ライフサイエンスコーパス: blocking agent

1 eous breathing (prevented by a neuromuscular blocking agent).

2 ded medications (aspirin and beta-adrenergic blocking agents).

3 id DCs that secrete the potent costimulation blocking agent.

4 hexamethonium (10 mg/kg, i.v.), a ganglionic blocking agent.

5 DS and had been treated with a neuromuscular blocking agent.

6 ses the impact of a cell cycle mitotic phase blocking agent.

7 d without injecting pharmacologic doses of a blocking agent.

8 d, or when using bovine serum albumin as the blocking agent.

9 FU/ml was achieved when 2% BSA was used as a blocking agent.

10 th myasthenia gravis receiving neuromuscular-blocking agents.

11 in a 1: 1 ratio with steroidal neuromuscular blocking agents.

12 lmonary fibroblasts were incubated with CTGF blocking agents.

13 ors are affected by the use of neuromuscular blocking agents.

14 ectively encapsulate steroidal neuromuscular blocking agents.

15 anslate these insights into prototypical DQ2 blocking agents.

16 ing different non-depolarizing neuromuscular blocking agents.

17 eiving continuous infusions of neuromuscular-blocking agents.

18 r nonresponders (n = 12) to therapy with TNF blocking agents.

19 may affect the outcome of treatment with TNF blocking agents.

20 nor the varying properties of different TNF-blocking agents.

21 xtracellular ion concentrations or potential blocking agents.

22 anding barriers to the effective use of beta-blocking agents.

23 , are relevant for the design of therapeutic blocking agents.

24 lity to block this passage with gap junction blocking agents.

25 channel in the context of ion permeation and blocking agents.

26 tubation in patients receiving neuromuscular-blocking agents.

27 ination with variable doses of neuromuscular blocking agents.

28 heart failure patients with beta-adrenergic blocking agents.

29 continuation of treatment with neuromuscular blocking agents.

30 ceiving continuous infusion of neuromuscular-blocking agents.

31 nt as demonstrated by studies with secretion blocking agents.

32 surgery or were treated with calcium channel blocking agents.

33 pha-2 adrenergic agonists or beta adrenergic blocking agents.

34 , shared to some extent with calcium channel blocking agents.

35 ing the treatment of heart failure with beta-blocking agents.

36 atients receiving infusions of neuromuscular-blocking agents.

37 g continuous administration of neuromuscular-blocking agents.

38 retion led to successful treatment with IL-1-blocking agents.

39 reaction, importantly, without the need for blocking agents.

40 who are increasingly treated with complement blocking agents.

41 ut beta-blockers or renin-angiotensin system blocking agents.

42 nts associated with the use of neuromuscular blocking agents.

43 respond dramatically to treatment with IL-1 blocking agents.

44 80 mg/dL in patients receiving neuromuscular-blocking agents.

45 , 2% BSA in 1.0 x 10-2 M, pH 7.4, PBS as the blocking agent, 0.5 mL/h as the sample flow rate, 1.0 x

46 han long-acting intraoperative neuromuscular blocking agents (1 RCT) reduce risk.

47 Paradoxically, the potassium channel blocking agent 4-aminopyridine (4AP) can sometimes cause

48 001) and more often received beta-adrenergic blocking agents (49% vs. 14%, p < 0.0001).

49 BALB/c mice were given small molecule GRP blocking agent 77427, or GRP blocking antibody 2A11, bef

50 ng enzyme inhibitors or angiotensin receptor blocking agents 85.3% versus 77.4% (AOR, 1.62; 95% CI, 1

51 of xemilofiban, an oral platelet GP IIb/IIIa blocking agent, administered to patients after percutane

52 col should include guidance on neuromuscular-blocking agent administration in patients undergoing the

53 or the subset of patients on beta-adrenergic blocking agents after CABG, there was a trend toward les

54 Encouraging early clinical results using blocking agents against components of the PD-1 pathway h

55 s corticosteroids and neuromuscular junction-blocking agents, although the exposure to the latter dru

56 e, treatment with the interleukin-1 receptor blocking agent anakinra 100 mg/d was started.

57 myocarditis with the interleukin-1 receptor blocking agent anakinra.

