ライフサイエンスコーパス: blocker

1 yme (activator) and turn off the activation (blocker).

2 opyridine, a voltage-gated K(+) (KV) channel blocker.

3 rld and Cmpd-15 is the first allosteric beta-blocker.

4 967, a potent, unconventional sodium channel blocker.

5 tor, or losartan, an angiotensin II receptor blocker.

6 rents inhibited by Psora-4, a KV 1.5 channel blocker.

7 a NEP inhibitor and an angiotensin receptor blocker.

8 arting block phosphate buffer saline-tween20 blocker.

9 ents who have never received calcium channel blockers.

10 suggesting that the hydride anions act as pi-blockers.

11 antagonist or various nitric oxide synthase blockers.

12 ed survival of patients on nonselective beta-blockers.

13 egardless of heart rhythm or receipt of beta-blockers.

14 an "agonist" in functional screens for VGSC blockers.

15 protective effect of angiotensin II receptor blockers.

16 ial likelihoods of receiving calcium channel blockers.

17 ee solutions and divalent cation Cav channel blockers.

18 d peptide-nucleic acid (PNA) oligonucleotide blockers.

19 ng enzyme inhibitors or angiotensin receptor blockers.

20 psies and lack of response to sodium channel blockers.

21 analyzed, 18.6% of whom used calcium channel blockers.

22 The potassium channel blocker 4-aminopyridine reliably induces seizure-like ev

23 guinea pig brain with the potassium channel blocker 4-aminopyridine.

24 diphenylphosphine oxide-1 and the KV1.3/1.5 blocker 5-(4-phenylbutoxy)psoralen reduced H2O2-elicited

25 kers (66% versus 68%; P=0.04) and early beta-blockers (56% versus 60%; P=0.01).

26 rting enzyme inhibitors/angiotensin receptor blockers (66% versus 68%; P=0.04) and early beta-blocker

27 locking the Nav1.8 channel with its specific blocker A-803467 in the LSG reduces sympathetic activity

28 Bisindolylmaleimide (BIM; a protein kinase C blocker), a protein kinase C inhibitory peptide or bafil

29 Pre-treatment of TG-con rats with the ETA blocker ABT-627 for 1 week prior to tunicamycin injectio

30 ic tone and modulated by treatment with beta-blockers; acute afterload stress induces a deeper impair

31 giotensin receptor blockers [ARBs], and beta-blockers adjusted for blood pressure, statins adjusted f

32 The exposure of interest was beta-blocker administration initiated during the hospitalizat

33 on was eliminated by splenectomy, ganglionic-blocker administration or beta2-adrenergic receptor bloc

34 Exposure to beta-blockers after TBI was associated with a reduction of in

35 ared with placebo plus beta-blocker and beta-blocker alone.

36 no active therapy in 47 (8%) patients, beta-blockers alone in 350 (58%) patients, implantable cardio

37 in A53T mutant or dopamine transporter (DAT) blockers also differentially affects the dopamine output

38 Treatment with the epithelial Na(+) channel blocker amiloride, improving airway surface hydration an

39 ants (five antibiotics, an herbicide, a beta-blocker, an antidepressant, and an antineoplastic) frequ

40 rescriptions included male sex, filling beta-blocker and antiplatelet agent prescriptions, and attend

41 ing exercise compared with placebo plus beta-blocker and beta-blocker alone.

42 d in the presence of the Na(+)/H(+) exchange blocker and micropinocytosis inhibitor amiloride, sugges

43 gate the association between the use of beta-blockers and 1-year mortality.

44 of compounds varying in polarity, such as UV blockers and biocide compounds in water, and the data we

45 ith obstruction is medical therapy with beta-blockers and calcium antagonists.

46 ommended treatment to prevent VRB using beta-blockers and ligation.

47 ere more commonly prescribed calcium channel blockers and long-acting nitrates at discharge (DM versu

48 We obtained information about use of beta-blockers and other medications through linkage with the

49 randomized controlled trials comparing beta-blockers and placebo.

