MI has not only been disputed,

228 To date, no robust clinical trial of ARBs in Alzheimer's disease has been performed.

229 ncer or cancer-related death with the use of ARBs, ACEi, beta blockers, diuretics, and CCBs.

230 with inflammatory bowel disease who were on ARB therapy compared to patients not receiving ARB thera

231 d trials that compared high doses of ACEI or ARB against low doses among patients with HF with reduce

232 monotherapy is more efficacious than ACEI or ARB monotherapy.

233 d increased prednisone dose (n = 2), ACEI or ARB only (n = 2).

234 addition of eplerenone to background ACEI or ARB therapy attenuates the progressive decline in left v

235 ormal renal function treated with an ACEi or ARB.

236 ion despite treatment with either an ACEi or ARB.

237 renal function and are receiving ACEi and/or ARB therapy.

238 Compared with low dose, high-dose ACEI or ARBs decreased all-cause mortality modestly (relative ri

239 nt evidence about the association of ACEI or ARBs with mortality in patients with CKD.

240 recommend substitution of ACE inhibitors or ARBs with ARNIs in appropriate patients.

241 ns, 42.5% versus 20.8% for ACE inhibitors or ARBs, and 75.1% versus 27.0% for insulin analogues.

242 antidiabetic treatment and ACE inhibitors or ARBs, for at least 8 weeks before study entry.

243 o standard care, including ACE inhibitors or ARBs.

244 r placebo as an adjunct to ACE inhibitors or ARBs.

245 ients with heart failure compared with other ARBs.

246 reduction in major cardiovascular outcomes: ARB (odds ratio [OR] 1.02; 95% credible interval [CrI] 0

247 e were no severe adverse events, and partial ARB decolonization was observed in 20/25 (80%) of the FM

248 oints included safety assessment and partial ARB decolonization.

249 1.10; 95% CrI 0.90-1.40), ACE inhibitor plus ARB (0.97; 95% CrI 0.72-1.29), DR inhibitor plus ACE inh

250 nterval [CrI] 0.90-1.18), ACE inhibitor plus ARB (0.97; 95% CrI 0.79-1.19), DR inhibitor plus ACE inh

251 2; 95% CrI 0.96-1.81), and DR inhibitor plus ARB (1.00; 95% CrI 0.73-1.38).

252 9; 95% CrI 0.65-1.57), and DR inhibitor plus ARB (1.18; 95% CrI 0.78-1.84).

253 rols (1.43%; 1.08, 0.78-1.46), and ACEi plus ARBs (1.45%; 1.10, 0.90-1.32).

254 eased risk with the combination of ACEi plus ARBs (2.30%, 1.14, 1.02-1.28); however, this risk was no

255 It was found that the two Gram-positive ARBs (MRSA and VRE) were more resistant to UV disinfecti

256 ar rescue of losartan, a commonly prescribed ARB, in a mouse model of AD.

257 caribe arenavirus, and HHV-8, and we propose ARB as a broad-spectrum antiviral drug that may be usefu

258 Patients randomly assigned to receive ARBs had a significantly increased risk of new cancer oc

259 her in patients randomly assigned to receive ARBs than in those assigned to receive control (0.9%vs 0

260 drug in 30,014 (85.7%) patients who received ARBs as part of the trials with new cancer data.

261 B therapy compared to patients not receiving ARB therapy.

262 ccine administrator, and study statistician (ARB) were unmasked.

263 Studying ARB from different environmental conditions will allow u

264 These results suggest ARB as a promising fat substitute, capable of maintain t

265 400 mJ/cm(2) for 3- to 4-log reduction) than ARB inactivation (10-20 mJ/cm(2) for 4- to 5-log reducti

266 at are inhibited by ARB and demonstrate that ARB suppresses in vitro infection of mammalian cells wit

267 graphically diverse locations indicates that ARB thrive in a wide range of ecosystems.

268 We have previously shown that ARB inhibits in vitro hepatitis C virus (HCV) by blockin

269 Our work has suggested that ARB use is associated with decreased amyloid deposition

270 vational studies have further suggested that ARB use is associated with decreased risk of Alzheimer's

271 Studies in animal models suggest that ARBs have cognitive protective effects that are related

272 Overall, our data suggest that ARBs with dual AT(1)R-blocking and PPARgamma activation

273 f randomised controlled trials suggests that ARBs are associated with a modestly increased risk of ne

274 nd comprehensive meta-analyses suggests that ARBs, while effective antihypertensive agents that prote

275 The ACEI captopril and quinaprilate and the ARB candesartan significantly increased plasma renin con

276 e surface attributed the removal of both the ARB and ARGs to adsorption, which was facilitated by an

277 ows long-term declining flows throughout the ARB.

278 I) injury on mice to investigate whether the ARB candesartan would mitigate any effects of TBI.

279 hibitor and each of the remaining therapies: ARB (OR 1.10; 95% CrI 0.90-1.40), ACE inhibitor plus ARB

280 clinical trials of antihypertensive therapy (ARBs, angiotensin-converting-enzyme inhibitors [ACEi], b

281 Thus, ARBs represent a valuable option to reduce CV mortality

282 Increased nosocomial BSI rates due to ARB occur in addition to infections caused by ASB, incre

283 :1; block size of six [Malian] or four [US]; ARB produced computer-generated randomisation lists; cli

284 Docking simulations of the clinically used ARBs into the AT(1)R structure further elucidated both t

285 VALUE) trial, in which the use of valsartan (ARB) was compared with amlodipine in patients at high ca

286 lightly increased recurrence hazard, whereas ARBs were not associated with recurrence (adjusted ACE i

287 We assessed whether ARBs affect cancer occurrence with a meta-analysis of ra

288 The definitive answer of whether ARBs are effective, if at all, in preventing MI remains

289 largely laid to rest the question of whether ARBs contribute to cardiovascular risk.

290 However, the manner by which ARBs mediate their beneficial effects is unknown.

291 d in the Prospective Comparison of ARNI With ARB on Management of Heart Failure With Preserved Ejecti

292 Participants colonized with ARB were treated with intraduodenal FMT according to a p

293 cooking, formulations without ARB (F0), with ARB 5 g/100 g (F5) and ARB 10 g/100 g (F10) presented 4.

294 ry branching was augmented in glomeruli with ARB-induced regression of sclerosis.

295 ear period, mainly caused by infections with ARB.

296 ded no difference in the risk of cancer with ARBs (proportion with cancer 2.04%; odds ratio 1.01, 95%

297 nificant increase in the risk of cancer with ARBs when compared with control, eliciting a safety revi

298 Concomitant therapy with ARBs, angiotensin-converting enzyme inhibitors, and anti

299 In addition, treatment with ARBs might result in less decline in pCBF than other ant

300 After cooking, formulations without ARB (F0), with ARB 5 g/100 g (F5) and ARB 10 g/100 g (F1