ライフサイエンスコーパス: blocker

1 ASIS-HF trial (ACE inhibitor or ARB and beta blocker).

2 rence from antihypertensive medication (beta-blockers).

3 inhibitor or an angiotensin type 1 receptor blocker.

4 ce and a role for carbenoxolone as a channel blocker.

5 antagonistic game between an Attacker and a Blocker.

6 he preferred tautomeric state of the channel blocker.

7 d by an N-methyl-D-aspartate (NMDA) receptor blocker.

8 suggesting bupropion is not an open channel blocker.

9 ere mitigated by verapamil, a Ca(2+) channel blocker.

10 ific conjugation with a photoswitchable pore blocker.

11 po, bound to sodium ions only, substrate, or blockers.

12 for select patients who do not tolerate beta-blockers.

13 g enzyme inhibitors and angiotensin receptor blockers.

14 d merbarone, which are two well-known topoII blockers.

15 may be a possible target of channel-specific blockers.

16 hma, we compared IL-4 vs IL-13 vs IL-4Ralpha blockers.

17 combinatorial partner for immune checkpoint blockers.

18 current was inhibited by known IKCa channel blockers.

19 al therapeutic application of quorum-sensing blockers.

20 ngiotensin receptor blockers (ARBs) and beta blockers.

21 CI, -4.99 to -1.44) for angiotensin receptor blockers.

22 %) were exposed to regular preoperative beta-blockers.

23 fects of oral adenosine diphosphate receptor blockers.

24 r conditions of intended use as bitter taste blockers.

25 increasingly combined with immune-checkpoint blockers.

26 k-out (KO) mice and a panselective T-channel blocker 3,5-dichloro-N-[1-(2,2-dimethyltetrahydro-pyran-

27 tail current decay, sensitive to the I (Ks) blocker (3R,4S)-(+)-N-[3-hydroxy-2,2-dimethyl-6-(4,4,4-t

28 ment with the FDA-approved potassium channel blocker 4-aminopyridine (4-AP) improves motor behavior i

29 meabilized myofibres with 2 mm Cl(-) channel blocker 9-anthracenecarboxylic acid (9AC) inhibited both

30 We tested the effect of the chloride channel blocker 9-anthracenecarboxylic acid (9AC) on P(i) entran

31 Treatment of diabetic mice with the NFAT blocker A-285222 reduced NFATc3 nuclear accumulation and

32 y ligation, treated with the specific S100A9 blocker ABR-238901 for 7 or 21 days.

33 ti-PD-1 Abs and their synergy with classical blocker Abs may be instrumental in potentiating immunoth

34 Because angiotensin II receptor blockers, ACE inhibitors, and mineralocorticoid receptor

35 rting enzyme inhibitors/angiotensin receptor blockers (ACEI/ARB) in acute myocardial infarction (AMI)

36 nts were receiving target doses of MRA, beta-blocker, ACEI/ARB, and ARNI therapy, respectively.

37 ty than those receiving angiotensin receptor blockers (all p < 0.001).

38 0 person-years [py]) was not reduced by beta-blockers alone (1.37 per 100 py; p = 1.00), or in combin

39 ne-treated animals, the combination of these blockers along with compound 101 was required to block a

40 e effects observed with brain-penetrant CB1R blockers, ameliorate obesity and its multiple metabolic

41 itional impairment (from the calcium channel blocker amlodipine).

42 ond, we explored outcomes associated to beta-blocker among advanced CKD participants with preserved (

43 was performed in a 4-year-old patient; beta-blocker and exercise restriction were recommended in 4 p

44 We hypothesized that angiotensin receptor blocker and neprilysin inhibitor, sacubitril/valsartan (

45 nts with HFrEF should be treated with a beta-blocker and one of an angiotensin receptor-neprilysin in

46 g patients with heart failure, combined beta-blocker and renin-angiotensin antagonist medication rate

47 ighly selective and potent TRPC1/4/5 channel blocker and T1E3, a TRPC1 blocking antibody.