58 sociation between receipt of a neuromuscular blocking agent and in-hospital mortality among mechanica

59 alcium channel blockers if already on a beta-blocking agent and rate-limiting calcium channel blocker

60 Whether the type of neuromuscular blocking agent and the duration of use are important det

61 (age 4 months), treated with a neuromuscular blocking agent and ventilated: control, hyperoxia-treate

62 dical treatments, including alpha-adrenergic blocking agents and 5 alpha-reductase inhibitors mean th

63 Without their use, dosing of neuromuscular blocking agents and anticholinesterases is often inappro

64 derivatives can be ablated by Ca(2+)-channel blocking agents and by the calcium chelator 1,2-bis(o-am

65 The newer vasodilating beta-blocking agents and calcium antagonists appear to be met

66 treatment with nondepolarizing neuromuscular blocking agents and corticosteroids in the intensive car

67 Using both CTLA-4/B7-blocking agents and CTLA-4-deficient T cells, we found t

68 lth outcomes associated with beta-adrenergic blocking agents and diltiazem treatment for unstable ang

69 als (n = 23) using pretreatment with various blocking agents and doses.

70 amined the association between neuromuscular blocking agents and ICU-acquired weakness, critical illn

71 The relationship between neuromuscular blocking agents and neuromuscular dysfunction acquired i

72 s a modest association between neuromuscular blocking agents and neuromuscular dysfunction acquired i

73 ot show an association between neuromuscular blocking agents and neuromuscular dysfunction acquired i

74 mice were simultaneously exposed to activity-blocking agents and neurotrophins for 2 weeks.

75 lso associated with the use of neuromuscular blocking agents and prolonged mechanical ventilation, su

76 ous ELISA assay involves multiple steps with blocking agents and secondary reporters that ultimately

77 elationship between the use of neuromuscular blocking agents and skeletal muscle weakness.

78 l the potential use of porins as targets for blocking agents and suggest that polyamines may act as e

79 is of the different orders of potency of the blocking agents and the differential response to 1-EBIO

80 been proposed based on the use of molecular blocking agents and transgenic animals to elucidate dise

81 7 years) who were not taking beta-adrenergic blocking agents and were referred for symptom-limited ex

82 operitoneal fibrosis include the use of beta-blocking agents, and connective tissue disease processes

83 Amiodarone, sedation, sodium channel-blocking agents, and ventricular pacing were effective i

84 acologic probes (lidocaine [a sodium channel blocking agent] and cesium [an outward potassium channel

85 The use of aspirin, beta-adrenergic blocking agents, angiotensin-converting enzyme inhibitor

86 Does nurse-led titration of beta-adrenergic blocking agents, angiotensin-converting enzyme inhibitor

87 Neuromuscular blocking agents are commonly used in critical care.

88 capability when aspirin and beta-adrenergic blocking agents are given appropriately and transfer is

89 Neuromuscular blocking agents are routinely used in the operating room

90 Although currently available Notch-blocking agents are showing anti-tumor activity in precl

91 beta-Blocking agents are the mainstay of treatment.

92 nd protocols could ensure that neuromuscular blocking agents are used and monitored appropriately.

93 Beta-adrenergic blocking agents are used in most patients for symptomati

94 s problem, many protein and surfactant-based blocking agents are used.

95 data prompt the future development of an FSH-blocking agent as a means of uncoupling bone formation a

96 r patients with AMI, such as beta-adrenergic blocking agents, aspirin and immediate reperfusion thera

97 al variable found receipt of a neuromuscular blocking agent associated with a 4.3% (95% CI, -11.5%, 1

98 ethylmethanethiosulfonate (AEMTS) as a thiol-blocking agent at 25 degrees C and pH 8.0.

99 to a peripheral site of action of the nAChR-blocking agents at the neuromuscular junction (NMJ), bec

100 bility of four nondepolarizing neuromuscular blocking agents (atracurium, gallamine, metocurine, and

101 was to assess the effect of the inflammasome blocking agents BAY 11-7082 (30 mg/kg, i.p.) and Brillia

102 1) We suggest that a neuromuscular-blocking agent be administered by continuous intravenous

103 ests that a reduced dose of an neuromuscular-blocking agent be used for patients with myasthenia grav

104 10) We suggest that neuromuscular-blocking agents be discontinued at the end of life or wh

105 linical practice suggests that neuromuscular-blocking agents be discontinued prior to the clinical de

106 ctic ester, followed by incorporation of the blocking agent bovine serum albumin.