50 25.5% [P=0.01], respectively), whereas beta-blockers and ranolazine were prescribed at similar rates

51 angiotensin II receptor blockers (ARB), beta-blockers and statins are recommended after acute myocard

52 ng enzyme inhibitors or angiotensin-receptor blockers and statins), and adverse clinical outcomes (em

53 at disease onset, response to sodium channel blockers and the functional properties of mutations in c

54 ciation between prior use of calcium channel blockers and the outcome of patients admitted to the ICU

55 : synergistic combination of selective TRPV4 blockers and vasoinhibins can be proposed to mitigate di

56 tolbutamide and glibenclamide (KATP channel blockers), and diazoxide (KATP channel opener).

57 nt thermal environment), pharmacologic (beta-blockers), and genetic (beta2-AR knockout mice) to reduc

58 ge-conductance Ca(2+)-activated K(+) channel blocker, and by 4-aminopyridine, a voltage-gated K(+) (K

59 d by selective UTR antagonist, TRPC4 channel blocker, and CaMKII and CREB-binding protein/p300 inhibi

60 tipsychotic drugs, selective calcium channel blockers, and antiepileptics.

61 rting enzyme inhibitors/angiotensin receptor blockers, and beta-blockers, respectively.

62 hibitors/angiotensin receptor blockers, beta-blockers, and dual antiplatelet therapy, respectively.

63 hibitors/angiotensin receptor blockers, beta-blockers, and dual antiplatelet therapy.

64 lockers, thiazide diuretics, calcium channel blockers, and metformin.

65 , angiotensin receptor blockers (ARBs), beta blockers, and mineralocorticoid receptor antagonists, an

66 ibitors, angiotensin-receptor blockers, beta-blockers, and mineralocorticoid-receptor antagonists.

67 fs in adherence to ACE inhibitors/ARBs, beta-blockers, and statins on survival among older people aft

68 prescriptions for ACE inhibitors/ARBs, beta-blockers, and statins, and survived >/=180 days after AM

69 Moreover, although the SK blocker apamin (200 nm) strengthened the input-output fu

70 Moreover, the SK channel blocker apamin enhanced the input-output function in sha

71 Inhibition of SK channels with the specific blocker apamin prolonged action potentials (APs) in isol

72 king glutamate reuptake with TBOA and the Sk blocker apamin, only 4-aminopyridine increased the frequ

73 ere inhibited by pretreatment with the ASIC3 blocker APETx2 and enhanced by pretreatment with the ASI

74 e inhibitors (ACEI) and angiotensin receptor blockers (ARB) doses on outcomes in patients with heart

75 zyme inhibitors (ACEI), angiotensin receptor blockers (ARB), beta-blockers (BB), mineralocorticoid re

76 yme (ACE) inhibitors/angiotensin II receptor blockers (ARB), beta-blockers and statins are recommende

77 The use of angiotensin receptor blockers (ARBs) correlates with reduced onset and progre

78 nzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta blockers, and mineralocorticoid re

79 yme inhibitors [ACEIs], angiotensin receptor blockers [ARBs], and beta-blockers adjusted for blood pr

80 ut heart failure (HF), it is unclear if beta-blockers are associated with reduced mortality.

81 Angiotensin II receptor blockers are beneficial in patients with acquired left v

82 Thus, current life-prolonging beta-blockers are contraindicated in patients with both heart

83 RSV entry blockers are in clinical trials, but escape mutations ch

84 uggest that the molecular effects of beta-AR blockers are not based on a modulation of CaMKII.

85 l by NK cells, demonstrating that checkpoint blockers are not only applicable to enhance T cell-media

86 renergic receptor antagonists, known as beta-blockers, are amongst the most prescribed drugs in the w

87 rity, among users of angiotensin II receptor blockers, as compared to non-users, we used multivariabl

88 ns the mechanism of action of several KCa3.1 blockers at the molecular level and could be used for st

89 ibitor/angiotensin receptor blocker, or beta-blocker) at baseline; these patients had 33% lower HF ho

90 red in the presence of the vesicle-refilling blocker bafilomycin indicated that spontaneous and evoke

91 n2 levels, which were rescued with mitophagy blocker, bafilomycin, in FECD.