48 duced by administration of a pharmacological blocker and when CFTR was fully functional.Conclusions:

49 tigations and appropriate initiation of beta blockers and angiotensin-converting-enzyme inhibitors (A

50 pinephrine infusion rate and the use of beta-blockers and plasma cytokines was assessed in 195 patien

51 The prescribed dosages of beta-blockers and renin-angiotensin system inhibitors were si

52 ents both in sensitivity to specific channel blockers and their current-voltage (I-V) relationships,

53 ble data regarding potential effects of beta-blockers and/or ACE inhibitors in coexisting venom aller

54 enzyme] inhibitor or angiotensin II receptor blocker) and a newer, but more expensive, heart failure

55 55.2% on PPIs, 24.3% on histamine-2 receptor blockers, and 24.4% on antacids).

56 Utilization of statins, beta-blockers, and angiotensin-converting enzyme inhibitors/a

57 ammatory conditions, hyperphosphatemia, beta-blockers, and epoetin.

58 beta-Blockers, calcium channel blockers, and mineralocorticoid receptor antagonists did

59 nhibition experiments, the use of amino acid blockers, and site-directed mutagenesis of UCP1, we prop

60 Exercise restriction, beta-blockers, and surgical intervention were discussed with

61 doxorubicin) and immune checkpoint inhibitor blocker (anti-PD-1 antibody) were more effective in S1pr

62 o-transformations, including beta-adrenergic blockers, antivirals, antibiotics, and pesticides.

63 03-3.96) and dihydropyridine calcium channel blockers (aOR 1.91, CI 1.03-3.55) were associated with d

64 ital use vs. non-use of angiotensin receptor blockers (aOR 2.02, CI 1.03-3.96) and dihydropyridine ca

65 antagonist (DCPP-ene) or by an NMDAR channel blocker applied through the recording pipette (MK-801).

66 PAH rats with dofetilide, an Kv11.1 channel blocker approved by the US Food and Drug Administration

67 zyme (ACE) inhibitor or angiotensin receptor blocker (ARB) affected the results.

68 yme inhibitor (ACEI) or angiotensin receptor blocker (ARB) influences disease outcomes.

69 tensive activity to the angiotensin receptor blocker (ARB) losartan.

70 ms data to characterize angiotensin receptor blocker (ARB) prescription trends to evaluate whether re

71 inhibitors (ACEi) or angiotensin II receptor blockers (ARB) during hospitalization of 614 hypertensiv

72 tion between the use of angiotensin-receptor blockers (ARBs) and angiotensin-converting-enzyme (ACE)

73 yme (ACE) inhibitors or angiotensin receptor blockers (ARBs) and beta blockers.

74 Angiotensin II type 1 receptor (AT1R) blockers (ARBs) are among the most prescribed drugs.

75 inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) both increased significantly (37% versus

76 inhibitors (ACEI) or angiotensin II receptor blockers (ARBs) does not increase susceptibility to SARS

77 (ACEs) inhibitors or angiotensin II receptor blockers (ARBs) in CKD is lacking.

78 inhibitors (ACEIs) and angiotensin-receptor blockers (ARBs) in coronavirus disease 2019 (COVID-19) s

79 me (ACE) inhibitors and angiotensin-receptor blockers (ARBs) in this clinical context.

80 E inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) may be beneficial in COVID-19.

81 zyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs) may make patients more susceptible to co

82 inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs), may be associated with decreased PTSD s

83 g enzyme inhibitors and angiotensin-receptor blockers are not associated with greater illness severit

84 users with cardiac disease suggest that beta-blockers are not unsafe and that may be effective in the

85 ockers or nondihydropyridine calcium channel blockers are reasonable drugs in patients with normal ve

86 tatins, vitamin D, and tumor necrosis factor blockers are unintentionally modulating the Treg compart

87 r weight 94.1146 g/mol), a potassium-channel blocker as a growth factor alternative to enhance the ra

88 ng enzyme inhibitor, or angiotensin receptor blocker as foundational therapy, with addition of a mine

89 es these learning deficits, suggesting Kcnn2 blockers as a new intervention for learning disabilities