107 tan, and intravenous injection of a ganglion blocking agent, but not an arginine vasopressin V1 recep

108 ated by hexamethonium, an autonomic ganglion blocking agent, but was abolished by CGRP-(8-37), an ant

109 (23%) who were treated with a neuromuscular blocking agent by hospital day 2.

110 of concomitant medications (beta-adrenergic blocking agents, calcium channel blocking agents or digo

111 A/1LacJ mice that were administered the CD80 blocking agents, called CD80-binding competitive antagon

112 nhibit DC maturation, whereas co-stimulation-blocking agents can also promote the induction of antige

113 luorescent dyes, the presence of these toxic blocking agents can be observed as a decrease in fluores

114 Here we show that transcription-blocking agents can induce phosphorylation of the Ser-15

115 Sodium channel blocking agents can provide effective protection of axon

116 demonstrate that treatment with inflammasome-blocking agents can significantly reduce the development

117 +, Sr2+, Mg2+, and La3+) and by gap junction blocking agents (carbenoxolone, octanol, heptanol, flufe

118 studies with the alpha- and beta-adrenergic blocking agent carvedilol demonstrated a significant sur

119 The third-generation beta-blocking agent carvedilol has substantially different ef

120 he use of nondihydropyridine calcium channel blocking agents (CCBs) appears to reduce reinfarction in

121 tudy, we report the efficacy of a novel CD80-blocking agent CD80-competitive antagonist peptide (CD80

122 e the first evidence that a cyclooxygenase 2 blocking agent, celecoxib, possesses strong chemoprevent

123 ffects of the potent selective 5-HT reuptake blocking agent, citalopram (10 mg/kg, i.v.), on local ce

124 However, N-ethylmaleimide, a thiol-blocking agent, completely eliminated its formation.

125 kness and included charges for neuromuscular blocking agents, continuous mechanical ventilation, ICU

126 perative administration of the costimulatory blocking agent CTLA4 immunoglobulin exhibited >100-day s

127 kg), together with the B7-CD28 costimulation blocking agent CTLA4Ig, 7 days before renal transplantat

128 Because most of the familiar Ca2+ channel blocking agents currently used in cardiology, such as ni

129 Dose-response studies with a translational blocking agent demonstrate that the cellular oxidative r

130 genation improved by beta-blockade and beta1-blocking agent did offset the adverse effect of epinephr

131 ce of female gender, greater calcium channel blocking agent, digoxin and diuretic use, lower heart ra

132 over another when calculating neuromuscular-blocking agent doses in obese patients.

133 body weight) when calculating neuromuscular-blocking agents doses for obese patients.

134 Thus, in addition to being an effective blocking agent during the initiation phase, these findin

135 However, use of neuromuscular blocking agents during emergent airway management outsid

136 ith nicotinic acetylcholine receptor (nAChR)-blocking agents [e.g., curare or alpha-bungarotoxin (alp

137 Several available blocking agents effectively suppressed this erroneous si

138 The short-acting beta1-selective adrenergic blocking agent, esmolol, was administrated during cardio

139 responded dramatically to the sodium channel blocking agent flecainide.

140 ed with that of the classical sodium channel blocking agent, flecainide, which has no recognized mono

141 otected by application of the sodium channel-blocking agent, flecainide.

142 The effects of the blocking agent, flow rate of samples and substrates, buf

143 lockade are relevant to the choice of a BAFF blocking agent for the treatment of autoimmune and malig

144 atients and have led to the approval of IL-1-blocking agents for a number of autoinflammatory conditi

145 Intensivists use neuromuscular blocking agents for a variety of clinical conditions, in

146 endation on the routine use of neuromuscular-blocking agents for patients undergoing therapeutic hypo

147 l examples of pharmacologically suitable DQ2 blocking agents for the potential treatment of Celiac Sp

148 dings indicate the possible utility of IL-1R-blocking agents for the treatment of ocular inflammatory

149 l therapy with a diuretic or beta-adrenergic blocking agent, for which reductions in morbidity and mo

150 , including their sensitivity to replication-blocking agents, growth defects, and inefficient chromat

151 ing drug reserpine and the adrenergic neuron-blocking agent guanethidine.