92 ), angiotensin receptor blockers (ARB), beta-blockers (BB), mineralocorticoid receptor antagonists (M

93 ell-known anti-migraine calcium channel (CC) blocker - being able to diminish intracellular Angpt-2 p

94 thought to be harmful in HF, beta-adrenergic blockers (beta-blockers) have consistently been shown to

95 rting enzyme inhibitors/angiotensin receptor blockers, beta-blockers, and dual antiplatelet therapy,

96 rting enzyme inhibitors/angiotensin receptor blockers, beta-blockers, and dual antiplatelet therapy.

97 ting-enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, and mineralocorticoid-receptor

98 tment with statins, renin-angiotensin system blockers, beta-blockers, dual antiplatelet therapy, and

99 nzyme inhibitors and angiotensin II receptor blockers, beta-blockers, thiazide diuretics, calcium cha

100 f hypertrophied myocytes to the Orai channel blocker BTP2 caused a reduction of AP duration and reduc

101 inflammatory effect of tumor necrosis factor blockers, but a 52-week study conducted by Bissonnette a

102 ting enzyme inhibitors, angiotensin-receptor blockers, calcium channel blockers, or beta blockers) wa

103 imental studies suggest that calcium channel blockers can improve sepsis outcome.

104 urally distinct T-type - but not L-type - CC blockers can suppress Angpt-2.

105 .7-selective, state-dependent sodium-channel blocker, can be administered at therapeutic doses withou

106 n, and could be inhibited by the ion channel blocker, capsazepine.

107 uralgia is treatment with the sodium channel blockers carbamazepine and oxcarbazepine, which although

108 Furthermore, beta-blocker carvedilol-mediated beta-arrestin-dependent ERK

109 ciated with long-term use of calcium channel blockers (CCBs) or angiotensin-converting enzyme inhibit

110 m of action of nifedipine, a calcium-channel blocker clinically used in patients with cardiovascular

111 Further, a good response to sodium channel blockers clinically was found to be associated with a re

112 impact of 3 generic angiotensin II receptor blockers commercialization on adverse events: hospitaliz

113 ity was lower for patients who received beta-blockers compared with those who did not (4.9% vs. 11.2%

114 Addition of carbenoxolone, a PANX1 channel blocker, completely abolished ATP release in Calhm1 knoc

115 Frequency of administration of H1 and H2 blockers, corticosteroids, and epinephrine was similar i

116 el), which is a tumour necrosis factor alpha blocker currently used to treat rheumatoid arthritis.

117 In contrast, estrogen receptor blocker did not affect BMP2 action.

118 Polymyxin B, an LPS blocker, did not affect ESAT-6 stimulated macrophage IL-

119 The selective KV1.5 blocker diphenylphosphine oxide-1 and the KV1.3/1.5 bloc

120 rtantly, human HF subjects receiving beta1AR-blockers display elevated circulating S1P levels, confir

121 the overhang sequence and the complementary blocker DNA, which consequently leads to the recovery of

122 n then be turned off through addition of the blocker dodecyl sulfate.

123 by combining effects of a hormone and a hERG blocker, dofetilide, or hERG mutations.

124 tolerance and the evidence behind using beta-blocker dose and heart rate as therapeutic targets.

125 e been stable on a "maximally tolerated beta-blocker dose," but this definition and how to achieve it

126 more commonly were not receiving target beta-blocker dose.

127 ins, renin-angiotensin system blockers, beta-blockers, dual antiplatelet therapy, and long-term cardi

128 03, in contrast to the reduced effect of IKr blocker E-4031.

129 sence of the IKs blocker JNJ-303 and the IKr blocker E-4031.