90 asses (statins, antiglaucoma drugs, and beta blockers) as an approach to reducing confounding by frai

91 loration of isradipine, an FDA-approved LTCC blocker, as a potential therapeutic for the prevention o

92 5% CI: 0.04 to 0.55) and regular use of beta-blockers at 6-month follow-up (HR: 0.20; 95% CI: 0.09 to

93 5% CI: 0.47 to 0.92) and regular use of beta-blockers at 6-month follow-up (HR: 1.62; 95% CI: 1.17 to

94 In vivo injection of vesamicol-a VAChT blocker-at the cholinergic synapse, suppressed forced wa

95 Pivotal trials of beta-blockers (BB) and angiotensin converting enzyme inhibito

96 Beta-blockers (BB) have been traditionally associated with im

97 beta-Blockers (BBs) are mainstay therapy for heart failure wi

98 nt with ACE inhibitors, angiotensin-receptor blockers, beta-blockers, calcium-channel blockers, or th

99 Such aryl sulfonamide Nav1.7 channel blockers bind to the extracellular surface of the S1-S4

100 ippocampal administration of reconsolidation blockers, both of which were restored by concomitant the

101 Treatment with the CCC blocker bumetanide prevented neuronal swelling via a rev

102 Accordingly, HER2 blockers, but not c-MET inhibitors, are paradoxically ef

103 beta-Blockers, calcium channel blockers, and mineralocorticoi

104 nsin system as it did not replicate for beta-blockers, calcium channel blockers, or diuretics.

105 ibitors, angiotensin-receptor blockers, beta-blockers, calcium-channel blockers, or thiazide diuretic

106 's preferred spatial location, whereas AMPAR blockers caused a more general suppression.

107 Calcium channel blockers (CCB) improve TB treatment outcomes in pre-clin

108 of oral hypoglycemic agents, calcium channel blockers (CCB), insulin, and diuretics were significantl

109 and omega-conotoxin-GVIA and to metal cation blockers Cd(2+) and Ni(2+) Also absent was the capacity

110 idly activating delayed rectifier K+ current blocker consistent with the increase of rapidly activati

111 ing conditions: carbenoxolone (gap junctions blocker), control, and picrotoxin (GABA-A receptor antag

112 icted poor outcomes, and regular use of beta-blockers correlated with late survival and LV functional

113 ce and absence of the acetylcholine receptor blockers d-tubocurarine and alpha-bungarotoxin.

114 In contrast, AMPAR blockers decreased activity elicited by the memory of bo

115 rting enzyme inhibitors/angiotensin receptor blockers decreased from 89%, 84.9%, and 72.2% on dischar

116 Applying specific potassium channel blockers diminished the hyperexcitability.

117 e were treated with >=50% of the target beta-blocker dose.

118 ght-at-night exposure and/or the use of beta-blocker drugs.

119 vivo sequestration agents for neuromuscular blockers, drugs of abuse (methamphetamine and fentanyl),

120 ultiorgan injury treated with the complement blocker eculizumab.

121 High-dose beta-blockers (eg, 100 mg of metoprolol succinate) administer

122 se inhibitor (GSK2606414) or the translation blocker emetine did not prevent TDP-43 ubiquitylation an

123 re subdivided according to preoperative beta-blocker exposure status.

124 ed in our patient with the addition of an H2-blocker for GERD, or addressing potentially serious unde

125 The development of effective channel blockers for Hv1 can lead to new therapeutics for the tr

126 phenotypes by administering the KATP channel blocker glibenclamide.

127 in Inhibitor] with ARB [Angiotensin Receptor Blocker] Global Outcomes in HFpEF), we assessed the risk

128 ant drug development, including NMDA channel blockers, glycine site agents, and allosteric modulators

129 e tested the effects of the selective I(NaL) blocker GS967 on PVT induction in a transgenic rabbit mo

130 mp inhibitors (PPIs) or histamine-2 receptor blockers (H2RBs) are often prescribed for patients as st

131 deficient ESCs or cells treated with an NFAT blocker had enhanced expression of dickkopf WNT-signalin

132 However, no ghrelin receptor blockers have been administered to heavy alcohol drinkin

133 iple Na(V)1.7-specific and Na(V)1.8-specific blockers have undergone clinical trials, with others in

134 Although immune checkpoint blockers have yielded significant clinical benefits in p

135 e of TRPV4 channels with the selective TRPV4 blocker, HC067047, prevented the loss of endothelial cel

136 were still treated by methotrexate, 3 by TNF-blockers, highlighting long-term Chikungunya-related pat

137 ](i) , as well as by the specific K(Ca) 1.1 blocker iberiotoxin.