152 In addition, the specificity of the blocking agents has been assessed by determining the ext

153 Chronic treatment with beta-adrenergic blocking agents has been shown to improve left ventricul

154 n the clinical pharmacology of neuromuscular blocking agents have advocated routine intraoperative us

155 Beta-adrenergic blocking agents have been revalidated in recent studies

156 beta-Blocking agents have beneficial effects on survival of p

157 ong-term safety of the tumor necrosis factor blocking agents have prompted investigators to take a cl

158 stage gametocytes and identify transmission-blocking agents have, until now, been hindered by a lack

159 e likely to receive aspirin, beta-adrenergic blocking agents, heparin and nitrates (all p < 0.0001).

160 Two other blocking agents, heterophilic blocking reagent and immun

161 intravenous administration of the ganglionic blocking agent hexamethonium (5 mg/kg) or an arginine va

162 and non-responses to tumour necrosis factor blocking agents, however, together with the increasing c

163 ent broth media was reported as an effective blocking agent; however, the natural background fluoresc

164 utants - hypersensitivity to the replication blocking agent hydroxyurea (HU).

165 ne, along with potentiation by neuromuscular blocking agents, immobilization, and probably also concu

166 Beta-blocking agents improve functional status and reduce mor

167 4-amino-pyridine (4-AP), a potassium channel-blocking agent, improves symptoms in some patients with

168 nd provides a rationale for the use of IL-22-blocking agents in B-cell-mediated autoimmune conditions

169 The addition of TGF-beta blocking agents in clinical trials of immunotherapies ma

170 These data strongly support testing of PD-1-blocking agents in combination with standard-of-care che

171 such as aspirin, statins and beta-adrenergic blocking agents in conjunction with comprehensive lifest

172 3) We suggest a trial of a neuromuscular-blocking agents in life-threatening situations associate

173 o recommendation on the use of neuromuscular-blocking agents in pregnant patients.

174 tiated by ATP-sensitive K(+) (K-ATP) channel blocking agents in STN neurons but not in dopamine neuro

175 perior blocking efficacy compared with other blocking agents in terms of high signal-to-noise ratio w

176 The use of sedatives and neuromuscular blocking agents in the ICU is positively associated with

177 nt] and cesium [an outward potassium channel blocking agent]) in 26 swine.

178 The application of selective SK blocking agents (including apamin, scyllatoxin and newer

179 T-cell costimulatory blocking agents inhibit allospecific T-cell responses in

180 This includes the injection of neuromuscular blocking agents into anterior scalene muscles to help co

181 ed in the prone position and a neuromuscular blocking agent is administered, without improvement in h

182 ection, early treatment with a neuromuscular blocking agent is associated with lower in-hospital mort

183 s patches (R(2) > 0.99), suggesting that the blocking agent is closely associated with the channel.

184 e hypothesized that the use of neuromuscular blocking agents is associated with a decreased prevalenc

185 opathy patients treated with beta-adrenergic blocking agents is controversial.

186 kin's battery, by topical application of Na+ blocking agents leads to inhibition or disruption of nor

187 4) We suggest that neuromuscular-blocking agents may be used to manage overt shivering in

188 ls suggest that treatment with neuromuscular blocking agents may improve survival in patients requiri

189 -AW and provides evidence that neuromuscular blocking agents may not be a major cause of weakness in

190 studies have suggested that calcium channel-blocking agents may prevent new coronary lesion formatio

191 our data suggest that therapeutic CD40-CD40L blocking agents may prove efficacious not only in early

192 However, potent CCR5 blocking agents may select for HIV-1 variants that use a

193 d mechanism for understanding how Na channel-blocking agents may suppress the pathologic, sustained N

194 suppress the sensitivity to the replication-blocking agent methylmethane sulfonate (MMS) in smc6 mut

195 ere reduced by the beta1-adrenergic receptor blocking agent metoprolol (1.5 mg/kg, intravenous), whic

196 to treatment with a beta-adrenergic-receptor blocking agent (metoprolol or carvedilol) or placebo.

197 some pairs of nondepolarizing neuromuscular blocking agents might be more efficacious because the hi

198 ective of chemical structural, neuromuscular blocking agents might produce prolonged paralysis in pre

199 toring and use of sedative and neuromuscular blocking agents, more mechanical ventilation days, and l

200 The thiol-blocking agent N-ethylmaleimide was applied in order to

201 The Ca2+ channel-blocking agents Nd3+ and nifedipine partially inhibited

202 ing use of continuous-infusion neuromuscular blocking agents (NMB) in the intensive care unit (ICU).