130 ee solutions and divalent cation Cav channel blockers, eliminate the outwardly rectifying current, wh

131 aining the properties of MK-801 binding site blockers, exert microtubules stabilizing properties, and

132 We have previously shown that Wnt pathway blockers exhibit potent combinatorial activity with taxa

133 ecific sodium, potassium and calcium channel blockers for their ability to improve the efficacy of Me

134 vented with the non-selective cation channel blocker Gadolinium (Gd(3+)).

135 ine mRNA expression were blocked by the Cx43 blockers Gap26 and carbenoxolone.

136 In the presence of ML297 or the G-protein blocker GDP-beta-S, DA induced a further decrease in spi

137 bolish high-affinity sensitivity to the KATP blocker glibenclamide in both intact cells and excised p

138 We used the new Kv2 blocker Guangxitoxin-1E (GTx) to study Kv2 functions in

139 We used the new Kv2 blocker Guangxitoxin-1E (GTx; 10-100 nm) in rat brain sl

140 rs of PPIs (n = 105,305) and new users of H2 blockers (H2B; n = 9578); data on renal outcomes were co

141 and patients receiving angiotensin receptor blocker had higher plasma Ang II with lower Ang-(1-7) le

142 In contrast, the Kir7.1 blocker had no effect on the ex-vivo isolated mouse reti

143 Beta-blockers had no effect on mortality in patients with AF

144 t Valsartan (Val) as an angiotensin receptor blocker has renoprotective effects, but the molecular me

145 Use of calcium channel blockers has been found to improve sepsis outcomes in an

146 ; however, current clinically available beta-blockers have poor selectivity for the cardiac beta1-adr

147 armful in HF, beta-adrenergic blockers (beta-blockers) have consistently been shown to reduce mortali

148 es mellitus and anemia, be treated with beta-blockers, have higher ejection fraction, relative wall t

149 tion were antagonized by the selective TRPV4 blocker HC 067047.

150 a significant mortality advantage with beta-blockers; however, quality of evidence is very low.

151 patients in sinus rhythm randomized to beta-blockers (HR: 0.73 vs. placebo; 95% CI: 0.67 to 0.79; p

152 Immune checkpoint blockers (ICB) have become pivotal therapies in the clin

153 shed reports on the mechanisms by which beta-blockers improve clinical outcomes.

154 To determine if beta-(beta)-blockers improve outcomes after acute traumatic brain in

155 4161, a potent MEK1/2 inhibitor, is an HIF-1 blocker in Ang II-treated VSMC.

156 e strategic use of clinically available beta-blockers in patients to improve responses to immunothera

157 m repressors of miR-1 as treatment with beta-blockers in pressure-overloaded mouse hearts prevented i

158 ize the current knowledge on the use of beta-blockers in pulmonary hypertension.

159 t differential increases in the PDC for beta-blockers in the 2012 entry cohort (adjusted differential

160 p containing G604 or with common TdP-related blockers in the intra-cavity binding site.

161 By analogy with the key role of beta-blockers in the management of left heart failure, some a

162 afety of adjunctive lanicemine (NMDA channel blocker) in the treatment of major depressive disorder (

163 vement disorder induced by dopamine receptor blockers, including antipsychotics.

164 Although beta-blockers increase survival in patients with heart failur

165 ollowing a potentially toxic calcium channel blocker ingestion (1D); 2) as first-line therapies (prio

166 Guangxitoxin, a Kv2 blocker, inhibited the whole-cell current by approximate

167 account for limited/null efficacy in beta1AR-blocker-insensitive HF subjects.

168 ype of surgery, and preoperative use of beta-blockers, intra-aortic balloon pump, or catecholamines.

169 etermines whether the use of calcium channel blockers is associated with a decreased risk of mortalit

170 stress, for which current therapy with beta-blockers is incompletely effective.

171 One family of potential autophagy blockers is the quinoline-derived antimalarial family, i

172 o 20 mum nifedipine, a l-type Ca(2+) channel blocker, is sufficient to trigger RRP but not SRP exocyt

173 he rate-lowering effect of the HCN selective blocker, ivabradine, was significantly correlated with t

174 durations (APDs) in the presence of the IKs blocker JNJ-303 and the IKr blocker E-4031.