138 Despite expectations, immune checkpoint blockers (ICBs) are poorly active in patients with HR(+)

139 ng enzyme) inhibitor or angiotensin receptor blocker if left ventricular ejection fraction <40% and/o

140 tors of a good response to immune checkpoint blockers in independent patient cohorts.

141 y for the Administration of P2Y(12) Receptor Blockers In Non-ST Elevated Acute Coronary Syndromes Wit

142 ng enzyme inhibitors or angiotensin receptor blockers in patients with COVID-19.

143 The necessity of neurohumoral blockers in patients with heart failure who demonstrate

144 imal dose of ACE inhibitors or ARBs and beta blockers in patients with HFrEF.

145 ional therapy (ACE inhibitor or ARB and beta blocker) in patients with chronic HFrEF by making indire

146 ic mechanism of dupilumab, a dual IL-4/IL-13 blocker, in multiple type 2 diseases.

147 reatment with carvedilol, but not other beta-blockers, indeed enhances contractile force in skeletal

148 The response to sodium channel blockers indicates a therapeutic overlap with trigeminal

149 ter ACE inhibitor or angiotensin II receptor blocker initiation was not associated with a lower risk

150 beta-blocker related side effects (ie, beta-blocker intolerance) in 56/64 patients (88%).

151 of the channel-forming toxins with targeted blockers is a promising drug design approach.

152 Immunotherapy using programmed death-1 blockers is a promising modality for non-small cell lung

153 ctivity in vivo in conjunction with the LTCC blocker, isradipine, we find that LTCCs drive differenti

154 ltage-gated L-type Ca(2+) channel (Ca(v)1.2) blockers (LCCBs) are major drugs for treating hypertensi

155 ed breakthrough cardiac events while on beta-blockers, LCSD as 1-time monotherapy for certain patient

156 The angiotensin type 1 receptor blocker losartan could fully inhibit this response.

157 iding the anti-fibrotic angiotensin receptor blocker losartan to mice in drinking water reduced both

158 ndependent predictors for stop/switch of ADP blocker: major surgery, need for oral anticoagulation (O

159 ugs and predicting that dopamine transporter blockers may be an adjunct treatment to reverse antipsyc

160 suggest that dihydropyridine calcium-channel blockers may be associated with reduced risk for Parkins

161 Furthermore, we propose that T-channel blockers may be further explored as a valuable adjunct t

162 ble that the ACE inhibitors and ACE receptor blockers may have the potential to prevent and to treat

163 eculated that renin-angiotensin system (RAS) blockers may promote COVID-19 by increasing ACE2, which

164 e agents and were insensitive to the channel blocker mecamylamine.

165 ticity were tested with application of NMDAR blockers (memantine/D-AP5).

166 Application of the dopamine transporter blocker, methylphenidate, significantly increased dopami

167 We also demonstrated that the TTCC blocker mibefradil induces apoptosis and impairs migrati

168 CGRP pathway blockers might thus aggravate coincidental cerebral isch

169 roundwork for future studies on adapting the blocker molecule for more effective inhibition of Hv1.

170 NMDAR blockers mostly decreased persistent firing associated w

171 support the combination use of an ARNI, beta blocker, MRA, and SGLT2 inhibitor as a new therapeutic s

172 odifying pharmacological therapy (ARNI, beta blocker, MRA, and SGLT2 inhibitor) versus conventional t

173 ensin-aldosterone system inhibitors and beta-blockers, n = 20).