203 4 (23%) lacked BSACI compliant neuromuscular blocking agent (NMBA) panels and 17/44 (39%) lacked a NA

204 Eleven patients received a neuromuscular blocking agent (NMBA) without a sedative/analgesic agent

205 anaphylaxis but not exposed to neuromuscular blocking agents (NMBA) were included.

206 Anaphylactic reactions to neuromuscular blocking agents (NMBAs) can be severe and even fatal.

207 on of analgesic, sedative, and neuromuscular blocking agents (NMBAs) for each patient.

208 Neuromuscular blocking agents (NMBAs) induce dose-dependent muscle rel

209 Allergy to neuromuscular blocking agents (NMBAs) is the most important caue of pe

210 use of sedatives, opioids, and neuromuscular blocking agents (NMBAs) may delay weaning and prolong in

211 use of allergic anaphylaxis to neuromuscular blocking agents (NMBAs).

212 a, was synchronized with the use of the G2/M blocking agent nocodazole.

213 Our results support the use of VEGF-C/VEGF-D-blocking agents not only to inhibit metastatic progressi

214 of sedative, analgesic, and/or neuromuscular blocking agents; nurse administration of these medicatio

215 Complementary experiments involving a blocking agent of cell wall pores and water root transpo

216 e of monoclonal antibody QCRL-4, a selective blocking agent of the MRP1 pumps.

217 ion with rAd encoding a potent costimulation blocking agent offers promise for therapy of allograft r

218 ry artery disease, nonuse of calcium channel blocking agents, older donor age, posttransplantation cy

219 Subjects taking a hydrogen pump blocking agent (omeprazole) develop bacterial overgrowth

220 to examine the effects of a beta-adrenergic blocking agent on the ischemic response to dobutamine st

221 of specific nonpeptide angiotensin receptor blocking agents on survival after myocardial infarction

222 enzyme (ACE) inhibitors and beta-adrenergic blocking agents on the remodeling process.

223 angina pectoris receiving a beta-adrenergic blocking agent or calcium antagonist, or both.

224 -adrenergic blocking agents, calcium channel blocking agents or digoxin).

225 ither timolol, a nonspecific beta adrenergic blocking agent, or with para-aminoclonidine, an alpha-2

226 y more likely to have received neuromuscular blocking agents (p = .004) or propofol (p =.026) for >1

227 s with first MI, patients on beta-adrenergic blocking agents, patients with LVEF < or =30%, patients

228 or vasopressors, sedatives, or neuromuscular blocking agents, percentage of patients that achieved un

229 Tumor necrosis factor-alpha blocking agents play an important role in the treatment

230 An analysis using the hospital neuromuscular blocking agent-prescribing rate as an instrumental varia

231 Phentolamine, an alpha-adrenergic blocking agent, prevents the C75-induced increases of sk

232 ravenous injections of the beta-adrenoceptor blocking agent, propranolol.

233 Novel retinoic acid metabolism blocking agents (RAMBAs) have been synthesized and chara

234 re sedative, analgesic, and/or neuromuscular blocking agent, range 1-9 drugs, mean 2.5 (+1.5) drugs.

235 iving a continuous infusion of neuromuscular-blocking agent receive a structured physiotherapy regime

236 Beta-blocking agents reduce the risk of hospitalization and d

237 All blocking agents reduced the number of N-cadherin-positiv

238 blockade: encapsulation of the neuromuscular blocking agent, resulting in inactivation.

239 A concentration response curve of this blocking agent revealed a half maximal inhibitory concen

240 in immature female rats using estradiol as a blocking agent revealed specific uptake of [18F]FEDPN in

241 hypoxia exposure, and the use of a ganglion blocking agent should inhibit activity within all branch

242 0-year period, increasing evidence that beta-blocking agents should or actually did improve the natur

243 terference with the Tie-2 pathway by diverse blocking agents such as soluble Tie-2 receptors, anti-Ti

244 cluded from most trials of immune checkpoint blocking agents, such as anti-PD-1 and anti-PD-L1, becau

245 ghtly to several commonly used neuromuscular blocking agents, such as rocuronium, in aqueous solution

246 Cell cycle-blocking agents, synchronization of cells stably express

247 illation was abolished by the sodium channel blocking agent tetrodotoxin (0.1-1 microM).