175 on significantly augmented the effect of IKs blocker JNJ-303, in contrast to the reduced effect of IK

176 Other NMDA open channel blockers ketamine and memantine showed a similar effect.

177 Further, the AT1 R blocker losartan (1 mum) diminished myogenic tone and bl

178 mulations of the angiotensin type 1 receptor blockers losartan and valsartan and the angiotensin-conv

179 C and had a greater impact than did the CCR5 blocker maraviroc, confirming the use of CXCR6 in primar

180 s to investigate mechanisms by which channel blockers may distinguish NMDAR subpopulations.

181 Moreover, antiepileptics and calcium channel blockers may provide repurposing opportunities.

182 or the clinically used broad-spectrum Panx1 blockers, mefloquine or probenecid, suppressed ATP relea

183 ansgenic mice were treated with the beta1-AR blocker metoprolol (270 mg/kg*d).

184 ndicates that use of angiotensin II receptor blockers might be associated with a lesser risk of acute

185 Experiments with the use-dependent NMDAR blocker, MK-801, indicate that potentiated NMDARs reside

186 Here, we used a newly identified Sec61 blocker, mycolactone, to analyze Sec61's contribution to

187 Patients who used beta-blockers (n = 522) had a lower cancer-specific mortality

188 Infusion of the CP-AMPAR-specific blocker Naspm into the NAc shell reversed the cocaine an

189 Combined angiotensin receptor blocker neprilysin inhibitors (ARNIs) have been associat

190 ive sensitivity to the l-type Ca(2+) channel blocker nifedipine.

191 By creating a competitive peptide blocker of AP-2-Slack binding, we demonstrated that this

192 and competes with that by amiloride, a pore blocker of ASICs.

193 lux was inhibited by MK-801, a specific pore blocker of N-Methyl-D-aspartic acid receptor (NMDAR) cha

194 interesting lead compound for high-affinity blockers of ASICs.

195 in the presence of bumetanide and amiloride (blockers of electroneutral Na(+) movement), the action p

196 The PD neuron MPR is sensitive to blockers of H- (IH) and calcium-currents (ICa).

197 r antiseizure agents and identifying channel blockers of interest to insecticide discovery or biosecu

198 agonists of D2R, antagonists of 5-HT6R, and blockers of SERT.

199 ified trihydroxyphenolic compounds as potent blockers of TGF-beta1 responses (IC50 50 nM), Snail1 ex

200 Small molecule mitochondrial import blockers of the Carla Koehler laboratory (MB)-10 inhibit

201 its receptor and persists in the presence of blockers of VIP, GABA or neuronal firing.

202 Treatment of TBI patients with beta-blockers offers a potentially beneficial approach.

203 rting enzyme inhibitors/angiotensin receptor blockers on outcome in patients with MINOCA, a trend tow

204 The effect of angiotensin II receptor blockers on right ventricular (RV) function is still unk

205 pathway, and IWP2, a wide action Wnt signal blocker, on the growth and differentiation of the limbal

206 type (P=0.421) were receiving selected beta-blockers, only 58.8% and 67.3% (P<0.001) were on >50% of

207 nsducer current, via pharmacological channel blockers or disruption of tip links, leads to stereocili

208 erting enzyme inhibitor/angiotensin receptor blocker, or beta-blocker) at baseline; these patients ha

209 arget actions of Cd(2+), a nonselective VACC blocker, or other variations in experimental conditions.

210 giotensin-receptor blockers, calcium channel blockers, or beta blockers) was significantly better tha

211 = -0.43, P = 0.003), and treatment with beta-blockers (P = 0.001).