174 ystem inhibitors, n = 20; withdrawal of beta-blockers, n = 20; and withdrawal of renin-angiotensin-al

175 failure medication (angiotensin II receptor blocker neprilysin inhibitor).

176 relaxation, we show that the calcium channel blocker nifedipine and the Rho-kinase inhibitor ROCKi si

177 ere, we found that the L-type Ca(2+) channel blocker nimodipine could hyperpolarize the membrane pote

178 utions against the use of non-selective beta-blockers (NSBB) in patients with refractory ascites or s

179 However, re-initiation of neurohumoral blockers occurred in 17 subjects because of hypertension

180 um) but were blocked by the connexin channel blockers octanol (1 mm) and carbenoxolone (100 mum).

181 bath sodium and application of amiloride, a blocker of ASIC channels, whereas the non-desensitizing

182 e of EPSC block by IEM-1460, an open channel blocker of Ca(2+)-permeable AMPARs, we propose a novel m

183 Leronlimab, a monoclonal antibody blocker of CCR5 originally developed to treat HIV-1 infe

184 Using a selective open channel blocker of CP-AMPARs, IEM-1460, we estimate that ~80% of

185 re to 10 or 25 uM ivabradine-an open channel blocker of HCNs-for 24 h resulted in a dose-dependent hi

186 nce and absence of TAK779, an effective CCR5 blocker of HIV entry.

187 the antioxidant trolox and to nifedipine, a blocker of L-type voltage-dependent Ca(2+) channels (LVD

188 od-brain barrier, thus acting as a selective blocker of peripheral ORs.

189 Barium (Ba(2+)) is a classic permeant blocker of potassium (K(+)) channels.

190 Iscalimab appears to be a promising blocker of the CD40-CD154 costimulatory pathway with pot

191 4-Aminopyridine (4AP) is a specific blocker of voltage-gated potassium channels (K(V)1 famil

192 discovery, we explore glucosylpolyphenols as blockers of Abeta-induced Fyn kinase activation while lo

193 actions, with implications for the design of blockers of chemokine function.

194 nsitive to postsynaptic Ca(2+) chelation and blockers of nicotinic receptors.

195 Blockers of the NMDARs decreased persistent firing assoc

196 Together, our results suggest that TTCC blockers offer a potential targeted therapy in resistant

197 vely insensitive to mammalian Ca(V)2 channel blockers omega-agatoxin-IVA and omega-conotoxin-GVIA and

198 binding free energies of a prototypical Hv1 blocker on a model of human Hv1 in an open state.

199 g enzyme inhibitors and angiotensin receptor blockers on the risk and outcomes of sepsis in patients

200 ntrathecal administration of a KV1.3 channel blocker or a glutaminase inhibitor ameliorated disabilit

201 he effect was seen both when applying a CPT1 blocker or by using a Cpt1a P479L mutant mouse strain.

202 Patients receiving beta-blockers or angiotensin-converting enzyme inhibitors had

203 aldosterone system with angiotensin receptor blockers or angiotensin-converting enzyme inhibitors.

204 f medical treatment is selected, either beta-blockers or nondihydropyridine calcium channel blockers

205 t compared to use of angiotensin II receptor blockers (OR = 0.70, 95% CI 0.54-0.92) or angiotensin-co

206 replicate for beta-blockers, calcium channel blockers, or diuretics.

207 tor blockers, beta-blockers, calcium-channel blockers, or thiazide diuretics and the likelihood of a

208 in (p < 0.001), statin (p < 0.001), and beta-blockers (p = 0.002).

209 ts involving cGMP/cGK axis by repressing CDK blockers p21(Cip1) and p27(Kip1) .

210 The present study examined the role of CDK blockers, p21(Cip1) /p27(Kip1) in the progression of ren

211 ood NK cells, these NKG2A Protein Expression Blockers (PEBLs) abrogated NKG2A expression.

212 ionization source is demonstrated using beta-blockers, peptides, and proteins.

213 The cationic beta-blocker pindolol was injected electrokinetically, and de

214 The beta-blocker positive group had significantly better survival

215 protein phosphatase 1 and decreased by beta-blocker pretreatment.