248 fines potential therapeutic target sites for blocking agents that could interfere with this interacti

249 By using a variety of different nAChR-blocking agents that target specific muscle or neuronal

250 On day 13, neuromuscular blocking agent therapy was discontinued, but severe prox

251 centration, incubation times and the type of blocking agent to achieve a low limit of detection (LOD)

252 etermined the ability of a selectin receptor blocking agent to affect neutrophil deposition in tissue

253 vine serum albumin (BSA) which served as the blocking agent to prevent non-specific adsorption.

254 Short-chain PDL was further used as a blocking agent to prevent readsorption of the hydrolyzed

255 c interventions in clinical disease by using blocking agents to ameliorate the systemic manifestation

256 c interventions in clinical disease by using blocking agents to ameliorate the systemic manifestation

257 e the capability to administer neuromuscular blocking agents to facilitate intubation (i.e., rapid se

258 e routine administration of an neuromuscular-blocking agents to mechanically ventilated patients with

259 examined the efficacy of two sodium channel blocking agents to protect white matter axons in two for

260 Use of tumor necrosis factor-alpha blocking agents to treat chronic pediatric uveitis is be

261 r treatment guidelines limit the use of HER2-blocking agents to tumors with HER2 gene amplification,

262 out of the sample zone and a small plug of "blocking agent" to negate the cells' mobility and induce

263 ctionalize portions of a gold surface with a blocking agent, typically 1-hexadecanethiol.

264 mportant implications for the safety of CCR5-blocking agents under development for HIV/AIDS.

265 ients had significantly less beta-adrenergic blocking agent use and higher ejection fraction (EF) (p

266 performed to assess whether beta-adrenergic blocking agent use is associated with reduced mortality

267 analysis, the association of beta-adrenergic blocking agent use with reduced mortality remained signi

268 djusting for age, gender and beta-adrenergic blocking agent use, multiple logistic regression analysi

269 or myocardial infarction and beta-adrenergic blocking agent use.

270 e, addiction, epilepsy and for neuromuscular blocking agents used during surgery.

271 ded demographics, sedation and neuromuscular blocking agents used, mechanical ventilation, hemodynami

272 anaesthetized, injected with a neuromuscular blocking agent, vagotomized and artificially ventilated.

273 D. discoideum can be reversed by the channel-blocking agent verapamil.

274 he effects of novel retinoic acid metabolism blocking agent, VN/14-1, in overcoming letrozole resista

275 ty for treatment, receipt of a neuromuscular blocking agent was associated with a reduced risk of in-

276 n to a single cell, an alternative synthetic blocking agent was sought.

277 ion of the CRP system with several different blocking agents was also studied, and 2.0% bovine serum

278 The use of neuromuscular blocking agents was associated with a lower prevalence o

279 Use of neuromuscular blocking agents was associated with significantly improv

280 erting enzyme inhibitors and calcium channel blocking agents was determined at discharge for all pati

281 eration in the presence of TNF-alpha or TNFR blocking agents was partially rescued by a TLR2 agonist,

282 Using cell cycle-blocking agents, we demonstrate that activated T cells a

283 ministration for sedatives and neuromuscular blocking agents were abstracted from ICU flow sheets.

284 Beta-adrenergic blocking agents were administered concurrently to all pa

285 erting-enzyme inhibitors and beta-adrenergic-blocking agents were administered if the patients could

286 Interestingly, when integrin-blocking agents were included in these assays, adhesion

287 he no-AAD group, only atrioventricular nodal blocking agents were prescribed.

288 Various potential blocking agents were screened including salts, polypepti

289 ffects of various gene deletions or chemical blocking agents were tested by investigating the express

290 Patients who received neuromuscular blocking agents were younger (mean age, 62 vs 68), more

291 A short-acting beta1-selective adrenergic blocking agent, when administered during cardiopulmonary

292 The use of neuromuscular blocking agents, when used by intensivists with a high l

293 Pharmacological blocking agents which are relatively selective for L- (v

294 nd another segment of solution containing a "blocking agent", which serves to stop the cell migration

295 Total body weight dosing of neuromuscular blocking agents will result in a prolonged effect.

296 gest that coformulation of this transmission-blocking agent with asexual stage antimalarials such as

297 Sotalol, a beta-adrenergic blocking agent with class III antiarrhythmic properties,

298 ty of carvedilol, a "third-generation" beta -blocking agent with vasodilator properties, in chronic h

299 tion for clinical trials combining autophagy-blocking agents with antitumor drugs and radiation.

300 comes of patients treated with neuromuscular blocking agents within the first 2 hospital days to thos