212 ,2-a]pyridine class of K(+)-competitive acid blockers (P-CABs), have potential application as acid-su

213 was eliminated by the selective BKCa channel blocker paxilline (100 nm), iberiotoxin (10 mum), Ca(2+)

214 BKCa channel blockers paxilline and iberiotoxin, as well as Ca(2+) fr

215 as 4-aminopyridine, but the selective KV1.3 blocker phenoxyalkoxypsoralen-1 was without effect.

216 The channel blockers picrotoxin, fipronil, and tetramethylenedisulfo

217 ent approach for adults with calcium channel blocker poisoning.

218 iously unrecognized mechanism by which beta1-blockers prevent HF progression in patients with ischemi

219 ressing Hybrid toxin and AaIT (Na(+) channel blocker) produced synergistic effects, requiring 45% few

220 a placebo or the noradrenergic beta-receptor blocker propranolol (40 mg).

221 and enhanced by pretreatment with the ASIC1a blocker psalmotoxin-1.

222 eurons with the intracellular sodium channel blocker QX-314 also disrupted premotor rhythms, as did b

223 beta-Blockers reduce mortality and improve symptoms in people

224 Beta-blockers reduced ventricular rate by 12 beats/min in bot

225 Ranolazine, a late Na(+) current blocker, reduced the electromechanical dysfunction of hu

226 t of GERD include potassium-competitive acid blockers, reflux-reducing agents, bile acid binders, inj

227 or beta-adrenergic antagonists, such as beta-blockers, relatively little is yet known about its regul

228 systemic corticosteroid and calcium channel blocker, remarkable improvement was noticed after the in

229 542 (96.4%) and 81,933 (93.2%) received beta-blockers, respectively.

230 tors/angiotensin receptor blockers, and beta-blockers, respectively.

231 In both groups, HVPG and acute beta-blocker response were evaluated at baseline and HVPG mea

232 cardiac surgery (n=12) treated with beta-AR blockers revealed no difference in CaMKII activity when

233 icular Zn(2+) transporter, ZnT3) and channel blockers revealed substantial differences in relevant Zn

234 ith cholinergic receptor muscarinic (ChRM)-3 blocker reversed the progression of AHR in the neonatal

235 RPV1, TRPC3 or TRPC6, nor by the TRP channel blocker Ruthenium Red.

236 ment of ProTx II (a selective Nav1.7 channel blocker)-sensitive sodium currents.

237 enzyme inhibitor or an angiotensin receptor blocker, should generally be included in the pharmacolog

238 of patients with CPVT, flecainide plus beta-blocker significantly reduced ventricular ectopy during

239 , diuretics, stimulants, narcotics, and beta-blockers) spiked in human urine and plasma samples.

240 icial effects of angiotensin type 1 receptor blockers, suggesting a role for angiotensin subtype 2 re

241 optosis as did treatment with the purinergic blocker suramin.

242 Three chemically diverse ERG channel blockers (terfenadine, ErgToxin-1, and E-4031) abolished

243 after 48 h silencing with the Na(+) channel blocker tetrodotoxin.

244 ly useful NMDA receptor (NMDAR) open channel blockers that inhibit NMDARs with similar potency and ki

245 ns actively initiating and up-titrating beta-blockers that may aid in achieving maximally tolerated d

246 and in vivo using glucose, nifedipine (VDCC blocker), the sulfonylureas tolbutamide and glibenclamid

247 to beta-blocker therapy is superior to beta-blocker therapy alone for the prevention of exercise-ind

248 l cohort study, preadmission calcium channel blocker therapy before sepsis development was associated

249 Patients who responded to calcium channel blocker therapy had metabolic profiles similar to those

250 osed to therapeutic levels and added to beta-blocker therapy is superior to beta-blocker therapy alon

251 est while receiving maximally tolerated beta-blocker therapy that was continued throughout the trial.

252 s and angiotensin II receptor blockers, beta-blockers, thiazide diuretics, calcium channel blockers,

253 on-steroidal mineralocorticoid receptor (MR) blocker, through two experimental protocols: In Protocol

254 r the stepwise management of calcium channel blocker toxicity.