216 We also found that NMDA receptor channel blocker produced a deficit in prepulse inhibition which

217 (+) impedes the forward translocation of the blocker, provides a powerful avenue to investigate the s

218 ssion and prognosis, and we showed that TTCC blockers reduce migration and invasion rates because of

219 It is unknown if beta-blockers reduce mortality/morbidity in patients with hea

220 We demonstrate that kink blockers reduce the line tension of step edges, which fa

221 otensin-converting enzyme inhibitors or beta-blockers reduce the rate of trastuzumab-induced cardioto

222 Recombinant C1q protein increased while C1q blockers reduced ethanol-induced C3a/b, C4, and membrane

223 cceptable quality of life stemming from beta-blocker related side effects (ie, beta-blocker intoleran

224 m Hg receive more often triple therapy (beta-blocker, renin-angiotensin system inhibitor, and mineral

225 ng enzyme inhibitors or angiotensin receptor blockers requires further investigation.

226 ning signals further correlate strongly with Blocker response times.

227 oton pump inhibitors vs histamine-2 receptor blockers resulted in hospital mortality rates of 18.3% v

228 Celiprolol, a barely studied beta-blocker, revealed the most distinct EFr among all invest

229 es, with no patients on target doses of beta-blocker, sacubitril/valsartan, and mineralocorticoid rec

230 Using six template/blocker scaffolds and the polymerase/dNTPs, the P(1)-gui

231 sequence engineering of the set of template/blocker scaffolds and their coupling to a nicking/polyme

232 A set of four DNA template/blocker scaffolds coupled to the polymerase/dNTP replica

233 set of six appropriately engineered template/blocker scaffolds, coupled to the polymerase/dNTP machin

234 Also, sequence-engineered template/blocker scaffolds, coupled to the polymerase/dNTP machin

235 ddition, by further engineering the template/blocker scaffolds, the hierarchical control over the com

236 cal therapy, mostly beta-adrenergic receptor blockers (specifically, propranolol and nadolol) and sod

237 prevention medications (antiplatelets, beta-blockers, statins, and renin-angiotensin-aldosterone sys

238 ol) and sodium and transient outward current blockers (such as quinidine), or surgical interventions,

239 s, with attention to angiotensin II receptor blockers, such as olmesartan, along with travel historie

240 2) bicuculline (a preferent GABA(A) receptor blocker), suggesting a GABAergic activation induced by O

241 ACE inhibitor ramipril nor the AT1 receptor blocker telmisartan affected lung or kidney ACE2 or TMPR

242 K(V)7.2 in the axons, using the K(+) channel blocker tetraethylammonium ions, we suggest this may exp

243 pecific voltage-gated sodium (Na(V)) channel blocker tetrodotoxin.

244 sensitivity to the highly selective 4D-Na(v) blocker tetrodotoxin.

245 089771 is an aryl sulfonamide Nav1.7 channel blocker that binds to the inactivated state of Nav1.7 ch

246 However, effective TAS2R8 blockers that can either suppress or reduce the bitterne

247 For cationic beta-blockers the theoretical plates achieved in the capillar

248 enzyme inhibitor or angiotensin II receptor blocker therapy and glucose-lowering treatment for at le

249 th FBN1 pathogenic variants who receive beta-blocker therapy and who limit strenuous exercise, aortic

250 ing ACE inhibitor or angiotensin II receptor blocker therapy between January 1, 2007, and December 31

251 ratio [OR], 0.94 [95% CI, 0.69-1.27]), beta-blocker therapy if prior myocardial infarction or left v

252 (Systematic Withdrawal of Neurohumoral Blocker Therapy in Optimally Responding CRT Patients [ST

253 nical study that examines the impact of beta-blocker therapy in patients with dystrophinopathies.

254 ing ACE inhibitor or angiotensin II receptor blocker therapy were matched 1:1 to patients without fol

255 beta-blocker therapy while highly effective for heart failure

256 among 4 groups (continuation of neurohumoral blocker therapy, n = 20; withdrawal of renin-angiotensin

257 ith sequential dilatation and maintenance H2-blocker therapy, she achieved significant symptomatic im

258 enzyme) inhibitor or angiotensin II receptor blocker therapy.