255 This idea was tested by applying the pore blocker toxin maurocalcine on the cytoplasmic side of Ry

256 MKII activity when compared with non-beta-AR blocker-treated patients.

257 ompassing 2005 unique TBI patients with beta-blocker treatment and 6240 unique controls.

258 Angiotensin receptor blocker treatment may blunt the harm associated with hig

259 e investigated the effect of chronic beta-AR blocker treatment on CaMKII activity in human and experi

260 The lack of CaMKII modulation by beta-AR blocker treatment was confirmed in healthy wild-type mic

261 CA, a trend toward a positive effect of beta-blocker treatment, and a neutral effect of dual antiplat

262 ts who can benefit from angiotensin receptor blocker treatment.

263 o explore the impact of angiotensin receptor blocker treatment.

264 s, of which, 19,742 received calcium channel blocker treatments prior to the admission.

265 Superfusion of SKCa and IKCa channel blockers UCL 1684 + TRAM 34 attenuated ROV, implicating

266 ing enzyme inhibitor or angiotensin receptor blocker usage were not significantly different.

267 week, 561 [52.8%]; P < .001), and lower beta-blocker use (73 [6.9%]; P < .001) compared with lower qu

268 ortality between those with and without beta-blocker use (average treatment effect [ATE] coefficient:

269 as to determine the association between beta-blocker use and mortality in patients with AMI without H

270 The association between calcium channel blocker use and sepsis outcome was determined by multiva

271 sed (hazard ratio: 2.46; p = 0.011) and beta-blocker use diminished (hazard ratio: 0.36; p = 0.004) r

272 ncer-specific mortality associated with beta-blocker use during the 90-day period before cancer diagn

273 onal outcome, and quality of life after beta-blocker use for TBI.

274 Prior calcium channel blocker use is associated with reduced mortality in pati

275 Although systemic beta-blocker use was associated with lower IOP and systemic A

276 Systemic beta-blocker use was independently associated with an IOP of

277 ing enzyme inhibitor or angiotensin receptor blocker use, and nonsmoking status-was evaluated among 1

278 baseline differences between calcium channel blocker users and nonusers, a propensity score matched c

279 erse events for 1000 angiotensin II receptor blocker users before and after generic commercialization

280 ohort (20.2% vs 32.9% in non-calcium channel blockers users; p = 0.009) and in multivariate analysis

281 Use of calcium channel blocker was associated with a reduced 30-day mortality a

282 ine the influence of healthy user bias, beta-blocker was used as an active comparator.

283 Chronic treatment with angiotensin receptor blockers was associated with better control of systolic

284 Prior use of calcium channel blockers was associated with improved 30-day survival in

285 rols, current use of angiotensin II receptor blockers was followed by a decreased risk of acute pancr

286 We find that the use of sodium channel blockers was often associated with clinically relevant s

287 blockers, calcium channel blockers, or beta blockers) was significantly better than thiazides and th

288 the EPA approved Hybrid (Ca(++)/K(+) channel blocker), was studied for pre-lethal effects.

289 bor mechanotransducer channels, recover upon blocker washout or tip link regeneration and can be repl

290 All four BTK blockers were found to inhibit anti-IgE-induced histamin

291 LTCC blockers were neuroprotective in mouse neurotoxin models

292 In contrast, sodium channel blockers were rarely effective in epilepsies with later

293 Recently, VACC blockers were reported to reduce spontaneous release of

294 Of the two, PNA blockers were the only efficient blocking strategy, allo

295 ins some of the side effects elicited by D2R blockers when used in neurological and psychiatric condi

296 ics the hypertrophy seen with broad TGF-beta blockers, while avoiding the adverse effects due to inhi

297 These PNA blockers will facilitate taxonomic profiling of the euka

298 or the development of selective inflammasome blockers with potential therapeutic benefit in a wide ra

299 eening approaches to identify activators and blockers with strong, specific binding for engineering a

300 ng enzyme inhibitors or angiotensin receptor blockers with well controlled BP and eGFR<90 ml/min per