259 a cardiovascular specialist or receive beta-blocker therapy.

260 oxicosis are monitored and treated with beta-blockers to control symptoms given that most of these co

261 r, despite the frequently proposed use of QS blockers to control virulence(8), the mechanisms underly

262 that the administration of immune checkpoint blockers to HIV-infected individuals on ART may facilita

263 KCl and the potassium channel blocker tolbutamide also stimulated primiR-199a2 promote

264 f the 88 carriers, 93% met criteria for beta-blocker treatment and 5/88 (5.7%) were on medications th

265 cal response to adrenergic agonists and beta-blocker treatment.

266 <60-30 mL/min per 1.73 m(2)), for whom beta-blocker trials demonstrate benefit.

267 nced disease than prior angiotensin receptor blocker trials in HCM.

268 survival benefit in patients exposed to beta-blockers undergoing non-cardiac surgery.

269 amined the adjusted association between beta-blocker use (and dose) at 3 years and the cardiovascular

270 ellitus type II (OR, 4.1, P=0.046), and beta-blocker use (OR, 3.8, P=0.049) in univariate regression

271 We used Part D data to calculate beta-blocker use after discharge and beta-blocker use over ti

272 The association between beta-blocker use and outcomes were analyzed using Poisson reg

273 Of the 6893 patients >=65 years age, beta-blocker use at 3 years was 72.2% (n=4980); 43% (n=2162)

274 Preoperative beta-blocker use is strongly associated with improved surviva

275 te beta-blocker use after discharge and beta-blocker use over time.

276 iinflammatory cytokine balance, whereas beta-blocker use was associated with a more proinflammatory c

277 Among patients with HFrEF, beta-blocker use was associated with lower risk of death (adj

278 We first explored associations between beta-blocker use, 5-year death, and the composite of cardiova

279 croalbuminuria, higher mean pulse rate, beta-blocker use, and sustained albuminuria.

280 g enzyme inhibitor use, angiotensin receptor blocker use, BMI z-score for age and sex, and urinary cr

281 e, higher mean systolic blood pressure, beta-blocker use, estimated glomerular filtration rate <60 mL

282 er risk of stroke (1.0% vs 0.5% without beta-blocker use; P = .005) and mortality (3.1% vs 2.3% witho

283 05) and mortality (3.1% vs 2.3% without beta-blocker use; P = .03) and should not be routinely used.

284 g enzyme inhibitors and angiotensin receptor blockers use, was similar between cohorts.

285 We show that phenytoin, a Na channel blocker used clinically for treatment of epilepsy, is a

286 ignificant association was observed for beta-blocker users in advanced CKD with HFpEF (death: 0.88 [0

287 gan failure were significantly lower in beta-blocker users, as were the incidences in postoperative i

288 nhibitor sacubitril and angiotensin receptor blocker valsartan on myocardial remodeling and cardiac p

289 in-aldosterone system inhibitors and/or beta-blockers versus continuation of treatment.

290 ayers' response to hERG ion channel specific blocker was Torsades de Pointes (TdP) reentrant arrhythm

291 patients with advanced CKD, the use of beta-blockers was associated with lower morbidity and mortali

292 Recently, immunotherapy with checkpoint blockers was shown to effectively induce vascular normal

293 roup and in the groups in which neurohumoral blockers were discontinued.

294 cle nicotinic acetylcholine receptor (nAChR) blocker with a significantly lower affinity at the neuro

295 roved pain Losartan, an angiotensin-receptor blocker with anti-fibrotic abilities, recapitulates the

296 potent and selective Cav2.2 calcium channel blocker with proposed antinociceptive action suggesting

297 t of novel genetically encoded Ca(V) channel blockers with unique properties; including, chemo- and o

298 ising member of the family of Ca(2+) channel blockers, with possible application to the inhibition of

299 e the feasibility and safety of neurohumoral blocker withdrawal in patients with normalized ejection

300 However, neurohumoral blocker withdrawal was hampered by cardiac comorbidities